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pharm 2 final > Bleeding disorders > Flashcards

Bleeding disorders Flashcards

1
Q

what are the 3 components of the “hemostasis tripod”?

A
  • Primary Hemostasis, mediated by platelets
  • Coagulation, a chemical process
  • Vasoconstriction, a mechanical process
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2
Q

Platelets adhere to disrupted vessel wall via:

A

A) Platelet surface membrane glycoprotein receptor Ib

B) vonWillebrand factor

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3
Q

Platelets adhere to one another via:

A

– surface receptor glycoprotein IIb/IIIa

– fibrinogen

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4
Q

what are the 2 Arachidonic acid vasoconstrictors?

A

– thromboxane A2

– prostaglandins (PGs).

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5
Q

Platelet surface provides a site for what to occur?

A

– generation of thrombin

– subsequent fibrin formation

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6
Q

what are the steps in the “extrinsic pathway” for clotting?

tissue factor- factor VII pathway

A

A) tissue factor exposed to blood
B) tissue factor forms complex with factor VII
C) factor VII activated- Factor VIIa
D) whole complex binds to factor X
E) Xa converts prothrombin (factor II) into Thrombin (IIa)
- this step requires factor V as a c-factor

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7
Q

what happens in the “secondary”/alternate clotting pathway?

A

A) factor IX activated by tissue-factor/VIIa complex

B) factor IXa and cofactor VIII activates factor X

C) thrombin formation proceeds

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8
Q

what is the 3rd coagulation pathway?

A

A) Thrombin itself activates factor XI

B) Factor XIa activates factor IX

C) Pathway proceeds to additional thrombin formation

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9
Q

____________ is essential for the conversion of fibrinogen into fibrin

A

Thrombin

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10
Q

what are the 4 main roles of thrombin?

A

1) conversion of fibrinogen into fibrin
2) Activates coagulation factors and cofactors, facilitating its own formation
3) Strong activator of platelet aggregation
4) Mediates Fibrinogen cleavage

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11
Q

what are the 3 main anti-coagulation mechanisms?

A

1) Tissue factor pathway inhibitor (TFPI)
2) Protein C
3) Antithrombin III

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12
Q

how does Protein C work?

A

1) Circulating protein C activated by endothelial cell-bound enzyme thrombomodulin in association with thrombin
2) Activated protein C degrades the important cofactors V and VIII
3) Activation requires an essential cofactor: protein S

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13
Q

____________ will inhibit both Thrombin and factor Xa

A

Antithrombin III

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14
Q

Antithrombin III is Strongly enhanced by presence of what molecule?

A

Heparin

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15
Q

Fibrinolysis is mediated by what molecules? what causes their activation?

A

A) tPA and uPA found in endothelial cells

B) Released by several stimuli, including hypoxia, acidosis

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16
Q

what are the 2 ways in which Fibrinolysis is inhibited?

A

1) Activator inhibitors (PAIs)

2) Circulating protease inhibitors, e.g. α2-antiplasmin

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17
Q

____________ is the most common CONGENITAL coagulation DISEASE

A

von Willebrand Disease

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18
Q

what are the 3 subtypes of von Willebrand disease?

A

1) Type I: reduced concentration (10-45% normal levels)
2) Type II: dysfunctional vWF
3) Type III: absent vWF (homozygous for gene defect)

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19
Q

Desmopressin (DDAVP) is used to treat what types of von Willebrand disease?

A

Type 1

Type 2a

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20
Q

how are severe forms of von Willebrand disease treated?

A

replacement with transfused factors

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21
Q

For von Willebrand disease, treatment must continue for _______ days after surgery

A

4 to 7 days

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22
Q

_____________ is the most commonly INHERITED coagulation DISORDER

how is this disease inherited?

A

Hemophilia A

  • Sex-linked recessive, 1 of 10,000 male births
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23
Q

Hemophilia A is caused by a reduction in what molecule?

A

Factor VIII

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24
Q

Patients with factor VIII levels greater than ___% rarely bleed spontaneously, but will have bleeding problems after surgery or trauma

A

5%

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25
Q

Mild Hemophilia A patients can have Factor VIII levels of ___% or less, while severe forms have less than ___%

A

Mild = 40%

severe = less than 1%

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26
Q

how is Hemophilia A treated?

A

Mild cases: DDAVP (desmopressin)

Severe cases: transfusion

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27
Q

Hemophilia B is similar to Hemophilia A but affects _________

A

factor IX

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28
Q

what are the 2 types of Hypercoaguable diseases?

A

A) Protein C Deficiency, Protein S Deficiency

B) Factor V Leiden

29
Q

what causes Factor V Leiden syndrome?

A

Polymorphic factor V which resists inactivation by activated protein C

30
Q

All Hypercoaguable conditions put the patient at risk for __________

A

thrombosis

31
Q

what clotting-related compounds are produced by the liver?

