Cardiology Practice Questions

Q: Which of the following does NOT increase the chances of Deep Vein Thrombosis?

Superficial thrombophlebitis. **Explanation:** Deep Vein Thrombosis (DVT) occurs due to the components of **Virchow’s Triad**: endothelial injury, stasis of blood flow, and hypercoagulability [1]. **Why Superficial Thrombophlebitis is the correct answer:** Superficial thrombophlebitis involves inflammation and thrombosis of the veins near the skin surface (e.g., great saphenous vein). While it causes local pain and redness, it is generally considered a benign, localized condition. Unlike DVT, it does not typically involve the deep venous system and is **not** a major independent risk factor for developing DVT, although the two can occasionally coexist in patients with systemic hypercoagulability. **Analysis of Incorrect Options:** * **Oral Contraceptive Pills (OCPs):** Estrogen increases the hepatic synthesis of clotting factors (VII, X, and fibrinogen) and decreases anticoagulant levels (Protein S), creating a **hypercoagulable state**. * **Hypertension:** Chronic hypertension causes **endothelial dysfunction** and vascular remodeling, which triggers the extrinsic coagulation pathway, increasing the risk of venous thromboembolism (VTE). * **Myocardial Infarction (MI):** MI leads to DVT through **stasis** [1]. Reduced cardiac output (pump failure) and the subsequent period of prolonged bed rest/immobility lead to sluggish venous return in the lower limbs [1]. **NEET-PG High-Yield Pearls:** * **Most common site for DVT:** Calf veins (Soleal sinuses) [1]. * **Most common inherited risk factor for DVT:** Factor V Leiden mutation (activated protein C resistance). * **Strongest clinical risk factor:** Major orthopedic surgery (especially hip and knee arthroplasty) [1]. * **Trousseau’s Sign:** Migratory superficial thrombophlebitis associated with visceral malignancy (most commonly pancreatic cancer).

Q: Increased risk of coronary heart disease is seen in which type of hyperlipidemia?

Type II hyperlipidemia. The risk of **Coronary Heart Disease (CHD)** is most strongly associated with elevated levels of **Low-Density Lipoprotein (LDL)**, which is the primary characteristic of **Type II Hyperlipidemia** (Fredrickson Classification) [1]. 1. **Why Type II is Correct:** * **Type IIa:** Characterized by isolated elevation of LDL due to a deficiency in LDL receptors [1]. * **Type IIb:** Characterized by elevations in both LDL and Very Low-Density Lipoprotein (VLDL). Since LDL is highly atherogenic, it undergoes oxidation within the arterial wall, leading to foam cell formation and plaque buildup. Therefore, Type II carries the highest risk for premature atherosclerosis and myocardial infarction [1]. 2. **Why Other Options are Incorrect:** * **Type I (Hyperchylomicronemia):** Involves an increase in Chylomicrons due to Lipoprotein Lipase (LPL) deficiency. While it causes extremely high triglycerides, it is **not** associated with increased CHD risk. The primary clinical risk here is **acute pancreatitis**. * **Type IV (Hypertriglyceridemia):** Involves elevated VLDL. While high triglycerides are a minor risk factor, they are not as strongly or directly linked to CHD as the LDL elevations seen in Type II. * **Type V:** Involves elevations in both Chylomicrons and VLDL. Like Type I, the predominant clinical concern is pancreatitis rather than accelerated atherosclerosis. **High-Yield Clinical Pearls for NEET-PG:** * **Type IIa** is associated with **Tendon Xanthomas** (especially the Achilles tendon) and Xanthelasma. * **Type III (Dysbetalipoproteinemia)** is associated with **Palmar Xanthomas** and also carries an increased risk of CHD and peripheral vascular disease. * **Mnemonic for Fredrickson:** "1-2-3-4-5" corresponds to "C-L-B-V-M" (Chylomicrons, LDL, Broad-beta, VLDL, Mixed). * **Most common type:** Type IV is the most common in the general population, but Type II is the most significant for CHD [2].

Q: A mid-diastolic murmur with presystolic accentuation is typically heard in which condition?

