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Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define pharmacology

A

Study of drug effects

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2
Q

Define pharmacokinetics

A

How the body affects the drug (ADME)

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3
Q

Define pharmacodynamics

A

How the drug affects the body

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4
Q

Define druggability

A

Ability of a protein target to bind to a small molecule (drug) with high affinity

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5
Q

What are most drug targets?

A

Proteins

e.g. Receptors, enzymes, ion channels, transporters

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6
Q

What are the 3 types of receptor targets?

A 
NT receptors (e.g. mACHR)
Autocoid receptors (e.g. cytokines, histamine)
Hormone receptors (e.g. steroid)
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7
Q

What are 4 receptor types?

A

Ligand-gated ion channels (e.g. nACHR)
GPCR (e.g. mACHR, beta-adrenergic receptors)
Tryptase kinase-linked (e.g. growth factors, insulin)
nuclear/cytosolic (e.g. steroid)

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8
Q

Define potency

A

measure of how well a drug works (basically binding affinity)
e.g. a more potent drug would have a higher receptor response at EC50

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9
Q

Define EC50

A

The concentration at half the maximum response (Emax)

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10
Q

What is the difference between a full and partial agonist?

A

Full agonist can achieve 100% response
Partial agonist has an Emax
Partial agonists are less efficacious

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11
Q

Define intrinsic activity of a drug

A

proportionality factor between the receptor occupacy and tissue response
(Emax/100% response)
Full agonist=1, antagonist=0

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12
Q

what is the difference between selective/competitive antagonism and non-competitive antagonism?

A

Competitive antagonists bind to orthosteric sites so increasing the concentration of the agonist would eventually achieve Emax.
Non-competitive antagonists bind to allosteric sites so increasing the concentration of the agonist would have no effect on the tissue response

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13
Q

What effect do irreversible antagonists have?

A

Permanently block the receptor so can no longer be stimulated. It can only then be endocytosed.

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14
Q

Define affinity

A

How well a ligand binds to a receptor

Shown by both agonist and antagonist

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15
Q

Define efficacy

A

How well a ligand activates a receptor

Only shown by agonists

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16
Q

What equation is used to calculate the no. of available receptors?

A

Furchgott Equation

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17
Q

What does an increase in receptors at a tissue mean for the drug dose?

A

A lower dose would achieve the same response

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18
Q

What do many tissues have a receptor reserve for?

A

Full agonists

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19
Q

Define allosteric modulation

A

Inactivates receptors
Affinity modulation: alters EC50
Efficacy modulation: alters Emax

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20
Q

Define inverse agonism

A

When a ligand binds to orthosteric site causing the opposite effect e.g. propanolol + cimetidine

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21
Q

Define tolerance

A

Down regulation of receptor with prolonged use. Require higher dose to achieve same effects.

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22
Q

Define receptor desensitisation

A

This is when the receptor can’t interact with the G protein –> endocytosed + degraded

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23
Q

Define specificity

A

Relates to the number of certain targets a drug binds to

no drug is completely specific

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24
Q

Define selectivity and give examples of selective and non-selective drugs.

A

Relates to the different effects a drug can cause.

Non-selective: isoprenaline (beta 1 + 2 agonist)
Selective: salbutamol (beta 2 agonist) –> however with continual high doses it can lose its selectivity and activate both beta 1 + 2 receptors.

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25
Q

What are 3 enzymes as drug targets?

A
  1. NSAIDS–> COX
  2. ACEi –> ACE
  3. Beta-Lactam Abs –> inhibit specific enzymes required for peptidoglycan cell wall biosynthesis
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26
Q

How does aspirin affect COX isotypes?

A

Irreversibly inhibits them (forms covalent bonds)

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27
Q

Describe the process of prostanoid synthesis

A

membrane phospholipid –PLA2–> Arachidonic acid –COX–> PGH2 –specific synthases–>
PGD2, (Mast cells)
PGI2, (vascular endothelial cells)
TXA2, (Platelets)
PGE2(Macrophages - mediates most body effects)

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28
Q

What are the 2 COX isotypes?

A

COX-1: Found widely in body

COX-2: induced - by inflammation

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29
Q

What are 2 examples of ACEi?

