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L47 Anticoagulation
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1An overview of the clotting cascade:
1. Initiation:
Platelets adhere to vessel and [blank_start]recruit[blank_end] more circulating platelets to [blank_start]aggregate[blank_end]. This provides a surface
where clotting factors assemble. Some clotting factors are [blank_start]released[blank_end]. TF initiates coagulation. TF activates [blank_start]X and IX[blank_end], forming Xa and IXa.
2. Amplification
IXa amplifies the activation of [blank_start]X[blank_end]. The [blank_start]Xa/Va[blank_end] complex is a critical component, activating [blank_start]FIIa[blank_end] (thrombin)
3. Propagation
A burst of activated thrombin then converts [blank_start]fibrinogen to fibrin[blank_end], to form a mesh.- Arecruit
- Baggregate
- Creleased
- DX and IX
- EX
- FFIIa
- GXa/Va
- Hfibrinogen to fibrin
2The clotting cascade has an "[blank_start]intrinsic[blank_end] pathway" activated by trauma inside the vascular system. It is [blank_start]slower[blank_end] than the “extrinsic pathway”. The initiation involves XII, XI, IX, VIII.
- Aintrinsic
- Bslower
3Warfarin is a Vitamin K “antagonist” that targets Vitamin K epoxide reductase in the liver.
- ATrue
- BFalse
4NOACs (novel oral anticoagulants) like dabigatran and rivaroxaban target thrombin and Xa.
- ATrue
- BFalse
5Choose the incorrect statement.
- AIt is a racemic mixture.
- BIt is highly protein bound (>99%) and well absorbed.
- CIt is renally metabolised.
- DS-warfarin has a greater clearance and shorter half life than R-warfarin.
6By inhibiting vitamin K epoxide reductase, warfarin increases the production of clotting factors II, VII, IX, X.
- ATrue
- BFalse
7The half-life of the FII is longer than warfarin and is the rate limiting step in the time course of the warfarin effect.
- ATrue
- BFalse
8Unfractionated heparin is found naturally in [blank_start]mast[blank_end] cells. It is a large [blank_start]polymer[blank_end] with alternating disaccharide units of variable lengths.
- No [blank_start]intrinsic[blank_end] anticoagulant activity
- Not [blank_start]orally[blank_end] available so given intravenously and subcutaneously
- Half-life of about [blank_start]1[blank_end] hour
The antidote is a reversal agent called [blank_start]protamine sulphate[blank_end].
It binds to [blank_start]antithrombin II[blank_end]I, and induces a conformational change that enhances binding to [blank_start]activated[blank_end] clotting actors, helping to inhibit coagulation.- Amast
- Bpolymer
- Cintrinsic
- Dorally
- E1
- Fprotamine sulphate
- Gantithrombin II
- Hactivated
9Low molecular weight heparins (LMWH)
• Given [blank_start]subcutaneous[blank_end]
• Enoxaparin halfe life ~ [blank_start]5hrs[blank_end]
• Mainly [blank_start]renally[blank_end]-cleared
• Effect [blank_start]partially[blank_end] reversed by giving protamine sulphate
• Target is mostly anti-[blank_start]Xa[blank_end], some anti-IIa- Asubcutaneous
- B5hrs
- Crenally
- Dpartially
- EXa
10Novel oral anticoagulants (NOACs):
1. Dabigatran etexilate
• Competitive and reversible inhibition of free and clot bound [blank_start]thrombin[blank_end]
• Prodrug converted to active compound (dabigatran)
• [blank_start]Low[blank_end] oral availability (~7%)
• ~80% [blank_start]renally[blank_end] cleared, ~20% glucuronidation
• Half life: ~12 hours
2. Rivaroxaban
• Competitive and reversible inhibition of free and clot bound [blank_start]Xa[blank_end]
• [blank_start]Good[blank_end] oral availability (>80%)
• ~35% renally cleared, ~65% [blank_start]metabolised[blank_end] (CYP3A4 and others)
• Half life: ~7-10 hours- Athrombin
- BXa
- CLow
- DGood
- Erenally
- Fmetabolised by liver
11PT, prothrombin time, is the time taken for plasma to clot in [blank_start]vitro[blank_end] after the addition of [blank_start]tissue factor & CaCl[blank_end]. Normally it is 12-15 seconds. The PT ratio is the [blank_start]patient's[blank_end] PT over the normal [blank_start]average[blank_end] PT.
The International Normalised ratio (INR) is a “correction” of the PT ratio, or rather a correction of the large variability in the [blank_start]sensitivity of the reagents[blank_end].
Low INR indicates a risk for [blank_start]clotting[blank_end] while high INR indicates a risk for [blank_start]bleeding[blank_end]. The usual range is 2-3.- Avitro
- BTF & CaCl
- Cpatient's
- Daverage
- Esensitivity of the reagents
- Fclotting
- Gbleeding
12Which of these is not a major determinant of warfarin dose requirements:
- AVitamin K status
- BDrug Interactions
- CGenetic differences (CYP2C9, VKORC1)
- DAge
- EBody size
- FSex
13Most clinically important interactions with warfarin are well understood and can be predicted.
I.e these drugs:
• Inhibition of CYP2C9, e.g. [blank_start]amiodarone, fluconazole[blank_end]
• Induction of CYPs, e.g. [blank_start]phenytoin, rifampin[blank_end]
• Inhibition if CYP3A4, 1A2 e.g. [blank_start]quinolones, macrolides, azoles[blank_end]
Will affect the warfarin metabolism significantly.- Aamiodarone, fluconazole
- Bphenytoin, rifampin
- Cquinolones, macrolides, azoles
14Occasional consumption of vitamin K rich food is unlikely to be important in most patients but in the elderly and malnourished, vitamin K deficiency may increase risk of bleeding.
- ATrue
- BFalse
15Thrombolytic drugs (also called fibrinolytics) work by activating [blank_start]plasminogen[blank_end], to produce plasmin. [blank_start]Plasmin[blank_end] breaks cross-links between [blank_start]fibrin[blank_end] molecules, disrupting the structural integrity of blood clots. They restore blood flow more [blank_start]quickly[blank_end] than anticoagulants but carry a much higher [blank_start]risk[blank_end] of bleeding.
- Aplasminogen
- BPlasmin
- Cfibrin
- Dquickly
- Erisk
16t-PA binds to fibrin, converts plasmin to plasminogen, which digests fibrin.
- ATrue
- BFalse
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- User has deleted their subject information Quiz on L47 Anticoagulation, created by Deleted user on 26/05/2019.
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- Created on 26 May 2019 · updated on 26 May 2019
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