ICS Pharmacology Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Give an example of a proton pump inhibitor.

A

Omeprazole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give an example of a statin.

A

Simvastatin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give an example of an ACE inhibitor.

A

Enalapril.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give an example of a COX inhibitor.

A

Aspirin and paracetamol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Give an example of a β2 adrenoceptor agonist.

A

Salbutamol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give an example of a β1 adrenoceptor blocker.

A

Atenolol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give an example of a Ca2+ channel blocker.

A

Amlodipine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give an example of a broad spectrum antibiotic.

A

Amoxicillin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give an example of an opiate analgesic.

A

Tramadol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do most drugs target?

A

Proteins!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name 4 receptors that drugs target.

A
  1. Ligand gated ion channels.
  2. GPCR.
  3. Kinase linked.
  4. Cytosolic/nuclear.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give an example of a ligand gated ion channel.

A

Nicotinic Ach receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give an example of a GPCR.

A

Muscarinic and β2 adrenoceptor.

GPCR’s usually interact with adenylate cyclase or phospholipase C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give an example of a kinase linked receptor.

A

Receptors for growth factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give an example of a cytosolic/nuclear receptor.

A

Steroid receptors; steroids affect transcription.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are agonists?

A

Agonists bind to a receptor and to activate it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are antagonists?

A

Antagonists decrease the effect of an agonist. They show no response at a receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the shape of a log dose-response curve.

A

Sigmoidal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does EC50 tell us about a drug?

A

Its potency!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is EC50?

A

The concentration of drug that gives half the maximal response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Greater potency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does Emax tell us about a drug?

A

Efficacy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
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 RHS. The drug therefore becomes less potent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Drug action: define affinity.

A

How well a ligand binds to a receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Drug action: define efficacy.

A

How well a ligand activates a receptor; how well it induces a conformational change.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

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

A

Less signal amplification gives a reduced drug response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe allosteric modulation.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is inverse agonism?

A

Where an agonist has a negative effect at a receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Does an antagonist show efficacy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Can aspirin be described as a selective drug?

A

No. Aspirin is non-selective, it acts on COX1 and COX2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the function of COX1 and COX2?

A

They cyclise and oxygenate arachidonic acid and produce prostaglandin H2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What does prostaglandin H2 form when it interacts with synthases?

A

Prostanoids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Define pro-drugs and give an example of one.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do ACE inhibitors work?

A

Angiotensinogen is converted to angiotensin 1 via renin. Angiotensin 1 is then converted to angiotensin 2 via ACE. ACE inhibitors prevents angiotensin 1 binding and so you don’t get angiotensin 2 formation.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Give an example of a β lactam antibiotic.

A

Penicillin and amoxicillin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How do β lactam antibiotics work?

A

The inhibit transpeptidase and so prevent bacterial cell wall synthesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How do diuretics work?

A

They inhibit ‘synporters’ in the loop of henle. This leads to increased H2O excretion and decreased salt reabsorption and so BP decreases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Give an example of loop of henle diuretics.

A
  • Furosemide, act on the ascending loop.

- Thiazides, act on the distal tubule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How can drugs be developed?

A
  1. Serendipity, by chance. e.g. penicillin.

2. Rational drug design. e.g. propranolol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe how rational drug design works.

A

Rational drug design is focused on developing an antagonist from an agonist. It looks at solubility, electrostatic charge and bulk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How do you determine whether insulin is long or short acting?

A

Small changes in amino acid sequence will determine whether insulin is long or short lasting - RECOMBINANT PROTEIN!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Name 3 things that the chemical properties of a drug can influence?

A
  1. Administration.
  2. Distribution.
  3. Elimination.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

As the difference in concentration falls what happens to the rate of reaction?

A

The rate of reaction will slow down.

Rate is proportional to the concentration of drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the association between diffusion and concentration gradient?

A

Diffusion is proportional to concentration gradient; this is a first order process and represents an exponential function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How many litres of water are there in the following body compartments:

a) Plasma.
b) Interstitial space.
c) Intracellular space.

A

a) 3L.
b) 11L.
c) 28L.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the 5 ways by which fluid can move between compartments?

A
  1. Simple diffusion.
  2. Facilitated diffusion.
  3. Active transport.
  4. Movement through extra-cellular spaces.
  5. Non-ionic diffusion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What can influence the degree of ionisation of weak acids and weak bases?

A

pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What equation can be used to determine the degree of ionisation at a specific pH?

A

Henderson Hasselbach.

pH = log[A-]/[HA] + pKa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What can enhance non ionic diffusion?

A

Non ionic diffusion can be enhanced if adjacent compartments have pH difference.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

In terms of ionisation, what happens to Aspirin in the stomach?

