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PR3154 > IC3 - Blood pharmacology > Flashcards

IC3 - Blood pharmacology Flashcards

1
Q

Name four antiplatelet agents.

A

Dipyridamole, Aspirin, Clopidogrel, Ticagrelor

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2
Q

Which class of drugs does dipyridamole belongs to?

A

Adenosine uptake and PDE3 inhibitor

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3
Q

How does Dipyridamole works?

A
  1. Increases the plasma adenosine and activation of A2 receptors on platelets
  2. Inhibits the PDE3 inhibitor and decrease cGMP degradation within platelets

1+2 = increase cAMP = decrease platelet activation and aggregation

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4
Q

Dipyridamole is a _______ and it affects the vascular smooth muscle.

A

vasodilator

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5
Q

Why is dipyridamole used as an adjunct antiplatelet?

A

It causes hypotension when used at planned dose as it is a vasodilator.

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6
Q

List 2 common side effects of dipyridamole.

A

Hypotension, Headache

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7
Q

How is dipyridamole given?

A

Oral (modified-release preparation)

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8
Q

Why is dipyridamole given as a modified release preparation?

A

Short duration of action of 3 hours

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9
Q

Which population should dipyridamole be used with caution in?

A

Hypotension and severe coronary artery disease (due to vasodilating effects)

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10
Q

List the DDI for dipyridamole.

A
  1. Increases adenosine, increased cardiac adenosine levels and effects (heart problems)
  2. Decreases Cholinesterase inhbitor = increase myasthenia gravis
  3. Heparin = increase risk of bleed
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11
Q

Which class of drugs does aspirin belong to?

A

NSAID (irreversible COX inhibitor)

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12
Q

Why is a low dose aspirin favored as antiplatelet?

A
  1. Aspirin inhibits COX1 better than COX2.
  2. TXA2 production favoring platelet aggregation restores in 7 to 10 days.
  3. PGI2 production inhibiting platelet aggregation restores in 3 to 4 hours.
  4. Giving in lower dose, PGI2 can be restored quickly to exert its antiplatelet effect as new COX2 will not be inhibited.
  5. Meanwhile TXA2 will continue to be inhibited as time is need to restore new COX1
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13
Q

How does aspirin works?

A

It inhibits platelet production of TXA2.

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14
Q

What are the adverse effects related to aspirin?

A
  1. Upper GI events (ulcers, bleed) - COX1 which has protective prostaglandin is inhibited.
  2. Bruising and bleeding
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15
Q

Which population should aspirin be used in caution with?

A

Platelet and bleeding disorders

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16
Q

What are the DDI related to aspirin?

A

Increased bleeding when used with other antiplatelet and anticoagulant

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17
Q

What are the two ADP P2Y12 receptor inhibitors?

A

Clopidogrel and Ticagrelor

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18
Q

How does ADP P2Y12 receptor inhibitors work?

A

It blocks the ADP from platelets from binding to ADP P2Y12 receptors, so that GP IIb/IIIa receptors are not activated and platelets will not be recruited for aggregation

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19
Q

Why is loading dose given for ADP P2Y12 receptor inhibitors?

A

It reaches peak clinical effect faster, hence it is given to reach the steady state faster.

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20
Q

Clopidogrel binds _____ while Ticagrelor binds _______.

A

Irreversibly, reversibly

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21
Q

Clopidogrel binds directly on the _____ on the P2y12 receptor while Ticagrelor does not.

A

ADP binding site

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22
Q

Which of the ADP P2Y12 receptor inhibitors have interindividual variability?

A

Clopidogrel (CYP2C19-mediated metabolism) - reduces effect

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23
Q

What is the main adverse effect of clopidogrel and ticagrelor?

A

Hemorrhage and bleeding

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24
Q

Which of the populations should not take clopidogrel and ticagrelor?

A

Current or history of active pathologic bleeding/ intracranial hemorrhage

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25
Q

Which of the populations should take clopidogrel and ticagrelor with caution?

A
  1. Risk of bleed
  2. Elderly (Ticagrelor)
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26
Q

List the DDI for Clopidogrel.

A
  1. Warfarin, NSAIDs - increase bleed risk
  2. Macrolides - reduce effect
  3. CYP2C19 inhibitor (mod and strong) - i.e. PPI - reduce effect
  4. Rifamycins - increase effect
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27
Q

List the DDI for Ticagrelor.

A
  1. Anticoagulants, fibrinolytic, long-term NSAIDs - bleeding risk
  2. Aspirin > 100mg - decrease effect, increase bleed
  3. CYP3A inducers (decrease) and strong inhibitors (increase)
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28
Q

What class of drugs is Warfarin under?

A

Vitamin K antagonist

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29
Q

How does wafarin works?

A

Inhibits Vitamin K reductase enzyme and hence prevent the reactivation of oxidized Vitamin K. This in turn prevent the activation of coagulation factors 2,7,9,10.

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30
Q

How is warfarin administered?

A

Orally

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31
Q

How fast does warfarin peak in plasma?

