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Pharm 2 final > Bleeding Disorders and Assessment > Flashcards

Bleeding Disorders and Assessment Flashcards

1
Q

what mediates primary hemostasis?

A

platelets

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2
Q

coagulation is what type of process?

A

chemical

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3
Q

vasoconstriction is what type of process?

A

mechanical

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4
Q

hemostasis tripod

A
  1. primary hemostasis
  2. coagulation
  3. vasoconstriction
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5
Q

hemostasis tripod is balanced by what?

A

anticoagulant activity

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6
Q

anticoagulant activity prevents what?

A

prevents excessive coagulation and keeps blood flowing appropriately

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7
Q

in primary hemostasis, how does platelets adhere to disrupted vessel wall?

A
  1. platelet surface membrane glycoprotein receptor Ib

2. von Willebrand factor

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8
Q

other than vessel wall, platelets also adhere to one another in primary hemostasis via what?

A
  1. surface receptor glycoprotein IIb/IIIa

2. fibrinogen

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9
Q

platelets also produce which arachidonic acid vasoconstrictors?

A
  1. thromboxane A2

2. prostaglandins (PGs)

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10
Q

which proteins are released from platelet storage granules?

A
  1. platelet agonists ADP and serotonin
  2. coagulation factors von Willebrand factor and coagulation factor V
  3. heparin-binding proteins platelet factor 4 and beta-thromboglobulin
  4. growth factor/chemokines PDGF, platelet TGF-β, TPO
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11
Q

platelet surface provides a site for what?

A
  1. generation of thrombin

2. subsequent fibrin formation

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12
Q

coagulation: tissue factor-factor VII pathway “extrinsic system”

A
  1. tissue factor exposed to blood
  2. complex forms between tissue factor and factor VII
  3. factor VII is activated: factor VIIa
  4. tissue factor-factor VIIa complex binds and activates factor X
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13
Q

after tissue factor-factor VIIa complex binds and activates factor X, factor Xa converts what?

A

prothrombin (factor II) to thrombin (factor IIa)

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14
Q

what is required for factor Xa to convert prothrombin (factor II) to thrombin (factor IIa)?

A

factor V as a cofactor

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15
Q

when is factor Xa more efficient at converting prothrombin (factor II) to thrombin (factor IIa)?

A

in the presence of a phospholipid surface (i.e. activated platelet)

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16
Q

alternate “secondary” pathway to coagulation

A
  1. activation of factor IX by tissue factor-factor VIIa complex
  2. factor IXa and cofactor VIII activate factor X
  3. thrombin formation
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17
Q

third coagulation pathway

A
  1. thrombin itself activates factor XI
  2. factor XIa activates factor IX
  3. pathway proceeds to additional thrombin formation
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18
Q

thrombin is essential for what?

A

conversaion of fibrinogen into fibrin

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19
Q

what does thrombin activate?

A

coagulation factors and cofactors

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20
Q

thrombin is a strong activator of what?

A

platelet aggregation

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21
Q

thrombin mediates what in the coagulation pathway?

A

mediates fibrinogen cleavage

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22
Q

what happens after fibrinogen is cleaved in coagulation pathway?

A
  1. forms fibrin monomers and subsquent polymers

2. crosslinking of fibrin takes place by thrombin-activated factor XIII

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23
Q

what is the ultimate step in the coagulation cascade?

A

crosslinking of fibrin by thrombin-activated factor XIII

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24
Q

what are some natural anticoagulation mechanisms?

A
  1. tissue factor pathway inhibitor (TFPI)
  2. protein C
  3. antithrombin III
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25
Q

circulating protein C is activated by what?

A

endothelial cell-bound enzyme thrombomodulin in association with thrombin

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26
Q

activated protein C degrades what important cofactors?

A

V and VIII

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27
Q

what is required in order to activate protein C?

A

protein S

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28
Q

antithrombin III inactivates what?

A

thrombin and factor Xa

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29
Q

what strongly enhances antithrombin III?

A

presence of heparin

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30
Q

where are tPA and uPA (plasminogen activators) found?

A

in endothelial cells

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31
Q

how are tPA and uPA (plasminogen activators) released during fibrinolysis?

A

by several stimuli, including hypoxia, acidosis

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32
Q

at which levels are fibrinolysis inhibited?

A
  1. activator inhibitors (PAIs)

2. circulating protease inhibitors (e.g. alpha2-antiplasmin)

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33
Q

what is the most common congenital coagulation disease?

A

von Willebrand disease

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34
Q

what are the 3 major subtypes of von Willebrand disease?

A
  1. type 1
  2. type 2
  3. type 3
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35
Q

type 1 von Willebrand disease

A

reduced concentration of vWF (10-45% normal levels)

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36
Q

type 2 von Willebrand disease

A

dysfunctional vWF

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37
Q

type IIa von Willebrand disease

A

variable qualitative defect in GP-1 binding and multimer formation

38
Q

type IIb von Willebrand disease

A

“gain in fxn” defect, excessive binding to platelet GP-1

39
Q

type IIm von Willebrand disease

A

monomers have decreased GP-1 binding, multimers normal

40
Q

type IIn von Willebrand disease

A

defect in binding to factor VIII

41
Q

type IIn von Willebrand disease may be diagnosed as what?

