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Phase 2A > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the enteral routes of systemic drug administration?

A

Via the GI tract:
- oral (PO)
- rectal (PR)
- sublingual

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2
Q

What are the parenteral routes of systemic drug administration?

A

(Not via the GI tract)
- Intravenous (IV)
- Intramuscular (IM)
- Subcutaneous (SC)
- Inhalation (Inh)
- Transdermal

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3
Q

What the routes of local drug administration?

A
  • Topical
  • Intranasal
  • Eye drops
  • Inhalation (Inh)
  • Transdermal
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4
Q

Give 4 groups of drug targets.

A

Receptors, enzymes, transporters, ion channels

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5
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.

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6
Q

What are ligands?

A

Molecules that bind to receptors to cause an effect, they can be exogenous (drugs) or endogenous (hormones, neurotransmitter, etc.)

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7
Q

Name and give an example of 4 types of receptor.

A
  • Ligand-gated ion channels (nicotinic ACh receptor)
  • G protein coupled receptors (beta-adrenoreceptors)
  • Kinase-linked receptors (receptors for growth factors)
  • Cytosolic/nuclear receptors (steroid receptors)
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8
Q

How do ligand-gated ion channels work?

A

They are pore-forming membrane proteins that allow ions through the pore so that the cell undergoes a shift in electric charge distribution.

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9
Q

How do GPCRs work?

A

G protein coupled receptors are integral membrane proteins that are used by cells to convert extracellular signals into intracellular responses, including responses to hormones, neurotransmitters, as well as responses to vision, olfaction and taste signals

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10
Q

How do kinase-linked receptors work?

A

Transmembrane receptors are activated when the binding of an extracellular ligand causes kinases on the intracellular side to catalyse phosphorylation and cause a change in the cell.

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11
Q

How do nuclear receptors work?

A

They modify gene transcription when ligands bind.

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12
Q

Steps of therapeutic development

A
  1. Identify the receptor involved in a pathophysiological response.
  2. Develop drugs that act at that receptor.
  3. Quantify drug action at that receptor.
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13
Q

What is an agonist?

A

A compound that binds to a receptor and activates it.
- mimics endogenous ligand
- can be full or partial

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14
Q

What is an antagonist?

A

A compound that reduces the effect of an agonist.

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15
Q

Define affinity

A

How well a ligand binds to the receptor.

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16
Q

Define efficacy

A

How well a ligand activates the receptor.

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17
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.

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18
Q

Define tolerance

A

Reduction in agonist effect over time, usually after repeated or continuous use, or high concentrations of the drug.

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19
Q

Define specificity

A

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

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20
Q

Define selectivity

A

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

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21
Q

What is the difference between competitive vs non-competitive inhibition?

A

A competitive inhibitor structurally resembles the substrate for a given enzyme and competes to bind to the enzyme active site whereas non-competitive inhibitors bind at a different site to the substrate.

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22
Q

Define bioavailability

A

The proportion of a drug which enters the circulation and so is able to have an active effect in the body.

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23
Q

What is an irreversible enzyme inhibitor?

A

A molecule that reacts with an enzyme, causing it to change chemically so that it cannot catalyse its reaction.

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24
Q

What is a reversible enzyme inhibitor?

A

A molecule that binds non-convalently to an enzyme producing different types of inhibition depending on whether these inhibitors bind to the enzyme, the enzyme-substrate complex, or both.

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25
Q

What is the action of statins?

A

They inhibit the HMG-CoA reductase enzyme, blocking the rate limiting step in the cholesterol pathway so less cholesterol is produced.

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26
Q

What is EC50?

A

The concentration of drug that gives half the maximal response.

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27
Q

Would a drug with a lower EC50 have a lower or greater potency?

A

Great potency

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28
Q

What does Emax tell us about a drug?

A

Efficacy

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29
Q

Which is more efficacious, a full or partial agonist?

A

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

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30
Q

Would an antagonist shift a dose-response curve to the left or right?

A

The antagonist would shift the dose-response curve to the right because it reduces the potency of the drug.

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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

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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33
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.
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34
Q

Define pharmacodynamics

A

The effect the drug has on the human body.

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35
Q

Define pharmacokinetics

A

The action of the body on the drug (how it’s broken down).

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36
Q

What is first pass metabolism?

