Family Medicine EOR PDF

Family Medicine EOR Cardiovascular 15% About Risk Factors Primary Prevention Secondary Prevention Coronary ▪leading cause of mortality...

Family Medicine EOR Cardiovascular 15% About Risk Factors Primary Prevention Secondary Prevention Coronary ▪leading cause of mortality in US ▪age: women >65yo or w/ premature menopause, men >55yo Primary prevention = risk factor reduction Secondary prevention = pharmacologic therapy Artery ▪MCC: atherosclerosis ▪family HX: first-degree ♀relative 30kg/m2) & physical inactivity ▪HTN (BP goal 3mg/L is an independent risk factor for Antianginal TX: Atypical angina, “anginal equivalents” myocardial ischemia » First line: beta blockers (also secondary prevention) Canadian Cardiovascular Society: ▪dyspnea, N/V, fatigue, diaphoresis, faintness ▪all patients w/ stable angina (⇣ mortality), esp. post-MI » Class I: angina w/ strenuous activity » women, diabetics, elderly ▪⊖cardiac enzymes ▪greatest reduction in number/duration of ischemic episodes » Class II: slight limitation of normal activity » Second line agents: nitrates, CCBs, ranolazine » Class III: severe limitation of normal activity Chest pain classification: EKG: resting EKG normal ➀ Nitrates » Class IV: unable to perform any activity w/o SXS ➀ substernal » ischemic EKG findings: ▪short-acting (SL NTG): prevent exertional/relieve acute angina ➁ provoked by exertion/emotional stress ▪T wave flattening, peaked T waves ▪long-acting (ISDN, ISMN): adjunct/alternative to BBs Myocardial ischemia: O2 demand > O2 supply ➂ relieved w/ rest/NTG ▪T wave inversions, ST depressions ➁ CCBs: used if intolerant to beta blockers » 3/3 = typical angina (definite) ➂ Ranolazine: alternative to beta blockers, refractory EKG Ischemia Findings: » 2/3 = atypical angina (probable) Stress testing: » Combination TX: BB + CCB, BB + ISDN, CCB + ISDN ▪T wave flattening, hyperacute T waves (peaked) » 0-1/3 = noncardiac chest pain ▪exercise stress test (EKG), ST ⇣ >1mm = ⊕ ▪T wave inversions (TWI) ▪myocardial perfusion scintigraphy Indications for Revascularization: ▪ST depressions ▪stress ECHO ▪left main stenosis >50% or equivalent (proximal LAD & LCx >70%) ▪triple-vessel disease, particularly w/ LVEF 3s = sinus arrest (+/- escape rhythm) First search for reversible causes “Sick Sinus ▪beta blockers, CCBs, digoxin ➃ SA nodal exit block ▪Type I: progressively shorter P-P intervals followed by dropped P wave Syndrome” ▪ischemia, autonomic imbalance ▪Type II: pauses in sinus rhythm that are multiples of basic sinus rates ➄ Chronotropic incompetence: inability to ⇡ HR to match demand from ⇡ activity Asymptomatic: intermittent examinations Symptomatic: permanent pacemaker MCC: sinus node degeneration & fibrosis; often involves other parts of conduction system ▪Meds: BBs, non-DHP CCBs, digoxin, antiarrhythmics, AChE inhibitors (donepezil, rivastigmine) ▪Infiltrative diseases: amyloidosis, sarcoidosis, scleroderma, hemochromatosis ▪Inflammatory disorders: rheumatic fever, pericarditis, diphtheria, Chagas disease ▪Other: SA nodal artery disease, cardiac trauma, hypothyroidism About Clinical Manifestations/EKG Management AV Blocks Block occurs IN the AV node: ▪First-degree & Mobitz I: typically benign, rarely produces symptoms First-degree, Mobitz I: ▪first-degree ▪Mobitz II & third-degree: almost always d/t pathologic disease involving the infranodal conduction system ▪no treatment ▪second-degree Mobitz type I (Wenckebach) » S/SXS: fatigue, dyspnea, presyncope, syncope ▪Third-degree (complete) AV block: “escape rhythms” drive the ventricle from below the block site; escape rhythm is slower Mobitz II: more serious Block occurs BELOW the AV node: than sinus (200ms) Second-degree, Mobitz I (Wenckebach): progressively longer PR ▪ALL atrial impulses conducted interval followed by non-conducted P wave (dropped QRS) Third-degree (complete): Etiologies: ⇡ vagal tone, meds (beta blockers, non- ▪permanent pacemaker imperative DHP CCBs), ischemic heart disease, cardiomyopathies, myocarditis, congenital heart disease Third-degree AV block: NO atrial impulses reach ventricles Second-degree, Mobitz II: random dropped QRS, stable PR interval PATHO: delayed conduction through AV node > ▪complete dissociation between P waves & QRS complexes ▪often 2:1, 3:2 prolonged PR interval > eventual dissociation of atrial & ventricular rhythms if completed blocked Blocks About Diagnostics Management Bundle Branch 2 key features of both left & right BBBs: RBBB: QRS ≥120ms Bundle Branch Blocks: Block (BBB) & ➀ prolonged QRS duration ▪terminal R wave in V1/V2 (rSR’) w/ discordant ST/T waves ▪asymptomatic: no further tx Fascicular ➁ terminal conduction delay » direct opposite of R’ (i.e., ST ⇣ or T wave inversion) ▪symptomatic: permanent pacemaker Block ▪broad S waves in V5/V6 ▪Complete BBB: QRS ≥120ms Fascicular Blocks: no specific treatment ▪Incomplete BBB: QRS 110-120ms ▪treat underlying disorder Right Bundle Branch Block (RBBB): delay in depolarization of RV LBBB: QRS ≥120ms *CAN occur in a healthy heart ▪broad, notched, or slurred R waves (rR’/RR’) in leads I, aVL, V5/V6 ▪dominant S wave in lead V1 Etiologies: congenital heart disease (e.g., ASD), acquired (e.g., valvular, ischemic) ▪absence of Q waves in lateral leads, appropriate ST/T discordance Left Bundle Branch Block (LBBB): delay in depolarization of LV; entire sequence of ventricular activation is altered, affecting both the initial septal & subsequent ventricular forces *does NOT occur in a healthy heart LAFB: QRS 200bpm, irregularly irregular rhythm *may precipitate VFIB pathway & retrograde conduction up AV node ▪anterograde conduction through both AV node & accessory pathway – unstable: electrical cardioversion » Wide QRS, rate controlled by accessory pathway refractory period (short) » occasional narrow QRS reflects AV node conduction – stable: IV procainamide or ibutilide *capable of rapid ventricular response, can precipitate VFIB » wide QRS d/t anterograde conduction through accessory pathway (rates – AFIB w/ antegrade conduction down accessory pathway & RVR close to 300bpm) TOC: electrophysiologic study & catheter ablation of bypass tracts S/SXS: if ⊕arrhythmia, may have palpitations, dizziness, or mild chest pain SVTs About Diagnostics Management Wandering