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Pharmacology > ANTITHROMBOTIC DRUGS > Flashcards

ANTITHROMBOTIC DRUGS Flashcards

1
Q

Antithrombotic drugs

A

are a group of drugs used in the prophylactic and curative treatment of thromboembolic disorders.

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2
Q

Vascular thrombosis can be arterial or venous.

A

• arterial thrombosis - an endothelium injury triggers platelet aggregation with white thrombus formation.
• venous thrombosis - the coagulation process is activated by the blood stasis, with the formation of the red thrombus.
In the case of thrombosis from the level of the valvular or vascular prostheses, both the platelet aggregation and the coagulation process are involved, with obliteration and reduction of local circulation or risk of embolism.

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3
Q

Fibrinolysis

A

is the process of activation of plasminogen in plasmine, which hydrolyzes fibrin and some coagulation factors (including fibrinogen) with clot lysis.

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4
Q

Antithrombotic drugs may be:

A
  • anti-platelets
  • anticoagulants
  • fibrinolytic.
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5
Q

Anti-platelet drugs

A

inhibit platelet functions and prevent white thrombus formation.
In arterial thrombosis there is an injury of the vascular endothelium (atheroma plaques) which
causes the increase of platelet adhesivity and aggregability.
As a result of these processes, thromboxane A2 (TXA2), ADP, Platelet Activating Factor - PAF begins to be released, with exposure of glycoprotein receptors IIb / IIIa (GP IIb / IIIa), from which fibrinogen binds, a
process that activates platelet aggregation and white thrombus formation.
- TXA2 promotes platelet adhesivity and has vasoconstrictor action.
- Prostacyclin (prostaglandin I2; PgI2) is formed in the normal vascular endothelium, and has an anti aggregating and vasodilating effects.

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6
Q

Anti-platelets drugs may have several mechanisms of action.

A
  • inhibition of cyclooxygenase (acetylsalicylic acid)
  • inhibition of ADP-induced aggregation (ticlopidine, clopidogrel)
  • blocking membrane glycoprotein receptors – GP IIb / IIIa (abciximab, tirofiban)
  • blocking thromboxane A2 receptors (terutroban)

The main indication is prophylaxis of arterial thrombosis in patients with ischemic heart disease, acute myocardial infarction, bypass, angioplasty, history of stroke.

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7
Q

Acetylsalicylic acid

A

has a long-lasting anti-aggregating effect. It blocks irreversibly by acetylation the platelet cyclooxygenase 1 (COX 1), decreasing TXA2 synthesis, inhibiting
platelet aggregation and prolonging bleeding time.

The platelet anti-aggregating effect is manifested at low doses of acetylsalicylic acid (75-300mg). At higher doses (500 mg) endothelial cyclooxygenase is also inhibited, limiting the anti-aggregating effect by decreasing prostacycline synthesis.

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8
Q

Acetylsalicylic acid It is indicated in the treatment and prophylaxis of

A

acute myocardial infarction, stroke, peripheral arteriopathy. It is well tolerated, with few adverse reactions - digestive bleeding in people with ulcer, gastritis.
It is contraindicated in case of allergy to salicylates, recent bleeding, ulcer.

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9
Q

Ticlopidine

A

irreversibly inhibits platelet receptors for ADP, inhibiting adhesivity and platelet aggregation.

It is indicated in the prophylaxis of arterial thrombosis (patients at risk or a history of stroke or acute myocardial infarction), in patients with peripheral arteriopathy, hemodialysis, coronary stent angioplasty

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10
Q

Ticlopidine Produces

A

haematological adverse reactions: thrombocytopenia, neutropenia, agranulocytosis, bleeding. Monitoring of the hemogram within the first 2-3 months of
treatment is required.
Neutropenia may be severe, but is reversible if is stopped the treatment.
It can also cause diarrhea, nausea, abdominal pain, ulcer.
Contraindications - bleeding, ulceration, liver failure.

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11
Q

Clopidogrel

A

irreversibly inhibits ADP receptors - subtype P2Y12 in platelets with irreversible inhibition of platelet functions.

Adverse reactions of clopidogrel are lower than
ticlopidine.