A

Aspirin is a weak acid and so becomes less ionised in the stomach due to the low gastric pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the advantage of aspirin becoming less ionised in the stomach?

A

This allows rapid non-ionic diffusion across the gut membrane into the plasma. Once in the plasma aspirin becomes more ionised again.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the effect of an increase in pH on a weak acid?

A

The weak acid will become more ionised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the effect of an increase in pH on a weak base?

A

The weak base will become less ionised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the effect of a decrease in pH on a weak acid?

A

The weak acid will become less ionised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the effect of a decrease in pH on a weak base?

A

The weak base will become more ionised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Define bioavailability.

A

The amount of drug taken up as a proportion of the amount administered. It is a reflection of uptake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What route of drug administration has a bioavailability of 1?

A

IV infusion, all the drug administered will go into the plasma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Explain what would happen to the bioavailability of aspirin if gastric pH increased.

A

The bioavailability would decrease. Aspirin would be more ionised and so wouldn’t diffuse across the gut into the plasma as rapidly this would mean aspirin uptake would decrease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Give 2 factors that drug distribution in the plasma depends upon.

A
  1. Chemical properties.

2. Molecular size.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Write an equation for the volume of distribution (Vd).

A

Vd = amount of drug administered/concentration of drug in plasma.

66
Q

If a drug had a high Vd what would that tell us about the drug?

A

This would indicate that the drug was highly lipid soluble and that most of the drug had moved into the intracellular space, less was in the plasma.

67
Q

What is the relationship between plasma concentration and Vd?

A

Plasma concentration is inversely proportional to Vd.

68
Q

Give 3 factors that can increase gastric pH.

A
  1. Ingesting alkaline foods.
  2. Antacids.
  3. Omeprazole (PPI).
69
Q

Give the two definitions for clearance.

A
  1. The volume of plasma from which a drug is completely removed per unit time.
  2. The rate at which plasma drug is eliminated per unit plasma concentration.
70
Q

Write an equation for renal clearance.

A

Renal clearance = Rate of appearance in urine / plasma concentration.

71
Q

What are the two ways by which drugs can be eliminated in the kidneys?

A
  1. Glomerular filtration.

2. Active secretion.

72
Q

What are the possible dangers of kidney damage with regards to renal clearance?

A

Kidney damage results in decreased renal clearance and so there is danger of accumulation, over dosage and toxicity.

73
Q

What compound do many lipid soluble drugs combine with to increase their hydrophilicity?

A

Glucuronic acid.

74
Q

Define hepatic extraction ratio (HER).

A

The proportion of a drug removed by one passage through the liver.

75
Q

What is the limiting factor when a drug has a high HER?

A

Hepatic blood flow, perfusion limited.

76
Q

What is the limiting factor when a drug has a low HER?

A

Diffusion limited. A low HER is slow and not efficient.

77
Q

What happens to high and low HER drugs when enzyme induction is increased?

A

The clearance of low HER drugs increases. There is minimal effect on high HER drugs.

78
Q

Where do phase 1 hepatic metabolism reactions occur?

A

In the smooth endoplasmic reticulum.

79
Q

What enzyme usually catalyses phase 1 reactions?

A

CYP450.

80
Q

What is a phase 2 hepatic metabolism reaction?

A

Phase 2 reactions involve conjugation and glucuronidation etc.
They usually inactivate products and increase hydrophilicity for renal excretion.

81
Q

Give 3 advantages of IV infusion.

A
  1. Steady state plasma levels are maintained.
  2. Highly accurate drug delivery.
  3. IV infusion can be used for drugs that would be ineffective when administered via an alternative route.
82
Q

Give 3 disadvantages of IV infusion.

A
  1. Expensive.
  2. Needs constant checking.
  3. Calculation error likely.
83
Q

Give an advantage of a drug having a low Vd.

A

It is easy to reach steady state and plasma concentration is ‘responsive’ to dose rate.

84
Q

Give 4 properties of the ‘ideal drug’.

A
  1. Small Vd.
  2. Drug broken down effectively by enzymes.
  3. Predictable dose:response relationship.
  4. Low risk of toxicity.
85
Q

What are the advantages of pulsatile secretion as opposed to steady state?

A
  1. Enhanced responsiveness.

2. More information can be conveyed.

86
Q

What is the principal neurotransmitter in the body?

A

Acetylcholine.

87
Q

What receptor does Ach interact with in the somatic nervous system?

A

Post-synaptic nicotinic receptors at the neuromuscular junction.

88
Q

What type of receptor are nicotinic receptors?

A

Ligand gated ion channels.

89
Q

Briefly describe how Ach is synthesised.

A

Acetyl CoA, choline and choline acetyl trasnferase combine to form acetylcholine. Ach is taken up into a vesicle in the presynpatic cleft and will be released following Ca2+ influx.

