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Emily Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacology?

A

The study of the effect of drugs

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2
Q

Define druggability

A

Used in drug discovery to describe a biological target that is predicted to bind with high affinity to a drug.

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3
Q

What are the 4 types of drug targets?

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

Define receptor.

A

A component of a cell that interacts with a specific ligand (exogenous or endogenous) and initiates a change of biochemical events leading to the ligands observed effects.

(ligand receptor only present on certain cells)

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5
Q

What are 3 types of chemical signals that use receptors?

A
  1. Neurotransmitters
    e.g., acetylcholine, serotonin
  2. Autacoids
    e.g. cytokine , histamine
  3. Hormones
    e.g. testosterone, hydrocortisone
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6
Q

What are 4 types of receptors?

A
  1. Ligand-gated ion channels
    e.g. nicotinic ACh receptor
  2. G protein coupled receptors
    e.g. beta-adrenoceptors
  3. Kinase-linked receptors
    e.g. receptors for growth factors
  4. Cytosolic/nuclear receptors
    e.g. steroid receptors
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7
Q

Explain what ligand gated ion channels are?

A

Are pore forming membrane proteins that allow ions to pass through the channel pore so that the cell undergoes a shift in electric charge

  • change in charge can be mediated by an influx of cation or efflux of anion
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8
Q

What receptors do ligand-gated ion channels have?

A

Nicotinic ACh receptors

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9
Q

Explain how G protein coupled receptors work.

A

Guanine Nucleotide-binding proteins
- Largest group of membrane receptors
- needs to interact with a G protein
- guanosine triphosphate (GTP) and guanosine diphosphate (GDP) binding are controlled
- G proteins act as switches

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10
Q

Explain the function of Kinase-linked receptors.

A

Kinases catalyse the transfer of phosphate groups between proteins - phosphorylation
- substrate gains a phosphate group ‘donated’ by ATP
- causes conformational change

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11
Q

What receptors do G protein coupled receptors have?

A
  • M3R (muscarinic receptor)
  • Beta-2-adrenorecepto. Produces second messenger cyclic-AMP
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12
Q

What are kinase-linked receptors targets for?

A

Growth factors

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13
Q

Explain the function of nuclear/cytosolic receptors.

A

Work by modifying gene transcription
(steroid hormones - require ligand binding site)

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14
Q

What are cytosolic receptors targets for?

A

Steroids

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15
Q

Define agonist

A

A compound that binds to a receptor and activates it

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16
Q

Define antagonist.

A

A compound that reduces the effect of an agonist.

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17
Q

Define the two state model of receptor activation.

A

Drugs activate receptors by inducing or supporting a conformational change in the receptor from ‘off’ to ‘on’

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18
Q

Define efficacy

A

How well a ligand activates a receptor
How well it induces a conformational change

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19
Q

Define potency

A

The amount of drug needed to produce a given effect.

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20
Q

What is the difference between a competitive and non-competitive antagonist?

A

Competitive = binds to the same site

Non = Binds to an allosteric site on the receptor to prevent activation of receptor

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21
Q

What is EC50 and what does it tell us about a drug?

A

EC50 = the conc of drug that give half the maximal response

Its potency!

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22
Q

What does Emax tell us about a drug?

A

Efficacy - The maximum response achievable

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23
Q

What is intrinsic activity?

A
  • Emax of partial agonist/Emax of full agonist
  • Basically, how well a drug works against something that fully works
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24
Q

Does an antagonist show efficacy?

A

No.
An antagonist has affinity but zero efficacy.
An agonist however demonstrates affinity and efficacy.

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25
Q

Which is more efficacious, a full agonist or partial agonist?

A

A full agonist is more efficacious because a full agonist can give a 100% response.

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26
Q

Define affinity.

A

How well a ligand binds to the receptor.

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27
Q

What 2 main factors govern drug action?

A
  1. Receptor-related
    - affinity
    - efficacy
  2. Tissue related
    - receptor number
    - signal amplification
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28
Q

What is the effect of fewer receptors on drug potency?

A

Fewer receptors will shift the dose-response curve to the RHS, this means drug potency will be reduced.

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29
Q

What is the effect of fewer receptors on receptor response?

A

Receptor response is still 100% due to receptor reserve. (Partial agonists don’t have receptor reserve).

