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MOD-E1 > Chapter 4: Hemodynamics and shock > Flashcards

Chapter 4: Hemodynamics and shock Flashcards

1
Q

edema vs effusion

A

edema - interstitial space

effusion - potential space (body cavities)

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2
Q

mechanisms of edema

A

increased intravascular hydrostatic pressure
reduced plasma oncotic pressure
increased vascular permeability
lymphatic obstruction

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3
Q

what can cause increased intravascular hydrostatic pressure

A

sodium and water retention

congestion

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4
Q

hyperemia vs congestion

A

hyperemia - too much blood arriving (physiological, arterial) (precapillary sphincter helps control)
congestion - not enough blood leaving (pathologic)

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5
Q

results of heart failure

A

increased capillary hydrostatic pressure

decreased renal blood flow

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6
Q

what can cause decreased oncotic pressure

what is lost

A

liver failure
malnutrition
nephrotic syndrome

albumin (protein) is lost

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7
Q

PE and imaging signs of heart failure

A

soft tissue and pulmonary edema and pleural effusions

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8
Q

what causes the increase in hydrostatic pressure in heart failure

A

retention of sodium and water –> increased volume = decreased oncotic pressure due to dilution

decreased pump activity –> backup of pulmonary venous circulation (congestion)

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9
Q

2 mechanisms of edema/ascities in liver failure

A 
decreased production of albumin
portal hypertension (congestion)
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10
Q

two ways renal failure can lead to edema

A 
retained sodium and water (RAAS)
nephrotic syndrome (excess protein loss in urine)
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11
Q

what is kwashiorkor

A

protein deficiency bc of malnutrition

–> decreased albumin –> edema

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12
Q

what would result in UNILATERAL(localized) edema

A

lymphatic obstruction – lymphedema

removal of lymph nodes (breast cancer example for UE)

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13
Q

what is elephantiasis

A

localized edema caused by parasitic filariasis (wuchereria) in lymph channels and nodes

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14
Q

describe heart-failure cells

A

hemosiderin-laden macrophages

result of chronic congestion. appears in lungs

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15
Q

what is congested in hepatic congestion

most common cause of hepatic congestion

A

central vein obstruction/flow reduction

advanced heart failure

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16
Q

signs of chronic hepatic congestion

A

“nutmeg liver”
hepatocyte necrosis, centrilobular pattern
central vein obstruction/flow reduction

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17
Q

what occurs in primary hemostasis

A

formation of platelet plug

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18
Q

steps in primary hemostasis

A

adhesion
activation
aggregation

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19
Q

primary player in primary hemostasis

A

platelets

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20
Q

what is important in the adhesion of platelets to endothelial wall

A

vWF (von willebrand factor) – on subendothelial surface

Gp1b (glycoprotein 1b) receptor – on platelet

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21
Q

useful marker of endothelial cells

A

weibel-palade bodies

significant source of vWF (houses it in the cell)

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22
Q

Bernard-soulier syndrome

A

deficiency of Gp1b receptor

giant platelets

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23
Q

von Willebrand factor disease

A

deficiency of vWF

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24
Q

what occurs to platelets after adhesion?

activation

A

conformational change
Gp2b-3a change – fibrinogen links
secretion of ADP and TxA2 – initiated by thrombin

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25
Q

function of ADP and TxA2 after adhesion

A

ADP - more activation

TxA2 - more aggregation

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26
Q

what inhibits TxA2

A

aspirin

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27
Q

what allows for aggregation

A

conformational change of Gp2b-3a

bivalent binding of fibrinogen and subsequent cross-linking

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28
Q

Glanzmann thrombasthenia

A

deficiency of Gp2b-3a complex

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29
Q

clinical findings of primary hemostasis problem

A

mucocutaneous bleeding (nosebleeds, gum bleeds)

30
Q

adhesion disorders

A

von Willebrand factor disease

bernard-soulier syndrome

31
Q

aggregation disorders

A

glanzmann thrombasthenia

32
Q

what happens in secondary hemostasis

A

coagulation cascade

33
Q

vitamin K dependent intermediates of coagulation cascade and anticoagulants

why are they vitamin K dependent

A

factor 2, 7, 9, 10
Protein C, S

Can’t bind Ca, so they rely on vitamin K-dependent carboxylation

34
Q

what is the major initiator of coagulation in vivo

A

TF

35
Q

what occurs with a deficiency of factor VIII

A

hemophilia A

factor VIII - antihemophilic A factor (AHF)

36
Q

f(x)s of thrombin

A 
stabilize thrombin
activates platelets (protease-activated receptor)
activates receptors on inflammatory cells and endothelium

anti-thrombotic fxn

37
Q

medical terminology for different sizes of bruises

A

petechiae - small
purpura - larger
ecchymosis - palpable

38
Q

plasmin f(x)

A

breaks apart fibrin

39
Q

anti-thrombotic effects of endothelium

A

no exposed TF (undamaged)
platelet inhibition
anticoagulation (thrombomodulin)
fibrinolysis tPA

40
Q

endothelial methods of platelet inhibition

A

adenosine diphosphatase

prostacyclin, NO

41
Q

effects of thrombin binding to thrombomodulin

A

activation of protein C (vitamin K dependent)

