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hemostasis and thrombosis Flashcards

1
Q

thrombosis

A

inappropriate activation of normal processes in uninjured vessels or thrombotic occlusion of a vessel after relatively minor injury

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2
Q

hemorrhage

A

defects in hemostatic plug formation

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3
Q

four stages of normal hemostasis

A

1 - vasoconstriction after injury to epithelium
2 - primary hemostasis - platelet aggregation
3 - secondary hemostasis - coagulation cascade (clot)
4 - thrombus and anti-thrombotic events

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4
Q

role of endothelial cells

A

maintain blood fluidity

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5
Q

how do endothelial cells regulate vessel tone?

A
  • secrete endothelia - vasoconstriction
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6
Q

how do endothelial cells prevent platelet aggregation and promote vasodilation?

A
  • secrete prostacyclin, nitric oxide
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7
Q

how do endothelial cells act as anticoagulants?

A

1 - prevent interaction with adhesive proteins such as collagen, vWF, tissue factor
2 - modulate fibrinolysis by synthesizing both plasminogen activator (tPA) and plasminogen activator inhibitor (PAI)

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8
Q

what is tissue factor?

A
  • membrane protein
  • in smooth muscle, fibroblasts, macrophages
  • initiates coagulation
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9
Q

prothrombotic properties of endothelial cells

A
  • synthesis, storage, release of vWF
  • storage and release of FVIII
  • synthesis of tissue factor
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10
Q

primary hemostasis (the three A’s)

A

1 - adhesion - to subendothelium mediated by vWF at site of injury
2 - activation - metabolic - membrane shape change, surface GPIIb/IIIa alteration
3 - aggregation - fibrinogen cross-links via GPIIb/IIIa

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11
Q

concept of anti-platelet therapy

A
  • prevention of inappropriate platelet activation to prevent stroke, ischemic heart disease, re-stenosis after angioplasty or stent.
  • aspirin irreversibly inhibits platelet cyclo-oxygenase-1 (COX-1)
  • NSAIDs reversibly inhibit COX-1
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12
Q

Clopidogrel

A
  • anti platelet therapy

- blocks ADP receptor

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13
Q

Abciximab

A
  • anti platelet therapy

- blocks GPIIb/IIIa

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14
Q

Where is VonWillebrand factor synthesized and stored?

A

endothelial cells and megakaryocytes (in platelet a granules)

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15
Q

vWF secretion and stimulation

A
  • secretion is constitutive from endothelium into plasm
  • stimulated by thrombin, fibrin, histamine, DDAVP from endothelium
  • from platelet a granules in megakaryocytes when they are activated
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16
Q

functions of vWF

A
  • adhesion
  • aggregation (bind to GPIIb/IIIa
  • FVIII binding - protects FVIII from proteolytic cleavage and brings it to site of hemorrhage
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17
Q

vitamin k dependent coagulation enzymes

A

factors 2, 7, 9, 10

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18
Q

what are the three lab coagulation pathways?

A
  • intrinsic
  • extrinsic
  • common (both feed into it)
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19
Q

what starts the lab intrinsic pathway?

A

factors XII and XIIa

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20
Q

what starts the lab extrinsic pathway?

A

TF and VIIa - stimulate X to Xa conversion directly

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21
Q

the lab common pathway starts with the conversion of:

A

X to Xa

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22
Q

what from the lab intrinsic pathway stimulates the first step of the lab common pathway?

A

VIIIa and Ca

23
Q

what stimulates the conversion from fibrinogen to fibrin in the lab common pathway?

24
Q

what stimulus the conversion from fibrin to cross-linked fibrin in the lab common pathway?

