Ischemic Heart Disease Histology

Question 1

hypoxia

Answer 1

reduced oxygen supply to a tissue with normal perfusion

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

Question 2

clinical syndromes that can result from ixchemia

Answer 2

angina pectoris

myocardial infarction

chronic ischemic heart disease

sudden cardiac death

Question 3

risk factors of HD

Answer 3

Heredity

Age

Sex

Lipidemia

Increased weight

Pressure

Inactivity

Diabetes

Smoking

“HAS LIPIDS”

Question 4

reperfusion injury

Answer 4

reversible or irreversible injury caused by repurfusion

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

Question 5

factors reducing coronary blood flow

Answer 5

decreased aortic diastolic pressure

increased intraventricular pressure and myocardial contraction

coronary artery stenosis

aortic valve stenosis and regurgitation

increased right atrial pressure

Question 6

etiologies of coronary artery stenosis

Answer 6

fixed coronary stenosis

acute plaque change (rupture, hemorrhage)

coronary artery thrombosis

vasoconstriction

Question 7

What is the most sensitive region to ischemia?

Answer 7

subendocardium

wave front moves outward from there

Question 8

most common sites for thrombosis

Answer 8

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

Question 9

complications of an MI

Answer 9

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

Question 10

1-4 hours of MI

Answer 10

usually no major changes

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

Question 11

6-12 hours of MI

Answer 11

coagulative necrosis beings to appear

Question 12

12-24 of MI

Answer 12

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

Question 13

4-24 hours of MI

Answer 13

pale

swelling

contraction band necrosis

PMNs

Question 14

3-5 days of MI

Answer 14

mottled yellow, red

hemorrhage

heavy PMNs

lowest degree of mechanical integrity and most prone to rupture

Question 15

5-7 days of MI

Answer 15

mottled

macrophages and fibroblasts

lowest degree of mechanical integrity and most prone to rupture

Question 16

2-4 weeks of MI

Answer 16

mottled

granulation tissue

Question 17

5-8 weeks of MI

Answer 17

scarring

gradual replacement with fibrotic tissue

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

can billow out forming an aneurism

Question 18

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

Answer 18

1-4 hours of MI

Question 19

What time do these events happen?

coagulative necrosis beings to appear

Answer 19

6-12 hours of MI

Question 20

What time do these events happen?

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

Answer 20

12-24 of MI

Question 21

What time do these events happen?

pale

swelling

contraction band necrosis

PMNs

Answer 21

4-24 hours of MI

Question 22

What time do these events happen?

mottled yellow, red

hemorrhage

heavy PMNs

lowest degree of mechanical integrity and most prone to rupture

Answer 22

3-5 days of MI

Question 23

What time do these events happen?

mottled

macrophages and fibroblasts

lowest degree of mechanical integrity and most prone to rupture

Answer 23

5-7 days of MI

Question 24

What time do these events happen?

mottled

granulation tissue

Answer 24

2-4 weeks of MI

Question 25

# 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

Answer 25

5-8 weeks of MI

Question 26

coagulation necrosis

Answer 26

cells are dead but can still see outlines nuclei are gone

Question 27

contraction band necrosis

Answer 27

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

Question 28

calcification of the coronary arteries

Answer 28

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

Question 29

most frequent cause of coronary occlusion

Answer 29

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

Question 30

cardiac allograft vasculopathy

Answer 30

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

Question 31

inciting agents of CAV

Answer 31

autoimmune response to allograft CMV ischemia reperfusion injury baseline HLD, HTN

Question 32

early CAV histology

Answer 32

diffuse fibrous intimal thickening or vasculitis

Question 33

late CAV histology

Answer 33

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

Question 34

complications of angioplasty

Answer 34

causes tearing and usually when effective causes dissection

Question 35

complications of stents

Answer 35

thrombogenic

Question 36

complications of vein grafts

Answer 36

grafts undergo arterialization

Question 37

complications of allografts

Answer 37

recipients lose their hearts due to diffuse arteriosclerosis

Question 38

creatine kinase

Answer 38

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

Question 39

lactic dehydrogenase (LD or LDH)

Answer 39

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

Question 40

myoglobin

Answer 40

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

Question 41

troponin T and I

Answer 41

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