# embeddings_queue

created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d36b-7265-11ef-9805-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 334, "chroma:document": "Some 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 ) \no Osteosclerosis  : enhanced bone density in the upper and lower margins \nof vertebrae \n3. Cardiovascular complications  \na) Congestive heart failure and/or pulmonary edema  : it may be due to \n\u2022 Volume over load  \n\u2022 Increase pulmonary capillary permeability \nb) Hypertension :  \n\u2022 Is the most common complication of end stage renal disease.  \n\u2022 It results from fluid overload."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d36c-7265-11ef-8544-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 335, "chroma:document": "Internal Medicine \n \n 320\u2022 Sometimes sever form of hypertension may occur. \nc) Pericarditis:  metabolic toxins are responsible for pericarditis. \n\u2022 The finding of a multicomponent friction rub strongly supports the \ndiagnosis \n\u2022 The pericardial effusion is often hemorrhagic  \n4. Hematologic abnormalities :  \na) Normocytic normochromic anemia : which may be severe ( Hgb 4-6 gm/dl) \n  The cause of anemia is multifactorial \n\u2022 Decreased synthesis of erythropoietin (the most important factor ) \n\u2022 Toxins suppressing bone marrow function \n\u2022 Blood loss ( mainly GI blood loss ) \n\u2022 Decreased life span of RBC \nb) Bleeding tendency  : attributed to platelet dysfunction \n\u2022 Patients may manifest with bleeding and easily bruiseablity \n\u2022 GI bleeding  \n\u2022 Intracranial hemorrhage  \nc) Susceptibility to infection : is due to  \n\u2022 Change in leukocyte formation and function  \n\u2022 Lymphocytopeneia and atrophy of lymphoid tissue  \n5. Neuromuscular abnormalities  \nEarly stage : irritability, inability to concentrate drowsiness, insomnia  \nIntermediate stage:  \n\u2022 Mild behavioral change , poor judgment  \n\u2022 Neuromuscular irritability: hiccup , cramps  , fasciculation , twitching of muscles \nTerminal stage:  \n\u2022 Asterixis, myoclonus, chorea, seizure  \n\u2022 Stupor which may even lead to coma \n\u2022 Peripheral neuropathy : distal sensory polyneuropathy  \no Restless leg syndrome : ill defined sensation of discomfort on the legs  \n6. Gastro intestinal abnormalities"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d36d-7265-11ef-8428-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 335, "chroma:document": "\u2022 Stupor which may even lead to coma \n\u2022 Peripheral neuropathy : distal sensory polyneuropathy  \no Restless leg syndrome : ill defined sensation of discomfort on the legs  \n6. Gastro intestinal abnormalities  \n\u2022 Early symptoms : anorexia , hiccup , nausea and vomiting  \n\u2022 Uremic fetor: the patient\u2019s breathe smells like urine.  \n\u2022 Mucosal ulceration leads to GI bleeding and peptic ulcer diseases."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d36e-7265-11ef-a63c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 336, "chroma:document": "Internal Medicine \n \n 3217. Endocrine and Metabolic abnormalities  \n\u2022 Hypogonadism is common  \no In men : decreased plasma testosterone level , impotence m oligospermia  \no In women: amenorrhea, inability to carry pregnancy to term. \n8. Dermatologic abnormalities ; \n\u2022 Pallor due to anemia  \n\u2022 Echymosis, hematoma  \n\u2022 Pruritis, and excoriation (Ca++ deposits and 20 hyperparathyroidism) \n\u2022 Yellowish declaration of skin : urochromes  \n\u2022 Uremic frost: is seen in advanced uremia  \no It is due to high concentration of urea in the sweat, and after evaporation of \nthe sweat, a fine white powder can be found on the skin surface. \n \nDiagnostic approach \nDifferentiate acute from chronic renal failure : the following findings characterize CRF   \n\u2022 Reduced kidney size on ultrasonography \n\u2022 Long standing nocturia and pruritis \n\u2022 Finding of broad tubular casts on urine analysis \n\u2022 Anemia (not always) \n\u2022 Renal osteodystrophy \nIdentification of aggravating factors (acute or chronic)  \n\u2022 Hypovolemia or hypotension \n\u2022 Hypertension  \n\u2022 Congestive heart failure \n\u2022 Sepsis \n\u2022 Nephrotoxins \n \nEvaluation of reversible underlying etiology \n\u2022 Malignant hypertension \n\u2022 Obstructive uropathy \n\u2022 Systemic lupus erythematosis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d36f-7265-11ef-9bab-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 337, "chroma:document": "Internal Medicine \n \n 322Establishing the underlying cause  \nHistory  \n\u2022 Of special importance in establishing the etiology of CRF are a history of: \no Hypertension \no Diabetes mellitus  \no Systemic infectious or  inflammatory diseases  \no Metabolic diseases \no Exposure to drugs and toxins \no Family history of renal and urologic disease.  \n\u2022 In evaluating the uremic syndrome, questions about appetite, diet, nausea, and vomiting, \nhiccoughing, shortness of breath, edema, weight change, muscle cramps, bone pain, \nmental acuity, and activities of daily living are especially helpful. \n \nPhysical Examination:  -  \n\u2022 Particular attention should be paid to: \n\u2022 Blood pressure \n\u2022 Funduscopy \n\u2022 Precordial examination \n\u2022 Examination of the abdomen for bruits and palpable renal masses \n\u2022 Extremity examination for edema \n\u2022 Neurologic examination for the presence of asterixis, muscle weakness, and \nneuropathy  \n\u2022 In addition, the evaluation of prostate size in men and potential pelvic masses in \nwomen should be undertaken by appropriate physical examination. \nDiagnostic work up   \n\u2022 These should also focus on a search for clues to an underlying disease process and \nits continued activity.  \n\u2022 Other tests to determine the severity and chronicity of the disease include : \no Serial measurements of serum creatinine and blood urea nitrogen \n\u2022 Hemoglobin \n\u2022 Electrolytes : calcium, phosphate, and alkaline phosphates to assess metabolic \nbone disease.  \n\u2022 Urinalysis:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d370-7265-11ef-bfb5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 338, "chroma:document": "Internal Medicine \n \n 323o May be helpful in assessing the presence of ongoing activity of the underlying \ninflammatory or proteinuric disease process, and when indicated should be \nsupplemented by a 24-h urine collection for quantifying protein excretion.  \no The presence of broad casts on examination of the urinary sediment is a \nnonspecific finding seen with all diverse etiologies and reflects an advanced stage of CRF.  \n\u2022 Ultrasonography of kidneys:  \no An ultrasound examination of the kidneys verifies the presence of two \nsymmetric kidneys, provides an estimate of kidney size, and rules out renal \nmasses and obstructive uropathy.  \no The documentation of symmetric sma ll kidneys supports the diagnosis of \nprogressive CRF with an irreversible component of scarring. The occurrence of normal kidney size suggests the possibility of an acute rather than chronic process. However in some diseases, chronic renal failure may be present with normal sized or even enlarged kidneys. E.g.  Amyloidosis , polycystic \nkidney diseases , Diabetic nephropathy \n \nManagement of chronic renal failure  The general management of the patient with chronic \nrenal disease involves the following issues \n \n1) Treatment of reversible causes of renal dysfunction \n2) Preventing or slowing the progression of renal disease 3) Treatment of the complications of renal dysfunction 4) Identification and adequate preparation of the patient in whom renal replacement \ntherapy will be required"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d371-7265-11ef-9310-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 338, "chroma:document": "2) Preventing or slowing the progression of renal disease 3) Treatment of the complications of renal dysfunction 4) Identification and adequate preparation of the patient in whom renal replacement \ntherapy will be required \n \n1. Treating reversible causes of renal dysfunction  \u2013 In addition to exacerbation of \ntheir original renal disease, patients with chronic renal disease, with a recent decrease in renal function may be suffering from an underlying reversible process \nsuch as : \no Hypotension or dehydration  \no Administration of nephrotoxic drugs  \no Urinary tract obstruction"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d372-7265-11ef-ab95-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 339, "chroma:document": "Internal Medicine \n \n 324o Sever hypertension \no Infection  \n\u2022 Correcting these reversible causes can improve the renal function. \n2. Slowing the rate of progression  of renal diseases :  \n\u2022 Angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor \nblockers (ARBs) slows the progre ssion of chronic renal failure .  \n\u2022 Blood pressure control : decreases progression of CRF \nTarget BP for patients with: \n\u00be Proteinuria is 125/75 mmHg  \n\u00be for patients without proteinuria is 130/85 mmHg  \n\u2022 The possible efficacy of dietary protein restriction, in slowing progression \nof renal diseases, is less clear.   \n \n3. Treatment of the complications of renal dysfunction  : \na) Volume overload  \u2013 \n\u2022 Dietary sodium restriction  \n\u2022 Diuretic therapy, usually with a loop diuretic given daily.  \nb) Hyperkalemia : \n\u2022 Low-potassium diet or concurrent use of a loop diuretic (to increase urinary \npotassium losses) often ameliorates the degree of hyperkalemia. \n\u2022 Calcium gluconate ; 10 ml of 10% solution over 5 minutes  \n\u2022 Glucose plus insulin:  \n\u2022 Correction of acidosis : administration of bicarbonate  \n\u2022 Potassium exchange resins: Kayaxalate  \n \nc) Metabolic acidosis : \n\u2022 Alkali therapy is advocated to maintain the plasma bicarbonate \nconcentration above 22 mEq/L. If alkali is given, sodium bicarbonate (in a \ndaily dose of 0.5 to 1 mEq/kg per day) is the agent of choice. \nd) Hyperphosphatemia: \n\u2022 Dietary phosphate restriction may limit the development of secondary"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d373-7265-11ef-a098-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 339, "chroma:document": "concentration above 22 mEq/L. If alkali is given, sodium bicarbonate (in a \ndaily dose of 0.5 to 1 mEq/kg per day) is the agent of choice. \nd) Hyperphosphatemia: \n\u2022 Dietary phosphate restriction may limit the development of secondary \nhyperparathyroidism in patients with chronic renal failure. An intake of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d374-7265-11ef-b9a1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 340, "chroma:document": "Internal Medicine \n \n 325about 800 mg/day may be desirable but can be accomplished only by \nlimiting protein intake. \n \n \ne) Hypertension : \n\u2022 Salt restriction \n\u2022 Diuretics: loop diuretics are recommended for the treatment of \nhypertension and edema in patients with chronic renal failure. Thiazide \ndiuretics have additive effect when administered with a loop diuretic for \nrefractory edema.  \n\u2022 Anti hypertensive drugs  \nf) Anemia : \n\u2022 Blood transfusion in selected patients  \n\u2022 Recombinant Erythropoietin may be given. \ng) Malnutrition: \n\u2022 The desire to maintain adequate nutrition among patients with chronic \nrenal failure clearly competes with attempts to slow the progression of \nrenal dysfunction with the use of a low protein diet.  \n\u2022 Although the benefits of slowing progressive renal failure with marked \ndietary protein restriction remain controversial, it is probably reasonable to restrict intake to 0.8 to 1.0 g/kg of high biologic value protein (plant source) \n\u2022 Since this level of restriction avoids protein malnutrition and may slow \nprogressive disease. Overall, the diet of most patients with chronic renal failure should provide approximately 30 to 35 kcal/kg per day.  \n \n4. Preparation for renal replacement Therapy \no Education  \no Informed choice of renal replacement therapy \ni. Chronic Hemodialysis \nii. Kidney transplantation"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d375-7265-11ef-91b8-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 341, "chroma:document": "Internal Medicine \n \n 326References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nChronic renal failure, pages 1653-1662. \n2) Myers R. Allen , National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Chronic renal failure, pages 285-286."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d376-7265-11ef-b712-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 342, "chroma:document": "Internal Medicine \n \n 3276. Urinary Tract infection  \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define urinary tract infections.    \n2. List the etiologies of urinary tract infections.      \n3. Describe the epidemiology of urinary tract infections.  \n4. Explain the pathogenesis of urinary tract infections.     5. Describe the clinical features of urinary tract infections.     6. List the common complications urinary tract infections.  \n7. Describe the most commonly used tests for the diagnosis of urinary tract infections.      \n8. Make an accurate diagnosis of urinary tract infections.       9. Treat urinary tract infections with appropriate antibiotics.   10. Design appropriate methods of prevention and control of urinary tract infections.     \n \nDefinitions \nUTI: is an acute infection of the urinary tract, and is subdivided into two general anatomic \ncategories:  \n\u2022 Lo wer urinary tract infection: which includes urethritis and cystitis and  \n\u2022 Upper urinary tract infection: includes acute pyelonephritis, prostatitis, and intrarenal and perinephric abscesses).   \n \nFrom a microbiologic perspective, urinary tract infection (UTI)  \n\u2022 Exists when pathogenic microorganisms are detected in the urine, urethra, bladder, \nkidney, or prostate. In most instances, growth of more than 10\n5 organisms per milliliter \nfrom a properly collected midstream \"clean-catch\" urine sample indicates infection."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d377-7265-11ef-98c5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 342, "chroma:document": "kidney, or prostate. In most instances, growth of more than 10\n5 organisms per milliliter \nfrom a properly collected midstream \"clean-catch\" urine sample indicates infection. \n\u2022 Especially in symptomatic patients, a smaller number of bacteria (102 to 104/mL) may \nsignify infection.  \n\u2022 In urine specimens obtained by suprapubic aspiration or \"in-and-out\" catheterization and \nin samples from a patient with an indwelling catheter, colony counts of 102 to 104/mL \ngenerally indicate infection.  \nRecurrence of UTI after treatment \n\u2022 Infections that recur after antibiotic therapy can be due to the persistence of the \noriginally infecting strain (as judged by species, antibiogram, serotype, and molecular"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d378-7265-11ef-9b8b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 343, "chroma:document": "Internal Medicine \n \n 328type) that become evident within 2 weeks of cessation of therapy termed relapse, or to \nreinfection with a new strain that become evident after 2 weeks of cessation of therapy. \n \nChronic pyelonephritis : refers to chronic interstitial nephritis believed to result from bacterial \ninfection of the kidney. Manifested by calyceal dilatation & cortical scarring.  \n \nAcute Urinary tract infection  \nEpidemiology  \nEpidemiologically, UTIs are subdivided into: \n1. Non-catheter-associated (or community-acquired) infections.  \n2. Catheter-associated (or nosocomial) infections and  \n\u2022 The vast majority of acute symptomatic infections involve young women.  \n\u2022 Acute symptomatic UTIs are unusual in men under the age of 50.  \n\u2022 The development of asymptomatic bacteriuria parallels that of symptomatic infection and is \nrare among men under 50 but common among women between 20 and 50.  \n\u2022 Asymptomatic bacteriuria is more common among elderly men and women, with rates as \nhigh as 40 to 50% in some studies.  \n\u2022 A study done by Messele Gedebou in 1980\u2019s showed that among patients with bacteruria E. \ncoli was identified in 80% of the patients with symptomatic UTI, in Ethiopia.  \n \nEtiology \n1. Etiologic agents for community acquired cases \n\u2022 Commonest causes are E. coli (80%), S. saprophyticus(10%), Klebsiella \npneumoniae (5%) and other (5%)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d379-7265-11ef-9eea-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 343, "chroma:document": "coli was identified in 80% of the patients with symptomatic UTI, in Ethiopia.  \n \nEtiology \n1. Etiologic agents for community acquired cases \n\u2022 Commonest causes are E. coli (80%), S. saprophyticus(10%), Klebsiella \npneumoniae (5%) and other (5%) \n\u2022 In acute uretheral syndrome (Sexually transmitted organisms: N. gonorrhea, Chlamydia trachomitis, Trichomonas, Candida, and herpes \nsimplex virus may cause lower UIT) \n\u2022 In elderly Enterococcus fecalis may be a cause for UTI. \n\u2022 Bacteremia is often due to S. aureus. \n2. Hospital acquired/ catheter associated UTI \n\u2022 E. coli (30%) \n\u2022 Enterococci (15%) \n\u2022 Pseudomonas (10%)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d37a-7265-11ef-b185-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 344, "chroma:document": "Internal Medicine \n \n 329\u2022 S. aureus, yeasts, and other Enterobacteriacea \n \nPathogenesis and source of infection \nRouts of inoculation  \n\u2022 Urethral inoculation : The urinary tract should be viewed as a single anatomic unit that \nis united by a continuous column of urine ex tending from the urethra to the kidney. In the \nvast majority of UTIs, bacteria gain access to the bladder via the urethra. Ascent of \nbacteria from the bladder may follow and is probably the pathway for most renal parenchymal infections. Whether bladder infection ensues depends on interacting effects of the pathogenicity of the strain, the inoculum size, and the local and systemic \nhost defense mechanisms. \n \n\u2022 Hematogenous spread: pyelonephritis occurs most often in debilitated patients who are \neither chronically ill or receiving immunos uppressive therapy. Metastatic staphylococcal \nor candidal infections of the kidney may follow bacteremia or fungemia, spreading from \ndistant foci of infection in the bone, skin, vasculature, or elsewhere. \n \nConditions affecting pathogenesis /risk factors for UTI \n1. Gender and Sexual Activity:  \n\u2022 The female urethra appears to be particularly prone to colonization with colonic"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d37b-7265-11ef-8786-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 344, "chroma:document": "distant foci of infection in the bone, skin, vasculature, or elsewhere. \n \nConditions affecting pathogenesis /risk factors for UTI \n1. Gender and Sexual Activity:  \n\u2022 The female urethra appears to be particularly prone to colonization with colonic \ngram-negative bacilli because of its proximity to the anus, its short length (about 4 cm), and its termination beneath the labia. Sexual intercourse causes the introduction of bacteria into the bladder and is temporally associated with the onset of cystitis; it thus appears to be important in the pathogenesis of UTIs in younger \nwomen.  \n\u2022 In males who are <50 years old and who have no history of heterosexual or \nhomosexual rectal intercourse, UTI is exceedingly uncommon, and this diagnosis \nshould be questioned in the absence of clear documentation.  \n\u2022 An important factor predisposing to bacteriuria in men is urethral obstruction due to \nprostatic hypertrophy.  \n\u2022 Men (and women) who are infected with HIV and who have CD4+ T cell counts of \n<200/\u03bcL are at increased risk of both bacteriuria and symptomatic UTI."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d37c-7265-11ef-abdf-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 345, "chroma:document": "Internal Medicine \n \n 330\u2022 Finally, lack of circumcision has been ident ified as a risk factor for UTI in both \nneonates and young men. \n \n2. Pregnancy :  \n\u2022 Is clearly associated with altered uretheral smooth muscle function and higher \nincidence of asymptomatic bacteriuria and 20 to 30% of pregnant women with \nasymptomatic bacteriuria subsequently develop pyelonephritis. \n\u2022 UTIs are detected in 2 to 8% of pregnant women. Symptomatic upper urinary tract \ninfections, in particular, are unusually common during pregnancy.  \n\u2022 Bladder catheterization during or after delivery causes additional infections. \nIncreased incidences of low-birth-weight infants, premature delivery, and newborn mortality result from UTIs during pregnancy, particularly those infections involving the upper tract. \n \n3. Vesicoureteral reflux:  \n\u2022 Defined as reflux of urine from the bladder cavity up into the ureters and \nsometimes into the renal pelvis.  \n\u2022 Vesicoureteral reflux occurs during voiding or with elevation of pressure in \nthe bladder.  \n\u2022 Vesicoureteral reflux is common among children with anatomic \nabnormalities of the urinary tract as well as among children with anatomically normal but infected urinary tracts. In the latter group, reflux disappears with advancing age and is probably attributable to factors other \nthan UTI.  \n\u2022 Vesicoureteral reflux may promote ascending infection in several ways, including"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d37d-7265-11ef-aa74-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 345, "chroma:document": "than UTI.  \n\u2022 Vesicoureteral reflux may promote ascending infection in several ways, including \nincreased delivery of bacteria  , increased size of inoculum , incomplete bladder emptying  \n4.  Obstruction : Any impediment to the free flow of urine caused tumor, stricture, stone, or \nprostatic hypertrophy results in hydronephrosis. This results in urinary stasis and impairs \nhost defense,  which  greatly increased the frequency of UTI.  \n5. Neurogenic Bladder Dysfunction:  - Interference with the nerve supply to the bladder, \nas in spinal cord injury, tabes dorsalis, multiple sclerosis, diabetes, and other diseases, \nmay be associated with UTI."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d37e-7265-11ef-879f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 346, "chroma:document": "Internal Medicine \n \n 3316. Diabetes mellitus:  is associated with high rate of infection. Part of the risk is mediated \nthrough neurogenic bladder disturbance, and partly due to other immune disorders in \ndiabetes. \n7. Immune deficiency:  congenital, acquired or drug induced immunodeficiencies are \nassociated with increased susceptibility to infection. \n8. Bacterial Virulence Factors : - Not all strains of E. coli are equally capable of infecting \nthe intact urinary tract. Bacterial virulence factors markedly influence the likelihood that a \ngiven strain, once introduced into the bladder, will cause UTI.  \n9.  Genetic Factors:  increasing evidence suggests that host genetic factors \ninfluence susceptibility to UTI. A maternal history of UTI is more often found \namong women who have experienced recurrent UTIs than among controls. \n \nClinical presentation  \nCystitis:  \n\u2022 Patients with cystitis usually report dysuria, frequency, urgency, and suprapubic \npain.  \n\u2022 The urine often becomes grossly cloudy and malodorous, and it is bloody in about \n30% of cases. \n\u2022 If a genital lesion or a vaginal discharge is evident, then pathogens that may cause \nurethritis, vaginitis, or cervicitis, such as C. trachomatis, N. gonorrhoeae, \nTrichomonas,  Candida,  and herpes simplex virus , should be considered. \nAcute Pyelonephritis :  \n\u2022 Symptoms of acute pyelonephritis generally develop rapidly over a few hours or a \nday and include a fever, shaking chills, nausea, vomiting, and diarrhea."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d37f-7265-11ef-b7bc-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 346, "chroma:document": "Acute Pyelonephritis :  \n\u2022 Symptoms of acute pyelonephritis generally develop rapidly over a few hours or a \nday and include a fever, shaking chills, nausea, vomiting, and diarrhea.  \n\u2022 Symptoms of cystitis may or may not be present.  \n\u2022 Physical examination:  fever, tachycardia, and generalized muscle tenderness, \nmarked tenderness on deep pressure in one or both costovertebral angles or on deep abdominal palpation ( Costvertebral angle tenderness ).  \n\u2022 In some patients, signs and symptoms of gram-negative sepsis predominate.  \nUrethritis :  \n\u2022 Approximately 30% of women with acute dysuria, frequency, and pyuria have \nmidstream urine cultures that show either no growth or insignificant bacterial growth."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d380-7265-11ef-a2b3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 347, "chroma:document": "Internal Medicine \n \n 332\u2022 Clinically, these women cannot always be readily distinguished from those with \ncystitis. In this situation, a distinction should be made between women infected with \nsexually transmitted pathogens, such as C. trachomatis, N. gonorrhoeae, or herpes simplex virus, and those with low-count E. coli or staphylococcal infection of the urethra and bladder.  \n\u2022 Chlamydial or gonococcal  infection should be suspected in women with a gradual \nonset of illness, no hematuria, no suprapubic pain, and more than 7 days of symptoms.  \n\u2022 The additional history of a recent sex-partner change, especially if the patient's \npartner has recently had chlamydial or gonococcal urethritis, should heighten the suspicion of a sexually transmitted infection, as should the finding of mucopurulent \ncervicitis.  \n\u2022 Gross hematuria, suprapubic pain, an abrupt onset of illness, a duration of illness of \n<3 days, and a history of UTIs favor the diagnosis of  E. coli UTI.  \n \nCatheter-Associated UTIs :  \n\u2022 Bacteriuria develops in at least 10 to 15% of hospitalized patients with indwelling \nurethral catheters. The risk of infection is about 3 to 5% per day of catheterization.  \n\u2022 Clinically, most catheter-associated infections cause minimal symptoms and no \nfever and often resolve after withdrawal of the catheter.  \n\u2022 Gram-negative bacteremia, which follows catheter-associated bacteriuria in 1 to 2% \nof cases, is the most significant recognized complication of catheter-induced UTIs."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d381-7265-11ef-996f-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 347, "chroma:document": "fever and often resolve after withdrawal of the catheter.  \n\u2022 Gram-negative bacteremia, which follows catheter-associated bacteriuria in 1 to 2% \nof cases, is the most significant recognized complication of catheter-induced UTIs.  \n\u2022 The catheterized urinary tract has repeatedly been demonstrated to be the most \ncommon source of gram-negative bacteremia in hospitalized patients, generally \naccounting for about 30% of cases. \n \nDiagnostic work up  \n1. Urinalysis: \n\u2022 Urinary sediment :  \n\u2022 Leukocytes are found in the urine : > 5 WBCs/ high power field in centrifuged urine \nor > 10 WBCs/ higher power field in unspun urine suggests UTI \n\u2022 Microscopic bacteruria: single microorganism per oil immersion field of unspun urine \nis indicative of a colony growth on culture of more than 10\n5 colonies /ml."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d382-7265-11ef-89fa-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 348, "chroma:document": "Internal Medicine \n \n 333\u2022 Gram stain of urethral discharge may be help full in patients suspected of having \nSTI associated urethritis. \n2. Culture of the urine:  is a definitive means for diagnosis \n\u2022 A clean catch , mid stream urine specimen should be collected \n\u2022 The growth  of more than 105 colonies /ml in the presence of symptoms signifies \ninfection that needs treatment  \n3.  Blood:  increased WBCs in the blood  \n4. Radiologic urologic evaluation:  may be help full in identification of some \npredisposing conditions such as urolithiasis, BPH, vesicoureteral reflux  \n \nTherapy  \nThe following principles underlie the treatment of UTIs: \n1. Except in acute uncomplicated cystitis in women, a quantitative urine culture, rapid \ndiagnostic test should be performed to confirm infection before treatment is begun.  \n2. Factors predisposing to infection, such as obstruction and calculi, should be \nidentified and corrected if possible. \n3. Relief of clinical symptoms does not always indicate bacteriologic cure. \n4. In general, uncomplicated infections confined to the lower urinary tract respond to \nshort courses of therapy, while upper trac t infections require longer treatment \n\u2022 The anatomic location of a UTI greatly influences the success or failure of a \ntherapeutic regimen. Bladder bacteriuria (cystitis) can usually be eliminated with nearly any antimicrobial agent to which the infecting strain is sensitive."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d383-7265-11ef-b685-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 348, "chroma:document": "\u2022 The anatomic location of a UTI greatly influences the success or failure of a \ntherapeutic regimen. Bladder bacteriuria (cystitis) can usually be eliminated with nearly any antimicrobial agent to which the infecting strain is sensitive. \n\u2022 Treatment of pyelonephritis  \u2013 Treatment decisions include whether or not to \nhospitalize the patient, which therapy to  administer empirically, and when to order \nimaging studies to determine whether an infection is complicated  \n \nDecision to hospitalize : Indications for admission to the hospital in acute pyelonephritis  \n1. Inability to maintain oral hydration or take medications 2. Concerns about patient compliance 3. Uncertainty about the diagnosis 4. Severe illness with high fevers, pain, and marked debility \nEmpiric antibiotic choices  \u2013 \no The initial antibiotic therapy is selected on the basis of urinalysis and an \nunderstanding of epidemiology and bacteriology of the infection."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d384-7265-11ef-93a1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 349, "chroma:document": "Internal Medicine \n \n 334o Knowledge of the antimicrobial susceptibility profile of uropathogens in the \ncommunity helps to guide therapeutic decisions. \no Ampicillin and sulfonamides should not be used for empiric therapy because of the \nhigh rate of resistance among causative uropathogens.  \no In comparison, resistance to the fluoroquinolones and aminoglycosides is very low \nin uncomplicated UTIs and Aminoglycosi des and fluoroquinolones achieve higher \ntissue levels. So these drugs are preferred for empiric treatment.  \no All pregnant women should be screened for bacteriuria in the first trimester and \nshould be treated if bacteriuria is demonstrated. \n1. Acute Uncomplicated lower UIT in women :  may be treated with  \n\u2022 Trimethoprim \u2013Sulfamethoxazol : 480 mg 2 tabs PO BID for 3-5 days \n\u2022 Norfloxacin 400 PO BID or Ciprofloxacin 500 mg PO BID for 5-7 days  \n2. Acute uncomplicated pyelonephritis in women  : E. coli , P. mirabilis , S. saprophyticus \nare the common causes  \n\u2022 Norfloxacin 400 PO BID or Ciprofloxacin 500 mg PO BID for 7-14 days or  \n\u2022 Single dose of Ceftriaxon 1gm or Gentamicin 80 mg IV followed by \nTrimethoprim \u2013Sulfamethoxazol : 480 mg 2 tabs PO BID for 14 days \n3. Complicated UTI in men and women:  E. coli , Proteus , Klebsiella , Pseudomonas , \nSerratia , enterococci, staphylococci are the common etiologies.  \n\u2022 Mild to moderate illness, no nausea or vomiting: outpatient therapy \n\u2022 Norfloxacin 400 PO BID or Ciprofloxacin 500 mg PO BID for 10-14 days or"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d385-7265-11ef-840b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 349, "chroma:document": "Serratia , enterococci, staphylococci are the common etiologies.  \n\u2022 Mild to moderate illness, no nausea or vomiting: outpatient therapy \n\u2022 Norfloxacin 400 PO BID or Ciprofloxacin 500 mg PO BID for 10-14 days or \n4. Severe illness or possible urosepsis: hospitalization is required . \n\u2022 Ceftriaxone 1gm IV daily or BID  \n\u2022 Gentamicine 80 mg IV TID  \n\u2022 Ampicillin  1gm IV QID and then 500 mg IV QID \n\u2022 IV quinolones such as Ciprofloxacin 200-400 mg IV BID can also be used if \navailable  \n\u2022 If enterococcus is suspected based upon the Gram stain, ampicillin (1 to 2 g IV \nQ6h) plus gentamicin (1.0 mg/kg IV Q8h or adjusted for renal function). \nNote:  IV medication should be changed to PO as soon as the patient became afebrile and \nthen give PO TMP-SMX or Ciprofloxacin or Norfloxacin   for 10- 21 days.  \nParenteral therapy \u2013 For hospitalized patients, aminoglycosides (3 to 5 mg/kg) given once \ndaily are cost effective , associated with low toxicity when used for short durations, and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d386-7265-11ef-852b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 350, "chroma:document": "Internal Medicine \n \n 335may provide a therapeutic advantage compared with beta lactams, because of their marked \nand sustained concentration in renal tissue .  \nUrologic evaluation .  \n\u2022 Routine urologic investigation of young healthy women with acute uncomplicated \npyelonephritis is generally not recommended.  \n\u2022 Urologic consultation and evaluation of the upper urinary tract with an ultrasound \nshould be considered if the patient remains febrile or has not shown signs of \ndemonstrable clinical improvement after 72 hours of treatment to rule out the \npresence of obstruction, renal or perinephric abscesses, or other complications of \npyelonephritis.  \n\u2022 It is reasonable to perform a urologic evaluation, starting with renal ultrasound to \nrule out nephrolithiasis or obstructive uropathy, after two recurrences of pyelonephritis or if any complicating factor is identified.  \nPrognosis \n\u2022 In patients with uncomplicated cystitis or  pyelonephritis, treatment ordinarily results \nin complete resolution of symptoms. When repeated episodes of cystitis occur, they are nearly always reinfections, not relapses. \n\u2022 Acute uncomplicated pyelonephritis in adults rarely progresses to renal functional \nimpairment and chronic renal disease. Repeated upper tract infections often represent relapse rather than reinfection, and a vigorous search for renal calculi or an underlying urologic abnormality should be undertaken. If neither is found, 6"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d387-7265-11ef-acb1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 350, "chroma:document": "impairment and chronic renal disease. Repeated upper tract infections often represent relapse rather than reinfection, and a vigorous search for renal calculi or an underlying urologic abnormality should be undertaken. If neither is found, 6 \nweeks of chemotherapy may be useful in eradicating an unresolved focus of \ninfection. \n\u2022 Repeated symptomatic UTIs in children and in adults with obstructive uropathy, \nneurogenic bladder, structural renal disease, or diabetes may progress to chronic renal disease with unusual frequency. Asymptomatic bacteriuria in these groups as well as in adults without urologic disease or obstruction predisposes to increased numbers of episodes of symptomatic infection but does not result in renal \nimpairment in most instances."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d388-7265-11ef-96f6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 351, "chroma:document": "Internal Medicine \n \n 336References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nUrinary tract infection and pyelonephritis ,  pages 1715-1721. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Urinary tract infection, Pages 284-285."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d389-7265-11ef-b678-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 352, "chroma:document": "Internal Medicine \n \n 337CHAPTER FIVE \nDISEASES OF THE GASTRO INTESTINAL SYSTEM \n \n1. Approach to a patient wi th gastrointestinal disorder \n \nLearning objectives: at the end of this unit the student will be able to \n1. List the symptoms of gastrointestinal diseases  \n2. Characterize each symptom of gastrointestinal diseases \n3. Describe the investigations for gastrointestinal diseases 4. Outline the steps in paracentesis 5. Describe the difference between exudates and transudates and their clinical use 6. List the different radiological and endoscopic investigations and their clinical use \nPatients with gastrointestinal disorders may present with a variety of symptoms that are specific to the gastrointestinal tract and/or general systemic symptoms. Disorders of the gastrointestinal tract also give a variety of signs. \n \nCommon symptoms include:  \n\u2022 Abdominal pain, abdominal distension  \n\u2022 Dyspepsia \n\u2022 Diarrhea or constipation  \n\u2022 Gastrointestinal bleeding    \n\u2022 Jaundice      \n\u2022 Change in weight and change in appetite  \n\u2022 Nausea vomiting  \n\u2022 Change in stool color \n\u2022 During history taking, detailed analysis of the above symptoms should be done, \nand history of medications should also be elicited.  \n\u2022 The usual techniques and steps of physica l examination of the gastrointestinal \nsystem should be followed, that include: inspection, auscultation, percussion, and \npalpation"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d38a-7265-11ef-9eeb-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 353, "chroma:document": "Internal Medicine \n \n 338Diagnostic work up of patients  with gastrointestinal diseases \n1) Stool microscopy  for i ntestinal parasite; ova, cyst or trophozoites, pus cells and red \nblood cells \n2) Stool culture  - indicated in certain cases of infectious diarrhea  \n3) Chemical analysis of stool  test for fecal fat and occult blood  \n4) Aspiration of peritoneal fluid (abdominal paracentesis) could be:- \n\u2022 Diagnostic  \u2013 for evaluation of clinically evident ascites  \n\u2022 Therapeutic  \u2013 to remove fluid in case of refractory ascites with respiratory \nembarrassment.  \nTechnique  \n\u03bf Empty the urinary bladder \n\u03bf Patient lying flat or slightly probed up  \n\u03bf Give local anesthetics if available \n\u03bf Site of aspiration is the right iliac fossa, a little outside the midpoint of a \nline joining the umbilicus to anterior superior iliac spine. \n\u03bf For diagnostic purpose 10cc syringe may be used  \n\u03bf For therapeutic purpose trocar and flanged cannula are used. If this is not \navailable intravenous set with needle may be used. \nThe fluid is analyzed biochemically, bacteriol ogically, cytologically and physically.  \n\u03bf Biochemical \u2013 protein, glucose, Lactate dehydrogenase (LDH) \n\u03bf Bacteriology   \u2013 Gram staining, AFB staining  \n\u03bf Culture  \n\u03bf Cytology \u2013 cell count and differential; look for malignant cells \n\u03bf Physical \u2013 color, specific gravity  \nBased on the above analysis, ascites is classi fied into two: exudative and transudative, and \nthe main differences are outlined below:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d38b-7265-11ef-988c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 354, "chroma:document": "Internal Medicine \n \n 339Table V-1-1, Main differences between exudative and transudative ascetic fluids  \n \n Exudative  Transudative  \nSpecific gravity  > 1.018  < 1.018  \nProtein  > 2.5 gm/dl  < 2.5 gm/dl  \nSerum ascetic \nalbumin gradient)  < 1.1                         > 1.1 \n \nCauses  Bacterial peritonitis  \nTB peritonitis  \nMalignancy  CHF  \nCirrhosis  \nNephrotic syndrome  \n \n5) Radiology of the gastrointestinal tract  \n\u2022 Plain x-ray  \u2013   no contrast is used and can be taken erect (to see for air fluid level) \nor supine.  \n\u2022 Contrast x-rays  \u2013 barium is used to outline the lumen of the gastrointestinal tract. \nDifferent terminologies are used to describe barium studies of the different parts of the gastrointestinal tract:   \no For esophagus - Barium swallow.  \no For stomach     - Barium meal. \no For intestine     - Barium meal and follow through.  \no For Rectum      -  Barium enema     \n\u2022 Indications for x-ray of the GI tract include  \no Intestinal obstruction (plain films) \no Dysphagia \no Peptic ulcer disease \no Inflammatory bowel disease \n6) Endoscopy is visualization of the lumen of the GI tract with endoscope. \nEndoscopes are of two types depending their flexibility  \n\u03bf Rigid  used for removal of foreign body  \n\u03bf Fibro-optic  is flexible and used for visualization of the GI tract \nDepending on the structures to be visualized endoscopes can be divided into  \nA) Upper GI endoscopy:-   \no It is used to visualize structures up to the second part of the duodenum."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d38c-7265-11ef-8392-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 355, "chroma:document": "Internal Medicine \n \n 340o It can be used for diagnostic and therapeutic purposes (to stop bleeding \nvarices, ulcers, or to dilate esophageal strictures) \nB) Lower GI endoscopy: there are three different types of lower GI \nendoscopies, to visualize the different parts of the large intestine:  \no Colonoscopy : for diagnosis and management of colonic polyps and \nulcers \no Sigmoidoscopy : to visualize the sigmoid colon.  \no Proctoscopy : to visualize the rectum and anus. \n \n \nDiagnostic work up of patients wit h diseases of hepatobiliary system  \n1. Biochemical tests: \n\u2022 Tests for the detoxification capacity of the liver : \n\u03bf Serum ammonia level \n\u03bf Serum bilirubin, urine bilirubin level \n\u2022 Tests for synthetic function of the liver:  \n\u03bf Serum albumin level \n\u03bf Prothrombin time  \n\u2022 Tests indicating hepatocellular damage  \n\u03bf Transaminases (serum glutamic oxalate transferase (SGOT) and serum \nglutamic pyruvate transferase (SGPT)) \n\u2022 Tests which show cholestasis  \n\u03bf Alkaline phosphatase \n\u03bf (Direct) bilirubin level. \n2. Ultrasound  is a noninvasive procedure that may be help full in diagnosing the following \ndiseases: \no Cirrhosis     \no Metastasis  \no Fluid filled lesions \u2013 cysts, abscess  \no Cholelithiasis \n3. Biopsy \u2013  can be done in two forms  \n\u03bf Open biopsy is done during laparatomy and allows to take adequate tissue \nsamples"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d38d-7265-11ef-84d5-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 356, "chroma:document": "Internal Medicine \n \n 341\u03bf Needle biopsy is done percutaneously  \n4. Cholangiography:  is contrast study of the biliary tree. The contrast can be given orally, \npercutaneously, intravenously, or by using endoscope; the last is known as \nEndoscopic Retrograde Cholangiopancreaticography (ERCP) \n  \nReferences:  \n2) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nApproach to patients with Gastrointestinal diseases , pages 1725-1729."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d38e-7265-11ef-9d6f-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 357, "chroma:document": "Internal Medicine \n \n 3422.  Gastritis and peptic ulcer diseases  \n \nObjectives: at the end of this unit the student will be able to:- \n1. Define gastritis and peptic ulcer diseases (PUD). \n2. List the etiologies of gastritis and PUD.    3. Describe the epidemiology of PUD. \n4. Explain the pathogenesis gastritis and PUD.    \n5. Describe the clinical features of gastritis and PUD.    6. List the common complications gastritis and PUD. 7. Describe the most commonly used methods for the diagnosis of gastritis and \nPUD. \n8. Make an accurate diagnosis of gastritis and PUD.    9. Treat gastritis and PUD at the primary care level with appropriate drugs. 10. Refer those presenting with complications of gastritis and PUD to hospitals. \n \n2.1 Gastritis \n\u2022 Gastritis refers to histologically confirmed inflammation of the gastric mucosa. It \nis not synonymous with dyspepsia or gastric erythema seen during endoscopy. \nIt is classified into:  \n \nAcute gastritis   \n\u2022 Commonly caused by: Helicobacter pylori .  \n\u2022 Other causes include : \no Drugs like ASA, NSAID ,  \no Alcohol in high doses,  \no Severe stress, and  \no Other infections such as viruses (CMV, Herpes simplex), mycobacterium, \nand syphilis.  \n\u2022 Patients are usually asymptomatic but at times they may present with sudden \nonset of epigastric pain, with neutrophilic infiltration, edema and hyperemia of the \ngastric mucosa."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d38f-7265-11ef-8672-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 358, "chroma:document": "Internal Medicine \n \n 343\u2022 If not treated, H. pylori  gastritis may progress to one of the chronic gastritis. No \nspecific treatment of acute gastritis is indicated. Removal of the offending agents \nmay be adequate.  \nChronic gastritis \n\u2022 Defined as a histological demonstration of lymphocytic and plasma cell infiltration \nof gastric mucosa.  \n\u2022 Course:  Superficial gastritis is followed by  atrophic gastritis (characterized by \ndistortion and destruction of gastric glands) progressing to gastric atrophy (with \nloss of gastric glands), which then undergo intestinal metaplasia (replacement of \ngastric mucosal cells by intestinal epithe lial cells) and finally progressing to gastric \ncarcinoma. \nChronic gastritis is classified into two: \n\u2022 Type A gastritis  (chronic fundal gastritis)   \n\u03bf The inflammation is limited to gastric fundus and body with antral sparing.  \n\u03bf Associated with pernicious anemia, with circulating autoantibodies to \nparietal cells, which is why it is also known as autoimmune gastritis. \n\u2022 Type B- gastritis (chronic antral gastritis)   \n\u03bf It is more common than type gastritis.  \n\u03bf It commonly involves the antrum and mostly associated with H. pylori  \ninfection. However, the inflammation may progress to involve the gastric fundus and body causing pangastritis usually after 15 - 20 \nyears.   \n\u03bf Histology improves with eradication of H. pylori.  \n \nTreatment of chronic gastritis : is aimed at controlling the sequellae, not the \ninflammatory process."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 358, "chroma:document": "years.   \n\u03bf Histology improves with eradication of H. pylori.  \n \nTreatment of chronic gastritis : is aimed at controlling the sequellae, not the \ninflammatory process.  \n\u2022 Lifelong parenteral Vitamin-B 12 is recommended for patients with pernicious \nanemia.  \n\u2022 There is no need to treat H. pylori , unless there is ulcer or MALT Lymphoma."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d391-7265-11ef-b878-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 359, "chroma:document": "Internal Medicine \n \n 3442.2 Peptic ulcer diseases \n \nDefinition:  An ulcer is a break in the mucosal surface, bigger than 5mm in size with depth to \nsub- mucosa.  \n\u2022 Peptic ulcer is caused by discrete tissue destruction caused by acid and pepsin.  \n\u2022 Ulcers occur most commonly in the stomach (GU) and proximal duodenum (DU), \nand less commonly in the esophagus, and rarely on the other portions of small \nintestine. \nIncidence:   \n\u2022 Duodenal ulcers occur more frequently than gastric ulcers. This is probably due to \nthe likelihood of gastric ulcers being silent and presenting only after complications. \nAutopsy studies suggest similar incidence of gastric ulcers and duodenal ulcers.  \n\u2022 Peptic ulcer disease occurs more commonly in males than females. \n\u2022 Gastric ulcers occur later in life than duodenal ulcers (peak is in the sixth decade).  \n\u2022 About 90 -100% of duodenal ulcers and 75 - 85% of gastric ulcers are associated \nwith H. pylori  infection.  \n\u2022 About 15 - 20% of patients have both gastric and duodenal ulcers.  \n\u2022 Patients with gastric ulcers have a 33% chance of developing subsequent duodenal \nulcers. \nThe most important risk factors are: \n1. Helicobacter pylori infection: \n\u2022 H. pylori  is a gram negative microaerophilic rod bacteria found attached to gastric \nepithelium, without invading the gastric epithelium.  \n\u2022 The bacterium produces lots of factors, which enable its existence in the acidic \nenvironment that include:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d392-7265-11ef-84d6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 359, "chroma:document": "epithelium, without invading the gastric epithelium.  \n\u2022 The bacterium produces lots of factors, which enable its existence in the acidic \nenvironment that include: \n\u03bf Urease: which splits urea to CO 2 and ammonia, and  alkalinize the acidic \nenvironment  \n\u03bf Catalase, adhesins, lipase, platelet activating factor, etc. \n\u2022 The prevalence of H. pylori  infection varies throughout the world and depends to a \ngreat extent on the overall standard of living. \n\u2022 In developing countries 80% of the population may be infected by age 20. \n\u2022 Transmission of H. pylori  occurs from person to person following an oral-oral or \nfecal-oral route."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d393-7265-11ef-ac41-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 360, "chroma:document": "Internal Medicine \n \n 345Pathophysiology:  \n\u2022    H. pylori  infection is virtually associated with chronic active gastritis, but only 10 - \n15% of the infected individuals develop frank peptic ulcerations. The basis for this \ndifference is unknown. The end results are dependent upon the interplay between bacterial and host factors.  \n\u2022  H. pylori  infection is present in 90 - 100% of duodenal ulcers and 75 - 85% of \ngastric ulcers. \n\u2022   The end results of H. pylori  infection are:- \n\u03bf Gastritis   \n\u03bf Mucosa associated lymphoid tissue  Lymphoma  (MALT lymphoma)  \n\u03bf peptic ulcer diseases    \n\u03bf Gastric cancer  \n\u03bf  \n2. Non-steroidal anti inflammatory drugs  \n\u2022 These are among the commonly used over-the-counter and prescription drugs. \n\u2022 The spectrum of morbidity ranges from nausea and dyspepsia (50 - 60%) to serious \ngastrointestinal complications, such as frank peptic ulceration complicated by perforations or bleeding in as many as 3 - 4% of users per year.  \n\u2022 These drugs inhibit prostaglandin synthesis, which maintains gastro- duodenal \nmucosal integrity and repair.  \n\u2022 Gastric ulcers occur at somewhat higher frequency than duodenal ulcers. \n3.  Miscellaneous factors  \n\u2022 Cigarette smoking  - Higher incidence of peptic ulcer disease and complications in \nsmokers, with delayed ulcer healing.  \n\u2022 Generic factors , personality, and diet  may be associated with PUD; however the \nmechanisms are not yet established."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d394-7265-11ef-ae72-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 360, "chroma:document": "smokers, with delayed ulcer healing.  \n\u2022 Generic factors , personality, and diet  may be associated with PUD; however the \nmechanisms are not yet established.                 \n\u2022 Corticosteroids alone do not predispose to ulcers; but they increase the risk of \nulcer development if given with NSAIDS.  \n \nPathophysiology of Ulcer Diseases \nPeptic ulcers develop as a result of an imbalance between protective mucosal defensive \nfactors and aggressive factors  \n\u2022 Defensive factors include"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d395-7265-11ef-bec5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 361, "chroma:document": "Internal Medicine \n \n 346\u03bf Prostaglandins,  \n\u03bf Mucus  \n\u03bf Bicarbonates  \n\u03bf Mucosal blood flow  \n\u2022 Aggressive factors  \n\u03bf Pepsin \n\u03bf Hydrochloric acid. \nWhereas acid-peptic injury is necessary for ulcer to develop, acid secretion is normal in \nalmost all patients with gastric ulcers and increased in approximately a third of patients with duodenal ulcers. \n \nClinical presentations  \n\u2022 Manifestations are dependent on ulcer location and patient age.  \n\u2022 Course is usually chronic and recurrent.  \n\u2022 Pain is the most common symptom, and described as burning, gnawing or felt as \nhunger, often localized to epigastrium and relieved by food or antacids \nGastric ulcer   \n\u2022 Symptoms often do not follow a consistent pattern, especially when ulcer is located in \npyloric channel, where symptoms of obstruction may predominate (bloating, nausea, vomiting due to edema and scarring). \nDuodenal ulcer  \n\u2022 Pain tends to be consistent, usually absent when patient wakes up but appears in \nmidmorning, and relieved by food but recurs again 2 - 3 hours after a meal.  \n\u2022 Pain may be severe enough to awaken patient at night."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d396-7265-11ef-9afe-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 362, "chroma:document": "Internal Medicine \n \n 347Table V-2-1. Some differences in the clinical manifestations between DU and GU \n \n  Duodenal ulcer  Gastric ulcer  \nAge Uncommon before age \n15 yrs  \n May develop in children as young as 5 \nyrs, but peak incidence is later than DU.\n \nRelation of pain to food/antacids\n Pain is relieved by food or antacids  \n Pain aggravated by ingestion of food\n \nRelation of pain to food timing\n The pain characteristically comes 90 minutes to 3 \nhr after ingestion of \nfood (hunger pain)\n The pain comes within 30 minutes of ingestion of food \n \n \nNausea and vomiting\n Not  common  \n Common  \n \nWeight loss  Uncommon  Common because of \nfear to eat  \nPerforation  more common  Less common  \nBleeding  Less common  more common  \nChange in the character of pain may herald development of complications:  \n\u2022 Duodenal ulcer pain that becomes const ant, is no longer relieved by food or \nantacids, or radiates to the back or to either upper quadrant, may signal penetration of \nthe ulcer to the pancreas. \n\u2022 Duodenal ulcer pain accentuated rather than relieved by food, and/or \naccompanied by vomiting often indicates gastric outlet obstruction (G.O.O). \n\u2022 Abrupt, severe or generalized abdominal pain is characteristic of free ulcer \nperforation into the peritoneal cavity. \nPhysical finding  \n\u2022 Epigastric tenderness is most frequent finding.  \n\u2022 Signs of peritonitis may be found in ulcer perforation. \n\u2022 Succussion splash is often detected in gastric outlet obstruction."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d397-7265-11ef-b61b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 363, "chroma:document": "Internal Medicine \n \n 348Complications of PUD: All patients with the following complications need special care at \nreferral hospitals \n\u2022 Haemorrhage   \no Is the most common complication of PUD, and patients present with \nhematemesis, passage of tarry stools, w eakness, hypotension, syncope, thirst \nand sweating resulting from associated blood loss.  \no Immediate treatment can be given via endoscopy (electrocautery, \ninjection of alcohol/sclerosant etc.) or surgery. \n\u2022 Penetration (confined perforation)  \n\u03bf Is entering of adjacent confined space (e.g. lesser sac) or organ (e.g. \npancreas, liver).  \n\u03bf Adhesions prevent leakage into peritoneal cavity.  \n\u03bf Radiographic evaluation with contrast study is usually needed to confirm the \ndiagnosis.  \n\u03bf When medical therapy does not produce healing, surgery is recommended. \n\u2022 Free perforation   \n\u03bf Usually presents as acute abdomen with sudden, intense, steady epigastric pain. \n\u03bf Diagnosis is confirmed with upright or lateral decubitus x-ray of abdomen.  \n \n\u2022 Gastric outlet obstruction (GOO)  \n\u03bf May be caused by scarring, spasm, or inflammation.  \n\u03bf Symptoms include recurrent large volume vomiting, persistent bloating, fullness \nafter eating, loss of appetite; weight loss, dehydration and alkalosis due to \nprolonged vomiting.  \n\u03bf Succussion splash for over 6 hrs after a meal, gastric aspiration or x - rays may \nhelp in the diagnosis.  \n\u03bf Treat such patients with nasogastric tube aspiration and acid suppression if"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d398-7265-11ef-8632-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 363, "chroma:document": "prolonged vomiting.  \n\u03bf Succussion splash for over 6 hrs after a meal, gastric aspiration or x - rays may \nhelp in the diagnosis.  \n\u03bf Treat such patients with nasogastric tube aspiration and acid suppression if \ncauses are temporary. But if the pyloric canal scarred, do endoscopic pyloric balloon dilatation or surgical relief of obstruction. \n\u2022 Stomach cancer  \n\u03bf Is intestinal type adenocarcinoma of  gastric body and antrum and commonly \nassociated with H. pylori infection."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d399-7265-11ef-be1a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 364, "chroma:document": "Internal Medicine \n \n 349\u03bf Moreover, the incidence of MALT lymphoma (MALT=mucosa-associated \nlymphatic tissue) is increased in PUD.  \n\u03bf Treating H. pylori  might cure lymphoma, but chemotherapy or radical surgery \nmust be used when such treatment fails to cure the tumour. \n\u03bf For adenocarcinoma, surgery is always treatment of choice  \n \nDiagnosis of PUD 1)  Barium examination of the upper gastrointestinal tract : sensitivity of this \ninvestigation to detect ulcers ranges from 70 \u2013 90% \n2) Endoscopy : is most sensitive and specific method for the diagnosis of PUD. \n Advantages  \na) Direct visualization and photographic documentation of the ulcer is possible.  b) Permits mucosal biopsy for detection of H. pylori infection.  c) Provides baseline reference for the assessment of ulcer healing. \n3) Tests for H. pylori  There are two categories of tests for the diagnosis of this bacterium: \ni) Invasive tests (endoscopy required) \n\u2022 Rapid urease test \n\u2022 Histology \n\u2022 Culture \nii) Non invasive tests \n\u2022 Urea breath test - simple, rapid; useful for early follow up, false negative with \nrecent therapy. \n\u2022 Serology \u2013 inexpensive, convenient, not useful for early follow-up \nTreatment  \nObjectives of treatment:  \n\u2022 Relief of symptoms (pain, dyspepsia) \n\u2022 Eradication of H. pylori  to prevent recurrence  \n\u2022 Promote ulcer healing \nMedical treatment \nI. Treatment of H. pylori (see table VII-2-2)  \nIndications: the following diseases with documented H. pylori infection"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d39a-7265-11ef-931e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 364, "chroma:document": "\u2022 Eradication of H. pylori  to prevent recurrence  \n\u2022 Promote ulcer healing \nMedical treatment \nI. Treatment of H. pylori (see table VII-2-2)  \nIndications: the following diseases with documented H. pylori infection \n\u03bf PUD                           \n\u03bf MALT lymphoma"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d39b-7265-11ef-acf6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 365, "chroma:document": "Internal Medicine \n \n 350\u2022 No single agent is effective for eradication of H. pylori ; hence a combination of \nmultiple drugs is essential. Proton pump inhibitors (omeprazole) are added to \nantibiotics or H 2 blockers (e.g.  Ranitidine) can be used alternatively.  \n Table V-2-2 Regimens recommended for eradication of H. pylori infection \nTriple therapy\n Dose   Duration  \nBismuth subsalicylate plus\n 2 tabs QID  2 weeks  \nMetronidazole plus  250 mg QID   \nTetracycline  500 mg QID   \n   \nOmeperazole plus  20 mg, BID  2 weeks  \nChlarithromycin plus \n  250 or 500mg BID   \nMetronidazole or \namoxicillin  500 mg BID/1 gm BID   \n   \nQuadruple therapy    \nOmeperazole +  20 mg, BID  2 weeks  \nBismuth subsalicylate\n + 2 tabs QID   \nMetronidazole +  250 mg QID   \nTetracycline  500 mg QID   \n \nII.  Acid Neutralizing/Inhibitory Drugs  \nA) Antacids  \n\u2022 Are the most frequently used drugs before the advent of antihistamines (H 2 - \nblockers). They are now rarely, if ever, used as the primary therapeutic agent, \nhowever are often used by patients for symptomatic relief of dyspepsia.  \n\u2022 A combination of magnesium hydroxi de and aluminum hydroxide (marketed as \nMaalox or other brands) are widely used at a dose of 15 -30 ml at 1 hour and 3 hours after each meal and at bedtime."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d39c-7265-11ef-bb49-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 366, "chroma:document": "Internal Medicine \n \n 351B) H  2 receptor antagonists   \n\u2022 Include cimetidine, famotidine, ranitidine and nizatidine.  \n\u2022 Cimetidine is the most commonly used drug. The dose is 800 mg at bedtime or \n400mg twice a day for 4 - 6 weeks.  \n\u2022 Ranitidine is used at a dose of 150 mg or ally twice a day or 300mg at bedtime for \n4 \u2013 6 wks. \nC) Proton pump inhibitors   \n\u2022 They inhibit the H+-pump, which is important for   synthesis of hydrochloric acid. \n\u2022 Omeperazole: 20mg orally daily for 4 - 8 weeks. \n\u2022 When these drugs are used for anti- H. pylori  treatment, it has direct antimicrobial \neffect on the organism. \nD) Dietary advice  \n\u2022 There is no specific diet recommended for patients with peptic ulcer disease.  \n\u2022 Patients are generally advised to avoid smoking, coffee, and foods that cause or \naggravate their symptoms. \nSurgical treatment  is indicated for:  \n\u2022 Perforation:  immediate surgery is recommended for acute perforation. If this is not \npossible, admit the patient to ICU and put on continuous nasogastric suction and \nbroad-spectrum antibiotics. \n\u2022 Obstruction not responding to medical therapy \n\u2022 Uncontrolled/recurrent bleeding \n\u2022 Suspected malignancy \n\u2022 Symptoms refractory to medical management  \nN.B.  For the types of surgical procedures and their complications, please refer Surgical \ntextbooks.  \nDyspepsia   \n\u2022 Is the classic symptom of PUD and is defined as pain centered in the upper \nabdomen or discomfort characterized by fullness, bloating, distension or nausea."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d39d-7265-11ef-a4a9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 366, "chroma:document": "textbooks.  \nDyspepsia   \n\u2022 Is the classic symptom of PUD and is defined as pain centered in the upper \nabdomen or discomfort characterized by fullness, bloating, distension or nausea.  \n\u2022 It\u2019s a common clinical problem and may be seen in 25 - 40% of adults.  \n\u2022 Only 15 - 25% patients with dyspepsia are found to have either gastric or duodenal \nulcers. \n\u2022 Other causes include: \n\u03bf Gastroesophageal reflux disease"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d39e-7265-11ef-899f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 367, "chroma:document": "Internal Medicine \n \n 352\u03bf Gastric cancer \n\u03bf Gastroparesis \n\u03bf Gastritis \n\u2022 In up to 60% of dyspeptic patients no cause is identified ( Functional or non ulcer \ndyspepsia ) - a condition most likely related to an abnormal perception of events \nin the stomach caused by afferent visceral hypersensitivity. \nNon gastritis mucosal Injury  \n1. NSAIDS  \n\u2022 Acute ingestion: increases mucosal permeability and back diffusion    of H+ leading \nto hyperemia, sub epithelial hemorrhage and superficial erosions. \n\u2022 Chronic ingestion: inhibition of gastro duodenal mucosal prostaglandin synthesis \nleading to decreased mucus and bicarbonate production and mucosal blood flow \nfinally resulting in frank ulceration may occur. \n2. Stress Related mucosal Damage \n\u2022 Mucosal ischemia caused by decreased blood flow (from shock, Catecholamine \nrelease) impairs mucosal resistance to acid back diffusion. Hyperemia of the \nmucosa evolves & erosions and then frank ulceration in the stomach and duodenum \nthat go on to bleeding. \nClinical features  \n\u2022 May be absent  \n\u2022 Epigastric pain  \n\u2022 Hemorrhage (hematemesis, melena)  \nDiagnosis  \u2013 History of drug ingestion  \n\u2022 Endoscopy  \nTreatment:   \n\u2022 Removal of offending agent.  \n\u2022 Antacids, H2-blokcer and surface acting agents (Sucralfate) are helpful. \n\u2022 In patients with hemorrhage \u2013 Volume replacement and endoscopic control of the \nbleeding."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d39f-7265-11ef-b778-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 368, "chroma:document": "Internal Medicine \n \n 353References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Peptic \nulcer diseases and related disorders, pages 1746-1762. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Peptic ulcer diseases, pages 210-215."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d3a0-7265-11ef-8e03-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 369, "chroma:document": "Internal Medicine \n \n 3543. Malabsorption syndromes  \n \nLearning Objectives: at the end of this chapter the student will be able to \n1. Define malabsorption syndromes \n2. List the etiologies of malabsorption syndromes 3. Explain the mechanisms of malabsorption syndromes \n4. Describe the clinical features of malabsorption syndromes    \n5. List the common nutritional complications malabsorption syndromes. 6. Make a diagnosis of malabsorption syndrome   7. Refer the patient to hospitals for better diagnosis and treatment \n \nDefinition:  Syndromes resulting from impaired absorption of one or more dietary nutrients \nfrom the small bowel.  \n\u2022 Many diseases or their consequences can cause malabsorption.  \n\u2022 The mechanism may be direct impairment of absorption or abnormalities of digestion \nthat finally leads to impaired absorption.  \n\u2022 Malabsorption may occur for specific nutrients such as carbohydrates, fats, or \nmicronutrients or may affect many nutrients at the same time. \nEtiologies  \n1) Maldigestion: refers to a defect either in the intraluminla hydrolysis of triglycerides, or in \nmicelle formation , which results from the following conditions  \na) Pancreatic insufficiency  due to chronic pancreatitis  , pancreatic carcinoma  \nb) Deficiency of conjugated bile salts  due to cholestatic or obstructive liver diseases  \nc) Bile salt deconjugation due to bacterial overgrowth in blind loop ( after Billroth-II \ngastrectomy ) or jejuna diverticulitis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d3a1-7265-11ef-ad3b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 369, "chroma:document": "b) Deficiency of conjugated bile salts  due to cholestatic or obstructive liver diseases  \nc) Bile salt deconjugation due to bacterial overgrowth in blind loop ( after Billroth-II \ngastrectomy ) or jejuna diverticulitis  \nd) Inadequate mixing of gastric contents  with bile salts and pancreatic enzymes as \na result of previous  gastric surgery \n2) Intrinsic bowl diseases  ( damage to the absorptive surface of the intestine ) \na) Celiac disease  causing flattening of the intestinal villa and inflammatory cell \ninfiltration. \nb) Whipple\u2019s diseases:  is a systemic disease that may cause intestinal mucosal \ndamage and lymphatic obstruction."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d3a2-7265-11ef-81ab-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 370, "chroma:document": "Internal Medicine \n \n 355c) Collagenous sprue : deposition of collagen substance in the lamina propia of the \nintestine  \nd) Non granulomatous ulcerative ileojejunitis a rare condition of unknown etiology \ncharacterized by fever, weight loss and features of absorption. \ne) Eosinophilic gastroenteritis:  characterized by peripheral eosipnophilia, and \ninfiltration of the wall of the stomach, small intestine or colon by eosinophils. Many \npatients present with specific food allergy.  \nf) Amylodosis :  amyloid infiltration of the submucosa of the small intestine  \ng) Crohn\u2019s diseases :  an inflammatory bowel diseases which may cause mucosal \ndamage  \n3) Inadequate absorptive surface:  from extensive small bowel resection. Resection of 50 \n% of small intestine is well tolerated, if the remaining bowel is normal.  \n4) Lymphatic obstruction  \na) Intestinal lymphangiectasia  \nb) Intestinal lymphoma \n5) Multiple defects  \na) After gastrectomy : which may result in poor mixing of gastric contents with \npancreatic enzymes and stasis in the afferent loops with bacterial overgrowth ( as in Billroth II gastrectomy) can cause malabsorption. \nb) Radiation enteritis : interferes with the blood supply of the intestine. Bacterial \novergrowth may occur secondary to radiation stricture , lymphatic obstruction may \noccur due to edema or fibrosis  \nc) Diabetes mellitus : alter gut motility from diabetic neuropathy, bacterial overgrowth"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d3a3-7265-11ef-9bff-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 370, "chroma:document": "overgrowth may occur secondary to radiation stricture , lymphatic obstruction may \noccur due to edema or fibrosis  \nc) Diabetes mellitus : alter gut motility from diabetic neuropathy, bacterial overgrowth \nand exocrine pancreatic insufficiency may lead to malabsorption. \n6) Other causes \na) Infections :  viral , bacterial or parasitic in fections may cause malabsorption  \ni) In HIV infected patients  malabsorption may be caused by Cryptosporidiosis , \nIsosporiosis or intestinal mucosal atrophy due to HIV virus itself (HIV  \nenteropathy ) \nii) Tropical sprue:  endemic malabsorption disorder occurring in the tropics. It is \nbelieved to have an infectious cause. \niii) Parasitic cause of malabsorption : include Hookworm, tapeworm and \nstrolgyloidiasis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d3a4-7265-11ef-8f4e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 371, "chroma:document": "Internal Medicine \n \n 356b) Hypoparathyroidism \nc) Drugs:  neomycin, kanamycine may cause malabsorption.  Phenytoin causes a \nselective folic acid malabsorption      \n \nClinical features  \nSigns and symptoms \n\u2022 Symptoms of malabsorption are caused either by the effects of osmotically active \nsubstances within the gastrointestinal tract or the resulting nutritional deficiencies.  \n\u2022 Patients may present with some or all of the following clinical manifestations. \nGeneral symptoms:   \n\u2022 Steatorrhea: passage of abnormal stools, which are greasy soft , bulky , and foul \nsmelling  and may float in the toilet because of their increased gas content : a film of \ngreasy or oil droplets may be seen on the surface of the water . This is often associated with abdominal distension, bloating, or discomfort and flatulence resulting \nfrom increased intestinal bulk and gas production \n\u2022 Weight loss:  which may be severe and involve marked muscle wasting. \n Secondary nutritional deficiencies:   \n\u2022 Deficiency of iron, folic acid, or B12  leading to anaemia \n\u2022 Calcium deficiency (common) partly due to  lack of vitamin D causing rickets, \nosteomalacia ,  paresthesia , tetany and carpopedal spasms. \n\u2022 Thiamine (vitamin B\n1) and B 12 deficiency may cause neuropathy, \n\u2022 Malabsorption of vitamin K (mainly fat-soluble) can lead to hypoprothrombinemia \nwith bruising and a bleeding tendency.  \n\u2022 Severe riboflavin (vitamin B 2) deficiency may cause a sore tongue and angular \nstomatitis,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3d3a5-7265-11ef-a4f1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 371, "chroma:document": "\u2022 Malabsorption of vitamin K (mainly fat-soluble) can lead to hypoprothrombinemia \nwith bruising and a bleeding tendency.  \n\u2022 Severe riboflavin (vitamin B 2) deficiency may cause a sore tongue and angular \nstomatitis,  \n\u2022 Vitamin A, C, and niacin deficiencies seldom cause clinical problems. \n\u2022 Protein malabsorption may lead to hypoproteinemic edema, usually of the lower \nlimbs.  \n\u2022 Dehydration, potassium loss, and muscle weakness can follow profuse diarrhoea.  \n\u2022 Secondary endocrine deficiencies may result from malnutrition."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa4c-7265-11ef-837b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 372, "chroma:document": "Internal Medicine \n \n 357Some causes of malabsorption may have distinct clinical features:  \n\u2022 Lactase deficiency  manifests with  explosive diarrhoea, abdominal bloating and gas \nafter milk ingestion \n\u2022 Pancreatic lipase deficiency: greasy stools with undigested dietary fat (triglycerides) \n\u2022 Dermatitis herpetiformis is often associated with a mild degree of celiac-like \nenteropathy \n\u2022 Biliary cirrhosis and pancreatic cancer may cause jaundice \n\u2022 Mesenteric ischemia may cause abdominal angina \n\u2022 Chronic pancreatitis may cause boring central abdominal pain \n\u2022 Patients with Zollinger-Ellison syndrome frequently manifest with severe  persistent \nulcerative dyspepsia.  \nDiagnostic workup \n\u2022 Symptoms and signs may point to the diagnostic impression of malabsorption.  \n\u2022 Any combination of weight loss, diarrhoea, and anaemia should raise the suspicion of \nmalabsorption.  \n\u2022 However, laboratory studies are essential to confirm the diagnosis \nCommon laboratory tests: \n1) Direct measurement of faecal fat:  3 - 4 days stool collection is required for this \nmeasurement. Faecal fat over 6 g/day is abnormal.   \n2) Stool inspection, microscopic examination: look for undigested food fragments, \nand do direct microscopy for ova and parasites, and Sudan III staining for the \npresence of grease/fat in the stool. \n3) Absorption tests help to define the site of the lesion; D-xylose absorption test is specific for proximal small-bowel (jejunal) absorption. Five grams of D-"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa4d-7265-11ef-a4ae-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 372, "chroma:document": "presence of grease/fat in the stool. \n3) Absorption tests help to define the site of the lesion; D-xylose absorption test is specific for proximal small-bowel (jejunal) absorption. Five grams of D-\nXylose is given orally to the fasting pat ient, and urine is collected for the next 5 \nhours. Smaller than 1.2 grams of D-xylose in the 5-hours urine collection is considered abnormal. \n4) Iron malabsorption: low serum ferritin and serum iron levels with adequate diet \nand lack of blood loss indicates iron malabsorption. Diminished iron storage on bone marrow examination may also be found. \n5) Folic acid absorption:  is suggested by low serum or RBC folate level with \nadequate diet and little alcohol intake. \n6) Schilling test is used to diagnose Vit B-12 malabsorption."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa4e-7265-11ef-af18-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 373, "chroma:document": "Internal Medicine \n \n 3587) Abdominal X-rays:  upper GI series with small-bowel follow-through may be helpful. \nPlain abdominal x-ray may show pancreatic calcification as a sign of chronic \npancreatitis. \n8) Small-bowel biopsy  can be taken during endoscopy to show mucosal changes. \nTreatment   \n\u2022 Is individualised according to underlying disease.   \n\u2022 However, if the underlying cause is not treatable as in short bowel syndrome, \nadequate substitution of missing nutrients must be ensured and diet adjusted appropriately. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nDisorders of absorption , pages 1763-1775."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa4f-7265-11ef-8bca-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 374, "chroma:document": "Internal Medicine \n \n 3594. Pancreatic diseases \n \nLearning objectives: at the end of this unit the student will be able to \n1. Define acute and chronic pancreatitis \n2. List the etiologies of acute and chronic pancreatitis 3. Explain the mechanisms of acute and chronic pancreatitis  \n4. Describe the clinical features of acute and chronic pancreatitis \n5. List the common complications acute and chronic pancreatitis  6. Make a diagnosis of acute and chronic pancreatitis &  7. Refer patients to hospitals for better diagnosis and treatment \n \n4.1. Acute Pancreatitis \nEtiology:  \n1) Biliary tract disease especially stones \n2) Alcoholism \n3) Drugs (furosemide, valproic acid, azathioprine, sulfasalazine) 4) Infection (e.g. mumps) 5) Hypertriglyceridemia \n6) Structural abnormalities of pancreatic duct (stricture, cancer, pancreas divisum) \n7) Abnormalities of common bile duct and ampullary region 8) Surgery of stomach, biliary tract 9) Vascular disease 10) Trauma \n11) Hyperparathyroidism, hypercalcemia \n \nSigns and symptoms: \n\u2022 Fever \n\u2022 Severe abdominal pain radiating to the back; sudden in biliary pancreatitis, \ndeveloping over weeks in alcoholism. Pain is steady, boring, persistent, \nrelieved by leaning forward, and accentuated by coughing, movement and deep breathing. \n\u2022 Abdominal tenderness with muscular rigidity, and sometimes board like \nabdomen"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa50-7265-11ef-8722-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 375, "chroma:document": "Internal Medicine \n \n 360\u2022 Hypoactive bowel sounds \n\u2022 Nausea, vomiting \n\u2022 Tachycardia, tachypnia \n\u2022 Jaundice may be present \n\u2022 Lung examination may reveal lim ited diaphragmatic excursions and \nevidence of atelectasis \n \nComplications: \n\u2022 Early death may be due to cardiovascular instability or respiratory failure; later death due \nto pancreatic or pseudocyst infection. \n\u2022 Pancreatic infection of devitalized retroperitoneal tissue with sepsis \n\u2022 Pancreatic pseudocyst may be secondarily infected, bleed or rupture \nDiagnosis: \n\u2022 Increased serum amylase, lipase  \n\u2022 WBC : usually between 12,000 to 20,000/mm3 \n\u2022 Hematocrit  may be as high as 50-55 % due to third-space losses. \n\u2022 Hyperglycaemia  \n\u2022 Serum calcium  is decreased \n\u2022 Bilirubin  may be increased \n\u2022 X-rays of the abdomen (Supine and upright plain x-rays); Chest x-ray  \n\u2022 Ultrasound of the abdomen (if available CT)  \nDifferential diagnosis:   the following diseases can mimic acute pancreatitis  \n\u2666 Perforated gastric or duodenal ulcer \n\u2666 Mesenteric infarction \n\u2666 Strangulating intestinal obstruction \n\u2666 Ectopic pregnancy \n\u2666 Dissecting aneurysm \n\u2666 Biliary colic \n\u2666 Appendicitis \n\u2666 Diverticulitis \n\u2666 Inferior wall myocardial infarction \n\u2666 Haematoma of abdominal muscles or spleen."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa51-7265-11ef-aaf8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 376, "chroma:document": "Internal Medicine \n \n 361Prognosis \nRanson's 11 prognostic signs  help estimate the prognosis of acute pancreatitis.  \n\u2022 Five signs can be documented at admission:  \n\u03bf Age more than 55 yr \n\u03bf Serum glucose over 200 mg/dl (> 11.1 mmol/L),  \n\u03bf Serum LDH over 350 IU/L  \n\u03bf AST over 250 units/L and  \n\u03bf WBC count over 16,000/\u00b5L.  \n\u2022 The development of the following within 48 h after admission indicates worsening \nprognosis:  \n\u03bf Hct drop by more than 10% \n\u03bf BUN rise greater than 5 mg/dl (> 1.8 mmol Urea/L) \n\u03bf Serum Ca less than 8 mg/dl (< 2 mmol/L) \n\u03bf Arterial Po 2  less than 60 mm Hg \n\u03bf Base deficit over 4 meq/l \n\u03bf Estimated fluid sequestration more than 6 L \n\u2022 Mortality increases with the number of positive signs:  \n\u03bf If fewer than three signs are positive, the mortality rate is less than 5%;  \n\u03bf If three or four signs are positive, mortality is between 15 to 20%. \n\u03bf The presence of 7 \u2013 8 of these criteria is associated with 100% mortality.  \n\u2022 Acute pancreatitis associated with necrosis and haemorrhage has a mortality rate of \nabout 10 to 50%. This diagnosis is suggested by  \n\u03bf A progressive decrease in Hct,  \n\u03bf The presence of hemorrhagic fluid within ascites,  \n\u03bf The reduction of serum Ca++ level,  \n\u03bf The presence of Grey Turner's  and/or Cullen's sign  (indicating extravasations of \nhemorrhagic exudates to the flanks or umbilical region, respectively). \nTreatment \nMild oedematous pancreatitis:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa52-7265-11ef-bb21-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 376, "chroma:document": "\u03bf The reduction of serum Ca++ level,  \n\u03bf The presence of Grey Turner's  and/or Cullen's sign  (indicating extravasations of \nhemorrhagic exudates to the flanks or umbilical region, respectively). \nTreatment \nMild oedematous pancreatitis:   \n\u2022 Keep patient NPO (nothing per os) until manifestations of acute inflammation subside \n\u2022 Give sufficient intravenous fluids \n\u2022 Insert nasogastric tube."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa53-7265-11ef-99c6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 377, "chroma:document": "Internal Medicine \n \n 362Severe acute pancreatitis:   \n\u2022 Refer to hospitals for admission to intensive care unit \n\u2022 Vital signs and urine output are monitored at least every 1 hr \n\u2022 Accurate metabolic flow sheet which should be checked every 8 hrs. \n\u2022 Arterial blood gases are determined as necessary \n\u2022 Hct, glucose, electrolytes (Ca, Mg), CBC, platelet count, coagulation parameters, \ntotal protein with albumin, BUN, creatinine, amylase, and lipase studies performed \ndaily. \n\u2022 Keep patient NPO with NG tube insertion  \n\u2022 Give H 2 receptor blockers IV \n\u2022 Fluids may be given up to 6 - 8 L/d.  \n\u2022 Give oxygen as needed \n\u2022 Severe pain should be treated with Pethidine 50 to 100 mg IM every 4 to 6 hrs and \nas needed in patients with normal renal function (morphine causes the sphincter of \nOddi to contract and should be avoided).  \n\u2022 Treat hyperglycaemia if over 250 mg/dl.  \n\u2022 If symptoms of calcium depletion appear give calcium gluconate 10 - 20 ml IV in 1 \nliter of replacement fluid. \nSurgery  is indicated for  \n\u2022 Trauma \n\u2022 Uncontrolled biliary sepsis \n\u2022 Inability to distinguish acute pancreatitis from other causes of acute abdomen \n\u2022 To drain a pseudocyst that is expanding rapidly, secondarily infected, or associated \nwith bleeding or impending rupture. \n \n4.2. Chronic pancreatitis \nEtiology: \n\u2022 Alcoholism : 70 -80% of chronic pancreatitis is associated with alcoholism \n\u2022 Idiopathic \n\u2022 Hereditary \n\u2022 Microlithiasis \n\u2022 Hyperparathyroidism"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa54-7265-11ef-80ae-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 377, "chroma:document": "with bleeding or impending rupture. \n \n4.2. Chronic pancreatitis \nEtiology: \n\u2022 Alcoholism : 70 -80% of chronic pancreatitis is associated with alcoholism \n\u2022 Idiopathic \n\u2022 Hereditary \n\u2022 Microlithiasis \n\u2022 Hyperparathyroidism \n\u2022 Obstruction of the main pancreatic duct due to stenosis, stones, or cancer"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa55-7265-11ef-8312-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 378, "chroma:document": "Internal Medicine \n \n 363Signs and symptoms :  \n\u2022 Persistent or recurrent epigastric or left upper abdominal pain, nausea, vomiting, \nanorexia, constipation, flatulence and weight loss are common.  \n\u2022 In advanced disease, patients may develop steatorrhea, recurrent acute attacks of \npain which become more constant later and insulin secretion is diminished with \nimpaired glucose tolerance. \nDiagnosis:  \n\u2022 Laboratory tests are frequently normal, but inflammation markers may be \nminimally elevated. \n\u2022 Plain abdominal x-ray may demonstrate  pancreatic calcification in 30% of cases \n\u2022 Abdominal ultrasound or CT to detect calcifications, dilated ducts and atrophic \ngland \n\u2022 ERCP is most sensitive test and may show dilated ducts, intraductal stones, \nstrictures or pseudocyst \n\u2022 Tests of pancreatic function:  assess endocrine and exocrine function, including \nglucose tolerance test (see chapter on diabetes mellitus). For exocrine function do ecretin test. \n\u2022 Stool tests:  faecal chymotrypsin \nTreatment  \n\u2022 Alcohol intake should be avoided.  \n\u2022 At times, IV fluids and fasting prove beneficial.  \n\u2022 Use of oral pancreatic enzymes (30.000 U of lipase) with each meal may improve \nsymptoms.  \n\u2022 If steatorrhea is particularly severe and refractory, medium chain triglycerides, \nwhich are absorbed without pancreatic enzymes, can be provided as an alternative source of fat.   \n\u2022 Supplementation with fat-soluble vitamins (A, D, K) is sometimes required."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa56-7265-11ef-9c75-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 378, "chroma:document": "which are absorbed without pancreatic enzymes, can be provided as an alternative source of fat.   \n\u2022 Supplementation with fat-soluble vitamins (A, D, K) is sometimes required.  \n\u2022 Relapse may require treatment similar to that of acute pancreatitis.  \n\u2022 A pancreatic pseudocyst, which causes chronic pain, needs referral to centres with \nsurgical facilities and expertise, where it can be decompressed into a nearby \nstructure to which it firmly adheres (e.g., the stomach) or into a defunctionalized loop of jejunum."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa57-7265-11ef-920c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 379, "chroma:document": "Internal Medicine \n \n 364\u2022 Diabetes mellitus rarely occurs in chronic pancreatitis. For most patients, serum \nglucose level of 200 to 250 mg is acceptable and doesn\u2019t require treatment. It is \nbetter to maintain the patient in a slightly hyperglycaemic range than run a risk hypoglycaemia caused by overzeal ous administration of insulin. \n\u2022 Patients with chronic pancreatitis are at increased risk for pancreatic cancer. \nWorsening of symptoms, especially with devel opment of a pancreatic duct stricture, \nshould prompt an examination for malignancy.  \n  \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Acute \nand chronic pancreatitis, 1895-1906. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Diseases of the pancreas, pages 240-244."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa58-7265-11ef-9eb9-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 380, "chroma:document": "Internal Medicine \n \n 3655. Hepatitis \n \nLearning objectives: at the end of this unit the student will be able to \n1. Define acute and chronic hepatitis \n2. List the etiologies of acute and chronic hepatitis  3. Explain the routes of transmission of the different hepatitis viruses \n4. Describe the clinical features of acute and chronic hepatitis  \n5. List the common complications acute and chronic hepatitis 6. Identify the antigens and antibodies used for the diagnosis of viral hepatitis 7. Make a diagnosis of acute and chronic hepatitis &  8. Refer patients to hospitals for better diagnosis and treatment \n \n\u2022 Hepatitis is a broad category of clinico-pathologic conditions resulting from viral, toxic, \npharmacologic or immune mediated damage to the liver.  \n\u2022 Hepatocellular necrosis and inflammatory cell infiltration of the liver are common \npathologic features.  \n\u2022 There are two types of hepatitis, which are defined based on duration: \nI. Acute hepatitis:  lasts for about 6 months or less. \nII. Chronic hepatitis:  sustained inflammatory response for over 6 months. \n \n    5.1 Acute hepatitis  \nEtiologies:   \n1) Viruses are the commonest causes, and include hepatitis A, B, C, D, E, G, viruses and \nother viruses such as EBV, CMV etc. \n2) Toxins (amanita phylloides in mushroom poisoning; carbon tetrachloride). \n3) Drugs:  acetaminophen, INH, halothane, chlorpromazine, erythromycin, heavy alcohol \nintake \n4) Others  \na. Wilson\u2019s disease \nb. Herbs"}


