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PR3154 Midterms > IC3a (standard drugs) > Flashcards

IC3a (standard drugs) Flashcards

1
Q

what is the mechanism of action of dipyridamole?

A

adenosine binds to A2 receptor = acitvated = ATP converted to CAMP by AC then to AMP by PDE3. CAMP also reduces calcium ion concentration.

Dipyridamole inhibits reuptake of adenosine, increasing plasma adenosine levels and activation of the A2 receptor.

Dipyridamole inhibits PDE3 reducing CAMP degradation

both lead to increased CAMP levels resulting in decreased ca2+

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2
Q

what is the other effect of dipyridamole

A

will inhibit adenosine reuptake and pde in vascular smooth muscle causing vasodilation.

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3
Q

in view of the effect, what is the other indication for dipyridamole

A

vasodilator properties used to stimulate exercise for myocardial perfusion imaging (induce reflex tachycardia and increase cardiac perfusion)

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4
Q

what is the onset and peak effect of oral dipyridamole

A

onset 20-30min
peak 2-2.5 hours

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5
Q

what is DOA of dipyridamole

A

3 hours

need to be modified release/

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6
Q

ADR dipyridamole and caution

A

headache, hypotension, dizzy, flush, GI distrubance (diarrhoea, N/V)

caution bleeding with other anticoauglants/platelets, esp heparin

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7
Q

c/i of dipyridamole

A

1)hypersx
2) hypotension or severe CAD
- reflex tachycardia = mi, angina, ecg…

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8
Q

ddi of dipyridamole

A

adenosine = increase cardiac adenosine levels

cholinersterase inhibitors (eg donepezil, rivastigmine: aggravate myasthenia gravis

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9
Q

what is the moa of aspirin (description of the drug class also) AND DOSING

A

it is a reversible cox inhibitor with selectivity for cox 1 over cox 2
inhibition of cox 1 = inhibits txa2 production. txa2 promotes platelet aggregation and vasoconstriction. (7-10 days for new platelet to form)

however, cox 2 inhibition inhibits pgi2 formation. pgi2 inhibits platelet aggregation as well.

therefore low dose OD dosing preferred over TDS-QDS to allow cox 2 enzyme synthesis (3-4 hours)
- 75-325mg loading, 40-160mg daily

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10
Q

ADR of aspirin (and reason)

A

upper gi events like gastric ulcer, bleeding due to inhibition of cox1 causing inhibition of production of protective prostaglandin in the stomach.

increased bleeding

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11
Q

c/i and caution for aspirn

A

caution in platelet and bleeding disorders

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12
Q

role of adp in platelet aggregation

A

adp binds to p2y12 receptors on platelet = promote the adp mediated increase in cell surface expression of gp2b-3a receptors = inhibit platelet aggregation via fibrinogen and activation of platelet (for release of agonists)

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13
Q

ddi of aspirin

A

caution bleeidng iwth other antiplatelets and anticoagulants

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14
Q

clopidogrel vs ticagrelor vs prasugrel
- moa and binding
- onset
- reversibility

A

clopidogrel is a product with active metabolite binding irreversibly to the adp binding site of p2y12
- delayed onset 6-8 hours and interindividual variability due to cyp2c19 mediated metabolism
- duration of action 7-10 days (lifetime of platelt)

VS

ticagrelor (not a prodrug) with reversible inhibtion (NOT at the same binding site) to inhibit g protein action and signalling
- faster onset
- recovery depends on serum conc of parent and active metabolite = 2-3days

vs

prasugrel is a prodrug with irreversible inhibition of p2y12
- more ptoent
- depend on 3a4, 2b6 metabolism

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15
Q

adr clopidogrel and ticagrelor

A

bleeding, haemorrhage (esp intracranial)., dyspepsia, rash

bronchospasm, dyspnoea, hypotension (due to p2y12 receptors of lungs and heart)

