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Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacodynamics?

A

The biochemical, physiological + molecular effects of a drug on the body

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2
Q

What is pharmacokinetics?

A

The fate of a chemical substance administered to a living organism

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3
Q

What are the 4 steps of the pharmacokinetic process?

A

-Absorption
-Distribution
-Metabolism
-Excretion

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4
Q

What is absorption of a drug?

A

The transfer of a drug molecule from the site of administration to the systemic circulation

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5
Q

What do these acronyms stand for?
-IV
-IA
-IM
-SC
-PO
-SL

A

-Intravenous
-Intra-arterial
-Intramuscular
-Subcutaneous
-Oral
-Sublingual

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6
Q

What do these acronyms stand for?
-INH
-PR
-PV
-TOP
-TD
-IT

A

-Inhaled
-Rectal
-Vaginal
-Topical
-Transdermal
-Intrathecal

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7
Q

In what modes of administration does 100% of the dose reach systemic circualtion?

A

IV + IA

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8
Q

What are the 3 mechanisms by which drugs can permeate across cell membranes?

A

-Passive diffusion through hydrophobic membrane (lipid soluble molecules)
-Passive diffusion through aqueous pores (small water soluble molecules)
-Carrier mediated transport (proteins transport sugars, a.a., neurotransmitters + trace metals)

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9
Q

What 2 factors affect drug absorption?

A

-Lipid solubility
-Drug ionisation

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10
Q

Why are ionised drugs poorly absorbed?

A

Have poor lipid solubility

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11
Q

Where are weak acid drugs best absorbed?

A

Stomach

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12
Q

Where are weak base drugs best absorbed?

A

Intestine

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13
Q

What 5 factors affect drug absorption in the stomach?

A

-Gastric enzymes may digest drugs
-Low pH may degrade drug
-Food-full stomach slows absorption
-Gastric motility
-Previous surgery

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14
Q

What is first pass metabolism?

A

Metabolism of drugs preventing them reaching systemic circulation-varies between ppl

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15
Q

How does first pass metabolism occur?

A

-Drug degraded by enzymes in intestinal wall
-Absorbed from intestine into HPV + metabolism via liver enzymes

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16
Q

How can you avoid first pass metabolism?

A

Give drugs by routes that avoid splanchnic circulation e.g. rectal

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17
Q

What is bioavailability?

A

The proportion of a drug that reaches the systemic circulation-expressed as a % or decimal

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18
Q

What is bioavailability dependent on?

A

-Extent of drug absorption
-Extent of first pass metabolism

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19
Q

Give an example of a drug delivered PR

A

Diazepam suppositories for epilepsy

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20
Q

Give an example of a drug delivered INH

A

Salbutamol inhaler

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21
Q

Give an example of a drug delivered S/C

A

Long acting insulins for T1

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22
Q

Give an example of a drug delivered TD

A

Fentanyl patches for severe chronic pain

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23
Q

What compartments of the body do drugs end up in + what %

A

-ICF-35%
-Fat-20%
-Interstitial fluid-15%
-Plasma-5%

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24
Q

What drug properties increase distribution?

A

-Small molecule size
-Lipophilic molecule
-Protein bound

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25
Q

What is Vd?

A

Volume of distribution-theoretical vol a drug will be distributed in the body
-Well distributed drugs=high Vd

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26
Q

What is the BBB?

A

Blood brain barrier-layer of epithelial cells with tight junctions that separates foreign substances in the blood from CNS

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27
Q

Name 3 ways drugs can reach the CNS

A

-Have high lipid solubility
-Be administered intrathecally
-In cases of inflammation BBB becomes leaky

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28
Q

With what patients should more care be taken when prescribing + why?

A

-Obese patients-drugs with small Vd not always delivered to fat-use ideal body weight rather than actual
-Septic patients-leaky blood vessels increases distribution, penetrates BBB better
-Liver impaired patients-hypoalbuminemia
-Older patients-smaller Vd of water soluble drugs=higher plasma concs

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29
Q

What are the 2 steps of metabolising a drug?

