# embeddings_queue

created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4885f-7265-11ef-ae3e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 507, "chroma:document": "Internal Medicine \n \n 4925. Extra cranial lesions \n\u2022 Paranasal sinusitis \n\u2022 Dental problems \n\u2022 Ear problems \n\u2022 Ocular problems \n\u2022 Cervical problem \nEvaluation of patients presenting with Headache \nWhen evaluating a patient with headache, the goal is to: \n\u2022 Distinguish serious headache from benign headache syndrome  \n\u2022 Give appropriate treatment. \nAppropriate History  is critical in evaluating a patient with headache. \n\u2022 Characterize the headache:  the quality, location, duration, time course, the conditions \nthat produce, exacerbate or relieve it should be reviewed.  \n\u2022 Look also for associated symptoms, medication history and psychiatric history. \nPhysical Examination:  is important to search for underlying serious illnesses.  It should include \n\u2022 Vital signs  (Blood pressure, temperature)    \n\u2022 Head and neck examination : scalp tenderness, sinus tenderness, examination of the \noral cavity and tempromandibular joint. \n\u2022 Ophthalmologic evaluation including  : fundoscopic examination pupillary size, \ncorneal clouding \n\u2022 Systematic evaluation of other systems  (Glands, chest, CVS, abdomen, GUS, MSS, \nand Integumentary system) \n\u2022 Neurological examination  including change in mental status, focal neurological deficit, \nneck stiffness and other meningeal signs \nInvestigation \n\u2022 Diagnosis of common primary headache syndromes  is clinical. No specific test is \navailable. \n\u2022 Occasionally investigations including N euro-imaging studies are important if the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48860-7265-11ef-b36c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 507, "chroma:document": "neck stiffness and other meningeal signs \nInvestigation \n\u2022 Diagnosis of common primary headache syndromes  is clinical. No specific test is \navailable. \n\u2022 Occasionally investigations including N euro-imaging studies are important if the \nheadache is atypical or it is associated with abnormalities on physical examination. \nAfter appropriate evaluation of the headache the following clinical features should be considered as indicators of serious underlying disease. \n1. First severe headache ever described as the worst type of headache in the patient\u2019s life  \nmay suggest subarachnoid hemorrhage"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48861-7265-11ef-9428-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 508, "chroma:document": "Internal Medicine \n \n 4932. Subacute worsening over days or weeks (tumor) \n3. Disturbs sleep or present immediately upon awakening (tumor) 4. Abnormal neurological exam (space occupying lesions) \n5. Fever or other unexplained systemic signs (meningitis) \n6. Vomiting precedes headache  \n7. Headache induced by bending, lifting or  cough 8. Known systemic illnesses \n9. Onset of headache in patients older than 55 yrs.  \n \nCommon Headache syndromes \n1. Vascular headache \n\u2022 Vascular headaches refers to a group of headache syndromes, of unknown cause ,in \nwhich pain results from dilation of one or more of branches of carotid arteries.   \n\u2022 Migraine headache and cluster headache account for the majority of the cases. \n \nA)  Migraine Headache \n\u2022 Definition:  migraine headache is a benign and episodic disease, characterized by \nheadache, nausea, vomiting and/ or other symptoms of neurological dysfunction. \n\u2022 It is the most common cause of vascular headache. It approximately affects 15% of \nwomen and 6% men. \n\u2022 It usually begins in childhood or young adult life. \nEtiology : the cause of migraine is often unknown, but several common precipitants have been \nobserved.  \n1) Family history  of migraine present in nearly 2/3 of patients. \n2) Environmental, dietary and psychological factors. \n\u2022 Emotional stress , depression  \n\u2022 Altered sleep pattern or sleep deprivation \n\u2022 Menses , Oral contraceptives \n\u2022 Alcohol intake especially red wine  \n\u2022 Caffeine withdrawal"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48862-7265-11ef-b8e4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 508, "chroma:document": "2) Environmental, dietary and psychological factors. \n\u2022 Emotional stress , depression  \n\u2022 Altered sleep pattern or sleep deprivation \n\u2022 Menses , Oral contraceptives \n\u2022 Alcohol intake especially red wine  \n\u2022 Caffeine withdrawal  \n\u2022 Various food staffs ( e.g. . chocolates, nuts, aged , cheese , meals containing \nnitrates"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48863-7265-11ef-a110-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 509, "chroma:document": "Internal Medicine \n \n 494\u2022 Perfumes \n3) It may develop after seemingly minor head injury. \n \nPathogenesis:  different hypothesis are proposed including: \n1) Vascular theory:  in this theory it is said that migraine and neurological symptoms are \nresults of extracranial vasodilatation and intracranial vasoconstriction. \n2) Neuronal theory : a slowly spreading neuronal depolarization is considered as a cause. \n3) Trigeminovascular system abnormality : this theory says dysfunction of trigeminal \nnucleus caudalis leads to release of vasoactive neuropeptides resulting in migraine. \n \nClinical feature \nMigraine may be precipitated by some of the factors mentioned above. It is relieved by sleep \nand exhilaration, Sumatriptan and pregnancy. \nThe syndrome of Classical migraine has five phases: \n\u2022 Prodromal phase : characterized by lassitude, irritability difficulty in concentrating \n\u2022 Aura phase: patients with aura often report visual complaints, vertigo, aphasia or other \nneurological deficit before the onset of the headache  \n\u2022 Headache phase  \u2013 characteristic migraine headache \n\u2022 Headache termination  \u2013 usually occurs within 24 hours \n\u2022 Post headache phase  \u2013 feeling of fatigue.  Sleepiness and irritability \nCharacteristic Migraine head ache is:  \n\u0083 Moderate to severe head pain , pulsating quality often unilateral ( affecting half part of \nthe head )  \n\u0083 It is exacerbation by physical activity and relived by sleeping"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48864-7265-11ef-8ccf-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 509, "chroma:document": "Characteristic Migraine head ache is:  \n\u0083 Moderate to severe head pain , pulsating quality often unilateral ( affecting half part of \nthe head )  \n\u0083 It is exacerbation by physical activity and relived by sleeping  \n\u0083 It is often associated with Nausea and/or vomiting, photophobia, phonophobia/ \nsonophobia (dislike ad avoidance of laud sounds or noises).  \n\u0083 Multiple attacks may occur, each lasting 4 \u2013 72 hrs. \nThere are different variants of Migraine  Common migraine \n\u2022 This is the commonest variation of migraine headache \n\u2022 No focal neurological disturbance precedes the recurrent headache"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48865-7265-11ef-8af9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 510, "chroma:document": "Internal Medicine \n \n 495Classic migraine \n\u2022 It is associated with characteristic premonitory  sensory, motor or visual symptoms.  Most \ncommon symptoms reported are visual which include scotomas and/or hallucinations. \nComplicated migraine \n\u2022 Migraine associated with dramatic transient neurological deficit, or a migraine attack that \nleaves a persisting residual neurological deficit. \n \nTreatment  \nTherapy should first involve removal of inciting agents when possible. \n1.  Acute/abortive tr eatment of migraine \nThese are lists of drugs effective for acute management of migraine attack  \na) NSAIDS (Nonsteroidal antinflamatory agents): such as  ASA, paracetamol, Ibuprofen, \nDiclofenac may reduce the severity and duration of migraine attack. These drugs are \neffective for mild to moderate attack s and are most effective when taken early. \nSide effects:  Dyspepsia and GI irritation are common side effects. \nb)  5-Hydroxytryptophan-1 Agonists: is a serotonin agonist that decreases substance P \nrelease at the trigeminovascular junction.  \ni. Nonselective (Ergot preparations: Ergotamine and dihydro-ergotamine)  \no Widely used for relief of acute attacks \no Has oral, sublingual, rectal, nasal and parentral preparation.  Parentral forms are \nused for rapid relief of the attack. \no Usually prepared combined with caffeine which potentiates the effect by \nimproving absorption. \no Dose: Initial  dose: 1 \u2013 2 mg oral /SL/ rectal and repeat every hour if there is no"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48866-7265-11ef-9b04-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 510, "chroma:document": "used for rapid relief of the attack. \no Usually prepared combined with caffeine which potentiates the effect by \nimproving absorption. \no Dose: Initial  dose: 1 \u2013 2 mg oral /SL/ rectal and repeat every hour if there is no \nrelief of headache to a maximum of 6 \u2013 8 mg over 24 hrs \no Side effects: are nausea, vomiting, myalgias, chest discomfort, peripheral \nischemia and even angina. Excess use may lead to rebound headache and dependency  \no Contraindication: patients  with vascular diseases like coronary heart disease \nii. Selective - Triptans including (Naratriptan, Ritatriptan, Sumatriptan, and \nZolmitriptan): are new drugs in management of migraine. \no Sumatriptan \u2013  single 6 mg SC dose is effective in 70 \u2013 80% of patients \nc) Dopamine agonists: are used as adjunctive therapy."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48867-7265-11ef-8345-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 511, "chroma:document": "Internal Medicine \n \n 4962. Prophylactic Treatment: includes drug regimens and changes in patients behavior  \nMedical therapy:  \n\u2022 These are drugs that have capacity to stabilize migraine. Prophylactic treatment is \nindicated if the patient has three or more attacks per month. \n\u2022 Drugs used for this purpose include \u03b2-blockers (propranolol), Tricyclic \nantidepressants (amitriptyline), and Calcium channel blockers (Verapamil), Valproic \nacid. \n\u2022 Start with low dose and gradually increase if there is no adequate response. \n        Biofeedback therapy \n\u2022 It is simple and cost effective. It lessens migraine attacks by helping patients deal more \neffectively with stress \n \nB)  Cluster Headache  \n\u2022 Cluster head ache is a vascular headache syndrome, characterized by severe, acute \nheadache that occurs in clusters lasting several weeks followed by pain free intervals that averages a year. \n\u2022 Common in men than women.  Male: Female ratio is 8:1 \n\u2022 Usually begins 3\nrd to 6th decades \n\u2022 Cluster headache is periorbital less commonly temporal.  It has rapid onset without \nwarning.  It is also severe and explosive in quality lasting 30 min to 2hrs, subsiding abruptly. \n\u2022 Clusters characteristically occur in the spring and fall several times a day particularly at \nnight and stay for 3 \u2013 8 weeks \n\u2022 During attack patients often have associated nasal stiffness, lacrimation and redness of \nthe eye ipsilateral to the headache. \n\u2022 Alcohol provokes attacks in about 70% of patients \n \nTreatment"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48868-7265-11ef-aa39-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 511, "chroma:document": "night and stay for 3 \u2013 8 weeks \n\u2022 During attack patients often have associated nasal stiffness, lacrimation and redness of \nthe eye ipsilateral to the headache. \n\u2022 Alcohol provokes attacks in about 70% of patients \n \nTreatment \nAcute attack /abortive therapy (Treatment) \n\u2022 Inhalation of 100% oxygen and \n\u2022 Sumatriptan 6 mg S.C. stat said to be helpful and ergotamine or other analgesics may \nalso be used. \nPreventions/prophylactic therapy: clusters attacks can be prevented effectively by:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48869-7265-11ef-ab57-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 512, "chroma:document": "Internal Medicine \n \n 497\u2022 Prednisolone , Lithium, Methysergide, Ergotamine, Sodium valproate and verapamil \n \nC) Tension headache (Tension type headache ) \n\u2022 Most common cause of headache in adults \n\u2022 Common in women than men \n\u2022 Can occur at any age, but onset during adolescence or young adulthood is common. \n \nEtiology: various precipitating factors may cause tension headache in susceptible individual \nincluding.  \n\u2022 Stress \u2013 usually occurs in the afternoon after long stressful work hours \n\u2022 Sleep deprivation \n\u2022 Uncomfortable stressful position and/or bad posture \n\u2022 Hunger (Irregular meal time) \n\u2022 Eye strain resulting from continuous TV watching, working on computer screen for a long \ntime. \nClinical feature  \n\u2022 Tension headache is characterized by mild or  moderate, bilateral pain.  Headache is a \nconstant, tight, pressing or band like sensation in the frontal, temporal, occipital or \nparietal area. \n\u2022 Usually lasts less than 24 hrs but can persist for days or weeks. \n\u2022 Prodromal symptoms are absent some patients have neck, jaw or tempromandibular \njoint discomfort. \n\u2022 On examination some patients may have tender spots in the pericranial or cervical \nmuscles. \n \nTreatment:  management of tension headache consists:-  \n1. Pharmacotherapy \n\u2022 Abortive therapy/acute treatment  \no Stop or reduce severity of individual attacks \no This can be done with simple analgesics like paracetamol, ASA, Ibuprofen, and"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4886a-7265-11ef-9558-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 512, "chroma:document": "Treatment:  management of tension headache consists:-  \n1. Pharmacotherapy \n\u2022 Abortive therapy/acute treatment  \no Stop or reduce severity of individual attacks \no This can be done with simple analgesics like paracetamol, ASA, Ibuprofen, and \nDiclofenac.  If treatment is unsatisfactory addition of caffeine or other analgesic is \nbeneficial."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4886b-7265-11ef-adc5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 513, "chroma:document": "Internal Medicine \n \n 498\u2022 Long term preventive therapy \no Main form of therapy for chronic form of tension headache \no This kind of treatment is indicated if the headache is : \n\u0083 Frequent (> 2 attacks / week ),  \n\u0083 Of long duration (> 3hrs)  \n\u0083 Severe (cause significant disability)  \n\u0083 Associated with overuse of abortive medication \no Commonly used drug for long term treatment is Amitryptilline. \n2. Physical Therapy:  different techniques can be used including  \n\u0083 Hot or cold application \n\u0083 Positioning \n\u0083 Stretching exercises \n\u0083 Traction \n\u0083 Massage \n3. Psychological Therapy \n\u2022 Includes reassurance, Counseling, relaxation, stress management programs and \nbiofeedback techniques reduce both the frequency and severity of chronic headache. \n \nD)  Headache Associated with Brain Tumor \n\u2022 About 30% of patients with brain tumor present with headache. \n\u2022 Brain tumor can affect all ages and both sexes.  Headache of brain tumor is usually \nintermittent dull aching, moderate intensity which worsens with time.  It disturbs sleep \nin about 10% of patients, exacerbated by exertion and postural changes.  With time \npatients can develop nausea and vomiting. \n\u2022 Upon examination focal neurological deficit may be detected. \nE) Temporal Arteritis \n\u2022 It is also called giant cell arteritis.  It is an inflammatory disorder of the carotid artery \nand its branches. \n\u2022 It is common in elderly, and women account for 65% of cases. \n           Clinical feature"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4886c-7265-11ef-ac58-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 513, "chroma:document": "E) Temporal Arteritis \n\u2022 It is also called giant cell arteritis.  It is an inflammatory disorder of the carotid artery \nand its branches. \n\u2022 It is common in elderly, and women account for 65% of cases. \n           Clinical feature \n\u2022 Typical presenting symptom includes headache, polymyalgia rheumatica, jaw \nclaudication, fever and weight loss."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4886d-7265-11ef-9803-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 514, "chroma:document": "Internal Medicine \n \n 499\u2022 Headache is located to temporal or occipital area, described as dull and boring. It is \nusually worse at night and is often aggravated by exposure to cold. \n\u2022 Scalp tenderness is often found over temporal artery. \n\u2022 50% of patients with untreated temporal arteritis develop blindness due to \ninvolvement of ophthalmic artery and its branches. \n  Diagnosis \n\u2022 ESR is often elevated. \n\u2022 Biopsy of temporal artery confirms the diagnosis. \n         Treatment \n\u2022 Prednisolone 80 mg /day for 4 \u2013 6 weeks \n \nF) Lumbar Puncture headache \n\u2022 Occurs in 10 \u2013 30% of patients having LP \n\u2022 Usually begins within 1 \u2013 2 days and persists for 3 \u2013 4 days. \n\u2022 Headache of lumbar puncture is usually bifrontal or occipital, dull aching \naggravated by sitting or standing, head shaking, jugular vein compression and \ndisappears in prone or supine position. \n\u2022 Treatment:  simple analgesics and lie the patient supine. \n  \nReferences:  \n3) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nHeadache,      pages 85-93. \n4) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nHeadache, pages 61\u2014613."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4886e-7265-11ef-9e65-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 515, "chroma:document": "Internal Medicine \n \n 5002. Diseases of the Spinal cord \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Identify the characteristic features of diseases of the spinal cord. 2. Describe the Etiologies of diseases of the spinal cord. 3. Identify the clinical manifestation of common diseases of the spinal cord. \n4.  Understand the diagnostic wok up for common diseases of the spinal cord. \n5. Understand the management of common diseases of the spinal cord. \n \n\u2022 Spinal Cord is part of the central nervous system contained in the spinal canal.   The adult \nspinal cord is 18 cm long, oval or round in shape in cross section. It has two parts, white \nmatter and gray matter, with central canal at the center. The white matter contains ascending sensory and descending motor fibers and gray matter contains nerve cell bodies. Spinal cord is organized into 31 somatotropic segments, i.e.  8 cervical, 12 thoracic, 5 Lumbar, 5 sacral \nand 1 coccygeal segments. \n\u2022 Diseases of the spinal cord are frequently devastating, because the spinal cord contains, in a \nsmall cross-sectional area, almost the entire motor output and sensory input of the trunk and \nthe limbs. \n Generally diseases of spinal cord are characterized by:  \n\u2022 The presence of a level below which motor/sensory and/or autonomic function is \ndisturbed.   \n1. Motor disturbance causes weakness (paraplegia, quadriplegia), spasticity,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4886f-7265-11ef-a7ae-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 515, "chroma:document": "the limbs. \n Generally diseases of spinal cord are characterized by:  \n\u2022 The presence of a level below which motor/sensory and/or autonomic function is \ndisturbed.   \n1. Motor disturbance causes weakness (paraplegia, quadriplegia), spasticity, \nhypereflexia and extensor plantar response, which is due to disruption of descending   corticospinal fibers.   \n2. Impaired sensation  results from disordered func tion of ascending spinothalamic \nand dorsal column pathways.   \n3. Autonomic disturbance  leads to disturbed sweating, bladder, bowel and sexual \ndysfunction."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48870-7265-11ef-bbd5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 516, "chroma:document": "Internal Medicine \n \n 501Some causes of spinal cord diseases \n1) Compressive : lesions may be epidural, intradural or intramedullary  \ni) TB spodylitis    \nii) Neoplasms    \niii) Epidural abscess   \niv) Epidural hemorrhage v) Cervical spondylosis vi) Herniated disc /disc prolapse \nvii) Fractured / displaced vertebral body \n2) Vascular \ni) AV \u2013 malformation \nii) Spinal artery thrombosis or embolization \n3) Inflammatory \ni) Transverse myelitis, Borrelia, Syphilis  ii) MS (multiple sclerosis) iii) Vasculitis \n4) Infections \ni) Viral : Varicella zoster virus , HSV-1 and HSV-2 , CMV , HIV  ii) Bacterial : Myocobaterial ,  iii) Parasitic : Schistosomaisis , Toxoplasmosis  \n5) Developmental :  syringomyelia , meningomyelocel \n6) Metabolic \ni) V-B 12 deficiency ii) Neurolathrism: that is a spastic parapares is resulting from consumption of \u201cGuaya\u201d, \nwhich grows in the northern part of Ethiopia. This cereal has neurotoxin which causes paraparesis when consumed in large amount for relatively long period of \ntime. \n \nCommon Spinal Cord Diseases  \nA. Neoplastic spinal cord compression \nMay be classified as: \n1) Extramedullary:  tumor outside the spinal cord. \ni) Epidural:  outside the dural layer"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48871-7265-11ef-83e2-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 517, "chroma:document": "Internal Medicine \n \n 502\u0083 Commonest cause of neoplastic compression of spinal cord in adults. Usually \nresults from metastasis to adjacent vertebral bone or direct compression of the \nspinal cord. \n\u0083 Commonest neoplasm  include: breast, lung, prostate, kidneys, lymphoma and \nmultiple myeloma \n\u0083 Most frequently involved site is thoracic cord \nii) Intradural:  inside the dural layer \n\u0083 These are slowly growing benign tumors like meningioma, neuroblastoma, \nlipoma   \n2) Intra medullary:  tumors within the spinal cord. \n\u0083 These are uncommon tumors , including ependymoma, hemangioblastoma low \ngrade astrocytoma \nClinical feature \n\u2022 Initial symptom is backache, which is localized, and which worsens with movement, coughing or sneezing.  The pain may radiate to the legs, trunk or following dermatomal distribution. \n\u2022 The pain may be sever and awaken the patient at night. \n\u2022 As compression progresses patient devel ops progressive weakness, sensory \nabnormalities and autonomic disturbances change in bladder function and constipation. \nPhysical findings include: \n\u2022 Weakness, spasticity, hyperreflexia \n\u2022 Loss of or decreased sensations to pinprick in the lower extremities \n\u2022 Extensor plantar response , and loss of abdominal reflexes and anal sphincter tone \n\u2022 Urinary retention  \nInvestigations \n\u2022 Check for primary tumor sites \n\u2022 Plain X-ray of the spine \n\u2022 Myelography  \n\u2022 Radionuclide bone scan \n\u2022 CT/MRI \n\u2022 Biopsy \n\u00c6 usually unnecessary in patients with known pre-existing cancer."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48872-7265-11ef-9817-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 517, "chroma:document": "\u2022 Urinary retention  \nInvestigations \n\u2022 Check for primary tumor sites \n\u2022 Plain X-ray of the spine \n\u2022 Myelography  \n\u2022 Radionuclide bone scan \n\u2022 CT/MRI \n\u2022 Biopsy \n\u00c6 usually unnecessary in patients with known pre-existing cancer. \nTherapy: depends on site and type of tumor. \nTreatment modalities include"}


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": 518, "chroma:document": "Internal Medicine \n \n 503Steroids : help to reduce the interstitial edema \n Should be started immediately with in the first 12 hrs of occurrence of symptoms \nPrednisolone 40 mg PO BID ,  or Dexamethason 12 mg IV followed by 4 mg IV QID may \nbe used \nRadiotherapy. \n Is effective even for classically radio-resistant tumors   \n Prevents new weakness and may give recovery of function \nSurgery: decompression or vertebral body resection \n Useful especially for intradural and intramedullary tumors \nNote: Treatment should be started as soon as possible (with in 12 hrs). Fixed motor deficits \n(paraplegia or quadriplegia), once established for > 12 hrs, do not usually improve, and beyond \n48 hrs the prognosis for substantial motor recovery is poor. \n \nB. Tuberculosis of the spine (Pott\u2019s disease) \n\u2022 One of commonest causes of myelopathy in  developing countries where Tuberculosis is \nendemic, Ethiopia. \n\u2022 Often Involves two or more adjacent vertebral bodies \n\u2022 Commonest site is lower thoracic and upper lumbar vertebrae \nClinical features \n\u2022 Patients present with insidious on set of back pain, which progressively get worse. \n\u2022 Gibus deformity (kyphotic swelling over the back) \n\u2022 Numbness and loss of sensation with a sensory level \n\u2022 Weakness of the lower limbs, often spastic in nature, with exaggerated deep tendon \nreflexes and up going plantar (Babinisky\u2019s sign)  \n\u2022 Bladder and /bowel dysfunction (Urinary retention with overflow incontinence, constipation or fecal incontinence)"}


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": 518, "chroma:document": "reflexes and up going plantar (Babinisky\u2019s sign)  \n\u2022 Bladder and /bowel dysfunction (Urinary retention with overflow incontinence, constipation or fecal incontinence)  \n\u2022 In about 65% of cases evidences of extra spinal tuberculosis is present  \nDiagnostic workup:  \n1. Imaging studies \n\u2022 Plain radiograph show characteristically destructive process of the vertebrae, \ninvolvement of disc space with deformity. \n\u2022 CT/MRI may show the lesion more clearly"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48875-7265-11ef-8ce7-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 519, "chroma:document": "Internal Medicine \n \n 504Treatment  \n\u2022 Medical Therapy \no DOTS: short course anti tuberculosis chemotherapy  is mainstay of therapy.  \no Steroids  can be added it there is neurological deficit  \n\u2022 Surgery:  is indicated if there is spinal instability or deformity and unresponsiveness to \nmedical treatment. \n \nC. Prolapse of intervertebral disc \n\u2022 It occurs due to trauma, sudden severe strain or degenerative changes. \n\u2022 Commonest site of for disc prolapsed is the lumbar region. \nClinical feature \nLocalized back pain aggravated by straining with or without \n\u2022 Radiculopathy \n\u2022 Segmental sensory loss \n\u2022 Changes in deep tendon reflexes (asymmetrical) \nStraight leg raising sign is positive:  the patient will have back pain, when stretched leg is \nraised / flexed at the hip joint. \nDiagnostic workup \n\u2022 Myelography: may help to localize the site of prolapse  \n\u2022 CT/MRI: can easily demonstrate the prolapsed disk  \nTherapy:  \nMedical therapy : is often supportive ad include \nBed rest, adequate analgesics and physical therapy \nSupporting belts or corsets \nSurgery : is the definitive treatment for disk prolapse. \n \nD. Transverse Myelitis   \nIt is an acute or sub acute inflammatory disorder of the spinal cord.  \nIt occurs   associated with; \n\u2022 Antecedent infection ( either viral or Mycoplasmal .)  \n\u2022 Recent vaccination \n\u2022 Multiple sclerosis \n\u2022 Collagen vascular disease (SLE)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48876-7265-11ef-82e3-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 520, "chroma:document": "Internal Medicine \n \n 505Clinical feature \n\u2022 Initial symptom is localized back or neck pain or radicular pain followed by various \ncombinations of paresthesia, sensory loss, motor weakness and sphincter disturbances, \nwhich can evolve within hours to several days. \nInvestigation \n\u2022 CSF: may be normal or show pleocytosis and increased protein. \nTreatment \n\u2022 Steroids can be used in moderate to severe cases. \n \nE. Metabolic and toxic myelopathies  \n \ni) Subacute combined dege neration of spinal cord \n\u2022 Neurologic disease mainly affecting the spinal cord, resulting from severe Vit-B 12 \ndeficiency. \n\u2022 Vit-B 12 deficiency results abnormalities on myelin basic protein leading to swelling of \nmyelin sheath followed by demyeliniation and gliosis.  \n\u2022 These changes mainly affect the posterior and lateral columns of spinal cord. \nClinical Feature: patients present with;- \n\u2022 Paresthesia in the hands and feet. \n\u2022 Early loss of position and vibration senses (loss of propioreceptor sensations). \n\u2022 Progressive spastic and ataxic weakness \n\u2022 Some patients may develop optic atrophy and encephalopathy \nTreatment \n    Vitamin B 12:  1000\u03bcg IM/d for 5 \u2013 10 days, followed by   \n1000 \u03bcg IM/week for 1 month, and then \n1000 \u03bcg IM month lifelong. \n \niii) Neurolathrism \n\u2022 Neurolathrism is syndrome that affects the nervous system of man due to consumption \nof peas of the lathyrus species (\u201cGuaya\u201d seeds) that contains neurotoxic amino acid."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48877-7265-11ef-8c31-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 520, "chroma:document": "1000 \u03bcg IM month lifelong. \n \niii) Neurolathrism \n\u2022 Neurolathrism is syndrome that affects the nervous system of man due to consumption \nof peas of the lathyrus species (\u201cGuaya\u201d seeds) that contains neurotoxic amino acid. \nExcessive consumption of these (Guaya) seeds occurs during times of food shortage, in Northern parts of Ethiopia (Gondar, Tigray, Wello and part of Gojam)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48878-7265-11ef-8166-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 521, "chroma:document": "Internal Medicine \n \n 506\u2022 It affects predominantly young men. \n \nClinical feature \nOnset can be acute /subacute usually precipitated by manual labour, febrile illness or diarrhea \nthen the patients will develop weakness, spastici ty and rigidity progressively preventing them \nfrom walking. Usually no sensory abnormality is seen. Some of severely affected cases may \ndevelop incontinence and impotence. Investigation \n\u2022 No specific laboratory test required.   \n\u2022 Diagnosis of neurolathrism is by exclusion of other causes and taking proper dietary \nhistory and understanding the geographic distribution of the diseases.  \n \nTreatment \n\u2022 No cure once established \nPrevention \n\u2022 Banning cultivation and consumption of the seed (\" Guaya\u201d).  \n\u2022 Breeding of nontoxic variant if possible. \n\u2022 Use of certain preparation methods (Cooking or soaking in excess water) makes the \nseed less toxic. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Diseases \nof the Spinal cord, pages 2438-2446. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nMyelopathy and other spinal cord disorders, pages 635-637."}


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": 522, "chroma:document": "Internal Medicine \n \n 5073. Cerebrovascular diseases  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define cerebrovascular diseases/stroke. 2. Understand   the epidemiologic significance of stroke. 3. Understand the classification of stroke and the etiologies. \n4. Identify the clinical manifestation of different types of stroke. \n5. Understand the diagnostic approach of patients with stroke. 6.  Understand the principles of management of patients with stroke.  \n7. Understand the preventive strategies for stroke.  \n Definition : Syndrome of an abrupt onset of nonconvulsive, focal neurologic deficit resulting \nfrom sudden interruption of the blood supply to parts of the brain, lasting 24 hours or longer. \n \nClassification of stroke  \nI. Etiologic classification  \n1) Ischemic   -stroke accounts for 80 \u2013 90% of all stroke in developed countries \na) Embolic \nb) Thrombotic \ni) Large vessel disease: resulting from narrowing of cerebral arteries doe to \natherosclerosis. \nii) Small vessel disease (Lacunar infarct) iii) Miscellaneous: E.g. Vasculitis resulting thrombus formation  \n2) Hemorrhagic Stroke: accounts for 10-20 % of cerebrovascualr accidents in developed \nnations. It is a much more commoner cause of stoke in developing countries , mainly associated with unrecognized or poorly controlled hypertension  \na) Primary Intracerebral Hemorrhage (PICH) b) Subarachnoid Hemorrhage (SAH) \nII. Classification based on the duration of stroke"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4887a-7265-11ef-896c-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 522, "chroma:document": "a) Primary Intracerebral Hemorrhage (PICH) b) Subarachnoid Hemorrhage (SAH) \nII. Classification based on the duration of stroke  \n1) Transient Ischemic attack:  TIAs are   focal neuralgic deficit lasting < 24 hrs confined to \nan area of brain perfused by specific artery , and neurologic deficit resolves in less than 24 hours"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4887b-7265-11ef-a73e-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 523, "chroma:document": "Internal Medicine \n \n 5082) Reversible Ischemic neurologic deficit:  sudden onset focal neurologic deficit which \nlasts for more than 24 hours, but the neurologic deficit recovers / resolves /. \n3) Stroke in evolution:  a focal neurologic deficit, the degree of which is progressing over \na couple of hours or days. \n4) Complete stroke:  sudden onset of focal neurologic deficit, in which the deficit neither \nimproves nor gets worse over time. It is oft en associated with infarction of part of the \nbrain. \n \nEpidemiology and risk factor  \nStroke is prevalent all over the worldwide. It is third commonest cause of death in developed \nworld following Coronary heart diseases and cancer. It is a leading cause of disability. The prevalence and incidence of stroke is also on the rise in developing countries. \nMajor risk factors associated with stroke include \n\u2022 Incidence is higher in men and old age \n\u2022 Hypertension \n\u2022 Smoking \n\u2022 Diabetic mellitus \n\u2022 Hyperlipidemia \n\u2022 Atrial fibrillation \n\u2022 Myocardial infarction \n\u2022 Congestive heart failure \n\u2022 Acute alcohol abuse \nApproach to a patient with stroke: \nGoals /Steps  \n1. Assessment and maintenance of vital functions  \n2. Determination of presumptive diagnosis of stroke subtype \n3. Confirmation of stroke subtype \n4. Management of a patients with stroke  \n \n1. Initial Assessment and maintenance of vital functions/stabilizing the patient"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4887c-7265-11ef-9cbd-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 523, "chroma:document": "2. Determination of presumptive diagnosis of stroke subtype \n3. Confirmation of stroke subtype \n4. Management of a patients with stroke  \n \n1. Initial Assessment and maintenance of vital functions/stabilizing the patient  \nStroke should be considered as medical emergency, as it affects vital functions of an individual.  For this reason the initial step in management of patients with acute stroke should be rapid \nassessment and maintenance of vital functions. This includes:"}