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30
Q

What is the affect of less signal amplification on drug response?

A

Less signal amplification gives a reduced drug response.

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31
Q

Describe allosteric modulation.

A

An allosteric modulator binds to a different site on a receptor and influences the role of an agonist.

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32
Q

What is inverse agonism?

A

Where an agonist has a negative effect at a receptor.

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33
Q

Pharmacology: define tolerance.

A

A reduction in the effect of a drug overtime. This can be due to continuous use of repeatedly high concentrations.

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34
Q

Why is selectivity used to describe drug targeting rather than specificity?

A

Because no compound is truly specific

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35
Q

Give an example of a drug that is highly selective and one that is not?

A
  1. Isoprenaline is a non-selective B-adrenoreceptor agonist it activates both heart (B1) and lung (B2) receptors
  2. Salbutamol is a selective B”-adrenoreceptor and only activates lung (B2) receptors
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36
Q

What 3 ways can a receptor be desensitised?

A
  1. Uncoupled (an agonist would be unable to interact with a GPCR).
  2. Internalised (endocytosis, the receptor is taken into vesicles in the cell).
  3. Degraded. (no longer functions properly)
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37
Q

What is signal transduction and amplification?

A

Transduction = process involving conversion of a signal from outside the cell to a functional change within the cell

Amplification = to increase the strength of a signal

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38
Q

What are the 2 types of enzyme inhibitors?

A
  1. Irreversible inhibitors
    - react with the enzyme and change it chemically
    - covalent bond
  2. Reversible
    - bind non-covalently and induce different inhibitions depending on location of bond
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39
Q

Explain how statins work?

A
  • Block the rate limiting step in cholesterol pathway
  • reduces level of ‘bad cholesterol’
  • reduce cardiovascular disease
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40
Q

How do ACE inhibitors work?

A
  1. Angiotensinogen (liver) is converted to angiotensin 1 via renin (kidney).
  2. Angiotensin 1 is then converted to angiotensin 2 via ACE (lungs).
  3. ACE inhibitors prevents angiotensin 1 binding and so you don’t get angiotensin 2 formation.

(Angiotensin 2 is a vasoconstrictor and so ACE can be used in the treatment of hypertension).

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41
Q

Name a drug that targets enzymes?

A

NSAIDs

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42
Q

What is the action of NSAIDs?

A
  • They inhibit the COX enzyme (competitive inhibitors)
  • COX is responsible for the breakdown of arachidonic acid to prostaglandin H2 (PGH2)
  • reduce prostaglandin production = can lead to stomach ulcers
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43
Q

How is Aspirin different to other NSAIDs?

A

It irreversibly blocks the active site of COX resulting in irreversible inactivation

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44
Q

Give an example of a disease where the enzymes target multiple step in the pathway.

A

Parkinson’s Disease

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45
Q

Define synergy

A

Interactions of drugs such that the total effect is greater than the sum of individual effects
e.g. paracetamol & morphine/ibuprofen
(1+1>2)

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46
Q

Define pharmodynamics.

A

the effect of the drug on the body

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47
Q

Define pharmacokinetics

A

What the body does with the drug

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48
Q

What is an example of a physiochemical reaction?

A

the adsorption of paracetamol by activated charcoal as a treatment of paracetamol overdose

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49
Q

Define summation.

A

Different drugs used together to increase the effect of a single drug
(1+1=2)

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50
Q

How can some drug interactions be antagonistic?

A

When 2 drugs are given but they act against each other and blocks the action
(1+1=0)

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51
Q

Define potentiation.

A

enhancement of one drug by another so that one drug becomes more potent but the other one stays the same
(1+1=1+1.5)

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52
Q

What is the mechanism of pharmacokinetics?

A

AD ME
Absorption
Distribution
Metabolism
Excretion

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53
Q

Define bioavailability

A

The fraction of an administered drug that reaches the systemic circulation.
e.g. IV is always 100% but orally less

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54
Q

What are the factors affecting absorption?

A
  1. Motility - if the gut has slowed digestion, the drugs won’t work as well. A drug interaction that affects speed of absorption
  2. Acidity - all drugs are either ionised or unionised, can affect whether a drug passes through membrane
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55
Q

Explain drug distribution

A

Drugs can go into the proteins, other tissues or the effected site

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56
Q

How does protein binding affect strength of drugs?

