(Academy for Foreign edhical Graduates) (CI SCREENING PROGRAM | For Regular Course Crash Course Postal Course SANIOIGSW [2 9810 608460 9810 686970 _ Hebline | E-mail: contact@atmg. co. ink. {GAn Academy for the Doctors by the Doct AFMG (Academy for Foreign Medical Graduates) Medicine Contents Cardiology Part-I 01-05 Cardiology Part —Ii 06-12 Cardiology Part -III 13-17 Respiratory System 18-31 Connective Tissue Disorder 32-36 Neurology 37-49 Endocrinology 50-58 GIT 59-73 Infectious Disease 74-103 Nephrology 104-10 Multi— Choice Question 01-14 visit us at: www.afmg.co.in, E-mail: contact@afmg.co.in 24hr. Helpline 9810608460, 9810686970 a gk ne a eeAFMG (Academy for Foreign Medical Graduates) CARDIOLOGY Dyspnoea: - Abnormally uncomfortable awareness of breathing is called Dyspnoea, Acute - Left ventricular failure - Bronchial asthma - Pneumothorax - Acute M1 Chronic; os : Pleuraleffusion | a a - CHF — ~ NYHA classification | — Dyspnea occurring at a activity much more than ordinary. It Dyspnea occurring at ordinary activity. Ill- Dyspnea occurring at activity less than ordinary. IV- Dyspnea at rest. PND (Paroxysmal Nocturnal Dyspnea) is a form of interstitial pulmonary edema. Angina - - Chest pain or discomfort that is substemal and frequently associated with heaviness or constricting feeling, It is the most common presenting symptoms in patients with acute MI. Syncope - Transient loss of consciouseness due to cerebral hypoperfusion, Most common cause is vasovagal (Neurocardioganic) syncope. Other causes are sick sinus syndrome, carotid sinus hypersensitivity, ventricular arrhythmias. Palpitation — Awareness of forceful beating of heart. Common cause are extrasystoles, tachyarhythmias, drugs like pseudoephedine, salbutamol, Theophylline. Clubbing — Bullous enlargement of distal phalanges is called clubbing. ~ Causes ~ Cyanotic congenital heart disease lung disease, bronchogenic carcinoma, bronchiectasis, infective endocarditis, G.I causes like crohn's disease cirrhosis. Cyanosis — Bluish discoloration of skin and mucous membranes. Central Cyanosis ~ Hypoxemia is the most common cause. Right to left shunting of blood is another important cause. a. Reduced Hb > 4g/d! ‘24 hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, e-mail: contact@afmg.co.in \AFMG (Academy for Forcign Medical Graduates) b. Meth Hb > 1.5 g/dl c. Sui Hb > 0.5g/dl All of these conditions can cause central cyanosis. Causes ~ Chronic bronchitis - High altitude ~ Cyanioic congential heart disease Peripheral cyanosis — Most common cause is CHF. It can also occur due to exposure to cold and peripheral vascular disease. Differential cyanosis is seen in patent ductus arteriosus with reversal of shunt. Ahiremnd f a PULSE: - _ fo 2 ChaFaetér of pulsé'ts best felt in arotid ‘Btlery. - Pulsus parvus et tardus- Aortic stenosis. Pulsus bisferiens — Aortic regurgitation, hypertrophic cardiomyopathy. - Pulsus alternans ~ Severe LV dysfunction. - Pulsus Paradoxus — Cardiac tamponade, acute severe asthma, pneumothorax. - Collapsing pulse — Aortic regurgitation, anemia, Thyrotoxicosis, Beri-Beri. Jugular venous Pulsation (JVP) JVP is seen in right internal jugular vein. Reference point for clinical examination is taken as sternal angle Scm + vertical distance from sternal angle). Large ‘a' wave ~ Tricuspid stenosis, pulmonic stenosis. Cannon ‘a’ wave — A-v dissociation ( complete heart block, Ventricular tachycardia) Absent ‘a’ wave — Atrial fibrillation. Large ‘V' wave — tricuspid regurgitation, atrial septal defect. Steep 'y’ descent — Tricuspid regurgitation, constrictive pericarditis JVP normally falls with inspiration but may rise (Kussmaul’s sign) in constrictive Pericarditis, and right-sided heart failure. Precordial palpation — cardiac impulse is Normally localized in fifth intercostal space, mid clavicular line. Abnormalities include. Tapping apex- Mitral stenosis Hyperkinetic apex ~ Mitral regurgitation, aortic regurgitation 24 hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, e-mail: contact@afmg.co.inAFMG (Academy for Foreign Medical Graduates) Sustained or heaving apex — Aortic stenosis Double systolic apical impulse — Hypertrophic cardiomyopathy. Dyskinetic impulse — Ventricular aneurysm. Auscultation — Heart Sounds - 81 loud — Mitral stenosis, short PR interval, tachycardia. $1 soft — Long PR interval, mitral regurgitation Bradycardia. S2— Normally A2 precedes P2 splitting increases with inspiration Abnormalities inclyde-— z y / iWide splitting RBBB, puoi nae ~~ iWide & Fixed splitting ; Atrial’septal-defect.! |. Paradoxical splitting: Aortic stenosis, LBBB, CHE. ~ $3~Low pitched, heart best with the bell of stethoscope at apex following S2. Physiological $3 can occur in athletes, children and pregnancy. It is always pathological after the age of 40 years. Causes are CHF, mitral regurgitation, - $4- Low pitched, heard best with bell at apex, preceding S1, reflects atrial contraction into a noncompliant vent side. Causes include AS, hypertension, hypertrophic cardiomyopathy. Heart Murmurs — Systolic Ejection type = Aortic outflow tract AS HOcM + Pulmonary out flow tract PS Holosystolic © Mitral regurgitation © Ventricular septal defect © Tricuspid regurgitation. Late Systolic © Mitral or tricuspid value Prolapse. Diastolic Early diastolic * AR = PR 24 hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, e-mail: contact@afmg.co.in \)AFMG _ ___ (Academy for Foreign Medical Graduates) Mid to Tate diastotic = MS - Ts Continuous © Patent ductus arteriosus © Coronary AV fistula © Ruptured sinus of valsaiva aneurysm © Venous hum ° Mammary soufflé } if Arthythmias. = Drugs (William V Vaughan classincation) 1A ~ Quinidine, Procainamide, Disopyramide IB- Lidocaine, Phenytoin, Mexiletene. IC — Flecainide, propafenone Il- Beta blockers Il — Amiodarone, sotalol, ibutidlide, Dofetilide, Bretylium. IV ~ calcium channel blockers Others — Digoxin, Adenosine. Atrial fibrillation * Causes include, mitral value disease, Thyrotoxicosis, CAD, Pericardilis, post cardiac surgery. + Atrial P waves, irregular R-R interval on ECG. + Absent a waves in JVP, variable first heart sound, irregularly irregular pulse. * Treatment Treat underlying cause © Control rate with Beta blockers or calcium channel blockers. © Cardioversion can be performed with Quinidine, ibutilide. D.C. shock is used in highly unstable patient. o In chronic AF, anticoagulation is required if risk factores for stroke are present. Atrial Flutter * Causes include post cardiac surgery, hypoxia, Myocarditis. * Atrial rate = 250-350/min. * A/V block of 2:1 or 4:1 is present. * Saw-tooth appearance of P waves on Ecc. * Treatment 24 hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, e-mail: contact@afmg.co.in |AFMG (Academy for Foreign Medical Graduates) oD, Cardioversion is the treatment of choice. Paroxysmal Supra ventricular tachycardia - Most individuals do not have underlying heart disease. - Atrial rate = 130-250 Initial or retrograde P waves - Initial treatment is carotid sinus massage. - Drug of choice is adenosine. - Radio frequency ablation is the treatment of choice for recurrent PSVT. - To prevent recurrences of PSVT Beta blockers, calcium channel blockers can be used. Ventricular tachycardia - There or more than three consecutive ventricular premature complexes at a fate more than 100/min is yentricular tachycardia, ~ (Causes — Myocardial, ischemia, Mydcarditis, flecrevte imbalafice, -I-can cause sudden death. Importar{t features are} "Av dissociation * ORS > 0.14 seconds * QRS concordance. + Atypical RBBB/L_BBB. Treatment + D.C. shock minimum 1004 if patient is unstable. * LV lidocaine , amiodarone, procainamide in stable patients. Torsades de pointes - _ Itis also called as polymorphic ventricular tachycardia. ~ Causes include long QT syndrome, hypokalemia, hypomagnesemia, drugs prolonging QT interval on ECG, - QT> 0.60sec in the sinus beats preGeding torsades de pointes. - Cardiac pacing and magnesium sulfate 1.V is the treatment for drug/electrolyte induced polymorphic VT. ~ Beta blockers are indicated for patients with congenital long QT syndrome. 24 hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, e-mail: contact@afmg.co.in jyAFMG Academy for Foreign Medical Graduates. CARDIOLOGY PAR’ DILATED CARDIOMYOPATHY Symmetrically dilated left ventricle (LV), with poor systolic contractile function, right ventricle (RV) commonly involved Previous Myocarditis or idiopathic most common cause. Ethanol, dexocubocin, muscular dystrophy, peripartum state are other causes, Dyspnea on exertion, paroxysmal noctumal dyspnea, Jugular venous distension, rales, diffuse and dyskinetic LV apex, S; hepatomegaly, peripheral edema, murmurs of mitral & tricuspid regurgitation aré common ~ _Echo-Left bundle branch block and ST-T wave abnromalities common - CXR - Cardiomegaly, pulmonary vascular redistribution, pleural effusion common - Echocardiogram — LV & RV enlargement with globally impaired contraction - Treatment — ACE inhibitors, diuretics are used. Beta-blockers should be used in ambulatory patients. Chronic anticoagulation with warfarin is recommended for very low ejection fraction (<25%), Antiarrhythmic drugs eg. Amiodarone is indicated for ‘symptomatic or sustained arrhythmias (implanted internal defibrillator is often a better alternative). RESTRICTIVE CARDIOMYOPATHY ~ _ Ethnologies include infiltrative diseases (Amyloid, sarcoidosis, hemochromatosis, Eosinophilic disorders) - Increased myocardial “stiffness” impairs ventricular relaxation, diastolic ventricular pressures are elevated ~ Symptoms are of CHF, although right - sided heart failure often predominates, with peripheral edema and ascites ~ Signs of right ~ sided heart failure -: Jugular venous distension, hepatomegaly, and ~ Peripheral edema, murmur of tricuspid regurgitation. Left signed may also be present - ECG: Low Jirnb lead voltage, sinus eee 'ST-T way6 abnormalities CXR: Mig LV enlargement Sf - Echo: Bilateral atrial enlargement: “Speckled pattern” in amyloidosis. Systolic is normal. - Treatment: Salt restriction and diuretics ameliorate pulmonary and systemic congestion; anticoagulation is often indicated, particularly in patients with Eosinophilic endo Myocarditis. HYPERTROPHIC CARDIOMYOPATHY ~ Marked LV hypertrophy, asymmetric, without underlying cause, Systolic functi normal, increased LY stiffness results in elevated diastolic filing pressures. 24hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, E-mail: contact@afmg.co.inAFMG Academy for Foreign Medical Graduates ~ Dyspnea on exertion, angina, syncope, sudden death may occur ~ Brisk carotid upstroke with pulsus bisferiens, S., harsh systolic murmur along left sternal border, blowing murmur of mitral regurgitation at apex. Ejection murmur increases with standing of valsalva ECG-LV hypertrophy with prominent Q waves in leads I, aVl, Leg ~ Echocardiogram — Asymmetric septal hypertrophy and >1.3X thickness of LV Posterior wall. LV systolic function is good with small end systolic volume LV out flow tract obstruction is accompanied by systolic anterior motion of the mitral value - TREATMENT - Strenuous exercise should be avoided Beta-blockers, Verapamil, or disopyramide are used to reduce symptoms. Digoxin, diuretics and vasodilators are contraindicated. ACUTE PERICARDITIS Causes — Idiopathic, infections (viral), Acute Ml, Metastatic neoplasm, chronic renal failure, SLE, Dressler's syndrome. History- Chest pain, sharp, pleuritic, and positional relieved by leaning forward); fever & palpitations are common Physical examination - Rapid or irregular pulse, coarse pericardial friction tub, which is loudest with patient sitting forward ECG- Diffuse ST elevation (concave upward) usually present in all leads except aVR & V1. PR segment depression may be present OXR- Cardiomegaly if large (250ml) pericardial effusion is present, with ‘water bottle” configuration. Echocardiogram — Most sensitive test fro detection of pericardial effusion. Treatment: Aspirin 650-975mg QID for several weeks depending upon the cause. CARDIAC TAMPONADE life threatening emergency resulting from accumulation of pericardial fuid under pressure, impaired filing of cardiac chambers and decreased cardiac output Causes- Most commonly metastatic tumour, uremia, acute Ml, viral pericarditis, cardiac trauma, myocardial perforation during catheter or pacemaker placement. History — Dyspnea, weakness, confusion. Examination- Tachycardia, Hypotension, pulsus paradoxus, jugular venous distension with Preserved x descent but loss of y descent, heart sounds distant. Beck's triad ~ Hypotension, raised JVP, and distant heart sounds. ECG- Electrical alternant (alternating size of ORS comply due to swinging of heart CXR- Enlarged cardiac silhouette. Echocardiogram — RA & RV collapse during diastole. 9810686970 contact@afmg.co ~ MI 24hr. Helpline 9810608460 visit us at: www.afmg.co.in, E-mail:AFMG Academy for Foreign Medical Graduates Immediate pericardiocentesis and IV volume expansion CONSTRICTIVE PERICARDITIS Rigid pericardium leads to impaired cardiac filing, elevation of systemic and pulmonary venous pressures, and decreased cardiac output. Causes: Tuberculosis is the most common cause in India. Viral, uremia, neoplastic Pericarditis are other common causes, (Imp- Rheumatic fever never causes constrictive Pericarditis) History — Gradual onset of dyspnea, fatigue, pedal edema, abdominal swelling (Imp-symptoms of LV failure are uncommon) Physical examination ~ Tachycardia, Jugular venous distention (Prominent y descent), which increases further on inspiration (Kussmau's sign), Hepatomegaly, pedal edema, ascites are common. Pericardigl- knock following Sa sometimes presents. / ECG- Low limb voltage, atrial antyahmnias are gommoh, t eo CXR- Rim of pericardial classification in up to 50% of patients. Echocardiogram.- Thickened pericardium, normal ventricular contraction, abrupt halt in ventricular filling in early diastole. CT or MIR is more precise than echocardiogram. Treatment — Surgical stripping of the pericardium. Acute Myocardial Infarction Chest pain similar to angina but is more intense and persistent (*30 minutes) 25% of the Ml are clinically silent Silent Ml occurs in diabetic patients and elderly Physical examination 7 - Palllor, diaphoresis, Tachycardia S4, dyskinetic cardiac impulse may be present IF CHF is present, S3, released present RVMI: JVP is raised ECG. Quwave MI Non- Q-wave MI Cardiac enzymes Myoglobin is the first enzymes to rise ~ Creatinine phosphokinase (CK) rises within 4-8 hours, peaks at 24 hi returns to normal by 48-72 hours. 24hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, E-mail: contact@afmg.co MiAFMG Academy for Foreign Medical Graduates - CK-MB is more specific for MI - CK-MB mass: (K activity > suggests acute Ml) - CK MB2: CK MBI > 1.5 very specific ~ Tropin T and Troponin | are more specific and remained elevated for 10-14 days after MI Treatment 1. Relief of pain (Morphine 2-4 mg iv) 2. Aspirin 160-325 mg to be chewed 3. Early thrombolysis with streptokinase is essential in ST elevation MI Dose STK =1.5 milion units tpA-100 mg Contraindications to thrombolysis - _H/O cerebrovascular hemorrhage at any time - Anonhemorrhagic stroke or TIA is past one year - Marked hypertension BP> 180/110 mmHg - Suspected aortic dissection Active internal bleeding (excluding menses) - Known bleeding diathesis - Active peptic ulcer disease ~ Recent (<2week) invasive or surgical procedure or CPR (> 10minutes) - Pregnancy Patient should not receive STK if that agent had been received within the precedmg 5 days to 2 years 4. Pecutaneous Transluminal Coronary Angioplasty (Primary PTCA is indicated in) - _ Patients with contraindications to thrombolysis - Cardiogenic shock - Pt 70 years old and in Hypotension Rescue angroplasty, Elective angioplasty B-blockers Heparin ACE inhibitors 9. Lipid lowering drugs (if LDL>130 mg/dl) Complication of Acute Myocardial Infarction 1. Bradyarrhythimias and AV block a. Inferior Ml-Heightened vagal tone If hemodynamically compromised treat with atropine 0.5 mg IV q 5 mi 2 mg). If no response use temporary external or transverse pacemaker Sx Oa 24hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, E-mail: contact@afmg.co.in I MAFMG Academy _for Foreign Medical Grad b. Anterior MI-AV conduction defects usually represent ext ive tissue necrosis consider temporary external or transverse pacemaker for i. Complete heat block ji, Mobitz type ll block fii, New bifascicular block 'v. Any bradyarrhythmia associated with Hypotension or CHE 2. Cardiogenic shock Severe IV failure - Systolic BP<80 mmHg - PCWP> 18 mmHG - Cardiac index < 1.8 Limin jm2 Treatment 1. Swan -Ganz catheter & intrarterial BP. Monitoring 2. Intraortic ballon pump counterpulsation may be necessary for maintaining BP. 3. Primary PTCA improver the outcome markedly. 3. Acute Mechanical complication Ventricular septal defect and acute mitral regurgitation due to papillary muscle ischemiafinfarct occur during the first week following Ml They are characterized by sudden onset CHF and new systolic murmur Treatment: - ~ Acute medical therapy requires vasoditates therapy (IV nitroprusside) ~ _Intraaortic ballon pump may be required ~ Surgical correction is postponed for 4-6 weeks after acute MI in stable patients. 4. Pericarditis: Pleuritic positional pain associated with pericardial sub, Atrial arrhythmias are common Treatment 1. Aspirin 650 mg qid 2. Withhold anticoagulants 5. Ventricular Ancurysm ~ Localized bulge of LV chamber due to infracted myocardium - True aneurysm — Consists of scar tissue ECG-Persistent ST elevation >2 weeks after initial intact CHF-Thrombs formation and ventricular arthythimias can occur ‘Thrombus within the aneurysm, or large aneurysmal segment due to anterior Mi, warrants oral anticoagulation with warfarin for 3-6 months. 24hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, E-m contact@afmg.co V }oAFMG Academy for Foreign Medical Graduates _ Pscudoancurysm — A form cardiac rupture contained to local area of pericardium and organized thrombus surgical repair is usually necessary to prevent rupture. 6. Dresslar's syndrome — Autoimmune etiology ~ _ Itis characterized by fever, pleuritic chest pain, and pericardical effusion. - Pericarditis is of fibrinous type Treatment 1. Aspirin 650 mg QID 2. Glucocorticoids in refractory cases. Avoid within first 4 weeks after MI. Atrioyentricular Block 1. First Degree Prolonged constant PR interval (>0.20sec) May be normal or secondary to increased vagal tone or digitals. No treatments required, 2. Second Degreé Mobitz | (Wénckebach)- i /f 5 es i Narrow QRS, progressive increase in PR interval until a ventricular beat is dropped then sequence is repeated. Itis seen with drug intoxication (digitalis, beta blockers), increased vagal tone, inferior MI. itis usually transient and no treatment is required. It symptomatic atropine IV 0.6 mg or temoporary pacemaker Mobitz tl- Fixed PR interval with occasional dropped beats, the ORS complex is usually wide. It is seen in Ml or degenerative conduction system disease. It may progress suddenly to complete AV block, pacemaker is indicated 3. Third degree (Complete AV block) Absial activity is not transmitted to ventricle atria & ventricle contract independently, t is seen in MI, digitalis, toxicity, and degenerative conduction system disease. Permanent pacemaker is indicated except when associated transiently with inferior MI or in asymptomatic congenital heart block. Class | indication for implantation of a permanent pacemaker 1. Atrioventricular block a. Third — degree AV block associated with symptoms ©. Third-degree AV block with pauses > 3 sec or with an escape rate < 40 beats per minute in awake patient. Postoperative AV block Second-degree AV block associated with symptoms ©. Chronic bifascicular or trifascicular block with intermittent third deg block or type II second -degree AV block. 24hr. Helpline 9810608460, 9610686970 ‘ visit us at: www.afmg.co.in, E-mail: contact@afmg.co.in I)AFMG Academy for Foreign Medical Graduates 2. AV block associated with myocardial infarction a. Second or third degree AV block in His ~ Purkinje system 6. Transient second or third degree intranodal AV block and associated bundle branch block ¢. Persistent symptomatic second or third degree AV block 3. Sinus Node Dysfunction a. Symptomatic sinus Bradycardia or sinus pauses b. Symptomatic chronotropic incompetence 4. Carotid sinus syndrome - Recurrent ‘syncope or near syncope 24hr. Helpline 9810608460, 9810686970 R visit us at: www.afmg.co.in, E-mail: contact@atmg.conin ” MBBSHELAFMG Academy for Foreign Medical Graduates CARDIOLOGY PART RHEUMATIC FEVER Group A streptococci (Lancefield Classification) Peak incidence 6-15 years of age more common in society & economically backward population Serotype 1,3,5,6,8 is most commonly associated Jones criteria for RF (Updated in 1992) Major criteria Carditis Migratory polyarthritis Sydenham’s chorea dus nodules -———? 5. Erythemé marginatum _| Minor criteria Roopa ‘Subcuten 1. Clinical Fever - Arthaigia 2. Laboratory ~ Elevated acute phase reactants - Prolonged PR interval Plus Supporting evidence of a recent group A streptococcal infection (e.g positive throat culture or rapid antigen detection test; and /or elevated or increasing streptococcal antibody test) ~ _ Migratory polyarthritis is the most common presentation (75% of patients) ~ _ Milral valve involvement is the most common, followed by aortic valve. ~ Rheumatic Pericarditis does not lead to constrictive Pericarditis, ~ Sydenham’s chorea occurs several months after intial streptococcal infection ~ 80% of the. patients with acute fever have raised antistreptolysin O titer at presentation. Treatment 1. Anti streptococcal therapy 2. Therapy for clinical manifestation s Secondary prophylaxis 1. Benzathine penicillin G 1.2 units i.m once every 4 weeks 2. Oral peniciliin V 250 mg BD 3. Oral sulfadiazine 1.0 gm daily 24hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, E-mail: contact@afmg.co MiAFMG Academy for Foreign Medical Graduates 4. Oral erythromycin 250 mg BD RF with Carditis 10 years or at least until age 40 RF without Carditis - 5 years or until 21, whichever is longer Valvular Heart Disease Mitral stenosis Most common etiology is rheumatic heart disease More common in females Critical MS is valve area < 0.6 cm’/m? BSA Manifestation: Principal symptoms are dyspnoea and pulmonary edema precipitated by fever, excitement, anaemia pregnancy etc. - _Palpable SI; opening snap (OS/follows A2 by 0.05 to 0.12 sec) - _A2-0S interval in inversely proportional to severity of obstruction - Duration of the murmur correlates with severity of obstruction ECG -Artial fibrillation, LA enlargement when sinus rhythm is present, RAD and RVH when pulmonary HT is present. CXR-LA and RV enlargement and-kecley Blines. 