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Drugs Used In Coagulations Disorders II: Anticoagulant Drugs Flashcards

1
Q

What are the endogenous inhibitors of coagulation?

A

Protein C
Protein S
Antithrombin III
Tissue factors pathway inhibitor (TFPI)

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2
Q

What type of enzyme is Antithrombin III?

A

Serine protease inhibitor

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3
Q

What is the mechanism of action of ATIII?

A

It inactivated Thrombin and Xa

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4
Q

What is the mechanism of action of Heparin?

A

Heparin forms a complex with ATIII, thereby inactivating thrombin and factor Xa

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5
Q

Where is heparin produced?

A

Mast cells

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6
Q

What is the chemical nature of heparin?

A

Large polysaccharide

Water soluble

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7
Q

What is the clinical indication of UFH and LMWH?

A

The prevention of fibrin formation

  1. Acute thromboembolism (DVT, PE and arterial emboli)
  2. Prophylaxis of post-op VT and recurrent TE
  3. ACS (MI, unstable angina)
  4. Anticoagulant therapy during pregnancy
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8
Q

What is the dosage of UFH in prophylactic use?

A

Prophylactic use: 2-3 x 5000-7500 IU or 5-7 IU/kg/h (IV infusion)

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9
Q

What is the dosage of UFH in acute therapy?

A

Starts with 5000 IU bolus — later 1000-15000 IU/h (IV infusion)

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10
Q

What is the dosage of LMWH in prophylactic use?

A

2500-5000 IU 1/day

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11
Q

What is the dosage of LMWH in acute treatment?

A

175-200 IU/Kg S.C. 1 or 2/day

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12
Q

What is the half life of UFH?

A

60-90 min half life

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13
Q

What is the half life of LMWH?

A

2-4h half life (longer in kidney insufficiency)

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14
Q

Does UFH and LMWH have good or bad absorption?

A

Bad

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15
Q

How are UFH and LMWH administered?

A

Only parenteral: IV or SC

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16
Q

What is the bioavailability of UFH after SC administration?

A

30%

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17
Q

What is the bioavailability of LMWH after SC administration?

A

90%

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18
Q

Do LMWH and UFH cross the placenta?

A

No

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19
Q

What anticoagulant drug should be used in pregnancy?

Why?

A

UFH and LMWH

Because both are large, water soluble polysaccharides that are unable to cross the placenta.

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20
Q

What does UFH bind to?

A

Binds to endothelium, macrophages, plasma proteins. These sites must be saturated 1st - this complicates elimination

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21
Q

What does LMWH bind to?

A

Limited binding to endothelium, macrophages and plasma proteins. Therefore there is a more predictable dose effect relationship and elimination.

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22
Q

How do we monitor UFH?

What is the control value

A
  • aPTT

- 1.5-2.5

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23
Q

Does UFH or LMWH have more predictable pharmacokinetics?

A

LMWH

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24
Q

Is heparin used for rapid or long term anticoagulation?

A

Rapid

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25
Q

What is the antagonist of heparin?

What type of antagonism is this?

A

Protamine sulfate

Chemical antagonism (no receptor required)

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26
Q

In which are side effects less frequent?

A

LMWH

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27
Q

What are the severe adverse affects of UFH and LMWH?

A

Bleeding
HIT
Osteoporosis
Hypersensitivity

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28
Q

What are the rare adverse affects of UFH and LMWH use?

A 
Hair loss
Hypersensitivity 
Mild transaminase elevation
Hypoaldosterone (at high doses)
Hyperkalemia
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29
Q

Bleeding as a side effect of UFH or LMWH use is associated with what?

A

IV therapy

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30
Q

What is the clinical indication of Fondaparinux?

A

DVT
PE
Prophylaxis of VTE in orthopaedic surgery

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31
Q

What is the half life of Fondaparinux?

A

15-17h

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32
Q

How is Fondaparinux administered?

A

Parenteral (S.C)

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33
Q

What is the bioavailability of Fondaparinux when administered SC?