A

Captopril
Enalapril
Both are peptides that mimic the final AA sequence of angiotensin I (preventing it from binding to ACE)

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30
Q

What are some transporters as drug targets? (4)

A

1) PPIs –> H+/K+ ATPase
2) H2 antagonists –> H2 receptor
3) Diuretics: Thiazides = NCC on DCT, Furosemide (loop diuretics) = NKCC2 on LoH)
4) Neuronal uptake inhibitors –> inhibit synaptic reuptake of NTs

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31
Q

What are 4 synaptic reuptake inhibitors?

A

1) Fluoxetine (prozac) = serotonin
2) Imipramine = serotonin + dopamine (non-selective)
3) Cocaine = dopamine
4) Tiagabine = GABA

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32
Q

Give 2 examples of ion channels as drug targets.

A

1) Calcium channel blockers e.g. amlodipine

2) Local anaesthetics = sodium channel blockers

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33
Q

What is amplodipine used to treat?

A

Calcium channel blocker used for angina, arrhythmias and hypertension

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34
Q

How do lidocaine and procaine work?

A

They inhibit post synaptic voltage gated sodium channels.

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35
Q

What are the 4 phases of pharmacokinetics

A

1) Absorption/uptake
2) Distribution
3) Metabolism
4) Elimination

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36
Q

What is the order of diffusion?

A

First order reaction

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37
Q

Give 5 forms of transport across membranes

A

1) Simple diffusion
2) Facilitated diffusion
3) AT (starts as 1st order –> 0 when fully saturated)
4) Via extracellular spaces (e.g. pores)
5) Non-ionic diffusion

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38
Q

Define non-ionic diffusion and give an example of a drug that utilises this transport mechanism.

A

When a molecule becomes less ionic when it diffuses across a membrane. E.g. ASPIRIN

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39
Q

How does pH effect the diffusion of weak acids across a membrane?

A

Higher pH: weak acid is MORE ionised, so rate of diffusion decreases.
Lower pH: weak acid is LESS ionised so rate of diffusion increases.
So weak acids are best absorbed in acidic environments where there is a lower pH outside cells than inside cells.

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40
Q

How does pH effect the diffusion of weak bases across a membrane?

A

Higher pH: weak base is LESS ionised, so rate of diffusion decreases.
Lower pH: weak base is MORE ionised so rate of diffusion increases.

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41
Q

Why do local anaesthetics not work on abscesses?

A

Because local anaesthetics are weak bases and abscesses have an acidic internal environment.

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42
Q

Define bioavailability (F)

A

The proportion of the volume of drug administered that is taken up by the plasma.
F = [drug uptake into plasma]/[drug administered]

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43
Q

What form of drug administration has a bioavailability of 1?

A

Intravenous

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44
Q

Give an example of a drug administration route

A
  • ORAL
  • SUBLINGUAL
  • NASAL
  • INHALATION
  • TOPICAL
  • TRANSCUTANEOUS
  • SUBCUTANEOUS
  • IV
  • IM
  • INTRATHECAL
  • RECTAL
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45
Q

Why is oral administration the most unpredictable?

A

Because drug absorption depends on various factors including pH (most drugs HA/A-), surface area, diarrhoea.

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46
Q

What drugs can alter the uptake of aspirin?

A

Any drugs that increase the pH of the stomach e.g. PPIs H2 antagonists, antacids.

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47
Q

What effect do drugs decreasing gut motility have of drug absorption?

A

Decrease absorption

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48
Q

What properties affect drug distribution?

A

Drug size and molecular properties.

pH of the compartment and membrane permeability.

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49
Q

Define volume of distribution (Vd)

A

Vd= (total amount of drug in body in body)/[drug in plasma]

Vd (L/kg)= (dose (mg))/[drug in plasma(mg/L)]

Finds how much of the drug is required in the body to get a certain concentration in the plasma (can also be used to calculate dose if you have the Vd and concentration required in the plasma)

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50
Q

Give an example of a drug with a high Vd. What does this mean?

A

Amiodarone (anti-arrhythmatic).
The drug is highly lipid soluble and it can easily be taken up by most body compartments. So a high dose is required to get a certain response from the effect site.
Adjusting infusion rates + achieving steady state plasma levels takes long time.

