Cardiology Practice Questions

Q: A newborn with a marked congenital heart defect (CHD) and decreased pulmonary vascularity should be treated with which of the following medications?

Prostaglandin E1. ### Explanation **Correct Answer: C. Prostaglandin E1 (Alprostadil)** **Medical Concept:** The clinical presentation of a newborn with a cyanotic congenital heart defect (CHD) and **decreased pulmonary vascularity** on X-ray indicates a **ductal-dependent pulmonary circulation**. In conditions like Pulmonary Atresia, Tricuspid Atresia, or severe Tetralogy of Fallot, pulmonary blood flow is restricted. The infant relies entirely on the **Ductus Arteriosus** to shunt blood from the aorta to the lungs for oxygenation. As the ductus naturally begins to close within the first hours or days of life, these infants develop profound cyanosis and shock. **Prostaglandin E1 (PGE1)** is life-saving because it maintains the patency of the ductus arteriosus, ensuring adequate pulmonary perfusion until surgical intervention (like a Blalock-Taussig shunt) can be performed. **Why Incorrect Options are Wrong:** * **A. Digoxin:** This is an inotrope used for heart failure or certain arrhythmias (SVT). It does not address the anatomical obstruction to pulmonary blood flow. * **B. Indomethacin:** This is a prostaglandin synthesis inhibitor used to **close** a Patent Ductus Arteriosus (PDA) in preterm infants. In this scenario, closing the ductus would be fatal. * **D. Epinephrine:** While used in resuscitation for cardiac arrest or severe shock, it does not solve the underlying problem of restricted pulmonary blood flow in a ductal-dependent lesion. **High-Yield Clinical Pearls for NEET-PG:** 1. **Ductal-dependent Systemic Circulation:** Conditions like Hypoplastic Left Heart Syndrome or Coarctation of the Aorta also require PGE1 to maintain systemic output. 2. **Side Effect of PGE1:** The most common high-yield side effect to watch for is **Apnea**; always be prepared for endotracheal intubation. 3. **X-ray Finding:** "Decreased pulmonary vascularity" (Oligemic lung fields) is a classic sign of right-to-left shunts with pulmonary obstruction.

Q: Which of the following is FALSE regarding Kawasaki disease?

Unilateral, suppurative cervical lymphadenopathy. **Explanation:** Kawasaki Disease (KD) is an acute, self-limiting systemic medium-vessel vasculitis. The diagnosis is clinical, based on the presence of high-grade fever for ≥5 days along with specific diagnostic criteria. **Why Option D is False:** While **unilateral cervical lymphadenopathy** (usually >1.5 cm) is a classic diagnostic criterion for KD, it is characteristically **non-suppurative**. If a lymph node is fluctuant or draining pus (suppurative), it points toward a bacterial etiology (like *Staphylococcus aureus* lymphadenitis) rather than Kawasaki disease. **Analysis of Other Options:** * **Option A (Strawberry tongue):** This is a classic finding of oral mucosal involvement in KD, caused by the sloughing of filiform papillae and hypertrophy of fungiform papillae. * **Option B (Periungual desquamation):** This is a hallmark of the **subacute phase** (occurring 2–3 weeks after fever onset). Skin peeling begins under the fingernails and toenails. * **Option C (Self-limiting febrile illness):** KD is indeed self-limiting; the fever and acute inflammation usually resolve even without treatment. However, treatment (IVIG) is mandatory to prevent the serious complication of coronary artery aneurysms. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Complication:** Coronary artery aneurysms (occurs in 20–25% of untreated cases). * **Treatment of Choice:** High-dose **IVIG** (2g/kg) plus **Aspirin**. (Note: This is one of the few pediatric conditions where Aspirin is indicated despite the risk of Reye syndrome). * **Cardiac Screening:** Echocardiography should be performed at diagnosis, at 2 weeks, and at 6–8 weeks. * **Incomplete Kawasaki:** Suspect in infants with prolonged fever and fewer than 4 criteria; check ESR/CRP and Echo.

Q: Which of the following can cause congenital heart block?

