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Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is medicine optimisation?

A

looks at the value which medicines deliver, making sure they are clinically-effective and cost-effective

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2
Q

What does medicine optimisation help patients do?

A

Improve their outcomes
Take their medicines correctly
Avoid taking unnecessary medicines
Improve medicines safety
Reduce wastage of medicines

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3
Q

What are some examples of medicine non-adherance?

A

Not taking prescribed medication
Taking bigger/smaller doses than prescribed
Taking medication more/less often than prescribed
Stopping the medicine without finishing the course
Modifying treatment to accommodate other activities(work, social)
Continuing with behaviours against medical advice(diet, alcohol, smoking)

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4
Q

Unintentional examples of medicine non-adherance

A

Difficulty understanding instructions
Poor dexterity
Inability to pay
Forgetting

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5
Q

Intentional examples of medicine non-adherance

A

Patients’ beliefs about their health/condition
Beliefs about treatments
Personal preferences

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6
Q

What is adherance?

A

the degree to which a patient correctly follows medical advice

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7
Q

What are the impacts of good doctor-patient communication?

A

Better health outcomes.
Higher adherence to therapeutic regimens in patients.
Higher patient and clinician satisfaction.
Decrease in malpractice risk.

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8
Q

What is pharmacokinetics?

A

The fate of a chemical substance administered to a living organism

What the body does to the drug

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9
Q

What is pharmacodynamics?

A

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

What the drug does to the body

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10
Q

What 12 ways can drugs be administered?

A

IV (intravenous)
IA (intra-arterial)
IM (intramuscular)
SC (subcutaneous)
PO (oral)
SL (sublingual)
INH (inhaled)
PR (rectal)
PV (vaginal)
TOP (topical)
TD (transdermal)
IT (intrathecal)

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11
Q

Which 2 ways of administering a drug ensure 100% of dose reach systemic circulation?

A

Intravenous
Intraarterial

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12
Q

How can drugs permeate across membranes?

A

Passive diffusion through hydrophobic membrane
Passive diffusion through aqueous pores
Carrier mediated transport

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13
Q

What factors can affect drug absorption?

A

Lipid solubility (affecting diffusion)
Drug ionisation (ionised drugs have poor lipid solubility and are poorly absorbed)

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14
Q

What factors affect oral drug absorption?

stomach

A

Drug ionisation
Low pH in stomach might degrade molecule
Gastric enzymes might digest
Full stomach will slow absorption
Gastric motility
Previous surgery

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15
Q

Where are weak acids and bases best absorbed?

A

Weak acids: best absorbed in the stomach
Weak bases: best absorbed in the intestine

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16
Q

What factors affect oral drug absorption?

Intestine

A

Drug structure (large or hydrophilic molecules are poorly absorbed)
Medicine formulation (coating can control time between administration and drug release)
P-glycoprotein (substrates are removed from intestinal endothelial cells back into lumen)

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17
Q

What is first pass metabolism?

A

Metabolism of drugs preventing them reaching systemic circulation

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18
Q

What happens in first pass metabolism?

A

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

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19
Q

What is bioavailability?

A

proportion of administered dose that reaches the systemic circulation

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20
Q

How can you avoid first pass metabolism?

A

giving via routes that avoid sphlanchnic circulation (eg rectal)

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21
Q

What is bioavailability dependent on?

A

Dependent on extent of drug absorption and extent of first pass metabolism

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22
Q

Pros and cons of rectal administration

A

Pros: Local administration
Avoids first pass metabolism
Nausea and vomiting

Cons: Absorption can be variable
Patient preference

e.g. diazepam in epileptic seizure

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23
Q

Pros and cons of inhaled administration

A

Pros: Well perfused large surface area
Local administration
Cons: inhaler techniques can limit effectiveness

e.g. salbutamol for asthma

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24
Q

Pros and cons of subcut administration

A

Pros: Faster onset than oral
Formulation can be changed to control rate of absorption

Cons: not as fast as IV

e.g. long lasting insulin

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25
Q

What affects drug distribution?

A

Molecule size (smaller distributes easier)
Lipid solubility
Protein binding (if drug molecule bound to albumin it can’t do its action or permeate across barriers)

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26
Q

Pros and cons of transdermal administration

A

Pros: Provides continuous drug release
Avoids first pass metabolism

Cons: Only suitable for lipid soluble drugs
Slow onset of action

e.g. fentanyl patches for chronic pain

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27
Q

What is the volume of distribution?

A

Volume of plasma required to contain the total administered dose

Theoretical volume a drug will be distributed in the body

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28
Q

Link between volume of distribution and drug distribution

A

Drugs that are well distributed will have high Vd
Drugs that are poorly distributed will have low Vd

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29
Q

How can drugs reach the CNS?