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": 381, "chroma:document": "Internal Medicine \n \n 3665.1.1 Acute viral Hepatitis  \n\u2022 Is the most common form of acute hepatitis; Caused by hepatitis viruses (designated as \nHV) HAV, HBV, HCV, HDV, HEV, HGV (Non A. Non B virus), all of which are RNA \nviruses except HBV, which is a DNA virus. \n\u2022 HDV is an incomplete RNA virus and requires the presence of HBV to cause infection. \nThus, it causes hepatitis when HDV infection occurs at the same time  as HBV infection (HDV co-infection) or in patients with chronic hepatitis B infection (super infection). \n\u2022 The complete HBV (Dane particle) consists of several antigenetically distinct \ncomponents, including a surface coat (hepatitis B surface antigen [HBsAg]) and a core of circular DNA, DNA polymerase, hepatitis B core antigen (HBc Ag), and hepatitis B \nenvelope antigen (HBe Ag).  \n \n  \n  \n \n    \n \nTransmission  \n\u2022 In HAV and HEV transmission is feacooral. Both viruses are implicated in most \ninstances of water borne and food transmitted infection, and in epidemics of viral \nhepatitis. \n\u2022 HBV is mainly transmitted by parentera l (via blood and blood products, contaminated \nneedles), sexual contacts and perinatal route. The virus is found in all body fluids and excreta.  \n\u2022  Like HBV, HCV is largely transmitted parenterally. It is the main cause of post \ntransfusion hepatitis, especially before the discovery of anti HCV antibodies. The virus is transmitted less frequently through the sexual and perinatal routes.  \n \nClinical and laboratory manifestations"}


