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Blood & Lymph > Antiplatelets, Anticoagulants & Thrombolytics 1 > Flashcards

Antiplatelets, Anticoagulants & Thrombolytics 1 Flashcards

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1
Q

3 classes of drugs that keep platelets in control

A
  1. Anti-platelet
  2. Anti-coagulant
  3. Fibrinolysis
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2
Q

Which polymorphisms must you be aware of in platelet drugs (2)?

A
  1. warfarin
  2. clopidogrel
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3
Q

Where do platelet clotting factors assemble?

A

On the surface of platelets → change shape to spiny structure increasing surface area & charge. This helps the factors assemble and expose phosphatidyl C ring → Ca2+ binds surface & clotting factors

(w/o activation → no clotting)

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4
Q

Aspirin MOA

A

Irreversible inhibition of COX-1 & COX-2 → suppress thromboxanes & prostaglandins

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5
Q

How does Aspirin inhibit COX enzymes

A

attaches acetyl group → steric hindrance → cannot come into contact w/arachidonic acid → no Thromboxane A2

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6
Q

Aspirin indications (2)

A
  1. TIA
  2. Acute coronary syndrome (NSTEMI or STEMI MI)

(fever, pain & headache)

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7
Q

Aspirin contraindications (5)

A
  1. GI ulcer
  2. Hx of asthma
  3. Children: chicken pox of flu → reye’s syndrome
  4. Combo w/methotrexate
  5. Last trimester of pregnancy
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8
Q

Why can aspirin not be used w/methotrexate (15 mg/week)?

A

reduces methotrexate elimination → decreases renal clearance & displaces it from protein binding sites → hematologic toxicity

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9
Q

Why is aspirin not given to women in the 3rd trimester of pregnancy?

A

acetylation of fetal enzymes

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10
Q

How does aspirin cause GI bleeding?

A

blocking prostaglandin synthesis → decreased renewal of epithelium cells → decreased mucus production & protection of the stomach lining.

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11
Q

Aspirin Adverse Effects (7)

A
  1. Hemolytic anemia
  2. Bleeding: GU, gingiva
  3. GI inflammation, heartburn
  4. Asthma, anaphylaxis, nasal congestion
  5. Mental confusion, drowsiness
  6. Tinnitis, hearing loss
  7. Dizzy, vertigo
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12
Q

Hemolytic anemia may occur when ______ patients are given aspirin

A

G6PD deficient

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13
Q

At low dose, aspirin _____ (increases/decreases) gout attack; high dose ______ (increases/decreases) the risk of gout attack.

A
  • increases
  • decreases
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14
Q

P2Y12 receptor antagonist MOA: stops GPIIb/IIIa activation → decreases platelet aggregation by ______ (2).

A
  1. decreases Ca release
  2. increases cAMP levels
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15
Q

Clopidogrel MOA

A
  1. prodrug metabolized by CYP2C19
  2. Irreversible blocks ADP receptor on platelets (lasts 7 days; life of platelet)

(dose-dependent; metabolized by CYP450)

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16
Q

Clopidogrel drug interactions (3)

A
  1. CYP2C19 inhibitors (omeprazole or Esomeprazole)
  2. Opioids
  3. Repaglinide

(may need to genotype your patient first)

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17
Q

Prasugrel is a prodrug, like clopidogrel, and is converted to active metabolite by _____ (2) enzymes. It irreversibly inhibits ______.

A
  • CYP3A4, CYP2B6
  • P2Y12

(indicated for acute coronary syndrome)

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18
Q

Prasugrel contraindications (2)

A
  1. pathological bleeding
  2. Hx TIA/stroke
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19
Q

Which 2 P2Y12 antagonists are reversible inhibitors?

A
  1. ticagrelor (also p-glycoprotein inhibitor)
  2. Cangrelor

(clopidogrel & prasugrel are irreversible inhibitors)

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20
Q

Which is the only antiplatelet drug that is NOT given orally?

A

Cangrelor (IV)

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21
Q

Why would you give cangrelor instead of another P2Y12 antagonist?