4 Echocardiogram -Madequate Separation, cal fey and ticking of en Valve area can be calculated. 5 tg Treatment 1. Prophylaxis for rheumatic fever infective endocarditis. 2. Medical therapy for heart failure. 3. Digitalis, Beta blockers, or Verapamil to slow ventricular rate in AF 4. In uncomplicated MS, percutaneous baloon mitral valvuloplasty is the procedure of choice. Closed and open surgical valvotomy 6. Mitral valve replacement. Mitral Regurgitation RHO, mitral value prolapse, IHD with papillary muscle dysfunction, hypertrophic cardiomyopathy, infective endocarditis, congenital Manifestations - Fatigue weakness and exertional dyspnoea. - Soft SI, loud holosystolic murmur - $3 are common findings - Hyperdynamic apex 24hr. Helpline 9810608460, 9810686970 * 14 visit us at: www.afmg.co.in, E-mail: contact@afmg.co.inAFMG Academy for Foreign Medical Graduates _ Echocardiogram: Enlarged LA: Doppler is helpful in diagnosing and assessing severity of MR Treatment 1. Diuretics and digoxin 2. After load reduction (ACE inhibitors, Hydralazine on iv nitroprusside) 3. Prophylaxis for endocarditis. 4. Surgical treatment, either mitral repair or Teplacement in the presence of symptoms or evidence of LV dysfunction a. LVEF < 60% or b. End -systolic LV diameter > 45 mm/m, Mitral valve prolapse Idiopathic, Marfan syndrome. Redundant mitral valuve tissue with myxomatous degeneration and elongated chordae tendinea Manifestation More common in females - Most patients are asymptomatic ~ Atypical chest pain and SV and ventricular arrhythmias are common. - Most imporfant is severe MR resulting in LV failure - Sudden death is very rate complication ~ Mid or late systolic click followed by late systolic murmur exaggeratedby valsalva and standing Echocardiogram Posterior displacement of posterior mitral leaflet late in systole Treatment 1. Asymptomatic pts should be reassured 2. Prophylaxis for IE in pts with significant Valve repair on replacement for pts with severe MR Aortic Stenosis Congenital, RHD, idiopathic calcification AS in elderly — More common in males Manifestations - _ Dyspnoea, angina, and syncope are cardinal symptoms ~ _Heaving apex, soft A2, S4 common, crescendo-decrescendo systolic murmur ECG & CXR -LV hypertrophy Echocardiogram — Thickening of LV wall, calcification and thickening of aortic valve cusps. Critical AS, valve area < 0.5 cm2/m2 BSA Treatment 4. Avoid strenuous activity 2. Treat heart failure but avoid after load reduction 24hr. Helpline 9810608460, 9810686970 Is visit us at: www.afmg.co.in, E-mail: contact@afmg.co.inAFMG Academy for Foreign Medical Graduates 3. Surgical replacement of valve is indicated in - Symptomatic patients with angina, syncope on heart failure eae ee - Value area < 0.5 em2im2 - Peak systolic pressure gradient, 50 mmHg Prognosis: IN patients not treated surgically the average time to death after onset of various symptoms is Angina - 3years : Syncope -3 years Dyspnoea - 2 years CHF- 1.52 years Aortic Regurgi nm More commen in males, Rheumatic in 70%, syphilis, and infective endocarditis are other causes. Manifestations Exertional dyspnoea and awareness of heart beat angina pectoris, and signs of LV failure collapsing pulse, Quincke's sign, de Musset’s signs pistol shots over femoral artery are common Decrescendo, diastolic, blowing murmur along left sternal border. Austin flint's murmur. Echocardiogram LV & LA enlargement. Doppler studies are careful in detection and quantification of AR Treatment 1. Standard therapy for LV failure 2. Surgical therapy is indicated in ‘Symptomatic patient - Asymptomatic points with LV dysfunction i. Surgical therapy is indicated in = Symptomatic patient - Asymptomatic pts with LV dysfunction i, LVEF < 55% ji, LV end systolic volume > 55 mlm, ili. LV end systolic diameter > 55 mm TRICUSPID STENOSIS - Usually rheumatic, most common in females, almost invariably associated with MS. - Hepatomegaly, ascites, edema, jaundice, jugular venous distension with slows by decent. g ~ Diastolic rumbling murmur along left sternal border increased by inspiratio presystolic component. 24hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, E-mail: contact@afmg.co. 16AFMG Academy for Foreign Medical Graduates ~~ Right atrial and superior vena caval enlargement on x-ray Severe Ts requires valve replacement surgery. TRICUSPID REGURGITATION ~ Usually functional and secondary to marked RV dilatation of any cause often associated with pulmonary hypertension ~ Severe RV failure, hepatomegaly and prominent s wayps in jugular venous puise - Systolic murmur along sternal ah is hreas hdl by ity - Intensive diuretic therapy is useful tion (Carvallo’s sign) Infective Endocarditis Acute Hectic febrile illness associated with damage to cardiac structures, seeding of extracardiac sites, and progression to death within weeks if left untreated. Subacute — Indolent illness associated with slow or no destruction of cardiac structures and rare Metastatic infection Etiology Acute- Staphylococcus aureus ‘Subacute — streptococcus viridans Early PVE — Coagulase negative ‘staphylococcus IV drug user — Staphylococcus aureus Late onset PVE -Streptococous viridans. 24hr. Helpline 9810608460, 9810686970 visit us at: www.afmg.co.in, E-mail: contact@afmg.co. M ieAFMG (Medicine) (Academy for foreign Medical Graduates) Respirato tem Chest Examination Condition Percussion Frenitus Breath Voice Adventitious sounds transmission sounds Consolidation Dull Increased Bronchial + Whispered Crackles pectoriloquy Asthma Resonant Normal Vesicular Normal Wheezing Interstitial lung Resonant Normal Vesicular. Normal Crackles disease Pneumothorax Hyper Decreased Decreased Decreased Absent resonant Pleural effusion Stony dull Decreased Decreased Decreased; Pleural rub. egophony at upper part Disturbance in ventilatory functions Two major patters are restrictive and obstructive patterns. In obstructive pattern + Hallmark is decrease in expiratory fl «Ratio FEA1/FVC is reduced + TLC igrormal or increased « RVis elevated due to trapping of air during expiration of air during expiration. In Restrictive pattern ¢ Hallmark is decrease in TLC ad (== * May be caused by pulmonary parenchymal disease or extraparenchymal. * Pulmonary parenchymal Reduced RV, Extraparenchymal - Increased RV Obstructive * Asthma * Chronic obstructive lung disease (chronic bronchitis, emphysema * Bronchiectasis * Cystic fibrosis © Bronchiolitis 24hr. Helpline 9810608460, 9810686970 www.afmg.co.in Pn pn ey teAFMG (Medicine) (Academy for foreign Medical Graduates) _ Restrictive Parenchymal Extraparenchymal * Sarcoidosis - Neuromusculer * Pneumoconiosis - GBS * Interstitial lung disease - Myasthenia gravis - Chest wall - Kyphoscoliosis - Obesity - Ankylosing - Spondylitis ASTHMA ~ Increased responsiveness of lower airways to multiple stimuli: episodic, and with reversible obstruction Severs obstruction persisting for days ar weeks is known as status asthmaticus, * Allergic asthma ~ Personal/ family history of alleray - Worsening of symptoms on exposure to allergens. - Skin test to allergens are positive ~ Serum IgE may be high. * Idiosyncratic asthma - No history of allergy - Most patients develop noone after a URI. + Some patients develop attacks of exposure exercife. disorders. * Signs ~ Tachypnea, tachycardia, use of accessory respiratory muscles, cyanosis (in very late stage), pulsus paradoxus, prolongation, wheezing * Silent chest is a sign of poor prognosis. * Sputum examination shows eosinophilia, Curschmann's spirals (casts of small airways), and Charcot- Leyden crystals. * CXR may show hyperinflation. It may show infiltration in ABPA and Churg Strauss syndrome. © PFT-Reduced FEV1/FVC. 24hr. Helpline 9810608460, 9810686970 1G) www.afing.co.iAFMG (Medicine) (Academy for foreigm Medical Graduates) Treatment 1, B adrenergic agonists ~ Epinephrine 0.3ml of 1:100 solution 8.C. - Inhaled route provides most rapid effect, salbutamol, terbutaline may be used 2. Methylxanthines-Theophylline (adjust dose to maintain blood level between 5 and 15 mg/m. 3. Anticholinergics — Inhaled tiotropium and ipratropium, 4. Glucocorticoids 5. Cromolyn sodium and Nedocromil sodium are useful in chronic therapy for prevention, not useful during acute attacks. 6. Leukotriene modifiers: 5-lipooxygenase inhibitors - Zileuton and leuktriene D4 receptor antagonists - Zafirlukast and motelukast are. useful for chronic therapy. They can precipitate Churg Strauss syndrome. OCCUPATIONAL EXPOSURES & PULMONARY DISEASE. 4. Asbestosis - - Exposure occurs in mining milling and manufacture of asbestos products - Asbestosis is a diffuse interstitial fibrosing disease of the lung requiring >, 10 years of moderate to severe exposure. PFT shows restrictive pattem. CXR reveals irregular or linear opacities, greatest in lower lung fields. - Lung cancer can occur 15 to 20 years after asbestos exposure. Smoking substantially increases risk of lung cancer a asbestos exposure. a) plaques and mesqfheliaml can also eS a oe - Exposure occurs in mining, stone cutting abrasive industries, blasting. - Short term high intensity exposure may produce acute silicosis-rapidly fatal pulmonary fibrosis with radiographic picture of profuse miliary infiltration or consolidation. - Longer-term, less intense exposures are associated with upper lobe fibrosis and hilar adenopathy more than 15 years after exposure - Pts with silicosis are at higher than normal risk for tuberculosis, and pts with chronic silicosis and a positive PPD warrant anti tuberculosis treatment. 