Mitral stenosis. ### Explanation **1. Why Mitral Stenosis (MS) is Correct:** 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 [2]. * **Mid-diastolic component:** Caused by turbulent blood flow across the narrowed mitral valve during the passive filling phase of the left ventricle [2]. * **Presystolic accentuation:** This occurs during **atrial systole** (atrial kick), which increases the pressure gradient across the valve just before the first heart sound ($S_1$) [3]. * *Note:* Presystolic accentuation disappears if the patient develops **Atrial Fibrillation**, as there is no coordinated atrial contraction [3]. **2. Why Other Options are Incorrect:** * **Mitral Regurgitation (MR):** Characterized by a **holosystolic (pansystolic) murmur** that radiates to the axilla. It occurs during ventricular systole, not diastole [4]. * **Aortic Stenosis (AS):** Presents as a **crescendo-decrescendo systolic ejection murmur** radiating to the carotids [1]. * **Mitral Valve Prolapse (MVP):** Typically presents with a **mid-systolic click** followed by a late systolic murmur [1]. **3. NEET-PG High-Yield Pearls:** * **Opening Snap (OS):** A high-pitched sound heard after $S_2$ in MS [1]. The shorter the $A_2-OS$ interval, the more severe the stenosis. * **Loud $S_1$:** A hallmark of MS (unless the valve is heavily calcified) [3]. * **Graham Steell Murmur:** An early diastolic decrescendo murmur heard in severe MS due to functional pulmonary regurgitation (secondary to pulmonary hypertension). * **Austin Flint Murmur:** A mid-diastolic murmur heard in **Aortic Regurgitation** that mimics MS but lacks an opening snap.

Q: Sinus tachycardia is seen in which of the following conditions?

Severe anaemia. ### Explanation **Correct Option: D (Severe Anaemia)** Sinus tachycardia is a physiological response to maintain adequate tissue oxygenation. In **severe anaemia**, the oxygen-carrying capacity of the blood is significantly reduced. To compensate for this deficit and maintain a stable **Cardiac Output (CO = Stroke Volume × Heart Rate)**, the sympathetic nervous system is activated [1]. This leads to an increase in heart rate (tachycardia) to ensure that the remaining hemoglobin circulates more frequently to meet the metabolic demands of the tissues [2]. **Why the other options are incorrect:** * **A. Beta blocker therapy:** Beta-blockers (e.g., Propranolol, Metoprolol) antagonize the $\beta_1$ receptors in the SA node, leading to a decrease in heart rate (**Bradycardia**). * **B. Athletes:** Well-trained athletes often exhibit **Physiological Bradycardia**. This is due to high vagal tone (parasympathetic dominance) and an increased stroke volume, allowing the heart to maintain cardiac output at a lower rate. * **C. Hypothyroidism:** Low levels of thyroid hormones lead to decreased expression of $\beta$-adrenergic receptors and reduced metabolic demand, typically resulting in **Sinus Bradycardia**. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** Sinus tachycardia is defined as a sinus rhythm with a rate **>100 beats/minute**. * **Common Causes:** Fever (most common), thyrotoxicosis, hypovolemia, anxiety, exercise, and drugs like caffeine or sympathomimetics [1]. * **Rule of Thumb:** For every 1°F rise in body temperature, the heart rate increases by approximately 10 beats/minute. * **Relative Bradycardia:** If a patient has a high fever but a normal or slow heart rate, consider **Typhoid fever (Faget’s sign)**, Legionnaire’s disease, or Yellow fever.

Q: Which of the following is a feature of first-degree AV block?