A

100%

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34
Q

What are the side effects of Fondaparinux?

A

Bleeding

Not HITII, thus no reversal by protamine sulphate

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35
Q

What is HIT type 1?

A

Reversible
Transient
5-10%

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36
Q

What is HIT type 2?

A

0.5-3% occurrence
Very dangerous 20-30% lethality
Ab mediated thrombocyte aggregation - paradoxically thromboembolic complications

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37
Q

What is the treatment of HIT type 2?

A

Protamine sulfate

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38
Q

What is the mechanism of action of Fondaparinux?

A

It is an analogue of the heparin binding site on antithrombin III
Selective inhibition of factors Xa by binding and potentiating antithrombin III
- higher specificity than LMWH

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39
Q

What is the mechanism of action of Danaparoid?

A

Inactivates factor Xa by accelerating antithrombin III

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40
Q

What is the half life of Danaparoid?

A

25h

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41
Q

How is Danaparoid administered?

A

Parenteral (SC)

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42
Q

What is the bioavailability of Danaparoid when administered SC?

A

100%

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43
Q

What is the side effect of Danaparoid?

A

Bleeding (not antagonised by protamine sulphate)

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44
Q

What is the side effect of Hirudin?

A

Bleeding

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45
Q

What is the side effect of Bivalirudin?

A

Bleeding

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46
Q

What is the side effect of Argatroban?

A

Bleeding

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47
Q

What is the side effect of Dabigatran etexilate?

A 
Bleeding
GI discomfort (abdominal pain, esophagus is, GI bleeding)
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48
Q

What is the mechanism of action of Hirudin?

A

Direct thrombin inhibitor

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49
Q

How is Hirudin eliminated?

A

Through the kidney

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50
Q

What is the half life of Hirudin?

A

1-1.5h

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51
Q

How is Hirudin eliminated?

A

Through the kidney

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52
Q

How is Hirudin administered?

A

Parenteral use (SC)

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53
Q

What is the bioavailability of Hirudin when administered SC?

A

100%

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54
Q

How is Hirudin monitored?

A
  • aPTT

- Should be 1.5-3 x higher than control

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55
Q

What is the mechanism of action of Bivalirudin?

A

Direct thrombin inhibitor

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56
Q

What is the clinical indication of Bivalirudin?

A

Used during PCR in patients having or at risk of having HIT

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57
Q

How is Bivalirudin administered?

A

IV

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58
Q

How is Bivalirudin monitored?

A
  • aPTT
  • Hemoglobin
  • Hematocrit
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59
Q

How is Bivalirudin eliminated?

A

Elimination is mostly independent from the kidney

60
Q

What is the onset and duration of action of Bivalirudin?

A

Faster onset and shorter duration of action than Hirudin

61
Q

What is the mechanism of action of Argatroban?

A

Direct thrombin inhibitor

62
Q

What is the clinical indication of Argatroban?

A

HIT type II
Prophylaxis of treatment of VTE in patients with HIT
Used during PCI in patients having or at risk of having HIT

63
Q

What is the half life of Argatroban?

A

Short half life

64
Q

What is the administration of Argatroban?

65
Q

How is Argatroban eliminated?

A

Elimination is independent from the kidney (influenced by liver disease)

66
Q

What is the mechanism of action of Dabigatran etexilate?

A

Direct thrombin inhibitor

Direct oral anticoagulant prodrug

67
Q

What are the clinical indications of Dabigatran etexilate?

A

Prophylaxis of stroke and systemic embolism in patients with non-valvular atrial fibrillation

68
Q

How is Dabigatran etexilate administered?

A

Oral

1-2 x day

69
Q

What is the antidote for Dabigatran etexilate?

A

Idarucizumab (Ab)

70
Q

How is Dabigatran etexilate activated?

A

After absorption, conversion to dabigatran and activation

71
Q

What is the mechanism of action of Rivaroxaban and Apixaban?

A

Direct Xa inhibitors

Direct oral anticoagulant (DOA)

72
Q

What is the antidote for Rivaroxaban and Apixaban?