3. Coal worker’s pneumoconiosis (CWP) - Symptoms of siriple CWP are additive to the effects of cigarette smoking on Ci 24hr. Helpline 9810608460, 9810686970 www.afmg.co.in ais oeAFMG (Medicine) (Academy for foreign Medical Graduates) —__ ~ Xray signs simple CWP are small, irregular opacities (reticular pattem) that may progress to smalll, rounded opacities (nedular pattern), - DLCOis reduced 4. Cotton Dust (Byssinosis) - Chest tightness occurs typically on first day of work (Monday chest tightness) - After 10yrs. Recurrent symptoms are associated with irreversible airflow limitation. ‘Treatment + Avoidance of toxic substance - Acute organic dust exposures may respond to Glucocorticoids. Chronic Obstructive Pulmonary disease Two types co Chronic Bronchitis co Emphysema - Emphysema is characterized by destruction of enlargement of the lung alveoli. ~ Cigarette smoking and a1 antitrypsin deficiency are major causes of emphysema. There are 3 histological subtypes. + Centriacinar (Smokers) * Panacinar (a 1 amtitrypsin deficiency) * Paraseptal — Chronic bronchitis is clinically defined condition with chronic cough and sputum production for at least 3 months in a year for 2 consecutive years. — Cigarette smoking is the most common cause of COPD. — Ried index is based on ratio of thickmess of the submucosal glands to that of bronchial walls. Normal value — 0.44 = 0.09 — In patients with chronic bronchitis -0.52=0.08. Patients with chronic bronchitis have early development of cyanosis and hence also known as “blue bloaters”, — Patients with emphysema do not dewelop cyanosis until very late, types of disease and hence also known as pink puffers. Lab Findings: - : ~The hallmark of COPD is airflow obstruction characterized by reduction in FEV1 and FEV1/FVC ratio on PFT. GOLD criteria for COPD severity 1 Mild FEV1 >80% predicted i Moderate 50%60years) * Comorbid conditions * Altered mental state * Respiratory rate >30min. * Systolic BP < 90 mm Hg * Temperature <38°C or <,40°C. © Pulse > 130/min * PO22/SroF Upper limit of Exudate Transudate - CHE - Cirrhosis - Exudate - Nephrotic syndrom Measure PF glucose, amylase PF cytology, and culture PF mark 24hr. Helpline 9810608460, 9810686970 www.afmg.co.in ae et) ee een iaAFMG (Medicine) (Academy for foreigm Medical Graduates) ‘Amylase Elevated Gitucose <60mgidl - Esophageal rupture - Rheumatoid arthritis - Pancreatitis - bacterial infection - malignancy No Diagnosis Y PF adenosine deaminase PCR for MTB Yes No - Treat for TB Pleural biopsy Acute Respiratory Distress Syndrome (ARDS) « Acute diffuse Infiltrative lung lesions of diverse etiologies with severe arterial hypoxemia * Most commen cause is sepsis. Other causes are diffuse pulmonary infections, aspiration, inhalation of toxins and irritaints, narcotic overdose, trauma. * Pathologically there is - Damage to alveolar capillary membrane - Increased alveolar capillary permeability - Pulmonary edema with hyaline membrane - Destruction of type | pneumocytes. - Proliferation of type Il pneumocytes later on. - Pulmonary fibrosis. * Earliest sign is often tachypnea followed by dyspnea. Crackles are audible diffusely. Cyanosis is evident * Chest X- ray shows diffuse, bilateral interstitial and alveolar infiltrates. * _ABG shows reduction of PO, and PCO» with widened alveolar —arterial O, difference. Diagnostic Criteria - PaO, /FIO, < 200 mm Hg - Acute onset - Bil alveolar or interstitial infiltrates PCWP < 18 mm Masts no clinical “at left atrial pressure. <—- ae el. of stmatiom fe jen may suffi but iriansantl mechanical ventilatory support is necessary. 24hr. Helpline 9810608460, 9810686970 www.afmg.co.inAFMG (Medicine) _ (Academy for foreigm Medical Graduates) _ IV Fluids and inotropic agents. - Glucocorticoids may be used Prognosis - Overall mortality rate is 50 %, new ventilator strategies reduce the mortality rate. Arterial blood gas analysis Metabolic acidosis - Reduction in PH, PCO; and HCO.is seen in ABG. - High anion gap © Diabetic Keto acidosis © Lactic acidosis © Poisoning (alcohol, methanol, ethylene glycol, salicylates) © Chronic renal failure Normal anion gap - Diarrhoea - Renal tubular acidosis - _ Ureterosigmiodstomy Treatment - Correct the underlying cause - IVNaHCO3 If PH <7.2 Metabolic alkalos' - PH, PCO, and HCO, all increase om ABG. - Causes - GL causes — vomiting 2 - Nasogastric suction - Diuretic therapy - Adrenal disorders - Cushing's syndrome ~ Hyperaldosteronism - Alkali ingestion -Treatment 24hr. Helpline 9810608460, 9810686970 www.afng.co.inAFMG (Medicine) (Academy for foreigm Medical Graduates) -Correct the underlying cause ~ Mild alkalosis requires Nacl infusion Severe alkalosis requires Hcl and Axcetazolamide Respiratory acidosis — * PCO2 increases, HCO3 increases and pH falls. ° Causes - COPD - Sedative overdose - Severe pulmonary edema - Hypoventilation * Confusion, asterixis and obtundation are common Treatment - Improve ventilation with bronchodilators - Mechanical ventilation may be necessary in acute cases. Respiratory Alkalosis * Reduction in CO2 reduction in HCO3, and increase in PH * Cause - _ Hyper ventilation disorder ( psychogenic ) - Asthma - Fever = Salicylates - Hepatic Failure - Mechanical over ventilation. - Pregnancy + Severe respiratory alkalosis may cause seizures, tetany, cardiac arrhythmias or loss of consciousness. Treatment - Treat underlying cause - _ Inpsychogenic cases, sedation or rebreathing bag may be required. we Fl & cami ons ‘*” Peak incidence 55-69 years of age 24hr. Helpline 9810608460, 9810686970 www.afmg.co.inAFMG (Medicine) : (Academy for foreign Medical Gradu > Most common type is Adenocarcinoma other histologic varieties are squamous cell, large and small cell (oat cell) carcinoma. + Major cause of lung cancer is cigarette smoking. * Central endobronchial tumours cause cough, haemoptysis, wheeze, stridor, dyspnoea, Pneumonitis, peripheral lesion cause pain, cough dyspnoea, symptoms of lung abscess resulting from cavitations. * Dysphagia, hoarseness, Horner's syndrome can occur due to Metastatic spread + Paraneoplastic syndromes = SIADH + Lambert Eaton's syndrome = Hypercalcemia, Stage TNM description ! 11-2 NoMo 11-2 N1Mo MA T3 No-1 Mo HIB 4 or N3, Mo Vv Any Mt Primary Tumor (T) T1 Tumor <3 cm 12 Tumor >3 cm 3 Tumor with extension into chest wall, diaphragm, Pericardium or mediastinal pleura. TA Tumor invading mediastinum or presence of malignant pleural effusion. Reginonal lumph Nodes (N) No - No node involvement Nt - Ipsilateral hilar nodes N2 - Ipsilateral mediastinal nodes. N3 ~ Contralateral hilar/mediastinal nodes or Supraciavicular nodes. Distant Metastasis (M) Mo- No Known distant metastasis. 24hr. Helpline 9810608460, 9810686970 ‘o www.afmg.co.in °AFMG (Medicine) (Academy for foreigm Medical Graduates) M1 — Distant metastasis present. Treatment 4. Non small cell lung cancer Respectable (I, II, IIIA) = Surgery - Radiation therapy for non-operable case Nonresectable (IIIB, IV) i. Radiation therapy / ii. Cisplatin bgeed-ehemothi ny | ‘dear . Surger * as eet ae oy tf ce - Combination chemotherapy is the standard mode of therapy = Combination of radiotherapy to chemotherapy prolongs survival. 24hr. Helpline 9810608460, 9810686970 www.afmg.co.in MBBSHELP.MEDICINE (Academ CONNECTIVE TISSUE DISORDER RHEUMATOID ARTHRITIS A chronic multisystem disease of unknown etiology characterized by persistent inflammatory synovitis, usually involving peripheral joints in a symmetric fashion. Cartilaginous destruction, bony erosions, and joint deformity are hallmarks; the course of RA can be variable. - Women are affected 3 times more often than men are; prevalence increases wilh age, onset most frequent in fourth & fifth decades. _Arlicular manifestations — Symmetric polyarthritis of peripheral joints with pain, tendemess, and swelling of affected joints, moming stiffness is common PIP and MCP joints frequently involved joint deformities may develop after persistent inflammation. Joint determities. © Zdetormity © Swan neck deformity © Boutonneire deformity EXTRAARTICULAR MANIFESTATIONS. - Cutaneous — Rheumatoid nodules, vasculitis = Pulmonary ~ Nodules, pleural disease, Caplan's syndrome (Seropositive RA with pneumonoconiosis) - Ocular~ Keratoconjunetivitis sicca, episcleritis, scleritis. - Hemalological- Anernia, Felty's syndrome (RA + splenomegaly + Neutropenia) - Cardiac — Pericarditis, Myocarditis. ~ Neurologic- Myelopathies secondary to cervical spine disease, entrapment, vasculitis. - Diagnosis is based on ACR criterig-Freurnatoid nk is a ‘inst Fc portion of 196. tis present in 4 gonora ion and B/S cages\of rheunfatoid arttyitis. ts, presence correlde with sbvere exjaarioular dsfase, TREATMENT 1. NSAIDs (Cox -2 selective inhibitors are preferred) 2. Glucocorticoids 3. Disease modifying antirheumatic drugs (DMARDs) Methotrexate, gold salts, hydroxychloroquine, sulfasaizine, d-penicillamine. At present, the preferred agent is methotrexate. Immunosuppressive therapy — Azathioprine, Leflunamide, Cyclosporine, Cyclophosphamide. 5. ‘TNF-a neutralizing agents — Etanercept, Infliximab, Adalimumab. ANKYLOSING SPONDYLITIS Marie-Strumpell disease / Bechterew disease M Onset at 15-25 y PATH: ENTHESITIS Entheses: site of soft tissue (tendinous / ligamentous) attachment to bone Helpline: 9810608460, 9810686970 32 Visit us at: www.aimg.co.in, E-mail: contact @afmg.co.im@BSHE ‘AFMG MEDICINE (Academy for Foreign Medical Graduat Ist manifestation: sacroiliitis Early inv of SI joint -> lower lumbar spine > ascending progression -> upper spine is involved LATE ‘Moming backache with stiffness -> improves with activity; In months --> persistent pain NOCTURNAL PAIN Constitutional features in FEW pts & ELDERLY pts Peripheral joint inv in 30% pts; usually asymmetrical EXTRA-ARTICULAR DISEASES IN AS - Acute anterior uveitis (MC extra-articular manifestation) ~ Aortic Regurgitation; 3rd degree heart block - _Inllarnmatory Bowel Disease Poor prognostic factor: early severe hip inv Disease progresses very slowly in females COMPLICATIONS: Spine fracture, cauda equina syndrome, upper tobe lung fibrosis "Modified New York criteria” used for diagnosis 1. Radiographic sacroilits plus any one of the following 2. History of inflammatory back pain 3. Limited spinal movement 4. Limited chest expansion Treatment: 1. NSAIDs can be used for temporary relief 2. Corticosteroids don't have any role in the management 3. TNF a antagonists like Infliximab and men the only agents which are effective snra of in preyentiig the progressiii OF Gijease but sériols side ptfects of these ageAS prevert bee gt Progi prev 1. _M:F=1:9 (mostly females of age 15-44) +2. UV-B causes flares (sometimes A) = 3, Clinical Features: a. ACR criteria (1992) - Malar rash: FIXED rash, spares nasolabial fold = Discoid rash: raised, scaling + ; atrophic scarring + - Photosensitivity ~ _ Uleers: oral / nasopharynx; usually painloss - Arthritis: NON-EROSIVE - Serosit : pleural effusion / pericarditis / ascites - Renal disorder: proteinuria > 3+ OR > 0.5 g/d OR casts - Neurological manifestations like psychosis, seizures, ‘strokes, excruciating headaches ~ Hematological manifestations: Hemolytic anemia, thrombocytopenia, lymphopenia, leukopenia -Immunotogical: anti- dsDNA / Anti-Sm / Anti-phospholipid antibodies (APLA). ~ ANA: by Immunofluorescence (>1:40) Helpline: 9810608460, 9810686970 33 Visit us at: www.aimg.co.in, E-mail: contact@afmg.co.iniae@ AFMG MEDICINE (Academy for Foreign Medical Graduates) reqt liagnosis 0 Disease characteristically has periods of remission and exacerbation ‘Systemic symptoms (common to all CTD) : fever, fatigue, weight loss, anorexia ‘Symmetrical, non-erosive arthritis + myopathy ’ Alopecia 5. DLE: scalp, ears, face; sun-exposed areas a. -Circular lesions with raised, scaly, erythematous margins; with central atrophy & scarring 1. DRUG-INDUCED LUPUS: 1. Procainamide , 2. Hydralazine 3. INH Drug induced lupus Vs. Idiopathic lupus Met ANA, Anli-histone antibodies are present. Anti-dsDNA, hypocomplementemia, CNS and renal disease are not seen LUPUS INDUCING DRUGS ARE NOT CONTRA-INDICATED IN PATIENTS WITH IDIOPATHIC SLE. ANTIBODIES RELATED TO SLE Most sensitive antibody for SLE: ANA (98%) Most specific for SLE: anti Sm (only 20%) Anti-dsDNA: assoc with nephritis Anti-Sm: ‘relatively specific for SLE Anli-Roo: Heart block, elderly, neonatal lupus, sjogren’s, ana —ve lupus Anti-La: always assoe with ar i-Ro; lower tisk for nephritis AAPLA include: Lupus Anticoagulant, Anti Cardipfipin, ant 82 glycoprotein 2. MIXED comecfive su TISSUE DISE! / fo | = Females in 1 rd decades -Consists of features of Sclerodema, SLE, Rheumatoid arthritis, Polymyositis ~MC presents with features of Scleroderma - MC cause of death is PAH Characteristic antibody: Anti-U1 RNP (Ribonucleoprotein) VASCULITIS SYNDROMES: 1). Polyarteritis Nodosa (PAN) Classic type Microscopic type © Classic type never involve lungs * Microscopic Polyangitis involves lungs * PAN shows -HbsAg 4ve in 30% cases * Diagnosis by - biopsy, TESR, anemi Hyporgammaglonulinemia 2). Chure- Strauss disease: - this is granulomatous vascults with eosinophilia Helpline: 9810608460, 9810686970 1BBS Visit.us at: www.afmg.co.in, E-mail: contact@afmg.co.il’ >AFMG MEDICINE (Academy for Foreign Medical Graduates) infiliratés in tung fields on CXR Clinical course is dominated by recurrent attacks of bronchial asthma ~ _ This disease can be precipitated or unmasked by use of Montelukast and Zafirlukast Most common cause of death is myocardial involvernent - Treatment: Steroids 3). Wegener's granulomatosis: _- It is characterized by Vasculitis in upper & lower respiratory tract Pulmonary cavities + glomerulonephritis ~ _ Diagnosis: Biopsy of the lung is the best. Kidney biopsy and cANCA antibodies can also be used. - Treatment: Cyclophosphamide and Prednisone 4),Giant cell arterit - Also known as temporal arteritis ~ Involves medium & large sized artery ~ Occurs in elderly fernale & in familial - CIF fever / headchae / anaemia (1 ESR ~ _ Diagnosis:- Temporal artery biopsy ~ Treatment: Sterokis 5). Takayasu's arteritis: - aortic arch syndrome ~ _ Painin arteries associated with loss of pulse - AR Ieardiomegaly / CCF MTN + Death due to CCF / CVA - Diagnosis: - aortogram / TESR / tigG. ~ Treatment: Steroids; Methotrexate can be added in cases not responding to steroids. 