A

High lipid solubility. e.g. psychiatric drugs usually very lipid soluble (therefore large Vd)
Intrathecal administration to bypass blood brain barrier (e.g. baclofen in MS and spinal cord injury, chemotherapy)
Inflammation of BBB (causes barrier to become leaky) so drugs thata can’t normally permeate it can

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30
Q

Things to consider when prescribing: distribution

A

Changes in distribution caused by disease states (e.g. sepsis increases leakyness and increases distribution)
Age related changes leads to smaller volume of distribution
Drugs able to cross BBB more likely to cause CNS side-effects
Caution dosing drugs with a small Vd using actual body weight in obese patients

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31
Q

What is drug elimination?

A

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

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32
Q

What is drug metabolism?

A

modification of chemical structure to form new chemical structure

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33
Q

What are the 2 phases of drug metabolism?

A

Phase 1: Oxidation/reduction/hydrolysis to introduce reactive group to chemical structure
Phase 2: Conjugation of functional group to produce hydrophilic, inert molecule

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34
Q

What happens in phase 1 drug metabolism?

A

Cytochrome P450 (CYP450) enzymes are responsible for majority of phase 1 metabolism
Located mostly in the liver (extrahepatic: small intestine, lung)
Lipophillic, unbound drug molecules will readily cross hepatocyte membrane
Produces a reactive metabolite by creating or unmasking a reactive functional group

introduce reactive group to chemical structure

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35
Q

How can CYP enzyme function vary?

A

Genetic variation
Reduced function in severe liver disease
Interactions enzyme inhibiting/inducing drugs or food can reduce/increase enzyme activity

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36
Q

What happens in phase 2 drug metabolism?

A

Conjugation of an endogenous functional group (glycine, sulfate, glucuronic acid) to produce a non-reactive polar (therefore hydrophilic) molecule
Hydrophyllic metabolite can then be renally excreted

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37
Q

Things to consider when prescribing: metabolism

A

In severe liver impairment may need reduced dose/frequency, additional monitoring or avoidance
CYP450 enzyme induction/inhibition drug interactions (to be discussed in detail in Drug Interactions lecture)
Saturation of metabolic pathways can lead to accumulation/toxicity of drug and or metabolites

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38
Q

How can drugs and metabolites be excreted?

A

Liquids (small, polar molecules): urine, bile, sweat, tears, breast milk
Solids (large molecules): faeces (through biliary excretion)
Gases (volatiles): expired air

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39
Q

How does renal excretion work?

A

Glomerular filtration
Active tubular secretion: drug molecules transported from blood into tubule by carrier systems (OAT, OCT)
Passive reabsorption: diffusion down the concentration

OAT: organic anion transporter OCT: organic cation transporter

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40
Q

Things to consider when prescribing: drug elimination/excretion

A

Kidneys excrete drugs and drug metabolites (active and inactive)
Reduced kidney function can lead to accumulation and toxicity of renally cleared drugs

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41
Q

What are the 4 pharmacokinetic processes?

A

Absorption
Distribution
Metabolism
Excretion

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42
Q

What happens in first order kinetics?

A

Rate of elimination is proportional to the plasma drug concentration (processes involved in elimination do not become saturated)

A constant % of the plasma drug is eliminated over a unit of time

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43
Q

What happens in zero order kinetics?

A

Rate of elimination is NOT proportional to the plasma drug concentration (metabolism processes become saturated)

A constant amount of the plasma drug is eliminated over a unit of time

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44
Q

What is the half life of a drug dependent on?

A

Dependent on clearance (CL) of drug from body by all eliminating organs (hepatic, renal, faeces, breath)
Dependent of volume of distribution (Vd) - A drug with large Vd will be cleared more slowly than a drug with a small Vd

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45
Q

What is drug half life not dependent on?

A

not dependent on drug dose or drug formulation

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46
Q

When is a drug cleared from the body?

A

A drug will be 97% cleared from the body after 5 x half lives (considered ‘cleared’ in clinical practice)

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47
Q

What is the relevance of drug half life in clinical practice?

A
  • Drug dosing (short t1/2 will need more frequent dosing)
  • Organ dysfunction (t1/2 may be increased)
  • Adverse drug reactions or management of toxicity (how long will drug take to be removed and symptoms to resolve)
  • Short t1/2 increases risk of discontinuation/withdrawal symptoms (such drugs may need dose weaning on cessation)
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48
Q

What is drug steady state?

A

rate of drug input is equal to rate of drug elimination

49
Q

What is Css and the time to Css?

A

Css = drug plasma concentration at steady state
Time to Css = 5 x t1/2 (after treatment initiation and after a dose increase)

50
Q

How can you reduce time to reach steady state?

A

Give a loading dose

51
Q

When would continuous IV infusion be used?