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": 381, "chroma:document": "transfusion hepatitis, especially before the discovery of anti HCV antibodies. The virus is transmitted less frequently through the sexual and perinatal routes.  \n \nClinical and laboratory manifestations  \n\u2022 The prodromal phase  lasts for several days and characterized by malaise, fatigue, \nanorexia, nausea, vomiting, myalgia and headache.  Patients will have aversion to smell \nof food and cigarette with mild fever and flue like symptoms.  Surface antigen (HBsAg) \nCore antigen (HBc Ag) \nDNA polymerase  HBV DNA"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa5b-7265-11ef-b28d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 382, "chroma:document": "Internal Medicine \n \n 367\u2022 Arthritis and urticaria may be present particularly in HBV which are attributed to \nimmune complex deposition.  \n\u2022 Jaundice appears late , usually when the patients start to improve in their sense of  \nwell being. It may be absent (Nonicteric hepatitis) in some patients.  \n\u2022 Dark urine and pale stool is common in cholestasis  \n\u2022 The liver is usually tender and enlarged, and splenomegaly occurs in 20% of the \ncases.  \nLaboratory   \n1) Liver enzymes:  Damage to hepatocytes causes release of intracellular enzymes like \nalanine transaminase (ALT), and aspartate transaminase (AST). Normal levels range \nbetween 0 and 35 U/L.  In acute hepatitis, they often rise to 20 fold or more.   \n2) Serum bilirubin:  normal levels range between 0.3 and 1 mg/dl. when  levels go above \n2.5 -3.0 mg/dl jaundice appears (called icteric hepatitis)    \n3) Alkaline phosphatase  may be increased by about 3 fold except in cholestatic hepatitis, \nin which the increment is very much higher.  \n4) CBC: leucopenia with atypical lymphocytes (relative lymphocytosis) is common. \n5) Serodiagnosis: serodiagnosis involves antigen/antibody detection.  \n\u2022 It allows the identification of etiologic agents  \n\u2022 It helps in planning of preventive and other public health measures for close \ncontacts of infected people  \n\u2022 It helps in evaluating the prognosis.  \na) Diagnosis of HAV  can be made by detection of anti HAV antibody, which is IgM"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa5c-7265-11ef-91e2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 382, "chroma:document": "\u2022 It helps in planning of preventive and other public health measures for close \ncontacts of infected people  \n\u2022 It helps in evaluating the prognosis.  \na) Diagnosis of HAV  can be made by detection of anti HAV antibody, which is IgM \ninitially and IgG later on. The IgG antibody confers lifelong immunity.  \nb) Diagnosis of HBV infection  The following antigens and antibodies can be \ndetected to HBV infection  and help in diagnosis , monitor disease progress , \ninfectivity, and predict the prognosis: \ni)  Antigens  \n(1) HBsAg   : \n\u2022 Usually cleared within 3 months. It may persist in some patients for 6 \nmonths to one year without complications.   \n\u2022 Its clearance from the blood precedes the appearance of anti-HBs antibody \nwith a time gap in between (known as the window period), during which the \nonly evidence of HBV infection may be anti-HBc antibody."}


