Cardiovascular, Pulmonology, GI/Nutritional, Orthopedics/Rheumatology, Endocrinology, Neurology, Urology/Renal, Hematology, Oncology, Infectious Disease

Flashcards for Internal Medicine topics including Cardiovascular, Pulmonology, GI/Nutritional, Orthopedics/Rheumatology, Endocrinology, Neurology, Urology/Renal, Hematology, Oncology, and Infectious Disease.

Coronary Artery Disease (CAD)

Leading cause of mortality in the US; most commonly caused by atherosclerosis.

Ischemic Heart Disease

Spectrum including Asymptomatic ",Silent" CAD, Stable Angina Pectoris, Unstable Angina, NSTEMI, and STEMI.

Acute Coronary Syndrome (ACS)

Acute ischemia, including Unstable Angina (UA), NSTEMI, and STEMI.

Risk Factors for CAD

Age (>65 for women or premature menopause, >55 for men), family history (female

Primary Prevention of CAD

Risk factor reduction: smoking cessation, low-fat/high-grain diet, BP goal (

Secondary Prevention of CAD

Pharmacologic therapy: ASA 81mg QD, clopidogrel & ticagrelor, statins, beta blockers, ACEI (ARB if not tolerated).

Stable Angina Pectoris

Manifestation of stable atherosclerotic CAD where myocardial oxygen demand exceeds supply, causing predictable chest discomfort with physical or emotional stress.

EKG Ischemia Findings

T wave flattening, hyperacute T waves, T wave inversions, ST depressions.

Atypical Angina (",anginal equivalents")

Dyspnea, N/V, fatigue, diaphoresis, faintness; more common in women, diabetics, and the elderly.

Typical Angina

Substernal chest pain provoked by exertion/emotional stress and relieved by rest/NTG (3/3 criteria).

Atypical Angina

Substernal chest pain provoked by exertion/emotional stress or relieved by rest/NTG (2/3 criteria).

Noncardiac Chest Pain

0-1/3 of the typical angina criteria.

Stress Testing for Angina

Nuclear perfusion imaging and ECHO.

Gold Standard for Angina Diagnosis

Cardiac catheterization, coronary CT angiography.

Acute Treatment for Angina

Sublingual nitroglycerin q5min up to 3x.

First-line Prevention Therapy for Angina

Beta blockers.

Indications for Revascularization with CABG

Chronic stable angina with 3-vessel disease, 2-vessel disease with prominent LAD involvement, 1/2-vessel disease with high-risk features (LV dysfunction), >50% stenosis of left artery, or refractory symptoms.

Vasospastic Angina (Prinzmetal or Variant Angina)

Focal or diffuse spasm of epicardial coronary artery leading to dynamic high-grade obstruction due to vascular smooth muscle hyperreactivity.

Vasospastic Angina Symptoms

Chest pain indistinguishable from obstructive CAD, predominantly at rest, often 12am to early morning, lasting 5-15 minutes, and responding rapidly to NTG.

Vasospastic Angina Triggers

Changes in autonomic activity, cocaine, amphetamines, marijuana, alcohol, ephedrine-based products, triptans, 5-FU, ergonovine, Mg deficiency, hyperventilation, allergic reactions, exposure to extreme cold.

EKG in Vasospastic Angina

Normal between episodes; transient ST-elevation/depression during episodes. Troponins are negative.

Vasospastic Angina Management

Sublingual NTG, smoking cessation, ASCVD risk factor modification. CCBs (diltiazem, amlodipine) are used to prevent vasoconstriction and promote vasodilation. Nonselective beta blockers (e.g., propranolol) should be avoided.

Beta Blockers (β1-Selective)

Bisoprolol, Betaxolol, Atenolol, Metoprolol, Acebutolol. MOA: β1 receptor antagonism, decreasing myocardial oxygen demand. Indications: chronic stable angina, unstable angina (mortality benefit). Contraindications: vasospastic angina, acute HF, 2nd/3rd degree heart block. Do not stop abruptly (rebound angina).

