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Pharmacology > Antithrombotic and Thrombolytic drugs > Flashcards

Antithrombotic and Thrombolytic drugs Flashcards

1
Q

Warfarin - MoA

A

Vit. K antagonist

Inhibit the synthesis of coagulation factors whose formation is dependent on vit K, factor II (Prothrombin), VII, IX and X.

Also it inhibits the synthesis of proteins C and S, which are endogenous anticoagulants that inactivates factor V and VIII and promote fibrinolysis.

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2
Q

Warfarin - Indication and goal of treatment

A

Long term treatment: Deep vein thrombosis, prevention of thrombosis in pt with atrial fibrillation or an artificial heart valve.

Pulmonary embolism

Used with heparin type anticoagulant for treatment of MI

Goal of treatment: prevent thrombus formation or expansion and to prevent embolization and other potentially fatal consequences of thrombosis.

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3
Q

Warfarin - Adverse Effects and Contraindication

A

Bleeding (mild nose bleed to life threatening hemorrhage)

Fetal warfarin syndrome(bone deformities and bleeding. Malformations are partly a result of antagonism of vit K-dependent maturation of bone proteins during a process in which these proteins are carboxylated. Vit K antagonists and Warfarin block this process –> birth defects

Contraindication: Pregnancy (Crosses the placenta and can cause fetal hemorrhage + fetal warfarin syndrome), Hypertension –> Increased risk of stroke

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4
Q

Warfarin - Interactions and special considerations

A

Special considerations:
Delayed onset of action, max effect is observed 3-5 days after started therapy –>
Pt with acute thromboembolic disorders can be treated with low molecular weight heparin plus warfarin, LMWH can be withdrawn once warfarin acts.

Prothrombin time should be monitored when adding/discontinuing drugs that interact with warfarin

Interactions:
Interacts with drugs that induce or inhibit cyt P450.

Most serious interactions are with drugs that increase the anticoagulant effect and place the patients at risk of hemorrhage, ex: Salicylates (by reducing prothrombin), cephalosporins

Decrease anticoagulant effect by inducing CYP enzymes that metabolize warfarin: rifampin, barbiturates

Cholestyramine inhibit absorption of warfarin from gut.

Amiodarone, cimetidine, erythromycin, fluconazole, gemifibrozil, isoniazid, metronidazole, sulfinpyrazone inhibit metabolism of warfarin increase the risk of bleeding.

Phytonadione (vit K1) directly antagonize the effect of warfarin, used to treat hemorrhage caused by anticoagulant activity.

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5
Q

Heparin - MoA

A

Inactivates clotting factors by potentiating the activity of an endogenous anticoagulant called antithrombin III (most powerful endogenous inhibitor of thrombin (factor II) ) and active factor X

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6
Q

Heparin - Indication

A

Acute thromboembolic disorders, peripheral and pulmonary embolism, venous thrombosis, disseminated intravascular coagulation.

Prevent clotting in arterial and heart surgery, during blood transfusions, renal dialysis and blood sample collection

Prevent embolization of thrombi that might cause cerebrovascular events in patients with acute atrial fibrillation.

Low doses (subc): prevent DVT and pulmonary embolism in high risk patients.

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7
Q

Heparin - Special consideration and interactions

A

Treatment of bleedings by heparin and LMWHs consist of adm protamine sulfate (positively charged protein that binds to negatively charged heparin and inactivates it) given IV. Severe bleeding may req adm of fresh plasma or clotting factors.

Risk of bleeding increased by salicylate

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8
Q

Heparin - Adverse effects

A

Bleeding caused by excessive anticoagulation
Hyperkalemia (because of suppression of aldosterone secretion).

Heparin induced thrombocytopenia(HIT)
Type 1 HIT: in 25% of pat treated with heparin. Caused by direct interaction between heparin and platelets –> platelet aggregation. It is usually mild and reversible within 4 days despite continued heparin treatment.

Type 2 HIT: less common, caused after 2-14 days, caused by immunoglobulin (IgM or IgG) mediated platelet inactivation –> high risk of thrombotic complications and mortality. In this case heparin must be stopped.