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51
Q

Give an example of a drug found in the plasma compartment. (CAW)

A

Proteins and large molecules e.g.

  • Crystalloids and colloids (plasma expanders)
  • Antibodies
  • Warfarin
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52
Q

Give an example of a drug found in the interstitial fluid compartment. (MAN)

A

Water soluble drugs e.g.

  • NSAIDs
  • Muscle relaxants
  • Antibiotics
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53
Q

Give an example of a drug found in the ICF compartment. (COALS)

A
  • CNS drugs Steroids
  • Opiods
  • Amiodarone
  • Local anaesthetics
  • Steroids
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54
Q

What 2 main organs are involved in elimination?

A

Liver and kidneys

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55
Q

Define clearance

A

clearance(ml/mg) = (rate of drug elimination (mg/min))/[drug]p (mg/L)

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56
Q

Define renal clearance and name the common marker used.

A

Renal clearance = [drug]U x urine volume/[drug]P

Creatinine (Cr)

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57
Q

What properties do renally excreted drugs commonly have?

A

They are small water-soluble molecules

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58
Q

What can renal impairment lead to?

A
  • Increased plasma urea and creatinine
  • Hypoalbuminaemia
  • Oedema in compartments - unpredictable drug reactions
  • DECREASED CLEARANCE AND ELIMINATION
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59
Q

How should you treat patients with renal impairment? (4)

A

1) Avoid nephrotoxic drugs
2) Replace renal eliminated drugs by liver eliminated drugs.
3) Correct their drug dosage based of their creatinine clearance (normally ≈ 125ml/min)
4) Measure [drug]P if toxicity risk

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60
Q

What is the HER?

A

The proportion of a drug metabolised by 1 pass through the liver.

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61
Q

What does a high HER mean?

A

These drugs are cleared rapidly via liver first pass metabolism.
Perfusion limits rate of elimination.
E.g. Propanolol, Lidocaine

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62
Q

What does a low HER mean?

A

These drugs are inefficiently metabolised by first-pass metabolism in the liver.
Diffusion limits their rate of elimination.
Drugs with a low HER induce liver enzyme synthesis to increase clearance.
E.g. Warfarin, Erythromycin

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63
Q

How are large hydrophilic drugs excreted as opposed to large lipophilic drugs?

A

Large hydrophilic drugs are DIRECTLY removed via BILE.
Large lipophilic drugs are conjugated with UGT (+UDPGA) via phase II detoxification reactions to a hydrophilic glucuronide that can then be removed via BILE.

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64
Q

What happens to pro-drugs in the liver?

A

They are activated via phase I functionalisation reactions which may involve microsomal CYP450 enzymes which oxidise drugs via a heme cofactor.

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65
Q

What 4 main factors does an ideal drug have?

A

1) Low Vd
2) Low toxicity risk
3) Broken down regardless of hepatic/renal function
4) Predictable dose-response relationship

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66
Q

Define steady state plasma levels

A

When uptake rate is in equilibrium with rate of elimination

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67
Q

What is the difference between continuous and pulsatile GnRH delivery?

A 
Continuous = contraception
Pulsatile = fertility treatment
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68
Q

What type of receptor is a nicotinic cholinergic receptor (nAChR) and where is it found?

A

It is a ligand gated ion channel.
Autonomic NS= post-synaptic neuron
Somatic NS= NMJ

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69
Q

What type of receptors are muscarinic cholinergic receptors (mAChR) and where are they found?

A

GPCRs

Found at the autonomic NMJ.

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70
Q

What are the 5 stages of ACh action at the NMJ?

A

1) Synthesis (Acetyl CoA + Choline –> CoA + ACh)
2) Storage (vesicle)
3) Stimulation + release (Na+ IN, Ca2+ IN, vesicle + membrane fuse)
4) Receptor binding (ACh + AChR –> Na+ IN)
5) Inactivation (ACh –AChE–> Acetate + choline (taken up)

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71
Q

How does the botulinum toxin (BOTOX) work at the NMJ?

A

1) Uses proteases to degrade ACh vesicles
2) No ACh released on stimulation
3) Paralysis

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72
Q

What is curare?

A

A competitive nAChR antagonist.

Causes paralysis.

