Medicine Revision 6.5 PDF

10 02 Medicine ----- Active space ----- CVS REVISION-2 Physiology of Pulse 00:00:11...

10 02 Medicine ----- Active space ----- CVS REVISION-2 Physiology of Pulse 00:00:11 Wave Coincides with Percussion wave S1 P wave Peak Tidal wave Aortic recoil Dicrotic notch S2 Dicrotic wave Peripheral (Reflected wave) resistance (PR) Applied aspect : Central/Augmented Systolic BP is Best indicator of Target Organ Damage (TOD). NOTE : Pulse apex deficit : Atrial Fibrillation (A-fib). Radio femoral delay : Coarctation of aorta. Abnormalities in Pulse 00:04:30 Rate abnormalities : Relative Bradycardia : For every 1˚F → in HR by 1o bpm. If in HR is < than this, then it’s said to be relative bradycardia. Causes : Infectious : Typhoid, Q-fever, Legionnaires’, Brucellosis. Non infectious : Lymphoma, Drug fever. Note : Leptospirosis, Dengue & malaria are very rare causes. Rhythm abnormalities : Irregularly irregular : A-fib. Regularly Irregular : VPC (Ventricular Premature Complex). Volume abnormalities : High volume ( Stroke volume) Low volume ( Stroke volume) Collapsing pulse AR Hypokinetic pulse LV dysunction Pseudo-collapsing pulse MR Pulsus tardus Severe AS - Pulsus parvus et tardus Very severe AS Medicine Revision v1.0 Marrow 6.5 2023  CVS Revision 2 02 11 Contour abnormalities : ----- Active space ----- 1. Pulsus bisferiens 2. Pulsus dicroticus Systolic peak + Prominent dicrotic peak. Seen in LV systolic failure. HCM d/t SAM. Severe AR ± Mild AS 3. Pulsus alternans 4. Pulsus bigemini Regular alternate high & low volume Irregular alternate high & low volume pulse. pulse. Seen in LV systolic failure. Seen in VPC. HCM : Hypertrophic Cardiomyopathy; SAM : Systolic Ant. Motion of mitral valve; VPC : Ventricular Premature Complex Note : Brockenbrough sign : In HCM → Pulse volume after post VPC pause d/t SAM. Variations in pulse with respiration : Reverse Pulsus Pulsus Normalis Aggregans/ Pulsus paradoxus paradoxus SBP falls by > 10 mmHg with inspiration. SBP with inspiration Seen in : Seen in : Cardiac Tamponade (M/c) IPPV. I/3rd cases of CCP. HCM. Hyper inflated lung. SVC Obstruction. Pulmonary Embolism. Note : very rare in Restrictive cardiomyopathy. CCP : Chronic Constrictive Pericarditis; IPPV : Intermittent Positive pressure ventillation Jugular venous pulse 00:13:53 Normal JVP waveform : waveform Corresponds to a wave RA contraction. Measures active filling of diastole (30% of filling). x descent Atrial relaxation Upward bulge of Tricuspid valve into atrium. c wave Coincides with S1. v wave Atrial filling. Coincides with S2 Emptying of Atria. y descent Measures passive filling of diastole (70% of filling) Medicine Revision v1.0 Marrow 6.5 2023  12 02 Medicine ----- Active space ----- JVP abnormalities : Abnormality Conditions Prominent a waves Pulm HTN, Rt. atrial thrombus/mass, TS, RVH. Cannon a waves Complete AV block, AVNRT junctional rhythm, Vent. tachycardia. Absent a waves Atrial fibrillation Absent x descent Severe TR, RV failure. Prominent/Rapid X Cardiac tamponade (CT), Chr. constrictive pericarditis (CCP) descent Dominant v waves TR, ASD, Vena caval pressure. Prolonged y descent Tricuspid stenosis (TS) Prominent y descent CCP, isolated severe TR, RCM Absent y descent Cardiac tamponade. Note : Kussmaul’s Sign : Inspiratory rise in JVP. Seen in : CCP, Restrictive cardiomyopathy, Right ventricular MI, TS. Not seen in cardiac tamponade. Abd. Jugular reflex (>3cm or >15 s) : Marker of impending Right Heart Failure. Heart sounds 00:34:36 Mixed murmur Low pitched murmurs Low pitched heart sounds 1. Aortic stenosis : 1. MS 1. S3 Carotids (low pitch) 2. TS 2. S4 Apex of heart (High pitch) 3. Austin flint murmur 3. Tumor plop Rest all are high pitched sounds. S1 & S2 : S1 S2 (A2-P2) Occurs just prior to isovolumetric contraction (IVC). A2 -P2 closure interval is called Due to coaptation of mitral & tricuspid valves Hangout Interval (HI). Normally A2 occurs prior to P2. 1. Soft S1 1. Loud A2 : MR. Bicuspid aortic valve producing Good filling of heart. AS. AR. Root pathologies in AR. 2. Loud S1 2. Soft A2 : MS. Elderly AS. Valve pathologies in AR. 3. Loud P2 : Pulmonary HTN. 4. Soft P2 : Pulmonary stenosis. Medicine Revision v1.0 Marrow 6.5 2023  CVS Revision 2 02 13 Split S2 : ----- Active space ----- Wide variable split Wide fixed split Paradoxical split Early A2 or Split fails to move P2 first followed by A2. delayed P2. with respiration. Commonly accompanied by loud P2. Cause : Causes : Causes : MR. RV failure. AR. ASD. AS. S3 : S3 in AS/AR is always with heart failure. S3 in MR can be heard with or without heart failure. Never heard in MS. S4 : Seen only in AS. Added diastolic sounds : Mnemonic : OP Time 3-4. 1. Early diastolic sound : Opening snap (High pitch) : a. Snapping open of mitral valve. b. S2-OS gap shortens with severity of MS/↑ left atrial pressure. Pericardial knock (High pitch). Tumor plop (Low pitch). 2. Middiastolic sounds : S3 (Low pitch). 3. Late diastolic sound : S4 (Low pitch). Added systolic sounds : 1. Ejection clicks : Aortic ejection click : Seen in bicuspid aortic valve. Pulmonary ejection click. Note : All right sided heart sounds ↑ with respiration → Carvallo’s sign, except pulmonary ejection click. 2. Non ejection clicks : Seen in mitral valve prolapse. Medicine Revision v1.0 Marrow 6.5 2023  14 03 Medicine ----- Active space ----- CVS REVISION 3 Heart Failure 00:00:27 Structural or functional impairment of the ventricle to pump out/fill itself with blood. Classification : HF with reduced EF (HFrEF) (< 40%) : Guideline based management. HF with preserved EF (HFpEF) (> 50%) : Comorbidity based management. HF with mid range EF (HFmEF) (40-50%). Staging of HF : A : Only risk factors present. Best prognosis. B : Risk factors + Structural abnormalities. M/c cause of mortality : C : Present or prior symptoms. Sudden cardiac death D : Advanced HF (Mortality cause is pump failure). NYHA grading of symptoms : For angina, palpitation & dyspnea. Class 1 Symptoms at exertion, no limitation. Class 2 Mild symptoms at ordinary physical activity, slight limitation. Class 3 Symptoms at less than ordinary physical activity, marked limitation. Class 4 Symptoms at rest, severe limitation. Symptoms : LV systolic failure LV end diastolic pressure Increase in RVEDP Cachexia (TNFα). ↑ LAP → ↑ PCWP → Abdomino jugular reflex ↓ Urine output (Cardiorenal Dyspnea → Orthopnea → (AJR) → Impending RV syndrome). PND → Acute pulmonary failure. Altered sensorium. edema. JVP. Cold extremities. O/E : Rales & S4. Ascites. Narrow pulse pressure. Hepatomegaly. O/E : S3 & cardiomegaly. Edema. Framingham criteria : Major symptoms : 1. Dyspnea/orthopnea/PND. 5. JVP. 2. Acute pulmonary edema. 