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GT BSN/CNL PHARM > Hematology & Anticoagulant Drugs > Flashcards

Hematology & Anticoagulant Drugs Flashcards

1
Q

Hemophilia A involves a deficiency in:

A

factor VIII

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2
Q

hemophilia B involves a deficiency in:

A

factor IX

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3
Q

What % of hemoglobin is normal in mild hemophilia? In moderate? In severe?

A

mild = 6-49% is normal
moderate = 1-5% is normal
severe <1% is normal

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4
Q

Medications for treating hemophilia A

A

factor VIII concentrate
DDAVP
antibody therapy
gene therapy

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5
Q

B12 deficiency causes:

A

bone marrow suppression
decreased GI tract mucosa
*neuronal demyelination of the CNS

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6
Q

When are B12 injections preferred?

A

If neurologic deficits (d/t neuronal demyelination of the CNS)

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7
Q

Consequences of folic acid deficiency

A

bone marrow suppression
GI tract mucosa decrease
fetal neural tube defects

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8
Q

is folic acid or folinic acid replacement preferred

A

folic acid (the folinic acid active form is more expensive & not any more effective)

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9
Q

Why is B12 given in severe folic acid deficiency?

A

B12 is utilized in converting folic acid to its active form

**folic acid can also be converted to its active form via a different pathway too!

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10
Q

erythropoietin (EPO) results in:

A

stimulation of RBC production in one marrow

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11
Q

adverse effects of exogenous EPO

A

HTN
CV events

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12
Q

what increases the risk of CV events with exogenous EPO?

A

Hgb>11
or
Hgb increase >1 in 2 weeks

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13
Q

formulations of exogenous EPO

A

epoetin alfa
darbepoetin (longer 1/2 life)

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14
Q

What are leukopoietic growth factors?

A

substances that stimulate WBC proliferation

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15
Q

adverse effects of leukopoietic growth factors?

A

leukocytosis
bone pain

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16
Q

formulations of leukopoietic growth factors

A

G-CSF: filgrastim
GM-CSF: sargramostim

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17
Q

What do thrombopoietin receptor agonists do?

A

stimulate platelet production

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18
Q

Two main steps in forming a clot

A
  1. platelet plug
  2. fibrin mesh
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19
Q

fibrinogen connects activated platelets by binding:

A

GPIIb/IIIa receptors

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20
Q

platelet activation occurs upon exposure to an agonist such as:

A

ADP
TXA2
thrombin
collagen
platelet activation factor

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21
Q

What is fibrin?

A

threadlike protein that reinforces the platelet plug

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22
Q

What does antithrombin do?

A

inhibits some of the coagulation factors so clotting doesn’t get out of control

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23
Q

Which factors depend on vitamin K for their synthesis?

A

II, VII, IX, X

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24
Q

what degrades the fibrin mesh?

A

plasmin

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25
Q

What happens with arteriole thrombosis formation?

A

Lack of adequate blood flow (oxygenation) to distal tissues

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26
Q

What happens with venous thrombosis formation?

A

Possibility of pieces breaking off (emboli) and traveling to lungs/brain.

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27
Q

Which drugs activate antithrombin?

A

heparin
LMWH (enoxaparin, dalteparin)

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28
Q

How does heparin work?

A

activates antithrombin –>
increased inhibition of some clotting factors
–> decreased ability to create fibrin mesh

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29
Q

Which major step in coagulation does heparin inhibit?

A

Fibrin mesh formation

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30
Q

What type of drug is warfarin?

A

Anticoagulant
Vitamin K antagonist

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31
Q

How does warfarin work?

A

inhibits VKORC1 (vitK epoxie reductase complex 1)
vitK cannot be converted to active form

factors II, VII, IX, X are decreased = fibrin mesh formation is decreased

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32
Q

Which major step in coagulation does warfarin inhibit?

A

fibrin mesh formation

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33
Q

How do direct thrombin inhibitors work?

A

Bind & inhibit thrombin
Thus fibrin can’t be formed & factor XIII can’t be activated.

Decreased fibrin mesh formation

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34
Q

What major step in coagulation do direct thrombin inhibitors inhbit?

A

Fibrin mesh formation

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35
Q

Name a couple direct thrombin inhibitors

A

dapigatran
desirudin
bivalrudin
argatroban

36
Q

How do direct factor Xa inhibitors work?

A

bind & inhibit factor Xa = decreased thrombin production

= decreased fibrin mesh formation

37
Q

What major step in coagulation do direct factor Xa inhibitors inhibit?

A

fibrin mesh formation

38
Q

List a couple direct factor Xa inhibitors

A

rivaroxaban
apixaban

39
Q

What is the primary source of thrombi in veins?

A

fibrin
*thus anti-fibrin drugs are especially helpful for preventing DVTs

40
Q

How is heparin administered?

A

IV or subQ

41
Q

Why do IV infusions of heparin have to be monitored with PTT checks?

A

widely variable protein binding, so effects amongst various patients are unpredictable

42
Q

What is normal PTT

A

40 sec

43
Q

What is often the therapeutic goal of heparin infusion?

A

PTT 60-80sec

44
Q

antidote for heparin

A

protamine

45
Q

How does protamine work?

A

binds heparin, inactivating it

46
Q

adverse effects of high dose heparin?