A

Critical care patients
Antibiotics
Unfractionated heparin
General anaesthetics

52
Q

What drugs require a loading dose?

A

Digoxin
Vancomycin
Teicoplanin
Amiodarone
Heparin

53
Q

Where should the steady state lie?

A

Aim for Css which lies between the Maximum safe concentration (MSC) and minimum effective concentration (MEC)

54
Q

What drugs follow zero order kinetics?

A

ethanol
phenytoin

55
Q

What does drug clearance (CL) mean?

A

rate of drug elimination by all eliminating organs

56
Q

What does half-life (t1/2) mean?

A

time taken for plasma drug concentration to fall 50%

57
Q

What does a narrow therapeutic window mean?

A

Drugs with a narrow window between minimum effective concentration and maximum safe concentration

58
Q

Examples of drugs with a narrow therapeutic window

A

vancomycin
gentamicin
phenytoin
digoxin
theophylline
lithium

59
Q

What does pharmacogenomics mean?

A

The use of genetic and genomic information to tailor pharmaceutical treatment to an individual

60
Q

Benefits of pharmacogenomics

A

Improved patient outcomes
Cost efficiency

61
Q

How can genomics affect medicines use?

pharmacokinetics

A

variations in drug metabolism (eg CYP450 enzymes)
- variations in efficacy
- increased incidence in adverse drug reactions

62
Q

How can genomics affect medicines use?

pharamcodynamics

A

variations in drug receptor
- variations in efficacy (‘on’ targets)
- increased incidence of adverse drug reactions (ADRs) (‘on’ and ‘off’ targets)

63
Q

What is a 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

ligand can be exogenous or endogenous (e.g. drugs or hormones)

64
Q

What are the different types of receptors?

A

Ligand-gated ion channels
G protein coupled receptors
Kinase-linked receptors
Cytosolic/nuclear receptors

65
Q

What do Kinase-linked receptors do?

A

Kinases catalyze the transfer of phosphate groups between proteins
Phosphorylation

65
Q

How do G protein coupled receptors work?

A

Largest and most diverse group of membrane receptors in eukaryotes
Activated by peptides, lipids, sugars
Activity is regulated by ability to bind and hydrolyze GTP to GDP

65
Q

How do nuclear receptors work?

A

Modify gene transcription

66
Q

What is an agonist?

A

a compound that binds to a receptor and activates it

67
Q

What is an antagonist?

A

a compound that reduces the effect of an agonist

prevents receptor activation by agonists

68
Q

Examples of endogenous ligands

A

Neurotransmitters
Hormones

69
Q

Example of an exogenous ligands

A

drugs

70
Q

What is an enzyme inhibitor?

A

a molecule that binds to anenzymeand (normally) decreases itsactivity

71
Q

How does an enzyme inhibitor work?

A

prevents the substratefrom entering the enzyme’sactive site and prevents it fromcatalyzingits reaction

72
Q

What are the 2 types of enzyme inhibitors?

A

Irreversible inhibitor: usually reacts with enzyme and changes it chemically
Reversible inhibitor: binds non-covalently and different types of inhibition are produced depending on what it binds to

73
Q

How do statins work?

A

Block the rate limiting step in the cholesterol pathway
HMG-CoA reductase inhibitors

74
Q

Why are statins used?

A

primary prevention of cardiovascular disease
lipid lowering (reduce cholesterol levels)

75
Q

What doe ACE inhibitors do?

A

Inhibiting ACE reduces ATII production and therefore causes a reduction in blood pressure

76
Q

What are the naturally occuring opioids?

A

Morphine
Codeine (weak)

77
Q

What are the synthetic opioids?

A

Fentanyl
Pethidine
Alfentanil
Remifentanil

78
Q

Example of an opioid agonist

A

Naloxone

79
Q

What is the difference between injecting opioids and giving them orally?

A

50% bioavailability orally
10mg orally = 5mg IV/IM/SC

80
Q

What are the side effects of opioids?

A

Respiratory depression
Sedation
Nausea and vomiting
Constipation
Itching
Immune supression

81
Q

What receptors are in the sympathetic nervous system?

A

Alpha 1 and 2
Beta 1 and 2

82
Q

What is affinity?

A

How strongly a drug binds to a receptor

83
Q

What is potency?

A

amount of medication needed to elicit an effect

84
Q

What’s the link between potency and affinity?

A

higher affinity = higher potency
higher affinity = effect at a lower dose

85
Q

What is intrinsic activity?

A

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

86
Q

What is efficacy?

