2nd Exam: Pathology of Cardiovascular Disease

Question 1

diaphoresis:

Answer 1

heavy sweating, usually due to drugs

Question 2

rales throughout systole:

Answer 2

could be mitral valve rupture

Question 3

afebrile:

Answer 3

without fever

Question 4

wavy fiber change, nuclei faded out:

Answer 4

MI only 4-12h old, recent cardiac necrois, new ischemic necrosis, wavy at border of infarct

Question 5

dense pink typical of:

Answer 5

ischemic necrosis

Question 6

neutrophoils, acute inflammatory response:

Answer 6

2-3 d old necrosis, that’s when papillary m. ruptured

Question 7

Next step after neutrophil infiltration:

Answer 7

granulation tissue formation

Question 8

palor within the anterior wall of LV, think:

Answer 8

LAD MI

Question 9

you can save m. __ hours

after 3 hours you almost never see repurfusion

Answer 9

6+

Question 10

Lactic acid and ATP changes during acute MI:

Answer 10

ATP dec, lactic acid inc (both curved arcs)

Question 11

Duration of reversible phase of acute MI:

Answer 11

30min

Question 12

Time at which ischemic myocardium is potentially salvageable by timely intervention after acute MI:

Answer 12

about 1.25h

Question 13

Time at which there is cumulative dead myocardium after acute MI:

Answer 13

about 1.75h

Question 14

Irreversible injury after acute MI starts after:

Answer 14

30min

Question 15

Molecular level changes during reversible phase of acute MI:

Answer 15

glycogen depletion, mito swelling, myofibril relaxation

Question 16

Molecular level changes during irreversible phase of acute MI:

Answer 16

sarcolemma disruption, mito amorphous densities

Question 17

Wavy fiber syndrome begins at borders:

Answer 17

1-2h after acute MI

Question 18

coagulation necrosis, edema, focal hemorrhage, neutrophilic infiltrate begins:

Answer 18

3-10h after acute MI

Question 19

Continuing coagulation necrosis, palor, shrunken nuclei, eosinophilic cytoplasm, myocyte contraction bands:

Answer 19

10-18 after acute MI

Question 20

Coagulation necrosis w loss of nuclei and striations, neutrophilic infiltrate, pallor, sometime hyperemia, yellowing at periphery:

Answer 20

1-2d after acute MI

Question 21

Disintegration of myofibers and phagocytosis by macs, hyperemic border, central yellow-brown softening:

Answer 21

2-8d after acute MI

Question 22

completion of phagocytosis, prominent granulation tissue w neovascularization and fibrovacsular reaction, maximally yellow and soft vascularized edges, red-brown and depressed:

Answer 22

8d-6wks

Question 23

Duration to form mature fibrous scar after an acute MI:

Answer 23

about 6wks

Question 24

Image of of 1-3d old acute MI:

Answer 24

necrosis, many PMNs

Question 25

3d old infarct:

Answer 25

look at edge to place a time frame on occurence, inflammatory change from living to dead, then another episode of ischemia, junction is all necrotic, inflammatory response stops, frozen in time 3d old inflammatory response several areas of different age infarctions 2nd episode caused mv regurgitation 3rd episode of myocardial necrosis

Question 26

acute MI, 7-10d:

Answer 26

removal of dead myocytes by macs

Question 27

granulation tissue transforming to scar tissue indicates that the acute MI:

Answer 27

probably older than 7-10 d

Question 28

How many days after acute MI are there capillaries growing in but no red blood cells?

Answer 28

7-10d

Question 29

contraction bands;

Answer 29

transverse dark pink bands in cytoplasm of dead myocytes lethally injured by ischemia, hypercontracted sarcomeres that form at the time of reflow during a reperfusion procedure (thrombolysis, angioplasty, CABG, etc.), Z lines pile up w the hypercontraction

Question 30

Effects of reprefusion:

Answer 30

save reversible injuries, reprefusion injuries

Question 31

Reprefusion injuries:

Answer 31

stunned myocardium (some form of contractile abnormality), microvascular injury, no reflow, arrhythmia (malfunction of electric system of h.), hemorrhage, micro-contraction bands

Question 32

When do contraction bands form?

