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DYS: Pharmacology + ADME > Clinical pharmacology + ADME > Flashcards

Clinical pharmacology + ADME Flashcards

1
Q

Pharmacokinetics

A

Time course of a drug from absorption to elimination
Determines drug regimen
- Dose
- How often

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2
Q

Therapeutic drug monitoring

A

Measuring plasma concentration after patient takes drug

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3
Q

Absorption mechanism

A

Active Transport
Bulk flow of water
Passive diffusion

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4
Q

Active transport

A

Drugs structurally-related to endogenous chemical

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5
Q

Bulk flow of water

A

Small water-soluble drugs

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6
Q

Passive diffusion

A

Movement of drugs

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7
Q

Small Intestines

A

Large surface area = 200m^3
Good blood flow
Long residence time
- High levels of unionised drugs

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8
Q

First-pass metabolism

A

Drug absorbed from small intestines to liver via hepatic portal vein

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9
Q

Calculate Bioavailability (F)

A

F = AUC oral / AUC iv

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10
Q

Clearance (Cl)

A

Volume of plasma cleared of drug per unit of time

  • ml/min
  • l/hr
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11
Q

Calculate Clearance

A

Clearance = Renal clearance + Hepatic clearance

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12
Q

Volume of distribution (Vd)

A

Apparent volume in which a drug is dissolved in the body

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13
Q

Regimens

A

Convenient dosing to obtain stable plasma concentration within window

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14
Q

How does the presence of food affect stomach?

A

Prescence of food increases time in stomach

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15
Q

Acid stable drugs

A

Slowed absorption

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16
Q

Acid labile drugs

A

Stay longer + more readily broken down

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17
Q

Example of Acid labile drugs

A

PPIs - they are given in gastro-resistant capsules

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18
Q

Half life

A

Time for plasma concentration to decrease by 50%

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19
Q

Calculate half life

A

t1/2 = 0.693 / K = 0.693Vd / Cl

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20
Q

K

A

Rate constant = fraction eliminated per unit time

K = Clearance / Vd

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21
Q

Calculate dose given

A

Dose given = Amount needed / F

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22
Q

Where does absorption take place

A

After taken an oral dosage form: it crosses gastrointestinal tract to blood stream

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23
Q

What alters absorption

A

Food / gastric emptying

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24
Q

First order kinetics

A

Rate of elimination is proportional to concentration of drug

Ct = Coe^-kt

25
Q

Ct (in first order of kinetics)

A

Conc at t=t

26
Q

Co (in first order of kinetics)

A

Conc at t=0

27
Q

K (in first order of kinetics)

A

Rate constant

28
Q

T (in first order of kinetics)

A

Time

29
Q

Resources to find out drug interactions

A

BNF
Stockley’s drug interactions
Computer alerts

30
Q

What inhibits CyP450

A 
Cimetidine
Antifungal agents (Ketoconazole)
Erythromycin / clarithromycin (macrolide)
Ciclosporin
Psolaralen
31
Q

What is the speed of the onset of CYP450 inhibition

A

1-2 days = Rapid onset

Reverses quickly on stopping

32
Q

What makes clopidogrel less effective

A

Omeprazole

- therefore avoid omeprazole and esomeprazole

33
Q

Types of drug interactions

A

Drug - drug

Drug - food

34
Q

Enzyme induction

A

Increase activity of metabolising enzyme

35
Q

What drugs have an effect on metabolism

A

Metoprolol - enhance action of poor metabolisers
Fluoxetine
Codeine - reduced response in poor metabolisers ( needs to be metabolically converted)
Tamoxifen -

36
Q

GI tract interactions

A
  • pH (drugs are passively absorbed best unionised; rise in pH can influence absorption of other drugs)
  • Absorption (2 drugs may alter absorotion)
  • GI motility/emptying (affect - absorption = metoclopramide acclerates absoription of other drugs)
  • Binding (colestyramine binds bile in GI Tract to prevent its reabsorption)
37
Q

What can increase pH

A

Antacids, PPIs, H2RAs

38
Q

MDR 1 (+other known names)

A

multiple drug resistance is an efflux transporter or pump which pumps drugs out into lumen (P-glycoprotein / ATP binding cassette = ABC)

  • Digoxin is a substrate
  • Rifampicin = inducer
  • Verapamil = inhibits (also psoralen
39
Q

Why does omeprazole make clopidogrel less effective

A

Due to being biotransformed by same Cyt P450

  • includes esomeprazole
  • clopidogrel no longer converted to active metabolite
40
Q

What is the current advice to take clopidogrel

A

Use another H2RA / PPI

  • not cimetidine
  • pantoprazole does not affect Cyt P450 + evidence suggest that it does not interact
41
Q

Most common polymorphism

A

SNP - single nucleotide polymorphism

  • mutations
  • lead to amino acid substitution (sickle cell)
42
Q

Therapeutic monitoring window for induction + inhibition

A

Inhibitor
Therapeutic window
Inducer

43
Q

What drugs are enzyme inducers + what do they do

A 
Barbiturates
Rifampicin
Griseofulvin
Phenytoin
Ethanol
Carbamazepine -  autoinduction
St John's wort

They reduce conc of a range of drugs as the increase metabolism of OCs

44
Q

How long is the onset of enzyme inducers

A

1-2 weeks

- effects can still continue after stopping inducer

45
Q

What increases drug interactions

A

Polypharmacy
Conditions e.g. renal impariment
- problem for drugs with narrow therapeutic window

46
Q

CYP2D6

A 
Genetic polymorphism
- poor metaboliser of debrisoquine
- homozygous for recessive genes
Extensive metaboliser = wild type
Ultrarapid metabolisers = multiple copies of CYP2D6 gene
47
Q

How do you report an ADR?

A

Yellow card Scheme
In BNF, submit to CSM (committee on safety of medicines) who monitor ADRs
- especially new meds + ADRs resulting in hospital admission

Report all black triangle drugs

48
Q

Type A ADR

A

Augmented responses - Undesirable pharmacological response
Dose-related
Predictable

49
Q

Type B ADR

A 
Bizarre
Unrelated to pharmacology 
Unpredictable
Rare
Severe 
Related to genetic or immunology
50
Q

Ulcerogenic effects of NSAIDs

A

NSAIDs + corticosteroids associated with peptic ulceration/damage

51
Q

State how ulcerogenic effects of NSAIDs can be minimised

A

Use paracetamol instead for pain-relief

Use PPI with Misoprostol (stable PGE1 analogue, acts on prostanoid receptors to inhibit gastric H+ secretion)

52
Q

Example of an immunological

A

Penicillin allergy

  • Treat with H1 - antagonist
  • allergic to one means likely to be allergic to all
53
Q

NSAIDs

A

Non-steroidal anti-inflammatory drugs

  • aspirin, ibuprofen, diclofenac
  • inhibit cyclooxygenase
  • pain-relief
  • anti-platelet
  • aniti-pyretic
  • anti-inflammatory
54
Q

How can you manage Type A

A

Managed by dose adjustment

55
Q

Most important ADR

A

NSAIDs

56
Q

% of hospital admissions ADR-related

A

5%

57
Q

% of hospital patients that suffer an ADR

A

10-20%

58
Q

% of patients who die from ADR

A

0.1%

DYS: Pharmacology + ADME (6 decks)

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