A

If you give 2 highly protein bound drugs, they will make each other stronger and increase their effect
- the drug bound to the protein has no effect, but the drug bound to that drug is then free to have an effect
(make sure you check what other drugs a patient is on)

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57
Q

How does drug inhibition effect drug metabolism?

A

inhibition = Drug A blocks metabolism of Drug B, leaving more free drug B in the plasma so it has an increased effect

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58
Q

How do drug interactions effect excretion?

A

Weak bases - cleared faster if urine acidic

Weak acids - cleared faster if urine alkali

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59
Q

What drugs cause acute kidney injury?

A

NSAIDs
ACEi
Gentimicin
Furosemide

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60
Q

How does enzyme induction effect drug metabolism?

A

Induction
- Drug C induced CYP450 isoenzyme leading to increased metabolism of Drug D so it has decreased effect
- drugs can cause an increase in liver enzyme activity
- broken down into metabolite quickly so now have decreased efficacy (unless metabolite is active)

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61
Q

Examples of diseases that are due to imbalance of chemicals/receptors

A

Chemicals
- Allergy; increased histamine
- Parkinson’s; reduced dopamine

Receptors
- Myasthenia gravis; loss of Ach receptors
- Mastocytosis; increased c-kit receptors

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62
Q

Define selectivity.

A

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

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63
Q

Define specificity.

A

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

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64
Q

Give 2 types of cholinergic receptors?

A
  1. Muscarinic
  2. Nicotinic
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65
Q

What are the 2 types of ion transport?

A
  1. Passive
    - symporter (transport in 2 in same direction)
    - channels
  2. Active
    - ATP-ases
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66
Q

What are uniporters?

A

Use energy from ATP to pull molecules in

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67
Q

What are symporters?

A

Use the movement of one molecule to pull in another molecule against a concentration gradient

(transport 2 molecules at same time in same direction)

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68
Q

What are antiporters?

A

One substance moves against its gradient, using energy from the second substance moving down its gradient

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69
Q

Example of symporter

A

Na-K-Cl cotransporter is a protein that transports Na, K and Cl into cells
- all move in same direction

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70
Q

Explain epithelial sodium channels?

A
  • selectively permeable to Na+ ions
  • causes reabsorption at collecting ducts
  • blocked by amiloirde
  • used as anti-hypertensive
71
Q

Explain voltage gated calcium channels

A
  • Found in membrane of excitable cells
  • at resting membrane potential closed
  • activated by depolarised membrane potential
  • Ca2+ enters the cell
72
Q

What drug inhibits voltage gated calcium channels?

A

Amlodipine (calcium channel blocker)
- inhibits movement of Ca ions
- inhibiting contraction of muscles
-lowering blood pressure

73
Q

Define xenobiotics

A

Compunds that are foreign to an organism’s normal biochemistry, such as a drug or poison

74
Q

What is the role of cytochrome P450?

A
  • Metabolise drugs
  • deactivate molecules so they can be excreted
75
Q

Define afferent

A

Carries signals towards the brain or spinal cord

76
Q

Define efferent

A

Carries signals away from the brain or spinal cord

77
Q

Define adrenergic.

A

Relating to adrenaline or noradrenaline and their receptors.

78
Q

Define cholinergic

A

Relating to acetylcholine and its receptors.

79
Q

Define autonomic

A

Acting or occurring involuntarily
- then divide into parasympathetic and sympathetic

80
Q

What are muscarinic and nicotinic?

A

Types of ACh receptors

81
Q

Define ganglion

A

A group of nerves

82
Q

What are the differences between somatic and autonomic NS?

A

Somatic:
- single neurone between CNS and skeletal muscle
- innervates skeletal muscle
- leads to muscle excitation

Autonomic:
- 2 neurone chain
- cranial nerve 3,7,9,10
- smooth muscle, cardiac muscle, glands
- leads to excitation or inhibition

83
Q

Is the postganglionic neuron closer to the effector organ in the sympathetic or parasympathetic nervous system

A

Parasympathetic

84
Q

Explain the different nervous system fibres?

