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Pathology Exam 2 > Hemostasis 1 > Flashcards

Hemostasis 1 Flashcards

1
Q

Components of normal hemostasis (3)

A
  1. vasculature
  2. platelets
  3. coagulation factors
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2
Q

What 4 things does circulation require?

A
  1. functional pump
  2. regulation of fluid balance and oncotic pressure
  3. normal plumbing and vascular tone
  4. blood maintained in fluid state
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3
Q

Alterations in factors affecting hemostasis can result in what two effects? (2)

A

hemorrhage (deficient coagulation/hemostasis)

thrombosis (excessive coagulation/hemostasis)

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4
Q

Normal hemostasis is because of what 3 properties that allow the endothelium to antagonize clot formation?

A

promotes vasodilation
inhibits platelet adhesion and aggregation
inhibits coagulation

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5
Q

Characteristics of laminar flow

A
  1. minimizes vascular trauma
  2. dilutes local accumulation of procoagulants
  3. minimizes platelet interaction with endothelium
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6
Q

What can cause vascular injury?

A 
physical trauma
endotoxins
cytokines
infectious agents
immune reactions
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7
Q

What is primary hemostasis?

A

platelets and vasculature

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8
Q

What is secondary hemostasis?

A

coagulation cascade

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9
Q

What is endothelin?

A

a potent vasoconstrictor released from injured endothelial cells (results in temporary decrease on blood flow)

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10
Q

How does primary hemostasis occur?

A
  • endothelial injury exposes subendothelial matrix
  • platelets adhere and become activated
  • platelet aggregation leads to formation of unstable platelet plug
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11
Q

How does secondary hemostasis occur?

A
  • tissue factor III (a procoagulant) is released from endothelial cells
  • formation of meshwork of cross-linked fibrin containing platelets, erythrocytes, leukocytes
  • fibrin network stabilizes platelet plug
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12
Q

Characteristics of prostacyclin (PGI2) and nitric oxide (NO)

A
  • maintain vascular relaxation (vasodilation)

- inhibit platelet adhesion and aggregation

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13
Q

What do membrane-associated heparin-like molecules do?

A

potentiate the actions of antithrombin III (AT III), a potent anticoagulant

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14
Q

Thrombomodulin

A

binds thrombin (a potent procoagulant)

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15
Q

Protein C and S

A

degrade clotting factors

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16
Q

Tissue plasminogen activator (t-PA)

A

promotes fibrinolysis (clot dissolution)

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17
Q

Adenosine-Diphosphatase

A

enzyme that degrades ADP (a stimulant of platelet aggregation)

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18
Q

von Willebrand factor (vWF)

A

needed for platelet binding to subendothelial surface

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19
Q

Plasminogen activator inhibitors (PAIs)

A

inhibit fibrinolysis (procoagulant)

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20
Q

Name procoagulants associated with endothelium (3)

A

tissue factor (factor III)
von Willebrand factor (vWF)
plasminogen activator inhibitors

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21
Q

Characteristics of platelets

A
  • membrane bound
  • can change shape
  • contain granules with pro-coagulants, vasoactive substances, and growth factors
22
Q

4 events platelets go through following vascular injury

A

adhesion
secretion
activation
aggregation

23
Q

Adhesion of platelets to the subendothelial extracellular matrix is mediated by what?

A

von Willebrand factor

24
Q

Secretion event following vascular injury involves what?

A

release of contents of alpha granules and dense bodies containing Ca2+, ADP, and other vasoactive/inflammatory mediators

25
Q

Activation event following vascular injury leads to what?

A

expression of phospholipid complex on platelet surface (binding site for Ca2+ and coagulation factors)

26
Q

What creates the primary hemostatic plug?

A

platelet aggregation mediated by ADP and thromboxane A2

27
Q

What creates the secondary hemostatic plug?

