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Phase 2a Medicine > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is synergy?

A

When the drug effects add up

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2
Q

Give two drugs that use synergy

A

Co-amoxiclav - amoxicillin and clavulanic acid

Co-codamol - paracetamol and codeine

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3
Q

Name 4 foods that monoamine oxidase inhibitors react with

A
  1. Chocolate
  2. Cheese
  3. Wine
  4. Marmite
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4
Q

Give 5 patient risk factors for drug interactions

A
  1. Genetics (also racial genetic differences) - people handle drugs differently
  2. Hepatic disease
  3. Renal disease
  4. Polypharmacy
  5. Age
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5
Q

Give 3 drug risk factors for drug interactions

A
  1. Narrow therapeutic index (small window between therapeutic effect and toxic effect)
  2. Steep dose-response curve
  3. Saturable metabolism e.g. alcohol (alcohol dehydrogenase saturated), paracetamol
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6
Q

What does ‘pharmacokinetic’ mean?

A

What the body does to the drug

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7
Q

Give 4 examples of pharmacokinetic actions

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion
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8
Q

Why do antacids reduce the absorption of antiretrovirals?

A

Antacids increase the pH in the stomach, which affects the ionisation of the antiretroviral drug compounds, making them more difficult to absorb

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9
Q

What 5 things can affect absorption of a drug?

A
  1. Motility
  2. Acidity
  3. Solubility
  4. Complex formation
  5. Direct action on enterocytes
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10
Q

How is grapefruit juice pharmacologically active?

A

It inhibits P-glycoprotein (transporter that affects drug uptake)

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11
Q

Why are drugs more likely to have toxic effects at lower levels in critically ill patients?

A

If the liver is failing, less albumin is being produced, which means less of the drug is bound to albumin and there are more free drug compounds in circulation.

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12
Q

Why is it important not to drink alcohol when taking metronidazole?

A

Metronidazole inhibits alcohol dehydrogenase –> alcohol cannot be broken down –> leads to accumulation of formalin-like products

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13
Q

What is CYP450?

A

A haemoprotein that plays a key role in the metabolism of various drugs

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14
Q

What happens if drug A inhibits metabolism of drug B?

A

There will be more free drug B in the plasma, leading to increased effects (unless drug B is a pro-drug and needs to be metabolised in order to work)

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15
Q

What happens if drug C induces the CYP450 enzyme, leading to increased metabolism of drug D?

A

Drug D will see decreased therapeutic effects, unless it is a pro-drug, in which case the effects will instead be increased.

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16
Q

Which iso-enzyme breaks down caffeine, theophylline, phenacetin, clomipramine, clozapine and thoradazine?

A

CYP 1A2

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17
Q

Name 4 drugs that inhibit CYP 1A2

A
  1. Omeprazole
  2. Nicotine
  3. Cimetidine
  4. Ciprofloxacin
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18
Q

Name 4 drugs that induce CYP 1A2

A
  1. Phenobarbital
  2. Fluvoxamine
  3. Venlafaxine
  4. Ticlodipine
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19
Q

Why does avocado affect warfarin?

A

It is a CYP450 inductor

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20
Q

Why might people in poorer countries take grapefruit juice alongside drugs such as Ca2+ channel blockers?

A

Grapefruit juice inhibits CYP450, meaning that less of the drug is broken down. This allows the patient to take a lower dose of the drug.

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21
Q

Give 2 ways in which drugs can be excreted

A
  1. Renal (in most cases)

2. Biliary excretion (e.g. morphine)

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22
Q

How do things that change the pH of urine affect the excretion of drugs?

A

Renal excretion is pH dependent - weak bases are cleared faster if the urine is acidic and weak acids are cleared faster if the urine is more alkaline.

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23
Q

What problem might an asthmatic with hypertension have with regard to medication?

A

Beta blockers used to treat hypertension can reduce the effectiveness of salbutamol because salbutamol is a beta-2 agonist.

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24
Q

What problem can beta blockers cause for diabetics?

A

Beta blockers can suppress the ability of a diabetic to sense a hypoglycaemic episode.

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25
Q

What three things make up the ‘triple whammy’ that causes renal failure?

