Anatomic Pathology Flashcards
what are the mechanisms of sudden cardiac death?
lethal arrythmias (asystole or VF)
What are the 6 acyanotic CHD
ASD, VSD, PDA, PS, AS, CoA
What are the reperfusion changes or associated pathology
Arrythmias, Myocardial hemorrhage, Irreversible cell injury (reperfusion injury), microvascular injury, prolonged ischemic dysfunction (myocardial stunning)
what are the 3 factors that trigger acute plaque change
Inflammation
Coronary Thrombosis
Vasoconstriction
How does chrinic IHD Present?
Large heart secondary to LV hypertrophy
discrete grey white scars
moderate to severe stenosing atherosclerosis
microscopic: myocardial hypertrophy, diffuse endocardial vacuolation, scar tissue.
What is the microscopy timeline of MI
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
what may cause sudden cardiac death?
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
What are the 4 IHD?
MI, Angina Pectoris,Chronic IHD, Sudden cardiac death
Differentiate between the diagnosis of acute and chronic PHHD
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.
What are the classic signs of a cardiac tamponade?
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 key complication in the first 24 hours of an MI?
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 is the most commonly involved coronary artery in myocardial infarction (MI)?
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 heart condition is Turner’s syndrome associated with?
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 is the TTC timeline of MI
<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
what are the clinical presentations of MI
Rapid pulse, diaphoresis, dyspnea
Raises serum myoglobon, troponin T&I, CK-MB, LD
ECG-new Q waves
What is the main complication of the macrophage phase (4 to 7 days) after an MI?
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.
Distinguish the 3 types of Angina
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)
Which of the following conditions is Marfan’s syndrome most commonly associated with?
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.
What are the 4 defects comprising the tetralogy of Fallot
ventricular septal defect
pulmonary stenosis
misplaced aorta
right ventricular hypertrohy
What is Ebstein’s anomaly?
An abnormal and mispositioned tricuspid valve
What does the ECG show in prinzmetal angina?
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 most common cause of sudden cardiac death (SCD)?
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 are the characteristics of stable angina?
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).
What is Acute Heart Failure
Reversible lack of myocardial contractility within a brief period of a MI Initiation
What is the etiology of Acute Infective Endocarditis
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
What is the morphologic presentation of a sudden cardiac death
Marked coronary atherosclerosis
healed infarcts at post mortem
Describe the diagnosis of SHHD
Concentric Left Ventricular Hypertrophy, cardiomegally.
Microscopy: increased transverse diameter of myocyte, cellular and nuclear size variation and interstitial fibrosis.
What is usually the first sign of SHHD
Atrial Fibrillation due to atrial dilatation or CCF due to dilatation or both
What is most commonly associated with VSD
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.
With respect to metabolism, state the effect of MI
Cessation of aerobic glycolysis. ATP falls to 50% within 10 minutes and to 10% within 40 minutes. There is accumulation of lactic acid
How are the Acute Coronary Syndromes initiated
Abrupt conversion of a relatively stable atheromatous plaque into a big lesion potentially life threatening.
what is a likely cause of Chronic IHD?
Post infarction decompensation due to exhausion of compensatory hypertrphy and other obstructive CAD
What are the 7 cyanotic CHD
TOF, TGA, tricuspid atresia, Truncus, TAPVR, Ebstein’s, single ventricle
what are some complications of MI
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
Differentiate etiology of acute and chronic PHHD
Acute PHHD is due to massive pulmonary thromboembolism; chronic is due to pulmonary artery obstruction or hypertention eg primary pulmonary hypertension, and emphysema
what is the pathogenesis of ACS
Diminished coronary perfusion relative to myocardial demand
What is the pathogenesis of MI
Coronary arterial occlusion through sudden disruption of artheromatous plaque, PLT aggregation, vasospasms, thrombosis.
What is the most common cause of right-sided heart failure?
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 best description of Eisenmenger’s syndrome?
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
What gross histological change correlates with white blood cells’ (WBCs) invasion into cardiac tissue during the first week after an MI?
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.
