Anatomic Pathology

Question 1

what are the mechanisms of sudden cardiac death?

Answer 1

lethal arrythmias (asystole or VF)

Question 2

What are the 6 acyanotic CHD

Answer 2

ASD, VSD, PDA, PS, AS, CoA

Question 3

What are the reperfusion changes or associated pathology

Answer 3

Arrythmias, Myocardial hemorrhage, Irreversible cell injury (reperfusion injury), microvascular injury, prolonged ischemic dysfunction (myocardial stunning)

Question 4

what are the 3 factors that trigger acute plaque change

Answer 4

Inflammation
Coronary Thrombosis
Vasoconstriction

Question 5

How does chrinic IHD Present?

Answer 5

Large heart secondary to LV hypertrophy
discrete grey white scars
moderate to severe stenosing atherosclerosis
microscopic: myocardial hypertrophy, diffuse endocardial vacuolation, scar tissue.

Question 6

What is the microscopy timeline of MI

Answer 6

4-12 hrs: light microwavy fibres in periphery of infarct; vacuolar degeneration (myolysis)
2-3 days: Inflammatory response, nuclear loss, loss of striations
2-4 weeks: Granulation tissues growing in
6 weeks: Scar

Question 7

what may cause sudden cardiac death?

Answer 7

congenital structural or coronary artery abnormality
Aortic Valve Stenosis
delayed or hypertrophic cardiomyopathy
mitral valve prolapse
pulmonary HT
hereditary or acquired abnormality of conduction system
Isolated Hypertrophy or HT of unknown cause

Question 8

What are the 4 IHD?

Answer 8

MI, Angina Pectoris,Chronic IHD, Sudden cardiac death

Question 9

Differentiate between the diagnosis of acute and chronic PHHD

Answer 9

Acute- RV dilatation without hypertrophy
chronic- RV Hypertrophy with dilatation and thickening of muscle bundles in outflow tract below pulmonary valve or moderator band. Secondary compression of LV and tricuspid regurgitation with fibrosis.

Question 10

What are the classic signs of a cardiac tamponade?

Answer 10

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.

Question 11

What is the key complication in the first 24 hours of an MI?

Answer 11

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.

Question 12

What is the most commonly involved coronary artery in myocardial infarction (MI)?

Answer 12

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.

Question 13

What heart condition is Turner’s syndrome associated with?

Answer 13

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.

Question 14

what is the TTC timeline of MI

Answer 14

<12 hrs: pale infarcted areas surrounded bybrick red viable myocardium
12-24 hrs: Red blue hue with dark mottling
>24 hrs: Yellow tan, mottling infarct at the center
10-14 days: Hyperemic ream around red grey infarcted center which later evolves into a scar

Question 15

what are the clinical presentations of MI

Answer 15

Rapid pulse, diaphoresis, dyspnea
Raises serum myoglobon, troponin T&I, CK-MB, LD
ECG-new Q waves

Question 16

What is the main complication of the macrophage phase (4 to 7 days) after an MI?

Answer 16

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 17

Distinguish the 3 types of Angina

Answer 17

Stable/typical: due to chronic stenosing atherosclerosis. Precipitated by increasing oxygen demand
Prinzmetal: Due to vessel spasm. occurs at rest
unstable: progressively worsens. Also called pre-infarction angina ( a prodrome of MI)

Question 18

Which of the following conditions is Marfan’s syndrome most commonly associated with?

Answer 18

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 an 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 19

What are the 4 defects comprising the tetralogy of Fallot

Answer 19

ventricular septal defect
pulmonary stenosis
misplaced aorta
right ventricular hypertrohy

Question 20

What is Ebstein’s anomaly?

Answer 20

An abnormal and mispositioned tricuspid valve

Question 21

What does the ECG show in prinzmetal angina?

Answer 21

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 22

What is the most common cause of sudden cardiac death (SCD)?

Answer 22

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 23

What are the characteristics of stable angina?

Answer 23

Stable angina is a type of ischaemic 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, dyspnoea and diaphoresis. Symptoms are relieved by rest or glyceryl trinitrate (GTN).

Question 24

What is Acute Heart Failure

Answer 24

Reversible lack of myocardial contractility within a brief period of a MI Initiation

Question 25

What is the etiology of Acute Infective Endocarditis

Answer 25

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 valve

Question 26

What is the morphologic presentation of a sudden cardiac death

Answer 26

Marked coronary atherosclerosis
healed infarcts at post mortem

Question 27

Describe the diagnosis of SHHD

Answer 27

Concentric Left Ventricular Hypertrophy, cardiomegally.
Microscopy: increased transverse diameter of myocyte, cellular and nuclear size variation and interstitial fibrosis.

Question 28

What is usually the first sign of SHHD

Answer 28

Atrial Fibrillation due to atrial dilatation or CCF due to dilatation or both

Question 29

What is most commonly associated with VSD

Answer 29

VSD is associated with fetal 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.

Question 30

With respect to metabolism, state the effect of MI

Answer 30

Cessation of aerobic glycolysis. ATP falls to 50% within 10 minutes and to 10% within 40 minutes. There is accumulation of lactic acid

Question 31

How are the Acute Coronary Syndromes initiated

Answer 31

Abrupt conversion of a relatively stable atheromatous plaque into a big lesion potentially life threatening.

Question 32

what is a likely cause of Chronic IHD?

Answer 32

Post infarction decompensation due to exhausion of compensatory hypertrphy and other obstructive CAD

Question 33

What are the 7 cyanotic CHD

Answer 33

TOF, TGA, tricuspid atresia, Truncus, TAPVR, Ebstein’s, single ventricle

Question 34

what are some complications of MI

Answer 34

contractile dysfunction in LV causing: LV hypotension, Pulmonary edema, Pulmonary congestion
Arrythmias - sinus bradycardia, heartblock or asystole, tachycardia, ventricular tachycardia/fibrillation, myocardial rapture with tamponade
Ventricular septum rupture, papillary rupture causing mitral regurgitation

Question 35

Differentiate etiology of acute and chronic PHHD

Answer 35

Acute PHHD is due to massive pulmonary thromboembolism; chronic is due to pulmonary artery obstruction or hypertention eg primary pulmonary hypertension, and emphysema

Question 36

what is the pathogenesis of ACS

Answer 36

Diminished coronary perfusion relative to myocardial demand

Question 37

What is the pathogenesis of MI

Answer 37

Coronary arterial occlusion through sudden disruption of artheromatous plaque, PLT aggregation, vasospasms, thrombosis.

Question 38

What is the most common cause of right-sided heart failure?

Answer 38

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.

Question 39

What is the best description of Eisenmenger’s syndrome?

Answer 39

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 40

What gross histological change correlates with white blood cells’ (WBCs) invasion into cardiac tissue during the first week after an MI?

Answer 40

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.