Pathoma Cardiac Pathology Flashcards
Three subtype of angina and what each is all about
1. Stable Angina: CP that arises with exertion or emotional stress. >70% stenosis. REVERSIBLE injury to myocytes w/o necrosis. Lasts <20 min. ST depression. Tx: rest, nitro
2. Unstable Angina: CP that occurs at rest. Due to rupture of atherosclerotic plaque with thrombosis and INCOMPLETE occlusion of coronary artery. REVERSIBLE injury. ST depression. High risk to progress to MI. Tx: nitro
3. Prinzmetal Angina: episodic CP unrelated to exertion. REVERSIBLE injury. Due to coronary artery vasospasm. ST elevation due to transmural ischemia. Tx: nitro, CCB
Myocardial Infarction and what are 3 most common arteries involved
- Necrosis of cardiac myocyte.
- Due to rupture of atherosclerotic plaque with thrombosis and COMPLETE occlusion of a coronary artery.
1. Left anterior descending artery (LAD) –>anterior wall and anterior septum (45% of cases)
2. Right Coronary Artery (RCA) –> posterior wall, posterior septum, papillary muscles LV (2nd most common)
3. Left Circumflex Artery (LCA) –> infarction lateral wall of LV
Treatment of MI
- ASA w/ w/o heparin, limits thrombosis
- O2 to minimize ischemia
- Nitrates: vasodilate veins* and coronary arteries
- B-blocker: slow HR, decrease demand of heart
- ACE-I: decrease blood volume, decrease TPR
- fibrinolytics (tPA) or angioplasty (stent)
Two complications after angioplasty of coronary vessels after an acute MI
1. Contraction band necrosis: reperfusion leads to an influx of calcium, leading to hypercontraction of myofibrils (despite cell being dead with no nucleus)
2. Reperfusion injury: return of O2 and inflammatory cells may lead to free radical generation. (often see an additional increase in troponin after angioplasty due to formation of free radicals)
<4 hours after MI
- NO gross changes, NO microscopic changes
- Can see cardiogenic shock (massive infarction), CHF, arrhythmia
4-24 hours post MI
-Dark Discoloration
-Coagulative necrosis
-Complication of arrhythmia
1-3 days post MI
-Yellow pallor
-Neutrophils due to Acute Inflammation
-Complication of fibrinous pericarditis that presents as CP with friction rub
4-7 days post MI
- Yellow pallor
- macrophages present that are eatingup necrotic debris.
Risk of rupture of ventricular free wall HIGHEST now can lead to cardiac tamponade. Risk of rupture of interventricular septum leading to shunt, rupture of papillary muscle leading to mitral insufficiency (esp if RCA infarct)
1-3 months post MI
and Months after MI
1-3 months
- Red border emerges as grnaulation tissue enters from edge of infarct
- Granulation tissue with plump fibroblasts, collagen (type 1 Collagen), and blood vessels
Months
White scar, with fibrosis, risk of aneuysm, mural thrombus or Dressler syndrome (Ab against pericardium)
Causes of left sided HF
- Ischemia
- hypertension
- dilated cardiomyopathy
- MI
- Restrictive cardiomyopathy
Clinical features of left sided HF
-pulm congestion leading to pulmonary edema
-dyspnea, paroxysmal nocturnal dyspnea (due to increased venous return when lying flat), orthopnea, crackles
- Small congested capillaries burst, leading to intraalveolar hemorrhage marked by hemosiderin-laden macrophages
- decreased blood flow to kidneys resulting in activation of RAAS
-tx: ACE-I
Right sided heart failure causes and presentation
Causes: left sided heart failure, left to right shunt, cor pulmonale
Clinical: JVD, hepatosplenomegaly (with nutmeg liver) leading to cardiac cirrhosis, pitting edema (due to increased hydrostatic pressure)
Right sided HF vs Left sided HF
Ventricular Septal Defect (VSD)
-Defect in septum that divides right and left ventricles.
-most common congenital heart defect
L–> R shunt
Can result in Eisenmenger syndrome (reversal of shunt)
Tx: surgical closure
Associated with fetal alcohol syndrome****, Cri-du-chat syndrome
Atrial Septal Defect
-Most common type is ostium secundum (90% of cases)
-Ostium primum type is associated with Down Syndrome
-Results in L –> R shunt, split S2 on auscultation due to increased blood in right heart delays closure of pulmonary valve
-Paradoxical emboli can occur (instead of going to lung to cause PE, go to left side of circulation, end up going to brain or other circulation places)
-Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.