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1 STEP Uworld coagulation > Antiplatelet AMBOSS > Flashcards

Antiplatelet AMBOSS Flashcards

1
Q

Glycoprotein IIb/IIIa inhibitors.

Drugs? i/v

A

Abciximab (Fab region fragments of monoclonal antibodies against glycoprotein IIb/IIIa receptors)
Eptifibatide
Tirofiban

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2
Q

Glycoprotein IIb/IIIa inhibitors. Mechanism?

A

Gp IIb/IIIa inhibitors bind to and block glycoprotein IIb/IIIa receptors (fibrinogen receptor) on the surface of activated platelets → prevention of platelets binding to fibrinogen → inhibition of platelet aggregation and thrombus formation

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3
Q

glycoprotein IIb/IIIa receptors. How they are called?

A

FIBRINOGEN RECEPTOR

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4
Q

glycoprotein IIb/IIIa receptors. Indications?

A

Prevention of thrombotic complications in high-risk patients with unstable angina/NSTEMI planned for PCI within 24 hours

*High risk:High-risk factors include age > 75 years; diabetes; chest pain lasting > 20 minutes; elevated troponin I (and other markers); ST depression on ECG; development of pulmonary edema; and left ventricular dysfunction.

NOT IN CAD (t.y NOT IN STABLE)

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5
Q

Glycoprotein IIb/IIIa inhibitors. Adverse.

A

Acute profound thrombocytopenia (t.y.Sudden drop in platelet count to < 50,000/mm3 within 24 hours of Gp IIb/IIIa inhibitor administration)

Hemorrhage

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6
Q

(Fab region fragments of monoclonal antibodies against glycoprotein IIb/IIIa receptors).
What drug?

A

Abciximab

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7
Q

!!!!Abciximab and tirofiban are contraindicated in patients with thrombocytes …………………. mm3

A

!!!!Abciximab and tirofiban are contraindicated in patients with thrombocytes < 100,000/mm3!

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8
Q

P2Y12 receptor antagonists. What agents? p/o

A 
Clopidogrel
Prasugrel
Ticagrelor (reversible)
Ticlopidine
Cangrelor (iv)
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9
Q

P2Y12 receptor antagonists. Mechanism?

A

Inhibition of P2Y12 receptor on platelets (ADP receptor) → ↓ expression of Gp IIb/IIIa receptors (fibrinogen receptor) on platelets → inhibition of platelet aggregation

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10
Q

Hemostasis. Activated PLT release ADP. Whats then happens?

A

ADP usually binds to P2Y12 receptors, leading to activation of Gp IIb/IIIa receptors and subsequent platelet aggregation.

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11
Q

What P2Y12 receptor antagonists agent IRREVERSIBLE inhibition?

A

clopidogrel, prasugrel, ticlopidine

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12
Q

What P2Y12 receptor antagonists agent REVERSIBLE inhibition?

A

ticagrelor

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13
Q

P2Y12 receptor antagonists. INDICATIONS?

A

DUAL ANTIPLATELET THERAPY!!!! (WITH ASA - ty. aspirinu):
1. STEMI
2. Unstable angina/NSTEMI
3. Secondary prevention of cardiac events in patients post PCI and/or stenting
Before PCI

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14
Q

Diagnosed MI. What we prescribe from antiplatelets?

A

Aspirin and P2Y12 receptor antagonists are administered as soon as MI is diagnosed.

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15
Q

Why give dual therapy in unstable/NSTEMI?

A

To prevent further clot progression

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16
Q

Why need and how long for therapy post PCI?

A

Secondary prevention of cardiac events in patients post PCI and/or stenting.
Aspirin and P2Y12 receptor antagonists should be continued for at least 12 months (if tolerated) after the acute event.

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17
Q

We prescribe aspirin, but there is intolerance. What to prescribe then?

A

P2Y12 receptor antagonists.

Alternative to aspirin in cases of intolerance: to prevent recurrence of thromboembolic events, including ischemic stroke, MI, and symptomatic peripheral arterial disease.