6) Kawasaki disease: - mucocutaneous lymph nodes syndrome Acute febrile multisystem disease in children Associated with: . ~ Coronary artery aneurysm - CCF /Ml ~ Edema of mucosal fining of lip, mouth ~ Congested conjunctiva ~ Treatment: Intravenous immunoglobulins 2mg/Kg body weight as single slow iv infusion plus aspirin 100 mg/Kg bw daily for 14 days - Steroids are not beneficial. 7). Bechet’s - More common in young males ~ Associated with HLA BS: - _ Diagnosis: Oral ulcers plus any 2 of the following: -__ Recurrent genital ulcers Helpline: 9810608460, 9810686970 35. Visit us at: www.afmg.co.in, E-mail: contact @aimg.co.inais ease:* @ ae $ AFMG MEDICINE ‘ Eye lesions ‘ ~ Skin lesions - Pathergy test ‘ CNS involvement is the most serious manifestation ( 10-20% of cases can develop recurrent DVT Treatment: Thalidomide is the most effective agent for oral ulcers, |! Steroids are indicated only in cases of uveitis. Patients with recurrent DVT should be managed with oral anticoagulant therapy. Helpline: 9810608460, 9810686970 36 tus at: www.afmg.co.in, E-mail: contact @afmg.co. isnt ELP.C!AFMG MEDICINE n Medical Graduates NEUROLOGY Cranial nerve Exam CN (Olfactory) ~ Occtude each nostril sequentially and ask pt of gently shift and correctly identify @ mild test stimulus, such correctly identity a mild test stimulus, such as soap, toothpaste, cotfee or lemon, CN (Optic) ~ Check visual acuity with or without correction using a snellen chart (distance) and Jaeger’s test type (near). Map visual fields by confrontation testing in each quadrant of visual field for each eye individually. Light reflex (direct and consensual) CNL IV, VI (Oculometor, trochlear and abducens) ~ Direct and consensual light reflex and convergence. Ask pl. Follow your finger as you move it horizontally to left and right and vertically with each eye. GN (Trigerminal)- Fee! the masseter and temporalis muscles as pl. Bites down and test jaw opening, protrusion, and lateral motion against resistance. Examine sensation over entire face and comeal reflex should be tested. CN Vil (Facial)- Look for asymmetry of face at rest with spontaneous as well as emotion-induced (e.g. laughing) movements. Test eyebrow, elevation, forehead wrinkling, eye-closure, smiling , frowning. Taste on the anterior two thirds of tongue can be affected by lesions of the VII CN Proximal to the chorda tympani. CN VIII (Auditop “check ability to earthy fork. Ct eck \for airjvs, mastoid bone gomduction> (Rinne) and tderaization of anion on the onl id (Weber, lee Laas acta ONIX, X (Glossopharyngeal, Vagus)- Check for symmetric elevation of palate-uvula with Phonation (‘ahh’), as well as positions of uvula and palatal arch at rest. Sensation in region of tonsils, posterior pharynx and tongue may also require testing. Gag rellex should be tested, La ie CN XIl (Hypogiossal) — Examine bulk and power of tongue. Look for deviation of tongue with protrusion. MOTOR EXAM Power 0 Nomovernent 1 Flicker or trace of contraction 2 Movement prosent but cannot be sustained against gravity, e 10608460, 9810686970 37 pline: tus at: www.afmg.co.in, E-mail: contact @atmg.co.in MBBS!MEDICINE al pplied resistance. Movement against some degree of resistance Graduates ‘Movement agai Full power. Loss in bulk and size of muscle (atrophy) should be noted. Tone should be evaluated and Presence of rigidity be evalualed and presence of rigidity or spasticity should be identified, Deep tendon reflexes should be tested. Biceps (L5, 6) triceps (7,8), Supinator (6,6) patellar (L2, 34), ankle (S1, 2) The plantar reflex should be tested by using a blunt ended object such as the using of a key to stroke the outer border of the sole of the foot frorn the heel towards the base of the great toe. ‘An abnormal response (Babinski sign} is extension of the great toe at the metatarsophalangeal joint. Normal response is flexion of toes. Sensory Exam: Itis sufficient to test sensation to pinprick, touch, position , and vibration in each of the four extremities. Discase of the spinal Cord Approach to the patient General considerations Spinal cord anatomy relevant to clinical signs. The spinal cord is a thin, tubular extension of the central nervous system contained within the bony spinal canal, The spinal cord is somatotropically organized consisting of 31 segments, each containing an exiting ventral motor root and entering dorsal sensory root. During embryologic development, growth of the cord lags behind that of the vertebral column, and in the adult the spinal cord ends at approximately the first lumbar vertebral body. The approximate relationship b/w spinal cord segments and the corresponding vertebral is as follows. Spinal Gord level | Corresponding vertebral bday > Upper cervical | Same as cord level Lower cervical | 1 level higher Upper thoracic | 2 levels higher Lower thoracic | 2 to 3 levels higher Lumbar THo-TI2 Sacral Tau Coceygeal u Features suggestive of spinal cord involvement: While approaching a patient with Neurologic disorder (esp. of UMN) type), there are certain features, which suggest the involvement of spinal cord. * Presence of paraplegia of quadriplegia Helpline: 9810608460, 9810 Visit us at: wwwafmg.co.in, E-mail: contact@afmg.co.in MBBSHMEDICINE Acade Presence of a definite sensory ievel + Brown Sequard syndrome Bladder bowel involvernent Level of the Lesion — The presence of a level below which sensory, motor, and/or autonomic funclion és distributed is a hallmark, of spinal cord disease. A sensory level is sought by asking the patient to identify as sharp a pinprick stimulates or as cool a cold stimulus applied to the low back and sequentially moved up toward the neck on each side, The uppermost level of a spinal cord lesion is often localized by attention to segmental signs corresponding to disturbed motor or sensory innervations by an individual cord segment, Various cord syndromes, The anatomic relationships of various fiber tracts and nuclei produce distinctive clinical syndrome that are pathognomonic of spinal disease and that often provide clues to the underlying disease process Brown-Sequard Hemicord Syndrome — this syndrome consists of ipsilateral weakness (pyramidal \ract) and loss of joint position and vibratory sense (posterior column), with contralateral loss of pain and temperature sense (spinothalamic tract) below the lesion, Central Cord Syndrome - this syndrome results from disorders of gray matter nerve cells and crossing spinothalamic tracts near the center canal. In the cervical cord, the central cord syndrome produce ‘21m weakness out of proportion to leg weakness and a “dissociated” sensory loss consisting of loss of pain and temperature sense over the shoulders, lower neck, and upper trunk with intact light touch, Joint position, and vibration sense. Trauma, syringomyelia, tumors and anterior spinal artery ischemia are common causes of the central cord syndrome. Anterior Two-thirds syndrome: This syndrome resulls form extensive bilateral disease of the s| cord thal spares the posterior columns. All spinal cord functions motor sensory and autonomic are lost below the level of the lesion, with the: ga exception of i eae ind position sensation, The etiology is vasoylar, either ttronboen Baar lism of the ~e jin “7 fotipmee po ae vessel by mass lesions within the spinal c ‘ntramedullary and Extramedullary Syndromes: the diagnosis of spinal cord disorders frequently requires that intramedullary processes, which arise within the substance of the cord, be distinguished form extramedullary processes that compress the spinal cord or ils vascular, supply. With extramedullary lesions, radicular pain is often prominent, and there is early sacral sensory loss (lateral spinothalamic tract) and spastic weakness in the legs (corticospinal tract) due to the superficial location of these fibers in thee lateral spinal cord, which renders them susceptible to external compression. With extramedullary lesions, the distinction between extradural masses is important, as the former are generally malignant and the later benign, a long duration of symptoms favors an intradural origin. Specific Locatizing sings Semvical Cord: High comvical cord lesions are frequently life threatening, producing, Helpline: 9810608460, 9810686970 Visit us at: www.afmg.co.in, E-mail: contact@afmg.co.in ‘ MBBSHMEDICINE, weakness of respiratory muscles innervated by the Phrenic nerve (C3-C8), Lesi 5 pr ‘quadriplegia with preserved respiratory {unetion. tn general cervical cord disorders are best localized by the pattern of weakness that ensues, whereas sensory loss has less localizing value. Thoracic cord: Lesions of the thoracic cord are best localized by identification of a sensory level on the trunk. Weakness of the legs and disturbances of bladder, bowel or sexual function may also accompany damage to the thoracic cord. Lumbar cord: The lumbar and sacral cord segments progressively decrease in size, and focal lesions of these segments are less easily localized than in cervical and thoracic regions. Sacral cord/Conus Medullaris: The conus medullaris is the tapered caudal termination of the spina cord, comprising the lower sacral and single coccygeal segments. Isolated lesions of the conus medullaris spare motor and reflex, functions in the legs. It consists of bilateral saddle anesthesia, prominent bladder and bowel dysfunction and impotence. Cauda equina lesions are characterized by severe low back or radicular pain, asymmeliic leg weakness of sensory loss, variable arretlexia in the lower extremities, and relative sparing of bowel and bladder function, Mass lesions in the lower spinal canal may produce a mixed clinical picture in which elements of both cauda equina and conus medullaris syndromes are present. Seizures and Epilepsy A seiawe is a paroxysmal event due to abnormal, excessive, hypersynchronous discharges from an aggregate of CNS neurons. Epilepsy is diagnosed when there are recurrent seizures due to a chronic, underlying process. Common causes 1. Neonates (< 1 mo) Perinatal hypoxia of ischemia Intracranial hemorrhage of trauma 2. Infanis.