A
  1. NSAID/Cox-2 inhibitor
  2. ACE inhibitor
  3. Dehydration/furosemide
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26
Q

What is ‘druggability’?

A

The concept of a biological target that is known to/predicted to bind with high affinity to a drug

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27
Q

What are the 4 main types of protein targeted by drugs?

A
  1. Receptors
  2. Enzymes
  3. Transporters
  4. Ion channels
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28
Q

What are kinases?

A

Enzymes that catalyse the transfer of phosphate groups between proteins (phosphorylation) –> phosphate group donated by ATP to substrate

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29
Q

How do nuclear receptors work?

A

By modifying gene transcription, e.g. by interacting with proteins to cause a conformational change that allows DNA binding domain to become accessible

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30
Q

What condition is caused by the loss of ACh receptors?

A

Myaesthenia gravis

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31
Q

What condition can result from increased c-kit receptors?

A

Mastocytosis

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32
Q

What is EC50?

A

The concentration of an agonist that gives half the maximal response

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33
Q

What can EC50 be used to measure?

A

Potency

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34
Q

What is Emax?

A

The maximum response possible

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35
Q

What is Emax used to measure?

A

Efficacy

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36
Q

How do non-competitive antagonists work?

A

Rather than competing for the same binding site, the non-competitive antagonist causes a conformational change to prevent agonist binding

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37
Q

What is the agonist and the antagonist of muscarinic cholinergic receptors?

A

Agonist: Muscarine
Antagonist: Atropine

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38
Q

What is the agonist and antagonist of nicotinic cholinergic receptors?

A

Agonist: Nicotine
Antagonist: Curare

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39
Q

How many types of histamine receptor are there?

A

4

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40
Q

What is the H1 receptor involved in?

A

Allergic conditions

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41
Q

What is the H2 receptor involved in?

A

Gastric acid secretion

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42
Q

What sort of disorders involve H3 receptors?

A

Mostly CNS disorders (e.g. narcolepsy, ADD, Alzheimer’s, schizophrenia)

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43
Q

In what sort of conditions is the H4 receptor implicated?

A

Immune system and inflammatory conditions (e.g. rhinitis, pruritus, asthma)

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44
Q

What 2 receptor-related factors affect drug action?

A

Affinity and efficacy

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45
Q

What 2 tissue-related factors affect drug action?

A

Receptor number and signal amplification

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46
Q

What is affinity of a receptor agonist?

A

How well a ligand binds to a receptor

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47
Q

What is efficacy of a receptor agonist?

A

How well a ligand activates the receptor once it has bound

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48
Q

Why might the same receptor and the same agonist lead to a different level of response in a different tissue?

A

Because of differences in signalling e.g. through the activation of transcription factors

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49
Q

What is inverse agonism?

A

When a drug binds to the same receptor as an agonist, but induces a pharmacological response opposite to that of the agonist.

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50
Q

What is tolerance?

A

Tolerance is developed slowly if a pathway is continuously blocked, resulting in a reduction in agonist effect over time. This means that a higher dose is required for effect.

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51
Q

What is densitisation?

A

Desensitisation occurs rapidly - receptors can be uncoupled, internalised and degraded

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52
Q

Why is it better to use salbutamol to treat asthma rather than isoprenaline?

A

Salbutamol is selective for B2 receptors in the lung, whereas isoprenaline antagonises B1 receptors as well, which are found in the heart –> could cause tachycardia

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53
Q

What is an enzyme inhibitor?

A

A molecule that binds to an enzyme and (normally) decreases its activity

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54
Q

How do enzyme inhibitors work?

A

By preventing the substrate from entering the active site, thereby preventing the enzyme from catalysing its reaction.

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55
Q

What is the difference in mechanism between irreversible and reversible enzyme inhibitors?

A

Irreversible inhibitors usually react with the enzyme and change it chemically (e.g. via covalent bond formation)

Reversible enzyme inhibitors bind non-covalently, either to the enzyme, enzyme-substrate complex or both

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56
Q

Statins are used for primary prevention of cardiovascular disease. How do statins work?

A

They inhibit the enzyme HMG-CoA reductase, which blocks the rate-limiting step in the cholesterol pathway, reducing levels of ‘bad’ cholesterol.

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57
Q

ACE inhibitors are used to treat hypertension. How do they work?