Atrial ▪≥3 ectopic atrial foci generating impulses that are all conducted to the ventricles EKG: ≥3 distinct P wave morphologies in the same lead WAP: benign, requires no treatment Pacemaker (WAP) ▪irregularly irregular rhythm w/ varying PR intervals ▪irregularly irregular rhythm, varying PP/PR/RR intervals & ▪isoelectric line between P waves (i.e., ⊘flutter waves) Pharmacotherapy for MAT indicated if: Multifocal Atrial Wandering Atrial Pacemaker (“multifocal atrial rhythm”) = HR ≤100bpm – Leads to sustained RVR that causes or worsens Tachycardia (MAT) Wandering Atrial Pacemaker: HR ≤100bpm myocardial ischemia, HF, peripheral perfusion, or Multifocal Atrial Tachycardia = HR >100bpm oxygenation – MAT associated w/ COPD! ▪Verapamil: COPD (d/t bronchospasm) – hypoxia, electrolyte abnormalities (e.g., hypokalemia, hypomagnesemia) ▪Metoprolol – Magnesium & potassium repletion even in patients w/ normal levels has shown to convert a significant % Multifocal Atrial Tachycardia (MAT): HR >100bpm of pts to NSR ▪Magnesium oxide or chloride ▪Potassium chloride – AADs & cardioversion NOT useful Ventricles About Clinical Manifestations/Diagnostics Management Ventricular VT: ≥3 consecutive PVCs S/SXS: CP, dyspnea, syncope, sudden cardiac death Unstable: assume VT Tachycardia – Nonsustained: lasts 100bpm Monomorphic VT (MC): uniform QRS pattern, consistent morphology; rate 150-200bpm MCC: acute MI, dilated cardiomyopathy Stable VT: IV amiodarone first line Others Causes: chronic CAD, electrolyte abnormalities, drug toxicities – DCC if VT fails to terminate/sxs worsen Monomorphic VT (MC): Polymorphic: IV magnesium ▪regular, broad complex tachycardia ▪uniform QRS complexes within each lead (i.e., each QRS is identical) Polymorphic VT: QRS morphology continuously varies Pulseless ⇢ ACLS ▪usually associated w/ myocardial scar Recurrent, refractory: overdrive pacing Polymorphic VT: – Internal cardiac defibrillator (ICD) ▪QRS morphology continuously varies (requires >1 EKG lead to see variation) ▪most often d/t ischemia in absence of QT prolongation Brugada Pattern: pseudo-RBBB + persistent ST segment ⇡ (coved) in V1-V2 Brugada Syndrome: hereditary, characterized by structurally normal heart ▪associated w/ ventricular dysrhythmias ⇢ syncope & sudden cardiac death – d/t mutation in cardiac Na gene channel (“sodium channelopathy”) ▪Asian men predominantly Torsades de ▪paroxysmal form of polymorphic VT Torsades de pointes (“twisting of the points”): ▪IV magnesium sulfate pointes ▪occurs secondary to QT prolongation, can be acquired (MC) or congenital ▪paroxysmal form of polymorphic VT, sinusoidal; rates >200bpm Unstable: DCC *polymorphic Acquired QT Prolongation: VT – RX: haloperidol, TCAs, abx (e.g., macrolides), methadone, antihistamines, Refractory: ICD antiemetics, anticonvulsants – Electrolyte Abnormalities: hypokalemia, hypomagnesemia, hypocalcemia Ventricular ▪total disorganized ventricular depolarization Ventricular Fibrillation: chaotic irregular zigzag pattern of varying amplitude ACLS Algorithm: Fibrillation ▪ventricle impulse rates up to 500bpm ▪no identifiable P waves or QRS complexes, rates varying between 150-500bpm – CPR, defibrillation (VFIB) ▪total loss of synchronized ventricular contraction, complete loss of CO ▪as times passes, amplitude typically decreases (coarse ⇢ fine) – Epinephrine 1mg – Amiodarone Etiologies: MI, cardiomyopathy, degradation of VT, PE, hypothermia, downing, electrical impulses ANTIARRHYTHMICS ABOUT Class Ia: MOA: Na-channel blockers; also block K-channels which prolongs the AP duration; ⇣ conduction velocity, ⇡ refractory period, ⇣ ADRs: torsades, hypotension, tachycardia, tinnitus Dipyridamole automaticity; widen QRS Quinidine Procainamide ▪Disopyramide: life threatening ventricular arrhythmias ▪Quinidine: AFIB-prophylaxis/TX for conversion to NSR; conversion ▪Procainamide: life threatening ventricular arrhythmias of PVCs to NSR; life threatening ventricular arrhythmias Class Ib: MOA: Na-channel blockers (fast); ⇣ conduction and automaticity at high HRs ADRs: lightheadedness, dizziness, incoordination, N/V, tremor, Lidocaine Indications: only used for ventricular arrhythmias (no efficacy in supraventricular arrhythmias) hearing disturbances, slurred speech, hallucinations Mexiletine ▪Lidocaine: special efficacy in prevention of ventricular arrhythmias associated w/ AMI Warnings (Mexiletine): blood dyscrasias, DRESS Class Ic: MOA: Na-channel blockers (slow); significantly reduce conduction & automaticity ADRs: dizziness, visual disturbances Flecainide Indications: life-threatening ventricular arrhythmias, PSVT, conversion/maintenance of NSR in paroxysmal AFIB/flutter in symptomatic ▪Propafenone: metallic taste, N/V Propafenone patients w/ NO structural heart disease ▪Flecainide: dyspnea Class II: beta blockers MOA: block response to adrenergic stimulation (NE, E) at the beta receptor; indirectly block Ca-channels in SA/AV nodes resulting in ⇡ refractoriness, ⇣ automaticity, & ⇣ conduction velocity Indications: used to slow ventricular rate in SVTs, such as AFIB Class III: MOA: K-channel blockers; delays phase 3 repolarization resulting in marked prolongation of AP duration & refractory period ADRs: QT prolongation Dronedarone Dofetilide Sotalol Ibutilide ▪Dronedarone: paroxysmal or persistent AFIB to reduce the ▪Dofetilide: conversion to/maintenance of NSR in AFIB ▪Amiodarone: photosensitivity (blue discoloration), neurotoxicity, Amiodarone risk of hospitalization; already in NSR ▪Ibutilide: recent onset of AFIB/flutter for conversion to NSR hypothyroidism, corneal microdeposits, DILE ▪Sotalol: life-threatening ventricular arrhythmias; maintenance ▪Amiodarone: DOC in pts w/ heart failure of NSR in AFIB Class IV – CCBs: MOA: block L-type calcium channels, slowing AV/SA node conduction velocity; ⇣ automaticity, ⇡ ERP ADRs: edema, HA, dizziness, constipation, gingival hyperplasia Verapamil Indications: ventricular rate control for supraventricular arrhythmias Diltiazem *should NOT be used in presence of LV systolic dysfunction (HFrEF) or decompensated HF due to ⊖ inotropic effects Miscellaneous AADs ABOUT Adenosine MOA: slows conduction through the AV node via activation of adenosine-I receptors; ⇣ conduction velocity, ⇡ ERP ADRs: transient, new