A

-Oxidation/reduction/hydrolysis to introduce reactive group
-Conjugation of functional group to produce hydrophilic, inert molecule

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30
Q

What enzyme is involved with most of phase 1 metabolism?

A

Cytochrome P450

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31
Q

What is the aim of phase 1 metabolism?

A

To create a reactive molecule

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32
Q

What is the aim of phase 2 metabolism?

A

To create a hydrophilic molecule that can then be renally excreted

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33
Q

How are drugs/metabolites excreted?

A

-Liquids (small polar molecules) e.g. urine, bile, sweat, tears, breast milk
-Solids (large molecules) e.g. faeces
-Gases (volatiles) e.g. expired air

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34
Q

How does glomerular filtration remove drugs?

A

Plasma filtered + very large drug molecules removed

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35
Q

How does active tubular secretion in the kidneys remove drugs?

A

Removes protein bound drugs

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36
Q

What kind of drugs does passive reabsorption in the kidneys remove?

A

Highly polar drugs

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37
Q

What is an advantage of PR administration?

A

Avoids first pass metabolism

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38
Q

What is an advantage of INH administration?

A

Well perfuses a large s.a.

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39
Q

What is an advantage of S/C administration?

A

-Faster onset than PO
-Can change formulation to control rate of absorption

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40
Q

What is an advantage of TD administration?

A

-Continuous drug release
-Avoids first pass metabolism

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41
Q

What is a disadvantage of PR administration?

A

-Variable absorption
-Patient preference

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42
Q

What is a disadvantage of INH administration?

A

Inhaler technique can limit effectiveness

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43
Q

What is a disadvantage of S/C administration?

A

Not as quick as IV

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44
Q

What is a disadvantage of TD administration?

A

-Only suitable for lipid soluble drugs
-Slow onset

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45
Q

What is first order kinetics?

A

When the rate of elimination is proportional to the plasma drug conc-metabolism processes do not become saturated-most drugs

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46
Q

What is zero order kinetics?

A

Rate of elimination is not proportional to the plasma drug conc-metabolism processes are saturated

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47
Q

Describe the elimination of a drug with first order kinetics

A

A constant % of the plasma drug is eliminated over time

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48
Q

Describe the elimination of a drug with zero order kinetics

A

A constant amount of the plasma drug is eliminated over time

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49
Q

What is Cmax?

A

Maximum plasma concentration

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50
Q

What is tmax?

A

Time taken to reach Cmax

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51
Q

What is clearance?

A

Removal of a drug by all eliminating organs

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52
Q

What is half life (t1/2) of drug elimination dependent on?

A

-Clearance
-Vd (large Vd takes longer to clear)

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53
Q

At what % of clearance is a drug considered ‘cleared’ in medical practice?

A

97% = 5x half lives

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54
Q

What must you consider when administering drugs with a short t1/2?

A

-Will need more frequent dosing
-Short t1/2 drugs may need dose weaning on cessation as risk of withdrawal symptoms

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55
Q

What does a steady state of drug delivery mean?

A

rate of drug input=rate of drug elimination

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56
Q

What is Css?

A

Drug plasma conc at a steady state

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57
Q

Why is a steady state important?

A

Need to deliver drug at concentration which lies between MSC (maximum safe conc) + MEC (minimum effective conc)

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58
Q

What is the purpose of a loading dose?

A

Decrease initial time to reach steady state-important as detrimental to wait to reach steady state

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59
Q

Name 5 drugs that require a loading dose

A

-Digoxin
-Vancomycin
-Teicoplanin
-Amiodarone
-Heparin

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60
Q

Give an example of a drug metabolised with zero order kinetics

A

Ethanol

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61
Q

Name 2 drugs with a narrow therapeutic window

A

-Lithium
-Digoxin

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62
Q

How to you deal with drugs that have a narrow therapeutic window?

