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ICS/GP/ILA > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Definition of physiochemical drug interactions?

A

How different drugs interact with each other

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2
Q

Definition of pharmacodynamic drug interactions?

A

How a drug affects the body

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3
Q

Definition of pharmacokinetic drug interactions?

A

What the body does to the drug (eg. whether it’s absorbed)

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4
Q

What is the physiochemical way of drug interaction?

A

Adsorption - solutes absorbed by solid or liquid surfaces

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5
Q

What is summative/additive pharmacodynamics?

A

Two drugs have the same effect, so the total effect is the sum of 2 drugs put togehter (with the same effect as a single drug would)

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6
Q

What is synergism in pharmacodynamics?

A

Putting two drugs together has a bigger effect than individual effects predicted. Eg. paracetamol and morphine

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7
Q

What is antagonism/blockade in pharmacokinetics?

A

Drugs that block the effects of each other, eg. beta-blockers

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8
Q

What is potentiation in pharmacokinetics?

A

Adding two drugs together and just one of the drugs having an increase in effect, the other drug isn’t affected

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9
Q

What is ADME in pharmacokinetics?

A

Absorption, Distribution, Metabolism, Excretion

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10
Q

Is the time of absorption quicker intravenously or orally?

A

intravenously

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11
Q

Definition of bioavailability?

A

How much drug is available over a given time in the systemic circulatuon (usually measuring oral in comparison to IV)

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12
Q

What are 3 factors that affect absorption of drugs?

A
  1. motility in the gut - if gut has slowed digestion, drugs won’t work as well
  2. acidity - whether ionised or unionised, pH and pKa interactions
  3. physiochemical - solubility and complex formation
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13
Q

How can drugs be distributed?

A

Into proteins, tissues, or effect sites

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14
Q

How does protein binding of drugs work?

A

A drug that is bound to a protein doesn’t have an effect because it’s stuck. So when 2+ drugs are given that are protein bound, one will be free and EXTRA ACTIVE

Eg. warfarin and amiodarone

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15
Q

What does protein binding depend on?

A

Albumin levels

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16
Q

Where are drugs usually excreted?

A

Renally and is pH dependent - weak bases cleared faster if urine is acidic and vice versa

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17
Q

What is used to prevent aspirin overdose?

A

Bicarb because it forces aspirin to remain in collecting system

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18
Q

Where are majority of drugs metabolised and excreted?

A

hepatically metabolised, renally excreted

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19
Q

Definition of a drug?

A

A medicine or other substance which has a physiological effect when ingested or introduced to the body

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20
Q

Definition of druggability?

A

Describes a biological target that is known or predicted to bind with hgh affinity to a drug

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21
Q

What is a drug receptor?

A

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

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22
Q

What can drug receptor ligands be?

A

Exogenous (drugs) or endogenous (hormones, neurotransmitters)

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23
Q

What types of drug chemicals use receptors?

A

Most - neurotransmitters (ACh, seratonin), autacoids (cytokines, histamine), hormones (testosterone, hydrocortisone)

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24
Q

What are some examples of chemical imbalances leading to pathology?

A

allergy - increased histamine
parkinson’s - reduced dopamine
myasthenia gravis - loss of ACh receptors

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25
Q

What are ligand-gated ion channels?

A

Pore-forming membrane proteins that allow ions to pass through

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26
Q

What form do drug receptors mostly come in?

A

proteins

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27
Q

How do ligand-gated ion channels work?

A

cause a shift in charge distribution which is mediated by influx of cation (+ve) or efflux of anion (-ve)

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28
Q

Example of a ligand-gated ion channel?

A

nicotinic ACh receptors

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29
Q

What is the largest group of membrane receptors?

A

G protein coupled receptors

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30
Q

What type of ligands do G protein coupled receptors use?

A

Light energy, peptides, lipids, sugars, proteins

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31
Q

What do G protein coupled receptors transmit signals from?