A

Idarucizumab

73
Q

How are Rivaroxaban and Apixaban administered?

A

Oral 2x/day

74
Q

What is the clinical use of Rivaroxaban and Apixaban?

A

Prophylaxis and treatment of DVT and PE in patients having knee or hip replacement surgery
Prophylaxis of systemic embolism with non-valvular A fib

75
Q

Name the Coumarin drugs

A

Acenocoumarol
Warfarin
Phenprocoumon

76
Q

What is the half life of warfarin?

77
Q

What is the half life of Acenocoumarol?

78
Q

What is the half life of Phenprocoumon?

79
Q

What are the clinical indications of coumarin like drugs?

A

Continuation of heparin therapy

Prophylaxis for TE (in long term treatment: A-fib and DVT)

80
Q

What is the dose of Warfarin?

81
Q

What is the dose of Acenocoumarol?

82
Q

What is the dose of Phenprocoumon?

83
Q

What is the mechanism of action of Coumarin type drugs?

A

They block vitamin K epoxide reductase resulting in functionally inactive clotting factors II, VII, IX, X protein S and Protein C.

Synthesis of these clotting factors requires a gamma carboxylation on glutamate residues necessary for Calcium binding and thus binding to phospholipids.

Gamma carboxylation is coupled with oxidation of reduced vitamin K to epoxide form

84
Q

How are the Coumarin type of drugs administered?

85
Q

What is the cause of Coumarin sensitivity?

A

Genetic polymorphism of the Coumarin metabolising enzyme CYP2C9 resulting in its decreased activity

86
Q

What is the coumarin metabolising enzyme?

87
Q

How are the Coumarin type drugs eliminated?

A

Through the urine and bile

88
Q

Where are the Coumarin type drugs metabolised?

A

Liver (glucuronidation)

89
Q

What is the absorption of coumarin type drugs?

A

Good absorption - almost 100%

90
Q

What is the antidote for Coumarin type drugs?

A

Rapid antidote - fresh frozen plasma (as it contains the active coagulant factors)
Delayed antidote - antagonised effect by vitamin K1 administration

91
Q

What is the normal INR?

92
Q

How is Coumarin monitored?

A

INR

and PT

93
Q

What is the therapeutic INR goal in Coumarin use?

94
Q

What is the INR goal in prophylactic use of coumarin?

95
Q

When are Coumarin type drugs contraindicated?

A

Pregnancy
Nursing women
Active bleeding
Increased risk of dangerous bleeding

96
Q

Is there a possibility to develop a resistance to coumarin?

97
Q

Why is it possible to develop a resistance to coumarin?

A

Due to a mutation of Vit K epoxide reducatase

98
Q

When is there a strong risk of bleeding in Coumarin administration?

A

If the INR >4

99
Q

What are the side effects of Coumarin?

A

Bleeding (minor: 10-20%, major: 5%, lethal: 1%)
Teratogenic malformations, death of Fetus
Necrosis of subcutaneous tissue and skin (rare)

100
Q

What is the cause of the necrosis of subcutaneous tissue and skin in coumarin use?

A

Protein C is also Vit K dependent. Protein C is an endogenous anti-coagulant and has a short half life (the shortest after factor 7) - therefore there is a prominent inhibition of protein C in the 1st week which results in a hypercoaguable state the increased risk of TE.

101
Q

What are the rare side effects of coumarin administration?

A

Allergic reactions
GI symptoms
Alone is
Purple toe syndrome

102
Q

What does vitamin K concentration in the blood depend on?

A

Diet and intestinal bacterial flora

103
Q

At absorbtion, what are Coumarin type drugs inhibited by?

A

Antacids

Cholestyramine

104
Q

What CYP450 enzyme inhibitors?

A 
Phenylbutazone
Sulfinpyrazone
Metronidazole
Fluconazole
Sulphonamides
Amiodarone
Disulfiram
Citemidine
105
Q

What are CYP450 enzyme inducers?

