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FA - Hematology and Oncology > Hem & Onc - Pharm (Heme Drugs) > Flashcards

Hem & Onc - Pharm (Heme Drugs) Flashcards

Pg. 398-401 in First Aid 2014 or Pg. 367-369 in First Aid 2013 Sections include: -Heparin -Argatroban, bivalirudin -Warfarin (Coumadin) -Direct factor Xa inhibitors -Heparin vs. warfarin -Thrombolytics -Aspirin (ASA) -ADP receptor inhibitors -Cilostazol, dipyridamole -GP IIb/IIIa inhibitors

1
Q

What is the mechanism of heparin? What coagulation factors does it effect, and in what way?

A

Cofactor for the activation of antithrombin; (1) Thrombin - decrease (2) Factor Xa - Decrease

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2
Q

What is important to remember about the half-life of heparin?

A

Short half-life

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3
Q

What are important things to remember about the clinical use of heparin?

A

(1) IMMEDIATE ANTICOAGULATION - PE, acute coronary syndrome, MI, DVT (2) Used during pregnancy (does not cross placenta) (3) Follow w/ PTT

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4
Q

What toxicities/side effects should you associate with heparin?

A

(1) Bleeding (2) Thrombocytopenia (HIT) (3) Osteoporosis (4) Drug-drug interactions

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5
Q

What is used as an antidote for heparin, and how does it work?

A

Protamine sulfate; Positively charged molecule binds negatively charged heparin

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6
Q

What are examples of low molecular weight heparins?

A

Enoxaparin, dalteparin;

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7
Q

List 6 major ways that low molecular weight heparins compare/contrast to heparin.

A

(1) Act more on factor Xa (2) Better bioavailability (3) 2-4 times longer half-life (4) Can be administered subcutaneously (5) Do not require laboratory monitoring (6) Not easily reversible

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8
Q

What is HIT? What is its mechanism? What symptoms/signs result?

A

Heparin-induced thrombocytopenia; Development of IgG antibodies against heparin bound to platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets –> thrombosis & thrombocytopenia

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9
Q

Argatroban and bivalrudin are derivates of what chemical? What purpose does this chemical of origin serve? What mechanism do they all share?

A

Derivates of hirudin = the anticoagulant used by leeches; Inhibit thrombin

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10
Q

How is bivalirudin used clinically? What is another example of a drug used like bivalirudin?

A

Used as an alternative to heparin for anticoagulating patients with HIT; Argatroban

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11
Q

What is another name for Warfarin?

A

Coumadin

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12
Q

What is the mechanism of Warfarin?

A

Interferes with normal synthesis and gamma-carboxylation of vitamin-K dependent clotting factors II, VII, IX, and X and proteins C and S

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13
Q

What metabolizes Warfarin?

A

Cytochrome P-450 pathway

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14
Q

What coagulation pathway does Warfarin effect? What is used to monitor it?

A

Extrinsic pathway; PT (increased); Think: “the EX-PresidenT went to war.”

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15
Q

What is important to remember about the half life of Warfarin?

A

Long

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16
Q

What are important things to remember about the clinical use of warfarin?

A

(1) CHRONIC ANTICOAGULATION (after STEMI [FYI - ST elevation myocardial infarction], venous thromboembolism prophylaxis, & prevention of stroke in atrial fibrillation) (2) NOT used in pregnant women (because warfarin, unlike heparin, can cross the placenta) (3) Follow with PT/INR values

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17
Q

What are the toxicities/side effects associated with warfarin?

A

(1) Bleeding (2) Teratogenic (3) Skin/tissue necrosis (4) Drug-drug interactions

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18
Q

How is Warfarin reversed? How is rapid reversal of severe warfarin overdose achieved?

A

Vitamin K; Fresh frozen plasma

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19
Q

Compare/contrast the structure of Heparin and Warfarin.

A

HEPARIN - large anionic, acidic polymer; WARFARIN - small lipid-soluble molecule

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20
Q

Compare/contrast the route of administration of Heparin and Warfarin.

A

HEPARIN - parenteral (IV, SC); WARFARIN - Oral

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21
Q

Compare/contrast the site of action of Heparin and Warfarin.

A

HEPARIN - blood; WARFARIN - liver

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22
Q

Compare/contrast the onset of action of Heparin and Warfarin.

A

HEPARIN - Rapid (seconds); WARFARIN - Slow (limited by half-lives of normal clotting factors)

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23
Q

Compare/contrast the mechanism of action of Heparin and Warfarin.

A

HEPARIN - Activates antithrombin, which decreases action of IIa (thrombin) and factor Xa; WARFARIN - Impairs the synthesis of vitamin K-dependent clotting factors II, VII, IX, and X (vitamin K antagonist)

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24
Q

Compare/contrast the duration of action of Heparin and Warfarin.

A

HEPARIN - Acute (hours); WARFARIN - Chronic (days)

25
Q

Does Heparin and/or Warfarin inhibit coagulation in vitro?

A

HEPARIN - Yes; WARFARIN - No

26
Q

What is the treatment of active overdose for Heparin versus Warfarin?

A

HEPARIN - Protamine sulfate; WARFARIN - IV vitamin K and fresh frozen plasma

27
Q

Compare/contrast the monitoring for Heparin and Warfarin.

A

HEPARIN - PTT (intrinsic pathway); WARFARIN - PT/INR (extrinsic pathway)

28
Q

Does Heparin and/or Warfarin cross the placenta?

