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Haematology Drugs Flashcards

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1
Q

Definition of venous thrombosis and treatment

A

Intravascular clot(red) forms in deep veins, particularly of the legs, when flow is sluggish. Fragment may bud of (embolus) and block blood vessels, often pulmonary artery

Therapy : anticoagulant drugs

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2
Q

Definition of arterial thrombosis and treatment

A

Platelets aggregate (white) usually at site of ruptured atherosclerotic plaque, then encapsulated by clot (red)

Therapy:

  • *Immediate-** dissolve existing clots with thrombolytics(fibrinolytics)
  • *long term** – antiplatelet drugs (anti-thrombolytics)
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3
Q

Haematolgical drugs categories

A

Thrombolytic drugs

  • rt-PA
  • streptokinase

Anticoagulant drugs

  • Heparins- (Unfractionated/ low molecular weight)
  • Warfarin -
  • Rivarobiban, apixaban - Factor Xa anatagonists
  • Dabgigatran - direct thrombin inhibitors

Antiplatelet drugs

  • Aspirin
  • Clopidogrel
  • Dipyridamole
  • Tirofiban
  • Abciximab
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4
Q

Oral anti-coagulants/ vitamin K antagoinst Example

A

Warfarin

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5
Q

Warfarin mechanism of action

A
  • Extrinsic pathway
  • Inhibits vitamin K epoxide reductase
  • Prevents recycling of Vitamin K to reduced form after carboxylation of coagulation factors II, VII, IX and X
  • Prevents thrombus formation
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6
Q

Indication of warfarin

A
  • Treatment of venous thromboembolism
  • Thromboprophylaxis in: AF/metallic heart valves/ Cardiomyopathy
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7
Q

Side effects of warfarin

A
  • Bleeding (risk increases with increasing INR)
  • Warfarin necrosis
  • Osteoporosis
  • crosses BBB
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8
Q

Important pharmacokinetics/pharmacodynamics of warfarin

A
  • Orally active (more convenient than heparin)
  • Numerous drug interactions / food interactions
  • Reversal by giving vitamin K
  • Polymorphisms in key metabolising enzymes (VKORC1 and CYP2C9)
  • Needs therapeutic drug monitoring and monitored loading regimen
  • Monitored with INR and dose adjusted according to indication
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9
Q

Patient information of warfarin

A
  • Need for compliance / attendance at visits for monitoring
  • Care needed with alcohol
  • Must inform doctor before starting new drugs – avoid over the counter aspirin preparations
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10
Q

How to reverse side effects of warfarin

A
  • Transfuse with plasma or coagulation factor concentrates
  • Oral vitamin K- but reversal is slow- require carboxylation to resume (1-3days)
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11
Q

Two types of heparin

A
  • Unfractionated heparin
  • Low molecular weight heparin
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12
Q

Unfracionated heparin mechanism

A
  • Intrinsic pathway
  • Enhances activity of antithrombin III. (natural anticoagulant)
  • Antithrombin III inhibits thrombin.
  • Heparins also inhibit multiple other factors of the coagulation cascade.
  • Immediate inhibition of clotting
  • This produces its anticoagulant effect.
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13
Q

Indication of unfractionated heparin

A
  • Treatment and prophylaxis of thromboembolic diseases, including induction of vitamin K antagonists.
  • Renal dialysis (haemodialysis)
  • Acute Coronary Syndrome treatment
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14
Q

Side effects of unfractionated heparin

A
  • Bleeding (Major haemorrhage risk can be as high as 3.5%)
  • Heparin-induced thrombocytopenia
  • Osteoporosis
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15
Q

Important PD/PK of unfractionated heparin

A
  • Administered by continuous intravenous infusion or subcutaneous injection
  • Complex kinetics - non-linear relationship between dose / half-life and effect – needs TDM
  • Effect monitored using activated partial thromboplastin time (aPTT)
  • Anticoagulant effect can be reversed with protamine.
  • Unfractionated heparin has a shorter duration of action than LMW Heparin.
  • Used in preference to LMW Heparin, in selected patients, due to the shorter duration of action and reversability with protamine (for example, Peri-operatively.
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16
Q

