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Disease Mechanisms > Ch. 4: Hemodynamic Disorders, Thromboemboylic Disease, and Shock > Flashcards

Ch. 4: Hemodynamic Disorders, Thromboemboylic Disease, and Shock Flashcards

1
Q

define effusion

A

accumulation of fluid in cavities

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2
Q

define transudate

A

fluid deficient in proteins

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3
Q

define exudate

A

fluid rich in proteins

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4
Q

define pitting edema

A

accumulating of low protein fluid in the interstitial space
*tissue pits when pressure is applied

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5
Q

define dependent (nonpitting) edema

A

accumulation of high protein fluid in the interstitial fluid
*tissue does not pit when pressed on because the proteins prevent the fluid from moving

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6
Q

disorders of what three systems can cause edema and effusions

A

cardivascular, renal, and hepatic

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7
Q

what causes impaired venous return

A

DVT
widespread heart failure
can cause increased hydrostatic pressure

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8
Q

what causes increased hydrostatic pressure

A

impaired venous return
arteriolar dilation

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9
Q

define hypoproteinemia

A

reduced plasma albumin due to either increase loss for decrease in synthesis

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10
Q

what causes reduced plasma osmotic pressure

A

reduced plasma albumin

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11
Q

how does the reduction of plasma osmotic pressure lead to edema and effusions

A

number of plasma proteins goes down
intravascular volume goes down
renal hypoperfusion (less blood flow to kidney)
secondary hyperaldosteronism (too much aldosterone)
salt and water retention
edema

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12
Q

what is filariasis

A

a type of parasite that blocks lymphatic drainage and leads to extreme edema, espeically in the lower limbs

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13
Q

what is hyperemia

A

ateriole dilation leading to an increase in blood flow
affected areas turn red (erythema)

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14
Q

what is congestion

A

reduced venous blood outflow leads to accumulation of deoxygenated hemoglobin
affected tissues turn a blue-red color (cyanosis)

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15
Q

define hemostasis

A

blood clotting at sites of vascular injury

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16
Q

what are platelets made of

A

granules which contain clotting factors, enzymes, mitochondria, and glycogen

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17
Q

what does the cytoskeleton of a platelet contain

A

microtubules that have actin and myosin filaments

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18
Q

what is the important surface receptor on platelets

A

GpIb (glycoprotein 1B)

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19
Q

explain how platelets are formed

A

hematopoietic stem cell
myloid cell
megakaryoblast
megakaryocyte
fragmentation

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20
Q

what is thrombopoietin

A

hormone made in the liver that stimulates megakaryoctes to make cytoplasmic extensions to go through clefts in the basement membrane
extensions break off to create platelets

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21
Q

what is the lifespan of a platelet and which 2 organs remove them

A

7-10 days
liver and spleen

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22
Q

what is the name for excessive clotting disorders

A

thrombotic disorders

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23
Q

explain how vascular spasm works

A

injured, bleeding vessel spasms and vasoconstricts
less blood flow allows less blood loss

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24
Q

explain primary hemostasis (platelet plug formation)

A

endothelial cells produce von Willebrand factor (vWF) in response to exposed collagen fibers of the injured vessel
vWF binds to platelets which activates them and causes them to stick to the exposed collagen
activated platelets releases granules
granules attract more platelets which aggregate to form the patch

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25
Q

what are the 3 main platelet granules released during primary hemostasis (platelet plug formation)

A

TXA2, calcium, and clotting factors

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26
Q

what is the main purpose of the coagulation cascade

A

getting fibrinogen activated to fibrin

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27
Q

which clotting factors require Vitamin K to be synthesized

A

clotting factors 2, 7, 9, and 10 and proteins C and S

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28
Q

what happens during the intrinsic pathway of secondary hemostasis (coagulation)

A

slower
exposed collagen fibers activate factor 12
factor 12a activated factors 9 and 11
factor 9a and 8a combine with calcium to activate factor X