A

GPCRs

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32
Q

How is activity of G protein coupled receptors regulated?

A

Factors control ability to bind and hydrolyse guanosine di/triphosphate - these act as switches

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33
Q

Example of G protein couple receptor?

A

Beta-adrenoceptors

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34
Q

What are kinase linked receptors?

A

Enzymes that catalyse the transfer of phosphate groups between proteins (phosphorylation)

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35
Q

When are kinase-linked receptors activated?

A

when binding of extracellular ligand causes enzymatic activity on intracellular side

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36
Q

Example of kinase-linked receptors?

A

Receptors for growth factors

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37
Q

How do cytosolic/nuclear receptors work?

A

Modify gene transcription

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38
Q

Example of cytosolic/nuclear receptors?

A

Steroid receptors

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39
Q

Definition of an agonist?

A

A compound that binds to a receptor and activates it

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40
Q

What is the two state model of receptor activation?

A

Describes how drugs activate receptors by inducing or supporting confirmatinal change of the receptor

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41
Q

How is drug potency measured?

A

logarithmic curve

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42
Q

What is EC50?

A

The concentration that gives half the maximal response

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43
Q

Definition of efficacy?

A

(intrinsic activity) - ability of a drug-receptor complex to produce a maximum functional response

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44
Q

Definition of an antagonist?

A

A compound that reduces the effect of an agonist - doesn’t activate receptors but reverses agonist effect

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45
Q

What is the difference between competitive and non-competitive antagonism?

A

competitive binds to the same site so is selective, non-competitive binds to an allosteric site on the receptor

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46
Q

Cholinergic receptor characterisation?

A
  1. agonist = muscarine, antagonist = atropine, receptor = mAChR
  2. agonist = nicotine, antagonist = curare, receptor = nAChR
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47
Q

Definition of affinity? (ligands)

A

Describes how well a ligand binds to the receptor

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48
Q

Does affinity apply to agonists or antagonists?

A

both

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49
Q

Definition of efficacy? (ligands)

A

describes how well a ligand activates the receptor

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50
Q

Does efficacy apply to antagonists or agonists?

A

agonists

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51
Q

What is receptor reserve for agonists?

A

some FULL agonists only need to activate a small amount of receptors to produce maximal response (reserve can be small or large)

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52
Q

What is signal transduction of drugs?

A

Signalling cascade that causes conversion of a signal from outside the cell to a functional change within the cell

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53
Q

What is signal amplification of drugs?

A

Increasing strength of a signal

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54
Q

What is allosteric modulation?

A

allosteric ligand binds to a different site on the molecules and prevents it from being transmitted

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55
Q

What is inverse agonism?

A

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

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56
Q

Defintion of drug tolerance?

A

reduction in agonsit effect over time due to continuous/repeated/high concentrations of the drug

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57
Q

Definition of desensitisation of drugs?

A

Complete changes in receptors due to uncoupled, internalised, degraded

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58
Q

Difference between tolerance and desensitisation?

A

tolerance is a slow process, desensitisation is fast

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59
Q

Definition of enzyme inibition?

A

A molecule that binds to an enzyme and decreases its activity by preventing substrate from binding to active site and catalysing

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60
Q

What are the two types of enzyme inhibition?

A

Irreversible inhibitors and reversible inhibitors?

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61
Q

What is the difference between irreversible and reversible inhibitors?

A

Irreversible react with enzyme and change it chemically (eg. via covalent bond formation), whereas reversible inhibition has different types depending on whether the inhibitor binds to the enzyme, enzyme-substrate complex, or both (non-covalent)

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62
Q

How are statins an example of enzyme inhibitors?

A

They block the rate limiting step in the cholestrol pathway to reduce levels of LDLs

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63
Q

What happens whenangiotensin converting enzyme (ACE) inhibited?

A

Reduces angiotnesin II production so blood pressure is reduced

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64
Q

How is parkinson’s treated?

