Ischemic Heart Disease Histology Flashcards Preview

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Flashcards in Ischemic Heart Disease Histology Deck (41):
1

hypoxia

reduced oxygen supply to a tissue with normal perfusion

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

2

clinical syndromes that can result from ixchemia

angina pectoris

myocardial infarction

chronic ischemic heart disease

sudden cardiac death

3

risk factors of HD

Heredity

Age

Sex

Lipidemia

Increased weight

Pressure

Inactivity

Diabetes

Smoking

"HAS LIPIDS"

4

reperfusion injury

reversible or irreversible injury caused by repurfusion

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

5

factors reducing coronary blood flow

decreased aortic diastolic pressure

increased intraventricular pressure and myocardial contraction

coronary artery stenosis

aortic valve stenosis and regurgitation

increased right atrial pressure

6

etiologies of coronary artery stenosis

fixed coronary stenosis

acute plaque change (rupture, hemorrhage)

coronary artery thrombosis

vasoconstriction

7

What is the most sensitive region to ischemia?

subendocardium

wave front moves outward from there

8

most common sites for thrombosis

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

9

complications of an MI

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

10

1-4 hours of MI

usually no major changes

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

11

6-12 hours of MI

coagulative necrosis beings to appear

12

12-24 of MI

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

13

4-24 hours of MI

pale

swelling

contraction band necrosis

PMNs

14

3-5 days of MI

mottled yellow, red

hemorrhage

heavy PMNs

lowest degree of mechanical integrity and most prone to rupture

15

5-7 days of MI

mottled

macrophages and fibroblasts

lowest degree of mechanical integrity and most prone to rupture

16

2-4 weeks of MI

mottled

granulation tissue

17

5-8 weeks of MI

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

usually no major changes

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

1-4 hours of MI

19

coagulative necrosis beings to appear

6-12 hours of MI

20

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

12-24 of MI

21

pale

swelling

contraction band necrosis

PMNs

4-24 hours of MI

22

mottled yellow, red

hemorrhage

heavy PMNs

lowest degree of mechanical integrity and most prone to rupture

3-5 days of MI

23

mottled

macrophages and fibroblasts

lowest degree of mechanical integrity and most prone to rupture

5-7 days of MI

24

mottled

granulation tissue

2-4 weeks of MI

25

scarring

gradual replacement with fibrotic tissue

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

can billow out forming an aneurism

5-8 weeks of MI

26

coagulation necrosis

cells are dead but can still see outlines

nuclei are gone

27

contraction band necrosis

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

calcification of the coronary arteries

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

most frequent cause of coronary occlusion

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

cardiac allograft vasculopathy

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

inciting agents of CAV

autoimmune response to allograft

CMV

ischemia reperfusion injury

baseline HLD, HTN

32

early CAV histology

diffuse fibrous intimal thickening or vasculitis

33

late CAV histology

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

34

complications of angioplasty

causes tearing and usually when effective causes dissection

35

complications of stents

thrombogenic

36

complications of vein grafts

grafts undergo arterialization

37

complications of allografts

recipients lose their hearts due to diffuse arteriosclerosis

38

creatine kinase

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

lactic dehydrogenase (LD or LDH)

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

myoglobin

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

troponin T and I

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