It is indicated in the treatment and prophylaxis of acute myocardial infarction or ischemic stroke and in patients with stent coronary angioplasty.

Clopidogrel is a prodrug that is activated in the liver via the cytochrome P 450 pathway.
The antithrombotic effect is maintained for 7-10 days after discontinuation of treatment.

Contraindications: active bleeding lesions (gastric or duodenal ulcer, cerebral hemorrhage), liver failure.
Due to metabolism in cytochrome P450, drug interactions are possible.

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12
Q

Prasugrel

A

irreversibly inhibits P2Y12 platelet receptors with antiplatelet effects.
It is a prodrug, which is activated by hepatic metabolism in cytochrome P450

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13
Q

Ticagrelor

A

reversibly blocks the P2Y12 receptor. As P2Y12 receptor binding is reversible, platelet activity returns rapidly after stopping treatment

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14
Q

Glycoprotein receptor antagonists IIb / IIIa - Abciximab, Eptifibatide, Tirofiban,

A

are substances that inhibit platelet functions by blocking long-acting membrane glycoprotein
IIb / IIIa receptors, used in the treatment of coronary syndromes.

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15
Q

Dipiridamol

A

has anti-platelet effect by inhibiting platelet phospho-diesterase, with subsequent increase in platelet cAMP concentration and inhibition of adenosine reuptake and metabolism.

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16
Q

Cilostazole

A

inhibits platelet phosphodiesterase and produces also vasodilation.

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17
Q

Anticoagulants

A

are drugs that prevent the coagulation process: indirect thrombin inhibitors (heparins, direct factor Xa inhibitors), direct thrombin inhibitors and coumarin
anticoagulants.

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18
Q

Indirect thrombin inhibitors - heparin

A

binds to antithrombin III (alpha2 plasma globulin), increases its inhibitory effect on factor Xa and increases the ability of antithrombin III to inactivate thrombin (factor IIa).

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19
Q

Unfractionated heparin - standard heparin or conventional heparin

A

or conventional heparin has glycosaminoglycan-like molecule; the anticoagulant effect is produced by the pentazaharidic sequence.

It binds to antithrombin III, which physiologically inhibits coagulation factors IIa, IXa and Xa, which increase its activity about 1000 times.

It has a rapid, intense, short-term effect, in vivo and in vitro.
The in vitro anticoagulant effect is used in the collection of blood samples

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20
Q

Heparin in high doses inhibits

A

platelet aggregation, promoting bleeding; clarifies
lipemic plasma - increases the release of lipoprotein lipase from tissues with triglyceride lysis.
It has a polar molecule and is inactivated in the intestine. It is administered intravenously or
subcutaneously. It cannot be administered intramuscularly, as it produces hematomas. It has a
short half-life (30-60 minutes).
Urinary elimination, partially inactive; caution is advised in patients with renal impairment. It can be used in pregnancy because it does not cross the placenta

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21
Q

Heparin

Adverse reactions:

A

bleeding, thrombocytopenia, decreased mineralocorticoid hormone synthesis, osteoporosis, allergic reactions.

Overdose of heparin is treated with protamine sulfate, which chemically inactivates heparin.

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22
Q

Heparin

Contraindications :

A

thrombocytopenia, hemophilia, thrombocytopenic purpura, active gastric or duodenal ulcer, intracranial hemorrhage, abortion, genital bleeding, endocarditis,
heparin hypersensitivity, recent surgery, uncontrolled hypertension.

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23
Q

Heparin sodium salt

A

may be administered intravenously by infusion or
subcutaneously.
Verification of the efficacy and safety of the treatment is performed by monitoring APTT (activated partially thromboplastin time )which should be maintained at values 1.5-2.5 times higher than normal.

24
Q

Heparin

Indications:

A

prophylaxis of venous thrombosis, pulmonary thromboembolism, acute coronary syndromes and in some cases of acute peripheral ischemia.

25
Q

Heparin calcium salt

A

is administered subcutaneously in the prophylaxis of

thromboembolic disorders.

26
Q

Low molecular weight heparins (enoxaparin, dalteparin, nadroparin, reviparin, tinzaparin)

A

are obtained by depolymerization of heparin. It stimulates antithrombin III and inhibits factor Xa. Are administered subcutaneously and have a long half-life (16-18 hours).