A

with multiple enzymatic inibitor drugs

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65
Q

How does peripheral DDC inhibitor increase dopamine in parkinson’s?

A

blocks DDC in periphery which means more is available in the CNS

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66
Q

How does peripheral COMT inhibitor increase production of L-DOPA in parkinson’s?

A

Prevents breakdown of L-DOPA so more available in CNS

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67
Q

How do central COMT inhibitors help in parkinson’s?

A

maintain dopamine levels in CNS

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68
Q

How does mono amine oxidase B inhibitor help parkinson’s?

A

prevents dopamine breakdown in CNS so increases availability

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69
Q

Difference between passive and active ion transport?

A

passive uses symporters and channel proteins, active uses carrier proteins and ATPases

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70
Q

How do uniporters work?

A

use energy from ATP to pull molecules in

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71
Q

How do symporters work?

A

use movement of one molecule to pull in another molecule against its concentration gradient

Eg. Na-K-Cl (NKCC) cotransporter

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72
Q

What is an antiporter?

A

Uses energy from second substrate moving down its gradient to move another substance against its concentration gradient

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73
Q

What are the different types of ion channels used in passive transport of drugs?

A

epithelial, voltage-gated, metabolic, receptor activated

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74
Q

What is an epithelial ion channel and what does it transport?

A

apical membrane bound heterotrimeric ion channel. selectively permeable to Na+ so is often used in heart failure

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75
Q

What is a voltage gated ion channel?

A

in membranes of excitable cells so closed at resting membrane potential and activated during an action potential

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76
Q

What does activation of calcium voltage-gated channel result in?

A

muscular contraction and excitation of neurons

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77
Q

What does a sodium voltage gated channel result in?

A

increases Na+ into the cell and has 3 conformational states - closed, open, inactivated

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78
Q

What are calcium/sodium voltage-gated channels used to treat?

A

nerve arrhythmias

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79
Q

What is a receptor activated ion channel?

A

igand-gated ion channel that allow ions to pass through the membrane in response to binding to a chemical messenger

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80
Q

Example of a receptor activated ion channel?

A

GABA inhibitory neurotransmitter inhibits GABA A which causes hyperpolarisation - eg. chloride in epilepsy

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81
Q

How are sodium pumps (active) used to decrease heart rate?

A

inibition causes increase in intracellular Na which also increases intracellular Ca, increasing length of cardiac action potential

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82
Q

How are proton pumps (active) used to treat acidifcation of the stomach?

A

proton-pump inhibitors are irreversible and inhibit acid secretion

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83
Q

What does drug metabolism occur through?

A

specialised enzymatic systems and biotransformation

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84
Q

What determines the duration and intensity of a drug’s pharmacologic action?

A

rate of metabolism

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85
Q

What does drug metabolism and biotransformation do?

A

generates compounds that are more readily excretable

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86
Q

What is the main enzyme involved in drug metabolism?

A

CYPs (CYP450)

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87
Q

How do CYPs help metabolise drugs?

A

deactivates or bioactivates drugs, either directly or by facilitated excretion

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88
Q

What are the different types of opioids and examples of each? (x4)

A
  • naturally occuring, eg. morphine
  • simple chemical modifications, eg. diamorphine
  • synthetic opioids, eg. pethidine
  • synthetic partial agonists, eg. buprenorphine
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89
Q

What are some routes of administration of drugs?

A
  • oral (bioavailability)
  • parenteral - subcutaneous, IV, IM, IA
  • inhalational
  • topical
  • sublingual
  • rectal
  • intrathecal
  • IV patient controlled analgesia
  • epidural into CSF
  • trans-fermal patches
  • first pass metabolism by the liver
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90
Q

What is first pass metabolism by the liver?

A

Eg. 50% oral morphine metabolised by first pass so needs to be halved if giving IV

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91
Q

How long does a single dose of morphine last?

A

3-4 hours but can be slow release twice a day in palloative patients

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92
Q

What existing pain modulation systems do opioids use?