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9
Q

Heparin related drugs/ LMWH + Adverse effects

A

Fondaparinux
Enoxaparin
Dalteparin

Bleeding caused by excessive anticoagulation

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10
Q

Fondaparinux - MoA

A

Most selective active factor X inhibitor

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11
Q

Fondaparinux - Indications

A

Prophylaxis of DVT in pat having hip fracture or hip replacement surgery or knee-replacement surgery.

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12
Q

Enoxaparin and Dalteparin - MoA

A

Inactivate factor X because the LMWH-AT-III complex has less afifnity for thrombin than does the heparin-AT-III complex

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13
Q

Enoxaparin and Dalteparin - Indications

A

Prevent venous thromboembolism associated with abdominal surgery or knee or hip replacement.

Prevent ischemic complications of unstable angina or non-ST segment elevation (non Q wave) MI, used in acute coronary syndrome and angioplasty

Enoxaparin: DVT and prevent thromboembolism caused by severely restricted mobility during acute illness

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14
Q

Bivalirudin and Argatroban - MoA

A

Directly inhibit thrombin without needing AT-III as a cofactor

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15
Q

Bivalirudin - Indication

A

Prevent Thrombosis in pt with unstable angina and acute MI, including those undergoing coronary angioplasty and stent insertion.

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16
Q

Argatroban - Indication

A

Prophylaxis and treatment thrombosis in pat with HIT, including persons undergoing percutaneous coronary interventions for MI

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17
Q

Dabigatran - MoA

A

Potent, competitive, reversible inhibitor of thrombin, a protease enzyme that converts fibrinogen to fibrin in the final step of blood coagulation.
Inhibits both fibrin-bound and unbound (free) thrombin.

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18
Q

Dabigatran - Indication

A

Reduce the risk of stroke and systemic embolism in patients with nonvalvular atrial fibrillation (–> lower rate of stroke and intracranial bleeding in these pat then with warfarin)
Treatment and prevention of DVT and PE in pt who have been treated with a parenteral anticoagulant for 5-10 days

Prevention of DVT in those undergoing hip-replacement sugery.

Alternative to warfarin for pt who have been poorly controlled or not well monitored

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19
Q

Dabigatran - Special consideration

A

Prodrug (dabigatran etexilate) –> converted to dabigatran by esterases in gut, blood and liver)

Reduce dose in pt with renal impairment –> prolongation of half-life.

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20
Q

Dabigatran - Adverse effects

A

Increased risk of bleeding (including GI) there is no antidote–> give plasma or RBC.

GI complains, dyspepsia, gastritis like symptoms. (taking drug with food or H2 blocker may prevent symp)

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21
Q

Dabigatran - Interactions

A

Idarucizumab: reverse dabigatran’s anticoagulant effect in cases of life-threatening or uncontrolled bleeding or emergency surgery

Rifampin and P-glycoprotein

Pgp inhibitors (verapamil, amiodarone, quinidine, clarithromycin): can be given, but 2 or more hours before/after dabigatran.

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22
Q

Direct thrombin inhibitors

A

Bivalirudin
Argatroban
Dabigatran

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23
Q

Active factor X inhibitors (Xa inhibitors)

A

Apixaban
Rivaroxaban
Edroxaban

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24
Q

Active factor X inhibitors - Indication

A

Decrease risk of stroke and systemic embolization in persons with nonvalvular atrial fibrillation + prevention of DVT and PE in persons undergoing knee- or hip-replacement surgery.

DVT and PE to decrease risk of recurrences of DVT and PE in persons with previous episodes.

Arterial fibrillation where warfarin has not been effective

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25
Q

Apixaban - Contraindication and Adverse effects

A

Potent inh of CYP3A4 and P-glycoprotein –> increased plasma concentrations

Bleeding and thrombocytopenia

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26
Q

Rivaroxaban - Interaction

A

Metabolized by P450, 3A4 –> OBS pat taking 3A4 inhibitors.

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27
Q

Antiplatelet drugs

A

Aspirin
Dipyridamole
Cilostazol

28
Q

Aspirin - MoA

A

Inhibit the synthesis of prostaglandins (the most important prostaglandin affecting platelet aggregation is prostacycline and TXA2).

Prostacycline: synthesized by vascular endothelial cells and inh platelet aggregation and thrombosis

TXA2: synthesized by platelets and promotes platelet aggregation.

Aspirin is a nonselective irreversible cox inhibitor. –> inhibits platelet aggregation for the life of the platelet.