A

They block conversion of angiotensin I to angiotensin II, thereby inhibiting the renin-angiotensin-aldosterone system and decreasing blood pressure.

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58
Q

Parkinson’s disease is caused by the degeneration of dopaminergic neurons. Name 3 enzymes involved in the dopamine pathway that could be targets for Parkinson’s treatment.

A
  1. Dopamine decarboxylase (DDC) - inhibiting this in the periphery means more L-dopa is able to cross the BBB into the CNS
  2. Catechol-O-methyl transferase (COMT) - converts L-dopa into 3-methyl dopa (3MT) - inhibiting this means more L-dopa can be converted to dopamine.
  3. Monoamine oxidase B - inhibiting this prevents dopamine breakdown, increasing dopamine availability.
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59
Q

Furosemide is a loop diuretic. How do loop diuretics work?

A

They inhibit the NKCC channels in the thick ascending loop of Henle, preventing reabsorption of Na, Cl and K and therefore increasing urine output

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60
Q

Amiloride is a high affinity diuretic, often used with thiazide. How does it work?

A

It blocks ENaC (epithelial sodium channel) in the collecting ducts of the nephrons (also in colon, lung and sweat glands), preventing reabsorption of sodium, thereby increasing urine output

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61
Q

What is the target of thiazide diuretics?

A

The Na/Cl co-transporter in the distal convoluted tubule

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62
Q

How does amlodipine decrease blood pressure?

A

Amlodipine is an angioselective calcium channel blocker, which inhibits the influx of calcium ions, particularly in vascular smooth muscle cells. This results in vasodilation, a reduction in peripheral resistance and therefore decreased blood pressure.

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63
Q

How can lidocaine be used to regulate arrhythmias of the heart?

A

It blocks transmission of action potentials by blocking voltage-gated sodium channels.

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64
Q

Explain how repaglinide, nateglinide and sulfonylureas can be used to treat type II diabetes

A

They block ligand-gated K channels in pancreatic beta cells. As the channel is closed, potassium cannot leave the cell and the membrane depolarises, causing the voltage-gated calcium channels to open, which stimulates exocytosis of insulin-containing vesicles

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65
Q

Explain how barbiturates cause depression of the central nervous system.

A

Barbiturates bind to the GABA-A complex (ligand-gated Cl- channel), increasing its permeability to chloride and thereby inducing hyperpolarisation, making depolarisation and therefore the conduction of action potentials more difficult.

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66
Q

Digoxin is used to treat atrial fibrillation, atrial flutter and heart failure by lengthening the cardiac action potential. How does it do this?

A

Digoxin inhibits Na/K ATPase, mainly in the myocardium. As Na/K ATPase normally pumps 3 Na out and 2 K in against concentration gradients, inhibition leads to an increase in intracellular Na, leading to decreased activity of the Na/Ca exchanger and therefore increase in intracellular Ca.

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67
Q

Explain how PPIs such as omeprazole work

A

They inhibit hydrogen/potassium ATPase in the stomach, meaning there is less H+ available to form HCl –> reduces stomach acid secretion

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68
Q

Organophosphates include insecticides such as diazinon and nerve gases such as sarin. How do these work?

A

They are irreversible inhibitors of cholinesterase, which results in ACh not being broken down.

69
Q

What are the symptoms caused by too much ACh at muscarinic receptors?

A

Salivation, defaecation, urination, bradycardia and hypotension

70
Q

What are the symptoms caused by too much ACh at nicotinic receptors?

A

Twitching, severe weakness and paralysis of the diaphragm

71
Q

What 3 categories can the autonomic nervous system be divided into?

A
  1. Sympathetic
  2. Enteric (GI)
  3. Parasympathetic
72
Q

Give 3 differences between the somatic and autonomic divisions of efferent peripheral nervous system

A
  1. Somatic: single neuron between CNS and skeletal muscle
    Autonomic: two neuron chain (separated by autonomic ganglion)
  2. Somatic: innervates skeletal muscle
    Autonomic: innervates smooth muscle, cardiac muscle and glands
  3. Somatic: leads to muscle excitation only
    Autonomic: leads to excitation or inhibition
73
Q

In general, which receptors does ACh act on in the preganglionic neuron?

