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Phase 2 > Pharmacology 2 > Flashcards

Pharmacology 2 Flashcards

1
Q

What is Pharmacodynamics?

A

How the drug affects the body

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2
Q

What is pharmacokinetics?

A

How body affects the drug
ADME Absorption, Distribution, Metabolism, Excretion

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3
Q

Drug Receptor types

A

Ligand-gated ion channels - nicotinic ACh receptors

G Protein Coupled receptors (GPCR’s) - beta-adrenoceptors

Kinase-linked receptors - for growth factors

Cytosolic/nuclear receptors - steroid

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4
Q

What questions should you ask when prescribing a drug, with pharmacokinetics in mind?

A

How quickly will drug reach its site of action? How quickly will I see a response?
Drug interactions likely?
Is a dose adjustment needed in certain disease states?
What monitoring is required?

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5
Q

What mechanisms do drugs use to permeate membranes?

A
  1. Passive diffusion through hydrophobic membranes - lipid soluble molecules
  2. Passive diffusion through aqueous pores - only v small soluble drugs, e.g. lithium
  3. Carrier mediated drugs - quite unusual, basically when proteins that usually transport sugars, amino acids etc transport drugs
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6
Q

How does drug ionisation affect drug absorption?

A

Ionised drugs have poor lipid solubility
∴ only unionised drugs can pass

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7
Q

Why are the majority of medications PO?

A

Convenient
Cost-effective

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8
Q

Where are medications that are weak bases best absorbed? Why?

A

In the small intestine
bc small intestine has a pH of ~ 6.5 ∴ more likely to be similar pH to pKa of medication (the pH at which ionised & unionised drug is 50/50)

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9
Q

Where are medications that are weak acids best absorbed? Why?

A

In stomach
bc stomach has a pH of ~ 3 ∴ more likely to be similar pH to pKa of medication (the pH at which ionised & unionised drug is 50/50)

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10
Q

What factors affect the oral drug absorption in the stomach?

A

Gastric enzymes - digest the drug, esp large protein drugs e.g. insulin (∴ never given orally)

Low pH - can degrade

Full stomach = slower absorption

Gastric motility - can be altered by drugs/disease

Prev. surgery

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11
Q

What factors affect the oral drug absorption in the small intestine?

A

Drug structure - large/hydrophillic molecules are poorly absorbed

Medicine formulation - i.e. capsule has a coating to control release
Modified release slows rate of absorption (bc less freq dosing)

P-glycoprotein - will remove substrates from endothelial cells back into lumen lol

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12
Q

What is first pass metabolism?

A

Metabolism of drugs which prevents them from reaching systemic circulation
(The fraction of drug lost at absorption)

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13
Q

How does first pass metabolism occur?

A

Degradation by enzymes in intestinal wall
&
Absorption from intestine into hepatic portal vein and metabolism via liver enzymes

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14
Q

What is bioavailability?

A

Proportion of administered dose which reaches the systemic circulation

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15
Q

What is bioavailability (F) dependent on?

A

Dependent on extent of drug absorption and extent of first pass metabolism
NOT dependent on rate of absorption

Varies w/ route of administration and between individuals
e.g. tablet has lower bioavailability (F) than IV

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16
Q

What is bioavailability expressed as?

A

% or fraction

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17
Q

Pros of PR route

A

Local administration
Avoids first pass metabolism
Helps if patients has severe N/V ∴ can’t take meds orally

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18
Q

Cons of PR route

A

Absorption is variable
Patient preference

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19
Q

Example of PR medication

A

Diazepam suppositories for epileptic seizures

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20
Q

Pros of INH route

A

Well perfused large SA
Local administration

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21
Q

Cons of INH route

A

Inhaler technique might be ineffective

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22
Q

Example of INH route meds

A

Gaseous anaesthetic
Salbutamol inhaler

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23
Q

Pros of SC route

A

Faster onset than PO
Formulation can be changed to control absorption rate

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24
Q

Cons of SC route

A

Not as rapid as IV

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25
Q

Examples of SC route meds

A

Long acting insulin for T1DM and T2DM

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26
Q

Pros of TD route

A

Provides continuous drug release
Avoids first pass metabolism

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27
Q

Cons of TD route

A

Only suitable for lipid soluble drugs
Slow onset of action

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28
Q

Examples of TD route medication

A

Fentanyl patches for severe chronic pain

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29
Q

What factors influence distribution?