Nitrates (Vasodilators)

Short-acting (NTG SL, TL spray) and long-acting (NTG ointment/patch, ISMN, ISDN). MOA: release NO, causing vasodilation, decreasing preload and increasing myocardial O2 supply. Indications: immediate relief for all angina patients (short-acting), add-on or alternative therapy (long-acting). Contraindications: use with PDE-5 inhibitors.

Calcium Channel Blockers (CCBs)

DHPs (Nifedipine, Amlodipine) and Non-DHPs (Verapamil, Diltiazem). MOA: inhibit calcium entry into myocardial cells, decreasing cardiac workload and O2 demand, increasing myocardial blood supply. Indications: stable angina, Prinzmetal. Specific contraindications for Non-DHPs: SBP <90, cardiogenic shock, AV block, acute MI, pulmonary congestion.

Ranolazine (Ranexa)

Anti-anginal medication that may decrease myocardial O2 demand by decreasing late phase Na current. Useful for chronic angina despite standard therapy. No mortality benefit. Warnings: prolongs QT interval (do NOT use if prolonged QT).

Acute Coronary Syndrome (ACS) Spectrum

Unstable Angina (UA), Non-ST Elevation Myocardial Infarction (NSTEMI), and ST-Elevation Myocardial Infarction (STEMI).

Unstable Angina (UA)

Ischemia without necrosis, partial obstruction. +/- EKG findings, negative biomarkers.

Non-ST Elevation Myocardial Infarction (NSTEMI)

Ischemia with necrosis, partial obstruction. +/- EKG findings, positive biomarkers.

ST-Elevation Myocardial Infarction (STEMI)

Ischemia with necrosis, complete obstruction. Positive EKG findings, positive biomarkers.

Pathophysiology of ACS

Progressive growth of atherosclerotic lesions leading to decreased luminal diameter and blood flow. Acute coronary plaque disruption leads to exposed thrombogenic endothelium, platelet aggregation, and thrombus formation.

Universal MI Classification

Type 1 (spontaneous), Type 2 (secondary to ischemic imbalance), Type 3 (death without biomarkers), Type 4 (PCI related), Type 5 (CABG related).

Early Complications of MI

Heart failure, cardiogenic shock, bradyarrhythmias, AV block, tachyarrhythmias, LV free wall rupture, interventricular septum rupture, papillary muscle rupture.

Late Complications of MI

LV thrombus, LV aneurysm, Pleuropericarditis (Dressler Syndrome).

Unstable Angina (UA) Clinical Presentation

New-onset angina, angina with increasing frequency or duration, angina with minimal exertion or at rest.

Most Common MI Symptom

Substernal chest tightness/pressure, radiating to L arm, neck/jaw, epigastrium, occurring at rest, lasting >30min (Levine sign).

Atypical MI Presentation

Dyspnea, weakness, sweating, N/V, epigastric pain, palpitations, dizziness, fatigue. Common in women, elderly, diabetics.

EKG for ACS

Obtained within 10 minutes of arrival. STEMI: ST elevations ≥1mm in 2 contiguous leads, new LBBB, new Q waves. UA/NSTEMI: normal, T wave inversions, ST depressions.

Inferior Lead EKG Changes

Suggest RV infarction; requires R-sided EKG. ST elevation in V4R indicates RV infarction. ST depression in V1 & V2 suggests posterior infarction.

Cardiac Enzymes for MI

High sensitivity cardiac troponins I & T are preferred (rise 2-3h, peak 12-24h, normalize 7-10d). CK-MB (rise 3-4h, peak 12-24h, normalize 1-2d). Myoglobin (rise 1-2h, peak 4-6h, normalize 24h).

AMI Protocol

EKG within 10min, door-to-PCI within 90min (120min with travel to PCI facility).

Immediate Measures for All ACS Patients (ANOM)

Aspirin 162-325mg chewed, 0.4mg SL NTG q5min x3 (avoid in inferior MI, PDE-5 inhibitor use), O2 (if SpO2 <90%), morphine (if refractory to NTG).