6. AJR. 3. Rales. 7. Cardiomegaly. 4. S3. Note : No ascites, edema, hepatomegaly in major Framingham criteria. Medicine Revision v1.0 Marrow 6.5 2023  CVS 3 03 15 1. Dyspnea : ----- Active space ----- Types of dyspnea : Bendopnea Trepopnea Seen in advanced HF (left & right HF). Preferred to lie on right side. A/w ↑ JVP & PCWP. Pleural effusion more on right side. Along with dyspnea, crepitations (Fine gravitational creps a/w cold extremities) + S4 can be seen. 2. Angina : D/t ↑ LV mass or LVOT obstruction (not a mandatory symptom of HF). 3. Palpitations : D/t cardiomegaly. 4. Syncope : D/t LVOT obstruction. Diagnosis : ECG : Other symptoms : Low voltage in limb leads. Sinus tachycardia → ↑ mortality. High voltage in chest leads. JVP (RHF) : ≥ 3 cm elevated from sternal angle. Poor R wave progression. AJR (Impending RHF). Echo : To evaluate ejection fraction. Edema, Ascites. Cardiac MRI : Gold standard for EF. Decompensation : Factors that precipitate acute HF in a patient with underlying HFrEF/HFpEF : Patient related (Non compliant/diet). Arrhythmias (A. Fib). Infection related (Infective endocarditis). MI. Anemia. NSAIDs & beta blockers. Mx of HFrEF : 1. Block SNS ( decrease HR & FOC) 2. Block RAAS β blockers. ARNI (Angiotensin II receptor Metoprolol/carvedilol/bisoprolol. blocker + Neprilysin inhibitor). Bisoprolol (β1 selective) : 1.25 mg - 10 mg. eg. Valsartan + Sacubitril. Started at lowest dose. ARNI > ACE inhibitors > ARBs. Patient should not have edema. 4. SGLT 2 antagonist 3. Mineralocorticoid receptor antagonist (MRA) Dapagliflozin/empagliflozin. Spironolactone/eplerenone/finrenone. Produce natriuresis & diuresis Side effects : Hyperkalemia,gynecomastia. without tachycardia. FOC : Force of contraction. Mortality benefit : β blockers > ARNI > MRA > Hydralazine + nitrate. Note : Hydralazine + nitrate is used in renal failure patients with heart failure. Medicine Revision v1.0 Marrow 6.5 2023  16 03 Medicine ----- Active space ----- Other drugs : Diuretics : For symptomatic relief. Ivabradine : Used only if HR > 70 bpm & patient on maximum dosage of β blockers. MOA : Inhibits funny currents (Na+). S/E : Visual field abnormalities. No role : ACE inhibitor + Neprilysin inhibitor : Omapatrilat. Digoxin. Dysfunction of ventricles 00:29:29 Systolic dysfunction Diastolic dysfunction Pumping defect Filling defect Left sided issues Right sided issues (RV > LV) Always followed by diastolic dysfunction Normal systole possible. Diastolic dysfunction with normal systole. Constrictive Restrictive (more severe) Chronic constrictive pericarditis Restrictive cardiomyopathy Diastolic dysfunction : ↑ RVEDP → ↑ RAP → Transmitted to SVC, IVC → Right sided HF (Ascites precox, edema, JVP & hepatomegaly). It has a chronic course. Acute pericarditis (D/d for MI) Clinical features : Elevated ST + chest pain. ECG : Global ST elevation (Concave) except lead V1, no reciprocal changes, PR depression. Cause : Post viral (Coxsackie virus), uremia. Multiple relapses → Rigid, calcific, thickened pericardium with adhesions (Rock like pericardium) → Chronic constrictive pericarditis. Medicine Revision v1.0 Marrow 6.5 2023  CVS 3 03 17 Chronic Constrictive Pericarditis (CCP) Restrictive cardiomyopathy ----- Active space ----- Causes : Causes : Multiple relapses of acute pericar- Intercellular accumulation : ditis. Amyloidosis (Most important cause). Post viral > TB. Intracellular accumulation : Iron Features : Chronic RHF symptoms. (Hemochromatosis), glycosphingolipids Cachexic + malnourished (TB) with (Fabry’s disease) and glycogen ascites, edema, hepatomegaly. (Pompe’s disease). Transmyocardial filling pressure No accumulation : DM, scleroderma. = Intracavitary pressure - Intra Features : pericardial pressure. It is reduced Stiff hypertrophic, non compliant, non in CCP. dilated ventricle. Diastolic dysfunction → Slow, chronic RHF symptoms. Normal systole. Normal chamber size. ECG : Low voltage complexes. Kussmaul sign (↑ in JVP on inspiration) : Fall in intrathoracic pressure is not transmitted to heart chambers d/t pericardial issue (normally JVP falls with inspiration). JVP : JVP : Sharp prominent rapid x descent. Holodiastolic restriction → No y Sharp prominent rapid y descent : descent, no square root sign. Frederichs sign. Atrial relaxation not adequate → x Ventricular pressures during diastole descent not prominent. : Fall → rise → abrupt halt : Square root sign. Elevation & equalisation of diastolic Elevation & equalisation of diastolic pressures after 1/3 of diastole. rd pressures not seen. Pulsus paradoxus seen in 1/3rd of Pulsus paradoxus absent. patients. Pericardial knock can be heard. S3 can be heard. Broadbent sign : Indrawing of 11th & No pericardial knock. 12th ribs (systolic retraction of apex). Ix : MRI (IOC). Ix : Echo. Rx : Pericardiectomy. Rx : Medical management (Manage cardiomyopathy/HF). Medicine Revision v1.0 Marrow 6.5 2023  18 03 Medicine ----- Active space ----- Cardiac tamponade 00:57:25 Cause : Acute post traumatic event. Features : Acute rise in intrapericardial pressure. Presentation : Obstructive shock (Hypotension + shock + disproportionate dyspnea + tachycardia). Beck’s Triad : Hypotension + muffled heart sounds + ↑JVP. JVP : Holodiastolic restriction → Absent y descent, no square root sign, no pericardial knock. Systolic phase of venous return (Coupled constraint) : X descent is prominent. Holodiastolic elevation & equalisation of diastolic pressures present. Transmission of pressure to cardiac chambers can be seen → ↓JVP on inspiration → No Kussmaul sign. Small chambers (as compressed from all sides). Pulsus paradoxus (Fall of SBP > 10 mm Hg on inspiration). ECG : Low voltage complexes (Electrical alternans). Rx : Emergency pericardiocentesis. Medicine Revision v1.0 Marrow 6.5 2023  CVS Revision 4 04 19 CVS REVISION 4 ----- Active space ----- Cardiomyopathy : Myocardial disease in which heart is structurally & functionally abnormal in the absence of valvular heart disease, congenital heart disease, CAD & HTN. Classification of cardiomyopathy : 1. Dilated cardiomyopathy (DCM). 2. Hypertrophic cardiomyopathy (HCM). 3. Restrictive cardiomyopathy (RCM). 