Pathology - cardiac Flashcards
Right-to-left shunts in early cyanotic babies
5 T's Truncus arteriosus (1 vessel) Transposition (2 switched vessels) Tricuspid atresia (3 = tri) Tetralogy of Fallot (4 = tetra) TAPVR (anomalous pulmonary venous return) (5 letters)
Generally caused by defects in aorticopulmonary septum (derived from neural crest)
Tetralogy of Fallot pathology
Caused by anterosuperior displacement of the infundibular septum
Four defects: pulmonary stenosis, RVH, overriding aorta, VSD
Pulm stenosis causes right-to-left shunting across VSD and RVH
Squatting increases systemic resistance, decr. R-to-L shunt, improves cyanosis
Late cyanosis in babies
VSD > ASD > PDA
ASD pathology
usually ostium secundum defects
distinct from PDA: pathology is missing tissue rather than unfused septa
End-stage effects of Eisenmenger syndrome
Late cyanosis, clubbing**, polycythemia
Associations with coarctation of the aorta
Bicuspid aortic valve, Turner syndrome (45 X)
aortic narrowing near insertion of ductus arteriosis (juxtaductal)
Look for delayed pulses in the lower extremities
Hypertension pathology
Primary (essential) - 90%, related to incr. CO or TPR
Secondary - 10%, related to renal/renovascular dz, primary hyper-aldosterone
Cause of hypertension in young woman
Fibromuscular dysplasia - string of beads in renal artery
Hypertensive nephropathy
Renal arterial hyalinosis
Evidence of end-organ damage in hypertensive emergency
Encephalopathy, stroke, retinal hemorrhages/exudates, papilledema, MI, HF, aortic dissection, kidney injury, MAHA, eclampsia
Hyperlipidemia signs
Xanthoma/xanthelesma - lipid-laden histiocytes in the skin
Tendinous xanthoma - seen particularly in Achilles
Corneal arcus - common in elderly
All appear in familial hypercholesterolemia
Arteriosclerosis
Arterial wall thickening and loss of elasticity
Includes arteriolosclerosis and medial calcific sclerosis
Arteriolosclerosis (two types)
Hyaline - thickening of vessel walls, seen in essential HTN/DM
Hyperplastic - proliferation of smooth muscle cells (onion skinning), seen in severe HTN
Medial calcific sclerosis
calcification of elastic lamina or arteries
Leads to vascular stiffening without obstruction
Intima not involved!
Atherosclerosis pathology progression
endothelial cell dysfunction –> macrophage/LDL accumulation –> foam cell formation –> fatty streaks –> smooth muscle migration (PDGF/FGF), ECM deposition –> fibrous plaque –> complex atheroma –> arterial occlusion or plaque rupture
Look for cholesterol crystals
Aortic aneurysm (abdominal vs. thoracic)
Localized pathologic dilatation of aorta
Abdominal: assoc. with atherosclerosis, older men
Thoracic: cystic medial degeneration, assoc. with bicuspid aortic valve, Marfan, tertiary syphillis (obliterative endarteritis)
Aortic dissection
intimal tear forming a false lumen
end results: rupture, pericardial tamponade, death
Type A: Ascending aorta, proximal, treat with surgery
Type B: involves descending aorta, treat with b-blockers then vasodilators
Coronary steal syndrome
phenomenon where administration of vasodilators (CCBs) dilates normal vessels and shunts blood to well-perfused areas, leading to decreased flow and ischemia in post-stenotic region
Pathologic evolution of MI
4-24 hrs
early coagulative necrosis, neuts appear, contraction bands with reperfusion
Pathologic evolution of MI
1-3 days
Extensive coagulative necrosis
Tissue surrounding infarct shows acute inflammation with neutrophils
Watch for pericarditis
Pathologic evolution of MI
3-14 days
Macrophages, then granulation tissue (thus, mac-mediated structural degradation)
Watch for free wall rupture (tampondade), pap muscle rupture (MR), septal rupture
LV pseudoaneurysm also appears