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73
Q

What can be used to reverse the effects of curare?

A

SUGAMMADEX

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74
Q

What is the mechanism of action of suxamethonium?

A

DEPOLARISING BLOCKADE (anaesthetic)

1) Binds to nAChR
2) Desensitises it
3) Paralysis

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75
Q

What is an example of a reversible cholinesterase inhibitor?

A

NEOSTIGMINE (MG treatment)

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76
Q

What is an example of an irreversible cholinesterase inhibitor?

A

ORGANOPHOSPHATES (insecticides + sarin)

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77
Q

What effects do organophosphates have at different cholinergic receptors?

A

1) nAChR: twitching, seizures, muscle weakness, paralysis
2) mAChR: salivation, bradycardia, hypotension, urination, defecation
3) CNS: confusion, convulsions, coma, reflex loss

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78
Q

What are 4 therapeutic targets of muscarinic ligands?

A

1) Eyes: glaucoma - PLIOCARPINE
2) Lungs: asthma/COPD - TRIOTROPIUM (LAMAs)
3) GI: IBS - MEBEVERINE
4) Bladder: BETHANECHOL(agonist - contraction), OXYBUTININ (antagonist - relaxation)

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79
Q

What are some adverse effects of muscarinic ligands?

A

DUMBELS

1) Diarrhoea
2) Urinary incontinence
3) Miosis
4) Bradycardia
5) Emesis (vomitting)
6) Lacrimation (tearing)
7) Salivation + sweating

80
Q

What is HEXAMETHONIUM and what effects does it have?

A

NEURONAL nAChR COMPETITIVE ANTAGONIST

  • PSNS effects: less secretions, constipation, blurred vision urine retention
  • SNS effects: Hypotension (anti-hypertensive)
81
Q

Give 3 examples of AChR ligands in the CNS. (SBD)

A
  1. SCOPOLAMINE (motion sickness) - inhibits ACh at mAChR in vomitting centre
  2. BENZATROPAMINE (Parkinson’s) - inhibits ACh stimulated DA reuptake
  3. DONEPEZIL (Alzheimer’s) - inhibits AChE
82
Q

Describe the synthesis of catecholamines

A

Phenylalanine –> L-tyrosine –> L-DOPA –> dopamine –> adrenaline and noradrenaline (–COMT–> metadrenaline + normetadrenaline)

83
Q

What are 2 enzymes that inactivate catecholamines release?

A

MAO (mono-amine oxidase)

COMT (catechol-o-methyltransferase)

84
Q

What type of receptor are adrenoceptors?

A

GPCRs

85
Q

How do alpha-1 adrenoceptors work?

exactly like M2

A

1) NAd binds to a1
2) Activates Gq protein
3) Activates PLC breakdown of a membrane phospholipid to DAG + IP3
4) DAG activates PKC
5) IP3 acts to increase intracellular Ca2+

VASOCONSTRICTION, PUPIL DILATION, BLADDER RELAXATION

Agonist: PHENYLEPHRINE
Antagonist: DOXAZOSIN

86
Q

How do alpha-2 adrenoceptors work?

like B2Ad

A

1) NAd binds to a2
2) activates Gi protein
3) activates AC (ATP –> cAMP)
4) activates PKA

INHIBITS PRESYNAPTIC NAd RELEASE (negative feedback)

Agonist: CLONIDINE
Antagonist: YOHIMBINE

87
Q

How do beta adrenoceptors work?

A

1) NAd binds to a2
2) activates GS
3) activates AC (ATP–> cAMP)
4) activates PKA

88
Q

What effects does B1 stimulation have? Drug examples?

A

HEART: +ve chronotropism, +ve inotropism, renin secretion

Agonist: DOBUTAMINE
Antagonist: ATENOLOL (beta-blockers)

89
Q

What effects does B2 stimulation have? Drug examples?

A

LUNGS: Broncodilation, vasodilation, increased gut motility

Agonist: SALBUTAMOL (SABAs)

90
Q

What effects does B3 stimulation have? Drug examples?