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18
Q

Why antiplatelets needed in PCI?

A

to prevent restenosis

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19
Q

P2Y12 receptor antagonists. adverse 5.

A 
Allergic reactions (rash, pruritus, anaphylaxis)
Hemorrhage 
Gastrointestinal upset (rare)
Possibly TTP (all)
Ticlopidine: neutropenia/agranulocytosis
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20
Q

ASA versus P2Y12 receptor antagonists. Which have lower bleeding risk?

A

P2Y12 receptor antagonists

the risk of hemorrhage is lower than that of acetylsalicylic acid.

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21
Q

Neutropenia/agranulocytosis. What drugs?

A

ticlopidine (P2Y12 rec antag)

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22
Q

P2Y12 receptor antagonists. Which drug is dependent on hepatic CYP?

A

Clopidogrel

Activation is dependent on hepatic cytochrome P enzymes.

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23
Q

P2Y12 receptor antagonists. Which can have interactions in liver?

A

Clopidogrel - ACTIVATION is dependent on CYP, therefore not effective in individual with drug-induced inhibition of CYP enzymes (e.g., cimetidine, amiodarone, omeprazole, etc.)

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24
Q

Genetic polymorphisms of CYP enzymes. Which P2Y12 receptor antagonists will not work?

A

Clopidogrel

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25
Q

Clopidogrel vs prasugrel. Which one is faster acting and more potent?

A

Prasugrel

26
Q

Clopidogrel vs ticagrelor. Which one is faster acting and more potent?

A

Ticagrelor

27
Q

Which P2Y12 receptor antagonist is i/v?

A

Cangrelor

28
Q

ANTIPLATELET CONTRAINDICATIONS?

A

Allergy
Active/recent bleeding within the past 30 days (e.g., gastric ulcers, intracranial bleeding)
Major surgery/severe trauma within the past 30 days
Severe hypertension
Aortic dissection
Thrombocytopenia

29
Q

Why antiplatelets contraindicated in severe HT (>180/90)?

A

Increases risk of hemorrhagic stroke

30
Q

Irreversible cyclooxygenase inhibitors. Agents?

A

Acetylsalicylic acid (ASA, aspirin)

31
Q

Aspirin what is low dose?

A

below 300 mg/day

32
Q

Aspirin what is intermediate dose?

A

300-2400 mg/day

33
Q

Aspirin what is high dose?

A

2400-4000 mg/day

34
Q

Low dose indication?

A

Inhibition of platelet aggregation

35
Q

Intermediate dose indication?

A

Antipyretic and analgesic effect

36
Q

High dose indication?

A

Anti-inflammatory effect

37
Q

How ASA attaches COX? and what group?

A

ASA covalently attaches an acetyl group to COX.

38
Q

ASA Irreversible COX1 inhibition? mechanism

A

Irreversible COX-1 inhibition → TXA2 synthesis in platelets → inhibition of platelet aggregation (antithrombotic effect)

39
Q

ASA Irreversible COX1 and COX2 inhibition? mechanism

A

Irreversible COX-1 and COX-2 inhibition → inhibition of prostacyclin and prostaglandin synthesis → antipyretic, anti-inflammatory, and analgesic effect

40
Q

aspirin Irreversible COX1 inhibition. Onset?

A

within minutes

41
Q

aspirin Irreversible COX1 inhibition. Duration of antiplatelet action?

A

7-10 days

42
Q

!!!!Why aspirin effect on COX1 lasts 7-10 days?

A

Platelets are anuclear and are therefore unable to resynthesize COX enzymes.
The antiplatelet effect of aspirin lasts as long as the lifespan of a platelet, which is 7–10 days. This timeframe should be considered if aspirin is discontinued before a planned procedure.

43
Q

The antiplatelet effect of aspirin lasts as long as the lifespan of a platelet, which is 7–10 days!!!!

A

.