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29
Q

what happens during the extrinsic pathway of secondary hemostasis (coagulation)

A

subendothelial cells display tissue factor
tissue factor activates factor 7
factor 7a combines with calcium to activate factor 10

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30
Q

what happens during the common pathway of secondary hemostasis (coagulation)

A

clotting factors 10a and 5a combine with calcium to change prothrombin into thrombin
thrombin turns fibrinogen into fibrin fibrin glues plug together

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31
Q

where are factors 5a and 8a coming from during the coagulation cascade

A

there is some thrombin already activated floating around that activates factors 5 and 8

32
Q

explain clot retraction

A

actin and myosin fibers in the platelet cytoskeleton contract, bringing the edges of the wounded vessels closer together
serum is squeezed out of the clot

33
Q

what is serum

A

fluid consisting of plasma without clotting proteins

34
Q

what is thrombolysis

A

process that begins after injury has healed and blood clotting is no longer necessary
process of fibrinolysis

35
Q

what is fibrinolysis

A

process that breaks down fibrin glue

36
Q

what happens during fibrinolysis

A

endothelial cells release tissue plasminogen activator (tPA)
tPA activates plasminogen
plasmin degrades fibrin and clot dissolves

37
Q

what is urokinase and what does it do

A

enzyme produced in the kidney that can initiate thrombolysis (fibrinolysis)

38
Q

what three chemicals do endothelial cells produce and secrete

A

nitric oxide
prostacyclin
anticoagulants

39
Q

what is nitric oxide and what does it do

A

chemical released by endothelial cells
turns off hemostasis, specifically it counteracts the first and second events, vascular spasm and platelet plug formation
causes vasodilation and inhibits platelet adhesion and aggregation

40
Q

what is prostacyclin and what does it do

A

prostaglandin released by endothelial cells
counter act the second event, platelet plug formation
inhibits platelet aggregation

41
Q

what produces anticoagulants and what do they do

A

produced by the endothelial cells and liver
inhibit third event, coagulation

42
Q

what are the four types of anticoagulants produced by the liver and endothelial cells

A

antithrombin 3
tissue factor pathway inhibitor
heparin sulfate
protein C

43
Q

what does antithrombin 3 (AT-111) do

A

protein that binds and inhibits activity of clotting factors 9 and 10 and thrombin
also prevents making of new thrombin

44
Q

what does tissue factor pathway inhibitor do

A

blocks the events of the tissue factor in the extrinsic pathway

45
Q

what does heparin sulfate do

A

polysaccharide that enhances antithrombin activity

46
Q

what does protein C do

A

type of anticoagulant
is activated by protein S and thrombomodulin complex
catalyzes reactions that degrade clotting factors 5 and 8

47
Q

what are three types of procoagulants

A

clotting factors
fresh frozen plasma
cryoprecipitate

48
Q

what are three types of anticoagulants

A

heparin
warfarin
asprin

49
Q

what are three types of fibrinolytic drugs

A

tPA
streptokinase
urokinase

50
Q

what is the name of bleeding disorders

A

hemorrhagic diathesis

51
Q

what are petechiae

A

1-2mm hemorrhages on skin
caused by an increase in intravascular pressure or decrease in platelet count or function

52
Q

what are purpura

A

3 mm hemorrhages on skin
caused by increase in intravascular pressure or a decrease in platelet count or function
can also be seen in vascular trauma, inflammation, or increased vascular fragility

53
Q

what is eccymoses

A

1-2cm hemorrhages on the skin
subcutaenous hematomas (bruises)

54
Q

how do infections affect vessel walls

A

microbes cause damage to blood vessels (vasculitis)

55
Q

how do drug reactions affect vessel walls

A

deposition of drug induced immune complexes causes damage to blood vessels (vasculitis)

56
Q

how does Ehlers-Danlos syndrome affect vessel walls

A

collagen defects weaken vessel walls causing microvascular bleeding

57
Q

how does Henoch-Schonlein purpura affect vessel walls

A

this is a systemic immune disorder in which there is a deposition of immune complexes within a vessel