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": 383, "chroma:document": "Internal Medicine \n \n 368(2) HBeAg   indicates HBV replication and high chance of infectivity to others \nii) Antibodies  \n(1) Anti HBs antibody  \u2013 confers long term immunity  \n(2) Anti HBc   - IgM  indicates recent infection , IgG indicates remote infection  \n(3) Anti HBe : active infection \nN.B. Anti-HBc and Anti-HBe do not provide immunity.  \nc) HDV can be diagnosed by detection of anti HDV antibody.  \nd) HCV is diagnosed by detecting anti HCV antibody.  \n \nTable V -5-1. Comparisons of   some features of hepatitis A, B, and C  \nFeature  Hepatitis A  Hepatitis B  Hepatitis C\nIncubation  15 to 45 days \n(mean 30)  30 to 180 days (mean 60 to 90)\n 15 to 160 days (mean \n50)\n \nOnset  Acute  Often insidious  Insidious  \nAge preference\n Children, young adults\n Any age  Any age but \nmore \ncommon in \nadults  \nTransmission Route  \nFecal-oral  + + +  - Unknown  \nOther non-\npercutaneous \nroutes  \u00b1 + + + + \nPercutaneous  \u00b1 + + +  + + +  \nOther Characteristics  \nSeverity  Mild Often severe  Variable  \nPrognosis  Generally good  Worse with age, debility\n Moderate"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa5e-7265-11ef-a8fe-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 384, "chroma:document": "Internal Medicine \n \n 369Progression \nto chronicity  None  Occasional (5% to 10%)\n Frequent (65% -85%)\n \nProphylaxis  Immunoglobulin /hepatitis A vaccineStandard IG (not documented), HBIG, HB vaccine\n None  \nCarrier  None  0.1% to 30%  Exists but prevalence unknown\n \n \nComplications   \n1)  Cholestatic hepatitis  \u2013  \n\u2022 Occurs most commonly during HAV and HEV infection  \n\u2022 Self limited  \n\u2022 Pruritus is a common symptom  \n\u2022 Marked conjugated hyperbilirubinemia presenting with dark urine and pale stool  \n\u2022 Increased alkaline phosphatase  \n2) Fulminant hepatitis  : in about 1% of cases  \n\u2022 Is defined as the onset of encephalopathy occurring within 8wks in a patient with \nacute liver disease \n\u2022 Associated with massive hepatocellular necrosis  \n\u2022 Commonly follows  HAV, HBV (usually super infection of HBV infection by HDV), \nHCV and HEV (in pregnancy) \n3) Chronic hepatitis  \n\u2022 Occurs in HBV and HCV infection  \n\u2022 Manifest with persistently increased AST and ALT for over 6 months,  \n\u2022 Slowly resolving HBV infection  may persist for 6-12 m with eventual complete \nresolution  \n\u2022 Persistent HBV infection  (persistence of HBsAg) without evidence of liver \ndamage resulting in asymptomatic or \u201chealthy\u201d HBV carriers."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa5f-7265-11ef-9bff-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 385, "chroma:document": "Internal Medicine \n \n 370Management  \n\u2022 Mainly supportive  \n\u03bf Rest to limit fatigue  \n\u03bf Maintain hydration \n\u03bf Adequate dietary intake   \n\u2022 Vitamin supplementation has no proven value but vitamin K can be given if there is \nprolonged cholestasis. \n\u2022 Alcohol should be avoided until serum transaminases normalize  \n\u2022 Metochlopromide (plasil) \u2013 for nausea \n\u2022 Admission \n\u03bf  Patients with severe nausea and vomiting. \n\u03bf  Patients with deteriorating liver function, especially those with \nencephalopathy or prolonged prothrombin time. \n\u2022 In general HAV may be regarded as non-infectious after 2 - 3 wks. HBV is potentially \ninfectious to contacts throughout its course, although the risk is low once HBS \nantigen has cleared.   \n\u2022 Interferon treatment is effective for HCV infection \n \nPrevention  \nPrevention of HAV and HEV \n\u2022 General hygienic measures \u2013 Hand washing after toilet use; careful handing, \ndisposal and sterilization of excret a and contaminated clothing and utensils. \n\u2022 For close contacts of HAV infected people  \n\u03bf Immune serum globulin (IgG) as soon as possible but no later than 6 wks after \nexposure \n\u03bf Active immunization  \nPrevention of HBV infection \n\u2022 Meticulous disposal of contaminated needles and other blood contaminated utensils  \n\u2022 For close contacts of HBV infected patients, give HBIG within 7 days and \nsubsequently HBV vaccine ( \u223c HBsAg) \n\u2022 Dose   of HBV vaccine \n\u03bf 2.5\u03bcg for < 11 yr (when mother is HBsAg - Ve)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa60-7265-11ef-835a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 385, "chroma:document": "\u2022 For close contacts of HBV infected patients, give HBIG within 7 days and \nsubsequently HBV vaccine ( \u223c HBsAg) \n\u2022 Dose   of HBV vaccine \n\u03bf 2.5\u03bcg for < 11 yr (when mother is HBsAg - Ve) \no 5 \u03bcg for 11 \u2013 19 yr & children < 11 yr born to HBsAg positive mother"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa61-7265-11ef-85dd-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 386, "chroma:document": "Internal Medicine \n \n 371o 10\u03bcg for immunocompetent adult. \n \n5.1.2 Alcoholic Fatty liver and Hepatitis \nAlcohol abuse is the most common cause of liver disease in the western world. Three major \npathologic lesions resulting from alcohol abuse and appearing as stages/spectrum of the disease:  \n1. Fatty liver 2. Alcoholic hepatitis  3. Cirrhosis  \nThe first two are potentially reversible, but the last one is not.  \n1. Alcoholic fatty liver : is characterized by \n\u0083 Right upper quadrant pain  \n\u0083 Incidentally discovered tender hepatomegally \n\u0083 Jaundice is rare, transaminases are mildly elevated (< 5X normal). \n\u0083 Completely reversible on cessation of alcohol  \n2. Alcoholic Hepatitis : is severe and prognostically ominous lesion and \ncharacterized by the following pathologic triads:  \n\u2022 Mallory bodies (intracellular eosinophilic aggregates  of cytokeratins), \nusually seen near or around nuclei  \n\u2022 Infiltration by polymorphnuclear leukocytes  \n\u2022 A network of interlobular connective tissues surrounding hepatocytes and \ncentral veins (spider fibrosis) \nClinical manifestations of alcoholic hepatitis:  include \n\u2022 Weight loss, anorexia, nausea, vomiting and abdominal pain are common \npresenting symptoms. \n\u2022 Hepatomegally is found in 80% and splenomegaly is often present  \n\u2022 Fever \n\u2022 Jaundice, spider angioma, palmar erythema, gyneacomastia and loss of \nbody hair. \n\u2022 Ascites and encephalopathy may be present and indicate severe disease."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa62-7265-11ef-911c-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 386, "chroma:document": "\u2022 Hepatomegally is found in 80% and splenomegaly is often present  \n\u2022 Fever \n\u2022 Jaundice, spider angioma, palmar erythema, gyneacomastia and loss of \nbody hair. \n\u2022 Ascites and encephalopathy may be present and indicate severe disease.  \n\u2022 CBC strikingly elevated. Transaminases modestly increased (200 \u2013 400 \nIU/l)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa63-7265-11ef-83e2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 387, "chroma:document": "Internal Medicine \n \n 372\u2022 The ratio of ASAT to ALAT frequently exceeds one in contrast to viral \nhepatitis in which the ratio is approximately one.  \n\u2022 Prolonged prothrombin time, hypoalbum inemia and hyperglobulinemia may \nbe found. \nComplications and prognosis  \n\u2022 Alcoholic Hepatitis can reverse with cessation of alcohol, but more \ncommonly progresses to cirrhosis.               \n \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Acute \nhepatitis, pages 1822-1842. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Diseases of the liver, pages 249-264."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa64-7265-11ef-9ec5-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 388, "chroma:document": "Internal Medicine \n \n 3736. Chronic Liver Diseases \n \nLearning objectives: at the end of this unit the student will be able to \n1. Define chronic liver diseases \n2. List the etiologies of chronic liver diseases 3. Describe the clinical features of chronic liver diseases \n4. List the common complications of chronic liver diseases \n5. Make a presumptive diagnosis of chronic liver diseases 6. Refer patients to hospitals for better diagnosis and treatment \nChronic liver diseases include:  \nA. Chronic hepatitis \nB. Liver cirrhosis \nC. Hepatocellular carcinoma (Hepatoma) \n \nA. Chronic hepatitis   \nDefinition: Chronic hepatitis is d efined as a hepatic inflammatory process that fails to resolve \nafter 6 months.  \nEtiologies: \n1) Except HAV and HEV, all hepatitis viruses can cause chronic hepatitis 2) Other causes             \na) Drugs like methyldopa b) Autoimmune disorders  c) Idiopathic causes  \nPathological classification  \n1. Chronic persistent hepatitis  - inflammatory activity is confined to portal areas. \n2. Chronic lobular hepatitis   \n\u03bf Inflammatory activity and necrosis are scattered throughout the lobule.  \n\u03bf Limiting plates of periportal hepatocytes are intact and no periportal fibrosis. \n3. Chronic active hepatitis :  \n\u03bf Inflammatory activity in portal areas spills out into the lobule (periportal \nhepatitis, piecemeal necrosis) in association with necrosis and fibrosis.   \n\u03bf Thought to have a significant risk for progression to cirrhosis and hepatic \nfailure."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa65-7265-11ef-abbd-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 389, "chroma:document": "Internal Medicine \n \n 374Chronic viral hepatitis  \n\u2022 Complicates about 1% of acute hepatitis B (young, immunocompetent) and 85-90% \nof acute hepatitis C will develop chronic hepatitis. About 20% of the later will develop \ncirrhosis in 10-20yrs. \n\u2022 Subjects with either HBV or HCV infection have greater risk of developing \nhepatocellular carcinoma       \nTreatment  can suppress hepatic inflammatory activity in 30-40% \n\u2022  Hepatitis B - therapy is indicated for patients positive for HBsAg and HBcAg (High \nreplicative phase). Treat with interferon \u03b1 and Lamivudine.  \n\u2022  Hepatitis C can be treated with interferon \u03b1 and ribavirin \n              \nB.   Cirrhosis of the liver and its complications \n\u2022 It is the end result of fibrous scarring and hepatocellular regeneration, that constitute \nthe major responses of the liver, to a variety of long standing inflammatory, toxic, metabolic and congestive insults. \n\u2022 The normal hepatic lobular architecture is replaced by interconnecting bands of fibrous \ntissue surrounding nodules derived from foci of regenerating hepatocytes.   \n\u2022 The following pathologic changes are the cause of the clinical manifestations and  \ncomplications of cirrhosis \n1) Fibrous scarring and disruption of hepatic architecture distort vascular bed leading to                 \nPortal hypertension and intrahepatic shunting \n2) Disturbed hepatocellular function  \n Clinical and laboratory features resulting from Hepatocellular dysfunction  \n\u2022 Hypoalbuminemia"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa66-7265-11ef-819c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 389, "chroma:document": "Portal hypertension and intrahepatic shunting \n2) Disturbed hepatocellular function  \n Clinical and laboratory features resulting from Hepatocellular dysfunction  \n\u2022 Hypoalbuminemia  \n\u2022 Decreased coagulation factors resulting in prolonged prothrombin time \n\u2022 Hyperbilirubinemia \n\u2022 Increased  blood ammonia level  \n\u2022 Hepatic encephalopathy \n\u2022 Ascites \n Portal HTN  \n\u2022 Ascites."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa67-7265-11ef-8d55-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 390, "chroma:document": "Internal Medicine \n \n 375\u2022 Varices \n\u2022 Splenomegaly causing thrombocytopenia and leucopenia. \n\u2022 Hepatic encephalopathy \nMajor causes of Cirrhosis \n1) Alcohol and HCV are major causes in western world  \n2) HBV is the commonest cause in developing countries  3) Other causes include: \no Biliary obstruction (Intrahepatic and extrahepatic) leading to Biliary cirrhosis \no Autoimmune hepatitis. \nMajor complications of cirrhosis \n1) Portal Hypertension (HPN)  \n\u2022 Normal portal pressure gradient 10 -15cm of saline  \n\u2022 Portal hypertension is said to exist when the portal pressure gradient is over 30 cm of \nsaline  \n\u2022 Portal hypertension leads to the formation of venous collateral vessels between the \nportal and systemic circulation. Collateral vessels may form at several sites, the most important clinically being those connecting the portal vein to the azygous vein that form dilated, tortuous veins (varices) in the submucosa of the gastric fundus and \nesophagus. \nTypes of portal hypertension \ni. Presinusoidal portal HPN  \u2013 increased resistance to portal blood flow into the liver  \nE.g.  Schistosomiasis causes periportal fibrosis and presinusoidal portal HPN \nii. Sinusoidal portal HPN  \u2013 is the commonest and found in cirrhosis. The resistance is \nin the sinusoids of the liver. \niii. Post sinusoidal portal HPN  \u2013 increased resistance to hepatic venous outflow from \nthe liver and causes include hepatic vein thrombosis and congestive heart failure.  \n2) Variceal hemorrhage"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa68-7265-11ef-a344-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 390, "chroma:document": "in the sinusoids of the liver. \niii. Post sinusoidal portal HPN  \u2013 increased resistance to hepatic venous outflow from \nthe liver and causes include hepatic vein thrombosis and congestive heart failure.  \n2) Variceal hemorrhage  \n\u2022 Esophageal varices \u2013 has a mortality of 30-60% if it bleeds \n\u2022 May present with hematemesis, melena, hematochezia  \nTreatment of Variceal hemorrhage  depends on the speed and volume of bleeding.  \n\u2022 Acutely bleeding patients should be referred to hospitals for intensive care. \n\u2022 Resuscitation"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa69-7265-11ef-acb6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 391, "chroma:document": "Internal Medicine \n \n 376Medical Therapy  \n\u2022 Somatostatin (or octreotide)  reduces splanchnic blood pressure when given \nintravenously  \n\u2022 Vasopressin with nitroglycerin help to minimize systemic vasoconstriction \n\u2022 Endoscopic therapy includes injection of sclerosing agent and/or band ligation of \nvarices.  \n\u2022 Balloon tamponade \u2013 compressing bleeding varices temporarily  \nSurgery:  portosystemic shunt \nPrevention of variceal hemorrhage :- the following drugs can be given for patients diagnosed \nto have CLD. They are not given during active variceal bleeding.  \n\u2022 Non selective \u03b2-blockers (propranolol and nadolol) \n\u2022 Mononitrates (Isosorbide mononitrate) decrease portal blood flow and pressure  \n3) Ascites  \n\u2022 Transudative  \n\u2022 Serum to ascitic albumin gradient  is > 1.1 \n\u2022 Clinically detectable when larger than 500 ml \n\u2022 Most sensitive clinical sign is shifting dullness \n\u2022 Subclinical ascites can be detected by ultrasound examination. \nManagement of ascites     \n\u2022 Salt restriction to less than 2g/day  \n\u2022 Fluid restriction if serum Na+ level is below 120 meq/l \n\u2022 Spirinolactone (aldactone) is an aldostrone antagonist, is often effective when given \nwith loop diuretics.  \n\u2022 Duiresis should be monitored because vigorous duiresis leads to hypovolemia and \nhypokalemia and precipitate hepatic encephalopathy. The goal of duiresis should be \ndependent on the extent of edema and be monitored by daily body weight \nmeasurement i.e."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa6a-7265-11ef-b9c9-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 391, "chroma:document": "hypokalemia and precipitate hepatic encephalopathy. The goal of duiresis should be \ndependent on the extent of edema and be monitored by daily body weight \nmeasurement i.e. \no  Decrease weight by 0.5 kg/day if no peripheral edema and \no  Decrease weight by 1kg/day if peripheral edema is present. \nRefractory ascites :  \n\u2022 Is defined as persistent tense ascites despite maximal diuretic therapy \n(Spirinolactone 400 mg/d, Furesemide 160 mg/d), or if azotemia develops (creatinine > 2mg/dl) while the patient is receiving sub maximal doses."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa6b-7265-11ef-bbf7-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 392, "chroma:document": "Internal Medicine \n \n 377\u2022 It occurs in 10% of ascites of CLD origin. Such patients should be referred to \nhospitals for treatment:  \n\u03bf Repeated large volume paracentesis (with intravenous albumin replacement if \navailable). But the following two modalities of therapy are available in \ndeveloped countries. \n\u03bf Surgical treatment (Porto-systemic shunt)   \n\u03bf Liver transplantation \nComplications of ascites \n\u03bf Spontaneous bacterial peritonitis \n\u03bf Hepatopulmonary syndrome  \n\u03bf Hepatorenal syndrome  \n\u03bf Rupture of the umbilicus  \na) Spontaneous bacterial peritonitis(SBP) \n\u2022 Usually due to enterobacteriacae  or pneumococci  \n\u2022 Characterized by fever, abdominal pain and tenderness. Hepatic \nencephalopathy may be precipitated by the infection. \n\u2022 Diagnosis is suspected when ascitic polymorphonuclear cell count is over \n250/\u03bcl. and confirmed by ascitic fluid culture.  \n\u2022 Treatment is with third generation cephalosporin for 5 -7 days.  \n \nProphylaxis for SBP \nIndications   \n\u2022 Previous history of SBP \n\u2022 Patient admitted with gastrointestinal hemorrhages. \n\u2022 Ascitic protein less than 1gm/dl \n\u2022 Candidates of liver transplantation \nDrugs  \n\u2022 Norfloxacin \u2013 400 mg/day \n\u2022 Ciprofloxacin \u2013 750 mg/once weekly or  \n\u2022 Co-trimoxazole - 960mg/d for 5 days ( Monday \u2013 Friday)  \nb) Hepatorenal syndrome(HRS) \n\u2022 Functional renal failure in the presence of cirrhosis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa6c-7265-11ef-9ce3-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 393, "chroma:document": "Internal Medicine \n \n 378\u2022 Occurs when there is significant hepatic synthetic dysfunction and severe \nascites.  \n\u2022 Vigorous duiresis , paracentesis and sepsis may predispose to HRS \n\u2022 Typically the kidneys are histologically normal with the capacity of regaining \nnormal function in the event of recovery of liver function. There is severe \ncortical vasoconstriction  \n\u2022 Characterized by declining GFR, oliguria, low urine sodium (< 10 mg/l), normal \nurinary sediment and azotemia often with disproportionately high levels of blood urea nitrogen and creatinine  \n\u2022 Diagnosed   after prerenal cause of renal failure is excluded. \n\u2022 Mortality rate from HRS is 95% \n   Management of HRS \n\u2022 Volume expansion to rule out volume depletion \n\u2022 Low dose vasopressin, octreotide or norepinephrine may be given  \n\u2022 Liver transplantation is the accepted management.  \n4) Hepatic encephalopathy (Hepatic coma or portosystemic encephalopathy)  \nIt is a complex neuropsychiatric syndrome that may complicate advanced liver disease and/or extensive portosystemic shunt. It manifest s in two major forms:  acute and chronic.  \nAcute  \n\u2022 Occurs in the setting of fulminant hepatitis \n\u2022 Cerebral edema plays a more important role  \n\u2022 Mortality rate is very high  \nChronic  \n\u2022 Occurs in chronic liver disease \n\u2022 Often reversible \nPathogenesis  \n\u2022 The hepatocellular dysfunction and portosystemic shunt leads to inadequate \nremoval of nitrogenous compounds and toxins ingested or produced in the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa6d-7265-11ef-aa84-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 393, "chroma:document": "Chronic  \n\u2022 Occurs in chronic liver disease \n\u2022 Often reversible \nPathogenesis  \n\u2022 The hepatocellular dysfunction and portosystemic shunt leads to inadequate \nremoval of nitrogenous compounds and toxins ingested or produced in the \ngastrointestinal tract, getting access to the brain and causing hepatic \nencephalopathy.  \n\u2022 The compounds commonly incriminated in causing hepatic encephalopathy include \n\u03bf Ammonia  is very well known and studied  \n\u03bf GABA"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa6e-7265-11ef-adc5-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 394, "chroma:document": "Internal Medicine \n \n 379\u03bf Mercaptans \u2013 a cause of fetor hepaticus in CLD \n\u03bf Short chain fatty acids  \nClinical Features may involve \n\u2022 Disturbance of higher neurologic function  \n\u2022 Intellectual and personality disorder  \n\u2022 Dementia, inability to copy simple diagrams (constructional apraxia) \n\u2022 Disturbance of consciousness \n\u2022 Disturbance of neuromuscular function (ast erixis, hyperreflexia, myoclonous)   \n\u2022 The findings are usually asymmetrical, but can also be symmetrical \n\u2022 The manifestations depend on the stage of hepatic encephalopathy \n \nTable V-6-1. Stages of chronic hepatic encephalopathy and their manifestations \n \nStage    Clinical manifestation  \n \nI Apathy, restlessness, reversal of sleep rhythm, slowed  intellect, impaired \ncomputing ability, impaired hand writing  \nII Lethargy, disorientation, drowsiness, asterixis  \n \nIII Stupor (arousable), hyper active reflexes, extensor plantar responses  \nIV Coma  \n \nTreatment of chronic hepatic failure is based on four principles  \n1) Identify and treat precipitating factors including  \n\u2022 GI bleeding                                     \n\u2022 Increased dietary protein                  \n\u2022 Constipation                                          \n\u2022 Alkalosis         \n\u2022 Hypovolemia           \n\u2022 Infection   \n\u2022 Azotemia \n\u2022 Hypokalimia from overduiresis"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 395, "chroma:document": "Internal Medicine \n \n 380\u2022 CNS depressant  drugs                                                                                                                \n                     \n2) Reduce and eliminate substrates for the generation of nitrogenous compounds. \n\u2022 Restrict dietary protein  \n\u03bf For patients in coma  no protein should be given  \n\u03bf For non comatose patients restriction of protein to 40 - 60 gm/d is enough. \n\u2022 Cleanse the bowel with  enema in patient with gastrointestinal hemorrhage  \n3) Reduce colonic bacteria that generate ammonia using oral preparations of  Neomycin \nor Metronidazole   \n4) Prevent diffusion of ammonia from the bowel lumen to the blood by \nadministering oral  lactulose, lactitol, or lactose (in lactase deficient patients) all of which \nare fermented by colonic bacteria to organic acids and reduce stool PH. The hydrogen ion \nproduced traps ammonia in the colon and changes it to nondiffusable NH 4+ ions.  \nHepatopulmonary syndrome  \n\u2022 Characterized by abnormal arterial oxygenation in a patient with cirrhosis and/or portal \nHTN. \n\u2022 Pathogenesis is thought to be due to intrapulmonary vasodilatation leading to impaired \nO2 transfer that improves with 100% O 2 \n\u2022 Clinical features range from sub clinical abnormalities in gas exchange to profound \nhypoxemia causing dyspnea at rest.  \n\u2022 It is a functional disorder that reverses with liver transplantation. \n \nC. Hepato cellular carcinoma (Hepatoma)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa70-7265-11ef-9b6d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 395, "chroma:document": "\u2022 Clinical features range from sub clinical abnormalities in gas exchange to profound \nhypoxemia causing dyspnea at rest.  \n\u2022 It is a functional disorder that reverses with liver transplantation. \n \nC. Hepato cellular carcinoma (Hepatoma) \n\u2022 One of the most frequent malignancies and important cause of mortality particularly \nin middle aged men in developing countries. The incidence is less in developed countries  \n\u2022 Arises in cirrhotic liver and is closely associated with chronic hepatitis B or C. \n\u2022 Hepatitis B DNA has been shown to integrate in to the host cell genome, where it \nmay disrupt the tumor suppressor genes and/or activate oncogenes. \n\u2022 Vaccination prevents  hepatitis B infection, thereby reducing the incidence of \nhepatoma  \n\u2022 More common in males (male to female ratio 4:1 to 8:1)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa71-7265-11ef-860e-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 396, "chroma:document": "Internal Medicine \n \n 381Clinical and Laboratory findings  \nCommon symptoms and findings \n\u2022 Abdominal pain \n\u2022 Weight loss \n\u2022 Abdominal mass                                 \n\u2022 Derangement of  liver function  \nUnusual manifestations  \n\u2022 Bloody ascites    \n\u2022 Tumor emboli          \n\u2022 Jaundice    \n\u2022 Gyneacomastia \n\u2022 Hepatic bruit or friction rub  \n\u2022 Metabolic effect \no Erythrocytosis  \no Hypercholesterolemia  \no Hypoglycemia  \no Hypercalcemia \no Acquired porphyria \n\u2022  High serum \u03b1 fetoprotein level (> 400 mg/dl) \n\u2022  Ultrasonography :Mass lesion with varying echogenicities but usually \nhypoechoic  \n\u2022  Tissue specimen: may be required to confirm the diagnosis \n\u2022  Median survival rate is less than 6 months from the time of diagnosis \nTreatment : is usually unsatisfactory but some options include: \n\u2022 Chemotherapy \n\u2022 Radiotherapy \n\u2022 Liver transplantation. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nChronic Hepatitis , Cirrhosis and it complications, pages 1844-1868. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Diseases of the liver, pages 249-264."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa72-7265-11ef-b2cf-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 397, "chroma:document": "Internal Medicine \n \n 3827. Diarrheal diseases  \n \nLearning objectives: at the end of this unit the student will be able to \n1. Define diarrhea \n2. List the etiologies of acute and chronic diarrhea 3. Explain the mode of transmission of organisms causing diarrhea \n4. Describe the clinical features of diarrhea \n5. List the common complications acute and chronic diarrhea 6. Make a diagnosis of acute and chronic diarrhea 7. Manage  patients with diarrhea at the primary care level \n \nDefinition : Diarrhea is defined as an increase in stool frequency and volume. The stool is \nusually liquid, and 24 hrs output exceeds 250 gm/day  Objective definition  \u2013 Stool weight greater than 200gm/day.  \n\u2022 Normal stool weight is about 100 - 200 gm/d for people in developed countries who \nusually consume diets containing less fiber. \n\u2022 Stool weight is affected by fiber contents of diet, gender (higher in males), medications, \npossibly exercise and stress. \n\u2022 Normal bowel habit ranges from 3 times/day to 3 times/wk. Thus, one has to know the \nnormal bowel habit of the individual and the nature of the current symptoms before the diagnosis of diarrhea \n\u2022 About 9 liters of fluid is presented to the GIT daily (7 liters from the secretion and 2 liters \nfrom diet). Of this only 100 - 200 ml of fluid is excreted with feces and the rest will be reabsorbed. Fluid absorption follows Na\n+ absorption, which is co-transported with \nchloride ion, glucose, and aminoacids and through Na+ channels."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa73-7265-11ef-9033-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 397, "chroma:document": "from diet). Of this only 100 - 200 ml of fluid is excreted with feces and the rest will be reabsorbed. Fluid absorption follows Na\n+ absorption, which is co-transported with \nchloride ion, glucose, and aminoacids and through Na+ channels. \n\u2022 Na \u2013 glucose co-transport is unaffected by many diarrheal diseases \n\u2022 Secretion follows chloride ion secretion in crypt cells, with Na+, K+ and water following \npassively through tight junctions. \n Classification of diarrhea  \n1. Based on the duration of illness diarrhea can be classified into acute and chronic  \nA) Acute diarrheal disease   \n\u2022 Lasts for 2 - 4 wks"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa74-7265-11ef-8dda-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 398, "chroma:document": "Internal Medicine \n \n 383\u2022 It is usually infectious in origin  \n\u2022 Resolves with or without intervention  \nB) Chronic diarrheal diseases  \n\u2022 Lasts for more than 4 wks  \n\u2022 The common causes include malabsorption, in flammatory Bowel Diseases (ulcerative \ncolitis), irritable Bowel syndrome, colonic cancer, and HIV/AIDS.  \n\u2022 Infectious causes are not common causes of chronic diarrhea  \n2. Based on the nature of diarrheal stool, acute diarrhea could be inflammatory or non-\ninflammatory \nA) Non-inflammatory diarrhea   \n\u2022 Is watery, non bloody diarrhea associated with periumblical cramps, nausea, and \nvomiting \n\u2022 It is small intestinal in origin \nB) Inflammatory diarrhea -  \n  Dysentery  is bloody diarrhea \n3. Pathophysiologic classification   \nMost diarrheal states are caused either by inadequate absorption of ions, solutes and water or \nby increased secretion of electrolytes that result in accumulation of water in the lumen.  Based on this concept diarrhea can be classified as: \nA) Secretory diarrhea:  \n\u2022 Occurs when the secretion of fluid and electrolytes is increased or when the normal \nabsorptive capacity of the bowel is decre ased. It usually follows stimulation by \nmediators like enteric hormones, bacterial enterotoxins (E.g. Cholera,  heat labile E. \ncoli toxin, Salmonella enterotoxin ), vasoactive intestinal peptides ( VIP )  or laxatives \n. These agents activate the adenyl cyclase \u2013cAMP system"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa75-7265-11ef-8d5b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 398, "chroma:document": "mediators like enteric hormones, bacterial enterotoxins (E.g. Cholera,  heat labile E. \ncoli toxin, Salmonella enterotoxin ), vasoactive intestinal peptides ( VIP )  or laxatives \n. These agents activate the adenyl cyclase \u2013cAMP system \n\u2022 These mediators block Nacl absorption and induce chloride secretion. These events \ncan result in massive diarrhea, without evidence of cell injury, as shown by the ability of the cell to absorb Na\n+ if coupled to nutrients (Na+ to glucose, Na+ to amino acids). \nThat is why cholera and other forms of secretary diarrhea can be treated with oral solutions containing sodium and glucose. \n\u2022 Diarrhea of secretary origin persists even if the patient fasts. \nB) Osmotic diarrhea:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa76-7265-11ef-91db-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 399, "chroma:document": "Internal Medicine \n \n 384\u2022 It occurs  due to the presence of poorly absorbed or nonabsorbable substance in the \nintestine which is osmotically active , resulting secondary accumulation of fluid and \nelectrolytes. Such nonabsorbable substances include lactose in patients with lactase deficiency.  \n\u2022 This type of diarrhea is usually caus ed by malabsorption and disappears when \npatient fasts for 48-72 hrs. \nC) Abnormal intestinal motility : causes or contributes to diarrhea seen in Diabetes \nmellitus , irritable bowel syndrome , postv agotomy states , carcinoid syndrome and \nhyperthyroidism, Mechanism of abnormal intestinal motility includes the following  \n\u2022 If small bowel peristalsis is too rapid , an abnormal large amount of fluid and partially \ndigested foodstuffs may be delivered to the colon  \n\u2022 Extremely slow peristalsis may allow bacterial overgrowth to occur, and bile salts \ndeconjugation to cause secondary malabsorption \n\u2022 Rapid colonic motility may not allow adequate time for the colon to absorb fluid \ndelivered to the cecum (Normally 90 % of the fluid is absorbed )      \nD)  Exudation : inflammations or infectious conditions that result in damage to the \nintestinal mucosa can cause diarrhea by a number of mechanisms. There is loss of \nblood, mucous proteins and serum proteins. Mucosal damage can interfere with \nabsorption, induce secretion and affect motility, all of which contribute to diarrhea.                                     \n \nInfectious Diarrhea"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa77-7265-11ef-8b57-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 399, "chroma:document": "blood, mucous proteins and serum proteins. Mucosal damage can interfere with \nabsorption, induce secretion and affect motility, all of which contribute to diarrhea.                                     \n \nInfectious Diarrhea  \nMicrobes cause diarrhea either directly by invasion of gut mucosa or indirectly through elaboration of different types of toxins: Secretory enterotoxins, cytotoxins and inflammatory \nmediators. \nI) Secretory toxin induced diarrhea \n\u2022 Patients seldom have fever or  major systemic symptoms.  \n\u2022 Little or no inflammatory response. \n\u2022 The organisms colonize the intestinal mucosa but don\u2019t invade the intestinal wall.  \n     Examples:   \na) Vibrio cholerae  produces enterotoxins which stimulate adenylate cyclase which results in \nmassive intestinal secretion.  \nb) Enterotoxigenic E. coli  is the major cause of traveler\u2019s diarrhea \nc)   Non typhoidal salmonella like S. typhimarium"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa78-7265-11ef-91a8-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 400, "chroma:document": "Internal Medicine \n \n 385d) Shigella dysenterae  may initially cause secretary diarrhea. \nII) Cytotoxin induced Diarrhea Cytotoxins are soluble factors that directly destroy mucosal \nepithelial cells. Examples:  \na) Shigella dysenterae  produces Shiga toxin which causes destructive colitis. \nb) Enterohemorrhagic E.coli  \nc) Clostridium perifringens, Vibrio parahemolyticus  \nd) Clostridium defficile  causes psudomembraneous  colitis in individuals treated with \nantibiotics.  \nIII) Diarrhea caused by invasive pathogens. \n\u2022 Characterized by fever and other syst emic symptoms like headache and myalgia. \n\u2022 The diarrhea is frequent but small in volume. It is associated with crampy abdominal \npain and tenesmus.  \n\u2022 These pathogens induce marked inflammatory response and stool usually contains \npus cells, proteins and often gross blood. \nCommon causes include :  \nAcute shigellosis \n\u2022 Feaco-orally transmitted, as few as  10 - 100 bacteria are enough to  cause diarrhea \n\u2022 Initially multiplies in the small intestine causing secretary diarrhea. Later it invades \ncolonic epithelium causing bloody diarrhea.  \n\u2022 Usually resolves spontaneously after 3 - 6 days. \nAcute Salmonellosis  \n\u2022 Transmitted by ingestion of contaminated meat, dairy or poultry products. \n\u2022 The non typhoidal salmonellae invade primarily the distal ileum.  \n\u2022 Causes short lived (2 \u2013 3 days) illness characterized by fever, nausea, vomiting and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa79-7265-11ef-8fa6-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 400, "chroma:document": "\u2022 Transmitted by ingestion of contaminated meat, dairy or poultry products. \n\u2022 The non typhoidal salmonellae invade primarily the distal ileum.  \n\u2022 Causes short lived (2 \u2013 3 days) illness characterized by fever, nausea, vomiting and \ndiarrhea. This is in marked contrast to the 3 - 4 wks febrile illness caused by Salmonella typhi and paratyphi, which are not usually associated with diarrhea. \nCampylobacter jejuni   \n\u2022 It may be responsible for up to 10% of acute diarrhea world wide. It invades both \nthe small and large intestines. \nEnterohemorrhagic E. coli  ; \n\u2022 It produces bloody diarrhea without evidence of mucosal inflammation (grossly \nbloody stool with few or no leucocytes)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa7a-7265-11ef-9672-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 401, "chroma:document": "Internal Medicine \n \n 386 Viral causes of diarrhea  e.g. Norwalk and Rota viruses  \n\u2022 Invade and damage villous epithelial cells  \n\u2022 Cause diarrhea by interfering with absorption through selective destruction of \nabsorptive villous tip cells with sparing of secretary crypt cells. \n\u2022 Stool is usually watery and its content resembles those of noninvasive diarrhea, with \nfew inflammatory cells, probably because of absence of colonic damage.  \n \nProtozoal cause of diarrhea \na) Giardia lamblia. \n\u2022 few organisms are necessary to cause infection \n\u2022 Multiplies in the small intestine, attach to and occasionally invade the mucosal cells. \n\u2022 Its clinical features span from an acute diarrheal illness to chronic diarrhea \nassociated with malabsorption and weight loss \n\u2022 Diagnosis  is based on  identification of the organism either in the stool or duodenal \nmucus or by small intestine biopsy. Cysts or trophozoites can be identified in the \nstool, and treatment should be given in both cases. \nb) Entamoeba histolytica  may cause syndromes ranging from mild diarrhea to \nfulminant amoebic colitis with multiple bloody stools, fever and severe abdominal pain.  \nc) Cryptosporidium parvum and Isospora belli  occasionally cause self limited acute \ndiarrheal illness in otherwise healthy individuals. They may cause voluminous life threatening diarrheal diseases in patients with acquired immunodeficiency syndrome. \nModified acid fast staining of the stool will identify both organisms."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa7b-7265-11ef-86a6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 401, "chroma:document": "diarrheal illness in otherwise healthy individuals. They may cause voluminous life threatening diarrheal diseases in patients with acquired immunodeficiency syndrome. \nModified acid fast staining of the stool will identify both organisms. \n \nEvaluation of a patient with diarrhea \nCareful interview of patients with diarrhea contributes in etiologic diagnosis, evaluation of \nseverity of illness, and in designing treatment and preventive measures. Thus, the history \nshould include \n Duration of illness:  if the diarrhea lasts for 2 - 4 wks, acute diarrheal diseases are said to \nexist. These are usually infectious in origin  and resolve with or without intervention. \nHowever, if it lasts for more than 4 wks, consider chronic diarrheal diseases and infectious \ncauses are unlikely. In such cases the common causes include malabsorption,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa7c-7265-11ef-acec-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 402, "chroma:document": "Internal Medicine \n \n 387inflammatory Bowel Diseases (ulcerative colitis), irritable Bowel syndrome, colonic cancer, \nand immuno suppressions like AIDS.  \nDiurnal variation \u2013 is there any relation to any part of the day? \n\u0083 Nocturnal \u2013 organic causes  \n\u0083 Non nocturnal \u2013 functional causes like irritable bowel syndrome \nIs the diarrhea watery or bloody? \n       Bloody diarrhea is usually inflammatory  or ischemic in origin and caused by invasive \norganisms, ulcerative colitis, or neoplasms     \nVolume of diarrhea  \nLarge volume diarrhea indicates small bowel or proximal colonic diseases  \nScanty, frequent stools associated with urgency suggest left colon or rectal diseases  \nAny association with specific meal ?  If diarrhea is associated with intake of \n Fat \u2013 it is due to fatty intolerance \n Sweet diet \u2013 it is due to osmotic diarrhea  Milk and milk products - it is due to lactase deficiency  \nIs there history of drug intake?  \nPenicillin may be associated with psudomembraneous colitis.  \nLaxatives Chemotherapeutic agents \n       7) Presence of underlying diseases (like diabetes mellitus) or systemic symptoms  \nPhysical examination:  Assess severity of dehydration, Wight loss and other associated signs \nin patient with chronic diarrhea.  \nDiagnosis:  \nLaboratory tests: \n1) Culture and sensitivity testing to detect a pathogenic bacterial strains. A positive \nstool culture is found for 40 % of patients who have  WBC in the stool  and fever"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa7d-7265-11ef-b7a8-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 402, "chroma:document": "in patient with chronic diarrhea.  \nDiagnosis:  \nLaboratory tests: \n1) Culture and sensitivity testing to detect a pathogenic bacterial strains. A positive \nstool culture is found for 40 % of patients who have  WBC in the stool  and fever \n2) Microscopic examination:  to identify ova and parasites  \n3) Guaiac :  to detect occult blood  \n4) Sudan staining:  to detect fat droplets. \n5) Wright or methylene blue staining: to detect WBC, which are indicative of invasive \ninfectious causes of diarrhea. \nProctosigmoidoscopy:  to exclude of confirm the diagnosis of inflammatory bowel diseases. \n \nManagement"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa7e-7265-11ef-afd8-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 403, "chroma:document": "Internal Medicine \n \n 3881. Rehydration \n\u2022 In patients with massive diarrhea and vomiting with hypotension intravenous fluids \nlike Ringer\u2019s lactate or Normal saline should be given in adequate amount. \n\u2022 For patients without hypotension oral fluid containing sodium, glucose, potassium and \nchloride ions (ORS) are preferred. \n2. Antimicrobial therapy \nAntibiotics:  \n\u2022 Most acute infectious diarrheal diseases do not require antibiotic therapy because \nmajority of them are self limited and viral in nature.  \n\u2022 Of the non invasive bacterial diarrhea, antibiotics decrease the volume of diarrhea \nonly in cholera. Doxycycline 300mg single dose is the drug of choice. \n\u2022 For invasive bacterial diarrhea caused by E. coli  and Shigella  (bacillary dysentery)   \nCiprofloxacin 500 mg or Norfloxacin 400mg twice a day for 3-5 days is indicated. \nAnti-protozoal: \n\u2022 For Entamoeba histolytica : Metronidazole 500mg PO TID for 7 days  \n\u2022 For Giardia lamblia:  Metronidazole 250mg thrice a day for 5 days or Tinidazole 2g \nonce. \n\u2022 For Isospora belli:   Co- trimoxazole 960mg four times a day for 10 days then 960mg \ntwice a day for additional three wks . In immunocompromized patients continue maintenance dose of the same drug three times a week. \n\u2022 When no specific therapy is available or no cause is identified it\u2019s appropriate to give \nempirical therapy E.g. \no Antibiotics for possible bacterial overgrowth or Metronidazole for Giardia, \ncholesteramine for bile acid malabsorption or"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa7f-7265-11ef-99f8-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 403, "chroma:document": "\u2022 When no specific therapy is available or no cause is identified it\u2019s appropriate to give \nempirical therapy E.g. \no Antibiotics for possible bacterial overgrowth or Metronidazole for Giardia, \ncholesteramine for bile acid malabsorption or  \no Non specific therapy with constipating agents such as loperamide, diphenoxylate \nand in more severe cases codeine or long acting somatostatin analogue.  \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Diarrhea,    \npages 225-229. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nDiarrhea, 210-224."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa80-7265-11ef-8d3a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 404, "chroma:document": "Internal Medicine \n \n 389CHAPTER SIX \nHEMATOLOGIC DISORDERS \n \n1. Anemia \nLearning objectives:   At the end of this topic the student we be able to:-   \n1. Define anemia and describe the diagnostic criteria of anemia in adults. \n2. Understand  factors that influence Hematocrite / Hemoglobin values \n3. Evaluate cases of anemia with appropriate history, physical examination and proper \nlaboratory studies \n4. Describe classification of Anemia. \n5. Understand the adaptive mechanisms to chronic anemia. 6. Understand the principles of management of anemia.                                        \n           \nAnemia: General approach  \na) Definition  \n\u2022 Functional definition : A significant reduction in red cell mass and a corresponding \ndecrease in the 0 2 carrying capacity of the blood. \n\u2022 Laboratory definition : A reduction of the Hemoglobin concentration, red cell mass \nor Hematocrite, to below normal levels. \n\u2022 In women of the child bearing age, their blood values are 10% lower than men. \nTherefore, Anemia may be defined as a HCT of less  than 10% below the mean values for age, sex and altitude  \n \nTable VI-1-1 Criteria of anemia in adults at sea level  \n                           \nFactor\n \n Women  Men \nRBC x 1012/ L < 4.0 < 4.5 \nHgb (g/dl)  < 12  < 14 \nHCT (% )  < 37 < 40 \n NB:  blood values may not accurately reflect alteration in red cell mass. For instance;"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa81-7265-11ef-b449-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 405, "chroma:document": "Internal Medicine \n \n 390\u2022 Hgb or Hematocrite could be falsely elevated ( \u2193 plasma volume) e.g. \nhemorrhage, burns, vigorous diuresis, dehydration all leading to \nHemoconcentration  \n\u2022 Hgb or Hct may be falsely low ( \u2191 plasma volume) leading to  Hemodilution  \nE.g.  Spleenomegaly, CHF, Cirrhosis, pregnancy  \n \nEpidemiology \n\u2022 In Ethiopia, a study conducted by Zein Ahmed Zein in Gondar, rural  population \nindicated a  prevalence rate of anemia to be very high ( 40.5%, ), and  anemia was the fourth leading cause of hospitalization and hospital deaths in 1982 in Gondar. \n\u2022 Another study done in Black lion Hospital in 1987 G.C. showed that anemia is the 3\nrd \ncause of hematology admissions.  \n\u2022 Analysis of admissions to hospitals in Ethiopia showed that anemia accounted for 0.5 - \n4% of all admissions and 25% of hematological diseases related admissions. \n\u2022 Iron deficiency anemia is the commonest ty pe of anemia globally, mainly in developing \ncountries like Ethiopia.   \n\u2022 Sickle cell disease and thalassemias are not reported in Ethiopia but common in other \nAfrican countries. Hereditary hemolytic anemias aren\u2019t common in our country . \n \nClinical approach to the Patients with anemia  \nAnemia is a manifestation of an underlying pathological condition.  \nIt results from:  \n1. Under production  \n2. Increased destruction/Hemolysis   \n3. Blood loss /bleeding 4. Multifactorial :  a combination of these"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa82-7265-11ef-9a15-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 405, "chroma:document": "Anemia is a manifestation of an underlying pathological condition.  \nIt results from:  \n1. Under production  \n2. Increased destruction/Hemolysis   \n3. Blood loss /bleeding 4. Multifactorial :  a combination of these              \nHistory:  Accurate history provides information crucial to the diagnosis of the underlying cause.                   \n\u2022 Nutritional /Dietary history       \n\u2022 Underlying diseases   \n\u2022 Blood loss : GI or Genito uirinary blood loss      \n\u2022 Family history of anemia     \n\u2022 Exposure to drugs/toxins E.g.  - Methyldopa  \n\u2022 Ggeographical location"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa83-7265-11ef-be53-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 406, "chroma:document": "Internal Medicine \n \n 391\u2022 Pregnancy \n      \nSymptoms :   \n\u2022 Depend on the rapidity of development of anemia, age of the patients, the presence of \nan underlying disease .They are often non-specific  \n\u2022 Fatigue, dizziness, dyspnea, palpitation, syncope, exercise and cold intolerance, angina,  \n\u2022 Tinnitus, vertigo, throbbing head ache,  \n\u2022 Anorexia, indigestion, nausea, bowel irregularity (due to shunting of blood from the \nsplanchinic bed) \n\u2022 Irritability, difficulty in concentration, worsened dementia and. \n\u2022 Impotence or decreased libido \n\u2022 Intermittent claudication \nPhysical Examination: \n       A comprehensive examination with em phasis to the following findings should be made. \n\u2022 Skin and mucous membrane: look for pallor, icterus, bleeding sites, leg ulcer \n\u2022 Spooning of fingernails \u2192 in iron deficiency anemia  \n\u2022 Atrophy of the tongue, sore tongue (glossitis), angular stomatitis which may be seen in \niron deficiency anemia. \n\u2022 Abdomen: spleenomegaly, hepatomegaly, evidence of gallstone. \n\u2022 Pelvic and rectal examination: to look for possible site of bleeding. \n\u2022 Bone tenderness and Lymphadenopathy to rule our hematologic malignancies and  \n\u2022 Neurological: gait, reflexes, vibration and position sense which may help to look for \nneurologic changes associated with Vit B- 12 deficnecy.  \n\u2022 Fundoscopy: retinal hemorrhage \n\u2022 Cardiovascular system; modest tachycardia, wide pulse pressure hyper dynamic"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa84-7265-11ef-96c6-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 406, "chroma:document": "neurologic changes associated with Vit B- 12 deficnecy.  \n\u2022 Fundoscopy: retinal hemorrhage \n\u2022 Cardiovascular system; modest tachycardia, wide pulse pressure hyper dynamic \nprecordium, flow murmur. In severe form of Chronic anemia patients may develop CHF \nwith S3 gallops. \n \nLaboratory study \n1. Complete blood count  \nHgb, Hct, ESR, Platelet count, WBC with differential"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa85-7265-11ef-86a7-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 407, "chroma:document": "Internal Medicine \n \n 3922. Red blood cell indices  \na. Mean Corpuscular volume ( MCV): Hct/RBC : normal value is 80 \u2013 95 fl \nb. Mean corpuscular Hemoglobin( MCH ) : Hgb/RBC : 27 \u2013 32 pg \nc. Mean corpuscular Hemoglobin (MCHC): Hgb/Hct 32 \u2013 36%               \n3. Examination of the peripheral blood smear: examine a cellular morphology, shape, \nsize, color, abnormality of other cells. \n             Red cell morphology       \n\u2022 Normochromic Normocytic  RBCs are aeen in normal individuals and in anemia of \nchronic diseases \n\u2022 Anisopoikilocytes: Variation in size a nd shape may be seen in iron deficiency anemia  \n\u2022 Hypochromic microcytic anemia: is seen in iron defeciency anemia , anemia of \nchronic diseases  , thalassemia and sideroblastic anemia (SBA) \n\u2022 Macrocytic RBCs : Macro \u2013 ovalocytes with hyper segmented neutrophils \u00c6 indicate \nmegaloblastic anemia and myelodysplasia  \n\u2022 Schistocytes (fragmented RBC/Helmentcells):- microangiopathies , DIC, vasculitis, \nprosthetic heart valve \nClassification of anemia  \nA. Pathophyisiologic Classifications  (based on underlying disease) \n1) Anemia associated with impaired RBC Production \na) Aplastic anemia                        \nb) Iron deficiency                                                     \nc) Myelodysplastic syndrome.                    \nd) Megaloblastic anemia  \ne) Anemia of CRF \nf) Anemia of chronic diseases  \ng) Drug related      \n2) Anemia associated with increased RBC loss or destruction  \na) Bleeding"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa86-7265-11ef-a84d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 407, "chroma:document": "c) Myelodysplastic syndrome.                    \nd) Megaloblastic anemia  \ne) Anemia of CRF \nf) Anemia of chronic diseases  \ng) Drug related      \n2) Anemia associated with increased RBC loss or destruction  \na) Bleeding  \nb) Hereditary hemolytic anemia  \ni) Hemoglobinopathies,  sickle cell disease, Thalassemia \nii) Primary disorder of RBCs iii) RBC erythropathies (G6 PDH, PK deficiency) \nc) Acquired hemolytic anemia"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa87-7265-11ef-8ad5-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 408, "chroma:document": "Internal Medicine \n \n 393i) Autoimmune     \nii) Drug induced hemolytic anemia                iii) Microangiopathies (e.g. DIC) \niv) Traumatic \nB. \nMorphological classification  \n1) Hypochromic microcytic anemia  \na) Inherited: Thalassema, sideroblastic anemia  \nb) Acquired: IDA, Anemia of chronic diseases \n2) Macrocytic anemia :  (MCV > 100 fl) \na) With megaloblastic marrow: megaloblastic anemia  \nb) With normoblastic marrow: Hemolysis, acute bleeding,  \n3) Normchromic normocytic:-   \na) Anemia of chronic disease  \nb) Early iron deficiency anemia  \nc) Aplastic anemia  \nd) Anemia of CRF  \nAdaptation to chronic anemia : the main consequence of anemia is tissue hypoxia  \nCompensatory mechanisms:  \n1.  Intrinsic red cell adjustments (adaptations) \n\u2022 Modulation of O 2 affinity by increased generation of 2,3- diphosphoglycerate in \nerythrocytes  \n\u2022 It bounds to Hgb, causing a right ward shift in O 2- Hgb dissolution curve \n\u21d2 This allows more O 2 to be unloaded from the RBC at any given blood O 2 tension \n2. Cardiovascular adjustment  \n\u2022 Increased in cardiac  output occurs at Hgb level of 7-8 gm% : the increased in cardiac \noutput coupled with modest tachycardia  creates a  hyperdynamic state and hence \nsystolic ejection murmur  \n\u2022 Peripheral vascular resistance decreases there by  facilitating tissue perfusion; \nclinically is evidenced by wide pulse pressure. \n3. Local changes in tissue perfusion:  Redistribution of blood flow to vital organs at the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa88-7265-11ef-a778-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 408, "chroma:document": "\u2022 Peripheral vascular resistance decreases there by  facilitating tissue perfusion; \nclinically is evidenced by wide pulse pressure. \n3. Local changes in tissue perfusion:  Redistribution of blood flow to vital organs at the \nexpense of reduced blood flow to less vital organs. \n4.  Reduction of mixed venous O 2 tension to increases the arterio\u2013venous O 2 difference \u21d2 \u2191 \nO2 extraction at peripheral tissues"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa89-7265-11ef-a40b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 409, "chroma:document": "Internal Medicine \n \n 394Individuals tend to survive at extremely low hemoglobin levels (even as low as 3 gm %) due to \nthese compensatory mechanisms.  \nTherapeutic considerations and indications \nIn the management of anemic patients carefully remember the following points  \n\u2022 Identify and correct the cause of anemia  \n\u2022 Administration of Hematinines such as Iron, Vit B 12 or folate without correct diagnosis \nof the cause of anemia is an unacceptable practice in the treatment of anemia  \n\u2022 Therapeutic modalities include: Iron, folate, Vit. B 12, pyridoxine (B 6) blood transfusion, \nsteroids (in hemolytic anemia) splenectomy, erythropoietin, bone marrow transplant (aplastic anemia), and androgens \n\u2022 Carefully weigh the risks of blood transfusion over its advantage. \nWhen to transfuse blood in chronic anemia  \n1. Anemia severe enough to cause CHF (congestive heart failure) 2. Hypoxic manifestations: Irritability, unconsciousness, angina  3. Surgical or gynecologic patient awaiting surgery  \nNB:  no threshold of Hct/Hgb that mandates transfusion; the decision to administer blood must \nbe based on the functional status and symptomatology of the patient. \n\u2022 Consider risk of blood transfusion \n\u2022 Adhere to blood component transfusion (packed RBC, FFP, cryoprecipitate, \nplatelets) \n\u2022 Consider whole blood only when there is volume loss due to hemorrhage. \n \nI. Micorocytic Anemias \nA) Iron deficiency anemia (IDA)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa8a-7265-11ef-a476-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 409, "chroma:document": "\u2022 Adhere to blood component transfusion (packed RBC, FFP, cryoprecipitate, \nplatelets) \n\u2022 Consider whole blood only when there is volume loss due to hemorrhage. \n \nI. Micorocytic Anemias \nA) Iron deficiency anemia (IDA) \nLearning objectives: at the end of this topic the student will be able to:-  \n1. Understand iron metabolism 2. Describe the characteristic features of iron deficiency anemia (IDA)  3. List the various causes of iron deficiency anemia ( IDA) 4. Know the clinical manifestations and common specific laboratory findings of iron \ndeficiency anemia (IDA) \n5. List some of the differential diagnosis of iron deficiency anemia (IDA) 6. Understand the management of  iron deficiency anemia (IDA)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa8b-7265-11ef-a7de-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 410, "chroma:document": "Internal Medicine \n \n 3957. Identify possible reasons for inadequate response to therapy and indications for \nparenteral iron administration \n8. List the possible causes of anemia of chronic diseases with their features, \npathogenesis and principles of therapy   \n \nDefinition : - Iron deficiency anemia occurs when body iron stores become inadequate for the \nneeds of normal RBC production (erythropoiesis)   \nIt\u2019s characterized by: \no Hypochromia and microcytosis of the circulating erythrocytes ( RBCs) \no Low plasma iron and ferretine concentration. \no A transferrin saturation of < 15% (Normally \u223c 35%)  \n\u2022 Iron deficiency anemia is a manifestation of diseases, not by itself a complete diagnosis  \n\u2022 It is the commonest cause of anemia world wide  \nIntroduction \nIron metabolism:  \n\u2022 Daily 10-30mg iron ingested, 5-10% absorbed to balance precisely the amount lost \n(1mg) under physiologic condition  \n\u2022 Amount absorbed can increases up to five fold  if body iron store are depleted or \nerythropoiesis is accelerated.  \n\u2022 Absorbed as hem and non hem iron in the duodenum and proximal jejunum  \nIron absorption: \n\u2022 Is facilitated by: Stomach acidity, Ascorbic acid, citrates, while  \n\u2022 Is limited/reduced  by : Phosphates, Oxalates, TTC, Tannates (tea) and pyrates (plant \nfood) \nTransferrin is the transport protein that carries iron in the plasma and ECF.  \nSequences of events in the development of IDA \n1. Mobilization and depletion of iron stores"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa8c-7265-11ef-8f02-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 410, "chroma:document": "food) \nTransferrin is the transport protein that carries iron in the plasma and ECF.  \nSequences of events in the development of IDA \n1. Mobilization and depletion of iron stores  \n2. Decreased plasma Fe2+ and Ferretine concentration \n3. Iron deficient erythropoiesis  \n4. Iron deficiency anemia \u2013 Hypo chromic  microcytic cells   \nEtiologies of Iron deficnecy Anemia  \n1. Chronic blood loss  \n\u2022 Uterine"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa8d-7265-11ef-b390-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 411, "chroma:document": "Internal Medicine \n \n 396\u2022 Gastrointestinal, e.g. esophageal varices; Hi atal hernia; peptic ulcer disease; aspirin \ningestion;  Carcinoma of the stomach, ceacum, colon or rectum; hook worm \ninfestation ;  colitis; piles; Diverticulosis; etc \n\u2022 Rarely hematuria, hemoglobulinuria, pulmonary hemosiderosis, self inflicted blood \nloss  \n\u2022 Disorders of hemeostasis, intravascular hemolysis  \n2. Increased demands  \n\u2022 Prematurity in newborns  \n\u2022 Rapid growth ( as in adolescent ) growth spurt \n\u2022 Pregnancy  \n3. Mal absorption of iron  \n\u2022 Gastrectomy, Celiac disease  \n4. Poor diet \n        \u21d2  Contributory factor in many countries but rarely sole cause  \n \nClinical manifestation:  \n\u2022 Is insidious in onset and progressive in course \n\u2022 Patients often present with nonspecific symptoms mentioned above with/without \nsome specific symptoms. \nSpecific symptoms  \n\u2022 Pica: craving for unusual food substance (amylophagia, geophagia, pagophagia) \n\u2022 Increased GI absorption of lead \u2013 lead poisoning \n\u2022 Koilonychia \u2013 spooning of the finger nails  \n\u2022 Plummer \u2013 Vinson/Peterson - Kelly syndrome: characterized by IDA, koilonychia, \nand dysphagia due to post cricoid esophageal web)  \nLaboratory findings  \nA) Peripheral blood morphology and RBC indices  \n\u2022 \u2193MCV, \u2193MCH, \u2193MCHC  and hypochromic microcytic RBCs with occasional target \ncells and pencil-shaped poikilocytes  \n\u2022 \u2193 reticulocyte count  \n\u2022 Dimorphic peripheral films ( mixed Normal RBCs and microcytic hypochromic RBCs )"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa8e-7265-11ef-9232-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 411, "chroma:document": "\u2022 \u2193MCV, \u2193MCH, \u2193MCHC  and hypochromic microcytic RBCs with occasional target \ncells and pencil-shaped poikilocytes  \n\u2022 \u2193 reticulocyte count  \n\u2022 Dimorphic peripheral films ( mixed Normal RBCs and microcytic hypochromic RBCs )   \no Combined Iron and folate /B 12 deficiency \no On those with recent iron therapy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa8f-7265-11ef-af49-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 412, "chroma:document": "Internal Medicine \n \n 397o Those with recent blood transfusion  \nB) Serum iron and total iron \u2013 binding capacity (TIBC) \n\u2022 \u2193  serum iron and \u2191 TIBC (hence IBC is < 10% saturated). This is in contrast to other \nforms (e.g. ACD). \nC) Serum ferritine is decreased  \nD) Free erythrocyte protoporphyrine (FEP): non specific  \n\u2022 It increased during early phase of iron deficiency anemia, lead poisoning, \nsideroblastic anemia and in erythropoietic porphyria.  \nE) Bone marrow iron  \n\u2022 Complete absence of iron from stores (macrophages) and absence of siderotic iron \ngranules from developing erythroblasts  \nF) Investigation to establish the underlying  cause   \n\u2022 Stool for occult blood  \n\u2022 CXR to exclude pulmonary hemosiderosis \n\u2022 U/A for hematuria or hemosiderinuria \n\u2022 Pelvic \u2013 gynecologic studies  \n\u2022 Cr- labeling of RBCs with 5 day collection of stools \n\u2022 Upper and lower GI radiologic and Endoscopic studies  \n\u2022 Bronchoscopy \n \nDifferential diagnosis of hypochromic, microcytic anemia   \nA. With \u2193 body iron stores \u2013 IDA \nB. With normal body or \u2191 body iron store \ni) Impaired iron metabolism: Anemia of chronic diseases (ACD) \nii) Disorder of globin synthesis: Thalassemia iii) Disorders of hem synthesis: sideroblastic anemia \niv) Both impaired iron metabolism and defecti ve globin synthesis:  lead poisoning  \n \nTreatment of Iron deficiency Anemia  \n1. Identify underlying cause and treat it  \n2. Correct anemia  and replenish stores  by oral iron,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa90-7265-11ef-bd6f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 412, "chroma:document": "iv) Both impaired iron metabolism and defecti ve globin synthesis:  lead poisoning  \n \nTreatment of Iron deficiency Anemia  \n1. Identify underlying cause and treat it  \n2. Correct anemia  and replenish stores  by oral iron, \n\u2022  Ferous sulfate 300mg (60 mg elemental iron)   3x/day for  4-6 months"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa91-7265-11ef-8764-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 413, "chroma:document": "Internal Medicine \n \n 398Absorption increased by  giving between meals, but side effects are less if \ngiven with meals  \nCommon Side effects ; GI upset, nausea, dyspepsia, constipation /diarrhea. If \nthe side effects are not tolerable, reduced dose or change brand e.g. to ferrous gluconate or ferrous lactate syrup.  \n\u2022 Response to treatment;  an expected daily rise of hemoglobin by 0.1-0.2 gm /dl \nin  \n\u2022 Follow-up ; reticulocytosis will start at 3-4 days and peak on the 10\nth day of \ninitiation of treatment. \n\u2022 An increase in Hgb concentration of at least 2gm/dl after 3wks of therapy is \nconsidered as a good response. \n\u2022 Treatment should be continued for about 3 months after resolution of anemia to \nreplenish the iron store. \nInadequate  response  may imply \n\u2022 Continuing hemorrhage  \n\u2022 non compliance to therapy \n\u2022 Wrong diagnosis \n\u2022 Mixed deficiency \u2013 associated folate or vit.B 12 deficiency  \n\u2022 Another cause for anemia e.g. malignancy, inflammation  \n\u2022 Malabsorption \u2013 rare cause \n\u2022 Use of slow release preparations  \nParentral iron  \n Indications:  \n1. Oral Iron intolerance despite modification in dosage regimen \n2. Malabsorption 3. Inability or unwillingness to take orally  \n\u2022 Iron-dextran  complex  or iron sorbitol  citrate  can be used Intra-muscularly or intra-venous \nroute. \nDose (ml)  = 0.0442 (desired Hgb \u2013 Observed Hgb.) X weight (Kg.) + (0.26 x weight Kg.) \n \nB)  Anemia of chronic diseases (ACD)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa92-7265-11ef-918f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 413, "chroma:document": "\u2022 Iron-dextran  complex  or iron sorbitol  citrate  can be used Intra-muscularly or intra-venous \nroute. \nDose (ml)  = 0.0442 (desired Hgb \u2013 Observed Hgb.) X weight (Kg.) + (0.26 x weight Kg.) \n \nB)  Anemia of chronic diseases (ACD) \nIt occurs in association with a variety of chronic inflammatory and malignant diseases."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa93-7265-11ef-8416-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 414, "chroma:document": "Internal Medicine \n \n 399Etiologies   \n1) Chronic inflammatory diseases  \na) Infections e.g. pulmonary abscess, TB, Osteomyelitis, pneumonia, bacterial \nendocarditis  \nb) Non infectious , e.g. Rheumatoid arthritis, SLE (systemic lupus erythematous) and other \nconnective tissue diseases, sarcoidosis, Crohn\u2019s disease  \n2) Malignant diseases  \nE.g. carcinoma, lymphoma, sarcoma  \n Characteristic features are: \n\u2022 NCNC or mildly hypochromic indices and red cell morphology  \n\u2022 Mild and non progressive anemia (Hgb rarely < 9.0g/dl) : Severity being related to \nseverity of underlying disease \n\u2022 Both serum iron and TIBC are reduced \n\u2022 Serum ferritine is normal or raised and  \n\u2022 Bone marrow storage  iron is normal but erythroblast iron is reduced  \n \nPathogenesis is related to release of cytokines which mediate \n\u2022 Decreased release of iron from macrophages to plasma,  \n\u2022 reduced RBC life span ( \u223c 80 days) in effective erythropoiesis  \n\u2022 Inadequate erythropoietin response to anemia  \nTreatment of Anemia of Chronic Dideases: \n1. Correction of underlying disease \n2. Erythropoietin (40-80 % success rate) \n3. Correction of reversible contributors (iron, folate, cobalamine supplements if necessary) \n \nC) Sideroblastic anemia: \n\u2022 Refractory anemia with hypochromia with \u2191 marrow iron  \n\u2022 Many pathological ring sideroblasts are found in the bone marrow  \n\u2022 Is caused by defect in hem synthesis  \nClassification: \n\u2022 Hereditary (sex linked recessive trait) \n\u2022 Acquired"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa94-7265-11ef-9825-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 415, "chroma:document": "Internal Medicine \n \n 400o Primary :Myelodysplasia  \no Secondary : \n- Malignant diseases of the marrow  \n- Drugs e.g. cycloserin alcohol, lead \n- Others: hemolytic anemia, megaloblastic anemia, malabsorption  \n\u223c 15% of marrow erythroblasts are ring sideroblasts in hereditary and 10 acquired forms.  \nLead poisoning  \n\u2022 Inhibits both hem and globin synthesis  \n\u2022 Interferes with breakdown of RNA by inhibiting the enzyme pyrimidine- 5 \nnucleotidase \u21d2 accumulation of denatured RNA in red cells giving rise to Basophilic \nstippling . \n\u2022 Hypo chromic/Hemolytic anemia with bone marrow ring sideroblasts \n\u2022 Free erythrocyte protoporphyrin is raised  \nManagement:  \n\u2022 Pyridoxine, folic acid therapy : may bring some response  \n\u2022 Repeated transfusion is ultimate choice  \n \nII. Macrocytic Anemia \nLearning objectives : at the end of the student will be able to:- \n1. Define Megaloblastic anemia (MA) \n2. Understand the pathogenesis of Megaloblastic anemia (MA) 3. List causes of Megaloblastic anemia (MA) \n4. Compare and contrast various forms of MA \n5. Identify the possible underling cause of Cobalamine deficiency 6. Understand the management of Megaloblastic anemia and asses response to therapy \nproperly \n \nMegaloblastic Anemia and other Macrocytic Anemia \n Pathogenesis : It\u2019s a descriptive morphologic term in which maturation of the nucleus is delayed"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa95-7265-11ef-a892-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 415, "chroma:document": "properly \n \nMegaloblastic Anemia and other Macrocytic Anemia \n Pathogenesis : It\u2019s a descriptive morphologic term in which maturation of the nucleus is delayed \nrelative to that of cytoplasm. The delay in maturation of the nucleus is attributed to defective DNA synthesis. This condition leads to Megalobl astic marrow and ineffective erythropoiesis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d3fa96-7265-11ef-81c5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 416, "chroma:document": "Internal Medicine \n \n 401The immature erythroblasts are destroyed within the bone marrow leading (Intramedulary \nhemolysis) which results Megaloblastic anemia .  \nEtiologies of megaloblastic anemia  \n1. Vitamin B 12 deficiency  \n2. Folate deficiency 3. Abnormalities of vitamin B\n12 or folate metabolism, transcobalamine deficiency,  \nantifolate-drugs  \n4. Other defects of DNA synthesis: congenital enzyme deficiency, alcohol, treatment with \nhydroxyurea, etc. \nCells primarily affected are those with rapid turnover: \n\u2022 Hematopoietic cells (RBCs, granulocytes, megakaryocytes) \n\u2022 Cells derived from Respiratory tract and  GIT etc \nMacrocytic RBCs appear before the onset of anemia  \n Table VI-1-2 Difference in between Cobalamine and Folate physiology and daily \nrequirement   \nFeature  Cobalamine  Folate  \nSource Animal products (meat, diary \nproduct) Vegetables, fruits  and  \nanimal product  \nDaily requirement 2-5 \u00b5g   100 mg (50-200mg) \nBody store 3-5(4) mg 5-20 mg \nTime to develop anemia after the underlying cause for deficiency  3-4 years 4-6 months \nCooking Little effect easily destroyed \nPlasma transport Specifically bound by \nTranscobalamine ( Tc. I, II, III) 2/3 easily bound to albumin, 1/3 is free \nUsual therapeutic form Hydroxocobalamine   Folic acid"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4208a-7265-11ef-8c18-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 417, "chroma:document": "Internal Medicine \n \n 402Causes of Vit. B 12 deficiency  \n1) Nutritional : especially in vegans  \n2) Malabsorption  \na) Gastric causes  \ni) Adult (addisonian) pernicious anemia  \nii) Congenital lack or abnormality of intrinsic factor  iii) Total or partial gastrectomy  \nb) Intestinal causes  \ni) Intestinal stagnant loop syndrome, jejunal diverticulosis, blind loop, stricture etc. \nii) Chronic tropical sprue  iii) Ileal resection and Crohn\u2019s disease  iv) Congenital selective mal absorption with proteinuria  \nv) Fish tapeworm : Diphlobotrium \n \nPernicious anemia: \nResults from immunologic destruction of the Parietal cells in the stomach, which produce \nintrinsic factors, as in chronic atrophic gastr itis, which results impaired production of intrinsic \nfactors. Nearly 90% of patients show parietal ce ll antibody, 50% have type I or blocking antibody \nto intrinsic factor (IF) and 35% show type II or precipitating antibody to IF. \n\u2022 MCV is increases  \n\u2022 Bone marrow : Hyper cellular and megaloblasts \n\u2022 Peripheral film : neutrophilic hypersegmentation indicated by  \n 1 neutrophil with 7 segments  \n 2-3 neutrophils with 6 segments or    \n > 5 neutrophils with 5 segments  To differentiate from folate deficiency biochemical tests should be done: \n\u2022 Serum folate would be normal in patients given over-night dose or  \n\u2022 Determination of RBC folate level  \nSchilling test (3 phases)  helps to identify the underlying cause of Vit.B\n12 deficiency."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4208b-7265-11ef-9ed0-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 417, "chroma:document": "\u2022 Serum folate would be normal in patients given over-night dose or  \n\u2022 Determination of RBC folate level  \nSchilling test (3 phases)  helps to identify the underlying cause of Vit.B\n12 deficiency. \n1) Radioactive cobalamine is given orally + un labeled cobalamine intra muscularly (to saturate \nbody needs). Then 24 hours urine cobalamine excr etion is should be determined . Normally \n>8% should be excreted. If the excretion rate is < 8% , it may indicate malabsorption to Vit B\n12 ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4208c-7265-11ef-a5f8-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 418, "chroma:document": "Internal Medicine \n \n 4032)    Labeled cobalamine  bound to IF is given orally  \nIn pernicious anemia Vit B 12 absorption is corrected i.e. the daily urinary excretion rate is \n>8% \nIn patients with abnormal in terminal ileum or pancreatic insufficiency Vit B 12 absorption will \nnot be corrected  \n3) Phase 2 repeated after 2 weeks of antibiotics  \n\u2022 Vit B 12 absorption is corrected in patients with bacterial over growth such as (blind loop \nsyndrome) \n\u2022 Administration of pancreatic extract corrects pancreatic insufficiency. \n\u2022 Lack of/by pass of ileal intrinsic factor receptor (terminal ileal disease) or defective trans \nenterocyt cobalamine transport can\u2019t be corrected. \n \nTreatment of megaloblastic anemia  \n1. Vit B12 Deficiency:   is treated with  Hydroxocobalamine  which is given parentraly   \n\u2022 Dose: Initial dose: 6 x 1000 \u00b5g over 2-3 weeks and Maintenance : 1000 \u00b5g every 3 \nmonths \n\u2022 Prophylactic therapy  is indicated in patients with Total gastrectomy and Ileal resection \n2. Folate deficiency:  is treated with Folic acid preparation which is given orally   \n\u2022 Dose : 5 mg Po daily  \n\u2022 Prophylactic therapy  is indicated in pregnancy, sever hemolytic anemia, in patients \nwith dialysis, and premature newborns  \n3. Additional measures: \n\u2022 Correct underlying cause \n\u2022 Antibiotics for bacterial over growth and treatment of fish tapeworm  \nResponse to therapy  \n\u2022 Feeling of general well being is restored  in 48 hrs  \n\u2022 Reticulocytosis begins in 3-4 days and peaks in 7-10 days."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4208d-7265-11ef-a772-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 418, "chroma:document": "\u2022 Correct underlying cause \n\u2022 Antibiotics for bacterial over growth and treatment of fish tapeworm  \nResponse to therapy  \n\u2022 Feeling of general well being is restored  in 48 hrs  \n\u2022 Reticulocytosis begins in 3-4 days and peaks in 7-10 days. \n\u2022 If both folate and cobalamine deficiency present give cobalamine first"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4208e-7265-11ef-9f30-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 419, "chroma:document": "Internal Medicine \n \n 404References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of In ternal medicine, 16th Edition,  Anemia,      \npages 586-624.  \n2) Myers R. Allen, National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Anemia,  pages 109-115."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4208f-7265-11ef-bfe3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 420, "chroma:document": "Internal Medicine \n \n 4052. Leukemias \n \nLearning Objective: At the end of this unit the student will be able to \n1) Define leukemia   2) Classify the different types of leukemias    3) Describe the possible etiologies and epidemiology of leukemia. \n4) Identify the clinical features of leukemia \n5) Make presumptive diagnosis and refer to hospitals where special investigations can be \ndone \n \nDefinition \n\u2022 Leukemias are neoplasms of hematopoitic cells proliferating in the bone marrow initially \nand then disseminate to peripheral blood,  lymph nodes, spleen, liver etc.   \n\u2022 Lymphomas differ from leukemias in that, lymphomas arise primarily from lymph nodes \nbut spread to blood and bone marrow only in \"leukemic phase\u201d of the diseases. \nClassification of leukemias - is based on \n1. Cell of origin : there are two types of leukemias \n\u2022 Lymphoid leukemias \n\u2022 Myeloid leukemias \n      2. Clinical course of the disease  - two forms of presentation of leukemias \n\u2022 Acute leukemias \n\u2022 Chronic leukemias \nThus, combining the above two criteria, there are have 4 main types of leukemias \nA) Acute lymphoblastic leukemia (ALL) \nB) Chronic lymphoid leukemia (CLL) \nC) Acute myelogeneous leukemia (AML) \nD) Chronic myeloid leukemia (CML) \nEtiology \nThe etiologies of leukemias are unknown in most of the cases. But studies have demonstrated \nthat both genetics and environmental factors are important in the causation of these diseases. 1. Genetics"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42090-7265-11ef-acbd-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 420, "chroma:document": "D) Chronic myeloid leukemia (CML) \nEtiology \nThe etiologies of leukemias are unknown in most of the cases. But studies have demonstrated \nthat both genetics and environmental factors are important in the causation of these diseases. 1. Genetics \n\u2022 There is a greatly increased incidence of leukemia in the identical twin of patients \nwith leukemia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42091-7265-11ef-a415-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 421, "chroma:document": "Internal Medicine \n \n 406\u2022 Increased incidence of leukemia also occurs in people with chromosomal \nabnormalities such as Down\u2019s syndrome (trisomy 21).  \n2. Environmental factors like \n\u2022 Ionizing radiation : The relation between acute leukemia and ionizing radiation, has \nbeen established in those having occupational radiation exposure, patients receiving \nradiotherapy and Japanese survivors of atomic bomb explosions.  Radiation \nexposure increases the risk of CML, AML and ALL.  No known relation with CLL. \n\u2022 Chemicals  like benzene, aromatic hydrocarbons, and treatment with alkylating \nagents and other chemotherapeutic drugs.  Exposure to such chemicals is associated with increased risk of developing AML. \n\u2022 RNA based retroviruses Infection with HTLV - I is related to human T-cell leukemia & similarly Epstein Barr virus is related to ALL (T\n3 subtype) and aggressive lymphoma. \n \nEpidemiology \n\u2022 Globally the incidence of all leukemias is 13/100,000/ year usually affecting men more \nthan women.   \n\u2022 Certain leukemias are more common in a particular age group than the other, i.e. acute \nlymphoblastic leukemia (ALL) is common in children and young adults whereas AML, \nCLL and hairy cell leukemia are common in adults with peak between the 6th & 7th \ndecade.  \n\u2022 A Study conducted in one of the teaching hospitals in Ethiopia has shown that leukemias \nwere the commonest, accounting for about 35.5% of hematological admissions and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42092-7265-11ef-80a7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 421, "chroma:document": "decade.  \n\u2022 A Study conducted in one of the teaching hospitals in Ethiopia has shown that leukemias \nwere the commonest, accounting for about 35.5% of hematological admissions and \nacute leukemias were the leading cause of mortality, accounting for 78.1%of all \nhematological deaths.     \n \n Acute Leukemias  \nAcute leukemias are characterized by the presence of immature white blood cells in the marrow and peripheral blood.  \nThere are two types of acute leukemias: \n1. Acute lymphoblastic leukemia ( ALL ) \n2. Acute myeloblastic leukemia ( AML ) \nSuch a classification of acute leukemias and further sub typing is done by using"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42093-7265-11ef-b565-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 422, "chroma:document": "Internal Medicine \n \n 407\u2022 Morphology of the cells \n\u2022 Immuno-phenotypic characteristics \n\u2022 Cytochemical characteristics \nDifferentiation between ALL and AML is critical because the two have different  \n\u2022 Natural history \n\u2022 Prognosis \n\u2022 Response to treatment \n \nA) Acute lymphoblastic leukemia (ALL) \nIs common in children:  85 % of cases of ALL occur in children, and 90 % of leukemia that occur \nin children is ALL. \nLymphoblasts are abnormal white blood cells that are found both in the bone marrow & the peripheral blood of patients with ALL. They are characterized by\n \n\u2022 Smaller size (10-15mm) than myeloblasts \n\u2022 Thin rim of dark blue cytoplasm with no granules \n\u2022 Nucleus is round or convoluted, and centrally located and has 1 or 2 nucleoli \nwhich are less prominent \nMorphologically ALL is categorized into 3 subtypes (FAB classification) \n1) L1 homogeneous population of small cells (childhood), a small nucleolus \n2) L2 - more heterogeneous population of larger cells (more often seen in adults) with \u2265 \n1 prominent nucleoli \n3) L3 - uncommon (constituting <5% of ALL), more mature subtype, large vesicular \nnucleus with basophilic often vacuolated cytoplasm.  \nImmuno phenotypic classification  of ALL  \n1) Common ALL  (L1, L2) account 75% of ALL, derived from precursors of B-cell. \n2) T-ALL  (L1, L2) account for 20%of ALL: common in adolescent males, associated with \nhigh WBC count, anterior, mediastinal  mass and central nervous system \ninvolvement."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42094-7265-11ef-8f31-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 422, "chroma:document": "2) T-ALL  (L1, L2) account for 20%of ALL: common in adolescent males, associated with \nhigh WBC count, anterior, mediastinal  mass and central nervous system \ninvolvement. \n3) B-cell ALL  (L 3) accounts for 5% ALL. Extramedullary presentation with metabolic \nabnormality."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42095-7265-11ef-83bb-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 423, "chroma:document": "Internal Medicine \n \n 408B) Acute myeloblastic leukemia(AML) \nMyeloblasts are abnormal cells that predominantly make up AML. These cells are larger than \nlymphoblasts   and have:- \n\u2022 Lower nuclear to cytoplasmic ratio \n\u2022 Prominent multiple nucleoli \n\u2022 Auer rods (stick like structures in the cytoplasm)  in 50% of AML  \n\u2022 Granules in the cytoplasm \n \nThe FAB group divided AML into 8 subtypes based on \n1. Degree of differentiation 2. Maturation of predominant cells towards granulocytes, monocytes erythrocytes or \nmegakaryocytes \nSubtypes of AML \n1) M\n0 (also called undifferentiated AML)  \n- Composed of primitive cells without cytochemical stains \n- Account for 3% of AML  \n2) M 1 (AML without maturation)  \n- Few if any azurophilic granules \n- Account for 20% of AML \n3) M 2 (AML with maturation)  \n- Blasts with promyelocytic granules  \n- Auer rods present \n- Strong avidity to perixidase and Sudan black   \n- Account for  25% of AML \n4) M 3 (promyelocytic leukemia)  \n- Hyper granular promyelocytes often with   \n- Auer rods per cell \n5) M 4 (Acute myelomonocytic leukemia)  \n- Monocytoid appearing cells in peripheral blood. \n- Strong avidity to non-specific esterase  \n- account for  20% of AML \n- M 5 (acute monocytic leukemia)  \n- 2 subtypes"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42096-7265-11ef-84e4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 424, "chroma:document": "Internal Medicine \n \n 4096) M5a \u2013 undifferentiated M5b - differentiated with 80% promyelocytes and  monocytes                         \n- Both have avidity to non specific esterase and account for 20% of AML \n7) M 6 (acute erythroleukemia)  \n- Erythroblasts are more than 50% of all nucleated cells \n- Avidity to periodic acid Schiff stain \n- Account for  5% of AML \n8) M 7 (acute megakaryocytic leukemia)  \n- Megakaryoblasts are more than 30% of all nucleated cells                    \n- Account for 5% of AML.  \n- Activity to PAS. \nPathophysiology \nAcute leukemias are characterized by clonal proliferation of immature hematopoietic cells.  The \nmost important characteristic is a defect in maturation beyond the myeloblast or promyelocyte \nlevel in AML, and beyond lymphoblast in ALL. Proliferation of these immature cells in the bone marrow leads to  \n\u2022 Appearance of these blast cells in the ci rculation where they aren't normally seen and \nocclusion of microcirculation by blast cells (leukostasis) \n\u2022 Infiltration of the tissues i.e. lymph nodes liver, spleen, skin, gum, viscera and central \nnervous system etc - causing enlargement  of lymph nodes, liver, spleen, gum etc. \n\u2022 Accumulation of blasts in the bone marrow has two major effects on the normal blood \ncell formation (hematopoisis) causing bone marrow failure.   \no They suppress the normal hematopoisis \no They replace the normal elements in the bone marrow"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42097-7265-11ef-9953-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 424, "chroma:document": "\u2022 Accumulation of blasts in the bone marrow has two major effects on the normal blood \ncell formation (hematopoisis) causing bone marrow failure.   \no They suppress the normal hematopoisis \no They replace the normal elements in the bone marrow  \nThese bone marrow changes will decrease the normal blood cells in the circulation and cause \no Infection  - due to decreased WBC \no Anemia - due to decreased RBC \no Bleeding - due to decreased platelets \nClinical Features ALL and AML share many clinical features.  In the majority of cases the initial symptoms are present for less than 3 months and are the consequence of bone marrow failure, i.e. \n\u2022 Symptoms of anemia  such as tiredness, weakness, shortness of breath on exertion \n\u2022 Recurrent infection  of any part of the body is common due to  \no Low neutrophil count in the circulation"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42098-7265-11ef-ab2c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 425, "chroma:document": "Internal Medicine \n \n 410o Functionally abnormal neutrophils \no Disruption of mucosal barriers \n\u2022 Bruising and/or bleeding  related to low platelet count \n\u2022 Occasionally, lymph node enlargement  and/or symptoms relating to enlargement of \nthe liver and spleen. \n\u2022 Symptoms related to hypoperfusion of the lungs and brain due to occlusion of \nmicrocirculation of these organs by blast cells. \nPhysical findings:  but some patients may have \n\u2022 Pallor \n\u2022 Bruises, petechial hemorrhages, purpura \n\u2022 Signs of infection like fever \n\u2022 Peripheral lymphadenopathy in ALL, not common in AML \n\u2022 Enlarged liver and spleen in ALL and small percentage of AML \n\u2022 Testicular involvement in ALL (T. variant) \n\u2022 Bone pain and sternal tenderness which are due to expanding malignant cell mass, \noccur in more than half of the patients with acute leukemias. \n\u2022 Symptoms related to involvement of the c entral nervous system (meningitis, etc) and the \nkidneys. \nLaboratory Investigation \nThe definitive diagnosis of acute leukemia is made on the basis of peripheral blood film and \nbone marrow aspirate examination. The following tests should be done to detect the disease & \nother associated abnormalities.    \n1) Complete blood count will show \n\u2022 Hemoglobin -low \n\u2022 WBC count -often very high, but occasionally decreased or normal  \n\u2022 Platelet count -low \n2) Peripheral blood film  shows characteristic leukemic cells, which are distinct from each other \nmorphologically, i.e."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d42099-7265-11ef-8193-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 426, "chroma:document": "Internal Medicine \n \n 411Table VI-2-1 Showing the main features of acute leukemic cells \n \n Lymphoblast  Myeloblast  \n \nCell size  Smaller  Larger  \nNucleus shape  Round , central  Irregular, eccentric  \nNucleoli  1 or 2 in number and not prominent\n More than two & prominent  \nAuer rods  absent  Present in 50%  \nCytoplasm  Dark blue rim  Pale blue, granular  \n \n3) Bone marrow aspiration  is mostly done on the sternum using a special needle and a smear \nprepared and stained  with Wright stain , shows  \n\u2022 Increased cellularity with abnormal lymphoid or myeloid blast cell population. \n\u2022 Replacement of the normal bone marrow elements \n  Management of acute leukemias \nA) Chemotherapeutic agents , that have the capacity to kill leukemic cells, are used to treat \nleukemia.  \nChemotherapy  of acute leukemia\u2019s is divided in to four phases  \na. Remission induction  is characterized by intensive syst emic chemotherapy with the goal of \nreducing leukemic cell below the level of clinical detection called complete remission. \nb. Consolidation/ early  intensification  phase   \nAfter complete remission if there is no further  treatment given, leukemia cells will expand \nand lead to relapse. In this phase intensive chemotherapy is given. \nc. Maintenance phase  here lower dose chemotherapy is  given over several years. \nd. Central nervous system prophylaxis  in this phase local chemotherapy or radiation is \ngiven to sites of frequent relapse like CNS. This prevents leukemic meningitis."}


