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SS- Cardio > Ischemia > Flashcards

Ischemia Flashcards

1
Q

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

A

20 minutes

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2
Q

transmural MI

A

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)

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3
Q

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

A

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

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4
Q

nuclear dust

A

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

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5
Q

myocytolysis

A

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

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6
Q

early sub acute MI

A 
4-10 days
see first few cells coming from the periphery
day 2: lymphocytes
day 3: macrophages
day 4: fibroblasts
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7
Q

subacute MI

A

2-3 weeks after MI

lots of fibroblasts, neovascularization

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8
Q

late subacute MI

A

mostly scar tissue

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9
Q

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

A 
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
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10
Q

subendocardial infarction

A

involves inner portion of wall

more likely to be patch and have episodic extension

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11
Q

reperfusion effects of MI

A
  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
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12
Q

reperfused subacute MI

A

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

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13
Q

neutrophilic response to acute MI

A

12 hours

max at 2 days

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14
Q

stunned myocytes

A

injured by acute ischemia

look normal but need several days to work normally

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15
Q

reperfusion injury

A 
bring oxygen (free radicals) and Ca to injured tissue
target mPTP: opens mPTP and collapses mitochondrial function
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16
Q

mPTP

A

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
Q

VDAC

A

voltage-dependent anion channel

located on outer mitochondrial membrane

18
Q

ANT

A

adenine nuucleotide translocator

located on inner mitochondrial membrane

19
Q

CypD

A

cyclophilin D

matrix side of mitochondrial membrane

20
Q

ischemic preconditioning

A

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

21
Q

How does ischemic preconditioning work?

A

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
Q

reperfusion injury salvage kinase (RISK) pathway

A

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

23
Q

acute rheumatic heart disease

A

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
Q

sydenham’s chorea

A

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

25
Q

erythema marginatum

A

pink rings on inner surface of limbs and trunk

26
Q

aschoff bodies

A

fibrinoid necrosis with histiocytes and anitschkow cells

27
Q

anitschkow cells

A

caterpillar cells: clumped chromatin

28
Q

chronic rheumatic heart disease

A

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
Q

marantic endocarditis

A

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
Q

treadmill test

A

see if angina upon exertion is heart related

Do NOT use for patients that have angina at rest/sleep

31
Q

stable angina pectoris

A

chest discomfort on exertion

32
Q

unstable angina

A

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

33
Q

STEMI

A

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

34
Q

major determinants of MvO2 demand

A

HR and BP

35
Q

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

A

70%

36
Q

factors contributing to plaque vulnerability

A

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

SS- Cardio (16 decks)

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