A

maximum response that can be achieved with a drug

87
Q

What are competive antagonists?

example

A

meds reversibly bind to same receptor site as the agonist but doesn’t activate it
binds and dissociates quickly
inhibition when more ligands are present
decreases potency but not efficacy

beta-blockers

88
Q

What are non-competitive antagonists?

example

A

bind to allosteric sites not to the same as agonist’s site
alters receptor shape so unrecognisable for ligand
irreversible or slow dissociation
receptor won’t activate despite how many agonists present

decreases efficacy

botox affecting ACh receptors

89
Q

Difference between competitive and non-competitive antagonists

A

Comp affect agonist potency
Non-comp affect agonist efficacy

Comp bind and dissociate quickly
Non-comp are irreversible or dissociate slowly

90
Q

What is inverse agonism?

A

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

91
Q

Example of a selective and non-selective agonist

A

Salbutamol is a b2-adrenoceptor agonist (selective for beta 2)
Isoprenaline is a b-adrenoceptor agonist
(non-selective for all beta)

92
Q

What is an adverse drug reaction?

A

noxious and unintended response to medicinal product

93
Q

What are the impacts of an adverse drug reaction on patients?

A
  • Reduced QoL
  • Poor compliance
  • Reduced confidence in clinicians and the healthcare system
  • Unnecessary investigations or treatments
94
Q

What is the impact of adverse drug reactions on the NHS?

A
  • Increased hospital admissions
  • Longer hospital stays
  • GP appointments
  • Inefficient use of medication
95
Q

What are the different types of ADRs?

(ABCDEFG)

A

Augmented
Bizarre
Chronic
Delayed
End of use
Failure of treatment
Genetic

96
Q

What is an augmented ADR?

example

A

exagerrated effect of a drug at therapeutic dose

respiratory depression in opiates

97
Q

What is a bizarre ADR?

example

A

not related to pharmacology of the drug or the dose

anaphylaxis

98
Q

What is an end of use/withdrawal ADR?

example

A

ADR after stopping drug

e.g. rebound tachycardia after stopping beta blockers

99
Q

What is a chronic ADR?

example

A

Continue after drug has been stopped

osteonecrosis of the jaw with bisphosphonates

100
Q

What is a failure of treatment AR?

example

A

unexpected treatment failure

drug-food or drug-drug interaction

101
Q

What is a genetic ADR?

example

A

drug irreversibly damages genome

thalidomide

102
Q

What is specificity of a drug?

A

the extent to which a drug produces only the desired therapeutic effect without causing any other physiological changes

High specificity less side effects

103
Q

What is drug selectivity?

A

a drug’s strong preference for its intended target over other targets

104
Q

How can ADRs be classified?

not A-G

A

Dose-related
- hypersusceptibility: ADRs at subtherapeutic doses (e.g. anaphylaxis with penicillin)
- collateral: at intended dose
- toxic effects: supratherapeutic (paracetamol overdose)
Time dependent
Susceptibility

105
Q

Who is at an increased risk of ADRs?

A

Atopic individuals- greater risk of immune mediated ADRS
Children and neonates- limited data, weight based dosing
Reduced drug clearance due to organ dysfunction
Extremes of weight- does adjustments may be needed to avoid under/over dosing
Females
Polypharmacy
Advanced age
Genetic variants- CYP450 altered metabolism

106
Q

How are ADRs detected?

A

Pre-clinical testing
Clinical trial data
Post-marketing surveillance
Pharmacovigilance (overseen by MHRA, yellow card scheme)

107
Q

When did the yellow card scheme start and what are the strengths?

A

1963
Confidential
No fear of litigation
Quick
Accessible

108
Q

What are the weaknesses of the yellow card scheme?

A

Underreporting: only 5% of ADRs
Relies on HCPs recognising ADRs
Doesn’t indicate incidence

109
Q

What changes can be made when an ADR is confirmed?

A

Adding ADR info to product (BNF)
Restrictions in use
Changes in legal classification
Increased monitoring
Withdrawal from market

110
Q

What is the definition of pain?

A

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

111
Q

What are the steps of the WHO analgesic ladder?

A

1: NSAID or paracetamol
2: weak opiods (codeine, tramadol)
3: strong opiods (morphine, fentanyl, oxycodone)

112
Q

What are the main side effects of NSAIDs?

A

Gastritis with dyspepsia (indigestion)
Stomach ulcers
Exacerbation of asthma
Hypertension
Renal impairment
Coronary artery disease, heart failure and strokes (rarely)

113
Q

When might NSAIDs be inappropriate?

A

Asthma
Renal impairment
Heart disease
Uncontrolled hypertension
Stomach ulcers

114
Q

What is commonly prescribed with an NSAID?

A

PPI

115
Q

What are the side effects of opioids?

A

Constipation
Skin itching (pruritus)
Nausea
Altered mental state (sedation, cognitive impairment or confusion)
Respiratory depression (usually only with larger doses in opioid-naive patients)

116
Q
A

Phase 2a (14 decks)

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