Adverse reactions, especially the risk of bleeding, are lower. Are used in the treatment of venous thrombosis, pulmonary thromboembolism, acute myocardial infarction, prophylaxis of venous thrombosis in patients undergoing surgery, immobilized.

27
Q

Fondaparine

A

selectively inhibits factor Xa; does not inhibit thrombin activity, does not influence platelet activity and does not alter coagulation assays.
It is administered subcutaneously in acute myocardial infarction, pulmonary thromboembolism, deep vein
thrombosis or for thrombosis prophylaxis after surgery.

28
Q

Idraparin

A

is a preparate similar to fondaparine, with a longer half-life

29
Q

Sulodexid

A

has antithrombotic action by inhibiting factor Xa. It inhibits platelet adhesivity, normalizes blood viscosity, activates lipoprotein lipase, and can normalize
increased plasma lipid concentrations.

30
Q

Direct inhibitors of factor Xa – rivaroxaban, apixaban

A

– are selective inhibitors of factor Xa, without inhibitor effect on thrombin (factor IIa) and without effect on platelets.

Are indicated in the prevention of venous thromboembolism, prevention of stroke in patients with
chronic atrial fibrillation

31
Q

Direct thrombin inhibitors

A

It binds directly to the active site of thrombin and inhibits its effects. It can be given parenterally (lepirudin, bivalirudin, agatorban) or orally (ximelgatran, dabigatran).

32
Q

Direct thrombin inhibitors

A
  1. Hirudin
  2. Lepirudine
  3. Bivalirudine
  4. Argatroban
  5. Dabigatran
33
Q

Hirudin

A

is a natural substance that irreversibly inhibits thrombin. It has high toxicity - it is administered only locally in the treatment of hematomas

34
Q

Lepirudine

A

is administered injectable in the treatment of thrombosis.

35
Q

Bivalirudine

A

is a synthetic derivative of hirudin, which also inhibits platelet activation.

It is given intravenously to patients with acute coronary syndrome who undergo invasive therapy.

36
Q

Argatroban

A

is useful in patients with heparin-induced thrombocytopenia.

37
Q

Dabigatran

A

is a thrombin inhibitor, which is administered orally. It is indicated for thromboembolic accidents prophylaxis in hip or knee surgery and stroke in patients with
chronic atrial fibrillation.

Adverse reactions: gastrointestinal disorders (nausea, vomiting), bleeding especially in elderly patients.

Contraindications: severe renal failure, active bleeding,
severe hepatic failure, pregnancy and lactation.

38
Q

Coumarin anticoagulants - antivitamins K

A

inhibit hepatic activation of vitamin K dependent coagulation factors - IIa, VIIa, IXa, Xa.

  1. They block epoxireductase, inhibit the restoration of vitamin K’s active form, and thus inhibit the activation of coagulation factors.
  2. These anticoagulants are active only in vivo. The anticoagulant effect slowly settles, after 24- 72 hours, during which time the consumption of the vitamin K-dependent factors in the plasma occurs, and it persists for 2-10 days after the discontinuation of the treatment, the interval needed to restore the coagulation factors.
39
Q

Coumarin anticoagulants - Pharmacokinetics:

A

are well absorbed in the digestive tract, bind 90-99% on albumin (90-99%) and are metabolized by the liver, cross the placenta and passes into breast milk.

40
Q

Coumarin anticoagulants

Indications :

A

curative treatment of thrombophlebitis and prophylaxis of thromboembolism in patients with chronic atrial fibrillation or in those with mechanical valve prostheses.
Are administered orally and the INR (international normalized ratio) is monitored.

41
Q

Coumarin Anticoagulants

Adverse reactions:

A

bleeding through overdose or interactions with drugs or food.
The increased risk of bleeding is also due to the prolonged effect of oral anticoagulants.
In the case of bleeding by overdosage of oral anticoagulants, vitamin K, fresh plasma or prothrombin
complex concentrate is given.
Hepatic disorders (insufficient synthesis of coagulation factors), heart failure (through liver stasis), vitamin K deficiency, hyperthyroidism increase the effect
of anticoagulants.

