๐ŸŒ SMLE ยท subject

SMLE Medicine Syllabus

The Medicine syllabus for SMLE in full: 2 chapters and 6 topics, every one listed below, plus 51 Medicine flashcards with answers.

2Chapters
6Topics
51Flashcards

Medicine syllabus: all 2 chapters

Expand any chapter to see its topics and sub-topics.

  1. Cardiology

    3 topics
    • Ischemic Heart Disease
    • Heart Failure
    • Arrhythmias
  2. Respiratory

    3 topics
    • Chronic Obstructive Pulmonary Disease
    • Asthma
    • Pneumonia

SMLE Medicine flashcards โ€” 51 questions with answers

  1. What is the underlying pathophysiology of ischemic heart disease (IHD)?

    An imbalance between myocardial oxygen supply and demand, most often caused by atherosclerotic narrowing of the coronary arteries, leading to myocardial ischemia.

  2. Differentiate stable angina from unstable angina based on symptom pattern.

    Stable angina: predictable chest pain on exertion, relieved by rest or nitroglycerin within minutes. Unstable angina: new-onset, rest, or crescendo pain that is more frequent/severe and NOT reliably relieved by rest โ€” an acute coronary syndrome.

  3. How do you distinguish unstable angina from NSTEMI?

    Both show no persistent ST elevation. Unstable angina has NORMAL cardiac troponins, whereas NSTEMI shows ELEVATED troponins (myocardial necrosis has occurred).

  4. What ECG finding defines STEMI, and what does it indicate?

    Persistent ST-segment elevation (or new left bundle branch block) indicating full-thickness (transmural) myocardial infarction from complete coronary occlusion.

  5. Which cardiac biomarker is most sensitive and specific for myocardial infarction, and its time course?

    Cardiac troponin (T or I). It rises within 3-4 hours, peaks at ~24-48 hours, and remains elevated for up to 7-14 days.

  6. What is the reperfusion strategy of choice for STEMI and its key time targets?

    Primary percutaneous coronary intervention (PCI). Target door-to-balloon time <90 minutes; if PCI is unavailable, give fibrinolysis within 30 minutes (door-to-needle) provided presentation is within 12 hours of symptom onset.

  7. List the components of initial medical therapy (MONA-BASH) for acute coronary syndrome.

    Morphine (if needed), Oxygen (if $SaO_2 < 90\%$), Nitrates, Aspirin, plus Beta-blocker, ACE inhibitor, Statin (high-intensity), and Heparin/anticoagulation. Add a second antiplatelet (P2Y12 inhibitor) for dual antiplatelet therapy.

  8. ECG leads II, III, and aVF show ST elevation. Which artery and wall are affected?

    Inferior wall myocardial infarction, usually from occlusion of the right coronary artery (RCA).

  9. Which coronary artery supplies the anterior wall, and which leads show its infarction?

    The left anterior descending (LAD) artery; anterior MI shows ST changes in the precordial leads $V_1$-$V_4$.

  10. Define heart failure.

    A clinical syndrome in which the heart cannot pump blood at a rate sufficient to meet the metabolic demands of tissues, or can do so only at elevated filling pressures.

  11. How are HFrEF and HFpEF distinguished by ejection fraction?

    HFrEF (reduced EF / systolic failure): $LVEF \leq 40\%$. HFpEF (preserved EF / diastolic failure): $LVEF \geq 50\%$ with impaired ventricular relaxation. An EF of 41-49% is HF with mildly reduced EF.

  12. State the formula for ejection fraction.

    $$EF = \frac{SV}{EDV} \times 100\% = \frac{EDV - ESV}{EDV} \times 100\%$$ where $SV$ is stroke volume, $EDV$ end-diastolic volume, and $ESV$ end-systolic volume. Normal is $\geq 55\%$.