Patient information of pharmacokinetics/ pharmacodynamics

A
  • Risk of bleeding
  • Regular blood monitoring required
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17
Q

Low molecular weight heparin mechanism of action

A
  • Enhances activity of antithrombin III.
  • Antithrombin III inhibits thrombin.
  • Heparins also inhibit multiple other factors of the coagulation cascade.
  • This produces its anticoagulant effect
  • LMWH inhibits factor X only
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18
Q

Indication of low molecular weight heparin

A
  • Treatment and prophylaxis of thromboembolic diseases, including induction of vitamin K antagonists.
  • Renal dialysis (haemodialysis)
  • Acute Coronary Syndrome treatment
  • low-molecular-weight heparins do not prolong the APTT; they have a predictable anticoagulant effect and do not require monitoring unless in long-term use; in this case use the factor Xa assay to assess the degree of anticoagulation
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19
Q

Side effects of LMWH

A
  • Bleeding (Major haemorrhage risk can be as high as 3.5%)
  • Heparin-induced thrombocytopenia (Less risk than unfractionated heparin)
  • Osteoporosis (Less risk than unfractionated heparin
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20
Q

Important pharmacokinetcis/ pharmaco dynamics of LMWH

A
  • Subcutaneous injection - not orally active
  • More predictable dose-response relationship than Unfractionated Heparin.
  • 2-4 times longer plasma half-life than Unfractionated Heparin
  • Clearance is mostly via a renal pathway, thus the half-life can be prolonged in patients with renal failure, so dose adjustment may be needed.
  • Regular coagulation monitoring is not required.
  • Less readily reversed with protamine, than Unfractionated Heparin.
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21
Q

Patient information of LMWH

A
  • Risk of bleeding
  • Requires injection
  • Will need blood testing in prolonged therapy (Full Blood Count, to monitor for thrombocytopenia)
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22
Q

How are the anticoagulants monitored?

A

Warfarin- measured using INR ratio

Heparin measured using the APTT (activated partial thromboplastin time) test

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23
Q

Anti-platelet drugs examples

A
  • Aspirin
  • clopidogrel
  • dipyrimadole
  • Ticagrelori
  • Tirofibran
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24
Q