Maternal Systemic Lupus Erythematosus (SLE). **Explanation:** **Correct Answer: A. Maternal Systemic Lupus Erythematosus (SLE)** Congenital Heart Block (CHB) is most commonly associated with maternal autoimmune diseases, specifically **SLE** and **Sjögren’s syndrome**. The underlying mechanism involves the transplacental passage of maternal IgG autoantibodies, specifically **anti-Ro (SS-A)** and **anti-La (SS-B)**. These antibodies cross the placenta and cause inflammatory damage (myocarditis) and subsequent fibrosis of the fetal AV node and conduction system. This damage is typically irreversible and occurs between 18 and 24 weeks of gestation. **Analysis of Incorrect Options:** * **B. Down’s Syndrome (Trisomy 21):** Most commonly associated with **Atrioventricular Septal Defects (AVSD)** or Endocardial Cushion Defects, followed by VSD and ASD. It does not typically cause heart block. * **C. Edward’s Syndrome (Trisomy 18):** Frequently associated with **Ventricular Septal Defects (VSD)** and Polyvalvular heart disease. * **D. Phenylketonuria (PKU):** Maternal PKU (untreated) is associated with an increased risk of microcephaly, intellectual disability, and cardiac defects like **Tetralogy of Fallot (TOF)** and VSD, but not isolated heart block. **High-Yield Clinical Pearls for NEET-PG:** 1. **Neonatal Lupus:** Presents with a characteristic "raccoon-eye" or periorbital rash and CHB. While the rash is transient (disappears as maternal antibodies wane), the **heart block is permanent**. 2. **Treatment:** If detected in utero, maternal steroids (Dexamethasone) may be used. Postnatally, most symptomatic infants require a **permanent pacemaker**. 3. **Bradycardia:** Congenital heart block is a classic cause of persistent fetal or neonatal bradycardia.

Q: All are features of Kawasaki disease, except?

Peak incidence at age > 5 years. **Explanation:** Kawasaki Disease (KD) is an acute, self-limiting systemic medium-vessel vasculitis. It is the leading cause of acquired heart disease in children in developed nations. **Why Option A is the correct answer (The "Except"):** The peak incidence of Kawasaki Disease is in children **younger than 5 years** (specifically between 6 months and 2 years of age). It is rare in infants under 3 months or children older than 8 years. Therefore, "Peak incidence at age > 5 years" is factually incorrect. **Why other options are incorrect (Features of KD):** * **Option B (Coronary Artery Aneurysm):** This is the most serious complication, occurring in 20–25% of untreated cases. It typically develops in the subacute phase. * **Option C (Enlarged Lymph Nodes):** Cervical lymphadenopathy (usually >1.5 cm and unilateral) is one of the five classic diagnostic criteria. * **Option D (Fever):** High-grade, spiking fever lasting for at least 5 days is the mandatory hallmark for diagnosis. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Criteria (CRASH and Burn):** **C**onjunctivitis (bilateral, non-purulent), **R**ash (polymorphous), **A**denopathy (cervical), **S**trawberry tongue (and oral mucosal changes), **H**ands/feet (edema/erythema/desquamation), and **Burn** (Fever ≥ 5 days). * **Treatment:** High-dose **IVIG** (2g/kg) and **Aspirin**. IVIG is most effective if given within the first 10 days to prevent coronary aneurysms. * **Incomplete Kawasaki:** Common in infants; requires high clinical suspicion as they are at high risk for aneurysms despite not meeting all criteria. * **Echo:** Should be performed at diagnosis, at 2 weeks, and 6–8 weeks.

Q: The clinical features associated with coarctation of the aorta in older children are the following, except?

Absence of flow murmurs over the scapular region. **Explanation:** Coarctation of the aorta (CoA) is a localized narrowing of the aortic lumen, typically occurring near the insertion of the ductus arteriosus. In older children, the clinical presentation is dominated by the development of **collateral circulation** and upper-body hypertension. **Why Option D is the Correct Answer:** In older children with significant coarctation, the body develops extensive collateral vessels (intercostal, internal mammary, and scapular arteries) to bypass the obstruction. These dilated, tortuous vessels produce **continuous or systolic flow murmurs** and bruits that are characteristically heard over the **scapular region** and back. Therefore, the "absence" of these murmurs is incorrect; their presence is a hallmark sign. **Analysis of Incorrect Options:** * **A. Upper body hypertension:** This is the classic finding. Obstruction leads to high pressure proximal to the coarctation, resulting in hypertension in the arms. * **B. Prominent pulsation in the neck:** High stroke volume and pressure in the carotid arteries often lead to visible suprasternal or carotid pulsations. * **C. Fatigability and tiredness in the legs:** Due to the narrowing, there is reduced distal perfusion (lower body ischemia), leading to leg pain or "claudication" during exercise. **NEET-PG High-Yield Pearls:** * **Physical Exam:** Look for the "Radio-femoral delay" and a significant BP pressure gradient between the upper and lower limbs. * **X-ray Findings:** "Rib notching" (due to dilated intercostal arteries eroding the lower borders of the 3rd–8th ribs) and the **"3 sign"** on the barium swallow/chest X-ray. * **Association:** Strongly associated with **Turner Syndrome** (15-20% of cases) and **Bicuspid Aortic Valve** (most common cardiac anomaly). * **Gold Standard Diagnosis:** CT Angiography or MRI; however, Echocardiography is the initial screening tool.