4. Unclassified. Dilated cardiomyopathy 00:00:12 Autosomal dominant. Thin walled dilated LV → Has poor contractility. Symptoms : 1. Systolic heart failure symptoms : Cachectic. Cold extremeties. Altered sensorium. Renal failure symptoms. Narrow pulse pressure. S3 +ve. 2. Diastolic failure symptoms : Dyspnea. 3. Right sided failure symptoms : JVP, ascites, edema, hepatomegaly. Causes : 1. 30% genetic : Truncated variant (Tv) Titin mutation (M/c) > myh7 mutation. 2. Peripartum cardiomyopathy : Best prognosis. D/t anti-angiogenic factors : SFLT 1. Risk factors : a. ↑ Age at pregnancy. b. HTN with pregnancy. c. Multiple pregnancy. Medicine Revision v1.0 Marrow 6.5 2023  20 04 Medicine ----- Active space ----- 3. Alcohol induced cardiomyopathy : Good prognosis (Reversible). Patients with ACE polymorphism are at ↑ed risk. Precipitated by : Selenium deficiency (Keshan’s disease), thiamine deficiency & magnesium deficiency. 4. Drug induced cardiomyopathy : Worst prognosis. Attributed to high dose Anthracycline. 5. Autoimmune : Sarcoidosis & hemochromatosis (DCM > RCM). 6. Endocrine : Pheochromocytoma, thyrotoxicosis & acromegaly. 7. Myocarditis : Acute post inflammatory DCM which can occur along with the infection/post infection period. Good prognosis. M/c cause : HHV 6 > Chagas disease. Investigations : 1. ECG findings : Triad a. Low voltage in limb leads. b. High voltage in chest leads. c. Poor ‘R’ wave progression. 2. Echo : Global LV hypokinesia. 3. MRI : Gold standard for ejection fraction. To look for ischemia vs infract. 4. Angiography. Restrictive cardiomyopathy 00:14:30 Seen in amyloidosis of heart. Bad prognosis. Types of amyloidosis : 1. Primary amyloidosis 2. Secondary amyloidosis : No cardiac involvement. 3. Transthyretin induced a. Senile systemic amyloidosis (Wild type) → Seen in elderly with carpal tunnel syndrome. b. Familial amyloid polyneuropathy (Mutant type) → Severe ANS symptoms + cardiac symptoms seen. Medicine Revision v1.0 Marrow 6.5 2023  CVS Revision 4 04 21 Features : ----- Active space ----- Biatrial enlargement. Biventricular hypertrophy. Interatrial septal thickening. Low voltage complexes. Investigations : IOC : Cardiac MRI (Glittering of myocardium). ECG : Pseudo infarct pattern (Infarct pattern on ECG with normal echo). Unclassified cardiomyopathy 00:17:02 Takotsubo cardiomyopathy : Aka stress induced cardiomyopathy/neurogenic myocardial stunning/transient apical ballooning. M/c : Middle aged females. Cause : Sympathetic overactivity. Presents with : ACS like presentation. Investigations : ECG : ST elevation. Trop I elevated (Not as much as in ACS). NT Pro BNP is high. On angiography : a. Normal coronary arteries. b. Base is hypercontractile. c. Bulging apex. Prognosis : Short term complications same as MI. No long term complications. Hypertrophic cardiomyopathy 00:20:12 M/c genetic cardiovascular disease. Autosomal dominant. Myosin heavy chain mutation > myosin binding protein C mutation. Males = females (Females have poorer prognosis). Medicine Revision v1.0 Marrow 6.5 2023  22 04 Medicine ----- Active space ----- Course of HCM : 95% -99% → Stable course. 1% - 5% → Develop complications like : 1. Progressive heart failure. 2. Arrhythmias (Atrial fibrillation). 3. Sudden cardiac death. Note : Pompe’s disease mimics HCM. Features of hypertrophy : LV thickness ≥15 mm with no cause & no dilatation. Asymmetric hypertrophy : Only septum + anterior wall hypertrophies. Inappropriate hypertrophy : Absence of any factor causing ↑ in afterload. Concentric LVH → ↓ Cavity size → ↑ LVEDP. Left ventricular outflow tract (LVOT) obstruction : First 1/3rd : Fixed obstruction. Second 1/3rd : No obstruction. In last 1/3rd : Dynamic obstruction. Pathophysiology : 1. Diastolic dysfunction with normal systolic function : Concentric LVH → ↓Cavity size → ↑ LVEDP → ↑LAP → ↑PcWP → Dyspnea (M/c symptom). A-fib 2. Systolic motion of anterior mitral leaflet (SAM) : Asymmetrical septal hypertrophy → LVOT obstruction → ↑ Velocity of blood across the obstruction → Low pressure zones across the outflow tract → Anterior mitral leaflet sucked into septum (Occurs in mid to late systole). SAM will lead to 2˚ MR. 3. Angina (2nd m/c symptom) with normal coronaries : D/t microvascular dysfunction. Factors influencing obstruction : ↑ Preload →↓Gradient ↓ LVOT obstruction ↑ Afterload →↓Gradient ↑ Force of contraction →↑ Gradient → ↑ LVOT obstruction. Clinical features : Most patients are asymptomatic. Atrial fibrillation. Angina, syncope, & dyspnea (Features of LVOT obstruction). Medicine Revision v1.0 Marrow 6.5 2023  CVS Revision 4 04 23 Findings : ----- Active space ----- Pulse : Pulses bisferiens ( In HCM p wave > t wave). JVP : Normal Apex : Double /triple apex (d/t SAM). S1 : Normal S2 : Normal/reverse split. S3 : May be heard. S4 : May be heard. Murmurs : a. Lower left sternal border : Ejection systolic murmur (D/t SAM). b. Apex : Pan systolic murmur (D/t 2˚ MR). Biopsy : Myofibre disarray. Dynamic auscultation : All the murmurs in cardiology ↓se with valsalva or standing except : 1. MVP : ↑Duration of murmur. 2. HCM : ↑ Intensity of murmur. To differentiate b/w MVP & HCM Post VPC pulse volume Increased Decreased (Brocken brough sign) MVP HCM Rx : DOC : β blockers (Propranolol). 2nd DOC : Verapamil > diltiazem. If no adequate response : Add Disopyramide (Class 1a). Side effects of disopyramide : a. QT prolongation. b. Anticholinergic side effects. c. Reduce ejection fraction by 5% - 10%. If medical Mx fails → Surgery : Septal myomectomy. If family h/o sudden cardiac death or spontaneous sustained VT → Im- plantable cardioverter-defibrillator (ICD). Medicine Revision v1.0 Marrow 6.5 2023  24 05 Medicine ----- Active space ----- CVS REVISION 5 Myocardial Infarction (MI) 00:00:20 Coronary circulation : Dominance of coronary circulation : Based on origin of posterior descending artery (which supplies Inferior wall) : Right dominant (80%) : If arises from right coronary artery (RCA). Left dominant (20%) : If arises from left circumflex artery (LCX). Origin of Acute marginal artery (AMA) demarcates RCA into Proximal & Distal segments. Acute marginal art. supplies RV free wall. Occlusion of AMA → RVMI. Inferior wall MI (IWMI), Right ventricular MI (RVMI), Posterior wall MI (PWMI) : Inferior Wall MI Can occur d/t Occlusion of Proximal RCA, Distal RCA or LCx. Involvement of Post. Descending artery : IWMI ± PWMI. In a right dominant person : Proximal RCA occlusion : RvMI + IWMI ± PWMI. Distal RCA occlusion : IWMI ± PWMI. Posterior wall can be supplied by obtuse marginal artery (branch of LCx), hence can be spared in RCA occlusion. In a left dominant person : LCX occlusion : Definitely IWMI + PWMI. Proximal RCA occlusion : Only RvMI. Distal RCA occlusion : No MI. Medicine Revision v1.0 Marrow 6.5 2023  CVS Revision 5 05 25 IWMI & RVMI Features : ----- Active space ----- SA nodal branch → Bradycardia. Clear lungs, ↑ JVP, hypotension in RVMI. Posteromedial papillary muscle rupture → 20 MR. ST elevation : II, III, aVF (Inferior wall). Identifying site of occlusion in IWMI : ST ↑ ST ↓ RCA Lead III > II aVL > aVR LCX Lead II > III aVR > aVL RVMI : V1 shows ST ↑ (or) flat/depressed ST which is discordant with V2, V3, V4. Findings : 1. ST elevation in leads II, III, aVF. IWMI 2. Reciprocal changes in V2,V3,V4. 