PR interval > 200 ms. **Explanation:** **First-degree Atrioventricular (AV) Block** is characterized by a delayed conduction through the AV node. The fundamental diagnostic feature is a **prolonged PR interval (>0.20 seconds or >200 ms)** that remains constant from beat to beat [1]. Importantly, every P wave is followed by a QRS complex (1:1 conduction), meaning there are no "dropped" beats. **Analysis of Options:** * **Option A (Correct):** The normal PR interval ranges from 120 to 200 ms. A PR interval exceeding 200 ms (5 small squares on ECG) signifies a conduction delay, defining first-degree AV block [1]. * **Option B (Incorrect):** T wave inversion is a sign of myocardial ischemia, ventricular hypertrophy, or bundle branch blocks, but is not a diagnostic feature of AV blocks. * **Option C (Incorrect):** Progressive *lengthening* (not shortening) of the PR interval until a QRS complex is dropped is the hallmark of **Mobitz Type I (Wenckebach) second-degree AV block** [1]. * **Option D (Incorrect):** U waves are most commonly associated with **hypokalemia**, though they can be seen in bradycardia or with certain drugs (e.g., Digoxin). **High-Yield Clinical Pearls for NEET-PG:** * **Location of Delay:** Usually occurs within the **AV node** itself. * **Clinical Significance:** Usually asymptomatic and benign; often found in athletes or due to increased vagal tone, medications (Beta-blockers, CCBs, Digoxin), or inferior wall MI [1]. * **Management:** No specific treatment is required unless the patient is symptomatic or the block is drug-induced. * **Rule of Thumb:** If the PR interval is long but constant and every P is followed by a QRS, it is 1st-degree block. If the PR interval is long and constant but some P waves are *not* followed by a QRS, it is Mobitz Type II [1].

Q: A 76-year-old woman presents with new-onset syncope and has noticed early fatigue on exertion for the past year. On examination, there is a systolic ejection murmur at the right sternal border that radiates to the carotids. What is the characteristic arterial pulse finding in this patient with suspected aortic stenosis?

Pulsus tardus. **Explanation:** The clinical presentation of syncope, exertional fatigue, and a systolic ejection murmur radiating to the carotids is classic for **Aortic Stenosis (AS)**. In severe AS, the narrowed valve orifice creates a mechanical obstruction to left ventricular outflow, leading to a characteristic arterial pulse known as **Pulsus parvus et tardus**. [1] * **Pulsus tardus** refers to a delayed upstroke (slow-rising pulse), while **pulsus parvus** refers to a small/low amplitude. This occurs because the blood is ejected slowly through the stenotic valve, prolonging the time to reach peak pressure. [1] **Analysis of Incorrect Options:** * **Pulsus paradoxus:** Defined as an exaggerated drop in systolic BP (>10 mmHg) during inspiration. It is characteristic of **Cardiac Tamponade**, severe asthma, or COPD, not valvular stenosis. * **Hyperkinetic pulse (Water-hammer pulse):** A rapid, forceful upstroke with sudden collapse. This is seen in **Aortic Regurgitation** or high-output states (e.g., thyrotoxicosis, anemia). [3] * **Bisferiens pulse:** A "double-peaked" systolic pulse. It is typically found in **AR combined with AS** or in **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Gallavardin Phenomenon:** In AS, the murmur may sound musical and be heard best at the apex, mimicking mitral regurgitation. [1] 2. **S2 Changes:** A paradoxical splitting of S2 or a soft/absent A2 component is a sign of severe AS. [1] 3. **The "SAD" Triad:** Symptoms of AS include **S**yncope, **A**ngina, and **D**yspnea (Heart Failure). [2] Once symptoms appear, the prognosis without valve replacement is poor.

Q: Hyperdynamic circulation is seen in all EXCEPT:

Cor pulmonale. **Explanation:** **Hyperdynamic circulation** is a state of increased cardiac output (CO) and decreased systemic vascular resistance (SVR). It is characterized by a "bounding pulse" and increased stroke volume [2]. **Why Cor Pulmonale is the Correct Answer:** Cor pulmonale refers to right ventricular hypertrophy and failure resulting from chronic pulmonary hypertension (usually due to lung disease like COPD) [3]. In this condition, there is **increased pulmonary vascular resistance**, which leads to a **low-output state** rather than a high-output state [1]. The heart struggles to pump blood through the lungs, eventually leading to decreased systemic cardiac output. **Analysis of Incorrect Options:** * **Anemia:** Reduced hemoglobin leads to tissue hypoxia, triggering compensatory vasodilation and increased stroke volume to maintain oxygen delivery. * **Beriberi (Wet):** Thiamine (Vitamin B1) deficiency causes systemic vasodilation and high-output heart failure due to impaired aerobic metabolism. * **AV Fistula:** An abnormal connection between an artery and a vein bypasses the high-resistance capillary bed, significantly reducing SVR and forcing the heart to increase CO to maintain systemic pressure. **NEET-PG High-Yield Pearls:** * **Common causes of Hyperdynamic Circulation:** Pregnancy, Thyrotoxicosis, Fever, Paget’s disease of the bone, Liver Cirrhosis, and Sepsis (early phase). * **Clinical Signs:** Water-hammer pulse (Corrigan’s pulse), wide pulse pressure, and a mid-systolic flow murmur [2]. * **Mnemonic:** Remember **"ABCD P"** for High Output: **A**nemia, **B**eriberi/BMR (Thyrotoxicosis), **C**irrhosis, **D**-AV fistula, **P**regnancy/Paget's.

Question 1

Which of the following does NOT increase the chances of Deep Vein Thrombosis?

Accepted Answer

Superficial thrombophlebitis

Answer

Oral contraceptive pills

Answer

Hypertension

Answer

Myocardial infarction

Question 2

Increased risk of coronary heart disease is seen in which type of hyperlipidemia?

Accepted Answer

Type II hyperlipidemia

Answer

Type I hyperlipidemia

Answer

Type IV hyperlipidemia

Answer

Type V hyperlipidemia

Question 3

A mid-diastolic murmur with presystolic accentuation is typically heard in which condition?

Accepted Answer

Mitral stenosis

Answer

Mitral regurgitation

Answer

Aortic stenosis

Answer

Mitral valve prolapse

Question 4

Sinus tachycardia is seen in which of the following conditions?

Accepted Answer

Severe anaemia

Answer

Beta blocker therapy

Answer

Athletes

Answer

Hypothyroidism

Question 5

Which of the following is a feature of first-degree AV block?

Accepted Answer

PR interval > 200 ms

Answer

Inversion of T wave

Answer

Progressive shortening of PR interval

Answer

Presence of U wave

Question 6

A 76-year-old woman presents with new-onset syncope and has noticed early fatigue on exertion for the past year. On examination, there is a systolic ejection murmur at the right sternal border that radiates to the carotids. What is the characteristic arterial pulse finding in this patient with suspected aortic stenosis?

Accepted Answer

Pulsus tardus

Answer

Pulsus paradoxus

Answer

Hyperkinetic pulse

Answer

Bisferiens pulse

Question 7

A 56-year-old woman presents with dyspnea, blurry vision, and headaches that began this morning and are worsening. Her past medical history includes hypertension and osteoarthritis. She discontinued her anti-hypertensive medications three months ago due to side effects. On examination, her blood pressure is 210/130 mm Hg, heart rate is 100 beats/min, and oxygen saturation is 95%. Fundoscopy reveals retinal hemorrhages and papilledema. Heart sounds are normal except for an S4, and lung auscultation reveals lower lobe crackles. Which of the following is the most appropriate agent to reduce her blood pressure?

Accepted Answer

IV nitroprusside

Answer

IV hydralazine

Answer

IV labetalol

Answer

Oral methyldopa

Question 8

What is the recommended management for essential hypertension?

Accepted Answer

Diet modification and pharmacotherapy are indicated.

Answer

No treatment is necessary.

Answer

Diet modification alone is sufficient.

Answer

Surgical intervention is the primary treatment.

Question 9

Hyperdynamic circulation is seen in all EXCEPT:

Accepted Answer

Cor pulmonale

Answer

Anemia

Answer

Beriberi

Answer

AV fistula

Question 10

Which of the following dietary interventions has shown to reduce mortality in patients with coronary heart disease?

Accepted Answer

Omega 3 polyunsaturated fatty acids

Answer

High Fibre diet

Answer

Stanol Esters

Answer

Potassium supplements

Cardiology — MCQs

Cardiology — MCQs

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