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": 524, "chroma:document": "Internal Medicine \n \n 509a) Maintenance of air way and ventilation \nb) Control of blood pressure \n\u0083 Acute stroke alters autoregulation of cerebral blood flow, compromising the blood \nsupply to an already damaged brain. Close monitoring of blood pressure and correction of both hypotension and hypertension reduces this risk. \n\u0083 If the patient is hypertensive treatment is recommend only when the DBP \u2265120 and \nSBP \n\u2265 200 mmHg.  Short acting antihypertensive drugs are preferred. \n\u0083 If the patient is hypotensive, it should be corrected by fluid administration and \ntreatment of the underlying cause for the hypotension.  \nc) Control of body temperature. \n\u0083 Fever occurs in 44% of patients with acute stroke.  The fever may be due to stoke or \ninfections.  Because fever worsens the prognosis of stroke body temperature should be controlled appropriately. \nd) Fluid management \n\u0083 Maintenance of euvolumic state and establishment of IV access using normal saline \n(rather than glucose solutions) is also important. Glucose is said to be neurotoxic and it is better avoided in patients with stroke. \nN.B Exclude causes of brain dysfunction, which mimic stroke like states like syncope, migraine, hysteria and trauma. \n \n2. Determine Presumptive Di agnosis of Stroke Subtype \nNumbers of clinical features are useful in determining the type of stroke. A good history taking, \nand proper physical examination may suggest the possible cause of the stroke. \nImportant historical information includes:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4887e-7265-11ef-8c05-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 524, "chroma:document": "Numbers of clinical features are useful in determining the type of stroke. A good history taking, \nand proper physical examination may suggest the possible cause of the stroke. \nImportant historical information includes: \n\u2022 Mode of onset and pattern of progression \no Embolisms usually occur suddenly when the patient is awake, most often early in \nthe morning, giving maximum deficit at onset. \no Hemorrhagic stokes also occur suddenly while the patient is awake, any may be \nphysically active or straining, and progresses within minutes to hours. \no Thrombosis often occurs during sleep hour or present upon arising from bed \nprogressing in a stepwise fashion. \n\u2022 Prior history of TIA  (transient ischemic attacks). These are often associated with \nthrombotic (atherosclerotic) vascular disease."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4887f-7265-11ef-b7d8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 525, "chroma:document": "Internal Medicine \n \n 510\u2022 Associated symptoms \no Headache, vomiting, reduced alertness suggest hemorrhagic stroke than \nischemic stroke. Very severe headache with altered consciousness without major \nneurologic deficit may suggest subarachnoid hemorrhage. \no If patient is having fever raises suspicion of infective endocarditis.   \no Seizure is common in embolic stroke. \n\u2022 Look for risk factors for stroke  \n\u2022 Looking for other medical conditions  associated with stroke such as hypertension, \ndiabetes, smoking and use of drugs like OCP* may suggest the diagnosis. \n \nPhysical Examination \n\u2022 Physical Findings may give clue to the type of stroke the patient is suffering from. \n\u2022 Absent/reduced peripheral pulses suggest atherosclerosis or embolism  \n\u2022 Presence of neck bruit suggests extra cranial occlusion of carotid arteries  \n\u2022 Cardiac abnormalities: such as atrial fibrillation, murmurs or cardiac enlargement may \nsuggest embolic stroke, the embolus originating from the heart. \n\u2022 Fever raises concern for infectious etiologies \n\u2022 Ophthalmoscopic examination: papilledma or retinal hemorrhage may suggest \nsubarachnoid hemorrhage or increased intracranial pressure. \n \nTable VIII-3-1.  Characteristic features of different types of stroke   \n \n Embolic \nstroke  Intracerebral hemorrhage Large vessel thrombosis  Lacunar \ninfarctions  Subarachnoid \nhemorrhage \nOnset \n  \n \n Sudden onset with maximum deficit at \nonset  Sudden (deficit  \nProgresses over minutes to \nhours)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48880-7265-11ef-92c3-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 525, "chroma:document": "Embolic \nstroke  Intracerebral hemorrhage Large vessel thrombosis  Lacunar \ninfarctions  Subarachnoid \nhemorrhage \nOnset \n  \n \n Sudden onset with maximum deficit at \nonset  Sudden (deficit  \nProgresses over minutes to \nhours) \n  Sudden,  Gradual, stepwise, or \nStuttering Sudden, \nGradual, Stepwise \nor \nStuttering  Sudden,  Usually few or not focal signs \n \n \nTime of \noccurrence When the \npatient is  \nAwake \n When the patient is  \nAwake and \nactive When the patient is  \nAsleep or \ninactive When the patient is  \nAsleep or  \ninactive When the patient is \nAwake and  \nactive"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48881-7265-11ef-b832-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 526, "chroma:document": "Internal Medicine \n \n 511  \n  \nWarning \nsigns (TIA) None  \n None \n \n Usually \n \n Variable, \nTIA\u2019s  \nmay occur None \n \n \nAssociated symptoms \n(Headache \nVomiting ) \n Sometimes \n \n Usually \n \n Sometimes \n \n No \n \n Always (stiff  \nneck) \nCT \nscan  \n Decreased \ndensity  \n Increased density\n \n \n Decreased  \ndensity  \n Usually \nnormal  \n \n Usually  \nabnormal  \n \nLP Usually clear  Usually bloody  \n Clear  Clear  Invariably \nblood  \n \nThese characterizations are generally accepted principles regarding stroke; however, it is good \nto remember that stroke can present atypically. \n3. Confirmation of Diagnosis:  different investigations are needed to confirm the \ndiagnosis. \n\u2022 Imaging studies (CT or MRI): are the most important initial diagnostic tests in patients \nwith stroke (if available and affordable by the patient).  CT can identify or excludes hemorrhagic stroke and other conditions which simulate stroke (like Neoplasm and abscesses).  Complete Infarction is usually seen after 24 hours. MRI is more sensitive than CT for early diagnosis of brain infarction. \n\u2022 Other Tests are:   \nLumbar puncture  \u2013 may be needed to make a diagnosis of small SAH which can be \nmissed by CT or MRI. \no Carotid Doppler studies : to look for carotid artery narrowing  \no Angiography : to identify the exact location and the specific artery blocked  \no Echocardiography : to look for cardiac sources of embolization  \no ECG: to look for arrhythmias such as atrial fibrillation"}


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": 527, "chroma:document": "Internal Medicine \n \n 512o CBC, ESR, VDRL \no Tests for HIV infection : stroke associated with vasculitis is common in HIV positive \npatients  \no FBS, Lipid profile : to look for diabetes and hyperlipidemia 9 risk factors for stroke  \no Coagulation profile: to look bleeding tendencies. \n \n4. Management of specific stroke  \nGoal of Treatment  \n\u2022 Interruption of further brain damage \n\u2022 Prevention and management of complication  \nA. General Measures \n\u2022 Admit the patients where close follow up can be given \n\u2022 Continue follow up and maintenance of vital functions. \no Airway and ventilation \no Controlling of blood pressure \no Controlling body temperature \no Fluid administration /Hydration \n\u2022 If the patient is comatose or has impaired mental status \no Changing the patients position every 2 hrs and avoid the occurrence of bed sores \no Bladder and bowel care: if the patient has incontinence \u2013 catheterize \n\u2022 Infections such as aspiration pneumonia should be treated with antibiotics \n \nB. Management of Specific Etiologies \n1) Atherosclerotic stroke (Thrombotic stroke  )  \ni) Thrombolytic therapy: in developed coun tries thrombolytic therapy with \nmedications such as rt-PA (plaminogen activator), to patients who present within \n3 hrs of onset of stroke, helps to lyse the thrombus and restore perfusion to the affected brain. \nContraindications:  \n\u2022 Extensive infarct on CT,  \n\u2022 Recent surgery, Head trauma \n\u2022 GI or urinary hemorrhage, bleeding disorders, Anticoagulation with"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 527, "chroma:document": "3 hrs of onset of stroke, helps to lyse the thrombus and restore perfusion to the affected brain. \nContraindications:  \n\u2022 Extensive infarct on CT,  \n\u2022 Recent surgery, Head trauma \n\u2022 GI or urinary hemorrhage, bleeding disorders, Anticoagulation with \nprolonged PT/PT"}


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": 528, "chroma:document": "Internal Medicine \n \n 513\u2022 Seizure at stroke onset \n\u2022 Severe uncontrolled hypertension.   \nii) Anticoagulants: use of Heparin and Warfarin is controversial. Low dose heparin \ncan be given for prevention of thromboembolism. \niii) Anti-platelet aggregation agents: \nAspirin reduces the incidence of stroke and vascular mortality. General \nrecommendation is to give 325 mg of ASA once daily. It may not help to resolve the already formed thrombus, but ASA prevents recurrence of stroke. \n2) Embolic stroke: (Cardiogenic embolus) \n\u2022 Anticoagulation is indicated to prevent recurrent embolic stroke. Anticoagulation \nwith heparin should be initiated when the acute phase of stroke is over. Care should be taken to avoid hemorrhagic transformation of infarct. Warfarin is used for chronic anticoagulation. \n3) Intracerebral hemorrhage \n\u2022 Continue supportive measures \n\u2022 Control very high blood pressure  \n\u2022 Surgical consultation is indicated for removing cerebellar hematoma, as it may \ncompress vital centers in the brainstem. \n4) Subarachnoid Hemorrhage \nMedical therapy:  \n(a) Supportive measures include bed rest, sedatives, analgesic, laxative,  \n(b) Control of hypertension and  \n(c) Nimodipin (calcium channel blocker) is given to prevent neurologic deterioration \ndue to vasospasm.   \nSurgical therapy : Saccular aneurysms are treated surgically \n \nC. Prevention of further stroke:  \n\u2022 Control of hypertension \n\u2022 Control blood sugar in diabetics \n\u2022 Ceasation of  smoking"}


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": 528, "chroma:document": "due to vasospasm.   \nSurgical therapy : Saccular aneurysms are treated surgically \n \nC. Prevention of further stroke:  \n\u2022 Control of hypertension \n\u2022 Control blood sugar in diabetics \n\u2022 Ceasation of  smoking \n\u2022 Physical activity and weight reduction  \n\u2022 Anticoagulation for atrial fibrillation \n\u2022 ASA 75 mg Po daily in individuals older than 50 and have history of TIA"}


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": 529, "chroma:document": "Internal Medicine \n \n 514\u2022 Surgery (Endarterioactomy): if a narrowed artery is detected  \nD. Rehabilitation:  is a very important part of management, and it shall be started early and \ninclude:- \n\u2022 Physiotherapy  \n\u2022 Occupational and speech therapy. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nCerebrovascular diseases, pages 2372-2392. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edtion Medicine, \nStroke, pages 619-625."}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 530, "chroma:document": "Internal Medicine \n \n 5154. Impairment of consciousness and Coma \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define different levels of Impairment of consciousness and Coma. 2. List the etiologies of Impairment of consciousness and Coma. 3. Understand the diagnostic approach of Impairment of consciousness and Coma. \n4. List differential diagnosis to Impairment of consciousness and Coma.  \n5. Understand the principles of management of patients with coma.  \n \nIntroduction \nMaintenance of conscious state requires proper functioning of the cerebral hemispheres, \nreticular activating system found in brain stem and corticothalmic connections.  If there is structural, metabolic or toxic insult of diffuse nature to these structures results in alteration of \nconscious level of different degree. \n\u2022 Coma  is severe degree of reduced consciousness (alertness and responsiveness) from \nwhich the patient cannot be aroused. \n\u2022 Stupor  is a sleep like unarousability, from which the patient can be awakened by vigorous \nstimuli. \n\u2022 Drowsiness:  is a state of reduced consciousness characterized by easy arousal that can be \nmaintained only for brief period of time. \n\u2022 Vegetative state:  is characterized by the patient\u2019s unawareness of self or external stimuli. \nAutonomic functions are relatively well maintained, and a sleep-wake cycle exists. The"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48888-7265-11ef-9173-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 530, "chroma:document": "maintained only for brief period of time. \n\u2022 Vegetative state:  is characterized by the patient\u2019s unawareness of self or external stimuli. \nAutonomic functions are relatively well maintained, and a sleep-wake cycle exists. The \npatient cannot interact with others in a meaning full fashion. The patient can survive with medical and nursing support.  \n\u2022 Brain death:  This is a state in which there has been cessation of cerebral blood flow; as  a \nresult there is  global loss of brain function while respiration is maintained by artificial means and the heart continues to pump.  \nEtiologies  \n1. Diseases that cause no focal neurologic deficit or lateralizing neurologic signs . The \nloss of consciousness in such patients is diff use bilateral hemispheric impairment, and such \npatients have normal brainstem function. Some of the causes include :-"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d48889-7265-11ef-a048-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 531, "chroma:document": "Internal Medicine \n \n 516\u2022 Metabolic disturbances such as :  hepatic encephalopathy ,uremic encephalopathy \n,hypoglycemia, diabetic ketoacidosis. Electrolyte imbalance (hyponatremia, \nhypernatremia, Hyperkalemia, Hypoca lcaemia), Hypoxia, Hypercapnia etc \n\u2022 Intoxications:  alcohol, sedative drugs, opiates \n\u2022 Sever systemic or CNS infections  : meningitis, encephalitis, cerebral malaria, \ncerebral abscess \n\u2022 Post seizure state  : status epilepticus  \n\u2022 Hypertensive encephalopathy , eclampsia \n\u2022 Sever hyperthermia or hypothermia  \n\u2022 Head trauma:  brain concussion  \n2. Diseases that cause focal neurologic deficit: these disorders cause coma by affecting \nthe reticular activating system. They are classified in to two depending on the location of the lesion.    \na) Supratentorial ( hemispheric) lesions  \n\u2022 Epidural or subdural hematoma \n\u2022 Intraparenchymal hemorrhage (hemispherical hemorrhage) \n\u2022 Large ischemic infarction \n\u2022 Tumor , Abscess , Trauma  \nb) Infratentorial lesions  \n\u2022 Pontine or cerebellar hematoma \n\u2022 Basilar artery thrombosis \n\u2022 Ischemic cerebellar infarction  \n\u2022 Tumor , abscess \nApproach to a patient in Coma \nComplete and rapid assessment of the patient is critical for optimal care. \nA. Assessment and maintenance of vi tal function is the initial step \n\u2022 Maintain the air ways and ensure adequate  breathing ( ABC of life )  \n\u2022 Maintain circulation  \nB. Establishment of cause of coma : is done by taking a careful history, doing rapid but"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4888a-7265-11ef-8d9b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 531, "chroma:document": "\u2022 Maintain the air ways and ensure adequate  breathing ( ABC of life )  \n\u2022 Maintain circulation  \nB. Establishment of cause of coma : is done by taking a careful history, doing rapid but \nthrough physical examination and investigations. \nPatient History:  \nPast medical history:  looking for disease like diabetes, hypertension, cirrhosis, chronic renal \ndisease, malignancies and other diseases."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4888b-7265-11ef-99e0-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 532, "chroma:document": "Internal Medicine \n \n 517\u2022 History of medications: legal or illicit dr ugs (sedatives, hypnotics, narcotics ) and history \nof drug abuse \n\u2022 Circumstances and rapidity with which change in mental status developed (sudden \nonset indicating vascular causes, gradual onset indicating metabolic and infectious \ncauses  fluctuations suggest subdural hematoma) \n\u2022 Recent patient complaints preceding loss of consciousness: medical and neurologic \nsymptoms (fever suggesting infections, polyuria and polydypsia indicating DKA) \n\u2022 Details regarding the site where the patient was found ( e.g. the presence of empty drug \nvials or evidence of fall or trauma \nPhysical examination should be through. \n\u2022 Vital signs : Extremes of BP, pulse or temperature and abnormal pattern of breathing. \no Fever suggests systemic or CNS infections or Neurogenic fever \no Tachypnea \u2013 in pulmonary infections or acidosis \no Hypertension \u2013 hypertensive encephalopathy \n\u2022 Head and neck : evidence of trauma and the presence of meningismus  \n\u2022 Skin:  look for signs of trauma or injection.     \n\u2022 General systemic examination: looking for evidences of systemic illnesses like \ncirrhosis, chronic renal, failure, meningococcemia etc. \nNeurologic examination: is the cornerstone of assessment of comatose patient. It should be \ndescriptive and systematic.   \n1. Level of consciousness : can be assessed semi quantitatively using the Glasgow \ncoma Scale .  \n \nTable VIII-4-1 Glasgow coma Scale: \nEye opening     Score"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4888c-7265-11ef-aff8-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 532, "chroma:document": "descriptive and systematic.   \n1. Level of consciousness : can be assessed semi quantitatively using the Glasgow \ncoma Scale .  \n \nTable VIII-4-1 Glasgow coma Scale: \nEye opening     Score  \nSpontaneous   To verbal stimulus       \nTo painful stimulus \nNone  4 3 \n2 \n1 \nBest verbal response  \nOriented   Confused   5 4"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4888d-7265-11ef-bdbd-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 533, "chroma:document": "Internal Medicine \n \n 518 \n \n \n \n  \n  \n \n   \n Points are given for best response in each category and are added giving a score between 3 \n(deep coma) and 15(normal)  \n \n2. Brain stem reflexes  \nAssessment of brainstem functions helps to localize the cause of coma. This can be done using brain stem reflexes including, pupillary light response, ocular movements, corneal reflex and the \nrespiratory pattern.  If the brainstem functions are normal, coma must be ascribed to bilateral \nhemispherical disease.  \na) Pupillary light response \nPupillary reactions are examined with a bright, diffuse light. During examination size, shape, \nsymmetry and reaction to light should be noted on both eyes.  \no Normally reactive and round pupils of midsize (2.5 to 5 mm) essentially exclude \nmidbrain damage. \no Enlarged (>6mm) and unreactive pupil on one side signifies a compression or \nstretching of the third nerve from the effects of a mass above. \no Bilaterally dilated and unreactive pupils, indicates severe midbrain damage, \nusually from compression by a mass. \no Bilaterally small (1 to 2.5 mm) and reactive pupils (not pinpoint) are seen in \nmetabolic encephalopathies or in deep bilateral hemispheral lesions such as hydrocephalus or thalamic hemorrhage. \no Very small but reactive pupils (< 1 mm)/pinpoint pupils, characterize narcotic or \nbarbiturate overdoses but also occur with extensive pontine hemorrhage the thalamus. Inappropriate words  Unintelligible words  None  3 2 1"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b0fb-7265-11ef-87b7-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 533, "chroma:document": "o Very small but reactive pupils (< 1 mm)/pinpoint pupils, characterize narcotic or \nbarbiturate overdoses but also occur with extensive pontine hemorrhage the thalamus. Inappropriate words  Unintelligible words  None  3 2 1 \nBest  motor response  \nObeys commands  Localizes pain   Withdrawal from pain   \nExtensor response  \nFlexor response  None  6 5 4 \n3 \n2 1"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b0fc-7265-11ef-9483-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 534, "chroma:document": "Internal Medicine \n \n 519b) Ocular Movements \nBefore maneuvers the eyes are observed by  elevating the lids and noting the resting \nposition and spontaneous movements of the eyeballs. \no Lid tone is tested by lifting the eyelids and noting their resistance to opening and \nthe speed of closure. Resistance to opening the eye lids may suggest hysteric \nconversion. Easy eyelid opening with slow closure indicates sever coma. \no Midline deviation suggests frontal/pontine damage. \no Dysconjugate gaze (abduction or adduction) suggests cranial nerve \nabnormalities. \no Spontaneous eye movements roving, dipping, bobbing suggest damages being \nat different sites. \no The eyes look towards a hemispheric lesion and away from a brainstem lesion. \ni. Occulocephalic reflex \nOculocephalic reflex is elicited by moving the head from side to side or vertically with eyes held open. In comatose patient with intact brainstem  \no If the eyeballs move to the opposite direction of the head movement \u00c6intact \nbrainstem function (\u201cdoll\u2019s eyes\u201d movement is positive.) \no If the eyeballs move to the same direction of the head movement \u00c6 Brainstem \ndysfunction. \nii. Caloric (occulovestibular) reflex \no This test is performed by irrigating the ear with ice (cold) to stimulate the \nvestibular apparatus. In patients with intact brain stem the eyes move to the irrigated ear. \nc)  Corneal reflex   \no This test assesses the integrity of dorsal midbrain and pontine. It is lost if the"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b0fd-7265-11ef-9f29-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 534, "chroma:document": "vestibular apparatus. In patients with intact brain stem the eyes move to the irrigated ear. \nc)  Corneal reflex   \no This test assesses the integrity of dorsal midbrain and pontine. It is lost if the \nreflex connections between the fifth (afferent) and the seventh (efferent) cranial nerves within the pons are damaged. \nd) Respiration:  \n\u2022 Abnormalities of respiratory pattern can help in coma diagnosis but are of less localizing \nvalue in comparison to other brainstem signs. \no Shallow, slow, but regular breathing  suggests metabolic or drug depression. \no Cheyne-Stokes respiration  signifies bihemispherical damage or metabolic \nsuppression, and commonly accompanies light coma."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b0fe-7265-11ef-a121-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 535, "chroma:document": "Internal Medicine \n \n 520o Rapid, deep (Kussmaul) breathing  usually implies metabolic acidosis but may \nalso occur with pontomesenephalic lesions and severe pneumonia. \no Agonal gasps  reflect bilateral lower brainstem damage and are indicators of \nsevere brain damage and a near death situation. \n3. Motor function /response \nPosture of the patient : \no Quadriparesis and flaccidity : suggest pontine or medullary damage  \no Decorticate posturing: flexion of the elbows and the wrists with supination of the \narms, and extension of the legs, suggests severe bilateral or unilateral \nhemispheric or diencephalic lesion (damage above the midbrain.) \no Decerebrate posturing  (extension of elbows and the wrist with pronation of the \nforearm and extension of the legs) indicates damage to the brainstem( midbrain or pontine compromise )    \no Spontaneous activities  \u2013 if the patient is yawning, swallowing, coughing or \nmoaning the coma is not deep. \no Abnormal body movements  \u2013 seizure, myoclonus may suggest the cause of \nthe coma is status epelepticus, uremia etc.  \no Assess tone, response to painful stimuli and presence of asterixes. Asymmetric \nmotor responses have localizing value. \nDifferential Diagnosis: \nPsychogenic Coma (hysteric coma):  patient often has history of psychiatric illness, and non \nphysiologic response on physical examination. \no Resistance to having the eyelids opened (the patient resists eyelid opening when the \nexaminer tries to open it)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b0ff-7265-11ef-a995-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 535, "chroma:document": "physiologic response on physical examination. \no Resistance to having the eyelids opened (the patient resists eyelid opening when the \nexaminer tries to open it)  \no Failure of the patient\u2019s arm, when held by the examiner over the patent\u2019s face, to fall \nup on the face when released by the examiner. \no Nystagmus when the ear is irrigated with cold water \no Adversive head and eye movements  \n \nLaboratory investigations \n\u2022 Blood film, CBC, urine analysis \n\u2022 Measurements of serum glucose level, renal and liver function test."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b100-7265-11ef-a1a9-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 536, "chroma:document": "Internal Medicine \n \n 521\u2022 Lumbar puncture and CSF examination  should be done as soon as possible unless \nincreased intracranial pressure is suspected to exclude infections and subarachnoid \nhemorrhage. \n\u2022 Measurements of serum electrolytes, cultur es, toxicological analysis, arterial blood gas \nanalysis, EEG and imaging studies are also helpful in diagnosis of coma if available.   \nManagement \nIdeally the, care of comatose patient is started together with the initial assessment to identify the etiology. \na) \nInitial therapy  : Maintaining an adequate airway, optimal ventilation and \nmaintaining adequate perfusion ( blood pressure) \no If there is possibility of cervical fracture, immobilization of the neck is \nessential \no Endothracheal intubation is often indicated to protect the airways  \no Blood samples for CBC, electrolyte glucose, RFT, LFT etc should be \nobtained. \no Intravenous thiamine: 100 mg IV with 50 % glucose solution is given. This \ntreatment is given if hypoglycemia is even remote possibility, and thiamine is \ngiven with glucose in order to avoid eliciting Wernicke disease in malnourished \no Naloxone(0.4mg ) is administered in case of opiate intoxication \no Flumazenil can be given if benzodiazepine or hepatic coma is suspected  \no Correct any associated problem  like hypertension, hypoglycemia \nhyperthermia and hypoxia \nb) Give care of comatose patient: \n\u2022 Monitor vital signs \n\u2022 Provide adequate ventilation and oxygenation."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b101-7265-11ef-99fe-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 536, "chroma:document": "o Correct any associated problem  like hypertension, hypoglycemia \nhyperthermia and hypoxia \nb) Give care of comatose patient: \n\u2022 Monitor vital signs \n\u2022 Provide adequate ventilation and oxygenation. \n\u2022 Maintain appropriate position and change position frequently \n\u2022 Catheterize and insert  nasogastric tube \nc)    Manage the primary cause of coma."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b102-7265-11ef-8df8-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 537, "chroma:document": "Internal Medicine \n \n 522References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Acute \nconfusional state and Coma, pages 1624-1630. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edtion Medicine, \nLoss of consciousness, pages 600-605."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b103-7265-11ef-8627-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 538, "chroma:document": "Internal Medicine \n \n 5235. Seizure and Epilepsy \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Seizure and epilepsy. 2. Describe the international classification of Seizure. 3. Understand   the epidemiology of Seizure and epilepsy. \n4. List the etiologies or risk factors for Seizure disorder. \n5. Identify the clinical manifestation of different types of Seizure disorders. 6. Understand the Evaluation and diagnostic approach to Seizure. 7.  Identify complications of Seizure. 8. List differential diagnosis for Seizure. \n9. Manage patients with Seizure or epilepsy.  \n10. Understand status epileptics and its management. \n \nDefinition: Seizure  is a paroxysmal event due to abnormal excessive discharge of cerebral \nneurons. The paroxysmal event may be subtle or dramatic. Depending on the distribution of the \ndischarge, the manifestations may be: \n\u2022 Motor \n\u2022 Sensory \n\u2022 Autonomic or \n\u2022 Psychiatric manifestation.  \nEpilepsy \u2013  is a syndrome characterized by recurrent  (two or more) unprovoked seizure attacks, \ndue to a chronic, underlying process in the brain. This definition implies that a person with a single seizure, or recurrent seizures due to correctable or avoidable circumstances, does not necessarily have epilepsy. \nInternational classification of seizures: \nEpileptic seizures can be classified in many different ways. Commonly used classification is the \none developed by International League against Epilepsy."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b104-7265-11ef-bbb3-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 538, "chroma:document": "International classification of seizures: \nEpileptic seizures can be classified in many different ways. Commonly used classification is the \none developed by International League against Epilepsy.  \n1) Partial seizures: beginning locally \na) Simple partial seizure: (with motor, somatosensory, autonomic or psychiatric symptoms  \nb) Complex partial seizure   \nc) Partial seizures with secondarily generalization"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b105-7265-11ef-9ddc-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 539, "chroma:document": "Internal Medicine \n \n 5242) Generalized seizures  \na) Absence seizures ( petit mal ) \nb) Tonic \u2013 clinical seizures ( grand mal ) \nc) Myoclonic seizures  \nd) Clonic seizures  e) Tonic Seizures  f) Atonic seizures  \n3) Unclassified  \na) Neonatal seizures  b) Infantile spasm  \nThe basis for this classification is manifestations during seizure attack and EEG feature between attacks. This classification is useful in understanding underlying etiology, selecting \nappropriate treatment and understanding the prognosis of seizure type.  Epidemiology \n\u2022 Epilepsy is estimated to affect 0.5-4% of the population around the world.  \n\u2022 The prevalence is said to be higher in developing countries.  \n\u2022 Grand mal seizure account for 40 to 80 %of all types of epileptic seizures.  \n\u2022 It is estimated that 5-10 % of the population will have at least one seizure attack in \ntheir life time, with the highest incidence occurring in early childhood and late adulthood. \n\u2022 In Ethiopia based on a study done by Teklehaymanot R\n. the prevalence of active \nepilepsy is estimated to be 5.2/1000. Analysis of 468 epileptics seen in neurology clinics of Addis Ababa showed highest incidence in males aged 11-20 years. The \ncommonest type of seizure was found to be grand mal seizure accounting for 60% of all cases.  \nEtiology of seizure or risk factors:  The causes of epilepsy/seizure are vary greatly in different age groups and across different regions of the world"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b106-7265-11ef-9bd3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 539, "chroma:document": "commonest type of seizure was found to be grand mal seizure accounting for 60% of all cases.  \nEtiology of seizure or risk factors:  The causes of epilepsy/seizure are vary greatly in different age groups and across different regions of the world \n\u2022 Idiopathic or cryptogenic : in which the cause is unknown,  accounts for the majority.   \n\u2022 Genetic factor  (Family History)  \n\u2022 Perinatal causes : perinatal asphyxia, birth trauma, perinatal infection  \n\u2022 CNS infections : encephalitis, toxoplasmosis, cerebral malaria,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b107-7265-11ef-8d50-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 540, "chroma:document": "Internal Medicine \n \n 525\u2022 Head trauma: penetrating head injury, depressed skull fracture, intracranial hemorrhage \nand prolonged post traumatic coma are associated with increased risk of having seizure \ndisorder. \n\u2022 Neoplasms : metastatic or primary brain tumors  \n\u2022 Vascular causes : Infarction or stroke, vascular malformations   \n\u2022 Metabolic abnormalities : hyponatremia, hypo or hyperglycemia, Uremia  \n\u2022 Inflammatory causes : Systemic lupus erythromatus  \n\u2022 Degenerative diseases:  Alzheimer\u2019s disease  \n\u2022 Drugs:  Thephylline, Cocaine, Lidocaine  \n \nClinical features   \nI. Partial Seizures:  these are seizures, which arise from localized region of the brain.  \na) Simple partial/focal seizures  \n\u2022 These are seizure activities in which consciousness is not impaired.  \n\u2022 Manifestation can be motor, sensory, autonomic or psychiatric.  \n\u2022 Motor manifestation is usually focal clonic or tonic movement of angle of mouth, finger or \nthumbs. This seizure activity may spread ov er one side of the body (Jacksonian march) \nto involve larger body part. (E.g. the convulsive activity can start in the face, move to \nipsilateral arm, and then to the leg) \n\u2022 The rest of manifestations include transient sensory abnormalities, flushing and sweating \nor odd feelings.  \nb) Complex partial seizure  \n\u2022 These are focal seizures activities accompanied by impairment of the patient\u2019s ability to"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b108-7265-11ef-8f93-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 540, "chroma:document": "\u2022 The rest of manifestations include transient sensory abnormalities, flushing and sweating \nor odd feelings.  \nb) Complex partial seizure  \n\u2022 These are focal seizures activities accompanied by impairment of the patient\u2019s ability to \nmaintain normal contact with the environment. The patient is unable to respond appropriately to visual or verbal commands during the seizure, and has impaired recollection or awareness of ictal phase. \n\u2022 The seizure frequently begins with an aura , which may  manifest with hallucination ( e.g. \nOlfactory . visual , auditory or gustatory ) and complex illusions ( e.g. having experienced a new event ) \n\u2022 The start of the ictal phase is often a sudden behavioral arrest or motionless stare, which \nis often accompanied by automatism, which is involuntary automatic behavior (repeated complex activities like chewing, lip smoki ng, \u201cpicking movement\u201d of the hands  , and \ndisplay of emotions)."}


