Path Flashcards
LAD
Anterior/anteroseptal wall of LV
LCx
Lateral wall LV
LAD+RCA
Septal wall
RCA
Posterior wall/posterior 1/3 of interventicular septum** SA node so infarct here can result in arrhythmia
Gross Changes Post MI0-12 h12-1824-721 wk2-3wk4-6wk
0-12 Hours – No changes 12-18 Hours – Pallor 24-72 Hours – White Infarct with Hyperemic Borders1 Week – Loss of Hyperemia 2-3 Weeks – Soft Gelatinous4-6 Weeks – Scarring/Fibrosis
Systolic Murmurs
Aortic StenosisPulmonic StenosisMitral Regurgitation/ProlapseTricuspid RegurgitationVentricular Septal DefectHypertrophic Cardiomyopathy
Histologic Time Sequence Post MI3-6 hr12-24 hr24 hr5-7d8-10d10-14d2-4wk4-6wk
3-6 Hours – Wavy fibers (non-contracting ischemic myocytes 12-24 Hours – Coagulation necrosis, hypereosinophilic myocytes24 Hours – Neutrophil infiltration peaking at 3-5 days5-7 Days – Macrophage infiltration and neutrophils regress 8-10 Days – Lipofuscin (wear and tear pigment)10-14 Days – Granulation tissue at infarct borders 2-4 Weeks – Fibroblasts depositing collagen4-6 Weeks+ - Mature Scar
Diastolic Murmurs
Aortic RegurgitationPulmonic RegurgitationMitral Stenosis Tricuspid Stenosis
Best to hear Aortic Valve
2nd-3rd R interspace
best to hear pulmonic valve
2nd-3rd L interspace
best to hear tricuspid valve
L sternal border
best to hear mitral valve
apex
Type I Atherosclerosis: Thickening of Intima
smooth muscle cells (HHF-35 positive) – you have more of these come inno macrophages (CD68 negative) and no lipids (oil-red-O negative)
Type II Atherosclerosis: Intimal Xanthoma
Progressive thickening with macrophagesCD68 positive and Oil-red-O positiveThis is when you have the formation of FOAMY CELLS (macrophages filled with lipids)
Type III Atherosclerosis: Pathologic Intimal Thickening
small cells of extracellular liquidNo symptoms at this point, because of positive remodeling Diameter of the artery changes, but the diameter of the lumen doesn’t changeThis is when you start to get worried, but this is not pathologic yet
Type IV Atherosclerosis: Fibroatheroma
core of extra-cellular lipid starts to formstart to get symptoms because lumen starts to be narrowed
Type V Atherosclerosis: Thin-cap fibroatheroma
Fibrous thickening of cap. Completion of formation of fibroatheroma. Fibroatheroma = well-formed lipid necrotic core surrounded by macrophages and lymphocytes with an overlying fibrous cap rich in SMCsThin-Cap Fibroatheroma = vulnerable plaque (i.e. vulnerable to disruption, leading to coronary thrombosis), since it has a thin fibrous cap infiltrated by macrophages (CD 68+) Cap – made of fibrin and smooth muscle cells, will start getting thin or thick, important to know if it is thin or thickLipid necrotic core
Type VI Atherosclerosis: Thrombus
Thrombus formation after surface defectOccurs either by plaque rupture or plaque erosion
6 Stages of Atherosclerosis
Thickening of IntimaIntimal XanthomaPathological Intimal ThickeningFibroatheromaThin-cap fibroatheromaThrombus
Most Common cause of death post-MI
Congenital Diseases predisposing to aneurysm
Marfan Syndrome: Fibrillin-1, elastinEhler’s Danlos Syndrome: mutation in collagen, procollagen Type III
Libman-Sacks endocarditis
Non-infectiousUndersurface of valvesAssoc w/ SLESmall, sterile emboli break offTricuspid, mitral
Aortic stenosis auscultation
Normal S1Ejection clickSystolic C-D murmurNormal S2Diastolic D murmur
Aortic regurg auscultation
Softer S1Ejection clickBrief, early systolic murmurSingle, softer S2S3 gallop*diastolic D murmur (low pitch = severe)
