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Blood Disorder Drugs
Kaplan
| Question | Answer |
|---|---|
| How does blood coagulates? | By transformation of soluble fibrinogen into insoluble fibrin. (Made in the liver) |
| How does Heparin works? | (anticoagulant) Inhibits activated clotting factors (2a and 10a) via ACTIVATION OF AT3 |
| How does Warfarin works? | (anticogulant) Inhibits hepatic synthesis of clotting factors (2,7,9,10) by INHIBITING VIT K EPOXIDE REDUCTASE (which prevents gamma-carboxylation of the clotting factors) |
| MOA of Protein C and S | (endogenous anticoagulant) Proteolysis of factors 5a and 8a |
| Which clotting factor is first to get affected by WARFARIN and why? | Factor 7 and protein C - which may lead to transient hypercoaguable state b/c it has the SHORTEST half life |
| What is the chemical nature (molecule size/solubility) of Heparin vs Warfarin? | HEPARIN: large (polysaccharide) water-soluble (safer in pregnancy d/t it being large- harder to cross the placenta) WARFARIN: small molecule, lipid-soluble (derived from vitamin K) |
| Which has a faster onset of action? (Heparin or Warfarin) | HEPARIN (faster onset) Heparin catalyzes the binding of antithrombin 3 (to 2a,9a,10a,11a,12a) Warfarin have to “warda” |
| What is the antagonist for Heparin? | Protamine sulfate (fast onset) |
| What is the antagonist for Warfarin? (2) | 1. Vitamin K- increase clotting factor synthesis (slow onset) 2. Fresh frozen plasma (fast onet) |
| Which Heparin has a low molecular weight, given subcutaneously and does not need to monitor the PTT? | ENOXAPARIN |
| What are the P450 inducers that DECREASE the PT while on Warfarin? (3) | 1. Barbs 2. Carbamazepine 3. Rifampin |
| What are the P450 inhibitors that INCREASE the PT while on Warfarin? (3) | 1. Cimetidine 2. Macrolides 3. Azole antifungals *they inhibit Warfarin so it works longer |
| What is the normal PT and INR? | PT: 12-15 sec INR: 0.8-1.2 (how long it takes for blood to clot) (if INR increases that indicates an increase in the plasma warfarin levels) |
| What are the direct thrombin inhibitors? (3) | 1. Argatroban 2. Dabigatran 3. Bivalirudin they do NOT require antithrombin 3 |
| What is an antidote for Dabigatran? | IDARUCIZUMAB |
| What are the direct Xa inhibitors? | "-xabans" Rivaroxaban |
| What is an antidote for the direct factor Xa inhibitor? | ANDEXANET ALFA |
| What are the thrombolytics/fibrinolytics? (2) | 1. Alteplase (tPA) 2. Streptokinase (not used anymore d/t antigenic proterties) |
| How does Alteplase (tissue plasminogen activator) works? | Rapidly converts plasminogen to plasmin |
| When (time wise) is a thrombolytic best used? | if used within 3 hours of post infarction |
| complication of thrombolytics? | Intracranial hemorrhage, bleeding |
| Whar are some antifibrinolytics (antidotes)? (2) | 1. Aminocaproic acid 2. Tranexamic acid |
| What are the (3) sites of platelet activation that gets blocked by antiplatelets drugs? | 1. TXA2 (inhibition of COX 1 and 2 by Aspirin) 2. GP2a/3b /Fibrinogen receptors (blocked by Abciximab) 3. ADP receptors (blocked by Clopidogrel) |
| Which drugs are ADP receptor blockers? (3) | “-grel” 1. Clopidogrel 2. Prasugrel 3. Ticagrelor |
| What are the GP2b/3a antagonists? (3) | 1. Abciximab 2. Eptifibatide 3. Tirofiban |
| Platelet aggregation is INCREASED by (5) | 1. ADP 2. 5HT (serotonin) 3. TXA2 (thromboxane) 4. Thrombin 5. alpha 2 agonists |
| Platelet aggregation is DECREASED by (5) | 1. PGI2 2. cAMP 3. ASA 4. Clopidogrel 5. GP 2a/3b |
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DVD27