  13. Contrast the typical clinical features of left-sided versus right-sided heart failure.

    Left-sided: pulmonary congestion โ€” dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pulmonary crackles. Right-sided: systemic congestion โ€” peripheral edema, raised JVP, hepatomegaly, ascites.

  14. Which biomarker aids in diagnosing heart failure and what does a low value suggest?

    BNP (or NT-proBNP), released from stretched ventricular myocardium. A low/normal BNP has a high negative predictive value, effectively ruling out heart failure as the cause of dyspnea.

  15. Name the four drug classes proven to reduce mortality in HFrEF (the 'four pillars').

    1) ARNI or ACE inhibitor/ARB, 2) Beta-blocker, 3) Mineralocorticoid receptor antagonist (e.g., spironolactone), 4) SGLT2 inhibitor. Diuretics relieve congestion but do not improve mortality.

  16. Describe the NYHA functional classification of heart failure.

    Class I: no symptoms with ordinary activity. Class II: slight limitation, symptoms with ordinary activity. Class III: marked limitation, symptoms with less-than-ordinary activity. Class IV: symptoms at rest.

  17. What compensatory mechanism initially maintains cardiac output in heart failure but becomes maladaptive?

    Neurohormonal activation โ€” the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). Chronically they cause vasoconstriction, salt/water retention, and adverse cardiac remodeling.

  18. State the relationship between cardiac output, heart rate, and stroke volume.

    $$CO = HR \times SV$$ Cardiac output equals heart rate multiplied by stroke volume (normal resting $CO \approx 4$-$8\ \text{L/min}$).

  19. What is the most common sustained cardiac arrhythmia, and its hallmark ECG features?

    Atrial fibrillation. ECG shows an irregularly irregular rhythm with absent P waves and a fibrillating (chaotic) baseline.

  20. What scoring system guides anticoagulation in atrial fibrillation, and its components?

    $CHA_2DS_2$-VASc: Congestive HF, Hypertension, Age $\geq 75$ (2 points), Diabetes, prior Stroke/TIA (2 points), Vascular disease, Age 65-74, Sex category (female). Anticoagulate when the score is $\geq 2$ in men or $\geq 3$ in women.

Show the other 31 Medicine flashcards
  1. Differentiate first-, second-, and third-degree AV block.

    First-degree: PR interval prolonged $> 200\ \text{ms}$, all beats conducted. Second-degree Mobitz I (Wenckebach): progressive PR lengthening until a dropped beat; Mobitz II: intermittent dropped beats with constant PR. Third-degree (complete): total AV dissociation โ€” atria and ventricles beat independently.

  2. What is the immediate management of pulseless ventricular tachycardia or ventricular fibrillation?

    Immediate unsynchronized defibrillation (shock) plus high-quality CPR, following the ACLS cardiac arrest algorithm; give epinephrine and consider amiodarone for shock-refractory rhythms.

  3. Define torsades de pointes and a key precipitating factor.

    A polymorphic ventricular tachycardia with a characteristic twisting-of-the-points QRS around the baseline, precipitated by a prolonged QT interval (from drugs, hypokalemia, hypomagnesemia). Treat with IV magnesium sulfate.

  4. How is the corrected QT interval (QTc) calculated by Bazett's formula?

    $$QT_c = \frac{QT}{\sqrt{RR}}$$ where $QT$ and $RR$ are in seconds. Prolonged if $QT_c > 440\ \text{ms}$ in men or $> 460\ \text{ms}$ in women.

  5. What ECG feature characterizes Wolff-Parkinson-White (WPW) syndrome?

    A short PR interval and a delta wave (slurred QRS upstroke) due to an accessory pathway (bundle of Kent) causing ventricular pre-excitation, predisposing to re-entrant tachycardia.

  6. What is the first-line management of stable, regular narrow-complex supraventricular tachycardia (SVT)?

    Vagal maneuvers first; if unsuccessful, IV adenosine (rapid push). If the patient is hemodynamically unstable, perform synchronized cardioversion.