arrhythmias; facial flushing, chest pain, Indications: rapid conversion to NSR in PSVT dizziness, transient ⇣ in BP, GI distress, dyspepsia Digoxin MOA: blocks at AV node = ⇣ conduction velocity, ⇡ nodal ERP ADRs: dizziness, mental disturbances, HA, N/V/D Indications: ventricular rate control in SVT; ineffective at controlling rate during exercise; used in combo w/ BB or CCB Contraindications: VFIB About Clinical Manifestations Diagnostics Management Dilated ▪dilation & impaired contraction of LV or both ventricles HF SXS: exertional dyspnea, fatigue, peripheral edema, ECHO: left ventricular dilation, thin ventricular HF TX: ACEI, BB, diuretics Cardiomyopathy » systolic dysfunction pulmonary congestion, cough, hepatomegaly walls, ⇣ LVEF, ventricular hypokinesis (DCM) ▪MC cardiomyopathy (95%), presents between 30-40yo ▪automated implantable defibrillator if ▪S3 gallop hallmark CXR: cardiomegaly, pulmonary edema, pleural LVEF L-sided HF ECHO: non-dilated ventricles w/ normal Treat the underlying disorder Cardiomyopathy ventricular filling (⇣ compliance); stiff ventricle fills w/ great ▪R-sided HF: peripheral edema, JVD, hepatomegaly, ascites thickness, diastolic dysfunction, marked (RCM) effort ▪L-sided HF: dyspnea, fatigue dilation of both atria Etiologies: infiltrative diseases (amyloidosis MCC, sarcoidosis, ▪Kussmaul’s sign: ⇡ JVP w/ inspiration hemochromatosis)  About Clinical Manifestations Diagnostics Management Myocarditis Inflammation of the heart muscle; MC in young adults Viral prodrome – fever, myalgias, malaise for CXR: cardiomegaly Supportive several days followed by sxs of systolic - systolic HF tx: ACEI, diuretics, BBs PATHO: myocellular damage leads to myocardial dysfunction (dilated cardiomyopathy) EKG: non-specific – sinus tachycardia MC necrosis & dysfunction, leading to HF HF sxs: dyspnea, fatigue, exercise intolerance, S3 Labs: may have + cardiac enzymes, ↑ ESR Etiologies: gallop infectious: viral MC (enteroviruses – Coxsackievirus Echo: ventricular systolic dysfunction B) Other: megacolon, pericarditis (pericardial friction autoimmune: SLE, RA rub, effusion) Endomyocardial bx: gold standard – infiltration uremia, medications (clozapine) of lymphocytes w/ myocardial tissue necrosis About Clinical Manifestations Diagnostics Management Pericarditis Inflammation of the pericardium, the outer layer of Chest pain: sudden onset EKG: diffuse ST elevations in the precordial leads Anti-inflammatory meds: NSAIDs or ASA + the heart pleuritic (sharp, worse w/ inspiration) w/ associated PR depressions in those leads colchicine x7-14d Fibrinous or serofibrinous: e.g., post-MI, infectious persistent postural (worse when supine & improved w/ Etiologies: sitting forward) Dressler Syndrome: ASA or colchicine 2 MCC – idiopathic, viral (Coxsackievirus & pain may radiate to back, shoulder, neck, arm, or - avoid NSAIDs because they can interfere w/ echovirus) epigastric area myocardial scar formation Dressler syndrome (post MI pericarditis + fever + pleural effusion) Pericardial friction rub: best heard at end expiration while upright & leaning forward Pericardial Accumulation of fluid in the pericardial space chest pain (if associated w/ acute pericarditis) Echo: test of choice – increased fluid in Treat the underlying cause (acute pericarditis) Effusion Normally, about 5-15ml of fluid is in the pericardial dyspnea, fatigue pericardial space Serial echo if needed space EKG: electrical alternans (alternating amplitudes Etiologies: viral, idiopathic, immune, malignancy – lung PE: decreased (muffled) heart sounds (due to of the QRS complexes); low QRS voltage Large effusions may need pericardiocentesis for cancer MC, breast second MC, aortic dissection, fluid) CXR: “water bottle” heart symptomatic relief uremia Cardiac Pericardial effusion causing significant pressure on Beck’s triad: distant (muffled) heart sounds + ↑ Echo: pericardial effusion + diastolic collapse of IMMEDIATE PERICARDIOCENTESIS to remove Tamponade the heart, impeding cardiac filling, leading to JVP + systemic hypotension cardiac chambers the pressure decreased CO & shock - volume resuscitation & pressor support if EMERGENCY Pulsus paradoxus: exaggerated (>10mmHg) ↓ in EKG: low voltage QRS complexes, electrical needed Etiologies: complication of acute pericarditis or systolic pressure w/ inspiration alternans - pericardial window drainage if recurrent trauma; malignancy MC non-traumatic cause Dyspnea, fatigue, peripheral edema, shock, reflex CXR: may show enlarged cardiac silhouette tachycardia, cool extremities Right heart catheterization: equalization of pressures in diastole Constrictive Loss of pericardial elasticity (thickening, fibrosis, dyspnea (MC), fatigue, orthopnea CXR: pericardial calcification may be seen esp. on Diuretics for symptom relief as well as Pericarditis calcification) leading to restriction of ventricular lateral view, clear lung fields reduction of edema & venous pressure diastolic filling Right-sided HF signs: normal or slightly increased heart size ↑ JVD, peripheral edema, N/V square root sign on cardiac catheterization Definitive: pericardiectomy PATHO: fibrosis limits ventricular filling, decreased ↑ hepatojugular reflex stroke volume & cardiac output Kussmaul’s sign (the lack of an inspiratory Echo: pericardial thickening &/or calcification decline or an ↑ in jugular vein pressure w/ (also used to r/o restrictive cardiomyopathy) Etiologies: any cause of acute pericarditis inspiration) ”square root” sign – early diastolic dip followed US – idiopathic & viral MCC by a plateau if diastasis worldwide – TB MCC Pericardial knock: high pitched diastolic sound similar to S3 (sudden cessation of ventricular CT scan/MRI: pericardial thickening or filling) calcification Heart Failure About Clinical Manifestations Diagnostics Management ACCF/AHA & HFSA: complex clinical syndrome that results L-side sxs: pulmonary venous congestion (Lungs, L-sided) DX: suspect if 1+ s/sxs of HF w/ no Lifestyle: smoking cessation, alcohol restriction, from any structural or functional impairment of ventricular dyspnea MC apparent non-cardiac cause sodium ≤3g/d, fluid ≤1.5-2L/d, weight loss filling or ejection of blood leading to cardinal manifestations *exertional, orthopnea, paroxysmal nocturnal dyspnea of