last minute review Flashcards
(36 cards)
1-4 hours after MI see on histology:
wavy fiber change (cells are not contracting, but are being pulled by other myocytes)
4-24 hrs after MI see on histology:
pale, swelling, coag necrosis, contraction band necrosis, PMNs
See cellular outline, but no nuclei
3-5 dys after MI see on histology
mottled, yellow, red; hemorrhage, many PMNs
5-7 days after MI see on histology
mottled, many MØ + fibroblasts present
2-4 weeks after MI see on histology
mottled granulation tissue
5-8 weeks after MI see on histology
scarring
Erzetimibe
blocks enterocyte NPC1L1 receptor, inh gut uptake of cholesterol
lowers LDL
good second line tx
Familial hypercholesterolemia (Fredrickson Type II)
i. Mutation in LDLR (can’t clear LDL)
ii. Autosomal dominant, haploinsufficient - heterozygotes have LDL around 250 (normal 130)
iii. Homozygotes have LDLC 1000-1200 (BAD)
iv. Get xanthomas (accumulations of cholesterol) in tendons & eyelids, get premature atherosclerosis, can see a defect in the cornea
Dysbetalipoproteinemia (Fredrickson type III)
i. Defect in ApoE2 synthesis (isoform of ApoE)
ii. Makes ApoE less able to bind lipoprotein receptors
iii. IDL accumulates, increases atherosclerotic risk
iv. Presents in adulthood as hyperlipidemia, xanthomas, premature CVD
Familial hypertriglyceridemia
i. Autosomal dominant
ii. Elevated fasting TG without clear 2ary cause, due to overproduction of VLDL
iii. Can cause pancreatitis when combined with 2ary cause like diet (high fat or excess EtOH), drugs, disease, metabolic changes
Familial chylomicronemia syndrome (Fredrickson Type I Hyperchylomicronemia)
High chylomicron levels –> high TG levels (>2000, normal is 150)
Creamy plasma
Deficiency of LPL or ApoC-II
bivalrudin
direct thrombin inhibitor
argatroban
direct thrombin inhibitor
what gps bind vwf?
GPIIbIIIa, GPIb-IX-V
what gps bind fibrinogen?
GPIIbIIIa
what gps bind fibronectin?
a5b1
what gps bind laminin
a6b1
what gps bind collagen
GPIaIIa, GPVI
what does norepi do?
bind a1, stimulate vasoconstr
what does epi do
bind a1 –> vasoconstr
bind B2 –> vasodilation of skeletal muscle
type I vs type II MI?
type I = ischemia due to 1ary coronary event (plaque erosion or rupture, fissuring or dissection). Type II = MI 2ary to ischemia due to imbalance of O2 supply and demand
medical tx for all people leaving hospital after MI
aspirin, ADP receptor antagonist, B blocker, statin, ACEi/ARB
anterior wall leads, what artery is occluded?
V1-V4 (think LAD)
septal wall leads, what artery is occluded?
V1-V2 (think LAD)