A

hemorrhage
heparin induced thrombocytopenia
hypersensitivity reactions

47
Q

What is HIT (heparin induced thrombocytopenia)?

A

immune response against heparin: antibodies are produced against heparin-platelet complexes

48
Q

What does HIT result in?

A

consumption of platelets (decreased platelets available to clot) = thrombocytopenia

increased platelet activation = increased thromboembolic events

49
Q

What lab values might you expect to change in heparin induced thrombocytopenia?

A

PTT increase
platelet decrease (drastically)

50
Q

Treatment for heparin induced thrombocytopenia?

A

d/c heparin
use alternative anticoagulant

51
Q

Why don’t LMWH require PTT monitoring?

A

decreased protein binding & slower clearance: predictable pharmacokinetics

52
Q

How is warfarin given?

A

PO only

53
Q

What might occur if another highly protein bound drug is given to your patient on warfarin?

A

Increased free warfarin = overdose
Increased bleeding risk

54
Q

What lab value is monitored during warfarin administration?

A

PT/INR

55
Q

What is the normal INR value?

A

0.8-1.1

56
Q

What is the goal INR in warfarin therapy?

A

2-3

57
Q

Why is warfarin not used for acute clotting issues?

A

Doesn’t inhibit the vitK factors that are already synthesized - thus effects take a few days

(just inhibits the formation of future vitK factors)

58
Q

Adverse effects of warfarin

A

hemorrhage
fetal hemorrhage (contraindicated in pregnancy)
infant hemorrhage (caution in breasfeeding)

59
Q

antidote of warfarin

A

vitamin K (phenytonadione)
FFP
plasma concentrates of factor II, VII, IX, X

60
Q

Dietary guidance for a patient being prescribed warfarin:

A

caution with excessive dietary vitK:
- leafy green veggies
- mayo
- canola oil

61
Q

What is unique about bivalrudin (compared with the other direct thrombin inhibitors)?

A

IV only (continuous infusion)
rapid onset
short duration

62
Q

adverse effects of direct thrombin inhibitors

A

hemorrhage (less than warfarin)
GI disturbances

bivalrudin can cause back pain, hypotension, and headache

63
Q

Do you need to monitor lab values for direct thrombin inhibitors or direct factor Xa inhibitors?

A

no

64
Q

adverse effects of rivaroxaban

A

hemorrhage (less than warfarin)
maternal hemorrhage risk + fetal effects (avoid in pregnancy)

65
Q

How does aspirin decrease clotting?

A

irreversibly inhibits cyclooxygenase = decreased thromboxane A2 (TXA2) formation

(TXA2 agonizes platelet activation & aggregation)

66
Q

What major step in clotting does aspirin inhibit?

A

platelet activation & aggregation

67
Q

what class of medication is aspirin?

A

COX inhibitor

68
Q

How do P2Y12 ADP receptor antagonists work?

A

block P2Y12 ADP receptors on platelet surface –> decreased activation and aggregation

69
Q

What major step in clotting do P2Y12 ADP receptor antagonists inhibit?

A

platelet activation & aggregation

70
Q

List some P2Y12 ADP receptor antagonists

A

clopidogrel
prasugrel
ticagrelor

71
Q

How do PAR-1 antagonists work?

A

inhibit PAR1 receptors on platelet surface = decreased platelet activation/aggregation

72
Q

What major step in coagulation do PAR1 antagonists inhibit?

A

platelet activation/aggregation

73
Q

Name a PAR1 antagonist

A

vorapaxar

74
Q

How do GP IIb/IIIa receptor antagonists work?

A

block GPIIb/IIIa receptors on platelet surface = inhibit FINAL COMMON STEP in platelet aggregation
(thus making them the MOST effective antiplatelet drug)

75
Q

list some GPIIb/IIIa receptor antagonists

A

abciximab
tirofiban
eptifibatide

76
Q

Which antiplatelet drug is most effective

A

GP IIb/IIIa receptor antagonists
(like abciximab)

77
Q

duration of action of single dose of aspirin

A

7-10 days (lifetime of platelet due to irreversible binding)

78
Q

duration of action of single dose clopidogrel (Plavix)

A

7-10 days (lifetime of platelet due to irreversible binding)

79
Q

Why are GPIIb/IIIa receptor antagonists the most powerful antiplatelet drug?

A

all other platelet activating/aggregating agonists (TXA2, etc.) require the GP IIb/IIIa receptor

80
Q

What do thrombolytic drugs do?

A

break down thrombi that have already formed

81
Q

list some thrombolytics

A

alteplase (tPA)
reteplase
tenecteplase

82
Q

how do thrombolytic drugs work?

A

activate plasmin which breaks down fibrin mesh
also degrades clotting factors

83
Q

route of administration of thrombolytic drugs

A

IV

84
Q

uses for thrombolytic drugs

A

acute MI, CVA, PE

85
Q

adverse effects of thrombolytic drugs

A

hemorrhage!

86
Q

How to prevent hemorrhage when administering thrombolytic drugs

A
  • minimize patient manipulations
  • avoid invasive procedures (even PIV placement!)
  • avoid subQ/IM injections
  • minimize concurrent use of other blood thinners

GT BSN/CNL PHARM (26 decks)

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