A

Reduced bioavailability of an orally administered drug due to metabolism of the drug by the gut and liver before it reaches the systemic circulation.

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37
Q

What is an example of a physicochemical drug reaction?

A

The adsorption of paracetamol by activated charcoal which is used to treat a paracetamol overdose.

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38
Q

What is the action of an inducer on drug metabolism?

A

Increase activity of cytochrome P450 and speed up metabolism of other drugs - may result in sub-therapeutic dose.

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39
Q

What are 3 examples of inducers?

A
  • Anti-epileptics (Phenytoin, carbamazepine)
  • Rifampicin (antibiotic)
  • Chronic alcohol intake
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40
Q

What is the action of an inhibitor on drug metabolism?

A

Decrease cytochrome P450 activity and reduce metabolism of other drugs - may result in toxicity.

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41
Q

What are 3 examples of inhibitors?

A
  • Ciprofloxacin, erythromyocin (antibiotics)
  • Isoniazid (antibiotic)
  • Amiodarone (for arrythmia)
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42
Q

What is first order elimination?

A

Catalysed by enzymes, rate of metabolism directly proportional to drug concentration.

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43
Q

What is zero order elimination?

A

Enzymes saturated by high drug doses, rate of metabolism is constant

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44
Q

What is synergy?

A

Interactions between drugs where the combined effect is greater than the sum of the individual effects. (1+1>2)

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45
Q

Define summation

A

Different drugs used together to have the same effect as a single drug would (1+1=1)

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46
Q

Define potentiation

A

Enhancement of one drug by another so that the combined effect is greater than the sum of each one alone. (1+1=1+1.5)

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47
Q

What are the pharmacokinetic actions? (ADME)

A

Absorption
Distribution
Metabolism
Excretion

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48
Q

What factors affect drug absorption?

A
  1. Motility
  2. Acidity
  3. (Physicochemical)
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49
Q

What are pro-drugs and what is an example of one?

A

Drugs that need to be activated enzymatically e.g. ACE inhibitors, enalapril.

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50
Q

How do ACE inhibitors work?

A

ACE inhibitors prevent angiotensin I binding to ACE so it can’t be converted to angiotensin II. (Prevents narrowing of blood vessels and so reduces BP)

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51
Q

Define adrenergic receptors

A

Receptors activated by catecholamines (adrenaline and noradrenaline) that help to trigger the fight or flight response.

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52
Q

Define cholinergic receptors

A

Receptors on the cell surface membrane that bind acetylcholine.

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53
Q

What kind of receptors does acetylcholine act on at the preganglionic nerve fibres?

A

Nicotinic receptors (both para and sympathetic ns)

54
Q

What kind of receptors does acetylcholine act on at the postganglionic nerve fibres?

A

muscarinic receptors (only parasympathetic)

55
Q

What is the mechanism of acetylcholine release and metabolism at the neurosynaptic junction?

A
  • Action potential arrives at the presynaptic terminal
  • ACh is release into the synapse and binds to postsynaptic receptor
  • ACh is broken down by AChesterase into acetate and choline
  • Choline is reuptaken by the presynaptic terminal and bind with acetyl CoA to form new acetylcholine
56
Q

Which branch of the autonomic nervous system does acetylcholine act upon?

A

parasympathetic nervous system

57
Q

What are some examples of acetylcholinesterase inhibitors?

A

Donepezil, rivastigmine and galantamine

58
Q

What are acetylcholinesterase inhibitors used to treat? What is their mechanism of action?

A

They prevent acetylcholinesterase from breaking down acetylcholine resulting in a higher concentration of acetylcholine in the brain whcih leads to better communication between nerve cells. They are used to treat Alzheimer’s and dementia

59
Q

What are the common side effects of acetylcholinesterase inhibitors?

A

nausea, diarrhoea, dizziness, bradycardia, insomnia, headaches, muscle cramps

60
Q

What is the mechanism of direct-acting cholinergic agonists? Give 3 examples and their actions.