  7. State the normal ranges for the PR interval and QRS duration on ECG.

    PR interval: $120$-$200\ \text{ms}$ (3-5 small boxes). QRS duration: $< 120\ \text{ms}$ (< 3 small boxes); a wide QRS $\geq 120\ \text{ms}$ suggests ventricular origin or a bundle branch block.

  8. Define chronic obstructive pulmonary disease (COPD).

    A chronic, largely irreversible airflow limitation caused by chronic bronchitis and/or emphysema, usually due to a noxious exposure โ€” most commonly cigarette smoke โ€” producing persistent respiratory symptoms.

  9. What spirometry criterion confirms an obstructive pattern in COPD?

    A post-bronchodilator $\frac{FEV_1}{FVC} < 0.70$, indicating airflow limitation that is not fully reversible.

  10. Contrast the classic 'pink puffer' and 'blue bloater' phenotypes of COPD.

    Pink puffer (emphysema-predominant): thin, marked dyspnea, pursed-lip breathing, relatively normal blood gases. Blue bloater (chronic bronchitis-predominant): overweight, cyanosis, cough with sputum, hypoxemia/hypercapnia, and cor pulmonale.

  11. Define chronic bronchitis clinically.

    A productive cough present for at least 3 months in each of 2 consecutive years, in the absence of other explanations.

  12. Which genetic deficiency causes early-onset emphysema, especially in non-smokers?

    Alpha-1 antitrypsin ($\alpha_1$-antitrypsin) deficiency, which allows unopposed neutrophil elastase to destroy alveolar tissue, classically causing panacinar, basal-predominant emphysema.

  13. What is the only intervention proven to reduce mortality and slow decline in COPD (besides smoking cessation)?

    Long-term oxygen therapy (LTOT) in patients with chronic resting hypoxemia ($PaO_2 \leq 55\ \text{mmHg}$, or $\leq 59\ \text{mmHg}$ with cor pulmonale/polycythemia), used $\geq 15$ hours/day. Smoking cessation is the single most effective intervention overall.

  14. What target oxygen saturation range is recommended during a COPD exacerbation, and why?

    $88$-$92\%$. Excessive oxygen can blunt hypoxic respiratory drive and worsen ventilation-perfusion matching, causing $CO_2$ retention and respiratory acidosis in chronic $CO_2$ retainers.

  15. List the core pharmacologic management of an acute COPD exacerbation.

    Short-acting bronchodilators (SABA + short-acting antimuscarinic), systemic corticosteroids (e.g., prednisolone ~5 days), antibiotics if increased sputum purulence/volume, controlled oxygen, and non-invasive ventilation (BiPAP) for hypercapnic respiratory failure.

  16. Define asthma.

    A chronic inflammatory airway disease characterized by reversible airflow obstruction, bronchial hyperresponsiveness, and airway inflammation, producing episodic wheeze, cough, chest tightness, and dyspnea.

  17. How does spirometry demonstrate reversibility in asthma?

    An obstructive pattern ($\downarrow FEV_1/FVC$) that improves after a bronchodilator, defined as an increase in $FEV_1$ of $\geq 12\%$ AND $\geq 200\ \text{mL}$.

  18. What is the preferred controller therapy foundation for asthma, and why not SABA alone?

    Inhaled corticosteroids (ICS), often combined with a long-acting beta-agonist (LABA) as needed or maintenance. SABA-only treatment is discouraged because it controls symptoms without treating underlying inflammation and is linked to increased exacerbation and mortality risk.

  19. List the clinical features that classify an asthma attack as life-threatening.

    $PEF < 33\%$ predicted, $SpO_2 < 92\%$, silent chest, cyanosis, poor respiratory effort, bradycardia/arrhythmia/hypotension, exhaustion, confusion, or a normal/rising $PaCO_2$ (a sign of impending respiratory failure).