3. ST ↑ in III > II RVMI with & ST ↓ in aVL > aVR proximal RCA 4. ST in V1 discordant to V2, V3. Diagnosis : IWMI + RVMI with proximal RCA occlusion. Anterior wall MI (AWMI) : 00:09:30 Left coronary artery (LCA) branches into : Left anterior descending (LAD) & LCX. Blood supply Area Corresponding leads LAD (D1) or LCX High lateral wall I, aVL LAD (S1) Septum V1 >> V2 LAD (D2) Anterior wall V2, V3, V4 LAD (D3) or LCX Lateral wall V5, V6 Findings : 1. ST elevation in V2, V3, V4. 2. Reciprocal changes in leads II, III, aVF. 3. ST ↑ in V1 → Above S1. 4. ST ↑ in I & aVL → Above D1. Diagnosis : Extensive antero high lateral MI. Medicine Revision v1.0 Marrow 6.5 2023  26 05 Medicine ----- Active space ----- Acute coronary syndrome Mx algorithm : Golden hour : 6 hours. First medical contact Diagnosis (preferably 0.16 s Origin : Above bundle of His. Origin : Above bundle of His. Origin : Ventricles. Atria : Atrial tachycardia (focal/ But, conducted with a Ventricular tachycardia. multifocal). bundle branch block AV node : Junctional tachycardia. AVNRT, AVRT, AF, atrial flutter. Note : Paroxysmal atrial tachycardia with AV block (d/t Digoxin). Medicine Revision v1.0 Marrow 6.5 2023  CVS Revision 5 05 27 Narrow QRS tachycardia : ----- Active space ----- Regular RR interval Irregular RR interval AVNRT : Atrial fibrillation. No P waves. Multifocal atrial tachycardia. P wave just outside QRS, with short RP & long PR interval (only in 1/3rd patients). AVRT : P wave just outside QRS, with short RP (> 80 to 100 ms) & long PR interval. Focal atrial tachycardia : Long RP, short PR interval with morphologically abnormal P waves. M/c narrow QRS tachycardia : Sinus tachycardia. Findings : 1. Narrow QRS tachycardia (Rate > 150/min). 2. P wave just before QRS complex → Long RP & short PR. Diagnosis : Atrial tachycardia. Findings : 1. Narrow QRS tachycardia. 2. P wave just after T wave. Diagnosis : Atrial tachycardia. Management : 1. AVNRT : Adenosine. In COPD → Verapamil → no response → Metoprolol. Defibrillation done in : Pulseless VT. Synchronised DC cardioversion. Ventricular fibrillation. 2. Atrial tachycardia : Verapamil, β blockers. Polymorphic VT. Multifocal atrial tachycardia : 3 different morphologically abnormal P waves can be identified. Can be precipitated by Theophylline Medicine Revision v1.0 Marrow 6.5 2023  28 05 Medicine ----- Active space ----- Atrial fibrillation (AF) : 00:35:27 Findings : 1. Irregular RR interval. 2. Fibrillatory waves. 3. No identifiable P waves. Diagnosis : AF. Valvular AF : AF seen in MS (or) prosthetic mitral valve. Types : 1. Paroxysmal : Lasts for < 7 days. Reverts back spontaneously (or) with drugs. 2. Persistent : Lasts for > 7 days. 3. Permanent : LA dilatation > 4 cm. Rhythm can’t be reverted back to normal. Complications : Thromboembolism. Management : Hemodynamically unstable : DC cardioversion (100 J → 100 J). Hemodynamically stable Transthoracic echo Normal Duration of AF LA > 4 cm Indicates : > 48 hours < 48 hours Structural heart disease (or) unknown Rhythm control : Rate control : CCBs. Transesophageal echo (or) Ibutilide. cardiac CT to visualise clot Amiodarone (Structural If clot + heart disease) 3 weeks anticoagulation f/b Rhythm control f/b 4 weeks anticoagulation Wide QRS tachycardia : Ventricular tachycardia : Sustained VT , rate > 100/min. ≥ 3 VPCs. Capture beat, fusion beat maybe present. Management Monomorphic VT. Unstable Stable Synchronised DC cardioversion Procainamide. (100 J → 100 J → 100 J → 60J) Amiodarone in structural heart disease. Lignocaine : Post MI. Medicine Revision v1.0 Marrow 6.5 2023  CVS Revision 5 05 29 Polymorphic VT + prolonged QT : Torsades de pointes. ----- Active space ----- Precipitating factors Class Ia, Ic, III anti arrhythmic drugs. Terbinafine. Macrolides. Hypokalemia, hypocalcemia, hypomagnesemia. Hypothermia. Torsades de pointes Mx (All patients unstable) : Defibrillation (200 J) + 2g I/v MgSO4. Hyperkalemia : 00:45:20 Causes : Renal failure (M/c). Hypoaldosteronism. Pseudo hypoaldosteronism : RTA type IV. Spironolactone. ECG findings Serum K+ (mEq/L) Tall T waves 6-7 ST segment ↓, 7-8 PR segment ↑ Wide QRS 8-9 P wave absent >9 Mx of hyperkalemia : Calcium gluconate. Hypokalemia : 00:47:22 Findings : 1. Sagging of ST segment. 2. Prominent U waves. Mx : I/v KCl. Medicine Revision v1.0 Marrow 6.5 2023  30 06 Medicine ----- Active space ----- RESPIRATORY SYSTEM REVISION 1 Weibel’s generation of airways : Total 23 generations of airway. First 16 generations → Conducting zone (Upto terminal bronchioles). Last 7 generations → Respiratory zone (Respiratory bronchioles + alveolar ducts + alveoli = Acinus). Classification of Lung Diseases 00:02:47 Lung diseases Obstructive lung diseases Vascular Restrictive lung disease COPD : Pulmonary hypertension. Chronic bronchitis. Pulmonary thromboembolism. Emphysema. Small airway disease ( 80%. Time (sec) Lung volumes in obstructive and restrictive lung disease : Obstructive lung disease Restrictive Lung disease Elastic recoil pressure (ERP) is low There is ventilation issue. d/t loss of alveolar attachments ERP is high d/t fibrosis → Difficult to → Hyperinflation→ Dynamic inflate alveoli. compression of airways. Medicine Revision v1.0 Marrow 6.5 2023  32 06 Medicine ----- Active space ----- Obstructive lung diseases Restrictive lung diseases Vascular Hyperinflation Air trapping Intra Extra parenchymal lung phase phase parenchymal diseases 1 FEV 1 ↓↓ ↓↓ Normal to ↑ Normal FVC 2 FEV 1 ↓↓ ↓↓ Normal Normal 3 FVC Normal ↓↓ ↓↓ Normal 4 DLCO Emphysema = ↓↓ ↓ Normal Very low NM Chest issues wall 5 RV ↑↑ ↑↑ ↓ Normal Normal Normal 6 TLC ↑↑ Normal ↓↓ ↓↓ Normal Normal 7 RV/ TLC - - - ↑↑ Normal - Lung volumes in smaller airway disease : FEV 1 /FVC : Normal Forced expiratory flow 25-75% (FEF 25-75) / Volume (l) Maximal Mid Expiratory Flow Rate (MMEFR) is used to identify small airway disease. Time (sec) DLCO 00:45:30 Measurement of lung’s ability to transfer gas (O2) across alveolocapillary membrane. Normal Value of DLCO : 20-30 ml/min/mm Hg. Normal Value of DLCO : 70 to 140 %. Carbon monoxide/CO used for measuring DLCO because : CO affinity to hemoglobin is very high. CO is diffusion limited gas. There is negligible amount of CO in the blood. Alveolocapillary membrane : Diffusion takes place across 1. Alveolar epithelium + Basement membrane. 