A

Somatic = one long fibre
Parasympathetic = 2 neurones, with ganglion within a chain adjacent to spinal cord

Sympathetic = 2 neurones with ganglion within or very close to effector organ

85
Q

What receptors are involved in parasympathetic nervous system?

A

Preganglionic = ACh (N2 receptor)
Post-ganglionic = Ach (Muscarinic receptor)

86
Q

What receptors are involved in sympathetic nervous system?

A

Preganglionic = ACh (N2 receptor)
Post-ganglionic = Noradrenaline (alpha and beta receptors)

87
Q

What does nicotine do?

A

Stimulates sympathetic and parasympathetic nervous system

88
Q

What does muscarine do?

A

Activates muscatinic receptors of the parasympathetic nervous system

89
Q

What are the 5 types of muscarinic receptors?

A

M1: Brain
M2: Heart (SA node)
M3: All organs with parasympathetic innervation
M4: Mainly CNS
M5: Mainly CNS

90
Q

Where are muscarinic receptors located?

A

Outside the cell and activate intracellular processes through G-proteins

91
Q

What affect do M2 receptors have on the body?

A

Activation on SA node
- decreases heart rate

Activation on AV node
- decrease conduction velocity
- induces AV node block (increase PR interval)

92
Q

What do M3 receptors do when stimulated in the respiratory system?

A

Stimulation in the respiratory system
- produces mucus
- induces smooth muscle contraction

93
Q

What do M3 receptors do when stimulated in the skin?

A
  • Only place where sympathetic system releases ACh
  • Stimulation causes sweating
94
Q

What do M3 receptors do when stimulated in the GI tract?

A

GI tract
- increase saliva production
- increase gut motility
- stimulates biliary secretion

95
Q

What do M3 receptors do when stimulated in the urinary system?

A
  • Contracts detrusor muscle
  • Relaxation of internal urethral sphincter
96
Q

What do M3 receptors do when stimulated in the eye?

A
  • Causes myosis (pupil constriction)
  • Increases drainage of aqueous humour
  • Secretion of tears
97
Q

What do muscarinic agonists do to the eyes?

A
  • increases drainage of aqueous humour
  • reduces ocular pressure
  • treats acute glaucoma (disease that damages optic nerve and reduces vision)
  • treat dry mouth
98
Q

Use of muscarinic antagonists

A
  • increase heart rate
  • treat bradyarrythmias
  • AV node block
  • reduce salivations
  • reduce bowel obstruction
99
Q

What are some functions of anti-muscarinics?

A
  • Bronchodilation
  • Dry mouth
  • urinary retention
  • slows gut contractibility -> treatment for irritable bowel syndrome
100
Q

Give some uses of ACh outside the ANS?

A
  • botulinum toxin (botox) prevents ACh release
  • cause flaccid paralysis and death
  • treat painful muscle spasms
101
Q

How is acetylcholine inhibited?

A

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

102
Q

Explain myasthenia gravis disease?

A
  • blockage of acetylcholine receptors
  • body makes antibodies that bind to these receptors
    –> repeated movements become difficult & tiring
103
Q

Name some Nicotinic antagonists and how they work

A
  • Curare, Pancuronium (relax skeletal muscles during surgery)
  • Compete with ACh for binding to the nicotinic receptor
104
Q

Where are noradrenaline and adrenaline released from?

A

Adrenaline = adrenal medulla
Noradrenaline = adrenal medulla + sympathetic nerve fibre ends

105
Q

What is the pathway from L.dopa to adrenaline?

A

It is the precursor to them

L-dopa –> dopamine –> noradrenaline –> adrenaline

106
Q

How many alpha and beta receptors are there?

A

Alpha 1 & 2
Beta 1, 2 & 3

107
Q

What is the function of alpha 1 receptors agonists?

A

Contracts smooth muscle

(pro-sympathetic)

  • vasoconstriction (in skin and abdominal beds)
    -> more blood can go to heart etc.
  • increase in peripheral resistance
  • increased blood pressure
  • increased closure of internal sphincter of the bladder

(greater affinity to bind to noradrenaline)

108
Q

When would Alpha 1 agonists be used?

A
  • Noradrenaline is given IV for shock
  • Also used to overcome anaesthetic agents
  • Adrenaline can be used to overcome anaphylaxis
  • Xylometazoline can be used as a nasal decongestion
109
Q

What is the function of alpha 2 agonists?