A

thrombin causes platelet contraction and converts fibrinogen to fibrin, which cements platelets together

28
Q

Coagulation cascade

A

series of enzymatic reactions that results in formation of thrombin and the conversion of fibrinogen into insoluble fibrin strands leading to clot formation

29
Q

How can the extrinsic coagulation cascade activate the intrinsic coagulation cascade?

A

factor 7 of extrinsic can activate factor 9 of intrinsic

30
Q

Intrinsic pathway of coagulation

A

Factors XII, XI, IX, VIII
(think of Wal-Mart: It’s not $12, it’s $11.98)
Factor XII initiates the pathway
Leads to activation of factor X and common pathway

31
Q

Extrinsic pathway of coagulation

A

Factors III and VII

Factor III initiates the pathway

32
Q

Common pathway of coagulation

A

Factors XIII, X, V, II, and I

Factor X activated by intrinsic and extrinsic pathways

33
Q

What does Factor X do?

A

converts prothrombin to thrombin followed by fibrinogen to fibrin

34
Q

What does Factor XIII do?

A

converts fibrin to cross-linked fibrin

35
Q

What does thrombin do?

A
  • promotes platelet aggregation and activation

- activates factors XI, VIII, V, and XIII

36
Q

Which factors are Vitamin K dependent?

A

factors II, VII, IX, and X

37
Q

What is plasmin?

A
  • derived from circulating plasminogen

- breaks down fibrin (clot dissolution)

38
Q

Plasmin results in formation of what?

A

Fibrin(ogen) degradation products (FDPs)

- have weak anticoagulant activity

39
Q

Clinical signs of defect in primary hemostasis

A

petechiae
ecchymoses
bleeding from mucosal surfaces

40
Q

Characteristics of thrombocytopenia (defect in primary hemostasis)

A
  • decreased platelet concentration
  • inadequate numbers to form primary hemostatic plug
  • can be due to decreased production or consumption/destruction
41
Q

Characteristics of abnormal platelet function (defect in primary hemostasis)

A
  • known as a thrombopathy
  • can be caused by von Willebrand disease (vWD), other inherited conditions, or acquired platelet dysfunction (from NSAIDs or renal failure)
42
Q

Characteristics of abnormal vasculature (defect in primary hemostasis)

A
  • can be from vasculitis

- can be from congenital or acquired abnormalities of vessel structure (rare)

43
Q

Evaluation of primary hemostasis

A
  • quantification of platelet concentration

- Buccal Mucosal Bleeding Time (BMBT)

44
Q

Clinical signs of defect in secondary hemostasis

A

hematomas
bleeding into body cavities
bleeding into joints

45
Q

Characteristics of liver failure (defect in secondary hemostasis)

A
  • decreased production of coagulation factors
  • decreased clearance of activated coagulation factors
  • altered blood flow in an extremely vascular organ
46
Q

Characteristics of congenital absence of clotting factors (defect in secondary hemostasis)

A
  • ex: hemophilia
47
Q

Characteristics of Vitamin K deficiency/antagonism (defect in secondary hemostasis)

A
  • rodenticide intoxication (vit K antagonists)

- moldy sweet clover (cattle)

48
Q

Evaluation of secondary hemostasis

A
  • partial thromboplastin time (PTT)
  • prothrombin time (PT)
  • thrombin time (TT)/fibrinogen concentration
  • activated clotting time (ACT)
  • fibrin(ogen) degradation products (FDPs)
49
Q

Clinical signs of mixed hemostatic disorder

A
  • evidence of both primary and secondary hemostatic defects
  • any type of bleeding
  • (clinical bleeding not always present)
50
Q

Characteristics of disseminated intravascular coagulation (DIC) (mixed hemostatic disorder)

A
  • systemic activation of coagulation, widespread thrombus formation, and hemorrhage
  • platelet numbers classically decreased due to consumption
  • coagulation factors are consumed in widespread thrombus formation (increased clot times)
51
Q

Name anticoagulants associated with endothelium (4)

A

thrombomodulin
proteins C and S
tissue plasminogen activator (t-PA)
ADPase

Pathology Exam 2 (5 decks)

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