A

Mimic ACh and bind to ACh receptors.
- Carbachol (constrict pupil)
- Bethanechol (increase smooth muscle tone in GI and GU tracts)
- Pilocarpine (stimulate saliva secretion)

61
Q

What is the mechanism of indirect-acting cholinergic agonists? Give 3 examples and their actions

A

Reversibly inhibit enzyme AChE, increasing the concentration of ACh available at the synapse.
- Neostigmine, Pyridostigmine (for myasthenia gravis, reverse anaesthesia)
- Donepezil (boost cholinergic activity in Alzheimer’s)

62
Q

What are the common side effects of cholinergic agonists?

A

Diarrhoea
Urination
Miosis/Muscle shrinkage
Bronchorrea (excessive watery mucus production)
Bradycardia
Emesis (vomiting)
Lacrimation
Salivation/Sweating

63
Q

What is the action of nicotinic antagonists? Give an example

A

compete with ACh for binding to the nicotinic receptor.
Curare and pancuronium are nicotinic antagonists used to relax skeletal muscles during surgery.

64
Q

What is the action of muscarinic antagonists? Give an example

A

Compete with ACh for binding to the muscarinic receptor.
Atropine is a muscarinic antagonist used to treat bradycardia, diarrhoea and bladder spasms.

65
Q

What kind of receptors does noradrenaline act on at the postganglionic fibres?

A

Alpha and beta receptors (sympathetic ns)

66
Q

What does the M2 muscarinic receptor affect?

A

The heart

67
Q

What does the M3 muscarinic receptor affect?

A

All organs with parasympathetic innervation

68
Q

What is the effect of M2 activation on the SA node?

A

Decreases heart rate

69
Q

What is the effect of M2 activation on the AV node?

A

Decreases conduction velocity, induces AV node block (increases PR interval)

70
Q

What is the effect of M3 receptor stimulation on the respiratory system?

A
  • produces mucus in the airways and nasopharynx
  • induces smooth muscle contraction (bronchoconstriction)
71
Q

What is the effect of M3 receptor stimulation on the GI tract?

A
  • increases saliva production
  • increases gut motility
  • stimulates biliary secretion
72
Q

What is the effect of M3 receptor stimulation on the skin?

A
  • only place where sympathetic system releases ACh
  • causes sweating
73
Q

What is the effect of M3 receptor stimulation on the urinary system?

A
  • contracts detrusor muscle
  • relaxation of internal urethral sphincter
74
Q

What is the effect of M3 receptor stimulation on the eyes?

A
  • causes myosis (pupil constriction)
  • increases drainage of aqueous humour
  • secretion of tears
75
Q

Examples of a muscarinic agonist and its effects

A

pilocarpine eye drops - increase drainage of aqueous humour, reduces ocular pressure, also used to treat dry mouth by stimulating saliva

76
Q

What is an example of a muscarinic antagonist?

A

hyoscine - used in palliative care to treat respiratory secretions and symptoms of bowel obstruction (anti-parasympathetic effect –> reduces mucus production, increases bowel motility)

77
Q

What are 4 examples of inhaled muscarinics?

A

Tiotropium, glycopyrronium, umeclidinium, aclidinium

78
Q

How does botulinum toxin affect the nervous system?

A

Prevents release of ACh, which causes paralysis and death from respiratory muscle involvement

79
Q

What happens in myaesthenia gravis?

A

Blockage of ACh receptors which results in skeletal muscle weakness

80
Q

What are the two main catecholamines and where are they released from ?

A

Noradrenaline - released from sympathetic nerve fibre ends
Adrenaline - released from the adrenal glands
(dopamine is the precursor of both)

81
Q

What is the main agonist, mechanism and consequence of alpha 1 receptor stimulation?

A

Main agonist = noradrenaline
Mechanism = increases intracellular Ca2+, Gq protein signalling
Consequence = vasoconstriction, increased peripheral resistance, increased blood pressure, increased closure of internal bladder sphincter, mydriasis (pupil dilation)

82
Q

What is the main agonist, mechanism and consequence of alpha 2 receptor stimulation?

A

Main agonist = Noradrenaline/Adrenaline
Mechanism = Gi signalling, inhibition of cAMP generation
Consequence = mixed effects on smooth muscle, inhibits release of noradrenaline, acetylcholine and insulin

83
Q

What is the main agonist, mechanism and consequence of beta 1 receptor stimulation?

A

Main agonist = noradrenaline/adrenaline
Mechanism = Gs signalling, raises cAMP
Consequence = tachycardia, increased lipolysis, increased myocardial contractility, increased renin release

84
Q

What is the main agonist, mechanism and consequence of beta 2 receptor stimulation?