2. Interstitium. 3. Capillary endothelium + Basement membrane. Surface area of alveolocapillary membrane : 70 m2 Thickness of alveolocapillary membrane : 0.2 - 0.5 micrometre. Medicine Revision v1.0 Marrow 6.5 2023  RS Revision 1 06 33 Factors affecting DLCO : ----- Active space ----- Factors that increase DLCO Factors that decrease DLCO ↑ Blood volume : Supine position, ↑cardiac output, Valsalva maneuver. congestive cardiac failure, polycythemia. Smoking (↑ CO Hb). ↓ PaO2 : High altitude. High flow O2 therapy (↑ OxyHb). Exercise and Obesity. Anemia. Left to right cardiac shunts. Clinical application of DLCO : Diseases with ↑ DLCO Diseases with↓ DLCO Diffuse alveolar hemorrhage: Helps in early diagnosis of ILD in Sensitive indicator for early rheumatological disorders: bleeding into alveoli. Eg: Rheumatoid arthritis (RA) Goodpasteur disease Scleroderma Wegener granulomatosis Mixed connective tissue disease Microscopic Poly Angiitis Polymyositis Dermatomyositis In asymptomatic patients → DLCO falls >15% within 6 months. → marker of progression of ILD Bronchial asthma Pulmonary vascular diseases Bronchitis Bleomycin toxicity Emphysema Pleura 01:00:42 Fluid in pleural cavity Detected 10 -30 mL Normal fluid in pleural cavity. 50 mL USG. 60- 80 mL Chest X-ray Lateral view. 200 mL Chest X-ray PA view. 300 mL Clinically. Pleural effusion : Light’s criteria distinguish transudates from exudates : The fluid is considered as exudative pleural effusion if any one of the following are found : 1. Ratio of pleural fluid to serum protein ≥0.5. 2. Ratio of pleural fluid to serum LDH ≥0.6. 3. Pleural fluid LDH ≥2/3rd of the upper limits of normal serum LDH. The fluid is considered a transudate if all the above are absent. Medicine Revision v1.0 Marrow 6.5 2023  34 06 Medicine ----- Active space ----- Causes of transudative pleural effusion : Congestive heart failure. Hypoalbuminemia. Cirrhosis. Budd Chiari Syndrome. Nephrotic syndrome. Urinothorax. Superior vena cava obstruction. Peritoneal dialysis. Hypothyroidism. Can cause Transudative/Exudative effusion : Chronic constrictive pericarditis. Pulmonary infarction. Pulmonary embolism. Acute pancreatitis. Note : Methotrexate causes HSP. Pleural fluid analysis : Cells : 1700 cells/μl (75% macrophages, 25% lymphocytes, < 1% mesothelial cells). LDH : 10 % eosinophils in pleural fluid) : Hemothorax /Pneumothorax. Drugs. Parasitic : Paragonimus westermani. Eosinophilic Granulomatosis with Histoplasmosis/Coccidioidomycosis. Polyangiitis (EGPA). Asbestosis. Pulmonary infarction. Pleural fluid abnormalities and associated diseases : 1. Empyema : 2. RA : LDH >1000 U/L pH 25% (or) b. Lung tissue eosinophilia (or) c. Peripheral eosinophilia + Lung infiltrates. Causes : Known causes Unknown causes 1. Parasite 1. Eosinophilic granulomatous polyangiitis a. Loeffler’s syndrome : Hypersensitivity to (EGPA). ascaris. 2. Acute eosinophilic pneumonia (ARDS like b. Lung fluke invasion. presentation). 2. Drugs : Nitrofurantoin. 3. Chronic eosinophilic pneumonia/CEP 3. Tropical pulmonary eosinophilia (d/t (Reverse batwing : Photographic negative microfilaria). of pulmonary edema on radiology). 4. Allergic bronchopulmonary aspergillosis (ABPA) 4. Idiopathic hyper eosinophilic syndrome. Note : HSP (Hypersensitivity pneumonitis). Bronchial asthma (A/w eosinophilia). Not eosinophilic lung diseases. Pulmonary eosinophilic granuloma diseases. BAL eosinophilia with > 40% : CEP & Tropical Pulmonary eosinophilia. Aspergillus in lung 00:06:56 Organism : Aspergillus fumigatus with septate hyphae (Forms mucus plug). Not a highly contagious disease. Presentations of aspergillus infection : 1. ABPA : Eosinophilic lung disease. 2. Aspergilloma : Seen in old tuberculosis cavity. 3. CCPA (Chronic cavitary pulmonary aspergillosis) : Thick walled cavities + bronchial wall invasion in COPD patients. Medicine Revision v1.0 Marrow 6.5 2023  46 08 Respiratory System ----- Active space ----- 4. Invasive aspergillosis : Neutropenic patients. CT : Halo sign (consolidation surrounded by ground glass opacities). ABPA : A. fumigatus colonizes airways in bronchial asthma or cystic fibrosis patients (Acute/remission/exacerbations/steroid dependent asthma/fibrosis). Type 1 + Type 3 hypersensitivity (type 1 > 3). Lung findings seen in 20% patients. Pathology : Bronchiectasis : Proximal bilateral cylindrical symmetrical central type. C/F of ABPA : Fever and cough with brownish thick mucosal plugs. Rarely gets converted to ILD (Involves upper lobe). Investigation : IgE >1000 (Part of obligatory criteria + used for Tram track lines in CXR follow up). Precipitin +ve. Imaging : a. Chest Xray : - Transient irregular parenchymal infiltrates. - Atelectasis. Finger in glove appearance - Tram track appearance. (d/t mucoid impaction - Finger in glove appearance. in distal bronchi) b. CT : Tree in bud appearance. Treatment : a. Steroids for 12 weeks (DOC). b. Steroid non responders : Itraconazole for 16 weeks. c. Omalizumab (Monoclonal antibody against IgE). HRCT showing central bronchiectasis (tree in bud pattern) Hypersensitivity pneumonitis (Extrinsic allergic alveolitis) : Inflammatory disorder of the lung involving the alveolar wall & terminal airways. Repeated exposure to organic dust Type 4 + Type 3 HS Involves airway > Parenchyma. Medicine Revision v1.0 Marrow 6.5 2023  RS Revision 3 08 47 Characterised by : ----- Active space ----- IgE/eosinophil absent + Precipitin +ve + Non caseating granuloma & infiltrates. If parenchyma is involved : Non fleeting Interstitial infiltrates. Subacute form (M/c) : A/w response to steroids. No systemic symptoms. HRCT : Mosaic/Head cheese pattern (Different kind of densities