created_at: 2024-09-14 06:50:03
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id: 71d4b109-7265-11ef-a801-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 541, "chroma:document": "Internal Medicine \n \n 526\u2022 They have also post-ictal confusion and transition to full recovery may take minutes to \nhours.  \n \nc)  Partial seizure with secondary generalization \n\u2022 These are focal seizures, which evolve into a generalized seizure. These are usually \ntonic-clonic type and difficult to different iate from primary generalized tonic-clonic \nseizure.  \n \nII. Generalized seizures  \nThere are seizure disorders which arise from bo th cerebral hemispheres simultaneously, with \nwithout any detectable focal onset.  \na) Absence seizure  : \n\u2022 It is characterized by sudden and brief lapses of consciousness without loss of postural \ncontrol.  \n\u2022 The seizure typically lasts for only few sec onds, consciousness returns as sudden as it \nwas lost. \n\u2022 It usually manifests with blank stari ng and they may have also subtle motor \nmanifestations like blinking of the eyes, chewing movements.  \n\u2022 There is no post-ictal confusion.  \n\u2022 The seizure may occur as many as hundreds of times per day  \n\u2022 It is usually detected by unexplained daydr eaming and decline in school performance.  \n\u2022 It usually begins in childhood (4- 8 yrs ) , and it often has a good prognosis, with 60-70 5 \nof such patients will have spontaneous remission during adolescence.  \nb) Generalized tonic clonic seizure (Grand mal) \n\u2022 Is the most common seizure type. \n\u2022 The seizure usually begins abruptly without warning (no aura or focal manifestations.)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b10a-7265-11ef-937f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 541, "chroma:document": "of such patients will have spontaneous remission during adolescence.  \nb) Generalized tonic clonic seizure (Grand mal) \n\u2022 Is the most common seizure type. \n\u2022 The seizure usually begins abruptly without warning (no aura or focal manifestations.) \n\u2022 The ictal phase  is begins with tonic contraction of muscles throughout the body , which \nis responsible for loud moan or cry (due tonic contraction of the muscles of respiration and the larynx), tonic posturing, respiration is impaired and the patient falls  to the \nground, and there may be  tongue biting due to tonic contraction of the jaw muscles. \nAfter 10 \u2013 20 seconds the tonic phase evolves to clonic phase characterized by bilateral \njerking clonic movement involving the whole body. This lasts for another 1 minute."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b10b-7265-11ef-b74a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 542, "chroma:document": "Internal Medicine \n \n 527\u2022 The post-ictal phase  is characterized by unres ponsiveness, muscle flaccidity, \nexcessive salivation and frothing of saliva which may cause stridorous breathing and \npartial airway obstruction. Bladder or bowel incontinence may occur at this point.  Patients gradually regain consciousness over mi nutes to hours, and during this transition \nthere is typically a period of postictal confusion, headache, muscle ache and fatigue that can last for many hours.  \nc) Atonic Seizures :  \n\u2022 Are characterized by sudden loss of postural muscle tone, lasting 1 to 2 seconds.  \n\u2022 Consciousness is briefly impaired. \n\u2022 It usually manifest as a head drop or nodding movement, while a longer seizure may \ncause the patient to collapse  \nd) Myoclonic  seizure  :  \n\u2022 Is characterized by a sudden and brief muscle contraction that may involve one part of \nthe body or the entire body.  \n\u2022 A normal common physiologic form of myoclonus is sudden jerking movement observed \nwhile falling asleep. \n\u2022 Pathologic myoclonus is most commonly seen with metabolic disorders, degenerative \ndiseases of the CNS or anoxic brain injury .  \n \nComplications \n\u2022 Status epilepticus  \n\u2022 Accidents \n\u2022 Hypoxic brain damage  \n\u2022 Mental retardation and impairment of intellectual function  \n\u2022 Sudden death  \n\u2022 Psychosocial (Social stigma).  \nDiagnostic approach/Evaluation"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b10c-7265-11ef-be14-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 542, "chroma:document": "Complications \n\u2022 Status epilepticus  \n\u2022 Accidents \n\u2022 Hypoxic brain damage  \n\u2022 Mental retardation and impairment of intellectual function  \n\u2022 Sudden death  \n\u2022 Psychosocial (Social stigma).  \nDiagnostic approach/Evaluation  \nPatient\u2019s history and physical examination can aid in the determination of whether or not a seizure or some other transient event was responsible for the patient\u2019s symptoms  \nHistory should include: - \nHistory of the event  \n\u2022 Presence of any prodromal symptoms  \n\u2022 Description of seizure by reliable observer"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b10d-7265-11ef-8874-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 543, "chroma:document": "Internal Medicine \n \n 528\u2022 Post ictal symptoms  \n\u2022 Urinary incontinence, myalgia and tongue bite or oral lacerations are clues to the \nproper diagnosis. \nHistory   of suggesting cause and risk factors  \n\u2022 Febrile convulsion (history of high grade fever )  \n\u2022 CNS infections (current /Previous)  \n\u2022 Head injury  \n\u2022 Stroke  \n\u2022 Developmental abnormality \n\u2022 Family history  \n\u2022 Social history (like alcohol abuse)  \nPhysical examination:  features that should be looked for include  \n\u2022 Skin for evidence of Neurofibromatosis  \n\u2022 Organomegaly: Metabolic storage diseases  \n\u2022 CVS/ carotid artery - stroke  \n\u2022 Complete neurological exam. \nInvestigations  \n\u2022 EEG (Electroencephalography)  is most useful test in diagnosis of seizure disorder. \nIt should be performed while the patient is asleep and awake. Abnormal EEG \nsupports the diagnosis of seizure and may give information about the type of seizure. However abnormal EEG is not adequate for diagnosis of seizure and normal EEG \ncan be found in epileptics.  \n\u2022 Neuroimaging preferably MRI  : may help to see any space occupying lesion in the \nbrain \n\u2022 Other routine laboratory assessment  may be required in management of patients \nwith epilepsy (CBC. Urinalysis, serum glucos e, liver function test, renal function test \nelectrolytes, toxicological screening).  \nDifferential Diagnosis for Seizure  \n\u2022 Syncope \n\u2022 Psychogenic seizure (hysteric conversion)  \n\u2022 Transient Ischemic attack \n\u2022 Migraine"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b10e-7265-11ef-b151-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 544, "chroma:document": "Internal Medicine \n \n 529Management:  \nGoal of therapy: \n\u2022 Complete control of seizure  \n\u2022 Prevent development of complications and socioeconomic consequences.  \nTreatment of seizure includes:-  \n1. Treatment of underlying condition  \n\u2022 Metabolic disorders such as hypoglycemia , hyponatremia or drug intoxication should \nbe corrected   \n\u2022 Structural CNS lesion lie tumors may be removed surgically.   \n2. Avoidance of precipitating factor  \n\u2022 Maintain normal sleep schedule  \n\u2022 Avoid taking  excess alcohol  \n\u2022 Reduce stresses using  , physical Exercise , meditation or counseling  \n3. Suppression or control of recurrent seizure  \nAntiepileptic drug therapy (AEDT)   \n\u2022 The Goal of antiepileptic therapy is to achieve complete control of seizure with no or \nminimal side effects, preferably using single agent and easy dosing schedule  \nWhen do we start anti epileptic drugs?  \n\u2022 Recurrent seizure of unknown cause or a known cause that cannot be \nreversed  \n\u2022 Single seizure due to  : \no Identified CNS lesion (tumor, infection, trauma)  \no With abnormal neurologic exam  \no Presenting as status epilepticus  \no With post-ictal Todd\u2019s paralysis \no With strong family history of seizure disorder \no With abnormal EEG"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b10f-7265-11ef-99a1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 545, "chroma:document": "Internal Medicine \n \n 530\u2022 Note:  anticonvulsant therapy is not often initiated in patients with a single, \nunprovoked convulsion, a normal neurologic examination, and a normal \nneuroimaging study and EEG unless they  experience a second seizure. \nGeneral principles :  \n\u2022 An attempt is usually made to prevent subsequent seizure using a single agent , in order \nto limit side effects.  \n\u2022 The drugs should be administered in progressive dose until seizure control has been \nachieved or until drug toxicity occurs.  \n\u2022 Only if monotherpay fails should a second drug be added to the patient\u2019s regimen. If \ncontrol is achieved, then the first agent might be carefully withdrawn. \n\u2022 A number of drugs are available for treatment of epilepsy and the choice of medication is \nbased on the seizure type   \n Table VIII-5-1 Selection of antiepileptic drugs  \n Primary GTCS  Partial  Absence  Atypical absence \n, myoclonic, \nAtonic  \nFirst line  Valproic acid  \nLamotrigine Carbamazepine  \nPhenytoin \nValproic acid  Valproic acid  \nEthusuximide Valproic acid   \nSecond line  \n  \n Phenytoin \nCarbamazepine  Phenobarbitone  Topiramate  Phenobarbitone Lamotrigin Clonazepam Lamotrigin Clonazepam Topiramate  \ni. Phenobarbitone  \n\u2022 In developing countries, Phenobarbitone is the drug of choice for the control of partial \nand GTC seizures, due to the wide availability and cheaper cost of the drug.  \n\u2022 Its efficacy is quite acceptable in comparison to most of the AEDS, but it has some side"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b110-7265-11ef-972e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 545, "chroma:document": "and GTC seizures, due to the wide availability and cheaper cost of the drug.  \n\u2022 Its efficacy is quite acceptable in comparison to most of the AEDS, but it has some side \neffects that might interfere with compliance. These side effects have to be explained to \nthe patient and his family early on.  \n\u2022  This drug is available in the following dosage forms: 15, 30, 60 and 100 mg tablets."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b111-7265-11ef-90d2-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 546, "chroma:document": "Internal Medicine \n \n 531Dosage:  \n\u2022 The usual starting dose for adults is 60 PO daily. If seizure is not controlled the dosage \nmay be increased gradually at intervals of no less than 2-3 weeks to a maximum dose of \n200 mg PO BID.  \nCommon side effects of Phenobarbitone  \n\u2022 Fatigue , Listlessness , depression  \n\u2022 Insomnia (especially in children)  \n\u2022 Distractibility and short attention span (especially in children) and Hyperkinesia , \nIrritability  \n\u2022 Poor memory  \n\u2022 Decreased libido  \nIn cases of treatment failure or poor control with maximum tolerable doses of drug, a second AEDS is often added to the regimen. The addition of a second drug is associated with worsening of adverse effects; hence care should be taken, before one decides to add a second drug to the original regimen. \nii. Phenytoin: is the usual prescribed as a second line drug in resource limited settings like \nours mainly because of its availability and cost.  \nDosage :  \n\u2022 100 mg PO BID or TID , which may be gradually increased to a maximum of 200 mg PO \nTID ( i.e. 600 mg daily ) \nSide effects: \n\u2022 CNS : nystagmus , ataxia  \n\u2022 Gingival hyperplasia  \n\u2022 Coarsening of facial feature \n\u2022 Toxic hepatitis and liver damage  \niii. Carbamazepine : is also available in Ethiopia. It is often given for the treatment of partial \nseizure  \nDosage:  a low initial dosage with gradual increase is advised. \n\u2022 200 mg Po BID and gradually increase the dos age by 2OO mg every week until the best"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b112-7265-11ef-ab4e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 546, "chroma:document": "seizure  \nDosage:  a low initial dosage with gradual increase is advised. \n\u2022 200 mg Po BID and gradually increase the dos age by 2OO mg every week until the best \nresponse is achieved or maximum dose of 1600 mg daily. \nSide effects  \n\u2022 Aplastic anemia \n\u2022 Dizziness drowsiness"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b113-7265-11ef-9725-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 547, "chroma:document": "Internal Medicine \n \n 532\u2022 Skin rash  \n\u2022 Transient diplopia \nWhen to stop antiepileptic drugs? \n\u2022 It is common practice to continue treatment until the patient has been seizure free for at \nleast 3 years.  \n\u2022 Thereafter, consideration of drug withdrawal is based on a number of factors like:-  \no The ease with which control was achieved starting from the time of AED drug \ninitiation.  \no The type of seizure  \no The presence of other neurological co-morbidity e.g. mental retardation, focal \nneurological deficit.  \n\u2022 The probability of relapse after stopping treatment is somewhere around 10-40%  \n\u2022 It is not known whether remissions for 3 or more years consist of \u201ccure\u201d or \u201c control\u201d and \nso drug withdrawals have to be gradual, over a period of months to minimize the risks of \nrelapse.  \n\u2022 Most relapses occur within a year of discontinuing of medications. The more severe and \nlong lasting a patient\u2019s active epilepsy before remission, the greater the risk of relapse.  \nWhen to refer patients to a neurologist or tertiary level hospital   \n\u2022 Failure to respond to treatment  \n\u2022 Recurrence of previously controlled seizure  \n\u2022 Change in clinical pattern of seizure  \n\u2022 Appearance of previously absent symptoms/sign  \n\u2022 Development of side effects of a drug  \n4. Managing psychosocial issues  \n\u2022 Social stigma  : avoid misconceptions in the public through health education \n\u2022 Psychiatric problems  : depression , psychosis  ,anxiety should be treated"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b114-7265-11ef-89c1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 547, "chroma:document": "\u2022 Development of side effects of a drug  \n4. Managing psychosocial issues  \n\u2022 Social stigma  : avoid misconceptions in the public through health education \n\u2022 Psychiatric problems  : depression , psychosis  ,anxiety should be treated  \n\u2022 Social problems  (education, employment, marriage): encourage patients to go \nschool /work to get married and establish family. \n\u2022 Educate Patients and families:  about the diseases and what precautions patient \nshould take.  \n\u0083 Seizure /epilepsy can be controlled by drugs  \n\u0083 Drug discontinuation creates problem and follow up is important  \n\u0083  Advice Patients to avoid"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b115-7265-11ef-bf23-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 548, "chroma:document": "Internal Medicine \n \n 533\u00be Alcohol/ other drugs or substances like \u201cChat\u201d                                                         \n\u00be Heights  \n\u00be Cooking with open fire \n\u00be Machineries that may cause  injury  \n\u00be Swimming  \n\u00be Driving  \n\u0083 What should families or attendants do during active seizure  \n\u00be No traditional treatment is beneficial  \n\u00be To be calm  \n\u00be Loosen patient\u2019s clothing \n\u00be Keep from injury  \n\u00be Turn head to side  \n\u00be Do not insert anything into  the month  \n \nSurgical Therapy: Patient\u2019s refractory to medical control of seizure may benefit from surgery \nto control the epilepsy. Surgical interventions include  \n\u2022 Temporal lobe resection \n\u2022 Corpus callosum sectioning   \nStatus epilepticus  \n\u2022 A condition characterized by continuous or repetitive discrete seizure with \nimpairment of consciousness during interictal period, which lasts for more than 30 \nminutes. It is a medical emergency  \nIt can be caused or precipitated by  \n\u2022 Non compliance with AED  \n\u2022 CNS infections  \n\u2022 Metabolic derangement  \n\u2022 Tumors  \n\u2022 Trauma  \n\u2022 Stroke \n\u2022 Refractory epilepsy"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b116-7265-11ef-9e61-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 549, "chroma:document": "Internal Medicine \n \n 534Clinical features: \nGeneralized status epilepticus is obvious when t he patient is having over convulsion, however \nafter 30-35 min of uninterrupted seizure, the signs may become increasingly subtle. Patients \nmay have mild clonic movement of only the fingers, or fine, rapid movement of the eyes. Complications of Status epilepticus: \n\u2022 Aspiration  \n\u2022 Hypoxia  \n\u2022 Metabolic acidosis  \n\u2022 Hypotension \n\u2022 Hyperthermia \n\u2022 Rhabdomyolysis and associated myoglobinuria  \n\u2022 Multiple physical injures including vertebral bone fracture \n\u2022 Irreversible neuronal injury   \n \nManagement  \n1. Emergency supportive measures  \nKeep Airway patent and maintain breathing  \nSecure IV line and take blood for laboratory investigation \nGive glucose IV with Thiamine   \n2. Control the seizure  with anticonvulsant  \n1\nst step: Lorazepam 0.1 mg/kg IC at a rate of 2mg/min or Give diazepam IV 5- 10 mg IV  \n2nd step: Phenytoin 20 mg/kg IV at a rate of 50 mg /min if seizure continues  \n3rd step: Phenobarbital 20 mg/kg IV at a rate of 50 -75 mg/min, if seizure still continues  \n4th Step: General anesthesia with Medazolam, Pr opofol or pentobarbitol, if seizure becomes \nrefractory  \nIn resource limited setting Diazepam 5-10 mg IV is given 2-3 times, and if the seizure is not \ncontrolled Phenytion 1000 mg PO is given through NG tube. Phenobarbitone can also be used. \n3. Treat the precipitating cause (metabolic abnormalities or infections)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b117-7265-11ef-b38a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 549, "chroma:document": "controlled Phenytion 1000 mg PO is given through NG tube. Phenobarbitone can also be used. \n3. Treat the precipitating cause (metabolic abnormalities or infections)  \n4.  Give maintenance antiepileptic drug: after the acute condition is controlled."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b118-7265-11ef-b4ae-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 550, "chroma:document": "Internal Medicine \n \n 535References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Seizure \nand Epilepsy, pages 2357-2371. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nSeizure, pages 626-628."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b119-7265-11ef-9c01-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 551, "chroma:document": "Internal Medicine \n \n 5366. Parkinson\u2019s Diseases and other movement disorders  \n \nLearning objectives: at the end of this lesson the student will be able to : \n1. Define Parkinsonism and Parkinson\u2019s disease. 2. List the etiologies or Parkinsonism. 3. Understand   the epidemiology and risk factors for Parkinsonism. \n4. Describe the clinical manifestation of Parkinson\u2019s diseases. \n5. Understand the principles of management of Parkinson\u2019s diseases.  \n6. Understand the basic clinical features of other movement disorders.  \n \nParkinsonism:  \nDefinitio n: Parkinsonism is a clinical syndrome characterized by :- \n\u2022 Bradykineisa : slowness and paucity of movement   \n\u2022 Tremor:  This occurs at rest  \n\u2022 Rigidity  \n\u2022 Snuffling gate and  \n\u2022 Flexed posture  \n Etiologies: \n1. Parkinson\u2019s Diseases: It is sporadic and idiopathic with unknown etiology.  \n\u2022 Is the commonest cause of Parkinsonism accounting for 75 % of all cases?  \n\u2022 It is characterized by degeneration of cells in the substantia nigra,  which causes \ndeficiency of dopamine (a neurotransmitter) in the CNS, leading to a series of changes in motor control pathways. These degenerative changes are believed to be due to accumulation of the presynaptic protein \u03b1-synuclien. \n2. Other known causes : account for 25 % of all cases   \na) Familial ( primary Parkinson\u2019s diseases ) \nb) Other neurodegenerative diseases \n\u2022 Shy-Drager  syndrome \n\u2022 Motor neuron disease with PD features  \n\u2022 Dementia with Lewy bodies"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b11a-7265-11ef-97e3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 551, "chroma:document": "2. Other known causes : account for 25 % of all cases   \na) Familial ( primary Parkinson\u2019s diseases ) \nb) Other neurodegenerative diseases \n\u2022 Shy-Drager  syndrome \n\u2022 Motor neuron disease with PD features  \n\u2022 Dementia with Lewy bodies \n\u2022 Progressive supranuclear palsy \n\u2022 Wilson\u2019s disease"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b11b-7265-11ef-8449-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 552, "chroma:document": "Internal Medicine \n \n 537\u2022 Huntington\u2019s diseases \nc) Miscellaneous acquired conditions \n\u2022 Vascular parkinsonism ( stroke affecting the extrapyramidal structures) \n\u2022 Normal pressure hydrocephalus  \n\u2022 Cerebral palsy \n\u2022 Repeated trauma:\u201c dementia puglistica\u201d with parkisonian features ( e.g. seen in \nprofessional boxers like Mohamed Ali ) \n\u2022 Infectious : post encephalitis PD , Neurosyphilis \n\u2022 Hypothyroidism or pseydohypoparathyriodism \n\u2022 Drugs:  \n\u2022 Neroleptics ( antipsychotics e.g. Haloperidol ,Chlorpromazine  \no Antiemetics : metoclopromide ,  \no Methyldopa \no Valproic acid  \n\u2022 Toxins : Cyanide , Methanol , Carbon monoxide, manganese  \n Epidemiology: \n\u2022 PD affect > 1 million people in US ( 1 % of those > 55 years ) \n\u2022 The peak age of onset is the 60s ( range is 35-85 years  )  \n\u2022 Familial PD tend to have an earlier age of ons et ( typically before the age of 50 year) \n \nRisk factors for Parkinsonism include  \n\u2022 Positive family history  \n\u2022 Male gender,  \n\u2022 Head injury  \n\u2022 Exposure to pesticides  \n\u2022 Consumption of well water  \n\u2022 Rural living  \nClinical Features  \nA diagnosis of PD can be made with some confidence in patients with some confidence in \npatients who present with at least 2 of the three cardinal signs \u2013rest tremor, rigidity and \nbradykinesia"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b11c-7265-11ef-95ba-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 553, "chroma:document": "Internal Medicine \n \n 538Motor Features  \nResting tremor:   \n\u2022 It is present in 85 % of patients with true PD, and a diagnosis of PD is difficult when \ntremor is absent. \n\u2022 It starts unilaterally and has a gradual onset, affecting first distally involving the digits \nand wrist where it may present with \u201cpill \u2013rolling\u201d character.  \n\u2022 Tremor usually spreads prox imally, ipsilaterally and occasionally to the leg, before \ncrossing to other side after a year or two. \n\u2022 It may appear later in the lips, tongue, and jaw but spears the head. \nBradykinesia/akinesia:  \n\u2022 It is the most disabling feature which interferes with all aspects of daily living. Patients \nhave trouble in walking, rising from seated posit ion, turning over in bed, dressing etc.  \n\u2022 Fine motor movement is also impaired as  evidenced by decreas ed manual dexterity and \nhand writing ( micrographia ) \n\u2022 Soft speech (hypophonia) is the other of bradykinesia. \n\u2022 Masked face , decreased eye blinking \nRigidity: \n\u2022 Is felt as a uniform resistance to a passive movement about a joint throughout the full \nrange of motion. Brief regular interruption of resistance during passive movement may \ngive rise to\u201ccogwheels rigidity. \nGait disturbance:  \n\u2022 Patients have shuffling short steps,  and a tendency to turn en bolc ,  \n\u2022 Festinating gait,  a typical feature of Parkinsonism, result from a combination of flexed"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b11d-7265-11ef-8883-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 553, "chroma:document": "give rise to\u201ccogwheels rigidity. \nGait disturbance:  \n\u2022 Patients have shuffling short steps,  and a tendency to turn en bolc ,  \n\u2022 Festinating gait,  a typical feature of Parkinsonism, result from a combination of flexed \nposture and loss of postural reflux, which causes the patient to accelerate in an effort to catch up with the body\u2019s centre of gravity. \n\u2022 Freezing of gait :  is a feature of more advanced PD, occurs commonly at the onset of \nlocomotion (start hesitation), when attempting to change direction to turn around and upon entering narrow space such as a doorway. \n\u2022 Abnormalities of balance and posturing:  tends to increase as the disease progress \n\u2022 Stooped posture : flexion of the head, stooping and tilting of the upper trunk, and \ntendency to hold the arm in flexed posture while waking is common.  \n\u2022 In advanced diseases postural instability may lead to frequent falls and injuries."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b11e-7265-11ef-a8ce-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 554, "chroma:document": "Internal Medicine \n \n 539Non motor features: \n\u2022 Loss of sense of smell  (anosmia) \n\u2022 Sensory abnormalities  often manifest as distressing sensation of inner restlessness  \nand aching pain in the muscles of the extremities which often develops as anti \nParkinson\u2019s medications are wearing  off. \n\u2022 Sleep disorders  are common in PD, which may manifest as day time drowsiness \nfrequent napping. This may result from disrupted sleep from night time worsening of symptoms and difficulty of turning over in bed  \n\u2022 Autonomic dysfunction: may manifest with orthostatic hypotension, constipation \nurinary urgency and frequency , excessive sweating  \nNeuropsychiatric System  \n\u2022 Depression  affects approximately half of patents  \n\u2022 Anxiety  disorders  \n\u2022 Cognitive abnormalities : affect many patients and it may manifest with difficulty of \ndoing complex tasks, long term planning, and memorizing or retrieving new information. \nDementia is 6X more common in PD patients than their age matched controls. \n\u2022 Psychotic symptoms : affect 6 \u2013 40 % of patients with PD, visual hallucination are \ncommon symptoms, and depression and dement ia are risk factors for developing \npsychiatric symptoms. \nTreatment  \n\u2022 The goal of therapy in PD is to maintain function and quality of life and to avoid drug \ninduced complications  \n\u2022 Parkinson\u2019s disease is a progressive di sease, therefore management protocols vary \ndepending on the patient symptoms and the extent of functional impairment."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b11f-7265-11ef-b2e6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 554, "chroma:document": "induced complications  \n\u2022 Parkinson\u2019s disease is a progressive di sease, therefore management protocols vary \ndepending on the patient symptoms and the extent of functional impairment. \n1. Pharmacotherapy of motor symptoms: \n\u2022 Therapy to control motor symptoms should be initiated as soon as the patient\u2019s \nsymptoms begin to interfere with the quality of life.  \nEarly Parkinson\u2019s disease:  \na) Selegilline  is selective and irreversible mono aminoxide (MAO) inhibitor.  \n\u2022 It may slow the clinical progression of Parkinson\u2019s diseases and delay the need \nfor other medication. This drug has minimal effect on symptoms when used as monotherapy or as an adjuvant to Carbidopa/levodopa."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b120-7265-11ef-b435-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 555, "chroma:document": "Internal Medicine \n \n 540\u2022 Selegilline is used as an initial therapy or added to alleviate tremor of \nCarbidopa/levodopa associated wearing effect  \nDose:   5 mg PO with breakfast and lunch  \nb) Dopamine agonists :  have direct post synaptic effect on do dopamine receptors. \n\u2022 Dopamine agonist monotherpay is well tole rated and significantly reduced the risk of \nlater treatment \u2013related complications such as motor fluctuation and dyskinesia \nassociated with Carbidopa/levodopa treatment. \nNon Ergot alkaloids: \no Rupinirole:  Initial dose 0.25 mg Po TID  to maximum target dose as \nmonotherapy is 12-24 mg/day \no Parmipexole  ; Initial dose 0.125 mg PO TID maximum target dose as \nmonotherapy is 1.5-4.5 mg /day \nErgot alkaloids  \no Pergolide ; Initial dose 0.05 mg PO TID to maximum dose 1.5-6 mg /day \no Bromocriptine : Initial dose 1.25 mg Po BID or TID, to maximum target \ndose as monotherapy 7.5-15 mg/day \n\u2022 When dopamine agonists are used as monotherapy, higher doses are required to control \nsymptom. However the dose should be titrated gradually.  \n\u2022 Most patients require the addition of levodopa or another agent, within 1-3 yrs of \ninitiating dopamine agonists \n\u2022 Older patients and those with akinetic rigidity have a low risk of motor complications and \ndyskinesia, and may be satisfactorily treated with levodopa as an initial therapy. \nAdvanced Therapy \nc) Levodopa/Carbidopa Formulation (Sinemet\u00ae, Atamet\u00ae)"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b121-7265-11ef-9817-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 555, "chroma:document": "dyskinesia, and may be satisfactorily treated with levodopa as an initial therapy. \nAdvanced Therapy \nc) Levodopa/Carbidopa Formulation (Sinemet\u00ae, Atamet\u00ae) \n\u2022 Levodopa : is converted to dopamine by presynaptic neuron and therefore increase the \namount of neurotransmitter available to the post synaptic dopamine receptor. \n\u2022 Carbidopa:  blocks systemic/peripheral conver sion of levodopa to dopamine, thereby \ndecreasing the undesirable systemic effects of levodopa such as nausea and orthostatic hypotension. \nDose:  \n\u2022 Carbidopa/levodopa  IR 25/100 mg Initial dose: t/2 tab PO TID, to maximum target \ndose of 3-6 25/100 mg tabs /day (i.e.  1 -2 tabs PO TID)  \n\u2022 Carbidopa/levodopa  CR 50/200 mg tabs : dose 1tab BID or TID"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b122-7265-11ef-845c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 556, "chroma:document": "Internal Medicine \n \n 541The dosage of these drags should be escalated gradually \nWearing- off effects:  management of Parkinson\u2019s disease becomes increasingly difficult \nas the disease progresses. Late treatment related complications include.  \n\u2022 Dsykineisa:  refers to choreiform and dytonic movements that occur as a peak \ndose effect or at the beginning or end of the dose.  \n\u2022 Motor fluctuation:  (on and off phenomenon) these are wide random swings in \nthe patient\u2019s mobility or exaggerated ebb and flow of Parkinsonian signs, experienced by many patients between doses of anti-Parkinson medication. \nMore than 50 % of patients with PD treated over five years with levodopa will develop \nthese complications  \nd) Levodopa Augmentation :  \ni) Catechol O-methytransferase (COMT) inhibitors  \n\u2022 Estacapone and tolcapone offer augmentation of the effect of levodopa by \nblocking enzymatic degradation of levodopa and dopamine. \n\u2022 These drugs are used in conjunction with Carbidopa/levodopa  , they alleviate the \nwearing off symptoms  \nii) Anti-cholinergics  :are given as adjuncts to  dopaminomimetic therapy \n\u2022 They are useful in controlling resting tremor and dystonia  \n\u2022 Bezhexol is a drug which is available and commonly used \niii)  Amantadine  : has anti-cholinergic and dopaminomimetic properties  \n\u2022 It helps to reduce drug induced dyskinesia  \n\u2022 Can be effective early in the course of the diseases, or as an adjunct therapy later"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b123-7265-11ef-858a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 556, "chroma:document": "iii)  Amantadine  : has anti-cholinergic and dopaminomimetic properties  \n\u2022 It helps to reduce drug induced dyskinesia  \n\u2022 Can be effective early in the course of the diseases, or as an adjunct therapy later \nin the diseases course  to help \u201c smooth out \u201c motor function  \n \n2. Neuroprotective therapy  \nReducing the progression of PD through neuroprotective or restorative therapy is a major focus \nof research. Some of the neuroprotecitve treatment trails arte  \n\u2022 Non steroidal anti-inflammatory agents  \n\u2022 Estrogens replacement therapy   in post menopausal women  \n\u2022 Selegilline therap y delays the need for levodopa therapy by 9 -12 months in newly \ndiagnosed patients. Studies demonstrated that patients who remain on Selegilline for 7 yrs experienced slower motor decline."