A

Mixed effects on smooth muscle

(anti-sympathetic)

  • exist in brain
  • increase concentration
  • reduces vascular tone
  • reduces blood pressure
  • inhibition of noradrenaline, ACh and insulin release

(same binding affinity to adrenaline and noradrenaline)

110
Q

Name an Alpha 2 agonist.

A
  • Clonidine can be used in ADHD to help concentration
111
Q

How are alpha 1 antagonists used?

A
  • lower blood pressure
  • block tamsulosin in benign prostatic hypertrophy
112
Q

How are alpha 2 antagonists used?

A
  • antidepressant
    Not used clinically.
113
Q

What is the use of beta 1 receptors?

A

Mainly in: heart, kidney, fat cells

  • tachycardia (positive chronotropic)
  • increase in stroke volume (positively ionotropic)
  • increase renin release
  • increase lipolysis and hyperglycaemia

(Same binding affinity to adrenaline and noradrenaline)

114
Q

What is the function of beta 1 blockers?

A
  • Reduce heart rate
  • Reduce stroke volume
  • Reduce myocardial oxygen demand and help remodelling in heart failure or post-myocardial infarction
    E.g. carvedilol, bisoprolol, atenolol…
  • bronchoconstriction (careful in asthma)
115
Q

What is the effect of beta 2 receptors on different tissues?

A

Vasodilation
Bronchi = bronchodilation
Bladder wall = inhibits micturition
Uterus = Inhibition of labour, relaxation of uterine muscles
Skeletal muscle = increase contraction speed
Pancreas = increase insulin and glucagon secretion

(greater binding affinity to adrenaline than noradrenaline)

116
Q

When is a beta 2 agonist useful?

A
  • Asthma/COPD (side effect hyperglycemia and tachyarrhythmia)
  • Can be used to delay labour
    Salbutamol is an example
117
Q

What are the characteristics of GABA receptors?

A
  • many different drugs binds to different places on the receptor
  • used in anxiety
  • in CNS
    e.g. Benzadiazepenes, ethanol, barbiturates
118
Q

What are the different histamine receptors?

A

H1 = allergies, IgE
H2 = Gastric acid secretion, GORD

119
Q

What are routes of administration of opioids?

A

Pharmacokinetics

  • oral -> bioavailability (first pass metabolism by the liver so only take in 50%)

Parenteral (given anywhere else in the body than the mouth)
- subcutaneous (Intravenous or Intramuscular)
- IV PCA (patient controlled analgesia - fall asleep before given too much)
- Epidural/CSF
- Transdermal patches

120
Q

How do opioids work?

A

Use the existing pain modulation system
- descending inhibition of pain (stops fight or flight)
- use G protein coupled receptors (act via second messengers)
- inhibit release of pain transmitters at spinal cord and midbrain (release endorphins instead)
- change pain perception in higher centre
- change emotional perception of pain

121
Q

Give some examples of opioid receptors

A

MOP (morphine - this is the one we actually use in drugs)
KOP (kappa receptors)
DOP (delta receptors)
NOP (nociceptin opioid-like receptors)

122
Q

What is the main opioid receptor, that all the drugs we currently use act on?

A

μ (Kappa) receptors
(MOP)

123
Q

Define tolerance

A

Down regulation of the receptors with prolonged use. Need higher doses to achieve the same effect.

124
Q

Define dependance: symptoms showing dependance.

A

Psychological = craving, euphoria
Physical effects

125
Q

Define the length of an opioid withdrawal?

A

Starts within 24 hours, lasts about 72 hours

126
Q

What are the side effects of opioids?

A
  • Respiratory depression
  • sedation
  • nausea + vomiting
  • constipation
  • itching
  • immune suppression
  • endocrine effects
127
Q

What are the risks of taking opioids?

A

ADDICTION
- slowly reduce dosage to reduce withdrawal effects

128
Q

Explain the metabolism of morphine?

A

Morphine –> morphine 6 glucuronide (more potent & usually excreted quickly)

  • in renal failure it will build up and cause respiratory depression
129
Q

What is respiratory depression?

A

Slow and ineffective breathing
- lungs fail to exchange carbon dioxide and oxygen

130
Q

What are opioids?