seen). Rx : Steroids. Mosaic attenuation/ Head cheese pattern Organic dust : Microorganisms serve as antigen in dust/animal proteins/chemicals : Disease Exposure Antigen Farmers lung Moldy hay Thermophilic actinomycete Bagassosis Moldy sugarcane (M/C antigen) : Mushroom worker’s lung Moldy compost/mushroom Thermoactinomycetes vulgaris Malt workers lung Barley Aspergillus clavatus Tobacco workers lung Mold on tobacco (2nd m/c) Compost lung Compost Wood workers lung Wood pulp Bird fancier’s lung (Obstructive/ Avian droppings emphysematous pattern) (Pigeon, parrot, chicken) Chemical workers lung Polyurethane foams (Isocyanates) Note : Disease Antigen Hot tub lung, or humidifier or Cladosporium, MAC air conditioner lung Wood trimmers lung Rhizopus Familial HP/wood workers Bacillus subtilis Medicine Revision v1.0 Marrow 6.5 2023  48 08 Respiratory System ----- Active space ----- Hypersensitive reactions to Aspergillus Extrinsic allergic Asthma ABPA alveolitis/HSP Colonization of airways, Lymphocytic infiltration of Hypertrophied Pathology viscid mucoid impaction, interstitium, noncaseating mucus gland tissue eosinophilia granuloma Radiographic features Migratory peripheral Normal Diffuse alveolar Early infiltrates, atelectasis, hyperinflation interstitial infiltrates bronchiectasis Normal Reticulonodular Late Fibrosis hyperinflation interstitial opacities Skin test reactions to Aspergillus antigens Immediate Positive Positive Positive Delayed Negative Positive Positive Other findings Peripheral Negative Positive Negative eosinophilia IgG aspergillus Positive Positive Positive precipitins Normal or Serum IgE levels Marked elevation Normal mildly elevated BAL lymphocytosis : CD4/CD8 (>2 : 1) : Sarcoidosis. CD8/CD4 (>2 : 1) : HSP. Bronchiectasis 00:23:50 Obstructive type of airway disease. Abnormal irreversible dilatation of bronchi + obliterative fibrosis of bronchioles. D/t destruction of smooth muscles and elastic tissue of lung. Types of dilatation : Tubular, cylindrical (M/C), varicose & cystic dilatation. Cystic dilatation : Seen in children & a/w clubbing. Traction bronchiectasis (Part of ILD) : Restrictive type. Causes for loss of smooth muscles & elastic tissue : 1. Idiopathic (30%). 2. Tuberculosis (40-50%). 3. Genetic causes : Alpha-1 antitrypsin deficiency. 4. Childhood infections : Measles & pertussis. 5. Genetic syndromes : Yellow nail syndrome, William Campbell syndrome. Medicine Revision v1.0 Marrow 6.5 2023  RS Revision 3 08 49 Pathophysiology : ----- Active space ----- Lt lobe > Rt; F > M; 50-70 yrs. Dry bronchiectasis (Sicca) : Tuberculosis. Right middle lobe bronchiectasis : K/a Brocks syndrome (d/t lymph node in TB). Middle lobe bronchiectasis : D/t MAC. C/F : Chronic cough. Foul smelling sputum. Hemoptysis. Early & mid inspiratory coarse crackles. Diffuse rhonchi. Imaging : 1. Volumetric multidetector helical CT scan (Best) : Absence of bronchial tapering. 2. Airway dilatation (Parallel lines or ring shadows) : 1-1.5 times adjacent vessel diameter : Signet ring sign. 3. Tram track sign. 4. Tree in bud pattern. 5. Central distribution, upper lobe & fibrotic band : ABPA. Bronchiectasis : Signet ring in CT s/o cylindrical bronchiectasis Rx : 1. Airway clearance with physiotherapy and postural drainage (Cornerstone of therapy). 2. Nebulized 7% hypertonic saline or steam inhalation to clear secretions. 3. Recombinant DNase for cystic fibrosis associated bronchiectasis. 4. Resection : If localized bronchiectasis with recurrent infection unresponsive to drugs. 5. Prophylaxis : Macrolides (Azithromycin) for 6-9 months. M/c organism causing infection : Pseudomonas. Medicine Revision v1.0 Marrow 6.5 2023  50 08 Respiratory System ----- Active space ----- Chronic obstructive pulmonary disease (COPD) 00:36:00 Acinus (Respiratory unit) : Respiratory bronchiole + Alveolar ducts + Alveoli. COPD has 2 diseases : 1. Chronic bronchitis (clinical) : Cough with sputum for 3 months for 2 consecutive years. 2. Emphysema (Pathological) : Dilatation of airspace distal to terminal bronchiole followed by destruction of walls of airspaces. Types of emphysema : Centriacinar Panacinar Paraseptal Most common. Complete involvement. Young, male, smokers. Respiratory Young, non smoker, α-1 Associated with bronchiole involved. antitrypsin deficiency & pneumothorax. Smoker & males. liver disease. Upper lobe Lower lobe predominant. predominant. α-1 antitrypsin Phenotypes : 1. Pimm : Normal phenotype. 2. Pizz : Severe deficiency. Medicine Revision v1.0 Marrow 6.5 2023  RS Revision 3 08 51 Chronic bronchitis Emphysema ----- Active space ----- Structure involved Parenchymal +++ Airway +++ Gaseous changes PaO2 PaO2 PaCO2 Normal PaCO2 Type of Respiratory failure Type 2 Type 1 Hypoxia More Less severe Pulmonary HTN/ More common Less common RV failure/ Infection Prognosis More mortality Better outcomes Complications : V/P mismatch (Characteristic of COPD) Severe chronic hypoxia Muscularization Intimal hyperplasia Pulmonary hypertension Fibrosis Obliteration Cor pulmonale Edema Death Rx : Based on categories. mMRC 0-1, CAT< 10 mMRC ≥2, CAT ≥10 0 to 1 moderate Group A Group B exacerbations A bronchodilator A long acting (Not leading to (Short acting bronchodilator hospital admission) bronchodilator) Dyspnea (LABA or LAMA) Exacerbation ≥2 moderate Group D exacerbations Group C LAMA or or LAMA LAMA + LABA ≥ 1 leading to (Long acting ± ICS hospitalization anti-muscarinic drugs) (If eosinophils ≥ 300). mMRC : modified medical research council dyspnea questionnaire ; CAT : COPD assessment test. For exacerbations : SABA + Short oral steroid therapy for 5-10 days. Medicine Revision v1.0 Marrow 6.5 2023  52 08 Respiratory System ----- Active space ----- LTOT (Long term oxygen therapy) : Given for 14-18 hrs/day. After exacerbation is over. Indications : a. PaO2 20%) Pneumonia Management 00:53:34 CURB score : Score of 1 to each point. Score 0, 1 : Outpatient management. C : Confusion. Score 2 : Inpatient management. U : Urea > 42 mg/dl. Score 3 : ICU management. : Respiratory rate >30/min. B : Acute crystal arthritis. CPPD). Relapsing polychondritis (RPC). Multicentric reticulohistiocytosis. Note : If erosions (+) in SLE → Rhupus syndrome (RA + SLE overlap). MAGIC Syndrome → Mouth and Genital ulcer (Behcet’s disease) + Inflammed cartilage ( RPC). b. Spondyloarthritis(SpA) : Synovitis + Enthesitis + Dactylitis. Axial predominant SpA → Ankylosing spondylitis (Bilateral sacroilitis) Peripheral predominant SpA Symmetrical polyarthritis (>5 joints) 1. Psoriatic arthritis : Assymetrical oligoarthritis (2-4 joints) 2. Reactive arthritis. c. Crystal arthropathy : Synovitis due to crystals. Monosodium urate monohydrate crystal (MSUM)/Gout : 1 st MTP > Knee joint. Calcium pyrophosphate dihydrate crystal (CPPD)/Pseudogout : Knee joint. Note : Symmetrical polyarthritis of small joints of upper limb. 1. Acute ( CPPD. Undifferentiated arthritis. 