A
  • G protein couple receptors and act via second messengers
  • descending inhibition of pain, produces fight or flight response rather than sustained activation
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93
Q

What do opioids inhibit?

A

pain transmitters at spinal cord and midbrain

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94
Q

How do opioids modulate pain perception in higher centres?

A

change emotional perception of pain (euphoria)

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95
Q

What type of receptors do opioids use?

A

μ receptors. Also: delta, kappa, nociception opioid-like receptors

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96
Q

What is the definition of drug potency?

A

Whether a drug is strong or weak relates to how well the drug binds to the receptor

97
Q

Definition of opioid drug efficacy?

A

Concept of full or partial agonists and maximal response with the drug

98
Q

Difference between tolerance and dependence?

A

tolerance occurs when there’s a downregulation of receptors with prolonged use, requiring higher doses to achieve the same effect. Dependence is a physiological response of craving and euphoria

99
Q

When does withdrawal from opioids start, and how long does it last?

A

starts within 24 hours and lasts about 72 hours

100
Q

Why do we get side effects from opioid use?

A

Side effects happen because opioid receptors exist outside the pain system (eg. digestive tract and respiratory control centre) and opioids are usually delivered systemically

101
Q

Why should you start with a small dose of opioids and titrate up?

A

Different patients have a range of sensitivity

102
Q

What complication can arise from overusing opioids?

A

Respiratory depression

103
Q

What are the side effects of respiratory depression?

A

sedation, nausea, vomiting, constipation, itching, immune suppression

104
Q

What is the medical response for respiratory depression?

A

Help –> ABC –> naxolone IV

105
Q

What is antagonist of opioids?

A

Naxolone - short half life so weary of overdose

106
Q

What are the disadvantages of using opioids in chronic non-cancer pain?

A
  • lose effectiveness quickly
  • addiction to drug leads to manipulative behaviour, easy to start, difficult to stop
107
Q

What needs to happen to codeine and tramadol in order for them to work?

A

They need to be metabolised by cytochrome CYP2D6 to morphine

108
Q

What does morphine have to be metabolised to in order to be excreted?

A

morphine 6 glucuronide which is more potent and renally excreted

109
Q

What patients do you have to be careful in giving morphine to?

A

Those with renal failure - it can build up and cause respiratory depression

110
Q

What is drug development?

A

Process of bringing a new pharmaceutical drug to the market

111
Q

What are the 4 steps of drug discovery?

A
  1. lead compound identification
  2. pre-clinical development
  3. clinical development and trials
  4. regulatory approval and marketing
112
Q

What have drugs been commonly developed from?

A

plants (morphine), organic chemistry (choloroform, anaesthetics), inorganic chemistry (anti-cancer), sulphonamide nucleus (hypertensives, diabetes), bacteria/mold/fungi

113
Q

What are stereoisomers?

A

Same molecular formula but with different orientation in space - cause differentpotencies in drugs

114
Q

What types of antibodies are used in immunotherapy?

A

Polyclonal and monoclonal

115
Q

How are recombinant proteins used clinically?

A

DNA enclosed protein inserted into plasmid vector and into bacteria to produce protein. Grown and purified –> used as therapeutic agent

116
Q

WHat other proteins are used in recombinant therapy?

A

insulin, erythropoietin, growth hormone, interleukin 2, gamma interferon

117
Q

Examples of drugs developed to target DNA?

A

methotrexate and protein kinase inhibitors (eg. vemurafenib)

118
Q

What is gene therapy in drug development?

A

Experiemental technique that uses genes to treat or prevent disease

119
Q

How can genes be used to prevent disease?

A
  • replacing mutated gene with healthy copy
  • inactivating mutated gene
  • introducing new gene to help fight disease
120
Q

How does high throughput screening help in drug discovery

A

Provides starting points for drug design and for understanding the interaction or role of a particular biochemical process

121
Q

What is rational drug design?

A

The process of finding new medications based on the knowledge of a biological target

122
Q

WHat type of drugs are commonly used in rational drug design?

