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Cardiac Pathology Quiz


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Elder

Want to put your knowledge of cardiac pathology to the test? Give this quiz a try!
Question 1
What are the characteristics of stable angina?
A

Chest pain that occurs with exertion and/or emotional stress

Severe and crushing chest pain (>20 mins)

C Chest pain that occurs at rest


D Bradycardia
Question 1 Explanation:
Stable angina is a type of ischemic heart disease which is due to atherosclerosis of coronary arteries with >70%
stenosis. 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 nitroglycerin.
Question 2
What is the pathogenesis of unstable angina?
A

Coronary artery vasospasm

Rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery

C Atherosclerosis of coronary arteries with >70% stenosis


D Rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery.
Question 2 Explanation:
Unstable angina is chest pain that occurs at rest. There is incomplete occlusion of the coronary artery
representing reversible injury to myocytes compared to a myocardial infarction(MI) where there is complete
occlusion of the artery resulting in necrosis (irreversible cell death) of the cardiac myocytes. The EKG will show
ST-segment depression due to subendocardial ischemia. Symptoms are relieved by nitroglycerin. It can progress
to MI. Coronary artery vasospasm (A) leads to prinzmental angina. Atherosclerosis with stenosis(C) causes
stable angina. Complete occlusion of a coronary artery by a thrombus (D) will lead to a MI.
Question 3
What does the ECG show in prinzmetal angina?
A

ST segment elevation

ST segment depression

C Absent P waves
D Prolonged PR interval
Question 3 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.
Question 4
What is the most commonly involved coronary artery in myocardial infarction (MI)?
A

Right coronary artery (RCA)

Left anterior descending artery (LAD)

C Left circumflex artery (LCA)


D Posterior descending artery (PDA)
Question 4 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. The PDA arises
from LCX and RCA.
Question 5
What is the most sensitive and specific marker for a myocardial infarction (MI)?
A

AST

LDH

C Troponin I
D CK-MB
Question 5 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. CK-MB elevations normalize within 3 days, allowing for detection of reinfarction. AST & LDH
were previously used to detect MI, prior to replacement by troponin I and CK-MB.
Question 6
Fibrinolysis and angioplasty are treatment options for MIs. An MI is usually due to rupture of an atherosclerotic
plaque with thrombosis and complete occlusion of a coronary artery. These treatments will open the blocked
vessels. What is the complication/s of fibrinolysis/angioplasty?
A

Reperfusion injury, contraction band necrosis

Palpitations

C Tachycardia / tachypnoea
D Hypertension

Question 6 Explanation:
Reperfusion injury occurs when there is free radical damage to myocytes. When the vessel is unblocked, there is
a flow of oxygen and inflammatory cells into the myocardium which generate the free radicals. Contraction band
necrosis is the hypercontraction of myofibrils due to the calcium influx that occurs when there is reperfusion of
irreversibly damaged cells.
Question 7
What is the key complication in the first 24 hours of an MI?
A

Fibrinous pericarditis

Coronary artery aneurysm

C Arrhythmia
D Mitral insufficiency
Question 7 Explanation:
Arrhythmia is the key complication in the first 4 to 24hrs after a MI. Coagulative necrosis is occurring (pyknosis,
karyorrhexis, karyolysis). This necrosis can damage the hearts conduction system resulting in arrhythmias.
Question 8
What gross histological change correlates with white blood cells (WBCs) invasion into cardiac tissue during the
first week after an MI?
A

Yellow pallor

Dark discolouration

C White scar
D Red border around yellow pallor
Question 8 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.
Question 9
What is the main complication/s of the macrophage phase in 4 to 7 days after an MI?
A

Fibrinous pericarditis

Arrhythmia

C Aneurysm / Mural thrombus / Dressler syndrome


D Cardiac tamponade / Shunt through the ventricular wall / Mitral insufficiency
Question 9 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.
Question 10
What is the most common cause of right sided heart failure?
A

Left sided heart failure

Chronic lung disease (Cor Pulmonale)

C Hypothyroidism
Question 10 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(B) and left to right shunt(C) are also causes of RHF.
Question 11
What is the most common cause of sudden cardiac death (SCD)?
A

Cocaine abuse

Mitral valve prolapse

C Cardiomyopathy
D Ventricular arrhythmia
Question 11 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.
Question 12
Ventricular septal defect (VSD) is the most common congenital heart defect, what condition is it most likely to be
associated with?
A

Congenital rubella

Down Syndrome

C Foetal alcohol syndrome


D Maternal diabetes
Question 12 Explanation:
VSD is associated with foetal alcohol syndrome. PDA is associated with congenital rubella. ASD (ostium primum
type) is associated with Down syndrome. Transposition of great vessels is associated with maternal diabetes.
Question 13
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)

C ASD, TAPVR, VSD


D PDA, Truncus arteriosus, tetralogy of fallot
Question 13 Explanation:
Remember the right to left shunts as the 5 Ts. The left to right shunts are ASD, VSD and PDA.
Question 14
What is the best description of Eisenmengers syndrome?
A

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.

C It is due to lack or aorticopulmonary septum formation.


D An initial left to right shunt becomes right to left due to increased pulmonary blood flow and eventual right
ventricular hypertrophy (RVH).
Question 14 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.
Question 15
What type of cardiomyopathy is seen in the sudden death of young athletes?
A

Hypertrophic Cardiomyopathy

Restrictive Cardiomyopathy

C Dilated Cardiomyopathy
Question 15 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.
Question 16
What heart condition is Marfans syndrome associated with?
A

Endocarditis

Restrictive Cardiomyopathy

C Arrhythmia

D Aortic dissection
Question 16 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 Marfans syndrome and Ehlers-Danlos syndrome. Marfans 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.
Question 17
What heart condition is Turners syndrome associated with?
A

Tricuspid atresia

Truncus arteriosus

C Coarctation of the aorta


D Patent ductus arteriosus
Question 17 Explanation:
Turners syndrome is a sex chromosome disorder of female sexual development (45, XO). Symptoms include
short stature, ovarian dysgenesis, lymphatic defects- cystic hygroma (webbed neck), lymphedema in feet, hands
and shield chest. In respect to cardiac pathology, it is most commonly associated with preductal coarctation of the
aorta which causes hypertension in upper extremities and weak, delayed pulse in lower extremities
(brachial>femoral) and lower extremity cyanosis in infants.
Question 18
What are the classic signs of a cardiac tamponade?
A

Hypotension, muffled heart sounds, increased jugular venous distension(JVD)

Tachycardia, dyspnoea, fever

C Bradycardia, weakness in arms, diaphoresis


D Hypertension, palpitations, chest pain
Question 18 Explanation:
The classic signs of cardiac tamponade are known as Becks 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 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.
Question 19

What is the most frequent etiologic agent of acute infective endocarditis in IV drug abusers?
A

Streptococcus viridans

Staphylococcus aureus

C Staphylococcus epidermidis
D Streptococcus bovis
Question 19 Explanation:
Staph aureus is the most common causative agent of endocarditis in IVDUs. 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. Strep bovis causes
endocarditis in patients with underlying colon cancer.
Question 20
What is the most common cause of mitral stenosis?
A

Chronic rheumatic valve disease

Acute rheumatic fever

C Congestive Heart Failure


D Infective endocarditis
Question 20 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- opening
snap followed by diastolic murmur best heard over apex in left lateral position, loud S1. 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.
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