2. 1st MTP : MSUM. 2. Chronic (>6 weeks) : Rheumatoid arthritis. Assymetrical oligoarthritis : Peripheral SpA. SLE/ SLE like arthritis. 1. Reactive arthritis. Psoriatic arthritis. 2. Psoriatic arthritis. Rheumatoid arthritis 00:25:40 M/c chronic inflammatory multisystem autoimmune connective tissue disease. Peak : 40-60 yrs. Female : male ratio → 3 : 1. Note : 2nd M/c connective tissue disorder : Sjogren’s syndrome. M/c Arthritis : Osteoarthritis. Medicine Revision v1.0 Marrow 6.5 2023  Rheumatology Revision 1 09 55 Etiology : ----- Active space ----- Genetic factors Environmental factors 1. HLA associated factors : 1. Smoking : HLA-DRB1*04 → QKRAA aminoacid motiff (AkA Strongest risk factor. shared epitope). Associated with bad prognosis. HLA-DRB1*13 : Protective. risk of ILD in RA. expression of PADI-4 in airway. 2. Non HLA associated factors : 2. Infection : Chronic periodontitis. PADI-4 (Peptidyl arginine deaminase 4) Caused by Porphyromonas Citrulline gingivalis. Arginine PADI-4 (Normal Aminoacid) (Abnormal aminoacid) 3. Alcohol/OCP : Mild protection. PTPN 22 Note : Smoking associated ILD is seen in : Desquamative interstitial pneumonia. Langerhans cell histiocytosis. ILD in rheumatoid arthritis. Respiratory bronchiolitis associated ILD. Pathogenesis : 1. Environmental & genetic factors → abnormal protein modification (citrullination). 2. Abnormal proteins→ presented by APC (Langerhans dendritic cells) to T cells → 20 activation of B cells & neutrophils → Migration to joint. 3. Synovial hypertrophy (Type A> type B synoviocytes)→ Pannus formation → Bone erosion. Autoantibodies in RA : Antibody Features Anti CCP/anti citrullinated poly- Seen in 80-90% cases of RA. peptide/mutated citrullinated Specificity : 95% for RA. vimentin. Best marker for Preclinical infection ↑ risk of extrarticular features Anti CarP Associated with palindromic rheumatism. Anti PADI-4 antibody - Rheumatoid factor (RF) IgM directed against Fc portion of IgG. ↑ titre a/w ↑ disease activity. Specificity : 75-80%. Also +ve in : a. Sjogren’s. b. Cryoglobulinemia type 2 & 3. c. Polyarticular JIA. Note : Markers for relapse in RA → ESR& CRP (Anti-CCP and RF hold no value). Medicine Revision v1.0 Marrow 6.5 2023  56 09 Medicine ----- Active space ----- Clinical features : Articular manifestations : Duration : > 6 weeks. B/l symmetrical. Intraarticular. Inflammatory (Indicated by morning stiffness > 45 mins). Peripheral small joint, upper limb polyarthritis. Disease starts at distal radioulnar joint. Joints Joints spared Joints involved/spared rheumatoid arthritis. involved Note : MCP. DIP. DIP joint is involved in : Wrist. 1st CMC, 1st Psoriatic arthritis PIP. MTP. C-spine Thoracolum- (Erosive arthritis : wrist, MCP, DIP, PIP). bar & sacral Osteoarthritis (Wrist and MCP joint spared). spine. Juvenile idiopathic arthritis. Multicentric reticulohistiocytosis. Progression of disease : Deformities Features Reversible 1. Zigzag deformity. Radial deviation of wrist + Ulnar deviation of MCP. 2. Subluxation of MCP joint. 3. Piano key styloid. Rupture of ulnar collateral ligament. 4. Hitchhiker thumb Abduction + Hyperextension of thumb. deformity Irreversible 1. Boutonniere deformity. Flexion of PIP + Hyperextension of DIP. 2. Swan neck deformity. Hyperextension of PIP + Flexion of DIP. 3. Opera glass hand. Arthritis mutilans. Other joints involved/deformities : TM joint. 5 th MTP : M.c involved C1-C2 joint : Odontoid process erosion. Pes planus. Cricoarytenoid : Change in voice. Forefoot varus. Ankle valgus. Medicine Revision v1.0 Marrow 6.5 2023  Rheumatology Revision 1 09 57 Extra-articular Manifestations : ----- Active space ----- Involvement Features Rheumatoid nodules m/c extraarticular manifestation : 40% cases. 20% develop within 1 yr of onset of RA. M/c site : Olecranon. Non tender nodules. ↑association in Smokers, Anti CCP/RF +ve, Early onset & long duration RA. Granulomatous reaction : Type 4 hypersensitivity. Size↓on treatment. Neuro ocular CNS No brain parenchymal involvement. manifestations C1-C2 myelopathy. Entrapment neuropathy. PNS RA related small fibre peripheral neuropathy. Ocular M/c : Dry eyes (Keratoconjunctivitis sicca). Episcleritis > scleritis. Thinning of sclera (scleromalacia perforans). Uveitis not a feature. Hematological M/c : Anemia of chronic disease. manifestation. Normal WBC count (In SLE : Leukopenia or lymphopenia).. Thrombocytosis. Rapidly progressive anemia → Warm IgG AIHA. ↑ risk of diffuse large B cell lymphoma. LGL leukemia. Felty syndrome : Seen later in the disease. Large granular Nodules, deformities +ve ; RF +ve, HLA-DRB1*04 +ve. lymphocytes (LGL) Antibody against citrullinated histones +ve. Features : RA + Neutropenia + Splenomegaly. Lung manifestations Pleuritis ± exudative effusion (Low sugars, Low pH). ILD : Usual interstitial pneumonia (UIP). Fibrosis. Traction bronchiectasis. Honeycombing. Loss of lung architecture. Cyst in the lung. Honeycomb app. Caplan syndrome : RA + nodules in lung + coal workers pneumoconiosis. (seen in UIP) Seen in active synovitis and RF +ve. CVS manifestations M/c cause of death in RA : MI (accelerated atherosclerosis). M/c presentation : Pericarditis w/o tamponade. M/c valvular disease : Mitral regurgitation. Renal manifestations M/c manifestation : 20 amyloidosis. GIT GI vasculitis. Vasculitis in RA Immune complex mediated small vessel vasculitis. M/c lesion : Purpura. Histology : Leucocytoclastic vasculitis. Dangerous forms : a. Medium vessel involvement : Gangrene. b. GI vasculitis. Rx : Rituximab c. Mononeuritis multiplex. Medicine Revision v1.0 Marrow 6.5 2023  58 09 Medicine ----- Active space ----- Involvement Features Others Flexor tendon tenosynovitis. Bursitis. Hypoandrogenism. Osteoporosis. Pyoderma gangrenosum. Note : ILD and Vasculitis in RA are more common in males. Presentation of RA : Presentation Features Preclinical RA Genetic & environmental risk factors +ve. Autoantibodies of RA +ve. Symptoms without clinical evidence of RA. Chronic symmetrical small joint Symptoms : Pain & inflammation. polyarthritis (M/c). D/d : SLE/SLE like illness.