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16
Q

c/i and caution of clopidogrel

A

1) hypersx
2) active apatholoigical bleeeding

caution: at risk of bleeding, cyp2c19 variants

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17
Q

ddi clopidogrel

A

warfarin, nsaid, salicylates = increase risk of bleeding

macrolide = reduce effect

strong 2c19 inhibitors eg ppi, fluoxetine, ketonazole) = reduce effect (cannot convert to active metabolite)

rifamycin - increase effect

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18
Q

ddi tiacgrelor

A

1) anticoagulants, fibrinolytics, & long-term NSAIDs may ↑bleeding risk

2) Aspirin doses >100 mg/day decrease ticagrelor effect but ↑bleeding risk

3) CYP3A inducers (e.g., dexamethasone, phenytoin, etc) may decrease ticagrelor level and antiplatelet effect

4) CYP3A strong inhibitors (e.g., clarithromycin, ketoconazole, etc) may
↑ticagrelor level and risk of adverse reactions

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19
Q

c.i and caution for ticagrelor

A

c/i hypersx, severe hepatic impairment, breast feeding
c/i hx of intracranial haemorrhage, active pathological bleeding (e.g. PUD)

caution: risk of bleeding, elderly, moderate hepatic failrue

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20
Q

moa of vit k antagonist warfarin

A

acts on all 3 pathways

warfarin inhibits vit k reductase enzyme (vkorc1) that reactivates oxidised vit k (epoxide) to the active form (hydroquinone)

prevents the carboxylation and activation of factor 2, 7, 9, 10. (which also converts active vit k to oxidised inactive form)

21
Q

warfarin onset, time to peak, full therapeutic effect, DOA, absorption speed

A

24-72 hours onset
peak 2-8h oral
full effect 5-7 days
duration 2-5 days
rapid and compleete oral absorption

22
Q

warfarin metabolism, t1/2, polymorphism

A

hepatic, 2c9 primarily
with 20-60 t1/2

polymorphism in 2c9 and vkorc1

23
Q

warfarin excretion

A

urine and faeces

24
Q

warfarin adr

A

haemorrhage/bleeding

hepatitis (increased with >60y, male, on warfarin<1month)

cutaneous necrosis and breast/butt/extremeties infarction (3-5days after initiation, due to reduced blood supply to adipose tissue)

25
Q

c/I warfarin

A

hypers

bleeding: active bleeding, risk of pathological bleeding, after recent major surgery

HTN: severe/malignant hypertension

renal/hepatic: several renal or hepatic disease

infection: severe bacterial endocarditis, pericarditis, pericardial effusion

pregnancy (teratogenic) = haemorrahgic disorder of foetus

26
Q

caution warfarin

A

breastfeeding

diverticulitis/colitis
mid-mod HTN
mid-mod hepatic or renal disease
drainage tubes in any orifice

27
Q

ddi warfarin

A

paracetamol long-term therapy (> 2 weeks) at high doses (> 2g/day) may increase bleeding

2c9 inhibitor
Numerous drugs (including allopurinol, NSAIDs, salicylates, proton
pump inhibitors, metronidazole, etc) may ↑risk of bleeding

Numerous traditional medicines, herbs, supplements, and foods (including gingko, ginseng, reishi mushrooms, cranberry juice, etc)
may ↑risk of bleeding

Numerous drugs (including barbiturates, rifampin corticosteroids, spironolactone, thiazide diuretics, etc)
*- diuretic increase concentration of clotting factors. *
- rest are 2c9 inducers
** may DECREASE efficacy of warfarin **

Numerous traditional medicines, herbs, and supplements (including supplements containing vitamin K, green tea, vitamin K-rich foods,
etc) may DECREASE efficacy of warfarin

28
Q

is warfarin used in pregnancy?