A

organic small molecules that activate or inhibit function of a biomolecule

123
Q

Why does rational drug design use drugs that are complementary in shape to biomolecular target?

A

So that they will interact and bind

124
Q

What does rational drug design rely on?

A

computer modelling techniques and knowledge of 3D structure of biomolecular target

125
Q

What is drug selectivity?

A

The degree to which a drug acts on a given site relative to other sites

126
Q

What is drug specificity?

A

The measure of a receptors ability to respond to a single ligand

127
Q

What is the principle of the pain analgesic ladder?

A

medications used in incremental fashion according to the patient’s reported pain intensity

128
Q

Why is the pain ladder unhelpful for persistant pain?

A

substantial reduction in pain is rarely achievable and requires other control methods

129
Q

Should the stepped pain ladder be used to make medication choices?

A

Can be considered but should ultimately aim to start with non-opioid drugs

130
Q

When can paracetamol overdose occur?

A

When patients take other drugs containing paracetamol without realising, eg. cocodamol

131
Q

What must most drugs do in order to enter general circulation?

A

Cross at least one membrane barrier from site of generation

132
Q

What are the different ways drugs can pass across membranes?

A
  • passive diffusion through lipid layer
  • diffusion through pores or ion channels
  • carrier mediated processes
  • pinocytosis
133
Q

What are ionizable groups essential for?

A

mechanism of action of most drugs because ionic forces are part of ligand receptor interaction

134
Q

What type of drugs is ionisation a basi property of?

A

drugs that are either weak acids or weak bases

135
Q

Which forms (ionised or unionised) are water soluble and lipid soluble?

A

ionised = water soluble
unionised = lipid soluble

136
Q

What feature of the small intestine allows rapid and complete absorption of oral drugs?

A

Large surface area and high blood flow

137
Q

What do drugs need to be in order to be absorbed from the gut?

A

lipid soluble

138
Q

Why do some drugs have to be given by an alternative route?

A

If unstable at low pH or in presence of digestive enzymes

139
Q

Why do some drugs have a capsule or coating?

A

Means they dissolve more slowly and are resistant to the acidity of the stomach

140
Q

What are the 4 metabolic barriers drugs have to pass in first pass metabolism?

A

intestinal lumen, intestinal wall, liver, lungs

141
Q

When are drugs given intradermally/subcutaneously?

A

allows small volume to be given, used for local effect, used to deliberately limit rate of absorption, avoids stratum corneum barrier

142
Q

What is intradermal/subcutaneous absorption limited by?

A

blood flow

143
Q

What does intramuscular absorption depend on?

A

blood flow and water solubility because increasing either can enhance drug removal

144
Q

What is a pro for inhalational absorption of drugs?

A

large SA and blood flow

145
Q

What are cons for inhalational absorption?

A
  • risks of toxicity to alveoli
  • largely restricted to volatiles, eg. anaesthetics and bronchodilators
  • asthma drugs non-volatile so have to be made aerosol
146
Q

Which type of drugs can readily cross placenta and BBB?

A

lipid soluble

147
Q

What is elimination of drugs?

A

Removal of drugs activity from the body which may involve metabolism or excretion

148
Q

Why are drugs converted to water soluble products to be excreted?

A

Lipid soluble would get reabsorbed

149
Q

Difference between phase 1 and phase 2 metabolism?

A

phase 1 - transformation to more polar metabolite, add functional group using CYP
phase 2 - formation of covalent bond between drug and endogenous substrate so more readily excreted

150
Q

What different forms are drugs excreted in?

A
  1. fluids - sweat, tears, breast milk
  2. solids - faecal elimination
  3. gases - expired air
151
Q

Difference between first order and zero order metabolic pharmacokinetics?

A

1st Order: decline is exponential, constant fraction of drug is eliminated per unit of time
Zero Order: once saturated, rate of removal is constant and unaffected by increase in concentration

152
Q

What is the half life of a drug?

