Cardiology — MCQs
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All of the following regarding the Universal Definition of Myocardial Infarction are true EXCEPT?
A 20-year-old girl presented with low-grade fever, malaise, night sweats, weight loss, arthralgia, and fatigue for 1 month. On examination, peripheral pulses were weak in the upper extremities and a bruit was present over the carotid and subclavian arteries. Investigations revealed dilatation of the proximal aorta. What is the most likely diagnosis?
Ventricular Tachycardia is represented by all, except:
A 57-year-old man comes to see you for follow-up 4 weeks after being discharged from hospital for unstable angina. His coronary angiogram showed moderate nonstenotic disease in two vessels. The cardiologist asks you to follow up on his fasting lipid profile since it was not checked in the hospital. His T-chol is 240 mg/dL, LDL 120 mg/dL, HDL 50 mg/dL, and triglycerides 130 mg/dL. For the above patient with dyslipidemia, select the most appropriate treatment?
Which of the following is seen in rheumatic fever?
All of the following statements about pulse deficit in Atrial Fibrillation are true, except?
CCF is associated with an increase in all of the following except?
A 40-year-old female G4P4L3A1, who delivered her third child 1 month ago, presented with recent onset of cough and palpitations associated with paroxysmal nocturnal dyspnea, orthopnea, and exertional intolerance. The patient also complained of a few episodes of hemoptysis 2 days prior. She had a history of pre-eclampsia in her last pregnancy. On examination, Jugular Venous Pressure was increased, with crepitations in bilateral basal lung fields and a shift of the apical impulse. Echocardiogram studies showed a left ventricular ejection fraction < 45%. Despite treatment, the patient did not survive. Histopathological examination was performed on the autopsied heart. Which finding would be most likely present on histopathological examination?
A young lady complains of sudden onset of palpitations, extreme weakness, and sweating. On examination, she was found to have a blood pressure of 90/70 mmHg with a regular pulse rate of 180/minute. Her symptoms disappeared after vomiting but she complained of polyuria. What is the most likely diagnosis?
JVP wave with absent y descent and prominent x wave is seen in which condition?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 381: All of the following regarding the Universal Definition of Myocardial Infarction are true EXCEPT?
- A. Sudden unexpected cardiac death with symptoms of ischemia
- B. New regional wall motion abnormality with raised cardiac biomarkers
- C. Three times increase in troponin levels are required for coronary artery bypass grafting (Correct Answer)
- D. Reinfarction can be diagnosed if increased troponin levels by 5-7% in serial samples
Explanation: The **Fourth Universal Definition of Myocardial Infarction (UDMI)** classifies MI into five types based on etiology and clinical context [1], [2]. ### **Explanation of the Correct Option** **Option C is the correct (false) statement.** According to the UDMI, **Type 5 MI** (related to CABG) is defined by an elevation of cardiac troponin (cTn) values **>10 times** the 99th percentile Upper Reference Limit (URL) in patients with normal baseline values, occurring within 48 hours post-procedure. A "three times" increase is insufficient for the diagnosis of Type 5 MI. ### **Analysis of Other Options** * **Option A (Type 3 MI):** This refers to sudden unexpected cardiac death involving symptoms suggestive of myocardial ischemia or new ECG changes, occurring before cardiac biomarkers can be measured or before they rise in the blood [1]. * **Option B (Type 1/2 MI):** The diagnosis of MI requires a rise and/or fall of cTn with at least one value above the 99th percentile URL, plus clinical evidence of ischemia, such as **new regional wall motion abnormalities** on imaging [1]. * **Option D (Reinfarction):** In patients where troponin levels are already elevated but stable or decreasing, reinfarction is diagnosed if there is a **≥20% increase** in the cTn value in a subsequent sample [1]. However, some guidelines and older iterations noted that even a minor significant rise (5-20% depending on the assay) in serial samples can be suggestive in the right clinical context. ### **High-Yield Clinical Pearls for NEET-PG** * **Type 1 MI:** Spontaneous MI (plaque rupture/erosion). * **Type 2 MI:** Demand-supply mismatch (e.g., anemia, tachycardia). * **Type 4a MI:** Related to PCI (requires cTn **>5 times** URL) [1]. * **Type 4b MI:** Related to Stent Thrombosis [1]. * **Gold Standard Biomarker:** Cardiac Troponin (I or T) is the preferred biomarker due to high sensitivity and tissue specificity [2].