A

-Monitor drug plasma levels to ensure efficacy + avoid toxicity
-Levels should be taken pre-dose

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63
Q

What is pharmacogenomics?

A

The use of genetic + genomic info to tailor pharmaceutical Tx to an individual

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64
Q

What is druggability?

A

The ability of a protein to bind to a specific drug, altering its function so it can give a therapeutic benefit to the patient

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65
Q

What is a receptor?

A

A component of a cell that interacts with a specific ligand + initiates a change of biochemical events leading to the ligands observed effects

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66
Q

Name 3 types of chemical that receptors help communicate + give an example for each

A

-Neurotransmitters e.g. acetylcholine, serotonin
-Autacoids e.g. cytokines, histamine
-Hormones e.g. testosterone, hydrocortisone

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67
Q

Name 4 types of receptor + examples

A

-Ligand-gated ion channel-nicotinic ACh receptor
-G protein coupled receptors-beta=adrenoceptors
-Kinase-linked receptors-growth factor receptors
-Cytosolic/nuclear receptors-steroid receptors

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68
Q

What are ligand gated ion channels?

A

Membrane proteins that allow ions to pass through the channel pore so cell has a change in electric charge distribution-change mediated by influx of cation/efflux of anion

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69
Q

What are GPCRs?

A

G/guanine protein coupled receptors-act as molecular switches

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70
Q

What regulates the activity of GPCRs?

A

Factors that control their ability to bind to + hydrolyse GTP to GDP

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71
Q

What are kinases?

A

Enzymes that catalyse the transfer of phosphate groups between proteins-phosphorylation

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72
Q

How are transmembrane receptors activated?

A

When an extracellular ligand binds + causes enzymatic activity on the intracellular site

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73
Q

What are nuclear receptors?

A

Steroid hormones that work by modifying gene transcription

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74
Q

Give 2 examples where an imbalance in chemical leads to pathology

A

-Allergy=increased histamine
-Parkinson’s=decreased dopamine

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75
Q

Give 2 examples where an imbalance with receptors leads to pathology

A

-Myasthenia gravis=loss of ACh receptors
-Mastocytosis=increased c-kit receptors

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76
Q

What is an agonist?

A

Compound that binds to a receptor + activates it

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77
Q

What is an antagonist?

A

Compound that reduces the effect of an agonist

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78
Q

What is the two state model of receptor activation?

A

Model that describes how drugs activate receptors by inducing a conformational change in the receptor from ‘off’ to ‘on’

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79
Q

What is Emax?

A

The maximum response from a Tx achievable-measure of efficacy

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80
Q

How do calculate intrinsic activity?

A

Emax of partial agonist/Emax of full agonist

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81
Q

What is intrinsic activity?

A

AKA efficacy-ability of a drug-receptor complex to produce a maximum functional response

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82
Q

What is competitive antagonism?

A

When antagonists bind to the same site as agonists

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83
Q

What are the 2 categories of cholinergic receptor?

A

-Nicotinic
-Muscarinic

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84
Q

Name 4 factors that affect drug action

A

-Receptor affinity
-Receptor efficacy
Receptor number
-Signal amplification

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85
Q

What is affinity?

A

How well a ligand binds to a receptor

86
Q

What is efficacy?

A

How well a ligand activates the receptor-is it possible to get a maximal response? Full vs partial agonists

87
Q

Compare agonists + antagonists in terms of affinity + efficacy

A

Agonists=have affinity + efficacy
Antagonists-have affinity but zero efficacy

88
Q

Give an example of an irreversible antagonist

A

Bromoacetyl alprenolol menthane (BAAM)

89
Q

What is a full agonist?

A

One with high efficacy, producing a full response while occupying a relatively low proportion of receptors

90
Q

What is a partial agonist?

A

One with a low intrinsic activity-can never see maximal response, even with 100% occupancy

91
Q

What is receptor reserve?

A

When an agonists can produce a maximal response with only a portion of available receptors being activated

92
Q

What can activation of a receptor do to a signal?