& children (@ Imo & 96 yrs) Cerebrovasular disease Brain tumour Alcohol withdrawal Simple partial seizures = Do not affect consciousness and may have motor, Sensory, autonomic, or psychic symptoms. Complex partial seizures - Include alteration in consciousness coupled with Automatisms (2.9. lip smacking, chewing ete.) Tonic-clonic seizures (grand mal) ‘ ~ Cause sudden loss of consciousness, loss of Posture control, tonic muscular contraction Producing teeth clenching, Helpline: 9810608460, 9810686970 40 Visit us at: www.afmg.co.in, E-mail: contact@afmg.co.in MBBSHAFMG MEDICINE, foreign Medical Graduates ) Followed by rhythmic Muscular jerking (clonic phase). Headache & Confusion are common postictal phenomenon, Absence seizures (Petit-mal) + There is sudden, brief impairment (5-10 seconds) Of consciousness without loss of postural conto. Other types - Infantile spasms, myoclonic seizures. Treatment: - Primary @TCS ~ Valproic acid -+ Lamotrigine — Phenytoin Partial = Carbamazepine Phenytoin Valproie acid Absence ~~ Valproie acid ~ Ethosuximde Aiypical absence, myoclonic Valproic acid Lamotrigine Patients with certain epilepsy syndromes (e.g. temporal lobe epilepsy) are often refractory to medical therapy and benefit from surgical excision of the seizure focus TREATMENT OF STATUS EPILEPTICUS Lorazepam (0.1 mg/kg IV at 2 mg/ min) Seizures continuing Phenyloin 20mg /kg IV infusion in NS @ 50 mg/min Seizures continuing Phenytoin addition 5- 10 mg / kg IV infusion Seizures continuing Phenobarbital 20 mg/kg IV infusion @ 60-75 m/min Seizures continuing . Phenobarbital additional S- 10 mg/kg Seizures continuing Anaesthesia with midazolam or Propofol ALZHEIMER'S DISEASE 1 Most common cause of dementia 2 Sublle recent memory loss, progressive 3 Death occurs from malnutrition or secondary infections 4 Pathology - Neuritic plaques composed of A f amyloid; Nourofibilary tangles composed of abnormally phosphorylated tau protein . 3. Rare genetic cause of Alzheimer’s disease is Down's syndrome (trisomy 21) elpline: 9810608460, 9810686970 4 Visit us at: www.afmg.co.in, E-mail: contact@afmg.co.in MBBS!AFMG MEDICINE, Academy for foreign Medical Graduates Treatment Donepezil 5-10 mg /d orally Estrogens in postmenopausal women Behavioural therapy VASCULAR DEMENTIA 1 Multiple stroke-tike episodes (mult-impact dementia). 2. Slowly progressive disease (diffuse white matter or Binswanger's disease). 3 Focal neurological deficits are usually present at presentation. NORMAL PRESSURE HYDROCEPHALUS Presentsasa | : 1. Ataxia 2. Dementia 3. Urinary incontinence: Gait improves in 20-50 % of patients following ventricular shunting, dementia and incontinence do not improve PARKINSON'S DISEASE Parkinsonism consists of 1. Tremor 2. Rigidity 3. Bradykinesia 1 Age of onset - 40-70 years “Pill-rolling* tremor of hands at rest. Cogwheel like rigid ‘Slowness of voluntary movement (bradykinesia) Fixed expressionless face (mask-like face) 2 3 4 5 6 Reduced frequency of blinking 7 Micrographia (small handwiiting) 8. Festinating gait (small steps with stooped posture while walking) 9 In Advanced PD- intellectual deterioration, aspiration pneumonia and bedsores are common. 10. Normal muscular strength, deep tendon reflexes and sensory examination. 11 CT scan, EEG, CSF examination do not reveal any abnormality. 12 Pathology ——- Degeneration of pigmented pars compacta neurons of the substatia nigra in the midbrain resulting in lack of dopaminergic input to striatum. Accumulation of Lewy bodies in neurons. Treatment 1. Levodopa / Carbidopa combination in the dose of 100/25 mg TDS or QID. Itis most helpful. for bradykinesia. 2. Trichexyphenidyi, benztropine are anticholinergic drugs and most use ful for tremors. Helpline: 9810608460, 9810686970 Visit us at: www.afmg.co.in, E-mail: contact@afmg.co.inAFMG ign Medical Graduates y potentiating the ‘elease of endogenous ‘Amaniadine is useful for dopamine. 4 Dopamine agonists (Bromocripiine, pergolide, pramipexole, ropinirole) may delay the emergence of late side effects with Levodopa use. 5. Surgery — Pallidotomy may be used in refractory cases. STROKE Asstroke is the sudden onset of a neurologic deficit from a vascular mechanism Hemorthagic (20 %) Ischemic (80 %) TIA --— An ischemic deficit that rapidly resolves within 24 hours is called transient ischemic attack, RIND -— An ischemic deficit that resolves within 7 days after onset is called reversible ischemic neurological deficit. 1 Ischemic stroke is most often due to embolic occlusion of large cerebral vessels, Source of the emboli may be heart, aortic arch, or carotids, 2 Hypertensive bleed typically occurs in © Putamen (most common site) 0 Thalamus CG Pons 0 Cerebellum 1 CT scan without contract is the initial study which is required to rule out hemorrhage or other mass lesion. 2 MAlis better for infarcts. 3. Treatment of ischemic stroke 1. Gradual reduction of BP 2. Osmotic therapy with mannitol in large infarcts. 3. Thrombolysis Ischemic deficit < 3 hours in duration No hemorrhage on CT scan No contrajndicatjons to Thrombpiysis—! | \ fae en Vv ee tissue plasminggemradtivator is uspd fo va is. JJ 4. Anticoagulatior with heparin-is ok paweanes ie stroke— s 5. Antiplatelet agents — aspirin & clopidogrel can be used. 1 For stroke prevention surgery used is carotid endarterectomy in symptomatic severe ({<70%) carotid stenosis. Treatment of Hypertensive bleed 4. Gradual control of BP Neurosurgical evacuation of hemorthage especially in cerebellar hemorthago Mannitol ) Glucocorticoids to reduce cerebral edema Helpline: 9810608460, 9810686970 Visit us at: www.afmg.co.in, E-mail: contact@afmg.co.in 43 MBBSHAFMG MEDICINE, Academy for foreign Medical Graduates dol aan oe 1 Most common cause is trauma. 2. Most common non-traumatic cause is rupture of an intracerebral aneurysm, 3. Sudden onset severe headache, often with transient loss of consciousness at onset, vorniting is common. Focal neurologic deficits are not common, but may result because of vasospasm (Day 4th to 14th). 4 Neck rigidity is common on physical examination. 5 Non-contract CT scan is the initial study of choice. CSF examination is required if. CT is non- diagnostic. F 6 Cerebral angiography is necessary to define the anatomy, location & type of vascular malformation. TREATMENT | q 1. Anticonvulsants- Phenytoin is used. . f 2, Sedation of the patient, 3. Neurosurgical clipping of the aneurysm neck should be done. { 4. Control of blood pressure | 5. Nimodipine is used to reduce vasospasm. MULTIPLE SELEROSIS. : 1 Demyetinating disease of the central nervous system. ‘ 2 Pathologically, the mulitocal-scarred lesions of the MS are termed plaques. 3. Most common presentation is recurrent attacks of focal neruologic dystunction, lasting weeks or months and followed by variable recovery. ( 4. Symptoms often transiently worsen with fatigue, stress, exercise, or heat. 5 Optic neuritis is most common manifestation in India (Devic's Disease) 6 Lhermitte’s symptom, a momentary electric shock-like sensation evoked by neck flexion, ‘ indicates in the cervical spinal cord. Diagnostic Criteria of MS 1. Objective abnormality of CNS on examination. 2, Disease of white matter long tracts usually Involving- pyramidal pathways, cerebellar pathways, medial longitudinal fascictlar, optic nerve. 3. Examination or history must indicate involvement of 2 or more areas of CNS. 4. Two or more separate episodes of worsening involving different sites of CNS, each lasting at least 24 hours and at least 6 months apart. 5. Age of onset 15-60 years. 6. The patient's neurological condition could not be better altributed to another disease. Intranuclear ophthalmoplegia is slowness or loss of adduction in one eye with nystagmus in the abducting eye in lateral gaze. It occurs because of involvement of Medial Longitudinal Fasciculus. Treatment 1._lV methylprednisone follow by oral prednisone for acute attacks. 2. Prophylaxis against relapses: _ a. Interferon Bib Helpline: 9810608460, 9810686970 Visit us at: www.afmg.co.in, E-mail: contaet@aimg.co.inAFMG MEDICINE, Academy for foreign Medical G b. Intericron Gta cc. Copolymer 1 3. Immunosuppressive drugs- - Mitoxantrone, Methotrexate, cyclophosphamide can be used for secondary progressive MS. 4. Spasticity may respond to baclofen, diazepam or tizanidine. 5. Dysesthesia may respond to carbamazepine, phenytoin or amitriptyline, DISEASES OF SPINAL CORD 1. Acute transverse myelitis 1 Sudden onset. 2 Motor and sensory involvement with bladder involvement, 3 Initially, there is spinal shock in which complete flaccid paralysis occurs. Below the level of lesion all reflexes (both Superficial and deep are absent). 4 Later on after gradual recovery from spinal shock UMN signs develop. Thoracic spine is commonly involved. Band like sensation is present at the spinal level. 6 The episodes commonly follow viral infections, vaccination, or may be sclerosis, 7 Treaiment of 1V methylprednisone followed by oral prednisone 2. Syringomyelia 1 Cavitary expansion of the spinal cord resulting in progressive myelopathy. 2 Chiari type 1- Hemiation of cerebellar tonsils into cervical spinal canal + syringomyelia. 3 Chiari type 2 - incomplete closure of spinal canal +syringomyelia. 4 Classic presentation is loss of pain and temperature sensation in neck, shoulders, forearm, or hands with areflexic weakness in the upper limbs and progressive spastic Para paresis, 5 Dissociative anesthesia - Loss of pain & temperature sensation while vibration, proprioception, and fine touch is preserved. 6 Diagnosis is made by MBI. 7 Treatment is surgical. 3. Sub acute combined degeneration (Vitamin B12 deficiency) 1 Earty loss of vibration /position sense, progressive spastic or ataxic weakness, and areflexia ‘due to associated peripheral neuropathy. Babinski sign (due to pyramidal tract involvement) is present with absence of Deep Tendon Reflexes (due to peripheral nerve involvement). 2 Mental changes “megaloblastic madness” may be Present 3. Diagnosis, cbqfimed bya lowsonim-B12 levels. Sok ne levels er peas Methyimdionie acid are eee teGh. ee 4 Folate Supplen tion cipitate Boal ities in a. nated vitamin B12 deficiency. 5 The most common cause of vitamin B12 deficiency is makabsorption. 6 Treatments vitamin replacement (Injection cobalamin 1 mg im. once a week for 8 weeks, thereafter 1 mg once monthly for the rest of life) Muscular Dystrophies Duchene Dystrophy: Helpline: 9810608460, 9810686970 Visit us at: www.afmg.co.in, E-mail: contact@afimg.co.in 4 MBBSHELP.AFMG MEDICINE. Academy for foreign Medical Graduates linked recessive mutation of the dystrophin gene that affects only males. Onset —5 years of age. By the age 12, most children are non-ambulatory. 