A

Nicotinic receptors; N1 for sympathetic, N2 for parasympathetic

74
Q

In general, which receptors does ACh act on in the postganglionic neuron?

A

Muscarinic receptors (parasympathetic)

75
Q

Which neurotransmitter acts on postganglionic alpha and beta receptors as part of the sympathetic nervous system?

A

Noradrenaline

76
Q

Why does nicotine stimulate both the sympathetic and parasympathetic nervous systems?

A

Because it acts on both N1 (sympathetic) and N2 (parasympathetic) receptors

77
Q

Muscarine is derived from a poisonous mushroom. Which receptors does it act on and which system does it affect?

A

Acts on muscarinic receptors, affects the parasympathetic nervous system.

78
Q

How many types of muscarinic receptors are there and where are they found?

A 
5 types:
M1 - brain
M2 - heart
M3 - all organs with parasympathetic innervation
M4 - mainly CNS
M5 - mainly CNS
79
Q

What sort of receptors are muscarinic receptors?

A

G protein coupled receptors

80
Q

What does activation of M2 receptors at the SA node do?

A

Decreases heart rate

81
Q

What does activation of M2 receptors at the AV node do?

A

Decreases conduction velocity

82
Q

What is the only place in the body where the sympathetic nervous system releases ACh and what happens?

A

The skin - stimulation of M3 receptors in the skin causes sweating

83
Q

What happens when M3 receptors in the respiratory system are activated?

A

Mucus production

Smooth muscle contraction

84
Q

What happens when M3 receptors in the GI tract are activated?

A

Increased saliva production, gut motility and biliary secretion

85
Q

What happens when urinary system M3 receptors are stimulated?

A

Detrusor muscle contracts

Internal urethral sphincter relaxes

86
Q

What effect does stimulation of M3 receptors have in the eye?

A

Myosis, increased drainage of aqueous humor, secretion of tears

87
Q

What are the 7 symptoms of muscarine poisoning?

A
  1. Myosis/blurred vision
  2. Hypersalivation
  3. Bronchoconstriction
  4. Bradycardia/heart block
  5. Diarrhoea
  6. Polyuria
  7. Hyperhidrosis
88
Q

How can pilocarpine eye drops be used to treat closed angle glaucoma?

A

Pilocarpine is an M3 agonist. It increases drainage of the aqueous humor, reducing ocular pressure.

89
Q

Atropine can be extracted from the atropia plant and is used to treat bradyarrythmias and AV node block. How does it work?

A

By antagonising M2 receptors, it blocks part of the parasympathetic pathway, increasing heart rate.

90
Q

What M3 antagonist is used in palliative care to reduce respiratory secretions and relieve symptoms of bowel obstruction?

A

Hyoscine

91
Q

Name 4 inhaled antimuscarinic drugs that can be used for bronchodilation

A
  1. Tiotropium
  2. Glycopyrronium
  3. Umeclidinium
  4. Aclidinium
92
Q

Why would you not give an inhaled antimuscarinic drug to a patient with glaucoma?

A

Some of the drug can end up in the eye and can worsen existing glaucoma by decreasing aqueous humor drainage

93
Q

How does solifenacin work and what is it used for?

A

Used to treat overactive bladder by blocking M3 receptors in the bladder, thereby inhibiting smooth muscle contraction

94
Q

How does mebeverine work and what is it used for?

A

Used to treat IBS, works by blocking M3 receptors in the gut, decreasing contractility and therefore slowing gut motility

95
Q

Rocuronium, suxamethonium and pancuronium are used as muscle relaxants during surgery. What kind of drugs are they?

A

Nicotinic (N1) receptor antagonists - inhibit ACh activity in the somatic nervous system

96
Q

Botox can be used locally to treat painful muscle spasms or can be used cosmetically. How does it work?

A

It blocks the release of ACh, preventing muscle contraction

97
Q

Why does myaesthenia gravis lead to skeletal muscle weakness?

A

The body produces antibodies to ACh receptors, preventing ACh from binding to receptors - blockage of normal transmission leads to skeletal muscle weakness

98
Q

What drug can be used to improve the symptoms of myaesthenia gravis?

A

Pyridostigmine (anti-cholinesterase) can be given to increase ACh availability at the neuromuscular junction

99
Q

Autonomic postganglionic transmission depends on which compounds?

