by mtoom

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Describe 2 factors that keep a clot localized
  • Platelets: Negatively charged phospholipid surfaces activate clotting pathways at site of injury
  • Protease inhibitors: (e.g. Antithrombin) Rapidly inactivate coagulation proteases (e.g. Factor Xa and IIa) as they leave the site of the clot
What does Factor Xa do?
Converts prothrombin into thrombin
What is another name for Factor IIa?
How do anti-platelets inhibit platelets?
Thromboxane A2 is involved in stimulating platelet aggregation

This is inhibited due to COX-inhibition (i.e. inhibition of the cyclooxygenase pathway)
How do both UH and LMWH work? Be very specific (about what 2 factors are inhibited).
By catalyzing antithrombin leading to the inhibition of:
  • Factor Xa
  • Factor IIa
Activity of antithrombin increases 1000x
At a molecular level, how does heparin work? (Basic explanation)
It forms Heparin-AT complexes, which more easily bind thrombin, inactivating it
Regarding the length of a heparin chain, any length of heparin chain is effective at doing what?
Inhibiting the action of Factor Xa by binding to antithrombin (AT)
What must be true about a heparin chain in order for it inactivate thrombin (Factor IIa)?
It must be sufficiently long to bind both thrombin (IIa) and antithrombin (AT)
  • LMWH has decreased anti-IIa activity (less than half of chains inhibit IIa)
Describe 6 advantages of LMWH over UH
  • Decreased "heparin resistance" (i.e. binding to non anticoagulant-related plasma proteins) as compared to UH
  • No need for laboratory monitoring (when given on weight-adjusted basis, LMWH response is predictable and reproducible)
  • Longer plasma half-life
  • More bioavailability
  • Less platelet inhibition
  • Less thrombocytopenia risk
Is heparin an anticoagulant by itself?
No, it requires the presence of antithrombin to function
How must heparin be administered?
Injection (it is highly charged)
What a serious, potentially fatal side effect of heparin use?
How can heparin be reversed?
When is the peak action for Warfarin reached? Why?
It may be delayed 72-96 hours

The half-life of the clotting factors that it inhibits are as long as 72h
Name 6 indications of Warfarin
  • Prophylaxis and treatment of venous thromboembolism
  • Prophylaxis and treatment of atrial fibrillation
  • Valvular stenosis
  • Heart valve replacement
  • Myocardial infarction
  • Antiphospholipid membrane
Name 5 side effects of warfarin
  • Hemorrhage
  • Skin necrosis
  • Purple toe syndrome
  • Microembolization
  • Teratogenicity
Give 2 important reasons why warfarin therapy must be monitored
  • Narrow therapeutic range
  • Can increase risk of bleeding
What are 6 contraindications and precautions for warfarin?
  • Hypersensitivity to warfarin
  • Condition with risk of hemorrhage
  • Inadequate lab procedures
  • Vitamin K deficiency
  • Intramuscular injections
  • NSAIDs (ASA)
Describe 6 factors that influence the warfarin dose
  • Inaccurate lab testing
  • Poor patient compliance
  • Concomitant medications
  • Levels of dietary Vitamin K
  • Alcohol
  • Hepatic dysfunction
What are 2 major advantages of using warfarin over heparin
  • Pill form (oral)
  • Inexpensive
Is warfarin active...
  • In vivo?
  • In vitro
  • In vivo... yes
  • In vitro... no

Warfarin influences the metabolism of Vitamin K which leads to effect on Glutamic acid residues and phospholipid membrane binding. All of this depends on pathways of the body (hence in vivo, but not in vitro)
Is heparin active...
  • In vivo?
  • In vitro
  • In vivo... yes
  • In vitro... yes
  • How long is the onset of action for Warfarin?
  • What dietary constituent can antagonize effects of Warfarin?
  • Does warfarin have a high or low degree of protein binding?
  • >3 days to peak effect
  • Vitamin K
  • High degree of protein binding
What test is used to monitor Warfarin use? What happens to the test when Warfarin use goes up?
  • Prothrombin time (PT)
  • Time increases
How does Warfarin work with regard to Vitamin K? Why does administering Vitamin K reduce the effect of Warfarin?
  • Vitamin K is essentially recycled from an active to inactive form
  • Warfarin inhibits/slows this recycling of Vitamin K
  • Dietary intake of Vitamin K is essentially in the activated form, so more active clotting effect is present despite presence of warfarin
How do thrombolytic agents work? Name 3 agents in this class
Activate plasminogen to plasmin (which is involved in dissolution of fibrin clots)
  • Streptokinase
  • Urokinase
  • Tissue Plasminogen Activator 
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