42
Q

Coumarin Anticoagulants

Contraindications:

A

hemorrhagic syndromes, ulcer, hypertension with stroke, pregnancy, liver failure, severe kidney failure.

Combination with heparin, anti-platelets drug,
NSAIDs, amiodarone, cimetidine, some antibiotics (penicillin, cephalosporins, erythromycin)
increases the effect of coumarin anticoagulants with high risk of bleeding.

43
Q

The decrease of the anticoagulant effect occurs when it is combined with

A

enzyme inducing drugs (barbiturates, rifampicin, griseofulvin, carbamazepine), by increasing the
hepatic metabolism of the anticoagulant.

All of these interactions require careful monitoring of
anticoagulant treatment Interactions with some foods. Foods rich in vitamin K (broccoli, cauliflower, soy, spinach, cabbage, green salad, liver, black tea, fish oil) decrease the anticoagulant effect, and the consumption of alcohol or certain vegetables and spices (garlic, ginger, ginseng extract) or Ginkgo biloba) increases the anticoagulant effect.

44
Q

Acenocoumarol

A

has high potency; the effect is installed 24-36 hours after the first dose and maintained 36-72
hours after stopping treatment. Warfarin - the effect settles slower (about 37-60 hours) and stays up to 5-7 days.

45
Q

Fibrinolytics (thrombolytics)

A
  1. are drugs that lysate fibrin clot by activating plasminogen in plasmin.
  2. Fibrinolytic drugs bind to the plasminogen in the fibrin clot, lyses fibrin and loosens the thrombus, with re-permeabilization and reperfusion.
    Thrombolysis is effective in the first hours-days of thrombosis.
46
Q

Plasminogen

A

an be activated in plasmin intrinsically by coagulation, dependent on factor XII of coagulation, by extrinsic pathway through tissue plasminogen activator, urokinase or exogenous drug activators

47
Q

Fibrinolytics

Indications:

A

acute myocardial infarction, pulmonary embolism, deep vein thrombosis and peripheral arterial occlusion, large vein thrombosis (superior vena cava).

48
Q

The recovery of the ischemic area is greater as the fibrinolytic administration becomes ____

A

earlier.
For acute myocardial infarction, the results are optimal if the administration is done within the first 4 hours after the onset of the infarction.

49
Q

The most common adverse reaction of fibrinolytics is hemorrhage

A

in which case it is necessary to interrupt fibrinolytic treatment, administer plasma infusions, and if necessary administer antifibrinolytic drugs such as aminocaproic acid or aprotinin. Invasive maneuvers
should be avoided.

They are contraindicated in the case of a history of strokes, recent head trauma, brain tumors, untreated hypertension, active gastric or duodenal ulcer, coagulopathies.

50
Q

Fibrinolytics

Administration :

A

Fibrinolytics are given intravenously.

51
Q

Fibrinolytics :

A
  1. Streptokinase
  2. Anistreplase
  3. Urokinase
  4. Alteplase
  5. Reteplase
  6. Tenecteplaza
52
Q

Streptokinase

A

is a protein obtained from the filtrate of beta-hemolytic streptococcus cultures.

It interacts with plasminogen, transforms plasminogen into plasma and has a thrombolytic effect.

Adverse reactions: bleeding, hypotension by vasodilation, allergic reactions.

53
Q

Anistreplase

A

(acylated plasminogen-streptokinase-activator complex; APSAC) is administered intravenously, attaches to fibrin chains, and produces proteolysis.

54
Q

Urokinase

A

directly activates plasminogen, transforming it into plasmin.
The presence of fibrin may increase its activity. It is not antigenic.

55
Q

Alteplase

A

(t-PA; tissue plasminogen activator) has high selectivity for fibrin, with poor plasma proteolysis.

56
Q

Reteplase

A
  • r-PA (recombinant plasminogen activator) is a recombinant plasminogen activator that converts plasminogen into plasma, with consecutive thrombus lysis.
57
Q

Tenecteplaza

A

is a recombinant plasminogen activator with increased specificity for fibrin from thrombus, converting plasminogen from thrombus into plasmin.

Pharmacology (12 decks)

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