Aspirin Mechanism of action

A
  • Irreversible inactivation of cyclooxygenase (COX) enzyme
  • This reduces platelet thromboxane (TXA2) production and endothelial prostaglandin (PGI2) production
  • Reduced platelet thromboxane production reduced platelet aggregation and thrombus formation
  • Reduced prostaglandin synthesis decreases nociceptive sensitisation and inflammation
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25
Indication of aspirin
* Secondary prevention of thrombotic events * Pain relief
26
Side effects of aspirin
* Bleeding (\<1% Patients) * Peptic ulceration * Angiooedema * Bronchospasm * Reye’s syndrome (very rare)
27
Important pharcokinetics/pharmacodyanmics of aspirin
Half life becomes longer with very large doses (pharmacokinetics may be non-linear in overdose)
28
Avoid over the counter preparations of aspirin
Avoid over the counter preparations that contain aspirin. Some patients may be advised to take a Proton Pump Inhibitor alongside long-term aspirin
29
Clopidogrel mechanism of action
* Irreversibly blocks the ADP-receptor on platelet cell membranes. * Consequently inhibits formation of GPIIb/IIIa complex, required for platelet aggregation. * Decreased thrombus formation.
30
Indication of clopidogrel
Secondary prevention of thrombotic events
31
Side effects of clopidogrel
* Bleeding (1-10% of Patients) * Abdominal pain / diarrhoea (1-10% of Patients
32
Important pharacokinetics/pharmacodynamics of clopidogrel
avoid in liver failure
33
patient information of clopidogrel
* Patients may be advised to stop clopidogrel before surgical procedures. * Patients should not stop clopidogrel without consulting their doctor if they have an arterial stent in-situ
34
Mechanism of action of dipyradimole
* Inhibits cyclic nucleotide phosphodiesterases à increase cyclin AMP and increases cGMP )potentiates prostacyclin and NO) * So inhibits platelet activation
35
Indication of dipyradimole
dipyridamole is used in conjunction with warfarin and other anti-coagulants in the prophylaxis against thrombosis associated with prosthetic heart valves
36
Adverse effects of dipyridamole
* hyoptension * nausea * diarrhoea * headache
37
Examples of glycoprotein IIb/IIIa inhibitors
* abciximab * tirofiban
38
Mechanism of action of abciximab
* monoclonal antibody fragment * directed towards the glycoprotein IIb/IIIa receptor of platlets * binding and inactivation of this receptor prevents platelet aggregation
39
Indication of abciximab
* Used during surgical exploration/ clearing of intravascular blockage e.g coronary artery thrombosis * Antigenic- can be used once only
40
Side effects of abciximab
* haemorrhage * nausea * vomitting * hypotension
41
Mechanism of action of tirofiban
* Tirofiban prevents the blood from clotting during episodes of chest pain or a heart attack, or while the patient is undergoing a procedure to treat a blocked coronary artery. * It is a non-peptide reversible antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, and inhibits platelet aggregation.
42
Indication of tirofiban
* For treatment, in combination with heparin, of acute coronary syndrome, * including patients who are to be managed medically and those undergoing PTCA or atherectomy.
43
Dabagitran mechanism of action
* Direct thrombin inhibitor; prevents conversion of fibrinogen to fibrin * prevents thrombus formation
44
Indication of dabigatran
Prophylaxis of venous thromboembolism (especially post-operative) Thromboprophylaxis in non-valvular A
45
Side effects of dabigatran
* Bleeding * Dyspepsia
46
Important PK/PD of dabagitran
* Rapid onset of action * No food / few drug interactions (not metabolised via CYP 450) * No need for therapeutic monitoring * Currently no available antidote
47
Patient information of dabagitran
risk of bleeding
48
Rivaroxaban mechanism of action
* Inhibits conversion of prothrombin to thrombin, reducing concentrations of thrombin in the blood. * This inhibits the formation of fibrin clots.
49
Indication of rivaroxiban
* Prophylaxis of venous thromboembolism (especially post-operative) * Thromboprophylaxis in non-valvular AF * Treatment of venous thromboembolism
50
Side effects of rivaroxiban
* bleeding * nausea
51
Important pharmacokinetics/pharmacodynamics of rivaroxaban
* Predictable drug interactions (metabolised via CYP 450, inc CYP3A4) * No need for therapeutic monitoring * Currently no available antidote
52
Patient information about rivaroxaban
risk of bleeding
53
Apixaban mechanism of action
* Inhibits conversion of prothrombin to thrombin; reducing concentrations of thrombin in the blood. * This inhibits the formation of fibrin clots
54
Indication of apixaban
* Prophylaxis of venous thromboembolism following hip or knee replacement surgery. * Thromboprophylaxis in non-valvular AF.
55
side effects of apixaban
* bleeding * nausea
56
Important pharmacokinetics/pharmaodynamics of apixaban
* Predictable drug interactions (metabolised via CYP 450 and substrate for p glycoprotein) * 75% is metabolised by the liver, the rest being renally excreted. * No need for therapeutic monitoring * Currently no available antidote.
57
Patient information of apixaban
risk of bleeding
58
Examples of recombinant tissue plasminogen activators (rtPA)
Tenecteplase alteplase **These drugs are thrombolytics/fibrinolytics**
59
Mechanims of action of rtPA
* Recombinant form of tissue plasminogen activator * Catalyses conversion of plasminogen to plasmin * Promotes fibrin clot lysis
60
Indication of rtPA
* Acute ischaemic stroke within 4.5 hours of onset * Myocardial infarction within 12 hours of onset * Massive pulmonary embolism * N.B Not all thrombolytic drugs are licenced for all of these indications
61
Side effecs of rtPA
Bleeding Allergic reaction / angiooedema (1%)
62
Important pharmacokinetics/pharmacodynamics of rtPA
* Bolus-infusion regimen is used for alteplase * Tenecteplase is given as a single bolus * Pharmacodynamic interactions with other blood thinners (antiplatelets / anticoagulants)
63
Patient information of rtPA
* When using thrombolytic drugs, patients should be made aware of the risk-benefit ratio, which should include reference to the rate of bleeding complications

Drugs (8 decks)

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