dyspnea, fatigue, fluid retention fatigue ECHO: assess LVEF Guideline-Directed Medical Therapy (GDMT): rales/crackles (less likely in chronic HF) LVEF ≥50% à workup for HFpEF diuretic PLUS Chronic HF: pts w/ longstanding (e.g., months-years) s/sxs LVEF 100pg/mL ACEI: if no hx of angioedema (“prils”) HFrEF: EF ≤40% PE: S3 gallop (+/- S4) ARB: for pts that cannot take ARNI or ACEI HFmrEF: EF 40-50% apical impulse displaced downward & to the left NT-proBNP: (“sartan”) HFpEF: EF ≥50% +/- pulsus alternans 450pg/mL 50-75y: >900pg/mL Beta blocker: carvedilol, metoprolol succinate, HFrEF Etiologies: Severe HF: anxious, diaphoretic, dyspneic, pallor, >75y: >1800pg/mL bisoprolol CAD (infarction/ischemia) duskiness, cool extremities, cyanosis valvular (AS, AR, MR, TR) EKG: can show AFIB, LA enlargement, ISDN-hydralazine: alternative to angiotensin congenital (shunts, systemic RV failure) NYHA Functional Classification: LVH, pathologic Q waves blockers (ARNI, ACEI, ARB) infectious (chagas, HIV) Class I: no limitation of activity, ordinary activity does not nonischemic CM (infiltrative, familial, tachycardia-induced) cause symptoms CXR: findings of pulmonary edema Secondary Therapy: toxic CM (chemo, immunotherapy, hydroxychloroquine, Class II: slight limitation; comfortable at rest, but cephalization of pulmonary vessels MRA (spironolactone, eplerenone): for pts who alcohol, cocaine) ordinary activity causes symptoms Kerley B lines are symptomatic (stages II-IV) + have EF ≤35% on chronic pulmonary vascular disease (cor pulmonale, Class III: marked limitation; only comfortable at rest, less peribronchial cuffing optimal initial pharmacologic therapy pulmonary arterial HTN) than ordinary activity causes symptoms pleural effusions autoimmune (giant cell myocarditis, lupus myocarditis) Class IV: symptoms at rest, unable to carry out any cardiomegaly Other secondary therapies depend on activity without symptoms indications: SGLT2-inhibitors, vericiguat, HFpEF Etiologies: Hemodynamic exercise test: RHC w/ ivabradine, digoxin HTN, CAD PCWP assessed at rest & w/ exercise valvular (AS, MS) PCWP ≥15mmHg at rest Acute HF: restrictive CM (amyloidosis, sarcoidosis, hemochromatosis) PCWP ≥25mmHg w/ exercise loop diuretic: first line for volume overload w/ hypertrophic CM, aging, myocarditis, obesity congestion endomyocardial fibroelastosis Labs: CMP, CBC, coagulation studies, vasodilators: used for pulmonary congestion UA for rapid relief of dyspnea High-Output HF: thyrotoxicosis, obesity, anemia, cirrhosis, elevated BUN/Cr *IV NTG, sodium nitroprusside, nesiritide AV shunt, chronic lung disease, vitamin B deficiency hyponatremia, hypo/hyperkalemia inotropic therapy: used for hypotension (beriberi), myeloproliferative disorder anemia *dobutamine, milrinone, dopamine position: sit pt up, have legs dangle over bed to PATHO: elevated cardiac filling pressure &/or inadequate decrease preload/venous return; positive peripheral oxygen delivery, at rest or during stress, caused by pressure (ventilation) cardiac dysfunction HEART FAILURE PHARM MOA Indications/Contraindications ADRs/Other Beta Blockers: MOA: antagonize ligand (NE, E) at beta-adrenergic receptors which ↓ Indications: reduce morbidity/mortality in HF pts; all HF pts should ADRs: ↓ HR/BP, fatigue, dizziness, decreased libido, Bisoprolol (β1) vasoconstriction receive a BB impotence, ↑ TGs, weight gain/edema Metoprolol succinate (β1) Beta-1: heart – increase HR & contractility Carvedilol (⍺1, β1/2) Beta-2: lungs/vascular smooth muscle – bronchodilation & Contraindications: severe bradycardia, 2nd/3rd degree heart block vasodilation ACEI: MOA: block angiotensin converting enzyme (ACE), reducing effects of Indication: reduce mortality rate in pts w/ HF; all HF pts should ADRs: cough, angioedema Enalapril AgII & decreasing stimulation of aldosterone receive an ACEI Lisinopril Warnings: angioedema, renal impairment, hyperkalemia, Quinapril Contraindications: pregnancy, hx of angioedema hypotension, renal artery stenosis (avoid use) Ramipril ARBs: MOA: block AgII from binding autonomic receptors, inhibiting Indication: reduce mortality rate in pts w/ HF; all pts should receive ADRs: dizziness, HA, rash Candesartan vasoconstriction and fluid retention if ACEI is contraindicated Losartan Valsartan ARNI: MOA: angiotensin receptor & neprilysin inhibitor Indications: ADRs: cough, dizziness Sacubitril/Valsartan neprilysin is an enzyme responsible for degradation of several Class II-IV pts to reduce hospitalization & cardiovascular death vasodilatory peptides, including natriuretic peptide & bradykinin Class II-III pts who are symptomatic & tolerate ACEI/ARB, in place of ACEI/ARB to further reduce mortality COMBO DRUG W/ ARB (valsartan) Contraindications: pregnancy, hx of angioedema, use w/ ACEI/ARB Aldosterone Receptor MOA: compete w/ aldosterone for binding at receptors at the distal Indication: reduce morbidity/mortality in HF pts; should be added to ADRs: hyperkalemia, increased serum creatinine, dizziness Antagonists: convoluted tubule & collecting ducts à decreased Na/water tx in pts w/ class II-IV Spironolactone retention Contraindications: hyperkalemia, anuria, significant renal Eplerenone impairment, diseases that cause increase in K (Addison’s) Loop Diuretics: MOA: Indications: no mortality benefit in HF pts; used to relieve sxs ADRs: ↓ Na, K, Cl, Mg, Ca, hyperuricemia, increased blood Furosemide block sodium/chloride reabsorption in the thick ascending loop of related to congestion/edema glucose, increased TG/total cholesterol, orthostatic Bumetanide Henle by interfering w/ the chloride-binding co-transport system hypotension, photosensitivity, increased urination Torsemide increases excretion of Na, K, Cl, Mg, Ca, & H2O Contraindications: anuria Ethacrynic acid reduces blood volume (decreases congestion/edema) Ethacrynic acid: ototoxicity – hearing loss, tinnitus, vertigo Hydralazine & Nitrates: MOA: Indications: Hydralazine: HA, reflex tachycardia, palpitations, fluid Hydralazine hydralazine is a direct arterial vasodilator (↓ afterload) decreases mortality (not as much as ACEI/ARB); indicated for pts retention, peripheral neuritis Isosorbide dinitrate (ISDN) nitrates increase the availability of NO which causes venous who cannot tolerate an ACEI/ARB