(No erosion). Psoriatic arthritis (No DIP involvement. CPPD (Pseudo RA) : Waxing & waning, non erosive. Palindromic rheumatism Intensely painful brief episodes of monoarticular arthritis. Mimics gout. Antibody involved : Anti CarP. Early morning stiffness of small joints + Normal examination & Xray findings. suspect Post viral arthritis (M/c : Parvo virus). If symptoms persist If symptoms 6 weeks. weeks. Suspect Undifferentiated arthritis. Diagnosis confirmed. Remission in Persists as UA Evolve into RA 1/3 rd cases. or progress to 1/3rd cases. other disease in 1/3rd cases. Medicine Revision v1.0 Marrow 6.5 2023  Rheumatology Revision 1 09 59 Scoring factors determining undifferentiated arthritis evolving into RA : ----- Active space ----- Age. Sex. Joint distribution. Morning stiffness. Tender & swollen joints. Markers : CRP, RF & anti CCP. Score >8 : Treat as RA. Management : DMARDS Biologic agents Small molecules Methotrexate (Mtx). Anti TNF-α : Etanercept. JAK 1/3 Leflunomide. Anti CD20 : Rituximab. inhibitor : Sulphasalazine. Anti IL-1 : Anakinra. Tofacitinib. Hydroxychloroquine Anti IL-6 : Tocilizumab. JAK 1/2 (HCQ). CTLA4/Fc IgG fusion inhibitor : molecule : Abatacept. Baricitinib. 1. Start DMARD : Methotrexate (Mtx) : 5mg weekly dose may go upto 25 mg weekly dose. CBC, LFT monitored. Side effects : Mucositis (m/c). Dose dependent bone marrow supression. Hypersensitivity pneumonitis ↑ size of nodules in 10% cases. 2. Remission assessment by Boolean score : Clinical assesment ≤ 1. Tender joint ≤1. Swollen joint ≤1. CRP ≤ 1mg/dl. 3. If no remission → Combination therapy used : Mtx + Sulphasalazine + HCQ or Mtx +TNF-α inhibitor or Mtx + JAK inhibitors. Medicine Revision v1.0 Marrow 6.5 2023  60 10 Medicine ----- Active space ----- RHEUMATOLOGY REVISION 2 Systemic Lupus Erythematosus 00:00:57 General features : Female : Male = 9 : 1 (Males → Severe disease). Family history +. Renal involvement in SLE : a. Adult SLE : 40% renal involvement. b. Childhood SLE : 100% renal involvement. c. Post-menopausal SLE : Mild disease with renal sparing. M/C cause of death : a. First 5 years : Infection/lupus nephritis. b. After 5 years : Accelerated atherosclerosis/MI. Risk factors : Genetic factors : 1. Non HLA & 2. HLA Non HLA HLA C1q (early complement) deficiency. C2, C3 deficiency. TREX gene on chromosome 3. HLA -DR2/DR3. Genes on X-chromosome : Klinefelter syn- drome has ↑risk. Environmental factors : ↑ estrogen (OCPs, HRP), EBV, UV-B. Pathogenesis : Defective clearance of apoptotic/NETosis debris → Innate immune system activation by IFN-α, IL-4 & Th2 Immune complex deposition (Type 3 HS reaction) in : Vessel wall → Vasculitis Synovium → Synovitis Glomeruli→ Glomerulonephritis Medicine Revision v1.0 Marrow 6.5 2023  Rheumatology Revision 2 10 61 Antibodies in SLE : Note : ----- Active space ----- 1. Anti-nuclear antibodies (ANA) : Conditions with 100% ANA positivity : SLE : 97% +. 1. Drug-induced lupus erythematosus. Sjogren’s syndrome : 85% 2. Type 1 autoimmune hepatitis. + (least positivity among CTD). 3. Mixed connective tissue disorder. ANA testing : Screening test for CTD. Method : Indirect immunofluorescence using Hep-2 cell line. Positive titre : ≥ 1/80. Patterns : Pattern Antibody Specific disease Homogenous Anti-ds DNA SLE Anti-histone Drug-induced lupus Dense fine speckled Rules out CTD Fine speckled Anti-Ro/SS-A & SS-B Sjogren’s syndrome Coarse speckled Anti-smith SLE Anti-U1RNP Mixed connective tissue disorder Nucleolar Anti-Pm-Scl-70 Sytemic sclerosis-dermatomyositis overlap syndrome Cytoplasmic Anti-Jo-1 Polymyositis & Dermatomyositis ANA-negative SLE (3% cases) : Anti-Ro/SS-A & anti-La/SS-B +. ANA profile : Done for ANA + patients. 2. Anti-ds DNA & 3. Anti-smith : Specificity for SLE : Anti-smith > anti-ds DNA. Anti-ds DNA is more clinically important : Titres measured by ELISA correlate with risk for nephritis/vasculitis. 4. Anti-Ro/SS-A & 5. Anti-La/SS-B : Indicates secondary Sjogren’s syndrome. If + in pregnancy → Neonatal lupus with complete heart block. Associated with better prognosis → ↓ risk for nephritis/vasculitis. Associated with sub-acute cutaneous lupus. Associated with shrinking lung syndrome. 6. Anti-phospholipid : Seen in 1/3rd of SLE patients. 7. Anti-RBC : Warm antibody (IgG) autoimmune hemolytic anemia. 8. Anti-platelet : 2° ITP (Idiopathic thrombocytopenic purpura). Medicine Revision v1.0 Marrow 6.5 2023  62 10 Medicine ----- Active space ----- 9. Anti-glutamate (aka anti-neuronal) : M/C antibodies in CNS lupus. M/C manifestation in CNS lupus : Cognitive dysfunction. 10. Anti-ribosomal-P : Pyschosis/depression in CNS lupus. Factors correlating with disease activity in SLE : Anti-ds DNA titres, ↓ C3 & C4,↑ ESR & ↓ CRP. Note : Overlap syndrome : Presence of features of > 1/6 CTD. 1. SLE. 4. Dermatomyositis. 2. Sjogren’s syndrome. 5. Systemic sclerosis. 3. Polymyositis. 6. Rheumatoid arthritis. Mixed connective tissue disorder : Overlap syndrome. 100% ANA +. Anti-U1RNP +. Diagnostic criteria for SLE : SLICC. Clinical features : Musculoskeletal manifestations : Chronic, inflammatory, b/l symmetrical polyarthritis of small joints in the up- per limb. Jaccoud arthropathy : Non-erosive + deforming arthritis. Mucocutaneous manifestations : A. Acute cutaneous lupus erythematosus (ACLE) : Malar rash/butterfly rash : Photosensitive. Erythematous. Scaling ±. Non-scarring. Associated with non-scarring alopecia. Associated with hard palate ulcers. Spares the nasolabial fold. Non-premalignant. Medicine Revision v1.0 Marrow 6.5 2023  Rheumatology Revision 2 10 63 B. Subacute cutaneous lupus erythematosus (SCLE) : ----- Active space ----- Annular (M/C) & psoriasiform SCLE. Highly photosensitive. Non-scarring. A/w anti-Ro/La. A/w HLA-DR3. ↓ risk for nephritis/vasculitis. Spares the mid-facial region. C. Chronic cutaneous lupus erythematosus (CCLE) : Discoid rash (M/C). 5% of patients with discoid rash have SLE. 20% of patients with SLE have discoid rash. Seen on the face, scalp and neck. Circular erythematous + dermal atrophy + follicular plugging. Premalignant lesion for squamous cell carcinoma. A/w scarring alopecia. Carpet track sign. CNS manifestations :. Small fibre neuropathy +, axial skeleton spared. Ocular manifestations : 2° Sjogren’s syndrome (M/C), absence of uveitis. Hematological ma