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Cardiovascular > Ischemic Heart Disease Histology > Flashcards

Ischemic Heart Disease Histology Flashcards

1
Q

hypoxia

A

reduced oxygen supply to a tissue with normal perfusion

ex. cyanotic congenital heart disease, severe anemia, carbon monoxide poisoning

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2
Q

clinical syndromes that can result from ixchemia

A

angina pectoris

myocardial infarction

chronic ischemic heart disease

sudden cardiac death

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3
Q

risk factors of HD

A

Heredity

Age

Sex

Lipidemia

Increased weight

Pressure

Inactivity

Diabetes

Smoking

“HAS LIPIDS”

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4
Q

reperfusion injury

A

reversible or irreversible injury caused by repurfusion

this includes myocardial stuning, srrythmias, microvascular injury, and irreversible cell damage

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5
Q

factors reducing coronary blood flow

A

decreased aortic diastolic pressure

increased intraventricular pressure and myocardial contraction

coronary artery stenosis

aortic valve stenosis and regurgitation

increased right atrial pressure

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6
Q

etiologies of coronary artery stenosis

A

fixed coronary stenosis

acute plaque change (rupture, hemorrhage)

coronary artery thrombosis

vasoconstriction

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7
Q

What is the most sensitive region to ischemia?

A

subendocardium

wave front moves outward from there

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8
Q

most common sites for thrombosis

A

LAD, right coronary, and left circumflex artery, in approximately a 3:2:1 ratio

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9
Q

complications of an MI

A

sudden cardiac death

congestive heart failure

aneurysm with mural thrombus formation

cardiac arrythmia

free wall rupture with resulting cardiac tamponade

Dresler’s syndrome (fibrinous pericarditis)

papillary muscle dysfunction with resultant valvular dysfunction usually of the mitral valve

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10
Q

1-4 hours of MI

A

usually no major changes

could be presence of wavy fibers due to inactive fibers being pulled on from the ends by live contracting myocytes

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11
Q

6-12 hours of MI

A

coagulative necrosis beings to appear

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12
Q

12-24 of MI

A

infarct becomes infiltrated by neutrophils, and the muscle cells begin to lose their nuclei and cross-striations

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13
Q

4-24 hours of MI

A

pale

swelling

contraction band necrosis

PMNs

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14
Q

3-5 days of MI

A

mottled yellow, red

hemorrhage

heavy PMNs

lowest degree of mechanical integrity and most prone to rupture

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15
Q

5-7 days of MI

A

mottled

macrophages and fibroblasts

lowest degree of mechanical integrity and most prone to rupture

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16
Q

2-4 weeks of MI

A

mottled

granulation tissue

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17
Q

5-8 weeks of MI

A

scarring

gradual replacement with fibrotic tissue

risk of rupture is low because the scar is thin but strong

can billow out forming an aneurism

18
Q

What time do these events happen?

usually no major changes

could be presence of wavy fibers due to inactive fibers being pulled on from the ends by live contracting myocytes

A

1-4 hours of MI

19
Q

What time do these events happen?

coagulative necrosis beings to appear

A

6-12 hours of MI

20
Q

What time do these events happen?

infarct becomes infiltrated by neutrophils, and the muscle cells begin to lose their nuclei and cross-striations

A

12-24 of MI

21
Q

What time do these events happen?

pale

swelling

contraction band necrosis

PMNs

A

4-24 hours of MI

22
Q

What time do these events happen?

mottled yellow, red

hemorrhage

heavy PMNs

lowest degree of mechanical integrity and most prone to rupture

A

3-5 days of MI

23
Q

What time do these events happen?

mottled

macrophages and fibroblasts

lowest degree of mechanical integrity and most prone to rupture

A

5-7 days of MI

24
Q

What time do these events happen?

mottled

granulation tissue

A

2-4 weeks of MI

25
Q

What time do these events happen?

scarring

gradual replacement with fibrotic tissue

risk of rupture is low because the scar is thin but strong

can billow out forming an aneurism

A

5-8 weeks of MI

26
Q

coagulation necrosis

A

cells are dead but can still see outlines

nuclei are gone

27
Q

contraction band necrosis

A

hyper dense eosinophilic bands

clearing of the cytoplasm - cells become hydropic

contractile proteins no longer present, instead hyper condensed in the band

calcium rushing into the cell through the leaky membranes cause the Z line to condense

28
Q

calcification of the coronary arteries

A

calcific atherosclerosis are typically stable

nut much lipid and not prone to rupture

a high number of stable placques indicates the presence of unstable placques

29
Q

most frequent cause of coronary occlusion

A

rupturing of mild to moderate stenoses (<80% of baseline)

this is because there are so many more of these stenoses as opposed to the highyl obstructive plaques

30
Q

cardiac allograft vasculopathy

A

major cause of death following cardiac transplantation as soon as 1 year following engraftment

many transplants fail to reinervate and angina is not common

clinical presentation includes arrythmias, CHF, or sudden death

affects intramural and epicardial coronary arteries and veins

thought to result form repeated endothelial injury followed by reiapr response

31
Q

inciting agents of CAV

A

autoimmune response to allograft

CMV

ischemia reperfusion injury

baseline HLD, HTN

32
Q

early CAV histology

A

diffuse fibrous intimal thickening or vasculitis

33
Q

late CAV histology

A

focal atherosclerotic plaques, diffuse intimal thickening, or a mixture of both

34
Q

complications of angioplasty

A

causes tearing and usually when effective causes dissection

35
Q

complications of stents

A

thrombogenic

36
Q

complications of vein grafts

A

grafts undergo arterialization

37
Q

complications of allografts

A

recipients lose their hearts due to diffuse arteriosclerosis

38
Q

creatine kinase

A

found in heart muscle, skeletal muscle, and brain

increased in over 90% after MIs

begins to rise 4-6 hours after MI and peaks at 24 hours

returns to normal in 3-4 days

MB fraction returns to normal in 2 days

39
Q

lactic dehydrogenase (LD or LDH)

A

found in heart muscle, skeletal muscle, liver, erythrocytes, kidney, and some neoplasms

increased in over 90% of MIs

begins to rise 24 hours after MI and peaks in 3 days

returns to normal in 8-9 days

40
Q

myoglobin

A

found in striated muscle

damage to skeletal or cardiac muscle releases myoglobin into circulation

rises 2 hours after MIs and peaks at 6-8 hours

returns to normal in 20-36 hours

41
Q

troponin T and I

A

high sensitivity, preferred markers

very specific for cardiac injury

rises in 4-6 hours

peaks in 12-16 hours

stays elevated for up to 10 days

Cardiovascular (46 decks)

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