due to poor renal function, hx of Isosorbide mononitrate vasodilation (↓ preload) angioedema, or hyperkalemia Nitrates: HA, dizziness, lightheadedness, flushing, Hydralazine + ISDN black pts w/ Class III-IV HF who are still symptomatic despite hypotension, tachyphylaxis, syncope optimal tx w/ ACEIs/BBs Contraindications: concurrent use w/ PDE-5 inhibitors (nitrates) Digoxin MOA: inhibits Na/K ATPase pump resulting in ↑ CO (positive Indication: ADRs: dizziness, mental disturbances, HA, N/V/D inotrope); exerts parasympathetic effect at AV node which ↓ HR no mortality benefit, but reduces hospitalizations; improves sxs, (negative chronotrope) exercise tolerance, & QOL Warnings: 2nd/3rd degree heart block (w/o pacemaker), pts who remain symptomatic despite optimal tx w/ ACEI/ARB & BB certain forms of AFIB (WPW) Contraindications: VFIB Ivabradine MOA: hyperpolarization-activated cyclic nucleotide gated channel Indications: no mortality benefit, but reduces hospitalizations ADRs: bradycardia, HTN, AFIB, luminous phenomena blocker (HCN-blocker); inhibits “funny channels” in the sinus node, ↓ Class II-III HF, LVEF ≤35% (seeing flashes of light) sinus rate which ↓ HR sinus rhythm w/ resting HF ≥70bpm either on maximally tolerated BB dose or have CI to BB Contraindications: ADHF, BP tricuspid > pulmonic *IVDU = tricuspid MC ▪repeat q24-48h until clearance » NVE: vancomycin + (ceftriaxone or cefepime) (IE) » PVE: vancomycin + gentamicin + cefepime RF: male, >60yo, IVDU, poor dentition, structural heart disease (e.g., MVP, ECHO: vegetations (hyperechoic), perivalvular abscess, new rheumatic heart disease), congenital heart disease (e.g., bicuspid AV, VSD, valvular regurgitation, prosthetic valve dehiscence (rocking) Targeted ABX therapy: *minimum of 4-6wks PDA), prior IE, indwelling IV, chronic hemodialysis, HIV⊕ » TTE within 12h of presentation, repeat after TX completed ▪MSSA » TEE indications: » NVE: nafcillin or oxacillin Acute Bacterial Endocarditis (ABE): ▪high risk (e.g., prosthetic valve, congenital heart disease, » PVE: nafcillin/oxacillin + rifampin + gentamicin » infection of healthy valves w/ highly virulent organism (S. aureus MCC) prior IE, new murmur, heart failure) ▪MRSA ▪rapid, fulminant progression; fatal within 6wks if left untreated ▪inconclusive TTE or concern for intracardiac complications » NVE: vancomycin Subacute Bacterial Endocarditis (SBE): » PVE: vancomycin + rifampin + gentamicin » infection of abnormal valves w/ less virulent organism (viridans streptococci MCC) Modified Duke Criteria: ▪viridans streptococci ▪indolent infection; progresses slowly over weeks to months ▪Pathologic Criteria: » (penicillin G or ceftriaxone) + gentamicin ➀ microorganisms shown by culture/histology of vegetation ▪enterococci Native Valve Endocarditis (NVE): IE Pathogens: ➁ features of active endocarditis present on histology » (ampicillin or penicillin G) + gentamicin » MCC: S. aureus, viridans streptococci, enterococci ▪S. epidermis (CoNS): peripheral venous catheters ▪HACEK: ceftriaxone ▪S. aureus: acute clinical course; common in IVDU ▪S. bovis: associated w/ colorectal cancer/IBD » Definite IE: ▪Viridans streptococci: subacute clinical course ▪HACEK (gram⊖): oral cavity/GI tract; mostly PVE ➀ 2 major Surgery consult: PVE, HF, uncontrolled IE, ▪Enterococci (E. faecalis): UTIs, GI/GU procedures perivalvular extension/complications, fungal IE, ➁ 1 major + 3 minor high embolic risk ➂ 5 minor Prosthetic Valve Endocarditis (PVE): IVDU: right-sided IE ⇢ tricuspid > pulmonic ▪valve replacement or repair » Early PVE (≤12mo postoperatively): » MCC: S. aureus (70%), streptococci, CoNS ➃ 1 pathologic criteria » Possible IE: ➀ 12mo postoperatively): » RF: immunodeficiency, IVDU, indwelling catheters ➁ 3 minor ➁ previous endocarditis ▪streptococci (viridans streptococci & S. bovis) Culture⊖ IE: Coxiella, Mycoplasma, Bartonella, ➂ unrepaired cyanotic congenital heart disease ▪S. aureus, CoNS, enterococci Legionella, Chlamydia spp., Brucella ➃ repaired CHD during first 6mo after repair Rejected DX (any one): ➄ repaired CHD w/ residual defects S/SXS: FEVER (90%, MC SXS); often associated w/ chills, anorexia, & weight loss ▪definite/possible IE criteria not met ➅ cardiac transplant recipients who develop ▪malaise, HA, myalgia/arthralgia, night sweats, abdominal pain, dyspnea ▪firm alternative diagnosis present cardiac valvulopathy » CV: MURMUR (new/change), HF, arrhythmias (suspect perivalvular abscess if new conduction delay) ▪IE symptoms resolve in ≤4d of ABX therapy Invasive Procedures: » Intraabdominal emboli: glomerulonephritis (hematuria), splenomegaly ▪no pathologic evidence of IE found at surgery or autopsy » dental procedures (e.g., tooth extraction) » Peripheral emboli & immunologic phenomena: petechiae, splinter (subungual) hemorrhages » respiratory tract procedures w/ mucosa incision ▪Janeway lesions: nontender erythematous macules on palms/soles (cutaneous septic emboli) Additional Evaluation: » procedures on skin/soft tissue infections ▪Osler nodes: painful nodules on finger/toe pads caused by immune complex deposition (“Osler, ouch”) ▪LABS: leukocytosis w/ left shift, ⇡ ESR/CRP, ⊕RF, anemia » tonsillectomy & adenoidectomy ▪Roth spots: round retinal hemorrhages w/ pale centers ▪baseline EKG w/ subsequent telemetry (conduction delay) REGIMEN: amoxicillin 2g PO 30-60min before » Neurologic: embolic stroke (visual loss, motor weakness, aphasia), intracerebral hemorrhage, abscess ▪CXR (septic emboli, infiltrate, CHF) » cephalexin 2g if PCN allergy  About Screening/Diagnostics Management Hyperlipidemia High TC only = hypercholesterolemia S/SXS: most are asymptomatic TX: lower LDL ▶ statins (HLD) High TGs only = hypertriglyceridemia – High LDL à xanthomas TX: lower triglycerides ▶ fibrates High TC + TGs = hyperlipidemia tendinous (e.g., Achilles, patellar, back of hand) palmar (yellowish plaques), tuberous (located over joints) Initiate statin therapy for: Primary Causes: familial genetic disorders eruptive (reddish papules all over body) 1) anyone w/ ASCVD (MI, stable/unstable angina, stroke, PAD, etc.) Secondary Causes: diabetes, alcohol, CKD, hypothyroidism, – High LDL à xanthelasma (smaller than xanthoma) 2) anyone w/ LDL ≥190mg/dL primary biliary cirrhosis/other liver