Cardiology Practice Questions

Q: What is the most common cause of death in patients with Marfan syndrome?

Annuloaortic ectasia. **Explanation:** **Marfan Syndrome (MFS)** is an autosomal dominant connective tissue disorder caused by mutations in the **FBN1 gene** on chromosome 15, leading to defective fibrillin-1 [1]. This defect results in cystic medial necrosis of the large arteries. **1. Why Annuloaortic Ectasia is Correct:** The most common cause of death in Marfan syndrome (accounting for >80% of cases) is cardiovascular complications. Specifically, **Annuloaortic ectasia** (dilation of the proximal ascending aorta and aortic root) is the primary underlying pathology. This progressive dilation leads to **Aortic Root Aneurysm**, which eventually results in fatal complications like aortic rupture or severe aortic regurgitation leading to heart failure. **2. Analysis of Incorrect Options:** * **B. Mitral Valve Prolapse (MVP):** While MVP is the most common *valvular* abnormality in MFS, it is rarely the cause of death unless it leads to severe infective endocarditis or acute heart failure. * **C. Aortic Dissection:** This is a major cause of mortality and often occurs as a *consequence* of annuloaortic ectasia. However, the primary structural abnormality and leading cause of death cited in standard textbooks (like Harrison’s) is the progressive dilation (ectasia) of the aortic root. * **D. Abdominal Aortic Aneurysm (AAA):** In MFS, the pathology predominantly involves the **ascending aorta** [1]. AAA is more commonly associated with atherosclerosis and smoking, not Marfan syndrome. **3. NEET-PG High-Yield Pearls:** * **Most common cause of death:** Annuloaortic ectasia/Aortic root dilatation. * **Most common valvular lesion:** Mitral Valve Prolapse (MVP). * **Diagnostic Criteria:** Revised Ghent Nosology (focuses on Aortic root Z-score and Ectopia lentis). * **Management:** Beta-blockers or ARBs (Losartan) are used to slow the rate of aortic dilatation. Prophylactic surgery is indicated when the aortic diameter exceeds **5.0 cm**.

Q: A mid-diastolic murmur with presystolic accentuation is typically heard in which of the following conditions?

Mitral stenosis. ### Explanation **Correct Option: A. Mitral Stenosis (MS)** The classic murmur of Mitral Stenosis is a **low-pitched, mid-diastolic rumbling murmur**, best heard at the apex with the bell of the stethoscope in the left lateral decubitus position [1]. * **The Mid-diastolic component** occurs due to the pressure gradient between the left atrium (LA) and left ventricle (LV) during the passive filling phase [2]. * **Presystolic accentuation** occurs during late diastole due to **atrial contraction** (atrial kick), which increases the velocity of blood flow across the narrowed mitral orifice just before the first heart sound (S1). **Why other options are incorrect:** * **B. Mitral Regurgitation:** Characterized by a **holosystolic (pansystolic) murmur** radiating to the axilla. It occurs during systole, not diastole [1][3]. * **C. Aortic Stenosis:** Characterized by a **crescendo-decrescendo systolic ejection murmur** radiating to the carotids [1]. * **D. Mitral Valve Prolapse:** Typically presents with a **mid-systolic click** followed by a late systolic murmur [1]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Loss of Presystolic Accentuation:** If a patient with MS develops **Atrial Fibrillation**, the presystolic accentuation disappears because there is no coordinated atrial contraction [2]. 2. **Opening Snap:** MS is often associated with an Opening Snap (OS) [1]. The shorter the **S2-OS interval**, the more severe the stenosis. 3. **Loud S1:** A hallmark of MS (provided the leaflets are mobile and not heavily calcified) [2]. 4. **Graham Steell Murmur:** An early diastolic murmur of pulmonary regurgitation heard in patients with MS due to secondary pulmonary hypertension.

Q: Paroxysmal AV block is associated with which of the following?