Medications Initiated within First 24h for ACS

Beta blocker (avoid in RVMI, acute HF, bradycardia, AV block), ACEI/ARB, high-intensity statin.

Additional Therapies for All ACS

Antiplatelet drug (P2Y12) + Anticoagulant (UFH, LMWH). GP IIb/IIIa antagonists not routinely used.

STEMI Reperfusion Therapy

PCI preferred (placement of drug-eluting stent). Fibrinolysis only if PCI unavailable within 120min.

UA/NSTEMI Management

TIMI score to assess need for PCI. Fibrinolysis NOT useful. Score ≥3 indicates benefit to early revascularization.

Discharge Medications for All ACS Patients

DAPT (ASA 81mg + P2Y12) for ≥1yr (ASA 81mg indefinitely), beta blocker + ACEI + statin indefinitely.

Aspirin (ASA) MOA

Irreversibly binds to/inhibits COX-1/COX-2 enzymes (cardioprotective effects at 75-160mg by inhibiting TXA2 and decreasing platelet activation).

Aspirin Indications

ACS (chewed), secondary prevention of CV death, MI, stroke (mortality benefit).

Aspirin Contraindications

NSAID/salicylate allergy, asthma, rhinitis, nasal polyps, children with viral infection (Reyes).

ADP Receptor Antagonists (P2Y12 Inhibitors)

Clopidogrel, Prasugrel (irreversible); Ticagrelor, Cangrelor (reversible). MOA: bind ADP P2Y12 platelet receptor, inhibiting ADP-induced platelet aggregation. Indications: ACS; secondary prevention of MI, stroke, PAD (Clopidogrel). Contraindications: serious active bleed.

Indirect Thrombin Inhibitors

UFH, Fondaparinux, LMWH (Enoxaparin, Dalteparin). MOA: bind to antithrombin III to accelerate its activity, enhancing inactivation of thrombin and factor Xa. Indications: ACS, VTE. Contraindications: history of HIT, active bleed, severe thrombocytopenia.

Direct Thrombin Inhibitor (Bivalirudin)

MOA: reversibly binds to both circulating and clot-bound thrombin, inhibiting fibrin activation. Indications: PCI as alternative to heparin. Monitor: ACT, aPTT, PT/INR.

Beta Blockers in ACS (Adjunctive)

β1-Selective (Bisoprolol, Metoprolol, Atenolol) and ⍺ + β blockers (Carvedilol, Labetalol). MOA: block sympathetic stimulation, decreasing myocardial oxygen demand/risk of VFIB, improving LV function. Indications: ALL ACS patients within first 24h indefinitely (mortality benefit). Contraindications: RV MI, active HF, 2nd/3rd degree block, asthma, hypotension, bradycardia, prolonged PR. Do not stop abruptly (rebound angina).

Statins in ACS (Adjunctive)

Simvastatin, Pravastatin, Lovastatin, Atorvastatin, Rosuvastatin. MOA: inhibit HMG-CoA reductase, increasing LDL receptors, promoting LDL clearance, reducing triglycerides. Indications: best drug to decrease LDL; decrease cardiovascular complications. Contraindications: active hepatic disease, elevated LFTs, pregnancy/breastfeeding.

Fibrinolysis/Thrombolytics

Tissue Plasminogen Activators (Alteplase, Reteplase, Tenecteplase). MOA: activate plasminogen to plasmin, which degrades fibrin. Indications: STEMI ONLY, if PCI unavailable within 120min and symptom onset ≤12h. Absolute contraindications: active internal bleed, history of ICH, CVA in past 1yr, intracranial neoplasm, suspected aortic dissection/pericarditis.

Sinus Tachycardia

HR 100 – (220 – age)bpm; gradual onset/termination, P wave identical to NSR. Usually physiologic response. Management: treat underlying etiology, beta blockers, CCBs.

