Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > 2nd Exam: Pathology of Cardiovascular Disease > Flashcards

2nd Exam: Pathology of Cardiovascular Disease Flashcards

1
Q

diaphoresis:

A

heavy sweating, usually due to drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

rales throughout systole:

A

could be mitral valve rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

afebrile:

A

without fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

wavy fiber change, nuclei faded out:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

dense pink typical of:

A

ischemic necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

neutrophoils, acute inflammatory response:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Next step after neutrophil infiltration:

A

granulation tissue formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

palor within the anterior wall of LV, think:

A

LAD MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

you can save m. __ hours

after 3 hours you almost never see repurfusion

A

6+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Lactic acid and ATP changes during acute MI:

A

ATP dec, lactic acid inc (both curved arcs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Duration of reversible phase of acute MI:

A

30min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

about 1.25h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

about 1.75h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Irreversible injury after acute MI starts after:

A

30min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Molecular level changes during reversible phase of acute MI:

A

glycogen depletion, mito swelling, myofibril relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Molecular level changes during irreversible phase of acute MI:

A

sarcolemma disruption, mito amorphous densities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Wavy fiber syndrome begins at borders:

A

1-2h after acute MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

3-10h after acute MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

10-18 after acute MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

1-2d after acute MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

2-8d after acute MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

8d-6wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Duration to form mature fibrous scar after an acute MI:

A

about 6wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Image of of 1-3d old acute MI:

A

necrosis, many PMNs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

3d old infarct:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

acute MI, 7-10d:

A

removal of dead myocytes by macs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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

A

probably older than 7-10 d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A

7-10d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

contraction bands;

A

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

30
Q

Effects of reprefusion:

A

save reversible injuries, reprefusion injuries

31
Q

Reprefusion injuries:

A

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

32
Q

When do contraction bands form?

A

at the time of reflow during a reprefusion procedure

33
Q

Cause of most acute MI’s (about 90%):

A

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

34
Q

2 causes of rapid growth of plaque:

A

hemorrhage, cholesterol rupture through plaque

35
Q

Plaque is:

A

lipid core, fibrous cap

36
Q

Pathogenesis of atherosclerosis:

A

endo injury, inflammation, lipid deposits, sm proliferation

37
Q

Factors affecting ath:

A

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

38
Q

1st step in ath pl formation:

A

endo injury

39
Q

Cholesterol efflux occurs into the lumen via:

A

HDL:

40
Q

foam cells:

A

Fat-laden macrophages seen in atherosclerosis

41
Q

Steps in pl formation:

A

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

42
Q

Large scale evolution of plaque:

A

fatty streak, fibrofatty plaque, catastrophic complication

43
Q

TF? Fatty streak always remains confined to the intima.

A

F. only at first

44
Q

Causes of endo damage:

A

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

45
Q

How are LDL’s oxidized in the intima?

A

free radicals

46
Q

Consequence of endo injury:

A

inc perm, wbc adhesion, monocyte adhesion and emigration

47
Q

Activates macros in the intima:

A

sm cell emigration

48
Q

Function of sm in the intima:

A

engulf lipids with macs

49
Q

Closer to the endo, external or internal elastic lamina?

A

internal

50
Q

Layers of normal a.:

A

endo, IMA

51
Q

Composition of fibrous cap:

A

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

52
Q

Composition of necrotic center

A

cholesterol crystals, calcium, debris, foam cells

53
Q

Causes of pl disruption:

A

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

54
Q

Most common cause of pl disruption:

A

Cap rupture

55
Q

Hemorrhage into pl comes from these vessels:

A

pl microvessels

56
Q

Dif types of vulnerable pl:

A

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

57
Q

Typical angina:

A

fixed coronary obstruction

58
Q

fixed coronary obstruction can progress to either:

A

severe fixed coronary obstruction or pl disruption (pl aggregation)

59
Q

severe fixed coronary obstruction:

A

chronic ischemic hd

60
Q

pl disruption can progress to either:

A

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)

61
Q

2 acute coronary syndromes:

A

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)

62
Q

Stages of healing of MI:

A

granulation tissue, scar

63
Q

Color that collagen in scar stains:

A

blue

64
Q

Complication of MI rupture syndromes:

A

free wall LV, papillary m., IV septum

65
Q

Complications of MI:

A

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

66
Q

Ranges of CHF:

A

mild to cariogenic shock

67
Q

etiology of kidney infarction:

A

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

68
Q

Sources of systemic emboli:

A

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

69
Q

Consequences of systemic emboli:

A

organ infarction

70
Q

Sites of systemic emboli:

A

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

Pathology (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions