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PCM Exam 1 > Drugs For Disorders Of Coagulation > Flashcards

Drugs For Disorders Of Coagulation Flashcards

1
Q

_____________ digests fibrin

A

Plasmin; inactive plasminogen must be converted to active plasmin

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2
Q

Families of drugs used to reduced clotting

A
  • platelet aggregation inhibitors (anti platelet drugs)
  • anticoagulants
  • thrombolytics
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3
Q

What are the 4 mechanisms of actions that allow for the inhibition of platelet aggregation

A
  • Cyclooxygenase inhibitors
  • ADP receptor blockers
  • phosphodiesterase inhibitors
  • blockers of platelet GP IIb/IIIA receptors
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4
Q

Aspirin inhibits the synthesis of ________ by _______________ of the enzyme ________

A 
Thromboxane A2 (causes platelet degranulation and aggregation) ; Irreverisble acetylation ; 
COX
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5
Q

What kind of protein receptor is involved in the aggreagation and activation of platelets?

A

Gq protein → Phosopholipase C → IP3 and DAG → release of calcium from ER activation PKC which then activates Phospholipase A2 → which activates the receptor (G2b/G3b) allowing for fribonrgen to bind and platelets aggregate

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6
Q

_______ forms bridges between adjacent pallets because it is ________

A

Fibrinogen; bivalent

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7
Q

What drugs are ADP receptor blockers?

A

Clopidogrel & Ticlopidine

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8
Q

Mechanism of ADP receptor blockers

A

Irreversible inhibitors of P2Y12 which is a subtype of ADP receptor

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9
Q

Of the ADP receptor blocker drugs, ___________ has fewer adverse effects than ____________

A

Clopidogrel; ticlopidine

Clopidogrel is preferred over ticlopidine

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10
Q

Clopidogrel is a prodrug that is converted to the active form by __________

A

CYP2C19

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11
Q

An individual who is a poor CYP2C19 metabolizer will have _________ plasma levels of clopidogrel

A

Low; CYP2C19 is used to convert the prodrug form to the active form of clopidogrel

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12
Q

Concurrent use of clopidogrel and ______________ should be avoided

A

Omeprazole (CYP2C19 inhibitor) because then cannot get the active form of clopidogrel

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13
Q

Drugs that are phosphodiesterase inhibitors

A

Dipyridamole: used for stroke prevention
Cilostazol: used for intermittent claudication

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14
Q

↑ _______ promotes dormant platelets while ↑ _________ leads to activation and aggregation of platelets

A

CAMP; calcium

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15
Q

Phosphodiesterase inhibitors cause an ↑ in _____________

A

CAMP; causes platelets to remain dormant

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16
Q

Drugs that are blockers of platelet GP 2B/3A receptors

A
  • Abciximab
  • Eptifibatide
  • Tirofiban (most popular)
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17
Q

Platelet GP 2B/3A receptor blockers are used for prevention of _____________

A

Cardiac ischemic complications after a MI

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18
Q

Classes of anticoagulant drugs based on mechanism (4)

A
  • indirect thrombin & factor Xa inhibitors
  • direct thrombin inhibitors
  • direct factor Xa inhibitors
  • Vitamin K antagonists
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19
Q

Drugs that are indirect thrombin and factor Xa inhibitors:

A

Heparin: unfractionated and low molecular weight (enoxaparin)
Fondaparinux

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20
Q

Administration method of heparin

A

Injected; rapidly active

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21
Q

UFH vs LMWH: Which one has higher, lower, or equal of the following

  • efficacy
  • bioavailability
  • half life
  • dosing requirements
A

Efficacy: equal
Bioavailability, half life: LMWH has higher (longer half life)
Dosing requirements: LMWH has less frequent dosing req.

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22
Q

Mechanism of action of heparin

A

Heparin acts a cofactor for antithrombin III and accelerates its normal function of inhibitor clotting factor pretenses: thrombin, IXa, and Xa

23
Q

What clotting factors does antithrombin III inhibit?

A

Thrombin, IXa, and Xa

24
Q

Difference in the mechanism of action between UFH and LWMH

A

UFH efficiently inactivates BOTH thrombin and Xa

LMWH has less effect on thrombin but efficiently inactivates Xa

25
Q

__________ is not necessary to accelerate the inactivation of clotting factor ______ by antithrombin III

A

Ternary complex; Xa

LMWH cannot form a ternary complex but this is why both UFH and LMWH efficiently inhibit factor Xa

26
Q

_____________ is used to monitor heparin levels

A

APTT assay (activated partial thromboplastin time) which tests for integrity of the intrinsic and common pathways

27
Q

Potency of LMWH can be assessed with __________ usually in ________ patients

A

Anti-factor Xa assays; obese

28
Q

Uses of heparin

A

DVT, pulmonary embolism, MI and drug of choice for pregnant women

29
Q

In heparin induced thrombocytpenia type II, ________ binds to the heparin causing it to be immunogenic and then ______ binds to the immune complex and activates platelets causing degranulation and activation and release of more platelet factor 4

A

Platelet factor 4; IgG

30
Q

Heparin induced thomrbocytopenia type 2 can result in thrombocytopenia and ________

A

Thrombosis

31
Q

Therapy for heparin induced thrombocytopenia type II

A

Discontinue heparin and administers a DTI or fondaparinux

32
Q

Antidote for excessive heparin administration

A

Protamine sulfate

33
Q

Warfarin inhibits ___________

A

Vitamin K epoxide reductase

34
Q

How long does it take to see the effect of warfarin?

A

6-60 hours because that is the half life of the circulating clotting factors

35
Q

Fondaparinux is a specific inhibitor of ___________ and is approved for prevention and treatment of _______

A 
Factor Xa (negligible antithrombin activity) 
DVT
36
Q

Peak warfarin effect is seen ________

A

72-96 hrs

37
Q

Antidote to excessive warfarin administration

A

Vitamin K

38
Q

Monitoring of warfarin levels is done by _____________ which tests the integrity of the ____________ pathways of coagulation

A

Prothrombin time; extrinsic and common pathways

39
Q

Adverse effects of warfarin

A
  • hemorrhage
  • cutaneous necrosisdue to ↓ activity of protein C which is an anticoagulant factor that requires vitamin K
  • teratogenic if taken during pregnancy
40
Q

Cutaneous necrosis is an adverse effect of taking what drug?

A

Warfarin

41
Q

Which one should be used for pregnant patients: heparin or warfarin

A

Heparin

42
Q

Drugs that are parenteral DTI’s (direct thrombin inhibitors) and how are they monitored?

A
  • desirudin
  • bivalirudin
  • argatroban

APTT

43
Q

Oral DTI drugs

A

Dabigatran etexilate (prodrug)

44
Q

Benefits of oral DTI

A

Produces a predictable response and does not need to be routinely monitored like you would need to with Heparin

45
Q

Drugs that are director factor Xa inhibitors

A

Apixaban & rivaroxaban

- do not req. monitoring and given orally

46
Q

Direct oral anticoagulants (DOAC’s) _________________ (3) are replacing warfarin for treating stroke and preventing embolism is atrial fibrillation because:

A

Dabigatran, apixaban, rivaroxaban

DOAC’s have equal efficacy and ↓ bleeding rates, dont need to be monitored, rapid onset of action, predictable pharmacokinetics, wider TW, and fewer drug interactions

47
Q

Thrombolytic drugs and mechanism

A 
Streptokinase
Urokinase
Alteplase 
Reteplase
Tenecteplase

Promote conversation of plasminogen to plasmin

48
Q

Urokinase is formed by ___________

A

Kidney; found in the urine

49
Q

_____________ causes the conversion of plasminogen to plasmin and is “fibrin selective” unlike streptokinase and urokinase;
Explain fibrin selective

A

T-Pa (tissue plasminogen activator) which is a serine protease produced by endothelial cells

T-Pa only converts plasminogen to plasmin when the plasminogen is bound to fibrin

50
Q

___________ and _________ are recombinant variants of t-Pa with a longer half life

A

Reteplase and tenecteplase

51
Q

Classes of drugs used to treat bleeding

A
  • Plasminogen activator inhibitors
  • protamine sulfate
  • vitamin K
  • plasma fractions
52
Q

Drugs that are plasminogen activation inhibitors

A

Aminocaproic acid and tranexamic acid

53
Q

Protamine sulfate can be used as an antidote for excessive administration of _________ because ______

A

Heparin;

Charge-charge antagonism: protamine sulfate is very positively charged while heparin is negatively charged

54
Q

Plasma fractions are given to __________

A

People with genetic defects such as factor XIII or Factor IX deficiencies (hemophilia)

PCM Exam 1 (22 decks)

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