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Pathology > 2nd Exam: Fluid and Hemodynamic Derangements > Flashcards

2nd Exam: Fluid and Hemodynamic Derangements Flashcards

1
Q

This kills more than the top 3 cancers combined:

A

HD

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2
Q

Greatest to least prevalance: lung, breast, colorectal cancers, stroke, HD:

A

HD, stroke, lung, colorectal, breast

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3
Q

2 ways to get too much blood in vascular bed:

A
  1. active hyperemia: excessive inflow (dilation of precapillary arterioles, autonomic stimulation, blushing, inflammatory process, 2: passive hyperemia/ congestion: something blocking flow out of bed, obstruction of vein, most common is congestive heart failure
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4
Q

What happens to red blood cells that enter the air spaces?

A

degenerate, macros will come and ingest them

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5
Q

most common blockage leading to hydrostatic pressure and fluid build up in lungs:

A

pulmonary vein to aorta blockage

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6
Q

Pulmonary edema, fluid that contains:

A

protein

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7
Q

What happens to the hemoglobin of RBCs that enter the alveolar space after RBC is degraded?

A

converted to hemosiderin, ingested by macs, these “heart failure cells” impart rusty color to lungs and spit

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8
Q

Inc p in sys caps leads to:

A

R sided CHF

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9
Q

Inc p in pulm caps leads to:

A

L sided CHF

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10
Q

Dec flow in pulm caps leads to:

A

hypoxemia

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11
Q

Dec flow in sys caps leads to

A

hypoperfusion

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12
Q

Dependent edema, chronic passive congestion: which type of heart failure?

A

R-sided CHF

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13
Q

Weakness, drowsiness, cyanosis, clubbing (deformity of fingers and toes), polycythemia (inc hemoglobin): hypoxemia or hypoperfusion?

A

hypoxemia

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14
Q

Dyspnea, orthopenia, hemoptysis: L or R-CHF?

A

L-sided CHF

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15
Q

Dyspnea:

A

difficult, labored breathing

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16
Q

orthopenia:

A

shortness of breath while laying down

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17
Q

hemoptysis:

A

coughing up blood

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18
Q

Syncope/coma, kidney failure, tissue necrosis: hypoxemia or hypoperfusion?

A

Hypoperfusion (shock)

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19
Q

Structures involved in R-sided CHF:

A

vena cava, R atrium/ vent, tricuspid valve, pulm valve, pulm a., intrinsic lung disease, L-sided CHF

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20
Q

causes of hypoxemia (low o2 concentration in blood)

A

heart malformations w R to L shunt, pulm arterial hypertension, Lung d. w inc resistance to blood flow

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21
Q

Structures involved in L-sided CHF:

A

pulm v., L atrium/ ven, mitral valve, aortic valve, systemic hypertension

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22
Q

Causes of hypoperfusion:

A

low P (vasod) or V (blood loss) , MI, fibrilation, sepsis

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23
Q

R-sided CHF leads to __ and L leads to __:

A

hypoxemia, hypoperfusion

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24
Q

Clinical presentation of R-sided CHF:

A

swollen ankles and legs

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25
Q

How can pregnancy lead to R-sided CHF?

A

compression of vena cava

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26
Q

mark of R sided CHF:

A

depressed area due to pressure, pitting edema, interference of blood flow

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27
Q

_-sided CHF will impede drainage of liver sinusoids to vena cava.

A

R, sinusoids will dilate, grossly dilated resembles cut nutmeg

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28
Q

First liver sinusoids to dilate with R-sided CHF:

A

those around centrilobular veins of liver

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29
Q

A clear image of this is not seen in liver slides with R-sided CHF:

A

portal triad

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30
Q

Nutmeg liver is indicative of:

A

R-sided CHF

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31
Q

Valve more likely to suffer from age related problems:

A

aortic, 2 cusps, L sided CHF

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32
Q

Age related stenosis presents with same symptoms as:

A

bicupsid (aortic) valve stenosis

33
Q

Age related stenosis:

A

lumps on aortic valves, rigid, harder to open, inc P, arteriosclerosis, more work for L ven, may fail

34
Q

Age related stenosis and aortic valve stenosis are both assoc w __-sided CHF:

A

L

35
Q

Blood supply to posterior L vent and posterior papillary of L vent:

A

L and R coronaries

36
Q

Diagonal cross hatching, diseased or normal heart?