Q: Which of the following is NOT seen in coarctation of the aorta?

Inability to augment cardiac output with exercise. **Explanation:** **Coarctation of the Aorta (CoA)** is a localized narrowing of the aorta, typically near the insertion of the ductus arteriosus. **Why Option D is the correct answer:** Patients with CoA **can** typically augment their cardiac output during exercise. While they may experience an exaggerated hypertensive response in the upper extremities during physical activity, the left ventricle is usually compensated (hypertrophied) enough to increase stroke volume and heart rate, thereby increasing total cardiac output. "Inability to augment cardiac output" is more characteristic of severe congestive heart failure or fixed obstructive lesions like critical aortic stenosis. **Analysis of Incorrect Options:** * **Option A:** If the coarctation is **pre-ductal** or involves the origin of the left subclavian artery, the blood pressure in the right arm will be significantly higher than in the left arm. * **Option B:** Persistent hypertension is a well-known long-term complication even after successful surgical repair. This is attributed to permanent changes in baroreceptor sensitivity and renin-angiotensin system activation. * **Option C:** The systolic murmur is produced by flow across the narrowing (heard at the back/interscapular area). The high-pitched diastolic murmur is often due to an associated **Bicuspid Aortic Valve (BAV)**, which occurs in up to 50-85% of CoA cases, leading to aortic regurgitation. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Sign:** Radio-femoral delay and upper limb hypertension. * **X-ray Findings:** "Figure of 3" sign on chest X-ray and **rib notching** (due to collateral flow through intercostal arteries; usually involves 3rd to 8th ribs). * **Association:** Strongly associated with **Turner Syndrome** (45, XO). * **Gold Standard Investigation:** CT Angiography or Cardiac MRI.

Q: What is the treatment for sudden worsening of Tetralogy of Fallot?

All of the above. **Explanation:** Sudden worsening of Tetralogy of Fallot (TOF) is clinically known as a **Hypercyanotic Spell** or **"Tet Spell."** This occurs due to an acute increase in right-to-left shunting, usually triggered by a decrease in systemic vascular resistance (SVR) or an increase in pulmonary vascular resistance (PVR) caused by infundibular spasm. **Why "All of the Above" is Correct:** The management of a Tet spell aims to increase SVR, decrease PVR, and relax the infundibular spasm. * **Oxygen therapy (B):** Acts as a potent pulmonary vasodilator, reducing PVR and improving oxygenation. * **Propranolol (C):** A beta-blocker used to relax the infundibular muscle spasm and slow the heart rate, allowing better ventricular filling. * **PGE1 infusion (D):** In neonates with severe TOF or pulmonary atresia, PGE1 is life-saving to maintain ductal patency (PDA), ensuring pulmonary blood flow. **Clinical Pearls for NEET-PG:** 1. **First-line physical maneuver:** Knee-chest position (increases SVR by kinking femoral arteries). 2. **Drug of choice for acute spell:** Morphine (sedates the child and reduces tachypnea). 3. **Vasopressor of choice:** Phenylephrine (increases SVR without increasing heart rate). 4. **Maintenance therapy:** Oral Propranolol is used to prevent future spells until definitive surgery. 5. **Definitive Treatment:** Total surgical correction (VSD closure and relief of RVOT obstruction). **Summary:** Management is a multi-modal approach involving positioning, oxygenation, sedation, and pharmacological intervention to restore hemodynamics.

Q: Wolff-Parkinson-White disease may be associated with which of the congenital heart defects?