A

Bladder relaxation, lipolysis

Agonist: MIRABEGRON

91
Q

Give an example of a non-selective adrenergic agonist

A

Adrenaline

Used in: anaphylaxis, acute hypotension, cardiac arrest

92
Q

Give an example of a non-selective adrenergic antagonist

A

1) PROPANOLOL: beta non-selective

2) CARVEDILOL: beta and alpha-1 (decreases BP, VD)

93
Q

What are certain features of PROPANOLOL?

A

Non-selective BAd antagonist.

Membrane stabilising activity (MSA) - can inhibit AP propagation so treat arrhythmias.

94
Q

What drug should you NEVER give to asthmatics?

A

BETABLOCKERS

95
Q

What are some indirect adrenergic agonists?

A
  • Amphetamines + cocaine

- MAO + COMT inhibitors

96
Q

Define pain and give 3 advantages.

A

An unpleasant sensory and emotional experience associated with actual/potential tissue damage

1) Warning of tissue damage
2) Immobilisation for healing
3) Memory establishment

97
Q

How do nociceptive/neuropathic pain differ?

A

Nociceptive involves nociceptor stimulation, neuropathic involves neuronal tissue damage.

98
Q

After how many weeks does acute pain become classed as chronic?

A

12 weeks

99
Q

What are the 4 main stages of the ascending pain pathway?

A

1) Noxious stimuli
2) Tissue damage (PG synthesis)
3) Nociceptor stimulation (Ad/c fibres + substance P)
4) Lateral spinothalamic tract (3 order) (2nd ON decussates)
5) Pain sensation

100
Q

Summarise the gate-controlled theory.

A

Non-noxious stimuli trigger larger A beta fibres, these override smaller pain fibres and ‘close the gate’ to pain transmissions to the CNS.

101
Q

What is the descending pain pathway an example of and where does it take place?

A

An endogenous pain control system activated under extreme stress.
Periaqueductal grey matter

102
Q

Summarise the descending pain pathway.

A

1) Serotonin + NAd neurons: inhibit the 1st ON (substance P release)
2) Opiod interneurons: release endogenous opiods (e.g. enkephalins and endorphins) which inhibit both the 1st and 2nd ON
3) These produce profound analgesia

103
Q

What is the basis of pain treatment? (3)

A

1) Decrease excitatory NTs (e.g. Local anaethetics)
2) Decease PGs (e.g. NSAIDs)
3) Increase inhibitory NTs (e.g. Antidepressants)

104
Q

What percentage can’t metabolise morphine or codeine?

A

10%

105
Q

Give 2 naturally occurring opiods.

A

Morphine

Codeine

106
Q

Give an example of an opiod which has had simple molecular modifications. (DOD)

A

Diamorphine (heroin)
Oxycodone
Dihydrocodeine

107
Q

Give an example of a synthetic opiod.

A 
Pithidine
Fentanyl (very potent)
Remifentanil (very potent)
Alfentanil (very potent)
Tramadol
108
Q

What is a synthetic partial opiod that DOESN’T cause respiratory depression but isn’t as potent?

A

Buprenorphine

109
Q

What is an opiod antagonist?

A

NALOXONE!!

110
Q

Why is it better to give morphine via IV infusion rather than orally?

A

Because morphine has a 50% oral bioavailability so only half the dose (5mg) is required via IV.

111
Q

If respiratory depression is such a devastating side effect of opiod OD, why can inpatients control their own administration?

A

Because they would fall asleep before it occurs.

Can only give 1mg every 5 minutes as well.

112
Q

What makes diamorphine (heroin) more dangerous than morphine?

A

More potent and faster acting.

Can cross the BBB

113
Q

What does opiod induced sustained activation of the descending pain pathway cause?

A

TOLERANCE + DEPENDENCE + ADDICTION

114
Q

What are the 4 types of opiod receptors

A

1) μ / MOP
2) delta / DOP
3) kappa / KOP
4) Nociceptin opiod-like receptor

115
Q

Which receptor do all current opiod drugs target?

A

MOP

116
Q

What is significant about the kappa / KOP receptor?

A

Causes depression instead euphoria

117
Q

What dose of morphine, diamorphine and buprenorphine have the same efficacy but different potency?

A

10mg morphine
5mg diamorphine
100mg buprenorphine

118
Q

How long do opiod withdrawal symptoms last?