Question 382: A 20-year-old girl presented with low-grade fever, malaise, night sweats, weight loss, arthralgia, and fatigue for 1 month. On examination, peripheral pulses were weak in the upper extremities and a bruit was present over the carotid and subclavian arteries. Investigations revealed dilatation of the proximal aorta. What is the most likely diagnosis?
- A. Polyarteritis nodosa
- B. Temporal arteritis
- C. Takayasu's arteritis (Correct Answer)
- D. Kawasaki's disease
Explanation: The clinical presentation is classic for **Takayasu’s Arteritis (TA)**, also known as "Pulseless Disease." It is a chronic, large-vessel vasculitis that primarily involves the **aorta and its major branches** [1]. 1. **Why it is correct:** The patient is a young female (typical demographic) presenting with systemic symptoms (fever, weight loss) followed by features of vascular inflammation. The **weak upper extremity pulses** and **bruit** over the carotids/subclavian arteries indicate arterial stenosis. The **dilatation of the proximal aorta** (aortitis) is a hallmark finding. According to ACR criteria, age <40, claudication, and decreased brachial artery pulses are key diagnostic features. 2. **Why the other options are wrong:** * **Polyarteritis nodosa (PAN):** A medium-vessel vasculitis that typically involves the renal and visceral arteries (sparing the lungs). It presents with hypertension, skin nodules, and mononeuritis multiplex, not absent pulses in the upper limbs. * **Temporal arteritis (Giant Cell Arteritis):** Also a large-vessel vasculitis, but it almost exclusively affects patients **over the age of 50**. It typically presents with headache, jaw claudication, and visual loss. * **Kawasaki's disease:** Primarily affects **children (<5 years)** [1]. It involves medium-sized vessels, most notably the **coronary arteries** (aneurysms), and presents with "strawberry tongue," conjunctivitis, and rash [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Demographic:** Most common in Asian females <40 years. * **Gold Standard Investigation:** Digital Subtraction Angiography (shows "string of pearls" or narrowing). * **Treatment:** Glucocorticoids are the first-line therapy. * **Key Sign:** A significant difference in blood pressure (>10 mmHg) between the two arms.
Question 383: Ventricular Tachycardia is represented by all, except:
- A. Wide QRS complex
- B. AV dissociation
- C. Capture Beats
- D. Typical RBBB QRS complex (Correct Answer)
Explanation: **Explanation:** Ventricular Tachycardia (VT) originates from an ectopic focus within the ventricles, bypassing the normal His-Purkinje conduction system. This leads to slow, cell-to-cell depolarization, resulting in a **Wide QRS complex (>0.12s)** (Option A) [1]. **Why Option D is the correct answer:** In VT, the QRS morphology is usually **atypical** or "bizarre" [1]. A **Typical RBBB or LBBB pattern** (Option D) suggests that the impulse is traveling through the normal conduction system, which is characteristic of **Supraventricular Tachycardia (SVT) with aberrancy**, not VT. In VT, the QRS morphology often shows "concordance" (all complexes in precordial leads are either positive or negative) or specific criteria like a Brugada sign. **Analysis of other options:** * **AV Dissociation (Option B):** This is a hallmark of VT. The atria and ventricles beat independently because the rapid ventricular rate prevents retrograde conduction to the atria [1]. * **Capture Beats (Option C):** These occur when a normal sinus impulse occasionally "captures" the ventricle amidst the tachycardia, resulting in a normal-looking, narrow QRS complex. Along with **Fusion beats**, these are pathognomonic for VT [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Brugada Criteria:** Used to differentiate VT from SVT with aberrancy. * **Northwest Axis:** An "extreme axis deviation" (between -90° and 180°) strongly suggests VT. * **Hemodynamic Stability:** Never use stability to rule out VT; stable VT is common and should be treated with Amiodarone or Procainamide, while unstable VT requires immediate DC cardioversion [2].