A

Catecholamines: Noradrenaline, adrenaline, dopamine

100
Q

Where is noradrenaline released from?

A

Sympathetic nerve fibre ends

101
Q

Where is adrenaline released from?

A

Adrenal glands

102
Q

What is the precursor of adrenaline and noradrenaline?

A

Dopamine

103
Q

What is the effect of alpha 1 receptor activation?

A

Vasoconstriction, mainly in the skin and splanchnic beds (abdomen)

104
Q

Does noradrenaline or adrenaline have a greater effect on alpha 1 receptors?

A

Noradrenaline

105
Q

Noradrenaline is given intravenously to treat shock in ITU or to overcome the alpha blocking effects of anaesthetic agents as it is a more powerful alpha 1 agonist than adrenaline. However, adrenaline is still used to treat anaphylactic shock. Why?

A

Adrenaline is stable at room temperature and can be given intramuscularly

106
Q

What is xylometazoline and what is it used for?

A

Topical alpha receptor agonist used to treat nasal congestion by causing vasodilation (and therefore decreased swelling) around the nose.

107
Q

Alpha 2 receptors have mixed effects on vascular smooth muscle. Where are they found?

A

In the brain

108
Q

How does clonidine help ADHD sufferers to concentrate?

A

It is an alpha-2 agonist, which causes vasodilation in the brain, reducing vascular tone and therefore blood pressure.

109
Q

What selective alpha 1a antagonist can be used to treat benign prostatic hypertrophy?

A

Tamsulosin

110
Q

Where are beta 1 receptors predominantly found?

A

In the heart, kidney and fat cells

111
Q

What are the effects of beta 1 agonism?

A

Tachycardia, increase in stroke volume, renin release (increase in vascular tone), lipolysis and hyperglycaemia

112
Q

Give 3 effects that beta 1 blockers have on the heart

A
  1. Reduced heart rate
  2. Reduced stroke volume
  3. Reduction of myocardial oxygen demand (helps remodelling in heart failure/ post myocardial infarction)
113
Q

Name a beta blocker that is selective for beta 1

A

Bisoprolol

114
Q

What can be used to treat beta blocker poisoning?

A

Glucagon - bypasses the beta-adrenergic receptor site and increases heart rate and myocardial contractility irrespective of the presence of beta blockers

115
Q

Where are beta 2 receptors found?

A

Bronchi, bladder wall, uterus, skeletal muscle, pancreas

116
Q

What is the effect of beta 2 agonists in the bronchi?

A

Bronchodilation

117
Q

What is the effect of beta 2 agonists in the bladder wall?

A

Inhibition of micturition

118
Q

What is the effect of beta 2 agonists in the uterus?

A

Inhibition of labour

119
Q

What is the effect of beta 2 agonists in skeletal muscle?

A

Increases contraction speed (induces tremor)

120
Q

What is the effect of beta 2 agonists in the pancreas?

A

Stimulates insulin and glucagon secretion

121
Q

Why do you need to be careful when giving beta blockers to asthmatics?

A

Antagonism of the B2 receptors in the bronchi can result in bronchoconstriction

122
Q

What is the antidote to opioid overdose?

A

Naloxone

123
Q

Name 4 synthetic opioids

A
  1. Pethidine
  2. Fentanyl
  3. Alfentanil
  4. Remifentanil
124
Q

Why doesn’t nuprenorphine cause respiratory arrest in cases of overdose?

A

It is a (synthetic) partial agonist of opioid receptors

125
Q

Why does a dose of morphine need to be halved if being given via a non-oral route?

A

50% of oral morphine is metabolised by first pass metabolism in the liver

126
Q

How do opioid analgesics work?

A

They use the existing pain modulation system by mimicking natural endorphins. They activate GPRCs to inhibit the release of pain transmitters at the spinal cord and midbrain to modulate pain perception in higher centres, resulting in changes in the emotional perception of pain

127
Q

Why are opioid analgesics so addictive?

A

The descending inhibition of pain is part of the fight/flight response and is not designed for sustained activation. Sustained activation leads to down-regulation of receptors, resulting in tolerance, addiction and withdrawal.