A

2 to 8 hours

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32
Q

How is warfarin metabolized?

A

Hepatically cleared via CYP2C9

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33
Q

What are the two genetic polymorphisms that results in inter-variability in Warfarin?

A
  1. CYP2C9
  2. VKORC1
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34
Q

What is the main adverse effects of warfarin?

A

Hemorrhage/ bleeding

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35
Q

Which group of patients is warfarin contraindicated in?

A
  1. Active bleeding
  2. Severe or malignant hypertension
  3. Severe renal or hepatic disease (CYP enzymes for metabolism affected)
  4. Pregnant (Pass placenta, teratogen)
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36
Q

What are the DDI related to warfarin?

A
  1. Paracetamol (>2weeks + >2g/day) - increase bleed
  2. PPI, NSAIDs - increase bleed
  3. Thiazides diuretics, steroids - decrease bleed
  4. Vitamin K , green tea - decrease effect
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37
Q

What class of drugs are dabigatran and rivaroxaban?

A

Non-vitamin K antagonists

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38
Q

How does Rivaroxaban works

A

Competitively and reversibly inhibits activated factor X (Xa)

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39
Q

How does Dabigatran works

A

Competitively and reversibly inhibits thrombin (IIa)

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40
Q

______ is used to reverse effects of Dabigatran while _____ is used to reverse Rivaroxaban’s effects.

A

Idarucizumab, Andexanet alfa

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41
Q

Why is Dabigatran extexilate given as a prodrug?

A

Low bioavailability of 3 to 7%

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42
Q

How does the half life of dabigatran etexilate affects the reversal of the drug effect as compared to rivaroxaban?

A

Dabigatran etexilate has a t1/2 of 12 to 17 hours whereas rivaroxaban has a t1/2 of 5 to 9 hours. Rivaroxaban effects will wear off in 1 to 2 days whereas dabigatran etexilate reverse in 3 to 5 days

43
Q

What are the adverse reactions of Dabigatran etexilate and Rivaroxaban?

A
  1. Bleeding
  2. GI symptoms (Dabigatran etexilate)
44
Q

How are Heparin and LMWH administered?

A

IV, SC

45
Q

How does parental anticoagulants work?

A

Potentiates action of antithrombin III by causing a conformation change (increases rapid interaction with proteases) and inactivating thrombin, thereby stopping fibrin and subsequently clot formation

46
Q

What are the coagulation factors inactivated by heparin-ATIII complex?

A

Thrombin (IIa) and Xa

47
Q

Give an example of LMWH.

A

Enoxaparin

48
Q

LMWH is more selective for ___ than ____

A

Xa, IIa

49
Q

In general LMWH has _____ bioavailability, t1/2 and ____ thrombocytopenia risk.

A

longer, lower

50
Q

List 2 adverses effect of Heparin and LMWHs.

A

Bleeding, thrombocytopenia

51
Q

Heparin and LMWH _______ cross the placenta.

A

do not

52
Q

What can be used to reverse effects of heparin and LMWHs?

A

Protamine sulfate IV infusion (partial reversal for LMWHs)

53
Q

Which population is heparin and LMWHs contraindicated in?

A
  1. Hypersensitive to heparins or pork products
  2. Active major bleeding
  3. Thrombocytopenia or antiplatelet antibodies
54
Q

What is the major DDI associated with Heparins and LMWHs?

A

SSRIs - increase bleeding risk

55
Q

What class of drugs are alteplase ?

A

Fibrinolytic (Recombinant tissue-type plasminogen activators)

56
Q

How does alteplase work?

A

It binds to and activate plasminogen to form plasmin, which then acts on the fibrin to dissolve blood clots.

57
Q

TPA can be inactivated by ________ and is uptake by the _______.

A

Plasminogen activator inhibitor 1 (PAI-1)
Liver

58
Q

How is alteplase given?

A

IV (long plasma half-life)

59
Q

What is the advantage of alteplase over kinases?

A

Preferential binding to clot associated plasminogen

60
Q

What are the adverse effect related to alteplase?

A

Bleeding, Embolism (if breakdown too fast)

61
Q

What are the two anti-fibrinolytic agents that can be used during excess fibrinolysis?

A

Tranexamic acid and aminocaproic acid

62
Q

How does anti-fibrinolytic agents work?

A

Complete for lysine sites on plasminogen and plasmin, blocking interaction with fibrin

63
Q

Which population should not be given alteplase?

A

Active bleeding

64
Q

What are the associated DDI with alteplase?

A
  1. Antiplatelet especially dipyridamole and aspirin - increase bleed
  2. Anticoagulants especially warfarin and heparin - increase bleed
  3. Nitroglycerin - decrease effect
65
Q

What are the two reasons behind aplastic anemia?

A

Dose-dependent direct drug or idiosyncratic by toxic metabolites

66
Q

What are the drugs that induces aplastic anemia?

A
  1. Dose-dependent direct drug: Cancer chemotherapies, chloramphenicol
  2. Idiosyncratic: Carbamazepine and phenytoin
67
Q

How to manage aplastic anemia?