A

normal

37
Q

Pathogenesis of L-CHF, acute MI:

A

One region of L-ven thinner, discolored, the rest hypertrophied, aortic valve may not be functioning

38
Q

determines the amount of force required to pump the blood:

A

Pressure of the blood

39
Q

Key finding in people with high BP:

A

hypertrophy of L ventricle

40
Q

Which came first in L-CHF, acute MI, thckening or thinning of L-vent?

A

thickening

41
Q

Greater L coronary artery supply is indicative of:

A

L-CHF, acute MI, needs more blood flow bc L-ven is working harder

42
Q

This surrounds the heart and is not of concern to us:

A

epicardial fat

43
Q

TF? Blood escapes because of congestion.

A

F.

44
Q

Virchow’s triad:

A

endo injury, hypercoagulability, abnormal blood flow - any can lead to thrombosis

45
Q

Factors that can lead to thrombosis:

A

endo injury, abnormal blood flow, hypercoagulability

46
Q

These are responsible for hypercoagulability:

A

coagulation factors

47
Q

__ occurs within the blood system, __ occurs when blood leaves system.

A

thrombosis, hematoma

48
Q

Demarcations of thrombi in aa. and vv.:

A

aa.: Lines of Zahn, vv.: valve markings

49
Q

TF? Thrombus formation can occur in living and dead.

A

F. living only

50
Q

How to tell if a clot occured in death or life by looking at it:

A

Lines of Zahn or Valve markings (stratified pattern formation) = living

51
Q

This type of thrombus,forms quickly, cylindrical, shiny, smooth bc it just formed:

A

artery (Lines of Zahn)

52
Q

Describe veinous thrombus:

A

grainy areas, while ago (1-2d), body tried to reorganize it

53
Q

post-mortem clots:

A

white head and a red tail, no Lines of Zahn, “currant jelly portion” (red tail) mostly RBCs, “chicken fat” upper portion (white head), shape of vessel, but does not fill vessel

54
Q

Fate of thrombi:

A

resolution, embolization to lungs, organized and incorporated into vessel wall, organized and recanalized

55
Q

What aides in thrombus organization?

A

adjacent, living tissue, tries to recanalize it

56
Q

This can lead to multi-channeled lumen:

A

recanalization of thrombi via macs

57
Q

embolus is likely to plug up

A

pulmonary system

58
Q

____ agents can lead to resolution of a thrombus.

A

thrombolytic

59
Q

mural thrombus:

A

thrombus in wall of atrium

60
Q

Factors that help thrombus attach to wall of atrium:

A

turbulence, stasis of flow, endo damage, hypercoagulability

61
Q

Failure to tx mural thrombus in L atrium results in:

A

stroke, after leaving L atrium

62
Q

Mural thrombi can form here:

A

wall of any vessel

63
Q

atrial fibrillation:

A

twitching movement, doesn’t propel blood, stasis, common rhythm promblem, 20% of 85yo have

64
Q

classic location for thrombus in L ventricle:

A

site of previous MI, bc of blood stasis in region of dead tissue from MI

65
Q

Most common reason for atrial fibrillation with a thrombus in the L atrium:

A

2 infarcts: 2 emboli (check)

66
Q

How to id leg thrombi:

A

indentations from venous valves

67
Q

Clot dislodged in location different from where it was formed:

A

embolus

68
Q

hemorrhagic lung infarct:

A

L sided CHF, block pulmonary artery, can’t infarct normal lung

69
Q

How can you tell if a thrombus has been there a while?

A

if attached to the wall

70
Q

Granulation tissue surrounding embolus indicates:

A

been there at least 1wk, GT trying to reorganize thrombus

71
Q

Main indication that an embolus has been there a while:

A

organization

72
Q

How to remove thrombus?

A

Merci thrombus removal device (catheter)

73
Q

Reopening of blood supply to an infarcted area can lead to:

A

hemorrhagic infart

74
Q

Common cause of BM emboli:

A

CPR

75
Q

BM emboli may lodge here:

A

lung

76
Q

How to tell how long a BM embolus has been lodged in lung:

A

you can’t

77
Q

Fat emboli may lodge:

A

kidney, lung

78
Q

edema of ankles and legs, affected by gravity and position, lower limbs affected if standing, butt affected if supine.

A

dependent edema

Pathology (23 decks)

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