128
Q

What is different about kappa opioid receptors?

A

Agonists cause depression instead of euphoria

129
Q

Which opioid receptors are targeted by drugs currently in use?

A

Mu receptors

130
Q

Why does opioid analgesia have side effects such as respiratory depression and constipation?

A

Mu receptors are also found in the respiratory system and the gut, as well as in the CNS.

131
Q

Codeine is a pro-drug. It needs to be metabolised by which enzyme in order to work?

A

CYP2D6

132
Q

Why is codeine not licensed for use in children under 12 or breastfeeding mothers?

A

In 5% of the population, CYP2D6 is overactive, meaning that individuals in this group are at increased risk of respiratory depression with codeine

133
Q

Why can morphine be particularly dangerous for patients with impaired renal function?

A

Because morphine is metabolised to morphine-6-glucuronide, which is more potent than morphine. With normal renal function, this is cleared quickly, but if renal function is impaired, it could build up and cause respiratory depression.

134
Q

What is tramadol?

A

A weak opioid agonist, which is slightly stronger than codeine

135
Q

How does tramadol work?

A

It is a pro-drug, which is metabolised by CYP2D6 to o-desmethyl tramadol (active form)

136
Q

Why should care be taken if prescribing tramadol to patients on anti-depressants?

A

Tramadol has a secondary effect: it inhibits reuptake of serotonin and noradrenaline, meaning that it interacts with SSRIs, tricyclic antidepressants and MAOIs.

137
Q

What is the difference between an adverse drug reaction and a side effect?

A

Both side effects and adverse drug reactions are unintended, but ADRs are always noxious, whereas side effects can sometimes be beneficial

138
Q

Adverse drug reactions are divided into what 3 categories?

A
  1. Toxic effects (beyond therapeutic range)
  2. Collateral effects (within therapeutic range)
  3. Hyper-susceptibility effects (below therapeutic range)
139
Q

What are the potential toxic effects of lithium?

A

Dysarthria and ataxia

140
Q

What are the potential toxic effects of animoglycosides (e.g. gentamicin)?

A

Nephrotoxicity and ototoxicity

141
Q

Why might a drug exert toxic effects?

A

If the dose is too high or if drug excretion is reduced as a result of impaired renal/hepatic function or interaction with other drugs

142
Q

What collateral effects can be caused by beta blockers?

A

Bronchoconstriction

143
Q

What collateral effects can be caused by broad spectrum antibiotics?

A

Clostridium difficile and pseudomembranous colitis

144
Q

What hypersusceptibility reaction can occur with penicillin?

A

Anaphylaxis

145
Q

Give 7 patient risk factors for adverse drug reactions

A
  1. Gender (F>M)
  2. Age (elderly and neonates)
  3. Polypharmacy
  4. Genetic predisposition
  5. Hypersensitivity/allergies
  6. Hepatic/renal impairment
  7. Adherence problems
146
Q

Give 3 drug risk factors for adverse drug reactions

A
  1. Steep dose-response curve
  2. Low therapeutic index
  3. Commonly causes ADRs
147
Q

Give 7 causes of ADRs

A
  1. Pharmaceutical variation
  2. Receptor abnormality
  3. Abnormal biological system unmasked by drug
  4. Abnormalities in drug metabolism
  5. Immunological
  6. Drug-drug interactions
  7. Multifactorial
148
Q

What are the 6 types of adverse drugs reactions according to the Rawlins Thompson classification?

A 
Type A - Augmented pharmacological
Type B - Bizarre/idiosyncratic
Type C - Chronic/Continuous
Type D - Delayed
Type E - End of treatment
Type F - Failure of therapy
149
Q

What 3 things need to be considered with regard to the possibility of ADRs when administering medication?

A
  1. Dose relatedness
  2. Timing (e.g. fast infusion of frusemide –> hearing loss)
  3. Patient susceptibility
150
Q

Individuals with glucose 6-phosphate dehydrogenase deficiency may experience what adverse drug reaction?

A

Primaquine causes haemolysis and haemolytic anaemia in these individuals.

151
Q

What causes malignant hyperpyrexia?