created_at: 2024-09-14 06:50:03
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id: 71d4209a-7265-11ef-84c5-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 426, "chroma:document": "d. Central nervous system prophylaxis  in this phase local chemotherapy or radiation is \ngiven to sites of frequent relapse like CNS. This prevents leukemic meningitis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4209b-7265-11ef-94b1-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 427, "chroma:document": "Internal Medicine \n \n 412Table VI-2-3. The treatment of acute leukemias (Cytotoxic drugs & phases of treatment).  \n  \nPhase of treatment  ALL AML \nRemission induction  Combination of vincristine \nPrednisolone and L asparaginase Daunorubucin for 4 weeks\n Daunorubucin+ cytosine arabinoside 4weeks (called 3+7 regimen\n \nContinuation/intensification phase\n Combination of 6-mercaptopurine & methotrexate+ Bone marrow transplantation\n 2-3 intensive cycles of the same as above or high dose of cytosine arabinoside+ bone marrow transplantation for young patients\n \nCNS prophylaxis  Radiation to the whole brain Combined with intra-thecal methotrexate (given by lumber puncture)\n No benefit because CNS relapse occurs only with systemic relapse. Therefore, it is not given. \n \nMaintenance  oral 6 -mercaptopurine &  Methotrexate\n No benefit  \n \nB) Supportive treatment  is applicable for both ALL & AML  \nb) For patients with severe anemia and thrombocytopenia  (especially platelet count \nbelow 20,000 /ML with the risk of bleeding) may be transfused with whole blood and platelet concentrates. \nc)  Infections are common in acute leukemias .  \nAppropriate preventive measures  should routinely be employed to prevent infections \nin such immunocompromised patients. These include   \n\u2022 Isolation of staff and visitors by the use of face masks  \n\u2022 Practice careful hand washing before coming in contact with the patient  \n\u2022 Advise the patient to eat only cooked foods"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4209c-7265-11ef-b440-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 427, "chroma:document": "in such immunocompromised patients. These include   \n\u2022 Isolation of staff and visitors by the use of face masks  \n\u2022 Practice careful hand washing before coming in contact with the patient  \n\u2022 Advise the patient to eat only cooked foods  \nWhen infections occur , gram negative sepsis is the commonest presentation, which \nrequires prompt evaluation and empirical antibi otic treatment until definitive diagnosis is \nmade by blood culture, after which the antibiotic(s) can be modified depending on the organism identified & its drug sensitivity."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 428, "chroma:document": "Internal Medicine \n \n 413Chronic Leukemias \n There are two main types of chronic leukemias \n1) Chronic lymphocytic leukemia \n2) Chronic myelocytic leukemia \n \nC) Chronic lymphocytic leukemia (CLL) \n \nDefinition:  \n\u2022 It is an incurable disease of older people characterized by an uncontrolled proliferation \nand accumulation of mature B-lymphocytes (98% of CLL) and T-lymphocytes in rare \ninstances. \n\u2022 Although, the disease remains asymptomatic in a proportion of cases; symptoms of \nanemia, infections and bleeding resulting from bone marrow failure are common in the majority of patients at presentation. \nClassification : FAB suggested 3 types of CLL \n1. Typical CLL: - where more than 95% of lymphocytes in the blood are small \nlymphocytes. \n2. Prolymphocytic CLL:-  If \u2265 51% of lymphocytes in the blood are prolymphocytes \n3. Atypical CLL  :- if < 10% of lymphocytes in the blood are small lymphocytes \nClinical Features \nIn 25% the diagnosis is made incidentally in asymptomatic individuals when WBC count is done \nfor other reasons.  However, the majority will have signs and symptoms resulting from:- \n1) tissue infiltration by leukemic cells \n2) Bone marrow failure with peripheral blood cytopenias and immune suppression. \nSymptoms   \nCLL is a disease of older adults and commonly present with  \n\u2022 Recurrent infections resulting from neutropenia & reduced immunoglobulin levels. \n\u2022 Symptoms of anemia \n\u2022 Painless lymph node enlargement \n\u2022 Spleen and liver enlargement \nSigns \n\u2022 Anemia"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 428, "chroma:document": "\u2022 Recurrent infections resulting from neutropenia & reduced immunoglobulin levels. \n\u2022 Symptoms of anemia \n\u2022 Painless lymph node enlargement \n\u2022 Spleen and liver enlargement \nSigns \n\u2022 Anemia \n\u2022 Enlarged lymph nodes, liver and/or spleen"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 429, "chroma:document": "Internal Medicine \n \n 414Laboratory Investigation  \n1. CBC  \n\u2022 Hemoglobin  is low or normal  \n\u2022 WBC count > 15,000/mm3  , of which 40% are lymphocytes, with a  minimum of \n5000/ mm3 mature lymphocytes in the circulation  \n\u2022 Platelets are low or normal \n2. Bone marrow  30% of the cellular elements would be mature B cells \n3. Serum immunoglobulins  are  low or normal \n4. Coomb's test  is positive in the presence of hemolysis. \n \nPromyelocytic leukemia differs from the ty pical CLL described above in that the disease \ncommonly present with \n\u2022 Massive spleen enlargement but no lymphadenopathy  \n\u2022 Very high WBC count (> 200,000/L) \n\u2022 Poor response to treatment \n\u2022 The cells are B cells, but they are larger  in size and have prominent nucleoli. \nStaging of CLL \nClinical course of the disease is variable, and prognosis is correlated directly with the stage of \nthe disease.  There are two different staging classifications i.e. \n1) RAl staging classification of CLL \nStage 0 : Lymphocytosis only (in blood and bone marrow)  \nStage I:  Lymphocytosis with lymphadenopathy  \nStage II : Lymphocytosis with liver and/or spleen enlargement \nStage III:  Lymphocytosis with anemia (Hgb <11 gm/dl) \nStage IV : Lymphocytosis with thrombocytopenia (platelets < 100,000/ L) \n Lymphocytosis is defined as  WBC count > 15,000/ L, of which 40% are lymphocytes \n \n2) Binet staging classification of CLL \n Stage A = < 3 involved lymphoid areas Hgb>10g/dl"}


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": 429, "chroma:document": "Stage IV : Lymphocytosis with thrombocytopenia (platelets < 100,000/ L) \n Lymphocytosis is defined as  WBC count > 15,000/ L, of which 40% are lymphocytes \n \n2) Binet staging classification of CLL \n Stage A = < 3 involved lymphoid areas Hgb>10g/dl \n Stage B= >3 involved lymphoid areas Platelets < 100,000/ L  Stage C = Any number of involved Hgb < 10 g/dl and/or Platelets < 100,000/ L         lymphoid areas"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 430, "chroma:document": "Internal Medicine \n \n 415NB: The cervical, axillary and inguinal lymph node groups (unilateral or bilateral), the spleen \nand the liver each counted as one area.  \nPrognosis \n\u2022 Stage 0 and 1 CLL has good prognosis. If a patient has stage 0 disease without \nother poor prognostic factors, the median survival would be more than 10 yrs without \ntreatment. \n\u2022 Stage II has Intermediate prognosis - median survival is 5 yrs \n\u2022 Stage III and IV has  worse prognosis - Median survival  is 3 years \n \nTreatment  \nPatients with CLL should be referred to centers where they can be treated and followed.  \nThe disease may remain stable for several years without treatment. Therefore, no \nadvantage in starting drugs before there is any clinical indication for treatment: \n \nIndication for initiating treatment include:  \n1) Hemolytic anemia 2) Cytopenias (neutropenia, thrombocytopenia, etc) with recurrent infections, bleeding \n3) Disfiguring lymphadenopathy 4) Symptomatic organomegally 5) Marked systemic symptoms 6) Advanced disease \n When treatment is required alkylating agents are often the drugs of choice: \n1) Chlorambucil: is given as small daily doses or larger pulse (intermittent) every 3-6 wks \nor \n2) Cyclophosphamide is also used in the same way (daily or pulses) \n3) Steroids (prednisolone) can be used in CLL if the patient develops autoimmune hemolytic anemia, autoimmune thrombocytopenia etc  \nOther modalities of treatment  which are rarely employed include"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 430, "chroma:document": "3) Steroids (prednisolone) can be used in CLL if the patient develops autoimmune hemolytic anemia, autoimmune thrombocytopenia etc  \nOther modalities of treatment  which are rarely employed include \n\u2022 Combined chemotherapy (similar to ly mphoma) is used for advanced disease  \n\u2022 Splenectomy/splenic irradiation \n\u2022 IV immunoglobulin for life threatening 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": 431, "chroma:document": "Internal Medicine \n \n 416Response to treatment can be assessed by \n\u2022 Declining WBC count \n\u2022 Increase Hgb, platelet count \n\u2022 Decrease size of Lymph nodes  \n \nD) Chronic Myelocytic Leukemia (CML) \n \nDefinition : It is disease of older adults and characterized by clonal expansion of hematopoitic \ncells of myliod origin, possessing Philadelphia chromosome .  It has a progressive clinical course \nwith three phases starting with chronic phase and evolving to accelerated phase and then to \nblast transformation. \n \nEpidemiology \nThe incidence of CML is 1.3/100,000 population /year, with men more affected than women, \nincreasing slowly with age until middle forties when the incidence rises rapidly.   \nIn the majority of cases the etiology is unknown.  However, CML has been one of the leukemias \nobserved to have an increased prevalence fo llowing atomic explosion at Hiroshima and \nNagasaki.  \nClinical Features \nThe clinical features of CML depend on the stages of the disease, and range from early \nasymptomatic phase to severe manifestations of the accelerated phase and blast transformation.  Therefore, manifestation can be described as follows:-  \n1. Chronic Phase: \n\u2022 The onset is insidious and some patients can be diagnosed while asymptomatic \nduring health screening visits.   \n\u2022 Others may present with fatigue, anemia, night sweating, fever, weight loss and \nsymptoms related to enlarged spleen i.e. left upper abdominal dull pain and early satiety."}


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": 431, "chroma:document": "during health screening visits.   \n\u2022 Others may present with fatigue, anemia, night sweating, fever, weight loss and \nsymptoms related to enlarged spleen i.e. left upper abdominal dull pain and early satiety.   \n\u2022 A few cases may show symptoms related to granulocytic or platelet dysfunction \ni.e. recurrent infections and thrombosis manifesting commonly with persistent \npainful erection of the penis (priapism) and cerebrovascular accidents."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 432, "chroma:document": "Internal Medicine \n \n 4172. Accelerated phase and blast transformation(or blast crisis) \nWith progression of CML from chronic phase to accelerated phase and then to blast \ntransformation patients will present with severe symptoms such as  \n\u2022 Unexplained fever \n\u2022 Progressive weight loss \n\u2022 Bone and joint pain \n\u2022 bleeding/ thrombosis \n\u2022 Recurrent infections \n\u2022 Increasing dose requirement of the drugs used for controlling the disease  \n\u2022 10-15% of patients may present for the first time with either the accelerated phase or \nblast transformation. \nPhysical examination may show \n\u2022 In the early stage 90% of or more of the cases may show  \no Moderately pale conjunctivae \no Enlarged spleen and mild liver enlargement. \n\u2022 Late in the disease process patients may develop \no Lymph node enlargement \no Chloromas \u2013 leukemic deposits on the skin & \no Tender sternum \n \nLaboratory Findings \n1) WBC count is increased of the granulocytic series with variable degrees of maturity i.e. \nmature neutrophils and band forms are seen in the peripheral blood film. Moreover immature granulocytes such as promyelocy tes, myelocytes and metamyelocytes are \nseen in the peripheral film with increased number. Some myeloblasts are also seen, and the percentage of blasts varies according to the stage of the disease, i.e.  \n\u2022 Chronic phase : blasts account for < 5% of granulocytes in the blood \n\u2022 Accelerated phase : blasts account for \n\u2265 15%  but < 30% of granulocytes in the \nblood"}


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": 432, "chroma:document": "\u2022 Chronic phase : blasts account for < 5% of granulocytes in the blood \n\u2022 Accelerated phase : blasts account for \n\u2265 15%  but < 30% of granulocytes in the \nblood  \n\u2022 Blast crisis:  blasts account for \u2265  30% granulocytes in the blood \nPhagocytic function is normal at diagnosis and remains normal in the chronic phase. Basopilia and monocytosis are commonly observed in the accelerated phase & blast transformation."}


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": 433, "chroma:document": "Internal Medicine \n \n 4182)  Patelet count  is elevated \n3)  RBC count  and hemoglobin concentrations are low, presenting with anemia \n4)  Bone marrow  aspiration: shows increased cellula rity primarily of the myeloid and \nmegakaryocytic lineage, but percentage of marrow blasts remains normal or slightly \nincreased   \nDepending on the laboratory findings the three stages can be defined as follows:- \nChronic Phase \n\u2022 <5% of circulating blasts \n\u2022 < 10% blasts + promyelocytes in the blood \n\u2022 Platelets are increased \n\u2022 Mild anemia \n\u2022 Increased cellularity of bone marrow with normal or increased percentage of blasts. \nAccelerated Phase \n\u2022 Worsening anemia \n\u2022 Blasts 15-30% of granulocytes (in the blood or bone marrow) \n\u2022 Blasts and promyelocytes \u2265 30% of granulocytes (in the blood or marrow) \n\u2022 Basophils \u2265 20% of granulocytes \n\u2022 Platelet counts < 100,000/L \nBlast Crisis \n\u2022 Blasts \u2265 30% of granulocytes (in the blood or marrow) \n\u2022 Hyposegmented neutrophils \nBlast cells may be   \n\u2022 Myeloid in 50% (AML) \n\u2022 Lymphoid in 30% (ALL) \n\u2022 Erythroid in 10% (erythroleukemia) \n\u2022 Undifferentiated in 10% \nTreatment \n\u2022 The goal of treatment is complete molecular remission and cure (i.e. achieving \nprolonged, durable non-neoplastic and non clonal hematopoisis).   \n\u2022 The treatment includes the following (used singly or in combination) \n1) Chemotherapy - hydroxyurea or busulphan - used in Ethiopia  \n2) Bone marrow transplantation - the only curative treatment but not available in this \ncountry"}


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": 434, "chroma:document": "Internal Medicine \n \n 4193) Interferon  treatment  \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th \nEdition, Acute and chronic Myeloid leukemia, Malignancies of Lymphoid cells, \npages 631-655. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd \nedition Acute leukemia, 123-126."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 435, "chroma:document": "Internal Medicine \n \n 4203. Lymphomas  \n \nLearning objectives : At the end of this lesson, the student will be able to:- \n1. Define lymphomas \n2. Understand the differentiating features of common lymphomas \n3. Identify clinical features of lymphomas including specific features \n4. Understand the clinical staging of lymphomas with its significance \n5. Principles of management of lymphomas \n Definition:   Malignant transformation of cells resi ding predominantly in lymphoid tissue.  \nLymphoma is broadly classified as  \n\u2022 Hodgkin\u2019s disease \n\u2022 Non-Hodgkin\u2019s lymphomas  \n \nA. Hodgkin\u2019s disease \n \nEpidemiology:  \n\u2022 It has bimodal age incidence (20-30 years and > 50 years).  \n\u2022 In developing countries young adults are commonly affected.  \n\u2022 Male to female ratio = 2:1  \nClinical manifestations \n\u2022 Most patients present with non-tender asymmetrical, firm, discrete and rubbery \nenlargement of superficial nodes: Cervical (60-70%), axillary (10-15%) inguinal (6-12%). Has waxing and waning feature.  \n\u2022 Mild spleenomegaly (50%), mediastinal Lym phadenopathy (6-11%) with or without plural \neffusion and superior venacaval syndrome may be present.  \n\u2022 Constitutional symptoms like fever, weight loss and sweating are common in widespread \ndisease. Fever is found in 30% of patients, and it described as Pel \u2013 ebsteins fever \ncharacterized by weeks of febrile period, interspersed by several weeks of afebrile \nperiod. \n\u2022 Pruritis is seen in 25%of patients"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 435, "chroma:document": "disease. Fever is found in 30% of patients, and it described as Pel \u2013 ebsteins fever \ncharacterized by weeks of febrile period, interspersed by several weeks of afebrile \nperiod. \n\u2022 Pruritis is seen in 25%of patients  \n\u2022 Alcohol induced pain in the affected area"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420ab-7265-11ef-91b6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 436, "chroma:document": "Internal Medicine \n \n 421\u2022 Others symptoms include Weight loss, profuse sweating, weakness, fatigue, anorexia, \ncachexia  \nHematological findings  \n\u2022 Normocytic normochromic  anemia \n\u2022 1/3rd of patients may have leukocytosis \n\u2022 Eosinophila \n\u2022 Lymphopenia may be found in advanced disease \n\u2022 Platelets count is variable (normal or increased in the early stage and decreased in the \nlate stage) \n\u2022 ESR is elevated \n\u2022 Bone marrow involvement \u2013 late in the course  \nImmunologic findings  \n\u2022 Progressive loss of immunologicaly compet ent T-lymphocytes leads to impaired cell \nmediated immunity which increases susceptibility to viral infections ( herpes zoster, \nCMV) and   fungal infections (e.g. Crypto coccus and Candida) infections . Moreover \npatients will have increased risk of reactivation of latent Tuberculosis infection. \n Biochemical findings  \n\u2022 \n\u2191Ca2+ , \u2193 Po 4-3, \u2191Alkaline Phosphatase, \u2191LDH indicates poor prognosis  \n\u2022 Hyperuricemia, \u2191 Transaminases and \u2191 bilirubin.  \nDiagnosis  \n\u2022 Lymph node biopsy:  histological ex amination of an excised lymph node. \n\u2022 Feature: the distinctive multinucleated, polyploidy cell with a characteristic Owel- eye  \nappearing Reed-Stern berg  (RS)  cells on an appropriate inflammatory background. \nClassification  Histologically Hodgkin\u2019s disease is classified in to four groups.  \nThese are listed depending on worsening order of prognosis as follows:  \n1. Lymphocytic predominant \n2. Nodular sclerosis 3. Mixed cellularity 4. Lymphocytic depleted"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 436, "chroma:document": "These are listed depending on worsening order of prognosis as follows:  \n1. Lymphocytic predominant \n2. Nodular sclerosis 3. Mixed cellularity 4. Lymphocytic depleted  \nClinical staging  \nStage 1:   Only affecting one lymph node area"}


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": 437, "chroma:document": "Internal Medicine \n \n 422Stage 2 :  2 or more lymph node areas on the same side of the diaphragm involved  \nStage 3:   Disease involving lymph nodes above and below diaphragm; splenic \ninvolvement is included here. \nStage 4:   Extra-nodal site involvement (Liver, bone marrow and other extra nodal sites) \nDepending on the presence or absence of constitutional symptoms the stages are further \nclassified as A (no constitutional symptoms) and B (presence of constitutional symptoms.) \n \nTreatment  \n1. Radiotherapy  \u2013 mainstay for stage I and II diseases; used for stage III and IV with \nchemotherapy . \n2. Chemotherapy  \n\u2022 Cyclical chemotherapy for stage III and IV diseases  \n\u2022 In stage I and II patient with bulky disease  \nE.g.  - Mediastinal widening by 1/3rd  \nLymph node > 10 cm in diameter \nThe commnly used combinations of chemotherapy include  \no MOPP: mustine, vincristine (oncovine), procarbatine, predinisolone  \no ABVD : adramycin, bleomycine, vinblastin, decarbazine  \no This combination therapy is either used alone or MOPP \u2013 ABVD hybrid given for \n6 cycles (or 4 cycles after full remission). \n3.  Relapse cases are  better treated with autologous Bone marrow transplantation with \ntotal body irradiation and high dose chemotherapy.   \nPrognosis \u2013 depends on stage  \nFive-year survival being  Stages I and II:  85%   Stage   III A:  70%  Stages III B & IV: 50%"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 438, "chroma:document": "Internal Medicine \n \n 423B. Non Hodgkin\u2019s Lymphoma (NHL) \n \nPredisposing diseases/ factors to NHL  \n\u2022 In HIV infected patients there is an increased incidence of lymphoma often at \nunusual sites like CNS; usually B-cell origin with high or intermediate grading. \n\u2022 Immunosuppression  increases the risk of developing  NHL  \n\u2022 Others : Celiac disease, dermatitis herpetiformis and angioimmunoblastic LAP \npredispose to T-cell lymphomas \n\u2022 Infections: e.g. Helicobacter infection  is associated with \u2191 frequency of MALTOMAS \n\u2022 Autoimmune diseases may cause NHL \nClinical features  \n\u2022 Superficial lymphadenopathy with a classic tr iangular  distribution (the three vertexes \nling over the cervical and the two epitroch lear lymph nodes, while the base lies over \nabdominal organs and lymph nodes.)  \n\u2022 Constitutional symptoms are encountered less commonly when compared with HD \nand if present indicates dissemination. \n\u2022 Oro-pharyngeal involvement is seen in 5-10% cases: have involvement of \nWaldeyer\u2019s ring including the tonsils adenoids and paratonsilar areas  \n\u2022 Anemia, neutropenia (infection) and thrombocytopenia may follow - bone marrow  \ninvolvement or may be autoimmune in origin \n\u2022 Abdominal organs and lymphnode involvement is more common in NHL than HD  \n\u2022 Other organs: skin, brain, testis, GIT, or thyroid involvement is frequent.  \nLaboratory findings:   \n1) Hematological findings  \n\u2022 Normocytic normochromic anemia due to autoimmune hemolytic anemia"}


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": 438, "chroma:document": "\u2022 Other organs: skin, brain, testis, GIT, or thyroid involvement is frequent.  \nLaboratory findings:   \n1) Hematological findings  \n\u2022 Normocytic normochromic anemia due to autoimmune hemolytic anemia \n\u2022 Cytopenias or leukoerythroblastic features  \n\u2022 Lymphoma cells in may be seen in the peripheral blood sometimes \n\u2022 Bone marrow biopsy may show focal or diffuse  involvement  \n2) Immunologic markers  are used for classification \n3) Chromosomal findings: various forms of translocations identified \nBlood chemistry  \n\u2022 Uric acid level is elevated \n\u2022 Liver enzymes are abnormally elevated"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 439, "chroma:document": "Internal Medicine \n \n 424\u2022 LDH \u2191 (in rapidly proliferating and extensive disease hence has prognostic \nimplication.) \nPrognostic features: \n\u2022 Histology  \n\u2022 Staging \n\u2022 Age > 60 years \u2013 unfavorable  \n\u2022 Poor performance status \n\u2022 Multiple sites of extra nodal involvement  \n\u2022 \u2191 LDH \n\u2022 Bulky disease (mass > 5 cm in diameter) \n\u2022 Prior history of low grade disease  \n\u2022 AIDS or other causes of imunosupression related \nTreatment  \nLow \u2013 grade  malignancy : \nNo need of treatment if the patient is asymptomatic  \n1) Local radiotherapy  is indicated for stage I, I\u03b5 or stage  II \n2) Combination chemotherapy  for advanced cases \nChlorambucil or cyclophosphamide  or repeated courses of fludarabine  \n3) BMT (bone marrow transplantation) \n4) INF - \u03b1 \nIntermediate \u2013 grade  malignancy  \n Localized disease  \nInitial combination  therapy with CHOP  (cyclophosphamide, Hydroxodunorubicin \n(Adriamycin), Vincristine (oncovin) and prednisolone) followed by irradiation .  \nDisseminated diseases : Combined Chemotherapy is the treatment of choice. \n     \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nMalignacies of Lymphoid cells, pages 641-655."}