A

-Signal transduction (signalling cascade)
-Signal amplification

93
Q

What is allosteric modulation?

A

Where a binding site is elsewhere on molecule to main (orthosteric) site, but a binding still alters shape of molecule

94
Q

What is an inverse agonist?

A

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

95
Q

What is the difference between tolerance + desensitisation?

A

Tolerance=slower, reduction in agonist effect over time vs desensitisation=much quicker degrading

96
Q

What is an enzyme inhibitor?

A

Molecule that binds to an enzyme + reduces its activity

97
Q

What is an irreversible inhibitor?

A

One that forms covalent bonds with the enzyme, changing it chemically

98
Q

What is a reversible inhibitor?

A

One that binds non-covalently, diff types of inhibition depending on where inhibitor binds

99
Q

What do statins inhibit?

A

HMG-CoA reductase

100
Q

How do statins work?

A

-Block rate-limiting step in cholesterol pathway
-Reduce levels of LDL
-Therefore reducing risk of CVD

101
Q

What drugs are used to treat hypertension?

A

ACE inhibitors

102
Q

How do ACE inhibitors reduce blood pressure?

A

-Inhibition of ACE, reduces production of angiotensin II
-Less ATII = less water + salt retention
-Decreases blood pressure

103
Q

What are the 3 types of protein ports?

A

-Uniporters
-Symporters
-Antiporters

104
Q

How do uniporters work?

A

They use energy from ATP to pull molecules in

105
Q

How do symporters work?

A

They use the movement in of 1 molecule, to pull in another molecule, against a conc gradien

106
Q

How do antiporters work?

A

On substance moves against it gradient, using energy from the 2nd substance moving down its gradient

107
Q

Give an example of a symporter

A

Na-K-Cl-co-transporter (NKCC)

108
Q

What does binding of the diuretic Furosemide to NKCC cause?

A

Loss of sodium, chloride = potassium ions in urine

109
Q

Name 4 types of ion channel

A

-Epithelial (sodium)
-Voltage-gated (calcium, sodium)
-Metabolic (potassium)
-Receptor activated (chloride)

110
Q

Give an example of an epithelial sodium channel (ENaC)

A

Reabsorption of Na+ at collecting ducts of kidney’s nephrons

111
Q

Give an example of a voltage-gated calcium channel

A

Membrane of excitable cells (glial, muscle, neurons etc)
e.g. vascular smooth muscle cells-Ca influx causes vasoconstriction + increases bp

112
Q

Give an example of voltage gated sodium channels

A

Transmission of action potential + signalling in heart

113
Q

Give an example of voltage gated potassium channels

A

Insulin regulation in Islets of Langerhans

114
Q

Give an example of a receptor-mediated (chloride) ligand ion channel

A

GABA A receptor

115
Q

Describe the action of the sodium pump (Na/K ATPase)

A

-x 3 Na’s pumped out, x2 K’s into cells, against conc gradients
-Energy required comes from ATP

116
Q

Describe the action of the stomach’s proton pump

A

-Hydrogen potassium ATPase exchanges potassium from intestinal lumen with cytoplasmic H+
-Causes acidification of stomach + activation of pepsin

117
Q

Name the irreversible inhibitors of cholinesterase

A

Organophosphates

118
Q

Name 2 drugs that are irreversible enzyme inhibitors

A

-Omeprazole
-Aspirin

119
Q

Give 3 examples of recombinant proteins in clinical use

A

-Insulin
-Erythropoietin
-Growth hormone

120
Q

Name 2 naturally occurring opioids

A

-Morphine
-Codeine

121
Q

Does morphine undergo first pass metabolism?

A

Yes-50% of morphine is metabolised by first pass metabolism if delivered orally

122
Q

What are the repercussions of morphine undergoing first pass metabolism by the liver?

A

Dose should be halved if given IV, s/c, IM

123
Q

What is diarmorphine?

