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Pathology - Cardiology > 2 - Hemodynamics and Coagulation > Flashcards

2 - Hemodynamics and Coagulation Flashcards

1
Q

total body water volume

A

36 L

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2
Q

how much water intracellular? how much extracellular?

A

24 L; 12 L

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3
Q

% of body weight intracellular fluid; % extracellular

A

40%; 16%

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4
Q

% of body weight serum is

A

4%

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5
Q

approximate blood volume

A

5 L

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6
Q

how much of blood V is cells? what is % (hematocrit)?

A

2 L; 40%

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7
Q

how much of blood volume is plasma?

A

3 L

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8
Q

sources of extracellular fluid

A

blood, interstitial, CSF, intraocular, GI (and other potential spaces)

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9
Q

how many units of blood in body?

A

10

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10
Q

how much plasma can you get from unit of blood?

A

300 mL

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11
Q

what determines osmolality?

A

M conc ions

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12
Q

equation for serum osmolality

A

1.86 x [Na] + glucose/18 + BUN/2.8

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13
Q

isotonic solutions

A

.9% sodium chloride, 5% dextrose solutions

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14
Q

60% of serum proteins is this

A

albumin

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15
Q

concentration of serum albumin

A

5g/dL

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16
Q

16% of serum proteins are these; what is concentration?

A

Ig; 1-1.5 g/dL

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17
Q

albumin: immunoglobulin ratio

A

3-4:1

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18
Q

main intracellular ion

A

K

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19
Q

generalized edema all over due to decreased protein

A

anasarca

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20
Q

collection of fluid in fallopian tubes

A

hydrosalpinx

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21
Q

collection of fluid in testes

A

hydrocele

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22
Q

collection of fluid within a potential space (transudate or exudate)

A

effusion

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23
Q

this can cause transudate

A

decreased protein and increased hydrostatic pressure

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24
Q

bloody fluid within a cavity; what are 2 main causes?

A

hemorrhagic effusion; neoplasms and TB

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25
Q

mechanisms of edema (increased delivery of fluid or decreased efflux of fluid from interstitial space)

A

increased VP, hydrostatic pressure, decreased protein, decreased lymphatic flow

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26
Q

what causes increased hydrostatic pressure?

A

obstruction flow on venous side of capillaries

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27
Q

what causes pulmonary edema?

A

thrombosis (localized) and left heart failure

28
Q

this causes increased pressure in venous pulmonary system and edema within alveoli

A

left heart failure

29
Q

what does R heart failure cause?

A

increased pressure vena cava, liver congestion, and peripheral edema

30
Q

this causes sodium and water retention (more wide spread)

A

reduction renal function, inadequate perfusion kidney (activates renin/angiotensin)

31
Q

protein calorie undernutrition

A

kwashiorkor

32
Q

possible mechanism of ascites related to cirrhosis

A

obstruction liver lymphatics

33
Q

causes of lymphatic obstruction

A

filariasis, neoplasia, scarring

34
Q

pathologic features of edema

A

swollen tissue, space between cells (within tissue), fluid filling spaces

35
Q

cause of hyperemia

A

arterial/arteriolar dilatation (active)

36
Q

increased blood flow into capillary beds

A

hyperemia

37
Q

what causes nutmeg liver?

A

right heart failure (obstruction vena cava or hepatic vein)

38
Q

coagulation factors required complexing with these (on surface of activated platelets)

A

phospholipids and Ca

39
Q

most coag factors circulate as these

A

inactivated serine proteases

40
Q

extrinsic coag cascade activates/forms this

A

VII

41
Q

intrinsic coag cascade activates/forms this

A

IX

42
Q

these activate factor X

A

VIIa or IXa

43
Q

what activates factor II (prothrombin)

A

Xa and co-factor Va

44
Q

this activates fibrinogen –> fibrin

A

thrombin

45
Q

responsible for cross-linking of fibrin

A

XIII

46
Q

this has central role to activation of multiple factors

A

thrombin

47
Q

inhibitors of coagulation cascade

A

thrombomodulin/Factor C, TFPI, antithrombin

48
Q

what activates VII in extrinsic cascade?

A

tissue factor (tissue or EC injury)

49
Q

what is initially activated in intrinsic cascade?

A

Hageman factor XII

50
Q

co-factor for activation of X by IXa

A

VIIIa

51
Q

what factors are activated after XII is activated in intrinsic cascade?

A

XI and IX

52
Q

hereditary absence of these factors causes hemophilia

A

VIII or IX

53
Q

factor IX can also be activated by this factor (in addition to XI)

A

VIIa

54
Q

central actions of thrombin in coagulation cascade

A

cleaves fibrinogen, activates VIII and V (co-factors), XIII, binds thrombomodulin (activating protein C -> inhibition)

55
Q

co-factors that are activated by thrombin

A

VIII, V, XIII

56
Q

thrombin acts on cells via these -> linked to 7 spanning G proteins

A

protease-activated receptors (clips end to cause conformational change and inflam effect)

57
Q

what occurs as a result of thrombin “clipping” end of protease-activated receptor –> induces local inflammatory cell effects

A

platelet aggregation, EC adhesion molecule expression, secretion NO, PGI2, tPA, PDGF (by EC), activation PMN/monocytes

58
Q

this inhibits activation of plasminogen by plasminogen activator (to form plasmin)

A

PAI-1

59
Q

this degrades fibrin to form fibrin degradation products –> chemotaxis, measure ongoing activation coag system (DIC)

A

plasmin

60
Q

antithrombin III (natural anticoagulant) inhibits these

A

thrombin, IXa, Xa, XIa, XIIa

61
Q

what activates natural anticoagulants (antithrombin III)?

A

binding heparin-like molecule on EC

62
Q

what are protein C and S (natural anticoags) dependent on? what do they inhibit?

A

vit K; Va and VIIIa (co-factors)

63
Q

this inactivates thrombin, but requires protein S for action

A

protein C (thrombomodulin)

64
Q

what does tissue factor pathway inhibitor (from endothelium) inactivate?

A

Xa and VIIa

65
Q

this promotes fibrinolysis and inhibits fibrin polymerization

A

plasmin

66
Q

two kinds of plasminogen activators (fluid phase, when bound to fibrin)

A

urokinase-like PA (fluid phase), tissue-type PA

67
Q

what produces tissue-type plasminogen activator (t-PA)

A

endothelium

Pathology - Cardiology (8 decks)

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