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