A

Crude form of heroin-developed from morphine-more potent + crosses BBB quickly

124
Q

How do opioids work?

A

They inhibit the release of pain transmitters at spinal cord + midbrain + modulate pain perception in higher centres-euphoria

125
Q

What does sustained inhibition of the pain pathways lead to?

A

Tolerance + addiction

126
Q

Name the 4 opioid receptors

A

-MOP (mu (μ)-opioid peptide)
-KOP (kappa opioid receptor)
-DOP (delta)
-NOP (nociceptin opioid-like receptor)

127
Q

Which opioid agonist causes depression instead of euphoria?

A

Kappa

128
Q

What kind of agonist are most opioids we use?

A

µ-mu

129
Q

What is potency?

A

Whether a drug is strong/weak in relation to how well it binds to the receptors-binding affinity

130
Q

What is tolerance?

A

Down regulation of the receptors with prolonged use-need higher doses to achieve same effect

131
Q

What is dependence?

A

Phycological-craving, euphoria
Physical symptoms

132
Q

When does opioid withdrawal start + how long does it last?

A

Starts within 24hrs, lasts 72hrs

133
Q

Name 7 side effects of opioid withdrawal

A

-Respiratory depression
-Sedation
-Nausea + vomiting
-Constipation
-Itching
-Immune suppression
-Endocrine effects

134
Q

What is the bioavailability for oral morphine?

A

50%

135
Q

Describe the 8 steps of a synaptic impulse

A

-Action potential arrives at axon terminal
-Voltage-gated Ca2+ channels open
-Ca2+ enters presynaptic neuron
-Ca2+ signals to neurotransmitter vesicles
-Vesicles move to membrane + dock
-Neurotransmitters released via exocytosis
-Neurotransmitters bind to receptors
-Signal initiate din postsynaptic cells

136
Q

What do α1 (postsynaptic)receptors do?

A

Vasocontriction

137
Q

What do β1
receptors do?

A

Increase heart rate + contractility

137
Q

What do α2 (presynaptic)
receptors do?

A

Negative feedback-suppresses norad release

137
Q

What do β2
receptors do?

A

Bronchodilation

138
Q

What do ACE inhibitors do?

A

Vasodilation, decreased IV remodelling

139
Q
A
140
Q

What do anti-platelet medication do?

A

Prevent clot formation

141
Q

What do statins do?

A

Reduce cholesterol

142
Q

What do beta blockers do?

A

-Decrease heart rate + contractility
-Prolong diastole-more time for coronary perfusion
-Reduce incidents of heart failure

143
Q

What do alpha 2 agonists do?

A

Act as hypertensives, sedatives + analgesics

144
Q

How do alpha 2 agonists work?

A

Act pre-synaptically to reduce amount of noradrenaline released

145
Q

Give an example of a β2 agonsist

A

Salbutamol

146
Q

Name a drug that stimulates all sympathetic receptors

A

Adrenaline

147
Q

Give an example of an α1 agonist

A

Phenylephrine

148
Q

How does organophosphate poisoning work?

A

Inhibits acetylcholinesterase-stops breakdown of ACh-accumulates + overstimulates nicotinic + muscarinic receptors

149
Q

What are the symptoms of organophosphate poisoning ?

A

-Increased saliva + tear production
-Diarrhoea
-Nausea + vomiting
-Sweating
-Muscle tremors
-Confusion

150
Q

How does atropine help with organophosphate poisoning?

A

It competes with ACh at muscarinic receptors

151
Q

How many muscarinic receptors are there?

A

5-M1-M5

152
Q

Describe nicotinic receptors

A

-Ligand gated ion channels
-Action increases membrane permeability to Na+, K+

153
Q

What are the 3 subgroups of nicotinic receptors?

A

-Ganglionic
-Neuromuscular
-CNS

154
Q

What are the nicotinic signs of acetylcholinesterase inhibitor toxicity?