A

Any drug the binds to opioid receptors in the brain
- derived from the morphine poppy

131
Q

What are the 4 types of opioids?

A
  1. Naturally occurring - opium poppy e.g. morphine, codeine
  2. Simple chemical modifications e.g. diamorphine (heroin)
  3. Synthetic opioids e.g. pethidine
  4. Synthetic partial agonists (weaker) e.g. buprenorphine
132
Q

How do people respond to opioids differently due to pharmogenetics?

A
  • 10% of people have a gene that makes opioids ineffective to them
  • 5% of people have gene that overreacts to opioids
133
Q

What is the antidote for morphine?

A

Anatgonist = Naloxone

134
Q

What does opium contain?

A

Morphine and codeine

135
Q

Where do opioid receptors exist?

A

In the brain - where we want to target

Also in:
- digestive tract
- respiratory control reserve
- spine
(this is why side effects occur)

136
Q

Define drug development

A

The process of bringing a new pharmaceutical drug to the market.

137
Q

Where are drugs developed from?

A
  1. Plants
  2. Inorganic elements
  3. Organic molecules
  4. Sulphonamide Nucleus
  5. Bacteria/fungi/moulds
  6. Stereoisomers
  7. Immunotherapy - antibody based vaccines, monoclonal antibodies
  8. Recombinant proteins/steroids - insulin
  9. Animals - insulin, steroids
  10. Drugs targeting DNA
  11. Gene therapy
  12. High throughput assays/rational design
138
Q

What are the pharmacokinetic issues for immunotherapy?

A
  1. Immunoglobulin - not filtered by kidney
  2. FcRn receptor - systemic receptors which absorb IgG into cells protecting them from metabolism
  3. Mouse antibodies - shorter half life
139
Q

What receptors do steroids use to work?

A

Work through nuclear hormone receptors

140
Q

What is a gene therapy?

A

Replacing a mutated gene that causes disease with a healthy copy of the gene
- inactivate or ‘knocking out’ mutated gene
- introduce new gene to help fight disease

141
Q

Define rational drug design.

A

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

142
Q

Define drug re-purposing

A

Drug repurposing or repositioning is a technique whereby existing drugs are used to treat emerging and challenging diseases

143
Q

Define adverse drug reaction

A

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug

144
Q

Side effect vs Adverse drug reaction

A

Side effect
- unintended effect of a drug due to pharmacological properties but can be BENEFICIAL

ADR
- Always NEGATIVE

145
Q

What are the 3 types of effects of ADR’s?

A
  1. Toxic effect (beyond therapeutic range)
  2. Collateral effects (therapeutic range)
  3. Hyper-susceptibility effects (below therapeutic range)
146
Q

What are some reasons for toxic effects?

A
  • dose is too high
  • drug excretion reduced by impaired renal or hepatic function
  • interaction with other drugs
147
Q

What are the causes of collateral drug effects?

A
  • standard therapeutic doses
  • beta blockers causing bronchoconstriction
148
Q

An example of a hypersusceptibility reaction?

A

Anaphylaxis and penicillin allergy

149
Q

What are risk factors for ADRs?

A
  • Female
  • elderly
  • neonates
  • polypharmacy
  • genetic predisposition
  • hypersensitivity/allergies
  • hepatic/renal impairment
  • adherence problems
150
Q

What are drug risk factors for ADRs?

A
  • steep dose response curve
  • low therapeutic index
  • commonly cause ADR’s
151
Q

What are some causes for ADR’s?

A
  1. Pharmaceutical variation—eosinophilia-myalgia syndrome with L-tryptophan
  2. Receptor abnormality—malignant hyperthermia with general anaesthetics
  3. Abnormal biological system unmasked by drug—primaquine induced haemolysis in patients deficient in glucose 6-phosphate dehydrogenase
  4. Abnormalities in drug metabolism—isoniazid induced peripheral neuropathy in people deficient in the enzyme N-acetyl transferase (that is, those who are slow acetylators)
  5. Immunological—penicillin induced anaphylaxis
  6. Drug-drug interactions—increased incidence of hepatitis when isoniazid is prescribed with rifampicin
  7. Multifactorial—halothane hepatitis
152
Q

What are the 6 types of time dependant reactions?