Question 384: A 57-year-old man comes to see you for follow-up 4 weeks after being discharged from hospital for unstable angina. His coronary angiogram showed moderate nonstenotic disease in two vessels. The cardiologist asks you to follow up on his fasting lipid profile since it was not checked in the hospital. His T-chol is 240 mg/dL, LDL 120 mg/dL, HDL 50 mg/dL, and triglycerides 130 mg/dL. For the above patient with dyslipidemia, select the most appropriate treatment?
- A. Fibric acid derivatives (clofibrate, gemfibrozil)
- B. Nicotinic acid
- C. Bile acid-binding resins (cholestyramine, colestipol)
- D. Hepatic hydroxymethylglutaryl coenzyme A (HMG-Co) reductase inhibitors (lovastatin, simvastatin, pravastatin) (Correct Answer)
Explanation: ### Explanation **1. Why the Correct Answer is Right:** The patient has established **Coronary Artery Disease (CAD)**, evidenced by his recent admission for unstable angina and angiographic findings of nonstenotic disease. According to current guidelines (AHA/ACC), any patient with clinical atherosclerotic cardiovascular disease (ASCVD) requires **high-intensity statin therapy** (HMG-CoA reductase inhibitors) for secondary prevention, regardless of their baseline LDL levels. Statins are the first-line treatment because they not only lower LDL-C but also provide **pleiotropic effects**, such as stabilizing atherosclerotic plaques, improving endothelial function, and reducing vascular inflammation. In this patient, even though the LDL (120 mg/dL) might seem "near-optimal" for a healthy individual, it is above the target for a post-ACS patient (ideally <55 or <70 mg/dL depending on risk stratification). **2. Why the Other Options are Incorrect:** * **A. Fibric acid derivatives:** These are primarily used to treat severe hypertriglyceridemia (TG >500 mg/dL) to prevent pancreatitis. They have a limited role in reducing major adverse cardiovascular events (MACE) compared to statins. * **B. Nicotinic acid (Niacin):** While it increases HDL and lowers LDL, large trials (AIM-HIGH, HPS2-THRIVE) failed to show a clinical benefit when added to statins, and it carries a high side-effect profile (flushing, hyperglycemia). * **C. Bile acid-binding resins:** These are second-line agents. They can increase triglyceride levels and are generally poorly tolerated due to GI side effects (constipation, bloating). They lack the robust mortality benefit evidence that statins possess. **3. NEET-PG High-Yield Pearls:** * **Statin Benefit Groups:** Always start a statin in patients with: 1) Clinical ASCVD, 2) LDL ≥190 mg/dL, 3) Diabetes (age 40-75) with LDL >70 mg/dL, or 4) 10-year ASCVD risk ≥7.5%. * **Mechanism:** Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, leading to up-regulation of LDL receptors on hepatocytes. * **Side Effects:** Monitor for **myopathy/rhabdomyolysis** (check CK if symptomatic) and **hepatotoxicity** (check LFTs before starting). * **Rule of 6:** Every doubling of the statin dose leads to an additional 6% reduction in LDL-C.
Question 385: Which of the following is seen in rheumatic fever?
- A. Sydenham's chorea (Correct Answer)
- B. Huntington's chorea
- C. Athetosis
- D. All
Explanation: **Explanation:** **Sydenham’s Chorea** (also known as St. Vitus' Dance) is a major criterion in the **Jones Criteria** for the diagnosis of Acute Rheumatic Fever (ARF) [1]. It is a delayed manifestation, often appearing months after the initial Group A Streptococcal (GAS) pharyngeal infection [1]. The underlying mechanism is **molecular mimicry**, where antibodies against streptococcal antigens cross-react with the **basal ganglia** (specifically the caudate and putamen), leading to involuntary, purposeless, non-repetitive movements [2]. **Why other options are incorrect:** * **Huntington’s Chorea:** This is an autosomal dominant neurodegenerative disorder caused by CAG repeat expansions in the HTT gene. It presents in mid-adulthood with chorea and progressive dementia, unrelated to streptococcal infections [2]. * **Athetosis:** This refers to slow, writhing, involuntary movements (often seen in cerebral palsy or basal ganglia lesions) [2]. While it involves the same brain region, it is clinically distinct from the rapid, jerky movements of chorea seen in ARF [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Jones Criteria (Revised):** Remember the mnemonic **J♥NES** (Joints-polyarthritis, ♥-Carditis, Nodules-subcutaneous, Erythema marginatum, Sydenham’s chorea). * **Clinical Signs:** Sydenham’s chorea is associated with **"Milkmaid’s grip"** (irregular contractions of hand muscles) and **"Darting tongue"** (inability to protrude the tongue steadily). * **Prognosis:** It is the only major manifestation of ARF that can occur in isolation and typically has a benign, self-limiting course, though it may require symptomatic treatment with valproate or carbamazepine.