44
Q

To achieve antipiretic/analgetic/antiinflammatory effect need COX2. Why need higher doses of this effect if to achieve inhibition of platelet aggregation is enough low dose of aspirin?

A

COX-2 is more resistant to inhibition than COX-1. Therefore, higher doses of aspirin are required to achieve the antipyretic, anti-inflammatory, and analgesic effects.

45
Q

Indications of ASA?

A

Acute MI
Acute ischemic stroke
Angina (stable and unstable)
Secondary prevention of CVD
Primary prevention of CVD and colorectal cancer
Symptomatic peripheral arterial disease
Giant cell arteritis
Prevention of stent thrombosis after revascularization procedures (e.g., PTCA, CABG, carotid endarterectomy)
See “Non-opioid analgesics” for indications in pain management and inflammation.

46
Q

Patient has stroke –> thrombolysis. When prescribe aspirin?

A

To prevent bleeding, aspirin should not be given in the first 24 hours after thrombolysis.

47
Q

Secondary prevention of CVD and aspirin. Its positive effect?

A

Lifelong aspirin administration decreases the risk of recurrent cardiovascular events in patients who have had an MI, ischemic stroke, or TIA.

48
Q

Primary prevention of CVD and colorectal cancer.

A

Current recommendation: low-dose aspirin for adults 50–59 years of age with a life-expectancy ≥ 10 years, no increased risk of bleeding, and a ≥ 10% risk of developing a CVD/colorectal cancer

49
Q

Why need aspirin in Giant cell arteritis?

A

To decrease the risk of blindness and/or stroke.

50
Q

Why need discontinue aspirin a week prior surgery?

A

The lifespan of a platelet is 7–10 days. If aspirin is held prior to surgery, it should be discontinued one week in advance.

51
Q

Aspirin adverse effects. Groups? 6

A 
GI (most common);
Coagulopathy and bleeding;
Tinnitus;
Renal;
Salicylate poisoning;
Allergic reactions
52
Q

Adverse. Aspirin. Coagulopathy and bleeding. What parameter increased and how long this adverse effect lasts?

A

These effects continue until new platelets are formed.
↑ Bleeding time
PT and aPTT are not affected.

53
Q

Adverse. Aspirin. Why Tinnitus?

A

Aspirin affects the vestibulocochlear nerve

54
Q

Adverse. Aspirin. When occur renal dysfunction? What kind?

A

In case of long-term use;

Acute kidney injury;
Acute interstitial nephritis

55
Q

Adverse. Aspirin. What allergic reactions?

A 
Cutaneous reactions (urticaria, angioedema)
Anaphylactoid reactions - A severe pseudoallergic reaction with symptoms of anaphylaxis (e.g., rash, angioedema). Not IgE-mediated; caused by direct mast cell degranulation (e.g., due to vancomycin or opioid use) or complement-mediated mast cell degranulation.
56
Q

Adverse. Aspirin. GI. What symptoms?

A

Dyspepsia; Gastric ulceration; hemorrhage; perforation

57
Q

Adverse. Aspirin. GI. What mechanism?

A

Gastrointestinal (most common): aspirin blocks COX-1 → inhibition of conversion arachidonic acid to PGH2 → ↓ formation of PGE2 → ↓ secretion of mucus and bicarbonate by epithelium → loss of protective layer on mucosa → gastric acid damages tissue → ↑ risk of ulcers, bleeding, and perforation.

58
Q

Adverse. Aspirin. GI. What element is absent and therefore gastric mucosa is damaged?

A

Decreased production of PGE2

59
Q

Contraindication of aspirin?

A

Febrile illness in individuals < 19 years of age (to avoid reye syndrome)

Acute gout attack (Aspirin use affects uric acid levels and may delay the cessation of symptoms.)

60
Q

What are complications of aspirin? groups of disease?

A

Aspirin-exacerbated respiratory disease (AERD);

Reye

61
Q

AMBOS REYE IR AERD NERA KORTOSE!!! buvo prie antiplatelets skyriaus amboss

A

.

1 STEP Uworld coagulation (6 decks)

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