A

hepatic disease; this drug is not metabolized by the liver

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22
Q

How do GP2b/3a inhibitors work?

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A

prevents fibrinogen from binding and bringing platelets together

23
Q

GP2b/3a inhibitors

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A
  1. Abciximab
  2. Eptifibatide
24
Q

Abciximab is intended for use with _______ (2)

Study These Flashcards
A
  1. aspirin
  2. heparin

(for coronary intervention)

25
Abciximab is a chimeric human-murine monoclonal ab against glycoprotein 2b/3a receptor of platelets. It is produced by \_\_\_\_\_\_\_.
continuous perfusion in mammalian cells
26
Abciximab onset? Platelet recovery?
1. rapid: half-life \< 10 min 2. platelet recovery w/in 48 hours
27
Thrombin inhibitors bind to \_\_\_\_\_\_. Why is this receptor unique?
* PAR1 * Carriers its own ligand (it just needs enzyme to cleave it → activation)
28
Vorapaxar is indicated for patients w/\_\_\_\_\_\_.
hx of MI or peripheral artery disease
29
Vorapaxar MOA
thrombin inhibitor: reversible antagonist of PAR-1 (protease-activated receptor-1) (long half life: 4 weeks!)
30
Cilostazol indicated to reduce \_\_\_\_\_\_\_
symptoms of intermittent claudication
31
Cilostazol MOA
inhibits phosphodiesterase III activity → inhibits platelet aggregation & vasodilation
32
Cilostazol contraindications
heart failure
33
Cilostazol: AE
1. tachycardia, palpitations 2. thrombocytopenia 3. leukopenia
34
What is the major targets of coagulation inhibition (2)?
1. Prevention of Thrombin IIa formation (inhibiting Xa) 2. second most effective is factor X
35
INR measures \_\_\_\_\_
warfarin activity (PT monitors this as well)
36
Normal prothrombin time
11-15 seconds ***_(prolonged in patients on warfarin; may double)_***
37
INR =
PT patient/ PT normal)ISIS (ISI determined by manufacturer of thromboplastin reagent)
38
Typical INR range
1.1
39
INR range of \_\_\_\_\_is an effective therapeutic range for warfarin
2-3
40
aPTT (activated partial thromboplastin time) uses (2)
1. heparin activity 2. investigate bleeding disorders
41
Normal PTT
35 seconds
42
How is [heparin] measured?
Anti-Xa activity
43
Which 2 classes of drugs are Direct/Novel Oral Anticoagulants (DOAC/NOAC)?
1. Factor Xa inhibitors 2. Thrombin (Factor IIa) inhibitors
44
List the factor Xa inhibitors (4)
1. Apixaban 2. Rivaroxaban 3. Edoxaban 4. Betrixaban (the -"xaban"s)
45
List the thrombin (factor IIa) inhibitor
Dabigatran
46
Rivaro**XA**ban reduces the risk of _______ & treats ______ (2).
1. stroke, systemic embolism in nonvalvular a-fib 2. DVT, pulmonary embolism
47
Patients with a renal clearance \< \_\_\_\_\_\_mL/min should not use RivaroXAban. Why?
* 15 * excretion is mainly via tubular & glomerular filtration
48
RivaroXAban discontinuation may increase risk of \_\_\_\_\_\_
stroke in nonvalvular a-fib ***_(Dabigatran also increases risk of thrombotic events if d/c early)_***
49
ApiXAban recommended dosage
5 mg 2xs/daily
50
ApiXAban contraindications (2)
1. Pregnancy & Lactation 2. Severe hepatic impairment
51
ApiXAban should NOT be used with ______ (Rx)
ELIQUIS (P-gp & strong CYP3A4 inhibitors also)
52
ApiXAban BetriXAban & EdoXAban inhibit \_\_\_\_\_(2).
1. free & clot-bound FXa 2. prothrombinase activity
53
EdoXaban reduces risk of \_\_\_\_\_
stroke & PE in patients w/nonvalvular a-fib

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