disease, medications yellow collection of cholesterol under skin, usually on/around eyelids 3) adults 40-75yo w/ ⊕ diabetes regardless of LDL (e.g., thiazides, BBs, retinoids, antiretrovirals, cyclosporine, – Hypertriglyceridemia 4) adults 40-75yo w/ LDL 70-189mg/dL & ≥7.5% 10y ASCVD risk estrogen, steroids) lipemia retinalis (cream-colored blood vessels in fundus) pancreatitis (>500mg/dL) Treatment goals: Traditional ASCVD Risk Factors: HTN, diabetes, family hx of – ≥50% LDL reduction for high-intensity statin premature ASCVD, cigarette smoking, CKD, obesity Screening Guidelines: determine if 1+ traditional RFs present & obtain – ≥30% LDL reduction for moderate-intensity statin baseline fasting lipid profile for individuals ≥20yo, reassess risk q4-6y Risk-Enhancing Factors: if 1+ traditional RF (HTN, obesity, diabetes, etc.): – family hx of premature ASCVD (M 0.5 Hemothorax: or neoplastic (MC lymphomatous) damage to thoracic duct ➂ pleural fluid LDH/serum LDH >0.6 ▪fluid resuscitation, PRBCs ▪small pleural effusion (50% peripheral Hct) d/t S/SXS: dyspnea, pleuritic CP (retrosternal), dry cough Additional PF markers: Exudative: trauma, spontaneous PTX, coagulopathy, etc. ⇣ tactile fremitus, ⇣ breath sounds, dullness to percussion ▪PF cholesterol >55mg/dL Malignant: » pleural friction rub (uncommon) ▪PF LDH >200U/L ▪therapeutic thoracentesis Empyema: pus in the pleural space; can occur as complication ▪PF protein >3.0g/dL ▪indwelling pleural catheter to pneumonia, abscess, etc. ▪PF glucose 0.3 Trapped Lung: encasement w/ fibrous peel ⇡ ⊖intrapleural pressure caused by empyema or tumor ⇢ transudation of fluid ▪Albumin gradient (serum-PF) 8mm blastomycosis, histoplasmosis neurofibroma, leiomyoma, angioma ▪subsolid: 2.5 ⇢ high probability of malignancy mucoid impaction Management MALIGNANT: Solid nodule: Low risk (65%) risk: ▪Bronchogenic carcinoma: adenocarcinoma, SCC, ▪Metastatic lesions (e.g., breast, head/neck, colon, 8mm ▪CT at 3mo, 9-12mo, & 18-24mo ▪FDG PET/CT &/or biopsy ▪Miscellaneous: plasmacytoma, schwannoma ⤷ ⊕growth at any f/u ⇢ biopsy » intermediate: FDG PET/CT ⤷ SUV > 2.5 ⇢ biopsy Initial assessment ⇢ probability of malignancy » high ⇢ biopsy or excision ▪low risk: 65% 50% risk ➁ Risk factors for lung cancer ▪current/former smoker** » ≤8mm: annual CT x5y ▪family history, female, emphysema » >8mm: FDG PET/CT ⇢ biopsy/resect if ⊕ ▪prior malignancy, asbestos exposure About DX Bronchogenic MCC of cancer-related deaths in the US Types ⇢ ➀ Small Cell Lung Cancer (SCLC) – 15% First ⇢ CXR Central: transbronchial biopsy Carcinoma Risk Factors: smoking, asbestos ➁ Non-Small Cell Lung Cancer (NSCLC) – 85% Then ⇢ CT w/ contrast Carcinoid: pink/purple, well-vascularized Adenocarcinoma (MC) Histopathology: S/SXS: cough, SOB, fever, weight loss, fatigue *Bronchoalveolar Carcinoma (adeno in situ) Adenocarcinoma: ▪neoplastic gland formation, pneumocyte marker expression (TTF-1), or Squamous Cell Carcinoma intracytoplasmic mucin Large Cell Carcinoma Squamous: ▪keratin production by tumor cells &/or intracellular desmosomes Small Cell Lung Cancer (SCLC): Carcinoid Tumors Large Cell: ▪sheets of round/polygonal cells w/ prominent nucleoli & abundant pale central, aggressive, often METS at presentation staining cytoplasm w/o differentiating features Paraneoplastic: Cushing’s, SIADH, SVC syndrome (face/neck swelling), Lambert-Eaton (proximal muscle weakness, dry mouth, hyporeflexia) Immunohistochemistry: ▪SCLC ⊕ TTF-1, high proliferation rate (Ki-67, MIB-1) Adenocarcinoma: *asbestos exposure Large Cell Carcinoma: ▪Adenocarcinoma ⊕ TTF-1, napsin A, CK 7, mucicarmine, PAS-D peripheral, slow growing, MC seen in non-smokers central or peripheral, rare ⊖ thyroglobulin Paraneoplastic: thrombophlebitis large peripheral mass w/ prominent necrosis MC ▪Squamous ⊕ p40, p63, CK 5/6, desmoglein Paraneoplastic: gynecomastia ⊖ CK 7 (usually) Squamous Cell Carcinoma: Management central, often associated w/ hemoptysis NSCLC: surgical excision, radiation + chemo hypercalcemia, +/- elevated PTHrp SCLC: chemo + radiation, no surgery! Pancoast syndrome: shooting arm pain/weakness, Horner’s (ipsilateral miosis, ptosis, anhidrosis) Screening: USPSTF recommends ANNUAL low-dose CT screening for those 55-80 who have no sxs of lung Carcinoid Tumors ⇢ excess secretion of serotonin, histamine, bradykinin cancer + a 30PPY smoking hx who currently smoke or have quit within 15yrs central, GI tract MC site, lung 2nd MC S/SXS: hemoptysis, focal wheezing, recurrent pneumonia Carcinoid syndrome: flushing, diarrhea, hypotension PULM About Clinical Manifestations Diagnostics Management Pneumonia Community-Acquired Pneumonia (CAP) CAP: acute onset fever, cough (+/- sputum), dyspnea LABS: CBC, CMP, CPR, procalcitonin CAP, outpatient: outside hospital or within 48h of admission EXAM: tachycardia, tachypnea, crackles (rales), rhonchi leukocytosis w/ left shift Amoxicillin + macrolide (preferred) – tactile fremitus, egophony, dullness to percussion procalcitonin – Doxycycline is macrolide alternative RF: older age, tobacco use, excessive ETOH use, 100mg/L interstitial infiltrates – Doxycycline is macrolide alternative cavitations FQ monotherapy (alternative) Mycoplasma *MC in ambulatory setting S/SXS: gradual onset HA, malaise, low-grade fever +/- sore throat VIRAL: bilateral, multifocal, patchy or CAP, inpatient, non-ICU: – cough (+/- sputum) follows, may have pleuritic CP/SOB ground-glass opacities antipneumococcal beta lactam + macrolide *chest soreness from persistent coughing common complaint *dense consolidations, pleural FQ monotherapy – ⊕ URI SXS (rhinorrhea, otitis media, sinusitis, cervical LAD) effusion & abscess should be Non-Respiratory Associated Disease: absent CAP, inpatient, ICU: autoimmune hemolysis (cold agglutinin disease), usually mild BACTERIAL: dense lobar or alveolar antipneumococcal beta lactam + Azithromycin Viral Pathogens (“Atypical” Presentation): mucocutaneous disease consolidations *preferred RSV, influenza, parainfluenza – erythema multiforme, SJS, other skin rashes, mucositis antipneumococcal beta lactam + FQ CMV, adenovirus, SARS-CoV-2 mild hepatic transaminase elevations CURB-65 Assessment (1pt each) arthralgias & myalgias C – confusion – Suspect MRSA: ⊕ Vancomycin or Linezolid Nosocomial Pneumonia