2 eo Pseudohypertrophy of calf muscles may be present. Survival beyond the age of 25 is rare 10 Lab evaluation, 0 Marked elevation of CPK ‘© Myopathic potentials on EMG. 11 Treatment © Glucocorticoids © Physiotherapy Becker's dystrophy ~ Less severe form of Duchene’s dystrophy. = Gower’s sign, pseudohypertrophy of calf muscles are clinical findings. Myotonic Dystrophy ~ The mest common adult muscular dystrophy. - Autosomal dominant ~ Onset -2” to 3" decade: - “Hatchet Face” appearance - Frontal boldness, posterior subcapsular cataract, gonadal atrophy, respiratory and cardiac problems. - Myotonia manifests as a peculiar inability to relax muscles rapidly following a strong exertion. - Treatment © Phenytoin to relieve myotonia © Pacemaker insertion for complete heart block. Limb Girdle muscular Dystrophy Most LGMDs are progressive and affect primarily the pelvic and shoulder girdle muscles. Respiratory insufficiency form diaphragm weakness may occur. In some patients, cardiac involvement results in congestive heart failure of arrhythmias, occasional patients present with a cardiomyopathy, intellectual function remains normal. An elevated serum CK level, myopathic EMG findings, and muscle biopsy features indicative of myopathy represent the characteristic change in limb-girdle dystrophy. Endocrine and Metabolic myopathies. Thyroid disorders. Abnormalities of i pcican causea iy of muscle} 15 thyrdid hormones So (50 timtate cnotoeres pi in iusce, iherease oar for vita rae ice muscle Lome to circulati rercatécholamines> Hypothyroidism: Hypothyroid patients have frequent muscle complaints, and proximal muscle ‘weakness occuts in about one-third of patients. Muscle cramps, pain, and sliffness occur commonly. ‘The relaxation phase of muscle stretch reflexes is characteristically prolonged. The serum CK level is ‘often elevated (up to 10 times normal), even when there is minimal clinical evidence of muscle Helpline: 9810608460, 9810686970 Visit us at: www.afmg.co.in, E-mail: contact@afmg.co.inAFMG MEDICINE, Academy for for n Medical Graduat disease. Hyperthyr ism: Thyrotoxic patients commonly have proximal muscle weakness and atrophy on examination, but they rarely complain of the deficit, Muscle stretch reflexes are preserved and often brisk. Serum CK levels ate ow in Thyrotoxic myopathy. The muscle histology usually shows only atrophy of muscle fibres. Parathyroid disorders Hyperparathyroidism: Muscle weakness is an integral part of primary and secondary heperparathyroidism. Proximal muscle weakness, muscle wasting, and brisk muscle stretch reflexes are the main features of this endocrinopathy. Serum Ck levels may be increased secondary to muscle damage following Tetany. Adrenal disorders, Conditions associated with glucocorticoid excess cause a myopathy and, in fact steroid myopathy is the most commonly diagnosed endocrine muscle disease, Muscle wasting may be striking. The clinical picture is one of persistent muscle weakness Serum CK levels may be elevated and a muscle biopsy may demonstrate degenerating fibers, some with vacuoles, Vitamin deficiency Vitamin D deficiency due to either decreased intake, decreased absorption, or impaired vitamin D metabolism (as occur in renal disease) may lead to chronic muscle weakness, systemic illness such as chronic respiratory. Cardiac or hepatic failures are frequently associated with severe muscle wasting and complaints of weakness. Strength testing often demonstrates mild weakness in such patients. There is proximal limb weakness with bone pain. Toxic myopathies Other drugs may include generalized muscle weakness; particularly affecting the proximal muscles, chloroquine administration may cause a vaculolar myopathy. (On muscle biopsy, Zidovudine myopathy demonstrates a distinctive pathologic alteration of skeletal ‘muscle, affecting mitochondria and resembling ragged red fibers. Drug induced myopathy ‘accompanied by proximal weakness occurs with glucocorticoid therapy. The clinical diagnosis of steroid induced muscle weakness can be difficult if the medication is being used to treat an underlying inflammatory myopathy. Common drugs causing true myalagia included Clotibrate, Lovastatin and Gemtibrozil. MOTOR NEURON DISEASE: ~ Amyotrophic lateral sclerosis (ALS) is the cet important of the motor neuron disease. TALS is causeytty degeneration pense olor ngurons at allovale of cluding ant =F hors of the Spinal cofd, brainstem fndtornucte, a oe x. | 2 Ons ets tually mistte with Progressi 3 Common initial symptoms are weakness, muscle wasting stiffness and ane and twitching in muscles of hands and arms. 4 Dysarthria and dysphagia can occur due to brainstem involvement. Fasciculation, hyperreflexia, spasticity, Babinski sign, atrophic limbs are present on physi 47 Helpline: 98 + 9810686970 Visit us at: www.afmg.co.in, E-mail: contact @afmg.co.in MBBSHan oa AFMG MEDICINE, Academy for foreign Medical Graduates examination. 6 No sensory abnormalities/ evidence of bladder involvement is found. 7 ENG provides objective evidence of muscle denervation. Treatment ~ Riluzole can be used, but results are not very good. TUMORS OF THE NERVOUS SYSTEM Brain tumors present with © Progressive focal neurolo: 0 Seizures © Non-focal neurological disorders. Most common tumors are secondaries. Most common site of origin of secondaries is ung. Astrocytomas- Most common primary intfactanial neoplasm. ‘Treatment ~ Surgery for diagnosis and to control masse effect Radiation therapy is useful, Meningiomas ~ Endo-axial mass attached to dura; dense and uniform contrast enhancement is diagnostic. = Total surgical resection of benign meningiomas is curative. Primary CNS Lymphomas = B cell malignancies = Occur in immunocompromized patients (AIDS, organ transplantation) - Present as single/multiple mass lesions most commonly in brain-stem. - Most of these tumors are posit 2 for EBV. In AIDS patients they are present in juals with a CD4 count less than 50/mm? ~ Poor prognosis. - Radiation & combination chenfotherapy. in he patient these tumors avery oor piognosis & survival i thaximum bapefled bythe ube of HAA =f 5 indi Guillain — Barre syndrome or Acute inflammatory Demyelinating Polyneuropathy ‘Acute, ascending usually demyelinating Polyneuropathy. LMN type moior paralysis without bladder involvement (symmetric involvement). Most cases are preceded by vial infections. ‘Sensory symptoms may be present but no sensory signs can be elicited. ween Respiratory paralysis may occur which may require ventilatory support. 6 CSF examination reveals elevated protein level without pleocytosis. Treatment. 1 Plasmapharesis is the treatment of choice. 2. Intravenous immune globulin {IVIG) 400 mg/kg/day for 5 days is the drug of choice. 3 Glucocorticoids are ineffective. Heipline: 9810608460, 9810686970 Visit us at: Www.afmg.co.in, E-mail: contact@afmg.co.inAFMG MEDICINE, ademy for foreign Medical Graduates © Autoimmune neuromuscular disorder resulting in weakness & fatigabilty of skeletal muscles, due to auto-antibodies directed against acetycholine receptors at neuromuscular junctions. © Symptoms are provoked by exertion, (Eyelids, extra ocular muscles, facial muscles, proximal limb muscles (asymmetric) are involved commonly. 0. Reflexes & sensation are normal. 0 May be exacerbated by some drugs like tetracyclines, aminoglycosides, propranolol which causes blocking of neuromuscular junction, G_ Thymoma or thymic hyperplasia is present in % of cases. O Itmay be seen in patients with Grave's disease. Lab. Evaluation * Ach Rantibodies + Tensiton (edrophonium) test. + EMG — Decremental response to repetitive stimulation, © CT'scan chest for Thymoma. + Thyroid function test. Treatment * Pyridostigmine 60 mg TDS orally. + Plasmapharesis & IV immune globulin can be used in acute crisi * Glucocorticoids for long-term use. + Azathioprine * Thymectomy improves the condition is most cases. DID. Lambert — Eaton Myasthenic syndrome Auto-antibodies to calcium channels in pre-synaptic motor norve terminals. Repeated testing increases power & deep tendon reflexes are absent, Associated with small cell carcinoma tung. EMG shows incremental response to repetitive stimulation. Helpline: 9810608460, 70 49 Visit us al: www.afmg.co.in, E-mail: contact@afmg.co.in » MBBS!AFMG MEDICINE _ Academy for Foreign Medic ‘ ENDO ( Anterior pituitary is referred to as the “master gland”, 't produces six major hormones ~ Prolactin, Growth hormone, Adrenocorticotropin hormone (ACTH), Latinizing hormone (LH), Follicle-stimufating hormone (FSH), and thyroid stimulating hormone (TSH). PITUITARY TUMORS: “ Benign monoclonal tumors = Most common are nonfunctional. Amongst the functional, prolactinomas are the most common. - Adenomas are classified as Microadenomas (< 10 mm) and Macroadenomas (2 10 mm). Other entiter that may present as a sellar mass include cranioptharyngiomas, Rathke’s Cleft cysts, sella chordomas, meningiomas, pituitary metastases, and gliomas. ‘Symptoms include headache, visual loss through compression of optic chiasma {Bitemporal hemianopia), diplopia, ptosis, ophthalmoplegia. Pituitary tumors are the most common cause of hypopituitarism as well as ; hyperpituitarism, ~ Contrast enhanced MAI of pituitary hypothalamie area is used lor diagnosis. Biochemical assays for hormone hypo or hypersecretion should be done. - __Trans-sphenoidal resection of the pituitary is the treatment. HYPERPROLACTINEMIA: Protactin acts to induce and maintain lactation and decrease reproductive function and Grive (via suppression of GnRH, Gonadotropins, and gonadal steroidogenesis). !tis uniqud.among pituitary horments in that the Bredominant fentral control snechanis roe (oem \ is inblbitory ia dopamine)., ‘ ~_Prggnaney and lactation ak the physiolo, :s¢s of Ayperp saga od) Prolactin levels > 100 gi. are most commonly caused by protactinoma (normal lovels 5- 25 pg/L). Less pronounced hyperprolactinemia is most commonly caused by medications (Chlorpromazine, haloperidol, metoclopramide, Hy antagonists, amitrypilino, selective ‘serotonin reuptake inhibitors, estrogens). Other causes include pituitary stalk damage (tumors, lymphocytic hypophysitis), primary ‘ hypothyroidism, or renal failure. - In women, amenomthea, galactorrhea, and infertility are the hallmarks of hyperprolactinemia. In men, symptoms of hypogonadism or mass effect are the usual Presenting symptoms. if Fasting moming prolactin levels and MRI of pituitary hypothalamic area are used for | diagnosis. Treatment: ~ tthe patient is on a drug known to cause hyperprolactinemia, stop the medicettion > 9810608460, 9810686970. tus at: www.afmg.co.in, EmMEDICINE, Graduate - Dopamine agonists are given for micro as well as mac rgoling is preferred over Bromocriptine. a woman is planning pregnancy Bromocriptine is preferred over catergoline and it should be stopped immediately after confirmation of pregnancy. : Surgery is requited for tumors not responding to medical therapy. ACROMEGALY: oF Most common cause is pituitary adenoma secreting Growth hormone (GH). In children, GH hypersecretion results in gigantism, Z In adults, acromegaly (Enlargement of acral parts) is seen, : Change in facial features, widened teeth spacing, deepening of voice, increased shoelglove size, frontal bossing, prognathism, macroglossia skin tags, thick heel pads, hypertensicn are the clinical features, Associated conditions include cardiomyopathy, left ventricular hypertrophy, diastolic dysfunction, sleep apnea, diabetes mottitus, colon polyps, and colonic malignancy. = Diagnosis: IGF-I levels are used for screening ‘The diagnosis is confirmed by demonstrating the failure of GH suppression to < 1 pot within 1 hof 784g oral glucose load, Treatment: 1. Trans-sphenoidal resection of pituitary adenoma is the therapy of choice. 