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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 440, "chroma:document": "Internal Medicine \n \n 4254.  Disorders of Hemostasis  \n \nBleeding Disorders \nLearning objectives: at the end of this topic students are expected to:-  \n1. Know common causes of hemiostatic disorders \n2. Differentiate clinically between primary and secondary hemiostatic disorders 3. Know possible causes of thrombocytopenia  4. Know clinical approach to a patient with thrombocytopenia  \n5. Understand how to approach a patient with drug induced thrombocytopenia \n6. Be able to recognize cases of ITP and refer to an appropriate set up 7. To be introduced with some of vascular causes of bleeding 8. Know commoner causes of coagulation abnormalities with their peculiarity and similarity   \n \nAbnormal bleeding may be due to:- \n1. Primary haemostatic disorders  : bleeding disorders resulting form either platlet or \nvascular abnormalities  \n\u2022 Vascular disorders \n\u2022 Thrombocytopenia \n\u2022 Functional platelet defect \n2. Secondary haemostatic disorder : resulting from problem in the coagulation pathway \n\u2022 Defective coagulation  \n \n1)  Disorders of the plat elet and vessel wall ( primar y haemostatic disorders) \n\u2022 Patients with platelet or vessel wall disorders usually bleed in to superficial sites such as \nthe skin, mucous membranes, or genitourinary or GI tract.  \n\u2022 Bleeding begins immediately after trauma, and either responds to simple measures such \nas pressure and packing or requires syst emic therapy with glucocorticoids, \ndesmopressin, plasma fractions and platelet concentrate."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420b2-7265-11ef-88f5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 440, "chroma:document": "\u2022 Bleeding begins immediately after trauma, and either responds to simple measures such \nas pressure and packing or requires syst emic therapy with glucocorticoids, \ndesmopressin, plasma fractions and platelet concentrate.  \nCommon platelet vessel wall disorders are: \n\u2022 Thrombocytopenia \n\u2022 Von willebrand\u2019s disease (VWD)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420b3-7265-11ef-87a7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 441, "chroma:document": "Internal Medicine \n \n 426\u2022 Drug induced platelet dysfunction  \n \nPlatelet Disorders  \n\u2022 Platelets are produced from fragmentation of megakaryocytes in the bone marrow \nresults in platelets of which 1/3 sequesters in the spleen, 2/3 circulates for 7-10 days.  \n\u2022 Platelet count in a normal adult ranges from 150,000 \u2013 450,000/ml. \n\u2022 When platelet count is reduced there will be reactive marrow megakaryocytosis  \n\u2022 Platelet count varies during menstruation i.e. rises during ovulation and failing during the \nonset of menses.  \n\u2022 It is also Influenced by nutritional state: decreased in sever fe2+, folic acid, or vitamin B 12 \ndeficiency.  \n\u2022 Platelets are acute phase reactants hence may be increased in patients with systemic \ninflammation, tumors, bleeding and mild iron deficiency hence the term secondary or \nreactive thrombocytosis is used. It is mediated by cytokines IL-3, 6, and 11. \n \nThrombocytopenia:  May follow any of the following three mechanisms  \n\u2022 Decreased bone marrow production  \n\u2022 Increased splenic sequestration or  \n\u2022 Accelerated destruction of platelets  \nTo determine the etiology one should do  \n\u2022 Careful examination of peripheral morphology \n\u2022 Assessment of marrow morphology by ex amination of an aspirate or biopsy \n\u2022 An estimate of splenic size by bed side palpation supplemented by ultrasonography. \nImpaired production of platelets:  \n\u2022 Is commonly associated with stem cell injury"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420b4-7265-11ef-8e91-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 441, "chroma:document": "\u2022 Assessment of marrow morphology by ex amination of an aspirate or biopsy \n\u2022 An estimate of splenic size by bed side palpation supplemented by ultrasonography. \nImpaired production of platelets:  \n\u2022 Is commonly associated with stem cell injury  \n\u2022 Affect multiple hematopoietic cell lines, hence there is varying degree of accompanying \nanemia and leucopoenia  \n\u2022 Bone marrow aspirate or biopsy show reduced number of megakaryocytes  \nCommon causes are:- \n\u2022 Marrow aplasia  \n\u2022 Fibrosis or  \n\u2022 Infiltration of the marrow with malignant cells"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420b5-7265-11ef-8e09-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 442, "chroma:document": "Internal Medicine \n \n 427Less commonly : \n\u2022 Cytotoxic drug use \n\u2022 Rarely congenital megakaryocytic hypoplasia and thrombocytopenia  \nSplenic sequestration:  usually follows conditions causing spleenomegaly such as  \n\u2022 Portal hypertension \n\u2022 Spleenic infiltration with tumor cells as in myeloproliferative disorders or lympho \nproliferative once) \nAccelerated destruction:  \n\u2022 Non immunologic :- associated with abnormal vessels, fibrin thrombi and heart \nvalve prosthesis \no Vasculitis, hemolytic uremic syndrome, TTP,  \no DIC \n\u2022 Immunologic:  platelets coated with antibody, immune complexes, or compliments are \nrapidly cleared by mononuclear phagocytes in the spleen or other tissues; may follow \nviral or bacterial infections, drugs, etc  \n\u2022 Drug \u2013 induced thrombocytopenia  \n       Drugs that may cause thrombocytopenia  \no Chemotherapeutic agents \u2013 especially carboplatin, alkylating agents, anthracyclines, \nantimetabolites \no Antibiotics \u2013 sulfonamides, penicillines, cephalosporines \no Heparins \u2013 Highest incidence is with unfractionated products  \no Cardiovascular agents \u2013 Thiazide diureti cs, rarely angiotensine converting enzyme \ninhibitors  \n\u2022 Most drugs induce thrombocytopenia by eliciting an immune response in which platelets are \ninnocent bystanders. The best proof of drug induced thrombocytopenia is prompt rise in the platelet count when the suspected drug is discontinued \n\u2022 Most recover within 7-10 days of discontinuation, some with platelet count of 10,000 to"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420b6-7265-11ef-971b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 442, "chroma:document": "innocent bystanders. The best proof of drug induced thrombocytopenia is prompt rise in the platelet count when the suspected drug is discontinued \n\u2022 Most recover within 7-10 days of discontinuation, some with platelet count of 10,000 to \n20,000/ml may have sever hemorrhage and hence need temporary support with glucocorticoid, plasmapheresis, or platelet transfusion; and patents should be instructed to avoid the offending drug in the future. \n\u2022 Heparin induces a paradoxical white th rombus formation leading to consumptive \nthrombocytopenia."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420b7-7265-11ef-a814-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 443, "chroma:document": "Internal Medicine \n \n 428Idiopathic /Immunologic Thrombocytopenic Purpura  \nImmunologic thrombocytopenias are divided on the basis of the pathologic mechanism, the \ninciting agent, and the duration of the illness. Accordingly they are classified as acute and \nchronic.  \nAcute ITP :  \n\u2022 Usually follows viral upper respiratory infection common in children aged 2-6 yrs  \n(accounts for 90% of pediatric cases) \n\u2022 60% recovers in 4 to 6 wks and > 90% recover within 3 to 6 months. \n \nChronic ITP:  \n\u2022 It is common in adults and run a more indolent course.  \n\u2022 Women age 20 \u2013 40 are afflicted most commonly and outnumber men by a ratio of 3:1.  \n\u2022 It presents acutely or more often with prior history of easy bruising and \nmennometrorhagia. \n\u2022 There is immune mediated platelet destruction as  well as functional platelet dysfunction.  \n \nInvestigation \n\u2022 Platelet count, complete blood count, serology for HIV, screening for SLE  \n\u2022 Bone marrow aspirate to look for reactive thrombocytosis ( increased megakaryocytes)  \n\u2022 Ultrasonography of the abdomen to look for spleenomegaly  \n \nNB- HIV infection is common cause of imm unologic thrombocytopenias in young adults. \n \nTreatment :  \nIt depends on age, severity, and anticipated natural history.  Specific treatment may not be necessary unless platelet count is < 20.000/ml  \n1) Steroids :  \n\u2022 Symptomatic patients with chronic ITP are placed on prednisone 60 mg/day for 4 to 6 \nwks; then tapered slowly over another few weeks."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420b8-7265-11ef-aca3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 443, "chroma:document": "1) Steroids :  \n\u2022 Symptomatic patients with chronic ITP are placed on prednisone 60 mg/day for 4 to 6 \nwks; then tapered slowly over another few weeks.  \n\u2022 Those patient who fail to maintain a normal platelet count after a course of steroid are \neligible to splenectomy (steroid responsive but dependent patients are most likely to \nrespond to splenectomy)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420b9-7265-11ef-aa76-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 444, "chroma:document": "Internal Medicine \n \n 4292) Intravenous immunoglobulines (IVIG)  or anti-Rho (win Rho) (reserved for those with \nsever thrombocytopenia and clinical bleeding who are refractory to other measures) \n3) Platelet transfusion  is considered only in those with eminent CNS bleeding as a temporary \nmeasure. \n4) Emergency splenectomy  (for those who are desperately ill and refractory to medical \nmeasures) \n5) Antiretroviral treatment  for those dually infected with HIV increases platelet count. \n \nNB: Failure to respond to splenectomy may signi fy presence of accessory spleen which may be \nevidenced by peripheral blood smear examination for Howell jelly body  which appears in the \ncirculation of asplenic patients. Such patients may need Immunosuppressive therapy or \nPlasmapheresis. \n \nVascular bleeding disorders  \n1) Hereditary hemorrhagic telangiectasia  : is an autosomal dominant disorder  \n2) Acquired vascular defects: \n\u2022 Simple easy bruising : benign disorder seen in women of child bearing age. \n\u2022 Senile purpura : due to atrophy of connective tissues of cutanous vessels  \n\u2022 Purpura associated with infection : follow vascular damage by infecting organs or \nimmune complex deposit e.g. meningococcemia, dengue fever. \n\u2022 Henoch \u2013 Schonlein\u2019s syndrome : is immune complex (type III) hypersensitivity. Is \ncharacterized by purpuric rash on the buttock and extensor surfaces; abdominal pain; painful joint swellings; hematuria. It is usua lly self limiting; however, some times may"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420ba-7265-11ef-9f4d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 444, "chroma:document": "characterized by purpuric rash on the buttock and extensor surfaces; abdominal pain; painful joint swellings; hematuria. It is usua lly self limiting; however, some times may \ncause renal failure.  \n \n2) Coagulation Disorders ( Secondary Hemostatic Disordrs ) \n\u2022 Hemophiliac A  \n\u2022 Hemophiliac B \n\u2022 Von will brand\u2019s disease  \nHemophilia A (hemophilia) \n\u2022 Commonest hereditary disorder  \n\u2022 Sex linked but 33% may not have family history and results from spontaneous \nmutations."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420bb-7265-11ef-8fb6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 445, "chroma:document": "Internal Medicine \n \n 430Defect : Absence or low level of plasma factor VIII \nClinical feature  \n\u2022 Profuse post circumcision hemorrhage in infants; \n\u2022 Recurrent painful hemarthroses and muscle hematomas  \n\u2022 Spontaneous intracerebral hemorrhage is important cause of death  \n\u2022 Transfusion related disorders: Hepatitis (HBV, HCV) and HIV infection are frequent \ncomplications of repeated Coagulation factor transfusions.  \n \nTable VI-4-1:  Correlation of coagulation factor activity and severity in hemophiliac and \nfactor IX deficiency  \nCoagulation factor \nactivity(% of normal)  Clinical manifestation   \n< 1 Sever disease  \nFrequent spontaneous bleeding \nEpisode from early life                     \nJoint deformity and crippling \n1-5  Moderate disease  \nPost traumatic bleeding  Occasional spontaneous episodes of bleeding \n5-20  Mild disease  \nPost-traumatic bleeding  \n \nDiagnosis \n1) Typical clinical presentation  \n2) Activated partial thromboplastin time(APTT) 3) Factor VIII clotting assay  \nTreatment :  \nFactor VIII replacement or treatment with Desmopressin. \nSpontaneous bleeding is usually controlled if patient\u2019s factor VIII activity is > 20%.  \nFor major surgery or serious post traumatic bleeding or hemorrhage occurring in dangerous sites Factor VIII level should be raised to 100% and maintained above 60% until healing occurs. Unit of Factor VIII needed can be calculated by the following formula:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420bc-7265-11ef-ba2d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 446, "chroma:document": "Internal Medicine \n \n 431X = % rise in factor VIII x weight (kg) \n K Where K = 1.5 for Factor VIII,  \n                  = 1 for Factor IX and 2 for Factor XI; 1 unit of Factor  VIII = 1% VIII activity  \n \nTable VI-4-2. Comparison between di fferent coagulation disorders  \n \n \nFeatures  Hemophiliac  Factor IX \ndeficiency  Von willi brand\u2019s disease \n \nInheritance  Sex linked recessive Sex linked recessive\n Autosomal dominant\n \nSite of bleeding  Body cavities, joint & intramuscular spaces\n Body cavities, joint & intramuscular spaces\n Both mucocutaneous  & other mentioned sites \n \nPlatelet count  N N N \nBleeding time  N N Prolonged  \nProthrombin time (Pt)  N N N \npartial thromboplastine time (PTT)\n Prolonged  Prolonged  Prolonged or normal \nVIII Low Normal  Low  \nVWF Normal  Normal  Low \nFactor IX  N Low Normal  \n \nVon will brand\u2019s disease  \n\u2022 Has both functional platelet abnormality (abnormal platelet adhesion) and low factor VIII \nactivity \n\u2022 Inheritance is autosomal dominant with variable degree of penetrance.  \n\u2022 Defect is reduced synthesis of VWF which facilitates platelet aggregation and carrier of \nFactor VIII (protecting it from premature destruction ).  \nTreatment:  \n\u2022 Intermediate \u2013 purity F VIII concentrates (containing both F VIII and VWF)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420bd-7265-11ef-8ec4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 447, "chroma:document": "Internal Medicine \n \n 432\u2022 Desmopressin  \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nDisorders of Hemostasis, pages 673-694. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition \nMedicine, Disorders of hemostasis and coagulation, pages 127-136."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420be-7265-11ef-9f26-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 448, "chroma:document": "Internal Medicine \n \n 433CHAPTER SEVEN \nDISEASE OF METABOLISM AND ENDOCRINE SYSTEM \n \n1. Introduction to Diseases of the Endocrine System \n \n\u2022 Like the nervous and the immune systems the endocrine system main function is being \na media of intercellular communication for a proper function of the body.  \n\u2022 This is achieved by organic compounds called hormones. Hormones are directly \nreleased into the blood therefore are said to be produced by \u201cductless glands\u201d. Some \nhormones are bound to carrier proteins for transport but it is the free form that is \nphysiologically active. These hormones first bind to plasma membrane of the target cells\u2019 \nreceptors .Then a series of cascade reactions (biochemical reactions that initiate and accelerate themselves which are mediated by cyclic AMP) or by direct enzyme induction \non the nucleus should occur before the nucleus of the cells is influenced to send a \ncommand for an action. \n\u2022 The release of hormones is controlled by feedback of serum level but also the \nphysiologic, morphologic and biochemical effects of hormones could play a role.  \n\u2022 These hormones are finally inactivated in target tissues with the exception of thyroid and \ninsulin which are degraded in the liver and kidneys as well. \n\u2022 The state of endocrine function is evaluated by level of hormone or the metabolic effects \nof the hormone. With few rare exceptions both high and low levels of hormone result in \ndisease."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420bf-7265-11ef-81f2-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 448, "chroma:document": "\u2022 The state of endocrine function is evaluated by level of hormone or the metabolic effects \nof the hormone. With few rare exceptions both high and low levels of hormone result in \ndisease.  \nE.g. High level of thyroid hormone results in hyperthyroidism while a low level of \nhormone results in hypothyroidism. \n\u2022 Endocrine functional assessment is very import ant in clinical practice but with serious \nchallenge for resource limited nations like ours. Hormone levels are too low making routine laboratory determination difficult and as a result very sensitive assay are needed \nwhich are not routinely available due to expense and special expertise needed. \n\u2022 The other challenge result from the very nature of pattern of hormone secretion during \nthe day making it necessary to take samples at specific times of the day  or doing interventions to suppress or stimulate hormone production whenever the levels are border line for decision making."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420c0-7265-11ef-a28d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 449, "chroma:document": "Internal Medicine \n \n 434Homeostasis \nFeed back control, both negative and positive, is a fundamental features of endocrine system. \nEach of the major hypothalamic \u2013pituitary hormone axes is governed by a negative feedback, a process that maintains hormonal levels within a relatively normal range.  \nThe Hypothalamus \nThe hypothalamus produces different releasing hormones that stimulate the pituitary gland.  \n\u2022 TRH stimulate the production of TSH \n\u2022 CRH stimulate the production ACTH \n\u2022 GnTH stimulate the production LH/FSH \n\u2022 GHRH stimulate the production GH \nThe hypothalamus is affected by negative (inhibitory) feedback from the pituitary gland as well \nas from serum level of different hormones or their metabolic effect.  \nThe hypothalamus produces antidiuretic hormone (ADH) which participates in control of fluid and electrolyte and Oxytocin which participate in uterine contraction after delivery. These two hormones are released in the posterior part of the pituitary gland. \n \nThe pituitary gland  produces trophic hormones that st imulate the peripheral endocrine glands. \n\u2022 Thyroid stimulating hormone(TSH) stimulates the thyroid gland to produce T\n3 and T 4 \n\u2022 Adrenocorticotrophic hormone (ACTH) stimulat es the adrenal cortex to produce cortisol. \n\u2022 Luteinizing hormone (LH)/Follicular stimul ating hormone stimulate the ovaries or the \ntestis.  \n\u2022 Growth hormone is also produced by the anterior pituitary and influence body growth"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420c1-7265-11ef-a01d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 449, "chroma:document": "\u2022 Luteinizing hormone (LH)/Follicular stimul ating hormone stimulate the ovaries or the \ntestis.  \n\u2022 Growth hormone is also produced by the anterior pituitary and influence body growth  \n\u2022 Prolactin is also produced by the anterior pituitary and influence lactation in females. \nThe peripheral glands produce specific hormones:  \n\u2022 The  thyroid glands produce Thyroid hormone (T 3 and T 4 ) \n\u2022 The adrenal glands produce Cortical \n\u2022 Ovary and testes produce hormones that control sexual activity and reproduction. \nOther endocrine organs   \n\u2022 Pancreas: produces insulin  and glucagon \n\u2022 Liver: produces  somatostatin  \n\u2022 Kidneys: produce : renin, angiotensin, erythropoietin, Vit-D \n\u2022 Stomach: produce gastrin  \nThe target cells  execute the command delivered by hormones."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d420c2-7265-11ef-8662-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 450, "chroma:document": "Internal Medicine \n \n 4352. Diabetes Mellitus \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Diabetes Mellitus . \n2. Describe the pathophysiology of  Diabetes  Mellitus. \n3. Understand   the epidemiologic significance of Diabetes Mellitus. \n4. Understand the different types of Diabetes Mellitus. \n5. Identify the clinical manifestation of Diabetes Mellitus. 6. Understand the diagnostic approach of Diabetes Mellitus. 7.  Identify acute and chronic complications of Diabetes Mellitus. \n8. Manage patients with acute complications Diabetes Mellitus . \n9. Understand the prevention  of chronic complications of  Diabetes Mellitus 10. Understand the course and prognosis of Diabetes Mellitus . \n \nDiabetes Mellitus:  is a common endocrine disorder characterized by: \n\u2022 Hyperglycemia \n\u2022 Manifesting often with symptoms and signs of osmotic diuresis such as polyuria and \npolydypsia \n\u2022 Calorie loss, generalized weakness, polyphagia and weight loss.  \nResulting from either an absolute deficiency (Type 1) or a relative deficiency (Type 2) of the \nhormone, Insulin.   \n\u2022 These disorders are associated with reversible and acute complications such as \nketoacidosis, which becomes fatal if treatment is delayed. \n\u2022 Disabling chronic complications affecting vision, kidneys, the nerves the vessels and the \nheart are common in those who are diagnosed very late, or in those who are not on \nproper medical follow up and care. \n \nEtiology and Classification:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4570e-7265-11ef-88e5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 450, "chroma:document": "\u2022 Disabling chronic complications affecting vision, kidneys, the nerves the vessels and the \nheart are common in those who are diagnosed very late, or in those who are not on \nproper medical follow up and care. \n \nEtiology and Classification:  \nType 1 DM  (formerly known as insulin-dependent DM)  \n\u2022 Usually occurs in childhood or early adulthood (age less than 30) \n\u2022 Patients are usually thin."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4570f-7265-11ef-9224-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 451, "chroma:document": "Internal Medicine \n \n 436\u2022 They require insulin for survival and develop ketoacidosis when patients are not on \nadequate insulin therapy.  \n\u2022 This accounts for 10% of cases of DM.  \n\u2022 Oral hypoglycemic agents will not be effective to lower the blood glucose level. \n\u2022 Type 1 DM is due to \u03b2-cell destruction, with absolute deficiency of insulin, which is of \nmultifactorial causes such as genetic predisposition, viral and autoimmune attacks on \nthe beta islet cells.  It may be immune mediated or idiopathic . \n \nType 2 DM  (formerly non insulin-dependent DM)  \n\u2022 Usually occurs in people >40 years of age \n\u2022 Most (about 60%) of the patients are obese.  \n\u2022 Type 2 DM occurs with intact beta islet cell function but there is peripheral tissue \nresistance to insulin.  \n\u2022 There may be some decrease in insulin production or a hyperinsulin state.  \n\u2022 These patients are not prone to develop ketoacidosis but may develop it under \nconditions of stress.   \n\u2022 Patients do not require insulin for survival at least in the earlier phase of diagnosis.  \n\u2022 The blood sugar level can be corrected by oral hypoglycemic agents. \nOther specific types   \nA. Genetic defects  of \u03b2-cell function:  MODY 1 , MODY 2 , MODY 3 etc \nB. Genetic defects in insulin action  : Type A insulin resistance  , Lipodsytrophy syndromes \nC. Diseases of the exocrine pancreas: Chromic pancreatitis , Pnactreatectomy , \nhemochromatosis \nD. Endocrinopathies : Cushing\u2019s syndrome, pheochromocytoma , acromegaly"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45710-7265-11ef-9204-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 451, "chroma:document": "C. Diseases of the exocrine pancreas: Chromic pancreatitis , Pnactreatectomy , \nhemochromatosis \nD. Endocrinopathies : Cushing\u2019s syndrome, pheochromocytoma , acromegaly  \nE. Drug- or chemical-induced DM (beta-blockers, oral contraceptives , glucocorticosteriods  \n Gestational onset DM  (GDM): is when diabetes onsets during pregnancy and resolves with \ndelivery. These patients are at a higher risk for developing DM at a later date. \n \nEpidemiology \n \n\u2022 Globally 124 million people are said to be affected by DM, of which 97% are type 2 \ncases."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45711-7265-11ef-b910-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 452, "chroma:document": "Internal Medicine \n \n 437\u2022 In USA 1 to 2% of the general population has abnormal fasting blood sugar level, and \n20% of above 60 years have diabetes.  \n\u2022 In Asia, particularly urban India, prevalence DM has climbed to 11%, while in South \nAfrican urban Indians it is as high as 18%.  \n\u2022 Amongst Pima Indians in America the prevalence of DM is very high (up to 50%) making \ngenetics predisposition an important factor. \n\u2022 Africa is not free from this disease which traditionally is considered the disease of the \naffluent societies of the first world. In Tunisia the prevalence of DM is 4%, in South Africa \n5%, in Tanzania 0.9%.  \n\u2022 In Ethiopia one community based study showed that the prevalence of DM in Gondar \narea of northern Ethiopia was found to be about 0.5%, and about 4.7% among older than 40 years.  \n\u2022 Emigrants from Ethiopia to Israel hav e shown a higher prevalence of 8.9%.These \nfindings imply that the incidence of disease increases with increasing age, as well as either the dietary habit or sedentary and stressful life style of the developed countries. \n \nMechanism of Disease in Diabetes Mellitus  \nInsulin is produced by the \u03b2-cells in the islets of Langerhans in the pancreas. Insulin secretion is \nstimulated by amino acids and parasympathetic nerves. It is inhibited by glucagon.  \nThe Biochemical actions of Insulin include: \n\u2022 Switches off hepatic glucose production (inhibits Gluconeogenesis) \n\u2022 Increase uptake and utilization of glucose by muscle"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45712-7265-11ef-b241-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 452, "chroma:document": "The Biochemical actions of Insulin include: \n\u2022 Switches off hepatic glucose production (inhibits Gluconeogenesis) \n\u2022 Increase uptake and utilization of glucose by muscle  \n\u2022 Inhibits lipolysis and by doing so prevents ketogenesis. \n\u2022 Enhances uptake of amino acids into muscle for protein synthesis and inhibition of \nbreakdown of proteins \nMechanism of disease in Type 1 Diabetes \nType 1 diabetes mellitus is believed to be due to autoimmune destruction of beta cells.  \n\u2022 The triggering agent (i.e. - a viral infection) will expose these cryptic (hidden) self \nantigens to which the immune system has not developed tolerance. Therefore an \nautoimmune process is set-up destroying self tissue, in this case the beta cells of the islets of Langerhans. \n\u2022 The other mechanism of injury is molecula r mimicry between trigger antigen (virus) and \n\u03b2-cell antigen. or instance Coxsackie virus antigen and that of glutamic acid"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45713-7265-11ef-b93e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 453, "chroma:document": "Internal Medicine \n \n 438decarboxylase (GAD) found within the \u03b2-cells  has similar chemical structure, so that the \nantibodies produced to fight the foreign antigen of the virus also cross react with \nantigens of self tissue bearing GAD hence destroying it . \n \nNatural history of type 1 diabetes \n\u2022 The disease is progressive going through phases of antibody production, then phase of \nimpaired GTT followed by an abnormal FBS, and finally culminating in an abnormal FBS \nwith Ketonemia.  \n Honeymoon period:  \n\u2022 In young people who are diagnosed for the first time to have overt DM, the DM may \nhave been precipitated by acute metabolic stressful conditions (such as infection or pregnancy).  In such circumstances, the increased metabolic demand for insulin, may \nlead to a relative insulin deficiency, and patients become symptomatic, and may need \nexogenous insulin to control their symptoms. \n\u2022 With the return to baseline metabolic demands, when the stressful event abates, the \npancreatic reserve may be adequate to maintain normal or near-normal blood glucose. Such patients may undergo a period of transient \u201ccure\u201d during which time they may not require exogenous Insulin to control their blood glucose level. Because of this, such patients are said to be in a \u201c HONEYMOON \u201d period.  \n\u2022 This is unfortunately is transient and the patients will be needing insulin again when the \nprogressive destruction of \u03b2-cells leads to absolute insulin deficiency.  \nMechanism of   Type 2 disease:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45714-7265-11ef-a7a5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 453, "chroma:document": "\u2022 This is unfortunately is transient and the patients will be needing insulin again when the \nprogressive destruction of \u03b2-cells leads to absolute insulin deficiency.  \nMechanism of   Type 2 disease:   \n\u2022 In Type 2 DM insulin resistance plays a central role in the pathogenesis.  \n\u2022 In obesity, increased production of non-esterified fatty acids, leads to resistant of \nperipheral organs to insulin which leads to increased gluconeogenesis in the liver, and decreased peripheral uptake and utilization of glucose by muscles . \n\u2022 Initially there is hypersecrtion of insulin by \u03b2-cells, to overcome the insulin resistance. \nBut later on \u03b2-cells fail to respond to the level resistance. Then \u03b2-cell number is \ndecreased and amyloid is deposited in islets."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45715-7265-11ef-a13b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 454, "chroma:document": "Internal Medicine \n \n 439 Predisposing factors for Type 2 DM \n1) Genetic Predisposition  plays an important role. The evidences are :- \n\u2022 Concordance among identical twins is upto100% \n\u2022 Concordance among fraternal twins is  20% \n\u2022 Familial aggregation history is common and up to 50% of siblings and 33% of \nchildren of diabetics develop diabetes. \n2) Environmental factors :  \n\u2022 Obesity  \n\u2022 Physical inactivity  \n\u2022 Diet  \n \nNatural history of type 2 diabetes  \nStage 1 : Insulin resistance:  increased glucose and Non Esterified Fatty Acids (NEFA ) \nStage 2 : Increased insulin secretion : compensatory hyperinsulinemia         \nStage 3: Impaired glucose tolerance                   \nStage 4 : Overt type 2 diabetes                         \n \nClinical features: \nFeatures of increased osmolality \n\u2022 Polyuria: increased volume and frequency of urination due to osmotic diuresis induced \nby hyperglycemia. \n\u2022 Polydepsia- increased feeling of thirst and drinking excess water/fluid due increased \nblood osmolality  \n\u2022 Blurring of vision: swelling of the lens due to increased osmolality. \nFeatures of calorie loss \n\u2022 Polyphagia:  feeling of hunger , a need to eat several times a day \n\u2022 Generalized weakness-  \n\u2022 Weight loss \nSome patients may be Asymptomatic mainly Type 2 patients and GDM  \nDiagnosis is made incidentally during routine medical checkup, ANC follow up etc.  \nTherefore it is advisable to screen patient for DM, if following risk factors are present:  \n\u2022 Obesity (BMI >25 kg/m2),"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45716-7265-11ef-a7cf-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 454, "chroma:document": "Diagnosis is made incidentally during routine medical checkup, ANC follow up etc.  \nTherefore it is advisable to screen patient for DM, if following risk factors are present:  \n\u2022 Obesity (BMI >25 kg/m2),  \n\u2022 First-degree relative with DM"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45717-7265-11ef-a559-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 455, "chroma:document": "Internal Medicine \n \n 440\u2022 History of gestational DM or delivered a baby weighing more than >4kg ( 9 lb ) \n\u2022 Hypertensive,  \n\u2022 Hyperlipidemia HDL <35 mg/dl or triglyceride level >250 mg/dl,  \n\u2022 History of impaired fasting glucose or impaired glucose tolerance glucose on prior \ntesting. \n Table VII-2-1 Criteria for the Diagnosis of Diabetes Mellitus:   \n \n \n \n \n   \n \n \n\u2022 Random  is defined as without regard to time since the last meal \n\u2022 Fasting is defined as no caloric intake for the last 8 hrs. \n\u2022 Oral glucose tolerance test : blood glucose is measured after ingestion of 75g \nanhydrous of glucose dissolved in water. \n\u2022 The patient is said to have impaired glucose tolerance (IGT) if the fasting plasma \nglucose is >110 mg/dl and <126 mg/dl. \nSource:  Modified from American Diabetes Association, 2004. \n \n \n  \n \n          \n \n \n \u2022 Symptoms of diabetes plus random blood glucose concentration \n\u226511.1 mmol/L ( 200 mg/dL )   OR \n\u2022 Fasting plasma glucose of  >126 mg/dl (7 mmol/L)  OR \n\u2022 2-hour postprandial plasma glucose >2 00 mg/dl after a glucose load \nof 75 g ( during oral glucose tolerance test) \n \nN.B. These criteria should be confirmed by repeat tests on a different day."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45718-7265-11ef-81b1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 456, "chroma:document": "Internal Medicine \n \n 441Somogyi phenomenon :  refers to hyperglycemia secondary to a period of drug-induced \nhypoglycaemia with metabolic compensation (increased gluconeogenesis and sympathetic \noutflow). If controlling high glucose becomes a pr oblem (especially a.m. glucose), consider \nchecking for hypoglycemia in the time leading up to high readings. \n \nTreatment: \nGoal of therapy . Eliminate symptoms and prevent the complications of diabetes.  \n\u2022 In resource limited setup preventing acute complications that result acute \ndehydration, coma and premature death.  \n\u2022 Prevention or delaying the occurrence of chronic complications: with tight blood \nglucose control to  to achieve a near normal  blood sugar level significantly \ndiminishes risk of developing chronic complications \n\u2022 In children one should also aspire to achieve normal growth and development. \nBiochemical Goals \n\u2022 FBS <130 or RBS<200 (Acceptable blood glucose control.) \n\u2022 FBS<100 or  RBS<160 ( ideal but usually di fficult to achieve by current technology) \nA. Non pharmacologic Therapy \n1) Diet therapy . Patients should be given proper advice about their diet.  \n\u2022 Maintenance of a normal Body Mass Index should be the prime target through \nrecommending calories intake according to age, sex and physical activity. \n\u2022 Alcohol ingestion should be limited  \n\u2022 Diet should include 60% to 65% carbohydrates, 25% to 35% fat, and 10% to 20% \nprotein.  \n\u2022 Patients are advised to significantly decrease cholesterol intake."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45719-7265-11ef-9aaa-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 456, "chroma:document": "\u2022 Alcohol ingestion should be limited  \n\u2022 Diet should include 60% to 65% carbohydrates, 25% to 35% fat, and 10% to 20% \nprotein.  \n\u2022 Patients are advised to significantly decrease cholesterol intake. \n\u2022 Avoid simple sugars (e.g. sugar, soft drinks, honey, and other sweets)  \n\u2022 High fiber diet such as vegetables slow the absorption of digested food in the form of \nsimple sugars \n\u2022 Fresh fruit such as water melon and lemon can be freely taken as opposed to \noranges bananas that must be taken with caution. \n\u2022 Dividing meal into four to six equal parts may helps in achieving stability in   some \ncases  \n2) Exercise : has multiple positive benefits to diabetic patients including : \no Cardiovascular risk reduction"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4571a-7265-11ef-bdd4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 457, "chroma:document": "Internal Medicine \n \n 442o Reduce blood pressure  \no Maintain muscle mass  \no Reduction in body fat and helps in losing weight. \no It is beneficial to both Type 1 and Type 2 patients  \n\u2022 Therefore regular exercise 20-30 minutes, aerobic exercise such as jogging, walking, \nswimming etc 3 \u2013 4 days is recommended. \n\u2022 N.B Patients on Insulin treatment should be cautious to avoid hypoglycemia \n3)  Weight reduction  \n\u2022 Maintain normal BMI of 20 and 25, Weight loss increase sensitivity to insulin and \nmay lead to decrease in the demand of exogenous insulin or the dose of Oral \nhypoglycemic agents. \n \n4)  Patient education . Involving patients in the their own treatment plan essential.The  \npatient  can be involved in his care through regular health education to achieve the ideal \nknowledge, attitude which is ccrucial to proper management of DM.  \nAreas of Patient Education  \no Patients should be made to understand DM is needs lifelong treatment and follow \nup  \no Goal of treatment should be set together with the patient \no To avoid excess alcohol intake and, smoking \no Benefit of weight reduction, diet and regular exercise \no Proper foot care \no Hypoglycemia causes , symptoms and simple first aid management \no Complications of diabetes \no Insulin injection technique  \no Self glucose monitoring \n \nB. Pharmacologic therapy . \n1. Insulin   \n\u2022 Beef, pork, and recombinant human insulin (Humulin) are available. Humulin is generally"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4571b-7265-11ef-99ec-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 457, "chroma:document": "o Complications of diabetes \no Insulin injection technique  \no Self glucose monitoring \n \nB. Pharmacologic therapy . \n1. Insulin   \n\u2022 Beef, pork, and recombinant human insulin (Humulin) are available. Humulin is generally \npreferable and tends to be less immunogenic than beef or pork insulin and therefore there is less insulin resistance secondary to anti-insulin antibodies.  \n\u2022 Type 1 DM patients must be started on insulin at the time of diagnosis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4571c-7265-11ef-98a4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 458, "chroma:document": "Internal Medicine \n \n 443\u2022 The average daily insulin requirement is appr oximately 0.3U/Kg/day (25 units /day) in a \nperson with type 1 diabetes in whom the production of endogenous insulin is assumed to \nbe nil. \n Table V-2-2 Different preparations of insulin based on their duration of action:  \nPreparation  Onset of \naction  Peak action and Duration of action  Clinical sue and rout of administration  \nShort acting (crystalline /regular)  30-60 min  P : 1-4 hrs D: 4-6 hrs  Used in ketoacidosis for rapid control of high sugar and acidosis.  It can be administered IV , IM or SC  \nIntermediate-acting insulin (NPH or \nLente)  1 to 3 \nhours  P: 6- 12 hrs  D:18-26 hrs  Used for ambulatory long term control of sugar level \nGiven not more than twice a day  \nRout of administration is limited to SC  \nLong-acting insulin (Ultralente PZI): \nLong acting (NPH, \nisophane)  Onset 4 to 8 P:14-  24 hrs D: 28- 36 hrs  Not available for use in our  country \n \n \nSide effects:  \n\u2022 The most serious complication of insulin is hypoglycemia. \n\u2022  Hypersensitivity, atrophy or hypertrophy of injection sites may also occur, sometimes. \n In type 1 DM  For patients diagnosed with DM presenting with Ketoacidosis  \n\u2022 Glucose control is initially obtained with a sliding scale using regular insulin. Measure \nserum glucose every 6 hours and give sub cutanous regular insulin depending on RBS measurement."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4571d-7265-11ef-8b3d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 459, "chroma:document": "Internal Medicine \n \n 444\u2022 Once the glucose is stabilized with regular insulin 6 hourly injections, 2/3 of the last 24 \nhrs insulin requirement is given, in the form of intermediate acting insulin, as S.C \ninjection per day.  \n\u2022 If the total daily requirement of insulin is greater than 40 units , 2/3 of the total insulin \nrequirement given as an AM dose ( in the mo rning ) and 1/3 third is  given as a PM \ndose( evening ).  \n\u2022 If the intermediate-acting agent does not give adequate control of daytime blood \nglucose, a short-acting agent may be added.  \nThe other option for patient diagnosed before developing acute complications \n\u2022 Start with 20- 25 units of Humulin  insulin (equivalent to daily insulin production by islets) \nS.C, daily \n\u2022 Gradually increase the dose by 3- 5 units very 4- 5 days till acceptable level of blood \nglucose is achieved \nIntensive insulin therapy : to achieve near normal blood glucose level  \n\u2022 An insulin pump , which administers continuous SQ insulin infusion with mealtime \nboluses, or  \n\u2022 Multiple daily insulin injections  with frequent blood glucose determinations. \n\u2022 Another option is the use of a long-acting insulin (such as Ultralente) to provide a base \nof insulin delivery augmented by regular insulin at mealtimes.  \n\u2022 This type of treatment approach needs a lot of commitment from the patient and the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4571e-7265-11ef-bd79-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 459, "chroma:document": "\u2022 Another option is the use of a long-acting insulin (such as Ultralente) to provide a base \nof insulin delivery augmented by regular insulin at mealtimes.  \n\u2022 This type of treatment approach needs a lot of commitment from the patient and the \nphysician. It helps to achieve near normal blood glucose level and thus delays the development of chronic complications. It may be complicated by frequent bouts of hypoglycaemia. \n  \n2. Oral hypoglycemic agents   \nThese groups of drugs are widely used in type 2 patients whose hyperglycemia has failed to be controlled with conservative measures. a) Sulfonylureas: s timulate pancreatic beta cells to secrete insulin.  \nDose:  Glyburide  2.5 to 20 mg PO or   \nGlipizide  5 to 20 mg PO  \n\u2022 Glyburide is more likely to result in glycemic control when used once a day \nthan is glipizide. Glyburide should be used in a twice-daily dosing if 20 \nmg/day total is required."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4571f-7265-11ef-b95b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 460, "chroma:document": "Internal Medicine \n \n 445\u2022 The effectiveness of sulfonylureas declines up to 10% annually as the failure \nof beta-cell function progresses.  \nb) Metformin : reduces blood glucose levels by improving hepatic and peripheral tissue \nsensitivity to insulin without affecting the secretion of insulin.  \n\u2022 Metformin is used as monotherapy or in combination with sulfonylureas or \ninsulin for type 2 DM.  \n\u2022 It is especially useful in overweight patients because it does not cause weight \ngain.  \n\u2022 Hypoglycaemia is not a problem with metformin.  \n\u2022 Metformin also appears to improve plasma lipid and fibrinolytic profiles \nassociated with type 2 DM.  \no Dose : Initial dosage is 500 mg PO daily until initial nausea and \nanorexia are tolerated and then increased to 500 mg BID. \no The dosage can be increased by 500 mg weekly to maximum dose of \n2500 mg if reasonable glycemic control couldn\u2019t be achieved. \no Use with or after food may lessen the GI side effects.  \n\u2022 Side effects : Lactic acidosis (rare). Risk is mi nimized if metformin is avoided \nin patients with renal disease, CHF or pulmonary disease.  \nc) Alpha-glycosidase inhibitors:   \n\u2022 Acarbose and Miglitol :  are oral agents that reduce the absorption of \ncarbohydrates, thus reduce postprandial hyperglycaemia. \n\u2022 Alpha-glycosidase inhibitors can be used as monotherapy or in combination \nwith insulin or sulfonylureas.  \n\u2022 Start with Acrarbose 25 mg with evening meal , may be increased to a \nmaximum dose of 50-100 in weeks"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45720-7265-11ef-aa53-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 460, "chroma:document": "\u2022 Alpha-glycosidase inhibitors can be used as monotherapy or in combination \nwith insulin or sulfonylureas.  \n\u2022 Start with Acrarbose 25 mg with evening meal , may be increased to a \nmaximum dose of 50-100 in weeks   \n\u2022 In general, this group of drugs is less effective than other classes \nd) Thazolidinediones  : reduce insulin resistance and increase peripheral glucose \nutilization  \nPioglitazone :   15- 45mg /day in a single daily dose  \nRosiglitazone :  2- 8 mg total daily dose given once or in two divided doses   \nThese new group of drugs decrease insulin and sulfonylurea requirement  Side effects: idiosyncratic hepatocelluar injury"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45721-7265-11ef-ba42-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 461, "chroma:document": "Internal Medicine \n \n 446The use of Insulin in type 2 DM ,  \n\u2022 Insulin is usually added to an oral agent when glycemic control is suboptimal at maximal \ndoses of oral medications.  \n\u2022 An intermediate-acting agent is used starting with a low dose and increasing as needed for \nglycemic control (such as 5 to 10 U of NPH increasing as needed).  \n\u2022 Adding NPH at bedtime is generally more efficacious than using it during the day.  \n\u2022 If using only insulin, start with an AM (morning) injection. The dose can be increased by 5 \nU every 3 to 7 days until adequate control is achieved.  \n\u2022 If early morning hyperglycemia is a problem, intermediate-acting insulin can be given twice \ndaily as a split dose.  \n \nFollow up of patients:- Since this is a lifelong disease regular follow up of patient is crucial.   \nPoints to give emphasis during follow up \n\u2022 Symptoms of hyper or hypoglycemia  \n\u2022 Wight  \n\u2022 Blood pressure \n\u2022 Visual acuity \n\u2022 Examine the oral cavity  \n\u2022 Examination of the feet \n\u2022 Examine Injection site \n\u2022 Laboratory tests: blood or urine sugar and urine albumin or protein.  \n \nAcute complications of  Diabetes Mellitus  \n1. Hypoglycemia \n2. Diabetic Ketoacidosis \n3. Hyperosmolar Comma \n \n1) Hypoglycemia  in the diabetic patient is caused by  \n\u2022 Overdose of insulin or hypoglycemic agents \n\u2022 Missing of meal  \n\u2022 Strenuous exercise"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45722-7265-11ef-8e26-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 462, "chroma:document": "Internal Medicine \n \n 447Clinical manifestations \nEarly : one may feel the effects of sympathetic stimulation such as cold sweat, tremor, hunger or \npalpitations.  \nLate:  If early symptoms are neglected then symptoms of the effect of hypoglycemia on the brain \n(Neurogenic manifestations) such as dizziness, blurring, headache, nightmares, and coma may \noccur.  \nManagement  \n\u2022 Any patient with diabetes losing consciousness should always be considered \nhypoglycemic until proven otherwise by blood sugar determination and should be \nmanaged by rapid IV  administration of gluc ose or PO/ NG tube administration of any \nconcentrated sugar solution.  \n\u2022 Prolonged unconsciousness requires continuous 10% IV glucose administration.  \n \n2)  Diabetic Ketoacidosis \nDefinition:  is an acute metabolic crisis in patients with diabetes mellitus characterized by: \n\u2022 Hyperglycemia (blood glucose level may range from 250-600 mg /dl )  \n\u2022 Metabolic acidosis (ketosis)  \n\u2022 Hypotension and features of dehydration  \n \nDKA was formerly considered as a hall mark of ty pe 1 DM. However, currently it is known that \nsome type 2 DM patients who are being treated by oral hypoglycemic agent may also develop \nDKA.  \n Precipitating factors:   \nDKA may occur after sever days of worsening diabetic control, or may appear suddenly within \nfew hours. Some of the precipitating factors are: \n\u2022 Intercurrent infection \n\u2022 Poor compliance with insulin or discontinuation of insulin \n\u2022 Dehydration"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45723-7265-11ef-a6ca-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 462, "chroma:document": "DKA may occur after sever days of worsening diabetic control, or may appear suddenly within \nfew hours. Some of the precipitating factors are: \n\u2022 Intercurrent infection \n\u2022 Poor compliance with insulin or discontinuation of insulin \n\u2022 Dehydration \n\u2022 Stressful conditions such as, trauma, surgery or of emotional crisis \n\u2022 Excessive alcohol ingestion"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45724-7265-11ef-a132-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 463, "chroma:document": "Internal Medicine \n \n 448Pathogenesis:  \nAny event that decrease insulin availability or   cause stress that increase the insulin demand, \nlead to sever insulin deficiency and the effect of counter regulatory hormones such as glucagon, \ncortisol, epinephrine and growth hormone becomes  overwhelming. This biochemical changes \nbring about:  \n\u0083 Increased production of glucose by the liver and increased glycogen degradation to \nglucose \n\u0083 Decreased glucose uptake and utilization by muscles \n\u0083 Lipolysis: enhanced break down of free fatty acids and subsequent ketogenesis.  This \nincreases blood levels of keton bodies such as acetoacetic acid, \u03b2-hydroxybutyric acid, \nand acetone, resulting in metabolic acidosis.  \n\u0083 The above biochemical processes result si gnificant hyperglycaemia and Ketoacidosis, \nwhich are responsible for the clinical manifestations of DKA. \n Signs and symptoms :  \n\u0083 Volume depletion : dehydration- dry tongue and bucal mucosa , poor skin turgor  and \nhypotension  \n\u0083 Kussmaul respiration : deep and fast breathing resulting from metabolic acidosis   \n\u0083 Acetone (\"fruity\") odour of breath: due too acetone  \n\u0083 Nausea and vomiting and frequent complaint of abdominal pain.  \n\u0083 Mental status changes : lethargy and confusion which may evolve into coma with sever \nDKA \n\u0083 Cerebral edema: an extremely serious complication of DKA is seen most frequently in \nchildren. \n\u0083 Signs of infection , which may be precipitating DKA , should be looked for"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45725-7265-11ef-8c45-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 463, "chroma:document": "DKA \n\u0083 Cerebral edema: an extremely serious complication of DKA is seen most frequently in \nchildren. \n\u0083 Signs of infection , which may be precipitating DKA , should be looked for \n\u0083 A history of diabetes (unless first presentation).  \n \nLaboratory Diagnosis: \n1. RBS: hyperglycaemia  can be diagnosed with RBS determination. Blood glucose  level is \nusually high ( averaging 500 mg /dl )  \n2. Urine dipstick for ketones :  ketosis  can be determined with bedside reagents. This test is \n97% sensitive. Serum keton level can also be measured to confirm hypereketonemia.  \n3. Arterial blood gas analysis  : can diagnose metabolic acidosis which is indicated by low \nserum bicarbonate level ( usually below 10 mEq / L )  and low blood PH ( < 7.35 )  \n4. Additional laboratory evaluation"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45726-7265-11ef-9174-0c9a3cb28fe6
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metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 464, "chroma:document": "Internal Medicine \n \n 449a) Electrolytes:  \n\u2022 Serum K+ level: look for hyperkalemia or hypokalemia \n\u2022 Serum Na+: tends to be low because of dilution as the osmotic effect of hypergycemia \nincreases ECF volume. \n\u2022 Serum osmolality is high  \nb) BUN, creatinine, \nc) CXR, urine culture and sensitivity, blood cultures should also be done to identify an \ninfectious process. \n \nTreatment of DKA: Acute management  \n1. Supportive therapy :  \n\u2022 Airway maintenance, supplemental oxygen as needed, and treatment of shock.  \n2. Fluid replacement :  \nFluid replacement corrects dehydration caused by glucose induced osmotic diuresis. The \nfluid deficit in patients with DKA averages 3-5 L, which should be promptly replaced. Hence give 5- 6 L of fluid in the 1\nst 24 hours. \no Initially 1 L of normal saline (0.9 % NaCl) is given over \u00bd an hour. \no Continue with 1 L of normal saline/hr for the first 2-3 hours \no Then \u00bd normal saline (0.45 % NaCl) at slower rate till the patient is well \nhydrated. \no This will rehydrate the patient and ensure adequate renal perfusion.  \no When the serum glucose level falls to 200-300 mg/dl, change the IV fluid to 5 % - \n10 % DW to prevent hypoglycaemia. \no Carefully monitor the urine out put  \n3. Insulin:  \nInsulin is administered to increase glucose use in the tissues, to inhibit ketogenesis, and to counter balance the effect of counter regulatory hormones. \nDosage and administration:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45727-7265-11ef-9111-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 464, "chroma:document": "o Carefully monitor the urine out put  \n3. Insulin:  \nInsulin is administered to increase glucose use in the tissues, to inhibit ketogenesis, and to counter balance the effect of counter regulatory hormones. \nDosage and administration:   \n\u2022 20 Units of regular insulin, 10 U IV and 10 U IM is given with the initial fluid resuscitation. \nThen 5-10 /hr units or regular insulin is given per hour till the blood glucose level drops \nto 250-300mg/dl"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45728-7265-11ef-a062-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 465, "chroma:document": "Internal Medicine \n \n 450\u2022 Blood glucose determination is done every hour. The expected rate of fall in serum \nglucose is 75-100 mg/dl/hr.  \n\u2022 When blood glucose reaches a range of 250 to 300 mg/dl, 5 -10 % glucose solution \nshould be infused to prevent hypoglycaemia. \n\u2022 Insulin infusion should not be stopped until the Ketonemia clears. It is preferable to give \n5% or 10% DW with insulin injection, rather than stop the insulin, because insulin is \nstill required to clear the acidosis and ketotic state.  \n\u2022 Shift to sliding scale when keton clears, until precipitating cause is well controlled.  \n\u2022 Shift to intermediate insulin when patient\u2019s blood sugar and precipitating factor is under \ncomplete control. \n4. Potassium replacement :  \n\u2022 Serum K+ level may be increased initially because of K+ ion movement from ICF to \nECF in metabolic acidosis.  Later, the serum K+ becomes low because of both renal \nloss of K+ and the movement of K+ ions back to ICF as the acidosis is corrected.  \n\u2022 Patients with DKA are expected to have a potassium deficit of 300-400 mEq, which \nshould promptly be replaced. \n\u2022 Start replacing potassium as soon as the patient has adequate urine output.  \n\u2022 Potassium chloride (KCl) is infused at a rate of 20 -40 mEq/hr. \n\u2022 Monitor serum K+ level closely.  \n\u2022 Oral potassium can be given if IV potassi um is not available. Encourage patients to \neat potassium rich fruits such us banana. \n5. Close follow-up of patients"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45729-7265-11ef-b1e7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 465, "chroma:document": "\u2022 Monitor serum K+ level closely.  \n\u2022 Oral potassium can be given if IV potassi um is not available. Encourage patients to \neat potassium rich fruits such us banana. \n5. Close follow-up of patients  \n\u2022 Monitor serum glucose and potassium  as well as urine output hourly.   \n\u2022 Maintenance fluids  should consist of 0.45% (\u00bd strength) saline with additives as \nindicated; 150 to 200 ml/hr adjusted according to urine output.  \n\u2022 Evaluate for potential precipitating factors,  including infection, pregnancy, Myocardial \ninfarction, inappropriate use of insulin.  \n\u2022 Diet.  Oral intake may resume when mental status of the patient improves and nausea \nand vomiting are controlled. Initial diet should consist of fluids, and solid diet is may not \nbe resumed until ketoacidosis is corrected.   \n3) Hyperglycemic Hyperosmolar State ( Non-Ketotic Hyperosmolar Coma  ) \n\u2022 Usually occurs in elderly type 2 DM patients that do not develop ketosis."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4572a-7265-11ef-ae55-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 466, "chroma:document": "Internal Medicine \n \n 451\u2022 It is often precipitated by serious intercurrent illnesses such as myocardial infarction, \nstroke, pneumonia, sepsis etc.  \nSymptoms : \n\u2022 Such patients present with several weeks history of polyuria, weight loss, and \ndiminished oral fluid intake that is followed by mental confusion, lethargy or \ncomma.  \nPhysical examination :  \n\u2022 Patients have extreme dehydration, hypot ension, tachycardia and altered state of \nconsciousness or comma. The dehydration is caused by a hyperglycemia induced osmotic diuresis, when it is not matched by adequate fluid intake. \nLaboratory : Very high serum blood glucose level (may range from 600- 1200mg/dl)  \nTreatment involves  \n\u2022 Fluid replacement : administration of IV fluids and  \n\u2022 Bringing down the blood sugar rapidly by using rapidly acting insulin preparations  \n\u2022 Identifying and treating the precipitating factor  \n \nChronic Complications of Diabetes Mellitus  \n\u2022 The chronic complications of DM affect many organ systems and are responsible for \nmajority of morbidity and mortality associated with the diseases. \n\u2022 Prevention of chronic complication is one of the major goals of care of the diabetic \npatients. This is attempted by achieving as near normal blood glucose level as possible.  \n\u2022 Several studies have shown that with tight blood glucose control, the occurrence of \nchronic complications can be delayed by several years. \n1. Retinopathy :"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4572b-7265-11ef-b6dc-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 466, "chroma:document": "\u2022 Several studies have shown that with tight blood glucose control, the occurrence of \nchronic complications can be delayed by several years. \n1. Retinopathy :   \n\u2022 Is one of the commonest chronic complications and one of the leading causes of \nblindness in developed countries. \n\u2022 Symptoms may include difficulty of reading , blurring of vision,  shadowing which \nmay later on progress to total blindness,  \nClassification of Diabetic retinopathy \na) Background retinopathy : early changes which is often asymptomatic \n\u2022 Microaneurysm: occlusion of capillaries gives rise to distention and eventual \nrupture of vessels"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4572c-7265-11ef-ba30-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 467, "chroma:document": "Internal Medicine \n \n 452\u2022 Dot hemorrhages: -increased permeability of capillaries and from ruptured \naneurysms  \n\u2022 Hard exudates: proteins and lipids leak due to increased permeability of \ncapillaries \nb) Maculopathy : which manifests with impairment of central vision loss \nc) Proliferative retinopathy: asymptomatic unless complicated by hemorrhage \n\u2022 Characterized by new vessels formati on which is stimulated by ischemia  \nd) Advanced diabetic disease :  may cause  severe vision loss  to the extent of \ncomplete blindness \n\u2022 Extensive fibrovascular proliferation  develops following ischemia and \nnecrosis. \n\u2022 Retinal detachment  results from the deformity created by extensive fibrosis \n\u2022 Vitreous hemorrhage  refers to blood in the vitreous hemorrhage. \nManagement              \n\u2022 Laser therapy \n\u2022 ASA 100 mg /day may prevents further  occlusion of small capillaries \n\u2022 Surgery : Viterotomy removes blood clots and fibrosis that obstruct vision \n \n2. Neuropathy \nSymptoms: include \n\u2022 Burning sensation, numbness \n\u2022 Constipation or nocturnal diarrhea \n\u2022 Impotence \n\u2022 Foot ulcer \nClassification of Diabetic Neuropathy \na) Polyneuropathy: \n\u2022 Is the commonest neuropathy, characterized by distal symmetrical, \npredominantly sensory impairment which manifests with tingling \nsensation, numbness, burning sensation etc.  \n\u2022 It is often progressive and may lead to total loss of sensation and \nabsence of deep tendon reflexes."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4572d-7265-11ef-8d37-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 467, "chroma:document": "predominantly sensory impairment which manifests with tingling \nsensation, numbness, burning sensation etc.  \n\u2022 It is often progressive and may lead to total loss of sensation and \nabsence of deep tendon reflexes. \nb) Radiculopathy : characterized by neurogenic pain. It is often self limiting \nc) Amyotropy : atrophy of proximal muscles mainly around the hip girdle"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4572e-7265-11ef-8651-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 468, "chroma:document": "Internal Medicine \n \n 453d) Autonomic Neuropathy: may manifest with :- \n\u2022 Postural hypotension \n\u2022 GI manifestations: gustatory sweating, gastroparesis, nocturnal diarrhea \n\u2022 Genitourinary manifestations: neuropathic bladder, erectile dysfunction \n(impotence) \ne) Mononeuropathy: paralysis of a specific nerve or nerves  \nE.g. diplopia due to of third and sixth nerves palsies  \n \nNeuropathy management \n\u2022 Symptomatic treatment : pain control \n\u2022 Diarrhea control \n\u2022 Treatment of impotence  \n \n3. Nephropathy : is a common complication in DM.  \n  Clincal fetures \n\u2022 Periorbital edema (eye or facial puffiness),pedal edema , anasarca \n\u2022 Anemia, Uremia and osteodystrophy in patients with end stage renal diseases \nLaboratory:  Progression from micro albuminuria \u00c6 Macroalbuminuria \nManagement \n\u2022 Tight blood pressure control \n\u2022 ACE- inhibitors:  decreases progression of renal diseases \n\u2022 Renal transplantation or Dialysis in End stage renal diseases \n4. Diabetic Foot Ulcer \nThe following are underlying mechanism for diabetic foot ulcers \n\u2022 Neuropathy   \no Loss of pain sensation exposes to injury \no Loss of sweating results dry skin that is susceptible to injury \n\u2022 Vascular:  poor blood supply to the foot causes decreased healing of wound poor \nrecovery from secondary infections. \n\u2022 Abnormal Pressure loading : due to neuropathy (Charcot\u2019s joints) or anatomical \ndeformity of the feet. Since the foot is not in a normal anatomic position it is exposed to"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4572f-7265-11ef-958f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 468, "chroma:document": "recovery from secondary infections. \n\u2022 Abnormal Pressure loading : due to neuropathy (Charcot\u2019s joints) or anatomical \ndeformity of the feet. Since the foot is not in a normal anatomic position it is exposed to \nabnormal load and pressure sores develop."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45730-7265-11ef-8574-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 469, "chroma:document": "Internal Medicine \n \n 454Symptoms and signs of foot ulcer : numbness and burning, aching pain, swelling, darkening, \nabscess and cold extremity \nFoot care: should be essential part of diabetes care  \n\u0083 Put on comfortable shoe \n\u0083 Check for pebbles in shoe \n\u0083 Examine the foot daily to detect problems earlier \n\u0083 Wash dry and oil the feet \n\u0083 Take caution during nail cutting \n\u0083 Treat athletes\u2019 foot or any other foot infection as early as possible \n\u0083 Remove corn  \n\u0083 Do not use hot water to wash the feet \n\u0083 Stop smoking  \n \nReferences:   \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nAsthma,     pages 2152-2180. \n2) Diabetes in Africa, Geoff Gill et al pp123-131 \n3) Management of Diabetes Mellitus, A Manual for Use in Ethiopia , Second edition, \nF.T. Lester \n4) Management of Diabetes Mellitus: coping with limited facilities, J. Abdulkadir, A. \nReja. , EMJ V39,N4 ,2001,pp 349-365 \n5) Clinical features, complications, and mortality in type 2 patients in Addis, Abeba, \nEthiopia 1976-1990. F.T.  Lester, EMJ 1993:31:109-125"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45731-7265-11ef-b6bb-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 470, "chroma:document": "Internal Medicine \n \n 4553. Thyroid disorder  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define different forms of thyroid disorders. 2. Describe the pathophysiology of diseases of the thyroid. 3. Understand   the epidemiologic significance of diseases of the thyroid. \n4. Identify the clinical manifestation of diseases of the thyroid, with special emphasis on \nhyperthyroidism and hypothyroidism. \n5. Understand the diagnostic approach of diseases of the thyroid.  \n6. Manage patients with common thyroid diseases. 7. Understand the prevention of some preventable thyroid diseases. \n \nIntroduction:  \n\u2022 The thyroid gland normally weighs 20gm and is visible in thin women. The basic unit of \nthyroid structure is a follicle which is spherical in shape, filled with colloid, and \nencompassed by single epithelial cell layer. The colloid consists of thyroglobulins in \nwhich thyroid hormones are stored. About 40 follicles form a lobule, a group of lobules form a gland.  The hormones produced by t he thyroid gland are referred to as tri-\niodothyronine (T\n3) and thyroxin (T 4).  \n Thyroid disorders: \n\u2022 Manifest with qualitative or quantitative alteration of thyroid hormone secretion, \nenlargement of thyroid, or both.  \n\u2022 Decreased production of these hormones leads to what is referred to as hypothyroidism, \nwhich results in a state of declined metabolic activity."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45732-7265-11ef-b8b6-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 470, "chroma:document": "enlargement of thyroid, or both.  \n\u2022 Decreased production of these hormones leads to what is referred to as hypothyroidism, \nwhich results in a state of declined metabolic activity.  \n\u2022 Increased production on the other hand leads to hyperthyroidism, which in turn results in \na state of increased metabolic activity.  \n\u2022 Goiter is a diffuse or focal enlargement of the thyroid gland that may be metabolically \nhyperactive, hypoactive, or normoactive  (Euthyroid) \n Transport and Metabolism of hormones    \n\u2022 Of the total hormone in the blood, 80% is found in the form of T4 and 20% in the form of \nT3\n."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45733-7265-11ef-83e2-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 471, "chroma:document": "Internal Medicine \n \n 456\u2022 Ninety nine percent of hormones is bound to carrier proteins (thyroglobulin) and is not \nphysiologically active, and it is only the remaining 1%, which is found free in the serum, \nwhich is physiologically active.          \nThe advantages of carrier proteins are: \n\u2022 They are reservoirs to replenish free hormone level \n\u2022 They buffer any fluctuation in gland secretion \n\u2022 They protect against hepatic degradation and renal excretion of the hormone  \n Standard lab tests measure protein bound hormone level so that results depend on the concentration of these proteins. Therefore the hormone level alterations could be apparent like \nwhen the thyroglobulin (TGB) level shifts or real when the TBG remains constant but hormone \nlevel varies.  \n\u2022 Conditions in which TBG is increased are  : pregnancy, contraceptive (estrogen ) , \nandrogen , infectious hepatitis         \n\u2022 Conditions in which TBG is decreased  are :  steroid, chronic liver diseases                                \n \n                  Metabolic actions of thyroid hormones:   \nActing through nuclear receptors, these hormones play a critical role in are to regulate        \n\u2022 Cellular  differentiation during development  \n\u2022 Maintain thermogenic and metabolic homeostasis in adults  \n  Regulation of hormone production: \n\u2022 Hypothalamic TRH stimulates pituitary production of TSH, which in turn stimulates \nthyroid hormone synthesis and secretion."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45734-7265-11ef-a3c7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 471, "chroma:document": "\u2022 Maintain thermogenic and metabolic homeostasis in adults  \n  Regulation of hormone production: \n\u2022 Hypothalamic TRH stimulates pituitary production of TSH, which in turn stimulates \nthyroid hormone synthesis and secretion.  \n\u2022 The presence of adequate thyroid hormone sends a negative feedback signal that \ninhibits TRH and TSH production.  \n\u2022 When the level of thyroid hormone in the serum decreases the production and release of \nTRH and TSH is enhanced. \nTSH,  secreted by thyrotrope cells of the anterior pituitary, plays a pivotal role in control of \npituitary - thyroid axis and serves as the most useful physiologic marker of thyroid hormone function."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45735-7265-11ef-9407-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 472, "chroma:document": "Internal Medicine \n \n 457 \nThyroid function tests:        \n1. Serum T 3 and T 4 level : measures the total bound (99 %) and free (1 %) hormone level in the \ncirculation. This gives some clue about serum level of thyroid hormone, but has limitation \nsince serum level of the hormone is influenced by conditions affecting the level of carrier \nproteins.  \nT3 and T4 levels are elevated in hyperthyr oidism and decreased in hypothyroidism. \n \n2. Serum TSH level:  is the most important test to asses thyroid hormone function. \n\u2022 In hypothyroidism , TSH level is elevated, as a result of feedback effects of low thyroid \nhormone level. It is a very sensitive test and, because it usually becomes elevated even \nbefore thyroid hormone (T3 and T 4) level decline below normal. \n\u2022 In hyperthyroidism , TSH level is decreased, because the elevated thyroid hormone \nconcentration, leads to suppression of TSH release, through a negative feedback mechanism. It is a very sensitive tes t, because TSH may be suppressed even when \nthyroid hormone level are not elevated above normal range. \n3. Radioactive iodine uptake (RAIU):   by the thyroid gland 24 hrs after administration of the \nIodine ( I\n131) isotope, assesses the rate of iodine uptake by the thyroid gland which \ndemonstrates the degree of glandular activity.  \n\u2022 Increased uptake in hyperthyroidism, and decreased uptake in hypothyroidism. \n\u2022 This test is especially useful in diagnosing ectopic hormone production"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45736-7265-11ef-b246-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 472, "chroma:document": "demonstrates the degree of glandular activity.  \n\u2022 Increased uptake in hyperthyroidism, and decreased uptake in hypothyroidism. \n\u2022 This test is especially useful in diagnosing ectopic hormone production  \n4.  Thyroid stimulating antibodies , circulating antibody against T 3 and T 4 is an evidence for \nautoimmune disease of thyroid glands.  \n \nCommon disorders of Thyroid gland                   \nA. Sick euthyroid syndrome (SES) \nB. Simple nontoxic goitre (SNG) \nC. Hypothyroidism D. Hyperthyroidism                                                  \ni. Graves    \nii. Toxic multinodular goiter(TMNG) \niii. Toxic solitary nodular (TSN) iv. Jodbasdow phenomena"}