A

Monday = Mydriasis
Tuesday = Tachycardia
Wednesday = Weakness
Thursday = Hypertension
Friday = Fasciculations

155
Q

What are the muscarinic signs of acetylcholinesterase inhibitor toxicity?

A

D = Defecation/diaphoresis
U = Urination
M = Miosis
B=Bronchospasm/bronchorrhea
E = Emesis
L = Lacrimation
S = Salivation

156
Q

Name a drug that blocks parasympathetic action

A

Atropine

157
Q

What is a drug interaction?

A

When a substance alters the expected performance of a drug

158
Q

Name the 2 types of drug interaction + what they are

A

Pharmacodynamic-drug effects same target
Pharmacokinetic-drug affects absorption, distribution, metabolism/excretion of another drug

159
Q

name the 2 types of pharmacodynamic drug interaction

A

-Synergistic
-Antagonistic

160
Q

Give an example of a beneficial pharmacodynamic drug interaction

A

Amlodopine + ramipril (both for hypertension) synergistic interaction-causes hypotension

161
Q

What are the risks of a pharmacokinetic absorption interaction?

A

Drug affects rate/extent of absorption of another drug
Bad if rapid effect needed + reduces steady state levels

162
Q

How can pharmacokinetic interactions reduce drug distribution?

A

-Only unbound drugs are distributed from plasma vol
-Interactions can cause competition for protein binding

163
Q

Give an example of a pharmacokinetic distribution interaction

A

Warfarin displaced by Amiodarone=warfarin has bigger effect on patient

164
Q

What substrates does CYP3A4 process?

A

simvastatin, warfarin, DOACs (apixaban, rivaroxaban etc), carbamazepine, diltiazem

165
Q

What enzyme processes ibuprofen + warfarin?

A

CYP2C9

166
Q

What does CYP2D6 process?

A

Codeine + warfarin

167
Q

What does CYP1A2 process?

A

caffeine, paracetamol, theophylline, warfarin

168
Q

What enzyme metabolises omeprazole + phenytoin?

A

CYP2C19

169
Q

Name 4 important drug-food interactions

A

-Grapefruit juice
-Milk
-High vitamin K foods
-Cranberry juice

170
Q

Describe the potential drug interaction with grapefruit juice

A

It is a CYP3A4 inhibitor so should be avoided for warfarin + statin patients

171
Q

Describe the potential drug interaction with milk

A

Milk forms insoluble complex with Ca-affects absorption of some drugs eg. doxycycline, levothyroxine, ciprofloxacin

172
Q

Describe the potential drug interaction with high vitamin K foods (spinach, kale, avocado etc)

A

These foods oppose action of warfarin

173
Q

Describe the potential drug interaction with cranberry juice

A

It’s a CYP2C9 inhibitor so should be avoided by patients on warfarin

174
Q

How should you manage drug interactions?

A

Moderate-additional monitoring-bloods, observation etc
High risk-initiate alternative, suspend interacting drug

175
Q

What are P-glycoproteins?

A

Drug transporter proteins-remove toxic substances from cells

176
Q

What is an ADR?

A

Adverse drug reaction-a response to a medicinal product/combination of products, which is noxious + unintended

177
Q

How do ADRs affects patients?

A

-Reduced QofL
-Poor compliance
-Reduced confidence in clinicians
-Unnecessary Tx/investigations

178
Q

How do ADRs affect the NHS?

A

-Increased admissions
-Longer stays
-GP appts
-Inefficient use of medication

179
Q

What are the 7 classification of ADRs?

A

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

180
Q

What is the most common type of ADR?

A

Augmented

181
Q

What is an augmented ADR + example?

A

Exaggerated effect of drugs pharmacology at a therapeutic dose-not normally life threatening
e.g. bleeding with anticoagulants

182
Q

What is a bizarre ADR + example?

A

Not related to pharmacology/dose-serious illness/mortality, symptoms don’t always resolve when drug stopped e.g. anaphylaxis with penicillin

183
Q

What is a chronic ADR + example?