U – BUN >19mg/dL (>7mmol/L urea) – Suspect Pseudomonas: – Hospital-Acquired Pneumonia (HAP) Nosocomial: new lung infiltrate + ≥2 clinical features of infection R – respiratory rate ≥30 beta lactam + FQ acquired >48h after admission S/SXS: new-onset fever, leukocytosis or leukopenia, purulent B – SBP 48h after endotracheal intubation 0-1: outpatient ABX REVIEW Pathogens (Nosocomial): Pseudomonas: IV antibiotics within past 90d, structural lung 2: admission Anti-MRSA: Vancomycin, Linezolid Pseudomonas aeruginosa (cystic fibrosis) disease (e.g., cystic fibrosis, bronchiectasis) ≥3: assess for ICU care (esp. if 4-5) Respiratory FQ Enterobacter spp. – Levofloxacin, Moxifloxacin, Gemifloxacin (PO) Acinetobacter spp. Microbiology (only need if inpatient) Antipseudomonal FQ: Ciprofloxacin, Levofloxacin S. aureus (esp. MRSA) blood culture x2 Antipneumococcal Beta Lactam: RF: recent abx use, prolonged hospitalization (≥5d) sputum gram stain + culture – Augmentin, Ampicillin-Sulbactam (Unasyn) S. pneumoniae urine antigen – Ceftriaxone, Cefotaxime, Ertapenem PCR for Legionella Antipneumo + Antipseudomonal Beta Lactam: PCR for pneumonia (BioFire PN) – Piperacillin-Tazobactam (Zosyn), Imipenem – Meropenem, Cefepime, Ceftazidime Macrolides: Azithromycin, Clarithromycin Nosocomial (Pseudomonas coverage): Zosyn or Cefepime – Risk of MRSA: ⊕ Vancomycin or Linezolid About Clinical Manifestations Diagnostics Management Pneumocystis PCP: interstitial pneumonia caused by the yeast-like S/SXS: gradual onset fever, dry cough, & dyspnea progressing CXR: diffuse, bilateral perihilar infiltrates TX: TMP-SMX x21d Alternatives: Pneumonia fungal organism Pneumocystis jirovecii over days to weeks ▪dapsone + trimethoprim (PCP) ▪fatigue, chills, CP, weight loss HRCT: bilateral patchy or nodular ground ▪primaquine + clindamycin Transmission: airborne ▪5-10% of patients are asymptomatic glass opacities HIV⊕ w/ moderate/severe PCP ⇢ add prednisone *AIDS-DEFINING ILLNESS ⇢ CD4 ♀ (2:1) ▪hepatic studies: Modest ⇡ AST & alk phos ▪treatment of underlying conditions MCC ⇢ ▪chronic viral hepatitis (HBV, HCV**) Others ⇢ ▪meds (e.g., MTX, APAP, ISN) ▪autoimmune hepatitis ⇡ bilirubin, ⇣ albumin, ⇡ GGT ▪alcohol-associated liver disease ▪primary biliary cirrhosis ▪Wilson disease ▪avoid hepatotoxic drugs: NSAIDs, opiates, ▪hemochromatosis ▪primary sclerosing cholangitis ▪right-sided HF ▪coagulation studies ⇡ PT, ⇡ INR BDZs (HE) ▪nonalcoholic fatty liver disease (NAFLD) ▪α1-antitrypsin deficiency ▪veno-occlusive disease i.e., Budd-Chiari ▪CBC: thrombocytopenia (MC), anemia, leukopenia ▪vaccinations: PPSV23, HAV/HBV, influenza Clinical Manifestations: ▪hyponatremia (common in cirrhosis + ascites) ▪adequate nutritional intake ▪muscle cramps (can be severe), easy bruising, LE edema ▪anovulation (♀): amenorrhea, menstrual irregularities ▪fever, diarrhea, pruritis, muscle wasting ▪hypogonadism (♂): gynecomastia, ⇣ libido, testicular atrophy IMAGING: Definitive ⇢ liver transplant ▪⇣ MAP (contributes to hepatorenal syndrome) ▪Skin: jaundice, dark urine, spider angiomata (telangiectasia) ▪U/S: surface nodularity, ⇡ echogenicity, small liver ▪indications: index complication (e.g., ▪hepatosplenomegaly, ascites ⇡⇡ bilirubin: jaundice usually not detectable until >2-3mg/dL ▪Caudate/left lobes: hypertrophy ascites, HE, variceal hemorrhage) &/or ▪caput medusae ⇢ dilated abdominal veins ▪Fetor hepaticus (sweet, pungent smelling breath): dimethyl ▪Right lobe: atrophy MELD score ≥15 ▪palmar erythema, clubbing (MC in 1° biliary cirrhosis) sulfide accumulation, suggests severe portal-systemic shunting ▪Dupuytren’s contractures (i.e., thickening/shortening of palmar LIVER BX ⇢ confirmatory Hemochromatosis: phlebotomy, fascia causes flexion deformities of fingers) Deferoxamine (iron-chelation) Hemochromatosis: Wilson Disease *ATP7B gene mutation Hemochromatosis (bronze diabetes) *HFE gene defect ▪transferrin sat ≥45%, ⇡ ferritin >200-300ng/mL Wilson: Penicillamine, avoid seafood & ▪copper accumulation results from impaired excretion ▪excess iron deposition as a result of ⇡ iron absorption ▪BX: ⇡ hemosiderin other high-copper foods ▪S/SXS: Parkinsonism, mood disturbances, cirrhosis ▪S/SXS: diabetes + dark (bronze) skin + cirrhosis ▪Kayser-Fleisher rings (corneal copper accumulation) Wilson: ⇣ ceruloplasmin, ⇡ urinary copper excretion ▪slit lamp (Kayser-Fleischer rings) COMPLICATIONS: ▪BX: ⇡ copper content Hepatic Encephalopathy ⇢ ammonia accumulation in brain Hepatic Encephalopathy: ▪cognitive deficits + impaired neuromuscular function ▪lactulose + rifaximin, liver transplant ▪asterixis: flapping tremor Portal Vein Thrombosis (PVT) ⇢ thrombus in the portal vein PVT: anticoagulation (enoxaparin) ▪contributes to development of portal HTN Cirrhosis Complications of Portal HTN Esophageal varices ⇢ UGIB Ascites ⇢ accumulation of fluid within the peritoneal cavity TX: therapeutic paracentesis S/SXS: hematemesis &/or melena S/SXS: abdominal distention/pain, early satiety ▪salt restriction ≤2g/d, +/- fluid restriction DX: EGD – prediction of variceal hemorrhage: location, size, appearance, clinical features, variceal pressure DX: paracentesis ▪diuretics (spironolactone, furosemide) ▪⊕red signs associated w/ ⇡ bleeding risk Spontaneous bacterial peritonitis (SBP) ⇢ infection of ascitic TX: IV cefotaxime 2g q8h x5d, IV albumin, TX: bleeding prophylaxis ⇢ beta blockers (e.g., propranolol or nadolol), endoscopic variceal band ligation fluid w/o an intraabdominal secondary source repeat paracentesis 48h later TX: variceal hemorrhage ⇢ PRBCs to maintain Hgb ≥7g/dL, octreotide (preferred) or vasopressin ▪common pathogens: E. coli, strep, Klebsiella ▪ABX prophylaxis: IV ceftriaxone x7d S/SXS: fever, abdominal pain/tenderness, AMS ▪endoscopic variceal band ligation** (1st line), sclerotherapy, balloon tamponade, TIPS (alternatives) DX: paracentesis ⇢ PMN (neutrophil) count ≥250 cells/mm3 Hepatorenal syndrome ⇢ development of renal failure in a patient who has advanced liver disease d/t Portopulmonary HTN ⇢ pulmonary HTN + portal HTN Cirrhotic cardiomyopathy ⇢ normal CO & cirrhosis, severe alcoholic liver disease, acute liver failure, etc. S/SXS: fatigue, dyspnea, peripheral edema, CP, syncope contractility at rest & a dysfunctional or blunted response to