A

Start within 24 hours and last ≈ 72

119
Q

What drug can be used to slowly and safely decrease opiod dosage?

A

METHODONE

120
Q

Give 3 side effects of opiods. (NICE SIR)

A 
Nausea + vomiting
Immune suppression
Constipation
Endocrine effects
Sedation
Itching
Respiratory depression
121
Q

What should you always do when starting IV opiods?

A

LOW DOSE + TITRATE UP

122
Q

Quick, there’s an opiod induced respiratory depression what do I do?

A

1) ABCDE

2) IV NALOXONE 400ug/ml - has a short half life so give DEPOT and titrate to effect

123
Q

What microsomal enzyme metabolises codeine to morphine?

A

CYP2D6

124
Q

What % of the population has less active CYP2D6?

A

10-15%

125
Q

What % of the population has overactive CYP2D6?

A

5%
So banned in children + pregnant/breast feeding mums
Titrated to effect

126
Q

What % of the population have no CYP2D6?

A

10%

127
Q

Why should you not give opiod to a patient with <30% renal function?

A

It can accumulate in the nephron and cause respiratory depression

128
Q

What is morphine metabolised by the liver?

A

Morphine-6-glucuronide

129
Q

What is tramadol?

A

A weak opiod agonist and also inhibits 5-HT and DA reuptake

130
Q

What is homeopathy?

A

‘treating like with like’
Symptom causing substances in healthy people, used to treat ill patients.
They don’t interfere with other meds but are prone to placebo effect.

131
Q

Give an advantage and a disadvantage of medicinal herbalism.

A

Advantage: Can be effective.
Disadvatages: Can interfere with other medications + are usually produced by an unregulated industry.

132
Q

What drug originates from the periwinkle plant and is used to treat cancer?

A

Vincristine

Vinblastine

133
Q

What drug originates from the poppy plant and is used as analgesia?

A

Morphine

Codeine

134
Q

What drug originates from the deadly nightshade and is used to treat scarlett fever?

A

Atropine

135
Q

What drug originates from the Foxglove plant and is used to treat AF?

A

Digitalis/Digoxin

136
Q

What are 2 forms of drug development?

A 
Fermentation (e.g. penicillin)
Rational design (e.g. propanolol)
137
Q

What are insulin analogues formed by?

A

Recombinant DNA

138
Q

How are monoclonal Abs (-mab) formed?

A

1) Mouse immunised against specific An
2) B cells checked for specific Ab production
3) Spleen removed + specific B cell obtained
4) Specific B cell + myeloma cell –> HYBRIDOMAs
5) Clonal expansion of hybridomas (infinite Ab production)
6) mAbs extracted

139
Q

What are the 3 forms of mAbs?

A

1) MURINE (mouse - derived) -mab
2) CHIMERIC (human + mouse mix) -ximab
3) HUMANISED (3 hyper-variable regions) -zumab

140
Q

Briefly describe the process of gene therapy drug production.

A

1) Combinatorial chemistry + biosynthesis produces a huge library of compounds
2) Compounds go through HTS (High throughput screening)
3) Generates HITs
4) Generates LEADs
5) Long, expensive, ^ attrition rate process –> DRUG

141
Q

What is the most common classification of ADRs (adverse drug reactions)?

A

Rawlin-Thompson ABCDE classification

142
Q

What are Type A ADRs?

A
  • Augmented
  • Most common
  • Dose-related extension of clinical effects
    E.g.
    PRIMARY: Anticoagulant –> bleeding
    SECONDARY: B blocker –> bronchoconstriction
143
Q

What are Type B ADRs?

A
  • Bizarre
  • Unexpected
  • Mostly hypersensitivity reactions
  • Idiosyncrasy
    E.g. Heparin –> hair loss
144
Q

What are Type C ADRs?

A
  • Chronic
  • After long-term use
    E.g. Steroids–> hyperglycaemia(DMT2) / Cushing’s syndrome
145
Q

What are Type D ADRs?

A
  • Delayed
  • Occur months-years after treatment
    E.g.
    Chemotherapy –6 weeks–> leukopenia
    Thalidomide + birth defects
146
Q

What are Type E ADRs?

A
  • End-of-use
  • Occurs after treatment stopped
    E.g. Opiod withdrawal symptoms
147
Q

What are the 5 questions asked to identify the ADR?

