Hemostasis Flashcards

1
Q

hemostasis

A

stopping blood loss in response to vascular injury

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2
Q

list the 4 general phases in the process of hemostasis

A
  1. vascular constriction
  2. formation of platelet plug
  3. formation of blood clot
  4. fibrous organization
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3
Q

describe and discuss vascular constriction

A

response to injury to help reduce blood flow/bleeding

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4
Q

describe and discuss formation of the platelet plug

A

primary hemostasis, platelet adhesion and aggregation, w/ help of vWF and fibrinogen (acts as a bridge for platelets)

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5
Q

describe and discuss formation of the blood clot

A

secondary hemostasis, activation of clotting factors (clotting cascade), enables fibrin to collect at site of platelet plug

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6
Q

describe and discuss fibrous organization

A

clot retraction and clot destruction. activation of lytic enzymes to break up clot and restore normal blood flow through healed vessel

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7
Q

thrombosis

A

formation of a clot, usually w/i lumen of vessel (can be arterial or venous)

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8
Q

embolus

A

an unattached thrombus fragment

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9
Q

atherosclerosis

A

pathologic deposition of lipids and smooth muscle proliferation inside an artery

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10
Q

infarction

A

dead tissue, can be caused by ischemia due to thrombosis that completely blocks lumen of blood vessel

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11
Q

petechiae

A

red-purple, non-blanchable discoloration less than 0.5cm in diameter (small purpura), caused by intravascular defects, infection

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12
Q

purpura

A

red-purple, non-blanchable discoloration larger than 0.5cm in diameter (large petechiae), caused by intravascular defects, inection

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13
Q

ecchymoses

A

red-purple, non-blanchable discoloration of variable size, caused by vascular wall destruction, trauma, vasculitis

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14
Q

vasculitis

A

inflammation of the vasculature

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15
Q

hematoma

A

collection of blood out of the vessels in tissues

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16
Q

discuss the 5 steps in the platelet activation process

A
  1. adhesion: vWB promotes platelet aggregation
  2. aggregation: fibrinogen bridges platelets
  3. spreading: platelets change shape
  4. granular secretion: secretion from platelets mediates plug formation
  5. pro-coagulant phospholipid exposure
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17
Q

life span of platelets

A

7-10 days

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18
Q

discuss how vWB factor and platelets interact w/ each other

A

platelets adhere to vWB factor via vWB factor receptors on their surface, this facilitates formation of the platelet plug in primary hemostasis.

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19
Q

discuss the breakdown of the fibrin clot

A

plasminogen is activated to plasmin (a bunch of factors act to do this), plasmin cleaves fibrin into fibrin degredation products, clot breaks down via fibrinolysis

20
Q

discuss the conversion of prothrombin to thrombin

A

prothrombin circulates in plasma, exposed TF activates prothrombin to thrombin. thrombin in turn activates fibrinogen into fibrin to create clot.

21
Q

discuss the conversion of fibrinogen to fibrin

A

fibrinogen is cleaved into fibrin by thrombin.

22
Q

discuss the role of thrombin in clot formation

A

fibrin binds platelets to help them change conformation. platelet plug forms by bridging of platelets via fibrinogen. thrombin also activates fibrinogen to fibrin to form the final product, a clot.

23
Q

intrinsic pathway

A

platelet factor pathway, activated by trauma inside vascular system, causes platelet factors to be released, slower than extrinsic pathway.

24
Q

extrinsic pathway

A

initiates the coag. cascade in vivo. TF is expressed on damaged endothelial cells of blood vessels, this initiates cascade of clotting factors. faster than intrinsic pathway.

25
Q

common pathway

A

convergence of intrinsic and extrinsic pathways, ultimately leads to formation of a fibrin clot.

26
Q

vitamin K is important for formation of which proteins?

A
  1. prothrombin
  2. factors VII, IX, X
  3. protein C
27
Q

what are two effects of vitamin K deficiency on clotting?

A
  1. affects intrinsic and extrinsic pathways

2. causes increased PT and PTT

28
Q

what are the 3 types of hemophilia we have studied?

A

hemophilia a: factor VIII deficiency
hemophilia b: factor IX deficiency
vWB disease: impaired platelet aggregation

29
Q

what are the clinical S/S of vWB disease?

A

muco-cutaneous bleeding. petechiae and easy bruising, most common cause of elevated PTT

30
Q

DVT

A

deep vein thrombosis, thrombus occurs in deep lower extremity vein, has potential to detach and become embolus

31
Q

pulmonary embolism

A

embolus migrates to pulmonary artery and become lodged there

32
Q

thrombocytopenia

A

abnormal decrease in platelets, may results in excessive bleeding

33
Q

disseminated intravascular coagulation

A

clotting condition, activation of both pathways causes small clots develop in blood stream and block vessels, depletes platelets and clotting factors, can lead to excessive bleeding.

34
Q

bleeding time

A

cause small cuts in pt. under BP cuff that is inflated on upper arm, blotted every 30 seconds

35
Q

platelet count

A

part of CBC, normal range ~150,000-300,000/microleter

36
Q

PTT

A

partial thromboplastin time, clotting time in seconds, measures intrinsic pathway, good test for monitoring heparin therapy

37
Q

PT

A

prothrombin time, clotting time in seconds, measures extrinsic pathway, good for monitoring warfarin therapy

38
Q

D-dimer

A

detects presence of d-dimer (fibrin degradation product), positive results may indicate presence of thrombus (e.g. DVT or PE)

39
Q

platelet function test

A

determines 3 things:

  1. platelet ability to aggregate
  2. strength of blot
  3. responsiveness of platelets to chemotactic signals

useful in diagnosing thrombotic deficiencies (e.g. vWB disease)

40
Q

what factors are involved in the intrinsic pathway

A

VIII, IX, X, XI, XII

41
Q

what factors are involved in the extrinsic pathway

A

VII

42
Q

describe how TFPI works to limit clot extension

A

targets factor VIIa-TF complex, inhibits extrinsic pathway

43
Q

describe how antithrombin works to limit clot extension

A

targets heparin and endogenous glycoconjugates, inhibits factors VIIa, IXa, XIa, and thrombin

44
Q

describe how activated protein C works to limit clot extension

A

targets factor V and VIII, inhibits formation of factor Xa and thrombin

45
Q

describe how plasmin works to limit clot extension

A

targets fibrin, causes fibrinolysis to occur

46
Q

factor V leiden

A

genetic mutation, increases pathogenic clot formation by 5-7x if heterozygous, 80x if homozygous, often goes undiagnosed. OCP, infection, smoking, surgery contribute to risk of developing a clot w/ this condition.