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unit 2 pharm > drug tx in thrombosis > Flashcards

drug tx in thrombosis Flashcards

1
Q

Unfractionated Heparin

A
  • indirect thrombin inhibitor
  • binds antithrombin –> formation of antithrombin-coagulation factor complex (Xa, IIa)
  • inhibits Xa and thrombin (IIa)
  • given initially (immediate-acting, short half-life, parenteral) followed by warfarin
  • unpredictable dosing because it binds to everything –> need to monitor via PTT (want 2-2.5X normal value)
  • adverse side effects: HIT, osteoporosis, bleeding
  • reversed by protamine
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2
Q

Low Molecular Weight Heparin

A
  • indirect thrombin inhibitor
  • mostly inihibits Xa, less effective against thrombin
  • (w/o the long tail the antithrombin complex can’t bind thrombin)
  • predictable dose-response –> less need to monitor but if you have to monitor via heparin assay (rather than PTT)
  • longer half-life
  • lower risk of inducing HIT
  • less effective reversal with protamine
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3
Q

Dalteparin (Fragmin)

A

LMWH

-“parin” = LMWH

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4
Q

Enoxaparin (Lovenox)

A
  • LMWH
  • drug of choice in pregnancy

“-parin” = LMWH

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5
Q

Tinzaparin (Innohep)

A
  • LMWH

“-aprin” = LMWH

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6
Q

Fondaparinux

A
  • Indirect thrombin inhibitor
  • synthetic polysaccharide that binds the active site of antithrombin
  • inhibits Xa (ineffective against thrombin!)
  • given for HIT patients
  • no antidote!
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7
Q

image of mech of action of unfractionated heparin, LMWH and fondaparinux

A
  • UFH binds antithrombin –> formation of antithrombin complex (Xa, IIa)
  • LMWH cant bind thrombin
  • fondaparinux doesn’t bind thrombin either
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8
Q

warfarin (coumadin)

A
  • Vitamin K antagonist –> blocks vitamin K-dependent carboxylation of factors II, VII, IX, X, Protein C and S
  • slow onset (often preceded by heparin)
  • oral, long-term use
  • may induce venous thrombosis at onset of tx because it inhibits anticoagulants protein C and S
  • drug interactions –> enhanced metab.
  • monitored by PT/ INR
  • reversed by Vit K, factor concentrates or FFP
  • contraindicated in pregnancy (teratogenic!)
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9
Q

direct thrombin inhibitors

A
  • Lepirudin, Bivalirudin (Angiomax), Argatroban and Dabigatran
  • inactivate fibrinogen-bound and unbound thrombin; irreversible
  • parenteral administration with rapid onset
  • monitored by PTT
  • no antidote!
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10
Q

Lepirudin

A

direct thrombin inhibitor

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11
Q

Bivalirudin (angiomax)

A

direct thrombin inhibitor

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12
Q

Argotroban

A

direct thrombin inhibitor

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13
Q

Dabigatran (Pradaxa)

A

direct thrombin inhibitor (oral)

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14
Q

direct Xa inhibitors

A
  • Rivaroxaban and Apixaban (have “X” in name)
  • oral
  • no methods to assess levels, no antidote
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15
Q

streptokinase

A
  • Fibrinolytic (thrombolytic)
  • lyses already formed clots by activating circulating plasminogen
  • not clot specific
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16
Q

Urokinase

A
  • Fibrinolytic/thrombolytic
  • lyses alreadly formed clots by activating circulating plasminogen
  • serine protease
17
Q

Reteplase and Tenecteplase

A
  • tissue plasminogen activator (t-PA) derivatives
  • lyse already formed clots by activating fibrin-bound plasminogen
  • more clot specific –> less systemic activation
18
Q

anticoagulants

A
  • used for venous thrombosis
  • Heparins (UFH, LWMH, Fondaparinux)
  • Vit K antags (warfarin)
  • Direct thrombin inhibs (Dabigatran, Bivalirudin, Argatroban, Lepirudin)
  • Direct Xa inhibs (Rivaroxaban)
19
Q

fibrinolytic drugs

A
  • used for acture thrombosis
  • streptokinase, urokinase, t-PA
20
Q

antiplatelet drugs

A
  • used for arterial thrombosis
  • asprin, clopidogrel, prasugrel, abciximab, eptifibatide, tirofiban
21
Q

aspirin

A
  • PGs have opposing effects on platelets (pro-coag) and endothelial cells (anti-coag)
  • low-dose baby asprin has greater effect on platelet COX-1 (new protein is continously being made in endothelial cells but no in anucleate platelets) –> higher doses affect endothelial cell COX-1
22
Q

dipyridamole

A
  • antiplatelet drug (weak effect)
  • phosphodiesterase inhibitor –> increases platelet cAMP

DIpyridamole –> phosphoDIesterase inhib

23
Q

Clopidogrel (plavix)

A
  • anti-platelet drug
  • inhibits platelet ADP receptor
  • irreversible binding –> antithrombotic effect lasts up to 10 days and can only be reversed with platelet infusion
  • give prasugrel (works by same mech but activiated by different P450) if resistant
24
Q

Abciximab

A
  • antiplatelet drug
  • MAb against GP IIb/IIIa (fibrinogen receptor)
  • may illicit immune response
25
Q

Eptifibatide (Integrilin) and Tirofiban (Aggrastat)

A
  • antiplatelet drugs
  • fibrinogen analog which competes with endogenous fibrinogen and vWF binding to IIb/IIIa

integrilin has integrity so it will compete fairly with fibrinogen

unit 2 pharm (12 decks)

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