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b124-7265-11ef-9edf-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 557, "chroma:document": "Internal Medicine \n \n 5423. Therapy of non motor symptoms  \n\u2022 Insomnia due to nocturnal akinesia  : treated with night time supplemental dose of \nCarbidopa /levodopa \n\u2022 Depression :  Responds to anti depressants like Amitriptyline  \n\u2022 Psychotic patients : first remove anticholinergics and amantadine if the patient is taking. \nReduce the dose of dopaminomimetic if the patient is not responding. If still the patient \nhas psychotic symptoms and signs, start antip sychotics with minimal extrapyramidal side \neffects. \n\u2022 Dietary manipulation  : limiting  protein intake during the day  may improve levodopa\u2019s \nefficacy \n\u2022 Physical therapy  and an exercise program help to optimize mobility. \n Surgical therapy \n\u2022 Pallidotomy , and thelamothomy  ; may be a therapeutic option for refractory \nParkinson\u2019s diseases \n\u2022 Neurotransplantation : Transplantation of fetal substantia nigra tissue or cells. \n \nOther movement disorders  \nHyperkinetic disorders: these are disorders associated with increased movement.  \n1. Tremor  \na) Benign essential tremor is characterized by  posture related 5-9 Hz oscillation of hands \nand forearms that impairs performance of fine motor tasks. \n\u2022 This type of tremor is familial and may be accompanied by titubation (head \ntremor/bobbing  ) \n\u2022 Consumption of alcohol may temporarily suppress the tremor: stress , caffeine or \nsleep deprivation may exacerbation the condition  \n\u2022 \u03b2-adrenergic blocking agents are effective in controlling tremor."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b125-7265-11ef-a56a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 557, "chroma:document": "tremor/bobbing  ) \n\u2022 Consumption of alcohol may temporarily suppress the tremor: stress , caffeine or \nsleep deprivation may exacerbation the condition  \n\u2022 \u03b2-adrenergic blocking agents are effective in controlling tremor. \na) An Action (kinetic) tremor is evident when the patient moves his or her arms; there may \nbe a relatively mild accompanying postural and intention component.  \u2022 Clonazepam treatment can be useful. \n2. Myoclonus \nDefinition:  a brief, lightning-like contraction of a muscle or group of muscles."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b126-7265-11ef-82a2-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 558, "chroma:document": "Internal Medicine \n \n 543Etiology: \n\u2022 Metabolic derangements (e.g. uremia) \n\u2022 Degenerative diseases (e.g. Alzheimer\u2019s) \n\u2022 Slow virus infections (Creuzfeldt-Jakob disease, subactue sclerosing panencephalitis) \n\u2022 Severe closed head trauma \n\u2022 Hypoxic-ischemic brain injury \nSigns and symptoms:   \n\u2022 Myoclonus may occur normally as a pers on falls asleep (nocturnal myoclonus).  \n\u2022 Common hiccup (singultus) is a form of myoclonus affecting the diaphragmatic muscles. \n\u2022 Action myoclonus: is a myoclonus that increases with intended movements, It occurs  \ntypically after brain injury;  \n\u2022 Palatal myoclonus is a continuous, rhythmic contraction of posterior pharyngeal \nmuscles. \n \nTreatment:   \n\u2022 Correct underlying metabolic abnormalities.  \n\u2022 Clonazepam 0.5-2 mg PO. TID or valproate may be effective. \n \n3. Tics \n\u2022 Brief, rapid, simple or complex involuntary movements, which are stereotypical and \nrepetitive, but not rhythmic .  \n\u2022 Simple motor tics  (e.g. blinking) often begin as nervous mannerisms in childhood or \nlater, and disappear spontaneously.  \n\u2022 Complex motor tics often resemble fragments of normal behaviour such as touching, \nsmelling and jumping. \n\u2022 Simple phonic tics  include throat clearing, sniffing and grunting and complex phonic \ntics include the repetition of words and coprolalia. \n\u2022 Tourette\u2019s syndrome : a complex type of tics disorder characterized by multiple motor \nand one or more phonic tics that may occur many times a day, nearly every day for more than 1 year."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b127-7265-11ef-90dd-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 558, "chroma:document": "tics include the repetition of words and coprolalia. \n\u2022 Tourette\u2019s syndrome : a complex type of tics disorder characterized by multiple motor \nand one or more phonic tics that may occur many times a day, nearly every day for more than 1 year. \nTreatment  \n\u2022 Education of patients and their family \n\u2022 Drugs: Clonidine, Haloperidol"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b128-7265-11ef-9ab2-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 559, "chroma:document": "Internal Medicine \n \n 5443. Chorea and Athetosis \nDefinition:  \n\u2022 Chorea:  is brief, purposeless involuntary movements of the distal extremities and face, \nwhich may merge imperceptibly into purposeful or semi purposeful acts that mask the \ninvoluntary motion. \n\u2022 Athetosis:  is writhing movements, often with alternating postures of the proximal limbs \nthat blend continuously into a flowing stream of movement. Both often occur together (choreoathetosis). \nEtiology:  \n\u2022 Huntington\u2019s disease (see below) \n\u2022 Thyrotoxicosis \n\u2022 SLE \n\u2022 Drugs (antipsychotics) \n4. Chorea gravidarum   \n\u2022 It is choreiform movement occurring during pregnancy, often in patients with a history of \nrheumatic fever.  \n\u2022 Chorea usually begins during the first trimes ter and resolves spontaneously by or after \ndelivery. Rarely, a similar disorder occurs  in women taking oral contraceptives.  \n\u2022 Treatment consists of sedation with barbiturates, because other drugs may harm the \nfetus. \n5. Hemiballismus   \n\u2022 It is violent, continuous proximal limb flinging movements confined to one side of the \nbody, usually affecting the arm more than the leg.  \n\u2022 It is caused by a lesion, usually an infarct, in the region of the contralateral sub-thalamic \nnucleus of Luys.  \n\u2022 Differential diagnosis includes acute hemichorea, usually due to tumor or infarct of the \ncaudate nucleus, and focal seizures. Although disabling, hemiballismus is usually self-\nlimited, lasting 6 to 8 wk."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b129-7265-11ef-9bc0-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 559, "chroma:document": "nucleus of Luys.  \n\u2022 Differential diagnosis includes acute hemichorea, usually due to tumor or infarct of the \ncaudate nucleus, and focal seizures. Although disabling, hemiballismus is usually self-\nlimited, lasting 6 to 8 wk.  \n\u2022 Treatment with antipsychotics is often effective. \n6. Huntington\u2019s Disease \nDefinition:  also called Huntington\u2019s chorea, chronic progressive chorea or hereditary chorea. \nIt is an autosomal dominant disorder characterized by choreiform movements and progressive \nintellectual deterioration, usually beginning in middle age."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b12a-7265-11ef-8b67-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 560, "chroma:document": "Internal Medicine \n \n 545Etiology:  Genetically determined.  \n \nSigns and symptoms:  Develop insidiously.  \n\u2022 Dementia or psychiatric disturbances may precede the disease or develop during the \ncourse (anhedonia, asocial behaviour).  \n\u2022 Motor manifestations: flicking movements of the extremities, a lilting gait, motor \nimpersistence (inability to sustain a motor act, such as tongue protrusion), facial grimacing, ataxia, and dystonia. Disorder is always progressive; patients ultimately lose physical and mental abilities to care for themselves. \nTreatment:   \n\u2022 No treatment for the underlying cause.  \n\u2022 Antipsychotics may control behaviour problems (e.g. chlorpromazine 100-900 mg/d PO \nor haloperidol 10-90 mg/d PO). \n \n7. Dystonia \nDefinition:  Sustained abnormal posture and disruptions of ongoing movement, resulting from \nalterations in muscle tone; it is classified as generalized, focal or segmental: \nGeneralized dystonia (dystonia musculorum deformans)   \n\u2022 It is a rare progressive syndrome characterized by movements that result in sustained, \noften bizarre postures.  \n\u2022 Symptoms usually begin in childhood with inversion and plantar fixation of the foot while \nwalking.  \n\u2022 Generalized dystonia is often hereditary.  \n\u2022 In its most severe form, the disorder can be relentlessly progressive. Severely affected \npatients may become twisted into grotesque fixed postures.  \n\u2022 Mental function is usually preserved."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b12b-7265-11ef-bf5f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 560, "chroma:document": "\u2022 Generalized dystonia is often hereditary.  \n\u2022 In its most severe form, the disorder can be relentlessly progressive. Severely affected \npatients may become twisted into grotesque fixed postures.  \n\u2022 Mental function is usually preserved. \n \nFocal dystonia  affects a single body region. Rarely, dystonic movements spread to an adjacent \nregion (segmental dystonia),  and even more rarely, the process generalizes."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b12c-7265-11ef-a48b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 561, "chroma:document": "Internal Medicine \n \n 546Treatment:   \nTreatment is often unsatisfactory. \n\u2022 For generalized dystonia,  high-dose anticholinergics and/or the dopamine-depleting \ndrug reserpine 0.1-0.6 mg/d PO are most often used. Levodopa and carbamazepine \nbenefit a few patients.  \n\u2022 For focal or segmental dystonias  or for generalized dystonia that severely affects \nspecific body regions, local injection of purified botulinum a toxin is the treatment of choice. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, \nParkinson\u2019s diseases and other movement disorders, pages 2406-2417. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edtion Medicine, \nMovement disorders, pages 629-633."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b12d-7265-11ef-b3cd-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 562, "chroma:document": "Internal Medicine \n \n 5477. Peripheral neuropathy \n \nDefinition:  A general term indicating peripheral nerve disorder of any cause.  \n Classification of neuropathies  \nNeuropathies may be classified based on: \n1. The type of symptoms and signs  : Sensory , Motor , Autonomic , Or any combination  \n2. Distribution  \n\u2022 Mononeuropathy:  single nerve affected  \n\u2022 Multiple mononeuropathy( mononeuritis multiplex) : two or more nerves in separate \nareas affected \n\u2022 Polyneuropathy:  many nerves simultaneously affected \n3. Course : ( acute , subacute or chronic )  \n4. Nerve conduction test (NCT ):  Axonal or Myelin sheath  \n Etiology: \nTable VIII-7-1 Etiologies of neuropathies based the predominant symptoms or signs    \n Causes  \nNeuropathy  Acute  Subacute of Chronic  \n  Sensory neuropathy   \n \n   \nDiabetes mellitus         Leprosy \nUremia \nAlcohol abuse \nVitamin deficiency: Vit B1, B6, B12 \nHIV \nHereditary neuropathies  \nDrugs : Cisplatin , Phenytoin \nParaneoplatic syndrome       \n \nMotor neuropathy     Guillain-Barre syndrome Porphyria  Critical illness Poliomyelitis  Chronic inflammatory demyelinating polyneuropathy ( CIDP ) Lead intoxication"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b12e-7265-11ef-9822-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 563, "chroma:document": "Internal Medicine \n \n 548Sensorimotor \nneuropathy  \n \n    \nDiabetes mellitus  \nUremia \nVasculitis  \nHypothyroidism  \nParaprotinemias \nCIDP \nDrugs  \nToxins  \n \nAutonomic neuropathy   Guillain-Barre syndrome Porphyria  \n Diabetes mellitus  \nAmyloidosis Familial dysautonomia  \n Etilogoies based on distribution  \n1. Mononeuropathy:  \n\u2022 Trauma : most common cause of localized injury to single nerve \n\u2022 Focal neuropathy : violent muscular activity, forcible overextension of joint, repeated \nsmall traumas \n\u2022 Pressure or entrapment paralysis:  affects superficial nerves at bony prominences or \nat narrow canals; also from tumors, bony hyperostosis, casts, crutches, prolonged \ncramped postures. \n\u2022 Haemorrhage  into a nerve, exposure to cold or radiation \n\u2022 Tumor invasion \nMultiple mononeuropathy ( mononeuritis multiplex) : \n\u2022 Collagen vascular disorders  (polyarteritis nodosa, SLE, Sj\u00f6rgen\u2019s, RA) \n\u2022 Sarcoidosis \n\u2022 Metabolic diseases  (diabetes, amyloidosis) \n\u2022 Infectious diseases  (e.g. HIV, leprosy) \nPolyneuropathy:  \n\u2022 Acute febrile diseases: from toxin (e.g. diphtheria), autoimmune reaction (Guillain-Barr\u00e9 \nsyndrome) \n\u2022 Immunization \n\u2022 Toxic agents: barbital, phenytoin, heavy metals, carbon monoxide etc."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b12f-7265-11ef-be83-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 564, "chroma:document": "Internal Medicine \n \n 549\u2022 Nutritional deficiencies, metabolic disorders: B vitamin deficiency, hypothyroidism, \nporphyria, sarcoidosis, amyloidosis, uremia, diabetes mellitus. \n\u2022 Malignancy \n \nSigns and symptoms : \nSpecific mononeuropathies: \nAre characterized by pain, weakness and paresthesias in distribution of affected nerve; multiple mononeuropathy is asymmetric; nerves may be involved all at once or progressively. \nUlnar nerve palsy:   \n\u2022 Often caused by trauma to nerve in the ulnar groove of the elbow, or due to compression \nat cubital tunnel;  \n\u2022 Paresthesia and sensory deficit in 5\nth and medial half of the 4th fingers is a common \nfinding.  \n\u2022 Thumb adductor, 5th finger abductor and interossei muscles are weak and atrophied.  \n\u2022 Claw hand deformity may occur. \nCarpal tunnel syndrome:   \n\u2022 Is compression of median nerve in volar aspect of wrist, may be unilateral or bilateral.  \n\u2022 Paresthesia in radial-palmar aspect of hand and pain over the wrist and palm; pain may \nbe more severe at night.  \n\u2022 Sensory deficit in palmar aspect of first three fingers may follow; thumb abduction and \nopposition may become weak and muscles atrophied. \n\u2022 For all, conservative treatment should be tried first, with surgical exploration taking place \nif no success or worsening of symptoms occurs. \nRadial nerve palsy:  \n\u2022 Is due to compression of nerve against humerus;  \n\u2022 Weakness of wrist and finger extensors (wrist drop),  \n\u2022 Sensory loss over dorsal aspect of 1st finger."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b130-7265-11ef-b539-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 564, "chroma:document": "if no success or worsening of symptoms occurs. \nRadial nerve palsy:  \n\u2022 Is due to compression of nerve against humerus;  \n\u2022 Weakness of wrist and finger extensors (wrist drop),  \n\u2022 Sensory loss over dorsal aspect of 1st finger. \nPeroneal nerve palsy:   \n\u2022 It is usually caused by compression of nerve against fibular neck.  \n\u2022 Weakness of foot dorsiflexion and eversion (foot drop) occurs;  \n\u2022 Sensory deficit over anterolateral aspect of lower leg and dorsum of foot or web space \nbetween 1st and 2nd metatarsals can occur."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b131-7265-11ef-8523-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 565, "chroma:document": "Internal Medicine \n \n 550Specific polyneuropathies:   \n\u2022 Are relatively symmetric, often affecting sensory, motor, and vasomotor fibers \nsimultaneously.  \n\u2022 They may affect the axon cylinder or the myelin sheath and, in either form, may be acute \n(e.g. Guillain-Barr\u00e9 syndrome) or chronic (e.g., renal failure). \nDiabetic neuropathy   \nSensory polyneuropathy  \n\u2022 Develops slowly over months or years.  \n\u2022 Sensory abnormalities are common, usually starting in the lower extremities, more \nsevere distally than proximally. \n\u2022 Peripheral tingling, numbness, burning pain, or deficiencies in joint proprioception and \nvibratory sensation are often prominent.  \n\u2022 Pain is often worse at night and may be aggravated by touching the affected area or by \ntemperature changes.  \n\u2022 In severe cases, there are objective signs of sensory loss, typically with stocking-and-\nglove distribution.  \n\u2022 Achilles and other deep tendon reflexes are diminished or absent.  \n\u2022 Painless ulcers on the digits or Charcot's joints may develop when sensory loss is \nprofound. Sensory or proprioceptive deficits may lead to gait abnormalities.  \nMotor neuropathy : results in distal muscle weakness and atrophy.  \nAutonomic neuropathy : Autonomic nervous system may be additionally or selectively \ninvolved, leading to: \n\u2022 Nocturnal diarrhoea \n\u2022 Urinary and faecal incontinence and impotence (erectile dysfunction)  \n\u2022 Postural hypotension.  \n\u2022 Vasomotor symptoms vary. The skin may be paler and drier than normal, sometimes"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b132-7265-11ef-9c19-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 565, "chroma:document": "involved, leading to: \n\u2022 Nocturnal diarrhoea \n\u2022 Urinary and faecal incontinence and impotence (erectile dysfunction)  \n\u2022 Postural hypotension.  \n\u2022 Vasomotor symptoms vary. The skin may be paler and drier than normal, sometimes \nwith dusky discoloration; sweating may be excessive.  \n\u2022 Trophic changes (smooth and shiny skin, pitted or ridged nails, and osteoporosis) are \ncommon in severe, prolonged cases.  \nPolyneuropathy due to nutritional deficiencies:   \n\u2022 Is commonly seen among alcoholics and the malnourished patients.  \n\u2022 Wasting and symmetric weakness of the distal  extremities is usually insidious but can \nprogress rapidly, sometimes accompanied by sensory loss, paresthesia, and pain."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b133-7265-11ef-b5a4-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 566, "chroma:document": "Internal Medicine \n \n 551\u2022 Aching, cramping, coldness, burning, and numbness in the calves and feet may be \nworsened by touch.  \n\u2022 Multiple vitamins may be given when etiology is obscure, but they have no proven \nbenefit.  \nDiagnostic approach to neuropathies  \n\u2022 History and physical examination  \n\u2022 CBC:  e.g. megaloblasts in pernicious anaem ia may suggest Vit-B12 deficiency or \nstippled RBCs indicate lead poisoning. \n\u2022 LFT, AP,  \n\u2022 Renal function test: creatinine to assess for renal function test   \n\u2022 glucose  \n\u2022 Urine analysis  \n\u2022 Serum protein and electrophoresis  (e.g. multiple myeloma) \n\u2022 TFT if suspicion of thyroid dysfunction \n\u2022 Electromyography, nerve conduction velocity tests  \n\u2022 Muscle biopsy, sural nerve biopsy  as needed \nTreatment:   \n\u2022 Treatment of the underlying cause or system ic disorder; recovery is usually slow \n\u2022 Traumatic lesions with complete transection of nerve require surgery.  \n\u2022 Entrapment neuropathies may require corticosteroid injections or surgical \ndecompression. Physical therapy and splints  reduce the likelihood or severity of \ncontractures. \n\u2022 If impaired sensation renders the patient prone to injury, protective measures should be \ntaken. \n\u2022 Autonomic insufficiency is difficult to manage ; orthostatic hypotension can be treated \nwith agents that expand blood volume ( e.g. fludrocortisone ) and increase vascular tone \n( epinephrine and yohimbine ) \n\u2022 Tricyclic antidepressants, carbamazepine, phenytoin and capsaicin can help patients"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b134-7265-11ef-8f65-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 566, "chroma:document": "with agents that expand blood volume ( e.g. fludrocortisone ) and increase vascular tone \n( epinephrine and yohimbine ) \n\u2022 Tricyclic antidepressants, carbamazepine, phenytoin and capsaicin can help patients \nsuffering room pain.   \n \nGuillain-Barr\u00e9 syndrome \nDefinition:  also called Landry\u2019s ascending paralysis \n\u2022 It is an acute inflammatory demyelinating polyradiculoneuropathy."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b135-7265-11ef-9c07-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 567, "chroma:document": "Internal Medicine \n \n 552\u2022 It is predominantly motor neuropathy charac terized by muscular weakness and arflexia \n(loss of deep tendon reflexes) \n\u2022 It has an acute onset and it is usually rapidly progressive in nature.  \n\u2022 There may be also mild distal sensory loss. \n \nEtiology and pathogenesis:  \nThe etiology is not known but it is believed to be due to  autoimmune damage to the myelin \nsheath of peripheral nerves.  \nIn about 2/3 of cases, the disease begins 5 days to 3 wk following an antecedent event such as: \n\u2022 Non specific viral syndrome \n\u2022 May be associated with HIV infection  \n\u2022 Campylobacter jejuni infection \n\u2022 Hepatitis , infectious mononucleosis  \n\u2022 Mycoplasma pneumonae infection \n\u2022 Vaccination \n\u2022 Surgery \n\u2022 Lymphoma or  \n\u2022 SLE \nIt is the most common acquired demyelinating neuropathy. \nSigns and symptoms:   \n\u2022 Relatively symmetric weakness with pares thesia usually begins in the legs and \nprogresses to the arms. \n\u2022 Weakness typically evolves over hours to a few days, and for 90% of patients, weakness \nis maximal at 3 wk after which the patent reaches a plateau, and further progression is \nunlikely.   \n\u2022 Weakness is always more prominent than sensory abnormalities and legs are usually \nmore affected than the arms.  \n\u2022 Deep tendon reflexes are lost.  \n\u2022 Sphincters (both bladder and bowel) are usually spared.  \n\u2022 More than 50% of patients with severe disease have weakness of facial muscles \n(diaparesis)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b136-7265-11ef-bd1d-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 567, "chroma:document": "more affected than the arms.  \n\u2022 Deep tendon reflexes are lost.  \n\u2022 Sphincters (both bladder and bowel) are usually spared.  \n\u2022 More than 50% of patients with severe disease have weakness of facial muscles \n(diaparesis).  \n\u2022 The lower cranial nerves are also frequently involved, causing bulbar weakness and \ndifficulty of swallowing difficulty of handling secretions and maintaining the airways."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b137-7265-11ef-acf4-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 568, "chroma:document": "Internal Medicine \n \n 553\u2022 Most patients need hospitalization, and almost 30 % require ventilator assistance at \nsome time during their illness due to possible respiratory failure. \n\u2022 Autonomic dysfunction: wide fluctuation in BP, postural hypotension, and inappropriate \nADH secretion, cardiac arrhythmias and pupillary changes occur in severe cases. These \ncomplications need close monitoring as they may be fatal. \n\u2022 Pain is another common feature of GBS. The usual type of pain is deep aching pain in \nthe weakened muscles. Back pain involving the entire spine may also be felt. \n\u2022 Respiratory paralysis and autonomic dysfunction may be life-threatening. \n\u2022 About 5% of patients die. \nDiagnosis:   \n\u2022 Presumptive diagnosis is made based on history and physical examination.  \n\u2022 CSF analysis:  elevated protein but few (<50 mononuclear cells) or no cells not cells \n(albumino-cytologic dissociation). \n\u2022 Nerve conduction test (NCT):  slow nerve conduction velocity, evidence of conduction \nblock, and prolonged distal latencies, which suggest demyelination is the usual finding. \nDifferential diagnosis:   \n\u2022 Toxins (organic phosphate, botulism),  \n\u2022 Acute poliomyelitis. \nTreatment: \nGuillain-Barr\u00e9 syndrome is a medical emergency,  requiring constant monitoring and support of \nvital functions.  \nGeneral supportive measures: \n\u2022 The airway must be kept clear, and vital capacity should be measured frequently, so that \nrespiration can be assisted if necessary."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b138-7265-11ef-8936-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 568, "chroma:document": "vital functions.  \nGeneral supportive measures: \n\u2022 The airway must be kept clear, and vital capacity should be measured frequently, so that \nrespiration can be assisted if necessary.  \n\u2022 Fluid intake should be sufficient to maintain a urine volume of at least 1 to 1.5 L/d.  \n\u2022 Extremities should be protected from trauma and from the pressure of bed rest.  \n\u2022 Heat helps relieve pain, making early physical therapy possible.  \n\u2022 Immobilization, which may cause ankylosis, should be avoided. Passive full-range joint \nmovement should be started immediately and active exercises begun when acute \nsymptoms subside.  \n\u2022 Heparin 5000 U SC BID may help to avoid thromboembolism in bedridden patients."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b139-7265-11ef-a9cc-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 569, "chroma:document": "Internal Medicine \n \n 554Immunotherapy:  \n\u2022 Plasmapheresis:  can shorten the length of time that the patient is dependent on \nrespirator and unable to ambulate. Criteria to initiate plamapheresis include the inability \nof the patient to walk or rapid progression of the diseases. \n\u2022 Immunoglobulin treatment:  it is also effective and decreases morbidity and hastens \nrecovery. Plasmapheresis and immunoglobulin treatment may be given in combination  \n\u2022 Steroids are not effective in GBS , but in chronic relapsing Polyneuropathy, \ncorticosteroids improve weakness and may be needed for a long time. Immunosuppressive drugs (azathioprine) and plasmapheresis benefit some patients. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  Nerve \nand muscle dioders, pages 2500-2540. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nNeuropathy: pages 638-640."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b13a-7265-11ef-828e-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 570, "chroma:document": "Internal Medicine \n \n 5558. CNS infections  \n \nI. Pyogenic (bacterial) meningitis \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define Bacterial meningitis.   \n2. List the etiologies of Bacterial meningitis.   \n3. Describe the mode of transmission Bacterial meningitis.     \n4. Describe the epidemiology of Bacterial meningitis.   \n5. Identify the clinical features of Bacterial meningitis.   \n6. List the common complications of Bacterial meningitis.   \n7. Describe the most commonly used tests for the diagnosis of Bacterial meningitis.   \n8. Make an accurate diagnosis of Bacterial meningitis.   \n9. Understand the management of Bacterial meningitis.   \n10. Understand methods of prevention Bacterial meningitis.   \n \nDefinition:  is an inflammation of the arachnoid layer of the meninges and the fluid that \ncirculates, in the ventricles and sub-arachnoid space (CSF), caused by bacterial infection \n \nEtiologic agents:   the causes of bacterial meningitis vary with age: \n\u2022 Infants (< 1 year) : E. coli, group-B streptococcus, Listeria monocytogenous  are the \ncommonest causative agents. \n\u2022 Young children/toddlers (age 1- 6 years ) : Haemophilus influenza, Meningococcus  \naccount for > 50 % of cases \n\u2022 Adolescents and Adults:  Meningococcus, Pneumococcus  are the commonest \netiologies \n\u2022 In immunocompromised hosts and cancer patients : Listeria, Staphylococcus, \nPseudomonas aeruginosa  etc. \nRout of infection:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b13b-7265-11ef-ba1c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 570, "chroma:document": "account for > 50 % of cases \n\u2022 Adolescents and Adults:  Meningococcus, Pneumococcus  are the commonest \netiologies \n\u2022 In immunocompromised hosts and cancer patients : Listeria, Staphylococcus, \nPseudomonas aeruginosa  etc. \nRout of infection: \n\u2022 Droplet infection through the upper airways:  E.g. In Meningococcus meningitis,  with \npossibly epidemic spread \n\u2022 Haematogenous spread:  e.g. in Pneumococcus pneumonia \n\u2022 Contagious spread from adjacent sites :  e.g. in otitis media , sinusitis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b13c-7265-11ef-9248-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 571, "chroma:document": "Internal Medicine \n \n 556\u2022 Direct:  e.g. in open head injury \nEpidemiology: \n\u2022 Bacterial meningitis is the most common form of suppurative CNS infection. \n\u2022 In the West due to the availability of vaccines for N. meningitidis  and H. influenza,  S. \npneumonae  has become the leading cause of bacterial meningitis. \n\u2022 However, in African and most developing countries, N. meningitidis is still the leading \ncause of bacterial meningitis in adolescents and adults. An outbreak of meningitis \nepidemic has been documented to occur every 7- 10 years in the meningitis belt in African, which includes our country Ethiopia. \nClinical presentation; \n\u2022 Incubation period:   the incubation period for Meningococcal meningitis may range from \n1-10 days, but mostly the clinical manifestations occur within in  2-4 days \n\u2022 Meningitis may manifest as an acute fulminant illness that progress rapidly in few hours  \nor as a subacute infection that progressively worsens over several days. \n\u2022 The classic clinical triad of meningitis is fever, headache and nuchal rigidity (neck \nstiffness) , which are seen in > 90 % of patients . \n\u2022 Alteration in metal status can occur in > 75 % of patients and can vary from lethargy to \ncomma.  \n\u2022 Nausea and vomiting are common symptoms. \n\u2022 Avoiding light (photophobia) is seen in some patients. \n\u2022 Seizure occurs as part of the initial presentation of bacterial meningitis, or during the \ncourse of the illness in 20-40 % of patients"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b13d-7265-11ef-bd53-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 571, "chroma:document": "\u2022 Nausea and vomiting are common symptoms. \n\u2022 Avoiding light (photophobia) is seen in some patients. \n\u2022 Seizure occurs as part of the initial presentation of bacterial meningitis, or during the \ncourse of the illness in 20-40 % of patients  \n\u2022 In Meningococcal meningitis of sudden onset with severe course, patients develop \ndiffuse erythromatus maculopapular rash which rapidly becomes petechial, purpural or bullos lesions. The petichiae are found on the trunk, lower extremities, in the mucous \nmembrane and the conjunctiva, and occasionally on the palms and soles.   \n\u2022 In older and debilitated patients the symptoms of meningitis may be subtle. \nMeningeal signs  are clinical signs often sound in patients with meningitis  \n\u2022 Neck stiffness  when head is flexed passively \n\u2022 Kerning\u2019s sign : when one leg which is flexed at the hip and knee joints, is passively \nextended at the knee joint, the other leg flexes at the knee.  \n\u2022 Brudzinski\u2019s sign:   Upon passively flexing the head, one notices flexion of both legs at \nthe knees"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b13e-7265-11ef-887d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 572, "chroma:document": "Internal Medicine \n \n 557Note:  These classic meningeal signs may not be seen in infants, old persons and patients in \ncoma. \nComplications:   \n\u2022 Brain edema,  \n\u2022 Hydrocephalus \n\u2022 Brain abscess, \n\u2022 Septic vein thrombosis \n\u2022 Hearing impairment  \n\u2022 Fulminant meningococcal sepsis: Waterhouse-Friedrichsen syndrome is a clinical \ncondition resulting from hemorrhagic necrosis of the adrenal gland, with multi-organ \nfailure. Patients are hypotensive or in sho ck.  Disseminated intravascular coagulation \n(DIC) with skin and mucosal purpura and bleedings are commonly seen associated features.  \nDiagnostic approach  \n\u2022 History, physical examination,  \n\u2022 Search for possible source of infection(pneumonia , otitis media , sinusitis , head injury)  \n\u2022 CSF analysis  \n\u2022 Identify the organism from CSF and blood (culture, PCR etc.) \n\u2022 Serologic antibody test : latex agglutination test  \n \nLaboratory findings: \nGeneral signs of inflammation: leukocytosis, CRP and ESR \u2191 \nCSF analysis: \n\u2022 Gross appearance and opening pressure : CSF looks turbid and the opening pressure is \nincreased ( due to raised intra cranial pressure ) \n\u2022 Cell count and differential : polymorphonuclear leukocytosis \n\u2022 Biochemical tests : glucose is decreases and  protein in the CSF is elevated   \n\u2022 Gram stain Culture and sensitivity  \no Meningococcus are seen as gram negative intracellular diplococcic"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b13f-7265-11ef-9a23-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 573, "chroma:document": "Internal Medicine \n \n 558Table VIII-8-1, CSF analysis findings in different types of meningitis  . \n Bacterial meningitis  Viral meningitis  Tuberculous \nmeningitis  \nAppearance  Turbid  Clear  Cob-web appearance\n \nCell count/\u00b5l  Several thousand  Several hundreds  Several hundreds  \nCell type  Granulocytes(PMNLs)  Lymphocytes  Lympho-, monocytes  \nGlucose  \u2193 (< 30 mg/dl)  Normal  \u2193 (< 30 mg/dl)  \nProtein  \u2191 (> 120 mg/dl)  Normal  \u2191 (> 120 mg/dl)  \nLactate dehydrogenase  ( LDH)\n > 3.5 mmol/L  < 3.5 mmol/l  > 3.5 mmol/l  \nDifferential diagnosis:   \n\u2022 Virally caused meningoencephalitis (Coxsackie- , Echo-, Mumps-virus, HIV, measles, \nCMV, VZV, HSV) \n\u2022 Chronic meningitis : Tuberculous meningitis , Cryptococcal meningitis  \n\u2022 Subarachnoid hemorrhage  \nTreatment:   \nA. Antibiotic Therapy  \n1. Empirical antibiotic therapy :  \nBacterial meningitis is a medical emergency and antibiotics should be initiated immediately before the results of the CSF gram stain and culture are known. Antibiotics should be given intravenously, at higher doses  \n\u2022 In adults without underlying disease: Ceftria xone 2 gm IV BID plus Ampicilline 2 gm IV \nQID for 2 weeks. \n\u2022 Crystalline Penicillin 3-4 million IU, IV ever y 4 hours plus Choramphnicole 1gm IV QID  \nare alternative antibiotics for a resource limited setting . \n\u2022 Patients with ENT infection or head injury: Ceftriaxone 2 gm IV BID and Vancomycin 1 \ngm IV BID + treatment of the underlying cause."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b140-7265-11ef-a041-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 573, "chroma:document": "are alternative antibiotics for a resource limited setting . \n\u2022 Patients with ENT infection or head injury: Ceftriaxone 2 gm IV BID and Vancomycin 1 \ngm IV BID + treatment of the underlying cause. \n\u2022 If suspected hospital-acquired infection: Ceftriaxone 2 gm IV BID plus Vancomycin 1 gm \nIV BID plus Gentamycin (80 mg TID) \n\u2022 In immunodeficient patients: Ceftriaxone 2 gm IV BID plus Vancomycin 1 gm IV BID plus \nAmpicillin (2g IV QID)"}