Question 386: All of the following statements about pulse deficit in Atrial Fibrillation are true, except?
- A. Usually more than 10/minute
- B. Increases with faster ventricular rates
- C. May be absent in digitalis intoxication
- D. Radial pulse rate may be more than ventricular pulse rate (Correct Answer)
Explanation: **Explanation:** The **Pulse Deficit** is defined as the difference between the apical heart rate (measured by auscultation) and the peripheral radial pulse rate. It is a hallmark clinical feature of **Atrial Fibrillation (AF)** [1]. **1. Why Option D is the Correct Answer (The False Statement):** By definition, the radial pulse rate can **never** be higher than the ventricular (apical) rate. A pulse deficit occurs because some ventricular contractions occur so prematurely (during the compensatory pause or short diastole) that the left ventricle has insufficient filling time. This results in a stroke volume too small to open the aortic valve or generate a palpable peripheral pressure wave. Therefore, the radial rate will always be equal to or less than the apical rate. **2. Analysis of Other Options:** * **Option A:** In untreated AF, the pulse deficit is typically significant, often **more than 10 beats per minute**. * **Option B:** As the ventricular rate increases, the diastolic filling time decreases further. This leads to more "ineffectual" contractions that do not reach the periphery, thereby **increasing the deficit**. * **Option C:** Digitalis (Digoxin) slows the ventricular rate by increasing AV nodal refractoriness [2]. As the heart rate slows and becomes more regular, diastolic filling improves, and the **pulse deficit may disappear**. **Clinical Pearls for NEET-PG:** * **Measurement:** To accurately measure pulse deficit, two examiners should ideally count the apical and radial pulses simultaneously for one full minute. * **Other Causes:** Besides AF, pulse deficit can be seen in **Premature Ventricular Contractions (PVCs)**. * **Significance:** A narrowing pulse deficit in an AF patient often indicates successful rate control therapy [3].
Question 387: CCF is associated with an increase in all of the following except?
- A. Right atrial mean pressure
- B. Serum sodium (Correct Answer)
- C. Serum urea
- D. Serum norepinephrine
Explanation: In Congestive Cardiac Failure (CCF), the primary pathophysiology involves a decrease in cardiac output leading to systemic venous congestion and compensatory neurohormonal activation [1]. **Why Serum Sodium is the Correct Answer:** In CCF, patients typically develop **Hyponatremia** (decreased serum sodium), not hypernatremia. This occurs due to: 1. **Non-osmotic ADH release:** Low effective arterial blood volume triggers the release of Antidiuretic Hormone (ADH), which causes excessive water reabsorption in the kidneys. 2. **Dilutional effect:** The retention of water is disproportionately greater than the retention of sodium, leading to "dilutional hyponatremia." This is a poor prognostic marker in heart failure. **Explanation of Incorrect Options:** * **Right Atrial (RA) Mean Pressure:** In CCF (especially right-sided failure), blood backs up into the venous system, leading to increased RA pressure, elevated JVP, and peripheral edema [1]. * **Serum Urea:** Decreased renal perfusion in CCF leads to "Prerenal Azotemia." The kidneys increase urea reabsorption to maintain osmotic pressure, resulting in elevated BUN/Urea levels [1]. * **Serum Norepinephrine:** Low cardiac output triggers the **Sympathetic Nervous System**. This leads to a compensatory increase in circulating norepinephrine to increase heart rate and contractility [1]. **High-Yield Clinical Pearls for NEET-PG:** * **BNP (B-type Natriuretic Peptide):** The gold standard biomarker to rule out CCF in acute dyspnea [1]. * **RAAS Activation:** CCF leads to increased Renin, Angiotensin II, and Aldosterone, contributing to fluid overload. * **Cardinal Sign:** The most specific sign of CCF is an elevated **Jugular Venous Pressure (JVP)** [1]. * **Electrolyte Triad in CCF:** Hyponatremia, Hypokalemia (often due to diuretics), and Hyperuricemia.