A

time taken for a concentration of a drug to reduce by half

153
Q

How is the apparent volume of distribution measured?

A

total amount of drug in body/plasma concentration

154
Q

What does a water soluble vs lipid soluble drug rate of distribution depend on?

A

water = rate of passage across membranes
lipid = blood flow to tissues

155
Q

What is the rate of elimination inversely proportional to?

A

volume of distribution

156
Q

What is drug clearance?

A

volume of blood or plasma cleared of a drug per unit of time

157
Q

What does it mean when a drug is in a steady state?

A

there is a balance between input and elimination of a drug

158
Q

What is most long term drug administration by?

A

Oral route - doses are intermittent so have peaks and troughs

159
Q

Difference between adrenergic and cholinergic?

A

adrenergic: relating to adrenaline or noradrenaline
cholinergic: relating to acetylcholine

160
Q

Difference between neuron chain of somatic and autonomic?

A

somatic - single neuron between CNS and skeletal muscle
autonomic - two neuron chain separated by autonomic ganglion

161
Q

Difference between somatic and autonomic innervation?

A

somatic - innervates skeletal muscle = excitation
autonomic - innervates smooth muscle = excitation or inhibiton

162
Q

What neurotransmitters and receptors do sympathetic NS use?

A

preganglionic: ACH on nicotine receptors
postganglionic: Nordadrenaline on alpha/beta receptors

163
Q

What neutrotransmitters and receptors do parasympathetic NS use?

A

preganglionic: ACh on nicotine receptors
postganglionic: ACh on muscarinic receptors

164
Q

Are muscarinic receptors adrenergic or cholinergic?

A

cholinergic

165
Q

Where are muscarinic receptors found and what do they activate?

A

found outside cell - M1 (brain), M2 (heart). activate intracellular processes though G proteins

166
Q

How do M2 receptors affect SA and AV node?

A

At SA: decrease heart rate
At AV: decrease conduction velocity and induce AV node block by increasing PR interval

167
Q

Where are M3 receptors activated?

A

resp system: produce mucus and induce bronchoconstriction
GI: increase saliva and gut motility
Skin: sweating

168
Q

Symptoms of muscarine poisoning?

A

blurred vision, hypersalivation, bronchoconstriction, bradycardia, diarrhoea, polyuria, hyperhidrosis (excessive sweat)

169
Q

Example of a muscarinic agonist?

A

pilocarpine eye drips increase drainage of aqueous humour to reduce pressure

170
Q

Example of muscarinic antagonists?

A

atropine eye drops dilate pupils and can also be used IV to increase HR

171
Q

What does local delivery of inhaled antimuscarinics result in?

A

bronchodilation

172
Q

Examples of M3 antimuscarinics in bladder and gut?

A

Solifenacin: blocks M3 and inhibits smooth muscle contraction
Mebeverine: blocks M£ and slows gut contractility

173
Q

Where is ACh used outside of the autonomic NS?

A

in CNS receptors and skeletal muscle

174
Q

What is a side effect of anticholinergics being used in CNS?

A

memory problems

175
Q

Botulinum toxin (BoTox) prevents ACh release - what does this cause?

A

flaccid paralysis and death from resp muscle involvement

176
Q

What is the pathology of myasthenia gravis?

A

blockage of normal transmission of ACh –> causes muscle weakness

177
Q

Are catecholamines present in cholinergic or adrenergic?

A

adrenergic

178
Q

What does post-atonomic ganglion neurotransmission depend on?

A

catecholamines: noradrenaline, adrenaline, dopamine

179
Q

What do alpha 1 receptors cause when activated?

A

vasoconstriction and contraction in smooth muscle of eye and blood vessels

180
Q

What are examples of agonists for alpha 1 receptors?

A

noradrenaline (shock) and adrenaline (anaphyalxis)

181
Q

Example of antagonist for alpha 1 receptors?

