Ischemia Flashcards Preview

SS- Cardio > Ischemia > Flashcards

Flashcards in Ischemia Deck (36):
1

How long does it take for cardiac myocytes to die when they are deprived of blood supply?

20 minutes

2

transmural MI

full thickness of wall
most due to occlusive thrombosis superimposed on atherosclerotic plaque
death starts in subendocardial zone and spreads to subepicardial zone (complete in 3 hours)

3

How long does it take for dead myocytes to show microscopic manifestations of their death?

4 hours: loss of striation, hypereosinophilia, nuclear pyknosis, karyorrhexis, karyolysis and loss
exception: dead thin wavy myocytes visible at 1/2 hour

4

nuclear dust

feature of infarcts 3-6 days: breakdown debris of nuetrophils

5

myocytolysis

hibernating myocardium
subendocardial myocytes get enough O2 from cardiac lumen to survive, but they catabolize their cytoplasmic contractile proteins

6

early sub acute MI

4-10 days
see first few cells coming from the periphery
day 2: lymphocytes
day 3: macrophages
day 4: fibroblasts

7

subacute MI

2-3 weeks after MI
lots of fibroblasts, neovascularization

8

late subacute MI

mostly scar tissue

9

How long does it take to see gross manifestations of MI? What does MI look like grossly?

12 hours
inflammation in from edges
can take up to 3 months to heal and form fibrous scar
acute (hrs): light brown to tan
subacute (days): yellow
old (wks to yrs): white

10

subendocardial infarction

involves inner portion of wall
more likely to be patch and have episodic extension

11

reperfusion effects of MI

1. smaller
2. patchy
3. hemorrhage
4. contraction band necrosis
5. accelerated inflammation and repair
6. diffusion of inflammation and repair
7. fewer neutrophils
8. more macrophages
9. more interstitial fibrosis

12

reperfused subacute MI

days 4-10
lymphocytes, then granulation, then collagen
appears older than non-reperfused MI
healing accelerated
PATCHES of preserved myocardium: make re-entry ventricular arrhythmias more common

13

neutrophilic response to acute MI

12 hours
max at 2 days

14

stunned myocytes

injured by acute ischemia
look normal but need several days to work normally

15

reperfusion injury

bring oxygen (free radicals) and Ca to injured tissue
target mPTP: opens mPTP and collapses mitochondrial function

16

mPTP

mitochondrial permeability transition pore
voltage-dependent channel
made of VDAC, ANT, and CypD proteins that provide path from mitochondrial matrix to cytoplasm
essential for generating ATP

17

VDAC

voltage-dependent anion channel
located on outer mitochondrial membrane

18

ANT

adenine nuucleotide translocator
located on inner mitochondrial membrane

19

CypD

cyclophilin D
matrix side of mitochondrial membrane

20

ischemic preconditioning

resistance to mild-moderate ischemia due to induction of protective proteins by brief episodes of ischemia

21

How does ischemic preconditioning work?

ischemia-> adenosine, bradykinin, opioids -> GPCR-> signaling cascade-> open K channels in mitochondrial membrane-> maintain mPTP and electrical potential of inner mitochondrial membrane -> maintainATP production

22

reperfusion injury salvage kinase (RISK) pathway

part of ischemic preconditioning
RISK-> PI-3K-> Akt-> mTOR
RISK-> MAPK-> ERK
both pathways prevent opening of mPTP

23

acute rheumatic heart disease

fibrinous pancarditis
after infection with group A beta-hemolytic streptococcal pharyngitis
Sx: fever, polyarthrits, Sydenham's chorea, subcutaneous nodules, erythema marginatum
vegetations, aschoff bodies

24

sydenham's chorea

rapid, uncoordinated jerking movements in primarily hands, feet and face

25

erythema marginatum

pink rings on inner surface of limbs and trunk

26

aschoff bodies

fibrinoid necrosis with histiocytes and anitschkow cells

27

anitschkow cells

caterpillar cells: clumped chromatin

28

chronic rheumatic heart disease

more common in carditis that is: severe, recurrent or at early age
Sx: 20 years after carditis, mitral stenosis (fibrous with thickening, retraction and fusion of chordae)
more common in women

29

marantic endocarditis

nonbacterial thrombotic endocarditis
common in: cancer (adenocarcinoma), DIC, hypercoaguability, long term cath
small platelet and fibrin thrombi: most common on atrial side of mitral valve; next ventricular side of aortic valve
precursor for infective endocarditis and embolism

30

treadmill test

see if angina upon exertion is heart related
Do NOT use for patients that have angina at rest/sleep

31

stable angina pectoris

chest discomfort on exertion

32

unstable angina

acute coronary syndrome
ruptured atherosclerotic thrombus
NO ST elevation
Tx: aspirin +heparin or clopidogrel

33

STEMI

crushing or squeezing chest pain
hyperadrenergic state: white as a ghost (vasoconstriction), diaphoresis, nausea, dyspnea
CK-MB, troponin, LDH
Tx: streptokinase

34

major determinants of MvO2 demand

HR and BP

35

How much of an artery is occluded before symptoms/angina occurs?

70%

36

factors contributing to plaque vulnerability

large lipid core, thin cap, lots of macrophages, low smooth muscle number