Sinus Bradycardia

HR <55-60bpm. Etiologies: rheumatologic, infectious, infiltrative, autonomic (increased vagal tone), iatrogenic (AVN blocking agents), metabolic. Management: stable (DC AV nodal blocking agents), unstable (atropine, dopamine/epinephrine, pacing).

Sick Sinus Syndrome (SND)

Abnormality in SA node action potential generation or conduction. Includes inappropriate sinus bradycardia, tachy-brady syndrome, sinus pause/arrest, SA nodal exit block, chronotropic incompetence. MCC: sinus node degeneration. Management: treat reversible causes, permanent pacemaker for symptomatic patients.

AV Blocks (First-Degree)

Delayed conduction through AV node, prolonged PR interval (>200ms). Typically benign, rarely symptomatic. No treatment needed.

AV Blocks (Second-Degree Mobitz Type I / Wenckebach)

Progressively longer PR interval followed by non-conducted P wave (dropped QRS). Block occurs IN the AV node. Typically benign. No treatment needed.

AV Blocks (Second-Degree Mobitz Type II)

Random dropped QRS, stable PR interval. Block occurs BELOW the AV node. More serious, can lead to complete block. Permanent pacemaker often required.

AV Blocks (Third-Degree / Complete Heart Block)

NO atrial impulses reach ventricles. Complete dissociation between P waves and QRS complexes. Block occurs BELOW the AV node. Permanent pacemaker imperative.

Atrial Flutter (AFL)

Second most common arrhythmia. Typically isthmus-dependent (single reentrant circuit around tricuspid annulus). Increased risk of thrombus formation. EKG: atrial rate ~300bpm, ventricular rate ~150bpm, ",sawtooth" pattern (negative in inferior leads, positive in V1). Management: unstable (cardioversion), stable (antiarrhythmics, rate control). Definitive: radiofrequency ablation.

Atrial Fibrillation (AFIB)

Most common arrhythmia. Multiple irritable atrial foci. MCC: uncontrolled HTN and CAD. Increased risk of thrombus formation/embolization. EKG: irregularly irregular rhythm, absence of discrete P waves (fibrillatory waves 350-600bpm). Management: immediate DCC (unstable), rate/rhythm control (stable). Anticoagulation therapy is crucial based on CHADS-VASc score.

AV Nodal Reentrant Tachycardia (AVNRT)

Most common PSVT (~60%). HR 120-200bpm; sudden onset/termination. Patho: reentry circuit via fast and slow pathways in AV node. EKG: P wave usually buried in QRS. Management: vagal maneuvers, IV adenosine (first line), catheter ablation. Prevention: AV nodal blocking agents.

AV Reciprocating Tachycardia (AVRT)

Less common reentry mechanism via bypass tract between atria/ventricles. Orthodromic (narrow QRS) or Antidromic (wide QRS, delta wave). Risk of VFIB. Management: vagal maneuvers, IV adenosine, AVN blocking agents. Refractory cases: catheter ablation.

Wolff-Parkinson White Syndrome (WPW)

Congenital accessory pathway (Bundle of Kent) with associated SVT. EKG: delta wave, short PR interval (

Wandering Atrial Pacemaker (WAP)

≥3 ectopic atrial foci generating impulses, irregularly irregular rhythm, varying PR intervals. HR ≤100bpm. Benign, requires no treatment.

Multifocal Atrial Tachycardia (MAT)

≥3 ectopic atrial foci generating impulses, irregularly irregular rhythm, varying PR intervals. HR >100bpm. Associated with COPD. Management: verapamil (COPD), metoprolol, magnesium/potassium repletion. AADs and cardioversion not useful.

Premature Atrial Contraction (PAC)

Typically normal variant. EKG: premature beat followed by normal QRS, P wave different morphology. Usually no treatment required.

Premature Ventricular Contraction (PVC)

Occasional in healthy adults. EKG: premature wide QRS without preceding P wave, followed by fully compensatory pause. Usually no treatment required. ≥3 PVCs = nonsustained VTACH.