+ protein S –> inactivate factors Va and VIIIa

42
Q

virchow’s triad of risk factors for thrombosis

A

endothelial injury
abnormal blood flow
hypercoagulability

43
Q

what happens with endothelial activation

virchow’s triad

A

Endothelial dysfxn –> decrease NO
Endothelial activation –> increased adhesion (vWF, Gp1b)

downregulation of thrombomodulin –> decrease active protein C
elaboration of plasminogen activator inhibitors

44
Q

primary genetic causes of hypercoagulability

deficiencies in which antithrombotic factors

A

Antithrombin III
Protein C
Protein S

rare

45
Q

primary genetic causes of hypercoagulability

increase in which prothrombotic factors

A

factor Va (activated protein C resistance; factor V leiden)
Prothrombin
increase in VIII, IX, XI and fibrinogen

common

46
Q

what happens if a thrombus dislodges?

A

–> embolus

47
Q

primary location an embolus can lodge post-DVT?

why?

A

lungs –> pulmonary embolism

bc not much can stop movement of embolus in venous circulation
lungs is first area narrow enough for the embolus to lodge
where it lodges depends on size of embolus

48
Q

what is so bad about a saddle embolus

A

LARGE embolus
lodges in pulmonary arteries near bifurcation
typically instantaneously fatal

49
Q

what is the most common heritable cause of hypercoagulability

A

factor V leiden (glu –> arg sub. that results in protein C resistance)

50
Q

APCR test

A

test clotting ability with increasing amounts of APC

tested w/ snake venom

51
Q

what happens in heparin-induced thrombocytopenia

A

administered heparin (unfractionated heparin) may induce the production of abs that recognize complexes of heparin-PF4(on platelets) and with heparin-like molecule

–> binding of ab to platelets –> activation aggregation and consumption –> pro-thrombic state

is a THROMBOTIC disease with thrombocytopenia due to platelet consumption

52
Q

what happens in antiphospholipid antibody syndrome

A 
LUPUS RELATED (secondary)
binding of ab to epitopes on proteins that are somehow induced or "unveiled" by phospholipids

primary –> exhibit only hypercoagulable state

vascular: arterial or venous thrombus
obstetrics: unexplained miscarriage/stillbirth

53
Q

how can you distinguish antemortem from postmortem blood clots

A

antemortem - lines of zahn

postmortem - dark red, gelatinous

54
Q

red vs. white thrombus

A 
white - most likely an infarct
platelet-rich
arterial
atherosclerosis
coronary as, cerebral as, femoral as
red - 
red cell rich
venous
stasis
LE
55
Q

what is a vegetation

A

thrombus on a heart valve

56
Q

why is tPA only effective when given during first few hours of a thrombotic event

A

more extensive fibrin deposition and cross-linking in older thrombi make it more resistant to lysis –> tPA is less effective

57
Q

fat emboli
what is it
what is it caused by
fat embolism syndrome

A

bone marrow introduced into circulation
caused by fracture or soft tissue trauma
fat embolism syndrome - respiratory distress, mental status changes

can be post mortem finding as a result of attempted resuscitation

58
Q

air embolism

A

iatrogenic
cardiac catheterization
the bends/”caisson disease”

59
Q

what happens in the bends/”caisson disease”

A

at high pressures, Nitrogen in air breathed dissolves into circulation
with rapid ascent, nitrogen in circulation comes out of solution in the tissues and blood (returns to gas form)
in lungs, gas bubbles can cause edema, hemorrhage, emphysema

chronic form of decompression syndrome - caisson

painful

60
Q

amniotic fluid embolism cause

A

infusion of amniotic fluid of fetal tissue into maternal circulation via a tear in placental membranes or rupture of uterine veins

anaphylactic rxn?

61
Q

septic emboli

A

bloodborne infective material
may occur in endocarditis – valve vegetations break off and manifest in other sites

skin microemboli: Janeway lesions (purpuric)
retinal microemboli: Roth spots
vascular damage in nail bed: splinter hemorrhage

62
Q

what kind of thrombosis would most likely cause an infarct in testis and ovaries and why

A

venous thrombosis

single efferent vein – no bypass channels

63
Q

factors that influence the development of an infarct

A

anatomy of the vascular supply – avail. of alt. blood supply
rate of occlusion – slower, less likely to infarct (bc of development of collateral pathways)
tissue vulnerability to hypoxia – how long tissue can stay viable without O2
hypoxemia – abnormally low o2 content

64
Q

definition of shock

A

tissue o2 and nutrient delivery is inadequate to meet physiological needs

65
Q

types of shock

A 
cardiogenic
hypovolemic
systemic inflammation
neurogenic
anaphylactic
66
Q

mechanism of cardiogenic shock

A

failure of heart resulting from intrinsic myocardial damage, extrinsic compression, or obstruction to flow

67
Q

mechanism of hypovolemic shock

A

inadequate blood or plasma volume

68
Q

mechanism of shock related to systemic inflammation

A

cytokine storm

69
Q

mechanism of neurogenic shock

A

vasodilation, decreased vascular resistance due to autonomic disruption

70
Q

mechanism of anaphylactic shock

A

IgE-mediated decrease in vascular resistance

71
Q

what can manifest as shock progresses

A 
heart failure
hypotension
renal failure
lung failure
coma

MOD-E1 (3 decks)

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