Type II second degree AV block. **Explanation:** **Paroxysmal AV block** is a clinical phenomenon characterized by the sudden, unexpected development of a high-grade or total AV block in a patient with previously stable conduction. It is most strongly associated with **Type II second-degree AV block (Mobitz II).** [1] **1. Why Type II Second-Degree AV Block is Correct:** Mobitz II block occurs due to disease in the **His-Purkinje system** (infra-nodal) [1]. Unlike Mobitz I, where the AV node gradually fatigues, Mobitz II involves an "all-or-nothing" failure of conduction. Because the underlying conduction system is severely diseased, it is highly unstable and prone to sudden, unpredictable failure, leading to paroxysmal complete heart block and Stokes-Adams attacks [1]. **2. Why Other Options are Incorrect:** * **First-degree AV block:** This is merely a delay in conduction (prolonged PR interval) at the AV node [1]. It is usually benign and rarely progresses directly to sudden paroxysmal block. * **Type I second-degree AV block (Wenckebach):** This occurs due to functional fatigue of the AV node. It is typically reversible, often physiological (seen in athletes), and progresses predictably rather than paroxysmally [1]. * **Third-degree AV block:** This is a permanent, established state of complete dissociation. It is not "paroxysmal" because the block is already constant. **Clinical Pearls for NEET-PG:** * **Site of Block:** Mobitz I is usually **Intra-nodal** (AV node); Mobitz II is **Infra-nodal** (Bundle of His) [1]. * **Vagal Maneuvers:** Carotid sinus massage worsens Mobitz II (by increasing AV delay) but may paradoxically improve Mobitz I. * **Management:** Mobitz II is an absolute indication for a **Permanent Pacemaker (PPI)**, even if asymptomatic, due to the high risk of progression to sudden cardiac death [1].

Q: All are absolute contraindications for fibrinolysis except?

Pregnancy. **Explanation:** In the management of ST-Elevation Myocardial Infarction (STEMI), distinguishing between absolute and relative contraindications for fibrinolytic therapy is a high-yield topic for NEET-PG. **Why Pregnancy is the Correct Answer:** **Pregnancy** is classified as a **relative contraindication**, not an absolute one. While there is an increased risk of placental abruption or maternal hemorrhage, fibrinolysis can be considered in life-threatening situations where Primary PCI is unavailable. **Analysis of Incorrect Options (Absolute Contraindications):** * **Upper Gastrointestinal Bleed:** Active internal bleeding (excluding menses) or a known structural gastrointestinal vascular malformation/malignancy is an absolute contraindication due to the risk of catastrophic hemorrhage. * **History of Ischemic Stroke 6 months prior:** Any ischemic stroke within the last **3 months** is an absolute contraindication. (Note: A history of any prior intracranial hemorrhage is an absolute contraindication regardless of timing). * **Systolic BP > 180 mmHg:** Severe, uncontrolled hypertension at presentation (SBP >180 mmHg or DBP >110 mmHg) is an absolute contraindication because it significantly increases the risk of hemorrhagic stroke during fibrinolysis. **High-Yield Clinical Pearls for NEET-PG:** * **Absolute Contraindications (The "Never" List):** Prior ICH, known structural cerebrovascular lesion, malignant intracranial neoplasm, ischemic stroke within 3 months, suspected aortic dissection, active bleeding, or significant closed-head/facial trauma within 3 months. * **Relative Contraindications:** Pregnancy, current use of anticoagulants, non-compressible vascular punctures, major surgery (<3 weeks), and poorly controlled chronic hypertension. * **Time Window:** Fibrinolysis is most effective when administered within **12 hours** of symptom onset if Primary PCI cannot be performed within **120 minutes** of first medical contact [1].