Ventricular Tachycardia (VT)

≥3 consecutive PVCs. Monomorphic (uniform QRS) or Polymorphic (varying QRS). MCC: acute MI, dilated cardiomyopathy. Management: unstable (cardioversion), stable (IV amiodarone). Pulseless: ACLS.

Torsades de Pointes

Paroxysmal polymorphic VT secondary to QT prolongation (acquired or congenital). EKG: sinusoidal, rates >200bpm. Management: IV magnesium sulfate. Unstable: DCC.

Ventricular Fibrillation (VFIB)

Total disorganized ventricular depolarization, complete loss of CO. Etiologies: MI, cardiomyopathy, degradation of VT. EKG: chaotic irregular zigzag pattern, no identifiable P waves or QRS complexes. Management: ACLS Algorithm (CPR, defibrillation, epinephrine, amiodarone).

Bundle Branch Block (BBB)

Characterized by prolonged QRS duration and terminal conduction delay. Complete (QRS ≥120ms), Incomplete (QRS 110-120ms).

Right Bundle Branch Block (RBBB)

Delay in depolarization of RV; can occur in healthy heart. EKG: terminal R wave in V1/V2 (rSR'), broad S waves in V5/V6.

Left Bundle Branch Block (LBBB)

Delay in depolarization of LV; entire sequence of ventricular activation is altered; NOT found in a healthy heart. EKG: broad, notched, or slurred R waves in I, aVL, V5/V6; dominant S wave in V1; absence of Q waves in lateral leads. Management for BBB: asymptomatic (no treatment), symptomatic (permanent pacemaker).

Fascicular Blocks (Hemiblocks)

Partial blocks in left bundle system (left anterior or posterior fascicular blocks). Generally do not prolong QRS but cause left/right axis deviation. No specific treatment, address underlying disorder.

Class Ia Antiarrhythmics (Na-channel blockers)

Disopyramide, Quinidine, Procainamide. MOA: block Na & K channels, prolonging AP duration. ADRs: torsades, hypotension, tachycardia, tinnitus.

Class Ib Antiarrhythmics (Na-channel blockers)

Lidocaine, Mexiletine. MOA: block Na channels (fast). Indications: ventricular arrhythmias only. ADRs: lightheadedness, dizziness, N/V, tremor.

Class Ic Antiarrhythmics (Na-channel blockers)

Flecainide, Propafenone. MOA: block Na channels (slow), significantly reducing conduction & automaticity. Indications: life-threatening ventricular arrhythmias, PSVT, AFIB/flutter (in pts without structural heart disease). ADRs: dizziness, visual disturbances.

Class II Antiarrhythmics (Beta Blockers)

MOA: block sympathetic stimulation, increasing refractoriness, decreasing automaticity and conduction velocity. Indications: slow ventricular rate in SVTs (e.g., AFIB).

Class III Antiarrhythmics (K-channel blockers)

Dronedarone, Dofetilide, Sotalol, Ibutilide, Amiodarone. MOA: delay phase 3 repolarization, prolonging AP duration and refractory period. Indications: various arrhythmias. ADRs: QT prolongation. Amiodarone: photosensitivity (blue discoloration), neurotoxicity, hypothyroidism, corneal microdeposits.

Class IV Antiarrhythmics (CCBs)

Verapamil, Diltiazem. MOA: block L-type calcium channels, slowing AV/SA node conduction velocity. Indications: ventricular rate control for supraventricular arrhythmias. Should NOT be used in LV systolic dysfunction or decompensated HF (negative inotropic effects).

Adenosine (Miscellaneous AAD)

MOA: slows conduction through AV node. Indications: rapid conversion to NSR in PSVT. ADRs: transient new arrhythmias, facial flushing, chest pain.

Digoxin (Miscellaneous AAD)

MOA: inhibits Na/K ATPase, increasing CO (positive inotrope), decreasing HR (negative chronotrope). Indications: ventricular rate control in SVT (not useful during exercise), often used with BB or CCB. Contraindications: VFIB.

