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CPT Summaries > Anticoagulants > Flashcards

Anticoagulants Flashcards

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1
Q

What is heparin?

A

An injectable, rapidly acting anticoagulant that is often used acutely to interfere with the formation of thrombi

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2
Q

What is unfractionated heparin?

A

A mixture of straight-chain, anionic glycosaminoglycans with a wide range of molecular weights

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3
Q

What are low-molecular weight heparins?

A

Heterogenous compounds (1/3 of size of unfractionated heparin) produced by the chemical or enzymatic depolymerisation of unfractionated heparin

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4
Q

What is the mechanism of action of the anti-coagulant effect of heparin?

A

Binds to antithrombin III, with subsequent rapid inactivation of coagulation factors

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5
Q

What is antithrombin III?

A

An alpha-globulin that inhibits serine proteases, including several clotting factors including thrombin and factor Xa

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6
Q

What is the mechanism of action of LMWH?

A

Complexes with antithrombin III, and inactivates factor Xa (but does not bind avidly to thrombin)

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7
Q

What are the indications for heparin?

A
  • Treatment of acute deep vein thrombosis and pulmonary embolism
  • Prophylactic prevention of post-operative venous thrombosis in patients undergoing elective surgery, and those in acute phase of MI
  • Use of extracorporeal devices, e.g. dialysis machines, to prevent thrombosis
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8
Q

Why is heparin and LMWH the treatment of choice when indicated in pregnancy?

A

Because these agents do not cross the placenta, due to their large size and negative charge

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9
Q

What is the advantage of heparin over LMWH?

A

Speedy onset of action, and rapid termination of action on suspension of therapy

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10
Q

What is the advantage of LMWH over heparin?

A
  • Convenient subcutaneous injection, predictable therapeutic effects, and more predictable pharmacokinetic profile.
  • Do not require same intense monitoring.
  • Good for inpatient and outpatient therapy.
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11
Q

How is heparin administered?

A

Parenterally, either in deep SC site or IV

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12
Q

Why must heparin be administered parenterally?

A

Because drug does not readily cross membranes

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13
Q

How is LMWH administered?

A

SC infection

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14
Q

Why is IM administration contraindicated in heparin and LMWH?

A

Haematoma formation

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15
Q

In whom might the dose of heparin need to be adjusted?

A

Renal failure

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16
Q

Why does heparin have unpredictable pharmacokinetics?

A

Because in the blood, it binds to many proteins that neutralise its activity, thereby causing resistance to the drug and unpredictable pharmacokinetics

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17
Q

What can prolong the half-life of heparin?

A
  • Hepatic cirrhosos
  • Renal insufficiency
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18
Q

Why does hepatic cirrhosis prolong the half life of heparin?

A

Because some heparin in the blood is taken up by the monocyte/macrophage system, and undergoes depolymerisation and desulfation in the liver to inactive products

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19
Q

Why does renal insufficiency prolong the half life of heparin?

A

The inactive metabolites, as well as parent heparin and LMWH, are excreted into urine

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20
Q

What are the ADRs of heparin?

A
  • Haemorrhage
  • Hypersensitivity reactions
  • Thrombosis
  • Thrombocytopenia
  • Abnormal
  • LFTs
  • Osteoporosis
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21
Q

What is required to minimise the problem of bleeding with heparin therapy?

A

Careful monitoring of bleeding time

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22
Q

How can excessive bleeding due to heparin be managed?

A

Ceasing administration of the drug, or treating with protamine sulfate

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23
Q

How can heparin cause thrombosis?

A

Chronic or intermittent administration can lead to reduction in antithrombin III activity, thus decreasing inactivation of coagulation factors, and increasing the risk of thrombosis

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24
Q

How is the risk of heparin induced thrombosis minimised?

A

Low-dose heparin therapy is typically used

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25
Q

What should be done if a patient on heparin displays severe thrombocytopenia?

A

Discontinue and replace with another anticoagulant

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26
Q

In whom is heparin contraindicated?

A

Those who are hypersensitive to it, have bleeding disorders, are alcoholics, or have had recent surgery of brain, eye, or spinal cord

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27
Q

What is the mechanism of action of rivaroxiban?

A

It binds to the active site of factor Xa, thereby preventing its ability to convert prothrombin to thrombin

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28
Q

How is rivaroxiban administered?

A

Orally

29
Q

What is the therapeutic use of rivaroxiban?

A
  • Treatment and prevention of DVT and PE
  • Prevention of stroke in non-valvular AF
30
Q

Is rivaroxiban protein bound?

A

Yes, highly

31
Q

What might increase the absorption of rivaroxiban?

A

Food

32
Q

How does rivaroxiban compare to warfarin, in terms of patient safety?

A

It has fewer drug interations, therefore there are no laboratory monitoring requirements for either agent

33
Q

What is the most serious adverse effect of rivaroxiban?