Question 388: A 40-year-old female G4P4L3A1, who delivered her third child 1 month ago, presented with recent onset of cough and palpitations associated with paroxysmal nocturnal dyspnea, orthopnea, and exertional intolerance. The patient also complained of a few episodes of hemoptysis 2 days prior. She had a history of pre-eclampsia in her last pregnancy. On examination, Jugular Venous Pressure was increased, with crepitations in bilateral basal lung fields and a shift of the apical impulse. Echocardiogram studies showed a left ventricular ejection fraction < 45%. Despite treatment, the patient did not survive. Histopathological examination was performed on the autopsied heart. Which finding would be most likely present on histopathological examination?
- A. Lymphocytic myocarditis (Correct Answer)
- B. Eosinophilic myocarditis
- C. Basophilic myocarditis
- D. Neutrophilic myocarditis
Explanation: ### **Explanation** The clinical presentation describes a classic case of **Peripartum Cardiomyopathy (PPCM)**. This is a form of dilated cardiomyopathy characterized by heart failure with a reduced ejection fraction (LVEF < 45%) occurring toward the end of pregnancy or in the first five months postpartum, in the absence of other identifiable causes. [1] #### **1. Why Lymphocytic Myocarditis is Correct** The pathogenesis of PPCM involves oxidative stress, which triggers the cleavage of the hormone **prolactin** into a 16-kDa fragment. This fragment is cardiotoxic, inducing endothelial damage and myocardial inflammation. Histopathological studies of autopsied hearts or endomyocardial biopsies in PPCM patients frequently reveal **Lymphocytic Myocarditis** (infiltration of lymphocytes associated with myocyte necrosis or edema). This inflammatory response is the hallmark histological finding in the acute phase of the disease. #### **2. Why Other Options are Incorrect** * **B. Eosinophilic Myocarditis:** Typically associated with hypersensitivity reactions (drugs), parasitic infections, or Loeffler’s endocarditis. It is not a feature of PPCM. * **C. Basophilic Myocarditis:** This is not a standard pathological entity in cardiomyopathy. Basophilic degeneration may be seen in some metabolic conditions, but not as an inflammatory infiltrate in PPCM. * **D. Neutrophilic Myocarditis:** Usually seen in the early stages of acute myocardial infarction or acute bacterial (pyogenic) myocarditis, rather than the immune-mediated process of PPCM. #### **3. Clinical Pearls for NEET-PG** * **Risk Factors:** Advanced maternal age (>30), multiparity, twin pregnancy, and pre-eclampsia (as seen in this patient). * **Diagnosis:** Requires LVEF < 45% + Heart failure symptoms + Timing (last month of pregnancy to 5 months postpartum). [1] * **Treatment High-Yield:** **Bromocriptine** (a dopamine agonist) is used to inhibit prolactin secretion, which has shown to improve LV recovery in PPCM. * **Prognosis:** About 50% of patients recover; however, future pregnancies are strictly discouraged if the LVEF does not normalize due to a high risk of recurrence and mortality.
Question 389: A young lady complains of sudden onset of palpitations, extreme weakness, and sweating. On examination, she was found to have a blood pressure of 90/70 mmHg with a regular pulse rate of 180/minute. Her symptoms disappeared after vomiting but she complained of polyuria. What is the most likely diagnosis?