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": 574, "chroma:document": "Internal Medicine \n \n 5592. Specific antibiotic therapy : is given when the specific etiologic agent is identified \nthrough gram stain or culture  \n\u2022 N. meningitidis  : Even though Ceftriaxone or Cefotaxim provide adequate empirical \ncoverage  , Penicillin G remains the drug of choice for N. Meningitides \nCrystalline Penicillin 3-4 million IU, IV every 4 hours for 7 -10 days may be adequate.  \n\u2022 Pneumococcal meningitis :  Antibiotic therapy in initiated with Cephalosporins plus \nVancomycine  \nCeftriaxone 2 gm IV BID and Vancomycin 1 gm IV BID for 2 weeks  \n\u2022 H. influenza  : Ceftriaxone 2 gm IV BID for 1- 14 days may be enough  \nChoramphnicole 1gm IV QID may be an alternative antibiotic, for patients who may not afford Ceftriaxone. \nB. Symptomatic and adjunctive Therapy \n\u2022 Steroids:  \no Dexamethason  when initiated before antibiotic therapy reduces the number of \nunfavourable outcomes, including death and neurologic complications. It is mainly advantageous in children, predominantly with meningitis due to H. \nInfluenza and S. Pneumoniae.  \nDose : Dexamethason10 mg IV 15-20 minutes before the first dose of antibiotics \nand 4 mg IV QID for 4 days   \n\u2022 Treat increased intracranial pressure : \no Elevation of the patients head to  30-45o  \no Intubation and hyperventilation  ( till PaCO 2 is lowered to 25-30 mmHg ) \no Mannitol IV infusion  \n\u2022 Regulate water and electrolyte balance,  \n\u2022 Thromboembolism prophylaxis \n\u2022 Patients with meningococcal meningitis should be isolated ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b142-7265-11ef-a0bc-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 574, "chroma:document": "o Intubation and hyperventilation  ( till PaCO 2 is lowered to 25-30 mmHg ) \no Mannitol IV infusion  \n\u2022 Regulate water and electrolyte balance,  \n\u2022 Thromboembolism prophylaxis \n\u2022 Patients with meningococcal meningitis should be isolated . \nChemoprophylaxis:  In case of N. Meningitides, all close contact to the patient should be given \nchemoprophylaxis with:- \n\u2022 Rifampicin 600 mg PO BID for 2 days in adults and 10mg/kg PO BID for children > 1 yr. \n\u2022 Ciprofloxacin 750 mg PO stat can be given as an alternative for adults."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b143-7265-11ef-9672-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 575, "chroma:document": "Internal Medicine \n \n 560II. Viral encephalitis  \n \nLearning Objective :  At the end of this unit the student will be able to  \n1. Define viral encephalitis.  \n2. List the etiologies of viral encephalitis.   3. Identify the clinical features of viral encephalitis.     \n4. Describe the most commonly used tests for the diagnosis of viral encephalitis.     \n5. Understand the management of viral encephalitis.     \n \nDefinition:  Inflammation of the brain parenchyma, with or without involvement of the meninges, \ncaused by virus. The spinal cord and/or nerve roots may also involved rarely.  \n Signs and symptoms:   \n\u2022 Acute febrile illness with evidence of meningeal involvement (meningeal signs) \n\u2022 Altered level of consciousness (ranging from lethargy to coma) \n\u2022 Abnormal mental state (hallucinations, agitation, personality change, behavioural \ndisorder, psychosis) \n\u2022 Evidence of either focal or diffuse neurologic signs or symptoms.  \n\u2022 Focal or generalized seizures occur in > 50 % of cases.  \n\u2022 Most common focal findings are aphasia, ataxia, hemiparesis (with hyperactive tendon \nreflexes), involuntary movements and cranial nerve deficits. \n \nOrganisms:  Viruses causing encephalitis \n \nCommon\n Less common  Rare \nArboviruses, enteroviruses, HSV-1, \nmumps\n CMV, EBV, HIV, \nmeasles, VZV  Adenoviruses, CTFV, influenza A, LCMV, \nparainfluenza, rabies, \nrubella"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b144-7265-11ef-8a01-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 576, "chroma:document": "Internal Medicine \n \n 561Laboratory findings: \n\u0083 CSF examination:  check for increased intracranial pressure first. Characteristic profile \nis undistinguishable from viral meningitis and consists of lympocytic pleocytosis, \nelevated protein, normal glucose level \n\u0083 CSF PCR, if available \n\u0083 CSF culture, usually negative (esp. in HSV-1 infections) \n\u0083 Serologic studies and antigen detection, if available \n\u0083 MRI, CT, and EEG: if available, done to exclude alternative diagnoses, and assist in \ndifferentiation between focal and diffuse encephalitic process (e.g. 90 % of patients with \nHSV-1 infection have abnormalities in the temporal lobe on MRI). \n\u0083 Brain biopsy:  reserved for patients with unclear diagnosis, lack of response to therapy \nand who have abnormalities on imaging techniques. \n \nTreatment: \nSupportive therapy (usually in ICU):  \n\u2022 Check vital signs, restrict fluid, and give antipyretics.  \n\u2022 Treat seizures and/or give prophylactic therapy (high risk for seizures!). \nMedication: \n\u2022 Acyclovir 10 mg/kg TID for at least 14 days (adult dose). \n\u2022 Gancyclovir (5 mg/kg BID) or Foscarnet (60 mg/kg TID) are especially \nrecommended for CMV infections. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Meningitis  \nand Encephalitis , pages 2471-2489. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nCNS infections, pages 644-645."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b145-7265-11ef-a44b-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 577, "chroma:document": "Internal Medicine \n \n 562CHAPTER NINE \nCONNECTIVE TISSUE DISORDERS AND DISEASES OF THE \nJOINTS  \n \nOverview:   \nThese are a group of medical disorders resulting from immunologic damage to the connective \ntissue of the body. \nThey overlap with each other, may affect many organ systems, and often respond to \nimmunosuppressives. Their pathologies vary. The following are some of connective tissue disorders:  \n1. Systemic lupus erythematosus (SLE),  \n2. Rheumatoid arthritis  \n3. Systemic sclerosis ( Scleroderma )  4. Polymyositis  5. Mixed connective tissue Disorder  \n6. Primary Sj\u00f6rgen\u2019s syndrome \n7. Beh\u00e7et\u2019s disease.  \n \n1. Systemic lupus erythematosus (SLE) \n \nDefinition:  SLE is a chronic immune disorder characterized by multisystem involvement and \nclinical exacerbations and remission.  \nCirculating immune complexes and autoantibodi es cause tissue damage and organ dysfunction. \nEpidemiology:  \n\u2022 The prevalence of SLE is approximately 15-5- cases per 100, 000 population \n\u2022 The prevalence in young women of child bearing age is 8- 10X that of men (F: M ratio is \n8:1 \u2013 10:1) \n\u2022 More common in black women than white women , more common in pregnancy \n\u2022 SLE has familial tendency and the concordance rate among identical twins is 50 % \nEtiology:  No single cause identified for SLE, it results from complex interaction of \nenvironmental, genetic factors and hormonal influences"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b146-7265-11ef-bb3f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 578, "chroma:document": "Internal Medicine \n \n 5631) Environmental factors: virus and drugs or toxins. It may be induced by drugs (isoniazid, \nhydralazine, chlorpromazine etc.) \n2) Genetic factors : there is genetic predisposition to SLE \n3) Autoimmunity : loss of tolerance to autoantigens  is central to the pathogenesis \n4) Hormonal influence : as the disease is more common in women of child bearing age , \nestrogen may play a role in the pathogenesis  \nClinical features : Signs and symptoms: \na) Systemic symptoms:  Fatigue , weight loss and fever are prominent systemic \ncomplaints  \nb) Skin:   \n\u2022 Photosensitive malar butterfly rash( facial erythema over the cheeks and nose ) ,  \n\u2022 The chronic potential scarring discoid lesions, alopecia,  \n\u2022 Livedo reticularis, Raynaud\u2019s phenomena, purpura, oral ulcers, urticaria, \nconjunctivitis, bullae.  \nc) Musculoskeletal:   \n\u2022 Joint/muscle pain, non-erosive polyarthritis \n\u2022 Myositis, proximal myopathy,   \n\u2022 Aseptic bone necrosis \nd) Renal:  SLE cause diffrent types glomerulonephritis which may manifest with  \nproteinuria, casts, edema, and later on to Cronic renal failure ( uremia)  \ne) CNS:  Focal or diffuse neurologic disordrs occur in approximatly 50 % of pateints  \n\u2022 Generalized manifestations  : Severe headache, reactive depression, \npsychosis, seizure , and cognitive disturbance \n\u2022 Focal:  focal seizure, hemiparesis, paraparesis, cranial nerve lesions, ataxia, \nchorea may also be seen. \n\u2022 Peripheral nerves : some pateints may have sensory or senorimotor"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b147-7265-11ef-b077-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 578, "chroma:document": "psychosis, seizure , and cognitive disturbance \n\u2022 Focal:  focal seizure, hemiparesis, paraparesis, cranial nerve lesions, ataxia, \nchorea may also be seen. \n\u2022 Peripheral nerves : some pateints may have sensory or senorimotor \nneuropathies   \nf) Lung:   \n\u2022 Pleurisy,  \n\u2022 Lupus pneumonitis,  \n\u2022 Fibrosing alveolitis \ng) CVS:   \n\u2022 Hypertension from renal involvment"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b148-7265-11ef-91f6-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 579, "chroma:document": "Internal Medicine \n \n 564\u2022 Pericarditis,  \n\u2022 Non infective endocarditis \n\u2022 Myocarditis \n\u2022 Coronaty vessle Vasculitis    \nh) Blood:  anemia, leukopenia, lymphopenia, thrombocytopenia, increased ESR \ni) Gastrointestinal tract:  intestinal vasculitis , Pancreatitis  \nj) Other:  fever, splenomegaly, lymphadenopathy, recurrent abortion \nDiagnosis: \n1) Hematology: Anemia, elevated ESR, decreased platelet count  \n2) Urinalysis:  proteinuria, hematuria   \n3) Renal function test : BUN and creatinin may be elevated  \n4) Serology  \n\u2022 ANA (antinuclear antibodies) nearly 99 % of patients with SLE have ANAs \n\u2022 Antibodies against double-strand DNA \n\u2022 Low complement components ( C3 and C4 ) \n \nTreatment:   \n1) If the SLE is believed to be due to be drug-induced, stop the drug.  \n2) Give sun-block creams or  sunscreens  \n3) NSAIDs  are used in full anti inflammatory dose for fever, joint complaints and serositis. \n4) Hydroxychloroquine if joint/skin symptoms are not controlled by NSAIDs, e.g. 400 mg/d PO for 6 mo, then 200 mg/d. \n5) Corticosteroids :  \n\u2022 High-dose predenisolone in life-threatening conditions, 1 mg/kg/d for 6 wks, then \ntaper. May be combined with other immunosuppressives. \n\u2022 Low-dose predenisolone is of value in chronic disease. \n6) Cytotoxic drugs: (E.g. azathioprine, cyclophsphamide) sometimes are employed to treat severe refractory features of SLE, particularly renal diseases. \nPrognosis  \n\u2022 Early diagnosis and treatment decreases morbidity and mortality"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b149-7265-11ef-aa99-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 579, "chroma:document": "6) Cytotoxic drugs: (E.g. azathioprine, cyclophsphamide) sometimes are employed to treat severe refractory features of SLE, particularly renal diseases. \nPrognosis  \n\u2022 Early diagnosis and treatment decreases morbidity and mortality  \n\u2022 Renal diseases and infectious complications are the major causes of death \n\u2022 CNS diseases can lead to severe disability"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b14a-7265-11ef-8acc-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 580, "chroma:document": "Internal Medicine \n \n 565References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  Asthma,     \npages 1508-1515 \n2) Myers R. Allen , National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Asthma, pages 75-78"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b14b-7265-11ef-a789-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 581, "chroma:document": "Internal Medicine \n \n 5662. Rheumatoid Arthritis ( RA ) \n \nLearning objectives:  at the end of this lesson the student will be able to: \n1) Define Rheumatoid arthritis  \n2) Describe the etiology and pathogenesis of Rheumatoid arthritis  3) Identify the clinical features of Rheumatoid arthritis \n4) Understand the diagnostic approach and investigations for Rheumatoid arthritis  \n5) Understand the management principles of Rheumatoid arthritis  6) Describe prognostic factors for Rheumatoid arthritis  \n \nDefinition:  it is a chronic multisystemic inflammatory disease of unknown cause, characterized \nby persistent inflammatory synovitis, usually involving peripheral joints in a symmetrical \ndistribution.  The potential of the synovial inflammation to cause cartilage damage and bone erosion and subsequent changes in joint integrity is the hall mark of the diseases.  \nEpidemiology \n\u2022 The prevalence of RA is approximately 0.8 in the population. \n\u2022 Women are more affected than men with F: M ratio of 3:1 \n\u2022 The prevalence increases with age and, and the sex difference diminishes in the older \nage group. \nEtiology:  \nTe cause of RA remains unknown. It is suggested that RA may be a manifestation of a \nresponse to an infectious agent in a genetically susceptible host.  \n1) Genetic factors  : genetic susceptibility to altered immune response may play a role \n\u2022 The concordance rate among monozygotic twins is 4X, and first degree relatives"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b14c-7265-11ef-ba85-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 581, "chroma:document": "response to an infectious agent in a genetically susceptible host.  \n1) Genetic factors  : genetic susceptibility to altered immune response may play a role \n\u2022 The concordance rate among monozygotic twins is 4X, and first degree relatives \nof patients with RA have a very high chance of developing RA \n\u2022 The presence of HLA-DR4 allogen is associated with high incidence of RA.  \n2) Infectious agent : may play a role in triggering an autoimmune reaction. Infectious \nagents such as rubella, Mycoplasma, CMV  and EBV virus may play a role in the pathogenesis  \nClinical Features  \nOnset: \n\u2022 Insidious onset : in about 2/3 of patients the RA begins insidiously with prodromal \nnonspecific symptoms such as fatigue, weight loss, anorexia, generalized body"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b14d-7265-11ef-ab5d-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 582, "chroma:document": "Internal Medicine \n \n 567weakness and vague musculoskeletal symptoms, for weeks or months before the \noccurrence of specific joint symptoms. \n\u2022 Acute onset:  in about 10 % of patients RA has an acute onset, with rapid development \nof polyarthritis, associated with constitutional symptoms, including fever, lymphadenopathy and splenomegaly. \n1) \nArticular ( joint )  manifestations:  result from persistent inflammatory  synovitis  \n\u2022 Pain , swelling and tenderness of involved joints , aggravated by movement \n\u2022 Generalized joint stiffness is often seen after a period of inactivity. Morning stiffness \nwhich lasts greater than 1 hr, which is a feature of inflammatory arthritis is a common complaint. \n\u2022 Bilateral, symmetrical small joint involvement is typical for RA \nCommonly affected joints are:- \n\u2022 Wrist joints, Metacarpo phalangal joints (MPJ) and proximal interphalangal PIP) \njoints  are often involved but distal interphal angal (DIP) joints are often spared. The \nelbow joint , and keen joints are also affected by RA.  \n\u2022 Wrist joint :  synovitis of wrist joint is very comm on is RA , and may lead to limitation of \nmovement , deformity and median nerve entrapment ( Carpal tunnel syndrome) \n\u2022 Elbow joint  involvement may lead to flexion contracture \n\u2022 Keen joint  is commonly involved with synov ial hypertrophy, chronic effusion and \nfrequent ligamentous laxity. Pain and swelling behind the knee may be caused by"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b14e-7265-11ef-8af1-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 582, "chroma:document": "\u2022 Elbow joint  involvement may lead to flexion contracture \n\u2022 Keen joint  is commonly involved with synov ial hypertrophy, chronic effusion and \nfrequent ligamentous laxity. Pain and swelling behind the knee may be caused by \nextension of inflamed synovium in to poplitial space ( Baker\u2019s cyst ) \n\u2022 Arthritis of the forefoot, ankles and subtalar joints  can produce sever pain with \nambulation and as well as a number of deformities. \n\u2022 Axial involvement is limited to cervical spines  ;  Atlantoaxial ligament involvement , \nin the cervical spine can lead to instability between  C1 and C2 vertebrae and potential neurologic complaints \nJoint deformities:  with persistent inflammation, a variety of characteristic joint changes \ndevelop due to damage or weakening of ligaments, tendons and joint capsule. These deformities include:- \n\u2022 Z- deformity:  radial deviation at the wrist with ulnar deviation of the digits \n\u2022 Swan neck deformity : hyperextension of the PIP joints, with compensatory flexion of \nDIP joints \n\u2022 Boutonier deformity : Flexion contracture of PIP joints and extension of DIP joints"}


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": 583, "chroma:document": "Internal Medicine \n \n 5682) Extraarticular features  : RA is a systemic diseases with a variety of extraarticular \nmanifestation  \n\u2022 Although these occur frequently, not all of them has clinical significance. However, \noccasionally they may be the major evidence of disease activity and source of morbidity. \n\u2022 More often, these manifestation occur in patients who have high titer of rheumatoid \nfactor and patients who have more severe and established diseases \na) Rheumatoid nodules:  are the most common features of extraarticular diseases and are \nfound in 20-25 % of patients.  \nThese firm subcutaneous masses typically are found in areas on periarticular structures and on areas exposed to of repetitive trauma (e.g. extensor surface of the forearm, the \nolecranion at the elbow, proximal ulna, Achilles tendon and the occipit).  \nIn some patients rheumatoid nodules may be found on the viscera (e.g. lungs, meningitis) \nb) Rheumatoid vasculitis : This can affect nearly any organ system and is seen in patients \nwith severe RA, and high titer of circulating Rheumatoid factor. \n\u2022 Peripheral nerves  : Distal sensory neuropathy or Mononuritis multiplex \n\u2022 Skin:  cutanous ulceration  , dermal necrosis  \n\u2022 Digital gangrene  \n\u2022 Visceral infarction  : Myocardial infarction , vasculitis involving the lungs , bowel \n, liver, spleen, pancreas ,kidneys etc \nc) Eye involvement : \n\u2022 Keratoconjuctivitis sicca is seen  in 10% -15 % of rheumatoid arthritis patients"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b150-7265-11ef-8b6f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 583, "chroma:document": "\u2022 Visceral infarction  : Myocardial infarction , vasculitis involving the lungs , bowel \n, liver, spleen, pancreas ,kidneys etc \nc) Eye involvement : \n\u2022 Keratoconjuctivitis sicca is seen  in 10% -15 % of rheumatoid arthritis patients \nwho have a secondary form of Sjogren syndrome  \n\u2022 Scleritis or episcleritis  occur less common \nd) Lungs  \n\u2022 Pleuritis and pleural effusion may be seen is some patients. The pleural fluid \ntypically has low glucose concentration. \n\u2022 Intestinal fibrosis \n\u2022 Rheumatoid nodules  may appear on the lung, single or multiple. \ne) Heart  \n\u2022 Asymptomatic Pericardits  is fund in 50% of patients on autopsy. It is often \nassociated pleural effusion.  \n\u2022 Myocarditis and Valvular dysfunctio n are rare findings"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b151-7265-11ef-9020-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 584, "chroma:document": "Internal Medicine \n \n 569f) Neurologic manifestations  : the CNS is not directly affected   \n\u2022 Peripheral nerves are affected  through Entrapment (carpal tunnel syndrome) or \nVasculitis related mononuritis multiplex \n\u2022 Atlantoaxial sublaxation  : may lead to compression of spinal cord  \ng) Hematologic features  \n\u2022 Anemia of chronic diseases \n\u2022 Thrombocytosis  \n\u2022 Felty\u2019s syndrome: chronic RA with splenomegaly and neutropenia, with an \noccasional thrombocytopenia and anemia. ,  \nConstitutional symptoms : like weight loss, fever anorexia and fatigue are common complaints \nand may be severe in patients with extraarticular manifestations  \nDiagnostic approach for RA  1) Proper history  taking  and Physical examination  play a crucial role in making the  \ndiagnosis of RA \n2) Laboratory findings  \na) Hematology: CBC may show normocytic, normoch romic anemia, leukocytosis and \nthorombocytosis. ESR is often raised indicating chronic inflammation \nb) Rheumatoid factor: It is autoantibodies against the Fc component of IgG. It is typically \npresent in 60 % of patients in the first year and 80% of patients with long standing diseases. Note that 30 -40 % of patients with rheumatoid arthritis may be sero-negative for Rheumatoid factor. \n3) Radiographic findings :  \n\u2022 Early  characteristic changes include soft tissue swelling and loss of bone in periarticular \nareas (periarticular osteopenia). \n\u2022 Late: sustained inflammation leads to loss of bones at joint margins (erosion) and joint"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b152-7265-11ef-b35f-0c9a3cb28fe6
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 584, "chroma:document": "\u2022 Early  characteristic changes include soft tissue swelling and loss of bone in periarticular \nareas (periarticular osteopenia). \n\u2022 Late: sustained inflammation leads to loss of bones at joint margins (erosion) and joint \nspace narrowing as a result of cartilage loss and joint deformity. \nRevised American revised Criteria for classification of RA \n1) Morning stiffness: lasting > 1 hr \n2) Arthritis of three or more joint areas:  \n3) Arthritis of hand joints: wrist, MCP and PIP \n4) Symmetrical athirst  \n5) Rheumatoid nodules: subcutaneous nodules over bony prominences \n6) Serum rheumatoid factor"}


created_at: 2024-09-14 06:50:03
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 585, "chroma:document": "Internal Medicine \n \n 5707) Radiologic changes : periarticular bony erosion and other fndigs  \n \nInterpretation: \n\u2022 Four of seven criteria are required to clas sify a patient as having Rheumatoid arthritis \n\u2022 Patients with two or more criteria, the clinical diagnosis of RA is not excluded. \nTherapy  \nGoals of therapy: \n1. Short term  : Controlling pain and reducing inflammation without causing undesired side \neffects \n2. Long term : Preservation of joint function and the ability to maintain life-style.  \nA) Pharmacotherapy  \n1) First line Treatment:  NSAIDs ( Non steroidal anti-inflammatory drugs ):  are the first line \ndrugs.  \n\u2022 They are used to control symptoms and signs of local inflammatory process.  \n\u2022 These agents are rapidly effective in alleviating pain and symptoms , but there effect on long term disease progression is minimal. \n\u2022 Aspirin, Ibuprofen, diclofenac, indometacin may be used  \n \nDose: Aspirine 900 mg PO TID, Ibuprofen 400 mg PO BID or Diclofenac 50 mg PO BID or \nTID \nSide effects : Dyspepsia, PUD, Renal dysfunction, bone marrow toxicity. \n2) Second line treatment:  low dose oral Corticosteroids have potent  anti-inflammatory effect  \n, but they have equally predictable unwanted side effects. \n\u2022 Systemic administration:  are given in sever progressive articular diseases and extra \narticular involvement  \nDose:  start 5-10 mg once daily in the morning. If patients improve, attempt should be \nmade to taper the dose."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b154-7265-11ef-95c6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 585, "chroma:document": "\u2022 Systemic administration:  are given in sever progressive articular diseases and extra \narticular involvement  \nDose:  start 5-10 mg once daily in the morning. If patients improve, attempt should be \nmade to taper the dose. \n\u2022 Local injection:  steroids may be injected occasional ly to joints which are severely \naffected  \n3) Third line: Disease modifying antirheumatic drugs- or slow acting antirheumatic drugs \n(DMARD) \n\u2022  This group of agents include Methotrexate , gold compounds , D-penicillamine , \nantimalarials and sulfasalazine"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b155-7265-11ef-82af-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 586, "chroma:document": "Internal Medicine \n \n 571\u2022 These are drugs which have no analgesic effect and generally require weeks to months \nbefore anti-inflammatory effects are evident. Hence, NSAIDs should continue during the \nadministration of DMARDs. \n\u2022 They have the capacity to alter the course of RA. \n\u2022 They are used in patients with rheumatoid arthritis, who are not responding to NSAIDs \n(with or without steroid).  \n\u2022 These drugs may be used singly mostly, but they may be prescribed in combinations in \npatients with bad prognosis or refractory diseases. \n\u2022 The disease progression is delayed with these drugs and acute phase reactants such as \nESR and C-reactive proteins frequently decline. \nMethotrexate  is the most frequently DMARD used, which is relatively rapidly acting  \nDose:  given in an intermittent low dose:  7.5-30 mg once weekly \nSide effects : GI upset, oral ulcer, liver function abnormalities and insidious liver fibrosis. \nAdministration of folic acid or folinic acid may diminish the frequency of some side effects,  \n4) Fourth line: Anti cytokine agents:  this are biological agents that bind and neutralize TNF. \nThese drugs are effective in controlling signs and symptoms of RA in patients who ailed to respond with DMARDs.  \n5) Fifth line : immunosuppressive therapy : \nThese include drugs such as Azathiopri ne, cyclsosporine, and cyclophosphamide."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b156-7265-11ef-a8be-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 586, "chroma:document": "These drugs are effective in controlling signs and symptoms of RA in patients who ailed to respond with DMARDs.  \n5) Fifth line : immunosuppressive therapy : \nThese include drugs such as Azathiopri ne, cyclsosporine, and cyclophosphamide. \nThey have the same therapeutic effect as DMARDs, but they are not more effective than DMARDs They are prescribed to patients who fail to respond to DMARDs \nB) Non pharmacologic therapy  \n1) Patient education:;  \n\u2022 Description of the illness : the chronicity of the diseases  \n\u2022 Rest and exercise  a. Patients should be advised to rest or splint acutely involved joints  b. Exersise is advised to srenghten muscle surrounding  involved joints , when the \narthritis is resolved  \n2) Physiotherapy and occupational therapy  to reduce disability"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b157-7265-11ef-82ec-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 587, "chroma:document": "Internal Medicine \n \n 572Assessment of response: \n\u2022 Resolution of symptoms : reduction or disappearance of joint pain, stiffness and \nswelling  \n\u2022 Functional status:  ability of the patient to perfo rm daily activities and living  \n\u2022 Laboratory:  anemia may be corrected and ESR  declines \n \nSurgical therapy:  \n\u2022 Early:  synovectomy may decrease the inflammato ry process in joints or tendon sheaths \nthat remain inflamed despite drug therapy \n\u2022 Late:  artheroplasy or total joint replacement may be appropriate to relive pain or help \nrestore function in structurally deformed joints.  \nPrognostic factors: poor prognostic factors include  \n\u2022 Many persistently inflamed joints  \n\u2022 Poor functional status  \n\u2022 Low educational status of the patient         \n\u2022 Rheumatoid factor positivity  \n\u2022 HLA-DR4 positivity \n\u2022 Extra-articular diseases \n\u2022 Persistently elevated acute phase reactants ( ESR, C-reactive protein ) \n\u2022 Radiologic evidence of erosion \n \n \n \nReferences:  \n3) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  Asthma,     \npages 1508-1515 \n4) Myers R. Allen , National Medical Series for independent Study ( NMS ) 3rd edition \nMedicine, Asthma, pages 75-78"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b158-7265-11ef-a1ed-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 588, "chroma:document": "Internal Medicine \n \n 5733. Other connective tissue diseases  \n3.1. Systemic sclerosis (Scleroderma)  \nIt is defined as a connective tissue characterized by widespread small vessel obliteration \ndisease and fibrois of the skin and multiple internal organs. \nClassification: \n\u2022 Limited cutaneous systemic sclerosis:  formerly called CREST syndrome ( calcinosis, \nRaynaud\u2019s, esophageal motility disorder, sclerodactyly and telangeictasia). \n\u2022 Diffuse cutaneous systemic sclerosis  with skin, renal and gut involvement; associated \nwith malignant hypertension, Raynaud\u2019s and myocardial disease. No effective treatment \nknown. \n\u2022 Localized (morphea=localized scleroderma):  localized skin sclerosis, progresses rarely. \nCharacteristic antibodies: topoisomerase, RNA polymerase, centromeres. \n \n3.2. Primary Sj\u00f6rgen\u2019s syndrome \n \nDefinition:  Association of a connective tissue disease (in 50 % rheumatoid arthritis) with \nkeratoconjunctivitis sicca (dry eyes) or xero stomia (dry mouth) due to lymphocyte and plasma \ncell infiltration into secretory glands. \n \nSigns and symptoms: \n\u2022 Dry eyes, mouth \n\u2022 Dyspareunia \n\u2022 Dry skin \n\u2022 Dysphagia \n\u2022 Otitis media \n\u2022 Pneumonia \n\u2022 Other: neuropathy, renal involvement, hepat osplenomegaly, drug reactions, lymphoma, \ndecreased well-being (headaches, GI symptoms, decreased concentration). \nDiagnosis: \n\u2022 History and physical examination \n\u2022 Schirmer\u2019s test to quantify tear production \n\u2022 Biopsy of salivary glands"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b159-7265-11ef-a5f9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 589, "chroma:document": "Internal Medicine \n \n 574Treatment:  artificial tears, occlusion of punctum which drains tears. Xerostomia may respond to \nfrequent cool drinks or artificial saliva spray. \n \n3.3. Idiopathic myopathies: pol ymyositis and dermatomyositis \n \nDefinition:  polymyositis is an idiopathic inflammatory muscle diseases characterized by \ninsidious, symmetrical, prominent proxim al muscle weakness resulting from muscle \ninflammation, elevated muscle enzymes and characteristic EMG finding.  \n\u2022 Signs and symptoms:   \n\u2022 Skin : The rash of dermatomyositis consists of erythematous paths which sometimes are \nscaling or atrophic and distributed over the face and, neck and upper chest and extensor surfaces. Rash on cheeks, eyelids and light-exposed areas may be seen. \n\u2022 Lung:  Chronic interstitial lung diseases \n\u2022 Joint:  mild symmetrical inflammatory arthritis   \n\u2022 Muscles : most patients have gradual but steady progression of muscle weakness. \nSome patients may have fulminant course that acute respiratory failure or myoglobinurin \nacute renal failure can ensue. \n\u2022 Pharyngeal muscle weakness  can lead to a problem in swallowing and aspiration and \nrespiratory muscle dysfunction. Patients may have also dysphonia, facial edema.  \n\u2022 Other features :  retinitis and myocardial involvement may occur. \n Diagnosis:   \n\u2022 Muscle enzyme (CK)is elevated  \n\u2022 EMG (electromyography) shoe characteristic features  \n\u2022 Muscle biopsy."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b15a-7265-11ef-90a6-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 589, "chroma:document": "\u2022 Other features :  retinitis and myocardial involvement may occur. \n Diagnosis:   \n\u2022 Muscle enzyme (CK)is elevated  \n\u2022 EMG (electromyography) shoe characteristic features  \n\u2022 Muscle biopsy. \n Treatment:  Rest, prednisolone (start with 1 mg/kg/d PO), other immunosuppressives. \n \n3.4. Mixed connective tissue disease \n\u2022 MCTD combines features of SLE, system ic sclerosis and polymyositis. Renal or CNS \ninvolvement is rare.  \n\u2022 Antibodies against ribonuclear protein are present."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b15b-7265-11ef-9571-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 590, "chroma:document": "Internal Medicine \n \n 575\u2022 Treat with immunosuppressives including steroids. \n \n3.5. Relapsing polychondritis \n\u2022 Relapsing polychondritis attacks pinna, nasal septum and larynx, the last causing stridor.  \n\u2022 It is associated with aortic valve disease, arthritis and vasculitis.  \n\u2022 Treat with steroids. \n \n3.6. Beh\u00e7et\u2019s disease \nDefinition:  A multiorgan disease associated with certain HLA-types and thromboses.  \nMore common in men M:f=2:1. \nSigns and symptoms:  \n\u2022 Joints:  arthritis \n\u2022 Eyes:  pain, decreased vision, floaters, iritis, retinal vein occlusion \n\u2022 Mouth, scrotum, labia : painful ulcers, heal by scarring \n\u2022 Gut: colitis \n\u2022 CNS:  meningoencephalitis, increased intracranial pressure, brainstem signs, dementia, \nmyelopathy, encephalopathy, cerebral vein thrombosis. \n Treatment:  Colchicine, steroids (topical and oral), other immunosuppressives. \n \nReferences:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition,  \nConnective tissue diseases , pages 1979-2015. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine,  \npages 570-581."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b15c-7265-11ef-9343-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 591, "chroma:document": "Internal Medicine \n \n 5764. Gout  \nLearning objectives:  at the end of this lesson the student will be able to: \n1) Define Gout   \n2) Describe the etiology and pathogenesis of Gout  \n3) Identify the clinical features of Gout \n4) Understand the diagnostic approach and investigations for Gout   5) Understand the management principles of different types Gout   \nDefinition:  A group of disorders of purine metabolism that are characterized by serum uric acid \nelevation (hyperuricemia), urate deposits in articular or extraarticular tissues. \nElevation of serum uric acid alone is not sufficient for the diagnosis of gout; only 10 % of patients with hyperuricemia develop gout. Some unknown factors predisposes some patients to \nurate deposition and articular inflammation, in the setting of sustained hyperuricemia \nEtiologic classification of Hyperuricemia \nAll gout syndromes are characterized by either epis odic or constant elevation of serum uric acid \nconcentration above 7 mg/dl. Patients with elevated serum uric acid are mainly due to  1) Overproduction: account for 10 % of patients. These patients synthesize greater than \nnormal amount of uric acid de novo. The urin ary excretion of urate is >1000mg/day (they \nhave normal urinary excretion of uric acid). The defect causing uric acid overproduction may be :- a) Primary : purine pathway enzyme defect  \nb) Secondary :  increased cell turn over or cellular destruction associated with alcohol use,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b15d-7265-11ef-9779-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 591, "chroma:document": "have normal urinary excretion of uric acid). The defect causing uric acid overproduction may be :- a) Primary : purine pathway enzyme defect  \nb) Secondary :  increased cell turn over or cellular destruction associated with alcohol use, \nhematologic malignancies , chronic Hemolysis , or cancer chemotherapy \n2) Under secretion of Uric acid : account for 90 % of patients. Decreased renal excretion of \nuric acid is the underlying reason for hyperuricemia (urinary excretion of uric acid is < 700mg/dl ) a) Drugs:  Diuretics , alcohol , Aspirin interfere with tubular handling of urate \nb) Renal diseases  ; chronic renal failure , lead nephropathy , inherited disorders  \nConditions associated with Gout  \n\u2022 Obesity:  serum uric acid level rises with body weight \n\u2022 Diabetes mellitus : more common in gout 576 patients \n\u2022 Hypertension:  is more common in gout patients  \n\u2022 Hyperlipidemia \n\u2022 Atherosclerosis"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b15e-7265-11ef-b716-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 592, "chroma:document": "Internal Medicine \n \n 577Clinical Stages of gout  \na) Asymptomatic hyperuricemia  : is characterized by an increased serum uric acid level \nin the absence of clinical evidences of deposition diseases (i.e. arthritis , tophi , \nnephropathy or uric acid stones) \n\u2022 These patients have an increased risk of having nephrolithiasis  or acute obstructive \nuropathy  \nb) Acute gouty arthritis :  is the second and primary manifestation of gout \u2013 is an \nextremely painful , acute onset arthritis \u2022 Most patients (80-90 %) are middle aged or elderly men who have had sustained \nasymptomatic hyperuricemia for 20-30 yrs before the first attack. \n\u2022 Premenopausal women are not affected by gouty arthritis, perhaps due to the effect \nof estrogen on uric acid clearance.  However gout may be seen in postmenopausal \nelderly women who have mostly associated hypertension. \n\u2022 Onset of acute gouty arthritis in teens or 20s is unusual, and when it occurs it is often \nassociated with primary or secondary causes of uric acid overproduction. \n\u2022 Several events may precipitate acute gouty arthritis including: dietary excess, \ntrauma, surgery, excessive alcohol ingesti on, ACTH or glucocorticoid withdrawal, \nhypouricemic therapy and serious medical illn esses like myocardial infarction and \nstroke . \n\u2022 Presentation:  an acute onset of severe, painful and tender joint swelling, affecting"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b15f-7265-11ef-b4d9-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 592, "chroma:document": "hypouricemic therapy and serious medical illn esses like myocardial infarction and \nstroke . \n\u2022 Presentation:  an acute onset of severe, painful and tender joint swelling, affecting \nthe first Metatarsoplalangal joint (called podagra). Other joints also may be affected including tarsal joints, ankle and knee. The fingers joints may be inflamed in elderly patients. \n\u2022 Many attacks occur suddenly at night with rapid evolution of joints with erythema, \nswelling, tenderness and warmth. Intense joint inflammation can extend in to the soft tissue and mimic cellulitis or phlebitis. Fever can occur in sever attacks. \n\u2022 Polyarticular involvement can occur in so me cases, and typically progression from \nmonoarticular to polyarticular involvement occurs by extension to adjacent joints. \n\u2022 Course:  acute attacks usually resolve spontaneously in few days 9 3-10 days), \nalthough some can extend over several weeks. The affected joint usually returns to normal between attacks and patients do not have residual symptoms until the next episode."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b160-7265-11ef-ada2-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 593, "chroma:document": "Internal Medicine \n \n 578c) Intercritical gout: The third stage of gout is an asymptomatic period after the initial \nattack. Recurrence of new attacks may occur during this stage. \n\u2022 Recurrence of monoarticular attacks: about 7% of patients never experience a new \nattack of acute gouty arthritis after the first attack. However 62% experience a \nrecurrence of gouty arthritis with in 1 yr. \n\u2022 Typically the patient is asymptomatic between attacks, but attacks become more \nfrequent and abate more gradually if urate deposition remains untreated. \n\u2022 Diseases progression:  Attacks tend to become polyarticular and more sever over \ntime. Some patients develop a chronic inflammatory arthritis without asymptomatic intervals leading to a condition which may resemble rheumatoid arthritis.   \nd) Chronic tophaceous gout:  develop in untreated patients and is the final stage of gout. \nThe tophus is a collection of urate crystal masses surrounded by inflammatory cells and fibrosis. \n\u2022 Typical locations for tophaceous deposits are   \no The pinna of the ear  \no The surfaces of chronically involved joints and subchondral bone as well as \nextensor surface of the forearm, olecranon , and the intrapatellar and Achilles \ntendons \ne) Renal complications : may arise at any stage of gout, but nephrolithiasis is the only"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b161-7265-11ef-8264-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 593, "chroma:document": "extensor surface of the forearm, olecranon , and the intrapatellar and Achilles \ntendons \ne) Renal complications : may arise at any stage of gout, but nephrolithiasis is the only \ncommon clinical presentation of renal involvement. Proteinuria and impaired ability to concentrate urine related to urate deposition in the renal interstitium have been described in gout patients. \nDiagnostic work up \nA) Acute gouty arthritis  ; \n\u2022 Laboratory findings  \n(1) Serum uric acid  value often is not helpful in the clinical diagnosis of acute gout. \nSerum uric acid concentration is normal in at least 10 % of patients at the time of \nan acute attack and an elevated serum uric acid is nonspecific for acute gout. It can be used to assess the effectiveness of hypouricemic therapy. \n(2) Synovial fluid analysis : The demonstration of urate crystals, especial \nintracellular crystals, in synovial fluid is diagnostic. Synovial fluid WBC of 10,000- \n60,000 /\u00b5l with predominant neutrophils are common in acute attacks."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b162-7265-11ef-be8b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 594, "chroma:document": "Internal Medicine \n \n 579B) Chronic tophaceous gout: \n\u2022 Physical appearance ; tophi are firm movable and superficial located. If they \nulcerate a chalky material extrudes. \n\u2022 Radiologic findings : tophaceous deposits appear as well defined large erosions \n(punched out erosions) of the sbchondral bone. These erosions are more common at \nthe first Metatarso phalangal joint (MTP), and at the base of the heads of phalanges: however any joint area can be affected. Typically gouty erosions have an overhanging edge of subchondral new bone formation  \n\u2022 Aspiration : tophi can be aspirated an crystals can be demonstrated  \n \nTherapy  \n1) Asymptomatic hyperuricemia : no need for treatment, other than correction of the \nunderlying causes. \n2) Acute gouty arthritis : drug treatment of acute  gouty arthritis is most effective  when \nstarted early after the symptoms begin \na) Colchicine  has anti-inflammatory effect, and if it  is given early, it is effective in \n85 % of patients. \nDose:   Colchicine 0.6 mg is given every hr until the relief of symptoms or \ngastrointestinal toxicity occurs. It may also be given intravenously during acute attack in patients who cannot take PO medication. \nb) NSAID:  are used in high but quickly tapered dose. Drugs like Aspirin that affect \nuric acid clearance should be avoided. Indomethacine:  25-50 mg PO TID,  \nIbuprofen: 800 mg Po TID \nDiclofenac: 25-50 mg PO TID   \nc) Corticosteroids :"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b163-7265-11ef-ac1f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 594, "chroma:document": "b) NSAID:  are used in high but quickly tapered dose. Drugs like Aspirin that affect \nuric acid clearance should be avoided. Indomethacine:  25-50 mg PO TID,  \nIbuprofen: 800 mg Po TID \nDiclofenac: 25-50 mg PO TID   \nc) Corticosteroids :  \nOral glucocorticoids:  Prednisolone, 30-50 mg/day as the initial dose and \ntapered over 5-7 days. Intraarticular injections  of steroids can be used to treat acute gout of single \njoint, particularly when the use of other agents is contraindicated. \nd) Drugs that alter serum uric acid concentration  (e.g. allopurinol, probenicide) \nshould be avoided during acute attack, because of lowering of serum uric acid"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b164-7265-11ef-9b42-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\Internal Medicine, Getachew Tizazu, Tadesse Anteneh.pdf", "page": 595, "chroma:document": "Internal Medicine \n \n 580level induces the release of crystals in to joint space and prolong the acute \nattack. \n3) Intercritical gout : Prophylactic treatment with small dose of colchicines (0.6 mg once or \n2X per day) or small doses of a NSAID can be used to prevent new attacks. \n4) Chronic tophaceous gout  : the aim of therapy is to control hyperuricemia( i.e. to reduce \nserum urate level to < 5 mg/dl ) \na) Uricosuric agents  (E.g. probenicide, Sulfinpyrazone). This drugs facilitate the renal \nexcretion of uric acid. It can be used in patients who excrete less than 700 mg of uric acid daily, who have normal renal function, and who have no history of urinary stones. Dose: Probenicide 200 mg PO Bid increased gradually as needed up to 2 gm \nb) Xanthine Oxide inhibitors:  include allopurinol; this drug competitively inhibits \nxanthine oxidase. This drug is preferred in patients with urate excretion greater than 1000 mg/day, creatinin clearance < 30 ml/min, tophaceous gout or history of nephrolithiasis. Dose: 300 mg single morning dose initially and may be increased up to 800 mg if \nneeded.  Dosage is reduced in the presence of renal failure to avoid toxicity. \n \n References:  \n1) Kasper L., Braunwald E., Harrison\u2019s principles of Internal medicine, 16th Edition, Gout,     \npages 2046-2050. \n2) Myers R. Allen, National Medical Series for independent Study (NMS) 3rd edition Medicine, \nGout, pages 727-532."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b165-7265-11ef-8fc4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 0, "chroma:document": "Abhishek Joshi  \nCorinne Ryan  \nSabe Sabesan  \nSuresh Varma  \nZulfiquer Otty  \n \n \nDEPARTMENT OF MEDICAL ONCOLOGY  \nTOWNSVILLE CANCER CENTRE  \nTOWNSVILLE UNIVERSITY HOSPITAL  \nTOWNSVILLE , AUSTRALIA  \n \n  \n \n \n \n \n \n \n \nMEDICAL ONCOLOGY HANDBOOK  \nFOR JUNIOR MEDICAL OFFICERS"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b166-7265-11ef-8b5f-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 1, "chroma:document": "Medical Oncology Handbook for Junior Medical Officers  \n5th Edition June 2020, \nTownsville, Australia.  \n \nTownsville Cancer Centre is a teaching partner of the James Cook University and \nresearch partner of the Australian Institute of Tropical Health &Medicine,  \nTownsville, Queensland, Australia ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b167-7265-11ef-b011-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 2, "chroma:document": "1 \n  \nINTRODUCTION:  \nWelcome to the Department o f Medical Oncology at the Townsville Cancer Centre. By \nthe end of the term, you should be able to identify and manage common side effects of \nchemotherapy and radiotherapy in the areas  of general practice, emergency departments \nand rural hospitals and general medical wards. Y ou will also have some understanding of \ntreatment principles and aims of cancer therapy for common malignancies. This \nhandbook is meant for the use of resident medical officers and basic physician trainees. \nIt may also be useful to advanced trainees in the ir first few months of training. We hope \nthat this experience will give you the skills to deal with cancer patients with positive and \nempathetic approach.  \nIf you are encountering emotional difficulties when dealing with poor prognosis, please \ntalk to one o f us earlier in the term to learn ways to deal with it effectively.  \n \nEnjoy the medical oncology rotation.  \n \n \nRegards,  \n \nCONSULTANT MEDICAL ONCOLOGISTS"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b168-7265-11ef-8fef-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 3, "chroma:document": "2 \n TABLE OF CONTENTS   \nORIENTATION TO MEDIC AL ONCOLOGY DEPARTME NT ............................  3 \nPRINCIPLES OF MANAGE MENT OF PATIENTS ON SYSTEMIC THERAPY  9 \nCommon side effects of systemic therapeutic agents  ................................ ................  13 \nChemotherapy related emesis  ................................ ................................ ....................  16 \nPRINCIPLES OF TARGET ED THERAPY  ................................ ..............................  19 \nPRINCIPLES OF CANCER  IMMUNOTHERAPY  ................................ .................  21 \nMedical Oncology Emergencies  ................................ ................................ ................  32 \nSUMMARY OF MANAGEMEN T OF COMMON CANCERS   ............................  33 \nBREAST CANCER  ................................ ................................ ................................ .... 33 \nCancers of the Gas tro-Intestinal Tract  ................................ ................................ ..... 37 \nGBM  ................................ ................................ ................................ ...........................  41 \nGERM CELL TUMOURS  ................................ ................................ .........................  41 \nHEAD AND NECK CANCER  ................................ ................................ ...................  43"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b169-7265-11ef-9efb-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 3, "chroma:document": "GERM CELL TUMOURS  ................................ ................................ .........................  41 \nHEAD AND NECK CANCER  ................................ ................................ ...................  43 \nLUNG CANCER  ................................ ................................ ................................ ........  43 \nMELANOMA  ................................ ................................ ................................ .............  45 \nGYNAECOLOGICAL CANCER  ................................ ................................ ...............  47 \nCANCERS OF GENITO URINAR Y SYSTEM  ................................ ........................  48"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b16a-7265-11ef-a2fe-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 4, "chroma:document": "3 \n ORIENTATION TO MEDICAL ONCOLOGY DEPARTMENT  \nJunior medical officers play an important role in the day-to-day care of patients in \nMedical Oncology Department . It is critical that you work in c lose collaboration with \nsenior medical, nursing and allied health staff , along with our administrative support \nofficers.  \nWe have outlined some useful practice poi nts will help you to settle into our department \nsmoothly.  \nEducational and training resources  \nElectronic medical records  \nTownsville Cancer Centre uses MOSAIQ as its EMR. Please become familiar with \nMOSAIQ by contacting the CNC for MOSAIQ on 32888 or through  our administrative \nsupport officers 44331671 prior to commencement. We assume that you are familiar with \nthe ieMR, the THHS -wide EMR.  \nChemotherapy protocol  \neviQ is a very useful website to learn chemotherapy protocols and side -effects. It also \ncontains in formati on about managing extravasation (www.eviq.org.au ). \nNB: RMOs and interns are not expected to write chemotherapy orders. When \nwriting oral chemotherapy, targeted agents and colony stimulating factors, please \nexercise caution and follow the advice of your registrars and consultants.  \nMedication prescribing  \nQuality of inpatient medication prescribing can be improved by adhering to the THHS \nguide for inpatient medication prescription . \nEnd of life care bedside tutorial and introduction to telehealth"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b16b-7265-11ef-87c2-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 4, "chroma:document": "Medication prescribing  \nQuality of inpatient medication prescribing can be improved by adhering to the THHS \nguide for inpatient medication prescription . \nEnd of life care bedside tutorial and introduction to telehealth  \nThese two topics are available on YouTube  (searchable using the titles)  and are useful \nresources for developing mental frameworks for approaching these topics.  \nBasic principles of oncology  \nClinical oncology for medical students is a useful resource for learning basic principles \nof oncology care.  \n \nhttp://wiki.cancer.org.au/oncologyformedicalstudents/Clinical_Oncology_for_Medical_\nStudents"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b16c-7265-11ef-a708-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 5, "chroma:document": "4 \n Documentation  \nSince funding for operations of medical departments are linked  to their clinical activities, \nit is important to use coding terminologies during documentation  of patient notes . \nIssues with central venous access devices  \nWe use central lines commonly in oncology and therefore, it is prudent to be aware of \nmanaging comp lications. As a rule , when it is difficult to draw blood from lines or inject \nfluids, it is important to use imaging (including chest -Xray and linogram) for checking \nthe position and viability before using the lines. Please seek advice when infection and \nthrombosis are  suspected /proven . We can rarely save lines using antibiotics   \nSelf-care  \nPlease maintain physical, emotional, mental and spiritual health. Take  regular  breaks  as \nmuch as possible and maintain effective work -life balance  (This doesn\u2019t mean work is \nbad and life is good; it is about having a balance that suits your needs) . Please seek help \nif you think you need help including emotional support and guidance.  \nDay unit  \n\u2022 Orientate with the Day -unit staff and introduce yourself t o senior nursing \nstaff and establish working relationships  with them .   \n\u2022 You are the first point of call for any issues in day unit and therefore, please \nmake sure that you are always available during rostered hours.  Day unit relies \non effective discharge o f patients to maintain flow. A delay due to one issue"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b16d-7265-11ef-ba33-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 5, "chroma:document": "\u2022 You are the first point of call for any issues in day unit and therefore, please \nmake sure that you are always available during rostered hours.  Day unit relies \non effective discharge o f patients to maintain flow. A delay due to one issue \ncould delay the whole day\u2019s operation and care of other patients.  \n\u2022 Infusion reactions are medical emergencies: You should always attend to a \npatient having a reaction, leaving everything else. If you are  not available, \nplease make sure another doctor can attend the patient immediately.  \nClinics  \n\u2022 Being \u201cOn Time\u201d is important! Clinics start on time so that patients can \nreceive their chemotherapy in day unit without delays.  \n\u2022 If a patient is seen by the consulta nt in clinic, please ask them to sign the blue \nform.  \nDealing with consultants and registrars  \nPlease don\u2019t hesitate to seek help from senior medical staff. All changes in management \nshould be discussed. Harass them even if they are busy!"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b16e-7265-11ef-b2ac-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 6, "chroma:document": "5 \n Dealing with nurses and other health professionals  \n\u2022 Advice from nursing staff is an important resource for patient care.  \n\u2022 When chemotherapy changes, delays or cancellation occur, it is prudent to \ninform the nursing and pharmacy staff. \nDealing with patients on chemothera py and chemotherapy orders  \n\u2022 When you see a patient for chemotherapy review, please prepare the care \nplans for the next cycle.  \n\u2022 Dose reduction: After consultation with senior medical staff, please document \ndose reductions and make changes on MOSAIQ scripts. I f there is  a dose \nincrease, it is possible only from the next cycle.  \n\u2022 All chemotherapy booking s are done through administration officers and day \nunit schedulers . \n\u2022 Initial c hemotherapy orders should be counter -signed by a consultant.  \n\u2022 Please be familiar with i mportant practice points for common medications as \ndescribed in this hand book.  \nAdmitted patients  \n\u2022 Make sure they are seen by consultants within 24 hours of admission and on a \nregular basis;  \n\u2022 Have an expected date of discharge and do the discharge planning , including \ntimely completion of high -quality discharge summaries; ideally on the day \nof discharge, using the national guide for discharge summaries . \n\u2022 If a patient undergoing chemotherapy is admitted with complications, inform \nthe day -unit and the treating consultant of any changes in treatment. It will \nalso be important to document this episode on MOSAIQ for continuity of"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b16f-7265-11ef-84ab-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 6, "chroma:document": "\u2022 If a patient undergoing chemotherapy is admitted with complications, inform \nthe day -unit and the treating consultant of any changes in treatment. It will \nalso be important to document this episode on MOSAIQ for continuity of \ncare and future planning includ ing dose changes and addition of GCSF.  \n\u2022 If any oncology patient is admitted in another department or another hospital \nwith complications, inform the treating consultant and document on \nMOSAIQ.  \n\u2022 In-patient consults from other departments need to be seen on th e same day, \ndiscussed with or seen by the consultant on call and documented on \nMOSAIQ.  \n\u2022 It is important to i nform the consultant on call of any patients admitted to \nmedical oncology.  \nRemember to use telehealth for appointments via our teleoncology coordinator. Telehealth is \nappropriate for  most rural &  selected metro patients"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b170-7265-11ef-b2e5-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 7, "chroma:document": "6 \n  \nCONSULTANT MEDICAL O NCOLOGISTS/ SENIOR M EDICAL \nOFFICERS  \nProfessor Sabe  Sabesan  \nBMBS (Flinders) , PhD, FRACP  \nSenior  Staff Specialist  \nClinical Dean, James Cook University &  \nTownville Hospital and Health Services  \n \nDr Suresh Varma  \nMBBS , MD, DM, FRACP  \nSenior Staff Specialist and senior lecturer  \n \nDr Abhishek Joshi  \nMBBS,  MD, DM, FRACP  \nSenior Staff Specialist and senior lecturer  \n \nDr Zulfiquer Otty  \nMBBS, MD, MRCP, FRACP  \nStaff specia list and senior lecturer  \n \nDr Corinne Ryan  \nMBBS (Hons), B  Appl  Sci, FRACP  \nStaff specialist and senior lecturer  \n \nDr Christine Mitchell  \nMBBS (Adelaide), FRACGP  \nSenior Medical Officer Medical Oncology"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b171-7265-11ef-a354-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 8, "chroma:document": "7 \n WEEKLY TIMETABLE  \nTime  Mon day Tues day Wed nesday  Thurs day Friday \n0745 -0830  GI MDT  \n(0800 -0900)   Breast MDT  \nGynae MDT \nevery three \nweeks  \n  Colorectal  \nMDT  \n(0800 -0900)  \n0900 -1200  Clinics  \nSV, ZO, \nCR Clinic  \nSV, ZO \nH&N MDT  Clinic  \nCM, SV,  AJ Clinic  \nCM, CR, AJ, \nZO Clinic  \nSV, ZO, AJ, \n1230 -1330  Grand rounds  \n(RDA)  Clinic  \nSS \n Radiology  \n(Weekly) /  \nUro MDT \n(fortnightly)  Clinical \nReasoning  \n(RDA)   \n1330 - Clinic \nSpill -over Clinic  \nAJ/SV  Skin MDT  \n(1300 -1400)   \n1400 -1500  Journal Club  \nReg training \nM&M   \n1500 -1600  \n1600 -1700   Neuro -MDT \n(monthly ) Lung MDT   \nEducational aims for this rotation:  \n\u2022 Management of complications of systemic therapy . \n\u2022 Familiarity with common systemic therapy  regimens . \n\u2022 Management of medical emergencies . \n\u2022 Management of quality of life issues . \n\u2022 Understanding of psychosocial issues related to cancer patients - discussing  \nprognosis, breaking bad news, family meetings etc. \n\u2022 Understanding of curative vs palliative intent therapy . \n\u2022 Familiarity  with the management of common maligna ncies including \nmultidisciplinary approach . \n 1430 -1530  \nLong case \npractice for \nBPT, RMO \nand Interns"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b172-7265-11ef-aaa1-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 9, "chroma:document": "8 \n Routine t asks:  \n\u2022 Managing inpatients \u2013 routine inpatient care, ward consultations, weekend \nroster (it is the responsibility of the registrars to do this roster).  \no Prior to consultant ward rounds, results should be available for imaging \nstudies, histology and blood tests.  \no (For interns, all the procedures except IV cannulation need to be initially \nsupervised by registrars or consultants).  \n\u2022 Review of day unit patients . \n\u2022 Review of clinic patients . \n\u2022 Phone consults  from GPs, other staff and the patients . \n\u2022 Participation in a long case practice session each Tuesdays (taking turn \namong BPT, RMO and Interns)  and other education sessions listed in the \ntime- table  \n\u2022 Participation in departmental Research and/or Quality Impro vement projects  \n \nDay unit and clinic patient review:  \n\u2022 To assess fitness for systemic therapy . \n\u2022 To assess symptoms and side effects of treatment.  \n\u2022 To address new concerns .  \n\u2022 To assess for treatment response -  \no tumour markers , \no scans - performed after 2 -3 cycles .    \n\u2022 To update systemic therapy  scripts ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b173-7265-11ef-82d3-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 10, "chroma:document": "9 \n PRINCIPLES OF MANAGE MENT OF PATIENTS ON \nSYSTEMIC THERAPY  \nAssessing fitness for systemic therapy  \nFitness for systemic therapy  depends on many  factors:  \n\u2022 performance status , \n\u2022 the type and severity of side effects from pr evious cycles or doses , \n\u2022 blood parameters , \n\u2022 co-morbidities  and \n\u2022 Patient choice  \nIf cure is the aim, it is usual to accept mild -to-moderate, non -life-threatening toxicities \nand continue treatment without delaying or reducing the dosage to minimise side effects. \nSometimes it is prudent to use supportive therapy such as  G-CSF to maintain  dose \nintensity. However, in patients with incurable metastatic disease where quality of life is \nparamount, dose delays or dose reductions are necessary.  \nPerformance status  \nThis is graded using the Eastern Cooperative Oncology Group (ECOG) scale.  \n \nGrade  ECOG performance status  \n0 Fully active, able to carry on all pre -disease performance without \nrestriction . \n1 Restricted in physically strenuous activity but ambulatory and able to \ncarry out work of a light or sedentary nature, e.g., light house work, \noffice work  \n2 Ambulatory and capable of all selfcare but unable to carry out any \nwork activities. Up and about more than 50% of waking hours  \n3 Capable of only limited selfcare, confined to bed or chair more than \n50% of waking hours  \n4 Completely disabled , cannot carry on any self -care, totally confined \nto bed or chair"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b174-7265-11ef-ac3b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 10, "chroma:document": "work activities. Up and about more than 50% of waking hours  \n3 Capable of only limited selfcare, confined to bed or chair more than \n50% of waking hours  \n4 Completely disabled , cannot carry on any self -care, totally confined \nto bed or chair  \n \nUsually, patients with ECOG grade > 2 are not fit for chemotherapy. The exception is \nchemotherapy -sensitive cancers such as lymphoma and small cell lung cancers. The \ndecision to offer chemotherapy must be individualised , depending upon factors such as  \nage of the patient, & comorbidities.  For example, a young patient with metastatic breast"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b175-7265-11ef-8e20-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 11, "chroma:document": "10 \n cancer with poor performance status could still be offered systemic treatments. Targeted \nagents and  endocrine therapy are usually tolerated better than chemotherapy.  \n \nToxicity from previous cycles of systemic therapy  \nClinicians must assess whether a side effect is affecting QOL, performance status  or is \nlife threatening:  \nFirst, determine the type and se verity of side effects.  \nFor example, in patients with early breast cancers undergoing taxane chemotherapy, mild \nperipheral neuropathy is acceptable. However, in patients undergoing fluorouracil -based \ntherapy, ongoing or severe diarrhoea necessitates a dose  delay and dose reduction of \nsubsequent cycles.  \nMid-cycle neutropenic fever usually requires dose reduction of the subsequent cycle \nunless the cancer is curable. If the cancer is curable or a substantial duration of remission \nis expected, prophylactic colo ny stimulating factors such as pegfilgrastim (neulasta) \nand/or antibiotics can reduce the risk of subsequent and opportunistic infection s. \n \nNext, determine the effects on important organs, such as:  \n\u2022 Fertility. Discuss semen cryopreservation with men. Option s for women \nshould also be discussed, particularly in young women of child -bearing \npotential and where curative intention treatment is planned.  Options include  \npreservation of egg, embryo and a piece of ovary is offered by some fertility \ngroups. Women who  wish to discuss this option should be referred to a"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b176-7265-11ef-9940-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 11, "chroma:document": "potential and where curative intention treatment is planned.  Options include  \npreservation of egg, embryo and a piece of ovary is offered by some fertility \ngroups. Women who  wish to discuss this option should be referred to a \nfertility specialist.  \n\u2022 Renal function, liver functions.  \n\u2022 Cardiac function. This may affect the dosage of anthracyclines (check \nejection fraction before treatment begins and after every 2 \u20133 cycles) and \ntrastuzumab (check ejection fraction before treatment begins and every 3 \nmonths during therapy).  \nToxicity is graded according to NCI common terminolo gy criteria for adverse events1. \n1. Blood parameters:  \na. Requires haematological and non-haematological parameters.  \n \n1 National cancer institute common toxicity criteria (CTCAE, version 4.03, June \n2010 ), National Institutes of Health, National Cancer Institute  . \nhttp://ctep.cancer.gov ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b177-7265-11ef-9116-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 12, "chroma:document": "11 \n For most regimens, a neutrophil count >1.5 x 109/L and platelet count > 100 x \n109/L are needed for safe administration of chemotherapy. For some regimens, \nlower levels may be acceptable.  \nSingle agent bleomycin and vincristine  are not myelotoxic and administration is \nnot affected by blood counts.  \nRenal function is important for cisplatin and carboplatin and liver function for \ndocetaxel , Magnesium levels especially  for cisplatin  and Calcium levels for \ndenosumab.  \nAction  - withhold treatment until recovery, then dose delay and/or dose reduction  \nafter discussion with senior staff . \nb. Pregnancy test: For women of child bearing potential, perform beta HCG \nbefore initiating treatment.  \n2. Non-haematological toxicity  \n(Also see the summa ry of common side effects for selected drugs on page 25). \na. Diarrhoea \u2013 mainly 5FU based, Irinotecan, Oxaliplatin, docetaxel . \nAction  - low threshold for withholding therapy if diarrhoea the day before , or \nmoderate diarrhoea for longer than expected duration , or nocturnal diarrhoea.  \nb. Mucositis/mouth care . \nc. Emesis . \n   Action  - (see anti -emetics) change class, change route, add another agent , or  \n   reduction of chemotherapy dose.  \nd. Skin Rash . \ne. Neuropathy - Cisplatin, Oxaliplatin, Taxanes and Vinca alkaloids . \n               Doses are delayed , reduced or omitted if neuropathy persists or interferes with  \n               function.  \nf. Autotoxicity - Cisplatin . \ng. Renal impairment - Cisplatin."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b178-7265-11ef-a6d8-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 12, "chroma:document": "Doses are delayed , reduced or omitted if neuropathy persists or interferes with  \n               function.  \nf. Autotoxicity - Cisplatin . \ng. Renal impairment - Cisplatin.  \nAction - prior to most agents, need to check creatinine especially if they are renally \ncleared  and Carboplatin  dose adjusted based on creatinine.  \nh. Pulmonary toxicity - bleomycin, methotrexate . \n3. Physical  examination -Routine exam and oral cavity, central lines and IV site \ninfections, lymph nodes and signs of recurrence and side effects."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b179-7265-11ef-b2ba-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 13, "chroma:document": "12 \n Symptom control  \nDiscussion or shared care with palliative care is helpful.  However, basic principles are as \nfollow s: \n(Also refer to the Guide for inp atient medication prescription)  \n1. Pain:    Always find out the cause of the pain before prescribing analgesics . \nTotal daily morphine requirement will guide the required daily slow release dose. \nWhen prescribing breakthrough, the dose is 1/6th of the daily do se. So, if you are \nincreasing the daily dose, break through need s to increase as well. If oral intake is \ndifficult \u2014patches or infusional morphine are options.  \n4. Dyspnoea:    Again, find out the cause, for cancer related dyspnoea \u2014nebulised \nmorphine and anxioly tics could be helpful.  \nWhen to stop cancer treatment  \nA decision to stop treatment prematurely depends on the aim of the treatment.  \nFor curable cancers, it is acceptable to continue treatment with dose modifications. \nHowever, life threatening or severe dose  limiting toxicities usually necessitate cessation \nof treatment (eg. moderate to severe peripheral neuropathy with taxanes and oxaliplatin, \nsevere enteritis from fluorouracil). Alternative regimens are sometimes available.  \nIf the cancer is incurable and th e toxicities severely interfere with the activities of daily \nliving, treatment may have to be stopped.  \nDeteriorating performance status and organ function usually require cessation of \ntreatment. Ongoing neutropenia or thrombocytopenia typically means the p atient is not"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b17a-7265-11ef-a878-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 13, "chroma:document": "living, treatment may have to be stopped.  \nDeteriorating performance status and organ function usually require cessation of \ntreatment. Ongoing neutropenia or thrombocytopenia typically means the p atient is not \ngoing to handle further chemotherapy.  \nIn case of patients with metastatic disease, palliative care team referral is done even when \nthey are on active treatment, to improve symptom management and supportive care."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b17b-7265-11ef-9892-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 14, "chroma:document": "13 \n Common side effects of systemic therapeutic agents  \n\u2022 Adriamycin/ Epirubicin    \nBe aware of cumulative dose, p erform cardiac function every 2-3cycles.  \n\u2022 Bleomycin -  \nLung functions every 3 weeks  (consider, discuss with consultant)  \n\u2022 Cisplatin  \nRenal function, Mg levels, peripheral neuropathy, hearing loss/tinnitus.  \n\u2022 Carboplatin  \nAdjust dose based on renal function; Dose  = AUC x (GFR+25).  \n\u2022 5-FU \nDiarrhoea -In severe cases, it can be life threatening.  \nBefore proceeding with treatment, please make sure no diarrhoea on the day an d \non the previous day of chemotherapy. When diarrhoea has been moderate to \nsevere, consider dose reduction or cessation.  \n5FU could also cause coronary artery spasm.  \nIn severe 5FU enteritis, admission for bowel rest +/ -TPN along with \naggressive anti diarrh oeal and antibiotics may be required.  \n\u2022 Gemcitabine  \nPneumonitis, peripheral edema.  \n\u2022 Irinotecan - Normal bilirubin is required.  \nDiarrhoea and flushing: acute symptoms related to parasympathetic system could \nsettle with atropine with chemotherapy.   \nFor chron ic symptoms, dose reduction may necessary.  \n\u2022 Taxol/ Paclitaxel  \nPeripheral neuropathy, flu like symptoms ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b17c-7265-11ef-8cdc-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 15, "chroma:document": "14 \n \u2022 Taxotere/Docetaxel  \nAdequate liver function, peripheral edema, neuropathy, rash.  \n\u2022 Oxaliplatin  \nCold induced paresthesia ( acceptable), but signs of peripher al Neuropathy may be \ndose limiting.  Laryngo spasm (cold induced) and bronchospasm are other acute \nside effects.  \n\u2022 Cyclophosphamide/ Ifosfamide  \nRenal function, hydration, confusion from encephalopathy.  \n\u2022 Capecitabine  \nMucositis, hand foot syndrome, rash, angina , diarrhoea.  \n\u2022 Trastuzumab  \nCardiac function every 3 months.  \n\u2022 Cetuximab/Panitumumab  \nAcneform rash.   \n\u2022 Methotrexate  \nFolinic acid rescue  for higher doses only . \n\u2022 Caelyx/ Liposomal doxorubicin  \nRash, hand foot syndrome, cardiac function.  \n\u2022 Avastin /Bevacizumab  \nHypertension and proteinuria.  \n\u2022 Denosumab  \nProlonged hypocalcaemia  (require calcium suppliments).  \n\u2022 Dabrafenib  (b-Raf inhibitor)  \nPyrexia, rash, s quamous cell carcinomas of skin.  \n\u2022 Mekinist \u2013 MEK inhibitor  \nUsually  combined with Dabrafenib to reduce in cidence of skin squamous cell \ncarcinoma  \n\u2022 Zolendronic acid  \nRenal function, hypocalcaemia, requires dose reduction for renal impairment.  \nNeed calcium supplements ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b17d-7265-11ef-bce3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 16, "chroma:document": "15 \n \u2022 Check point inh ibitors (Ipilumumab, nivolumab , Pembrolizumab ) \nAutoimmune complications such as  colitis, pneumonitis, hepatitis and \ninflammation  of pituitary gland leading to Addison\u2019s crisis require urgent medical \nattention.  \n\u2022 Alopecia  \nThis does not occur with every medication.  \nCommon with breast, ovarian, sarcoma, small cell, lung (Carbo/Taxol) canc er and \ntesticular regimens  \nCommon chemotherapy abbreviations  \nBreast Cancer   \nTAC  Docetaxel, Adriamycin, Cyclophosphamide  \nFEC  5Fluorouracil, Epirubicin, Cyclophosphamide  \nAC (inc DD) Adriamycin, Cyclophosphamide (DD for dose dense)  \nTC Docetaxel, Cyclophosphamide  \nColo -rectal Cancer   \nFOLFOX  Oxaliplatin, Continious infusion 5Fluorouracil and \nLeucovorin  \nXELOX  Oxaliplatin, Capecitabine  \nFOLFIRI  Irinotecan, Continious infusion 5 Fluorouracil and \nLeucovirin  \nXELIRI  Irinotecan, Capecitabine  \nGastric/Lower Oesophageal   \nECF  Epirubicin, Cisplatin, 5 Fluorouracil  \nEOX Epirubicin, Oxaliplatin , Capecitabine  \nFLOT  5FU, Leucovorin , Oxaliplatin, Docetaxel  \nHead and Neck Cancer   \nTPF  Docetaxel, Cisplatin, 5 Fluorouracil  \nTesticular Cancer   \nBEP  Bleomycin, Etoposide, Cisplatin  \nTIP Paclitaxel, Ifosfamide, Cisplatin"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b17e-7265-11ef-b930-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 17, "chroma:document": "16 \n Chemotherapy related emesis  \nCauses of nausea and vomiting in patients receiving chemotherapy:  \n\u2022 Chemotherapy related . \n\u2022 Other causes such as  gastro -oesophageal reflux disease or medications \nrelated.  \nPathways by which chemotherapeutic agents may produce an emetic \nresponse 2 \n \n \nChemotherapy -induced emesis  results from stimulation of a multistep reflex pathway that \nis controlled by the brain and triggered by afferent impulses to the vomiting centre  from \nthe chemoreceptor trigger zone, gastrointestinal tract (by way of vagal affere nt fibres ), \nand possibly, the cerebral cortex.   \n \n2 Hesketh, P. J. (2008). \"Chemotherapy -induced nausea and vomiting.\" New England \nJournal of Medicine  358(23): 2482 -2494."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b17f-7265-11ef-b55a-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 18, "chroma:document": "17 \n Emetogenic potential of chemotherapy agents  \n \nHigh  \n(>90%)  Moderate  \n(60-90%)  Moderate  \n(30-60%)  Low  \n(10-30%)  Minimal  \nCisplatin \n>50mg/m2  Carboplatin  Cyclophos \n<750mg/m2  Xeloda/5FU  Bleomycin  \nDacarbazine  \n Cisplatin  \n<50mg/m2  cabazitaxel  Docetaxel  Herceptin  \nCyclophos>  \n1.5g/m2  Doxorubicin  \n>60mg/m2  Doxorubicin  \n20-60mg/m2  Caelyx  Cetuximab  \n Epirubicin  \n>90mg/m2  Epirubicin \n<90mg/m2  Taxol  Vincristine  \n  Irinotecan,  \nOxaliplatin  Gemzar,  Vinorelbine  \n*Acute or early nausea and vomiting - within 24 hours of chemotherapy.  \n*Delayed/late \u2013 after 24 hours of chemotherapy. .  \nFor Cisplatin, emesis reaches its maximal intensity 48 -72 hours after chemotherapy and \ncan last up  to 6-7 days.  \n*Anticipatory nausea and vomiting - Nausea before chemotherapy  \nFive neurotransmitter receptor sites are of primary importance in the vomiting reflex: M1 \n\u2013 muscarinic, D2 \u2013 dopamine, H1 \u2013 histamine, 5 -hydroxytryptamine (HT) -3 \u2013 serotonin, \nNeurokinin 1 (NK1) receptor \u2013 substance P  \nAntiemetics  \n\u2022 Neurokinin 1 receptor antagonist - Aprepitant (emend), fosaprepitant  \n(Only for prophylaxis ). \n\u2022 5HT3 antagonists: ondansetron (zofran), granisetron & palonosetron  (aloxi) . \n\u2022 Dopamine antagonists: 1.  Phenothiazines - prochlorperazine, 2. Benzamides: \nMetoclopromide.  3.  Butyrophenons -haloperidol . \n\u2022 Glucocorticoids: active in early and delayed nausea.  \n\u2022 Anti-histamines: Promethazine ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b180-7265-11ef-ab8e-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 18, "chroma:document": "\u2022 Dopamine antagonists: 1.  Phenothiazines - prochlorperazine, 2. Benzamides: \nMetoclopromide.  3.  Butyrophenons -haloperidol . \n\u2022 Glucocorticoids: active in early and delayed nausea.  \n\u2022 Anti-histamines: Promethazine . \n\u2022 Benzodiazepins: Lorazepam (useful for anticipatory emesis) ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b181-7265-11ef-8ffb-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 19, "chroma:document": "18 \n High emetogenic drugs and anthracycline containing regime ns for breast \ncancer3  \n\u2022 NK1 inhibitors: eg Emend (Aprepitant)  \nDay 1: 165 mg pre chemotherapy with no subsequent doses . \nPlus \n\u2022 5HT3 antagonists: eg Aloxi (Palonosetron)  250 mcg IV on  Day 1 only or \nOndansetron 8mg twice daily for 2 -3 days starting the night of chemotherapy.  \nPlus \n\u2022 Dexamethasone  \n8-12 mg IV pre -chemo and 8mg oral mane for 2 -3 days.  \nNB- for patients who ex perience sudden decline in well -being when steroids are \nstopped, a weaning off regimen might be useful.  \n\u2022 Metoclopramide  \n10 mg Q6H PRN.  \nNB: 5HT antagonists can be constipating  - so warn patients about prevention of \nconstipation. No need to prescribe take -home 5HT antagonists after Palonosetron.  \nModerately emetogenic drugs or combination of drugs:  \n\u2022 5HT3 antagonist : eg Aloxi (Palonosetron)  250 mcg IV on day 1 Plus. \n\u2022 Dexamethasone  8 mg IV pre -chemo and 8mg oral mane 2 -3 days . \nNK1 inhibitors  can be added to the above regimen if the patients experience \nnausea & vomiting after moderately emetogenic chemotherapy.  \nMildly emetogenic drugs:  \nUsually premedication with metoclopramide 10 mg Q6H PRN would be adequate. \nIf nausea is not controlled, we may have to treat it like moderate drugs after \nexcluding other causes of nausea such as gastroesophageal  reflux and \nulcers/gastritis.  \nIf nausea persi sts, consider other causes.  \nAddition of lorazepam 1 mg Q6H PRN may be useful especially for anxious"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b182-7265-11ef-a0d3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 19, "chroma:document": "excluding other causes of nausea such as gastroesophageal  reflux and \nulcers/gastritis.  \nIf nausea persi sts, consider other causes.  \nAddition of lorazepam 1 mg Q6H PRN may be useful especially for anxious \npatients . \n \n3 Roila, F., J. Herrstedt, et al. (2010). \"Guideline update for MASCC and ESMO in \nthe prevention of chemotherapy - and radiotherapy -induced nausea and vomiting: \nresults of the Perugi a consensus conference.\" Annals of Oncology  21 Suppl 5 : v232 -\n243."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b183-7265-11ef-8bf7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 20, "chroma:document": "19 \n PRINCIPLES  OF TARGETED THERAPY   \n  \n \nIf we use analogy of pesticides : empiric chemotherapy would be \u201cRaid\u201d while targeted \ntherapy is \u201cR oach Hotel\u201d.   \nDr David Gandara  \nIt is like using a \u201csmart\u201d  bomb versus a \u201ccluster\u201d bomb.  \nDr Nevin Murray  \n \nThe figure below d epicts typical targets for anti -cancer drugs which could be pathways, \nprocesses and physiology which are uniquely dis rupted in cancer cells: receptors, genes, \nangiogenesis, tumour pH etc."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b184-7265-11ef-bddd-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 21, "chroma:document": "20 \n  \nTable 1 below depicts some targ ets and commonly available anti -cancer drugs in common \nsolid tumours . \n \nTable 1 Targets and examples of treatments for common solid tumours.  \nDisease  Target  Treatment  \nAdenocarcinoma of lung  EGFR exon 9, 11 mutation  Erlotinib, Gefitinib , Afatinib  \n T 790M  Osemertinib  \n ALK -EML4 fusion gene  Crizotinib /Alectinib  \nMelanoma  BRAF  Dabrafenib, Vemurafinib  \n MEK  Mekinist  \nColon Cancer  RAS  Cetuximab, Panitimumab  \nBreast Cancer  Her 2 neu amplification  Trastuzumab , Pertuzumab, \nLapatinib  \n ER and PR  Tamoxifen, Aromatase \nInhibitors  \nProstate Cancer  AR receptor  Enzalutamide, Abiraterone  \nGIST  CD 117 (c -kit) Imatinib Mesylate"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b185-7265-11ef-87e2-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 22, "chroma:document": "21 \n PRINCIPLES OF CANCER  IMMUNOTHERAPY  \n \n \n \n(CTLA4 outcompetes CD28 for CD80 and CD86, and the costimulatory signal ceases as \nthe target is eliminated, reducing the release of pro -effector cytokines such as IL -12 and \ncytotoxic enzymes such as perforin and granzyme B. Homeostasis is restored.)  \n \nIn a state of chronic antigen presentation, such as malignancy, the chronic presence of \nantigen or pro -inflammatory cytokines (IL -12, IFN  gamma, etc) can upregulate PD -1 \nexpression on the T cell; tumour  clones can also select for PD -L1 expre ssion. With PD -\n1-PD-L1 binding, even in the presence of the costimulatory molecule, \"peripheral \nexhaustion\" can occur.  \n \n \n \n \nThe anti -CTLA -4 antibody, ipilimumab  was the first immune checkpoint inhibitor to be \napproved based upon its ability to prolong survival in patients with metastatic mel anoma.  \nProgrammed cell death 1 (PD -1) is a trans -membrane protein expressed on T cells, B \ncells, and NK cells . It is an inhibitory molecule that binds to PD -ligand 1 (PD -L1; also \nknown as B7 -H1) and PD -L2 (B7 -H2). PD -L1 is expressed on the surface of multiple \ntissue types, including many tumour  cells, as well as hematopoietic cells; The IgG4 \nsubclass PD -1 inhibiti ng antibodies  like nivolumab  and pembrolizumab  prolonged \noverall survival in randomized trials in various cancers, including metastatic melanoma ,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b186-7265-11ef-b5d4-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 23, "chroma:document": "22 \n clear cell renal carcinoma, bladder cancer, head and neck cancer  and non-small cell lung \ncancer.  \nImmune Response Criteria : The patt erns of response to treatment with these \nimmunotherapy agents differ from those with molecularly -targeted agents or cytotoxic \nchemotherapy in several important respects . \nToxicities associated with checkpoint inhibitor immunotherapy  \nCheckpoint inhibition is  associated with a unique spectrum of side effects termed \nimmune -related adverse events (irAEs) or, occasionally, adv erse events of special \ninterest . IrAEs include dermatologic, gastrointestinal, hepatic, endocrine, and other less \ncommon inflammatory event s4. \nIn general, treatment of moderate or severe irAEs requires interruption of the checkpoint \ninhibitor and the use of corticosteroid immunosuppression. Treatment is based upon the \nseverity of the observed toxicity:  \n\u2022 For patients with grade 2 (moderate) imm une-mediated toxicities, treatment \nwith the checkpoint inhibitor should be withheld and should not be resumed \nuntil symptoms or toxicity is grade 1 or less. Corticosteroids should be started \nif symptoms do not resolve quickly . \n\u2022 For patients experiencing gra de 3 or 4 (severe or life -threatening) immune -\nmediated toxicities, treatment with the checkpoint inhibitor should be \npermanently discontinued. High doses of corticosteroids ( prednisone  1 to 2 \nmg/kg/day or equivalent) should be given. When symptoms subside to grade"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b187-7265-11ef-b5ab-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 23, "chroma:document": "mediated toxicities, treatment with the checkpoint inhibitor should be \npermanently discontinued. High doses of corticosteroids ( prednisone  1 to 2 \nmg/kg/day or equivalent) should be given. When symptoms subside to grade \n1 or less, steroids can be gradually tapered over at least one month.  \n\u2022 Patients who will benefit from corticosteroids generally do s o within days. If \nsymptoms do not clearly improve, particularly after approximately three days \nwith intravenous steroids, our approach is to administer infliximab  (5 mg/kg) \nrather than continue with a prolonged course of high -dose IV corticosteroids. \nIf symptoms persist after the first infliximab dose, a second dose of \ninfliximab (5 mg/kg) can be repeated two weeks after the initial dose.  \n \n \nDetailed management of various toxicities is covered by Cancer Institute of NSW\u2019s \neviQ:Cancer Treatments Online site . Free registration is required for login.\n \n4 Naidoo J et al.(2015) Toxicities of the anti -PD-1 and anti -PD-L1 immune checkpoint \nantibodies. Annals of Oncology 2015;26(12):2375"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b188-7265-11ef-9cd3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 24, "chroma:document": "23 \n Common side effects of oncology medications  \n Myelosuppression  Mucositis  Enteritis  Alopecia  Cardiac  Renal  Neuropathy  Liver  Rash  Lung \nAnthracyclines  ++ +  ++ +   +   \nCapecitabine  + ++ ++  angina     +HFS   \nCarboplatin  ++      +    \nCisplatin  +     ++ ++    \nCyclophosphamide  +   +  +  +   \n5FU  ++ ++  angina     +  \nGemcitabine  +  +       + \nIrinotecan  +  ++ +    +   \nOxaliplatin   + + +    ++    \nPaclitaxel  +   ++   ++    \nDocetaxel  +  + ++   ++ + +  \nPermetexed  +  +        \n \nExamples of Monoclonal antibodies and small molecules  \n Infusion reactions  cardiac  rash  thyroid  Proteinuria  diarrhea  Hypertension  \nTrastuzumab  + \n+ \n+ +      \nBevaczuzumab     +  ++ \nCetuximab/panitumab   ++     \nSunitinib   ++ + + + +"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b189-7265-11ef-a14b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 25, "chroma:document": "24 \n FEBRILE NEUTROPENIA  \nNeutropenic Fever 5 6 \nIt is a medical emergency. It is the responsibility of the MO to ensure prompt \nantibiotic administration.  \nWith diarrhoea and neutropenia, even if afebrile, it is advisable to use the \nsame protocol.  \nDefinitions  \n\u2022 A single oral temperature of 38.3  C.  \n\u2022 A temperature \u2265 38  C on two occasions over 1 hour . \n\u2022 ANC \u2264 500 or less \u2264 1000/\u00b5l with predicted rapid decline to less than 500/\u00b5l . \nSeptic Work -Up \n\u2022 Physical examination . \n\u2022 Blood cultures x 2 sets (venipuncture and indwelling venous catheter if \npresent), urine C&S, cultures from any  suspected sites, CXR ). \nTreatment of Neutropenic Fever 7 \nAntibiotics (early involvement of anti -microbial stewardship service is  \nbeneficial) . \n\u2022 Anti pseudomonal penicillins (Piperacillin/tazobactam & Ticarcillin) and \ncephalosporins (Cefepime) are used as single agents.  \nIn patients with hypersensitivity to pen icillins, seek expert advice.   \nModifications  \n\u2022 Aminoglycosides may be added  if patient is unstable to cover resistant \npseudomonal bacteremia.  \n \n5 Freifeld, A. G., E. J. Bow, et al. (2011). \"Clinical practice guideline for the use of \nantimicrobial agents in neutropenic  patients with cancer: 2010 Update by the \nInfectious Diseases Society of America.\" Clinical Infectious Diseases 52(4): 427 -\n431. \n6 National Comprehensive Cancer Network (NCCN) Clinical P ractice Guidelines in"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b18a-7265-11ef-ba89-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 25, "chroma:document": "antimicrobial agents in neutropenic  patients with cancer: 2010 Update by the \nInfectious Diseases Society of America.\" Clinical Infectious Diseases 52(4): 427 -\n431. \n6 National Comprehensive Cancer Network (NCCN) Clinical P ractice Guidelines in \nOncology, Prevention and treatmen t of cancer -related infections, Version 2.2011.  \nwww.nccn.org  . \n7 Therapeutic guidelines. online -tg-org-au.cknservices.dotsec.com"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b18b-7265-11ef-9069-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 26, "chroma:document": "25 \n \u2022 Add Vancomycin if clinically unstable, gram positive blood cultures before \nantibiotics, severe mucositis present, already on Quinolone prophylaxis, a \ncatheter associated cellulitis or tunnel  infection, past history, high prevalence \nor carrier of Methicillin -resistant staph aureus.  \n\u2022 Metronidazole for abdominal symptoms or suspected C. difficile infection.  \n\u2022 Persistent neutropenic fever on D5 \u2013 add antifungal therapy (Amphotericin B \n0.5mg/kg /day o r Fluconazole 400mg/day) . \nDiscuss with consultants first.  \nDuration of Antibiotics (variable)  \n\u2022 Low risk patient (clinically well, stable signs, no mucositis, ANC >100/\u00b5L, \nrising ANC, afebrile within 2 -3 days of starting antibiotics, negative cultures) \nconsid er early discharge on oral Ciprofloxacin and Augmentin for 5 days or \ncease antibiotics altogether when ANC >500/\u00b5L . \n\u2022 High risk patients,  who become afebrile within 3 days, should continue \nparenteral antibiotics, targeted to the specific pathogen, until reso lution of \nneutropenia .  \n\u2022 Specific pathogens need to be treated according to therapeutic guidelines \nwhile continuing broad coverage."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b18c-7265-11ef-8805-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 27, "chroma:document": "26 \n Patients with any of the following characteristics are considered to be  at \nhigh risk for serious complications during episodes of neutropenic fever  \n\u2022 Neutropenia (absolute neutrophil count <500 cells/microL) anticipated to last \n>7 days*   \nPresence of any comorbid medical problems, including, but not limited to:  \n\u2022 Hemodynamic instability  \n\u2022 Oral or gastrointestinal mucositis that interferes with swallowing or causes \nsevere diarrhoea   \n\u2022 Gastrointestinal symptoms, including abdominal pain, nausea and vomiting, \nor diarrhoea   \n\u2022 Neurologic or mental status changes of new onset   \n\u2022 Intravascular catheter infection, especially catheter tunnel infection  \n\u2022 New pulmonary infiltrate or hypoxemia  \n\u2022 Underlying chronic lung disease  \n\u2022 Complex infection at the time of presentation : \nInpatient status at the time of development of fever  \nUncontroll ed or progressive cancer  \nEvidence of hepatic insufficiency (defined as aminotransferase levels >5 times \nnormal values) or renal insufficiency (defined as a creatinine clearance of <30 \nmL/min)  \nMultinational Association for Supportive Care in Cancer (MASCC) risk index \nscore <21"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b18d-7265-11ef-acab-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 28, "chroma:document": "27 \n Guide to Febrile Neutropenia  \n \n \n \nColony stimulating factors (GCSF)  are generally not recommended in management of \nfebrile neutropaenia, with some exceptions."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b18e-7265-11ef-b027-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 29, "chroma:document": "28 \n Catheter -related infections  \nCatheter removal is recommended in addition to antibiotic therapy for at least 14 days. \nBut, if the infection is caused by coagulase -negative staphylococci and is important to \nsave the line, catheter could be retained using systemic antibiotics.  \nExtravasation of Chemotherapy  Drugs  8 \nIf it d oes occur, proper documentation should include the time, site of line insertion, \nneedle size, estimated amount of extravasated medication, technique used to manage the \nextravasation, appearance of site, photograph, patient \u2019s comments, and notification of \nphysician.  \nManagement  \n \nStop infusion.  Before removing cannula attempt to aspirate some of extravasated fluid.  \nIf antidote exists give it both IV through cannula and by SC infiltration see Table 2 below.  \n \nIntermittent local cooling is recommended, except for vinca alkaloids (warming packs).  \nRest and elevate the affected site for 48 hours.  Telephone contact daily and assess need \nfor plastic surgery.  \n \nDay unit nurses have protocols for managing extravasatio n and their input will be \nimportant for developing management plans.  \n \n8 Albanell, Joan, and Jose Baselga. \"Systemic therapy emergencies.\" Seminars in \noncology . Vol.  27. No. 3. 2000."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4b18f-7265-11ef-bf2a-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 30, "chroma:document": "29 \n Table 2 Example of Antidotes for Vesicant and Irritant Drugs  \n \nChemotherapy \nagent  Pharmacologic  \nantidote  Nonpharmacologic  \nAntidote  Method of  \nAdministration  \n\u2022 Mechlorethamine  \n(nitrogen \nmustard)  \n\u2022 Cisplatin  \n(large \nextravasation)  Sodium  \nthiosulfate  None  Prepare 1/6 molar solution: if \n10%Na thiosulfate solution,  \nmix 4 mL with 6 mL sterile \nwater for injection.  \nThrough existing IV line, \ninject 2 mL for every 1 mg \nextravasated.  Inject SC if \nneedle is removed.  \n\u2022 Vincristine  \n\u2022 Vinblastine  \n\u2022 Vindesine  \n\u2022 Etoposide  \n\u2022 Vinorelbine  Hyaluronidase  Warm packs. 15 -20 \nminutes at least \nfour times/day for \nthe first 24 -48 \nhours and elevate  Prepare hyaluronidase, 150 \nunits/mL with 1 -3 mL saline.  \nInject through existing IV \nline, 1 mL for each 1 mL \ninfiltrated.  Inject SC if needle \nis removed.  \n\u2022 Doxorubicin  \n(Adriamycin)  \n\u2022 Daunorubicin  \n\u2022 Idarubicin  \n\u2022 Mitomycin C  DMSO  Ice packs  Apply cold pad with \ncirculating ice water pack or \ncryogel pack for 15 -20 \nminutes at least four times/day \nfor first 24 -48 hours.  Some \nbenefit of 99% dimethyl \nsulfoxide (DMSO) 1 -2 mL \napplied to site every 6 hours.  \n\u2022 Paclitaxel  \n\u2022 Docetaxel  Hyaluronidase  Ice pac ks As for Vinca alkaloids.  \n\u2022 Mechlorethamine  \n(nitrogen \nmustard)  \n\u2022 Cisplatin  \n(large \nextravasation)  Sodium  \nthiosulfate  None  Prepare 1/6 molar solution: if \n10%Na thiosulfate solution, \nmix 4 mL with 6 mL sterile \nwater for injection.  \nThrough existing IV line,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ecdb-7265-11ef-ab9c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 30, "chroma:document": "\u2022 Mechlorethamine  \n(nitrogen \nmustard)  \n\u2022 Cisplatin  \n(large \nextravasation)  Sodium  \nthiosulfate  None  Prepare 1/6 molar solution: if \n10%Na thiosulfate solution, \nmix 4 mL with 6 mL sterile \nwater for injection.  \nThrough existing IV line, \ninject 2 mL for every 1 mg \nextravasated.  Inject SC if \nneedle is removed.  \n\u2022 Paclitaxel  \n\u2022 Docetaxel  Hyaluronidase  Ice packs  As for Vinca alkaloids."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ecdc-7265-11ef-8ef5-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 31, "chroma:document": "30 \n PREMEDICATIONS TO PR EVENT ALLERGIC REACT IONS  \nPaclitaxel Premedications  \n\u2022 Recommended schedule:  \nDexamethasone 20 mg oral, 12 hours and 6 hours before Paclitaxel (in practice \nthe night before and the morning of treatment).  \nPromethazine 25 mg IV 30 -60 minutes before therapy.  \nRanitidine 50 mg IV 30 -60 minutes before therapy.  \nAdditional Dexamethasone IV as antiemetic depending if Paclitaxel given alone \n(4mg IV) or in combination with other drugs.  \n \n\u2022 Modified regimen (in cases where the patient forgets to take premedication, \nor 2nd and subsequent cycles where no hypersensitivity reaction occurred \nwith 1st tr eatment an d steroids are not appropriate) . 9 10 11 \no Dexamethasone IV 20 mg 30 minutes before Paclitaxel.  \no Promethazine IV 25 mg IV 30 -60 minutes before therapy.  \no Ranitidine 50 mg IV 30 -60 minutes before therapy.  \n \n\u2022 Modified schedule for weekly regimen (where ster oids are not appropriate):  \no  1st Treatment   \n\u25aa  Dexamethasone 12 mg IV . \n\u25aa Promethazine 25mg IV . \n\u25aa Ranitidine 50mg IV . \nIf no hypersensitivity reaction, subsequent treatments may be given without \npremedications.12 \nDocetaxel Premedications13 \n\u2022 Recommende d schedule for 3 weekly regimen . 14 \nDexamethasone 8mg BD oral x 6 doses (starting night before treatment) . \n \n9 Product Information, 2001  \n10 Markman M. J Clin Oncol  15(12): 3517, 1997  \n11 Kintzel PE. Ann Pharmacother  35:1114 -7, 2001  \n12 Quock J. Proc ASCO  18 abstr 635, 1999"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ecdd-7265-11ef-895d-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 31, "chroma:document": "Dexamethasone 8mg BD oral x 6 doses (starting night before treatment) . \n \n9 Product Information, 2001  \n10 Markman M. J Clin Oncol  15(12): 3517, 1997  \n11 Kintzel PE. Ann Pharmacother  35:1114 -7, 2001  \n12 Quock J. Proc ASCO  18 abstr 635, 1999  \n13 Product Information, 2001  \n14 Jackisch C. Proc ASCO  19 abstr 417, 2000"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef87-7265-11ef-869b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 32, "chroma:document": "31 \n Additional Dexamethasone IV as antiemetic depending if Docetaxel used alone \n(4mg IV) or in combination with other drugs.  \n\u2022 Schedule for weekly regimen:  \nDexamethasone 8mg oral BD x 3 doses (starting night before treatment) . \nMonoclonal Antibodies  \n\u2022 Trastuzumab (Herceptin) may cause fever and chills, chest tightness and \ntachycardia with 1st infusion.  \n\u2022 Rituximab (Mabthera) may cause asthenia, chills, bronchospas m, \nhypotension, angioedema.  Premedicate with Paracetamol 1 g QID, \nPromethazine 25 mg IV and Hydrocortisone 200 mg IV 30 -60 minutes prior \nto drug.  \n\u2022 Cetuximab requires phenergan 12.5mg or 25 mg prior to infusion."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef88-7265-11ef-aee0-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 33, "chroma:document": "32 \n Medical Oncology Emergencies  \n(Management of Neutropaenic fever is discussed above. ) \nSpinal Cord -compression  \nNeurological symptoms and signs consistent with spinal cord compression necessitates .  \n\u2022 Urgent review and MRI of spine.  \n\u2022 Urgent neurosurgical and or radiotherapy referral . \n\u2022 Start Dexamethasone 8mg IV stat , followed by 16 -24 mg daily in divided \ndoses.  \nSVC Obstruction:  \n\u2022 If the patient presents with st ridor or respiratory compromise , emergency \ntreatment with endovascular stent and Radiotherapy is required.  \n\u2022 In other cases: a histologica l diagnosis is required prior to initiating specific \ntreatment.  \n\u2022 In chemotherapy -sensitive malignancies like small \u2013cell lung cancer, germ \ncell tumour or lymphoma, systemic chemotherapy is usually t he treatment. In \nmost other tum ours, including non -small c ell lung cancer, Radiotherapy is the \npreferred treatment.  \n\u2022 Endovascular stenting could achieve rapid relief of symptoms.  \nHypercalcemia:  \n\u2022 Saline hydration, IV zelodronic acid, IV frusemide after adequate hydration . \n\u2022 Steroids useful in hypercalcaemia due to lym phoma . \n\u2022 s/c calcitonin may be useful in resistant hypercalcemia . \nInfusion reactions and other acute reactions  \n\u2022 Mild to moderate infusion reactions with no features of anaphylaxis -  \n\u2022 IV hydrocortisone and phenergan. Stop infusion till reaction subsides and \nrestart at a lower rate, with close monitoring."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef89-7265-11ef-a5dc-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 33, "chroma:document": "Infusion reactions and other acute reactions  \n\u2022 Mild to moderate infusion reactions with no features of anaphylaxis -  \n\u2022 IV hydrocortisone and phenergan. Stop infusion till reaction subsides and \nrestart at a lower rate, with close monitoring.  \nSevere infusion reactions and anaphylaxis (hypotension, angioedema,  \nbronchospasm, generalised urticaria)  - Resuscitation  with epinephrine, \nhydrocortisone,  phenergan ranitidine and fluids.  \nDO NOT RE -CHALLENGE."