90
Q

What enzyme is responsible for acetylcholine breakdown in the synaptic cleft?

A

Acetylcholinesterase.

91
Q

Describe the action of botulinum toxin at the NMJ,

A

Botulinum toxin inhibits Ach release at the NMJ. Protease degrade vesicle proteins.

92
Q

Describe the action of competitive antagonists at the NMJ.

A

They block Ach receptors. Competitive antagonists are muscle relaxants, adjuncts to general anaesthesia.

93
Q

Describe the action of depolarising agonists (blockers) at the NMJ.

A

Depolarising agonists cause receptor desensitisation.

94
Q

Describe the action of anticholinesterases at the NMJ.

A

There is increased Ach in the synaptic cleft. Ach can then compete with depolarising blockers.

95
Q

What type of receptor are muscarinic receptors?

A

GPCR.

96
Q

Give examples of adverse muscarinic agonist effects.

A
  1. Diarrhoea.
  2. Urination.
  3. Miosis.
  4. Brachycardia.
  5. Emesis (vomiting).
  6. Lacrimation.
  7. Salivation.
97
Q

Give 2 examples of Ach action in the CNS.

A
  1. Motion sickness; Ach stimulates the vomiting centre in the brain.
  2. Ach leads to increase dopamine re-uptake and so can worsen the symptoms of Parkinson’s.
98
Q

Briefly describe catecholamine synthesis.

A

Tyrosine -> L-DOPA -> Dopamine -> Noradrenaline -> Adrenaline.

99
Q

Where does the conversion from Dopamine to Noradrenaline happen?

A

In a vesicle in the pre-synpatic neurone.

100
Q

Which enzymes inactivate catecholamines?

A

MAO and COMPT.

101
Q

Which protein does α1 interact with to activate phospholipase C?

A

Gq.

102
Q

What is the primary function of α1?

A

α1 leads to vasoconstriction.

103
Q

Which protein does α2 interact with in order to inhibit adenylate cyclase synthesis?

A

Gi.

104
Q

What is the primary function of α2?

A

α2 is responsible for pre-synaptic inhibition; it inhibits NAd release.

105
Q

What protein does β1,2,3 interact with in order to activate adenylate cyclase?

A

Gs.

106
Q

What is the role of adenylate cyclase?

A

It converts ATP to cyclic AMP, this then leads to PKA synthesis.

107
Q

What are the primary functions of β1?

A
  1. Increased cardiac effects e.g. force, rate and conduction.
  2. Increased renin secretion.
108
Q

What are the primary functions of β2?

A
  1. Bronchodilation.

2. Vasodilation.

109
Q

What are the primary functions of β3?

A
  1. Increase lipolysis.

2. Bladder relaxation.

110
Q

What would an α1 adrenergic antagonist do?

A
  1. Vasodilation.

2. Relaxation of bladder neck = reduced resistance to bladder outflow.

111
Q

What disease could an α1 adrenergic antagonist be used in the treatment of?

A

Benign prostatic hyperplasia.

112
Q

What would a β1 adrenergic antagonist do?

A
  1. Reduce CO.

2. Reduce renin secretion.

113
Q

What diseases could an β1 adrenergic antagonist be used in the treatment of?

A

Hypertension, angina and arrhythmia.

114
Q

Define pain.

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.

115
Q

Give 3 advantages of pain.

A
  1. Gives a warning for tissue damage.
  2. Immobilisation for healing.
  3. Memory establishment.
116
Q

Define acute pain.

A

Pain caused by nociceptor activation. It is of short duration,

117
Q

Define chronic pain.

A

Pain that is on-going or persistent, it lasts for >3-6 months.

118
Q

Define neuropathic pain.

A

Pain caused by a primary lesion or dysfunction of the nervous system.

119
Q

Define nociceptive pain.

A

Pain caused by actual or potential damage to non neural tissue, it is due to nociceptor activation.

120
Q

Are A delta fibres myelinated or unmyelinated?

A

Myelinated.

121
Q

Are C fibres myelinated or unmyelinated?

A

Unmyelinated.

122
Q

Describe the type of pain that A delta fibres conveys.

A

Quick, sharp, localised.

123
Q

Describe the type of pain that C fibres conveys.

A

Slow, dull, spread out.

124
Q

Describe pain wind up.

A

A perceived increase in pain intensity over time when a stimulus is repeatedly delivered. It is caused by C fibre stimulation.

125
Q

Describe the gate control theory.

A

Non-noxious stimuli trigger larger A beta fibres, these override smaller pain fibres and ‘close the gate’ to pain transmissions to the CNS.

126
Q

What is pain treatment focused on?