Q: A 27-year-old male has had hard-to-control hypertension for 2 years. He is taking clonidine, hydrochlorothiazide, verapamil, and lisinopril. His blood pressure is 170/105 mmHg, pulse 90 beats/min, and respirations 16/min. The cardiopulmonary exam is normal. Pedal pulses are intact and there is no edema or misdistribution of fat. Laboratories show potassium of 2.7 mEq/L, BUN 20 mg/dL, creatinine 1.2 mg/dL, bicarbonate 33 mg/dL, and fasting glucose 98 mg/dL. What is the most likely diagnosis?

Conn syndrome. The clinical presentation of a young patient with **resistant hypertension** (uncontrolled despite ≥3 drugs) and spontaneous **hypokalemia** (2.7 mEq/L) strongly suggests **Primary Hyperaldosteronism (Conn Syndrome)**. **1. Why Conn Syndrome is correct:** In Conn syndrome, an adrenal adenoma or hyperplasia produces excess aldosterone. Aldosterone acts on the principal cells of the renal collecting duct to reabsorb sodium and water (causing hypertension) and secrete potassium and hydrogen ions [1]. This leads to the classic triad seen here: * **Hypertension** (often resistant). * **Hypokalemia** (muscle weakness or asymptomatic). * **Metabolic Alkalosis** (elevated bicarbonate of 33 mg/dL). The absence of edema is due to the "Aldosterone Escape" phenomenon. **2. Why other options are incorrect:** * **Renal Vascular Hypertension:** While it causes resistant hypertension, it usually presents with an abdominal bruit or a significant rise in creatinine after starting an ACE inhibitor (Lisinopril) [3]. * **Cushing Syndrome:** Ruled out by the absence of physical findings like truncal obesity, striae, or "buffalo hump," and the normal fasting glucose (98 mg/dL). * **Carcinoid Syndrome:** Typically presents with flushing, diarrhea, and wheezing, rather than isolated resistant hypertension and hypokalemia. **High-Yield Clinical Pearls for NEET-PG:** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio > 20-30** is suggestive. * **Confirmatory Test:** Oral/Saline salt loading test (failure to suppress aldosterone) [2]. * **Management:** Surgical excision for Adenoma; Spironolactone/Eplerenone for bilateral hyperplasia [2]. * **Note:** Diuretics like Hydrochlorothiazide can worsen hypokalemia, but the severity here (2.7 mEq/L) in a young hypertensive patient should always trigger a workup for primary aldosteronism.

Q: Gibson's murmur is a feature of which cardiac condition?

Patent Ductus arteriosus. **Explanation:** **Gibson’s murmur** is the classic eponym for a **continuous machinery murmur**. It is the hallmark clinical finding of **Patent Ductus Arteriosus (PDA)** [1]. **Why Patent Ductus Arteriosus is correct:** In PDA, there is a persistent communication between the high-pressure aorta and the lower-pressure pulmonary artery [1]. Because the pressure in the aorta remains higher than in the pulmonary artery during both systole and diastole, blood flows continuously through the ductus [1]. This results in a murmur that begins in systole, peaks at the second heart sound (S2), and continues through diastole, creating the "machinery" quality. It is best heard at the **left infraclavicular area** (Gibson’s area). **Why the other options are incorrect:** * **Mitral Valve Prolapse (MVP):** Characterized by a mid-systolic click followed by a late systolic murmur. * **Pulmonary Regurgitation (PR):** Typically presents as a decrescendo diastolic murmur (Graham Steell murmur if secondary to pulmonary hypertension). * **Mitral Regurgitation (MR):** Presents as a pansystolic (holosystolic) murmur heard best at the apex, radiating to the axilla [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Best heard in the left 2nd intercostal space, just below the left clavicle. * **Differential for Continuous Murmurs:** Apart from PDA, consider Ruptured Sinus of Valsalva (RSOV), Aortopulmonary window, and Coronary AV fistula. * **Management:** Indomethacin or Ibuprofen (NSAIDs) are used for pharmacological closure in preterm neonates; surgical or device closure is indicated for persistent cases. * **Eisenmenger Syndrome:** If PDA develops right-to-left shunting, it leads to **differential cyanosis** (cyanosis and clubbing in the lower limbs, but not the upper limbs).

