# embeddings_queue

created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f5f-7265-11ef-b77d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 168, "chroma:document": "Pathogenesis:    \n\u2022 Cutaneous anthrax is initiated when spores of B. anthracis  are introduced through \nabrasions of the skin or insect bite.  \n\u2022 Inhalation anthrax is acquired by directly inhaling the agent to the alveoli.   \n\u2022 Gastrointestinal form usually occurs after i ngestion of raw or partially cooked meat that is \ncontaminated.  \nB. anthracis  goes to the blood stream and replicates rapidly.  It is resistant to phagocytosis.  It \nalso produces anthrax toxin, which causes edema and inhibition of polymorphonuclear \nleucocyte function.  Moreover, it causes release of cytokines, shock and death."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f60-7265-11ef-ae00-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 169, "chroma:document": "Internal Medicine \n \n 154Clinical Manifestations \nAbout 95% of anthrax is cutaneous form. 5% is inhalation, and that of gastrointestinal (GI) is \nvery rare. GI form is more common in areas where raw meat is ingested. \nCutaneous anthrax :  \n\u2022 The lesions are more common on exposed areas like face, neck and extremities.  \n\u2022 In the beginning, a small red macule develops within days.  This will become papular \nand pustular which then forms a central necrotic ulcer (black eshcar) with surrounding \nedema; it is painless.  \n\u2022 Usually there is associated painful regional lymphadenopathy and fever is uncommon.   \n\u2022 Most patients recover spontaneously but about 10% develop progressive infection, \nbacteremia, high grade fever and rapid death. \nInhalational anthrax (wool sorter\u2019s disease):   \n\u2022 This form resembles severe viral respiratory disease and thus diagnosis is difficult.   \n\u2022 This form may be used as biological warfare.  \n\u2022 Within 3 days of infection patients develop fever, dyspnea, stridor, hypoxemia, \nhypotension and may die within 24 hours once patients become symptomatic. \nGastrointestinal anthrax:  Patients may have nausea, vomiting, abdominal pain, bloody \ndiarrhea, and fever; they may develop ascites. \n Treatment \nCutaneous anthrax   \n\u2022 Can be treated with crystalline penicillin 2 million units 6 hourly until edema subsides \nthen oral penicillin for 7-10 days.   \n\u2022 For allergic patients, ciprofloxacin, erythromycin, TTC or chloramphenicol may be given."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f61-7265-11ef-afda-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 169, "chroma:document": "Cutaneous anthrax   \n\u2022 Can be treated with crystalline penicillin 2 million units 6 hourly until edema subsides \nthen oral penicillin for 7-10 days.   \n\u2022 For allergic patients, ciprofloxacin, erythromycin, TTC or chloramphenicol may be given.   \n\u2022 Wound should be cleaned, debrided and dressed.   \nInhalation or GI form   \n\u2022 Should be treated with high dose penicillin 8-12 million units per day, divided into 4-6 \ndoses. \nMortality rate  \n\u2022 Cutaneous Anthrax is 10-20%,  for and almost. \n\u2022 GI Anthrax can 50% \n\u2022 Inhalational anthrax 100% for"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f62-7265-11ef-8d69-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 170, "chroma:document": "Internal Medicine \n \n 155Prevention: \n\u2022 Mass vaccination of animals \n\u2022 Avoiding feeding on infected cattle \n\u2022 Proper disposal of dead animals and  \n\u2022 Keeping personal hygiene. \n \nReference: \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Anthrax \n,  pages 1280-1-83"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f63-7265-11ef-a505-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 171, "chroma:document": "Internal Medicine \n \n 1566.4 Brucellosis \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define brucellosis 2. List the etiologies of brucellosis 3. Describe the mode of transmission of brucellosis \n4. Explain the epidemiology of brucellosis  \n5. Describe the pathophysiology of brucellosis  6. Identify the clinical manifestations of brucellosis 7. Describe the most commonly used tests for the diagnosis of brucellosis  8. Make a diagnosis of brucellosis  \n9. Treat brucellosis at the primary care level \n10. Design appropriate methods of prevention and control of brucellosis \n \nDefinition:  Brucellosis is a zoonotic disease caused by Brucella species , which is characterized \nby remittent type of fever and multi-organ involvem ent.  It is transmitted to humans from infected \nanimals. \n \nEtiology : It is caused by four different types of Brucella. They are small aerobic gram-negative \nbacilli; they are non-motile and facu ltative intracellular parasites. \n\u2022 Brucella melitensis (the most common and most virulent type) acquired from goats, \nsheep and camels. \n\u2022 Brucella abortus from cattle \n\u2022 Brucella suis from hogs  \n\u2022 Brucela canis from dogs \n \nEpidemiology:   \n\u2022 It is found worldwide, but the true incidence is not known.  In communities where \nbrucellosis is endemic, it occurs in children and family members of infected persons are at risk.  Commonly affected are farmers, meat-processing workers, veterinarians, and \nlaboratory workers."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f64-7265-11ef-9c95-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 172, "chroma:document": "Internal Medicine \n \n 157\u2022 Brucella organism is transmitted commonly through the ingestion of untreated milk or \nmilk products; raw meat and bone marrow have been implicated.  But it can also be \ntransmitted by inhalation from close contact with animals. \nPathogenesis:  In the blood Brucella is ingested by polymorphonuclear leukocytes and \nmacrophages but they resist intracellular phagocytosis.  Severity of the disease is largely determined by the outcome of pathogen-phagocyte interaction.  The organisms multiply, reach \nblood stream via lymphatics, and then reside in different organs, the liver, spleen, bones, \nkidneys, lymph nodes, heart valves, nervous system and testes.  In infected organs there will be \ninflammatory responses or noncaseating granulomas. Serum IgM will appear within a week and later IgG and IgA will develop. \n Clinical manifestations and complications:    \n\u2022 Brucellosis is a systemic ill ness and its manifestations mimic other febrile illnesses.   \n\u2022 The incubation period is about 1-3 weeks.  The  illness may begin suddenly or it could be \ngradual.  \n\u2022 The most common symptoms are fever, chills, diaphoresis, headache, myalgia, fatigue, \nanorexia, joint and low back-pain, weight loss, constipation, sore throat and dry cough.   \n\u2022 Patients may look well with no findings or may exhibit physical findings related to the \norgan affected. \n\u2022 Fever of brucellosis has no distinctive features but it occurs in late afternoons or \nevenings."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f65-7265-11ef-bf19-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 172, "chroma:document": "\u2022 Patients may look well with no findings or may exhibit physical findings related to the \norgan affected. \n\u2022 Fever of brucellosis has no distinctive features but it occurs in late afternoons or \nevenings.   \n\u2022 Patients may have reactive asymmetric polyart hritis involving larger joints; and lumbar \nvertebral osteomyelitis.  \n\u2022 Cardiovascular complications of Bruce llosis include endocarditis, myocarditis, \npericarditis, thrombophlebites and pulmonary embolism.   \n\u2022 Brucella can have respiratory manifestations like sore throat, tonsillitis, dry cough and \neven pneumonia and lung abscess.   \n\u2022 Gastrointestinal manifestations are generally mild and include nausea, vomiting, \nabdominal pain and diarrhea; there is hepatosplenomegaly in about 15-20% of patients.   \n\u2022 Patients may have genitourinary infection and present with epididymoorchitis, prostatitis, \namenorrhea, tubo-ovarian abscess, salphingitis, acute pyelonephritis and \nglomerulonephritis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f66-7265-11ef-8226-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 173, "chroma:document": "Internal Medicine \n \n 158\u2022 Nervous system involvement is unco mmon but when involved patients may have \nmeningitis, meningoencephalitis, brain abscess, hemiplegia and cranial nerve deficit.   \n\u2022 Other manifestations are conjunctivitis, retinopathy, skin involvement, abortion, anemia, \nleukopenia and thrombocytopenia. \n \nDiagnosis  \nThe combination of history of exposure, clinical  features and significantly raised levels of \nBrucella agglutinin confirms the diagnosis of active brucellosis. \nTreatment   \n\u2022 The combination of doxycycline and aminoglycoside (gentamicin, or streptomycin) for 4 \nweeks followed by the combination of doxycycline and rifampin for 4 to 8 weeks is the most effective treatment modality. \n\u2022 Alternative regimen is combination of doxycycline and rifampin given for 8 to 12 weeks. \n\u2022 Patients with serious illness and complication need admission for treatment with \nintravenous medications and possible surgical intervention. \n \nPrevention  - Immunization of animals, boiling or pasteurizing milk are important in preventing \nthe disease.  \n \nReference: \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nBrucellosis , 914-917"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f67-7265-11ef-9819-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 174, "chroma:document": "Internal Medicine \n \n 159CHAPTER TWO \nDISEASES OF THE RESPIRATORY SYSTEM \n \n1. Common Symptoms of Respiratory System \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. List the common symptoms of diseases of the respiratory system \n2. Characterize each of the symptoms \n3. Describe the pathophysiology of each symptom 4. Identify disease conditions associated with each symptom 5. Describe the most commonly used investigations of the respiratory system \n \nCough  \nCough is an explosive expiration that provides  a protective mechanism for clearing the \ntrachiobronchial tree of secretions and foreign material.  However, when excessive, it is one of \nthe commonest presentations (complaint).  As a protective mechanism against foreign or noxious material, cough can be initiated by a variety of airway irritants, which enter the trachiobronchial tree by inhalation (smoke, dust, \nfumes) or by aspiration (upper airway secretions, gastric contents, foreign bodies). \n Any disorder resulting in inflammation, constriction, infiltration, or compression of airways can be associated with cough.   Inflammation commonly results from airway infections, ranging from. \nSome causes of cough are: \n\u2022 Inflammation-infection (viral  ,bacterial etc )  , bronchitis , bronchiectasis,  asthma etc  \n\u2022 Constriction - asthma (it is reversible)  \n\u2022 Infiltration \u2013 tuberculosis, neoplasm, granuloma, or sarcoidosis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f68-7265-11ef-bb7a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 174, "chroma:document": "Some causes of cough are: \n\u2022 Inflammation-infection (viral  ,bacterial etc )  , bronchitis , bronchiectasis,  asthma etc  \n\u2022 Constriction - asthma (it is reversible)  \n\u2022 Infiltration \u2013 tuberculosis, neoplasm, granuloma, or sarcoidosis  \nExamples of parenchymal lung disease potentially producing cough include pneumonia, \ninterstitial lung disease, and lung abscess. Patients with congestive heart failure may have cough, because of interstitial edema."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f69-7265-11ef-9900-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 175, "chroma:document": "Internal Medicine \n \n 160Approach to the Patient with cough \nA detailed history frequently provides the most valuable clues for etiology of the cough.  \nParticularly important questions include: \n\u2022 Is the cough acute or chronic? Factors influencing it? \n\u2022 Were there associated symptoms suggestive of a respiratory infection? \n\u2022 Is it seasonal or associated with wheezing? Dyspnea? \n\u2022 Is there nasal discharge or gastroesophageal reflux (heartburn)? \n\u2022 Is there fever or sputum?  If sputum is present, what is its character? \n\u2022 Does the patient have any associated disease or risk factors for disease (e.g. Cigarette \nsmoking, risk for HIV, environmental exposures eg. pollution)? \n The general physical exam  may point to a non-pulmonary cause of cough, such as heart \nfailure, malignancy, or AIDS. \n\u2022 Auscultation of the chest may demonstrate: inspiratory stridor (indicative of upper airway \ndisease), respiratory wheezing (indicating lower airway disease) or inspiratory crepitations (process involving the pulmonary parenchyma, such as interstitial lung disease, pneumonia, tuberculosis or pulmonary edema). \nComplications of cough: may precipitate syncope, fracture of the ribs etc \nDefinitive treatment of cough  depends on determining the underlying cause and then initiating \nspecific therapy. Different cough suppressants can be used in addition to specific therapy to decrease the duration of cough.  \nChest Discomfort/pain"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f6a-7265-11ef-973a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 175, "chroma:document": "Definitive treatment of cough  depends on determining the underlying cause and then initiating \nspecific therapy. Different cough suppressants can be used in addition to specific therapy to decrease the duration of cough.  \nChest Discomfort/pain \nChest discomfort is one of the most frequent complaint for which patients seek medical attention. There is little relation between the severity of chest discomfort and the gravity of its cause. \n \nCauses of Chest Discomfort Pleuritic chest pain  \u2013 It is usually a brief, sharp, knifelike pain that is precipitated by inspiration \nor coughing. It is very common and generally results from inflammation of parietal pleura. Typical example is pneumonia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f6b-7265-11ef-ba71-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 176, "chroma:document": "Internal Medicine \n \n 161Myocardial ischemia:   \n\u2022 Angina pectoris is usually described as a heaviness, pressure, squeezing or sensation of \nstrangling or constriction in the chest, but it also may be described as an aching or \nburning pain or even as indigestion.  \n\u2022 Typically, angina pectoris develops during emotion or physical exertion. The pain \ntypically resolves within 5-30 minutes. The pain is   more prolonged in myocardial \ninfarction (MI). \nChest pain due to pericarditis: -  \n\u2022 The pain arises from parietal pericardium and adjacent parietal pleura. Infectious \ndiseases and inflammation are the main causes of pain.  \n\u2022 Pericarditis can cause pain in several locations like the tip of the shoulder and the neck \nmore often the pain is located in the anterior part of the chest and is relieved by bending forward; but pain may also be in the upper part of abdomen or at corresponding region of the back.  \n\u2022 Pericardial pain commonly has a pleuritic component; i.e. it is aggravated by cough and \ndeep inspiration, because of pleural irritation. Sometimes there may be steady substernal discomfort that mimics acute myocardial infarction. \nVascular causes of chest pain:  \u2013  \n\u2022 Pain due to acute dissection of the aorta usually begins abruptly, reaches an extremely \nsever peak rapidly.  \n\u2022 It is felt in the center of the chest and/ or the back, lasts for hours and requires unusually"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f6c-7265-11ef-be39-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 176, "chroma:document": "Vascular causes of chest pain:  \u2013  \n\u2022 Pain due to acute dissection of the aorta usually begins abruptly, reaches an extremely \nsever peak rapidly.  \n\u2022 It is felt in the center of the chest and/ or the back, lasts for hours and requires unusually \nlarge amounts of analgesics for relief of pain. Pain is not aggravated by changes in position or respiration. Usually there is associated low blood pressure. \nChest pain due to pulmonary embolism: -  \n\u2022 The pain resulting from pulmonary embolism may resemble that of acute MI, because in \nmassive embolism pain is located substernally.  \n\u2022 In patients with smaller emboli, pain is located more laterally, is pleuritic in nature, and \nsometimes is associated with hemoptysis.  \nGastrointestinal causes of chest discomfort: -  \n\u2022 Esophageal pain commonly presents as a deep thoracic burning pain, which is the \nhallmark of acid-induced pain. Esophageal spasm has acute pain that may be indistinguishable from MI."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f6d-7265-11ef-9cb4-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 177, "chroma:document": "Internal Medicine \n \n 162\u2022 Other diseases like PUD, biliary disease, pancreatitis, and cholecystits may present as \nchest discomfort or pain. \n \nEmotional cause of chest pain  - Usually, the discomfort is experienced as a sense of \n\"tightness\", sometimes called \"aching\".  It is confused with myocardial   ischemia. Ordinarily, it \nlasts for half an hour or more.  There is usually associated emotional strain or fatigue. \n \nHemoptysis; is defined as expectoration of blood from the respiratory tract, which could be \nscanty and mixed with sputum or large amount of frank blood. Massive hemoptysis is defined as \nexpectoration of >600 ml of blood in 24 hours. Hemoptysis can have different causes. Some of the causes are: \n1) Tracheobronchial source \n\u2022 Neoplasm    \n\u2022 Bronchitis , Bronchiectasis \n\u2022 Foreign body   \n\u2022 Airway trauma \n2) Pulmonary parenchymal source \n\u2022 Pneumonia, tuberculosis \n\u2022 Lung abscess \n\u2022 Lung congestion \n3) Primary vascular source \n\u2022 Mitral stenosis  \n\u2022 Pulmonary embolism \n4)  Sources other than the lower respiratory tract \n\u2022 Upper airway (nasopharyngeal) bleeding \n\u2022 GI bleeding \n\u0099 Tuberculosis and pneumonia are the commonest causes of hemoptysis in developing \ncountries. But bronchitis and bronchogenic ca are common in developed regions. Up to \n30% of patients may not have identifiable cause even after complete investigation."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f6e-7265-11ef-a27c-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 178, "chroma:document": "Internal Medicine \n \n 163Approach to the patient with hemoptysis \nHistory:   \n\u2022 Blood streaked, mucopurulent sputum suggests bronchitis.  \n\u2022 If it is associated with fever pneumonia should be suspected.  \n\u2022 If sputum smell is putrid, lung abscess is likely.  \n\u2022 Hemoptysis that occurs suddenly with  chest pain and dyspnea suggests pulmonary \nembolism.  \n\u2022 Previous history of renal disease, SLE, or malignancy is all important for suggesting \nDDX.   \nPhysical examination : may reveal \n\u2022 Pleural friction rub, Localized or diffuse crackles \u00c6 lung paranchymal damage.  \n\u2022 Wheezing \u00c6Airflow obstruction (chronic bronchitis).  \n\u2022 Cardiac examination may reveal pulmonary hypertension, mitral stenosis or heart failure \nDiagnostic evaluation  :  \n\u2022 Chest X-ray which may show mass lesion suggestive of bronchiectasis, pneumonia.  \n\u2022 Sputum examination for Gm and AFB stain. \n\u2022 CBC, coagulation profile, urine analysis,  \n\u2022 BUN and creatinine and  \n\u2022 If possible bronchoscopy is useful in localizing and managing the site of bleeding \nTreatment : the rapidity of bleeding and its effects on gas exchange determine the urgency of \nmanagement. \n\u2022 If there is only blood streaking sputum with mid hemoptysis, first establish diagnosis. Put \nthe patient at rest and Giving cough suppressant may help to subside the bleeding  \n\u2022 If massive hemoptysis urgent treatment is necessary to stop bleeding and patients"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f6f-7265-11ef-b19a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 178, "chroma:document": "the patient at rest and Giving cough suppressant may help to subside the bleeding  \n\u2022 If massive hemoptysis urgent treatment is necessary to stop bleeding and patients \nshould be referred to a hospital. Massive hemoptysis may require endotracheal intubation and mechanical ventilation. If the bleeding side is known position the patient \nso that the source of bleeding is placed in dependent position to protect suffocation of \nthe unaffected lung."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f70-7265-11ef-9f94-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 179, "chroma:document": "Internal Medicine \n \n 164   2. Upper Respiratory Tract Infections  \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define upper respiratory infections \n2. List the etiologies of upper respiratory infections  3. Describe the mode of transmission of upper respiratory infections  4. Explain the epidemiology of upper respiratory infections   \n5. Describe the pathophysiology of upper respiratory infections  \n6. Identify the clinical manifestations of upper respiratory infections  7. Describe the most commonly used method of diagnosis of upper respiratory infections  8. Make a diagnosis of upper respiratory infections  9. Give supportive therapy at the primary care level \n10. Design appropriate methods of prevention of upper respiratory infections  \n \n2.1 The Common Cold (Acute coryza) \nIt is an acute, usually afebrile, viral infection of the respiratory tract, with inflammation in any or \nall airways, including the nose, paranasal sinuses, throat, larynx, and often trachea and bronchi. \nEtiology  - Many viruses cause the common cold including Picornavirus (rhinoVirus), Influenza \nand parainfluenza viruses, Respiratory syncytial virus, Corona- and adeno virus group.  Infections may be facilitated by excessive fatigue, emotional distress, or allergic naso \npharyngeal disorders and during the mid-phase of the menstrual cycle. \nSymptoms and signs  - onset is abrupt after a short (1 to 3 days) incubation period.  Illness"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f71-7265-11ef-adf0-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 179, "chroma:document": "pharyngeal disorders and during the mid-phase of the menstrual cycle. \nSymptoms and signs  - onset is abrupt after a short (1 to 3 days) incubation period.  Illness \ngenerally begins with nasal or throat discomfort followed by sneezing, rhinorrhea, and malaise.  \nThe disease is afebrile and pharyngitis is usually present. Nasal secretions, watery and profuse \nduring 1\nst or 2nd day of symptoms, become more mucous and purulent. Hacking cough \nassociated with scanty sputum often lasts into the 2nd week. When no complications occur, \nsymptoms normally resolve in 4 to 10 days. \nDiagnosis - Symptoms and signs are nonspecific. Bacterial infections, allergic rhinorrhea, and \nother disorders also cause upper respiratory tract symptoms at onset.  Differentiation depends \non the season and the course of the Symptoms. Fever more severe symptoms usual indicate influenza."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f72-7265-11ef-914a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 180, "chroma:document": "Internal Medicine \n \n 165Prophylaxis - Immunity is virus type-specific.  Because of numerous types and strains of known \nviruses causing URT, it is difficult to produce a useful vaccine. \nTreatment \n\u2022 A Warm, comfortable environment and measures to prevent direct spread of infection \nare recommended for all persons.  \n\u2022 Antipyretics and analgesics are given to control fever and malign.  \n\u2022 Nasal decongestants are used if patients have nasal congestion. Steam inhalation is \nalso used in nasal congestions to help mobilize secretions and relieve chest tightness. \n\u2022 Treat persistent cough with cough suppressants. \n\u2022 Ascorbic acid or high doses of citrus juices have no scientific benefit. \n\u2022 Antibiotics are not effective against viruses, so they are not recommended unless a \nspecific bacterial complication develops. \n2.2 Influenza \nInfluenza is a specific acute viral respirator y disease characterized by fever, coryza, \ncough, headache, and malaise and inflamed re spiratory mucous membranes. It usually \noccurs as an epidemic in rainy seasons.  \nEtiology : It is caused by influenza viruses, which are classified as orthomyxovirus.  There are \ntypes A, B & C \nEpidemiology :  \n\u2022 Influenza type A virus is the most frequent single cause of clinical influenza; other \ncauses include influenza B, paramyxovirus, pneumonia-virus and (rarely in adults) rhino and echoviruses.  \n\u2022 Spread is by person - to - person contact; airborne droplets spray infects people and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f73-7265-11ef-90ac-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 180, "chroma:document": "causes include influenza B, paramyxovirus, pneumonia-virus and (rarely in adults) rhino and echoviruses.  \n\u2022 Spread is by person - to - person contact; airborne droplets spray infects people and \ncontaminates articles with viruses that can transmit infection.  \n\u2022 Persons of all ages are affected, but prevalence is highest in school children.  \n\u2022 Persons at highest risk of developing severe disease are those with chronic pulmonary \ndisease and those with valvular heart disease, pregnant women, the elderly, the very young and the bed ridden. \n\u2022 Infection with influenza A is associated with significant morbidity and mortality.  \nSymptoms and Signs:  \n\u2022 During the 48-hour incubation period, transient asymptomatic viremia occurs.  \n\u2022 Then there is chills and fever up to 39 to 39.5 \n0c developing over 24 hr."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f74-7265-11ef-afd1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 181, "chroma:document": "Internal Medicine \n \n 166\u2022 Generalized aches and pains (most pronounced in the back and legs) appear early.  \n\u2022 Headache is prominent. \n\u2022 Respiratory tract symptoms may be mild initially but become prominent later.  \n\u2022 The soft palate, posterior hard palate, and tonsillar pillars may be reddened. Usually \nafter 2 to 3 days, acute symptoms rapidly subside and fever ends.  \n\u2022 Weakness, sweating and fatigue may persist for several days or occasionally for weeks.  \n\u2022 In severe cases, hemorrhagic bronchitis and pneumonia are frequent and can develop \nwithin hours.  \n\u2022 Fulminant, fatal viral pneumonia may occur and death may follow as soon as 48 hr after \nonset. This is usually during a pandemic caused by a new virus or in high-risk people. \nComplication:   \n\u2022 Secondary bacterial infection of the bronchus and pneumonia. With pneumonia, cough \nworsens and purulent or bloody sputum is produced.  Crepitations can be detected over \naffected segment. \n\u2022 Encephalitis, myocarditis, and myoglobinuria may occur as complications of influenza, \nusually during convalescence.  \nDiagnosis:   \n\u2022 Clinical influenza is a common experienc e and can easily diagnosed. Chest examination \nis usually normal in mild cases and may look like common cold. Pulmonary symptoms may be similar to those of bronchitis or atypical pneumonia. Fever and severe constitutional symptoms differentiate influenza from the common cold \n\u2022 The leukocyte count is normal in uncomplicated cases."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f75-7265-11ef-82ab-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 181, "chroma:document": "\u2022 The leukocyte count is normal in uncomplicated cases.  \n\u2022 Isolating the virus can make specific diagnosis of influenza. Serologic tests are also \nused. \n \nPrognosis:  Recovery is the rule in uncomplicated influenza. Viral pneumonia may cause death. \nProphylaxis:  Vaccines that include the prevalent strains of influenza viruses effectively reduce \nthe incidence of infection. Amantadine 100mg orally bid (for adults) can be used prophylactically \nagainst influenza A. \n \nTreatment: \n\u2022 Amantadine has a beneficial effect on fever and respiratory symptoms if given early in \nuncomplicated influenza."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f76-7265-11ef-b3c6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 182, "chroma:document": "Internal Medicine \n \n 167\u2022 Basic treatment for most patients is symptomatic with bed rest, antipyretics, nasal \ndecongestants & steam inhalation.  \n \n2.3 Acute Bronchitis \nIt is an acute inflammation of the tracheobronchial tree, generally self-limiting and with eventual \ncomplete healing and return to normal function. It could be caused by infections or irritants.  \nEtiology:   \n\u2022 Acute infectious bronchitis  is often part an acute upper respiratory tract infection (URTI). \nIt may develop after a common cold or other viral infection of the nasopharynx, throat or \ntracheobronchial tree, often with secondary bacterial infection.  \n\u2022 Acute irritative bronchitis  is caused by various mineral and vegetable dusts, volatile \nsolvents, tobacco or other smoke.  \nSymptoms and signs :  \n\u2022 Acute infectious bronchitis is often preceded by symptoms of URTI, coryza, malaise, \nchilliness, slight fever, back and muscle pain and sore throat.  \n\u2022 The onset of cough usually signals onset of bronchitis. Cough is initially dry but \nprogresses to be productive.  Purulent sputum suggests bacterial superinfection.  \n\u2022 In uncomplicated case, fever to 38.80c may be present upto 3-5 days, following which \nacute symptoms subside (though cough may continue for several weeks).   \n\u2022 Persistent fever may suggest complication like pneumonia.  \n\u2022 Pulmonary signs are few in uncomplicated acute bronchitis. Scattered rhonchi and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f77-7265-11ef-9688-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 182, "chroma:document": "acute symptoms subside (though cough may continue for several weeks).   \n\u2022 Persistent fever may suggest complication like pneumonia.  \n\u2022 Pulmonary signs are few in uncomplicated acute bronchitis. Scattered rhonchi and \nwheezes may be heard, as well as occasional crepitations at the bases.  Serious complications are usually seen only in patients with an underlying chronic respiratory \ndisorder. \nDiagnosis :  \n\u2022 It is usually based on the symptoms and signs.  \n\u2022 Chest X-ray is taken only to rule out serious conditions like pneumonia.  \n\u2022 In persons who do not respond to antibio tics, gram stain and sputum culture is \nnecessary. \nTreatment : \n\u2022 General Management  \n\u2022 Rest until fever subsides.  \n\u2022 Oral fluids should be taken more:- this  facilitates sputum expectoration."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f78-7265-11ef-b924-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 183, "chroma:document": "Internal Medicine \n \n 168\u2022 Antipyretics and analgesics (like aspirin or par acetamol) are given if there is fever or \nmyalgia.  \n\u2022 Symptomatic treatment of cough may shorten the duration of cough.                    \n\u2022 Specific Treatment  \n\u2022 Antibiotics should be given when purulent sputum and persistent fever are present.                        \nTTC or ampicillin can be given for 7 \u2013 10 days."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f79-7265-11ef-a405-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 184, "chroma:document": "Internal Medicine \n \n 1693. Pneumonia \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define Pneumonia  2. List the etiologic agents of Pneumonia occurring in different settings  3. Describe the mode of transmission of Pneumonia    \n4. Understand the epidemiology of Pneumonia.  \n5. Describe the pathophysiology of Pneumonia  6. Identify the clinical manifestations of Pneumonia    7. List the complications of  Pneumonia  8. Describe the most commonly investigations for the diagnosis of Pneumonia   \n9. Make an accurate diagnosis of Pneumonia   \n10. Manage most cases of Pneumonia  appropriately  11. Refer complicated  cases of Pneumonia  \n \nPneumonia is an acute infection of lung parenchyma  including alveolar spaces and interstitial \ntissue. \n\u2022 Involvement may be confined to an entire lobe -Lobar pneumonia \n\u2022 A segment of a lobe-Segmental or lobular pneumonia  \n\u2022 Alveoli contiguous to bronchi -  Bronchopneumonia  \n\u2022 Interstitial tissue - Interstitial pneumonia  \nThese distinctions are generally based on x-ray observations. Predisposing factors for pneumonia  include:- \n\u2022 Preceding respiratory viral infections \n\u2022 Alcoholism \n\u2022 Cigarette smoking \n\u2022 Underlying diseases such as Heart failure, COPD  \n\u2022 Age extremes \n\u2022 Immunosuppressive therapy and disorders \n\u2022 Decreased consciousness, comma , seizure etc  \n\u2022 Surgery and aspiration of secretions"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f7a-7265-11ef-9741-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 185, "chroma:document": "Internal Medicine \n \n 170The usual mechanisms to develop pneumonia are either to inhale droplets small enough to \nreach the alveoli, or to aspirate secretions from the upper airways.  Other means include \nhematogenous dissemination, via the lymphatics, or directly from contiguous infections. \nMicrobial Pathogen that cause Pneumonia: depend on the setting in which pneumonia is \nacquired \n1. Community-acquired  pneumonia \no Streptococcus pneumoniae ( pneumococcal pneumonia ) commonest cause  \no Mycoplasma pneumoniae  \no Chlamydia pneumoniae \no Haemophilus influenza  \no Oral anaerobic bacteria  \no Staphylococcus aureus  \no Legionella pneumophila \no Mycobacterium tuberculosis \n2. Aspiration pneumonia: This occurs when large amount of oropharyngeal or gastric \ncontents are aspirated into the lower respiratory tract. Aspiration occurs more frequently \nin patients with: \n\u2022 Decreased level of consciousness (alcoholism, seizure, strokes or general \nanesthesia)  \n\u2022 Neurologic dysfunction of oropharynx and swallowing disorders.  \n\u2022 People with periodontal disease are affected more.  \nCommon Etiologic agents of Aspiration pneumonia: It is often polymicrobial \no Anerobic organisms in the oral cavity  \no Enterobateriacae \no S. pneumoniae \no S.aureus \n Patients present with cough and foul smelling sputum. The cough may be chronic"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d35f7b-7265-11ef-b055-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 185, "chroma:document": "Common Etiologic agents of Aspiration pneumonia: It is often polymicrobial \no Anerobic organisms in the oral cavity  \no Enterobateriacae \no S. pneumoniae \no S.aureus \n Patients present with cough and foul smelling sputum. The cough may be chronic \nforming lung abscess and may resemble TB. There will be signs of cavity on physical exam and CXR. It is treated with crystalline penicillin and metronidazole IV for several \nweeks if lung abscess develops.   \n3. Community acquired Pneumonia in Immunocompromised hosts: \nImmunocompromised hosts such as transplant recipients, HIV infected patients, and \npatients on Chemotherapy etc. are prone to develop pneumonia. The etiologic agents are"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38518-7265-11ef-8149-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 186, "chroma:document": "Internal Medicine \n \n 171o Common bacterial causes of CAP : St. Pnumoniae , H.influenzae, \nMycoplasma  \no Gram negative organisms : enterobacteriaceae \no Funguses such as Pneumocystis carinii ( jerovecii ), C. neoformans , \nHistoplasmosis , Aspergillus \no Mycobaterium tuberculosis  \no Viruses : HSV , CMV \n4. Hospital-acquired pneumonia: a patient is said to have hospital acquired pneumonia if the \nsymptoms begin 48 hours after hospital admission and not incubating at the time of \nadmission. Common organisms that cause hospital-acquired pneumonia are:- \no Gram-negative bacilli including  Pseudomonas aeroginosa , K.pneumoniae  \no Staphylococcus aureus ( may ne drug resistant ) \no Oral anaerobes. \nClinical Presentation of community acquired pneumonia \n\u2022 Community acquired pneumonia can have typical or atypical presentations. This \nclassification is less distinct but it may have diagnostic value. More commonly patients have \u201ctypical\u201d presentation and it is mainly caused by S.Pneumonae .  But other \norganisms like H. influenza  and oral flora can be causes.  \n\u2022 Pneumonia is often preceded by a URTI. \nThe \u201ctypical\u201d Community acquired pneumonia:  is characterized by:- \n\u2022 Sudden onset with a single shaking chill. This is followed by high grade fever (upto \n40.5\n0c ) \n\u2022 Cough productive of purulent, blood streaked or rusty sputum \n\u2022 Pleurtic chest pain on the involved side worsened during inspiration and coughing  \n\u2022 Daphnia ( shortness of Breath )"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38519-7265-11ef-a5fa-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 186, "chroma:document": "40.5\n0c ) \n\u2022 Cough productive of purulent, blood streaked or rusty sputum \n\u2022 Pleurtic chest pain on the involved side worsened during inspiration and coughing  \n\u2022 Daphnia ( shortness of Breath ) \n\u2022 Headache , myalgia , arthralgia and fatigue   \nPhysical findings  \n\u2022 The Patient will have tachycardia (pulse 100 to 140/min)and  tachypnea (RR > 20/min).  \n\u2022 There will be pulmonary signs of consolidation (lobar pneumonia), which are  \n Increased tactile fremitus and vocal fremitus , dullness on  percussion  \n Bronchial breath sound, egophony, wispering pectoriloquy, crackles and pleural \nfriction rub."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3851a-7265-11ef-8790-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 187, "chroma:document": "Internal Medicine \n \n 172The \u201catypical\u201d pneumonia present with: \n\u2022 Atypical\u201d pneumonia is usually caused by M. pneumoniae , C.pneumoniae , oral \nanaerobes  and P. carinii (usually in HIV patients), as well as S. Pneumoniae. Some \nviruses like influenza virus, Varicella zoster virus and cytomegalovirus may cause \n\u201catypical\u201d pneumonia. Tuberculosis could also present in this form.   \n\u2022 More gradual onset of symptoms, dry cough, shortness of breath. \n\u2022 Prominence of systemic symptoms like headache, malign, fatigue, nausea, vomiting and \ndiarrhea.  \n\u2022 Chest findings on physical examination are minimal even though X-ray changes are \nmarked.  \nComplications:   \n\u2022 Local : Parapneumonic effusion or pus in the pleural space (empyema).  \n\u2022 Distant complications : include septic arthritis and meningitis. Pneumonia can progress \nto sepsis, sometimes with septic shock.   \nLaboratory findings:  \n1) CBC : leucocytosis with increased neutrophils is seen in most cases.  \n2) Gram stains from sputum  may show a predominant pathogen like Gram-positive \ndiplococci. \n3) Chest x-ray shows  pulmonary infiltrates or homogeneous opacity indicating lobar \npneumonia. Very early in the course, it may be normal.  \nDiagnosis: \n\u2022 Pneumonia should be suspected in patients with acute febrile illness, associated with \nchest pain, dyspnea and cough.  \n\u2022 Presumptive diagnosis can be made from hi story, changes on chest x-ray, blood and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3851b-7265-11ef-b82f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 187, "chroma:document": "Diagnosis: \n\u2022 Pneumonia should be suspected in patients with acute febrile illness, associated with \nchest pain, dyspnea and cough.  \n\u2022 Presumptive diagnosis can be made from hi story, changes on chest x-ray, blood and \nsputum culture and sputum Gram stains. An absolute diagnosis requires demonstration \nof S. pneumoniae or other etiologic agents in pleural fluid, blood, lung or transtracheal \naspirate. \nPrognosis:  The overall mortality rate is low, if treated early.  Factors that herald a poor \nprognosis include the following:-  \n\u2022 Extremes of age, especially < 1 yr or >60yrs,  \n\u2022 Positive blood culture \n\u2022 Involvement of more than one lobe  \n\u2022 Peripheral WBC < 5000/ml"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3851c-7265-11ef-bdac-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 188, "chroma:document": "Internal Medicine \n \n 173\u2022 Presence of associated diseases (e.g. cirrhosis, CHF, immunosuppression) \n\u2022 Development of extrapulmonary complicat ions like meningitis and endocarditis. \nManagement: \nMild form of CAP \nPatients with uncomplicated \u201ctypical\u201d pneumonia can be treated at OPD   \n\u2022 Amoxicillin 500 mg PO TID or  Ampicillin 500 mg PO QID for 7 to 10 days  OR.  \n\u2022 Procaine penicillin 600,000 IU IM every 12 hrs. \nIf \u201catypical\u201d pneumonia is suspected,   \n\u2022 Erythromycin 500 mg PO QID for 7-10 days or Doxycycline100 mg PO BID  \nSupportive Therapy : Patients should also get bed rest, adequate fluids and analgesics for \npleuritic chest pain and fever.  Response  \u2013 In mildly ill patients who are treated early, fever subsides in 24 to 48 hrs. Others \nmay require 4 days to respond. \n\u2022 If Patients are allergic to penicillins, cephalosporins, erythromycin, and clindamycin can \nbe given. TTC are less predictable and should not be used in seriously ill patients.  \n\u2022 If a patient does not improve, the following factors should be considered:  \n Wrong etiologic diagnosis \n Adverse drug reaction \n Far advanced case or superinfection \n Inadequate host defenses due to associated condition \n Non-compliance to the drug regimen in outpatients \n Antibiotic resistance of the strain and  \n Complications like empyema requiring drainage, or metastatic foci of infection \nrequiring higher doses (e.g. meningitis, endocarditis or septic arthritis)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3851d-7265-11ef-b285-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 188, "chroma:document": "Antibiotic resistance of the strain and  \n Complications like empyema requiring drainage, or metastatic foci of infection \nrequiring higher doses (e.g. meningitis, endocarditis or septic arthritis). \n \n\u2022 Persistent cough and infiltration on chest x-ray for more than 6 weeks after therapy \nsuggests possibility of an underlying bronchogenic neoplasm or tuberculosis. \nSevere forms of CAP \nIf patients are seriously ill they shoul d be admitted and treated as inpatient. \nCriteria for Hospitalization of patients with Pneumonia are:  \n1) Respiratory rate of  >28/min ( Tachypnea ) tachycardia >140/min \n2) Systolic blood pressure <90mm Hg (hypotension \n3) Hypoxemia (arterial PO 2 < 60mm Hg) while breathing room air or O 2 saturation < 90 %"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3851e-7265-11ef-900c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 189, "chroma:document": "Internal Medicine \n \n 1744) New onset of confusion or impaired level of consciousness . \n5) Unstable /Significant co-morbidity (e.g. Heart faiure , uncontrolled diabetes, Chronic \nRenal insufficiency ,alcoholism , immunosuppresion ) \n6) Multilobar pneumonia  is Hypoxemia is present 7) Pleural effusion and with analysis showing characteristics of  complication \n Other conditions in which inpatient management may be advisable  \n\u2022 Elderly patient >65 yrs of age \n\u2022 Leukopenia <5000 WBC/ml \n\u2022 Pneumonia caused by St. aureus or Gram negative bacilli \n\u2022 Suppurative complications e.g. empyema, arthritis, meningitis, endocarditis \n\u2022 Failure of Outpatient treatment  \n\u2022 Inability to take oral medication or persistent vomiting \nManagement of CAP \nSupportive management   \n\u2022 Ensure adequate oxygenation to patients with cyanosis, significant hypoxemia, sever \ndyspnea, circulatory disturbance or delirium.  \n\u2022 Patients should be well hydrated \n\u2022 Fever and pain should be managed \nAntibiotic Therapy \n\u2022 Admitted patients should be started on antibiotics empirically  \n\u2022 High dose of crystalline penicillin 3-4 million IU IV every 4-6 hours  \n\u2022 Alternatives are Ceftriaxone 1gm IV daily or  2X /day or Ampicillin 500 mg IV QID Or \nCefotaxime \n\u2022 In severely ill patients erythromycin or a flouroquinolone can be added. \n\u2022 Choice of Antibiotics may be modified based on culture and sensitivity results, if \navailable."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3851f-7265-11ef-97fe-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 189, "chroma:document": "Cefotaxime \n\u2022 In severely ill patients erythromycin or a flouroquinolone can be added. \n\u2022 Choice of Antibiotics may be modified based on culture and sensitivity results, if \navailable.   \n\u2022 If the patient improves, IV treatment can be changed to oral after 3-4 days to complete a   \n7-10 days course. \nPrevention \n\u2022 Cessation of smoking and alcoholism  \n\u2022 Vaccines : Influenza an Pneumococcal vaccines ( available in developed countries )"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38520-7265-11ef-8edb-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 190, "chroma:document": "Internal Medicine \n \n 175Pneumonia in the Compromised Host \n\u2022 Immunocompromised hosts include patients with AIDS, acute leukemia, cancer \nchemotherapy, diabetes, sickle cell disease, Hodgkin's disease, and corticosteroid \ntreatment. \n\u2022 The potential pathogens in compromised hosts are many, as it has been stated above.  \n\u2022 Pathogens like Streptococcus pneumonia, which cause pneumonia in immunocompetent \npeople, are still responsible for the majority of pneumonia in compromised patients.  \nDiagnosis:   \n\u2022 Sputum examination and culture are used but they are not specific.   \n\u2022 Transtracheal aspirate, bronchoscopy and biopsy have high accuracy; however these \nare done only in specialized hospitals.  \n\u2022 High index of suspicion from clinical pr esentation is important to diagnose pneumonia in \nimmunocompromised hosts.  \nTreatment :  \n\u2022 Acutely ill patients who have suspected bacterial infections are often treated with \nantibiotics selected on the basis of probabilities and the findings with sputum gram stain \nand culture. Later treatment is adjusted on the basis of more definitive diagnostic \nevaluation.  \n\u2022 In patients with HIV infection and \u201catypical\u201d pneumonia, PCP should be considered and \ntreated with high dose of co-trimoxazole ( 3 tablets every 6 hours for 3 weeks) if clinically considered. \n \nHospital acquired Pneumonia (HAP)  \nThe definition of HAP includes the presence of a new or progressive infiltrates of Chest X-ray ,  \nplus at least two of the following"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38521-7265-11ef-8610-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 190, "chroma:document": "Hospital acquired Pneumonia (HAP)  \nThe definition of HAP includes the presence of a new or progressive infiltrates of Chest X-ray ,  \nplus at least two of the following  \n\u2022 Fever >37.8 oC \n\u2022  Leukocytosis > 10,000/mm3 \n\u2022 Production of purulent sputum \nOther findings: dyspnea, hypoxemia and chest pain \nTreatment  \nAntibiotics: Should be initiated empirically which latter on may be modified based on culture and \nsensitivity result."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38522-7265-11ef-9af9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 191, "chroma:document": "Internal Medicine \n \n 176The selection of drugs should be guided by an understanding of local patterns of antibiotics \nresistance  Antibiotics should cover at least gram negatives and S. aureus  \n\u2022 Ceftriaxone 1gm IV daily or BID plus Cloxacillin or meticillin Or \n\u2022 Levofloxacin 500 mg IV /day  \nWhen resistant organisms are suspected  \n\u2022 Cefotaxime 750 mg IV TID plus Vancomycin 1gm IV BID  \nPrevention \n\u2022 Strict hand washing protocols by health care providers  \n\u2022 Extubate an entubated patient as soon as the patient is stable  \n\u2022 Remove NG tubes when the patient is stable \n\u2022 Proper aseptic handling of IV lines \n \nReferences: \n4) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nPneumonia,      pages 1528-1540"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38523-7265-11ef-b2c3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 192, "chroma:document": "Internal Medicine \n \n 1774. Bronchial Asthma \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define bronchial asthma  2. Understand the epidemiology of bronchial asthma. 3. Describe the etiology of bronchial asthma.     \n4. Understand the pathophysiology of bronchial asthma .   \n5. Identify the clinical manifestations of bronchial asthma.     6. List the signs of severity of bronchial asthma.   7. Make an accurate diagnosis of bronchial asthma.   8. Manage most cases of bronchial asthma.  \n9. Refer complicated cases of bronchial asthma.   \n \nDefinition : Bronchial asthma is defined as chronic inflammatory disease of airways \ncharacterized by increased responsiveness of t he tracheobronchial tree to a multiplicity of \nstimuli. It is associated with widespread airway obstruction that is reversible (but not completely in some patients), either spontaneously or with treatment \nEpidemiology:   \n\u2022 Asthma is a common disease The prevalence of asthma is rising in different parts of the \nworld.  \n\u2022 It can occur at any age; but it usually starts early in life. About 50% of patients develop \nasthma before the age of 10 and another 35% before the age of 40.  \n\u2022 Males are affected twice as common as females in early life; this sex difference \nequalizes by age 30. Most cases of asthma are associated with personal or family history of allergic disease such as eczema, rhinitis and urticaria."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38524-7265-11ef-b0d9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 192, "chroma:document": "\u2022 Males are affected twice as common as females in early life; this sex difference \nequalizes by age 30. Most cases of asthma are associated with personal or family history of allergic disease such as eczema, rhinitis and urticaria.  \nEtiology Asthma is a heterogeneous disease and genetic ( atopic )  and environmental factors \nsuch as viruses , occupational exposure and allegens contribute to its initiation and continuance \n. Atopy is the single most important risk factor for asthma \n Asthma can be classified in to 3 types Allergic (atopic) , Nonallergic ( idiosyncratic ) and Mixed"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38525-7265-11ef-b15f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 193, "chroma:document": "Internal Medicine \n \n 178Table II-4-1 Comparison of the two major types of Asthma  \n \n Allergic \n(Atopic) \nasthma   Non Allergic \n(idiosyncratic )  \nAge of onset  Early in life  Late in life \nFamily or personal history of \nallergy: rhinitis , urticaria eczemaPresent  Absent  \nSkin test with intradermal injection of allergens  Positive wheal-and -flare skin test Negative skin test \nSerum IgE level  Elevated  Normal \nResponse to inhalation provocative test positive  Negative  \n \nMany patients have disease that doesn\u2019t fit into either of the 2 categories, but instead fall into a \nmixed group with some features from each group. In general asthma which has its onset early in life tends to have strong allergic component, where as  asthma that develops late in life tends to \nbe nonallergic or to have mixed etiology.  \nFactors important for the genesis of asthma \n\u2022 Genetic factors  \no Asthma has strong genetic predisposition or familial tendency \nStimuli that incite Asthma  \n\u2022 Allergens :  Seasonal allergens such as pollen green \n\u0083 Non seasonal animal feathers , dust mites , molds  \n\u2022 Pharmacologic stimuli : Aspirin , Tatrazin (coloring agent), Beta blockers such as \nPropranolol etc \n\u2022 Environmental and air pollution : in industrial and heavily populated areas. The \ncommon pollutants are ozone, nitrogen dioxide and sulfur dioxide. \n\u2022 Infections : Respiratory infections are the most common of the stimuli that evoke acute"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38526-7265-11ef-b804-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 193, "chroma:document": "\u2022 Environmental and air pollution : in industrial and heavily populated areas. The \ncommon pollutants are ozone, nitrogen dioxide and sulfur dioxide. \n\u2022 Infections : Respiratory infections are the most common of the stimuli that evoke acute \nexacerbation of asthma. Respiratory viruses are the major factors."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38527-7265-11ef-a566-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 194, "chroma:document": "Internal Medicine \n \n 179\u2022 Exercise: is  a very common precipitant of acute episodes of asthma  \n\u2022 Emotional stress: psychological factors can worsen or ameliorate asthma  \nPathophysiology:  \nAsthma results from a state of persistent subacute inflammation of the airways.  The airways \nobstruction in asthma is due to a combination of factors. The cells thought to play important part \nin the inflammatory response are mast cells, eosinophils, lymphocytes and airway epithelial cells. These cells release inflammatory mediators which may result  \n\u2022 Bronchoconstriction  (spasm of airways smooth muscles ) \n\u2022 Vascular congestion and edema of airways mucosa \n\u2022 Increased mucus production  \n\u2022 Injury and desquamation of the airways epi thelium and impaired muco-ciliary transport  \nSymptom and Signs \n\u2022 The symptoms of each asthmatic patient differ greatly in frequency and degree.   \n\u2022 Some asthmatics are symptom free, with an occasional episode that is mild and brief; \nothers have mild coughing and wheezing much of the time, punctuated by severe exacerbations of symptoms following exposure to known allergens, viral infection, exercise etc. Psychological factors particularly those associated with crying, screaming \nor hard laughing may precipitate symptoms. \n\u2022 An attack usually begins acutely with paroxysms of wheezing, coughing, and shortness \nof breath, or insidiously with slowly increasing manifestations of respiratory distress."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38528-7265-11ef-8f1d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 194, "chroma:document": "or hard laughing may precipitate symptoms. \n\u2022 An attack usually begins acutely with paroxysms of wheezing, coughing, and shortness \nof breath, or insidiously with slowly increasing manifestations of respiratory distress.  \n\u2022 The asthmatic first notices dyspnea, tachypnea, cough and tightness in the chest and \nmay even notice audible wheezes.  \nOn physical examination  \u2013  \n\u2022 Varying degrees of respiratory distress tachypnea, tachycardia, and audible wheezes \nare often present.  \n\u2022 Dehydration may be present because of sweating and tachypnea.  \n\u2022 Chest examination shows a prolonged expira tory phase with relatively high pitched \nwheezes throughout inspiration and most of expiration.  \n\u2022 In more severe episodes, patients may be unable to speak more than a few words \nwithout stopping for breath.  \n\u2022 Cyanosis is usually a late sign of hypoxia.  \n\u2022 Confusion and lethargy may indicate the onset of progressive respiratory failure."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38529-7265-11ef-990a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 195, "chroma:document": "Internal Medicine \n \n 180\u2022 Less wheezing (silent chest) might indicate mucous plug or patient fatigue with less \nairflow. And it is a sign of impending respiratory failure. \n\u2022 The presence, absence, or prominence of wheezes does not correlate precisely with the \nseverity of the attack.   \n\u2022 The most reliable clinical signs include the degree of dyspnea at rest, cyanosis, difficulty \nin speaking and use of accessory muscles of respiration.  This is confirmed by arterial \nblood gas analysis. \n\u2022 Between acute attacks, breath sounds may be normal during quiet respiration. However, \nlow grade wheezing maybe heard at any time in some patients, even when they claim to be completely asymptomatic. \nComplications during an Acute Attack of Asthma \n\u2022 Pneumothorax : It may present as sudden worsening of respiratory distress, \naccompanied by sharp chest pain and on examinat ion, hyperresonant lung with a shift of \nmediastinum. Chest x-ray confirms the diagnosis.  \n\u2022 Mediastinal and subcutaneous emphysema  due to alveolar rupture \n\u2022 Atelectasis due to obstruction \n\u2022 Dilated right heart chambers  (Corpulmonale) : from ch ronic hypoxemia and pulmonary \nhypertension  \n\u2022 Respiratory failure  \n \nLaboratory Findings \n\u2022 Eosinophilia  is a common finding.  \n\u2022 Sputum  is tenacious, rubbery and whitish or may be yellowish; eosinophils are present \nin the sputum. \n\u2022 Chest x-ray:  varies from normal to hyperinflation.  Atelectasis and pneumothorax may \nbe seen in complicated cases."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3852a-7265-11ef-b83d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 195, "chroma:document": "\u2022 Sputum  is tenacious, rubbery and whitish or may be yellowish; eosinophils are present \nin the sputum. \n\u2022 Chest x-ray:  varies from normal to hyperinflation.  Atelectasis and pneumothorax may \nbe seen in complicated cases.  \n\u2022 Pulmonary function tests  are valuable in differential diagnosis and in known patients to \nassess the degree of airways obstruction. \n \nDiagnosis \nAsthma should be considered in anyone who wheezes. A family history of allergy, rhinitis or \nasthma can be elicited in most asthmatics."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3852b-7265-11ef-aa7f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 196, "chroma:document": "Internal Medicine \n \n 181Differential diagnosis includes :  \n\u2022 In children : foreign body obstruction, viral URTI involving the epiglottis (croup), and \nbronchiolitis (RSV infection);  \n\u2022 In adults : COPD, heart failure, endobronchial TB, and malignancies. Physical \nexamination should search for heart failure and signs of chronic hypoxemia (clubbing). \nUnilateral wheezes usually indicate obstruction by foreign bodies or tumor. \nPrevention of attacks \n\u2022 The role of environmental factors (e.g. animal dander, dust, airborne moulds, and \npollens) in acute exacerbations is clear. Allergens that can be controlled by avoidance \nshould be eliminated. \n\u2022 Nonspecific exacerbating factors (e.g. cigarette smoke, odors, irritant fumes, and change \nin temperature, atmospheric pressure, and humidity) should also be investigated and avoided if possible. \n \nTreatment \nGeneral principles \n\u2022 Assessing the severity of the attack is paramount in deciding management \n\u2022 Bronchodilators should be used in orderly progression \n\u2022 Decide when to start corticosteroids \nTreatment of the Acute Attack \nMild acute asthmatic attack: Most patients can be managed as an outpatient \n\u2022 Salbutamol aerosol (Ventolin\u00ae) two puffs every 20 minutes for three doses is the 1st line \nof treatment.  \n\u2022 Adrenaline 1:1000 can be given in doses up to a maximum of 0.2 ml in children and 0.3 \nml in adults, repeated once or twice in 20 to 30 min (if there is no hypertension or any other contra indication)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3852c-7265-11ef-801e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 196, "chroma:document": "of treatment.  \n\u2022 Adrenaline 1:1000 can be given in doses up to a maximum of 0.2 ml in children and 0.3 \nml in adults, repeated once or twice in 20 to 30 min (if there is no hypertension or any other contra indication).  \n\u2022 If the initial treatment fails, Aminophylline 250 mg IV diluted in dextrose in water should \nbe given slowly over 10-15 minutes, once.  \n\u2022 If the patient does not respond to one dose of aminophylline IV, then the patient is \ndeclared to have severe asthma, and should be admitted and managed as in-patient."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3852d-7265-11ef-871c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 197, "chroma:document": "Internal Medicine \n \n 182In patient management  \nPatients who are diagnosed to have severe and life threatening asthma need in patient \nmanagement. Some may even need admission to ICU. \n Signs of Severity of acute asthmatic attack \n1) Tachycardia HR > 120/min , Tachypnea RR.30 min \n2) Presence of pulsus paradoxus 3) Use of accessory muscles of  respiration \n4) Cyanosis \n5) Altered state of consciousness ( confusion , drowsiness ) 6) Silent chest  7) Paradoxical movement of the chest and the abdomen  8) Presence of complications : Pneumothorax , atelectasis \n9) Unable to finish a sentence with single breath ( frequent interruption of speech to take a \nbreath ) \n10) Laboratory parameters \no PEFR < 50 % or FEV\n1 < 60 % \no PaO 2   < 60mmof Hg or SaO 2  < 90 % \no PaCO 2 > 42 mmHg \n \nSpecific drug Treatment  \n\u2022 Aminoplylline in doses of 1mg/kg/hr in a continuous IV infusion should be given.  \n\u2022 Corticosteroids  should also be given IV e.g. Hydrocortisone 4mg/kg IV every 4 hrs. \nWhen the patient improves the hydrocorti sone be changed to Prednisolone PO and the \ndosage should be tapered up on discharge. \n\u2022 Patients who do not respond to aggressive drug therapy are candidates for endotracheal \nintubation and Mechanical Ventilation for which they should be admitted to an ICU. \n\u2022 Respiratory tract infections precipitating acute asthmatic attack are predominantly viral; \nbut if patients expectorate yellowish, green or brown sputum, antibacterial therapy is"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3852e-7265-11ef-bb44-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 197, "chroma:document": "\u2022 Respiratory tract infections precipitating acute asthmatic attack are predominantly viral; \nbut if patients expectorate yellowish, green or brown sputum, antibacterial therapy is \nindicated. Ampicillin is the first line; alternat ives are TTC, erythromycin or cotrimoxazole. \nChest x-ray is taken if there is suspicion of pneumonia or complications."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3852f-7265-11ef-aa8e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 198, "chroma:document": "Internal Medicine \n \n 183Supportive Treatment  \n\u2022 O 2 therapy is always indicated for hospitalized patients \n\u2022 Fluid and electrolyte balance requires special attention because of frequent occurrence \nof dehydration during   acute asthmatic attack. However, over hydration may cause \npulmonary edema and one should be cautious in fluid administration.  \n\u2022 Anxiety is common in patients with severe acute asthmatic attack. However this can be \novercome when underlying hypoxia and feeling of asphyxiation is treated. Health personnel should be considerate and reassure the patient. \n \nMaintenance Therapy for Asthma (Chronic Treatment) \nGoal of Therapy : To achieve a stable, asymptomatic state with the best pulmonary function, \nusing the list amount of medication .Drug selection is based upon the severity of illness. \n \nTable II-4-2. Step wise approach for managing Asthma in adults  \n \nSeverity Symptoms \nday/night  Medication  Alternative \ntreatment in \nresource limited setting \nMild \nintermittent  \u2264 2 days/wk and \u2264 2 \nnights /month  No daily medication needed  \nTreat when there is acute exacerbation   \nMild Persistent  > 2days /week but < 1 per day and > 2 \nnights/month Low dose inhaled steroids \nor \nCromolyn  Theophedrine tablets \nor Salbutamol tabs \nModerate Persistent  Daily symptoms and more than 1 night /wkLow-medium does inhaled steroid and long acting B-agonist inhaler \n Theophylline sustained release  Salbutamol Tabs  \nPrednisolone tablets \n(low dose"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38530-7265-11ef-9055-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 198, "chroma:document": "or Salbutamol tabs \nModerate Persistent  Daily symptoms and more than 1 night /wkLow-medium does inhaled steroid and long acting B-agonist inhaler \n Theophylline sustained release  Salbutamol Tabs  \nPrednisolone tablets \n(low dose  \nSever Persistent  Continual daily symptoms and High dose inhaled steroid and long acting inhaled B-Theophylline sustained release"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38531-7265-11ef-96b3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 199, "chroma:document": "Internal Medicine \n \n 184frequent night \nsymptoms agonists and Oral steroids (if needed ) Salbutamol Tabs  Prednisolone tablets (high dose) or \nCelestamine tabs \n \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  Asthma,     \npages 1508-1515 \n2) Myers R. Allen , National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Asthma, pages 75-78"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38532-7265-11ef-8912-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 200, "chroma:document": "Internal Medicine \n \n 1855. Chronic obstructive pulmonary diseases (COPD) \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define chronic obstructive pulmonary diseases (COPD 2. List the etiologies of COPD 3. Explain the epidemiology of COPD \n4. Describe the pathophysiology of COPD \n5. Identify the clinical manifestations of COPD 6. Outline the main differences between c. bronchitis and emphysema  7. Describe the most commonly used tests for the diagnosis of COPD  8. Make a diagnosis of COPD \n9. Give therapy to COPD at the primary care level \n10. Design appropriate methods of prevention of COPD  \n \nDefinition : Chronic obstructive pulmonary diseases are conditions characterized by chronic \nirreversible airway obstruction causing an increas ed resistance to outflow of air due to chronic \nbronchitis and emphysema. Both these diseases occur together in the same individual in a \nvariable proportion but the manifestations of one often predominates the clinical picture.  1) Chronic bronchitis : is a condition associated with excessive tracheobronchial mucus \nproduction sufficient to cause cough with expectoration of sputum for at least 3 months in a \nyear for over 2 consecutive years.  \n2) Pulmonary emphysema : is distension of the airspaces distal to the terminal bronchioles, \naccompanied by destructive changes of the alveolar septa. \nEtiology \n\u2022 Emphysema : Any factor leading to chronic alveolar inflammation would encourage"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38533-7265-11ef-9355-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 200, "chroma:document": "2) Pulmonary emphysema : is distension of the airspaces distal to the terminal bronchioles, \naccompanied by destructive changes of the alveolar septa. \nEtiology \n\u2022 Emphysema : Any factor leading to chronic alveolar inflammation would encourage \ndevelopment of an emphysematous lesion. Smoking has adverse effects on lung \ndefenses, leading to emphysematous change. Congenital enzyme defects such as \u03b1\n1- \nantitrypsin deficiency are also risk factors for the disease.  \n\u2022 Chronic bronchitis : with sufficient exposure to bronchial irritants, particularly cigarette \nsmoke, most persons develop some degree of chronic bronchitis with signs of \ninflammation of the airways. In developing countries household smoke from fire wood is said to be a major contributing factor."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38534-7265-11ef-b2ca-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 201, "chroma:document": "Internal Medicine \n \n 186Prevalence :  \n\u2022 COPD is a major health problem especially in western societies because of the effect \nof cigarette smoking and aging.   \n\u2022 Males are affected more than females which could be attributed to the higher \nprevalence of smoking in males. Nowadays, the incidence of this disease in females is \nincreasing because of the increasing smoking habit.  \n Pathological changes and pathophysiology  \n\u2022 Chronic bronchitis is characterized by hypertrophy of mucus glands in both large and \nsmall airways with thickening of walls and accompanying excess production of mucus \nand narrowing of airway lumen. In C. bronchitis, alveoli are often spared, and no vessel \nloss and lung perfusion remains normal but ventilation is very much reduced. This \nleads to abnormal V/Q (arteriovenous shunt) and patients usually suffer from hypoxemia (manifested with cyanosis) and acidosis, which causes pulmonary \nhypertension and right heart failure in the long term.  \n\u2022 On the other hand emphysema is characterized by destruction of alveolar septa and \ndistension of alveoli resulting in reduced surface area and loss of vessels, the later causing reduced perfusion. Moreover, emphysema causes mucus production and airway narrowing with accompanying reduction in ventilation. This leads to retention of \ncarbon dioxide in the blood and severe dyspnea from reduced tissue perfusion. \nHowever, these patients don\u2019t suffer from hypoxia and acidosis, and have less chance"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38535-7265-11ef-bc6f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 201, "chroma:document": "carbon dioxide in the blood and severe dyspnea from reduced tissue perfusion. \nHowever, these patients don\u2019t suffer from hypoxia and acidosis, and have less chance \nof development of pulmonary hypertension and cor-pulmonale. However, patients \nusually have a mixed picture of em physema and chronic bronchitis. \nClinical features:   \n\u2022 COPD is thought to begin early in adult life but significant symptoms and disability do \nnot appear until middle age.  \n\u2022 A mild \"smoker's cough\" is often present many years before onset of exertional \ndyspnea. Gradual progressive exertional dyspnea is the most common presenting complaint.  \n\u2022 Cough, wheezing, recurrent respiratory infections or, occasionally weakness, weight \nloss, or reduced libido may also be initial manifestations.  \nPhysical findings : in COPD are very variable especially in early stages."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38536-7265-11ef-b7e5-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 202, "chroma:document": "Internal Medicine \n \n 187\u2022 A consistent abnormality is obstruction to expiratory airflow manifested by prolonged \nforced expiration (normally < 4 seconds). \n\u2022 Typical findings including gross pulmonary hyperinflati on, prolonged expiration during \nquiet breathing, pursed-lip breathing, stooped posture, and marked use of accessory \nmuscles of respiration are seen in later stages of COPD.  \n\u2022 Other findings are rhonchi, diminished vesicular breath sounds, tachycardia, distant \nheart sounds, and decreased diaphragmatic excursion.  \n\u2022 The chest may be remarkably \"quiet\" in adv anced stages of emphysema but is usually \n\"noisy\" in patients with chronic bronchitis.  \n\u2022 In advanced cases, frank cyanosis may be there from hypoxemia; a plethoric \nappearance associated with secondary erythrocytosis and, signs of right-sided heart \nfailure in patients with cor-pulmonale.  Mild edema may be there even without heart failure. \nChest x-ray findings :- are very variable.   \n\u2022 In early stages it is normal.  \n\u2022 Hyperinflation (e.g. depressed diaphragm, generalized radio-lucency of the lung fields) \nis common usually late in the disease process.  \n\u2022 In patients with recurrent chest infections, a variety of non-descriptive post-\ninflammatory abnormalities (referred to as \u201cdirty lung\u201d) may be noted on the chest film. \nDiagnosis:  \n\u2022 COPD should be suspected in any patient with chronic productive cough and/or \nexertional dyspnea of uncertain etiology, or whose physical examination reveals"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38537-7265-11ef-90c0-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 202, "chroma:document": "Diagnosis:  \n\u2022 COPD should be suspected in any patient with chronic productive cough and/or \nexertional dyspnea of uncertain etiology, or whose physical examination reveals \nevidence of prolonged forced expiration. \n\u2022 Pulmonary function tests (spirometric testing) are done at specialized hospitals to \ndetermine the type of pulmonary obstruction.  \n\u2022 Red cell counts may reveal erythrocytos is and elevated hematochrit in chronic \nhypoxemic patients.  \n\u2022 The pattern of physiologic abnormality in each patient depends to some extent on the \nrelative severity of intrinsic bronchial disease and emphysema. In patients with severe \nemphysema, resting hypoxemia is usually m ild (i.e. no or less cyanosis). In patients \nwith chronic bronchitis, severe hypoxemia may be noted relatively early."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38538-7265-11ef-8259-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 203, "chroma:document": "Internal Medicine \n \n 188Table II-5-1 Summary of clinical manifestations of Chronic Bronchitis and Emphysema \n \n  \nPredominant emphysema  Predominant C. \nbronchitis \nAge  60 +/-  50+/- \nBody habitus Thin obese \nCough  After dyspnea  Before dyspnea  \nSputum  Scanty, mucoid Copious, purulent \nAppearance  Pink, tachypneic (pink puffers)  Cyanosed, normal RR \n(blue bloaters) \nP/E \u2191AP diameter, \nUse of accessory muscles of respiration Silent chest, Hyperresonant \nDecreased cardiac dullness +/- use of accessory muscles of respiration  \nNo hyperresonance  Rhonchi (changing)  Wheezing with cough \nCXR Long, narrowed tubular heart,  Low diaphragm (flat diaphragm) Dark lung fields (translucent) \nwith loss of peripheral vascular \nmarkings Enlarged heart  Large pulmonary artery  Increased bronchovascular markings \n \nHematology  Normal Hct Increased Hct \nBlood gases PaO 2  =65\u2013 75mmH  \nPaCO 2 = 35 \u2013 40mmHg PaO 2 = 40 \u2013 60mmHg \nPaCO 2 = 50 \u2013 60mmHg \nComplications  Less bronchial infection Terminal respiratory insufficiency \n+/- cor-pulmonale Frequent bronchial infection  Repeated respiratory insufficiency \nFrequent cor-pulmonale"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38539-7265-11ef-a465-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 204, "chroma:document": "Internal Medicine \n \n 189Course and Prognosis \nIn the early stage of COPD, some reversal of airway obstruction and considerable \nsymptomatic improvement can often be obtained with therapy, but the long-term prognosis is less favorable in such patients.  \nTreatment:  so far no curative treatment.  \n\u2022 Therapy is directed at relieving symptoms, controlling potentially fatal exacerbations, \nand slowing of the progression of the disorder.  \n\u2022 Avoidance of bronchial irritants, especially cessation of smoking, is of primary \nimportance.  \nThus, the treatment is outlined as follows:  \n1) Treatment of infection : COPD patients with purulent sputum should be treated with a \nbroad spectrum antibiotic. Commonly used drugs include co-trimoxazole 980mg POBID or TTC or Ampicillin 250 - 500mg four times a day for 10 days. The course can be repeated at the first sign of recurrence of bronchial infection.  \n2) Control of bronchospasm : \u03b2-agonists like salbutamol, or one of the theophyllines can \nbe used. Corticosteroids do not have a major role in maintenance treatment. \n3) Facilitation of drainage of bronchial secretion : adequate hydration with oral fluids is \nessential to prevent drying of secretions.  Inhalation of mist, postural drainage, and chest exercise may help. \n4) Hypoxemia:  this will lead to cor-pulmonale in patients with predominant c.bronchitis. \nOxygen should be given in such patients with hypoxia, and in severe cases a portable"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3853a-7265-11ef-a751-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 204, "chroma:document": "4) Hypoxemia:  this will lead to cor-pulmonale in patients with predominant c.bronchitis. \nOxygen should be given in such patients with hypoxia, and in severe cases a portable \noxygen therapy ( 16 hrs /day) for home use is recommended.                                 \n5) Control of heart failure : the most important measures are correction of hypoxemia, \nadministration of diuretics and restriction of sodium intake. \n6) Exercise : prolonged inactivity leads to exercise intolerance. Regular exercise as long \nas there is no severe heart disease is recommended. \n7) Depression : The nature of the disease should be well understood by both the patient \nand the family. Psychological support is very important. Antidepressants may be \nnecessary but they should be used cautiously to avoid sedation. \n8) Treatment of exacerbation : exacerbation requires prompt treatment. If sputum \nbecomes purulent, a course of broad-spectrum antibiotics should be given.  \n9) Phlebotomy:  hematochrit is usually high because of the chronic hypoxemia \n(polycythemia) especially in patients with predominant chronic bronchitis. Phlebotomy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3853b-7265-11ef-97f5-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 205, "chroma:document": "Internal Medicine \n \n 190should be done when the hematocrit level is very high (above 55%) and patients are \nsymptomatic. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  Chronic \nobstructive pulmonary diseases, pages 1547-1553 \n2) Myers R. Allen , National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Chronic obstructive pulmonary diseases , 70-74"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3853c-7265-11ef-bbdb-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 206, "chroma:document": "Internal Medicine \n \n 1916. Suppurative lung diseases  \n \n6.1 Bronchiectasis   \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define bronchiectasis  \n2. List the etiologies of bronchiectasis  3. Explain the epidemiology of bronchiectasis  4. Describe the pathophysiology of bronchiectasis  5. Identify the clinical manifestations of bronchiectasis \n6. Describe the most commonly used tests for the diagnosis of bronchiectasis   \n7. Make a diagnosis of bronchiectasis 8. Give treatment for bronchiectasis at the primary care level 9. Design appropriate methods of prevention of bronchiectasis   \nDefinition:  It is a pathologic, irreversible destruction and dilatation of the wall of bronchi and \nbronchioles, usually resulting from suppurative infection in an obstructed bronchus. \nEtiology and pathogenesis:   \n\u2022 Small bronchi of children are susceptible to recurrent infections and obstruction by \nforeign body, lymph node, or impacted secretions, all of which lead to persistent \ninfection and the development of bronchiectasis. However, bacterial pneumonia is the \ncommonest cause of bronchiectasis. Pr edisposing conditions include congenital \ndisorders (e.g. bronchial stenosis) and immunosuppressive disorders.  \nClinical features \n\u2022 Chronic cough productive of copious and of fensive purulent sputum is the cardinal \nfeature of bronchiectasis. The sputum typically forms three layers when collected in a"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3853d-7265-11ef-bd4b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 206, "chroma:document": "Clinical features \n\u2022 Chronic cough productive of copious and of fensive purulent sputum is the cardinal \nfeature of bronchiectasis. The sputum typically forms three layers when collected in a \nglass container: the upper layer is foam (mucus), the middle one is liquid and the lower \none is sediment.  \n\u2022 In the early stage of the disease cough and sputum production are related to cold \nexposure, with occasionally hemoptysis.  \n\u2022 In advanced disease patients have progressive dyspnea, massive hemoptysis and \ncough occurs at any time of the day and produces large volume of khaki colored \nsputum with accompanying cyanosis and clubbing."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3853e-7265-11ef-97ac-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 207, "chroma:document": "Internal Medicine \n \n 192\u2022 Complications in advanced cases include recurrent hemoptysis, cor-pulmonale, \nrespiratory failure, amyloidosis and recurrent pneumonia. \nDiagnosis \n\u2022 Diagnosis is largely based on clinical features. Obtaining a history of recurrent \npulmonary infections ultimately followed by chronic recurrent cough and production of \ncopious purulent sputum may suggest a diagnosis of bronchiectasis.  \n\u2022 Physical examination of the chest may s how only rales in early stages. Additional \nfindings like cyanosis, clubbing and signs of right heart failure appear late.  \n\u2022 Pulmonary function test may be normal in early disease.  \n\u2022 Chest x-ray usually shows peribronchial  fibrosis or it can have a honeycomb \nappearance. Segmental lung collapse may be observed in parts of the lung affected by \nbronchiectasis. \n\u2022 Definitive diagnosis of bronchiectasis is made by bronchography.  \n\u2022 CT scanning often identifies the lesions, eliminating the need for bronchoscopy and \ncontrast studies. \nTreatment \nGenerally, patients should avoid smoking and exposure to dust. Living in warm & dry \nclimatic condition is advisable. However, m edical therapy is the mainstay of treatment \nand include  \n \n1) Control of respiratory infections  : \na. Broad spectrum antibiotics that shou ld be given whenever signs of pulmonary \ninfection appear and symptoms are exacerbated (Ampicillin, tetracycline or \nerythromycin),  \nb. Immunization for influenza and S. pneumoniae  if available"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3853f-7265-11ef-8c81-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 207, "chroma:document": "a. Broad spectrum antibiotics that shou ld be given whenever signs of pulmonary \ninfection appear and symptoms are exacerbated (Ampicillin, tetracycline or \nerythromycin),  \nb. Immunization for influenza and S. pneumoniae  if available \n2) Improve drainage of secretion : using postural drainage, liquefaction and \nbronchodilators. \n3) O 2 therapy:  may be given in patients with hypoxemia. \n4) Surgical resection  of the affected part is indicated when bronchiectasis is localized, \nand in those with recurrent massive hemoptysis that fails to respond to conservative \ntreatment. This is effective if done early in life."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38540-7265-11ef-b790-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 208, "chroma:document": "Internal Medicine \n \n 1936.2 Lung abscess \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define lung abscess  2. List the etiologies of lung abscess  3. Explain the risk factors for lung abscess   \n4. Identify the clinical manifestations of lung abscess \n5. Describe the most commonly used methods for the diagnosis of lung abscess 6. Make a diagnosis of lung abscess  7. Identify the complications of lung abscess 8. Give treatment for lung abscess at the primary care level \n9. Design appropriate methods of prevention of lung abscess   \n \nDefinition:  lung abscess is defined as collection of pus within a destroyed portion of the lung. \nIt may develop following necrotizing infections of  the lung (bacterial pneumonia, TB, fungi), \nloss of blood supply to a part of the lung causing cavitary infarction due to septic or bland \nembolism, obstruction to airways or cavitations of malignancy. The anaerobic abscess is the \ncommonest and usually follows periodontal diseases (gingivitis, pyorrhea) or aspiration of oro-\npharyngeal/gastric contents. \nEtiology:   \n\u2022 Lung abscess is commonly caused by pyogenic bacteria: S.aureus, Klebsiella , mixed \nanaerobes, and Nocardia.   \n\u2022 Common risk factors include alcoholism, immunodeficiency, loss of consciousness, \nand periodontal diseases \nClinical features:   \n\u2022 In the early stage manifestations of lung abscess may resemble that of pneumonia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38541-7265-11ef-963f-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 208, "chroma:document": "anaerobes, and Nocardia.   \n\u2022 Common risk factors include alcoholism, immunodeficiency, loss of consciousness, \nand periodontal diseases \nClinical features:   \n\u2022 In the early stage manifestations of lung abscess may resemble that of pneumonia.  \n\u2022 The development of features of lung abscess within 1-2 weeks after bacterial \npneumonia, possible aspiration or bronchial obstruction is usually reported.  \n\u2022 Patients will have cough with sudden expectoration of massive purulent and foul \nsmelling sputum, high grade fever, and sweating with occasional hemoptysis.   \nDiagnosis :  \nWhen patients present with the typical manifestations outlined above, the diagnosis of lung \nabscess may not difficult.  However, it should be confirmed by chest x-ray by"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38542-7265-11ef-b0ab-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 209, "chroma:document": "Internal Medicine \n \n 194demonstrating parenchymal infiltrates with cavity  containing air-fluid level. Gram stain and \nculture of the sputum help to make etiologic diagnosis. \nComplications include   \n\u2022 Metastatic brain abscess \n\u2022 Fatal hemoptysis \n\u2022 Empyema \n\u2022 Secondary amyloidosis \nTreatment  \nMedical therapy is the main stay of treatment. Admit patients to hospitals and  the \nfollowing modalities of therapy can be given:  \n1) Antibiotics  \u2013 start empirical antibiotics until laboratory results are available and adjust \ndrugs accordingly. Start both crystalline penicillin and chloramphenicol high doses IV \nand treatment should be given for 4 \u2013 8 weeks. \n2) Drainage of abscess  \u2013 postural drainage can be effective but bronchoscopic drainage \nmay be used when airway obstruction by fo reign body or mass hinders drainage of pus \nby postural means. Bronchoscopes and experts who can do such procedures are \navailable only in specialized hospitals. \n3) Surgical treatment of lung abscess may be indicated in patients with  \n\u2022 Persistent or massive hemoptysis \n\u2022 Empyema or bronchopleural fistula \n\u2022 Failure of medical treatment  \n\u2022 Lung cancer \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nBronchiectasis, pages 1541-1542. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nBronchiectasis, 78-80."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38543-7265-11ef-9236-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 210, "chroma:document": "Internal Medicine \n \n 1957. Pleurisy and Pleural Effusion \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define pleurisy and pleural effusions 2. Classify pleural effusions 3. List the etiologies of pleural effusions \n4. Describe the pathophysiology of pleural effusions \n5. Identify the clinical manifestations of pleural effusions  6. Describe the most commonly used method of diagnosis of pleural effusions  7. Make a diagnosis of pleural effusions  8. Give treatment for pleural effusions at the primary care level \n \nDefinition: pleural effusion is the presence of excess fluid in the pleural space. Normally 10\u2013 \n20 ml of fluid is spread in a thin layer between the two layers of pleurae. Pleural effusions are \nclassified as transudates and exudates based on laboratory analysis of the fluid.  \nTransudative effusion:  results from elevations in hydrostatic pressure or decrease in oncotic \npressure. The following are some of the causes:-  \n\u2022 Heart failure \n\u2022 Cirrhosis of the liver \n\u2022 Nephrotic syndrome  \n\u2022 Myxoedema  \n\u2022 Hypoproteinemia  \nExudative effusion: is  due to pleural inflammation (pleurisy) with an increased permeability of \nthe pleural surface to protein. Pleurisy commonly occurs in infections such as pneumonia, \ninfections of the esophagus, mediastinum or s ub-diaphragmatic areas, traumatic injuries, and \nextension of infections from adjacent organs. Initially pleurisy tends to be dry but fluid starts to"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38544-7265-11ef-9566-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 210, "chroma:document": "infections of the esophagus, mediastinum or s ub-diaphragmatic areas, traumatic injuries, and \nextension of infections from adjacent organs. Initially pleurisy tends to be dry but fluid starts to \ncollect subsequently. It is found in association with:-  \n\u2022 Parapneumonic effusions \n\u2022 Empyema \n\u2022 Pulmonary embolism \n\u2022 Neoplasms  \n\u2022 Systemic lupus erythematosis and rheumatoid pleural effusion \n\u2022 Sub-diaphragmatic abscess"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38545-7265-11ef-9ab1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 211, "chroma:document": "Internal Medicine \n \n 196\u2022 Pancreatitis \n\u2022 Uremic pleural effusion \n\u2022 Hemothorax \n\u2022 Chylothorax (thoracic duct injury) \n\u2022 Radiation and drugs.  \nClinical findings and diagnosis  \n\u2022 Pleuritic chest pain and dyspnea are the most common symptoms, but many pleural \neffusions are asymptomatic and discovered on physical examination or chest x-ray.  \n\u2022 Underlying causes should be suspected from the history.  \n\u2022 Physical examination on the affected side discloses the presence of decreased chest \nmotion, absent tactile fremitus, percussion dullness, and decreased or absent breathes \nsounds.  \nDiagnosis and laboratory findings  \n\u2022 The diagnosis of pleural effusion can be suspected from a properly done physical \nexamination. \n\u2022 Chest x-ray is the most precise way to confirm the physical findings. It demonstrates \nthe presence of pleural fluid as homogenous opacity with a meniscus-sign and \nobliteration of the costophrenic angle. Large pleural effusions may result in complete \nopacification of the hemithorax and mediastinal shift to the opposite side. The best way \nto identify and localize a loculated pleural effusion is with ultrasonography. \n\u2022 Pleural thoracenthesis (aspiration of fluid) should be performed to confirm the presence \nof fluid and to determine its characteristics, including color and consistency.  \no Clear yellow fluid is described as serous \no Bloody or blood-tinged fluid as sanguineous or serosanguineous. Some of the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38546-7265-11ef-a5c4-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 211, "chroma:document": "of fluid and to determine its characteristics, including color and consistency.  \no Clear yellow fluid is described as serous \no Bloody or blood-tinged fluid as sanguineous or serosanguineous. Some of the \ncauses include pulmonary infarction and pleural carcinomatosis \no Translucent or opaque, thick fluid as purulent.  \n\u2022 Microscopic examination of the fluid is important including Gram stain and culture (if \npossible).  \n\u2022 Total and differential cell counts should be obtained.  \no The predominance of polymorphonuclear leukocytes suggests an underlying \npneumonia with a parapneumonic effusion.  \no The presence of many small mature lymphocytes, particularly with few \nmesothelial cells, strongly suggests tuberculosis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38547-7265-11ef-9ee9-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 212, "chroma:document": "Internal Medicine \n \n 197\u2022 It is important to determine whether pleural fluid is an exudate or a transudate; this \ngives a clue to the underlying cause. Ex udative effusions have at least one of the \nfollowing characteristics, whereas transudates have none of these: \no Pleural fluid protein/ serum protein > 0.5    \no Plural fluid LDH/serum LDH > 0.6 \no Pleural fluid LDH more than 2/3 normal upper limit for serum \n\u2022 If effusion is exudative, gross description of fluid, glucose level, amylase level, WBC \nand differential count, microbiologic st udies, and cytology should be obtained. \nTreatment:   \n\u2022 Therapeutic thoracenthesis should be done in massive effusion to relieve respiratory \ndistress. Removal should be limited to 1200 to 1500 ml at a time.  \n\u2022 Definitive treatment of pleural effusion requires identifying the underlying condition and \nadministration of specific therapy.  \no Tuberculous effusion is treated with a course of anti tuberculous drugs.  \no Parapneumonic effusions and other bacterial infections in the pleural space \nshould be treated with long course of antibiotics.  \no Empyema (purulent fluid in the pleural cavity) is treated with high doses of \nparenteral antibiotics coupled with surgical drainage (Chest tube insertion).  \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nDisorders of the pleura, pages 1565-1568. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38548-7265-11ef-b4c1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 212, "chroma:document": "References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nDisorders of the pleura, pages 1565-1568. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Diseases of the pleura, 88-91."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38549-7265-11ef-9579-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 213, "chroma:document": "Internal Medicine \n \n 1988. Neoplasms of the lung \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Classify lung neoplasms \n2. List the etiologies of lung neoplasms 3. Identify the clinical manifestations of lung neoplasms \n4. Describe the most commonly used method of diagnosis of lung neoplasms \n5. Make a diagnosis of lung neoplasms 6. Refer patients with lung neoplasms to hospitals for further investigations and treatment  \n \n\u2022 Metastatic tumors are more common than primary tumors of the lungs; the commonest \nprimary sites being the breasts, stomach, prostate, and ovary.  \n\u2022 Majority (90 \u2013 95%) of primary lung tumors are malignant epithelial tumors collectively \ncalled bronchogenic carcinomas. The remaining are bronchial carcinoids, mesenchymal tumors (lymphomas, sarcomas, liomyomas, lipomas, fibromas, liomyosarcomas) and bronchial hemartomas, the last being benign tumors with \naberrant differentiation of the bronchial tissues. The disease is common between the \nage ranges 65 \u2013 75 years, and affects men more than women, with M: F ratio of 2:1. \nEtiology : A number of factors have been found to be associated with lung cancer and include \n\u2022 Cigarette smoking  - cigarettes contain at least 55 carcinogens and the risk of lung \ncancer increases to 20 fold for people who smoke more than 40 cigarettes/d. Smokers have 10 times more risk of dyi ng from lung cancer than non-smokers."}


created_at: 2024-09-14 06:50:03
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id: 71d3854a-7265-11ef-9782-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 213, "chroma:document": "\u2022 Cigarette smoking  - cigarettes contain at least 55 carcinogens and the risk of lung \ncancer increases to 20 fold for people who smoke more than 40 cigarettes/d. Smokers have 10 times more risk of dyi ng from lung cancer than non-smokers. \n\u2022 Exposure to Radon in underground miners  (occupational) or indoors  \n\u2022 Exposures to other carcinogens :Ni, Co , Cr, Asbestos, Polycyclic aromatic \nhydrocarbons, Silica , Mustard gas (world war I) \nPathologic features of bronchogenic carcinomas: originate from the bronchial \nepithelium and have 4 histological types  \n\u2022 Adenocarcinoma (including bronchoalveolar carcinoma) account for 30 -\n35% of bronchogenic ca \n\u2022 Squamous cell carcinoma accounts for  25 -30% \n\u2022 Small cell (Oat cell) carcinoma  accounts for 15 \u2013 25% \n\u2022 Large cell carcinoma accounts for 10 \u2013 15%"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 214, "chroma:document": "Internal Medicine \n \n 199\u2022 Mixed cell type (Squamous & sm all cell or squamous cell & \nadenocarcinoma) account for 5 - 10% \n\u2022 Pleomorphic carcinoma (mixed carci noma & sarcomatoid pattern) 0.5%  \nDifferentiation between small cell and non-sma ll cell carcinoma (Adenocarcinoma, Squamous \ncell ca, large cell ca) is very important becaus e small cell carcinoma is responsive (at least \ninitially) to chemotherapeutic treatment.  \nAll lung neoplasms are very aggressive, invasi ve and widely metastasizing commonly to liver, \nadrenals brain and bones; they also produce bioactive hormones and other products.  Cigarette smoking is closely linked to squamous cell ca, small cell ca and large cell ca but not \nto adenocarcinoma Adenocarcinoma \n\u2022 More common in women than men & develop in the periphery of the lung \n\u2022 Commonest lung cancer in non-smokers \n\u2022 Some adenocarcinoma arise from an area of pulmonary fibrosis/scar (old infarcts, \nasbestosis, or on healed TB scars) which are referred to as  scar cancers \n\u2022 Distant organ metastases occurs in over 50% of cases, especially to the brain \n\u2022 Have poor prognosis \u2013 5 year survival is 10 -12% \n \nSquamous cell carcinoma \n\u2022 More common in males than females \n\u2022 Strongly associated with cigarette smoking \n\u2022 Arise centrally in the major or  segmental bronchi & spread to hilar lymph nodes  \nin 70 \u2013 90% of cases or to distant nodes in 50 -60% of cases or to viscera \n\u2022 Has poor prognosis \u2013 5 year survival  is only 5 \u2013 8% \nSmall cell carcinomas"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 214, "chroma:document": "\u2022 Arise centrally in the major or  segmental bronchi & spread to hilar lymph nodes  \nin 70 \u2013 90% of cases or to distant nodes in 50 -60% of cases or to viscera \n\u2022 Has poor prognosis \u2013 5 year survival  is only 5 \u2013 8% \nSmall cell carcinomas \n\u2022 Very aggressive and early metastasizing \n\u2022 More common in males than females \n\u2022 Strongly associated to cigarette smoking \n\u2022 Centrally located \n\u2022 Commonly associated with paraneoplastic syndromes \n\u2022 Poor prognosis \u2013 5 year survival  is only 5 \u2013 8% \nLarge cell carcinomas \n\u2022 Anaplastic (undifferentiated) tumors, and occur in smokers"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 215, "chroma:document": "Internal Medicine \n \n 200\u2022 Central or peripheral locations \n\u2022 Metastasizes very rapidly and widely \n \nClinical features of lung carcinomas are variable.  \n\u2022 Some may present with local pulmonary symptoms. Others present with symptoms \nreferable to metastasis before local pulmonary symptoms.  \n\u2022 About 10 - 15% of lung tumors are detected by chance (a coin shaped lesion on chest \nx-ray). Manifestations could be related to local obstruction, local tumor invasion, distant \nmetastasis or ectopic hormone secretions by tumor cells (paraneoplastic syndromes).  \n\u2022 Local symptoms depend on the location of the tumor. When tumors are endobronchial \ncough, hemoptysis, stridor, wheezes, dyspnea, and nonresolving pneumonia may predominate. Pleuritic chest pain is common with peripheral  tumors.   \nLocal tumor invasion and obstruction  may result in  \n\u0083 Recurrent laryngeal nerve palsy causing hoarseness of voice \n\u0083 Phrenic nerve paralysis with diaphragm paralysis \n\u0083 Esophageal obstruction causing dysphagia \n\u0083 Superior vena cava obstruction  presenting with edema of the face \n\u0083 Pancoast syndrome is said to exist when apical lung tumors infiltrate the spinal \nnerves (C8 \u2013 T1) and cause shoulder pain, & cervical sympathetic nerves causing Horner\u2019s syndrome which is characterized by  absence of sweating, eyelid drooping and \npupillary constriction on the affected side. \u0083 Pericardial or pleural effusions, and bronchial obstruction leading to atelectasis, \npneumonia, and lung abscess"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3854e-7265-11ef-ba03-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 215, "chroma:document": "pupillary constriction on the affected side. \u0083 Pericardial or pleural effusions, and bronchial obstruction leading to atelectasis, \npneumonia, and lung abscess  \n \nParaneoplastic syndromes: \n\u2022 Occur in 10 \u2013 15% of bronchogenic carcinoma and the manifestations are related to \nectopic hormone secretions by tumor cells . The manifestations could be systemic, or \nrelated to different systems.  \n\u2022 Systemic symptoms such as anorexia, cachexia, weight loss and fever may occur in \n30% of cases.  \n\u2022 Another third of patients with bronchogenic carcinoma may present with endocrine \nmanifestations like hypercalcemia or hy pocalcaemia (from ectopic secretion of \nparathormone or calcitonin), Cushing\u2019s syndr ome (from ectopic secretion of ACTH),"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 216, "chroma:document": "Internal Medicine \n \n 201gyneacomastia (from ectopic secretion gonadotrophins)  and inappropriate release of \nADH causing Na+ & water retention.  \n\u2022 Additionally patients may present with clubbing, migratory thrombophlebitis, cerebellar \ndegeneration, neuropathies and myopathies such as Eaton-Lambert syndrome or \nmyasthenia gravis, anemia, and thrombocytopenic purpura.  \n \nDiagnosis \nScreening  \n\u2022 Is mandatory for men over 45 years, and those smoking more than 40 cigarettes/day \n\u2022 Screened tumors were resectable in 62% of cases, and nonscreened tumors were \nresectable only in 20%.  \n\u2022 Can be done by sputum cytology (to detect malignant cells), and CXR. CXR usually \ndemonstrates solitary pulmonary nodule and about 35% of such cases are due to \nbronchogenic carcinoma.  \nOther investigations commonly used to make the diagnosis and staging of lung tumors, most of which are available in specialized hospitals  \n\u2022 Lymph node biopsy from enlarged scalene or supraclavicular LN to detect \nmetastasis \n\u2022 Mediastinoscopy  \n\u2022 Bronchoscopy \n\u2022 Thoracenthesis to collect fluid for cytology \n\u2022 Pleural biopsy  \nManagement \n1.  Non-small cell carcinoma  \n\u2022 Surgical excision is curative for patient with ipsilateral lymph node involvement but \nwithout local/distant spread or contralateral lymph node involvement. \n\u0083 Intrathoracic disease - radiotherapy is palliative  \n\u0083 Pancoast  syndrome \u2013 radiotherapy/chemotherapy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38550-7265-11ef-a531-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 216, "chroma:document": "without local/distant spread or contralateral lymph node involvement. \n\u0083 Intrathoracic disease - radiotherapy is palliative  \n\u0083 Pancoast  syndrome \u2013 radiotherapy/chemotherapy \n\u0083 Extrathoracic disease \u2013 analgesics, radiot herapy, dexamethasone, obliteration of the \npleural cavity \n2. Small cell carcinoma  \n\u0083 By the time of diagnosis 95% of these tumors have metastasized  \n\u0083 Responsive for chemotherapy +/- radiotherapy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38551-7265-11ef-89c2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 217, "chroma:document": "Internal Medicine \n \n 2023. Bronchial adenomas, carcinoids need surgical resection \n Prevention \u2013 Cessation of  smoking \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nNeoplasms of the lung, pages 506-515. \n2)  Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Carcinoma of the lung, 169-172."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38552-7265-11ef-a6f3-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 218, "chroma:document": "Internal Medicine \n \n 203CHAPTER THREE \nDISEASES OF THE CA RDIOVASCULAR SYSTEM \n \nIntroduction  \nThe epidemic of cardiovascular diseases (CVDs) is accelerating globally over all regions and \nsocial classes. This is reflected in the high burden as well as the estimated escalation of those \nburdens over the next two decades. Most current global burden of CVD as well as all of the expected future augmentation of this burden is attributable to the change in the life style of \npeople. Even in the setting of a 'double burden' of disease which is experienced by the \ndeveloping countries, CVD contributes to a large proportion of morbidity and mortality. \n  \n A major study by WHO and Harvard School of Public Health published in 1996, predicted \nmassive rise of non-communicable diseases (NCDs ), most of this rise taking place in the \ndeveloping world. Already, according to the author of this report, adults under the age of 70 in Africa face a higher probability of death from NCD than their counterparts in the West. The number of people living with a disability is also set to increase.  \n A number of reasons underlie the expected rise in CVD in the developing world:  \n1. An overall increase in the population.  \n2. Improved life expectancy is leading to more person living to the middle age and beyond , \nwhich increase the risk of CVD \n3. Lifestyle transition:-increase urbanization, industrialization, globalization and change in \nnutritional habit."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38553-7265-11ef-929d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 218, "chroma:document": "2. Improved life expectancy is leading to more person living to the middle age and beyond , \nwhich increase the risk of CVD \n3. Lifestyle transition:-increase urbanization, industrialization, globalization and change in \nnutritional habit. \n4. Past or current nutrition deprivation in utero and early childhood may affect \ncardiovascular health trend. Lack of weight gain in the first year of life and low birth weight in spite of maternal weight gain have been linked to coronary disease in adult life.  \nThe causes of cardiovascular diseases in developing countries include:- \n\u2022 Chronic rheumatic heart disease \n\u2022 Hypertensive heart disease \n\u2022 Cardiomyopathies \n\u2022 Congenital heart disease.  \n\u2022 Ischemic heart disease:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38554-7265-11ef-a5ee-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 219, "chroma:document": "Internal Medicine \n \n 204There are indicators of increasing prevalence of ischemic heart diseases due to the existence of \nrisk factors in some segment of the population: hypertension, smoking, diabetes, hypercholesterolemia, and obesity.  \nThere are very few studies about CVD in Ethiopia.  The prevalence of rheumatic heart disease \nis 6/1000 in school children. Analysis of admi tted cases, to medical ICU of Tikur Anbessa \nHospital from 1988 to 1997 (in Addis Ababa, Ethiopia) has showed that acute myocardial infraction (AMI) was the third cause of ICU admission, and AMI annual admission increased \nconsistently. Moreover, from one year (1998 - 1999) autopsy study done in Minilik II Hospital to \ninvestigate the cause of sudden death in Addis Ababa, 70% (44/63) deaths were found to be due to coronary artery disease.   The implication of a CVD epidemic is devastating to developing countries in general and to \nEthiopia in particular, as there are few community-based programs and government policies to \nlimit the spread of deleterious health behaviors.  Therefore, there is a need to carry out appropriate preventive strategies to tackle the problem."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38555-7265-11ef-915e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 220, "chroma:document": "Internal Medicine \n \n 2051.  Rheumatic Fever  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define rheumatic fever \n2. Understand the etiologic agents of rheumatic fever  3. Understand  the Epidemiology of rheumatic fever  \n4. Describe the pathogenesis of rheumatic fever   \n5. Identify the clinical manifestation of rheumatic fever  6. Understand the diagnostic approach of rheumatic fever 7. Manage patients having  rheumatic fever  8. Design strategies for prevention of rheumatic fever  \n Background: Rheumatic fever causes chronic progressive damage to the heart and its valves \n.The association between sore throat and rheumatic fever was not made until 1880. The dramatic decline in the incidence of rheumatic fever in the developed world is thought to be \nlargely owing to antibiotic treatment of streptococcal infection, though it stated to decline before \nthe era of antibiotic, probably due improvement of socioeconomic status.  \n \nEpidemiology  \n\u2022 Even though the overall incidence of RF and  RHD in developed countries has sharply \ndeclined, rheumatic fever is the commonest cause of heart disease in the developing countries. In those countries, more than 50% of heart disease is accounted for rheumatic \nheart disease (RHD). Even in developing countries, the prevalence of RF and RHD varies \nbetween rural and urban areas. \n\u2022 The Prevalence of RF ranges from 3 to 12/1000 population in the developing country with the \npeak age of 5-15 years."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38556-7265-11ef-9c5c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 220, "chroma:document": "heart disease (RHD). Even in developing countries, the prevalence of RF and RHD varies \nbetween rural and urban areas. \n\u2022 The Prevalence of RF ranges from 3 to 12/1000 population in the developing country with the \npeak age of 5-15 years.  \n\u2022 In adult the risk developing of RF is about 3% following group A Streptococcal (GAS) \nPharyngitis with a recurrence rate of 1/6. \n\u2022 The high attack rate of group A Streptococcal pharyngitis in families, institutions and military \nrecruits is the result of contact among susceptible persons living closely enough to ensure droplet transmission.  \n\u2022 Risk factors for RF include low socioeconomic status with associated over crowded living \ncondition. However, RF is not associated with streptococcal skin infection (pyoderma)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38557-7265-11ef-96ff-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 221, "chroma:document": "Internal Medicine \n \n 206Pathophysiology \n\u2022 Acute rheumatic fever is a sequel of a previous group A streptococcal infection, usually \nof the upper respiratory tract. One beta-streptococcal serotype (e.g., M types 3, 5, 18, \n19, 24) is linked directly to acute rheumatic fever. Rheumatogenicity of GAS is important \nfactor as not all GAS pharyngitis is associated with development of rheumatic fever. \n\u2022 Rheumatic fever follows Lancefield \u03b2 hemolytic streptococcus pharyngitis within the \ninterval of 2-3 weeks.   \nThe mechanism is elusive, but the followings are proposed ones: \n\u2022 Dysfunction of the immune Response   \n\u2022 Antigenic Mimicry  \no Similarity between the carbohydrate moiety if GAS and glycoprotein of heart \nvalve  \no Molecular similarity between some Streptococcal antigens and sarcolema or \nother moiety of human myocardial cells. \n\u2022 Several host related factors have been identified to have operated in relation to specific \ngenetic function and difference in the immune response of individuals.    \n\u2022 The disease involves the heart, joints, ce ntral nervous system (CNS), skin, and \nsubcutaneous tissues. It is characterized by  an exudative and proliferative inflammatory \nlesion of the connective tissue, especially that of the heart, joints, blood vessels, and subcutaneous tissue. \nClinical Manifestation \nAcute rheumatic fever is associated with 2 distinct patterns of presentation. \n\u2022 The first pattern of presentation is sudden onset. It typically begins as polyarthritis 2-6"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38558-7265-11ef-a101-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 221, "chroma:document": "Clinical Manifestation \nAcute rheumatic fever is associated with 2 distinct patterns of presentation. \n\u2022 The first pattern of presentation is sudden onset. It typically begins as polyarthritis 2-6 \nweeks after streptococcal pharyngitis, and it  is usually characterized by fever and \ntoxicity. \n\u2022 The second pattern is insidious or subclinical and the initial abnormality is mild carditis. \n\u2022 Age at onset influences the order of complications. Younger children tend to develop \ncarditis first, while older patients tend to develop arthritis first. \nDiagnosis :  \nDiagnosis of acute rheumatic fever requires a high index of suspicion. Jones criteria developed by the American Heart Association is used to make the diagnosis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38559-7265-11ef-9b4c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 222, "chroma:document": "Internal Medicine \n \n 207Table III -1 -1 Jones criteria for the diagnosis of acute rheumatic fever.   \n \nMajor Criteria   Minor Criteria  \nCarditis Migratory ply arthritis  Sydenham\u2019s Chorea Subcutaneous nodules  \nErythema marginatum Clinical  \n     Fever      Arthralgia Laboratory   \n     Elevated acute phase reactants : ESR, \nCRP       Prolonged PR interval \nPlus \nSupportive evidence of recent Group A streptococcal infection ( e.g. positive throat culture or \nrapid antigen detection test ; and/or elevated or increasing streptococcal antibody test : ASO \ntiter , Anti DNAase , Anti NADase etc ) \nJAMA: 268, 2069, 1992. \n \n In addition to evidence of a previous streptococcal infection, the diagnosis of acute rheumatic \nfever requires 2 major Jones criteria or 1 major plus 2 minor Jones criteria. \n 1) Carditis,  (pancarditis here), occurs in as many as 40- 60% of patients and may manifest as:  \na) New murmur \nb) Cardiomegaly \nc) Congestive heart failure  d) Pericarditis with or without a pericardial rub and resolve without squeal of constriction.   e) Valvular disease: mitral and aortic valves  are commonly affected. Healing of rheumatic \nvalvulitis will lead into fibrous thickening and adhesion, resulting in progressive valvular damage. But, about 80% of mild valvulitis wo uld resolve. There is a risk of developing \nendocarditis on a damaged valve.  \n2) Migratory polyarthritis  occurs in 75% of cases and involves many joints at a time. The \nlarger joints are mainly affected."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3855a-7265-11ef-a384-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 222, "chroma:document": "endocarditis on a damaged valve.  \n2) Migratory polyarthritis  occurs in 75% of cases and involves many joints at a time. The \nlarger joints are mainly affected. \n3) Subcutaneous nodules : occur in 10% of patients and are edematous fragmented collagen \nfibers. They are firm painless nodules on the ext ensor surfaces of wrists, elbows, and knees."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3855b-7265-11ef-801b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 223, "chroma:document": "Internal Medicine \n \n 2084) Erythema marginatum occurs in about 5% of cases. The rash is serpiginous and long \nlasting. \n5) Sydenham\u2019s chorea  (i.e., St Vitus\u2019 dance) is a characteristic movement disorder that \noccurs in 5-10% of cases. Sydenham\u2019s chorea consists of rapid purposeless movements of \nthe face and upper extremities. Onset may be delayed for several months to years and may cease when the patient is asleep. \nLaboratory Studies:  \n\u2022 No specific confirmatory laboratory tests exis t. However, several laboratory findings indicate \ncontinuing rheumatic inflammation. Some are part of the Jones minor criteria. \n\u2022 Supportive evidences                        \no Streptococcal antibody tests disclose preceding streptococcal infection \n ASO titer: positive in 80% of cases   \n Anti DNAase \u03b2 & Anti hyaluronidase is positive in 95 % of cases \no Isolate group A streptococci via throat culture which has 20-40% yield.  \n\u2022 Laboratory minor criteria  \no Acute phase reactants (e.g. raised ESR and  C-reactive protein [CRP])   \no Leukocytosis may be seen. \no Anemia usually is caused by suppression of erythropoiesis. \no ECG: PR interval prolongation is seen in 25% of all cases but is neither specific to nor \ndiagnostic. \nTreatment  \nMedical therapy involves the following 5 areas:  \n1. Treat group A streptococcal infection  regardless of organism detection.  \nAll patients with acute rheumatic fever should be given appropriate antibiotic."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3855c-7265-11ef-9437-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 223, "chroma:document": "diagnostic. \nTreatment  \nMedical therapy involves the following 5 areas:  \n1. Treat group A streptococcal infection  regardless of organism detection.  \nAll patients with acute rheumatic fever should be given appropriate antibiotic.  \no Ampicillin 500 mg PO QID or Amoxicillin 500 mg PO TID  for 10 days or \no Benzathin penicillin 1.2 million IU IM single dose or  \no Erythromycin 500 mg PO QID for 10 days ( for penicillin allergic patient) \n2. Therapy for manifestation of acute rheumatic fever   \nArthritis: \no ASA is given at dose 2 gm four times per day for 4-6 weeks, no indication for \nsteroids.  \nCarditis  \nSevere Carditis with congestive heart failure should be treated with"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 224, "chroma:document": "Internal Medicine \n \n 209o Prednisolone 60 to 80 mg /day, to be tapered as patient improves  \no Start ASA during tapering phase to be given for 4-6weeks \no But both have no influence on the future development of valvular heart disease \n(VHD).   \n \nCongestive heart failure: Treats by conventional therapy such as digoxin  and diuretics.    \nSydenham\u2019s chorea : In majority of the cases it is self-limiting. But in symptomatic patients \nbenzodiazepines (diazepam) or phenothiazines ( haloperidol) may be helpful in controlling \nsymptoms.  \n3.  Administer secondary prophylaxis:  is indicated for all patients with rheumatic fever.  \nTaking benzathin penicillin is the first choice for better compliance and longer prevention.  \n\u2022 Benzathin penicillin 1.2 million IU IM every 4 weeks , but if the there is high risk of \nrecurrence, it can be given every 3weeks  \nAlternative antibiotics  \n\u2022 Oral penicillin V (250mg twice/day)  \n\u2022 Oral sulfadiazine (1g/day)  \nN.B. In a patient with an established RHD, it is  advisable to get the prophylaxis lifelong.  \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nRheumatic fever , pages 1977-1978"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 225, "chroma:document": "Internal Medicine \n \n 2102. Congestive Heart Failure  \n \nLearning objectives: at the end of this lesson the student will be able to  : \n1. Define congestive heart failure. 2. List the etiologic agents of congestive heart failure.   3. Understand the Epidemiology of congestive heart failure.  \n4. Describe the pathophysiology of congestive heart failure.   \n5. Identify the clinical manifestation of congestive heart failure. 6. Understand the diagnostic approach of congestive heart failure. 7. Manage patients with congestive heart failure. \n8. Design strategies for prevention of congestive heart failure . \n \nDefinition: \n\u2022 Heart failure is a clinical syndrome charac terized by inadequate systemic perfusion to meet \nthe body's metabolic demands as a result of abnormalities of cardiac structure or function.  \n\u2022 This may be further subdivided into either systolic or diastolic heart failure.  \no Systolic heart failure: there is reduced cardiac contractility \no Diastolic heart failure there is impaired cardiac relaxation and abnormal \nventricular filling.  \n\u2022 The body, sensing inadequate organ perfusion, activates multiple systemic neurohormonal \npathways which compensate initially by redistributing blood flow to vital organs but later \nexacerbate the patient's symptoms and lead to clinical deterioration. \n Etiology:"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 225, "chroma:document": "pathways which compensate initially by redistributing blood flow to vital organs but later \nexacerbate the patient's symptoms and lead to clinical deterioration. \n Etiology:  \nThe most common cause of heart failure is left ventricular systolic dysfunction (about 60% to 70% of patients). The following are some of the underlying causes of heart failure . \n1) Decreased contractile function  \na. Valvular heart disease  \nb. Coronary Heart Disease : Myocardial ischemia \nc. Myocardial Disease : C adiomyopathy , Myocarditis  \n2) Increased after load   \na. Acute systemic hypertension  \n3) Abnormalities in preload"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 226, "chroma:document": "Internal Medicine \n \n 211a. Excessive preload  \nb. Reduced preload  \n4) Reduced compliance states: Constrictive pericarditis , Restrictive cardiomyopathy \nPrecipitating factors for heart failure:  \n\u2022 These are relatively acute disturbances t hat place an additional load on a myocardium \nthat is chronically and excessively burdened.  \n\u2022 In compensated state patients are asympt omatic; however as patients have little \nadditional reserve, they become symptomatic in the presence of these precipitating factors.  \n\u2022 Knowing the precipitating factors is important because most of the time they are \ntreatable and the cardiac function improves when these precipitating factors are treated \nor avoided. \nThe most important precipitating factors may be represented with the mnemonic, HEART \nFAILES    \nH- Hypertension (systemic)  \nE- Endocarditis (infections)  \nA- Anemia R- Rheumatic fever and myocarditis  T- Thyrotoxicosis and pregnancy  \nF- Fever (infections)  \nA- Arrhythmia  I- infarction (myocardial)  L- Lung   infection  E- Embolism (pulmonary)  \nS- Stress (emotional, physical, environment, dietary, fluid excess)  \nPathophysiology  \n\u2022 In left ventricular systolic dysfunction, regar dless of the etiology, cardiac output is low \nand pulmonary pressures are high, leading to pulmonary congestion. As a result, a series of adaptive mechanisms are activated. Initially, as a direct result of inadequate"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 226, "chroma:document": "and pulmonary pressures are high, leading to pulmonary congestion. As a result, a series of adaptive mechanisms are activated. Initially, as a direct result of inadequate \ncardiac output and systemic perfusion, the body activates several neurohormonal pathways in order to increase circulating blood volume.  \n\u2022 With continuous neurohormonal stimulation, the left ventricle undergoes remodeling with \nleft ventricular dilatation and hypertrophy, such that stroke volume is increased without"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 227, "chroma:document": "Internal Medicine \n \n 212an actual increase in ejection fraction. Thi s is achieved by myocyte hypertrophy and \nelongation. However, left ventricular chamber dilatation causes increased wall tension, \nworsens subendocardial myocardial perfusion, and may provoke ischemia in patients \nwith coronary atherosclerosis. Furthermore, left ventricular chamber dilatation may \ncause separation of the mitral leaflets and mitral regurgitation with worsening of pulmonary congestion. Enhanced neurohormonal stimulation of the myocardium also causes apoptosis, or programmed cell death, leading to worsening of ventricular \ncontractility. \n \nClinical Manifestations   \n\u2022 Progressive dyspnea which initially occurs with exertion and later occurs at rest. \nDyspnea on exertion has been found to be the most sensitive complaint, yet the specificity for dyspnea is less than 60%. \n\u2022 Orthopnea and paroxysmal nocturnal dyspnea (PND) are more specific symptoms; \nhowever, sensitivity for orthopnea and PND is only 20-30%. \n\u2022 Cough productive of pink, frothy sputum is highly suggestive of CHF. Wheezing may \nalso occur. \n\u2022 Peripheral edema and ascites  \n\u2022 Nonspecific complaints include the following: easy fatigability , light headedness , \nmalaise  anxiety abdominal pain , nausea etc \n\u2022 Past medical history  may include the following: rheumatic fever , alcohol use, \nhypertension , angina , previous history of  myocardial infarction  and familial history of heart disease \nPhysical findings:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38563-7265-11ef-b468-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 227, "chroma:document": "\u2022 Past medical history  may include the following: rheumatic fever , alcohol use, \nhypertension , angina , previous history of  myocardial infarction  and familial history of heart disease \nPhysical findings:  \n\u2022 Tachycardia and Tachypnea and signs of respiratory distress including use of accessory \nmuscles of respiration \n\u2022 Jugular venous distention (JVD) frequently is present and engorged neck veins  \n\u2022 Pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle \n[LV] function \n\u2022 Wheezing or rales may be heard on lung auscultation and there may be bilateral basal \ndullness. \n\u2022 Apical impulse frequently is displaced laterally \n\u2022 Cardiac auscultation may reveal aortic or mitral valvular abnormalities, S\n3 or S 4."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38564-7265-11ef-8795-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 228, "chroma:document": "Internal Medicine \n \n 213\u2022 Skin may be diaphoretic or cold, gray, and cyanotic \n\u2022 Lower extremity edema also may be noted, especially in the subacute process. \n \nNew York Heart Association Heart Failure Classifi cation scheme is used to assess the severity \nof a patient's functional limitations and correlates fairly well with cardiovascular prognosis.   Table III -2-1: New York Heart Association Heart Failure Symptom Classification System  \n \nGrade   Symptoms  \nI No symptom limitation with ordinary physical activity  \nII Ordinary physical activity somewhat limited by dyspnea (i.e., \nlong distance walking, climbing 2 flights of stairs)  \nIII Exercise limited by dyspnea at mild workloads (i.e., short distance walking, climbing one flight of stairs)  \nIV Dyspnea at rest or with very little exertion  \n \nDiagnostic    Workup  \n\u2022 Chest x-ray :  the main findings are cardiomegally, pulmonary edema, and pleural \neffusion. \n\u2022 Echocardiography : may help identify valvular abnormalities, ventricular dysfunction, \ncardiac temponade, pericardial constriction, and pulmonary embolus. \n\u2022 Electrocardiogram (ECG) : is a nonspecific tool but may be useful in diagnosing \nconcomitant cardiac ischemia, prior myocardi al infarction (MI), cardiac dysrhythmias, \nchronic hypertension, and other causes of left ventricular hypertrophy.   \n\u2022 Other laboratory tests : Hemoglobin, Urinalysis, BUN, Creatinine  \n Management of Heart Failure  \nPrinciples of management"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 228, "chroma:document": "chronic hypertension, and other causes of left ventricular hypertrophy.   \n\u2022 Other laboratory tests : Hemoglobin, Urinalysis, BUN, Creatinine  \n Management of Heart Failure  \nPrinciples of management  \n1. Identify and treat the precipitating factors \n2. Control the congestive state  \n3. Improve myocardial performance"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 229, "chroma:document": "Internal Medicine \n \n 2144. Prevention of deterioration of myocardial function (slowing  progression of heart \nfailure )  \n5. Treat the underlying cause  \nA. General measures :  \n\u2022 Dietary sodium restriction  should be implemented in all patients with congestive \nheart failure to < 3 g/d.  \n\u2022 Activity and life style modification   :  \no Meals should be small in quantity but more frequent. \no Reduce anxiety and emotional stress \no Avoid excess physical exertion ( NB exer cise may be advised within the limit of \nthe patient\u2019s cardiac function )  \no Weight loss in encouraged in obese patients. \no Cessation of smoking  \no Avoid other CVD risk factors  \nB. Control of the Congestive state  \nDiuretics: are useful in relieving congestion and reduce or prevent edema.  \nMost patients with heart failure have some degree of symptomatic congestion and \nbenefit from diuretic therapy.  \nUsually a loop diuretic is required, with the addition of a Thiazide diuretic in patients refractory to the loop diuretic alone.  1. Furosomide :   Initial dose 20-40 mg PO 1-2 X daily or 20 mg IV \nMaximum dose 400 mg PO/day or 80 mg IV /day \n2. Hydrochlorothiazide :  Initial dose 25 mg PO/day \nMaximum dose 100 mg PO/day  \n\u2022 N.B . Loop and thiazide diuretics are useful for symptomatic relief; however they \nhave not been shown to improve survival. \n\u2022 Side effects : Azotemia, hypokalemia, me tabolic alkalosis and elevation of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38567-7265-11ef-8dfa-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 229, "chroma:document": "Maximum dose 100 mg PO/day  \n\u2022 N.B . Loop and thiazide diuretics are useful for symptomatic relief; however they \nhave not been shown to improve survival. \n\u2022 Side effects : Azotemia, hypokalemia, me tabolic alkalosis and elevation of \nneurohormones   3. Spirinolactone : is an aldosterone inhibitor, reduces mortality in patients with \nadvanced heart failure. This drug should be reserved for patients with moderately \nsevere or severe heart failure  ( class IV symptoms ) \nInitial dose: 25 mg PO/day or every other day  \nMaximum dose: 50 mg PO BID or higher"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 230, "chroma:document": "Internal Medicine \n \n 215Side effects :  \n\u2022 Hyperkalemia  is common so monitoring K+ the serum potassium level is \nessential. As a result, this drug should not be used in patients with a \ncreatinine above 2.5 mg/dl.  \n\u2022 Gynecomastia  in men is the other side effect of this drug.  \n \nC. Enhancement of Myocardial contractility : \n1) Digoxin:  is a drug which has :  \n\u2022 Inotropic effect  and acts by inhibiting the Na+-K+ ATPase and increase \nintracellular calcium. This increases myocardial contractility. \n\u2022 Neurohormonal modulation  of centrally mediated parasympathomimetic and \nsympatholytic activity.  By doing so it blocks the AV node and delays AV \nconduction. \no Initial dose : 0.125 mg PO/day    \no Maximum dose : 0.25 mg PO/day  \n\u2666 The use of digoxin can improve symptoms, reduce the duration  and the need for \nhospitalization in patients with  heart failure,, but has no effect on long term survival. \n\u2666 Digoxin is renally excreted and so dose adjustment is necessary in renal failure.  \n\u2666 A low dose of the drug (0.125 mg daily) should be prescribed, especially in women.  \n\u2666 Digoxin use is recommended for patients with left ventricular systolic dysfunction, \nparticularly if they have atrial fibrillation.  \n\u2666 It is relatively contraindicated in some cardiac disease  \no Cardiac outflow obstruction in  MS (in the absence of atrial fibrillation  ) \no Corpulmonale  \n\u2666 Because of it narrow window of safety, digoxin is associated with different Side \neffects including:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 230, "chroma:document": "o Cardiac outflow obstruction in  MS (in the absence of atrial fibrillation  ) \no Corpulmonale  \n\u2666 Because of it narrow window of safety, digoxin is associated with different Side \neffects including: \no GI : anorexia , nausea, vomiting , weight loss \no Neuralgia, delirium \no Yellow vision  \no Gynecomastia \no Arrhythmias of different types"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 231, "chroma:document": "Internal Medicine \n \n 216o Electrolyte on toxicity is suspected, digoxin should be withheld, and has \nobserve for some days before reinitiate with a lower dose. One should also \ngive KCl, as hypokalemia is increase digoxin toxicity.  \n2) Vasodilators:  may be useful in patients with severe acute heart failure who demonstrate \nsystemic vasoconstriction despite ACE inhibitor therapy. Through vasodilatation they reduce the peripheral resistance and after load and improve cardiac performance. Hydralazine:  Initial dose:   25 mg PO TID \n              Maximum dose: 150 mg PO QID. \nIsosorbide dinitrate : Initial dose 10 mg PO TID \n               Maximum dose: 80 mg PO TID \n\u2666 Hydralazine and nitrates in combination are effective afterload reducing agents \nused in ACE-intolerant patients.  \nD. Prevention of deterioration of Myocardial function :  \n\u2022 The following drugs prevent deterioration in myocardial function by inhibiting the \nneurohumeral mechanism which causes cardiac remodelling and progression of heart failure. \n1) Angiotensin Converting Enzyme (ACE) Inhibitors \nAfterload reduction and neurohormonal modulation with ACE inhibitors ( e.g. Captopril, Enalapril, etc)    have been shown to improve mortality, symptoms, and hospitalizations.  \nThe dose of ACE inhibitors should be titrated to the maximum that can be tolerated symptomatically or the target dose. . \nInitial dose: Captopril 6.25 mg PO/day or every other day  \n          Enalapril 2.5 mg PO BID"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3856b-7265-11ef-afef-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 231, "chroma:document": "The dose of ACE inhibitors should be titrated to the maximum that can be tolerated symptomatically or the target dose. . \nInitial dose: Captopril 6.25 mg PO/day or every other day  \n          Enalapril 2.5 mg PO BID   \nMaximum dose: Captopril 50-100 mg PO QID         Enalapril 10- 20 mg PO BID \nSide effects of ACE inhibitors \no Angioedema  \no Acute renal failure I patients with bilateral renal artery stenosis. It is \ncontraindicated in a patient with creatinine >3mg/dl \no Cough  \nContraindications: \no Angioedema or anuric renal failure  \no Pregnancy  \no Hypotension"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3856c-7265-11ef-8a12-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 232, "chroma:document": "Internal Medicine \n \n 217o Creatinine > 265 mol/L (3mg/dl)  \nN.B The first two side effects are serious and necessitate immediate cessation of the \ndrug.  \n \n2) Angiotensin-II Receptor blocker  \nThese drugs are useful in patients who cannot tolerate ACE inhibitors due to different \nside effects like cough angioedema and lukopenia. \nLasortan:  Dose : - 25-50 mg once 0r twice daily \n3) Beta Adrenorecepter  blockers  \nAdministration of these drugs with gradually increasing dose has been reported to \nimprove symptoms of heart failure, the need fo r hospitalization  and reduce mortality. \nThey are indicated to moderately severe heart failure.  \nThey are not indicated in unstable heart failure , hopotensive states , severe fluid \noverload , sinus bradycardia , AV block and asthma. \nMetoprololol:  Initial dose 6.25 mg PO BID \n     Maximum dose: 75 mg PO BID \n   \nReferences:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Heart \nfailure, pages 1367-1377. \n2. Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nCongestive Heart failure,1-6."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3856d-7265-11ef-a6f2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 233, "chroma:document": "Internal Medicine \n \n 2183. Valvular Heart Diseases (VHD)   \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define valvular heart diseases. \n2. List the etiologies of valvular heart diseases.  3. Understand the Epidemiology of valvular heart diseases.  \n4. Describe the pathogenesis of valvular heart diseases.  \n5. Identify the clinical manifestation of different valvular heart diseases.  6. Understand the diagnostic approach of valvular heart diseases. 7. Understand the management of patients having valvular heart diseases.   \nIntroduction  \n\u2022 Valvular heart disease from chronic rheumatic fever is still the commonest cardiac \ndisease in the developing world, occurring at the younger age. \n\u2022 It causes significant morbidity and mortality due to lack of appropriate preventive and \ntherapeutic intervention.  \n\u2022 It accounts for 42 % of cardiac patients attending hospitals in Ethiopia.  \n\u2022 Generally, patients with stenotic valvular lesions can be monitored clinically until \nsymptoms appear. In contrast, patients with regurgitate valvular lesions require careful echocardiographic monitoring for left ventricular function and may require surgery even if no symptoms are present. \n\u2022 Aside from antibiotic prophylaxis, very little medical therapy is available for patients with"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3856e-7265-11ef-9302-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 233, "chroma:document": "\u2022 Aside from antibiotic prophylaxis, very little medical therapy is available for patients with \nvalvular heart disease; surgery is the treatment for most symptomatic lesions or for lesions causing left ventricular dysfunction even in the absence of symptoms. However surgical management is unavailable for most patients who are suffering from valvular \nheart diseases in Ethiopia.   \n \nAortic Stenosis (AS) \nAortic stenosis could be caused by \n\u2022 Rheumatic carditis \n\u2022 Congenital stenosis of aortic valve or \n\u2022 Senile/calcific aortic stenosis which is id iopathic results in calcification and degeneration \nof the aortic leaflets."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3856f-7265-11ef-8471-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 234, "chroma:document": "Internal Medicine \n \n 219\u2022 Persons born with a bicuspid aortic valve are predisposed to develop aortic stenosis. \n \nClinical features   \n Initially there is an extended latent period duri ng which the patient is asymptomatic. This is \nfollowed by the classic symptoms of AS: \n\u2022 Angina \n\u2022 Exertional syncope and  \n\u2022 Dyspnea \n Physical Examination  \n\u2022 The most common physical sign of aortic stenosis is a systolic ejection murmur at left at \nthe 2\nnd intercostals space that radiates to the neck. In mild aortic stenosis, the murmur \npeaks early in systole, but as the severity  of stenosis increases, the murmur peaks \nprogressively later in systole and may become softer as cardiac output decreases \n\u2022 As the stenosis worsens, the aortic component of the second heart sound may become \ndiminished.  \n\u2022 The timing and amplitude of the carotid pulse correlate with the severity of aortic \nstenosis. Later in the disease, the carotid upstrokes become diminished and delayed \n(parvus et tardus)  \n Echocardiography  \n\u2022 Echocardiography with Doppler provides an accurate assessment of aortic valve area \nand transvalvular gradient and also can be used to estimate left ventricular hypertrophy and ejection fraction. \n \nChest X-ray : may demonstrate valve calcification.  \nManagement  \nMedical Therapy : \n\u2022 Is not effective and treatments with digitalis or cautiously administered diuretics may only \nreduce symptoms.  \n\u2022 Patients with severe aortic stenosis should limit vigorous physical activity."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 234, "chroma:document": "Management  \nMedical Therapy : \n\u2022 Is not effective and treatments with digitalis or cautiously administered diuretics may only \nreduce symptoms.  \n\u2022 Patients with severe aortic stenosis should limit vigorous physical activity.  \n\u2022 Patients with aortic stenosis are at moderate risk for development of endocarditis and \nshould receive endocarditis prophylaxis before selected procedures."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38571-7265-11ef-a304-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 235, "chroma:document": "Internal Medicine \n \n 220Surgical Therapy   \n\u2022 Aortic valve replacement is the only effectiv e treatment that will relieve this mechanical \nobstruction.  \nPrognosis:  \n\u2022 The survival of patients with aortic stenosis is  nearly normal until the onset of symptoms, \nwhen survival rates decrease sharply.  \n\u2022 Although the rate of progression of aortic stenosis is variable and difficult to predict \napproximately 75 percent of patients with aor tic stenosis will be dead three years after \nthe onset of symptoms if the aortic valve is not replaced.  \n \nAortic Regurgitation (AR)  \nAortic regurgitation results from disease affecting the aortic root or aortic leaflets, preventing \ntheir normal closure.  \nCommon causes of aortic regurgitation include: \n\u2022 Endocarditis \n\u2022 Rheumatic fever \n\u2022 Collagen vascular diseases \n\u2022 Aortic dissection   \n\u2022 Syphilis \n\u2022 Bicuspid aortic valves are also prone to regurgitation. \n\u2666 In chronic aortic regurgitation, the stroke volume  is increased, which in turn causes systolic \nhypertension, high pulse pressure and increased afterload. The afterload in aortic \nregurgitation may be as high as that occurring in aortic stenosis.  \n\u2666 Patients may be asymptomatic until severe left ventricular dysfunction has developed. The \ninitial signs of aortic regurgitation are subtle and may include decreased functional capacity or fatigue. As the disease progresses, the typical presentation is that of left-sided heart failure: orthopnea, dyspnea and fatigue."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 235, "chroma:document": "initial signs of aortic regurgitation are subtle and may include decreased functional capacity or fatigue. As the disease progresses, the typical presentation is that of left-sided heart failure: orthopnea, dyspnea and fatigue.  \n\u2666 Systolic dysfunction is initially reversible, with full recovery of left ventricular size and function \nafter aortic valve replacement. Over time, how ever, progressive chamber enlargement with \ndecreased contractility make recovery of le ft ventricular function and improved survival \nimpossible, even with surgery."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 236, "chroma:document": "Internal Medicine \n \n 221Physical Examination :  \n\u2022 A diastolic blowing murmur heard along the left sternal border is characteristic of aortic \nregurgitation. A diastolic rumble may also be heard over the apex.  \n\u2022 The peripheral signs of hyperdynamic circulation indicate severe disease. Some of these \ninclude: \no Wide pulse pressure  \no Collapsing pulse ( water hammer pulse )   \no Quincke's pulse (alternating blanching and erythema of the nailbed with gentle \npressure applied)   \no De musset's sign (head bobbing) \no Pistol shot over the femoral artery  \nEchocardiography  \n\u2022 Echocardiography with Doppler ultrasonography provides information about aortic valve \nmorphology and aortic root size, and a semiquantitative estimate of the severity of aortic \nregurgitation .It provides valuable information about left ventricular size and function. \n \nManagement   \nMedical Treatment   \n\u2022 Diuretics  \n\u2022 Digoxine: may be indicated in patients with severe regurgitation and dilated left ventricle \nwithout frank LV failure. \n\u2022 Salt restriction  \n\u2022 Vasodilators: afterload reduction with vasodilators has been shown to improve left \nventricular performance and reduce aortic regurgitation. ACE inhibitors are the preferred \nvasodilators. Therapy with long acting nifedipine in particular has been shown to delay \nthe need for surgery by two to three years. \n\u2022 Endocarditis prophylaxis is essential for all patients with AR as their infection tolerance is \npoor."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38574-7265-11ef-8281-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 236, "chroma:document": "vasodilators. Therapy with long acting nifedipine in particular has been shown to delay \nthe need for surgery by two to three years. \n\u2022 Endocarditis prophylaxis is essential for all patients with AR as their infection tolerance is \npoor. \n \nSurgical management : aortic valve replacement is the definitive treatment for patients with AR. \nThere are two important points to consider in deciding the timing of surgery. \n1. Patients with chronic AR usually don\u2019t become symptomatic until after the development \nof myocardial dysfunction"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38575-7265-11ef-94d8-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 237, "chroma:document": "Internal Medicine \n \n 2222. When delayed too long, surgical treatment often does not restore normal LV function. \n\u2022 There for appropriate timing is necessary for surgical intervention.  \nAortic regurgitation should be corrected if the symptoms are more than mild. Compelling \nevidence supports surgical correction before the onset of permanent left ventricular damage, even in asymptomatic patients.\n \n \nMitral Stenosis (MS)  \n\u2022 Mitral stenosis is sequelae of rheumatic heart disease primarily affecting women.  \n\u2022 Mitral stenosis has a progressive, lifelong course that is slow and stable in the early \nyears, with rapid acceleration later in life.  \n\u2022 It is very common in the developing countri es manifesting below the age of 20 whereas \nthere is generally a latent period of 20 to 40 years between the occurrence of rheumatic \nfever and of mitral stenosis in developed countries.  \n\u2022 Elevated left atrial pressure eventually causes pulmonary vasoconstriction, pulmonary \nhypertension and compromise of right ventricular function.  \n\u2022 Many patients remain asymptomatic until atrial fibrillation develops or until pregnancy \noccurs, when there is increased demand on the heart.  \n\u2022 Symptoms are generally those of left-sided heart failure: dyspnea on exertion, orthopnea \nand paroxysmal nocturnal dyspnea. Patients may also present with hemoptysis, signs of \nright-sided heart failure, and embolic phenomena like stroke.  \nPhysical Examination"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38576-7265-11ef-9467-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 237, "chroma:document": "and paroxysmal nocturnal dyspnea. Patients may also present with hemoptysis, signs of \nright-sided heart failure, and embolic phenomena like stroke.  \nPhysical Examination  \n\u2022 An apical rumbling, mid-diastolic murmur is characteristic and will immediately follow an \nopening snap, if present. The rumble is loudest in early diastole but, in patients with mild mitral stenosis or mitral stenosis with low cardiac output, the murmur may be difficult to \nhear. It can be accentuated by placing the patient in the left lateral decubitus position \nand using the bell of the stethoscope. Brief exercise (such as walking in the hallway) may also accentuate the murmur.  \n\u2022 A loud first heart (S1) sound is common.  \n\u2022 A right ventricular lift, elevated neck veins, ascites and edema are later signs of right \nventricular overload with pulmonary hypertension."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38577-7265-11ef-92fd-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 238, "chroma:document": "Internal Medicine \n \n 223Complication of MS \n\u2022 Atrial fibrillation \n\u2022 Thromboembolism \n\u2022 Right sided hear failure  \nEchocardiography \n\u2022 Echocardiography is the study of choice for diagnosing and assessing the severity of \nmitral stenosis.  \nChest X-ray  may show left atrial enlargement and sign of pulmonary congestions.  \nManagement  \nIn asymptomatic patients   \n\u2022 Annual evaluation (history and physical exam ination, as well as a chest x-ray and \nECG).  \n\u2022 Endocarditis prophylaxis \n\u2022 Secondary prophylaxis for reumatic fever \nIn patients with symptoms : \nMedical treatment \n\u2022 Diuretics may be helpful in reducing left atrial pressure and decreasing symptoms.   \n\u2022 Digoxin: is indicated for patients with atrial fibrillation to control the heart rate, since \ntachycardia will further decrease left ventricular filling, reduce cardiac output and \nincrease left atrial pressure, leading to more symptoms.  \n\u2022 Anticoagulants such as Warferin may be indicated in patients with Left atrium and \natrial fibrillation. \nSurgical management:  improves survival and reduce symptoms.  \n\u2022 Open commissurotomy or  \n\u2022 Mitral valve reconstruction or  \n\u2022 Mitral valve replacement.  \n \nMitral Regurgitation (MR)  \nCauses of chronic mitral regurgitation include: \n\u2022 Rheumatic fever \n\u2022 Infective endocarditis \n\u2022 Degenerative valvular disease (mitral valve prolapsed).  \n\u2022 Myocardial infarction affecting papillary muscles."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38578-7265-11ef-b3e7-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 239, "chroma:document": "Internal Medicine \n \n 224Pathophysiology: \nChronic mitral regurgitation is a state of volume overload leading to the development of left \nventricular hypertrophy. The left atrium also enl arges to accommodate the regurgitate volume. \nThis compensated phase of mitral regurgitation varies in duration but may last many years. The \nprolonged state of volume overload may eventually lead to decompensate mitral regurgitation. This phase is characterized by impaired left ventri cular function, decreased ejection fraction and \npulmonary congestion.  \nThe common symptoms are: \n\u2022 Fatigue, Exertional dyspnea and orthopnea are the most common complaints. \n\u2022 Right sided heart failure with painful hepatic congestion, peripheral edema may occur in \npatients with MR who have associated pulmonary hypertension . \nPhysical Examination   \n\u2022 A soft first heart sound ( S1 is generally absent ) and a widely split second heart sound \nmay be present.  \n\u2022 An S 3 gallop  indicates severe disease but does not necessarily indicate heart failure \n\u2022 There may be displacement of the left ventricular impulse \n\u2022 A holosystolic murmur that may radiate to the axilla, the upper sternal borders or the \nsubscapular region is apparent on physical examination.  \nEchocardiography  \n\u2022 Echocardiography can be used to determine the etiology and morphology of mitral \nregurgitation, which are important in determining suitability for mitral valve repair."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38579-7265-11ef-8232-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 239, "chroma:document": "subscapular region is apparent on physical examination.  \nEchocardiography  \n\u2022 Echocardiography can be used to determine the etiology and morphology of mitral \nregurgitation, which are important in determining suitability for mitral valve repair.  \nChest X-ray : Enlargement of LA and LV , Pulmonary venous congestion and interstitial edema \nand Kerley-B lines .  \nManagement  \nMedical Treatment: \n\u2022 Diuretics  \n\u2022 Digoxin: may be indicated in patients with severe regurgitation and dilated left ventricle \nwithout frank LV failure. \n\u2022 Salt restriction  \n\u2022 Vasodilators: afterload reduction with vasodilators has been shown to improve left \nventricular performance.. ACE inhibitors are the preferred vasodilators. \n\u2022 Treatment of atrial fibrillation if it occurs  \n\u2022 Endocarditis prophylaxis is important essential.."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3857a-7265-11ef-97dc-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 240, "chroma:document": "Internal Medicine \n \n 225Surgical Treatment:  Mitral valve replacement  is the definitive treatment.   \n\u2022 In patients with chronic mitral regurgitation, left ventricular damage can occur while the \npatient remains asymptomatic. Therefore, surgery is indicated if left ventricular \ndysfunction has begun to develop, even in the absence of symptoms. \n\u2022 Patents with MR who are asymptomatic  and whose LV function are normal are not \nconsidered to be candidates for surgical treatment. \nTricuspid Regurgitation (TR) \n\u2022 TR is functional and secondary to marked dilatation of tricuspid annulus The most \ncommon cause of TR is pulmonary hypertension as result of left sided cardiac failure or pulmonary parenchymal/vascular disease.  \n\u2022 Less common causes include rheumatic HD, right sides myocardial infarction , and \nendocarditis in IV drug abusers.  \nClinical features  \n\u2022 In patients with pulmonary HTN symptoms of pulmonary congestion diminish, but the \nsymptoms of right sided heart failure are intensified such as peripheral edema and ascites.  \n\u2022 Patients will have prominent jaguar venous distention  \n\u2022 Holosystolic murmur at the left lower sternal border.  \n\u2022 Pulsatile liver and  \n\u2022 More prominent ascites than edema is a common finding. \nEchocardiography  \n\u2022 It is a very useful study, and it differentiates primary from secondary TR. \nManagement: \n\u2022 Treatment of the underlying cause of heart failure usually reduces the severity of \nfunctional TR."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3857b-7265-11ef-8484-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 240, "chroma:document": "Echocardiography  \n\u2022 It is a very useful study, and it differentiates primary from secondary TR. \nManagement: \n\u2022 Treatment of the underlying cause of heart failure usually reduces the severity of \nfunctional TR.  \n\u2022 Surgical treatment as indicated for primary TR.  \nMitral Valve Prolapse  \n\u2022 Mitral valve prolapse occurs when varying por tions of one or both leaflets of the mitral \nvalve extend or protrude abnormally above the mitral annulus into the left atrium.  \n\u2022 MVP has different causes \no Redundant or excessive  mitral valve tissue  \no Congenital diseases such as Marfan\u2019 s syndrome , osteogenesis imperfecta."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3857c-7265-11ef-b872-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 241, "chroma:document": "Internal Medicine \n \n 226\u2022 Although the prevalence of mitral valve prolapse was once thought to be as high as 15 \npercent in the general population, more recent studies using new echocardiographic \ncriteria for diagnosis have suggested a prevalence of approximately 2.4 percent.  \nClinical futures  \n\u2022 MVP is more common in females and more common in the age group of 14-30. \n\u2022 The clinical course is often benign \n\u2022 Most patients are asymptomatic and may remain so for their entire lives. \n\u2022 Some patients may manifest with features of Mitral regurgitation  \n\u2022 Arrhythmias like premature ventricular contractions and ventricular tacycardias may \noccur as complications. \n\u2022 The mid-systolic click, often accompanied by a late systolic murmur, is the auscultatory \nhallmark of mitral valve prolapse.  \nManagement  \n\u2022 Asymptomatic patients may need only reassurance \n\u2022 Symptomatic patients with thickening of mitral valve  \no Endocarditis prophylaxis is  \no B- blockers sometimes may relive chest pain \n\u2022 Sever symptoms from secondary MR: surgical treatment may be needed ( mitral valve \nrepair and or rarely replacement. ) \nSummery  \n\u2022 Even though the definitive management for mo st valvular heart diseases is surgical \nintervention to correct the underlying valvular abnormality ,  in the current Ethiopian \nsetup, surgical interventions are not affordable and not available in the country. Hence the general management is treatment of the congestive heart failure state."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3857d-7265-11ef-9759-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 241, "chroma:document": "setup, surgical interventions are not affordable and not available in the country. Hence the general management is treatment of the congestive heart failure state.  \n\u2022 The onset of symptoms in the developing world occurs at an earlier age because of \nrepeated attack of recurrent rheumatic fever. Increased left atrial pressure and decreased cardiac output produce the symptom. Therefore both primary and secondary preventions are paramount importance to reduce the morbidity and mortality  \n\u2022 Great progress has been made in improving rates of morbidity and mortality in patients \nwith valvular heart disease. Successful management of patients with valvular heart disease requires an evidence-based approach to echocardiography and to surgical \nintervention."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3857e-7265-11ef-8312-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 242, "chroma:document": "Internal Medicine \n \n 227\u2022 Echocardiography should assess not only the valvular lesion but also the compensatory \nchanges of the heart in response to the lesion.  \n\u2022 Timing of surgical intervention often correlates with outcome.  \n\u2022 Most patients with acquired valvular heart disease are at risk for developing endocarditis \nand should receive prophylactic antibiotics.  \nReferences:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Valvular \nHeart Diseases, pages 1390-1402. \n2. Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nValvular Heart Diseases, 29-37."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3857f-7265-11ef-b34f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 243, "chroma:document": "Internal Medicine \n \n 2284.  Infective Endocarditis  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1) Define valvular heart Infective endocarditis. 2) List the etiologic agents of Infective endocarditis.  3) Describe the different types of Infective endocarditis. \n4) Understand the Epidemiology of Infective endocarditis.  \n5) Describe the pathogenesis of Infective endocarditis.  6) Identify the clinical manifestation of Infective endocarditis.  7) Understand the diagnostic approach of Infective endocarditis. \n8) Understand the management of patients having Infective endocarditis .  \n \nDefinition:  Infective endocarditis (IE) is an infection of the endocardial surface of the heart. The \nintracardiac effects of this infection include severe valvular insufficiency, which may lead to intractable congestive heart failure and myocardial abscesses.  \nInfective endocarditis affects not only the heart,  but also produces a wide variety of systemic \nsigns and symptoms through several mechanisms, including both sterile and infected emboli \nand a variety of immunological phenomena.  \n \nClassification of Infective endocarditis:  depending on the type of valve affected \n1. Native valve endocarditis (NVE) : endocarditis that may develop on natural valve. The \naffected valve may be damaged or normal.  \n2. Prosthetic valve endocarditis : is when the endocarditis develops on \nprosthetic/\u2019artificial\u2019 valve. \n3. Endocarditis in intravenous drug abuser (IVDA)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38580-7265-11ef-be41-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 243, "chroma:document": "affected valve may be damaged or normal.  \n2. Prosthetic valve endocarditis : is when the endocarditis develops on \nprosthetic/\u2019artificial\u2019 valve. \n3. Endocarditis in intravenous drug abuser (IVDA). \n\u2022 There is a marked rise in cases of prosthetic valve endocarditis and endocarditis in IV drug \nabusers in different parts of the world. However Native valve endocarditis is the commonest \ntype of Infective endocarditis in Ethiopia and other developing countries. \n\u2022 The classic clinical presentation and clinical course of IE has been characterized as either \nacute or subacute.  \no Acute Infective endocarditis :  frequently involves healthy valves. It is a rapidly \nprogressive illness with destruction of valvular structures.."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d38581-7265-11ef-9aa2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 244, "chroma:document": "Internal Medicine \n \n 229o Subacute Infective endocarditis : typically affects only previously damaged \nvalves. The course is insidious even in untreated cases which may extend over \nmany months. \n Etiologic agent of Infective endocarditis  \n\u2022 Streptococcus viridans : is a bacterium which is a normal flora of the oral cavity. It \naccounts for approximately 50-60% of cases of subacute infective endocarditis.  \n\u2022 Group D streptococci:  the source for this bacterium is the gastrointestinal or \ngenitourinary tract. Most cases infective endocarditis due to this organism is subacute.  \n\u2022 S. aureus : is the leading cause of  Prosthetic valve endocarditis (PVE), acute infective \nendocarditis and endocarditis in IVdrug abusers. Approximately 35-60.5% of \nstaphylococcal bacteremia is complicated by infective endocarditis. In more than half of \ncases endocarditis due to S. aureus  occurs in the absence of underlying valvular \ndisease. Mortality rate may range 40-50% \n\u2022 Coagulase-negative S. aureus: it accounts for approximately 30% of PVE cases, fewer \nthan 5% of NVE cases. It causes subacute disease  \n\u2022 HACEK  organisms (i.e., Haemophilus species, Actinobacillus, actinomycetemcomitans, \nCardiobacterium hominis, Eikenella corrodens, Kingella species ) .These group of \norganisms usually cause subacute disease. It accounts for approximately 5% of infective \nendocarditis. \n\u2022 Fungus: Mostly frequently cause subacute disease. Candida albicans  is the commonest \nfungal etiology."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac2d-7265-11ef-b58c-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 244, "chroma:document": "organisms usually cause subacute disease. It accounts for approximately 5% of infective \nendocarditis. \n\u2022 Fungus: Mostly frequently cause subacute disease. Candida albicans  is the commonest \nfungal etiology.  \n Pathophysiology:  \nAll cases of infective endocarditis deve lop from a commonly shared process:  \n1. Bacteremia (nosocomial or spontaneous) that  delivers the organisms to the valve's \nsurface \n2. Adherence of the organisms to valvular structures \n3. Eventual invasion of the valvular leaflets and formation of vegetations.  \n\u2022 Infective endocarditis develops most commonly on the mitral valve, closely followed in \ndescending order of frequency by the aortic valve, the combined mitral and aortic valve, the tricuspid valve, and, rarely, the pulmonic va lve. Mechanical prosthetic and bioprosthetic \nvalves exhibit equal rates of infection."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac2e-7265-11ef-bccc-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 245, "chroma:document": "Internal Medicine \n \n 230\u2022 Turbulence in blood flow damages valvular surface and edocardium which creates a \nfavorable situation for formation of sterile thrombus (vegetation) made of platelets and fibrin. \n\u2022 The microorganisms that most commonly produce endocarditis (i.e., S. aureus; S.viridans;  \ngroup A, C, and Group D streptococci; enterococci) resist the bactericidal action of \ncomplement and possess fibronectin receptors for the surface of the fibrin and platelet \nthrombus.  \n\u2022 Either a spontaneous bacteremia or one that is the result of an invasive procedure gives \naccess to the bacteria to adhere to the sterile platelet/fibrin vegetation. Most cases of subacute disease are secondary to the bactermias that develop from the activities of daily living (e.g., brushing teeth, bowel movements) \n\u2022 The complications of acute bacterial endocarditis result from intracardiac disease and \nmetastatic infection produced by suppurative emboli. Because of their shortened course, \nimmunological phenomena are not a part of acute infective endocarditis.  \n \nClinical Features  \nA. Subacute infective endocarditis \n\u2022 The patient suspected of SBE should be asked about invasive procedures that may be \ncausing bacteremia. Most subacute disease caused by S.viridans  is related to dental \ndisease.  \n\u2022 The symptoms of early subacute NVE usually are subtle and nonspecific.  \n\u2022 SBE is suggested by a history of a slowly pr ogressive process characterized by fever,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac2f-7265-11ef-8538-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 245, "chroma:document": "disease.  \n\u2022 The symptoms of early subacute NVE usually are subtle and nonspecific.  \n\u2022 SBE is suggested by a history of a slowly pr ogressive process characterized by fever, \nfatigue, anorexia, back pain, and weight loss.  \n\u2022 Less common developments are a cerebrovascu lar accident or congestive heart failure.  \n\u2022 When appropriate therapy is delayed for weeks or months, additional clinical features, \nembolic or immunological in origin, develop. \n \nEmbolic manifestations of infective endocarditis include: \no Acute meningitis with sterile spinal fluid \no Hemiplegia due to embolization in the distribution of the middle cerebral artery \no Renal regional infarcts producing painless hematuria \no Splenic infarction   \no Unilateral blindness caused by occlusion of a retinal artery \no Myocardial infarction resulting from embolization to a coronary artery."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac30-7265-11ef-8255-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 246, "chroma:document": "Internal Medicine \n \n 231The risk of embolization is related to the type of the organism, the size of the vegetation and its \nrate of growth or resolution, and the location of the vegetation. \nImmunologic Manifestations of SBE: \no Acute glomerulonephritis \no Osler\u2019s nodes  \no Roth spots  \no Presence of rheumatoid factor \n \nCommon Physical findings in SBE \n\u2022 Fever:   most patients have low grade fever; however 3-15% of patients with SBE may \nhave normal or subnormal temperature.  \n\u2022 Murmurs : the vast majority of patients have detectable heart murmurs (99% of cases). \nThe absence of a murmur should cause clinicians to reconsider the diagnosis of IE. The \nmajor exception is right-sided infective endocarditis, in which only one third of cases \nhave a detectable murmur.  \n\u2022 The peripheral lesions of subacute infective endocarditis  are observed in only \napproximately 20% of patients as compared to 85% in the preantibiotic era. \no Petechiae  are the most common peripheral lesions. They may occur on the \npalpebral conjunctivae, the dorsa of the hands and feet, the anterior chest and abdominal walls, the oral mucosa, and the soft palate. \no Subungual hemorrhages  (i.e., splinter hemorrhages) are linear and red lesions \nthat do not extend for the entire length of the nail. \no Clubbing of fingers and toes  may be seen. It primarily occurs in those patients \nwho have an extended course of untreated infective endocarditis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac31-7265-11ef-976b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 246, "chroma:document": "that do not extend for the entire length of the nail. \no Clubbing of fingers and toes  may be seen. It primarily occurs in those patients \nwho have an extended course of untreated infective endocarditis. \no Arthritis  associated with subacute infective endocarditis is asymmetrical and \nlimited to 1-3 joints.  \no Splenomegaly  is observed more commonly in patients with long-standing \nsubacute disease. It may persist long after successful therapy. \no Osler nodes  are small tender nodules that range in color from red to purple and \nare located primarily in the pulp spaces of the terminal phalanges of the fingers and toes, soles of the feet, and the thenar and hypothenar eminences of the hands. \nB. Acute infective endocarditis: \n\u2022 History of antecedent procedures or illicit drug use must be investigated."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 247, "chroma:document": "Internal Medicine \n \n 232\u2022 Is a much more aggressive disease. The onset of illness is abrupt, with rapidly \nprogressive destruction of the infected valve. The valvular leaflets are destroyed rapidly \nby bacteria that multiply very fast  within the ever-growing friable vegetations.  \n\u2022 The clinical symptoms of acute infective endocarditis result from either embolic or \nintracardiac suppurative complications.  \n\u2022 There is an acute onset of high-grade fever and chills and a rapid onset of congestive \nheart failure.  \n\u2022 Complications develop within a week. These include the dyspnea and fatigue of severe \ncongestive heart failure and a wide spectrum of neuropsychiatric complications resulting from involvement of the CNS. \n\u2022 Roth spots  are retinal hemorrhages with pale centers. The Litten sign represents \ncotton-wool exudates. \n\u2022 Murmurs  are present in nearly two third of patients with acute infective endocarditis. \nThe most common type is murmur aortic regurgitation. Because of the rapid onset, the left ventricle does not have a chance to dilate. In this situation, the classic findings of increased pulse pressure that are seen in chronic AR are absent. \n\u2022 Janeway lesions  are irregular erythematous and painless macules (1-4 mm in \ndiameter). They most often are located on the thenar and hypothenar eminences of the hands and feet. They usually represent an infectious vasculitis of acute infective \nendocarditis resulting from S.  aureus  infection."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 247, "chroma:document": "diameter). They most often are located on the thenar and hypothenar eminences of the hands and feet. They usually represent an infectious vasculitis of acute infective \nendocarditis resulting from S.  aureus  infection. \n\u2022 Acute septic monoarticular arthritis  in patients with acute infective endocarditis most \noften is caused by S aureus  infection. \n\u2022 Purulent meningitis  may be observed in patients with acute infective endocarditis , as \ncompared to the aseptic type observed in patients with subacute disease.  \nC. Right-sided infective endocarditis:  is associated with a very low rate of congestive heart \nfailure and valvular perforation.   \no Pulmonary infarcts may result from emboli of right-sided infective endocarditis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 248, "chroma:document": "Internal Medicine \n \n 233   Table III-4-1: Frequencies of Occurrence of prominent Clinical and Laboratory \nManifestations in Endocarditis \n \nClinical manifestations % of occurrence  \nFever \nArthralgias and/or myalgias Murmur \nSplenomegaly \nSplinter hemorrhages Roth's spots Osler's nodes Janeway lesions \nClubbing \nClinically apparent emboli Neurologic manifestations > 95 25-45 > 85 \n25-60 \n20-40 < 5 10-25 < 5 \n10-20 \n25-45 20-40 \nLABORATORY MANIFESTATIONS   \nAnemia Leukocytosis Proteinuria Microscopic hematuria Elevated serum creatinine level \nElevated erythrocyte sedimentation rate \nRheumatoid factor Circulating immune complexes Decreased serum complement level 70-90 20-30 50-65 30-50 10-20 \n>90 \n50 65-100 5-40              \n \nDiagnostic work up:  \nLab Studies:  \n1. Blood Culture :  \n\u2022 The gold standard test for the diagnosis of infective endocarditis is the \ndocumentation of a continuous bacteremia (>30 min in duration) through  blood \nculture."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 249, "chroma:document": "Internal Medicine \n \n 234\u2022 For making diagnosing SBE draw 3-5 sets of blood cultures , at 3 different sites ,  \nover 24 hours.  \n\u2022 This detects 92-98% of cases in patients who have not received antibiotics \nrecently.  \n\u2022 In the case of Acute infective endocarditis, 3 sets may be drawn over 30 minutes \n(with separate venipunctures) to document a continuous bacteremia. \n2. Echocardiography \n\u2022 Has become the indirect diagnostic method of choice, especially in patients who \npresent with a clinical picture of infective endocarditis but who have \nnondiagnostic blood cultures. \n\u2022 The diagnosis of infective endocarditis can never be excluded by a negative \nechocardiogram. \n3. Other Tests:  \n\u2022 Electrocardiography  may detect the 10% of patients who develop a conduction \ndelay during infective endocarditis by documenting an increasing P-R interval. \nRheumatoid factor  becomes positive in 50% of patients with subacute disease. It becomes \nnegative after successful treatment.   \n  Table III -4-2. The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis  \n Major Criteria \n1. Positive blood culture:   for typical microorganism that causes infective \nendocarditis from two separate blood cultures.  ( Viridans streptococci , \nStreptococcus bovis , HACEK group , or Community-acquired Staphylococcus \naureus  or enterococci in the absence of a primary focus ) \n2. Positive echocardiogram :  \n\u2022 Definitive vegetation ( oscillating intracardiac mass on valve or supporting"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac36-7265-11ef-81e3-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 249, "chroma:document": "Streptococcus bovis , HACEK group , or Community-acquired Staphylococcus \naureus  or enterococci in the absence of a primary focus ) \n2. Positive echocardiogram :  \n\u2022 Definitive vegetation ( oscillating intracardiac mass on valve or supporting \nstructures )  \n\u2022 Abscess   \n\u2022 New partial dehiscence of prosthetic valve   \n\u2022 New valvular regurgitation (increase or change in preexisting murmur not \nsufficient)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac37-7265-11ef-b8c9-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 250, "chroma:document": "Internal Medicine \n \n 235 \nMinor Criteria \n\u2022 Predisposition : predisposing heart condition or IV drug abuse  \n\u2022 Fever >38.0 oC. \n\u2022 Embolic  phenomena : major arterial emboli, septic pulmonary infarcts, mycotic \naneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions \n\u2022 Immunologic phenomena : glomerulonephritis, Osler's nodes, Roth's spots, \nrheumatoid factor \n\u2022 Microbiologic evidence : positive blood culture but not meeting major criterion.  \nEchocardiogram : consistent with infective endocarditis but not meeting major \ncriterion \nSOURCE: Adapted from Durack et al. \n \nDefinitive Diagnosis can be made by documentation of: \n\u2022 Two major criteria or \n\u2022 One major and three minor criteria or  \n\u2022 Five minor criteria allows a clinical diagnosis of definite endocarditis.  \nTreatment: \nAll patients should be treated in the hospital to allow adequate monitoring of the development of \ncomplications and the response to the antibiotic therapy. \nGeneral measures: \n\u2022 Diet: No special diets are recommended for patients with endocarditis; however, if the \npatient has congestive heart failure, sodium-restriction may be necessary.  \n\u2022 Activity: Activity limitations are determined by the se verity of illness, complications (e.g., \nstroke), and the presence of significant congestive heart failure.  \nMedical  Treatment  \nThe major goals of therapy for infective endocarditis are  \n\u2022 Eradicating the infectious agent from the thrombus"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac38-7265-11ef-b98b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 250, "chroma:document": "stroke), and the presence of significant congestive heart failure.  \nMedical  Treatment  \nThe major goals of therapy for infective endocarditis are  \n\u2022 Eradicating the infectious agent from the thrombus  \n\u2022 Treating the complications of valvular infection \n1. Eradicating the infectious agent from the thrombus  \n\u2022 Antibiotics remain the mainstay of treatment for IE. In the setting of acute IE, \nantibiotic therapy should be instituted as soon as possible to minimize valvular"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 251, "chroma:document": "Internal Medicine \n \n 236damage. Three to five sets of blood cultures should be obtained within 60-90 \nminutes, followed by the infusion of the appropriate antibiotic regimen.  \n\u2022 By necessity, the initial antibiotic choice is empiric, determined by clinical history and \nphysical examination. \n\u2022 In the case of subacute IE, treatment may be safely delayed until cultures and \nsensitivities are available. Waiting does not increase the risk of complications in this form of the disease. \n\u2022 Eradicating bacteria from the fibrin-platelet thrombus is extremely difficult..  \n\u2022 Intravenous administration is the preferred to ensure reliable serum therapeutic \nlevels.  \n\u2022 The antibiotics should be bactericidal and are should be administered at higher dose \nfor prolonged period of time. \n \nEmpirical antibiotic treatment  \nNVE of sub acute nature:  \n\u2022 Crystalline penicillin 3-4 million IU IV every 4 hours for 4- 6 weeks plus \n\u2022 Gentamicin 1mg/kg ( 80 mg ) IV TID for 2 weeks plus  \nProsthetic Valve endocarditis: \n\u2022 Vancomycin 1gm IV BID  for 6 weeks Plus  \n\u2022 Gentamicin 1mg/kg ( 80 mg ) IV TID for 2 weeks plus \n\u2022 Refampicin 300 mg PO /TID for 6 weeks  \nAcute Infective endocarditis where S.aureus is suspected : E.g. hospital acquired infection    \n\u2022 Naficillin 1.5-2gm IV every 4 hours OR Vancomycin 1gm IV BID  for 6 weeks  Plus  \n\u2022 Gentamicin 1mg/kg (80 mg) IV TID for 2 weeks."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac3a-7265-11ef-a00b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 251, "chroma:document": "Acute Infective endocarditis where S.aureus is suspected : E.g. hospital acquired infection    \n\u2022 Naficillin 1.5-2gm IV every 4 hours OR Vancomycin 1gm IV BID  for 6 weeks  Plus  \n\u2022 Gentamicin 1mg/kg (80 mg) IV TID for 2 weeks. \nWhen the result of blood culture is made available the choice of antibiotics depend on the type of organism identified and the anti microbial sensitivity. \n2. Dealing with the complications of valvular infection. The latter includes both the intracardiac and extracardiac consequences of infective endocarditis.  \n\u2022 Mild congestive heart failure resulting from valvular insufficiency or myocarditis may be \nmanaged with standard medical therapy for CHF.  \n\u2022 Although thrombosis is a key element of infective endocarditis, anticoagulation with \nheparin or Warfarin is controversial, and it should be avoided. \n Surgical Treatment:  Approximately 15-25% of patients with IE eventually require surgery."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 252, "chroma:document": "Internal Medicine \n \n 237Indication for Surgery: \n\u2022 Acute AR with severe Heart failure  \n\u2022 Fungal endocarditis \n\u2022 Mobile vegetation > 10mm in size.  \n\u2022 Evidence of valve ring or myocardial abscess \n\u2022 Recurrent embolization despite adequate antibiotic therapy \n\u2022 Poor response to antibiotics \n\u2022 Prosthetic valve dysfunction  associated with CHF \n\u2022 Valve ring Abscess near a prosthetic valve  \n \nReferences:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  Infective \nendocarditis , pages 731-739."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac3c-7265-11ef-a521-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 253, "chroma:document": "Internal Medicine \n \n 2385. Cardiomyopathy  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Cardiomyopathy. 2. List the etiologies of Cardiomyopathies.  3. Describe the different types of Cardiomyopathies. \n4. Understand the Epidemiology of Cardiomyopathies.  \n5. Describe the pathogenesis of Cardiomyopathies.  6. Identify the clinical manifestation of Cardiomyopathies.  7. Understand the diagnostic approach of Cardiomyopathies. 8. Understand the management of patients Cardiomyopathies. \n Definition:  \nCardiomyopathies are a group of diseases that affect the myocardium and are not the result of \nhypertension, valvular, coronary or pericardial abnormalities. Cardiomyopathies are frequently \nassociated with myocardial dysfunction and su bsequently heart failure. With few exceptions, \nhistologic findings are nonspecific, with myoc yte hypertrophy, cellular necrosis, and fibrosis. \n \nEtiologic classification of Cardiomyopathies: \nPrimary Myocardial Involvement \n\u2022 Idiopathic  \n\u2022 Familial \n\u2022 Eosinophilic  endomyocardial diseases \n\u2022 Endomyocardial Fibrosis \nSecondary myocardial involvement: \n\u2022 Infective Myocarditis: Viral , bacterial , fungal , protozoal , Metazoal , Spirochetal \n\u2022 Metabolic : Thyrotoxicosis \n\u2022 Familial storage diseases: Glycogen storage diseases , Hemochromatosis ,  \n\u2022 Deficiencies : Electrolyte  , Nutritional ( Vitamin B 1 deficiency )  \n\u2022 Connective tissue diseases : SLE , polyarteritis nodosa , Rheumatoid arthritis ,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac3d-7265-11ef-a81b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 253, "chroma:document": "\u2022 Familial storage diseases: Glycogen storage diseases , Hemochromatosis ,  \n\u2022 Deficiencies : Electrolyte  , Nutritional ( Vitamin B 1 deficiency )  \n\u2022 Connective tissue diseases : SLE , polyarteritis nodosa , Rheumatoid arthritis , \nSystemic sclerosis  \n\u2022 Infiltration and granulomas ; Amyloidosis , sarcoidosis , malignancies  \n\u2022 Neuromuscular : muscular dystrophies ,myotonic dystrophies"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac3e-7265-11ef-b42a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 254, "chroma:document": "Internal Medicine \n \n 239\u2022 Sensitivity and toxic reactions : Alcohol , drugs , radiation   \n\u2022 Peripartum heart diseases  \n \nTable III-5-1 Clinical classification of Cardiomyopathies \nDISORDER  DESCRIPTION  \nDilated cardiomyopathy  Dilatation and impaired contraction of the left or both ventricles. \nCaused by familial/genetic, viral and/or immune, alcoholic/toxic, or unknown factors, or is associated with recognized cardiovascular disease.  \nHypertrophic cardiomyopathy  Left and/or right ventricular hypertrophy, often asymmetrical, which usually involves the interventricular septum. Mutations in sarcoplasmic proteins cause the disease in many patients.  \nRestrictive \ncardiomyopathy  Restricted filling and reduced diastolic size of either or both ventricles with normal or near-normal systolic function. Is \nidiopathic or associated with other disease (e.g., amyloidosis, endomyocardial disease)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac3f-7265-11ef-99e4-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 255, "chroma:document": "Internal Medicine \n \n 2405.1 Dilated  Cardiomyopathy   \n \nDefinition  \n\u2022 This condition may be defined as impaired left and/or right ventricular systolic \ndysfunction characterized by an ejection fraction <40% in the presence of increased left ventricular dimensions (left ventricular end-di astolic size >115% of that calculated for \nage and body surface area).  \nPathophysiology   \n\u2022 Dilated cardiomyopathy represents the final common morphologic outcome of a variety \nof biological insults. It is a combination of myocyte apoptosis and necrosis with \nincreased myocardial fibrosis, producing reduced mechanical function. Many causes are a result of direct toxicity (e.g., alcohol) or mechanical insults (e.g., chronic volume \noverload in mitral valvular regurgitation), infection (eg myocarditis).  \nClinical manifestations  \n\u2022 A careful history is essential , with particular emphasis on  \no Family history of similar illness  \no Exposure to cardio toxins such as alcohol \no Protracted \"flu-like illness\" or respiratory tract infection may suggest previous \nmyocarditis \no History of recent delivery or being in the last trimester of pregnancy  \n\u2022 Some patients may have left ventricular dilatation for months or even years and may \nremain asymptomatic and are diagnosed only by screening or postmortem examination.  \n\u2022 Symptoms of left and right sided congestive heart failure develop gradually in most \npatients. Unfortunately, the most common clinical presentation is one of progressive"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac40-7265-11ef-ab6a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 255, "chroma:document": "\u2022 Symptoms of left and right sided congestive heart failure develop gradually in most \npatients. Unfortunately, the most common clinical presentation is one of progressive \ndeterioration, with worsening heart failure and death occurring over a variable time \ncourse. \n\u2022 Syncope may result from arrhythmias  \n\u2022 Systemic embolization, often emanating from ventricular thrombus, may occur. \n \nPhysical examination :  \n\u2022 Hypotension , tachycardia  \n\u2022 Cardiomegaly ( displaced PMI ) \n\u2022 Findings of CHF : narrow pulse pressure , raised JVP and S\n3 and S 4 gallops"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac41-7265-11ef-b9d0-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 256, "chroma:document": "Internal Medicine \n \n 241\u2022 Functional mitral or tricuspid regurgitation. \nDiagnostic work up: \n\u2022 Chest radiograph : enlargement of cardiac silhouette and evidence of pulmonary \ncongestion \n\u2022 ECG : sinus tachycardia or atrial fibrillation , , ventricular arrhythmias, St segment and T \nwave abnormalities  \n\u2022 Echocardiogram:  Left ventricular dilatation and dysfunction (ejection fraction < 40 %) \n\u2022 Other laboratory investigation include  \no Complete blood cell count  \no Renal function test  \no Blood glucose ( fasting or random) \no Lipid profile  glucose \no Thyroid function tests  \n \nTreatment of Dilated Cardiomyopathy \nMedical Therapy : Standard therapy of heart failure  \n\u2022 Salt restriction \n\u2022 Diuretics  \n\u2022 Digitalis \n\u2022 ACE inhibitors or Angiotensin II receptor blockers  \n\u2022 Spirinolactone  \n\u2022 Alcohol should be avoided \n\u2022 Identify and treat the underlying cause if it is treatable  \nSurgical Therapy : Cardiac transplantation provides a medi an 10-year survival and is effective \npalliation in appropriately selected individuals. \nPrognosis. \n\u2022 In the absence of a specific remediable etiology (e.g., in peripartum cardiomyopathy, \nalcoholic cardiomyopathy, ischemic hibernat ing revascularizable myocardium), the \noverall outcome is poor in patients with cardiomyopathy. \n\u2022 Majority of patients have downhill course, and particularly those >55 years, die within 3 \nyears of onset of symptoms. The 5-year survival rate of patients diagnosed with heart \nfailure is 50%."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 256, "chroma:document": "\u2022 Majority of patients have downhill course, and particularly those >55 years, die within 3 \nyears of onset of symptoms. The 5-year survival rate of patients diagnosed with heart \nfailure is 50%. \n\u2022 Blacks are more likely to suffer progressive heart failure and death than whites"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac43-7265-11ef-8cb8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 257, "chroma:document": "Internal Medicine \n \n 2425.2 Hypertrophic Cardiomyopathy   \n \nDefinition:  \nHypertrophic cardiomyopathy is characterized by left ventricular hypertrophy (myocardial \nthickness greater than 1.5 cm), typically of none dilated chamber, without obvious causes. Other \netiologies of left ventricular hypertrophy, such  as long-standing hypertension and aortic stenosis \nneed to be excluded before one can diagnose HCM.   \n \nGenetic Predisposition: \n\u2022 HCM is the most common genetic cardiovascular disease. About half of patients with \nHCM have a positive family history wi th autosomal dominant transmission. \n\u2022 The prevalence in the general adult population for people with phenotypic evidence of \nHCM is estimated at 1 per 500.  \n Pathophysiology:  \nGenerally, ventricular hypertrophy involves the pr oximal portion of the interventricular septum. \nAs the septum thickens, it may narrow the outflow tract. In addition, systolic anterior motion of the mitral valve may occur and result in left ventricular outflow tract obstruction and mitral regurgitation. When systolic anterior motion occurs, the mitral valve leaflets are pulled or dragged anteriorly toward the ventricular septum, producing the obstruction. Consequently, the left ventricle has to generate much higher pressu res to overcome the out flow  obstruction and \nto pump blood to the systemic circulation. Prem ature closure of the aortic valve may occur and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac44-7265-11ef-9781-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 257, "chroma:document": "to pump blood to the systemic circulation. Prem ature closure of the aortic valve may occur and \nis caused by the decline in pressure distal to the left ventricular outflow obstruction.  \n Clinical Features  \n\u2022 The clinical course of HCM is variable. Most patients with HCM are asymptomatic.  \n\u2022 The most common symptom of HCM is dyspnea on exertion.  \n\u2022 Patients may also complain of chest pain with exertion, syncope or near syncope, or \npalpitations.. Congestive heart failure and atrial fibrillation along with their accompanying symptoms may be part of the natural history of HCM.  \n\u2022 Unfortunately, the first clinical manifestation of the diseases may be sudden cardiac \ndeath frequently occurring in young children and young adults. , often during or after \nphysical exertion."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 258, "chroma:document": "Internal Medicine \n \n 243Physical examination : \n\u2022 Unless congestive heart failure has developed, the lungs are usually clear and the \njugular venous pressure normal \n\u2022 Bisferiens pulse : rapidly rising carotid pulse followed by a collapse in the pulse and \nthen a secondary rise. \n\u2022 The point of maximal impulse may be double or triple, forceful and sustained.  \n\u2022 S4 gallop  may be present.  \n\u2022 Systolic murmur : the classic auscultatory finding for HCM is a crescendo-decrescendo \nsystolic murmur along the left sternal border t hat increases with the Valsalva maneuver. \nIn young adults, HCM is the most common etiology for sudden cardiac death. \nDiagnosis  \nLaboratory studies generally will be unremarkable.  \n\u2022 Chest radiograph  may suggest left ventricular hypertrophy but will often be normal \nbecause the hypertrophy in HCM involves the ventricular septum.  \n\u2022 The electrocardiogram  often shows left ventricular hypertrophy and occasionally may \nalso have a pseudoinfarct pattern.   Left atrial abnormality may be present if the patient \nhas had long-standing mitral regurgitation from systolic anterior motion of the mitral valve. Atrial fibrillation also may be present as one of the complications of HCM. \n\u2022 Echocardiography  is the gold standard for diagnosing HCM. On transthoracic \nechocardiography, the clinician should note the thickness of the septum; location and pattern of hypertrophy; site and degree of left ventricular outflow tract obstruction;"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac46-7265-11ef-89e1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 258, "chroma:document": "echocardiography, the clinician should note the thickness of the septum; location and pattern of hypertrophy; site and degree of left ventricular outflow tract obstruction; \npresence of systolic anterior motion of the mitral valve; presence of premature closure of \nthe aortic valve; and any change in severity of obstruction with amyl nitrite \nTreatment:  \nMedical Therapy \n\u2022 Competitive sport and probably str enuous exercise should be avoided. \n\u2022 Dehydration should be avoided and diuretics should be used with caution. \n\u2022 \u00df-blockers are considered first-line therapy. By decreasing contractile force, \u00df-blockers \ndecrease the outflow gradient and decrease oxygen demand. \u00df-blockers also lengthen diastolic filling by slowing the heart rates. They help to control chest pain. \n\u2022 Calcium channel blocker: Second-line therapy includes the verapamil and, Diltiazem can \nbe used. But Nifedipine, amlodipine and felodipine should be avoided because they"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac47-7265-11ef-a934-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 259, "chroma:document": "Internal Medicine \n \n 244cause peripheral vasodilatation, which may result in decreased left ventricular filling and \nworsening of symptoms of outflow tract obstruction. \n\u2022 Atrial fibrillation is a common complicati on of HCM. Treatment of persistent atrial \nfibrillation in HCM includes anticoagulation and rate control, preferably with \u00df-blockers. \n\u2022 Digoxin should be avoided in HCM patients, part icularly in those with resting or latent \nobstruction, because of its positive inotropic effect.  \n\u2022 Patients with HCM should receive prophylactic antibiotics for endocarditis prevention \nbefore dental or invasive procedures. Turbulent flow through the LVOT striking the aortic \nvalve as well as mitral regurgitation from systolic anterior motion of the mitral valve \npredispose to endocarditis. \nSurgical Therapy \n\u2022 Septal myomectomy/myotomy may cause lasting symptomatic relief in \u00be of severely \nsymptomatic patients. \n\u2022 Alcohol ablation: ethanol injection in to the septal artery has also been reported to \nreduce obstruction. \nPrevention : First degree relatives of patients with HCM should be screened with ECHO."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac48-7265-11ef-804d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 260, "chroma:document": "Internal Medicine \n \n 245Restrictive Cardiomyopathy  \nDefinition  \n\u2022 Restrictive cardiomyopathy is a disease of  the myocardium that is characterized by \nrestrictive filling and reduced diastolic volume of either or both ventricles with normal or \nnear-normal systolic function.  \n Pathophysiology: \nThese conditions result in impaired ventricular filling and primarily diastolic heart failure. They \npresent with a clinical heart failure syndrome t hat is frequently indistinguishable from that \ncaused by systolic dysfunction. Atrial fibrillation is poorly tolerated. It simulates other right side heart failure like cor pulmanale and diastolic dysfunction of constricted pericarditis.  \nClinical Features\n: \n\u2022 Exercise intolerance and dyspnea are the prominent symptoms. \n\u2022 Peripheral edema with predominant ascites  \n\u2022 Enlarged tender and pulsatile liver. \n\u2022 JVP is elevated and it doesn\u2019t fall norma lly during inspiration ( Kussmaul\u2019s sign ) \n\u2022 The heart sounds may be distant but apica l impulse is easily palpable unlike in \nconstrictive pericarditis. \nDifferential Diagnosis : The clinical features are very similar to constrictive pericarditis.  \nDiagnostic work up \n\u2022 Chest x-ray : mild cardiac enlargement   \n\u2022 ECG: low voltage and conduction defects   \n\u2022 Echocardiography: Increases left ventricular wall thickness, normal or mildly reduced \nsystolic function."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac49-7265-11ef-8b8a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 261, "chroma:document": "Internal Medicine \n \n 2466. Myocarditis  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Myocarditis. . \n2. List the etiologies of Myocarditis. 3. Describe the different types of Myocarditis. \n4. Understand the epidemiology of Myocarditis. \n5. Understand the pathophysiology of Myocarditis. 6. Identify the clinical manifestation of Myocarditis. 7. Identity consequences of Myocarditis.  8. Understand the diagnostic approach of Myocarditis. \n9. Understand the principle of management of Myocarditis.  \n \nDefinition:  Myocarditis is inflammation of the myocardium often resulting from infectious \nprocess, which subsequently leads to myocardi al destruction and a dilated cardiomyopathy.  \nThe acute picture is nonspecific unless overt congestive heart failure develops. Although the \ncauses of myocarditis are numerous, the most common association is an antecedent viral \nsyndrome.   \nEtiologies of Myocarditis  \n1. Infectious causes \n\u2022 Viral infections : Coxsackievirus B , HIV myocarditis ( overt involvement is seen \nin 10 % of HIV patients ) \n\u2022 Bacterial myocarditis:  \no Not common usually occurs as a complication of infective endocarditis. \no Diphtheric myocarditis may develop in \u00bc of patients with diphtheria \n\u2022 Fungal myocarditis \n\u2022 Protozoal myocarditis: Chaga\u2019s dis ease caused by a protozoon Trypanosoma \ncruzi and transmitted by an insect vector. It is one of the most common causes of \nheart disease in Central and South America."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac4a-7265-11ef-8af0-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 261, "chroma:document": "\u2022 Fungal myocarditis \n\u2022 Protozoal myocarditis: Chaga\u2019s dis ease caused by a protozoon Trypanosoma \ncruzi and transmitted by an insect vector. It is one of the most common causes of \nheart disease in Central and South America. \n\u2022 Rickettsial myocarditis :associated with Typhus , Lyme disease \n\u2022 Spirocheatal myocarditis: associated with Relapsing fever."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac4b-7265-11ef-9073-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 262, "chroma:document": "Internal Medicine \n \n 2472. Hypersensitivity and toxic reactions to : \n\u2022 Drugs : Doxorubicin ( anti- neoplastic agent )  \n\u2022 Radiation \n3. Giant cell myocarditis  : is a rare form of myocarditis of unknown etiology \n \nPathophysiology:   \nMyocarditis is defined as inflammatory changes in the heart muscle and is characterized by an \ninterstitial mononuclear cell infiltrate with an attendant myocyte necrosis.  It is not known whether the infiltrate is caused by a direct invasion of the infective agents or by a systemic immune response. In the chronic stage, cytotoxic T lymphocytes infiltrate the myocardium and mediate an autoimmune response with myocardial autoantibody activity \ndirected against cardiac myosin. This autoimmune process persists after the viral particles are no longer detected. Coronary artery thrombus formation, luminal obstruction, ischemia, and dysrhythmias compound the deleterious effects of the inflammatory response.  \n \nClinical features   \n\u2022 The clinical presentation of myocarditis is variable. Patients may present with a \nnonspecific illness characterized by fatigue, mild dyspnea, or fulminant congestive heart \nfailure (CHF). Myocarditis may even cause sudden death in some patients. \n\u2022 The majority of cases of myocarditis are subclinical; therefore, the patient rarely seeks \nmedical attention during acute illness. \n\u2022 An antecedent viral syndrome has been documented in 60% of patients with"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac4c-7265-11ef-9942-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 262, "chroma:document": "\u2022 The majority of cases of myocarditis are subclinical; therefore, the patient rarely seeks \nmedical attention during acute illness. \n\u2022 An antecedent viral syndrome has been documented in 60% of patients with \nmyocarditis. The typical time interval between the onset of the viral illness and cardiac \ninvolvement is 2 weeks. \n\u2022 Fever is present in 20% of cases. Fatigue , myalgia and,malaise are common symptoms  \n\u2022 Chest pain or chest discomfort is reported in 35% of cases. The chest pain is often \npleuritic quality with precordial pain of a sharp stabbing nature. Sometimes it may be substernal and squeezing, more typical of ischemic pain. \n\u2022 Dyspnea on exertion is common and orthopnea and shortness of breath at rest may be \nnoted if CHF is present. \n\u2022 Palpitations are common.  \n\u2022 Syncope signals development of AV block or malignant dysrhythmias and may lead to \nsudden death in patients with myocarditis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac4d-7265-11ef-9749-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 263, "chroma:document": "Internal Medicine \n \n 248Physical examination :  \n\u2022 Patients with mild cases of myocardi tis have a nontoxic appearance and simply may \nappear to have a viral syndrome. Tachypnea and tachycardia are common. Tachycardia \nis often out of proportion to fever. \n\u2022 More acutely ill patients have signs of left ventricular failure including:  \no Raised JVP, bilateral basal crepitations on the chest, ascites and pperipheral \nedema. S 3 gallop may be noted with significant cardiac enlargement (displaced \napical impulse). S 1 is soft or muffled. Cyanosis may be noticed. \no Hypotension caused by left ventricular dysfunction is uncommon in the acute \nsetting. A poor prognosis is indicated when hypotension is present. \no Cardiogenic shock is observed in fulminant cases and has a high mortality. \no Murmurs of mitral or tricuspid regurgitation may be present due to ventricular \ndilation. \n\u2022 In cases where a dilated cardiomyopathy has developed, signs of peripheral or \npulmonary thromboembolism may be found. \n\u2022 Associated pericarditis may manifest with a per icardial friction rub. Pericardial effusion is \ncommon, but signs of tamponade (e.g., hypotension, jugular venous distention, muffled heart sounds) are rare. \n\u2022 Pleural friction rub might be heard because pleuritis can occur with cases of acute \nmyocarditis. \n               \nDiagnostic workup  \nSince many cases of myocarditis are not clin ically obvious, a high degree of suspicion is"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac4e-7265-11ef-8ad3-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 263, "chroma:document": "\u2022 Pleural friction rub might be heard because pleuritis can occur with cases of acute \nmyocarditis. \n               \nDiagnostic workup  \nSince many cases of myocarditis are not clin ically obvious, a high degree of suspicion is \nrequired for the making a diagnosis of acute myocarditis.  \nLaboratory Studies:  \n\u2022 Erythrocyte sedimentation rate (ESR) is elevated in 60% of patients with acute \nmyocarditis. \n\u2022 Leucocytosis is present in 25% of cases. \nImaging Studies:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac4f-7265-11ef-bb7a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 264, "chroma:document": "Internal Medicine \n \n 249\u2022 Chest x-ray: often reveals a normal cardiac silhouette, but pericarditis or overt clinical \nCHF may be associated with cardiomegaly. Vascular redistribution, interstitial and \nalveolar edema and pleural effusion may also be noticed.  \n\u2022 Echocardiography: Dilated chambers and reduced ejection fraction indicating left \nventricular systolic dysfunction. \n\u2022 ECG:  Sinus tachycardia is the most frequent finding. ST-segment elevation without \nreciprocal depression, particularly when diffuse, is helpful in differentiating myocarditis \nfrom acute myocardial infarction \nTreatment of Myocarditis  \n\u2022 Patients with mild symptoms and no signs of cardiac failure or dysrhythmia may be \ntreated on an outpatient basis.  \n\u2022 The medical treatment of myocarditis is directed towards amelioration of associated \ncomplications including CHF and cardiogenic shock, arrhythmias, and \nthromboembolism. \n1. Left ventricular dysfunction with signs of CHF should be treated with; \n\u2022 Low sodium diet \n\u2022 Limitation or avoidance of exercise as exercise may have deleterious effect. \n\u2022 Diuretics \n\u2022 Digoxin: should be given with caution as patients with myocarditis are \nsensitive for digitalis toxicities. \n\u2022 ACE inhibitors and vasodilators \n\u2022 In general, sympathomimetic and beta-blocker drugs should be avoided \nbecause they increase the extent of myocardial necrosis and mortality. \n2. Arrhythmias :  \n\u2022 Detection of dysrhythmia with inpatient cardiac monitoring."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac50-7265-11ef-98ca-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 264, "chroma:document": "\u2022 In general, sympathomimetic and beta-blocker drugs should be avoided \nbecause they increase the extent of myocardial necrosis and mortality. \n2. Arrhythmias :  \n\u2022 Detection of dysrhythmia with inpatient cardiac monitoring.  \n\u2022 Medical therapy for arrhythmias  \n\u2022 Implantation of cardiac pacemakers. \n3. Avoiding risk of thromboembolism:;  \n\u2022 Anticoagulants such as Warfarin or Heparin may be given. \n\u2022 Nonsteroidal anti-inflammatory drugs (NSAIDs) are contraindicated in the \nearly course of disease because of inhibition of prostaglandin production, worsened myocyte function, and increased myocardial necrosis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac51-7265-11ef-bf40-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 265, "chroma:document": "Internal Medicine \n \n 250Prognosis:  \n\u2022 Majority of cases are believed to be clinically silent and resolve spontaneously \nwithout sequelae; therefore, it is difficult to make accurate statements concerning \nthe prognosis of myocarditis. \n\u2022 Patients presenting with CHF experience morbidity and mortality based on the \ndegree of left ventricular dysfunction, and the presence of arrhythmias and thromboemblic complications increase the risk of mortality from myocarditis. \n \nReferences:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nCardiomyopathy and Myocarditis,  pages 1408-1413. \n2. Myers R. Allen , National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Cardiomyopathies , pages 38-43"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac52-7265-11ef-9308-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 266, "chroma:document": "Internal Medicine \n \n 2517. Hypertension.  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Hypertension. \n2. List the etiologies of Hypertension. 3. Describe the different types of Hypertension. \n4. Understand the epidemiology of Hypertension. \n5. Understand the pathophysiology of Hypertension. 6. Identify the clinical manifestation of Hypertension. 7. Identity consequences of Hypertension.  8. Understand the diagnostic approach of Hypertension. \n9. Understand the management of chronic hypertension and hypertensive crisis.  \n \nDefinition: \n\u2022 Hypertension is defined as arterial blood pressure that exceeds 140/90mmHg at several \ndeterminations. This is an arbitrary definitio n because a diastolic pressure of even 85 \nmm Hg may be associated with increased cardiovascular morbidity and mortality. \n\u2022 Hypertension is one of the most common diseases afflicting humans throughout the \nworld. Because of the associated morbidity and mortality and the cost to society, hypertension is an important public health challenge.  \n\u2022 It is easily detectable, usually easily treatable, and often leads to lethal complications if \nleft untreated. \n\u2022 Hypertension is the most important modifiable risk factor for coronary heart disease,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac53-7265-11ef-a746-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 266, "chroma:document": "\u2022 It is easily detectable, usually easily treatable, and often leads to lethal complications if \nleft untreated. \n\u2022 Hypertension is the most important modifiable risk factor for coronary heart disease, \nstroke, congestive heart failure, end-stage renal disease, and peripheral vascular disease. Therefore, health care professionals must not only identify and treat patients with hypertension but also promote a healthy lifestyle and preventive strategies to decrease the prevalence of hypertension in the general population.  \nEpidemiology  \n\u2022 Overall, approximately 20% of the world's adults are estimated to have hypertension in \nexcess of 140/90 mm Hg. Some studies done in developed countries show almost 50 % \nof the population may have hypertension.  \n\u2022 The prevalence dramatically increases  in patients older than 60 years.  \n\u2022 The prevalence is higher among balks than whites."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac54-7265-11ef-b403-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 267, "chroma:document": "Internal Medicine \n \n 252\u2022 The age-adjusted prevalence of hypertension is slightly higher in men than in women. \nThe prevalence in women is closely related to age, with substantial increase occurring \nafter age 50. This may be related to hormonal changes associated with menopause. \n\u2022 There is paucity of data about prevalence of hypertension in Ethiopia , however some \nstudies have shown  that 6% of adolescent and young adults in urban area may have hypertension, and 11% of immigrant from Ethiopia to Israel ,  after 2- 4 years of stay were found to have developed hypertension \n \nClassification  \nBecause the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or \ntherapeutic interventions. \n \nTable III-7-1. Classification of blood pressure for adults and older children * \n \n   \nBLOOD PRESSURE ( in mm Hg)  \nCATEGORY  Systolic   Diastolic  \nOptimal <120  and  <80  \nNormal  <130  and  <85  \nHigh-normal  130\u2013139 or  85\u201389  \n \nHypertension   \nStage 1  140\u2013159 or  90\u201399  \nStage 2  160\u2013179 or  100\u2013109  \nStage 3  \n 180  or  N \n 110  \n \n\u2022 When systolic and diastolic blood pressure levels fall into different categories, the \nhigher category should be selected to classify the individual's blood pressure status.  \nE.g.       160/92 mm Hg should be classified as stage 2 hypertension \n 174/120 mm Hg should be classified as stage 3 hypertension."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac55-7265-11ef-bce5-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 268, "chroma:document": "Internal Medicine \n \n 253\u2022 Isolated systolic hypertension is defined as systolic blood pressure 140 mm Hg or \ngreater and diastolic blood pressure le ss than 90 mm Hg and staged approximately \n(e.g., 170/82 mm Hg is defined as stage 2 isolated systolic hypertension).  \n\u2022 In addition to classifying stages of hypertension on the basis of average blood \npressure levels, clinicians should specify the presence or absence of target organ \ndamage and additional risk factors. This specificity is important for risk classification and treatment. \n\u2022 Optimal blood pressure with respect to cardiovascular risk is \u2264 120/80 mm Hg.  \n\u2022 Hypertension should be diagnosed based on the average of two or more readings \ntaken at each of two or more visits after an initial screening.  \nThe natural history of essential hypertension :  \n\u2022 It evolves from occasional to established hypertension. After a long invariable \nasymptomatic period, persistent hypertension develops into complicated \nhypertension, in which target organ damage to the aorta and small arteries, heart, \nkidneys, retina, and central ner vous system is evident. \n\u2022 The progression begins with prehypertension in persons aged 10-30 years (by \nincreased cardiac output) to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent) to established hypertension in persons aged 30-50 years, and, finally, to complicated hypertension in persons aged 40-60 years."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac56-7265-11ef-8fc6-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 268, "chroma:document": "Etiologic Classificati on of Hypertension: Hypertension may be classified as either \nessential or secondary.  \nI.  Primary or essential hypertension (90-95%):   \no Essential hypertension is diagnosed in individuals in whom generalized or \nfunctional abnormalities may be the cause of hypertension but no specific \nsecondary causes are identified.  \no The pathophyisoliogy of essential hypertension is multifactorial and highly \ncomplex. A number of factors modulate the blood pressure. These factors include humeral mediators, vascular reactivity, circulating blood volume, \nvascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and \nneural stimulation."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac57-7265-11ef-abd5-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 269, "chroma:document": "Internal Medicine \n \n 254Some factors that may contribute for the development of essential hypertension \ninclude:  \n\u2022 Genetic predisposition :  the exact mechanism has not been established \n\u2022 Environment : a number of environmental factors have been implicated  \no Dietary salt intake and Salt sensitivity   \no Obesity \no Occupation  \no Family size and crowding  \n\u2022 Pregnancy-induced hypertension:  Toxemia of pregnancy   \n II. Secondary causes of hypertension:  \nIn 5-10 % of patients with hypertension, the hypertension is secondary to an identifiable disorder.   \nA. Renal Hypertension  (2.5-6%) a variety of renal diseases may be accompanied by \nhypertension  \n\u2022 Renal parenchymal disease  :  \no Chronic pyelonephritis  \no Acute and chronic glomerulonephritis  \no Polycystic kidney disease  \no Urinary tract obstruction  \no Renin-producing tumor  \n\u2022 Renovascular hypertension  (0.2-4%) \no Coarctation of aorta  \no Vasculitis  \no Collagen vascular disease \nB. Endocrine (1-2%)  \u2013  \n\u2022 Oral contraceptives \n\u2022 Adrenocoritical hypertension   \no Primary aldosteronism  \no Cushing syndrome \no Congenital adrenal hyperplasia \n\u2022 Pheochromocytoma  \n\u2022 Acromegally"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 270, "chroma:document": "Internal Medicine \n \n 255\u2022 Myxoedema  \n\u2022 Thyrotoxicosis \nC. Neurogenic :  \n\u2022 Psychogenic  \n\u2022 Increased intracranial pressure \n\u2022 Acute spinal cord section  \nD. Drugs and toxins  \n\u2022 Alcohol  \n\u2022 Adrenergic medications  \n \nConsequences of Hypertension (End organ /target organ damage) \nPatients with hypertension die prematurely, the most common cause of death is heart disease, \nwith stroke and renal failure also frequent, particularly in patients with retinopathy \n1. Effects on the Heart : \n\u2022 Left ventricular hypertrophy as a compensatory mechanism  \n\u2022 Coronary artery disease /Ischemic heart disease:  \no Angina Pectoris  \no Myocardial infarction which  may lead to heart failure \n2. Neurologic effects   \na. Retinal changes :  \ni. Exudates: hard and soft exudates  \nii. Hemorrhages: dot and bloat hemorrhages \niii. Thickening of arterioles \u2013 copper wiring \u00c6 silver wiring  \niv. Abnormalities on arteriolo \u2013venular crossings ( A/V crossings )  \nv. Papilledema \nb. Central nervous system dysfunction  \ni. Cerebrovascular disease \n\u0083 Transient ischemic attacks : episodic dizziness , unilateral \nblindness , hemiparesis etc \n\u0083 Stroke  \n\u2022 Ischemic stroke : due to atherosclerosis of cerebral blood \nvessels"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac59-7265-11ef-8a9e-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 271, "chroma:document": "Internal Medicine \n \n 256\u2022 Hemorrhagic stroke: as a result of elevated arterial \npressure and formation of vascular micro- aneurysms. \nii. Hypertensive encephalopathy : consists of severe hypertension, \naltered state of consciousness, increased intracranial pressure with \npapilledema and seizure. Focal neurologic deficits are not common. \n3. Effects on the kidneys  : \n\u2022 Arteriolosclerosis of the afferent and efferent arterioles and the glumerular \ncapillary tuft impairs renal function. Patients may have proteinuria and microscopic hematuria  and later on develop chronic renal failure.  \n \nRisk factors for an adverse pr ognosis in hypertension: \n\u2022 Black race  \n\u2022 Youth  \n\u2022 Male sex  \n\u2022 Smoking \n\u2022 Diabetes mellitus  \n\u2022 Hypercholesterolemia \n\u2022 Obesity  \n\u2022 Excess alcohol intake  \n\u2022 Evidence or of end organ damage  \n \nApproach to a patient with Hypertension:  \nDiagnosis of hypertension :  is confirmed after an elevated blood pressure \u2265 140/90 mm Hg, \nproperly measured, has been documented on at least 3 separate occasions (based on the \naverage of 2 or more readings taken at each of 2 or more visits after initial screening). An accurate measurement of blood pressure is the key to diagnosis . \n\u2022 Several determinations should be made over a period of several weeks.  \n\u2022 At any given visit, an average of 3 blood pressure readings taken 2 minutes apart \nusing a mercury manometer is preferable.  \n\u2022 Blood pressure should be measured in both the supine and sitting positions,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac5a-7265-11ef-8efe-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 271, "chroma:document": "\u2022 At any given visit, an average of 3 blood pressure readings taken 2 minutes apart \nusing a mercury manometer is preferable.  \n\u2022 Blood pressure should be measured in both the supine and sitting positions, \nauscultating with the bell of the stethoscope."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac5b-7265-11ef-80a3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 272, "chroma:document": "Internal Medicine \n \n 257\u2022 On the first visit, blood pressure should be checked in both arms and in one leg to \navoid missing the diagnosis of coarctation of aorta or subclavian artery stenosis.  \n\u2022 As the improper cuff size may influence blood pressure measurement, a wider cuff is \npreferable, particularly if the patient's arm circumference exceeds 30 cm.  \n\u2022 The patient should rest quietly for at least 5 minutes before the measurement.  \n\u2022 Although somewhat controversial, the common practice is to document phase V (a \ndisappearance of all sounds) of Korotkoff sounds as the diastolic pressure. \nPatient evaluation : In evaluating a patient with hypertension the initial history, physical \nexamination and laboratory should be directed at  \n1) Establishing pretreatment base line hypertension : \n2) Identifying correctable secondary caused of hypertension \n3) Determining if target organ damage is present: patients may have undiagnosed \nhypertension for years without having had their blood pressure checked. Therefore, a search for end organ damage should be made through proper history and \nphysical examination. \n4) Determining whether other cardiovascular risk factors are present  \n5) Assessing factors that may influence the type of therapy or be changed adversely \nby therapy \nClinical symptoms and History:   \n\u2022 Most patients with hypertension have no specific symptoms and are identified only \nin the course of physical examination"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac5c-7265-11ef-9e43-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 272, "chroma:document": "by therapy \nClinical symptoms and History:   \n\u2022 Most patients with hypertension have no specific symptoms and are identified only \nin the course of physical examination \n\u2022 If patients develop symptoms, the they may be attributable to   \n\u00be The elevated BP itself or \n\u00be The end organ damage associated with hypertension or  \n\u00be The underlying secondary disease  \nSome of the symptoms may be  \n\u2022 Headache:  though popularly considered symptom of high BP, it is a characteristic \nof only sever hypertension. Such headaches are localized to the occipital region  \nand present when the patient awakens in the morning  but subsides spontaneously \nafter several hours \n\u2022 Dizziness  , palpitation , easy fatigability and impotence  \n\u2022 Symptoms referable to vascular diseases or evidences of target organ damage include"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac5d-7265-11ef-9188-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 273, "chroma:document": "Internal Medicine \n \n 258o Epistaxiis , hematuria  \no Retinal changes \u00c6blurring of vision  \no Cerebrovascular damages : Transient ischemic attacks \u00c6 episodes of \nweakness or dizziness or Stroke may occur ( hemorrhagic or ischemic ) \no Cardiovascular damages : chest pain /angina pectoris or myocardial \ninfarction which may cause dyspnea due to  heat failure  \no Pain due to dissecting aorta \n \nSymptoms/history suggesting underlying disease \n\u2022 A history of known renal disease, abdominal masses, anemia, and urochrome \npigmentation.  \n\u2022 A history of repeated UTI may suggest chronic pylonephritis.   \n\u2022 A history of sweating, labile hypertension, headache, nervousness, postural \ndizziness, palpitations and weight loss may suggest the diagnosis of pheochromocytoma.  \n\u2022 A history of polyuria, polydiepsia and muscle weakness may be to secondary to \nhypokalemia associated with aldosteronism.  \n\u2022 A history of weight gain , emotional labiality may suggest Cushing\u2019s syndrome  \n\u2022  A history of cold or heat tolerance, sweating, lack of energy, and bradycardia or \ntachycardia may indicate hypothyroidism or hyperthyroidism. \n\u2022 A history of drug ingestion, including oral contraceptives, licorice, and \nsympathomimetics, should be looked for. \nPredisposing factors for hypertension  \n\u2022 Strong family history of hypertension  \n\u2022 Age : secondary hypertension often develops before the age of 35 or after 55 \n Associated cardiovascular risk factors: \n\u2022 Cigarette smoking"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac5e-7265-11ef-b1c3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 273, "chroma:document": "Predisposing factors for hypertension  \n\u2022 Strong family history of hypertension  \n\u2022 Age : secondary hypertension often develops before the age of 35 or after 55 \n Associated cardiovascular risk factors: \n\u2022 Cigarette smoking  \n\u2022 Lipid abnormality or hypercholesterolemia,  \n\u2022 Diabetes mellitus \n\u2022 Family history of early deaths due to cardiovascular diseases  \n\u2022 Alcoholism."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac5f-7265-11ef-9a42-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 274, "chroma:document": "Internal Medicine \n \n 259\u2022 Obtain a history of over-the-counter medication use, current and previous \nunsuccessful antihypertensive medication trials \n \nPhysical Examination:   \n\u2022 General appearance: \no Round face and truncal obesity suggests Cushing syndrome  \no Muscular development in the upper extremities out of the proportion of the  \nlower extremities suggests coarctation of the aorta \n\u2022 Proper measurement of blood pressure \no Compare the BP and pulses in the two  upper extremities and in supine and \nstanding position \no A rise in diastolic pressure when the patient goes from supine to standing \nposition is most compatible with essential hypertension while a fall in BP in the absence of antihypertensive medications suggests secondary hypertension. \n\u2022 Funduscopic evaluation of the eyes :  should be performed to detect any \nevidence of hypertensive retinopathy. Some of the findings may be flame-shaped hemorrhages and cotton wool exudates. The presence of papilledema and other neurologic signs raises the possibility of increased intracranial pressure \n\u2022 Palpation of all peripheral pulses should be performed . Mainly palpation and \nauscultation of carotid arteries. Femoral pulse should be felt and compared with radial pulse. Radio femoral delay suggests Coarctation of the aorta. \n\u2022 A careful cardiac examination:  is performed to evaluate signs of LVH. These \ninclude displacement of apex, a sustained and enlarged apical impulse, and the presence of an S"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac60-7265-11ef-bde4-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 274, "chroma:document": "\u2022 A careful cardiac examination:  is performed to evaluate signs of LVH. These \ninclude displacement of apex, a sustained and enlarged apical impulse, and the presence of an S\n4. Occasionally, a tambour S 2 is heard with aortic root dilatation. \n\u2022 Abdominal examination:  \no Look for renal artery bruit over the upper abdomen; the presence of a \nunilateral bruit with both a systolic and diastolic component suggests renal \nartery stenosis. \no Palpate for an abdominal aneurysm, enlarged kidneys of polycystic kidney \ndiseases."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac61-7265-11ef-8343-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 275, "chroma:document": "Internal Medicine \n \n 260Diagnostic workup \nLaboratory investigations:  \nUnless a secondary cause for hypertension is suspected, only the following routine \nlaboratory studies should be performed:  \n\u2022 CBC and Hematochrite \n\u2022 Urinalysis including microscopy , protein , blood and , glucose \n\u2022 Fasting blood glucose   \n\u2022 Serum electrolytes : serum K+  \n\u2022 Lipid profile (total cholesterol, low-density lipoprotein [LDL] and high-density \nlipoprotein [HDL], and triglycerides). \n\u2022 Serum creatinine,  uric acid,  \n\u2022 ECG \nImaging Studies:  \n\u2022 Echocardiography : to detect LVH  \nSpecial studies to screen for Secondary hypertension: should be requested only when \nsecondary hypertension is strongly suspected. \n\u2022 Renovascular disease  : ultrasound and Doppler flow study \n\u2022 Pheochromocytoma  : 24 hrs urine assay of metanehprines and catecholamine \n\u2022 Cushing\u2019s syndrome : overnight dexamethason suppression test or 24 hrs urine \ncortisol \n\u2022 Primary aldosteronism : plasma aldostrone  \n\u2022 Thyrotoxicosis  or Myxoedema  : Thyroid function test ( TSH , T 3 and T 4 ) \n \nTherapy of Hypertension  \nIndication for treatment: \n\u2022 Patients with a diastolic pressure >90mm Hg or systolic pressure > 140 mm Hg \nrepeatedly \n\u2022 Isolated systolic hypertension (systolic BP > 160 with diastolic BP < 89 mmHg) if the \npatient is older than 65 years. \nGoal of therapy :  \n\u2022 Reducing the diastolic BP to < 90 mmHg and systolic BP < 150mmHg.  \n1. General measures : non pharmacologic therapy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac62-7265-11ef-9c85-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 276, "chroma:document": "Internal Medicine \n \n 261a. Sodium restriction : intake not more than 100 mmol/d (2.4 g sodium or 6 g \nsodium chloride). \nb. Lifestyle modifications .  \n\u0083 Weight reduction in obese patients  \n\u0083 Limitation of  alcohol intake : alcohol potentiates the action of \ncatecholamines  and may exacerbate hypertension \n\u0083 Regular physical exercise: increase aerobic activity (30-45 min most \ndays of the week).  \n\u0083 Maintain adequate intake of dietary potassium, calcium and \nmagnesium for general health. ( healthy diet like fruits, vegetables, \netc) \n\u0083 Stop smoking  \n\u0083 Reduce intake of dietary saturated fat and cholesterol \n2. Pharmacologic therapy . \nA. Diuretics : are often the first line drugs , and reduce extra cellular fluid volume  \n\u2022 Thiazide diuretics : are more effective anti-hypertensive agents than loop \ndiuretics  Dose:  Hydrochlorothiazide  25 mg PO daily and may be increased \ngradually  \nSide effects:  hypokalemia, hyperuric emia, hyperglycemia \nContraindcation: Gout \n\u2022 Potassium-sparing diuretics (e.g. Spironolactone )   : is a competitive \ninhibitor of aldosteron and may be used in primary hyperaldosteronism (as an additional therapy in combination with thiazide diuretics) Dose: 25-50 mg PO 2 to 4 times daily \nB. \u03b2-adrenergic blocking agents  :  reduce cardiac output and rennin release  \n\u2022 \u03b2-blockers :  Propanolol  , Metoprolol  , Labetolol , Carvidolol , Atenolol \n  Doses: Propranolol 20 mg PO /day to Maximum of 120 mg PO 4X/day"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac63-7265-11ef-910e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 276, "chroma:document": "B. \u03b2-adrenergic blocking agents  :  reduce cardiac output and rennin release  \n\u2022 \u03b2-blockers :  Propanolol  , Metoprolol  , Labetolol , Carvidolol , Atenolol \n  Doses: Propranolol 20 mg PO /day to Maximum of 120 mg PO 4X/day \n               Metoprolol: 25 \u2013 150 mg PO BID \n  Atenolol: 25-100 mg PO/day \nSide effects:  bronchospasm, bradycardia, worsening of heart failure, \nimpotence, depression \nContraindication:  Asthma, peripheral vascular disease (severe)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac64-7265-11ef-92ed-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 277, "chroma:document": "Internal Medicine \n \n 262C. Centrally acting agents : These agents inhibit sympathetic out flow from the \nCNS. \n\u2022 Methyldopa  : 250 mg -1000 mg PO BID , TID or QID  \nSide effects:  postural hypotension, depression, gyneacomastia.  \nD. Vasodilators:  dilate arteriols and arteries, reducing peripheral vascular \nresistance which inturn reduces high blood pressure. \n\u2022 Hydrallazine  : Oral 10-75 mg PO QID  \n                            Paraneteral: 10-50 mg IV or PO every 6 hours. \nSide effects : \u2013 headache, lupus erythromatosis like syndrome  \n\u2022 Minoxidil : 2.5 -40 mg PO BID  \n  Side effects : Orthostatic hypotension \nE. Calcium channel blockers : by modulating calcium release in smooth muscles, \ncalcium channel blockers reduce smooth muscle tone, resulting vasodilatation. \nDihydropyridines:  Nifedipine, Felodipine, Amlodipine  \nNon dihydropyridines  : Diltiazime, and Verapamil \nDoses:  Nifedipine: 30 \u2013 90 mg PO daily \nAmlodipine: 2.5 -10 mg PO daily \nSide effects  : Dihydropyridines:  headache , tachycardia  , GI disturbance  \nNon dihydropyridines  have cardio depressant effect and their use \nmay be problematic in CHF patients   \nContraindication: Heart block, heart failure \nF. ACE inhibitors: inhibit the conversion of angiotensin I to angiotensin II (a potent"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac65-7265-11ef-b812-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 277, "chroma:document": "Non dihydropyridines  have cardio depressant effect and their use \nmay be problematic in CHF patients   \nContraindication: Heart block, heart failure \nF. ACE inhibitors: inhibit the conversion of angiotensin I to angiotensin II (a potent \nvasoconstrictor). By doing so ACE inhibitors reduce peripheral resistance. In addition they reduce aldosteron production, reducing the retention of sodium and water. Captopril , Nezapril , Enalapril , Fosinopril , Ramipril   \nDoses : Captopri  : 12.5 -75  mg PO BID  \nEnalapril : 2.5-40 mg daily \nSide effects : Cough, Leucopenia, angioedema, hyperkalemia. \nContraindicated in:  Bilateral renal artery stenosis, Renal failure.  \nG. Angiotensin receptor blockers : they block the angiotensin system without \ncausing some of the annoying side effects of ACE inhibitors such as cough. Losartan:  25-50 mg once or twice daily \nSide effects : hypotension"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac66-7265-11ef-99eb-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 278, "chroma:document": "Internal Medicine \n \n 263Stepwise prescription of anti -hypertensive medication: \n\u2022 Diuretics are often preferred as first line drugs. They may be effective alone in mild \nhypertension. However most of the time they are used in combination with other \ndrugs like: \u03b2 \u2013blockers, ACE inhibitors or Calcium channel blockers.  The addition of \n12.5 \u2013 25 mg of Hydrochlorothiazide will potentiate the activity of a number of antihypertensive drugs, particularly ACE inhibitors. Such combination has an additive effect, controlling blood pressure in up to 85% of patients \n\u2022 The dosage of be anti-hypertnsivedrugs should be escalated till BP is well controlled  \n\u2022 If one drug fails to control the BP consider changing the antihypertensive drug  \n\u2022 If the blood pressure is still uncontrolled consider using multiple drugs which act at \ndifferent sites and have additive effect. Most drug combinations, using agents that \nact by different mechanisms, have an additive effect. The combination of a calcium \nchannel blocker with either an ACE inhibitor or a dihydropyridine calcium channel blocker and a beta-blocker has additive effects. \n\u2022 Some combinations may not be additive, including a beta-blocker and ACE inhibitor, \na beta-blocker and an alpha1-blocker and an alpha2 stimulant. \n\u2022 Some combinations may have additive adverse effects; these include a beta-\nblocker combined with Verapamil or Diltiazem, which leads to cardiac depression, bradycardia, or heart block."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac67-7265-11ef-b5a8-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 278, "chroma:document": "\u2022 Some combinations may have additive adverse effects; these include a beta-\nblocker combined with Verapamil or Diltiazem, which leads to cardiac depression, bradycardia, or heart block.  \n\u2022 If the BP is still resistant to treatment add direct vasodilators."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac68-7265-11ef-80af-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 279, "chroma:document": "Internal Medicine \n \n 264Choice of anti hypertensive drugs in certain situations for which a specific class of drug \nmay be administered. \n\u2022 Thiazides (e.g.Hydrochlorothiazide) :is the preferred therapy for uncomplicated \nhypertension ,  systolic hypertension in elderly people and  older diabetic patients without nephropathy \n\u2022 ACE inhibitor:  should be the initial treatment in situations in which hypertension is \nassociated with congestive heart failure, diabetes mellitus with proteinuria, and post myocardial infarction with systolic left ventricular dysfunction. In patients who develop persistent cough while on ACE inhibitor therapy, an angiotensin II receptor \nantagonist may be substituted, but these agents' efficacy in lowering cardiovascular \nmortality rates has not yet been proven.  \n\u2022 \u0392-blockers :  are often preferred in post\u2013myocardial infarctionand useful also for \nuncomplicated hypertension.  \n\u2022 A diuretic or a long-acting calcium channel blocker  may be more effective in \nelderly patients with isolat ed systolic hypertension.  \n\u2022 Calcium channel blockers:  Nifedipine is preferred therapy for systolic hypertension \nand an alternative therapy in uncomplicated hypertension.  \n\u2022 Central acting agents  (e.g. Methyldopa) may be used as alternative therapy for \nuncomplicated hypertension. \n \nHypertensive crisis :  is defined as severe hypertension characterized by diastolic blood"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac69-7265-11ef-982d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 279, "chroma:document": "\u2022 Central acting agents  (e.g. Methyldopa) may be used as alternative therapy for \nuncomplicated hypertension. \n \nHypertensive crisis :  is defined as severe hypertension characterized by diastolic blood \npressure greater than 130 mmHg. Blood pressure elevation to such degree can cause vascular damage, encephalopathy, retinal hemorrhage, renal damage and death. 1 \u20132% of the hypertensive population develop this complication.  It is categorized into two:  \n\u2022 Hypertensive Emergency  in which there is acute impairment of an organ system (CNS, \nCVS, Renal). In these conditions, the blood pressure should be lowered aggressively over minutes to hours.  \n\u2022 Hypertensive Urgency  in which BP is high and there is potential risk but not yet caused \nacute end-organ damage. These patients require BP control over several days to weeks.  \nDiagnosis : A diastolic pressure of 130 mmHg, funduscopic finding of papilledema, change \nin neurologic and mental status and abnorma l renal sediments are the hallmarks of \nhypertensive crisis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac6a-7265-11ef-9e4f-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 280, "chroma:document": "Internal Medicine \n \n 265Approach to patients with hypertensive crisis : \n\u2022 Rapid assessment of the patient with brief history and targeted physical \nexamination (of the CNS, CVS , retina ),  \n\u2022 Laboratory investigations  : \no CBC \no Urinalysis  \no Renal function test \no ECG \nTreatment \u201ctreats the patient, not the number\u201d \nGeneral measures : \nInitial considerations: look if the patient is in a stressful situation .Place the patient in a quiet room and reevaluate after initial interview, some patient\u2019s BP lowers below a critical level after relaxation.  \nPharmacologic treatment:  \n\u2022 If the patient has Hypertensive emergency, lower the BP rapidly by 25% of the \ndiastolic BP and not less than 95mmHg.  \n\u2022 Use rapidly acting antihypertensive (IV hydrallazine, Soduim Niteroprusside or \nSublingual Nifedipine). \no Soduim Niteroprusside : is an effective treatment.  \n\u0083 Dose : 0.5-8 microgram/kg/min through continuous IV infusion till BP \nis lowered to the desired level \no Hydralazine  10 -20 mg IV stat to be repeated every 20 -30 minutes can also \nbe used \no Labetalol : 2mg /min through continuous IV infusion \n\u2022 As the patient\u2019s BP stabilizes start long term oral anti hypertensive agents. \n\u2022 Those patient with urgency, could be discharge with close follow \u2013up and oral \nmedication.  \n \nReferences:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nHypertensive vascular diseases, pages 1463-1480"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 280, "chroma:document": "\u2022 Those patient with urgency, could be discharge with close follow \u2013up and oral \nmedication.  \n \nReferences:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nHypertensive vascular diseases, pages 1463-1480 \n2. Myers R. Allen , National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Hypertension, 346-364."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac6c-7265-11ef-b384-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 281, "chroma:document": "Internal Medicine \n \n 2668. Pericarditis and Pericardial effusion                        \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Pericarditis.  \n2. List the etiologies of Pericarditis.  3. Describe the different types of Pericarditis. \n4. Understand the pathophysiology of Pericarditis. \n5. Identify the clinical manifestation of Pericarditis. \n6. Identity acute and chronic complications of Pericarditis.  \n7. Understand the diagnostic approach of Pericarditis. \n8. Understand the principle of management of Pericarditis.  \n \nDefinition: Pericarditis is an inflammation of the pericardium surrounding the heart. \nPercarditis and   cardiac tamponade are clinical problems involving the potential space surrounding the heart or pericardium. Pericarditis is one cause of fluid accumulation in this \npotential space and cardiac tamponade is the hemodynamic result of fluid accumulation.  \n \nPathophysiology: The pericardium consists of an outer fibrous layer (parietal pericardium) \nand an inner serous layer (visceral pericardium).  Normally the two layers are separated by \na small quantity of fluid (15-50 ml).The pericardium  serves as a protective barrier from the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac6d-7265-11ef-ab69-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 281, "chroma:document": "and an inner serous layer (visceral pericardium).  Normally the two layers are separated by \na small quantity of fluid (15-50 ml).The pericardium  serves as a protective barrier from the \nspread of infection or inflammation from adjacent structures. It also prevents sudden dilatation of the cardiac chambers during exercise and hypervolumia. It restricts the anatomic position of the heart and minimizes friction with the surrounding structures. Approximately 120 cc of additional fluid can accumulate in the pericardium without an \nincrease in pressure. Further fluid accumulation can result in marked increases in \npericardial pressure, eliciting decreased cardiac output and hypotension (cardiac tamponade). The rapidity of fluid accumulation influences the hemodynamic effect."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac6e-7265-11ef-a108-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 282, "chroma:document": "Internal Medicine \n \n 267Table \u2013III-8-1.  Classification of Pericarditis  \n \n \nClinical classification   Etiologic Classification  \nI.  Acute pericarditis (<6 weeks) \na. Fibrinous \nb. Effusive (serous or sanguineous) \nII.  Subacute pericarditis (6 weeks to 6 \nmonths) \na. Effusive-constrictive b. Constrictive \nIII. Chronic pericarditis (over 6 \nmonths) \na. Constrictive b. Effusive c. Adhesive (nonconstrictive) \n  I. Infectious Pericarditis \na. Viral b. Pyogenic \nc. Tuberculous \nd. Fungal   \nII. Noninfectious Pericarditis  \na. Uremia b. Acute myocardial infraction \nc. Neoplasm \nd. Idiopathic   \nIII. Hypersensitivity/autoimmune \na. Rheumatic fever \nb. Rheumatoid arthritis \nc. SLE  d. Posttraumatic    \nTB pericarditis is quite common in HIV positive patients.  \n \nClinical features  \nPericarditis \n\u2022 The most common symptom of acute pericarditi s is precordial or retrosternal chest \npain, usually described as sharp or stabbing. \no Pain may be of sudden or gradual onset and may radiate to the back (left \ntrapezial ridge), neck, left shoulder, or arm. \no Movement or inspiration may aggravate the pain. \no Pain may be most severe when the patient is supine and can be relieved \nwhen the patient leans forward while sitting. \n\u2022 Commonly associated symptoms include low-grade intermittent fever, dyspnea, \ncough, and dysphagia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac6f-7265-11ef-97ca-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 283, "chroma:document": "Internal Medicine \n \n 268\u2022 In tuberculosis pericarditis, fever, night sweats, and weight loss are commonly \nnoted (80%). \n\u2022 Some patients may present with acute abdominal pain. \nCardiac tamponade \n\u2022 Patients may present subacutely with symptoms of anxiety, dyspnea, orthopnea, \nfatigue, or altered mental status. \n\u2022 Patients may have a history of medical illnesses associated with pericardial \ninvolvement, particularly end-stage renal disease (ESRD). \n\u2022 Traumatic tamponade may present with acute dyspnea or altered mental status. \n\u2022 A waxing and waning clinical picture may be present in intermittently \ndecompressing tamponade. \n \nPhysical findings:  \nPericarditis \n\u2022 The classic sign of acute pericarditis is pericardial friction rub , which is scratchy, \nleathery sound heard during both systole and diastole. It is best, heard at the lower \nleft sternal border or apex when the patient is positioned sitting forward. Friction rub \nmay be transient from one hour to the next and is present in approximately 50% of \ncases. A friction rub may be distinguished from a cardiac murmur by its changing character from heartbeat to heartbeat and patient position changes. A friction rub is closer to the ear on auscultation than a murmur. \n\u2022 Fever: usually is low grade, but it may occasionally reach 39\n0 C. \n\u2022 Cardiac arrhythmias: Premature atrial and ventricular contractions occasionally are \npresent. \n\u2022 Tachypnea and dyspnea: Dyspnea is a frequent complaint and it may be severe"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac70-7265-11ef-844b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 283, "chroma:document": "\u2022 Fever: usually is low grade, but it may occasionally reach 39\n0 C. \n\u2022 Cardiac arrhythmias: Premature atrial and ventricular contractions occasionally are \npresent. \n\u2022 Tachypnea and dyspnea: Dyspnea is a frequent complaint and it may be severe \nwith myocarditis, pericarditis, and tamponade. \n\u2022 Ewart sign  (dullness and bronchial breathing between the tip of the left scapula and \nthe vertebral column) \n\u2022 Hepatomegally and ascites may be found. \nCardiac tamponade  \n\u2022 As the volume of pericardial fluid increases, the capacity of the atria and ventricles \nto fill is mechanically compromised, leading to reduced stroke volume and tamponade. It is influenced by volume and rate of accumulation."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac71-7265-11ef-9381-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 284, "chroma:document": "Internal Medicine \n \n 269\u2022 Beck triad  (jugular venous distention, hypotension, and muffled heart sounds) \n\u2022 Neck vein distension is a common finding: but Kussmaul\u2019s sign is absent  \n\u2022 Hypotension to the extent of shock: may occur when the cardiac stroke volume \nis significantly reduced and tissue perfusion is compromised   \n\u2022 Pulsus paradoxus : abnormal fall in blood pressure by more than 10 mm Hg during \ninspiration.  \n\u2022 Narrow pulse pressure : indicates reduced left ventricular stroke volume. \n\u2022 Cyanosis \n\u2022 Varying degrees of  altered consciousness \nDiagnostic workup \nLaboratory studies:  \n\u2022 CBC with differential \n\u2022 Elevated erythrocyte sedimentation rate (ESR) \n\u2022 HIV testing \n\u2022 Antinuclear antibody, rheumatoid factor \nImaging Studies:  \n\u2022 Chest radiography: A bottle\u2013shaped heart can be seen with excessive pericardial \nfluid accumulation. In cardiac tamponade (or large effusions), the chest x-ray may \ndemonstrate an enlarged cardiac silhouette after 200-250 ml of fluid accumulation. This occurs in patients with slow fluid accumulation, compared to a normal cardiac silhouette seen in patients with rapid accumulation and tamponade. Thus, the \nchronicity of the effusion may be suggested by the presence of a huge cardiac \nsilhouette. \n\u2022 ECHO:  minimal pericardial effusion in pericar ditis and significant pericardial effusion \nin Chonic pericarditis or Cardiac tamponade.   \n\u2022 ECG :  \no Acute pericarditis: diffuse ST segment elevation without reciprocal ST segment"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac72-7265-11ef-90b0-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 284, "chroma:document": "silhouette. \n\u2022 ECHO:  minimal pericardial effusion in pericar ditis and significant pericardial effusion \nin Chonic pericarditis or Cardiac tamponade.   \n\u2022 ECG :  \no Acute pericarditis: diffuse ST segment elevation without reciprocal ST segment \ndepression and depression of PR segment is unique to acute pericarditis \nreported in up to 80% of viral pericarditis cases..  \no Cardiac tamponade or massive effusion : electrical alternans is pathognomonic \nof cardiac tamponade and is characterized by alternating levels of ECG voltage \nof the P wave, QRS complex, and T waves. This is a result of the heart \nswinging in a large effusion. Low voltage of ECG."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac73-7265-11ef-a87c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 285, "chroma:document": "Internal Medicine \n \n 270Treatment  \n1. Acute Pericarditis : \nTreating pain and inflammation: \n\u2022 Nonsteroidal anti-inflammatory drugs (NSAID): ASA, Indomethacine and Ibuprofen \nare effective in reducing the inflammation and reliving the chest pain. \n\u2022 Steroid therapy: intractable cases of pericarditis that fail to respond to NSAID. \nSpecific therapy : should be directed towards the cause of pericarditis. \nE.g. Patients with TB pericarditis should be treated with ant TB along with steroid \n2. Cardiac tamponade \n\u2022 Patients with evidence of cardiac tamponade need emergency pericadiocentesis i.e. \nremoval of fluid from pericardial sac.  \nComplications of Pericarditis:  \n\u2022 Recurrence : pericarditis may recur in 15-32% of patients  \n\u2022 Cardiac tamponade  \n\u2022 Chronic constrictive pericarditis \n\u2022 Cardiac perforation at time of pericardiocentesis \n\u2022 Bronchopericardial fistula: This was noted as a complication of multi\u2013drug-resistant \nTB in a patient with HIV. \nPrognosis: The prognosis of pericarditis depends upon the etiology of the pericardial \ninfection or inflammation as well as the presence of a pericardial effusion and/or \ntamponade.    \n References:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nPericardial disease, pages 1414-1419."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac74-7265-11ef-ad49-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 286, "chroma:document": "Internal Medicine \n \n 2719. Ischemic Heart Diseases \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Ischemic Heart Diseases. \n2. List the etiologies of Ischemic Heart Diseases. 3. Describe the different types of Ischemic Heart Diseases. \n4. Understand the epidemiology of Ischemic Heart Diseases. \n5. Understand the pathophysiology of Ischemic Heart Diseases. 6. Identify the clinical manifestation of Ischemic Heart Diseases. 7. Identity consequences of Ischemic Heart Diseases hypertension.  8. Outline the diagnostic approach of Ischemic Heart Diseases. \n9. Understand the principles of management of Ischemic Heart Diseases.  \n10. Refer patients with Ischemic Heart Diseases to better facility. \n \nBackground  Ischemic Heart Diseases manifests due to an imbalance in myocardial oxygen supply and \ndemand, that results in myocardial hypoxemia. The most common cause of myocardischemia is atherosclerotic disease of the coronary arteries. \nEpidemiology   \n\u2022 IHD is the leading cause of morbidity and mortality in developed countries and it \nincurs greater economic cost. \n\u2022 The prevalence of IHD is also on the rise in developing countries as there is a \nchange in the life style associated with urbanization including sedentary life style, \nsmoking, obesity high fat and energy diet and the associated increased prevalence in Diabetes mellitus. \n\u2022 Larger increases in prevalence of  IHD through out the world are projected, and the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac75-7265-11ef-989a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 286, "chroma:document": "smoking, obesity high fat and energy diet and the associated increased prevalence in Diabetes mellitus. \n\u2022 Larger increases in prevalence of  IHD through out the world are projected, and the \nit is likely to become the most common cause of death worldwide by 2020 \n \nEtiology/Pathophysiology \nMyocardial ischemia reflects an imbal ance between myocardial oxygen supply and \ndemand. Myocardial oxygen demand is mainly determined by heart rate, the force of \nventricular contraction, and ventricular wall te nsion, which is proportional to the ventricular"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac76-7265-11ef-b0a4-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 287, "chroma:document": "Internal Medicine \n \n 272volume and pressure. Unless there is a proportionate rise in oxygen supply, conditions that \nincrease oxygen demand such as physical exertion result in ischemia Atherosclerosis of coronary artery (CAD) is the most common cause IHD.  \n Risk factors for Coronary artery disease / Ischemic heart diseases \n\u2022 Age: the risk of CAD increases progressively with age. The risk of death from CAD \nis 1.5 in 1000 individuals at age 50. \n\u2022 Gender  : IHD is more prevalent in men than in women >The difference is more \nmarked in premenopausal women compared to men of similar age \n\u2022 Lipid abnormalities  :  increased serum LDL level and reduced HDL level with \nhypertrigyceridemia favors the deposition of lipds and choletrol in atherosclerotic plaques \n\u2022 Smoking  : cigarette smokers are 60% more likely to develop CAD than non \nsmokers \n\u2022 Hypertension : increases the risk of CAD both in men and women. \n\u2022 Diabetes mellitus  : is associated with significant increase in the risk of CAD  \n\u2022 Family history : a familial predisposition to CAD exists \n\u2022 Oral contraceptive pills : use of OCP is associated with increased risk of CAD. \n\u2022 Other risk factors : Gout, Obesity.  \n Atherosclerosis is focal narrowing of arteries which results from a plaque formation. In \nCAD, atherosclerosis risk factors such as hyperlipidemia, cigarette smoking, diabetes \nmellitus, and hypertension apparently disrupt the normal functioning of the vascular endothelium.  Plaques are formed as a result of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac77-7265-11ef-93a1-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 287, "chroma:document": "CAD, atherosclerosis risk factors such as hyperlipidemia, cigarette smoking, diabetes \nmellitus, and hypertension apparently disrupt the normal functioning of the vascular endothelium.  Plaques are formed as a result of  \n\u2022 Intimal smooth muscle proliferation probably as a result of endothelial damage  \n\u2022 Lipids ( Cholesterol esters ) are deposited at the center of plaques and also with in \nsmooth muscle cells \n\u2022 A fibrous cup made of connective tissue covers the plaque \n \nAs the stenotic lesions grow, perfusion pressure distal to the lesions decreases; in response, coronary arterioles dilate to maintain adequate blood flow preventing ischemic symptoms at rest. During exertion the myocardial oxygen demand increases which couldn\u2019t be matched by"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac78-7265-11ef-b0d8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 288, "chroma:document": "Internal Medicine \n \n 273the perfusion via the narrowed coronary artery. The resulting myocardial ischemia results in \nchest pain, called angina pectoris, which is relived by taking rest.  Sometimes atherosclerotic plaques may rapture and a fibrin thrombus is formed overe the \nplaque which completely blocks the narrowed coronary artery and result in myocardial \ninfarction. \n Factors in CAD   \nClinical features of Coronary artery diseases. \n1. \nAngina pectoris : is a chest pain or pressure produced by myocardial ischemia.  \n\u2022 Anginal pain is often precipitated by exertion. Other factors that increase myocardial \noxygen demand (e.g. emotional stress, eating meal, sexual intercourse) may also precipitate angina. \n\u2022 The chest pain in angina is squeezing in type or a feeling of pressure or tightness in \nthe chest. Sometimes it can be burning in nature or felt as epigatric discomfort. \n\u2022 Radiation: the pain radiates to the left shoulder, left jaw, teeth or to the left arm. \nSometimes it may radiate to the right arm. \n\u2022 The pain in angina is often reproducible with the same degree of physical exertion. \nThe symptom usually begins with low intensity, increase over 2-3 minutes and often lasts less than 15 minutes. Episodes lasting morethan30 minutes suggest myocardial infarction may have occurred \nTypes of Angina  \nA. Chromic stable angina : angina which recurs under similar circumstances and with \nsimilar frequency over time."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac79-7265-11ef-8dc1-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 288, "chroma:document": "Types of Angina  \nA. Chromic stable angina : angina which recurs under similar circumstances and with \nsimilar frequency over time. \nB. Silent ischemia : for every episode of symptomatic ischemia that the patient suffers, \nthere are usually four to five episodes of silent (asymptomatic) ischemia. This \nepisode can be detected by ECG including stress ECG. Such episodes are less severe in nature and shorter in duration. \nC. Unstable angina : is a term applied to angina when a change in status occurs. \nUnstable angina is progressive and it may be ominous feature of imminent myocardial infarction. So physicians and patients should be aware that close \nobservation and intensive therapy are required. It represents a more serious \nsituation tan chronic stable angina.  \ni. New onset angina   is an angina that progresses in  severity  , duration or \nfrequency  over 1-or 2 months"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac7a-7265-11ef-b390-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 289, "chroma:document": "Internal Medicine \n \n 274ii. Resting angina : is particularly worrisome because it implies decreased \nsupply, rather that increased demand, is causing angina. This suggests \npossible occlusion is imminent. \n \nC. Varian ( Prinzmetal\u2019s ) angina  :  \n\u2022 This is a type of angina resulting from transient coronary spasm, which \nusually but not always associated with fixed atherosclerotic lesion. The \nspasm produces total but transient coronary occlusion. \n\u2022 It usually occurs at rest (often at night) and episodes are frequently \ncomplicated with ventricular arrhythmias. \nHistory   \n\u2022 In a patient presenting with a history of recurrent chest pain, obtain a detailed \nsymptom history, including onset, quality, location, duration, radiation, and precipitating and relieving factors.  \n\u2022 Determine the presence or absence of each of the three following symptom \ncomplex characteristics:  \n1. Substernal discomfort with a characteristic quality and duration 2. Symptoms provoked by exertion or emotional stress, and  3. Symptoms relieved by rest or nitroglycerin.  \n\u2022 Based on the number of symptom complex present, angina can be  classified as : \no Typical (definite)  angina if all three of the characteristics  are present \no Atypical angina (probable)  if two of the characteristics  are present or  \no Non-cardiac chest pain  if none or one of the characteristics is present.  \n\u2022 If the patient's symptoms are consistent with typical angina, sub-classify the angina"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac7b-7265-11ef-94f4-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 289, "chroma:document": "o Atypical angina (probable)  if two of the characteristics  are present or  \no Non-cardiac chest pain  if none or one of the characteristics is present.  \n\u2022 If the patient's symptoms are consistent with typical angina, sub-classify the angina \nas stable (unchanged for 2 or more months) or unstable (rest, new-onset, or \nincreasing) angina.  \n\u2022 In patients with typical (definite) or atypical (probable) angina, ask about functional \nlimitations  \n\u2022 Ask about any episodes of dyspnea, palpitations, or dizziness with or without chest \npain. If the patient has experienced any such episodes, ask about the same symptom variables that are applicable to typical angina  \n\u2022 Assess potential risk factors for CAD, includ ing those related to lifestyle, habits, past \nmedical history, family history, and hormone therapy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac7c-7265-11ef-a0d9-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 290, "chroma:document": "Internal Medicine \n \n 275\u2022 Ask about a history of symptoms, such as exertional dyspnea, orthopnea, and \nbilateral leg swelling, that suggest left ventricular (LV) dysfunction or heart failure \nand nocturia   \n\u2022 Ask about other potential causes of chest pain, especially if the symptoms have \nchanged, new symptoms have arisen, or the patient is at low risk for CAD.  \nPhysical Examination  \n\u2022 In a patient presenting with suspected stable angina, perform a complete physical \nexamination to help identify the cause of the chest pain and any comorbid disorder(s)  \n\u2022 Assess the vital signs, especially for hypertension, tachycardia, bradycardia, \narrhythmia, and tachypnea  \n\u2022 Closely examine the head and neck, especially for signs of anemia (mucous \nmembrane pallor), thyroid disease (exophthalmos, thyromegaly), \nhypercholesterolemia (Xanthelema which is the deposit of lipids in the skin of the \neyelids) or atherosclerosis (carotid bruit)   \n\u2022 Perform a general and peripheral vascular examination to identify signs of \ngeneralized or peripheral atherosclerosis (e.g., inequality of blood pressure in arms, diminished pedal pulse, and abdominal aneurysm).  \n\u2022 Carefully examine the heart for evidence of hypertrophy, murmurs, and third or \nfourth heart sounds (S3, S4).  \n\u2022 Examine the lungs for rales (crackles) and other abnormal breath sounds.  \n\u2022 Examine the lower extremities for dependent (ankle) edema, tendinous xanthomas"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 290, "chroma:document": "fourth heart sounds (S3, S4).  \n\u2022 Examine the lungs for rales (crackles) and other abnormal breath sounds.  \n\u2022 Examine the lower extremities for dependent (ankle) edema, tendinous xanthomas \n(lipid deposit), weak pulses, or cutaneous signs of ischemia or necrosis.  \n \n Diagnostic workup:  \nElectrocardiography: \nResting ECG : \n\u2022 ECG taken when the patient is not in pain may be normal. The presence of new \nhorizontal or down sloping of ST segment depression and new T-wave inversion are \nsuggestive of myocardial ischemia. \n\u2022 ST segment elevation associated with pain which returns to normal as the pain \nwanes suggest variant angina"}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 291, "chroma:document": "Internal Medicine \n \n 276Stress ECG :  \n\u2022 Recording ECG during exercise increases the sensitivity and specificity of ECG. \nThis helps to quantify the patient\u2019s exercise tolerance. The presence of new \nhorizontal or down sloping of ST segment depression has sensitivity of 70 % and specificity of 90 %. \nRadiologic/Imaging   \n\u2022 Chest-ray in patients with symptoms and signs of congestive heart failure  \n\u2022 Stress radionuclide ventricuography \n\u2022 Stress echocardiography \n\u2022 Cardiac catheterization  \n \nOther laboratory tests  \n\u2022 Hemoglobin or CBC, fasting blood glucose,  \n\u2022 Serum lipid profile  \nDifferential Diagnosis  \nConsider other cause of chest pain like  \n\u2022 Pleurisy  \n\u2022 Pneumonia \n\u2022 Pericarditis \n\u2022 Ischemia associated with aortic stenosis, or hypertrophic cardiomyopathy  \n \nTreatment for Angina  \nTherapy for angina should be directed either towards reducing myocardial oxygen demand, \nor to compensate for impaired flow through diseased coronary arteries or at increasing \nmyocardial oxygen supply (i.e. blood flow) \nGeneral measures  \nLifestyle Measures  \n\u2022 Counsel patients about cessation of smoking \n\u2022 Diet (\u2018healthy\u2019 diet like low fat  and low caloric diet with increased habit of eating \nfruits and vegetables) \n\u2022 Regular exercise \n\u2022 Weight reduction."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac7f-7265-11ef-80d5-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 292, "chroma:document": "Internal Medicine \n \n 277Medical therapy \na) Nitrates : this class of drugs produce venodilation and to lesser extent arteriolar \ndilation. These effects reduce blood pressure and reduce cardiac size. \nInstruct patients about how and when to use short-acting nitrates (e.g., 0.4 mg \nsublingual nitroglycerin) for acute attacks, unless nitrates are contraindicated \nConsider long-acting nitrates in patients who have refractory chest pain despite \nmaximal tolerated beta-blocker therapy, or in patients who would benefit from after load reduction  \nTo avoid nitrate tolerance in patients requiring long-acting nitrates, prescribe a 10- \nto 12-hour nitrate-free period daily.  Nitroglycerine 0.3-0.6 mg  sublingual as soon as the pain starts or 5 minutes \nbefore a stressful activity. Isosorbide dinitrate slow release : 10-60 mg PO TID or 2.5 -10 mg sublingual \nevery 4-6 hrs \nb) \u03b2-blockers : reduce heart rate and myocardial contractility. By doing so reduce \ncardiac oxygen demand. Propranolol, Atenolol, Nadolol, and Timolol may be used. \nPropranolol:  20 -80 mg PO BID to QID \nMetoprolol:  25-200 mg Po BID  \nAtenolol:  50 -150 mg PO daily \nN.B. Consider the patient's concomitant health problems, when selecting a specific beta-blocker Contraindicated  in patients with asthma and severe form of CHF \n \nc) Calcium channel blockers : decrease the tone of the smooth muscle of coronary \narteries.  These drugs are especially effective in preventing coronary spasm that cause \nvariant angina."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac80-7265-11ef-8d35-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 292, "chroma:document": "c) Calcium channel blockers : decrease the tone of the smooth muscle of coronary \narteries.  These drugs are especially effective in preventing coronary spasm that cause \nvariant angina. \nNifedipine XL : 30 mg PO O daily \nVerapamil: 180-240 mg daily \nAmlodipine:  5-10 mg daily \n\u2022 Consider calcium channel blockers when beta-blockers are contraindicated or \nare not tolerated."