2nd Exam: Pathology of Cardiovascular Disease Flashcards
diaphoresis:
heavy sweating, usually due to drugs
rales throughout systole:
could be mitral valve rupture
afebrile:
without fever
wavy fiber change, nuclei faded out:
MI only 4-12h old, recent cardiac necrois, new ischemic necrosis, wavy at border of infarct
dense pink typical of:
ischemic necrosis
neutrophoils, acute inflammatory response:
2-3 d old necrosis, that’s when papillary m. ruptured
Next step after neutrophil infiltration:
granulation tissue formation
palor within the anterior wall of LV, think:
LAD MI
you can save m. __ hours
after 3 hours you almost never see repurfusion
6+
Lactic acid and ATP changes during acute MI:
ATP dec, lactic acid inc (both curved arcs)
Duration of reversible phase of acute MI:
30min
Time at which ischemic myocardium is potentially salvageable by timely intervention after acute MI:
about 1.25h
Time at which there is cumulative dead myocardium after acute MI:
about 1.75h
Irreversible injury after acute MI starts after:
30min
Molecular level changes during reversible phase of acute MI:
glycogen depletion, mito swelling, myofibril relaxation
Molecular level changes during irreversible phase of acute MI:
sarcolemma disruption, mito amorphous densities
Wavy fiber syndrome begins at borders:
1-2h after acute MI
coagulation necrosis, edema, focal hemorrhage, neutrophilic infiltrate begins:
3-10h after acute MI
Continuing coagulation necrosis, palor, shrunken nuclei, eosinophilic cytoplasm, myocyte contraction bands:
10-18 after acute MI
Coagulation necrosis w loss of nuclei and striations, neutrophilic infiltrate, pallor, sometime hyperemia, yellowing at periphery:
1-2d after acute MI
Disintegration of myofibers and phagocytosis by macs, hyperemic border, central yellow-brown softening:
2-8d after acute MI
completion of phagocytosis, prominent granulation tissue w neovascularization and fibrovacsular reaction, maximally yellow and soft vascularized edges, red-brown and depressed:
8d-6wks
Duration to form mature fibrous scar after an acute MI:
about 6wks
Image of of 1-3d old acute MI:
necrosis, many PMNs
3d old infarct:
look at edge to place a time frame on occurence,
inflammatory change from living to dead, then another episode of ischemia, junction is all necrotic, inflammatory response stops, frozen in time 3d old inflammatory response
several areas of different age infarctions
2nd episode caused mv regurgitation
3rd episode of myocardial necrosis
acute MI, 7-10d:
removal of dead myocytes by macs
granulation tissue transforming to scar tissue indicates that the acute MI:
probably older than 7-10 d
How many days after acute MI are there capillaries growing in but no red blood cells?
7-10d
contraction bands;
transverse dark pink bands in cytoplasm of dead myocytes lethally injured by ischemia, hypercontracted sarcomeres that form at the time of reflow during a reperfusion procedure (thrombolysis, angioplasty, CABG, etc.), Z lines pile up w the hypercontraction
Effects of reprefusion:
save reversible injuries, reprefusion injuries
Reprefusion injuries:
stunned myocardium (some form of contractile abnormality), microvascular injury, no reflow, arrhythmia (malfunction of electric system of h.), hemorrhage, micro-contraction bands
When do contraction bands form?
at the time of reflow during a reprefusion procedure
Cause of most acute MI’s (about 90%):
sudden change of ath plaque in epicardial coronary a. causing occlusion
2 causes of rapid growth of plaque:
hemorrhage, cholesterol rupture through plaque
Plaque is:
lipid core, fibrous cap
Pathogenesis of atherosclerosis:
endo injury, inflammation, lipid deposits, sm proliferation
Factors affecting ath:
high lipids, high BP, smoking, toxins, blood stasis/ turbulence, immune reactions, viruses
1st step in ath pl formation:
endo injury
Cholesterol efflux occurs into the lumen via:
HDL:
foam cells:
Fat-laden macrophages seen in atherosclerosis
Steps in pl formation:
endo injury, endo express adhesion molecules, inflammation, macros and lymphos, lipids begin collects in intima, free radical oxidation, monocyte adhesion and emigration into intima, differentiation to macro, ingestion of lipids, now foam cell, cytokines, Gf, and sm cells come to intima from media, reactive sm proliferation
Large scale evolution of plaque:
fatty streak, fibrofatty plaque, catastrophic complication
TF? Fatty streak always remains confined to the intima.
F. only at first
Causes of endo damage:
smoking, high BP, diabetes, infection, high fats, homocysteine, rate of blood flow, toxins, immune reactions
How are LDL’s oxidized in the intima?
free radicals
Consequence of endo injury:
inc perm, wbc adhesion, monocyte adhesion and emigration
Activates macros in the intima:
sm cell emigration
Function of sm in the intima:
engulf lipids with macs
Closer to the endo, external or internal elastic lamina?
internal
Layers of normal a.:
endo, IMA
Composition of fibrous cap:
sm cells, macs, foam cells, lymphos, collagen, elastin, proteoglycans, neovascularization
Composition of necrotic center
cholesterol crystals, calcium, debris, foam cells
Causes of pl disruption:
Cap rupture (most common), pl erosion, hemorrhage into pl, ulceration of Ca2+ nodule
Most common cause of pl disruption:
Cap rupture
Hemorrhage into pl comes from these vessels:
pl microvessels
Dif types of vulnerable pl:
rupture-prone vulnerable, ruptured/healing vulnerable, erosion-prone vulnerable, eroded vulnerable, vulnerable w intra-pl hemorrhage, vulnerable w calcific nodules, critically stenotic vulnerable
Typical angina:
fixed coronary obstruction
fixed coronary obstruction can progress to either:
severe fixed coronary obstruction or pl disruption (pl aggregation)
severe fixed coronary obstruction:
chronic ischemic hd
pl disruption can progress to either:
TOMS: MURAL thrombus w variable obstruction (unstable angina or acute SUBENDOCARDIAL myocardial infarction or sudden death) OCCLUSIVE thrombus (acute TRANSMURAL myocardial infarction or sudden death)
2 acute coronary syndromes:
Both thrombus, TOMS: mural thrombus w variable obstruction (unstable angina or acute subendocardial myocardial infarction or sudden death) occlusive thrombus (acute transmural myocardial infarction or sudden death)
Stages of healing of MI:
granulation tissue, scar
Color that collagen in scar stains:
blue
Complication of MI rupture syndromes:
free wall LV, papillary m., IV septum
Complications of MI:
pericarditis, CHF, mural thrombus over older MI, LV aneurysm, LV aneurysm w mural thrombus, ischemic coagulation necrosis of kidney glom and tubules (?check)
Ranges of CHF:
mild to cariogenic shock
etiology of kidney infarction:
embolic occlusion, renal a. branch from mural thrombus over old MI
Sources of systemic emboli:
mural thrombi from heart or large arteries, old MI’s w aneurysms, hypokinetic areas, etc., vegetation on valve (IE, NBTE), ath pl
Consequences of systemic emboli:
organ infarction
Sites of systemic emboli:
75%: lower extremities, 10%: brain, intestines, kidneys, spleen