A
  1. Molecule size (small, ↑ distribution)
  2. Lipid solubility (if lipophillic, ↑ distribution)
  3. Protein binding (if NOT protein bound, ↑ distribution)
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30
Q

What is the volume of distribution (Vd)?

A

Also sometimes known as apparent volume of distribution

Theoretical vol a drug will be distributed in the body
Vol of plasma required to contain the total administered dose

If well distributed, high Vd
If poorly distributed, low Vd

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31
Q

What is the blood brain barrier?

A

Membrane that separates foreign substances in blood from CNS

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32
Q

Describe the physical aspect of the BBB

A

Continuous layer of endothelial cells with tight junctions
Has high number of efflux pumps that remove water soluble molecules

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33
Q

How can drugs reach the CNS?

A

High lipid solubility - can permeate and diffuse across BBB
Intrathecal route
Inflammation - causes BBB to be leaky ∴ drugs can cross

34
Q

In actuality, what must you think about when prescribing drugs, in relation to distribution?

A

Careful w dosing drugs with a small Vd - using actual body weight in obese patients
e.g. Aciclovir NOT distributed to fat ∴ should be dosed based on ideal body weight, not actual

Distribution changes in diff disease states (i.e. sepsis = leaky blood vessels = BBB penetration)

Age changes body composition, which changes Vd of water soluble drugs

Drugs that can cross BBB have CNS s/e

35
Q

What is drug elimination?

A

The process by which the drug becomes no longer available to exert its effect on the body

36
Q

Name 2 methods of drug elimination

A

Metabolism - modification of drug to new chemical entity
Excretion of unchanged drug

37
Q

What are the 2 phases of metabolism?

A
  1. Oxidation / Reduction / Hydrolysis to introduce reactive group to chemical structure
  2. Conjugation of functional group to produce hydrophillic, inert molecule

then excreted

38
Q

What cytochrome is mainly responsible for Phase 1 metabolism? Where are these located?

A

Cytochrome P450 (CYP450)
Mostly in liver (also small intestine, lung)

39
Q

When will CYP enzyme function vary?

A

Genetic variation
↓ Function in severe liver disease
Interactions w/ drugs/foods which can ↑ or ↓ activity

40
Q

How many CYP450 enzymes are there?

A

57

41
Q

What CYP enzyme has the substrates caffeine, paracetamol, theophylline and warfarin?

A

CYP 1A2

42
Q

What CYP enzyme has the substrates ibuprofen and warfarin?

A

CYP 2C9

43
Q

What CYP enzyme has the substrates codeine and warfarin?

A

CYP 2D6

44
Q

What CYP enzyme has the substrates simvastatin, warfarin, DOACs, carbamazapine and diltiazem?

A

CYP 3A4

45
Q

What substrates are associated with CYP1A2?

A

Caffeine, paracetamol, theophylline, warfarin

46
Q

What substrates are associated with CYP2C9?

A

Ibuprofen, warfarin

47
Q

What substrates are associated with CYP2C19?

A

Omeprazole, phenytoin

48
Q

What substrates are associated with CYP2D6?

A

Codeine, warfarin

49
Q

What substrates are associated with CYP3A4?

A

simvastatin, warfarin, DOACs, carbamazapine and diltiazem

50
Q

Which are the most signif CYP for drug metabolism?

A

3A4, 2C9, 2C19, 1A2, 2D6

51
Q

In actuality, what must you think about when prescribing drugs, in relation to metabolism?

A

If severe liver impairment, is metabolism reduced?
∴ reduced dose? additional monitoring? avoid??

Drug interactions

Saturation of metabolic pathways can lead to accumulation or toxicity (paracetamol overdose)

52
Q

If normal dose of paracetamol, how is it metabolised?

A

Via glucuronidation and sulphation to form a non-toxic metabolite

53
Q

If paracetamol overdose, how is it metabolised? What is the result? How do we treat this?

A

Normal pathway is saturated
∴ Oxidation by CYP2E1

Forms NAPQI (v toxic)
Causes hepatocyte necrosis ∴ liver failure

We would give IV n-acetyl cysteine (NAC)
Replenishes body’s stores of glutathione
∴ glutathione conjugation
∴ produces a non-toxic metabolite :)

54
Q

When would we give a reduced paracetamol dose?