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef8a-7265-11ef-977f-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 34, "chroma:document": "33 \n SUMMARY OF MANAGEMEN T OF COMMON CANCERS  15 16 \nThis section outlines the principles behind the management of common cancers.  \nFor metastatic cancers, enrolment into a clinical trial is the best treatment option.  \nSummaries provided below are developed using eviQ and NCCN guidelines as practical \nguidance.  \n \n \nBREAST CANCER  \nEarly breast cancers:  \n(Includes axillary node positive disease .) \n\u2022 Mostly curative intent therapy.  \nPost-operative systemic treatment depends on oestr ogen and/ or progestogen \nreceptor status, Her 2 st atus and the estimated risk of systemic relapse.  \n\u2022 Prognostic factors.  \nSize, age, grade, axillary nodes, receptor status and lympho -vascular invasion.  \n \n Low risk  Average risk  High risk  \nSize <1cm  1-2 cm  >2 cm \nAge   <35 \nNodes  Negative   Positive  \nGrade  Grade 1  Grade2  Grade3  \nER/PR  Positive   Negative  \nHer2  Negative   Positive  \nLVI Absent  present   \n \n\u2022 Low risk  - Hormonal manipulation or nil.  \n\u2022 Average  - Hormonal +/ - chemotherapy for ER/PR positive disease,  \n \n15 www.nccn.org . \n16 www.eviq.org.au"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef8b-7265-11ef-9551-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 35, "chroma:document": "34 \n  Chemotherapy for ER/PR negative disease.  \n\u2022 High risk - Chemotherapy + hormonal manipulation for ER positiv e disease.  \nChemotherapy for ER/PR negative disease.  \n\u2022 For Her-2 positive disease , Herceptin is given with chemotherapy for total of \n52 weeks (3 weekly).  \n\u2022 Hormonal manipulation -  \nIn premenopausal women; Tamoxifen alone may be an option . In patients who \nremain premenopausal after che motherapy  and have high risk disease , ovarian  \nsuppression with LHRH agonists or bilateral oophorectom y with exemestane or \nTamoxifen is better than Tamoxifen alone.  Aromatase Inhibitors are not used \nalone in premenopausal women.  \nConsider 10 years of tamoxifen over 5 years of treatment, particularly f or patients \nat highest baseline risk eg where chemotherapy was indicated.  \nIn post -menopausal women  - Aromatase inhibitors are the preferred endocrine \ntreatment unless contraindicated. In patients who cannot tolerate AI or where it is \ncontraindicated, Tamox ifen is used.   \nIn post -menopausal patients who start treatment with tamoxifen, switching to AI \nafter 2 -3 years is recommended.  \n5-10 additional years of aromatase inhibitors after 5 years of tamoxifen improves \nsurvival in high -risk patients.  \nFor patients on AIs and documented osteopaenia addition of bisphosphonates  \ndecreases the risk of decline in bone density.  They are also encouraged to take \nregular calcium and vitamin D tablets.  DEXA scans are done yearly to two yearly"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef8c-7265-11ef-9076-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 35, "chroma:document": "For patients on AIs and documented osteopaenia addition of bisphosphonates  \ndecreases the risk of decline in bone density.  They are also encouraged to take \nregular calcium and vitamin D tablets.  DEXA scans are done yearly to two yearly \nfor monitoring bone  health in patients on aromatase inhibitors.  \nChemotherapy regimens - \n\u2022 Lower risk/Average risk - 4x TC,  \n\u2022 High risk - 3x FEC - 3x D OR  AC-weekly Taxol  OR AC - dd Taxol . AC may \nbe given in dose dense fashion (preferred if possible).  \n\u2022 In Her-2 positive disease , Trast uzumab  is combined with Taxanes and not \nwith anthracyclines because of risk of cardiac toxicity. Eg FEC -D Herceptin \nor AC -Taxol Trastuzumab .  Pertuzumab may be added in treatment given \nneoadjuvantly.  \n\u2022 In Her2 positive disea se, a non -anthracycline regimen , eg TCarboH is an  \nalternative .17 \n \n17 Slamon, D., W. Eiermann, et al. (2011). \"Adjuvant trastuzumab in HER2 -positive \nbreast cancer.\" New England Journal of Medicin e 365(14): 1273 -1283"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef8d-7265-11ef-924d-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 36, "chroma:document": "35 \n \u2022 G-CSF prophylaxis - If severe neutropenia, cycles delayed because of \nneutropenia or complicated by neutropenic fever, add neulasta  (most of these \nprotocols now have upfront G -CSF)    \nNeoadjuvant chemotherapy:  \n\u2022 Chemotherapy regim ens are similar to adjuvant regimens.  \n\u2022 More effective in triple negative or Her -2 positive disease.  \n\u2022 May be used to achieve breast conservation in some cases, large primary \ntumour sizes, clinical nodal involvement (locally advanced disease) or if \nsurgical c oncerns for upfront surgery.  \n\u2022 Patients with residual cancer after neoadjuvant chemotherapy may require \nfurther chemotherapy treatment or a change in agent (eg capecitabine if triple \nnegative, TDMI (trastuzumab emtansine) if HER2 positive).  \nPost -operative  radiotherapy:  \n\u2022 After lumpectomy, radiotherapy decreases local recurrence rates.  \n\u2022 After mastectomy, indications include (but not limited to):  \no close or positive margins  \no >/=4 axillary nodes involved  \no tumour size >5 cm  \n\u2022 Extensive lymphovascular inva sion.  \nRadiotherapy is given after the chemotherapy is completed, but can occur \nconcurrently with Herceptin in Her2 positive disease  \nLocally advanced and inflammatory breast cancers  \n\u2022 The cure rate is lower than with early breast cancers.  \n\u2022 Chemotherapy is giv en before surgery to reduce the size of the primary and \neradicate micrometastases (see above for regimens).  \n\u2022 Radiotherapy is given after surgery.  \nMetastatic breast cancer"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef8e-7265-11ef-988b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 36, "chroma:document": "\u2022 Chemotherapy is giv en before surgery to reduce the size of the primary and \neradicate micrometastases (see above for regimens).  \n\u2022 Radiotherapy is given after surgery.  \nMetastatic breast cancer  \n\u2022 First line ER/PR + HER2 - bone only metastases - Endocrine therapy +/ - CDK \n4/6 inhibitor (eg palbociclib or ribociclib) . \n\u2022 Patients with bone metastases also benefit from monthly Bisphosphonates or \nDenosumab to reduce pain, skeletal events and hypercalcemia.  \n\u2022 First line chemotherapy is  usually Taxane or Anthracycline based (depending \nupon chemotherapy exposure in adjuvant setting) with combination therapies"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef8f-7265-11ef-9c11-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 37, "chroma:document": "36 \n generally reserved for patients with high volume disease (including visceral \ndisease) or suggestion of aggressive clinical course . \nLater lines of therapy can include taxanes, gemcitabine, capecitabine, \nvinorelbine and eribulin.  Choices may be influenced by patient and physician \npreferences, previous chemotherapy exposure and patient fitness.  For further \ndetailed information on these  protocols , visit eviQ website.  \n\u2022 In Her 2 positive disease, Taxanes can be combined with Trastuzumab  and \nPertuzumab as initial treatment.  \nSecond line treatment may include TDM1 (Trastuzumab emtansine ). If \nprogression on TDM -1, use Lapatanib/capecitabine a nd Herceptin/ \nchemotherapy ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef90-7265-11ef-9a6c-0c9a3cb28fe6
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 38, "chroma:document": "37 \n Cancers of the Gastro -Intestinal Trac t \nAnal Cancer  \n \nMajority of patients are treated with concurrent chemo -radiation. This requires PICC \ninsertion and CADD pump for delivery of continuous infusion 5 - Fluorouracil.  \n \nRegimen:  \nMitomycin C on Day 1 and 5 -Fluorouracil on Days 1 to 4 and 29 to 32 along \nwith radiation for 5 -6 weeks  (standard of care).  \n \nMitomycin C can be substituted with Cisplatin  (if patient has hypersensitivity to \nmitomycin or has any coagulation or bleeding disorders or thrombocytopenia).  \nIf patient cannot have PICC for some reason 5 -Fluorouracil can be substituted \nwith Capecitabine.  \n \nMetastatic Anal Cancer: Different chemother apies can be used such as, \nCarboplatin & Paclitaxel (weekly/three weekly), 5Fu & Cisplatin, FOLCIS \n(5Fu, leucovorin & Cisplatin), mFOLFOX, mDCF.  \n \nGastro -Oesophageal and Gastric Cancer  \n \nDefinitive Concurrent Chemo -Radiation  \n \nFor those not suitable for surgery:  \nCisplatin and 5 -Fluoruracil along with radiation (2 cycles)  \n \nNeo-adjuvant  chemoradiation : \n \nWeekly Carboplatin and Taxol  \nAlternatively, Cisplatin and 5 -Fluorouracil with radiation.  \n \nPeri-operative chemotherapy : \n \nFor aden ocarcinoma of lower oesophagus, gastro -oesophageal junction and stomach.  \n4 cycles FLOT pre and post resection.  \nor, 3 cycles of ECF / EOX  pre and post resection . \nor 2 x cis/5fu pre & post resection.  \n \nAdvanced or Metastatic Carcinoma of Gastro -oesophageal J unction/Stomach:"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef91-7265-11ef-82b1-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 38, "chroma:document": "4 cycles FLOT pre and post resection.  \nor, 3 cycles of ECF / EOX  pre and post resection . \nor 2 x cis/5fu pre & post resection.  \n \nAdvanced or Metastatic Carcinoma of Gastro -oesophageal J unction/Stomach:  \n \nDifferent single agent/combination regimens can be used depending on existing co -\nmorbidities. Many regimens can be used for both adenocarcino and squamous cell \ncarcinoma.  \nCombination : FOLFOX 6  or XELOX  \nSingle agents:  Docetaxel, paclitaxel, irinotecan  \n \nFor HER -2 positive adenocarcinoma \u2013 Add Trastuzumab (Herceptin)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef92-7265-11ef-8d25-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 39, "chroma:document": "38 \n  \nCERS OF THE GASTRO -INTESTINAL TRAC  \nBiliary and Gall Bladder  \nOutcome is usually poor in patients with multiple co -morbidities and poor performance \nstatus. In these cases, omitting chemotherapy from management plans may be prudent.  \n\u2022 Adjuvant therapy for node positive disease \u2013 fluoropyrimidine or Gemcitabine \nbased chemotherapy (eg: Cisplatin or Carboplatin /Gem citabine).  \nConsider chemoradiati on for margin -positive or node positive cancer.  \n\u2022 Metastatic/inoperable \u2013 Same regimens as adjuvant therapy.  \nHepatocellular carcinoma  \n\u2022 Limited disease: Operable or locoregional therapy available  \n\u2022 Inoperable  or not suitable for locoregional therapy:  Lenvatinib  or Sorafenib  \nin Child -Pugh A patients) . Role of systemic chemotherapy is not established.  \n \nMetastatic Neuro -endocrine Tumours of Gastro -intestinal Tract  \n\u2022 Grade I/II \u2013 Sandostatin/Lanreotide . On progression capecitabine and \ntemozolomide.  \n      Everolimus or sunitinib can be used for pancreatic Grade I/II tumours.  \n\u2022 Grade III \u2013 Carboplatin and etoposide or cisplatin and etoposide .  \nAdeno -carcinoma of Pancreas  \nRole of neoadjuvant therapy contin ues to evolve, and this is usually not standard practice \noutside of clinical trial settings except where an MDT strongly recommends this \napproach. Outcome is usually poor in patients with multiple co -morbidities and poor \nperformance status. In these cases,  omitting chemotherapy from management plans may \nbe prudent."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef93-7265-11ef-8f7b-0c9a3cb28fe6
encoding: FLOAT32
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{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 39, "chroma:document": "approach. Outcome is usually poor in patients with multiple co -morbidities and poor \nperformance status. In these cases,  omitting chemotherapy from management plans may \nbe prudent.  \n \n\u2022 Adjuvant \u2013 modified FOLFORINOX x 6 months or Capecitabine + \nGemcitabine . \n\u2022 Advanced/metastatic \u2013 If disease recurrence occurs after 6 months of \ncompleting adjuvant therapy, same regimen could be c onsidered. In good \nperformance patients with minimal co -morbidities, m FOLFIRINOX or \nGemcitabine and nab -Paclitaxel.  After 4 -6 months, less intensive components \ncould be maintained."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef94-7265-11ef-b067-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 40, "chroma:document": "39 \n In poor performance patients, BSC alone or single agent  regimens such as \ngemcitabine  may be appropriate.  \n \n \n Colon Cancer  \nStage I and II surgery alone.  \nStage II with adverse features is  treated as stage III with adjuvant chemotherapy. \nAdverse features are \u2013 poorly differentiated histology, lympho -vascular invasion, \nbowel obstruction, perforation, fewer than 12 lymph nodes in the resected \nspecimen, perineural invasion, close or positive m argins.  \nAdjuvant chemotherapy  is for six months. However, in low risk patients (T1 -3 \nN1) shorter duration (three months) of adjuvant XELOX (CAPOX) is equivalent \nto six months of XELOX in efficacy with less neurotoxicity . If using mFOLFOX \nrecommendation is for six months of treatment. For High risk features, \nrecommendation is for six months of treatment.  \nRegimens : Different schedules of calcium leucovorin and 5 fluorouracil, \nCapecitabine, FOLFOX  & XELOX . \nMetastatic cancer : Any adjuvant regimen can be used in metastatic setting. Other \nregimens are Irinotecan, FOLFIRI, FOLFOXIRI, XELIRI.  \nAssess patients with imaging after 3 cycles of chemotherapy for respectability  of \nlesions. Discuss  in GI multi -disciplinary meetings. Some of the patients with few \nmetastases ma y eventually be curable.  \nBevacizumab is usually combined to different chemotherapy regimens in \nmetastatic setting unless contra -indicated.  \nPatients with KRAS wild type tumours have additional option of having"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef95-7265-11ef-9e87-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 40, "chroma:document": "metastases ma y eventually be curable.  \nBevacizumab is usually combined to different chemotherapy regimens in \nmetastatic setting unless contra -indicated.  \nPatients with KRAS wild type tumours have additional option of having \nCetuximab/ Panitumumab added  to chemotherapy re gimen.  \n \nRectal Cancer  \nMost of the patient s are treated with neo -adjuvant concurrent chemo -radiotherapy.  \nChemotherapy consists of continuous infusion 5 -Fluorouracil through PICC line or oral \ncapecitabine. If the patient did not receive neo -adjuvant treatmen t it may be given post -\noperatively for T3/T4 or node positive tumours."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef96-7265-11ef-acbc-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 41, "chroma:document": "40 \n For those who had neo -adjuvant treatment further adjuvant chemotherapy is offered post -\noperatively in the form of leucovorin -5-Fluorouracil/capecitabine  to complete six months \nof perio perative chemotherapy.  \nFOLFOX is currently not approved for rectal cancer.  \n \nMetastatic rectal cancer  \nAll the regimens used in colonic cancer can be used in metastatic rectal cancer including \nBevacizumab, cetuximab and panitumumab.  \nAssess patients with imag ing after 3 cycles of chemotherapy for res ectability of \nlesions. Discuss  in GI multi -disciplinary meetings. Some of the patients with few \nmetastases may eventually be curable.  \n \nGastro-Intestinal Stromal Tumours (GIST)  \n\u2022 Adjuvant  \u2013 for those with high risk features \u2013 Imatinib for 3 years . \nHigh Risk Features are : Primary GIST greater than 5 cm with a mitotic count of \ngreater than 5/50 high power fields (HPF); or  \nPrimary GIST greater than 10 cm with any mitotic rate; or  \nPrimary GIST with a mitotic count of greater than 10/50 HPF  \n\u2022 Metastatic  -   Imatinib. Sunitinib can be used when progress on Imatinib."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef97-7265-11ef-87a3-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 42, "chroma:document": "41 \n GBM  \n\u2022 Surgery is for resectable disease.  \n\u2022 For resected GBM, Temazolamide with RT and 4 weeks later, 5days per \nmonth for 6 m onths of Temazolamide improves survival.   \nTemazolamide:  \n\u2022 With RT - 75mg/m2/day M -F. \n\u2022 After RT or on its own for palliation - 150-200 mg/m2/day for 5 days a \nmonth.  \nCheck platelets mid cycle as a caution.  \nUnresectable and incurable GBM - options include Temazolam ide & Avastin \nbased combinations.  \nGERM CELL TUMOURS   \nStage 1 -   \n\u2022 Normally for stage 1 seminoma  (make sure serum AFP normal)  - Single \ndose carbo platin AUC 7.  Check counts every week for 2 weeks post  \nchemotherapy . \nDiscuss sperm banking  with patient prior to g iving chemotherapy. However , \nfertility is unlikely to be affected  with one cycle of carboplatin.  \n\u2022 For stage 1 non -seminoma - wait and watch (6 weekly markers and 3 \nmonthly CTs first 2 years and later relax to 6 monthly scans and 3 monthly \nbloods for another 3 years).  \nor 2 cycles of BEP for patients who are not reliable for follow up  or who move \naround different towns . \nStage 2 onwards -  \nThis includes patients with normal scans but have the markers eleva ted few weeks \npost orchidectomy.  \nSeminoma:  \n\u2022 Stage 2 or stage 3: \nGood prognosis - 3 cycles of BEP . \nIntermediate prognosis - 4x cycles of BEP ( only first 3 cycles are with Bleomycin).  \n\u2022 Non seminoma   \nGood prognosis - 3 x cycles of BEP,"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef98-7265-11ef-86ef-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 43, "chroma:document": "42 \n Intermediate or poor prognosis - 4x cycles of BEP.  \nResidual disease /mass  after optimal chemotherapy needs to be resected.  \nPre BEP treatment:  \n\u2022 History of renal, auditory,  neuropathy and vascular issues,  \n\u2022 Lung function test - DLCO and lung volumes,  \n\u2022 Sperm banking  (Semen cryopreservation: In Townsville, this is performed by \nQFG) , ELFTS, FBC, LDH and markers.  \n(Please discourage smoking ). \n\u2022 Recurrent GCTs can still be cured by TIP or VIP chemotherapy.  \nPrognostic groups:  Seminoma:  \n \n Good prognosis  Intermediate prognosis  \nPrimary site  any any \nPresence of non \npulmonary met astasis no yes \nMarkers  (not AFP)  any any \n \nIf serum  AFP  is elevated, it is treated as non -seminoma.  \nNon -Seminoma:  \n \n Good  Intermediate  Poor  \nPrimary site  Non mediastinal  Non mediastinal  mediastinal  \nNon pulmonary \nmetastasis no no yes \nMarkers   \nAFP <1000  1000 -10000  >10000  \nB HCG  <5000  5000 -50000  >50000  \nLDH  <1.5 x ULN  1.5-10 x ULN  >10 x ULN"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef99-7265-11ef-98fe-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 44, "chroma:document": "43 \n  \nHEAD AND NECK CANCER  \n\u2022 Resectable disease - Surgery.  \nFor high risk disease, post op radiotherapy with chemotherapy improves survival.  \n\u2022 Unresectable  disease or organ preservation -  \nInduction chemotherapy followed by chemoradiotherapy.  \nInduction chemotherapy - 2 -3 cycles of T PF. \nChemoradiotherapy - weekly cisplatin 40mg/m2.  \n\u2022 *If not fit for weekly cisplatin , abnormal renal function or cardiac issues -  \nCetuximab ( Erbitux ) Loading dose 400mg/m2 one week prior to RT and then \nweekly 250mg/m2 weekly  (Discuss with Radiation oncologists for their \npreference ). \nThey need Phenergan 12.5mg or 25mg as premed ications .  \n\u2022 Metastatic H&N cancer - (Cisplatin or Carboplatin) and 5FU / Capecitabine  \nSecond -line -PDL1 antibody Nivolumab.  \nLUNG CANCER  \n\u2022 Non Small Cell Lung cancers:  \n*Stage I to III - Surg ical resection  offers the best chance of cure.  \n\u2022 For resected stage 1b, II or III  -  \nAdjuvant chemotherapy with cisplatin  & vinorelbine x 4 cycles to improve \nsurvival in fit and <70 years.  Carboplatin & paclitaxel  is other alternative.  \n\u2022 *Stage III - \nFor patients who are unresectable, chemo -radiation can improve survival.  \n\u2022 concurrent with radia tion-  \nCisplatin with Etoposide is the preferred regimen. Other alternativ es are used in \npatients who are unfit for Cisplatin (elderly, renal impairment etc) . \nEg - Carbo platin (AUC 2) and Paclitaxel (50mg.m2) weekly with radiation.   \nPost CRT immunotherapy improves outcomes."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef9a-7265-11ef-a6db-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 44, "chroma:document": "patients who are unfit for Cisplatin (elderly, renal impairment etc) . \nEg - Carbo platin (AUC 2) and Paclitaxel (50mg.m2) weekly with radiation.   \nPost CRT immunotherapy improves outcomes.  \n \nNon metastatic pan coast tumours  - chemo -radiotherapy followed by surgery.  \n\u2022 *Stage IV or incurable stage III b-  \nAlways test for oncogenic mutations like EGFR , ALK  and ROS -1 in Non \nSquamous  NSCLC. If either is positive, treat with EGFR inhibitor ( Afatinib is"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef9b-7265-11ef-83b7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 45, "chroma:document": "44 \n preferred or Erlotinib or Gefitinib) or ALK inhibitor (Alectinib is preferred or \nCrizotinib ).  \n\u2022 All NSCLCs (non squamous or squamous) should also be tested for PDL -1 by \nIHC (to check for eligibility of using immunotherapy alone as first line treatment). \nIf PDL -1 expression >50%  and there is no actionable mutation , then single agent \nPembrolizumab (anti PDL -1) can be offered as upfront treatment (without \nchemotherapy).  \n\u2022 For NSCLC patients with PDL -1 expression less than 50% and  with no actionable \nmutation, consider offering combination of immunotherapy (anti PDL -1) along \nwith platinum doublet chemotherapy if performance status is reasonable (ECOG \n<=2) . \n\u2022 Maintenance Pemetrexed  chemotherapy can be considered in patients with Non \nSquamous  NSCLC who have not progressed after first line combination \ntreatment.  \n\u2022 All these patients with incurable disease should be considered for clinical trial if \none is available.  \n\u2022 In select  patient  groups (e.g elderly with good PS, or patients who have \ncontraindication for immunotherapy like significant autoimmune disorder), single  \nagent chemotherapy alone is a reasonable option  \nOnce first line treatment with chemotherapy fails \u2013 consider treatment with  anti \nPDL -1 antibody  (e.g Nivolumab) for 2nd line treatment.  \n\u2022 Palliative best supportive care is reasonable for patients with poor (ECOG>2) PS. \nConsider early referral to palliative care for all stage IV lung cancer patients"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef9c-7265-11ef-91d5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 45, "chroma:document": "PDL -1 antibody  (e.g Nivolumab) for 2nd line treatment.  \n\u2022 Palliative best supportive care is reasonable for patients with poor (ECOG>2) PS. \nConsider early referral to palliative care for all stage IV lung cancer patients \nundergoing active treatment as this has shown to improve survival.  \nSmall cell lung cancer  \n\u2022 Limited stage -  \nCisplati n and etoposide x 4 cycles and radiation as early as possible or Carboplatin \nand etoposide for 6 cycles and radiation.  \nAt the end of the treatment, if no brain mets - Prophy lactic cranial irradiation to \nadd another 5% survival benefit.  \n\u2022 Extensive stage - \nCarboplatin and etoposide with immunotherapy for 6 cycles. If complete response \nthat last for 6 -12 months, could have re treated.  \n\u2022 Urgent chemotherapy (with or without  tumour ly sis prophylaxis ) for patients \npresenting with bulky disease and oncology emergency (e.g SVC obstruction)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef9d-7265-11ef-aecc-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 46, "chroma:document": "45 \n Mesothelioma  \nSurgical decortication can be useful in selected patients.  \nOtherwise, Carbo AUC 5 or Cisplatin and Pemetrex ed every 3 weeks.  \nImportant - 1 week before Pemetrex ed - start VitB12 1000mcg IM every 9 \nweeks and folic acid 0.5 mg daily until Pemetrex ed is stopped.  \nConsider Clinical trial for these patients if available.  \n \n \n \n \nMELANOMA  \n\u2022 Stage I to III - resection of the primary +/ - sentine l node biopsy and node \ndissection for node positive disease.  \no Stage IB or II can be considered for clinical trial with adjuvant \ntreatment if available otherwise ongoing surveillance.  \n\u2022 For stage III disease : \no Stage IIIA disease: consider imaging and BRAF muta tion testing. \nConsider systemic treatment on clinical trial, otherwise surveillance.  \no Resected stage IIIB/C/D disease: imaging to confirm staging and \nBRAF mutation testing. Immunotherapy  (anti PD -1) for BRAF WT \ndisease, or Dabrafenib (BRAFi) and Trametinib (MEKi) for patients \nwith BRAF V600 mutation. Observation is also an option. Treatment \nsubject to ECOG 1 or less.  \no Unresectable stage III disease: treat as unresectable stage IV disease.  \no Consider adjuvant radiotherapy in patients with involved surgical \nmargi ns. \n\u2022 Stage IV disease  \no Limited/oligometastatic (resectable) disease. Imaging to confirm \nstaging. BRAF mutation testing. LDH. Systemic treatment followed \nby imaging and resection OR resection followed by systemic \ntreatment."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef9e-7265-11ef-bc90-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 46, "chroma:document": "margi ns. \n\u2022 Stage IV disease  \no Limited/oligometastatic (resectable) disease. Imaging to confirm \nstaging. BRAF mutation testing. LDH. Systemic treatment followed \nby imaging and resection OR resection followed by systemic \ntreatment.  \n\u25aa Systemic treatment depending on BR AF and performance \nstatus.  \n\u25aa Systemic options are the same as resected stage III disease"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4ef9f-7265-11ef-830f-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 47, "chroma:document": "46 \n o Disseminated (unresectable) disease.  \n\u25aa In patients without brain metastasis: systemic therapy as \nabove, intralesional T -VEC, palliative resection or RT. Best \nsupportive care.  \n\u25aa With brain metastasis: Primary RT , Palliative resection with or \nwithout adjuvant RT , Followed by systemic therapy as above  \nor combination immunotherapy in low volume cases ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4efa0-7265-11ef-8568-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 48, "chroma:document": "47 \n GYNAECOLOGICAL CANCER  \n\u2022 Ovarian cancer  \nStage 1 - Surgery  (adjuvant chemotherapy for high risk patients such as with \ntumour rupture or positive peritoneal washings) . \nStage >/= 2 Debulking surgery, BSO/TAH.  \nPost debulking su rgery - Carbo AUC 5/6 and Taxol weekly or three weekly  (three \nweekly generally prefe rred) .   \nPatients who are unfit for surgery can be given neo adjuvant chemotherapy first \nand receive surgery after several cycles of chemotherapy (interval debulking) with \nsubsequent adjuvant chemotherapy.  This approach may reduce surgical morbidity \nof de bulking procedures without compromising outcomes.  \nIntraperitoneal chemotherapy may be used in selected stage3 disease, after \noptimal debulking surgery.  \nIn patients who have metastatic disease (stage 4) or those who do not achieve \noptimal debulking (residua l disease >1cm), bevacizumab for one year may be \nused on the PBS.   \n \n\u2022 Relapsed Disease  \nChoice of agent may depend upon interval since last exposure to platinum (ie \nplatinum sensitive versus resistant).  \nNewer agents such as PARP inhibitors may be used depending upon BRCA \nmutation status . \nProtocols include carboplatin/caelyx, carboplatin/gemcitabine and topotecan . \nCervical cancer  \n\u2022 Early disease - surgery  \n\u2022 Locally advanced - chemoradiotherapy with weekly cispla tin, \n\u2022 Metastatic - Platinum/ Taxol / Bevacizumab , Taxol/Topotecan , Gemcitabine ."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4efa1-7265-11ef-a724-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 49, "chroma:document": "48 \n CANCERS OF GENITO URINARY SYSTEM  \nPROSTATE CANCER  \nTreatment depends on disease stage and hormone sensitivity.  \n \n\u2022 Early stage disease  is treat ed with surgery, radiotherapy ( externa l beam and/ \nor brachytherapy) or observation. Treatment modality is individualised based \non several factors: age and co morbidities of the patient, serum PSA level, \nGleeson score, clinical stage and patient preference based on benefits and \nside effects of therapy.  \nFor example, a patient with clinically non apparent tumour with Gleason score of \n<6 who has a life expectancy of <10 years coul d be actively observed without any \nimpact on survival.  \nFor locally advanced inoperable disease, radical radiotherapy cou ld lead to cure. \nAndrogen deprivation therapy is sometimes used for short periods  (4-6 months) \nbefore/concomitantly/ after radiotherapy in selected high-risk patients.  \n \nMetastatic disease  is incurable and the aims are to prolong survival and improve \nquali ty of life.  \n \nHormone Sensitive disease:  \n\u2022 All Hormone sensitive tumours are treated with a GnRH agonist  (eg- \ngoserelin,  leuprorelin). To prevent flare, antiandrogens  (eg- flutamide,  are \nstarted 1-2 weeks before the injection  and continued for a total of 3-4 weeks ). \nWhether anti - androge ns are continued beyond that is  controversial.  \n\u2022 Chemotherapy wi th Docetaxel 75 mg/m2 x 6 doses , can be added to \nhormonal therapy  in fit patients with high volume (presence of visceral mets"}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4efa2-7265-11ef-972b-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 49, "chroma:document": "Whether anti - androge ns are continued beyond that is  controversial.  \n\u2022 Chemotherapy wi th Docetaxel 75 mg/m2 x 6 doses , can be added to \nhormonal therapy  in fit patients with high volume (presence of visceral mets \nor >= 4 bony mets)  metas tatic disease, as it improves survival significantly \n(CHAARTED, STAMPEDE trials).  \nHormone Refractory disease:  \n\u2022 Hormone refractory disease includes patients where the disease has \nprogressed despite hormonal manipulation.  GnRH agonists are usually \ncontinued.    \n\u2022 Chemotherapy improves median survival by up to 3 months and maintains \nimprovement in quality of life.   \n\u2022 Bone metastases are treated with intravenous bisphosphonates  (eg-zoledronic \nacid) or RANK -ligand inhibitor Denosumab monthly.  For asymptomatic and \nlow volume disease, chemotherapy is usually delayed."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4efa3-7265-11ef-99e5-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 50, "chroma:document": "49 \n \u2022 Symptomatic metastases or rapid rise in PSA (doubling time of <3 months) \nmay be treated with docetaxel  (75mg/m2)  and prednisone  5 mg BD.  On \nprogression after doc etaxel, newer androgen inhibitors (below) are effective.  \nPalliative care is another option.  \n\u2022 Localised bone pain responds to external beam radiotherapy very well. Men \nwith multifocal painful bone metastases and those with persistent or recurrent \npain despite receiving EBRT to maximal normal tissue tolerance may achieve \npalliation of their symptoms by treatment with bone -targeted radi oisotopes \nsuch as strontium -89. \nDisease progression after chemotherapy : Abiraterone , an andr ogen biosynthesis \ninhibitor or Enz alutamide an androgen receptor signalling inhibitor are effective . Median \nprogression free survival and overall survival are better compared to placebo.  \nRenal Cell Carcinoma  \n\u2022 Metastatic renal cell carcino ma with clear cell  histology is  treated based on \nrisk stratification  (example IMDC criteria) . \n\u2022 Low risk disease can be treated with tyrosine kinase inhibitors Sunitinib  or \nPazopanib. Cabozantinib or Sorafenib can be used after failure of these. \nSorefenib can also be used for  papillary carcinoma. Everolimus and axitinib \nare other second line options available.  \n\u2022 Intermediate and high -risk disease is treated with combination \nimmunotherapy Ipilimumab (anti CTLA4) and Nivolumab (anti PDL -1)."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4efa4-7265-11ef-8fd7-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 50, "chroma:document": "are other second line options available.  \n\u2022 Intermediate and high -risk disease is treated with combination \nimmunotherapy Ipilimumab (anti CTLA4) and Nivolumab (anti PDL -1). \n\u2022 Once progressed on first like VEGF TKI, immunotherapy is drug of choice \nfor second line treatment. Vice versa if disease progresses on immunotherapy \nthen VEGF TKI such as Cabozantinib or Sunitinib or Pazopanib can be used.  \nUrinary Bladder Cancer  \n\u2022 Non-muscle invasive disease is treated with surger y and adjuvan t intravesical \ntherapies (eg.  BCG  or Mitomycin ). \n\u2022 Muscle invasive disease is treated with surgery. Pre -op Cisplatin based (neo-\nadjuvant) chemotherapy improves survival.  \n\u2022 Adjuvant Cisplatin based Chemotherapy is considered for those at high ris k \nof recurrence such as T3/T4 tumours, lympho -vascular invasion or positive \nnodes  if neo -adjuvant therapy was not given .  \n \nInoperable disease may be managed with:  \n\u2022 Radiotherapy with or without radio -sensitising chemotherapy with weekly \ncisplatin or mitomyci n and infusional 5 -Fluorourcil."}


created_at: 2024-09-14 06:50:03
topic: persistent://default/default/3f492d3d-8f06-4f02-95f0-362c067678fe
id: 71d4efa5-7265-11ef-8e1c-0c9a3cb28fe6
encoding: FLOAT32
metadata:
{"source": "data/docs\\medical_oncology_handbook_june_2020_edition.pdf", "page": 51, "chroma:document": "50 \n \u2022 Chemotherapy alone (platinum and gemcitabine), or a  \n\u2022 Palliative care alone.  \n \nMetastatic disease  is managed with chemotherapy , immunotherapy  or palliative care \nalone.  \nPlatinum based chemotherapy is usually  the first line palliative treatment. One such \nregimen is Carboplatin and Gemcitabine.   \n \nImmunotherapy with Pembrolizumab is used as second line treatment after failure of \nplatinum -based  chemotherapy."}