  20. In an acute severe asthma exacerbation, what does a normal or rising PaCO2 indicate?

    Impending respiratory failure. Early in an attack $PaCO_2$ is low from hyperventilation; a normalizing or rising $PaCO_2$ signals the patient is tiring and cannot maintain ventilation โ€” a critical warning sign.

  21. Outline the emergency treatment of acute severe asthma.

    High-flow oxygen (target $SpO_2\ 94$-$98\%$), nebulized SABA (salbutamol) plus ipratropium, systemic corticosteroids, and IV magnesium sulfate for severe/life-threatening cases; escalate to ICU if not improving.

  22. Name the classic asthma triad known as Samter's triad (aspirin-exacerbated respiratory disease).

    Asthma, nasal polyps, and aspirin (NSAID) sensitivity.

  23. Contrast asthma and COPD on reversibility, age of onset, and typical trigger.

    Asthma: largely reversible airflow obstruction, often childhood onset, atopy/allergen triggers, eosinophilic inflammation. COPD: largely irreversible obstruction, onset usually after age 40, smoking-related, neutrophilic inflammation.

  24. Define pneumonia.

    An acute infection of the lung parenchyma (alveoli and distal airways) causing consolidation, typically presenting with fever, cough, sputum, dyspnea, and pleuritic chest pain.

  25. What is the most common bacterial cause of community-acquired pneumonia (CAP)?

    Streptococcus pneumoniae (pneumococcus).

  26. What does the CURB-65 score assess, and what do its components stand for?

    It estimates CAP severity and guides admission. Confusion, Urea $> 7\ \text{mmol/L}$, Respiratory rate $\geq 30$, Blood pressure (systolic $< 90$ or diastolic $\leq 60\ \text{mmHg}$), Age $\geq 65$. Each scores 1 point; $0$-$1$ outpatient, $2$ consider admission, $\geq 3$ hospital/ICU assessment.

  27. Differentiate typical from atypical pneumonia.

    Typical (e.g., S. pneumoniae): abrupt high fever, productive purulent sputum, lobar consolidation. Atypical (e.g., Mycoplasma, Legionella, Chlamydophila): gradual onset, dry cough, prominent extrapulmonary symptoms, and diffuse/interstitial infiltrates with milder-looking chest exam ('walking pneumonia').

  28. Which organism causes pneumonia associated with hyponatremia, GI symptoms, and exposure to contaminated water systems?

    Legionella pneumophila (Legionnaires' disease). Diagnosis is aided by the urinary Legionella antigen test.

  29. Distinguish hospital-acquired pneumonia (HAP) from community-acquired pneumonia (CAP) by definition.

    HAP develops $\geq 48$ hours after hospital admission; CAP is acquired outside the hospital or within the first 48 hours of admission. HAP more often involves gram-negative bacilli, S. aureus (including MRSA), and resistant organisms.

  30. Which pathogen classically causes 'currant jelly' sputum and cavitating pneumonia, especially in alcoholics/diabetics?

    Klebsiella pneumoniae โ€” associated with thick red-brown ('currant jelly') sputum, upper-lobe involvement, and abscess/cavity formation.

  31. What is the empiric outpatient antibiotic approach for community-acquired pneumonia in an otherwise healthy adult?

    A macrolide (e.g., azithromycin) or doxycycline; amoxicillin is also used. For patients with comorbidities, a respiratory fluoroquinolone or a beta-lactam plus a macrolide is preferred to cover typical and atypical organisms.

SMLE Medicine FAQ

What is in the SMLE Medicine syllabus?

SMLE Medicine is split into 2 chapters: Cardiology and Respiratory. Together they contain 6 topics.

How many chapters are in SMLE Medicine?

2 chapters, containing 6 topics. The largest chapter is Cardiology, with 3 topics.

Are there flashcards for SMLE Medicine?

Yes โ€” a 51-card Medicine deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.