29
Q

Aspirin - Indication

A

Prevent arterial thrombosis in pat with ischemic heart disease and stroke.

Reduces the risk of second MI and stroke.
Prevent MI in persons with coronary artery disease

Acute MI: to prevent enlargement of a coronary thrombus and reduce the severity of cardiac damage.

In pat with transient ischemic attacks- used to prevent an initial or subsequent stroke.

In pat who have artificial heart valves or undergoing percutaneous coronary angioplasty- used with other drugs to prevent thrombosis.

Also to treat peripheral arterial occlusive disease and chronic limb ischemia.

30
Q

Aspirin Low VS High dose and Interaction

A

Low doses of aspirin: selectively inhibits the synthesis of TXA2 without much effect on prostacycline.
Higher doses: inhibit synthesis of both prostaglandins.

Increases hypoglycemic effect pf sulfonylureas. Increases risk of GI bleeding, ulceration ass with methotrexate, valproate. Inhibits uricosuric effect of probenecid

31
Q

Aspirin - Adverse Effects

A

GI bleedings(due to inh of synthesis of prostaglandins that promotes secretion of bicarbonates to the mucus)
Hypersensitivity
Tinnitus
High doses: Hypoprothrombinemia –> increased risk of bleeding

32
Q

Dipyridamole - MoA

A

Inhibiting platelet adhesion to the vessel wall. It can also inhibit platelet aggregation by increasing the formation of cAMP (due to its action as phosphodiesterase inh) and lowering the level of platelet calcium.

33
Q

Dipyridamole - Indication

A

As vasodilator: used during myocardial perfusion imaging (to dilate and evaluate the arteries of pt with coronary artery disease)

In combo with aspirin to prevent ischemic (thrombotic) stroke in persons who prev had strokes.

34
Q

Cilostazol - MoA and Effect

A

Inhibits type 3 phosphodiesterase and the breakdown of cAMP, thereby increasing cAMP levels in platelets and blood vessels. This leads to inhibition of platelet aggregation and vasodilation.

Improves blood flow and reduces muscle pain, while increasing walking distance in persons with this condition.

35
Q

Cilostazol - Indication

A

Intermittent claudication (peripheral vascular disease- pain, weakness in a limb –> limping & lameness)

36
Q

Cilostazol - Adverse effect and Interaction

A

Headache

Metabolized by CYP3A4 –> inhibitors of this enzyme (erythromycin) may increase antiplatelet effect.

37
Q

ADP inhibitors

A

Clopidogrel
Prasugrel
Cangrelor
Ticagrelor

38
Q

Clopidogrel and Prasugrel - MoA

A

Block ADP P2Y12 receptors which inhibits activation of GP-2b/3a receptors and prevents ADP-induced platelet aggregation –> prevents thrombus formation and prolongs bleeding time

Irriversible antagonists.

39
Q

Clopidogrel and Prasugrel - Indication

A

Prevention of thrombosis and MI in persons with ACSs

Clopidogrel: Secondary stroke prevention

Clopidogrel: Prevent thrombosis in pt with intermittent claudication, chronic arterial occlusion, AV shunts or fistulas, open heart surgery, and sickle cell anemia.

Reduce thrombosis and MI in pt with ACS who are undergoing angioplasty and coronary artery stent insertion.

40
Q

Clopidogrel - Adverse effect

A

Bleeding and Neutropenia

41
Q

Prasugrel - Adverse effect

A 
Increased incidence of bleeding
GI-pain
Increased cholesterol and triglyceride levels
Nausea
Neutropenia
42
Q

Dipyridamole - Averse effects

A

GI distress
Headache
Mild/transient dizziness
Rash

43
Q

Dipyridamole - Interactions

A

Decreases metabolism of adenosine

Increases risk of bradycardia ass with beta adrenergic receptor antagonists

44
Q

Cangrelor and Ticagrelor - MoA

A

Block ADP P2Y12 receptors which prevent ADP-induced platelet aggregation by inhibiting expression of GP iib/iiia receptors for fibrinogen.

Reversible

45
Q

Cangrelor - Clinical use and Adverse effects

A

Adjunct to percutaneous coronary intervention (PCI) to reduce risk of thrombotic events during and after these prosedures.