Question 1

What is the most common cause of death in patients with Marfan syndrome?

Accepted Answer

Annuloaortic ectasia

Answer

Mitral valve prolapse

Answer

Aortic dissection

Answer

Abdominal aortic aneurysm rupture

Question 2

Which of the following is a poor prognostic factor in acute myocardial infarction?

Accepted Answer

Hypotension at diagnosis

Answer

Ventricular premature complexes (VPCs) in the first 24 hours

Answer

Chest pain

Answer

Hypertension

Question 3

Which of the following conditions is characterized by the absence of P-waves?

Accepted Answer

Wolff-Parkinson-White (WPW) syndrome

Answer

Ventricular Tachycardia

Answer

Ventricular Fibrillation

Question 4

A young asymptomatic female is observed to have a midsystolic click on routine examination. Which valve is likely to show myxomatous degeneration?

Accepted Answer

Myxomatous degeneration

Answer

Aschoff bodies

Answer

Calcific degeneration

Answer

Ruptured chordae tendinae

Question 5

A mid-diastolic murmur with presystolic accentuation is typically heard in which of the following conditions?

Accepted Answer

Mitral stenosis

Answer

Mitral regurgitation

Answer

Aortic stenosis

Answer

Mitral valve prolapse

Question 6

A 26-year-old woman presents with a 2-day history of worsening right leg pain and swelling. She recently completed an 8-hour car drive following a hiking trip. Initially, she attributed the pain to exertion, but it has progressively worsened. Her past medical history includes infertility and two spontaneous abortions. Physical examination reveals normal vital signs, heart, and lung findings. The right leg is swollen from the mid-thigh down and is tender. Doppler studies show a large deep venous thrombosis (DVT) in the femoral and iliac veins, extending into the pelvis. Laboratory results are unremarkable for electrolytes, WBC, platelet counts, and PT, but the aPTT is 3 times the normal value. A pregnancy test is negative. Low-molecular-weight heparin therapy has been initiated. What should be the subsequent management?

Accepted Answer

Warfarin with an INR goal of 2.5-3.5 for life

Answer

Rituximab 375 mg/m2 per week for 4 weeks

Answer

Warfarin with an international normalized ratio (INR) goal of 2.0-3.0 for 3 months

Answer

Warfarin with an INR goal of 2.0-3.0 for 12 months

Question 7

Paroxysmal AV block is associated with which of the following?

Accepted Answer

Type II second degree AV block

Answer

First degree AV block

Answer

Type I second degree AV block

Answer

Third degree AV block

Question 8

All are absolute contraindications for fibrinolysis except?

Accepted Answer

Pregnancy

Answer

Upper gastrointestinal bleed

Answer

History of ischemic stroke 6 months prior

Answer

Systolic blood pressure > 180 mm of Hg at presentation

Question 9

A 27-year-old male has had hard-to-control hypertension for 2 years. He is taking clonidine, hydrochlorothiazide, verapamil, and lisinopril. His blood pressure is 170/105 mmHg, pulse 90 beats/min, and respirations 16/min. The cardiopulmonary exam is normal. Pedal pulses are intact and there is no edema or misdistribution of fat. Laboratories show potassium of 2.7 mEq/L, BUN 20 mg/dL, creatinine 1.2 mg/dL, bicarbonate 33 mg/dL, and fasting glucose 98 mg/dL. What is the most likely diagnosis?

Accepted Answer

Conn syndrome

Answer

Renal vascular hypertension

Answer

Cushing syndrome

Answer

Carcinoid syndrome

Question 10

Gibson's murmur is a feature of which cardiac condition?

Accepted Answer

Patent Ductus arteriosus

Answer

Mitral Valve prolapse

Answer

Pulmonary regurgitation

Answer

Mitral regurgitation

Cardiology — MCQs

Cardiology — MCQs

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