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3/4: YX - CPT Summaries > Anticoagulants > Flashcards

Anticoagulants Flashcards

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
What should be done if a patient on heparin displays severe thrombocytopenia?
Discontinue and replace with another anticoagulant
26
In whom is heparin contraindicated?
Those who are hypersensitive to it, have bleeding disorders, are alcoholics, or have had recent surgery of brain, eye, or spinal cord
27
What is the mechanism of action of rivaroxiban?
It binds to the active site of factor Xa, thereby preventing its ability to convert prothrombin to thrombin
28
How is rivaroxiban administered?
Orally
29
What is the therapeutic use of rivaroxiban?
* Treatment and prevention of DVT and PE * Prevention of stroke in non-valvular AF
30
Is rivaroxiban protein bound?
Yes, highly
31
What might increase the absorption of rivaroxiban?
Food
32
How does rivaroxiban compare to warfarin, in terms of patient safety?
It has fewer drug interations, therefore there are no laboratory monitoring requirements for either agent
33
What is the most serious adverse effect of rivaroxiban?
Bleeding
34
Is there an antidote available to reverse bleeding caused by rivaroxiban?
No
35
What can increase the risk of bleeding with rivaroxiban?
Declining kidney function
36
Why is there an increased risk of bleeding caused by rivaroxiban in declining kidney function?
As the drug is eliminated renally
37
At what creatinine clearance should rivaroxiban not be used due to the risk of bleeding?
Less than 15mL/min
38
What is the INR?
The standard by which the anticoagulant activity of warfarin therapy is monitored
39
What does the INR correct for?
Variations that occur with different thromboplastin reagents used to perform testing at various institutions
40
With regards to INR, what is the goal of warfarin therapy?
To achieve an INR or 2 to 3, or 2.5 to 3.5 for some mechanical valves or other indications
41
Why is it important to keep INR within the optimal range as much as possible?
Because warfarin has a narrow therapeutic index
42
What clotting factors require vitamin K for synthesis?
II, VII, IX, and X
43
Where are clotting factors II, VII, IX, and X synthesised?
Liver
44
What is the mechanism of action of warfarin?
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
How long after administration are the anti-coagulant effects of warfarin observed?
72 to 96 hours
46
Why does it take 72-96 hours for the onset of anti-coagulant effects of warfarin?
This is the time required to deplete the pool of circulating clotting factors
47
How can the anti-coagulant effects of warfarin be overcome?
By administration of vitamin K
48
How long does warfarin reversal following the administration of vitamin K take?
24 hours
49
Why does warfarin reversal by the administration of vitamin K take 24 hours?
This is the time necessary for the degradation of already synthesised clotting factors
50
What are the therapeutic uses of warfarin?
* 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
How is warfarin administered?
Orally
52
What is the bioavailability of warfarin?
100%, with little individual patient variation
53
Is warfarin bound to plasma albumin?
Yes, highly
54
What is the result of the high protein binding of warfarin on its diffusion?
It prevents diffusion into cerebrospinal fluid, urine, and breast milk
55
What might displace warfarin from albumin binding sites?
Drugs that have a greater affinity for the albumin binding site, such as sulfonamides
56
What effect might drugs that displaced warfarin from albumin have?
They might cause a transient elevated activity, leading to variation in the therapeutic response to warfarin
57
Does warfarin cross the placental barrier?
Yes, readily
58
What is the half life of warfarin?
Mean half life is about 40 hours, but highly variable among individuals
59
How is warfarin eliminated from the body?
It is metabolised by the CYP450 system to inactive components, which are then excreted in urine and faeces
60
What might affect the therapeutic effects of warfarin?
Drugs that affect the metabolism of warfarin
61
What drugs might inhibit the metabolism of warfarin?
* Acute alcohol ingestion * Amiodarone * Fluconazole * Metronidazole * Trimethoprim
62
What drugs might stimulate the action of warfarin?
* Chronic alcohol ingestion * Barbiturates * Dicloxacillin * Rifampicin
63
What are the adverse effects of warfarin?
* Haemorrhage * Skin lesions and necrosis * Purple tow syndrome * Teratogenesis
64
What is required due to the risk of haemorrhage with warfarin therapy?
Frequent monitoring of INR, with dose adjustment if necessary
65
How can minor bleeding caused by warfarin be treated?
Withdrawal of the drug, or administration of oral vitamin K
66
How can major bleeding caused by warfarin be treated?
* Intravenous vitamin K * Whole blood * Frozen plasma * Plasma concentrates of blood factors
67
What is purple-toe syndrome?
A rare, painful, blue-tingled discolouration of the toe caused by cholesterol emboli from plaques
68
What can be used if anti-coagulant therapy is required during pregnancy?
Heparin or LMWH

3/4: YX - CPT Summaries (8 decks)

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