A

1) Predictable? [A]
2) Allergic reaction? [B]
3) Long-term use? [C]
4) Drug history? [D]
5) Withdrawing? [E]

148
Q

What can increase ADR susceptibility?

A

1) Pregnancy
2) Age >65
3) Female
4) Drug interactions
5) Diseases
6) Diet & alcohol
7) Genetics + hypersensitivity

149
Q

What are the 2 types of anaphylaxis?

A

IMMUNE: IgE-mediated

NON-IMMUNE: direct mast cell degranulation

150
Q

Are Type A ADRs drug allergies?

A

No!!

151
Q

What is used to report ADRs?

A

MHRA yellow-card scheme.
Strength: Continual safety monitoring
Limitation: Not all ADRs reported (only 10% severe reactions reported)

152
Q

Give 4 drug interactions

A

1) Summation: 1 + 1 = 2
2) Synergism: 1 + 1 > 2
3) Potentiation: 1 + 1 = 1 + 1.5
4) Antagonism: 1 + 1 = 0 (E.g. beta blocker and beta-2 agonist)

153
Q

What is the name for Amoxicillin + clavulonic acid

A

Augmentin (AB with less likely resistance)

154
Q

What are patient risk factors for drug interactions? (PHOG)

A

Polypharmacy
Hepatic/renal impairment
Old age
Genetics

155
Q

What are drug property risk factors for drug interactions?

A

1) Saturable metabolism (so low HER)
2) Steep dose/response curves
3) Narrow therapeutic index (between ED50 + TD50)

156
Q

Give examples of pharmacokinetic mechanisms of drug interactions.

A

1) Alter gut motility
2) Alter pH
3) Alter solubility of the other drug
4) Form non-absorbed complexes
5) Directly alter enterocyte function
6) Alter active drug distribution
7) Alter liver metabolism
8) Alter excretion

157
Q

Would a weak base be excreted faster if urine is acidic or alkali?

A

ACIDIC

158
Q

Would a weak acid be excreted faster if urine is acidic or alkali?

A

ALKALI

159
Q

What are 3 broad pharmacodynamic mechanisms of drug interactions?

A

1) Receptor based mechanisms (agonist etc)
2) Signal transduction (
3) Physiological system interactions (drugs affecting different receptors in same system)

160
Q

What can beta blockers e.g. propanolol cause in diabetics?

A

Can prevent detection of fall in BGL.

Beta-2 blocker: inhibits hyperglycaemic response
Beta-3 blocker: inhibits adipocyte detection and alteration of BGLs.

161
Q

What is the ‘triple whammy’ drug response? (DAN)

A

Diuretic
ACEi
NSAID

162
Q

How does grapefruit juice affect drugs?

A

Grapefruit juice is a CYP4A3 inhibitor, and modulates PGP in enterocytes.
Increases the bioavailibility + effectiveness of drugs e.g. Ca2+ channel blockers and anti-transplant rejection drugs.

163
Q

How does avocado affect the absorption of fat soluble drugs like warfarin?

A

It causes them to dissolve due to its high fat content, decreasing its effectiveness.

164
Q

What are 3 actions of NSAIDs?

A

AAA

1) Anti-inflamatory
2) Analgesic
3) Anti-pyrexic

165
Q

What is an adverse drug reaction?

A

A noxious and unintended response to a drug/combination of drugs

166
Q

Describe how rational drug design works.

A

Focuses on developing an antagonist from an agonist. Looks at electrostatic charge, solubility and bulk.

167
Q

Define a side effect.

A

An unintended effect of a drug related to its pharmacological properties. Can be beneficial.

168
Q

How does the drug dose related to its therapeutic range determine its ADR effect type?

A

Above therapeutic index = TOXIC EFFECTS
Within therapeutic index = COLLATERAL EFFECTS
Below therapeutic index = HYPERSUSCEPTIBILITY EFFECTS

169
Q

What is an example of a mild ADR?

A

Nausea, drowsiness, itchy rash

170
Q

What is an example of a severe ADR?

A

Respiratory depression, neutropenia, anaphylaxis, catastrophic haemorrhage

171
Q

What are some examples of time dependent reactions?