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": 473, "chroma:document": "Internal Medicine \n \n 458E. Thyroiditis \nF. Thyroid carcinoma             \n \nEpidemiology of Thyroid Diseases is Ethiopia \n\u2022 Simple nodular goiter is very common in areas where there is serious iodine deficiency. \n\u2022 Among 373 patients seen at the Endocrinology unit of Tikur Anbessa teaching hospital, \nbetween 1986 to 1991, 68% of all cases came for a thyroid disorder. Of these 44% were \nthyrotoxic, 24% has solitary nodules, 29% simple toxic goiter, while thyroiditis and hypothyroidism were rare.  \n\u2022 Among the thyrotoxics 42% were due to Graves\u2019 diseases, 32% due to Toxic \nmultinodular goiter, and 22% due to toxic nodule.   \n \nA. Sick Euthyriod Syndrome (SES)                                \n\u2022 This is a state in which serum level of thyroid hormones is abnormally low or high but \npatients are not symptomatic.  \n\u2022 Such clinical condition often results from severe illness, physical trauma, stress during \nwhich the thyroid hormone level may be low.  \n\u2022 In elderly patients taking drugs containing Iodine, serum level of thyroid hormones may \nbe abnormally high. Patients however remain asymptomatic probably due to decreased \nimpact on peripheral tissue.  \n \nB.  Hyperthyroidism \n \nDefinition:  Hyperthyroidism is a hypermetabloic state, resulting from excessive thyroid \nhormone function.   \nThyrotoxicosis  is defined as the sate of thyroid hormone excess. \nEtiology:   \nCommon causes of hyperthyroidism include: \n\u2022 Graves\u2018diseases \n\u2022 Toxic multinodular goiter \n\u2022 Toxic adenomas"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45738-7265-11ef-898a-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 474, "chroma:document": "Internal Medicine \n \n 459Graves\u2019 disease:   \n\u2022 Is the most common cause of hyperthyroidism in the third and fourth decades. It is \ncommon in women.  \n\u2022 This is an autoimmune diseases caused by abnormal thyroid stimulating immunoglobulin \nof IgG class which has long acting thyroid gland stimulating effect. \n\u2022 It causes a diffuse, symmetrically enlarged thyroid gland, with normal to slightly soft \nconsistency.   \n\u2022 It is associated with ophthalmopathy, dermatopathy and pretibial myxedema. \n\u2022 There is hyperthyroid state.  \n \nToxic multinodular goiter:   \n\u2022 It usually develops insidiously in a patient who has had a nontoxic nodular goiter for \nyears.  \n\u2022 The thyroid gland is irregular, asymmetric and nodular in nature. \n\u2022 This clinical condition may occur when a nontoxic multinodular goiter has been exposed \nto excess iodine intake or when one of the nodules become autonomous (fails to fall \nunder control of TSH-T 3 ,T4) feedback axis  \nSolitary hyperfunctioning adenomas:   \n\u2022 The thyroid gland contains a smooth, well-defined, soft to firm nodule that shows intense \nradioactive uptake on scan with absence of uptake in the rest of the gland.  \n\u2022 Most patients with solitary adenomas do not become thyrotoxic. When they do, they are \nusually less toxic than those with Graves\u2019 disease, and they do not develop \nophthalmopathy or pretibial myxedema.  \nAutoimmune thyroiditis/  Hashimoto\u2019s thyroiditis :  \n\u2022 Normal-sized or enlarged nontender thyroid gland."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45739-7265-11ef-aa24-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 474, "chroma:document": "usually less toxic than those with Graves\u2019 disease, and they do not develop \nophthalmopathy or pretibial myxedema.  \nAutoimmune thyroiditis/  Hashimoto\u2019s thyroiditis :  \n\u2022 Normal-sized or enlarged nontender thyroid gland.  \n\u2022 Thyroid antibodies, when present, are high in titer.  \n\u2022 This disorder improves spontaneously but frequently recurs.  \nExcess exogenous thyroid hormone administration:   \n\u2022 May occur because of dosage errors or occasionally in individuals taking large doses of \nthyroid hormones to lose weight or increase their energy.  \n\u2022 The thyroid gland is normal or small in size.  \nSubacute thyroidits and viral thyroiditis:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4573a-7265-11ef-9b6f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 475, "chroma:document": "Internal Medicine \n \n 460\u2022 Tender, diffusely enlarged thyroid gland with a normal or elevated T4 and an elevated \nESR.  \n\u2022 Probably of viral origin and may manifest as a sore throat.  \nRare causes:  Radiation thyroiditis, thyroid carcinoma, excessive TSH stimulation, excessive \niodine intake, struma ovarii, and trophoblastic disease.  \n \nClinical features: \n\u2022 Metabolic changes:  elevated basal metabolic rate, weight loss with increased appetite \nheat intolerance and sweating  \n\u2022 Cardiovascular effects:    \no Weakness, dyspnea on exertion \no Palpitation ,  sinus tachycardia  , atrial fibrillation in the elderly \no Systolic hypertension , high output failure  with wide pulse pressure  \n\u2022 Gastro Intestinal symptoms: loss stool or  diarrhea ( may be the first sign of thyroid \nstorm) \n\u2022 Skin and hair changes:  the skin  is warm and moist because of peripheral vasodilation \n, fine silky hair is characteristic finding  \n\u2022 CNS and neuromuscular effects  \no Nervousness, hyperactivity, irritabilit y, dysphoria, emotional lability, poor \nconcentration  \no Fine Tremor  \no Muscle weakness and fatigue proximal myopathy \n\u2022 Genitourinary manifestations  :Polyuria, dysmenorrhea, oligomenorrhea or \namenorrhea \n\u2022 Ophthalmopathy \no Wide stare and lid lag   ( i.e. slow closing of the upper  lid when the eye moves \ndown ward , revealing sclera between  the lid and cornea ) may occur in any form \nof hyperthyroidism  \no Exophthalmus: true thyroid exophthalmus is seen only in Graves\u2019 diseases,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4573b-7265-11ef-a6d4-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 475, "chroma:document": "down ward , revealing sclera between  the lid and cornea ) may occur in any form \nof hyperthyroidism  \no Exophthalmus: true thyroid exophthalmus is seen only in Graves\u2019 diseases, \noccurring in approximately 50 % of cases.  \n\u00be The eyes are pushed forward because of mucinous and cellular infiltration \nof extraocular muscles \n\u00be There is inflammation of the conjunctiva and surrounding tissue"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4573c-7265-11ef-a0e7-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 476, "chroma:document": "Internal Medicine \n \n 461\u00be The patient may complain tearing, eye irritation, pain and double vision. In \nsever case vision may be threatened. \n\u2022 Other findings \no Gioter \no Gynecomastia  \n \nFeatures specific to Graves\u2019 disease \n\u2022 Thyroid gland is diffusely enlarged  and smooth in consistency , bruit/thrill  may be \nheard over it \n\u2022 Ophthalmopathy :  exophthalmus  \n\u2022 Thyroid dermopathy : pretibial myxedema which is non inflamed indurataed plaque \n\u2022 Thyroid acropathy : clubbing \nDiagnosis: \n\u2022 TSH is elevated in 98 % of patients. It is the best screening test.  \n\u2022 Serum T3 and T4 level ( free or total ) may be raised  \n\u2022 Antithyroid antibodies: antimicrosomal antibody and antifollicular cell antibody, \nantithyroglobulin antibody, thyroid-stimulating antibody; elevated especially in autoimmune thyroiditis. \n \nTreatment : \nGraves\u2019 disease:  \n1. Antithyriod drugs: \n\u2022 Inhibit the oxidation of iodine and coupling of iodotyrosines, thus decrease the synthesis \nof thyroid hormone. PTU in addition decreases the conversion of T4 to T3 in peripheral \ntissues  Dose:   Propylthiouracil:  100 to 150 mg every 8 hours, or  \nMethimazole :  15 to 60 mg divided every 12 hours depending on severity of \nillness.  \n\u2022 Although blockade of hormones synthesis is rapid, clinical improvement occurs after few \nweeks or months, because a large pool of stored hormone continues to be released from thyroid.  \n\u2022 The patient becomes euthyroid 2 to 3 months after beginning therapy."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4573d-7265-11ef-9aa3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 477, "chroma:document": "Internal Medicine \n \n 462\u2022 Propylthiouracil may achieve results faster because it prevents the peripheral conversion \nof T 4 to active T 3.  \n\u2022 After clinical improvement, the dose of the medication is tapered to the lowest dose to \nmaintain euthyroid state and the drug is continued for 1 - 1 \u00bd yrs. \n\u2022 A free T 4 level should be checked after 1 month of therapy and then every 2 to 3 months.  \nSide effects /drug toxicity  \n\u2022 Skin rash or joint pain \n\u2022 Agranulocytosis \nAdvantages of Atithyroid drugs: \n\u2022 Hospitalization , surgery and anesthesia are avoided \n\u2022 The occurrence of post treatment hypothyroidism is less likely   \nDisadvantages:  \n\u2022 Permanent remission occurs in fewer than 50 % of patients  \n\u2022 Treatment success depends on patient compliance to treatment  \n2. Radioactive iodine  \n\u2022 Iodine 131, 5 to 15 mCi, a single dose of 131 I, causes a decrease in function and size of \nthe thyroid gland in 6- 12 weeks.  \n\u2022 Approximately 75 % of patients with Grav es\u2019 disease are made euthyriod by a single \ndose. \n\u2022 Those who are still thyrotoxic after 12 weeks are given a second dose. Additional dose \ncan be given if needed.  \n\u2022 Eventually, almost all patients are cured in this way.  \n\u2022 131 I treatment may be   preceded and followed by antithyroid drugs.  \nAdvantages: \n\u2022 Hospitalization , surgery and anesthesia are avoided \n\u2022 The rate of cure is almost 100% \n\u2022 Little patient compliance is required  \nDisadvantages: \n\u2022 There is a risk of treatment induced hypothyroidism"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4573e-7265-11ef-aea2-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 477, "chroma:document": "Advantages: \n\u2022 Hospitalization , surgery and anesthesia are avoided \n\u2022 The rate of cure is almost 100% \n\u2022 Little patient compliance is required  \nDisadvantages: \n\u2022 There is a risk of treatment induced hypothyroidism  \nPregnancy is an absolute contraindication to 131I therapy. \n \n3. Inorganic iodine  rapidly controls hyperthyroidism by inhibiting hormone synthesis and \nrelease from the gland."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4573f-7265-11ef-b78f-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 478, "chroma:document": "Internal Medicine \n \n 463\u2022 One drop of saturated potassium iodide solution in juice is taken daily.  \n\u2022 This should not be used as the sole form of therapy.  \n\u2022 It may be used alone for 7 to 10 days before surgery to decrease the vascularity of the \nthyroid gland. \nSurgery: Subtotal thyriodectomy  - usually reserved for those who are unable to take \nantithyroid drugs  \nPreparation for surgery: \n\u2022 Operation on thyrotoxic patient produces the risk of thyroid storm; therefore, treatment \nshould be initiated with atntithyriod drugs, long enough in advance for patients to return \nto a euthyriod state before surgery. Inorganic iodine may be given to decrease \nvascularisation before surgery. \nAdvantages of surgery \n\u2022 Cure of hypothyroidism is rapid \n\u2022 The success rate is high , most patient are cured  \n\u2022 Patient compliance is required for shorter period \nDisadvantages \n\u2022 The patient must be hospitalized , and surgical and anesthetic risks are incurred \n\u2022 Surgical complications include : hypothyroidism and recurrent laryngeal nerve paralysis \n \nOther symptomatic treatments:  \n\u2022 Propranolol:  80 to 200 mg/day in divided doses every 6 hourly, will reduce symptoms \nof tachycardia, palpitations, heat intolerance, and nervousness but will not normalize the metabolic rate. It should not be used alone except in the case of transient \nhyperthyroidism secondary to autoimmune (viral) thyroiditis. \n Ophthalmopathy:   \no Smoking can worsen ophthalmopathy. Ophthalmopathy may also worsen"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45740-7265-11ef-a229-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 478, "chroma:document": "hyperthyroidism secondary to autoimmune (viral) thyroiditis. \n Ophthalmopathy:   \no Smoking can worsen ophthalmopathy. Ophthalmopathy may also worsen \n(usually transiently) with radioactive iodine.  \no This can be prevented by treatment with prednisone (0.5 mg/kg PO for 3 months \nstarting 2 to 3 days after radioactive iodine). However, this carries the risk of \nprednisone exposure."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45741-7265-11ef-900f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 479, "chroma:document": "Internal Medicine \n \n 464o Symptomatic treatment for ophthalmopathy includes artificial tears or \nmethylcellulose drops for the discomfort, patching or prisms for diplopia, diuretics \nand raising the head of the bed for circumorbital edema. \n Treatment of other causes of hyperthyroidism  \n\u2022 Toxic multinodular goiter  is treated with surgery or I-\n131. \n\u2022 Solitary hyperfunctioning adenomas are treated with I-131 or surgery.  \n\u2022 Autoimmune thyroiditis  is transient and does not require definitive treatment except in \nthose patients with recurrent hyperthyroidism. Propranolol may be used alone if symptoms are mild. Antithyroid drugs may be needed for a short time in some patients. \n\u2022 Subacute thyroiditis  and viral thyroiditis generally self-limited but should be treated \nwith aspirin 650 mg QID. In more severe cases, prednisone may be used at 40 mg PO QD, tapering to 10 mg each day over 2 weeks, and then continued for 1 month after patient becomes asymptomatic. Resolution of symptoms usually occurs in 1 to 6 \nmonths, and relapse is common. Hypothyroidism may occur but is rare. \n \nThyroid storm \nDefinition:  A severe life-threatening form of hyperthyroidism. \nEtiology:  Increasing stress such as trauma or illness may cause this in a previously mildly \nhyperthyroid patient. \nSigns and symptoms:  Have signs and symptoms consistent with thyrotoxicosis (tachycardia, \nheat intolerance, weight loss), as well as fever, confusion, agitation, weakness, dyspnea, \ndiarrhea, and shock."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45742-7265-11ef-b3b1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 479, "chroma:document": "hyperthyroid patient. \nSigns and symptoms:  Have signs and symptoms consistent with thyrotoxicosis (tachycardia, \nheat intolerance, weight loss), as well as fever, confusion, agitation, weakness, dyspnea, \ndiarrhea, and shock. \nTreatment : \nWhen suspected, treatment should be instituted immediately.   \nSupportive therapy: \n\u2022 Control fever:  Fever is controlled with acetaminophen and a cooling blanket. If fever is \nnot controlled within several hours, concurrent infection should be suspected. Other \nsigns of hyperthyroidism may require seve ral days of therapy before improvement is \nseen. \n\u2022 Propranolol 20 to 40 mg QID to control tachycardia, tremor, \n\u2022 Fluid and electrolytes  : should be replaced"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45743-7265-11ef-8b51-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 480, "chroma:document": "Internal Medicine \n \n 465Antithyriod treatment  \n\u2022 Propylthiouracil:  250 mg PO QID (Or methimazole  20 to 40 mg PO or per NG Q6-8h).  \n\u2022 Alternative is 0.5 g of sodium iodide in 1 L of NS over 12 hours.  \n\u2022 Give steroids  equivalent to about 300 mg of hydrocortisone per day (100 mg IV TID \nQ8h). Dexamethasone has some theoretical advantage because it prevents conversion \nof T 4 to T 3 peripherally.  \n\u2022 Avoid aspirin  because it may increase circulating active T 3 and T 4 by reducing protein \nbinding. \n       \nC.  Hypothyroidism \n \nDefinition:   \nPrimary hypothyroidism:  refers to a thyroid hormone deficiency as a result of thyroid gland \ndisease. Secondary hypothyroidism : results from TSH deficiency.  \nTertiary hypothyroidism:  results from thyrotropin-releasing hormone (TRH) deficiency. \nEtiology: \nWithout thyroid enlargement \n\u2022 Hypothyroidism frequently develops following treatment of Graves\u2019 disease with 131I \ntherapy or thyriodectomy.  \n\u2022 Idiopathic hypothyroidism: is idiopathic atrophy of the thyroid gland. It is one of the \ncommonest causes of hypothyroidism. \n\u2022 Developmental defects and TSH or TRH deficiency are less common causes. \nWith thyroid enlargement \n\u2022 Chronic thyroiditis /Hashimoto\u2019s thyroiditis  is one of the most common causes of \nspontaneous hypothyroidism.  \n\u2022 Drugs, iodine deficiency, and inherited defects in thyroid hormone synthesis are rare \ncauses. \nSigns and symptoms: \n\u2022 Fatigue, weakness, lethargy, slow movement, cold intolerance"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45744-7265-11ef-a9ea-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 480, "chroma:document": "spontaneous hypothyroidism.  \n\u2022 Drugs, iodine deficiency, and inherited defects in thyroid hormone synthesis are rare \ncauses. \nSigns and symptoms: \n\u2022 Fatigue, weakness, lethargy, slow movement, cold intolerance \n\u2022 Slight to moderate weight gain , but appetite tends to be diminished  \n\u2022 Carpal tunnel syndrome, edema of the face and extremities, \n\u2022 Hearing loss, hoarseness of the voice  \n\u2022 Dry skin  , hair loss , sparse eyebrows with loss of the lateral half"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45745-7265-11ef-aa5f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 481, "chroma:document": "Internal Medicine \n \n 466\u2022 Pericardial effusion and ascites occasionally occur  \n\u2022 Constipation \n\u2022 Menorrhagia, \n\u2022 Memory impairment \n\u2022 Psychosis may develop with long-standing hypothyroidism and may be precipitated by \nthyroid hormone replacement \nPhysical examination  \n\u2022 Thickened, puffy features is due to accumulation of mucinous mucoplysaccharide-rich \nmaterial in tissues .This is known and myxedema \n\u2022 Yellowish dry skin  \n\u2022 Nonpitting edema \n\u2022 Hypothermia  \n\u2022 Bradycardia    \n\u2022 A delay in return phase of Achilles and other deep tendon reflexes is a specific finding. \n\u2022 Loss of the lateral portion of the eyebrows ( madarosis ) \nEffect of hypothyroidism on organ systems  \n\u2022 Cardiovascular system : Decrease in cardiac output ,Pericardial effusion  \n\u2022 Respiratory system : Hypoventilation  ,Plural effusion \n\u2022 Gastrointestinal tract : Constipation \n\u2022 Nervous system: Decreased mental function , Psychi atric changes ( e.g. psychosis , \ndepression )  \n\u2022 Blood: Normocytic normochromic anemia.  \nCretinism : is sever hypothyroidism beginning in infancy infants may have  \n\u2022 Hypotonia, umbilical hernia,  \n\u2022 Delayed mental and physical development, and mental retardation may result if \nhypothyroidism goes untreated in the first few years of life. \n\u2022 Shot limbs and a large head , with a bread flat nose , widely set eyes , and a large \ntongue characterize this form of dwarfism \n\u2022 Other signs and symptoms typical of adult patients may also be seen   \n \nDiagnostic workup:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45746-7265-11ef-bd40-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 481, "chroma:document": "\u2022 Shot limbs and a large head , with a bread flat nose , widely set eyes , and a large \ntongue characterize this form of dwarfism \n\u2022 Other signs and symptoms typical of adult patients may also be seen   \n \nDiagnostic workup:  \nThyroid function tests: \n1. Serum TSH level:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45747-7265-11ef-ad55-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 482, "chroma:document": "Internal Medicine \n \n 467\u2022 Increased serum concentration of TSH is the earliest and the most sensitive indicator \nof primary hypothyroidism.   \n\u2022 Low TSH value indicates a secondary (pituitary) or tertiary (hypothalamic) \nhypothyroidism.  Both are rare causes of hypothyroidism. \n\u2022 Serum T 3 and T 4 level are decreased   \n2. Other laboratory abnormalities may include  : \n\u2022 High AST, low sodium, low blood glucose, elevated CPK,  \n\u2022 Elevated cholesterol and triglycerides, \n\u2022 Mild normocytic normochromic  anemia,  \n\u2022 Elevated prolactin levels secondary to high TRH levels, and \n\u2022 ECG:  flat or inverted T waves with minor ST-segment depression and low amplitude  \n \nTreatment :  \nThyroid hormone replacement: L-thyroxin, a synthetic agent is the treatment of choice. \nThe goal of therapy is to normalize the TSH. \nInitiation of treatment:  \nSlow initiation:  \n\u2022 Patients with severe hypothyroidism, older patients and patients with cardiovascular \ndisease, may have an increased sensitivity to thyroid hormone, and are at risk of acute cardiovascular and other complications, if hypothyroidism is corrected too quickly.  \n\u2022 Therefore, these patients should be given a very small dose of thyroid hormone initially \n(25 \u03bcg of L-thyroxin) which is gradually increased (every 2 to 4 weeks) to a full \nmaintenance dose during 6-12 weeks period. \nRapid initiation  \n\u2022 Younger patients and patients with less sever hypothyroidism, may be started on slightly"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45748-7265-11ef-88d5-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 482, "chroma:document": "(25 \u03bcg of L-thyroxin) which is gradually increased (every 2 to 4 weeks) to a full \nmaintenance dose during 6-12 weeks period. \nRapid initiation  \n\u2022 Younger patients and patients with less sever hypothyroidism, may be started on slightly \nhigher dose ( 50 \u03bcg of L-thyroxin ) and advanced to a full replacement dose more quickly \n(e.g. , the dose may be raised to 100 \u03bcg two weeks and 125 -150 \u03bcg in another 2 weeks)  \n\u2022 Check the TSH 2 to 3 months after changing the L-thyroxin dose.  \nMaintenance therapy  \n\u2022 Most patients require 75 -100 \u03bcg of L-thyroxin daily \n\u2022 When symptoms of hypothyroidism hav e resolved, the dosage should be further \nadjusted  so that serum TSH and thyroid hormone level  are maintained in the normal range"}


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": 483, "chroma:document": "Internal Medicine \n \n 468Cautions  \n\u2022 Elective surgery should be avoided in hypothyroid patients because respiratory \ndepression commonly occurs.  \n\u2022 Increased sensitivity to narcotics and hypnot ics is also common in the hypothyroid \npatient.  \n \nMyxedema Coma \nDefinition:  Myxedema coma results from severe chronic hypothyroidism, which is left \nuntreated, and is life threatening clinical condition. \n \nThis serious condition may occur gradually ( over years)  or more acutely in response to  a \nprecipitating factor such as  exposure to cold, infection, hypoglycemia, respiratory depressants, allergic reactions, or other metabolic stress. \nClinical features:  \n\u2022 Hypothermia, hypoglycemia, shock, hypoventilation, and paralytic ileus \n\u2022 Severely impaired level of consciousness \n\u2022 The mortality rate is 50 % -75% \nTreatment:  must be started rapidly, despite the risk associated with sudden hormone \nreplacement  \nL-thyroxin (T\n4) 500 \u00b5g is given as IV bolus injection, followed by oral L- thyroxin 100  \u00b5g QID.  \nAncillary treatment:  \n\u2022 Temporary use of glucocorticosteriods  \n\u2022 Respiratory support  \n\u2022 Hypothermia and heat loss should be avoided \n \nD.  Thyroid enlargement \n \n Goiter \n\u2022 A goiter is a simple enlargement of the thyroid gland. \n\u2022 It is more common in females with the highest incidence in the second through sixth \ndecades of life."}