stress DX: ⇡ creatinine, normal urine sediment, no/minimal proteinuria ( scarring secondary to diverticulitis > volvulus dilated bowel loops w/ air-fluid levels in ladder-like appearance decompression of obstructed segment major factor in clinical course of LBO is competence of ileocecal valve ▪3-6-9 rule: small bowel >3cm, large bowel >6cm, cecum >9cm Options: ▪30% ⇢ incompetent ileocecal valve: allows decompression of large bowel into ileum ▪SBO dilated loops ⇢ central, LBO dilated loops ⇢ peripheral resection + primary anastomosis ▪MC ⇢ ileocecal valve does NOT allow reflux to occur: closed loop obstruction w/ rapidly ⇡ little/no air distal to obstruction resection + diversion, diversion alone intraluminal pressure ⇢ impaired capillary circulation, mucosal ischemia, bacterial translocation pneumoperitoneum ⇢ perforation endoscopic stent placement w/ systemic toxicity ⇢ gangrene, perforation SIGMOID Volvulus: coffee bean sign (bent inner tube, kidney bean) dilated loop w/ absent haustrae, arises in LLQ & extends ⇢ RUQ Cecal: ileocecal resection or R colectomy w/ VOLVULUS: torsion of bowel on its axis ⇢ closed loop obstruction; sigmoid MC (75%), cecal (25%) proximal colonic/small bowel dilation w/ air-fluid levels, ⊘distally ileocolic anastomosis torsion of mesenteric vascular pedicle ⇢ occlusion/thrombosis of mesenteric vessels ⇢ bowel CECAL Volvulus: Sigmoid: strangulation, ischemia, & gangrene dilated loop w/ maintained haustrae, arises in RLQ & extends ⇢ LUQ ⊘signs of peritonitis: upward displacement of appendix, ⊘colonic dilation distally sigmoidoscopy w/ rectal tube insertion for dilated small bowel loops w/ multiple air-fluid levels decompression, detorsion, & reduction CT (volvulus): whirl sign pathognomonic surgery if fails ⊕signs of peritonitis/ischemia: sigmoid colectomy & primary anastomosis  About Clinical Manifestations Diagnostics Management Colorectal Most arise from adenomatous polyps Iron deficiency anemia (fatigue, weakness), Colonoscopy w/ bx: diagnostic TOC Localized: surgical resection (radical vs. Cancer (CRC) MC cause of large bowel obstruction in adults rectal bleeding, abdominal pain, change in endoscopic) + post-op chemo to destroy bowel habits Barium enema: apple core lesion residual cells & micrometastases Risk Factors: age >50yrs (peak 65yrs), AA, family hx of CRC Advanced disease: ascites, abdominal masses, Labs: iron deficiency anemia, (CRC is MC cause of occult GI Metastatic: palliative chemo IBD: UC > Crohn hepatomegaly bleeding in adults) diet (low fiber, high in red or processed meat, animal fat) Chemotherapy: obesity, smoking, ETOH Right-Sided (Proximal): chronic occult bleeding Tumor markers: CEA is MC monitored FOLFOX (iron deficiency anemia, + guaiac), diarrhea -folinic acid (leucovorin calcium) Protective Factors: physical activity, regular use of ASA, NSAIDs Screening: any of the 3 approaches -fluorouracil Left-Sided (Distal): bowel obstruction; present fecal occult blood test annually starting at 50yrs -oxaliplatin Genetics: later & cause changes in stool diameter – may colonoscopy q10yrs for ages 50-75 FOLFIRI Familial Adenomatous Polyposis: genetic mutation of APC gene; develop Streptococcus bovis endocarditis flexible sigmoidoscopy q5yrs + fecal occult blood testing -folinic acid (leucovorin calcium) adenomas begin in childhood – almost all will develop colon q3yrs -fluorouracil cancer by age 45yrs; prophylactic colectomy best for survival ↓ risk: -irinotecan pedunculated Lynch Syndrome: colonoscopy q1-2yrs beginning at 20- VGEF inhibitor: bevacizumab Turcot Syndrome: FAP-like syndrome + CNS tumors tubular 25yrs (medulloblastoma, glial tumors) 1cm low risk: q5-10yrs type I: esp. seen on right side 1-2 polyps, 16,000/µL ➉ base deficit >4mEq/L ⑪ sequestration of fluid >6L Chronic Progressive inflammatory changes to the pancreas that lead to Amylase & lipase usually normal ETOH abstinence, pain control, low fat diet, vitamin Pancreatitis loss of pancreatic endocrine & exocrine function supplementation CT: calcification of the pancreas (often done in pts w/ acute pain to r/o other causes of Etiologies: ETOH abuse MC, idiopathic abdominal pain) Oral pancreatic enzyme replacement hypocalcemia, hyperlipidemia, islet cell tumors, familial, trauma, iatrogenic; gallstones not significant as in acute Abdominal x-ray: calcified pancreas Pancreatectomy only if retractable pain despite medical therapy S/SXS: ➀ calcification ➁ steatorrhea ➂ diabetes Endoscopic U/S or ERCP *seen in only 1/3 of patients ▪weight loss, epigastric/back pain may be atypical or absent Pancreatic function testing: fecal elastase most sensitive & specific; pancreatic HEPATITIS Transmission Acute/Chronic Incubation Period Clinical Manifestations Serology/Diagnostics Management HAV Fecal-oral ACUTE 15-45d (4wks) Prodromal sxs: Acute: IgM anti-HAV No treatment needed (self-limiting) anorexia, N/V Past exposure: IgG HAV Ab fatigue, malaise, arthralgias, myalgias Post-Exposure Prophylaxis: HA, photophobia LFTs: ↑ AST/ALT & bilirubin healthy, age 1-40: HAV vaccine preferred over pharyngitis, cough, coryza immunoglobulin (within 2wks of exposure) immunocomp, chronic liver disease: HAV vaccine + 1-2wks later à jaundice, +/- RUQ pain HAV immunoglobulin (within 2wks) HBV Sex & blood BOTH 30-180d (8-12wks) HBsAg (surface antigen): (+) in acute & chronic Supportive – majority will not become chronic Dark urine, clay-colored stools – may Anti-HBs (surface antibody): (+) if recovered/immunized appear 1-5d before onset of jaundice Anti-HBc (core antibody): Chronic Mgmt: acute: IgM antiviral therapy may be indicated if persistent, chronic/recovered: IgG severe sxs, marked jaundice, (bilirubin >10), HbeAg (envelope antigen): replicative (chronic) inflammation on liver bx, ↑ ALT or (+) HB envelope Anti-Hbe (envelope antibody): non-replicative (chronic) antigen present entecavir, tenofovir LFTs: ↑ bilirubin tx can be stopped after confirmation pt has cleared acute: AST/ALT in the thousands HBsAg chronic: AST/ALT in the hundreds Vaccine: derived from yeast, CI if allergic to baker’s HBV DNA: best way to assess viral replications activity yeast infant: given @ birth, 1-2mo, 6-18mo Liver bx adult: 3 doses @ 0, 1, 6mo HCV Blood (IVDU MC) BOTH 15-160d (7wks) Screening test: HCV antibodies