A 
Barbiturates
Rifampin 
Carbamazepine
Phenytoin
Griesofulvin
106
Q

What will warfarin administration do to the INR?

A

Increased INR

107
Q

What will the use of CYP450 inhibitors do to the INR when warfarin is also administered?

A

INR increased

108
Q

What will CYP450 inducers do to the INR if administered with warfarin?

A

INR will decreases

109
Q

What is the mechanism of thrombin?

A

It converts soluble fibrinogen to insoluble fibrin (clot)

110
Q

Why does HIT result in a hyper coagulable state?

A

Because the damaged platelets result factors that activate thrombin

111
Q

What is the pathomechanism of HIT?

A

Abs are generated against heparin and platelet factor 4

112
Q

What is the mechanism of Xa?

A

It converts prothrombin to thrombin

113
Q

When should LMWH be avoided?

A

In renal insufficiency. LMWH is eliminated in the kidney so renal insufficiency can lead to high plasma levels of LMWH that are hard to monitor.

114
Q

What does aPTT measure?

A

The common and intrinsic pathway

115
Q

When is heparin administered IV?

A

In acute cases:
DVT
PE
MI

116
Q

When is Heparin administered SC?

A 
In prophylactic cases:
Pregnancy
Surgery
Malignancy 
Immobilisation 
History of oral contraceptive use
117
Q

Why is hyperkalemia a side effect of UFH use?

A

UFH can lead to hypoaldosteremia leading to hyperkalemia

118
Q

What is the antidote of UFH?

A

Protamine sulfate (+)

119
Q

What is the mechanism of action of LMWH?

A

Forms a complex with ATIII and inactivates Xa

120
Q

What drugs is protamine sulphate less effective against?

121
Q

Does LMWH have a short or prolonged half life compared to UFH?

122
Q

Does LMWH require continuous and strict monitoring?

A

Not as much as UFH

123
Q

How is UFH eliminated?

124
Q

Is heparin safe in pregnancy?

125
Q

Which anti-coagulant infers the lowest risk of HIT?

A

Fondaparinux

126
Q

What are the indirect anticoagulants?

A

UFH
LMWH
Fondaparinux

127
Q

What are the direct thrombin inhibitors?

A
  • Bivalirudin
  • Argatroban
  • Dabigatran
128
Q

What are the direct factor Xa inhibitors?

A

Rivaroxaban

Apixaban

129
Q

How are Rivaroxaban and Apixaban administered?

130
Q

Is there need to monitor Rivaroxaban and Apixaban?

A

Not so much

131
Q

What are the Vitamin K dependent coagulation factors?

A

Factor 2, 7 9 and 10

Protein S and Protein C

132
Q

What does warfarin block?

A

Vit K epoxide reductase

133
Q

Which coagulation factor has the shortest half life? What is that half life

A

Factor VII

6 hours

134
Q

What is the serum half life of warfarin?

A

36-42 hours

135
Q

What does PT measure?

A

The function of the extrinsic pathway

136
Q

What is the extrinsic pathway dependent on?

A

Factor VII

137
Q

What is the clinical indication of warfarin?

A
  • A fib

- Tx and prophylaxis of DVT and PE.

138
Q

Why does warfarin have a delayed onset of action?

A

Because it works at the level of transcription. So you have to wait for circulating activated factors to be eliminated before it works.

139
Q

Can warfarin be used in pregnancy?

140
Q

When is warfarin induced tissue necrosis most likely?

A

In Protein C deficiency

141
Q

How can you reverse warfarin anticoagulation?

A

Vit K - but the response is delayed

142
Q

What enzyme metabolises warfarin?

143
Q

Which anti-coagulant drugs are part of an inactivation complex?

A

Heparin
LMWH
Danaparoid
Fondaparinux

144
Q

What anti-coagulants are direct thrombin inhibitors?

A

Hirudin
Bivalirudin
Argatroban
Dabigatran

145
Q

What are the direct factor Xa inhibitors?

A

Rivaroxaban
Apixaban
Endoxaban
Betrixaban

Pharma (23 decks)

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