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac81-7265-11ef-9935-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 293, "chroma:document": "Internal Medicine \n \n 278\u2022 Consider using combination therapy cautiously (e.g., a beta-blocker and \ncalcium antagonist or nitrate) for patients who fail to respond adequately to \nmonotherapy.  \nd) Anti-platelet agents :  \nAspirin:  small dose of aspirin is recommended for patients with angina to prevent \nthe occurrence of myocardial infarction. \nDose: 75 \u2013 150 mg PO daily. \ne) Lipid lowering drugs  :Generally, prescribe a lipid-lowering medication (statins) and \na low-fat, low-cholesterol diet for patients with CAD and elevated low-density \nlipoprotein (LDL) levels to achieve an LDL level of less than 100 mg/dl  \nf) ACE inhibitor  : may be beneficial in all patients with significant CAD by \nangiography or in those with previous MI who also have diabetes and/or LV systolic \ndysfunction  \ng) Treat comorbidities that can provoke or exacerbate angina (e.g., hypertension, \ndiabetes mellitus, hyperthyroidism, pulmonary disorders, anemia)  \n\u2022 N.B Acute Care/Hospitalization : Always refer patients presenting with new-onset, rest, \nor increasing angina to an emergency department, and hospitalize a patient with clinical \nevidence of unstable angina or myocardial infarction.  \nSurgical interventions:  \n\u2022 Percutanous transluminal coronary angioplasty \n\u2022 Artherectomey \n\u2022 Coronary artery bypass surgery \nComplications  \n\u2022 In patients with chronic stable angina, be sensitive particularly to accelerating \nsymptoms, indicating development of unstable angina. \nPrognosis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 293, "chroma:document": "\u2022 Artherectomey \n\u2022 Coronary artery bypass surgery \nComplications  \n\u2022 In patients with chronic stable angina, be sensitive particularly to accelerating \nsymptoms, indicating development of unstable angina. \nPrognosis  \nThe main prognostic indicators in patients with ischemic heart disease (IHD) are: \n\u2022 The status of left ventricular (LV) function \n\u2022 The location and severity of coronary artery narrowing \n\u2022 The severity or activity of myocardial ischemia \n\u2022 The presence of complex arrhythmias"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac83-7265-11ef-a52b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 294, "chroma:document": "Internal Medicine \n \n 279Acute Myocardial Infarction    (AMI)  \nAMI develops when the myocardium is deprived of its blood supply (Oxygen) for a significant \namount of time. \nAMI may be classified in to  \n\u2022 Transmural myocardial infarction  : results from obstruction of coronary arteries  \nby thrombus or coronary spasm \n\u2022 Non Transmural ( subendocardial ) myocardial infarction the cause of which \nremains uncertain \nSymptoms: \n\u2022 Chest pain : Sever squeezing or crushing type of chest pain that lasts for more than \n30 minutes and not relived by rest or sublingual nitroglycerine. The pain radiates in \na similar pattern to angina. The pain usually occurs when the patient is a rest or involved in minimal activity. Emotional  stress may also precipitate AMI. \n \n\u2022 Other associated symptoms ; Nausea, vomiting, diaphoresis and shortness of \nbreath, anxiety and sense of impending doom. \nPhysical examination \n\u2022 The patient is in pain and quite apprehensive often appears ashen \n\u2022 Hypotension and tachycardia may be present if the infarction is extensive  \n\u2022 There also may be signs of CHF (E.g.  elevation of JVP , pulmonary rales , and S\n3 \ngallop ) \n\u2022 A new murmur of mitral regurgitation may be present. \nComplications of AMI \nArrhythmias:  \n\u2022 Lethal ventricular arrhythmias are the commonest cause of death in the first hour. \nThis may include ventricular tachycardias and ventricular fibrillation \n\u2022 Atrial arrhythmias ; atrial fibrillation and atrial flutter"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac84-7265-11ef-bff6-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 294, "chroma:document": "Arrhythmias:  \n\u2022 Lethal ventricular arrhythmias are the commonest cause of death in the first hour. \nThis may include ventricular tachycardias and ventricular fibrillation \n\u2022 Atrial arrhythmias ; atrial fibrillation and atrial flutter \nAcute conduction system abnormality   \n\u2022 The conduction system may be part of the myocardium affected during infarction. \nThis may lead to bradycardia and heart block \n\u2022 Inferior wall MI occurs when the right coronary artery is occluded. Since it supplies \nthe AV node, Sinus bradycardia and varying degree of AV block occur during inferior myocardial infarction."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac85-7265-11ef-b908-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 295, "chroma:document": "Internal Medicine \n \n 280\u2022 Anterior myocardial infarction may lead to Right or left bundle branch blocks \nPump failure  \n\u2022 Congestive heart failure is most likely to occur, when 30 % of the myocardium is \ninfracted ,  \n\u2022 Cardiogenic shock , defined as Systolic BP < 90 mmHg: occurs if more than 40% \nof the myocardium is affected by infarction. \nMitral regurgitation:  may occur if the papillary muscles are affected by infarction. \nVentricular septal defect :  \n\u2022 The left ventricular septum may become infracted either in anterior or inferior AMI. , \nleading to rapture of the septum. \nCardiac rapture :  \n\u2022 Myocardial infarction of the free wall may lead to eventual perforation of the heart. \nThis complication, which results overwhelmingly cardiac tamponade, is nearly \nalways fatal. \nLeft ventricular aneurysm:   \n\u2022 The infracted myocardium may evaginate and heal with fibrous connective tissue. It \nmay be a source for cardiac emboli. \nPericarditis:  post AMI pericarditis (Dressler\u2019s Syndrome) which is believed to be \nautoimmune in origin. Diagnostic work up \n1. ECG:  is diagnostic in approximately 85% of cases. \n\u2022 Transmural MI/Q-wave MI  :  ST segment elevation in those leads reflecting \nthe area of myocardial infarction ,As ST segments fall , Q waves appear and T waves become inverted \n\u2022 Subendocadial infarction /Non Q wave MI ;  ECG findings are less certain \nand ST segment depression may be the only finding"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac86-7265-11ef-a28d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 295, "chroma:document": "the area of myocardial infarction ,As ST segments fall , Q waves appear and T waves become inverted \n\u2022 Subendocadial infarction /Non Q wave MI ;  ECG findings are less certain \nand ST segment depression may be the only finding \n2. Cardiac enzymes  : as myocardial necrosis occurs , the myocardium releases \ncardiac enzymes \n\u2022 Creatine phospho kinase ( CPK ) elevation appears 6 hours after infarction  \n\u2022 Aspartate aminotransfarase ( AAST or SGOT ) elevates 12 hrs after \ninfarction  \n\u2022 Lactate dehydrogenase (LDH): starts to elevate 24 hrs after infarction."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac87-7265-11ef-8dad-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 296, "chroma:document": "Internal Medicine \n \n 281\u2022 Cardiac specific troponin-T and cardiac specific troponin- I, are also elevated \nand they are very specific to cardiac muscles. (So this is the preferred \nbiomedical test in Developed countries.). These proteins are not normally detectable in the blood of healthy individuals , but rise > 20 X in patients with AMI. \n \n3. Cardiac Imaging  \n\u2022 Echo: Decrease myocardial function ( decrease ejection fraction ) and \nsignificant wall motion abnormality may be detected  \n\u2022 Radionuclide imaging techniques \n \nManagement of patients with acute myocardial infarction \nManagement of AMI is beyond your capacity and immediate referral to hospitals with \nintensive care unit (ICU) facility is mandatory. However, the management of acute MI is \noutlined as follows \nA. Emergency management  :Management of patients should start before they reach \nthe hospital emergency room \n1. General measures  \n\u2022 Reassure and make the patient comfortable  \n\u2022 Supply O 2  by mask \n\u2022 Secure IV line  \n\u2022 Give Aspirin 160-325 mg tablets \u2013helps to prevent further platelet \naggregation  \n2. Treatment of pain : \n\u2022 Nitroglycerin : sublingual up to three doses of 0.4 mg should be \nadministered at about 5 minutes interval for up to three doses. \n\u2022 Morphine sulphate:  is very effective analgesic for pain associated with AMI \norigin .It is administered in small doses of 2-4 mg IV every 5 minutes  \n3. Limitation of infarct size through reperfusion or revascularization.: \n\u2022 Thrombolysis/Fibrinolysis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac88-7265-11ef-a5ee-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 296, "chroma:document": "origin .It is administered in small doses of 2-4 mg IV every 5 minutes  \n3. Limitation of infarct size through reperfusion or revascularization.: \n\u2022 Thrombolysis/Fibrinolysis \n\u00be Thrombolytic agents : such as Streptokinase , t-plaminogen activator, \nurokinase : these drugs are given to  dissolve the occlusive thrombus \nand promote reperfusion of the infarct related artery reduces"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac89-7265-11ef-b30a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 297, "chroma:document": "Internal Medicine \n \n 282mortality from myocardial infarction when administered within 6 hours \nof the onset of chest pain. \nContraindication : History of Cerebrovascular hemorrhage, marked \nhypertension, bleeding disorder. \n\u2022 Direct percutanous transluminal coronary angioplasty:  in best facilities \nin the developed countries this is the preferred method to restore perfusion \nof occluded coronary artery. When perf ormed by experienced physicians the \nshort and long term outcomes are much better than what can be archived \nthrough thrombolysis or fibrinolysis. \nB. Hospital phase management:  patients should be referred and admitted to \ncoronary artery units or ICU. \n1. General measures  \n\u2022 Activity :  absolute bed rest for the first 12 hours , Sitting on their bed in the \nfirst 24 hours , the patient may ambulate in their rooms by the 2nd or 3rd day \n\u2022 Diet :  Because of the risk of emesis and aspiration soon after AMI , patients \nshould receive either nothing or only clear liquids by mouth for the first 4-12 hrs. The diet should be low fat low calori and rich in Potassium \n\u2022 Bowel motion : constipation is common and straining may precipitate AMI . \nFibrous diet and Stool softeners like bisacodyl or Dioctyl sodium sulfosuccinate 200 mg /day are recommended. If the patient remains \nconstipated laxatives can be prescribed. \n\u2022 Sedation:  many patients require sedation during hospitalization to withstand \nthe period of enforced inactivity with tranquility."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac8a-7265-11ef-b739-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 297, "chroma:document": "constipated laxatives can be prescribed. \n\u2022 Sedation:  many patients require sedation during hospitalization to withstand \nthe period of enforced inactivity with tranquility. \no Diazepam15 \u2013 30 mg or Lorazeam 0.5 to 2mg given 3-4 X daily. \n \n2. Pharmacological therapy \na) Antithombotic agents  and anti platelet agents : \n\u2022 Unfractionated heparin : may be given in patients where there is a risk of \ncardiac thrombus formation and subsequent emboli \n\u2022 Anti platelet agents : ASA 75-150 mg Po daily to prevent recurrence of AMI \nb) \u03b2-Blockers : have short term and long term benefits for patients with AMI. \n\u2022 The short term benefit is they relive pain and decrees the risk of malignant \narrhythmias"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac8b-7265-11ef-84b6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 298, "chroma:document": "Internal Medicine \n \n 283\u2022 Long term benefits are : improved myocardial performance and facilitate the \nhealing process in Post myocardial infarction patients \nMetoprolol: 25-200 mg BID \nAtenolol: 50-150 mg Po daily \n  Contraindication : Severe CHF, AV block \nc) ACE inhibitors  ; reduce the mortality rate and improve long term survival in post \nAMI patients by preventing cardiac remodeling which may have lead to progressive heart failure. Their effect is additive to what is archived with Aspirin and \u03b2-blockers. . The maximum benefit is seen in high risk patients  ( elderly \npatients , significant LV dysfunction ) . ACE inhibitors should be prescribed \nwithin 24 hours and maximum benefit is archived when they are given at higher \ndoses that are recommended. In patients with CHF ACE inhibitors are given indefinitely. \nCaptopril: Start with smaller dose 12.5 mg PO day to gradually escalate to 75 mg Po BID \nEnalapril: Start with 2.5 mg PO daily and escalate gradually to 40 mg Po \ndaily \nManagement of Complications  \nMalignant arrhythmias ;  \n\u2022 Cardiac defibrillation \n\u2022 Prophylactic lidocaine  \n\u2022 Other antiarrhythmic agent; bertyluim tosylate and procainamide \nTreatment of serous conduction disturbances; \n\u2022 Sinus bradycardia :Atropine  2mg IV  may restore conduction and restore heart rate \n\u2022 AV block : Trans cutanous cardiac pace makers  \nHeart failure: \n\u2022 Diuretics, Salt restriction, ACE inhibitors, vasodilators. Use of digoxin is \ncontroversial."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac8c-7265-11ef-9260-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 298, "chroma:document": "\u2022 Sinus bradycardia :Atropine  2mg IV  may restore conduction and restore heart rate \n\u2022 AV block : Trans cutanous cardiac pace makers  \nHeart failure: \n\u2022 Diuretics, Salt restriction, ACE inhibitors, vasodilators. Use of digoxin is \ncontroversial. \nCardiogenic shock:  do Echocardiography to assess the ventricular function \n\u2022 IV infusion of fluids to maximize left ventricular filling  \n\u2022 Use of vasopressors: Dubutamine, dopamine) in IV infusion. \n\u2022 Intraaortic balloon pumping  \n\u2022 Percutanous transluminal angioplasty"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 299, "chroma:document": "Internal Medicine \n \n 284Prognosis: depends on two factors  \nThe extent of coronary artery disease in terms of the number of vessels affected \n\u2022 Patents with uncorrected main left coronary artery disease have approximately a 20 \n% mortality in the first year  \n\u2022 Single vessel coronary artery has 2 % annual mortality. \n\u2022 Double vessel disease: have approximately a 2- 4 % annual mortality. \n\u2022 Triple vessel disease: have 5-8 % annual mortality. \nThe extent of ventricular damage: left ventricular ejection fraction  \n\u2022 An ejection fraction of <40 % doubles the yearly mortality rate at each level of extent \nof coronary disease. \nRevascularization:  significantly improves the short term and long term morbidity and, \nmortality when it is done at the right time by an expert hand.  \n \nReferences:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nIschemic heart disease, pages 1434-1448. \n2. Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Ischemic heart disease, pages 15-28."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 300, "chroma:document": "Internal Medicine \n \n 28510. Cardiac Arrhythmias \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Cardiac arrhythmias  \n2. List the etiologies of arrhythmias. 3. Classify the different types of arrhythmias. \n4. Understand the pathophysiology of arrhythmias. \n5. Identify the clinical manifestation of arrhythmias. 6. Identity consequences of arrhythmias.  7. Understand the diagnostic approach arrhythmias.  \n8. Understand the principle of management of arrhythmias.   \n9. Refer patients with arrhythmias to appropriate centers  \n \nDefinition : Cardiac arrhythmias are changes in the regular beating of the heart. The heart \nmay seem to skip a beat or beat irregularly or beat very fast or very slow. \nThe normal heart beat of a person ranges from 60 -100 beats/min. \n\u2022 Many arrhythmias occur in people who do not have underlying heart disease. \n\u2022 Most of the time, there may not be a recognizable cause of an arrhythmia.  \n\u2022 Heart disease may cause arrhythmias. Other causes include: stress, caffeine, \ntobacco, alcohol, diet pills,\u201dK hat\u201d, cough and cold medicines. \n\u2022 In some people, arrhythmias are associated with heart disease. In these cases, \nheart disease, not the arrhythmia, poses the greatest risk to the patient. \n\u2022 In a very small number of people with se rious symptoms, arrhythmias themselves \nare dangerous. These arrhythmias require medical treatment to keep the heartbeat \nregular."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac8f-7265-11ef-8126-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 300, "chroma:document": "\u2022 In a very small number of people with se rious symptoms, arrhythmias themselves \nare dangerous. These arrhythmias require medical treatment to keep the heartbeat \nregular.  \n\u2022 Arrhythmias occur commonly in middle-age adults. As people get older, they are \nmore likely to experience an arrhythmia. \n\u2022 Patients with arrhythmias often complain that they felt their heart beat very fast, \nexperienced a fluttering in their chest, or noticed that their heart skipped a beat. Almost everyone has also felt dizzy, faint, or out of breathe or had chest pains at one time or another."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 301, "chroma:document": "Internal Medicine \n \n 286Classification of Arrhythmias \n1. Bradyarrhythmias: are arrhythmias in which the heart beats slower than normal. \nThey result from inadequate sinus impulse  production or from blocked impulse \npropagation. They are not usually cause of concern unless the patient develops \nsyncope or presyncope.  \n\u2022 Sinus bradycardia \n\u2022 Sinus pause  \n\u2022 AV block \n2. Tachyarrythmias : are arrhythmias in which the heart beats faster than normal.  \nA. Atrial tachyarrhythmias: tachyarrhythmias originating from the atria.  \ni) Regular atrial tachycardias : the heart beats faster but the rhythm is regular  \n\u2022 Sinus tachycardia  \n\u2022 Paroxysmal atrial tachycardias \n\u2022 Atrial flutter with constant conduction  \nii) Irregular atrial tachycardias : the heart beats faster and the rhythm is \nirregular \n\u2022 Atrial fibrillation  \n\u2022 Multifocal atrial tachycardia \n\u2022 Atrial flutter with irregular conduction \nB. Ventricular Tachyarrhythmias: tachyarrhythmias originating from the ventricles.  \n\u2022 Premature ventricular contraction \n\u2022 Ventricular tachycardia \n\u2022 Ventricular fibrillation  \nBradyarrhythmias \n1. Sinus bradycardia:  \nCauses  \n\u2022 Physical conditioning in professional athletes \n\u2022 Hypothyroidism \n\u2022 Sinus node dysfunction \nTherapy \n\u2022 If  it is physiologic no need for treatment \n\u2022 If it is due to sinus dysfunction and severe  ( the HR  is < 35 beats/min) :"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 302, "chroma:document": "Internal Medicine \n \n 287o Atropine : 1mg IV  may temporarily increase the sinus rate \no Cardiac Pacemaker implantation. \n2. Sick sinus syndrome:  The sinus node does not fire its signals properly, so that \nthe heart rate slows down. Sometimes the rate changes back and forth between a \nslow (bradycardia) and fast (tachycardia) rate \n3. AV blocks:  all of the impulses generated from the sinus node are not conducted to \nthe ventricles \n2nd degree AV block:  Some atrial impulses are blocked and not transmitted to the \nventricles  \n\u2022 Mobitz Type I (Wenckebach) block : the PR interval is progressively \nprolonged until a generated P wave is not conducted. \n\u2022 Mobitz Type II block:  there is no prolongation of the PR interval before the \ndropped beat. Often conduction is in a ration of 2: 1and it  is prolonged enough to cause symptomatic bradycardia. \n3\nrd Degree (Complete) heart block : No atrial impulses are conducted and the atria \nand the ventricles are contracting independently. The heart rate drops significantly to a range of 20- 40 beats/min and patients become symptomatic. \nTherapy: \n\u2022 Pharmacologic therapy : reserved only for acute situations to temporarily increase \nthe ventricular rate. \no Atropine 0.5-2 mg IV or Isoproterenol 1-4 microgram/min IV  \n\u2022 Permanent cardiac pacemakers  : most symptomatic AV blocks need  permanent \npacing \nSinus tachycardia : the sinus node sends out electrical signals faster than usual,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac92-7265-11ef-9984-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 302, "chroma:document": "o Atropine 0.5-2 mg IV or Isoproterenol 1-4 microgram/min IV  \n\u2022 Permanent cardiac pacemakers  : most symptomatic AV blocks need  permanent \npacing \nSinus tachycardia : the sinus node sends out electrical signals faster than usual, \nspeeding up the heart rate. It represents physiologic or pathologic increase in the sinus rate \n\u2265100 beats/min. It rarely exceeds > 200 beats/min  \nSupraventricular tachycardia (SVT), paroxysmal atrial tachycardia (PAT) . A \nseries of early beats in the atria speed up the heart rate (the number of times a heart beats \nper minute). In paroxysmal tachycardia, repeated periods of very fast heartbeats begin and \nend suddenly. These arrhythmias are sudden onset, often occurring in patients with otherwise normal heart, and characterized by a heart rate of 150-250 beats /min"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac93-7265-11ef-afba-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 303, "chroma:document": "Internal Medicine \n \n 288Common causes  \n\u2022 Exercise , fever  \n\u2022 Anxiety ,thyrotoxicosis \n\u2022 Hyopoxemia ,hypotension \n\u2022 Heart Failure \nDiagnosis: ECG : Faster rate with P waves followed by narrow QRS complexes. \nTreatment:  \n\u2022 If patient is stable  \u2013 No need for treatment, identify and treat the underlying cause. \n\u2022 If the patient is hemodynamically unstable  \u2013 there is a need for treatment.  \n\u2022 The patient should be kept in a quiet room \nMechanical treatment  \no Carotid sinus massage  \no Valsalva maneuver \no Head immersion in cold water \nMedial therapy: \n\u0083 \u03b2-blockers, Calcium channel blockers ( Verapamil and Diltiazem ) or  \ndigoxin can be helpful. \nAtrial flutter : Rapidly fired signals cause the muscles in the atria to contract quickly, leading to \na very fast, steady heartbeat. Is characterized by an atrial rate of 240-400 beat/min and is \nusually conducted to ventricles with block so that the ventricular rate is a fraction of the atrial \nrate. The block is usually regular so the ventricular rate is regular. Sometimes there may be a \nvarying block resulting irregular ventricular beat. \nCauses of atrial flutter : often associated with antecedent hear diseases \n\u2022 Coronary artery diseases \n\u2022 Pericarditis  \n\u2022 Valvular heart diseases \n\u2022 Cardiomyopathy \nECG:  Classic saw tooth pattern: 2 or 3 P waves are followed by QRS complex. The block is \noften in a ratio of 2:1 with an atrial rate of 240 beats/min and ventricular rate of 120 beat/min"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac94-7265-11ef-bfbe-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 304, "chroma:document": "Internal Medicine \n \n 289Therapy: \n\u2022 Drugs :   \no Digoxin , Esmolol or Verapamil to control ventricular rate and  \no Quinidine or other ant arrhythmic agents to restore sinus rhythm. \n\u2022 Direct current cardioversion:  if the patient is hemodynamically unstable  \nAtrial Fibrillation: electrical signals in the atria are fired in a very fast and uncontrolled \nmanner. Electrical signals arrive in the ventricles in a completely irregular fashion, so the heart \nbeat is completely irregular.  \nCommon cause of atrial fibrillation \no Stress , fever  \no Excessive alcohol intake  \no Hypotension \no Pericarditis \no Coronary artery disease \no Myocardial infarction \no Pulmonary embolism \no Mitral valve diseases : Mitral stenosis , Mitral regurgitation  and Mitral valve \nprolapse \no Thyrotoxicosis \no Idiopathic (lone) atrial fibrillation. \nECG:  irregularly irregular pattern disorganized atrial activity without discrete P wave. \nTherapy  \nIf the patient is hemodynamically unstable: direct current synchronous cardioversion: \n \nIf the patient is hemodynamically stable \n\u2022 Identify and treat the underlying cause  \n\u2022 Control the ventricular rate : \u03b2-blockers , Calcium channel blockers ( Verapamil and \nDiltiazim ) , Digoxin \n\u2022 Restore sinus rhythm : Quinidine  \n\u2022 Anticoagulants : if the atrial fibrillation ahs stayed for more than 1 week to prevent \nthromboembolism"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac95-7265-11ef-acd4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 305, "chroma:document": "Internal Medicine \n \n 290Ventricular tachyarrhythmias :  \nPremature ventricular contractions (PVC)  : is a type of arrhythmia in which occasional \ncardiac impulses are originating directly from the ventricles by passing the normal conduction \nsystem. These are among the commonest arrhythmias. \nECG:  Wide and bizarre QRS appearing in a relatively normal looking ECG \nTherapy:  most isolated PVCs are benign and need no treatment. \nVentricular tachycardia : arises from the ventricles, it occurs paroxysmal and exceeds 120 \nbeats/min, with regular rhythm. There is AV dissociation and the ventricular arrhythmia \nproceeds independently of the normal atrial rhythm. During ventricular tachycardia, the \nventricles do not have enough time to relax, ventricular filling is impaired and the cardiac output \nsignificantly decreases. When ventricular tachycardia lasts for more than 30 seconds or requires control because of hemodynamic collapse it is called sustained Ventricular tachycardia. \nECG:  Bizarre and wide QRS complexes coming in succession with no constant relation to \nP waves. \nTherapy: since this is a life threatening situation urgent intervention is needed \n\u2022 Anti-arrhythmic drugs : intravenous administration of Beretylium, Lidocaine or \nProcainamide may be useful in returning the patient\u2019s rhythm to normal while preparation is being made for DC cardioversion. \n\u2022 DC cardioversion : is urgently required"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac96-7265-11ef-9e49-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 305, "chroma:document": "Procainamide may be useful in returning the patient\u2019s rhythm to normal while preparation is being made for DC cardioversion. \n\u2022 DC cardioversion : is urgently required  \nVentricular Fibrillation:   electrical signals in the ventricles are fired in a very fast and \nuncontrolled manner, causing the heart to quiver rather than beat and pump blood. It is characterized by lack of ordered contraction of the ventricles. Therefore there is no cardiac out \nput. Thus ventricular fibrillation is synonymous with death unless urgent conversion to effective rhythm can be accomplished.  \nTherapy:  patients need cardiorespiratory resuscitation  \n\u2022 Cardiac resuscitation  \n\u2022 Mechanical ventilation \n\u2022 Cardiac compression and intracardiac adrenalin \n\u2022 DC cardioversion using high voltage. \nThe place of Surgery in the management of Arrhythmias  \n\u2666 When an arrhythmia cannot be controlled by other treatments, there may be a place \nfor surgery. After locating the heart tissue that is causing the arrhythmia, the tissue is altered or removed so that it will not produce the arrhythmia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac97-7265-11ef-bf90-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 306, "chroma:document": "Internal Medicine \n \n 291Prevention \nIf the precipitating factor for arrhythmia is identified, one has to avoid what is causing it.  \nE.g. If caffeine or alcohol is the cause, the pati ent has to avoid drinking coffee, tea, colas, or \nalcoholic beverages . \n \nReferences:  \n1. Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nDisordrs of cardiac rhythm , pages 1333-1357. \n2. Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Cardiac arrhythmias, pages 7-14."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac98-7265-11ef-b4ae-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 307, "chroma:document": "Internal Medicine \n \n 292CHAPTER FOUR \nDISEASES OF THE KIDNEYS \n \n1. Introduction to Renal Disease \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. List common etiologies of renal diseases. \n2. Describe the calcification of renal diseases. \n3. Identify common clinical manifestation of renal diseases. \n4. Understand the diagnostic approach to renal diseases.   \n \n\u2022 Patients with renal disease may have a variety of different clinical presentations.  \n\u2022 Some have symptoms that are directly refe rable to the kidney (gross hematuria, flank \npain) or to associated extrarenal symptoms (edema, hypertension, signs of uremia).  \n\u2022 Many patients, however, are asymptomat ic and are noted on routine examination to \nhave an elevated plasma creatinine concentration or an abnormal urinalysis.  \n\u2022 Specific disorders are more likely to be either acute or chronic in duration, thereby \nnarrowing the differential diagnosis among pati ents presenting with similar clinical \nfindings related to the kidney. \n \nMajor causes of renal diseases .  \nRenal function is based upon four sequential steps, which are isolated to specific areas of the kidney or surrounding structures: \n \n1. First, blood from the renal arteries is delivered to the glomeruli. 2. The glomeruli form an ultrafiltrate, which subsequently flows into the renal tubules. \n3. The tubules reabsorb and secrete solute and/or water from the ultrafiltrate."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3ac99-7265-11ef-bd51-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 307, "chroma:document": "1. First, blood from the renal arteries is delivered to the glomeruli. 2. The glomeruli form an ultrafiltrate, which subsequently flows into the renal tubules. \n3. The tubules reabsorb and secrete solute and/or water from the ultrafiltrate. \n4. The final tubular fluid, the urine, leaves the kidney, draining sequentially into the renal             pelvis, ureter, and bladder, from which it is excreted through the urethra. \nThe causes of renal disease are traditionally classified based on the portion of the renal \nanatomy most affected by the disorder"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d33b-7265-11ef-9a04-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 308, "chroma:document": "Internal Medicine \n \n 2931. Prerenal disease  \u2013 Reduced glomerular perfusion is most commonly caused by \nvolume depletion and/or relative hypotension.  This may result from: \n\u2022 True hypoperfusion due to bleeding, gastrointestinal, urinary, or cutaneous \nlosses, or  \n\u2022 Effective circulatory fluid volume depletion in congestive heart failure, shock, or \ncirrhosis. \n2. Vascular disease  \u2013 The vascular diseases affecting the kidney can be divided into \nthose that produce acute and chronic disease.  \n\u2022 The major acute causes are vasculitis, malignant hypertension, scleroderma, \nand thromboembolic disease. \n\u2022 The major chronic disorders are benign nephrosclerosis and bilateral renal \nartery stenosis.  \n3. Glomerular disease:         \nThere are numerous idiopathic and secondary disorders that produce glomerular disease. \nTwo general patterns (with considerable overlap in some diseases) are seen:  \n\u2022 The nephritic pattern which is associated with inflammation on histologic \nexamination and produces an active urine s ediment with red cells, white cells, \ngranular and often cellular casts, and a variable degree of proteinuria;   \n\u2022 The nephrotic pattern which is not associated with inflammation on histologic \nexamination and is primarily manifested c linically by proteinuria, often in the \nnephrotic range. \n4. Tubular and interstitial disease  \u2013 As with vascular disease, the tubular and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d33c-7265-11ef-974e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 308, "chroma:document": "examination and is primarily manifested c linically by proteinuria, often in the \nnephrotic range. \n4. Tubular and interstitial disease  \u2013 As with vascular disease, the tubular and \ninterstitial diseases affecting the kidney can be divided into those that produce acute and chronic disease.  \n\u2022 The most common acute tubulointerstitial disorders are acute tubular necrosis, \nwhich typically occurs in hospitalized patients, acute interstitial nephritis, which is often drug-induced, and cast nephropathy in multiple myeloma.  \n\u2022 The major chronic tubulointerstitial disorders are polycystic kidney disease, \nvesicoureteral reflux, autoimmune disorders (such as sarcoidosis and Sj\u00f6gren's syndrome), and analgesic abuse. \n5.  Obstructive uropathy  \u2013 Obstruction to the flow of urine can occur anywhere from \nthe renal pelvis to the urethra. The development of renal insufficiency in patients"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d33d-7265-11ef-a9d1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 309, "chroma:document": "Internal Medicine \n \n 294without intrinsic renal disease requires bilateral obstruction and is most commonly \ndue to prostatic disease. \n \n Clinical manifestations  \u2013 Patients with renal disease may present with a variety of \nclinical manifestations: \n\u2022 Signs and symptoms resulting directly from alterations in kidney function, including \ndecreased or no urine output, flank pain, edema, or discolored urine. \n\u2022 Asymptomatic elevations in the plasma creatinine concentration or abnormalities \non urinalysis. \n\u2022 Symptoms and/or signs of renal failure, including anorexia, vomiting, mental status \nchanges (including seizures), edema, and hypertension. \n\u2022 The presence of certain symptoms or signs may suggest an underlying diagnosis.  \nE.g.  \n\u00be Unilateral flank pain is most consistent with a renal stone, renal infarction, \ninfection, or obstruction,  \n\u00be The total absence of urine (anuria) is primarily observed with bilateral \nureteral obstruction or shock. \n\u2022 A constellation of symptoms and signs may also favor a particular set of \ndisorders. \nE.g. A patient with edema, hypertension, red to brown colored urine due \nto hematuria (with red cell casts), and a rapidly rising plasma creatinine \nconcentration almost certainly has glomerulonephritis or vasculitis. \n\u2022 Other manifestations, however, are relatively nonspecific and can be observed \nwith a wide variety of disorders. \n Disease duration : An important aspect of the evaluation of the patient with renal"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d33e-7265-11ef-8493-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 309, "chroma:document": "\u2022 Other manifestations, however, are relatively nonspecific and can be observed \nwith a wide variety of disorders. \n Disease duration : An important aspect of the evaluation of the patient with renal \ndisease is the determination of disease duration. As noted above, the differential \ndiagnosis can frequently be narrowed if the disease duration is known. \n \n\u2022 Comparing the current urinalysis or plasma creatinine concentration with previous results: -  A patient with a current plasma creatinine of 4.0 mg/dL (354 \n\u00b5mol/L) but a plasma level of 1.0 mg/dL (88 \u00b5mol/L) one month previously has acute disease while the same patient with a prior plasma creatinine concentration"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d33f-7265-11ef-9e4b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 310, "chroma:document": "Internal Medicine \n \n 295of 3.0 mg/dL (265 \u00b5mol/L) two years ago has a slowly progressive chronic \ndisease. \n\u2022 When a previous urinalysis or plasma cr eatinine is unavailable, certain clinical \nelements may suggest the duration of disease. These include : \n\u00be The recent onset of symptoms or signs, such as fever and discolored urine, \nsuggests an acute process. \u00be An increasing plasma creatinine after the initial evaluation is indicative of at \nleast an acute component to the disease, while a stable value suggests a chronic disease. In addition, the rate of rise in the plasma creatinine concentration may help distinguish among possible disorders. \n \nDiagnostic work up of pa tients with Renal Diseases. \n1. Assessment of renal function \u2013 Once renal disease is discovered, the presence or \ndegree of renal dysfunction should be as sessed and the underlying disorder is \ndiagnosed.  \n\u2022 Glomerular filtration rate  \u2013 An estimation of the glomerular filtration rate (GFR), \nusually by the plasma creatinine concentration and less often by the creatinine \nclearance, is used clinically to assess the degree of renal impairment and to follow \nthe course of the disease. However, since all renal disorders variably affect renal \nfunction, estimation of the GFR has no diagnostic utility. \n \n2. Urinalysis : The urinalysis is the most important noninvasive test in the diagnostic \nevaluation, since characteristic findings on microscopic examination of the urine"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d340-7265-11ef-83a5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 310, "chroma:document": "function, estimation of the GFR has no diagnostic utility. \n \n2. Urinalysis : The urinalysis is the most important noninvasive test in the diagnostic \nevaluation, since characteristic findings on microscopic examination of the urine \nsediment strongly suggest certain diagnoses. E.g. \n\u00be The finding of red cell casts is diagnostic of vasculitis or glomerulonephritis, \nand  \n\u00be The presence of muddy brown granular casts and epithelial cell casts in a \npatient with acute renal failure is highly suggestive of acute tubular necrosis;  \n\u00be Even a normal urinalysis has diagnostic utility.  \nUrine volume : has little diagnostic value.  \n\u2022 Anuria (Complete absence of urine output): may be due to shock, complete \nbilateral urinary tract obstruction, renal cortical necrosis, and bilateral vascular"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d341-7265-11ef-b062-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 311, "chroma:document": "Internal Medicine \n \n 296occlusion (as with thrombotic thrombocytopenic purpura-hemolytic uremic \nsyndrome). \n3. Radiologic/imaging studies . They are principally required to assess urinary tract \nobstruction, kidney stones, renal cyst or mass, disorders with characteristic \nradiographic findings, renal vascular diseases, and vesicoureteral reflux. \nRenal ultrasonography : \no Showing small kidneys is most consistent with a chronic disease because \nof the progressive loss of renal parenchyma with time. However, the presence of normal-sized kidneys does not exclude chronic disease \no Obstructive uropathy: hydronephrosis, hydroureter, Stone, and the site of \nobstruction can be seen by U/S. \nPlain film of the abdomen (KUB):   A plain abdominal radiograph can detect renal \nstones and provide a rough approximat ion of kidney size and shape.  \n4. Other studies: may be ordered to make specific diagnosis \n1. Intravenous pyelogram  \n2. Renal biopsy has limited value. \n \nReferences:  \n1) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd \nedition Medicine, Clinical assessment of renal function, pages 279-280."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d342-7265-11ef-98cb-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 312, "chroma:document": "Internal Medicine \n \n 2972. Acute Nephritic Syndrome   \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define acute nephritic syndrome.  \n2. List the etiologies of acute nephritic syndrome.. 3. Describe the clinical features and diagnostic approach to patients with acute \nnephritic syndrome. \n4. Understand the pathogenesis of Poststreptococcal glomerulonephritis. 5. Identify the clinical manifestation of Poststreptococcal glomerulonephritis.. 6. Identity complications of nephritic syndrome..  7. Understand the diagnostic approach to Poststreptococcal  glomerulonephritis..  \n8. Understand the principle of management of Poststreptococcal glomerulonephritis.  \n \nDefinition \nThe acute nephritic syndrome is the clinical correlate of acute glomerular inflammation. In its \nmost dramatic form, the acute nephritic syndrom e is characterized by sudden onset (i.e., over \ndays to weeks) of acute renal failure and oliguria (<400 mL of urine per day) associated with \nhypertension, edema and the presence of active urinary sediments.  \n Clinical features  \n\u2022 Extracellular fluid volume expansion, edema, and hypertension develop because of \nimpaired GFR and enhanced tubular reabsorption of salt and water. Patients may \npresent with congestive heart failure and pulmonary edema.  \n\u2022 And pictures of acute renal failure may also occur (see later sections). \n\u2022 Evidence of the underlying cause can be detected (skin lesions, joint swelling, \nfever)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d343-7265-11ef-a6d1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 312, "chroma:document": "present with congestive heart failure and pulmonary edema.  \n\u2022 And pictures of acute renal failure may also occur (see later sections). \n\u2022 Evidence of the underlying cause can be detected (skin lesions, joint swelling, \nfever) \nLaboratory tests \n\u2022 Urinalysis: as a result of injury to the glomerular capillary wall, urinalysis typically \nreveals red blood cell casts, dysmorphic red blood cells, leukocytes, and subnephrotic proteinuria of <3.5 g per 24 h (\"nephritic urinary sediment\"). Hematuria \nis often macroscopic. \n\u2022 Renal function test :Elevated level of serum creatinine \n\u2022 Serology: Immunologic assays suggesting the underlying disease."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d344-7265-11ef-8392-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 313, "chroma:document": "Internal Medicine \n \n 298Etiology \nAcute nephritic syndrome can result from renal -limited primary glomerulopathy or from \nsecondary glomerulopathy complicating systemic  disease. In general, rapid diagnosis and \nprompt treatment are critical to avoid the development of irreversible renal failure.  \n \nImmune-complex glomerulonephritis may be: \n1. Idiopathic \n2. Represent a response to a known antigenic stimulus (e.g., post infectious \nglomerulonephritis) \n3. Part of a multisystem immune-complex disorder (e.g., lupus nephritis, Henoch-Schonlein purpura, cryoglobulinemia, bacterial endocarditis). \n \n \nPoststreptococcal glomerulonephritis \nEtiology and Epidemiology \n\u2022 This is the prototypical postinfectious glomerulonephritis and a leading cause of \nacute nephritic syndrome.  \n\u2022 Most cases are sporadic, though the disease can occur as an epidemic. \nGlomerulonephritis develops, on average, 10 days after pharyngitis or 2 weeks after a skin infection (impetigo) with a nephritogenic strain of group A \u03b2-hemolytic \nstreptococcus .  \n\u2022 Immunity to these strains is type-specific and long-lasting, and repeated infection \nand nephritis are rare. Epidemic poststreptococcal glomerulonephritis is most commonly encountered in children of 2 to 6 years of age with pharyngitis during the winter months. This entity appears to be decreasing in frequency, possibly due to \nmore widespread and prompt use of antibiotics."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d345-7265-11ef-a1b2-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 313, "chroma:document": "more widespread and prompt use of antibiotics.  \n\u2022 Poststreptococcal glomerulonephritis in association with cutaneous infections \nusually occurs in a setting of poor personal hygiene or streptococcal superinfection \nof another skin disease. \n Clinical picture \n\u2022 The classic clinical presentation of postst reptococcal glomerulonephritis is full-blown \nnephritic syndrome with oliguric acute r enal failure; however, most patients have \nmilder disease."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d346-7265-11ef-8952-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 314, "chroma:document": "Internal Medicine \n \n 299\u2022 Indeed, subclinical cases outnumber overt cases by four- to tenfold during \nepidemics. Patients with overt disease present with gross hematuria (red or \"smoky\" \nurine), headache, and generalized symptoms such as anorexia, nausea, vomiting, and malaise.  \n\u2022 Swelling of the renal capsule can cause flank or back pain. \nPhysical examination : Hypervolemia, edema, and hypertension.  \nComplications; \n\u2022 Congestive heart failure and Pulmonary edema \n\u2022 Acute renal failure  \n\u2022 Sever hypertension with hypertensive encephalopathy. \nLaboratory findings: \n\u2022 Urinalysis: the urinary sediment is nephritic, with dysmorphic red blood cells, red \ncell casts, leukocytes, occasionally leukocyte casts, and subnephrotic proteinuria. Fewer than 5% of patients develop nephrotic-range proteinuria.  \n\u2022 Renal function test : the serum creatinine is often mildly elevated at presentation. \n\u2022 Serology:  most patients (>90%) have circulating antibodies against streptococcal \nexoenzymes such as ASO, DNAase.  \nDiagnosis: \nAcute poststreptococcal glomerulonephritis is usually diagnosed on clinical and serologic grounds. The characteristic lesion is diffuse proliferative glomerulonephritis.  \nCourse and prognosis of the disease \n\u2022 Poststreptococcal glomerulonephritis is  typically an acute disease, with \nspontaneous recovery occurring in almost all patients, even those who develop renal insufficiency during the acute episode."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d347-7265-11ef-ba80-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 314, "chroma:document": "Course and prognosis of the disease \n\u2022 Poststreptococcal glomerulonephritis is  typically an acute disease, with \nspontaneous recovery occurring in almost all patients, even those who develop renal insufficiency during the acute episode.  \n\u2022 Resolution of the clinical manifestations of poststreptococcal glomerulonephritis is \ngenerally quite rapid, assuming concurrent resolution of the infection .  \n\u2022 Diuresis typically begins within one week and the plasma creatinine concentration \nreturns to the previous baseline by three to four weeks.  \n\u2022 Hematuria usually resolves within three to six months.  \n\u2022 The degree of proteinuria also falls during recovery, but at a much slower rate.  \n\u2022 Generally the long-term prognosis is good."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d348-7265-11ef-b63d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 315, "chroma:document": "Internal Medicine \n \n 300Treatment  \n1. Eliminating the streptococcal infection with antibiotics. \n2. Supportive therapy until spontaneous resolution of glomerular inflammation occurs. \na. Bed rest  b. Salt restriction  c. Diuretics and are employed to control extracellular fluid volume.  \nd. Antihypertensive drugs  to control high blood pressure  \n3. Dialysis : some patients may need dialysis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d349-7265-11ef-8833-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 316, "chroma:document": "Internal Medicine \n \n 3013. Nephrotic syndrome: \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define nephrotic syndrome.  \n2. List the etiologies of nephrotic syndrome. 3. Describe the clinical features of   nephrotic syndrome. \n4. Identity complications of nephrotic syndrome..  \n5. Understand the diagnostic approach of nephrotic syndrome.  \n6.  Understand the principle of management of nephrotic syndrome.  \n Definition The nephrotic syndrome is a clinical complex characterized by: \n\u2022 Significant proteinuria of >3.5 g/1.73m\n2/per 24 h (for practical purpose >3.0 to 3.5 g \nper 24 h) is the most important clinical feature  \n\u2022 Hypoalbuminemia \n\u2022 Edema \n\u2022 Hyperlipidemia and  lipiduria  and  \n\u2022 Hypercoagulability  \n \nEtiology \n1. Multisystem diseases account for 50 \u201370 % of adult nephrotic syndrome.  \na. Diabetes mellitus \nb. Collagen vascular diseases  \nc. Amyloidosis  \n2.  Neoplasms: - leukemias, lymphomas and solid tumors \n3.  Infections: - viral, bacterial, protozoan and helimenthic \n4.   Primary glomerulopathies( Idiopathic ): - account for 30 \u201350 % of adult nephrotic syndrome \n Clinical picture \n \n1. Proteinuria and hypoalbuminemia : - In general, the greater the proteinuria, the lower the \nserum albumin level. Hypoalbuminemia is co mpounded further by increased renal catabolism"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d34a-7265-11ef-aef1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 317, "chroma:document": "Internal Medicine \n \n 302and inadequate hepatic synthesis of albumin. The proteinuria is believed to be due to increased \npermeability of the glomerular basement membrane to proteins. 2. Edema : - Common sites for edema formation in the early stage include: dependent areas, \nface, peri-orbital areas and scrotum. Hypoalbuminemia and primary water and salt retention by kidneys are the postulated mechanisms for edema formation.  3. Hyperlipidemia : - is believed to be a consequence of increased hepatic lipoprotein \nsynthesis & decreased clearance. Hyperlipidemia may accelerate atherosclerosis and \nprogression of renal disease. \n \n4. Hypercoagulability : -  \n\u2022 It is mutifactorial: some of the mechanisms are loss of anti-thrombin III in the urine, \nincreased fibrinogen production by the liver , increased platelet aggregation.  \n\u2022 Spontaneous peripheral arterial or venous thrombosis, renal vein thrombosis, and \npulmonary embolism may occur. \n\u2022 Clinical features that suggest acute renal vein thrombosis include sudden onset of flank \nor abdominal pain, gross hematuria, a left-sided varicocele (the left testicular vein drains \ninto the renal vein), increased proteinuria, and an acute decline in GFR. Chronic renal vein thrombosis is usually asymptomatic. \n \n5. Other complications:  -  \n\u2022 Protein malnutrition  \n\u2022 Iron-resistant microcytic hypochromic anemia due to transferrin loss.  \n\u2022 Hypocalcemia as a consequence of vitamin D deficiency due to enhanced"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d34b-7265-11ef-89ac-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 317, "chroma:document": "5. Other complications:  -  \n\u2022 Protein malnutrition  \n\u2022 Iron-resistant microcytic hypochromic anemia due to transferrin loss.  \n\u2022 Hypocalcemia as a consequence of vitamin D deficiency due to enhanced \nurinary excretion of cholecalciferol-binding protein.  \n\u2022 An increased susceptibility to infection from urinary loss and increased \ncatabolism of immunoglobulin. \nDiagnosis \n1. Confirming significant proteinuria \n\u2022 Quantify 24 hours urine protein \n\u2022 Comparing with urinary creatinine level on a single void urine \n\u2022 Measurement of urinary protein by a dipstick (+3 or +4 diagnostic if the first two \nare not available)  \n2. Renal biopsy ( if available  ): to identify the underlying histopathologic abnormality"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d34c-7265-11ef-91bd-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 318, "chroma:document": "Internal Medicine \n \n 303\u2022 Minimal change diseases: accounts for 80 % nephrotic syndrome in children < 10 \nyrs.  \n\u2022 Membranous glomerulopathy: accounts for 60-70 % of nephrotic syndrome in \nadults. \n\u2022 Focal segmental glomerulosclerosis  \nTreatment \nThe treatment of nephrotic syndrome involves:-  \n1. Specific treatment of the underlying morphologic entity \n\u2022 Minimal change disease  : Steroids , and cytotoxic drugs  \n\u2022 Membranous nephropathy : Not steroid responsive \n2. Measures to control proteinuria: - \na. Dietary protein restriction: the potential value of dietary protein restriction for \nreducing proteinuria must be balanced against the risk of contributing to malnutrition.  \nb. Angiotensin-converting enzyme (ACE) inhibitors : decrease proteinuria by \ndecreasing glomerular filtration pressure \nc. Controlling hypertension: keeping BP below 130/80 reduces proteinuria. \n3.  Treatment of complications of nephrotic syndrome. \na. Edema : should be managed cautiously by : \ni. Moderate salt restriction , usually 1 to 2 g/day, and the judicious \nuse of  \nii. Loop diuretics  can be given in higher doses: It is unwise to remove \n>1.0 kg of edema per day as more aggressive diuresis may precipitate intravascular volume depletion and prerenal azotemia.   \nb. Thromboembolism : Anticoagulation is indicated for patients with deep \nvenous thrombosis, arterial thrombosis, and pulmonary embolism. Heparin may not be effective because of urinary loss of anti- thrombin III."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d34d-7265-11ef-9017-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 318, "chroma:document": "b. Thromboembolism : Anticoagulation is indicated for patients with deep \nvenous thrombosis, arterial thrombosis, and pulmonary embolism. Heparin may not be effective because of urinary loss of anti- thrombin III. \nc. Hyperlipidemia  : may need lipid lowering agents  \nd. Vitamin D deficiency : Vit-- D supplementation."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d34e-7265-11ef-8c19-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 319, "chroma:document": "Internal Medicine \n \n 304References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nGlomerular diseases,  pages 1508-1515 \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Glomerular diseases, pages 296-307."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d34f-7265-11ef-b58d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 320, "chroma:document": "Internal Medicine \n \n 3054. Acute Renal Failure  \n \nLearning objectives: at the end of this lesson the student will be able to  : \n1. Define acute renal failure. 2. List the etiologies of acute renal failure.   3. Describe the pathophysiology of acute renal failure.   \n4. Identify the clinical manifestation of acute renal failure. \n5. Identify complications of acute renal failure. 6. Understand the diagnostic approach of acute renal failure. 7. Understand the principles of management of acute renal failure.  \n8. Understand the course and prognosis of acute renal failure.  \n9. Refer patients with acute renal failure to hospitals with better facilities  \n Definition:  \nAcute renal failure is a syndrome characterized by: \n\u2022 Rapid decline in glomerular filtration rate (hours to days ) \n\u2022 Retention of nitrogenous wastes due to failure of excretion  \n\u2022 Disturbance in extracellular fluid volume and \n\u2022 Disturbance electrolyte and acid base homeostasis. \nBased on the amount of urine output acute renal failure may be classified as  \n\u2022 Anuric: - if urine volume is less than 100 ml/day  \n\u2022 Oliguric:  - if urine volume is less than 400 ml/day  \n\u2022 Non-oliguric : - if urine volume is greater than or equal 400 ml/day  \nEpidemiology: - \n\u2022 ARF complicates approximately 5% of hospital admissions and up to 30% of \nadmissions to intensive care units. Oliguria (urine output < 400 ml/d) is a frequent \nbut not invariable clinical feature (~50%)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d350-7265-11ef-a38d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 320, "chroma:document": "Epidemiology: - \n\u2022 ARF complicates approximately 5% of hospital admissions and up to 30% of \nadmissions to intensive care units. Oliguria (urine output < 400 ml/d) is a frequent \nbut not invariable clinical feature (~50%).  \n\u2022 ARF is usually asymptomatic and is  diagnosed when biochemical screening of \nhospitalized patients reveals a recent increase in plasma urea and creatinine \nconcentrations. \n\u2022 Most ARF is reversible, the kidney being relatively unique among major organs in its \nability to recover from almost complete loss of function."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d351-7265-11ef-8177-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 321, "chroma:document": "Internal Medicine \n \n 306\u2022 Nevertheless, ARF is associated with major in-hospital morbidity and mortality, in \nlarge part due to the serious nature of the illnesses that precipitate the ARF. \n\u2022 A prospective study in Ethiopian patients done by Worku Zewdu in 1992, sowed \nthat septic abortion was the leading cause of ARF followed by P.falciparum  malaria \nand nephrotoxic agents. \nAcute renal failure may complicate a wide range of diseases, which for purposes of \ndiagnosis and management are conveniently divided into three categories \n \nEtiologic classification of acute renal failure   \nA. Prerenal ARF  : account for nearly 55 % of all cases of acute renal failure \nI. Hypovolemia \n\u2022 Hemorrhage, burns, dehydration \n\u2022 Gastrointestinal fluid loss: vomiting, surgical drainage, diarrhea \n\u2022 Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus), \nhypoadrenalism \n\u2022 Sequestration in extravascular space: pancreatitis, peritonitis, trauma, burns, \nsevere hypoalbuminemia \nII.  Low cardiac output \n\u2022 Diseases of myocardium, valves, and pericardium; arrhythmias; tamponade \n\u2022 Other: pulmonary hypertension, massive pulmonary embolus \nIII.  Altered renal systemic vascular resistance ratio \n\u2022 Systemic vasodilatation: sepsis, anaphylaxis IV. Renal hypoperfusion with \nimpairment of renal autoregulatory responses \n\u2022 NSAIDS, angiotensin-converting enzyme inhibition  \nB. Intrinsic Renal ARF : account for nearly 40% of all ARF"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d352-7265-11ef-9d34-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 321, "chroma:document": "\u2022 Systemic vasodilatation: sepsis, anaphylaxis IV. Renal hypoperfusion with \nimpairment of renal autoregulatory responses \n\u2022 NSAIDS, angiotensin-converting enzyme inhibition  \nB. Intrinsic Renal ARF : account for nearly 40% of all ARF  \nI. Renovascular obstruction  (bilateral or unilateral in the setting of one functioning \nkidney) \nII. Disease of glomeruli or renal microvasculature \nIII. Acute tubular necrosis \n\u2022 Ischemia: as for prerenal ARF (hypovolemia, low cardiac output, renal \nvasoconstriction, systemic vasodilatation), obstetric complications (abruptio placentae, postpartum hemorrhage) \n\u2022 Toxins"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d353-7265-11ef-b607-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 322, "chroma:document": "Internal Medicine \n \n 307\u00be Exogenous: radio contrast, cyclosporine, antibiotics (e.g., \naminoglycosides), chemotherapy (e.g., cisplatin), organic solvents (e.g., \nethylene glycol), acetaminophen, illegal abortifacients \n\u00be Endogenous: rhabdomyolysis, hemolysis, ur ic acid, oxalate, plasma cell \ndyscrasia (e.g., myeloma) \nIV. Interstitial nephritis  \nPost renal ARF (OBSTRUCTION) : account for  ~5% of ARF. \nI. Ureteric \n\u2022 Calculi, blood clot, sloughed papillae, cancer, external compression (e.g., \nretroperitoneal fibrosis) \nII. Bladder neck \n\u2022 Neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clot \nIII. Urethra \n\u2022 Stricture, congenital valve, phimosis  \nPrerenal ARF  \n\u2022 Prerenal ARF is the most common form of ARF and represents a physiologic \nresponse to mild to moderate renal hypo perfusion.  \n\u2022 Prerenal ARF is rapidly reversible upon restoration of renal blood flow and \nglomerular ultrafiltration pressure.  \n\u2022 More severe hypoperfusion may lead to ischemic injury of renal parenchyma and \nintrinsic renal ARF. Thus, prerenal ARF and intrinsic renal ARF due to ischemia are part of a spectrum of manifestations of renal hypoperfusion.  \n\u2022 Prerenal ARF can complicate any disease that induces hypovolemia, low cardiac \noutput, systemic vasodilatation, or selective renal vasoconstriction. \nPathophysiology: \n\u2022 Hypovolemia  leads to glomerular hypoperfusion, but filtration rate are preserved"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d354-7265-11ef-ac76-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 322, "chroma:document": "output, systemic vasodilatation, or selective renal vasoconstriction. \nPathophysiology: \n\u2022 Hypovolemia  leads to glomerular hypoperfusion, but filtration rate are preserved \nduring mild hypoperfusion through several compensatory mechanisms. During states of more severe hypoperfusion, these compensatory responses are overwhelmed and GFR falls, leading to prerenal ARF. \n\u2022 Drugs that interfere with adaptive responses in the renal microcirculation may \nconvert compensated renal hypoperfusion into overt prerenal ARF or trigger \nprogression of prerenal ARF to ischemic intrinsic renal ARF (ACE-inhibitors, \nNSAIDS)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d355-7265-11ef-842a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 323, "chroma:document": "Internal Medicine \n \n 308 \nIntrinsic ARF \n\u2022 Intrinsic renal ARF can complicate many diverse diseases of the renal parenchyma.  \n\u2022 Most intrinsic renal ARF is triggered by  ischemia (ischemic ARF) or nephrotoxins \n(nephrotoxic ARF), insults that classically  induce acute tubular necrosis (ATN).  \n \nDiagnosis of ARF:  \nCareful history is essential  \n\u2022 Exposure to nephrotoxins and drugs  \n\u2022 Anuria may indicate post-renal causes  \n\u2022 Skin rashes may indicate allergic nephritis  \n\u2022 Evidences of volume depletion: diarrhea, bleeding  \n\u2022 Pelvic and per-rectal examinati on: look for evidence of abortion  \n\u2022 Ischemia or trauma to the legs or arms may indicate rhabdomyolysis  \n\u2022 Recent surgical or radiologic procedures  \n\u2022 Past and present use of medications   \n\u2022 Family history of renal diseases  \nPhysical examination: should be focused to rule out possible differential diagnosis  \nPrerenal ARF: is suggested by clinical signs of   \n\u2022 Intravascular volume depletion ( e.g. orthostatic hypotension , rapid pulse and \npoor skin turgor ) \n\u2022 Congestive heart failure (e.g. raised JVP , S3 , dependent edema , and pulmonary \nrales ) \nAcute allergic interstitial nephritis: is suggested by signs of allergy ( e.g. periorbital \nedema, esosinophilia , maculopapular rash , and wheezing ) \nLower Urinary tract obstruction: is suggested by suprapubic or flank mass or \nsymptoms of bladder  dysfunction (e.g. hesitancy, urgency)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d356-7265-11ef-8780-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 323, "chroma:document": "edema, esosinophilia , maculopapular rash , and wheezing ) \nLower Urinary tract obstruction: is suggested by suprapubic or flank mass or \nsymptoms of bladder  dysfunction (e.g. hesitancy, urgency) \nUremia : - clinical syndrome resulting from the adv erse effect of renal failure on other \norgan systems (only very few develop in acute renal failure)  \n \nComplications of ARF \n\u2022 Intravascular overload:  may be recognized by weight gain , hypertension , \nelevated central venous pressure ( raise JVP) , Pulmonary edema"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d357-7265-11ef-ac20-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 324, "chroma:document": "Internal Medicine \n \n 309\u2022 Electrolyte disturbance  \no Hyperkalemia:  (serum K+ >5.5 mEq/L) develops as a result of decreased \nrenal excretion combined with tissue necrosis or hemolysis. \no Hyponitremia :  ( serum Na+ concentration < 135 mEq/L ) results from \nexcessive water intake in the face of excretory failure \no Hyperphosphatemia :  ( serum Phosphate concentration of > 5.5 mg /dl ) \nresults from failure of excretion or tissue necrosis \no Hypocalcemia :  ( serum Ca++ < 8.5  mg/dl ) results from decreased Active \nVit-D , hyperposhphatemia , or hypoalbuminemia \no Hypercalcemia:  (serum Ca++ > 10.5 mg /dl) may occur during the recovery \nphase following rhabdomyolysis induced acute renal failure. \n\u2022 Metabolic acidosis : ( arterial blood PH < 7.35 ) is associated with sepsis or sever \nheart failure \n\u2022 Hyperuricemia:  due to decreased uric acid excretion \n\u2022 Bleeding tendency :  may occur due to platelet dysfunction and coagulopathy \nassociated with sepsis \n\u2022 Seizure: may occur related to uremia \n\u2022 Chronic Renal failure:  a modest degree of decline in filtration may exist in 10 % \nof patients for several months following ARF. In patients with underlying renal \ndiseases who experience ARF , progression to chronic renal failure is relatively \nlikely. \nDiagnostic work up  1. Urinalysis: Microscopic evaluation of urinary sediment. \n\u2022 Presence of few formed elements or hyaline casts is suggestive of prerenal or \npostrenal azotemia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d358-7265-11ef-838b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 324, "chroma:document": "likely. \nDiagnostic work up  1. Urinalysis: Microscopic evaluation of urinary sediment. \n\u2022 Presence of few formed elements or hyaline casts is suggestive of prerenal or \npostrenal azotemia. \n\u2022 Many RBCs may suggest calculi , trauma , infection or tumor \n\u2022 Eosinophilia : occurs in 95 % of patients with acute allergic nephritis  \n\u2022 Brownish pigmented cellular casts and many renal epithelia cells are seen in \npatients with acute tubular necrosis (ATN ) \n\u2022 Pigmented casts without erythrocytes in the sediment from urine but with positive \ndipstick for occult blood indicates hemoglobinuria or myoglobinuria"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d359-7265-11ef-8982-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 325, "chroma:document": "Internal Medicine \n \n 310\u2022 Dipstick test: trace or no proteinuria with pre-renal and post-renal ARF; mild to \nmoderate proteinuria with ATN and moderate to severe proteinuria with \nglomerular diseases.  \n\u2022 RBCs and RBC casts in glomerular diseases  \n\u2022 Crystals RBCs and WBCs in post-renal ARF.  \n2. Urine and blood Chemistry: most of these tests help to differentiate prerenal \nazotemia, in which tubular reabsorption function is preserved from acute tubular \nnecrosis where tubular reabsorption is severely disturbed.  \n\u2022 Osmolality or specific gravity: decreased in ATN and pos-renal ARF (urine is \ndiluted) , while increased in pre-renal ARF ( urine is concentrated .) \n\u2022 BUN/plasma creatinine ratio: the BUN/plasma creatinine ratio is normal at 10-15:1 \nin ATN, but may be greater than 20:1 in prerenal disease due to the increase in the \npassive reabsorption of urea that follows the enhanced proximal transport of \nsodium and water. Thus, a high ratio is highly suggestive of prerenal disease as \nlong as some other cause is not present. But this criterion is not highly specific. \n\u2022 Renal failure index: ratio of urine Na+ to urine to plasma creatinine ratio \n(UNa/Ucr/Pcr) . Values less than 1 % are consistent with prerenal ARF ,where as a \nvalue > 1% indicates ATN \n\u2022 Fractional excretion of Na+: is ration of urine-to-plasma Na ratio to urine-to-plasma \ncreatinine expressed as a percentage [ (U Na/PNa)/(U cr/Pcr )X 100]. Value below 1%"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 325, "chroma:document": "value > 1% indicates ATN \n\u2022 Fractional excretion of Na+: is ration of urine-to-plasma Na ratio to urine-to-plasma \ncreatinine expressed as a percentage [ (U Na/PNa)/(U cr/Pcr )X 100]. Value below 1% \nsuggest prerenal failure , and values above 1% suggest ATN \n\u2022 Serum K+ and other electrolytes \n3. Radiography/imaging  \n\u2022 Ultrasonography: helps to see the presence of two kidneys, for evaluating \nkidney size and shape, and for detecting hydronephrosis or hydroureter. It also helps to see renal calculi, and renal vein thrombosis. \n\u2022 Retrograde pyelography:  is done when obstructive uropathy is suspected  \n \nManagement of Acute renal failure: \n1. Prevention :   \n\u2022 Because there are no specific therapies for ischemic or nephrotoxic ARF, \nprevention is of paramount importance."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d35b-7265-11ef-83c6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 326, "chroma:document": "Internal Medicine \n \n 311\u2022 Many cases of ischemic ARF can be avoi ded by close attention to cardiovascular \nfunction and intravascular volume in high-risk patients, such as the elderly and \nthose with preexisting renal insufficiency.  \n\u2022 Indeed, aggressive restoration of intravascular volume has been shown to reduce \nthe incidence of ischemic ARF dramatically after major surgery or trauma, burns, or \ncholera.  \n\u2022 The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of \npotential nephrotoxins to body size and GFR; for example, reducing the dose or frequency of administration of drugs in pati ents with preexisting renal impairment.  \n2. Preliminary measures \n\u2022 Exclusion of reversible causes : Obstruction should be relived , infection should \nbe treated  \n\u2022 Correction of prerenal factors : intravascular volume and cardiac performance \nshould be optimized  \n\u2022 Maintenance of urine output : although the prognostic importance of oliguria is \ndebated, management of nonoliguric patients is easier. Loop diuretics may be \nusefully to convert the oliguric form of ATN to the nonoliguric form. High doses of \nloop diuretics such as Furosemide ( up to 200 to 400 mg intravenously) may \npromote diuresis in patients who fa il to respond to conventional doses.  \n3. Specific Therapies :  \n\u2022 To date, there are no specific therapies for established intrinsic renal ARF due to \nischemia or nephrotoxicity."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d35c-7265-11ef-ab88-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 326, "chroma:document": "promote diuresis in patients who fa il to respond to conventional doses.  \n3. Specific Therapies :  \n\u2022 To date, there are no specific therapies for established intrinsic renal ARF due to \nischemia or nephrotoxicity.  \n\u2022 Management of these disorders should focus on elimination of the causative \nhemodynamic abnormality or toxin, avoidanc e of additional insults, and prevention \nand treatment of complications.  \n\u2022 Specific treatment of other causes of intrinsic renal ARF depends on the underlying \npathology. \nPrerenal ARF :   \n\u2022 The composition of replacement fluids for treatment of prerenal ARF due to \nhypovolemia must be tailored according to the composition of the lost fluid.  \n\u2022 Severe hypovolemia due to hemorrhage should be corrected with packed red blood \ncells, whereas isotonic saline is usually  appropriate replacement for mild to \nmoderate hemorrhage or plasma loss (e.g., burns, pancreatitis)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d35d-7265-11ef-b904-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 327, "chroma:document": "Internal Medicine \n \n 312\u2022 Urinary and gastrointestinal fluids can vary greatly in composition but are usually \nhypotonic. Hypotonic solutions (e.g., 0.45% saline) are usually recommended as \ninitial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses, although isotonic saline may be more appropriate in severe cases.  \n\u2022 Subsequent therapy should be based on measurements of the volume and ionic \ncontent of excreted or drained fluids. Serum potassium and acid-base status should be monitored carefully.                                                                 \nPostrenal ARF:    \n\u2022 Management of postrenal ARF requires close collaboration between nephrologist, \nurologist, and radiologist.  \n\u2022 Obstruction of the urethra or bladder neck is usually managed initially by \ntransurethral or suprapubic placement of a bladder catheter, which provides temporary relief while the obstructing lesion, is identified and treated definitively.  \n\u2022 Similarly, ureteric obstruction may be treated initially by percutaneous \ncatheterization of the dilated renal pelvis or ureter.  \n4. Supportive Measures:  (Conservative therapy ) \n\u2022 Dietary management: adequate calorie intake is essential in patients with ARF.  \no Generally, sufficient calorie reflects a diet that provides 40-60 gm of protein \nand 35-50 kcal/kg lean body weight.  \no In some patients, severe catabolism occurs and protein supplementation to"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d35e-7265-11ef-9577-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 327, "chroma:document": "o Generally, sufficient calorie reflects a diet that provides 40-60 gm of protein \nand 35-50 kcal/kg lean body weight.  \no In some patients, severe catabolism occurs and protein supplementation to \nachieve 1.25 gm of protein /kg body weight is required to maintain nitrogen balance.  \no Restricting dietary protein to approximately 0.6 g/kg per day of protein of \nhigh biologic value (i.e., rich in essential amino acids) may be recommended \nin sever azotemia.  \n\u2022 Fluid and electrolyte management  : \nFollowing correction of hypovolemia, total oral and intravenous fluid administration should be equal to daily sensible losses (via urine, stool, and NG tune o surgical \ndrainage ) plus estimated insensible ( i.e. , respiratory and derma ) losses which usually equals 400 \u2013 500 ml/day. Strict input output monitoring is important. \n\u2022 Hypervolemia : can usually be managed by restriction of salt and water intake and \ndiuretics."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d35f-7265-11ef-bcd3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 328, "chroma:document": "Internal Medicine \n \n 313\u2022 Metabolic acidosis :  is not treated unless serum bicarbonate concentration falls \nbelow 15 mmol/L or arterial pH falls below 7.2.  \no More severe acidosis is corrected by oral or intravenous sodium \nbicarbonate. Initial rates of replacement are guided by estimates of \nbicarbonate deficit and adjusted thereafter according to serum levels.  \no Patients are monitored for complications of bicarbonate administration such \nas hypervolemia, metabolic alkalosis, hypocalcemia, and hypokalemia.  \no From a practical point of view, most patients requiring sodium bicarbonate \nneed emergency dialysis within days.  \n\u2022 Hyperkalemia: cardiac and neurologic complications may occur if serum K+ level is \n> 6.5 mEq/ L \no Restrict dietary K+ intake  \no Give calcium gluconate 10 ml of 10% solution over 5 minutes  \no Glucose solution 50 ml of 50 % glucose plus Insulin 10 units IV  \no Give potassium \u2013binding ion exchange resin  \no Dialysis: it medial therapy fails or the patient is very toxic \n\u2022 Hyperphosphatemia  is usually controlled by restriction of dietary phosphate and by \noral aluminum hydroxide or calcium carbonate, which reduce gastrointestinal absorption of phosphate.  \n\u2022 Hypocalcemia  does not usually require treatment. \n\u2022  Anemia : may necessitate blood transfusion if severe or if recovery is delayed.  \n\u2022 GI bleeding : Regular doses of antacids appear to reduce the incidence of \ngastrointestinal hemorrhage significantly and may be more effective in this regard"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d360-7265-11ef-85e7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 328, "chroma:document": "\u2022  Anemia : may necessitate blood transfusion if severe or if recovery is delayed.  \n\u2022 GI bleeding : Regular doses of antacids appear to reduce the incidence of \ngastrointestinal hemorrhage significantly and may be more effective in this regard \nthan H2 antagonists, or proton pump inhibitors.  \n\u2022 Meticulous care of intravenous cannulae, bladder catheters, and other invasive \ndevices is mandatory to avoid infections \n \nDialysis  \nIndications and Modalities of Dialysis: - Dialysis replaces renal function until regeneration \nand repair restore renal function. Hemodialysis and peritoneal dialysis appear equally effective for management of ARF. Absolute indications for dialysis include: \n\u00be Symptoms or signs of the uremic syndrome \n\u00be Refractory hypervolemia"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d361-7265-11ef-91fb-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 329, "chroma:document": "Internal Medicine \n \n 314\u00be Sever hyperkalemia \n\u00be Metabolic acidosis.  \nClinical course and prognosis \n\u2022 Stages: acute renal failure due to ATN typically occurs in three stages: Azotemic , \nDiuretic , and recovery phases. The initial azotemic stage can be either oliguric or \nnon oliguric type. \n\u2022 Morbidity and mortality: are affected by the presence of oliguria \no GI bleeding, septicemia, metabolic acidosis and neurologic abnormalities \nare more common in oliguric patients than in nonoliguric patients. \no The mortality rate for oliguric patients is 50 % where as that of nonoliguric \npatients is only 26 % \n Prognosis: \n\u2022 The mortality rate among patients with ARF approximates 50. It should be stressed, \nhowever, that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself \n\u2022 Mortality is affected by both severity of the underlying diseases and the clinical \nsetting in which acute renal failure occurs \n\u2022 E.g. the mortality of ATN is 60 % when it results from surgery or trauma, 30 % when \nit occurs as a complication of medical illnesses, and 10-15 % when pregnancy is involved. \n\u2022 Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN. \n\u2022 In agreement with this interpretation, mortality rates vary greatly depending on the \ncause of ARF: ~15% in obstetric patients, ~30% in toxin-related ARF, and ~60% following trauma or major surgery.  \n\u2022 Oliguria (<400 mL/d) at time of presentation and a rise in serum creatinine of >3"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d362-7265-11ef-96e3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 329, "chroma:document": "cause of ARF: ~15% in obstetric patients, ~30% in toxin-related ARF, and ~60% following trauma or major surgery.  \n\u2022 Oliguria (<400 mL/d) at time of presentation and a rise in serum creatinine of >3 \nmg/dl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness.  \n\u2022 Mortality rates are higher in older debilitated patients and in those with multiple \norgan failure \n\u2022 Patients with no complicating factors who survive an episode of acute renal failure \nhave a 90 % chance of complete recovery of kidney function."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d363-7265-11ef-9944-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 330, "chroma:document": "Internal Medicine \n \n 315References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Acute \nrenal failure, pages 1644-1652. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Acute renal failure, pages 280-284."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d364-7265-11ef-8e00-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 331, "chroma:document": "Internal Medicine \n \n 3165. Chronic Renal Failure  \n \nLearning objectives: at the end of this lesson the student will be able to  : \n1. Define chronic renal failure. 2. List the etiologies of chronic renal failure.   3. Describe the pathophysiology of chronic renal failure.   \n4. Identify the clinical manifestation of chronic renal failure. \n5. Identify common complications of chronic renal failure. 6. Understand the diagnostic approach of chronic renal failure. 7. Understand the principles of management of chronic renal failure.  \n8. Understand the course and prognosis of chronic renal failure.  \n9. Refer patients with Chronic renal failure to better facilities,  \n Definitions  \nChronic Renal failure : progressive and irreversible reduction of the renal function, over a \nperiod of more than 6 months, to a level less than 20 % of the normal, as a result of \ndestruction of significant number of nephrons.  \n\u2022 End stage renal disease (ESRD):  represents a clinical state or condition in which \nthere has been an irreversible loss of endogenous renal function, of a degree sufficient to render the patient permanently dependent upon renal replacement therapy (dialysis or transplantation) in order to avoid life-threatening uremia. \n\u2022 Uremia is the clinical and laboratory syndrome, reflecting dysfunction of all organ \nsystems as a result of untreated or undertreated acute or chronic renal failure. \n\u2022 Azotemia  refers to the retention of nitrogenous waste products as renal"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d365-7265-11ef-afd6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 331, "chroma:document": "\u2022 Uremia is the clinical and laboratory syndrome, reflecting dysfunction of all organ \nsystems as a result of untreated or undertreated acute or chronic renal failure. \n\u2022 Azotemia  refers to the retention of nitrogenous waste products as renal \ninsufficiency develops. \n Etiologies  1. Prerenal causes  \n\u2022 Sever long standing renal artery stenosis \n\u2022 Bilateral renal artery embolism \n2. Renal causes  \n\u2022 Chronic glomerulonephritis: -  primary or secondary forms (30%)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d366-7265-11ef-b882-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 332, "chroma:document": "Internal Medicine \n \n 317\u2022 Chronic tubulointerstitial disease:  - vesicouretral reflux, and chronic pyelonephritis \n(in adolescents) \n\u2022 Vascular disease:  - hypertensive nephrosclerosis \n\u2022 Diabetic nephropathy \n\u2022 Connective tissue diseases  : SLE , scleroderma \n\u2022 Hereditary disease:  -polycystic kidney disease \n3. Post renal cause  \n\u2022 Obstructive nephropathy:  - urolithiasis, benign prostatic hypertrophy, \n \n\u0099 Chronic glomerulonephritis , Hypertension and diabetic nephropathy are the commonest \ncauses for ESRD \n Stages of Chronic renal failure  \n1. Stage of decreased renal reserve  \n\u2022 Basal glomerular filtration rate (GFR ) may be normal or even elevated (hyper-\nfiltration). Adaptation increases the function of the remaining nephrons \n\u2022 Patients are symptom free  \n\u2022 BUN and creatinine are normal or slightly elevated.  \n2. Stage of Renal insufficiency  \n\u2022 GFR declines  by 70 %  ( i.e., GFR will be  30% of normal ) \n\u2022 Patients may remain asymptomatic  \n\u2022 Biochemical evidence of the decline in GFR, i.e., rise in serum concentrations of \nurea and creatinine. Early additional clinical and laboratory manifestations of \nrenal insufficiency may occur. These may include nocturia, mild anemia and loss \nof energy, decreasing appetite and early disturbances in nutritional status. \n\u2022 Sudden stress such as infection, urinary tract obstruction, dehydration, \nadministration of nephrotoxic drugs ma y induce signs and symptoms of uremia. \n3. Renal failure  \n\u2022 GFR falls to below 30% of normal"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d367-7265-11ef-97c4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 332, "chroma:document": "\u2022 Sudden stress such as infection, urinary tract obstruction, dehydration, \nadministration of nephrotoxic drugs ma y induce signs and symptoms of uremia. \n3. Renal failure  \n\u2022 GFR falls to below 30% of normal \n\u2022 An increasing number and severity of uremic clinical manifestations \n\u2022 Biochemical abnormalities raised NUN and creatinine.  \n4.  End stage renal diseases (ESRD ) \n\u2022 GFR falls below 5 to 10% of normal"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d368-7265-11ef-ba78-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 333, "chroma:document": "Internal Medicine \n \n 318\u2022 Continued survival without renal repl acement therapy becomes impossible. \n \nPathophysiology \n\u2022 Uremic manifestations occur mainly due to accumulation of nitrogenous wastes and \nthe reason for accumulation of these wastes is decreased renal excretion and reduced catabolizing capacity of the kidney  \n\u2022 Most toxins in uremia are by products of proteins and amino acid metabolism, \nbecause unlike carbohydrates and fats, which are metabolized to CO\n2 and H 2O, \nwhich can be excreted through the lungs and skin , by products of protein are non volatile organic acids  \nClinical manifestations and complications of Chronic Renal failure  \n1. Fluid, electrolyte and acid base disturbance \na) Volume expansion and contraction (edema, dehydration) \n\u2022 As long as water intake does not exceed the capacity for free water \nclearance, the extra cellular fluid volume expansion will be isotonic and the patient will remain normonatremic. On the other hand, hyponatremia will be the consequence of excessive water ingestion.  \n\u2022 Patients with CRF also have impaired renal mechanisms for conserving Na+ \nand H\n2O. When an extra renal cause for fluid loss is present (e.g., vomiting, \ndiarrhea, sweating, fever), these patients are prone to volume depletion and dehydration.  \n\u2022 In the face of Sodium intake patients may retain Na\n+ and water which may \nlead to congestive heart failure, eripheral edema and ascites . \nb) Potassium Homeostasis:  -"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d369-7265-11ef-a132-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 333, "chroma:document": "\u2022 In the face of Sodium intake patients may retain Na\n+ and water which may \nlead to congestive heart failure, eripheral edema and ascites . \nb) Potassium Homeostasis:  -  \n\u2022 Most commonly, clinically significant hyperkalemia does not occur until the \nGFR falls to below 10 mL/min \n\u2022 Factors that contribute to increased serum K+ level are \n\u2022 Endogenous a K+ load (e.g., hemolysis, trauma, infection) or  \n\u2022 Exogenous K+ (e.g., administration of stored blood, K+-containing \nmedications, K+-containing dietary salt substitute).  \n\u2022 Acidosis : facilitates influx of K+ form ICF to ECF \n\u2022 Drugs: potassium sparing diuretics, ACE inhibitors."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d36a-7265-11ef-97bf-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 334, "chroma:document": "Internal Medicine \n \n 319c) Metabolic Acidosis:  -  \n\u2022 Acidosis is a common disturbance during the advanced stages of CRF. With \nadvancing renal failure, total urinary net daily acid excretion is usually \nreduced markedly. \n \n2. Renal osteodetrophy and Metabolic bone disease: \n\u2022 Is due to disturbance in bone phosphate and calcium metabolism. \n\u2022 Hyperphosphatemia is a feature of advanced renal failure. The serum phosphate \nconcentration rises in patients with a GFR < 20 mL/min. \n\u2022 Calcium : - The total plasma Ca2+ concentration in patients with CRF is often \nsignificantly lower than normal. Patients with CRF tolerate the hypocalcaemia quite well; rarely is a patient symptomatic from the decreased Ca\n2+ \nconcentration. Note that the low serum level of Ca++ is attributed to secondary \nhyperparathyroidism. \n\u2022 Reduced synthesis of 1,25 (OH)2D3 during CRD plays a key role in the \npathogenesis of hyperparathyroidism, both directly and through hypocalcaemia. The abnormal vitamin D metabolism may be related to the renal disease itself \n(since the active vitamin D metabolite is normally produced in the proximal \ntubule) and to the hyperphosphatemia, which has a suppressive effect on the renal 1\u03b1-hydroxylase enzyme.  \nSome of the resulting bony abnormalities are  \no Ostitis fibrosa cystica  : is due to osteoclastic bone resorption of \nspecially  terminal phalanges , long bones and distal end of clavicle  \no Renal rickets  ( Osteomalacia )"}