A

In low body weight patients
Or if severe hepatic impairment

55
Q

In what forms can drugs/metabolites be excreted?

A

Liquids - small polar molecules e.g. urine, bile, sweat, tears, breast milk

Solids - large molecules e.g. faeces (thru biliary excretion)

Gases - volatiles e.g. expired air

56
Q

What is the first process that accounts for renal excretion?

A
  1. Glomerular filtration
    Free/unbound drug molecules will pass through
    V large molecules will be excluded and will go thru efferent arteriole
57
Q

What is the 2nd process of renal excretion?

A
  1. Active tubular secretion
    Drug molecules transported from blood into renal tubule thru carriers
    (organic anion transporter (OAT) & organic cation transporter (OCT))

Can clear protein bound drugs

Most effective renal clearance mechanism

58
Q

What is the 3rd process of renal excretion?

A
  1. Passive reabsorption
    Diffusion down conc gradient from tubule into peritubular capillaries

Hydrophobic drugs diffuse easily
Highly polar drugs will be excreted

59
Q

Types of Adverse drug reactions

A

ABCDEFG

Augmented
Bizarre
Chronic/continuing
Delayed
End of use/withdrawal
Failure of treatment
Genetic

60
Q

What is Augmented ADR caused by?

A

Exaggerated effect of drugs pharmacology at therapeutic dose
Usually not fatal

61
Q

What is the most common ADR?

A

Augmented (80%)

62
Q

When is Augumented ADR dependent on?

A

Dose dependent
Reversible when drug is withdrawn

63
Q

Give some examples of Augmented ADR

A

AKI w/ ACE-i
Bradycardia w/ beta blockers
Hypoglycaemia w/ gliclazide, insulin
Resp depression w/ opiates
Bleedings w/ anticoag

64
Q

Describe Bizarre ADRs

A

Not related to pharm
Not dose related
Can cause serious illness/death
Symptoms don’t always resolve when stopping drug

65
Q

Give examples of a Bizarre ADR

A

Anaphylaxis w/ penicillin
Tendon rupture w/ quinolone abx
Steven Johnson Syndrome w/ IV vancomycin

66
Q

What is a Chronic/Continuous ADR?

A

An ADR that continues after drug has been stopped

67
Q

Give examples of Chronic/Continuing ADR

A

Osteonecrosis of the jaw w/ bisphosphonates
HF w/ pioglitazone

68
Q

What is a delayed ADR?

A

ADRs that become apparent some time after stopping drug

69
Q

Give an example of a delayed ADR

A

Leucopenia w/ chemo

70
Q

What is an End of Use/Withdrawal ADR?

A

ADR that develops after drug has been stopped

71
Q

Give examples of End of Use/Withdrawal ADR

A

Insomnia after stopping benzodiazepine
Rebound tachycardia after stopping BB

72
Q

What could cause a Failure of treatment ADR?

A

Drug-drug or drug-food interaction
Poor compliance with administration instructions

73
Q

Give examples of a Type F ADR

A

Failure of bisphosphonates due to taking w/ food
Failure of DOAC due to enzyme inducer (e.g. carbamazepine)

74
Q

What is a Genetic ADR?

A

When drug causes irreversible damage to genome

75
Q

Give an example of a Genetic ADR

A

Phocomelia in children of women taking thalidomide

76
Q

Other than the ABCDEFG classification, what is another way of classifying ADRs?

A

DoTS

Dose-relatedness
Timing
Susceptibility

77
Q

Describe the Do in DoTS

A

Dose relatedness
Looks at the dose you might get a ADR

//
Hypersusceptibility reaction
When you get an ADR at a subtherapeutic dose
e.g. anaphylaxis w/ penicillin

Collateral effect
ADR at a therapeutic dose
e.g. hypokalaemia w/ loop diuretic

Toxic effects
ADR at subpratherapeutic dose
e.g. liver damage w/ paracetamol

78
Q

Describe the T in DoTS

A

Timing
When does ADR develop in relation to the drug taken

TYPES :
Rapid
First dose
Early
Intermediate
Late
Delayed

79
Q

Describe the S in DoTS

A

Susceptibility
Certain patients/groups have specific susceptibility to ADRs

Could be due to :
Age
Gender
Disease states
Physiological states

80
Q
A

Phase 2 (24 decks)

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