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Fundamentals 3- Heme > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

How does aspirin work as an anticoagulant?

A

It inhibits platelet aggregation but irreversible acetylating COX1 which blocks the synthesis of TXA2 (a promoter of platelet aggregation).
It also blocks PGI2 (an inhibitor of platelet aggregation) but PGI2 comes from endothelial cells which can synthesize more. TXA2 comes from platelets which don’t have nuclei to synthesize more.

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2
Q

How is aspirin administered?

What dose achieves maximum antithrombotic effect?

A

Orally- rapid action 2hrs.

80-325mg

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3
Q

What are the adverse effects of using aspirin?

A
  1. Hemorrhage- a single dose of aspirin increases the bleeding risk for 4-7 days
  2. GI ulcers (rare at 80-325mg) in ppl on steroids
  3. ASA intoxication
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4
Q

Aspirin use is contraindicated in what 4 patients?

A
  1. severe hepatic damage
  2. hypoprothrombinemia
  3. vit K deficient
  4. hemophilia

Basically people that were already at an increased bleeding risk

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5
Q

What are the 4 therapeutic uses of aspirin?

A
  1. prevent a stroke in patients with transient ischemic attack
  2. prevent occlusive cardiovascular diseas in patients with MI or unstable angina
  3. increase saphenous vein patency in bypass grafts
  4. prophylaxis in patients at risk for a myocardial infarction
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6
Q

What age should women start taking aspirin prophylactically to decrease risk of MI?
Men?
Why not younger?

A

Women- 55
Men- 45

If they were younger the benefit would be offset by the increased risk of hemorrhagic stroke

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7
Q

What is the mechanism of clopidogrel?

A

It inhibits platelet ADP receptors which prevents activation of GpIIb/IIIa.

This reduces:

  1. fibrinogen and vWF binding
  2. platelet aggregation
  3. clot retraction.
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8
Q 
Describe the pharmacokinetics of clopidogrel.
Administration
Mechanism
Time of onset
Duration
A

It is an orally administered prodrug that becomes converted to metabolites by hepatic cyp metabolism.
The metabolites irreversible bind ADP receptors which prevent GpIIb/IIIa activation.

Onset is slow (several days) because it needs to be converted before action
It has prolonged action after discontinuation

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9
Q

What are the adverse effects of clopidogrel?

A

rashes, diarrhea, neutropenia, bleeding

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10
Q

What are the therapeutic uses of clopidogrel?

A
  1. Reduce MI, stroke, vascular deaths in patients with coronary syndrome
  2. reduce stint occlusion
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11
Q

What is the mechanism of GpIIb/IIIa blockers?
How are they administered?
What is their major adverse effect?

A

They inhibit:

  1. fibrinogen and vWF binding
  2. prevent clot retraction
  3. block platelet binding in the presence of agonists like ADP, TXA2, thrombin and collagen)

They are administered IV with:

  1. Heparin and ASA
  2. clopidogrel

They can cause bleeding

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12
Q

What are the two main reasons to use anticoagulant drugs?`

How do they achieve their purpose?

A
  1. to reduce risk of thrombosis or embolism
  2. to prevent extension of current venous thrombus

They block coagulation cascade. They cannot dissolve an existing thrombus but can prevent extension of the thrombus and block formation of new thrombi.

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13
Q

What are the four major mechanisms of thrombin?

A
  1. Fibrinogen–> fibrin
  2. activate factors 5 and 8
  3. activate factor 11
  4. activate factor 13
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14
Q

What is the mechanism of Heparin?.

A

It is a sulfated mucopolysaccharide with an electronegative charge that interacts with antithrombin III to increase the ability of ATIII to neutralize factor Xa and thrombin.

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15
Q

What coagulation factors does thrombin affect?

A

Factor Xa and thrombin (ACTIVATED FACTORS)

It has no effect on factor X or prothrombin, the inactive precursors

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16
Q

What is LMWH? How is its action different from that of heparin?

A

Low molecular weight heparin is hydrolyzed heparin that has a MW of 4-5 kDalton instead of 15.
Like heparin, LMWH binds to antithrombin III to enhance its effects.
The difference is that LMWH and fondaparinux bind ATIII and inactivate Xa but they have little effect on thrombin.

17
Q

How must heparin, LMWH and fondaparinux be administered?

How frequently are they administered?

A

They have an electronegative charge and are large so they can’t be absorbed in the GI.
They are administered SC or IV.
Heparin IV is repeated every 4-8 hours
LMWH is SC every 12-24 hours

18
Q

What is the difference in IV heparin administration and SC administration?

A

IV is immediate

SC is delayed 20-60 minutes

19
Q

What are the two general adverse reactions to heparin or LMWH?