A
  1. Immunosuppressants
  2. GM-CSF/ G-CSF
  3. IL-14
68
Q

What are two drugs that can induce immune thrombocytopenia?

A

Heparin
Sulfonamides

69
Q

How to treat immune thrombocytopenia?

A

Immunosuppressants

70
Q

What causes agranulocytosis/ neutropenia?

A

Direct drug toxicity, toxic metabolite, immune (hapten/ complement mediated)

71
Q

List 3 drugs that induces agranulocytosis.

A
  1. Direct drug toxicity: Thiamazole
  2. Toxic metabolites: Clozapine
  3. Immune: Beta-lactams
72
Q

How can agranulocytosis be treated?

A
  1. G-CSF (Filgrastim)
  2. GM-CSF (Sargramostim)
73
Q

What causes immune haemolytic anemia?

A
  1. Drug induced true autoantibody
  2. Immune complex autoantibody production
  3. Hapten-induced hemolysis
74
Q

What drugs are associated with immune haemolytic anemia?

A
  1. Drug induced: Methyldopa
  2. Immune complex: Quinidine
  3. Hapten: Penicillin, cephalosporins, streptomycin
75
Q

What causes non-immune haemolytic anemia?

A

Protein adsoprtion

76
Q

What drugs are associated with non-immune hemolytic anemia?

A

Cisplatin, Oxaliplatin, Beta lactamase inhibitor

77
Q

What drugs can be given for hemolytic anemia?

A

Steroids, immunoglobulins, Rituximab

78
Q

What are the drugs used as nutrients supplements for anemia?

A
  1. Iron (Ferrous sulfate, iron sucrose)
  2. Vit B12 (Hydroxocobalamin)
  3. Folic acid
79
Q

What ESA agents can be given for anemia?

A

Epoetin alfa and darbepoetin alfa

80
Q

What are the drugs used in neutropenia?

A
  1. G-CSF: Filgrastim, Pegfilgrastim (+ plerixafor)
  2. GM-CSF (Sargramostim)
81
Q

What are the drugs used for thrombocytopenias?

A
  1. Recombinant IL11 (Oprelvekin)
  2. Fc fusion protein thrombopoietin receptor agonist (Romiplostim)
  3. Oral nonpeptide thrombopoietin receptor agonists (Eltrombopag)
82
Q

How is ferrous sulfate and iron sucrose given for anemia?

A

Ferrous sulfate: Oral
Iron Sucrose: Parental

83
Q

What is a chronic adverse effect of iron?

A

Haemochromatosis (deposition of iron in organs, leading to their failure and death)

84
Q

What are the two iron chelators that can treat iron overdose?

A

Deferoxamine (IV), Deferasirox (oral)

85
Q

How is hydroxocobalamin (vit b12) given?

A

Parenteral

86
Q

_____ may reduce oral absorption of vitamin B12

A

PPIs

87
Q

_______, a metabolite of folic acid undergoes enterohepatic circulation

A

5 methyltetrahydrofolate

88
Q

What is the main adverse reaction associated with folic acid?

A

GI disorders, Nausea (bitter/ bad taste)

89
Q

List 2 DDI associated with folic acid.

A

Aspirin - increase elimination
Co-trimoxazole/ chloramphenicol - interfere with folate metabolism

90
Q

How are ESAs administered?

A

Parental

91
Q

How does ESA works?

A

Stimulate division and differentiation of erythroid progenitor cells

92
Q

Who cannot be given ESAs?

A

Patients with uncontrolled HTN

93
Q

Which group of patients require special precaution when given ESAs?

A

HTN and history of seizures

94
Q

What are the adverse effects related to ESAs?

A

HTN, thrombosis

95
Q

How does G-CSF work?

A
  1. Stimulates proliferation and differentiation of progenitors committed to neutrophil lineage
  2. Activates phagocytic activity of mature neutrophils
96
Q

How does GM-CSF works?

A

Stimulates proliferation and differentiation of early and late
granulocytic, erythroid and megakaryocyte progenitors

97
Q

What are the adverse effects of G-CSF?

A

Reversible bone pain

98
Q

G-CSF is _________ tolerated than GM-CSF.

A

better

99
Q

Which group of patients should not use myeloid growth factors?

A

Chronic myeloid leukemia or myelodysplastic syndrome

100
Q

What are some adverse effects caused by both G-CSF, GM-CSF?

A

Sickle cell crisis and respiratory issues (use with caution)

101
Q

What are the adverse effects associated with megakaryocyte growth factors?

A
  1. Thromboembolic events
  2. Oprelvekin - fluid retention, peripheral edema, dyspnoea on exertion
102
Q

Which group of patients should take precaution when megakaryocyte growth factors are given to them?

A
  1. Cerebrovascular disease
  2. Thromboembolism risk
  3. Chronic HF (oprelvekin)
103
Q

_____ dose of eltrombopag is needed in non-East Asian ancestry.

A

Higher

PR3154 (16 decks)

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