Answer 32

at the time of reflow during a reprefusion procedure

Question 33

Cause of most acute MI's (about 90%):

Answer 33

sudden change of ath plaque in epicardial coronary a. causing occlusion

Question 34

2 causes of rapid growth of plaque:

Answer 34

hemorrhage, cholesterol rupture through plaque

Question 35

Plaque is:

Answer 35

lipid core, fibrous cap

Question 36

Pathogenesis of atherosclerosis:

Answer 36

endo injury, inflammation, lipid deposits, sm proliferation

Question 37

Factors affecting ath:

Answer 37

high lipids, high BP, smoking, toxins, blood stasis/ turbulence, immune reactions, viruses

Question 38

1st step in ath pl formation:

Answer 38

endo injury

Question 39

Cholesterol efflux occurs into the lumen via:

Answer 39

HDL:

Question 40

foam cells:

Answer 40

Fat-laden macrophages seen in atherosclerosis

Question 41

Steps in pl formation:

Answer 41

endo injury, endo express adhesion molecules, inflammation, macros and lymphos, lipids begin collects in intima, free radical oxidation, monocyte adhesion and emigration into intima, differentiation to macro, ingestion of lipids, now foam cell, cytokines, Gf, and sm cells come to intima from media, reactive sm proliferation

Question 42

Large scale evolution of plaque:

Answer 42

fatty streak, fibrofatty plaque, catastrophic complication

Question 43

TF? Fatty streak always remains confined to the intima.

Answer 43

F. only at first

Question 44

Causes of endo damage:

Answer 44

smoking, high BP, diabetes, infection, high fats, homocysteine, rate of blood flow, toxins, immune reactions

Question 45

How are LDL's oxidized in the intima?

Answer 45

free radicals

Question 46

Consequence of endo injury:

Answer 46

inc perm, wbc adhesion, monocyte adhesion and emigration

Question 47

Activates macros in the intima:

Answer 47

sm cell emigration

Question 48

Function of sm in the intima:

Answer 48

engulf lipids with macs

Question 49

Closer to the endo, external or internal elastic lamina?

Answer 49

internal

Question 50

Layers of normal a.:

Answer 50

endo, IMA

Question 51

Composition of fibrous cap:

Answer 51

sm cells, macs, foam cells, lymphos, collagen, elastin, proteoglycans, neovascularization

Question 52

Composition of necrotic center

Answer 52

cholesterol crystals, calcium, debris, foam cells

Question 53

Causes of pl disruption:

Answer 53

Cap rupture (most common), pl erosion, hemorrhage into pl, ulceration of Ca2+ nodule

Question 54

Most common cause of pl disruption:

Answer 54

Cap rupture

Question 55

Hemorrhage into pl comes from these vessels:

Answer 55

pl microvessels

Question 56

Dif types of vulnerable pl:

Answer 56

rupture-prone vulnerable, ruptured/healing vulnerable, erosion-prone vulnerable, eroded vulnerable, vulnerable w intra-pl hemorrhage, vulnerable w calcific nodules, critically stenotic vulnerable

Question 57

Typical angina:

Answer 57

fixed coronary obstruction

Question 58

fixed coronary obstruction can progress to either:

Answer 58

severe fixed coronary obstruction or pl disruption (pl aggregation)

Question 59

severe fixed coronary obstruction:

Answer 59

chronic ischemic hd

Question 60

pl disruption can progress to either:

Answer 60

TOMS: MURAL thrombus w variable obstruction (unstable angina or acute SUBENDOCARDIAL myocardial infarction or sudden death) OCCLUSIVE thrombus (acute TRANSMURAL myocardial infarction or sudden death)

Question 61

2 acute coronary syndromes:

Answer 61

Both thrombus, TOMS: mural thrombus w variable obstruction (unstable angina or acute subendocardial myocardial infarction or sudden death) occlusive thrombus (acute transmural myocardial infarction or sudden death)

Question 62

Stages of healing of MI:

Answer 62

granulation tissue, scar

Question 63

Color that collagen in scar stains:

Answer 63

blue

Question 64

Complication of MI rupture syndromes:

Answer 64

free wall LV, papillary m., IV septum

Question 65

Complications of MI:

Answer 65

pericarditis, CHF, mural thrombus over older MI, LV aneurysm, LV aneurysm w mural thrombus, ischemic coagulation necrosis of kidney glom and tubules (?check)

Question 66

Ranges of CHF:

Answer 66

mild to cariogenic shock

Question 67

etiology of kidney infarction:

Answer 67

embolic occlusion, renal a. branch from mural thrombus over old MI

Question 68

Sources of systemic emboli:

Answer 68

mural thrombi from heart or large arteries, old MI's w aneurysms, hypokinetic areas, etc., vegetation on valve (IE, NBTE), ath pl

Question 69

Consequences of systemic emboli:

Answer 69

organ infarction

Question 70

Sites of systemic emboli:

Answer 70

75%: lower extremities, 10%: brain, intestines, kidneys, spleen