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": 484, "chroma:document": "Internal Medicine \n \n 469\u2022 Diffusely enlarged goiters are caused by i odine deficiency or excess, congenital defects \nin thyroid hormone synthesis and drugs (e.g., lithium carbonate) dietary causes such as \ncabbage, soybean, cassava etc. \n\u2022 Most are asymptomatic. It is unusual to have pain and rare to have hoarseness and \ntracheal obstruction.  \n\u2022 Thyroid function tests should be performed on all patients with goiter because it can be \nassociated with hypothyroidism, euthyroidism, or hyperthyroidism. \n \nMultinodular Goiter \nEtiology:  most often caused by iodine deficiency. \nSigns and symptoms: Symptoms: \n\u2022 Thyromegaly, occasionally with rapid enlargement and tenderness secondary to \nhaemorrhage into a cyst.  \n\u2022 Rarely, tracheal compression may occur, causing coughing or choking.  \n\u2022 Some patients may complain of a feeling of lump in the throat. \nPhysical exam \n\u2022 Many nodules of varying sizes are usually pal pable. Occasionally it may be difficult to \ndistinguish from the typically lobulated, irregular Hashimoto\u2019s gland. \nDiagnosis:   \n\u2022 Thyroid function tests: Performed to rule out hypo or hyperthyroidism  \n\u2022 Malignant transformation is rare, but should be considered if the gland is enlarging \nrapidly or hoarseness develops. \nTreatment:   \nThe main indications for treatment are compression of the trachea or esophagus and venous-outflow obstruction.  For nontoxic multinodular goiter , the treatments include: \n\u2022 Surgery \n\u2022 Raradioiodine therapy ,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4574b-7265-11ef-b924-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 484, "chroma:document": "Treatment:   \nThe main indications for treatment are compression of the trachea or esophagus and venous-outflow obstruction.  For nontoxic multinodular goiter , the treatments include: \n\u2022 Surgery \n\u2022 Raradioiodine therapy ,  \n\u2022 L-thyroxin suppression therapy:  decreases TSH level and help to decrease the size of \nthe goiter.  \no Such therapy should not be given to patients with angina or other known heart \ndisease unless the patient is hypothyroid."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4574c-7265-11ef-a6a4-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 485, "chroma:document": "Internal Medicine \n \n 470o If thyroid enlargement persists despite adequate TSH suppression, a needle \nbiopsy or subtotal thyriodectomy should be considered. \nFor toxic multinodular goiter , options are \n\u2022 Antithyroid agent \n\u2022 Surgery \n\u2022 Radioiodine, and more recently  \n\u2022 Percutaneous injection of ethanol in to the toxic nodule  \n \n Solitary Nodules \n\u2022 They are usually benign. \n\u2022 One should, suspect malignancy in a patient with a history of radiation exposure, rapid \nenlargement, hoarseness or obstruction, and a solid nodule that is cold on scan. \nDiagnosis:   \n\u2022 History and  \n\u2022 Radio iodine thyroid scan should be done on every patient with a solitary nodule. Hot \nnodules that take up the radioisotope are generally benign but fine-needle aspiration of a \nsolitary nodule is prudent. \nTreatment:  \n\u2022 Is indicated if signs of compression of trachea, esophagus, significant growth, and \nrecurrence of a cystic nodule after aspiration.  \n\u2022 Similar to multinodular goiter: surgery, thyroxin, or radioiodine for nontoxic nodule; \nAntithyriod agent, Surgery, radioiodine for toxic nodule. \n \nSubacute Thyroiditis/granulomatous thyroiditis \nEtiology: the cause is generally considered as viral. Mumps and Coxackievarus have been suspected as causes.  Clinical features: \n\u2022 Early symptoms : prodromal phase of malaise, upper respiratory symptoms, and fever \nthat lasts 1-2 weeks. Then the Thyroid gland becomes enlarged, firm and tender, with \npain radiating to the ears, neck, or arms."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4574d-7265-11ef-b9a1-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 485, "chroma:document": "\u2022 Early symptoms : prodromal phase of malaise, upper respiratory symptoms, and fever \nthat lasts 1-2 weeks. Then the Thyroid gland becomes enlarged, firm and tender, with \npain radiating to the ears, neck, or arms. \n\u2022 Hyperthyroidism  may occur, due to thyroid hormone leaking from damaged follicles in \nto the circulation."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4574e-7265-11ef-a7a8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 486, "chroma:document": "Internal Medicine \n \n 471Disease course:  the thyroid pain and the hyperthyroidism subside in few weeks to months. The \ngland usually return to normal size, if enlarge ment persists, chronic thyroiditis should be \nsuspected. \nDiagnosis ; \n\u2022 Acutely swollen, tender an painful thyroid gland associated with symptoms of \nhyperthyroidism  \n\u2022 Radioactive uptake : low radioactive iodine uptake in the face of high serum T 3 and T 4 \nlevel. This is because the follicles are damaged are unable to trap iodine. \nTherapy is symptomatic : because the diseases are self limited \n\u2022 Aspirin , NSAID and Corticosteroids ( in severe cases ) to relive the pain and tenderness \n\u2022 \u03b2-blockers can be used to relive symptoms of hyperthyroidism .  \n \nChronic Thyroiditis (Hashimoto thyroiditis)  \n \nEtiology:  it is an autoimmune disorder that mainly affects women. Antithyriod antibodies are \npresent in most patients. \nClinical features  \n\u2022 Thyroid gland enlargement : is the main clinical manifestation, is the result of \nautoimmune damage that leads to lymphocytic in filtration, fibrosis and weakens ability of \nthe thyroid to produce hormone.  \n\u2022 Pain and tenderness  of the gland in subacute thyroiditis  \n\u2022 Hypothyroidism  is present in approximately 20 % of patients  \nDiagnosis:  is suspected in any patient with firm, nontoxic goitre \n\u2022 Serology : high titer of antithyroglobulin antibodies, antimicrosomal antibodies \n\u2022 Thyroid function tests  are often normal unless the patient has hypothyroidism"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4574f-7265-11ef-b725-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 486, "chroma:document": "Diagnosis:  is suspected in any patient with firm, nontoxic goitre \n\u2022 Serology : high titer of antithyroglobulin antibodies, antimicrosomal antibodies \n\u2022 Thyroid function tests  are often normal unless the patient has hypothyroidism  \nTherapy:  \n\u2022 L-thyroxin often decreases the size of the gioter and it is useful even in patients with \nnormal thyroid function \n \nMalignancies of the thyroid  \nEpidemiology:  \n\u2022 Thyroid cancer is common; it is found at autopsy in approximately 5 % of patients with \nno known thyroid diseases"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45750-7265-11ef-aa99-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 487, "chroma:document": "Internal Medicine \n \n 472\u2022 It is usually an indolent cancer and tends to  remain localized to the thyroid for many \nyears , which is the reason for the low morality rate   \nEtiology:   \n\u2022 Genetic factors  : one form of thyroid cancer , medullary c.a. has familial tendency  \n\u2022 Radiation exposure : the incidence of thyroid cancer is increased among atomic bomb \nsurvivors.  \nTypes/ Classification: \n\u2022 Papillary  carcinoma  : which accounts for 60 % of all thyroid cancer \no Affects younger age group \u2013 50 % of patients are younger than 40 years  \no Papillary Ca metastasize through the lymphatic system \n\u2022 Follicular carcinoma;  comprises 25 % of all thyroid cancer  \no Histologicaly resembles normal thyroid tissue ,  \no Follicular Ca metastasizes hematogenously \n\u2022 Medullary carcinoma : which accounts for 5 % of all thyroid cancers. Arises from \nparafollicular cells.  \no Produce calcitonin, patients may have diarrhea. \no  May be associated with multiple endocrine neoplasia syndromes, MEN type  II  \no Approximately 20 % of these carcinomas are familial. \n\u2022 Anaplastic carcinoma:  account for 10 % of thyroid cancer, usually affects patients \nolder than 50 years of age and is highly malignant.  \n\u2022 Other rare malignancies  (lymphoma, sarcoma etc.); secondaries of other tumours \nSigns and symptoms:   \n\u2022 A hard nodule in the thyroid is usually the first sign. \n\u2022 Late signs: hard, immobile thyroid, attached with skin, cervical or supraclavicular lymph"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45751-7265-11ef-82c6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 487, "chroma:document": "Signs and symptoms:   \n\u2022 A hard nodule in the thyroid is usually the first sign. \n\u2022 Late signs: hard, immobile thyroid, attached with skin, cervical or supraclavicular lymph \nnodes enlarged, hoarseness, Horner syndrome, throat/ear/head pain, stridor, dysphagia, \nvenous congestion. \nDiagnosis: \n\u2022 Ultrasound: nodules \n\u2022 Scintigraphy/radioiodine uptake: cold nodules without or little uptake \n\u2022 CT/MRI of neck  \n\u2022 FNA with cytology or biopsy  \n\u2022 Serum Calcitonin level ,  \n\u2022 Staging is based on : CXR, CT, bone scintigraphy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45752-7265-11ef-9708-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 488, "chroma:document": "Internal Medicine \n \n 473 \nTreatment:  Always combine  \n\u2022 Surgery:  total thyroidectomy and neck dissection \n\u2022 Radiotherapy: external radiation in Anaplastic carcinoma \n\u2022 Nuclear medicine: 131I ablative radiotherapy.  \n\u2022 Give T4, as high a dose as possible, to suppress TSH-effect on remaining metastases.  \n Reference  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Diseases of the thyroid gland, pages 2104-2126. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3\nrd edition \nDiseases of the thyroid gland, pages 457-467.  \n3) The pattern of adult diseases in Adult Ethiopians and experience in their management. M. Mulugeta, EMJ , 1993:31:25-35 \n4) Surgical goitre in Ethiopians Taye Mekuria ,Eth med jour 1977:15;169-172 \n5) Experience with thyroid scintigraphy in Ethiopian patients Solomon Demena,EMJ 1993,31:1-7"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45753-7265-11ef-810b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 489, "chroma:document": "Internal Medicine \n \n 4744. Diseases of the adrenal gland  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define different types of diseases of the adrenal gland. 2. Describe the pathophysiology of diseases of the adrenal gland. 3. Identify the clinical manifestation of diseases of the adrenal gland, with special emphasis \non Cushing\u2019s syndrome and Addison\u2019s diseases. \n4. Understand the diagnostic approach of diseases of the adrenal gland.  5. Manage patients with common diseases of the adrenal gland. \n \nCommon  Adrenal gland diseases  \n1. Disease of the adrenal cortex  a) Resulting from excess production of hormones  \n\u2022 Cushing\u2019s syndrome : excess cortisol production \n\u2022 Primary hyperaldosteronism : excess production of aldosteron \nb) Inadequate production ; \n\u2022 Addison\u2019s diseases : inadequate production of cortisol and aldosteron  \n2. Disease of the adrenal medulla \n\u2022 Pheochromocytoma : excess production of catecholamine  \n \nCushing\u2019s Syndrome ( Hypercortisolism) \n \nCushing\u2019s syndrome : is caused by excessive concentration of cortisol or other glucocorticoid \nhormones in the circulation \nEtiology:   \na) Bilateral adrenal hyperplasia (Cushing\u2019s diseases)  is the commonest cause of \nCushing\u2019s syndrome. It is caused by increas ed pituitary secretion of ACTH. Pituitary \ntumors large enough to be seen by skull x-ray, are present in more than 10 % of these \npatients, and smaller basophilic adenomas are found in more than 50 % of patients."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45754-7265-11ef-aac2-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 489, "chroma:document": "tumors large enough to be seen by skull x-ray, are present in more than 10 % of these \npatients, and smaller basophilic adenomas are found in more than 50 % of patients. \nb) Adrenal adenomas and adrenal carcinoma  may produce excess cortisol"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45755-7265-11ef-a5d5-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 490, "chroma:document": "Internal Medicine \n \n 475c) Ectopic ACTH production by tumors  , such as oat cell carcinoma of the lung, \ncarcinoma of the pancreas , bronchial carcinod tumors , and other, cause adrenal \nhyperplesia and Cushing\u2019s syndrome \nd) Iatrogenic Cushing\u2019s syndrome : is seen more often than spontaneous occurring \nsyndrome. It is an expected complication in patients receiving long term glucocorticiod \ntreatment for asthma, arthritis, and other conditions. \nClinical features  \n\u2022 Central obesity  is caused by the effect of excess cortisol on fat distribution. Fat \naccumulation in the face, neck and trunk, while thelimns remain thin. The \u201cmoon face \u201d , \n\u201cbuffalo hump\u201d  ( cervical fat pad ) and supraclavicular fat pads  contribute to the \nCushingiod appearance  \n\u2022 Hypertension : result from the vascular effects of cortisol and sodium retention \n\u2022 Decreased glucose tolerance : is common, 20 % of patients have overt diabetes. This \nis a result of hepatic gluconeogenesis, and decreased peripheral glucose utilization. \n\u2022 Symptoms of androgen excess  (e.g. oligomenorrhea, hirsutism, and acne) may occur \nin women with Cushing\u2019s diseases, because  of stimulation by ACTH of adrenal \nandrogen production. \n\u2022 Purple striae : are linear marks on the abdomen, where the thin, wasted skin is \nstretched by underlying fat. Atrophic skin with senile purpura may also be seen. \n\u2022 Muscle wasting and weakness:  reflects the catabolic effect of cortisol on muscle \nprotein."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45756-7265-11ef-9c74-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 490, "chroma:document": "stretched by underlying fat. Atrophic skin with senile purpura may also be seen. \n\u2022 Muscle wasting and weakness:  reflects the catabolic effect of cortisol on muscle \nprotein. \n\u2022 Osteoporosis:  is caused by increased bone catabolism. \n\u2022 Susceptibility to bruising:  is probably caused by enhanced capillary fragility. \n\u2022 Psychiatric disturbance , especially depression, are frequently seen. \n\u2022 Poor wound healing: due to impaired immune function.   \n\u2022 Growth retardation  in children may be severe.  \n       Diagnosis:  \n1.  Overnight Dexamethasone suppression test :  is recommended as an initial screening test  \nAdminister dexamethasone 1 mg PO at 11 PM at midnight and measure serum cortisol at 8:00 AM the following day  The serum cortisol level should be <5 \u00b5g/dl in most individuals, indicating normal \nsuppression of ACTH and cortisol by dexamethasone. Because this test is sensitive, the \ndiagnosis of Cushing\u2019s syndrome need not be considered further in these cases."}


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": 491, "chroma:document": "Internal Medicine \n \n 476Patients with Cushing\u2019s syndrome will have cortisol level > 5 \u00b5g/dl usually greater than 10 \n\u00b5g/dl .This result indicates further study is needed.  \n2.     The standard dexamethasone suppression test:  is the most relied up on test for Cushing\u2019s \nsyndrome  \n \nTable VII-3-1 Standard Dexamethasone Suppression Test in the diagnosis of Cushing\u2019s \nsyndrome \n \n Method \nDay Dosage of Dexamethasone Measurement \n1 \n  2,3  \n \n4,5 None ( baseline )    Low dose ( O.5 mg dexamethasone \nPO QID ) \n High dose dexamethasone 2 mg every  QID 24 hrs urinary 17-hydroxycorticosteriod and 4 PM serum cortisol level  Repeat measurement on day 3  \n \nRepeat measurement on day 5\n  \n \nResponse \nDiagnosis  Suppression with low \ndose Suppression with \nhigh dose  \nNormal  Yes  Yes  \nCushing\u2019s diseases  No Yes \nAdrenal tumor  or ectopic ACTH \nproduction  No No \n \n3. ACTH measurement : may help to differentiate the cause of Cushing\u2019s syndrome  \na. High normal or slightly elevated A CTH\u00c6Cushing\u2019s diseases \nb. Markedly elevated ACTH  \u00c6 Ectopic ACTH production \nc. Extremely low ACTH level \u00c6 automatically functioning adrenal tumor is the \nsource of excess cortisol. Pituitary secretion of ACTH is suppressed due to the excess cortisol"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45758-7265-11ef-95db-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 492, "chroma:document": "Internal Medicine \n \n 4774. Serum cortisol level: in normal in individuals is highest in early morning and decreases \nthroughout the day, reaching a low point at about midnight. Although the morning level may \nbe increased in patients with Cushing\u2019s syndrome, a loss of the normal diurnal variation and \nan increase in the evening level are more consistent findings.  \n5. The 24 hrs urinary free cortisol excretion rate : is increased in most patients with \nCushing\u2019s syndrome  \n6. Other tests: lukocytosis , with relatively low percentage of lymphocytes and eosinophils  \n7. Radiologic findings  \na. Skull x-ray: enlargement of sella turcica in 10 % of patients with Cushing\u2019s \nsyndrome who have macroadenoma.  \nb. CT scan with injection of contrast medium : detect approximately 50 % of \npituitary adenomas \nc.  CT scan of the adrenal gland:  reveal most adrenal tumors. Uniform \nenlargement of both adrenal glands suggests an ACTH dependent Cushing\u2019s \nsyndrome ( ether Cushing\u2019s diseas e o r the ectopic ACTH syndrome  ) \nTherapy  \n1. Adrenal adenoma : complete surgical resection of the adenoma cures the disease , but \npatients may need cortisol replacement post operatively for several month s \n2. Ectopic ACTH syndrome: can be cured by treating or removal of the tumor that is \nproducing the ectopic ACTH. \n3. Cushing\u2019s Disease \na. Pituitary radiation : is effective in children but it cures fewer than 1/3 of adult \npatients \nb. Bilateral adrenalectomy cures Cushing\u2019s diseases ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45759-7265-11ef-88cf-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 492, "chroma:document": "producing the ectopic ACTH. \n3. Cushing\u2019s Disease \na. Pituitary radiation : is effective in children but it cures fewer than 1/3 of adult \npatients \nb. Bilateral adrenalectomy cures Cushing\u2019s diseases . \nDisadvantages  \n\u2022 Patients will develop Addison\u2019s disease  and need lifelong Cortisol \nreplacement \n\u2022 Nelson\u2019s syndrome : in which pituitary adenomas undergo rapid growth, \nperhaps because it is no longer inhibited by above normal level of cortisol . \nc. Transphenoidal pituitary surgery: \n\u2022 Is the treatment of choice, even when tumor cannot be seen on CT scan \nor MRI , transspheniodal exploration may disclose a microadenoma."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4575a-7265-11ef-b4a1-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 493, "chroma:document": "Internal Medicine \n \n 478\u2022 Surgery is successful in 50%-95% of cases and is followed by normal \npituitary and adrenal function as well as cure of Cushing\u2019s diseases.  \n \nA. Hyperaldosteronism  \nAldosteronism : is a syndrome associated with hypersecretion of the mineralocorticoid, \naldosterone. \nEtiology:   \n1. Primary aldosteronism:  the cause of excess aldosterone production resides with in the \nadrenal gland \n\u2022 Aldosterone producing adrenal adenoma (Conn\u2019s  syndrome) : in most cases , \nunilateral small adenoma which can occur on either side  \n\u2022 Adrenal carcinoma:  rare cause of aldosteronism  \n\u2022 Bilateral cortical nodular hyperplasia /idiopathic hyperaldosteronism \n \n2. Secondary aldosteronism : the stimulus for excess aldosterone production is outside the \nadrenal gland. It refers to a appropriately increased production of aldosterone in response to \nactivation of the renin-angiotensin system \n\u2022 Accelerated phase of hypertension \n\u2022 Pregnancy \n\u2022 Congestive heart failure \n\u2022 Other edema states : nephritic syndrome , CLD etc \nPathophysiology:  The excess  aldosterone increase the reabsorption of sodium and excretion \nof potassium and hydrogen ions, in the distal renal tubules, which results progressive depletion of potassium and leads to hypokalemia. \nSigns and symptoms: \n\u2022 Moat patients have diastolic hypertension  resulting from sodium retention.  Patients \nmay complain headache and symptoms of other organ damage"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4575b-7265-11ef-809a-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 493, "chroma:document": "Signs and symptoms: \n\u2022 Moat patients have diastolic hypertension  resulting from sodium retention.  Patients \nmay complain headache and symptoms of other organ damage \n\u2022 Hypokalemia and associated symptoms : muscle weakness and fatigue.   \n\u2022 Impairment of urinary concentrating ability\n\u00c6polyuria and polydipsia. \n\u2022 Metabolic alkalosis  with paresthesia, possibly tetany \nECG: \n\u2022 Evidences of left ventricular enlargement  \n\u2022 ECG signs of hypokalemia : prominent U waves and cardiac arrhythmias"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 494, "chroma:document": "Internal Medicine \n \n 479Laboratory Diagnosis:  \n\u2022 Hypokalemia in hypertensive patients  is often the clue that triggers the search for \nprimary aldosteronism :  \n\u2022 Metabolic alkalosis  \n\u2022 Serum aldosteron level : elevated aldosteron and metabolites in 24-h urine \n\u2022 Plasma renin activity : is the most important useful indicator of whether elevated \naldosterone is primary or secondary. Increased plasma renin activity favours the \ndiagnosis of secondary aldosteronism. While raised aldosteron level with reduced plasma renin activity suggests primary aldosteronism. \n\u2022 CT scan and MRI : may detect aldosteron secreting adenomas. \nTreatment: \n1. Surgery:  removal of solitary adenoma results cure of hypertension in about 60 % of \ncases and improvement in another 25 %.  Adrenalectomy is done after 4 week treatment \nwith spironolactone (in case of adenoma, hyperplasia)  \nIn contrast only 20%-50 % of patients with bilateral hyperplasia are improved with \nsurgery, even if bilateral adrenalectomy is performed. \n2. Medical Therapy: Spironolactone  inhibits the effects of aldosteron on renal tubule.  \nIn idiopathic form: Spironolactone (50-100 mg/d), possibly combined with potassium-sparing diuretics correct the hypokalemia and with  anti-hypertensive medication , high blood pressure can be controlled. \n \nReferences:  \n3) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nDisorders of  the adrenal cortex , pages 2127-1508-1515"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4575d-7265-11ef-9896-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 494, "chroma:document": "References:  \n3) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nDisorders of  the adrenal cortex , pages 2127-1508-1515 \n4) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nDisorders of the adrenal gland, pages 492-501."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4575e-7265-11ef-9842-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 495, "chroma:document": "Internal Medicine \n \n 4804. Diseases of the pituitary gland \n \n1. Anterior pituitary diseases may result from:- \ni) Insufficient production of pituitary hormones: hypopituitarism  \nii) Excess production of pituitary hormones:  \na. Acromegaly,  \nb. Cushing\u2019s diseases \nc. Hyperprolactinoma  \niii) Local effect of pituitary tumours  \n \n2. Posterior Pituitary diseases  \n \nI) Hypopituitarism ( Insufficient production of  anterior pituitary \nhormones) \n\u2022 Hyposecretion may be generalized (hypopituitarism) or caused by the selective loss \nof one or more pituitary hormones. \nGeneralized hypopituitarism \nDefinition:  Endocrine deficiency syndromes due to partial or complete loss of anterior lobe \npituitary function.  \nEtiology: 1. Pituitary tumours  \n\u2022 Chromophbic adenomas \n\u2022 Craniopharyngioamas \n2. Infarction of ischemic necrosis of the pituitary \n\u2022 Shock , especially post partum ( Sheehan\u2019s syndrome ) or in Debates mellitus or \nSickle cell anemia  \n\u2022 Vascular thrombosis or aneurysm of the anterior cerebral artery \n\u2022 Hemorrhagic infarction : pituitary apoplexy  \n3. Inflammatory /infectious process : meningitis ( tuberculus )  , pituitary abscess  \n4. Infiltrative diseases: Sarcoidosis , hemochromatois ,  \n5.  Iatrogenic : irradiation or Surgical removal of pituitary tumours or during operation for other \nbran tumours"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4575f-7265-11ef-b560-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 496, "chroma:document": "Internal Medicine \n \n 481Clinical features: \n\u2022 The onset is usually insidious and may not be recognized as abnormal by the patient, \nbut occasionally it may be sudden or dramatic. The function of all target glands will \ndecrease when all hormones are deficient (panhypopituitarism). \n\u2022 With slow progressive destruction of pituitary tissue , \no Failure of GH and gonadotrophin secretion occurs early \no TSH failure comes next  \no ACTH level falls finally  \n \n1) Growth hormone deficiency  \n\u2022 In children growth failure \n\u2022 In adults: increases adipose tissue and decreases lean body mass , leading to \nreduced strength and exercise capacity \n2) Gonadotrphine ( LH and FSH ) deficiency : \n\u2022 In women : amenorrhea and genital atrophy and  infertility, if there is associated loss \nof adrenal androgens , because of concomitant ACTH, deficiency , pubic and axillary \nhair may be lost , in women \n\u2022 In men:  loss of potency and libido, testicular atrophy, regression of secondary sexual \ncharacteristics, and decreased spermatogenesis with consequent infertility \n3) TSH deficiency:  symptoms and signs of hypothyroidism \n4) ACTH deficiency : leads to secondary type of adrenal insufficiency. This type of adrenal \ninsufficiency differs from primary adrenal insufficiency in that :  \n\u2022 There is no hyperpigmentation of skin and mucous membrane  \n\u2022 Hyponatremia and Hypokalemia are minimal, since aldosteron production, which"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d45760-7265-11ef-a4bb-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 496, "chroma:document": "insufficiency differs from primary adrenal insufficiency in that :  \n\u2022 There is no hyperpigmentation of skin and mucous membrane  \n\u2022 Hyponatremia and Hypokalemia are minimal, since aldosteron production, which \ncontrols the balance of these electrolytes, mainly depends on the renin-angiotensin system. \n5) Prolactine deficiency:  postpartum failure of lactation \nPituitary apoplexy  is a symptom complex caused by hemorrhagic infarction of either a normal \npituitary gland or, more commonly, a tumor.  \n\u2022 Acute symptoms may include severe headache, stiff neck, fever, and visual \ndisturbances."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4884e-7265-11ef-9791-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 497, "chroma:document": "Internal Medicine \n \n 482\u2022 Varying degrees of hypopituitarism may develop suddenly, and the patient may present \nin vascular collapse because of deficient ACTH and cortisol secretion. Often the CSF is \nhemorrhagic. \nDiagnosis: \n1) Evaluation of target organ function:  is often the first step in the diagnosis of \nhypopituitarism; this condition is often suspected because of failure o more than one target organ  \n\u2022 Evaluation of thyroid function: T4, T3, TSH \n\u2022 Evaluation of ACTH secretion  \n\u2022 Evaluation of prolactin levels : prolactin not regularly depressed \n\u2022 Evaluation of serum LH and FSH levels : helpful in postmenopausal women, not so \nmuch in others. \n\u2022 Measurement of GH hormone level:  may be undetectable under baseline \ncondition, provocative maneuvers are needed to prove inadequacy of hormone \nproduction \no Insulin induced hypoglycemia/ Insulin tolerance :  test is the most \nconsistent effective test : Regular insulin at a dosage of 0.1 U/kg body weight \nis given IV over 15 to 30 sec, and venous blood samples are obtained to \ndetermine GH, cortisol, and glucose levels at zero time (before insulin administration) and 30, 60 and 90 minutes  later. The fall in serum glucose level is maximal at 30 minutes, is followed by a rise in GH level to a level \ngreater than 8-10ng/ml n normal individuals. Blood cortisol level is also \nexpected to rise. Failure to rise in the level of both hormones may suggest hypopituitarism. \n2) Imaging studies"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4884f-7265-11ef-9f40-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 497, "chroma:document": "greater than 8-10ng/ml n normal individuals. Blood cortisol level is also \nexpected to rise. Failure to rise in the level of both hormones may suggest hypopituitarism. \n2) Imaging studies  \n\u2022 Skull x-ray of sella turcica (detects macroadenomas > 10 mm) \n\u2022 High-resolution CT or MRI if available \n3) Formal visual field testing \n \nDifferential diagnosis:   \n\u2022 Anorexia nervosa,  \n\u2022 Chronic liver disease (alcohol, hemochromatosis),  \n\u2022 Polyglandular autoimmune disease"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48850-7265-11ef-8733-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 498, "chroma:document": "Internal Medicine \n \n 483Therapy:  \n1) Treatment of the underlying cause the patients pituitary insufficiency  \nSurgery:  \n\u2022 If hypopituitarism is due to tumor and tumor is small and is not secreting prolactin, \nmost favour Transphenoidal removal of the neoplasm.  \n\u2022 Most endocrinologists consider bromocripti ne the initial treatment of prolactinomas, \nregardless of size.  \n\u2022 With larger tumours and suprasellar extension, resection of the entire neoplasm, \neither transsphenoidally or transfrontally, may not be possible, and adjunctive \nirradiation may be needed.  \n\u2022 After surgical or radiation treatment, other hormones may be lost as well, and \nreplacement may be needed accordingly. \n\u2022 In pituitary apoplexy, Transphenoidal decompression of the often hemorrhagic tumor \nshould be undertaken promptly \nMedical:  Treatment of granulomatous diseases \n2) Hormone replacement therapy  : treatment is directed toward replacing the hormones \nof the hypofunctioning target glands. \n\u2022 GH replacement : given for children with growth failure  \n\u2022 Thyroid hormone replacement : given in usual replacement dose \n\u2022 Cortisol is given in the usual replacement dose \n\u2022 Estrogens and progesterone combination : may be given to women to restore \nmenstrual function and Testosterone may be given to men to restore libido and \npotency \n \nII)  Selective pituitary hormone deficiencies \nDefinition:  A clinical condition in which one or more pituitary hormones are deficient; may"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48851-7265-11ef-98c6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 498, "chroma:document": "menstrual function and Testosterone may be given to men to restore libido and \npotency \n \nII)  Selective pituitary hormone deficiencies \nDefinition:  A clinical condition in which one or more pituitary hormones are deficient; may \nrepresent an early stage in the development of more generalized hypopituitarism so evaluate patient regularly.  \nForms: \n\u2022 Isolated GH deficiency  is responsible for many cases of pituitary dwarfism. \n\u2022 Isolated gonadotropin deficiency  occurs in both men and women and must be \ndistinguished from primary hypogonadism."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48852-7265-11ef-9dd1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 499, "chroma:document": "Internal Medicine \n \n 484\u2022 Isolated ACTH deficiency  is a rare clinical entity. Symptoms of weakness, \nhypoglycemia, weight loss, and decreased axillary and pubic hair suggest the diagnosis. \nPlasma and urinary steroid levels are low and rise to normal after ACTH treatment. Clinical and laboratory evidence of other hormonal deficiencies is absent. \n\u2022 Isolated TSH deficiency  is likely when clinical features of hypothyroidism exist, plasma \nTSH levels are not elevated, and no other pituitary hormone deficiencies exist. Plasma TSH levels are not always lower than normal, suggesting that the TSH secreted is biologically inactive. \n\u2022 Isolated prolactin deficiency  has been noted rarely in women who fail to lactate after \ndelivery. \n \nIII)  Hypersecretion of anterior pituitary hormones (hypopituitarism) \nThe anterior pituitary hormones that are most commonly secreted in excess are \n\u2022 GH hypersectretion: which manifests as an Acromegaly or, gigantism \n\u2022 Hyperprolactinoma:  \n\u2022 Excess secretion of ACTH : results as in the pituitary type of Cushing's syndrome \n \nGigantism and Acromegaly \nDefinition:  Syndromes of excessive secretion of GH (hypersomatotropism) nearly always due \nto a pituitary adenoma of the somatotrophs.  \nClinical features: excess GH secretion may cause changes in bone, soft tissue and metabolic \nprocess.   Bone and soft tissue changes: \n1. Gigantism:  GH hypersecretion beginning in childhood before closure of epiphyses may"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48853-7265-11ef-b06a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 499, "chroma:document": "Clinical features: excess GH secretion may cause changes in bone, soft tissue and metabolic \nprocess.   Bone and soft tissue changes: \n1. Gigantism:  GH hypersecretion beginning in childhood before closure of epiphyses may \ncause increase linear growth of long bones resulting gigantism. There is little bony \ndeformity, soft tissue swelling or enlargement of peripheral nerves.  \nDelayed puberty or hypogonadotropic hypogonadism may be present.  \n2. Acromegaly:  GH hypersecretion beginning after epiphyseal closure, in adults, result soft \ntissue growth and bony enlargement, especially in acral areas of the skeleton, which may \naffect the patient\u2019s appearance.  \n\u2022 Enlargement of hands  (especially fingertips) and feet: increased ring, gloves \nand shoe size. \n\u2022 Coarsening of facial features"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48854-7265-11ef-a722-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 500, "chroma:document": "Internal Medicine \n \n 485o Thick skin folds : brows and nasolabialfolds \no Enlargement of the nose \no Enlargement of mandible:  Prognathism, spreading of teeth  \n\u2022 Body hair increases and the skin thickens  and becomes darker. \n\u2022 Excessive perspiration , offensive body odour may be noted. \n\u2022 Voice becomes husky , tongue enlarged  and furrowed.  \n\u2022 Barrel chest deformity  may be noted.  \n\u2022 Joint symptoms are common , crippling degenerative osteoarthritis may occur.  \n\u2022 Galactorrhea may occur in women and menstrual irregularities/amenorrhea may \nbe noted. Impotence is common in men.  \n\u2022 Peripheral neuropathies  due to entrapment of peripheral nerves are common, \nas are headaches (due to pituitary tumor).  \n\u2022 Bitemporal hemianopsia  (visual field defect) may develop due to the pressure \neffect of pituitary adenoma.  \n\u2022 Enlargement of internal organs:  The heart, liver, kidneys, spleen, thyroid, \nparathyroid glands, and pancreas are also larger than normal. Cardiac disease in \n1/3 of patients.  \n3. Metabolic changes:  \nPoor glucose tolerance, a result of the anti-insulin actions of GH, is common. Over diabetes occurs in only 10% of acromegalic patients. \nDiagnosis: Diagnosis of Acromegaly depends on the clinical manifestations. \n\u2022 GH level : should be measured in the morning under basal condition. \n\u2022 A level higher than 10ng/dl favors the diagnosis of Acromegaly. \n\u2022 Glucose tolerance test:  to diagnose for possible DM"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48855-7265-11ef-952e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 500, "chroma:document": "\u2022 GH level : should be measured in the morning under basal condition. \n\u2022 A level higher than 10ng/dl favors the diagnosis of Acromegaly. \n\u2022 Glucose tolerance test:  to diagnose for possible DM \n\u2022 Skull x-ray:  in most cases the pituitary adenoma is large enough to distort the sella \nturcica and can be seen on lateral skull x-ray \n\u2022 CT or MRI (if available):  will help to visualize the tumor. \n\u2022 Other X-ray changes : Enlargement of sinuses \nTufting of distal phalanges, cortical thickening."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48856-7265-11ef-b473-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 501, "chroma:document": "Internal Medicine \n \n 486Treatment:   \n1. Ablative therapy ; \n\u2022 Transpheniodal pituitary adenomectomey : results  prompt normalization of GH in the \nmajority of patients  \n\u2022 Irradiation therapy radiation  is generally indicated, but be aware of danger of \nhypopituitarism. \n2. Medical therapy  is indicated if surgery and radiotherapy are contraindicated or have failed.  \n\u2022 Give bromocriptine up to 15 mg/d PO in divided doses. \n \nHyperprolactinoma /Galactorrhea \n \nDefinition:  Hyperprolactinoma is a clinical condition re sulting from excess secretion of prolactin  \nin men, or in women who are not breastfeeding. \nEtiology:  \n1. Prolactin secreting pituitary adenomas (Prolactinoma),  are more common in women \nthan in men, usually appearing during repr oductive years. Majority are microadenomas \n(< 10 mm in size). Men tend to have larger tumors (macroadenomas), which usually are \nsuspected because of neurologic impairment and hypogonadism.  \n2. Damage to the hypothalamus or the pituitary stalk: by tumors , granulomas and \nother process may prevent the normal regulatory effect of hypothalamic  dopamine on lactotrope activity , resulting hypersecretion of prolactin.  \n3. Drugs:  drugs that inhibit dopamine activity, and thus interfere with its regulatory activity \non prolactin secretion. Some of the drugs are phenothiazines, antidepressants, antihypertensives (methyldopa, reserpine) , opioids, cimetidine, metoclopromide, \ncontraceptives etc  \n4. Other rare causes :"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48857-7265-11ef-a06a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 501, "chroma:document": "on prolactin secretion. Some of the drugs are phenothiazines, antidepressants, antihypertensives (methyldopa, reserpine) , opioids, cimetidine, metoclopromide, \ncontraceptives etc  \n4. Other rare causes :   \n\u2022 Primary hypothyroidism  \n\u2022 Chronic liver disease  \n\u2022 Renal failure  \n\u2022 Ectopic prolactin production from  tumors (paraneoplastic syndromes)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48858-7265-11ef-aac6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 502, "chroma:document": "Internal Medicine \n \n 487Clinical features: \nIn women:  \n\u2022 Galactorrhea:  is the direct result of prolactin excess.  \n\u2022 Amenorrhea or menstrual irregularity  is due to inhibition of hypothalamic GnRH \nproduction by prolactin as well as the direct effect of prolactin on the ovaries.  \n\u2022 Signs of estrogens deficiency  may be seen such as hot flushes and dyspareunia. \nIn men: \n\u2022 Loss of libido and potency , hypogonadism.  \n\u2022 Headaches, visual difficulties  result from the compression effect of tumors, which are \noften larger in men.  \nDiagnosis: \n\u2022 Prolactin levels : are elevated. A serum prolactin level greater than 300ng/ml strongly \nsuggests the presence of prolactinoma. Func tional causes such as drugs seldom \nelevate the prolactin level above 100-200ng/ml  \n\u2022 Skull x-ray (lateral):  CT/MRI: are used to visualize the adenoma.  \n\u2022 Visual field examination \n \nTherapy: \nDepends on the size of the tumor, and its manifestation. \n1. Surgical therapy: transsphenoidal surgery : cures most patients with small adenomas. \n2. Medical: Bromocriptine is remarkably effective in decreasing prolactin level, usually, to \nnormal. It also reduces tumor size. \nDose:   initial dosage 1.25 mg once or twice daily may need to be increased to 10-20mg \ndaily for full effect. Side effects : headache, dizziness, fatigue. \n \nLarger tumors with suprasellar extension are not cured by surgery. Such"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48859-7265-11ef-a870-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 502, "chroma:document": "Dose:   initial dosage 1.25 mg once or twice daily may need to be increased to 10-20mg \ndaily for full effect. Side effects : headache, dizziness, fatigue. \n \nLarger tumors with suprasellar extension are not cured by surgery. Such \nmacroadenomas may be initially treated with bromocriptine. If the tumor shrinks, there is a greater chance for successful surgery. \n3. Radiotherapy  is reserved for therapy-resistant cases. It may be used in conjunction with \nsurgery and bromocriptine to further reduce tumor size and function."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4885a-7265-11ef-9cee-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 503, "chroma:document": "Internal Medicine \n \n 488IV) Posterior Pituitary lobe Disorders \n \nCentral Diabetes Insipidus  \nDefinition:  A temporary or chronic disorder of the neurohypophyseal system due to deficiency \nof vasopressin (ADH), and characterized by excretion of excessive quantities of very dilute (but \notherwise normal) urine, and by excessive thirst. \n ADH is produced by cells in the supraoptic a nd paraventricular nuclei of the hypothalamus, \ntravels down through the pituitary stalk and stored in the posterior lobe of the pituitary gland \n(neurohypophysis)  \n \nEtiology:   \n1. Primary/Idiopathic : account for approximately 50 % of the cases of diabetes insipidus. \n2. Injury to the hypothalamus  \u2013pituitary  area:  may result from head trauma, neurosurgical \nprocedures such as hypophysectomy.  \n3. Less common causes : neoplasms, histiocytosis, granulomas, vascular lesions, infections \n(encephalitis.) \nClinical features:  Onset insidious or abrupt; may occur at any age.  \n \n\u2022 Polyuria: with urine volume f 3-15 L daily, result from the inability to reabsorb free water \nand to concentrate urine. Nocturia is almost always present, which may disturb sleep and cause mild day time fatigue or somnolence.  \n\u2022 Thirst (polydipsia) : leads to increased fluid intake. A conscious patient with normal \nthirst mechanism and free access to water will maintain hydration.  However rapid and life threatening dehydration and hypovolemia ma y develop rapidly, if urinary losses are"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4885b-7265-11ef-86aa-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 503, "chroma:document": "thirst mechanism and free access to water will maintain hydration.  However rapid and life threatening dehydration and hypovolemia ma y develop rapidly, if urinary losses are \nnot continuously replaced, which may occur in unconscious patients or infants. \nIn primary DI, only polydipsia and polyuria are present.  In acquired DI, signs and symptoms of associated lesions are also found.  \n \nDiagnosis: \n1. Measurement of plasma osmolality:  in untreated patients helps to distinguish the cause \nof polyuria. In DI, the loss of free water leads to high osmolality (280-310 mOsm/kg). In psychogenic polydipsia excess fluid intake is primary and serum osmolality is low (255 -280 mOsm/kg )"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4885c-7265-11ef-b181-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 504, "chroma:document": "Internal Medicine \n \n 4892. Water deprivation test:  started in the morning by weighing the patient, obtaining venous \nblood to determine electrolyte concentrations and osmolality, and measuring urinary \nosmolality.  \nFluid intake is withheld, and voided urine is collected hourly and its osmolality is \nmeasured. Dehydration is continued until \n\u2022 Orthostatic hypotension and postural tachycardia appear,  \n\u2022 5% or more of the initial body weight has been lost, or  \n\u2022 The urinary concentration does not increase by more than 30 mOsm/L in \nsequentially voided specimens for 3 hrs.  \nAt this point, serum electrolytes and osmolality are again determined, and  Five (5 U) of aqueous  vasopressin or 2 \u00b5g of desmopression is then injected SC.  \nUrine osmolality is measured 1 hr later. \n Table VII-4- 2 Interpretations of Water deprivation test \n \nDisorder Urinary osmolality in \nresponse to water \ndeprivation Response to Vasopressin \ninjection \nNormal response  Urinary osmolality increases  > 280 mOsm/kg No further increment in urine osmolality \nCentral DI The urinary osmolality does not increase Urinary osmolality increases \nNephrogenic DI The urinary osmolality does not increase The urinary osmolality does not increase \n \n3. Measurement of circulating ADH concentrations by radioimmunoassay  \n \nDifferential diagnosis:  \n\u2022 Compulsive (psychogenic) water drinking \n\u2022 Nephrogenic diabetes insipidus. \nTreatment: \n1. Hormonal therapy:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4885d-7265-11ef-8f17-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 505, "chroma:document": "Internal Medicine \n \n 490\u2022 Aqueous vasopressin SC or IM in doses of 5-10 U.  Since effect lasts 6 h or \nless, use in chronic treatment is limited.  \n\u2022 Desmopresin:  DDAVP (synthetic vasopressin) in a dose of 0.05-0.2ml applied to \nthe upper respiratory mucous membrane twice daily by nasal cannula or nasal \nspray.  \nThe effect lasts 12-24 h, can be given intranasally, SC or IV and it is a preparation of choice for both adults and children.  \n2. Nonhormonal therapy:  to reduce polyuria \n\u2022 Chlorpropamide (an oral hypogycemic agent) may increase endogenous ADH \nin patients who have partial ADH deficiency.  Dose: 250-500 mg PO makes patients asymptomatic daily 3-5 mg/kg PO. \n\u2022 Thiazide diuretics : have paradoxical effect on decreasing urine output in \npatients with DI.  They are the preferred drugs for treating nephrogenic DI.  Thiazides are only partially effective, decreasing the urine volume by 30%-50 %. \n\u2022 Restricting salt intake may be helpful.  \n\u2022 Prostaglandin inhibitors such as indom ethacin (1.5-3 mg/kg/d PO in divided \ndoses) may be effective.  \n\u2022 Treatment of underlying causes of DI , if treatable.  \n \nReferences  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nDisorders of the anterior Pituitary and the neurohypophysis, pages 2076- 2103. \n2) Myers R. Allen , National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Diseases of the pituitary gland, pages 75-78"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4885e-7265-11ef-a289-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 506, "chroma:document": "Internal Medicine \n \n 491CHAPTER EIGHT \nDISEASE OF THE NERVOUS SYSTEM \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Understand   the epidemiologic significance of Headaches. \n2. Understand the classification of common headaches. \n3. Identify the clinical manifestation of common headaches. 4. Manage patients with acute common headache and prevention of recurrent attacks.  \n \n1. Headache \n\u2022 Headache is one of the commonest complaints in medical practice.  As many as 90% of \nindividuals have at least one episode of headache per year.  Severe disabling headache is reported to occur at least annually by 40% of individuals worldwide. \n\u2022 It results from distention, stretching, inflammation or destruction of pain sensitive cranial \nstructures.  These pain sensitive structures are the scalp, dura, sinuses, falx cerebri, \nmiddle meningeal arteries, proximal segments of  large pial arteries and cranial nerves 5, \n9 and 10.  Brain parenchyma is not pain sensitive.   \n\u2022 A pain (sensory stimuli) from these structures is conveyed to the brain either via \ntrigeminal nerve or first three cervical nerves. \nClassification of headaches \nHeadache can be clarified pathophysiologically as: \n1. Vascular headache \n\u2022 Migraine headache \n\u2022 Cluster headache \n\u2022 Miscellaneous (orgasmic, Hangover)  \n2. Cranial Neuralgias 3. Tension headache \n4. Traction \u2013inflammation headache \n\u2022 Cranial arteritis \n\u2022 Meningitis \n\u2022 Brain tumor \n\u2022 Increased /Decreased ICP"}