A

Main agonist = adrenaline
Mechanism = Gs signalling, raises cAMP
Consequence = relaxes smooth muscle (premature labour, asthma)

85
Q

What is the main agonist, mechanism and consequence of beta 3 receptor stimulation?

A

Main agonist = noradrenaline
Mechanism = Gs signalling, raises cAMP
Consequence = enhances lipolysis, relaxes bladder detrusor

86
Q

what are side effects of anti-cholinergic drugs?

A
  • worsen memory and can cause confusion
  • constipation
  • drying of the mouth
  • blurred vision, worsening of glaucoma
87
Q

What is the effect of alpha blockers?

A
  • block alpha 1 receptors to lower blood pressure (doxazosin)
88
Q

What is the effect of beta blockers?

A
  • slow heart rate, reduce tremor
  • lower blood pressure
89
Q

What is a cholinergic crisis and what effects does this cause?

A

Overabundance of acetylcholine.
Causes:
Salivation
Lacrimation
Urination
Defecation
Gastric upset
Emesis (vomiting)

90
Q

What are 2 naturally occurring opioids?

A

Morphine and codeine (weak)

91
Q

What is the bioavailability of morphine taken orally?

A

50%

92
Q

What enzyme is needed to metabolise codeine?

A

Codeine is a pro drug and needs to be metabolised by CYP2D6.

93
Q

What is morphine metabolised to?

A

Morphine 6 glucuronide

94
Q

10mg of morphine is taken orally. What is the equivalent dose if given parenterally?

A

5mg

95
Q

Give 5 side effects of opioid use.

A
  1. Respiratory depression
  2. Sedation
  3. Nausea
  4. Vomiting
  5. Constipation
96
Q

Describe the dose-response curve for morphine

A

As dose increases, response increases. This association is initially rapid and then plateaus

97
Q

Define opioid dependence

A

Psychological state of craving euphoria.

98
Q

What is the treatment for opioid induced respiratory depression?

A

Naloxone which is a competitive opioid inhibitor

99
Q

How do opioids cause respiratory depression?

A

They slow nervous activity in the brain which also slows down breathing and heart rate.

100
Q

Define potency

A

the amount of a drug needed to produce a given effect.

101
Q

How do opioids work?

A

They inhibit the release of pain transmitters at spinal cord and midbrain as well as modulating pain perception in higher centres.

102
Q

What is an adverse drug reaction?

A

An unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use.

103
Q

What is a side effect?

A

An unintended effect of a drug related to its pharmacological properties and can include unexpected benefits of treatment.

104
Q

What are the types of effects of ADRs?

A
  • Toxic effects (above therapeutic range)
  • Collateral effects (therapeutic range)
  • Hyper-susceptibility effects (below therapeutic range)
105
Q

What are 5 patient risk factors for ADRs?

A
  • gender (females more than men)
  • elderly
  • neonates
  • polypharmacy
  • hypersensitivity/allergies
106
Q

What are 3 drug-related risk factors for ADRs?

A
  • steep dose-response curve
  • low therapeutic index
  • commonly causes ADRs
107
Q

Causes for ADRs

A
  • pharmaceutical variation
  • receptor abnormality
  • abnormal biological system unmasked by drug
  • abnormalities in drug metabolism
  • immunological
  • drug-drug interactions
  • multifactorial
108
Q

What are the types of ADRs (Rawlins-Thompson)?

A

A - augmented = predictable, dose-dependent, common (80% of ADRs)
B - bizarre = not predictable or dose dependent, can be life-threatening (10-15% of ADRs)
C - chronic = osteoporosis and steroids
D - delayed = malignancies after immunosuppression
E - end of treatment = occur after abrupt drug withdrawal
F - failure of therapy = failure of OCP (pill) in presence of enzyme inducer

109
Q

Which drugs. most commonly have adverse drug reactions?

A
  • Antibiotics
  • Anti-neoplastics
  • Cardiovascular drugs
  • Hypoglycaemics
  • NSAIDS
  • CNS drugs
110
Q

What are the most common ADR presentations?

A

Confusion
Nausea
Balance problems
Diarrhea
Constipation
Hypotension

111
Q

What is the yellow card scheme?