Ebstein's anomaly. **Explanation:** **Ebstein’s Anomaly** is the congenital heart defect most classically associated with **Wolff-Parkinson-White (WPW) syndrome**. In Ebstein’s anomaly, there is a failure of delamination of the tricuspid valve leaflets, leading to their downward displacement into the right ventricle ("atrialization" of the RV). This structural abnormality is frequently accompanied by **accessory pathways** (Bundle of Kent), particularly located around the malformed tricuspid annulus on the right side of the heart. Approximately 10–20% of patients with Ebstein’s anomaly have WPW syndrome, often involving multiple accessory pathways. **Analysis of Incorrect Options:** * **Tetralogy of Fallot (TOF):** While TOF is associated with right bundle branch block (RBBB) and ventricular arrhythmias post-repair, it does not have a specific developmental association with accessory atrioventricular pathways. * **Patent Ductus Arteriosus (PDA):** PDA is an extracardiac shunt. It leads to volume overload of the left heart but is not associated with the conduction system abnormalities seen in WPW. **High-Yield Clinical Pearls for NEET-PG:** * **WPW in Ebstein’s:** Usually involves **Right-sided accessory pathways**. * **ECG Triad of WPW:** Short PR interval (<0.12s), Delta wave (slurred upstroke of QRS), and prolonged QRS complex. * **Drug of Choice:** For acute orthodromic SVT in WPW, Adenosine is used. However, for permanent destruction of the pathway, **Radiofrequency Ablation** is the definitive treatment. * **Avoid:** "ABCD" drugs (Adenosine, Beta-blockers, Calcium channel blockers, Digoxin) in patients with WPW and Atrial Fibrillation, as they can paradoxically increase conduction through the accessory pathway, leading to Ventricular Fibrillation.

Question 1

A 34-day-old baby presented with increased respiratory effort along with grunting. The infant is always irritable, feeds very poorly, and has not been able to gain weight. There is a history of frequent recurrent pneumonia requiring hospitalization. On examination, the findings include wide pulse pressure, bounding peripheral pulses, a hyperkinetic apex, a continuous thrill in the 2nd left intercostal space, and a continuous murmur localized to the 2nd left intercostal space and radiating down the left sternal border. Which of the following concomitant findings is most likely to be present in this child?

Accepted Answer

Nuclear cataract

Answer

Limb hypoplasias

Answer

Optic atrophy

Answer

Periventricular calcifications

Question 2

A newborn with a marked congenital heart defect (CHD) and decreased pulmonary vascularity should be treated with which of the following medications?

Accepted Answer

Prostaglandin E1

Answer

Digoxin

Answer

Indomethacin

Answer

Epinephrine

Question 3

Which of the following is FALSE regarding Kawasaki disease?

Accepted Answer

Unilateral, suppurative cervical lymphadenopathy

Answer

Strawberry tongue

Answer

Periungual desquamation

Answer

Self-limiting febrile illness

Question 4

Which of the following can cause congenital heart block?

Accepted Answer

Maternal Systemic Lupus Erythematosus (SLE)

Answer

Down's syndrome

Answer

Edward's syndrome

Answer

Phenylketonuria

Question 5

All are features of Kawasaki disease, except?

Accepted Answer

Peak incidence at age > 5 years

Answer

Aneurysm of coronary artery

Answer

Enlarged lymph nodes

Answer

Fever

Question 6

The clinical features associated with coarctation of the aorta in older children are the following, except?

Accepted Answer

Absence of flow murmurs over the scapular region

Answer

Upper body hypertension

Answer

Prominent pulsation in the neck

Answer

Fatigability and tiredness in the legs

Question 7

Which of the following is NOT seen in coarctation of the aorta?

Accepted Answer

Inability to augment cardiac output with exercise

Answer

High blood pressure in the right arm compared to the left arm

Answer

Persistent hypertension despite complete surgical repair

Answer

A systolic murmur heard best over the anterior chest and back, and a high-pitched diastolic murmur along the left sternal border

Question 8

What is the least common cause of endocarditis?

Accepted Answer

Atrial Septal Defect (ASD)

Answer

Patent Ductus Arteriosus (PDA)

Answer

Tetralogy of Fallot (TOF)

Answer

Ventricular Septal Defect (VSD)

Question 9

What is the treatment for sudden worsening of Tetralogy of Fallot?

Accepted Answer

All of the above

Answer

PGE1 infusion

Answer

Oxygen therapy

Answer

Propranolol

Question 10

Wolff-Parkinson-White disease may be associated with which of the congenital heart defects?

Accepted Answer

Ebstein's anomaly

Answer

Tetralogy of Fallot

Answer

Patent Ductus Arteriosus (PDA)

Answer

All of the above

Cardiology — MCQs

Cardiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?