A

does not cross placental, not associated with fatal malformations

29
Q

what are the properties of dabigatran etexilate

A

prodrug to dabigatran
dabigatran and acyl glucuronide metabolites are competitive, reversible non-peptide antagonists of thrombin (2a)

30
Q

what are the properties of rivaroxaban

A

competitive reversible antagonist of activate factor x (xa)

31
Q

what reverses dabigatran

A

idarucizumab
- humanised monoclonal atb = binds to dabs and metabolites with higher affinity than they have for thrombin.

emergency or urgent surgery; life threatening bleeiding

32
Q

what reverses rivaroxaban

A

andexanet alfa

recombinant modified human factor xa decoy protein

33
Q

pk dabigatran (ba, peak, metabolism, t1/2, excretion)

A

BA: 3-7%
peak: 3h
metabolism: excreted unchanged
t1/2: 12-17
excretion: urine

34
Q

pk Rivaroxaban (ba, peak, metabolism, t1/2, excretion)

A

BA: 80-100%
peak: 2.5-4h
metabolism: hepatic
t1/2: 5-9h
excretion: urine 66, faeces 28

35
Q

ddi dabigatran

A

↑risk of bleeding: antiplatelets,
anticoagulants, fibrinolytics,
NSAIDs, ketoconazole
DECREASE dabigatran level:
rifampin

36
Q

ddi Rivaroxaban

A

↑risk of bleeding: anitplatelets,
anticoagulants, NSAIDs, P-glyco-
protein (P-gp) & CYP3A4 inhibitors

DECREASE rivaroxaban level:
P-gp)& CYP3A4 inducers

37
Q

difference in pk of heparin vs lmwh

A

BA: 30 vs 86-98
t1/2: 1 vs 4
renal excretion: no vs yes
thrombocytopenia risk: <5 vs <1%

lmwh preferred due to longer half life, higher BA

38
Q

moa heparin and lmwh

A

potentiate antithrombin iii through binding + conformational change
= inactivate thrombin

heparin: 2a, 10a, (9a, 11a, 12a).
lmwh: 10a (and lesser extent, 2a)

39
Q

ADR of heparin and lmwh

A

bleeding

epidural /spinal hematoma and paralysis in those receiving epidural/spinal anesthesias/spinal puncture

heparin induced thrombocytopenia
- bind to pf4 on activated platelet surface = heparin-pf4 complex = ing antibody.

40
Q

what reverses heparin

A

protamine sulfate IV infusion
- highly basic peptide binds to negatively charged heparin neutralising it

(only partial in lmwh)

41
Q

heparin and lmwh c/i

A

hypersx pork products or heparin
active major bleeding
thrombocytopenia or antiplatelet antibodies

42
Q

caution for heparin / lmwh

A

elderly,

risk of bleeding: prosthetic heart valve, major surgery, regional or lumbar block anaesthesia, blood dyscrasia, recent childbirth,

pericarditis, pericardial effusion,

renal insufficiency (for lmwh)

43
Q

ddi heparin/lmwh

A

↑risk of bleeding: anitplatelets, anticoagulants, fibrinolytics,
NSAIDs, SSRIs

↑risk of bleeding: with various herbs/foods, including
chamomile, fenugreek, garlic, ginger, ginkgo, ginseng.

44
Q

what are r-tpa drugs and special properties

A

recombinant tissue plasminogen activator drugs ie alteplase. (ends with -teplase)
- the drugs have longer plasma t1/2 vs native tPA
- bind preferentially to clot associated plasminogen (compared to urokinase, streptokinase)

45
Q

ADR of alteplase

A

1) BLEEDING: haemorrhage/bleeding

2) CARDIAC: Ventricular arrhythmias, hypotension, oedema

3) EMBOLISM: Cholesterol embolization, venous thromboembolism

4) Hypersensitivity and anaphylaxis

46
Q

reversal agents for alteplase

A

trenaxamic acid OR aminocaproic acid

  • compete for binding at lysine on plasminogen and plasmin
47
Q

c/I of alteplase

A

active bleeding, prior intracranial haemorrhage, recent intracranial/spinal surgery (<3months), serious head injury, stroke

48
Q

caution of alteplase

A

Caution in patients with

major surgery within 10 days,

risk of bleeding
(e.g., peptic ulcer),

cerebrovascular disease, mitral stenosis, atrial
fibrillation,

acute pericarditis or subacute bacterial endocarditis

49
Q

ddi of alteplase

A

increase bleeding risk with antiplatelets esp dipyridamole, aspirin) and anticoags (esp warfarin and heparin)

decrease alteplase level: nitroglycerin

PR3154 Midterms (8 decks)

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