A

A receptor abnormality, which causes a sudden huge rise in calcium concentration, increase in muscle contraction and increase in metabolic activity and rise in body temperature if patient is given certain inhaled anaesthetics (halothane, isofluorane)

152
Q

What can occur if glucocorticoid therapy is withdrawn abruptly?

A

Adrenocortical insufficiency

153
Q

Under what 4 conditions should we suspect an ADR?

A
  1. Symptoms soon after a new drug is started
  2. Symptoms after a dosage increase
  3. Symptoms disappear when drug is stopped
  4. Symptoms reappear when drug is restarted
154
Q

What are the 6 most common drug types to cause ADRs?

A
  1. Antibiotics
  2. Anti-neoplastics
  3. Cardiovascular drugs
  4. Hypoglycaemics
  5. NSAIDs
  6. CNS drugs
155
Q

What are the 6 most common systems to be affected by ADRs?

A
  1. GI
  2. Renal
  3. Haemorrhagic
  4. Metabolic
  5. Endocrine
  6. Dermatologic
156
Q

What should be reported on a yellow card?

A
  1. All suspected reactions for herbal medicines and black triangle drugs
  2. All serious suspected reactions for established drugs, vaccines, contrast media and drug interactions
157
Q

What is a ‘serious’ reaction?

A

A reaction that:

  • is fatal
  • is life-threatening
  • is disabling/incapacitating
  • results in hospitalisation
  • prolongs hospitalisation
158
Q

What 4 pieces of information must be included on a yellow card?

A
  1. Suspected drug(s)
  2. Suspected reaction(s)
  3. Patient details
  4. Reporter details
159
Q

What are the 4 types of hypersensitivity reaction?

A

Type 1 - IgE mediated drug hypersensitivity
Type 2 - IgG mediated cytotoxicity
Type 3 - Immune complex deposition
Type 4 - T-cell mediated (delayed)

160
Q

Describe what happens in a type 1 hypersensitivity reaction

A
  • Prior exposure to antigen/drug
  • IgE antibodies formed after exposure to molecule
  • IgE becomes attached to mast cells/leukocytes and expressed as cell surface receptors
  • Re-exposure causes mast cell degranulation and release of substances like histamine, prostaglandins, leukotrienes, platelet activating factor etc.
161
Q

What is the most common cause of anaphylaxis?

A

Insect venom

162
Q

Describe what happens in a type 2 hypersensitivity reaction

A
  • Drug/metabolite combines with a protein
  • Body treats it as a foreign protein and forms antibodies (IgG, IgM)
  • Antibodies combine with the antigen and complement activation damages the cells
163
Q

Describe what happens in a type 3 hypersensitivity reaction

A
  • Antigen and antibody form large complexes and activate complement
  • Small blood vessels become damaged/blocked
  • Leukocytes attracted to the site of reaction, release pharmacologically active substances and trigger inflammatory process
164
Q

Describe what happens in a type 4 hypersensitivity reaction

A
  • Antigen specific receptors develop on T lymphocytes

- Subsequent administration leads to local or tissue allergic reaction

165
Q

What happens in non-immune anaphylaxis?

A

Direct mast cell degranulation, with no prior exposure

166
Q

What are the main features of drug-induced anaphylaxis?

A
  1. Rapid onset following exposure to drug
  2. Rash in 80-90% of cases
  3. Swelling of lips, face, oedema and central cyanosis
  4. Wheeze/shortness of breath
  5. Hypotension
  6. Can cause cardiac arrest
167
Q

Why is adrenaline used to treat anaphylaxis?

A
  1. It causes vasoconstriction, which increases peripheral vascular resistance and BP
  2. It acts on alpha 1 receptors and improves coronary perfusion
  3. It stimulates beta 1 adrenoreceptors in the heart –> increases HR and SV
  4. Reduces oedema and bronchodilates via beta 2 receptors
  5. Attenuates further release of mediators from mast cells and basophils by increasing intracellular cAMP, thereby reducing the release of inflammatory mediators
168
Q

What are the clinical criteria for allergy to a drug?

A
  • Does not correlate with pharmacological properties of the drug
  • No linear relation to dose
  • Reaction similar to those produced by other allergens
  • Induction period of primary exposure
  • Disappearance on cessation
  • Reappears on re-exposure
  • Occurs in a minority of patients on the drug

Phase 2a Medicine (13 decks)

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