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Pharmacology > Drugs in the bloodstream > Flashcards

Drugs in the bloodstream Flashcards

1
Q
A
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2
Q

What enzyme does warfarin inhibit

A

Vitamin K epoxide reductase

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3
Q

Warfarin Pharmacokinetic

A

99%plasma prtein bound
almost entirely metabolised by he liver, metabolites excreted in urine + faeces
Elimiation t1/2 35 to 45 hours
Significant drug interactions- either from being displaced from plasma proteins or liver indction/inhibition

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4
Q

What drugs cause inhibition of warfarin metabolism (and so potentiate effects)/

A

Cimetidine
ALcohol
Allopurinol
Erythromycin
Ciprofloxacin
Metronidazole

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5
Q

What can displace warfarin from plasma proteins?

A

NSAIDS

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6
Q

WHat drugs induce enzymes and thus inhibit warfarin action?

A

Barbituates
rifampacin
CArbamazepine

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7
Q

What does cholestyramine do with warfarin?

A

INhibits effect as decreased fat soluble lipid absorption

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8
Q

What is INR

A

the ratio of a patients prothrombin time to a normal control sample

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9
Q

How do you treat high INRs? (INR >8 and RF)

A

Stop warfarin
Can give FFP (15ml/kg) but does not fully revers
Administer Vit K 5mg- will work within 12 hours and 10mg will saturate stores, preventing re-warfarinisation
Prothrombin complex can be used for complete reversal

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10
Q

Risks of warfarin in pregnancy?

A
  • Crosses the placenta and may cause fetal haemorrhage
  • Spont. abortion
  • Stillbirth
  • Neonatal death
    -Teratogenicity (5% incidence of birth defects)
    In later pregnancy central nervous system disorders are more prevalent
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11
Q

What is heparin?

A

Heparin is a glycosaminoglycan, mucopolysaccharide
Organic acid and occurs naturally in the liver and mast cells,
mainly made from porcine intestinal mucosa
molecula weight is 12-15kDa

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12
Q

What is the MOA of heparin

A

Binds reversibly and potentiates antithrombin 3- plasma serine protease inhibitor.

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13
Q

What does ATIII inhibit

A

Mainly coag factors 2, 9 and 10 but can also inhibi 12, 11 and plasmin.
Antiplatelet effects also occur through effects on fibrin

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14
Q

Pharmacokinetics of UFH?

A

Only given SC or IV- negative charge stops oral absorption
Highly plasma protein boung, individual variation leading to differences in efficacy
Low lipid solubility- does not cross BBB or placenta
t1/2 is 30-60 mins
Metabolised by hepatic heparinase
Excreted in the urine

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15
Q

What are lmwh?

A

Short chain polysaccharides with a predictable anticoag action
Avg weight is <8000kDa

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16
Q

What does LMWH act on

A

Full anti xa action but less anti 2a action due to shorte chain lengths

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17
Q

Half life of LMWH and why

A

2-3x longer than unfractionated due to a lower affinity for heparin binding proteins

18
Q

How can you monitor effect of LMWH

A

Xa assays

19
Q

Advantages of LMWH?

A

ONce daily dosing
no need to monitor aptt
smaller risk of bleeding- less plt interaction
Smaller risk of osteoporosis
Smaller risck of HIT
LEss effect on thrombin

20
Q

Commonest adverse reactions to heparin ?

A

Haemorrhage, hyperkalaemia and hypotension if admin. quickly

21
Q

WHat is HIT

A

An immune mediated thromboctopenia where heparin is recognised as foreign.
Heparin binds to plt factor 4 stimulating IgG ab formation and predisposition to thrombosis.
Most are asymptomatic.

22
Q

WHen does the platelet count normally fall in HIT

A

5-14 days after heparin is started, or quicker if pt has received heparin in the last 3 months

23
Q

What is danaparoid?

A

Factor Xa inhibitor, heparinoid. Can be used in HIT. Mixture of heparan, dermatan and condroitin suphatea

24
Q

Advers effects of danaparoid?

A

Low platelets due to some structural similarities with heparin, exacerbations of asthma

25
Q

What is fondaparinux?

A

A synthetic pentasaccharide similar to heparin
Xa inhibition
T1/2 is 21hrs, renally excreted
Risk of HIT is substantially lower

26
Q

What is rivaroxaban?

A

Xa inhibitor

27
Q

What is normal plt turnover?

A

10% per day,

28
Q

WHen will plt function return to normal after aspirin?

A

7-10 days

29
Q

Aspirin pharmacokinetics?

A

Weak acid with a pKA of 3
REadily absorbed in stomach, but greater SA means more in SI
85% plasma protein bound
Half life 15-20 minutes
HYdrolysed to acetic acid and salicyclate.
Converted ot water soluble products in the liver and then excreted by the kidneys

30
Q

What are the water soluble products of aspirin

A

Salicykuric acid + glucuronide

31
Q

Aspiring does what in acute overdose?

A

Uncouples oxidative phosphorylation- increases o2 consumption and co2 production
Initially MV increases, then direct stimulation of resp centre increases RR and leads to a respiratory alkalosis
Impaired aerobic metabolism then leads toa metabolic acidosis

32
Q

Symptoms of aspirin ovedose

A

Tachycardia
Pyrexia
Swaeting
Blurred vision
HYperventilation
Tinnitus

33
Q

Treatment of aspirin OD?

A

ACtivated charcoal early
IV fluids
ALkalinisation of urine with sodium bicarb in significant OD
HD in severely poisoned patients ie
levels >100
neurotoxicity
renal failure
pulmonary oedema
CV instability

34
Q

What is clopidogrel and how does it work

A

Blocks the ADP induced platelet activation pathway (P2Y12ADP)
Prevents platelet activation caused by shear stress after surgery
Irreversible plt effects

35
Q

Pharmacokinetics clopidogrel

A

It is a prodrug activated by oxidation of the thiophene ring by CP450
Rapidly absorbed, extensively metabolised . half life around 8 hours

36
Q

Uses of clopidogrel?

A

POst MI
Prevention of thrombosis post stent
Prevention of vascular ishaemic events in pts with symptomatic atherosclerosis

37
Q

AT what dose of clopi does maximal plt inhibition occur?

A

400mg, can be fully reversed with a plt transfusion

38
Q

MOA of GP2b3a antagonists

A

Block common pathway preventing binding of fibrinogen
reduced plt activity, thrombin effects and neointima formation in damaged arteries
Reduces plt aggregation at 50% occupation and abolish aggregation at 80% occupancy

39
Q

What is Dipyridamole?

A

Pyrimidopyrimidine derivative
ANtiplt- inhibits adhesion to the vessel wall
Vasodilates- particularly at the coronary artery
Excreted by the bilary tree
Half life 1 hours

40
Q

MOA of dipyridamole?

A

PDE inhibito so potentiates prostacyclin
Stimulates prostacyclin
Inhibits the metabolism of adenosine

41
Q
A

Pharmacology (12 decks)

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