A

A) Liver is the source of coagulation factors

B) Liver is also the source of Protein C, Protein S, and fibrinogen

32
Q

Thrombocytopenia due to decreased liver function is the result of what conditions?

A

Result of portal hypertension and associated splenomegaly

  • liver failure causes drop in thrombocytes (platelets)
33
Q

T/F: Clinical bleeding in patients with liver disease is often worse than predicted by INR alone

A

True

34
Q

what is a MELD score? what is it based on?

A

Model for End-Stage Liver Disease (MELD) Score

Formula based on:
– Serum bilirubin
– Serum creatinine
– INR

35
Q

How do MELD scores correlate to mortality?

A 
– 40 or more = 71.3%
– 30–39 = 52.6%
– 20–29 = 19.6%
– 10–19 = 6.0%
– less than 9 = 1.9%
36
Q

how can renal disease effect coagulation?

A

attributed to impaired platelet adhesion, aggregation, and release

37
Q

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

A

DDAVP (Desmopressin)

38
Q

___________ is a Irreversible inhibitor of platelet membrane-associated cyclooxygenase

A

Aspirin

  • blocks the formation of thromboxane A2
  • Less inhibition of other PG’s
39
Q

_______ days are usually required after termination of aspirin use to restore adequate platelet function and effective hemostasis

A

5 to 7

40
Q

what are the most important adverse effects of aspirin?

A

1) bleeding

2) the occurrence of hemorrhagic gastritis or even gastric ulceration

41
Q

how does Clopidogrel (Plavix) function?

A
  • Blocks the ADP receptor on the platelet
42
Q

T/F: the combination of clopidogrel and aspirin was shown to be superior over aspirin alone

A

true

after an acute coronary event, percutaneous coronary interventions, and coronary stent placement

43
Q

T/F: Clopidogrel results in MORE clinical bleeding than aspirin

A

true

44
Q

how does Dipyramidole work?

A

antiplatelet effect by inhibition of phosphodiesterase

45
Q

T/F: Glycoprotein Receptor IIb/IIIa Inhibitors are effective orally

A

False

46
Q

Which vitamin-K dependent factors does Coumadin block?

A

factors II, VII, IX, and X

47
Q

how long does it take for coumadin to reach its full effect? how long does it take for the effects of coumadin to dissipate after therapy has been stopped?

A
  • the full effect of therapy is delayed for 2 or 3 days

- full restoration of normal coagulation after termination of Coumadin therapy requires at least 3 to 5 days

48
Q

which tests are used to monitor the effects of coumadin?

A

PT/INR

49
Q

T/F: factor Xa inhibitors do not require monitoring

A

true

50
Q

what is the onset time for Factor Xa inhibitors? how long is their half life?

A

Relatively rapid onset (2-3 hours) and short half life (8-12 hours

51
Q

what does Idarucizamab do?

A

acts as reversal agent for Dabigatran

52
Q

what drug will act as a reversal agent for factor Xa inhibitors?

A

Andexanet Alfa

  • Reverses anticoagultion in less than 5 minutes
53
Q

Heparin binds to ___________

A

antithrombin III

54
Q

T/F: The anticoagulant effect of heparin may be highly variable

A

true

55
Q

what test is used to monitor the effects of heparin?

A

aPTT

56
Q

what are the indications for the use of Pentasaccharides?

A

Indicated for DVT prophylaxis or DVT/PE treatment

57
Q

what is heparin-induced thrombocytopenia?

A

– an immunological response to heparin characterized by thrombocytopenia and thromboedema

  • occurs 5-7 days after first dose
58
Q

what are some clinical signs that a patient may have a defect in their coagulation system?

A

– Abnormal bruising
– Petechiae
– Splenomegaly

59
Q

normal PT averages ______ seconds

A

12 ± 2

60
Q

T/F: PT times will not vary depending on laboratories

A

FALSE

  • they can differ
61
Q

The PT is prolonged by deficiencies in:

A 
A) factor 7
B) factor 10
C) Factor 5
D) Prothrombin
E) Fibrinogen
62
Q

The PTT measures the slower “intrinsic” pathway: normal is roughly _______ seconds

A

25-40

63
Q

Deficiencies in factors _____ or _____ will not be detected with the PTT test

A

VII or XIII

64
Q

which lab test is used to monitor coumadin? which one is used to monitor heparin?

A

A) PT/INR is for Coumadin

B) aPPT is for heparin

65
Q

Platelet Function Analyzer-100 (PFA-100) is used in place of what type of test?

A

bleeding time tests

66
Q

__________________ is considered the gold standard for platelet function analysis

A

Platelet aggregometry (PAA)

67
Q

how does dabigatran (Pradaxa) function?

A

direct thrombin inhibitor

68
Q

name the factor Xa inhibiting drugs:

A

A) XARELTO (rivaroxaban)

B) ELIQUIS (apixaban)

C) SAVAYSA (edoxaban)

69
Q

What deficiency causes the rare coumadin-induced skin necrosis?

A

protein C deficiency

pharm 2 final (7 decks)

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