2, Somatostatin analogues, octreotide and lanreotide are used to suppress GH secretion and debulking of tumor. Dopamine agonists can be used. \ | 7 Poplecrenveat \ | Ct, sgvisomnt is a'GH mens \ | a] Cranial radiation for tumors not Fesponding to surgpry. ea HYPOPITUITARISM: Causes: Congenital © Traumatic (Pituitary ‘surgery, head injury) 7 © Neoplastic (Pituitary adenoma, craniopharyngioma metastases, meningioma) © Inlitrative (Hemochromatosis, lymphocytic hypophysitis, sarcoidosis, histiocytosis X) © Vascular (Pititary apoplexy, Sheehan's syndrome) © Infections (Tubercular, fungal) - Chronic pituitary damage due to tumors or Tadiation is in the following ‘sequence: GH > FSH/LH > TSH > ACTH (GH being the earliest and ACTH last to decrease) : {mn children, growth failure or short stature is the earliest manifestation, - In adults, hypogonadisi the earliest manifestation. = Diagnosis is made by demonstrating low or inappropriately normal levels of pituitary hormones in the setting of low ‘target hormone level. Initial testing should include an 8 A.M. cortisol level, TSH and free T,, IGF-1, testosterone in men, and an assessment. ‘menstrual cycles in women. elpline: 9810608460, 9810686970 51 Visit us at: www.afmg.co » E-mail: contact@afmg.co.impasuripAFMG MEDICINE cademy for Foreign Me al Graduate ‘ Hormone replacement therapy for adult hypopituitarism: 1. ACTH: Prednisone 5 mg A.M., 2.5 mg P.M. 2. TSH: L-Thyroxine (0.075-0.15 mg daily) 3. FSH/LH: Males — Testosterone enanthate 200 mg in every 2 weeks Female ~ Conjugated estrogen (0.65-1.25 mg OD for 25 days) For fertility ~ Menopausal gonadotropins, human chorionic gonadotropins. 4. GH: Somatotropin 0.3-1,0 mg SC OD. 5. Vasopressin: Intranasal desmopressin 5-20 mg BD. DISORDERS OF THE POSTERIOR PITUITARY: DIABETES INSIPIDUS - Central DI: Insufficient AVP is released in response to physiologic stimuli. Causes include head trauma, neoplastic or inflammatory condition affecting the posterior pituitary, Genetic. - Nephrogenic DI: Genetic, drug exposure (lithium, demeclocycline, amphoterecin B), metabolic conditions (hypercalcimia, hypokalimia) P Gestational DI: Aminopeptidase produced by placenta leads to Arginine Vasopressin deficiency. E Primary polydipsia: Secondary insufficiencies of AVP due to inhibition of AVP secretion by excessive fluid intake. - ‘Symptoms include polyuria, excessive thirst and polydipsia. = 24 hours urine output > 50 mVkg and a urine osmolality that is less than that of plasma (< 300 mosm/kg) ate characteristics. Diagnosis: 1. Fluid deprivation test 2. AVP levels before and after fluid deprivation test. i 3. MRI head (Presence of bright spot in the area of posterior pituitary ruler out central Dl). Treatment: 1. Central DI can be treated with desmopressin subcutaneously, via nasal spray, or orally. Chlorpropamide can also be used. 2. Nephrogenic DI can be treated with a thiazide diuretic, amiloride in conjunction with low sodium diet or prostaglandin synthesis inhibitors (2.9. indomethacin). SYNDROME OF INAPPROPRIATE ANTI DIURETIC HORMONE (SIADH) = Causes: © Neoplasms — Carcinoma lung, thymoma, carcinoids. © Head trauma, hydrocephalus, CVA, encephalitis. © Pneumonia, Lung abscess, TB. © Drugs ~ Desmopressin, chlorpropamide, carbamazepine. : It hyponatremia develops acutely, symptoms of water intoxication may include mild headache, confusion, anorexia, nausea, vomiting, coma, and convulsions. Helpline: 9810 : tus at: www.afmg.co.in, E-mail: contact@atmg.co. its7 Lab findings include low BUN, creatinine, uric acid, and albumin, serum Na = 130 mmol ~ AFMG MEDICINE Academy for Foreign Med and plasma osmolality < 270 mmolkg, Urine is almost always, hypertonic to plasma and urinary Na” is usually > 20 mmol/L. : Ww is a type Ill (Euvolemic) hyponatremia. (Type | ~ Hypervolemic, Type Il — hypovolemic).. Treatment: 1. Fluid restriction 2. Hypertonic (30%) saline should be given in care of CNS signs. Infusion rate should be less than 0.05 ml/kg body weight i.v. per minute. Fast infusion may cause Central Pontine Myelinolysis. 3, Chronic SIADH can be managed with Demeclocyeline or fludrocortisone. DISORDERS OF THE THYROID Hypothyroidism ‘Symptoms include lethargy, dry hair & skin, cold intolerance, hair loss, difficulty in concentrating, poor memory, constipation, mild weight gain, and menorthagia. Examination reveals bradycardia, mild diastolic hypertension, prolongation of the relaxation phase of deep tendon reflexes, and cool peripheral extremities. Pericardial effusion is common. Myxedema coma is a hypothermic, stuporous state with respiratory depression. Elevated TSH is a marker of primary hypothyroidism. Low T. occurs in all varieties of hypothyroidism. ‘Thyroid peroxidase (TPO) antibodies are increased in patients with autoimmune pati iy Treatment \ a 90-100 =e yotonina aa at does 50- 100 mg/d. Hydrocortisone 50 mg ss is given iii adrenal Thyrotoxicosis a: Visit us Primary hyperthyroidism — Grave's disease, toxic multinodular goiter, iodine excess. Extra thyroidal source of thyroid hormone ~ Thyrotoxicosis factitia, struma ovarit ‘Secondary hyperthyroidism ~TSH secreting pituitary adenoma, gestational thyrotoxicosis. ‘Symptoms include nervousness, irritability, heat intolerance, excessive sweating, palpitations, weight loss with increased apetite, frequent bowel movements, and oligomenorthea. In Grave's disease, the thyroid is usually diffusely enlarged to two to three limes ils normat size, and a bruit or thrill may be present, Infilterative ophthalmopathy (with variable degrees of proptosis, periorbital swelling and ophthalmoplegia) and dermopathy (pretibial Myxedema) may also be foun elpline: 9810608460, 9810686970 alt: www.afmg.co.in, E-mail: contact@afmg.coAFMG MEDICINE Foreign Medical Graduate 9 excesserbation of hyperthyroidism and can be accompanied by fever, delirium, Academy for syrotonic ens, 0 seizures, arrhythmias, coma, vomiting, diarrhoea, and jarmdice. Diagnosis - Serum TSH levels are tow in primary hyperthyroidism. - Radionuctide uptake is high in Grave's disease & low in extra thyroidal sources of thyroid hormone. Treatment ~ Ant thyroid drugs — propyithiouracil, carbimazole, methimazole. - Beta-blockers to control adrenergic symptoms. tial treatment. - Radioiodine can also be used as. = Subtotal thyroidectomy is the surgical treatment of Grave's disease. - Ophthalmopathy does not improve with antithyroid drugs and is treated with ghicocorticoids and orbital decompression surgery. = Inpregnaney, only propythipuracil can be used. Treatment of thyroid storm ~ Propylthiouracil 600 mg stat followed by 200 mg 6 hrly. ~ lodine orally one hour later. - Propranolol 40 mg 4 hily. - Dexamethasone 2 mg 6 hry. DISORDERS OF Gaile GLAND co \ sahil CUSHING’S SYNDROME: ‘Most common cause is iatrogenic. * Excessive AGTH secretion by pituitary is known as Cushing's disease. + Central obesity, hypertension, osteoporosis, emotional lability, amenorthea, and diabetes mellitus are common features. Specific features include easy bruising, purple stria, proximal myopathy, fat deposition in the face and interscapular region (moon facies and buffalo hump) and viriization, Diagnosis = For screening 24 hours urinary cortisol and 1 mg Dexamethasone suppression test (8. A.M. plasma cortisol < 5 mg/dt) is used. = Definitive diagnosis is made after low dose Dexamethasone (0.5 mg 6 hrly for 48 h) suppression test. - Plasma ACTH levels are also measured Low levels _ Adrenal adenoma / Carcinoma High levels — Pituitary / Ectopic source - High dose Dexamethasone suppression test (2 mg 6 h for 48 h) suppresses cortisol levels: case of pituilary micro adenomas but not in ectopic sources of ACTH. P = ” 54 Visit us at: www.afmg.co.in, E-mail: contact@afmg.co.imjaasyripAFM G MEDICINE Forei - Academy for TREATMENT ~ Adrenal adenoma or carcinoma requires surgery. Pituitary micro adenomas require Transsphenoidal surgery, Medical adrenalectomy © Metyrapone 2-3 g/d © Mitotate 2-3 mg/d © Ketoconazole 600-1200 mg/d Cohn’s syndrome * Primary aldosteronism refers to an adrenal cause and can be due to either and adrenal Adenoma or bilateral adrenal hyperplasia. * Most patient present with headache and hypertension. Edema is characteristically absent, * Biochemical investigations commonly reveal Hypokalemia, metabolic alkalosis and hypematremia, Serum aldosterone levels are high and renin levels are low. Treatment a i oes - Surgery for or adronal adenoma ~ “Real hyperpiasia is nvanaded with sodiunt Testric Orr ar eae 254100Tg TDS Addison's dis > Itis hypo function of the adrenal gland. » Most common cause is tuberculosis. Other causes include HIV, Cryptococeosis, B/L adrenal hemorrhage. > occurs when > 90 % of adrenal gland is destroyed. > Fatigue, weakness, anorexia, nausea, vomiting, weight loss, cutaneous and mucosal pigmentation, Hypotension and hypoglycemia are common manifestations. . Diagnosis is best made by Cosyntropin (ACTH) test. v ‘Treatment Hydrocortisone 20 mg ~ 2/3 rd dose in moming, 1/3 rd dose in the evening. - Fludrocortisone 0.05 ~ 0.4 long OD. Pheochromocytoma * These tumors produce, store, and secrete catecholamines. * 10% are bilateral, 10% are éxtra-adrenal, 10% are malignant most are <10 cm in diameter, & weigh <100gm. * Association with MEN 2A (Sipplo’s syndrome) and MEN 2B (Mucosal neuroma syndrome}, von Hippel- Lindau’s syndrome, and Neurofibromatosis (Type 1) ion is the most common manifestation. Pp 9810608460, 9310686970 55° Visit us at: www.aimg.co.in, E-mail: contact @afmg.co.ini...MEDICINE al Graduate x ‘Headache, profuse sweating palpitations, and apprehension often witha sense of impending doom are common. Paroxysm may be precipitated by any acitivity that displases abdominal contents. © Diagnosis > 24 hours urine catecholamines is the best screening test. > 24 hours metanephrines & VMA can also be tested. > MRI or CECT scan of the abdomen for diagnosis can be performed. «Treatment Surgery is curative Drugs For acute management lV phentolmmine is the DOC For long lasting management, oral phenoxy bezamine is the DOC. vvvv Diabetes Mettitus '* _DMtype 1 was previously known as IDDM and is characterized by insulin deficiency and a tendency to develop ketosis. * DM type 2 was previously known as NIDDM and is a disorder comprising of insulin resistance, impaired insulin secretion and increased glucose production, Genetic cause — Maturity onset diabetes of young (MODY) ‘* Other causes — Chronic pancreatitis, Acromegaly Cushing's syndrome, Hyperthyroidism. - Fasting plasma glucose >/ 126 mg / dl = Random blood glucose >! 200 mg/dl - 2 hour plasma glucose (afler 75 gm of oral glucose) >/ 200 mg a. - Impaired fasting glucose ~ 140 ta 146 mg/dl ss a * impated glucose Tolerance — Pladma glucosel between, 40 af 200 mol how after a 75 __gnyoratglucose load sexesel ~ =] Clinical features include polyuria, polydipsia, polyphagia, weight loss, fatigue, weakness, blurred vision, frequent superficial infections, and poor wound healing. Chronic complications ~ Ophthatmologic — background & Proliferative retinopathy. - Renal — Proteinuria, CRF — Neurologic ~ Polyneuropathy, mononeuropathy, antonomic neuropathy. - Gastrointestinal — Gastroparesis, diarrhoea. - Genitourinary — UTI, Erectile dysfunction. = Cardiovascular - CAD, Congestive heart failure, strokes. = Lower extremity — Diabetic foot, ulceration Treatment > Diet control and exercise. Helpline: 9810608460, 9810686970 Visit us at: www.afmg.co.in, E-mail: contact@afmg.co MBBSHELP