A
  1. Rapid reactions
  2. First dose reactions
  3. Early reactions
  4. Immediate reactions
  5. Late reactions - e.g, seizures on withdrawal
  6. Delayed reactions - pregnancy
153
Q

What are the 5 types of adverse drug reactions?

A
  • Augmented
  • Bizarre
  • Chronic
  • Delayed
  • End of use

ABCDE

154
Q

What is a type A adverse drug reactions?

A

Augmented

  • predictable
  • dose dependent
  • common
  • increase of normal side effects you would expect
  • high morbidity, low mortality
    e.g. drug abuse, overdose
155
Q

Type B

A

Bizarre

  • Not predictable
  • Not dose dependent
  • life threatening
  • can be allergy or hypersensitivity
  • low morbidity, high mortality
    (anaphylaxis)
156
Q

Type C

A

Chronic / continuous
- uncommon
- related to cumulative dose
- time related

e.g. osteoporosis and steroids
colonic dysfunction due to laxatives

157
Q

Type D

A

Delayed
- uncommon
- usually dose related
- shows itself some time after the use of the drug
- malignancies after immunosupression
e.g. in pregnancy only have effect later - thalidomide

158
Q

Type E

A

End of treatment
- uncommon
- occur after abrupt drug withdrawal
e.g. opiate withdrawal syndrome

159
Q

Type F

A

Failure of therapy
- common
- dose related
- often caused by drug interaction
e.g. failure of oral contraceptive in presence of enzyme inducer

160
Q

Which are the most common drugs to have ADR’s?

A

Antibiotics
Anti-neoplastics
Cardiovascular drugs
Hypoglycaemics
NSAIDS
CNS drugs

161
Q

Which body systems are most commonly affected?

A

GI
Renal
Haemorrhagic
Metabolic
Endocrine
Dermatologic

162
Q

What is the MHRA?

A

Medicines and healthcare products regulatory agency

  • responsible for approving medicines and devices for use
163
Q

What is the yellow card scheme?

A
  • 1964
  • ADR reporting scheme
  • collects spontaneous reports and suspect ADR’s
  • voluntary scheme
164
Q

Why report ADRs?

A
  • Important for patient safety
  • To identify ADRs not identified in clinical trials
  • To identify new ADRs ASAP
  • To compare drugs in the same therapeutic class
  • To identify ADRs in ‘at risk’ groups
165
Q

What to report on a yellow card?

A

All suspected reactions for:
- herbal medicines
- black triangle drug (a medicine undergoing ‘additional monitoring’)

All serious suspected reactions for
- established drugs, vaccines, and contrast media
- drug interactions

166
Q

Define hypersensitivity.

A

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

immunologic (allergic) or non-immunological mechanisms

167
Q

What are risk factors for hypersensitivity?

A

Medicine factors:
- protein or polysaccharide based macro molecules

Host factors:
- females
- HIV
- prep drug reactions
- uncontrolled asthma

Genetic:
- certain HLA groups
- acetylator status

168
Q

How is adrenaline useful in anaphylaxis?

A
  1. vasoconstriction - increase BP, increase in peripheral vascular resistance
  2. Stimulation of beta 1-adrenoceptors
  3. Reduces oedema and bronchodilates (beta 2)
  4. attenuates further release of mediators from mast cells
169
Q

Which vitamin has a reverse effect on warfarin?

A

Vitamin K - reverses anticoagulation

170
Q

How does a salbutamol inhaler act on the body to help with asthma?

A

Relaxes bronchial smooth muscle cells

171
Q

What effect does a alpha 1 antagonist have on blood vessels?

A

Dilation of venous capacitance vessels

172
Q

What characteristics should an anaesthetic drug have in terms of its protein binding and lipid solubility?

A

Low protein binding
- so higher conc of the drug is free in the plasma enabling it to have an effect
- when bound to proteins the drug cannot work

High Lipid solubility
- can readily cross the blood brain barrier (contains phospholipids) and reach its site of action in the brain

173
Q

Why is morphine bad for someone with renal failure?

A

Morphine is metabolised in the liver by CYP2D6 enzymes to Morphine-6-glucuronide
- this is more potent than morphine and needs to be readily excreted from the kidney
- if a patient has renal failure, this cannot be excreted so a lower dose of morphine needs to be given

Emily Phase 2a (15 decks)

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