A
  1. Reducing excitatory neurotransmitters and nerve excitation.
  2. Enhancing inhibitory neurones.
127
Q

What are released in the presence of pain?

A

Endorphines.

128
Q

What is an adverse drug reaction?

A

A noxious and unintended response to a drug.

129
Q

Rawlins-Thompson system: Describe a type A adverse drug reaction.

A
  • Augmented.
  • Very common.
  • Predictable from physiological effects of the drug.
  • Often dose related.
130
Q

Rawlins-Thompson system: Describe a type B adverse drug reaction.

A
  • Bizarre.
  • Unpredictable.
  • Immunological mechanisms and hypersensitivity.
  • Often there is a history of allergy.
131
Q

Rawlins-Thompson system: Describe a type C adverse drug reaction.

A
  • Chronic.

- Occurs after long term therapy.

132
Q

Rawlins-Thompson system: Describe a type D adverse drug reaction.

A
  • Delayed.

- Occurs many years after treatment.

133
Q

Rawlins-Thompson system: Describe a type E adverse drug reaction.

A
  • End of use.

- Withdrawal reaction after long term use; complications of stopping medication.

134
Q

What is the treatment for a type A adverse drug reaction?

A

Reduce the dose.

135
Q

What is the treatment for a type B adverse drug reaction?

A

Withdraw drug immediately!

136
Q

Why are drug interactions such a big problem today?

A
  1. Ageing population.
  2. Polypharmacy.
  3. Increased use of over the counter drugs.
137
Q

Give 5 patient risk factors for drug interactions.

A
  1. Old age.
  2. Polypharmacy.
  3. Renal disease.
  4. Hepatic disease.
  5. Genetics.
138
Q

Give 3 drug related risk factors for drug interactions.

A
  1. Narrow therapeutic index.
  2. Steep dose/response curve.
  3. Saturable metabolism.
139
Q

Name 3 types of drug interaction.

A
  1. Synergy; interaction of 2 compounds leads to a greater combined effect.
  2. Antagonism; one drug blocks another.
  3. Other.
140
Q

How might drug interactions affect drug metabolism?

A

If a drug inhibits or induces CYP450 it might affect the metabolism of another drug.

141
Q

How does avocado affect CYP450? And what drug might this impact on?

A

Avocado is a CYP450 inductor. Warfarin is likely to be affected and the risk of blood clots will be increased.

142
Q

How does grapefruit juice affect CYP450? And what drugs might this impact on?

A

Grapefruit juice is a CYP450 inhibitor, it affects CYP3A4 specifically and increases the bioavailability of some drugs e.g. Ca2+ channel blockers and immunosuppressants.

143
Q

Are weak acids cleared quicker if urine is more acidic or more alkali?

A

Weak acids are cleared quicker if urine is more alkali.

144
Q

Are weak bases cleared quicker if urine is more acidic or more alkali?

A

Weak bases are cleared quicker if urine is more acidic.

145
Q

What drug acts as an antagonist at the μ receptor?

A

Naloxone.

146
Q

What enzyme is needed to metabolise codeine?

A

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

147
Q

What is the bioavailability of morphine taken orally?

A

50%.

148
Q

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

A

5mg.

149
Q

What is morphine metabolised to?

A

Morphine 6 glucuronide.

150
Q

Where might μ receptors be found?

A

In the epidural space and CSF.

151
Q

Give 5 side effects of opioid use.

A
  1. Respiratory depression.
  2. Sedation.
  3. Nausea.
  4. Vomiting.
  5. Constipation.
152
Q

Describe the dose-response curve for morphine.

A

As dose increases response increases. This association is initially rapidly and then the graph plateaus. It is not sigmoidal!

153
Q

Name a protein that can inhibit apoptosis.

A

BCL-2; it inhibits pro-apoptotic proteins e.g. caspase and therefore inhibits apoptosis.

154
Q

What disease might develop in someone with a non-functional BCL-2 protein?

A

Cancer.

155
Q

Where are mast cells found?

A

They are only found in tissues, not in the blood!

156
Q

What is dobutamine used in the treatment of and at what receptor is it an agonist?

A

Dobutamine is a beta 1 agonist. It is used in the treatment of heart failure.

157
Q

Define physiological antagonism.

A

A substance that produces effects that counteract the effects of another substance.

158
Q

What are the 3 actions of NSAIDS?

A
  1. Anti-inflammatory.
  2. Analgesic.
  3. Anti-pyrexic.
    (AAA).
159
Q

Name a local anaesthetic.

A

Lidocaine.

160
Q

How do local anaesthetics work?

A

They inhibit pain by stopping impulse conduction in sensory nerves.

161
Q

What drug inhibits ACh release at the NMJ?

A

Botulinum toxin.

It is used to treat urinary incontinence and also cosmetically as a muscle relaxant.