A

1) Rapid
2) First dose
3) Early
4) Intermediate
5) Late
6) Delayed

172
Q

What is an example of a rapid reaction?

A

Red man syndrome.

Due to histamine release on rapid admin of vancomycin

173
Q

What is a common example of a first dose reaction?

A

Hypotension and ACEi

174
Q

What type of reaction is Stevens-Johnson syndrome?

A

Intermediate - delayed immunological reaction e.g. to carbamazepine.

175
Q

Other than the Rawlins Thompson ABCDE classification, how else can ADRs be classified?

A

DoTS

  • Dose related? (toxic, collateral, hypersusceptibility)
  • Timing? (e.g. fast infusion)
  • Suceptibility of patient?
176
Q

What are F type ADRs?

A
  • Failure of therapy

E.g. OCP failure in presence of enzyme inducers

177
Q

Define idiosyncrasy.

A

Inherent abnormal drug response.

E.g. Enzyme deficiency, abnormal receptor activity

178
Q

Give 3 of the most common drugs to have ADR’s.

A

1) Antibiotics
2) Anti-neoplastics
3) Cardiovascular drugs
4) Hypoglycaemics
5) NSAIDS
6) CNS drugs

179
Q

What are the most common systems affected by ADRs? (ReGIMED)

A 
Renal
GI
Metabolic
Endocrine
Dermatological
(+ haemorrhagic)
180
Q

What are some common ADRs?

A
  • Confusion
  • Nausea
  • Balance problems
  • Hypotension
  • Constipation/Diarrhoea
181
Q

What % of ADRs are preventable?

A

30-50%

182
Q

What are black triangle  drugs?

A

A drug undergoing additional monitoring

183
Q

What drugs MUST be reported on the Yellow card?

A

1) All suspected ADRs for: vaccines and black triangle drugs

2) All serious suspected reactions

184
Q

What 3 factors determine a serious reaction?

A

1) Fatal/life threatening
2) Disabling/incapacitating
3) Result in/prolong hospitalisation

185
Q

Define anaphylaxis.

A

Extreme allergic reaction

186
Q

Are non-immune anaphylactoid reactions considered a type 1 HS?

A

NO!
They do not involve prior exposure and IgE antibodies, despite being clinically identical to immune acute anaphylaxis.
They involve direct mast cell degranulation.

187
Q

Do anaphylactic reactions always involve urticaria?

A

NO!

Absent 10-20% of the time.

188
Q

What is the usual presentation of anaphylaxis?

A
  • Immediate
  • Swelling with central cyanosis
  • Wheezing, SOB
  • Urticaria
  • Hypotension
  • Cardiac arrest
  • Anaphylactic shock (lose consciousness)
189
Q

What is the alternative presentation of anaphylaxis?

A
  • CARDIORESPIRATORY ARREST
190
Q

What is the 4 step management of anaphylaxis?

A

1) ABCDE
2) Recovery position
3) Get help
4) ADRENALINE: 500ug IM
5) Establish airway (HIGH FLOW OXYGEN)
6) IV fluid, glucocorticoids + anti-histamines
7) Equipment: ECG, pulse oximetry, BP

191
Q

What is the most common antihistamine used in anaphylaxis?

A

IM CHLORPHENAMINE 10mg

192
Q

What is the most common glucocorticoid used in anaphylaxis?

A

IM HYDROCORTISONE 100-200mg

193
Q

Why do you give IV fluids e.g. 500-1000ml colloids in anaphylaxis?

A

Because blood volume is greatly reduced due to increased vascular permeability and exudation.

194
Q

Why is adrenaline given in anaphylaxis?

A

Non-selective adrenergic agonist.

Can vasoconstrict, bronchodilate, inhibit mast cells, myocardial contraction.

195
Q

Why might a second dose of adrenaline be required in anaphylaxis? And it what route must it be administered?

A

If there is no improvement in the patient.

IV administration must be started.

196
Q

What confirmatory blood test is taken to diagnose anaphylaxis?

A

MAST CELL TRYPTASE.

Ideally 3 timed samples.

1) Immediately
2) 1-2 hrs after symptom onset
3) <24 hrs post onset

Phase 2a (5 decks)

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