Bleeding

46
Q

Ticagrelor - Clinical use

A

Prevention of thrombosis and MI in persons with ACSs

Reduce thrombosis and MI in pt with ACS who are undergoing angioplasty and coronary artery stent insertion.

47
Q

Ticagrelor - Adverse effects

A

Bleeding
Dyspnea
Neutropenia –> rarely used

48
Q

Glycoprotein IIb/IIIa antagonists

A

Abciximab
Tirofiban
Eptifibatide

49
Q

Abciximab - MoA

A

Prevents platelet aggregation by binding to platelet GP 2b/3a receptors to prevent fibrinogen from binding and crosslinking with platelets.

50
Q

Abciximab - Clinical use

A

Prevent platelet aggregation and thrombosis in pat undergoing coronary interventions(coronary angioplasty, stent placement)

Prevent vessel restenosis, reinfarction and death.

51
Q

Abciximab - Adverse effects

A

Bleeding
Thrombocytopenia
Hypotension
bradycardia

52
Q

Tirofiban and Eptifibatide - MoA

A

Competitive reversible inhibitor of fibrinogen binding to GP 2b/3a receptors

Prevent platelet aggregation by preventing fibrinogen cross-linking of platelets.

53
Q

Tirofiban and Eptifibatide - Clinical use

A

Unstable angina and MI often in combo with LMWH

  • Prevent coronary thrombosis in persons with unstable angina or non-ST-segment elevation(non Q-wave) MI
  • Prevent thrombosis in persons having coronary angioplasty or stent placement for ST-segment elevation MI
54
Q

Tirofiban and Eptifibatide - Adverse effects

A

Bleeding

55
Q

Vorapaxar - MoA

A

Protease- activated receptor- 1 (PAR-1) antagonists  competitively inhibits thrombin access to its target receptor and prevents thrombin- mediated platelet aggregation.

56
Q

Vorapaxar - Clinical use

A

Pt with history of MI or with peripheral arterial disease (PAD)

Reduces thrombotic cardiovascular events and mortality

57
Q

Thrombolytic (Fibrinolytic) Drugs

A 
Alteplase
Reteplase
Tenecteplase
Streptokinase
Anistreplase
58
Q

Thrombolytic Drugs - MoA

A

Recombinant forms of human tissue plasminogen activator(t-PA) enzyme, converts plasminogen to plasmin and cause fibrinolysis

59
Q

Thrombolytic Drugs - Clinical use

A

Degrade thrombi in pat with MI, thrombotic stroke, pulmonary embolism

Open thrombosed renal dialysis and central venous catheters

Venous thromboembolism, such as in cases of extensive iliofemoral vein thrombosis, where catheter-directed thrombolysis is employed as an adjunct to anticoagulants

For patients with ST-segment elevation MI, thrombolytic drugs are used to restore coronary blood flow when patients are not eligible for angioplasty

60
Q

Thrombolytic Drugs - Adverse effects and Contraindications

A

Hemorrhage
Arrhythmias (Bradycardia, Tachycardia)

Contraindications: 
Hemorrhagic stroke 
Recent surgery
Recent trauma
Pregnancy
Uncontrolled hypertension
Cancer
Peptic Ulcer
Inflammatory Bowel Disease
Hypersensitivity
61
Q

Thrombolytic Drugs - Interactions

A

Antidote- aminocaproic acid inhibits fibrinolysis(given orally or iv, it can cause thrombosis, hypotension and arrhythmias)

62
Q

Aminocaproic acid - Clinical use

A

Stop bleeding caused by thrombolytic drugs

Prevent bleeding in patients who have hemophilia or are recovering from GI or prostate surgery

63
Q

Aminocaproic acid - Adverse effects

A

Thrombosis
Hypotension
Arrhytmias

64
Q

Tranexamic acid - Clinical use

A

Cyclic heavy menstrual bleedings

Injection in patients with hemophilia who need short-term treatment to prevent hemorrhage during and after tooth extraction

65
Q

Tranexamic acid - Adverse effects

A

Thrombosis, which is increased when hormonal contraceptives are used, especially in women who are obese and smoke cigarettes

66
Q

Aminocaproic acid and Tranexamic acid - MoA

A

They prevent degradation of plasmin to fibrin

Pharmacology (55 decks)

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