A

doxazosin and tamsulosin

182
Q

Where are alpha 2 adrenoreceptors located?

A

In brain so have mixed effects on vascular smooth muscle

183
Q

What effects do alpha 2 receptors have once activated?

A

reduce vascular tone and blood pressure

184
Q

Where are beta 1 receptors located?

A

heart, kidneys, fat cells

185
Q

What effects do agonists of beta 1 receptors cause?

A

tachycardia, increased SV, renin release, lipolysis, hyperglycaemia

186
Q

What are antagonists of beta 1 receptors known as?

A

beta blockers, eg. propranolol

187
Q

What effects do beta blockers have

A

reduce heart rate and SV, reduce oxygen demand and remodel in heart failure

188
Q

Where are beta 2 receptors located?

A

bronchi (dilate), bladder (inhibits micturition), uterus (inhibits labour), skeletal muscle (more contraction), pancreas

189
Q

Example of beta 2 agonists?

A

salbutamol use in asthma

190
Q

What is the definition of an adverse drug reaction?

A

unwanted or harmful reaction following administration of drug under normal conditions of use, and is suspected to be related to the drug

191
Q

What does a drug reaction have to be in order to be classed as adverse?

A

noxious and unintended

192
Q

Difference between mild and severe ADRs?

A

mild = nausea, drowsiness, itchy rash
severe = resp depression, anaphylaxis, haemorrhage

193
Q

How is a side effect different to an ADR?

A

unintended effect of drug related to its pharmacology and can include unexpected benefits of treatment. Side effects could be beneficial

194
Q

What are the three types of effects of an ADR?

A

toxic (above therapeutic range), collateral (therapeutic range), hyper-susceptibility (below theraputic range)

195
Q

When can toxic effects occur? Example?

A

When dose is too high or drug excretion is reduced by impaired renal/hepatic function. Eg. nephrotoxicity with high doses of aminoglycosides

196
Q

Example of collateral ADR effect?

A

beta blockers causing bronchoconstriction

197
Q

Example of hyper-susceptibility ADR effects?

A

penicillin and anaphylaxis

198
Q

Common patient risk factors for ADRs? (7)

A
  • gender F>M
  • age (elderly and neonates)
  • polypharmacy
  • adherence problems
  • genetic predisposition
  • hypersensitivity
  • hepatic/renal impairment
199
Q

What are common drug risk factors for ADRs? (4)

A
  • steep dose-response curve
  • low therapeutic index so easily toxic range
  • already causes adverse reactions
  • prescriber risks
200
Q

What can causes for ADRs be due to?

A
  • pharmaceutical variation
  • abnormal biological system unmasked by drug
  • abnormalities in drug metabolism
  • receptor abnormality
  • drug-drug interaction
201
Q

What are the time-dependent ADRs?

A

rapid, first dose, early, intermediate, late, delayed

202
Q

What is the classification of ADRs?

A

A - augmented pharmacological
B - bizarre/idiosyncratic
C - chronic
D - delayed
E - end of treatment
F - failure of therapy

203
Q

What are the main characteristics of a type A ADR?

A

predictable, dose dependent, common. high morbidity, low mortality

204
Q

What is the difference between a primary and secondary type A ADR?

A

primary effect eg. is bradycardia and propranolol
secondary effect eg. bronchospasm and propranolol

205
Q

What are main characteristics of type B ADR?

A

not predictable, dose dependent, not readily reversed, less common, low morbidity but high mortality

206
Q

What is a type B ADR often due to? and give an example.

A

idiosyncrasy, allergy, hypersensitivity. Eg. anaphylaxis and penicillin

207
Q

Common characteristics of type C ADR? and example.

A

uncommon, time related, related to cumulative dose. Eg. osteoporosis and steroids

208
Q

Common charcateristics of type D ADR? and example.

A

uncommon, dose related, shows some time after use of drug. Eg. malignancies and immunosuppression

209
Q

Characteristics of type E ADR? and example.