A

Reporting procedure for suspected ADRs and acts as an early warning system.

112
Q

What are 2 anti-platelet drugs and their actions?

A
  1. Aspirin -> COX1 inhibition - reduces thromboxane A2 which activates platelets resulting in reduced platelet activation
  2. Clopidogrel -> inhibits P2Y12 which is a receptor on platelets and its inhibition prevents platelet aggregation
113
Q

What are 4 anticoagulants and their actions?

A
  1. Heparin -> activates antithrombin 3 which inhibits factor X (a clotting protein) reduces clotting
  2. Warfarin -> antivitamin K, works by inhibiting vit K epoxide reductase
  3. DOACs (Direct oral anticoagulants) -> anti factor Xa (e.g. apixaban, rivaroxaban)
  4. Thrombolytics -> artificial form of tPa (tissue plasminogen activator) which activates plasmin to degrade fibrin (e.g. alteplase)
114
Q

What is the mechanism of action of NSAIDs?

A

Non-steroidal anti-inflammatory drugs inhibit COX 1 + 2 which prevents the production of prostaglandins.
COX-1 inhibition = decreased gastric mucosal protection + increased stomach pH
COX-2 inhibition = anti-inflammatory

115
Q

What are 3 examples of NSAIDs?

A
  • Ibuprofen (mild to moderate pain relief)
  • Naproxen (for rheumatoid arthritis)
  • Diclofenac (for RA and osteoarthritis)
116
Q

What is the mechanism of action of PPIs?

A

Proton pump inhibitors work by irreversibly binding to and inhibiting the H+-K+ ATPase pumps in the parietal cells of the stomach lining which inhibits the secretion of gastric acid.

117
Q

What are 3 examples of PPIs?

A
  • Lansoprazole
  • Omeprazole
  • Esomeprazole

Used to treat acid reflux and to prevent and treat duodenal and gastric ulcers.

118
Q

What is the mechanism of action of loop diuretics?

A

Reduce NaCl reabsorption in the thick ascending limb of the LoH by inhibiting the Na+-K+-2Cl carrier in the luminal membrane. This results in reduced water reabsorption and increased production of dilute urine.

119
Q

What are 3 loop diuretics?

A
  • Furosemide
  • Bumetanide
  • Torsemide
    Used to treat heart failure, hypertension and oedema.
120
Q

What is the mechanism of action of thiazide diuretics?

A

Inhibit the apical sodium/chloride transporters in epithelial cells of the distal convoluted tubules to reduce ECF and cardiac output.

121
Q

What are 3 examples of thiazide diuretics?

A
  • Hydrochlorothiazide
  • Chlorthalidone
  • Indapamide
    Used to treat hypertension.
122
Q

What is the mechanism of action of spironolactone?

A

It is a pharmacological antagonist of aldosterone which acts through competitive binding of receptors at the aldosterone-dependent Na+-K+ exchange site in the distal convoluted renal tubule and collecting duct. This causes increased excretion of sodium into the tubule and therefore increased water excretion resulting in increased production of urine.

123
Q

What is the common name for spironolactone?

A

Aldactone (used to treat heart failure and hypertension)

124
Q

What are 3 common side effects of NSAIDs?

A
  1. Stomach ulcers
  2. Indigestion
  3. Heart burn
125
Q

What are the common drug side effects of ACE-inhibitors?

A
  • Dry cough (caused by bradykinin accumulation in the lungs)
  • risk of AKI due to dilation of the afferent arteriole (glomerulus) which leads to decreased GFR
126
Q

What is a common side effect of PPIs?

A

Increased fracture risk with prolonged use due to decreased intestinal absorption of calcium

127
Q

What are 3 common side effects of opioids?

A
  1. Respiratory distress (antidote = Naloxone)
  2. Drug dependence
  3. Nausea and vomiting
128
Q

What is a common side effect of loop diuretics and thiazides?

A

Hypokalaemia due to increased elimination of potassium in the urine

129
Q

What is a common side effect of spironolactone?

A

Hyperkalaemia due to increased sodium excretion and potassium uptake.

130
Q

What is the volume of distribution?

A

Theoretical volume that the total amount of administered drug would have to occupy to provide the same concentration as it currently is in blood plasma.

Phase 2A (18 decks)

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