A

HEPARIN - No; WARFARIN - Yes (teratogenic)

29
Q

What are examples of thrombolytics?

A

(1) Alteplase (tPA) (2) Reteplase (rPA) (3) Tenecteplase (TNK-tPA)

30
Q

What is the mechanism of thrombolytics? What effect do they have on PT, PTT, and platelet count?

A

Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots; Increased PT, Increased PTT, no change in platelet count

31
Q

What are thrombolytics used for clinically?

A

(1) Early MI (2) Early ischemic stroke (3) Direct thrombolysis of severe pulmonary embolism

32
Q

What are the toxicities/side effects/contraindications associated with thrombolytics?

A

Bleeding, Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension

33
Q

How is thrombolytic toxicity treated, and what is the general mechanism of this treatment? What else can be used, and what exactly is it used for?

A

Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis; Fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies.

34
Q

What is the mechanism of aspirin (ASA)? How long does it effects last, and why?

A

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation; Last until new platelets are produced, because (drugged) platelets cannot synthesize new enzyme

35
Q

What lab measurements/changes should you associate with aspirin?

A

(1) Increased bleeding time (2) Decreased TXA2 (3) Decreased prostaglandins (4) No change in PT (5) No change in PTT

36
Q

How is aspirin used clinically?

A

(1) Antipyretic (2) Analgesic (3) Anti-inflammatory (4) Antiplatelet (decreased aggregation)

37
Q

What are the 2 major toxicities associated with aspirin?

A

(1) Gastric ulceration (2) Tinnitus CNVIII

38
Q

What can result from chronic use of aspirin?

A

(1) Renal failure (2) Interstitial nephritis (3) Upper GI bleeding

39
Q

What can aspirin cause in children with viral infection?

A

Reye’s syndrome (FYI - a potentially fatal disease that has numerous detrimental effects to many organs, especially the brain and liver, as well as causing a lower than usual level of blood sugar)

40
Q

What pH disturbance(s) does aspirin overdose cause?

A

Overdose causes respiratory alkalosis initially, which is then superimposed by metabolic acidosis

41
Q

What are examples of ADP receptor inhibitors?

A

(1) Clopidogrel (2) ticlopidine (3) Prasugrel (4) Ticagrelor

42
Q

What is the mechanism of ADP receptor inhibitors?

A

(1) Inhibit platelet aggregation by irreversibly blocking ADP receptors (2) Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

43
Q

How are ADP receptors used clinically?

A

(1) Acute coronary syndrome (2) Coronary stenting (3) Decrease incidence/recurrence of thrombotic stroke

44
Q

Which of the ADP receptor inhibitors is associated with a particular toxicity? What is the toxicity? What other toxicity may be seen with ADP receptor inhibitors?

A

Ticlopidine; Neutropenia; TTP/HUS may be seen

45
Q

What is a drug that shares the same mechanism as cilostazol? What kinds of drugs are these, and what are their mechanisms/effects)?

A

Dipyridamole; Phosphodiesterase II inhibitors; (1) Increase cAMP in platelets, thus inhibiting platelet aggregation (2) Vasodilators

46
Q

How are Cilostazol and dipyridamole used clinically?

A

(1) Intermittent claudication (2) Coronary vasodilation (3) Prevention of stroke or TIAs (transient ischemic attacks) (combined with aspirin) (4) Angina prophylaxis

47
Q

What are toxicities/side effects associated with cilostazol and dipyridamole?

A

(1) Nausea (2) Headache (3) Facial flushing (4) Hypotension (5) Abdominal pain

48
Q

What are examples of GP IIb/IIIa inhibitors?

A

(1) Abciximab (2) Eptifibatide (3) Tirofiban

49
Q

What is the mechanism of GP IIb/IIIa inhibitors and its effect?

A

Bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation

50
Q

What is abciximab? What effect does it have? How is it made?

A

GpIIb/IIIa inhibitor - binds glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation; Made from monoclonal antibody Fab fragments

51
Q

How are GpIIb/IIIa inhibitors used clinically?

A

(1) Acute coronary syndromes (2) Percutaneous transluminal coronary angioplasty

52
Q

What are the toxicities/side effects associated with GpIIb/IIIa inhibitors?

A

(1) Bleeding (2) Thrombocytopenia

53
Q

What kind of drug is Apixaban? What is another drug in this same class?

A

Direct factor Xa inhibitors; Apixaban, Rivaroxaban

54
Q

What is the mechanism of Apixaban and rivaroxaban?

A

Direct factor Xa inhibitors = bind and directly inhibit the activity of factor Xa.

55
Q

What are the clinical uses for direct factor Xa inhibitors (apixaban, rivaroxaban)?

A

Treatment and prophylaxis of DVT and PE (rivaroxaban), stroke prophylaxis in patients with atrial fibrillation. Oral agents do not usually require coagulation monitoring.

56
Q

What toxicity is associated with direct factor Xa inhibitors (apixaban, rivaroxaban)? What is the availability of interventions regarding this toxicity?

A

Bleeding (no specific reversal agent available).

57
Q

As it relates to direct factor Xa inhibitors, what is important to know about coagulation monitoring?

A

Oral agents do not usually require coagulation monitoring

58
Q

Which direct factor Xa inhibitor is particularly used in the treatment and prophylaxis of DVT and PE?

A

Treatment and prophylaxis of DVT and PE (rivaroxaban)

FA - Hematology and Oncology (17 decks)

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