Want to put your knowledge of cardiac pathology to the test? Give this quiz a try!
Cardiac pathology quiz
What type of cardiomyopathy is seen in the sudden death of young athletes?
Question 1 Explanation:
Hereditary hypertrophic cardiomyopathy is due to autosomal dominant mutations in beta myosin heavy chain. It causes massive hypertrophy of the left ventricle which results in diastolic dysfunction and subaortic stenois. Thus, there is an increased risk for ventricular arrhythmias which is a common cause of sudden death in young athletes.
What is the most sensitive and specific marker for a myocardial infarction (MI)?
Question 2 Explanation:
Troponin I is the gold standard for MI detection. Levels rise 2-4hrs after infarction, peak at 24hrs and return to normal by 7-10 days. AST AND LDH were previously used to detect MI, prior to replacement by troponin I.
What are the classic signs of a cardiac tamponade?
Hypotension, muffled heart sounds, increased jugular venous distension (JVD)
Tachycardia, dyspnoea, fever
Bradycardia, weakness in arms, diaphoresis
Hypertension, palpitations, chest pain
Question 3 Explanation:
The classic signs of cardiac tamponade are known as Beck’s triad which includes hypotension, muffled heart sounds and increased JVD. Cardiac tamponade is a pathological compression of the heart caused by excess fluid in the pericardial sac. Cardiac output is reduced as the myocardium cannot contract efficiently leading to hypotension. The accumulation of fluid in the pericardial sac has an insulating effect leading to the heart sounds becoming muffled. JVD is increased as a result of increased venous pressure due to the backflow of blood into veins which is due to the reduced cardiac output.
What is the most common cause of right sided heart failure?
Left sided heart failure
Chronic lung disease (Cor Pulmonale)
Question 4 Explanation:
Left sided heart failure (LHF) is the most common cause of right sided heart failure (RHF). There is a multitude of causes of LHF including ischemia, hypertension, dilated cardiomyopathy, restrictive cardiomyopathy and myocardial infarction. Chronic lung disease and left to right shunt are also causes of RHF.
What is the most common cause of sudden cardiac death (SCD)?
Mitral valve prolapse
Question 5 Explanation:
SCD is unexpected death due to cardiac disease. It occurs without symptoms or within 1 hour after symptoms arise. It is usually due to fatal ventricular arrhythmia- most patients have pre-existing severe atherosclerosis.
What is the most commonly involved coronary artery in myocardial infarction (MI)?
Right coronary artery (RCA)
Left anterior descending artery (LAD)
Left circumflex artery (LCA)
Posterior descending artery (PDA)
Question 6 Explanation:
The LAD is the most commonly involved artery in MI. It leads to the infarction of the anterior wall and anterior septum of the left ventricle (LV). Order of coronary artery involvement: LAD>RCA>Circumflex.
What is the key complication in the first 24 hours of an MI?
Coronary artery aneurysm
Question 7 Explanation:
Arrhythmia is the key complication in the first 4 to 24hrs after a myocardial infarction. Coagulative necrosis is occurring (pyknosis, karyorrhexis, karyolysis). This necrosis can damage the heart’s conduction system resulting in arrhythmias.
What are the characteristics of stable angina?
Chest pain that occurs with exertion and/or emotional stress
Severe and crushing chest pain (>20 mins)
Chest pain that occurs at rest
Question 8 Explanation:
Stable angina is a type of ischemic heart disease which is due to atherosclerosis of coronary arteries. The reduced blood supply cannot meet the demand of the myocardium during exertion which results in reversible injury to the myocytes. It presents as chest pain (<20mins) that radiates to the left arm or jaw, dyspnea and diaphoresis. Symptoms are relieved by rest or glyceryl trinitrate (GTN).
What gross histological change correlates with white blood cells’ (WBCs) invasion into cardiac tissue during the first week after an MI?
Red border around yellow pallor
Question 9 Explanation:
The yellow pallor is indicative of inflammation characterised by neutrophils and macrophages within the myocardium. In the first 24 hours after an MI, there is dark discolouration due to coagulative necrosis. During the first week, there is inflammation signified by the yellow pallor. After which (1 to 3 weeks), granulation tissue emerges marked by a red border entering from edge of infarct. Months after, white scar forms- this is due to fibrosis.
What heart condition is Marfan’s syndrome associated with?
Question 10 Explanation:
Aortic dissection begins as an intimal tear which then allows for blood to pass through the weakened media of the aortic wall. The most common cause of aortic dissection is hypertension but it can also be caused by connective tissue diseases such as Marfan’s syndrome and Ehlers-Danlos syndrome. Marfan’s syndrome is caused by a gene mutation in FBN1 on chromosome 15 leading to a defect in fibrillin (a glycoprotein that forms a sheath around elastin). It causes cystic medial necrosis of the media which is due to fragmentation of elastic laminae with accumulation of myxoid material in aortic media leading to aortic dissection. Other cardiac pathology associations include aortic valve incompetence and mitral valve prolapse. Other findings of the syndrome are tall stature with long extremities, hypermobile joints, pectus excavatum, arachnodactyly and upward/temporal subluxation of lenses.