A

hemophilia A

42
Q

type III von Willebrand disease

A

absent von Willebrand factor (homozygous for gene defect)

43
Q

what is the treatment for type I and IIa von Willebrand disease?

A

demopressin (DDAVP)

44
Q

demopressin (DDAVP) is analogue to what?

A

vasopressin

45
Q

what does demopressin (DDAVP) promote?

A

release of vWF stored in endothelial cell-associated Weibel-Palade bodies

46
Q

demopression (DDAVP) increases circulating vWF by how much?

47
Q

demopressin (DDAVP) is contraindicated in whaT?

A

type IIb vWD

48
Q

treatment for more severe forms of von Willebrand disease?

A

replacement of transfused factors

49
Q

people with severe von Willebrand disease who have had replaced their transfused factors, what does that result in?

A

late re-bleeding after fibrinolysis

50
Q

what is the most commonly inherited coagulation disorder?

A

hemophilia A (classic hemophilia)

51
Q

T/F: hemophilia A (classic hemophilia) is autosomal dominant

A

false, sex-linked recessive

52
Q

hemophiliac patients with factor VIII levels greater than 5% rarely bleed spontaneously but what will have what after surgery or trauma?

A

will have bleeding problems

53
Q

what develops in 10-15% of severely affected hemophiliacs?

A

anti-factor VIII antibodies (factor VIII inhibitors)

54
Q

why are factor VIII levels also decreased in patients with von Willebrand disease?

A

because vWF acts as a carrier molecule for factor VIII

55
Q

treatment of mild to moderate hemophilia A

A

demopressin (DDAVP)

56
Q

demopressin (DDAVP) causes release of endogenous factor VIII from what in patients with mild to moderate hemophilia A?

A

liver sinusoids and endothelial cells

57
Q

treatment for severe hemophilia A patients

A

factor VIII transfusion

58
Q

hemophilia B (Christmas disease)

A

similar to hemophilia A but affecting factor IX

59
Q

how is hemophilia B (Christmas disease) treated if severe?

A

with factor transfusion

60
Q

hypercoagulable coagulation diseases

A
  1. protein C deficiency, protein S deficiency

2. factor V leiden

61
Q

protein C and S are synthesized where?

62
Q

protein C and S are what type of proteins?

A

vitamin-K dependent proteins

63
Q

mild forms of protein C or S deficiency predispose patients to what?

A

thrombosis

64
Q

severe forms of protein C or S deficiency are not compatible with what?

65
Q

factor V leiden

A

polymorphic factor V which resists inactivation by activated protein C

66
Q

factor V leiden is present in about 5% of which population?

A

north american caucasians

67
Q

factor V leiden is rare in what population?

68
Q

factor V leiden predispose patients to what?

A

deep venous thrombosis

69
Q

which organ is the source of coagulation factors?

70
Q

the liver is also a source for what?

A
  1. protein C
  2. protein S
  3. fibrinogen
71
Q

what causes thrombocytopenia in patients with coagulation problems?

A

portal HTN and associated with splenomegaly

72
Q

thrombocyte fxn is impaired in what type of patients?

73
Q

formula for end-stage liver disease (MELD) score is based on what?

A
  1. serum bilirubin
  2. serum creatinine
  3. INR
74
Q

end-stage liver disease (MELD) score predicts what?

A

3-month mortality

75
Q

end-stage liver disease (MELD) score may be a more useful predictor of what?

A

bleeding complications than INR alone

76
Q

how do you manage patients with coagulation problems and liver disease?

A

may include transfusion with missing factors and/or platelets

77
Q

patients with renal failure often present with what?

A

coagulation abnormalities

78
Q

patients with renal failure are at risk for enhanced bleeding. why?

A

it’s attributed to impaired platelet adhesion, aggregation and release

79
Q

a low hematocrit in patients with renal failure may contribute to what?

A

impaired fxn of primary hemostasis

80
Q

how can the extent of impaired fxn of primary hemostasis in patients with renal failure be tested?

A

platelet fxn assay or comparable assay

81
Q

what has been shown to correct prolonged bleeding time in patients with uremia?

A

DDAVP (demopressin)

82
Q

aspirin is an irreversible inhibitor of what?

A

platelet membrane-associated cyclooxygenase

83
Q

what does aspirin block?

A

formation of thromboxane A2

84
Q

thromboxane A2

A

potent platelet agonist and vasoconstrictor

85
Q

aspirin inhibits less of what?

A

other PGs, such as platelet antagonist and vasodilator prostacyclin (PGI2)

86
Q

aspirin may be associated with what?

A

significant impairment of primary hemostasis and mild enhancement of bleeding

87
Q

life span of platelets

88
Q

how many days are usually required for termination of aspirin use to restore adequate platelet fxn and effective hemostasis?

89
Q

what are the most important adverse effects of aspirin?

A
  1. bleeding
  2. hemorrhagic gastritis
  3. gastric ulceration
90
Q

T/F: for most dental procedures, patients should discontinue aspirin us

A

false, it’s NOT indicated for it may pose greater risks than benefits

Pharm 2 final (10 decks)

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