A

ADR that continues after drug stopped e.g. osteonecrosis of jaw with bisphosphonates

184
Q

What is a delayed ADR + example?

A

ADR becomes apparent some time after drug stopped e.g. leucopenia with chemotherapy

185
Q

What is a end of use ADR + example?

A

ADR develops after drug stopped e.g. insomnia after stopping benzodiazepine

186
Q

What is a failure of Tx ADR + example?

A

Unexpected Tx failure, could be drug/food-drug interaction or due to poor compliance e.g. failure of bisphosphonate due to taking with food

187
Q

What is a genetic ADR + example?

A

Drug causes irreversible damage to genome e.g phocomelia in children of women taking thalidomide

188
Q

What is another way to classify ADRs?

A

DoTS

189
Q

What does DoTS stand for?

A

-Dose-relatedness
-Timing
-Susceptibility

190
Q

Name the 3 dose-related types of ADR

A

-Hypersusceptibility-dose is subtherapeutic
Collateral/side effects-ADRs at therapeutic doses
-Toxic effects-ADRs at higher than therapeutic levels

191
Q

What are the 6 time stages for ADRs?

A

-Rapid-rapid administration
-First dose-1st dose only
-Early-only early in Tx-resolves
-Intermediate-Occurs after some delay
-Late-risk increases with exposure
-Delayed-reaction some time after initial exposure

192
Q

Name 4 groups/populations with higher susceptibility for ADRs

A

-Age
-Gender
-Disease states
-Physiological states

193
Q

How are ADRs identified?

A

In stages of drug development:
-Pre-clinical
-Clinical trial
-Post-marketing surveillance
-Pharmacovigilance

194
Q

What symbol in the BNF/SPC/on patient info leaflet indicates a drug is under post-marketing surveillance?

A

Black triangle

195
Q

What body oversees ADRs?

A

MHRA (Medicines and Healthcare products Regulatory Agency)

196
Q

What is the yellow card system?

A

Voluntary + confidential reporting system for ADRs

197
Q

What is a GSL drug?

A

General sales list drug

198
Q

What is a POM drug?

A

Prescription only medication

199
Q

What is a P drug?

A

Pharmacy medication

200
Q

What are 2 genetic variations that can increase risk for ADRs

A

-Variation in expression of CYP450 enzymes (altered metabolism)
-HLA (human leucocyte antigen) alleles can increase risk of immune mediated idiosyncratic ADRs

201
Q

What is hypersensitivity?

A

Objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus at a dose tolerated by normal subjects

202
Q

What causes acute anaphylaxis?

A

Prior exposure to antigen/drug causes IgE antibodies to form
-IgE attaches to mast cells/leucocytes, expressed as cell surface receptors
-Re-exposure causes mast cell degranulation + release of histamine, prostaglandins, leukotrienes, platelet activating factor etc

203
Q

What is type 1 hypersensitivity?

A

Acute anaphylaxis

204
Q

What is a type 2 hypersensitivity reaction?

A

-Drug/metabolite combines with protein
-Body treats it as foreign + forms antibodies
-Antibodies combine with antigens + complement activations damages cells

205
Q

What is a type 3 hypersensitivity reaction?

A

-Antigen-antibody complex forms + activates complement
-Small blood vessels damaged/blocked
-Leucocytes attracted to site of reaction + release inflammatories

206
Q

What is a type 4 hypersensitivity reaction?

A

-Antigen-specific receptors develop on T-lymphocytes
-Later administration leads to local/tissue allergic reaction e.g. contact dermatits

207
Q

What is non-immune anaphylaxis?

A

Clinically identical to normal anaphylaxis but needs no prior exposure, due to to mast cell degranulation

208
Q

What does adrenaline do?

A

-Vasoconstriction, increases BP + coronary perfusion
-Stimulates beta1-adrenoreceptors
-Reduces oedema
-Reduces release of inflammatory mediators

Phase 2a (8 decks)

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