Dilated Cardiomyopathy (DCM)

Most common type. Reduced strength of contraction and systolic dysfunction, leading to ventricular enlargement and progressive heart failure. Etiologies: idiopathic, viral, genetic, HTN, alcohol, postpartum. ECHO: LV dilation, thin walls, decreased EF. Management: ACEI, BB, diuretics. AICD if EF <35-30%.

Hypertrophic Cardiomyopathy (HCM)

Autosomal dominant genetic disorder with inappropriate LV/RV hypertrophy and diastolic dysfunction. Subaortic outflow obstruction. Symptoms: dyspnea, fatigue, angina, syncope. Murmur: harsh systolic at LLSB, increases with decreased venous return (Valsalva, standing). ECHO: asymmetric wall thickness, systolic anterior motion of mitral valve. Management: BBs, CCBs, disopyramide. Avoid dehydration, exertion, digoxin, nitrates, diuretics.

Restrictive Cardiomyopathy (RCM)

Diastolic dysfunction in a non-dilated ventricle, impeding ventricular filling (stiff ventricle). Etiologies: infiltrative diseases (amyloidosis MCC, sarcoidosis, hemochromatosis). Symptoms: R-sided HF > L-sided HF. ECHO: non-dilated ventricles, diastolic dysfunction, marked atrial dilation. Management: treat underlying disorder.

Stress (Takotsubo) Cardiomyopathy

Transient regional systolic dysfunction of LV, mimicking MI in absence of obstructive CAD/plaque rupture. Risk factors: postmenopausal women with stress. Symptoms: substernal CP, dyspnea, syncope. EKG: ST elevation. ECHO: apical LV ballooning. Management: ASA, NTG, BB, heparin, ACEI, serial imaging.

ACCF/AHA Heart Failure Classification

Complex clinical syndrome from ventricular filling/ejection impairment, leading to dyspnea, fatigue, fluid retention. Includes HFrEF (EF ≤40%), HFmrEF (EF 40-50%), HFpEF (EF ≥50%).

Left-Sided Heart Failure Symptoms

Pulmonary venous congestion (lungs): dyspnea (exertional, orthopnea, PND), fatigue, rales/crackles.

Right-Sided Heart Failure Symptoms

Systemic venous congestion (SVC, IVC, hepatic): weight gain, lower extremity edema, abdominal bloating, anorexia, RUQ pain, hepatomegaly, splenomegaly, increased JVP.

NYHA Functional Classification (Heart Failure)

Class I (no limitation), Class II (slight limitation), Class III (marked limitation), Class IV (symptoms at rest).

Heart Failure Diagnostics

ECHO (assess LVEF), BNP/NT-proBNP (>100pg/mL for BNP), EKG (AFIB, LA enlargement, LVH), CXR (pulmonary edema, cardiomegaly), hemodynamic exercise test (RHC), labs (elevated BUN/Cr, hyponatremia, anemia).

Heart Failure Lifestyle Management

Smoking cessation, alcohol restriction, sodium ≤3g/d, fluid ≤1.5-2L/d, weight loss.

Guideline-Directed Medical Therapy (GDMT) for HFrEF

Diuretic + ARNI/ACEI/ARB + Beta Blocker. Secondary: MRA (spironolactone, eplerenone) for symptomatic pts (stages II-IV) with EF ≤35%. Other: SGLT2-inhibitors, vericiguat, ivabradine, digoxin.

Acute Heart Failure Management

Loop diuretic (first line for volume overload), vasodilators (IV NTG, sodium nitroprusside, nesiritide for pulmonary congestion), inotropic therapy (dobutamine, milrinone, dopamine for hypotension). Position: sit patient up with legs dangling.

Beta Blockers in Heart Failure (Pharmacology)

Bisoprolol, Metoprolol succinate, Carvedilol. MOA: antagonize beta-adrenergic receptors, reducing vasoconstriction, HR, and contractility. Indications: reduce morbidity/mortality in HF; all HF patients should receive. Contraindications: severe bradycardia, 2nd/3rd degree heart block.