58
Q

how does Hereditary Hemorrhagic Telangiectasia (webe osler-rendu syndrome) affect vessel walls

A

mutation which leads to dilated, tortuous vessels with thin walls
cause upper GI bleeds (nose, mouth, etc)

59
Q

what is thrombocytopenia and what are its four main causes

A

low blood platelet counts
caused by:
decreased platelet production
decreased platelet survival
sequestration (spleen removing too many)
dilution

60
Q

what causes decreased production of platelets

A

nutritional deficiencies: B12 and folate
aplastic anemia (bone marrow can’t make enough)

61
Q

what causes decreased platelet survival

A

certain drugs: quinidine, heparin, and sulfa compounds
disseminated intravascular coagulation (abnormal clotting)

62
Q

what is thrombotic thrombocytopenic purpura (TTP)

A

a thrombotic microangiopathy caused by dysfunction of the plasma metalloprotease ADAMTS13
excessive platelet activation and aggregation causes occlusion in small vessels
can be chronic (genetic) or aquired idiopathic (unsure of cause)

63
Q

what is the purpose of the plasma metalloprotease ADAMTS 13

A

breaks down large vWF proteins into smaller molecules

64
Q

what is a tell-tale symptom of thrombotic thrombocytopenia purport (TTP)

A

microangiopathic hemolytic anemia

65
Q

what is heparin-induced thrombocytopenia (HIT)

A

issue caused by treating a patient with unfractionated heparin
immune reaction directed against the complex of heparin and PF4
leads to platelet consumption
treated with LMW heparin (anticoagulant)

66
Q

explain the mechanism of heparin induced thrombocytopenia (HIT)

A

platelet factor 4 is released, binds to a platelet, and is activated
factor 4a binds to heparin to create a factor 4a+heparin complex
complex binds to IgG which causes complex to become anti-heparin
complex binds to Fc receptor on platelet
platelets become activated and is removed by splenic macrophages

67
Q

what is a hereditary deficiency in regards to clotting factors

A

deficiency that affects a single clotting factor such as 8 (hemophilia A) or vWF

68
Q

what is an acquired deficiency in regards to clotting factors

A

deficiency that involves multiple coagulation factors
ex. vitamin K deficiency, liver disease, and disseminated intravascular coagulation

69
Q

what is disseminated intravascular coagulation (DIC)

A

issue where multiple coagulation factors are consumed leading to their deficiency
usually occurs secondary to something else
leads to fibrinolysis, bleeding, occlusions from thrombi, and tissue hypoxemia

70
Q

what is von willebrand disease

A

most common inherited bleeding disorder
mutation of vWF leads to unnoticed bleeding tendencies
no platelet adhesion or stabilization of factor 8
diagnosed with ristocetin agglutination test
treated with desmopression or vWF

71
Q

what products are common in DIC

A

fibrin split products

72
Q

define shock

A

state of systemic circulatory failure which leads to impaired tissue perfusion and cellular hypoxia

73
Q

what are the three major types of shock

A

cardiogenic
hypovolemic
distributive

74
Q

explain cardiogenic shock

A

shock that is due to heart failure which leads to decreased cardiac output
shock specifically can be caused by things like MIs, arrhythmias,
valve insufficiencies, and obstructions

75
Q

what is hypovolemic shock

A

shock due to reduced intravascular volume, reduced preload, and reduced cardiac output
can be caused by bleeding (hemorrhagic) or reduced intravasular volume due to things like vomit (non-hemorrhagic)

76
Q

what is distributive (vasodilatory) shock

A

shock due to severe peripheral vasodilation and pooling of blood
tissue ends up being under perfused
different types of distributive shock: septic shock, neurogenic shock, anaphylactic shock, drug and toxin shock, or endocrine shock

Disease Mechanisms (19 decks)

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