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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
function of ADP and TxA2 after adhesion
ADP - more activation | TxA2 - more aggregation
26
what inhibits TxA2
aspirin
27
what allows for aggregation
conformational change of Gp2b-3a | bivalent binding of fibrinogen and subsequent cross-linking
28
Glanzmann thrombasthenia
deficiency of Gp2b-3a complex
29
clinical findings of primary hemostasis problem
mucocutaneous bleeding (nosebleeds, gum bleeds)
30
adhesion disorders
von Willebrand factor disease | bernard-soulier syndrome
31
aggregation disorders
glanzmann thrombasthenia
32
what happens in secondary hemostasis
coagulation cascade
33
vitamin K dependent intermediates of coagulation cascade and anticoagulants why are they vitamin K dependent
factor 2, 7, 9, 10 Protein C, S Can't bind Ca, so they rely on vitamin K-dependent carboxylation
34
what is the major initiator of coagulation in vivo
TF
35
what occurs with a deficiency of factor VIII
hemophilia A factor VIII - antihemophilic A factor (AHF)
36
f(x)s of thrombin
``` stabilize thrombin activates platelets (protease-activated receptor) activates receptors on inflammatory cells and endothelium ``` anti-thrombotic fxn
37
medical terminology for different sizes of bruises
petechiae - small purpura - larger ecchymosis - palpable
38
plasmin f(x)
breaks apart fibrin
39
anti-thrombotic effects of endothelium
no exposed TF (undamaged) platelet inhibition anticoagulation (thrombomodulin) fibrinolysis tPA
40
endothelial methods of platelet inhibition
adenosine diphosphatase | prostacyclin, NO
41
effects of thrombin binding to thrombomodulin
activation of protein C (vitamin K dependent) + protein S --> inactivate factors Va and VIIIa
42
virchow's triad of risk factors for thrombosis
endothelial injury abnormal blood flow hypercoagulability
43
what happens with endothelial activation | virchow's triad
Endothelial dysfxn --> decrease NO Endothelial activation --> increased adhesion (vWF, Gp1b) downregulation of thrombomodulin --> decrease active protein C elaboration of plasminogen activator inhibitors
44
primary genetic causes of hypercoagulability | deficiencies in which antithrombotic factors
Antithrombin III Protein C Protein S rare
45
primary genetic causes of hypercoagulability | increase in which prothrombotic factors
factor Va (activated protein C resistance; factor V leiden) Prothrombin increase in VIII, IX, XI and fibrinogen common
46
what happens if a thrombus dislodges?
--> embolus
47
primary location an embolus can lodge post-DVT? | why?
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
what is so bad about a saddle embolus
LARGE embolus lodges in pulmonary arteries near bifurcation typically instantaneously fatal
49
what is the most common heritable cause of hypercoagulability
factor V leiden (glu --> arg sub. that results in protein C resistance)
50
APCR test
test clotting ability with increasing amounts of APC | tested w/ snake venom
51
what happens in heparin-induced thrombocytopenia
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
what happens in antiphospholipid antibody syndrome
``` 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
how can you distinguish antemortem from postmortem blood clots
antemortem - lines of zahn | postmortem - dark red, gelatinous
54
red vs. white thrombus
``` white - most likely an infarct platelet-rich arterial atherosclerosis coronary as, cerebral as, femoral as ``` ``` red - red cell rich venous stasis LE ```
55
what is a vegetation
thrombus on a heart valve
56
why is tPA only effective when given during first few hours of a thrombotic event
more extensive fibrin deposition and cross-linking in older thrombi make it more resistant to lysis --> tPA is less effective
57
fat emboli what is it what is it caused by fat embolism syndrome
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
air embolism
iatrogenic cardiac catheterization the bends/"caisson disease"
59
what happens in the bends/"caisson disease"
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
amniotic fluid embolism cause
infusion of amniotic fluid of fetal tissue into maternal circulation via a tear in placental membranes or rupture of uterine veins anaphylactic rxn?
61
septic emboli
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
what kind of thrombosis would most likely cause an infarct in testis and ovaries and why
venous thrombosis | single efferent vein -- no bypass channels
63
factors that influence the development of an infarct
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
definition of shock
tissue o2 and nutrient delivery is inadequate to meet physiological needs
65
types of shock
``` cardiogenic hypovolemic systemic inflammation neurogenic anaphylactic ```
66
mechanism of cardiogenic shock
failure of heart resulting from intrinsic myocardial damage, extrinsic compression, or obstruction to flow
67
mechanism of hypovolemic shock
inadequate blood or plasma volume
68
mechanism of shock related to systemic inflammation
cytokine storm
69
mechanism of neurogenic shock
vasodilation, decreased vascular resistance due to autonomic disruption
70
mechanism of anaphylactic shock
IgE-mediated decrease in vascular resistance
71
what can manifest as shock progresses
``` heart failure hypotension renal failure lung failure coma ```

MOD-E1 (3 decks)

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