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Systemic Pharm > Blood Thinners > Flashcards

Blood Thinners Flashcards

1
Q

Why would you prescribe anticoagulants or fibrinolytics

A

for thrombotic disorders such as acute myocardial infarction, deep vein thrombosis, pulmonary embolism, and acute ischemic stroke

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2
Q

T/F Coagulation involves both cellular (platelet) and protein based (coagulation factors) components

A

True

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3
Q

what kind of thrombosis usually consists of a platelet rich clot

A

arterial thrombosis

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4
Q

what kind of thrombosis is commonly triggered by blood stasis or inappropriate activation of the coagulation cascade

A

venous thrombosis

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5
Q

What are the drug classes of anti hemostatic agents

A
  1. anticoagulants

2. platelet inhibitors

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6
Q

the coagulation process culminates in the generation of thrombin –> ______to the glycoprotein–> ______

A

fibrinogen; fibrin (the actual clot)

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7
Q

Drugs acting within the extrinsic pathway affect what?

A

the synthesis of vitamin K dependent coagulation factors (trauma)

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8
Q

drugs acting within the intrinsic pathway affect what

A

inhibit the activity of coagulation factors (more important in inflammation pathways)

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9
Q

In the intrinsic pathway, activation of factor ____ snowballs to the conversion of factor _____which plays final roles in the common pathway

A

X11; X

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10
Q

Factor ____ is common to both intrinsic and extrinsic pathways

A

X

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11
Q

what are the anticoagulant drug classes

A
  1. vitamin K antagonists

2. coagulation factor antagonists

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12
Q

T/F vitamin k antagonism involves direct action rather than inhibition of vitamin K recycling enzymes

A

F; it does not involve direct action, it rather inhibits the vitamin K recycling enzymes

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13
Q

which drug is a vitamin K antagonist

A

coumadin (warfarin)

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14
Q

what is the indication for coumadin

A

anticoagulation

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15
Q

what is the mechanism of action of coumadin

A

inhibits vitamin K dependent coagulation factor synthesis (II, VII, IX, X, proteins C and S)

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16
Q

what are the vitamin K dependent coagulation factors that are affected by coumadin

A

VII, IX, X, Prothrombin

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17
Q

what are the common adverse effects of coumadin

A
  1. bleeding/bruising
  2. headache
  3. dizziness
  4. pruritis
  5. edema
  6. dermatitis
  7. fever
  8. parethesias
  9. alopecia
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18
Q

what are serious adverse effects of coumadin

A
  1. syncope
  2. vasculitis
  3. hemorrhage
  4. cholesterol embolism
  5. anemia
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19
Q

what are drug interactions of coumadin

A
  1. azole antifungals, macrolids, fluoroquinolones, tetracyclines: impair coumadin metabolism
  2. NSAIDS, omega 3, and omega 6 FA: additive blood thinning effects
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20
Q

what are contraindications/cautions of coumadin

A
  1. recent ocular surgery
  2. hypertension
  3. diabetes
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21
Q

Which class of drugs have a suffix of -“parin” and -“xaban”

A

coagulation factor antagonists

22
Q

what is the indication for enoxoparin

A
  1. post op DVT prophylaxis

2. unstable angina

23
Q

what is the mechanism of action of enoxoparin

A

fractionated, heterogenous low MW heparin extracted from porcine intestinal mucosa. Binds to the circulating anticoagulant antithrombin and accelerates its irreversible inactivation of clotting Factor Xa much more so than Factor IIa

24
Q

what is factor IIa

A

thrombin

25
Q

heparin is a natural ______ which is complexed with histamine in mast cells where its physiologic role be antimicrobial

A

glycosaminoglycan

26
Q

what are the two factors that are targets of unfractionated heparin and LMWH

A

factor X and factor II (prothrombin)

27
Q

what is the difference between unfractionated heparin and fractionated (LMWH)?

A

Fractionated has a higher affinity for factor X.

28
Q

which is more predictable, heparin or LMWH?

A

LMWH; has a higher bioavailability and longer half life

29
Q

what are common adverse effects of enoxoparin

A
  1. hemorrhage

2. fever

30
Q

what are serious adverse effects of enoxoparin

A

anemia

31
Q

what are drug interactions of enoxoparin

A

NSAIDS, omega-3 and omega-6 FA’s are additive

32
Q

when should you use caution with enoxoparin

A
  1. recent ocular surgery
  2. diabetic retinopathy
  3. hypertension
  4. diabetes
33
Q

what is the indication for rivaroxaban

A
  1. DVT

2. Stroke prophylaxis

34
Q

how is enoxaprin administered? how is rivaroxaban administered?

A

enoxparin is via subcutaneous injection. Rivaroxaban is orally administered.

35
Q

what is the mechanism of action of rivaroxaban

A
  1. Factor Xa inhibitor

2. Selectively blocks the active site of Factor Xa, inhibiting blood coagulation.

36
Q

what are common adverse effects of rivaroxaban

A
  1. hemorrhage

2. pruritus

37
Q

what are serious adverse effects of rivaroxaban

A
  1. severe hemorrhage

2. SJS

38
Q

what are drug interactions of rivaroxaban

A
  1. macrolides, FQ, cyclosporine, and azoles cause increased rivaroxaban levels.
  2. NSAIDs: additive hemorrhage
  3. ophthalmic NSAIDs, omega FA’s: additive hemorrhage
39
Q

what are cautions of rivaroxaban

A

active major bleeding

40
Q

which two receptors are usually activated in the critical last phase of thrombus formation which serve to bind adhesive proteins like fibrinogen

A
  1. GP IIb

2. GP IIIa

41
Q

platelet stimulating agents that lead to GP IIb/IIIa receptor activation include:

A
  1. thromboxane A2
  2. ADP
  3. thrombin
  4. serotonin
  5. collagen
    * platelet inhibitors inhibit all of this
42
Q

aspirin prevents the production of ______A2

A

thromboxane

43
Q

what are platelet inhibitor drug classes

A
  1. adenosine receptor blockers

2. glycoprotein IIb/IIIa receptor antagonists

44
Q

what are the adenosine receptor blockers

A
  1. clopidogrel
  2. ticlopidine
  3. prasugrel
  4. dipyridamole
45
Q

what is the indication for clopidogrel

A
  1. acute coronary syndrome

2. thrombotic event prophylaxis

46
Q

what is the mechanism of action of clopidogrel

A

its a prodrug that gets metabolized in the body and causes irreversible inhibition of platelet ADP receptors which normally trigger platelet activation and aggregation via downstream activation of the GPIIb/IIIa complex

47
Q

Ticlopidine, clopidogrel, and prasugrel all inhibit ADP- mediated platelet aggregation by blocking ______ activation of GDP receptor.

A

calcium

48
Q

what are common adverse effects of clopidogrel

A
  1. hemorrhage
  2. pruritus
  3. cough
  4. bronchitis
  5. dizziness
  6. headache
49
Q

what are serious adverse effects of clopidogrel

A
  1. angioedema
  2. SJS
  3. TEN: toxic epidermal necrolysis
  4. TTP: thrombotic thrombocytopenic purpura
50
Q

what are drug interactions of clopidogrel

A
  1. evening primrose oil, flaxseed, omega 3 FA, NSAIDs: additive
  2. Ketoconazole: reduced metabolism/activation –> via inhibition of the CYP2C19 enzyme.
51
Q

what are cautions of clopidogrel

A

ocular disease

Systemic Pharm (9 decks)

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