What heart condition is Turner’s syndrome associated with?
Coarctation of the aorta
Patent ductus arteriosus
Question 11 Explanation:
Turner’s syndrome is a sex chromosome disorder of female sexual development (45, XO). Symptoms include short stature, ovarian dysgenesis, lymphatic defects, cystic hygroma, webbed neck and lymphoedema. In respect to cardiac pathology, it is most commonly associated with preductal coarctation of the aorta which causes hypertension in upper extremities and weak pulses in the lower extremities.
What does the ECG show in prinzmetal angina?
ST segment elevation
ST segment depression
Absent P waves
Prolonged PR interval
Question 12 Explanation:
ST elevation is due to transmural ischemia which occurs in prinzmetal angina. Prinzmetal angina is episodic chest pain that occurs at rest. It is due to coronary artery vasospasm.
What is the main complication of the macrophage phase (4 to 7 days) after an MI?
Aneurysm / Mural thrombus / Dressler syndrome
Cardiac tamponade / Shunt through the ventricular wall / Mitral insufficiency
Question 13 Explanation:
The main complication produced by the macrophages is rupture. They clear all the dead and necrotic debris thereby weakening cardiac tissue making it more susceptible to rupture. If the ventricular free wall is ruptured, a cardiac tamponade will develop. Rupture of the interventricular septum leads to a shunt and rupture of the papillary muscle leads to mitral insufficiency.
Ventricular septal defect (VSD) is the most common congenital heart defect, what condition is it most likely to be associated with?
Foetal alcohol syndrome
Question 14 Explanation:
VSD is associated with foetal alcohol syndrome. PDA is associated with congenital rubella. ASD (ostium primum type) is associated with Down's syndrome. Transposition of the great vessels is associated with maternal diabetes.
What is the most common cause of mitral stenosis?
Chronic rheumatic valve disease
Acute rheumatic fever
Congestive heart failure
Question 15 Explanation:
Mitral stenosis is the narrowing of the mitral valve orifice and is often as a result of chronic rheumatic disease, a late sequelae of acute rheumatic fever. The acute attack is a multisystem inflammatory disease (migratory polyarthritis, carditis, subcutaneous nodules, erythema marginatum and Sydenham chorea) following group A beta haemolytic streptococcal pharyngitis. The acute attack usually resolves but may progress to chronic disease especially with repeat exposure to group A beta haemolytic streptococci. In chronic disease, there is valve scarring and thickening of the chordae tendinae and cusps leading to stenosis. Physical exam findings include an opening snap followed by diastolic murmur best heard over apex in left lateral position. Complications of mitral stenosis include pulmonary congestion due to the backup of blood in the left atrium, pulmonary hypertension leading to right sided heart failure, atrial fibrillation due to dilation of left atrium disrupting the electrical signal and mural thrombi due to blood stasis.
Choose the complete and accurate grouping of right to left shunts
Atrial septal defect (ASD), Patent ductus arteriosus (PDA), Ventricular septal defect (VSD)
Truncus arteriosus, Transposition of great vessels, Tricuspid atresia, Tetralogy of Fallot, Total anomalous pulmonary venous return (TAPVR)
ASD, TAPVR, VSD
PDA, Truncus arteriosus, tetralogy of fallot
Question 16 Explanation:
Remember the right to left shunts as the ‘5 Ts’. The left to right shunts are ASD, VSD and PDA.
What is the most frequent etiologic agent of acute infective endocarditis in IV drug abusers?
Question 17 Explanation:
Staph aureus is the most common causative agent of endocarditis in IV drug users. It is highly virulent and affects native, undamaged valves, especially the tricuspid. It creates large vegetations that destroy the valves, often leading to tricuspid regurgitation. Strep viridans is the most common overall cause of endocarditis; it is low virulence and infects previously damaged valves. Staph epidermidis infects prosthetic valves.
What is the best description of Eisenmenger’s syndrome?
It occurs when a right to left shunt becomes left to right due to a build-up of pressure on the left side of the heart.
It is due to failure of the aorticopulmonary septum to spiral.
It is due to lack or aorticopulmonary septum formation.
An initial left to right shunt becomes right to left due to increased pulmonary blood flow and eventual right ventricular hypertrophy (RVH).
Question 18 Explanation:
Left to right shunts (ASD, VSD, and PDA) will cause increased flow in the pulmonary circulation leading to pathologic remodelling of vasculature and pulmonary hypertension. RVH occurs to compensate and the shunt is reversed (now right to left). This will present as late cyanosis, polycythaemia and clubbing.
There are 18 questions to complete.