A

Bleeding

34
Q

Is there an antidote available to reverse bleeding caused by rivaroxiban?

A

No

35
Q

What can increase the risk of bleeding with rivaroxiban?

A

Declining kidney function

36
Q

Why is there an increased risk of bleeding caused by rivaroxiban in declining kidney function?

A

As the drug is eliminated renally

37
Q

At what creatinine clearance should rivaroxiban not be used due to the risk of bleeding?

A

Less than 15mL/min

38
Q

What is the INR?

A

The standard by which the anticoagulant activity of warfarin therapy is monitored

39
Q

What does the INR correct for?

A

Variations that occur with different thromboplastin reagents used to perform testing at various institutions

40
Q

With regards to INR, what is the goal of warfarin therapy?

A

To achieve an INR or 2 to 3, or 2.5 to 3.5 for some mechanical valves or other indications

41
Q

Why is it important to keep INR within the optimal range as much as possible?

A

Because warfarin has a narrow therapeutic index

42
Q

What clotting factors require vitamin K for synthesis?

A

II, VII, IX, and X

43
Q

Where are clotting factors II, VII, IX, and X synthesised?

A

Liver

44
Q

What is the mechanism of action of warfarin?

A

It inhibits vitamin K epoxide reductase, which is required for the synthesis of vitamin K dependant clotting factors. This results in clotting factors with 10 to 40% of the normal activity, due to lack of gamma-carboxyglutamyl side chains

45
Q

How long after administration are the anti-coagulant effects of warfarin observed?

A

72 to 96 hours

46
Q

Why does it take 72-96 hours for the onset of anti-coagulant effects of warfarin?

A

This is the time required to deplete the pool of circulating clotting factors

47
Q

How can the anti-coagulant effects of warfarin be overcome?

A

By administration of vitamin K

48
Q

How long does warfarin reversal following the administration of vitamin K take?

A

24 hours

49
Q

Why does warfarin reversal by the administration of vitamin K take 24 hours?

A

This is the time necessary for the degradation of already synthesised clotting factors

50
Q

What are the therapeutic uses of warfarin?

A
  • Prevention and treatment of DVT and PE
  • Stroke prevention, including in the setting of atrial fibrillation and/or prosthetic heart valves, protein C or S deficiency, and antiphospholipid syndrome
  • Prevention of venous thromboembolism during orthopedic or gynecologic surgery
51
Q

How is warfarin administered?

A

Orally

52
Q

What is the bioavailability of warfarin?

A

100%, with little individual patient variation

53
Q

Is warfarin bound to plasma albumin?

A

Yes, highly

54
Q

What is the result of the high protein binding of warfarin on its diffusion?

A

It prevents diffusion into cerebrospinal fluid, urine, and breast milk

55
Q

What might displace warfarin from albumin binding sites?

A

Drugs that have a greater affinity for the albumin binding site, such as sulfonamides

56
Q

What effect might drugs that displaced warfarin from albumin have?

A

They might cause a transient elevated activity, leading to variation in the therapeutic response to warfarin

57
Q

Does warfarin cross the placental barrier?

A

Yes, readily

58
Q

What is the half life of warfarin?

A

Mean half life is about 40 hours, but highly variable among individuals

59
Q

How is warfarin eliminated from the body?

A

It is metabolised by the CYP450 system to inactive components, which are then excreted in urine and faeces

60
Q

What might affect the therapeutic effects of warfarin?

A

Drugs that affect the metabolism of warfarin

61
Q

What drugs might inhibit the metabolism of warfarin?

A
  • Acute alcohol ingestion
  • Amiodarone
  • Fluconazole
  • Metronidazole
  • Trimethoprim
62
Q

What drugs might stimulate the action of warfarin?

A
  • Chronic alcohol ingestion
  • Barbiturates
  • Dicloxacillin
  • Rifampicin
63
Q

What are the adverse effects of warfarin?

A
  • Haemorrhage
  • Skin lesions and necrosis
  • Purple tow syndrome
  • Teratogenesis
64
Q

What is required due to the risk of haemorrhage with warfarin therapy?

A

Frequent monitoring of INR, with dose adjustment if necessary

65
Q

How can minor bleeding caused by warfarin be treated?

A

Withdrawal of the drug, or administration of oral vitamin K

66
Q

How can major bleeding caused by warfarin be treated?

A
  • Intravenous vitamin K
  • Whole blood
  • Frozen plasma
  • Plasma concentrates of blood factors
67
Q

What is purple-toe syndrome?

A

A rare, painful, blue-tingled discolouration of the toe caused by cholesterol emboli from plaques

68
Q

What can be used if anti-coagulant therapy is required during pregnancy?

A

Heparin or LMWH

CPT Summaries (8 decks)

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