A

factor XIII

25
what starts the in-vivo coagulation pathway?
TF + Factor VIIa
26
prothrombin is also known as
factor II
27
thrombin is also known as
factor IIa
28
what stimulates the conversion of fibrinogen to fibrin in the in-vivo pathway?
thrombin (IIa)
29
what stimulates the conversion of fibrin polymers to a fibrin clot in the in-vivo pathway?
factor XIII
30
what enzyme is known as the master conductor?
thrombin (IIa)
31
how does factor XIII work?
stabilizes fibrin clot by cross linking lysine and glutamine side chains of fibrin to form homopolymers
32
four elements of the quaternary complex:
1 - enzyme 2 - cofactor 3 - phospholipid surface 4 - calcium ions
33
what does coumadin do?
blood thinner - antagonizes vitamin k, which inhibits factors 2, 7, 9, 10
34
what are the body's three anticoagulant mechanisms?
- antithrombin system - protein C system - fibrinolytic system
35
describe antithrombin action
AT + heparins neutralize thrombin and factors IX, X, XI, XII
36
describe protein C system
- thrombomodulin binds thrombin and protein C | - activated protein C and protein S inactivate factors V and VIII
37
describe the fibrinolytic system
plasminogen from the liver cleaves fibrin and fibrinogen
38
name four inherited hemorrhage disorders, their defect, mode of inheritance, and frequency
1 - vonWillebrand's disease, vWF, autosomal dominant, .1-1% 2 - hemophilia A, factor VIII, x-linked, 1/10,000 males 3 - hemophilia B, factor IX, x-linked, 1/50,000 males 4 - hemophilia C, factor XI, autosomal recessive, 1/100,000
39
four acquired hemorrhage disorders
1 - blood loss - platelet and clotting factor depletion 2 - excess anticoagulation - decrease or inhibition of factors 3 - disseminated intravascular coagulation (DIC) - consumption of clotting factors or platelets 4 - inhibitors - antibodies to clotting factors
40
Bernard Soulier syndrome
- hemorrhage disease - deficiency of GPIB - AR
41
Glanzmann's Thrombasthenia
- hemorrhage disease - deficiency of GPIIbIIIa - AR
42
thrombosis: Virchow's Triad
- endothelial injury - abnormal blood flow - hypercoagulability
43
APC resistance/factor V mutation
- AA replacement at one of three APC cleavage sites in factor Va molecule - factor V inactivation takes ten times longer so there is persistent thrombin generation and a hypercoagulable state
44
prothrombin 20210 mutation
second most common explanation for hyper coagulability
45
disseminated intravascular coagulation causes and treatment
causes - bacterial sepsis, viremia, trauma, tissue necrosis, leukemia, obstetric accidents treatment - treat underlying condition, break DIC cycle with heparin
46
heparin-induced thrombocytopenia syndrome
- antibodies that bind PF4/heparin/platelets causing clotting - depletion of platelet count - generally important when treating with heparin and it causes pre-existing clots to get worse - avoid by using low molecular weight heparin
47
antiphospholipid antibody syndrome (Hughes Syndrome)
- causes thrombosis, thrombocytopenia - possibly activates platelets directly, inhibits PGI2, or inhibits proteins C or S - treatment - warfarin, heparin, steroids
48
PT prolonged by
- deficiencies of VII, X, V, II, fibrinogen
49
important application of PT
- monitor warfarin therapy because warfarin interferes with vitamin k dependent factors II, VII, IX, X
50
reagents added for PT
- recombinant TF - Ca2+ - phospholipid
51
reagents added for PTT
- contact activator | - phospholipid
52
PTT prolonged by
- deficiencies in VIII, IX, XI, XII, (HMWK, pre-kallikrein) | - unfractionated heparin, lupus anticoagulant, factor inhibitors
53
what are mixing studies?
- when prolonged PT or PTT - used to figured out whether it is a factor deficiency or the presence of an anticoagulant - if fresh pooled normal plasma (PNP) mixed with patient plasma corrects PT/PTT, it is a factor deficiency - if PT/PTT does not correct it is an anticoagulant which also inhibits the added factor in the PNP.

pathology (15 decks)

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