- A. Primary thyrotoxicosis
- B. Acute anxiety state
- C. Paroxysmal atrial tachycardia (Correct Answer)
- D. Paroxysmal atrial flutter
Explanation: ### Explanation The clinical presentation is classic for **Paroxysmal Supraventricular Tachycardia (PSVT)**, specifically **Paroxysmal Atrial Tachycardia (PAT)**. **Why PAT is the Correct Diagnosis:** 1. **Sudden Onset & Regularity:** The patient presents with a sudden onset of palpitations and a regular heart rate of 180 bpm (typically 120–240 bpm in PSVT) [1]. 2. **Vagal Termination:** The disappearance of symptoms after vomiting is the key diagnostic clue. Vomiting induces a **vagal maneuver**, which increases parasympathetic tone and slows conduction through the AV node, abruptly terminating the arrhythmia. 3. **Post-episode Polyuria:** This is a high-yield clinical sign. Rapid atrial rates lead to atrial distension, which triggers the release of **Atrial Natriuretic Peptide (ANP)**, resulting in polyuria after the episode subsides [1], [2]. **Analysis of Incorrect Options:** * **Primary Thyrotoxicosis:** While it causes tachycardia, it is usually persistent (not paroxysmal) and associated with other signs like tremors, weight loss, and goiter. It would not terminate abruptly with vomiting. * **Acute Anxiety State:** Anxiety causes sinus tachycardia, where the heart rate rarely exceeds 150 bpm and shows a gradual (not sudden) onset and offset. * **Paroxysmal Atrial Flutter:** Atrial flutter typically has an atrial rate of 250–350 bpm with a ventricular response that is often irregular (due to variable AV block) or fixed (e.g., 2:1 block resulting in 150 bpm). It is less likely to terminate completely with a simple vagal maneuver. **NEET-PG High-Yield Pearls:** * **Acute Management:** Hemodynamically stable patients should first attempt vagal maneuvers (Valsalva, carotid sinus massage). The drug of choice is **Adenosine** (6mg IV rapid bolus). * **Hemodynamically Unstable:** If BP is low and the patient is symptomatic (as seen here with 90/70 mmHg), **Synchronized DC Cardioversion** is the treatment of choice. * **Definitive Treatment:** Radiofrequency ablation (RFA) of the bypass tract or slow pathway [3].
Question 390: JVP wave with absent y descent and prominent x wave is seen in which condition?
- A. Restrictive cardiomyopathy
- B. Cardiac tamponade (Correct Answer)
- C. Constrictive pericarditis
- D. Right ventricular failure
Explanation: **Explanation:** In **Cardiac Tamponade**, the heart is compressed by fluid within the rigid pericardial sac. This high intrapericardial pressure prevents the ventricles from expanding during early diastole. [1] * **Why the 'y' descent is absent:** The 'y' descent represents the rapid emptying of the atria into the ventricles after the tricuspid valve opens. In tamponade, the diastolic pressure in the ventricles is already extremely high (equilibrated with the pericardial pressure), which prevents rapid inflow. Thus, the **'y' descent is blunted or absent.** * **Why the 'x' wave is prominent:** The 'x' descent represents atrial relaxation and the downward pulling of the tricuspid annulus during ventricular systole. Since the heart is compressed, this is the only phase where the intrapericardial pressure momentarily drops, allowing for atrial filling. **Analysis of Incorrect Options:** * **Constrictive Pericarditis:** Characterized by a **prominent/steep 'y' descent** (Friedreich’s sign) due to rapid early diastolic filling followed by a sudden halt. * **Restrictive Cardiomyopathy:** Similar to constriction, it typically shows a **prominent 'y' descent** due to high venous pressure and rapid early filling. * **Right Ventricular Failure:** Usually presents with a prominent 'a' wave (due to decreased RV compliance) and a prominent 'v' wave if tricuspid regurgitation is present, but not an absent 'y' descent. **High-Yield Clinical Pearls for NEET-PG:** * **Kussmaul’s Sign** (paradoxical rise in JVP on inspiration): Seen in Constrictive Pericarditis and RCM, but **absent** in Cardiac Tamponade. * **Pulsus Paradoxus:** A hallmark of Cardiac Tamponade. [1] * **Beck’s Triad (Tamponade):** Hypotension, Muffled heart sounds, and Raised JVP. [1] * **Mnemonic:** Tamponade = **"x"** is present (e**x**tra fluid), **"y"** is absent (**y**ields to pressure).
Practice by Chapter
Coronary Artery Disease and Angina
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Acute Coronary Syndromes
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Heart Failure
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Cardiac Arrhythmias
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Valvular Heart Diseases
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Cardiomyopathies
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Pericardial Diseases
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Congenital Heart Disease in Adults
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Hypertension and Hypertensive Emergencies
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Pulmonary Hypertension
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Non-invasive Cardiac Diagnostics
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Preventive Cardiology
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