A

uncommon, occur after ubrupt drug withdrawal. Eg. opiate withdrawal

210
Q

Characteristics of Type F ADR? and example.

A

common, dose related, caused by drug interactions. Eg. failure of contraceptive pill in presence of enzyme inducer

211
Q

What does DoTS stand for?

A

DOse relatedness, Timing, patient Susceptibiltity

212
Q

Wht does idiosyncrasy mean?

A

Inherent abnormal response to a drug

213
Q

When should we suspect an ADR?

A
  • symptoms soon after a new drug is started or dosage changed
  • symptoms disappear when drug is stopped and reappear when restarted
214
Q

What is the recommended response to an ADR?

A

assess if urgent reaction, take a history, review meds, review adverse effect profile of drug, modify or stop drug, report drug

215
Q

What are some drugs that commonly cause ADRs?

A

antibiotics, anti-neoplastics, cardiovascular, hypoglycaemic, NSAIDs, CNS drugs

216
Q

What bodily systems are commonly affected by ADRs?

A

GI, renal, metabolc, endocrine, dermatologic, haemorrhagic

217
Q

What are common side effects of ADRs?

A

confusion, nausea, balance problems, diarrhoea, constipation, hypotension

218
Q

What is the Medicines and Healthcare Products Regulatory Agency (MHRA) responsible for?

A

Approving medicines and devices for use

219
Q

What is yellow card reporting?

A

voluntarily collects spontaneous reports and suspected ADRs

220
Q

Why are ADRs reported?

A

patient safety, to identify ADRs missed in clinical trials, compare drugs in same therapeutic class,identify ADRs in risk groups

221
Q

What should you report on a yellow card?

A
  • all suspected reactions for herbal medicines and black triangle drugs
  • all serious reactions for established drugs, vaccines, and interactions
222
Q

What is the optimisation of medicines?

A

looks at the value of medications to make sure they are clinically and cost-effective. Ensures people get right choice of medicines at the right time.

223
Q

Definition of adherence?

A

Extent to which patient’s actions match agreed recommendation

224
Q

Why is adherence better than compliance?

A

acknowledges importance of patients belief but recognises health professional is still expert

225
Q

What is compliance?

A

An old term that assumes doctor knows best and the patient should be passive and follow orders.

226
Q

Example of non-adherence?

A

not taking, taking smaller/bigger/more/less doses, stopping without finishing course

227
Q

What are some unintentional reasons for non-adherence?

A

difficulty understanding instructions, problems using treatment, financial

228
Q

What are some intentional reasons for non-adherence?

A

patient’s belief about their health/treatments, personal preferences

229
Q

What are necessity beliefs?

A

Perceptions of personal need for treatment and concerns about a range of potential adverse consequences.

230
Q

What is the aim of patient-centeredness?

A

Shift in focus from treatment to the process of care

231
Q

What does patient-centredness encourage?

A
  • focus in consultation on patient as a whole with preferences and social context
  • shared control and decisions about health management
232
Q

What are the benefits of good doctor-patient communication?

A

better health outcomes, higher adherence, higher doctor-patient satisfaction, reduced risk of malpractice

233
Q

How can communication be improved for drug adherence?

A

adapt consultation style to patient’s needs and encourage them to ask Qs

234
Q

How can patient involvement of treatment be increased?

A
  • explain condition and pros/cons of treatment
  • ideas, concerns and expectations
  • record patients decision if choose not to take medicine
235
Q

How can a doctor understand patient’s perspective of their treatment?

A

Ask what they know and believe, and if they have any concerns

236
Q

How can doctors increase adherence (3)?

A
  • provide clear and individualised info
  • assess adherence in non-judgemental way
  • review medicines
237
Q

What is concordance?

A

extension of patient-centered care that thinks of patients as equals who are expected to take part in treatments

238
Q

Why my patients not want to work in concordance about their treatment?

A

Might worry them more or medical decisions may be too complex

ICS/GP/ILA (9 decks)

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