A
  1. Hemorrhage

2. Thrombocytopenia

20
Q

What is the incidence of serious bleeding when given:

  1. heparin
  2. LMWH
  3. fondaparinux

How can bleeding by heparin or LMWH be reversed?

A
  1. 1-4%
  2. 1-3%
  3. 1-2%

Bleeding is reversed with protamine sulfate which is positively charged and binds the electronegative heparin molecule. NO reversal for fondaparinux.

21
Q

Who would the use of heparin be contraindicated in?

A
  1. recent brain or eye surgery
  2. thrombocytopenia
  3. uremia
  4. history of bleeding
  5. on current platelet inhibitor
22
Q

What causes HIT?

How can it be prevented?

A

Heparin induced thrombocytopenia is caused by the generation of heparin-dependent antibodies.
The antibodies cause platelet activation, thrombocytopenia, and thrombosis.

There are screening methods to detect the presence of heparin-dependent antibodies.

23
Q

What are the therapeutic uses of heparin?

A
  1. venous thrombosis and PE, manage MI, angina, during/after coronary angioplasty or stent placement, cardiopulmonary bypass surgery
  2. Prevention/treatment of venous thromboembolism in hip-replacement patients
  3. Anti-coagulation during pregnancy
24
Q

What is warfarin? What is the method of action?

A

Super warfarin is rat poison that causes internal bleeding and death in rats
Warfarin is an antagonist to Vitamin K which inhibits the synthesis of coagulation factors 2,7,9,10 in the liver. (it also inhibits the anti-coagulants protein C and S)

25
Q

Describe the vitamin K dependent reaction required by coagulation factors 2.7.9.10.

A

Vitamin K helps for the post-translational carboxylation of glutamate residues on the factors.
This is necessary to allow the AA to bind Ca required to bind PL and form coagulation complexes

26
Q

How is warfarin administered?
How long does it take to achieve full anticoagulant effect?
What is the duration of action?

A

It is given orally and takes 48 hours to achieve full effect because the active factors have to be depleted and then it inhibits the production of new factors.
The duration of action is 2 to 5 days.

27
Q

Why must you give heparin with warfarin for the first 2 days?

A

Because warfarin will inhibit protein C (anticoagulant) first. leading to excessive coagulation.
This is why you “bridge” with heparin

28
Q

What are the 6 types of drug interactions with warfarin?

A
  1. Absorption- cholestyramine interrupts enterohepatic circulation and excretes warfarin in stool
  2. Binding- drugs can displace warfarin bound to albumin increasing serum concentration
  3. Metabolism- drugs that induce p450 will lower blood warfarin. drugs that inhibit p450 will increase blood warfarin
  4. Diuretics increase clearance of warfarin
  5. Antibiotic kill vitamin K producing bacteria and increase anti-coagulation effect of warfarin
  6. Aspirin- worsens bleeding by inactivating platelets
29
Q

What is the major side effect of warfarin?

How can an overdose be reversed?

A

Hemorrhage.
Reversed by administration:
1. vitamin K - slow reversal for not that severe
2.FFP (that has all factors, not just vit K dependent ones) for immediate/fast reversal

30
Q

In addition to hemorrhage, what other serious adverse affect is associated with warfarin?

A

It can cause birth defects and abortions because it inhibits important vitamin K-dependent steps in fetal development

31
Q

What are the three main therapeutic uses of warfarin?

A
  1. prevent venous thrombosis and PE after trauma, surgery, disease. (use heparin bridge)
  2. treat overt thrombosis
  3. stop blood from coagulating on artificial surfaces like artificial heart valves, renal dialysis machines etc
32
Q

What are direct thrombin inhibitors (bivalirudin and argatroban) used for?

What is the major adverse effect?

A
  1. treatment of HIT
  2. prevent venous thrombosis, PE in patients where heparin is contraindicated

Major adverse effect is major bleeding

33
Q

What is the mechanism of action of tPA?

A

tissue-plasminogen activator is a recombinant thrombolytic protein that converts:

Plasminogen bound to fibrin clots–> plasmin–> dissolved clot

34
Q

t-PA is highly specific for plasminogen that is _____________.
It is more effective on _______clots than ______clots.

A

specific for plasminogen bound to clots.
More effective on recent clots than older clots.
Therapy should be started ASAP (within 6 hours for MI, 4.5 for stroke)

35
Q

How is tPA administered?
How soon after MI should it be given?
How soon after stroke?

A

It is a protein so NOT absorbed by GI.
Infused or injected IV.
within 6 hours of MI and 4.5 hours of stroke

36
Q

What is the main adverse effect of tPA?

A

bleeding

37
Q

What are the 5 therapeutic uses for tPA?

A
  1. acute MI
  2. acute ischemic stroke
  3. massive PE with blood flow <50%
  4. severe acute arterial thrombosis
  5. occluded A-V cannulae in dialysis patients

Fundamentals 3- Heme (19 decks)

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