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Phase 2A revision > PHARMACOLOGY > Flashcards

PHARMACOLOGY Flashcards

1
Q

what are pharmacodynamics?

A

what the drug does to the body

i.e. what does the drug do once it is in the body?

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2
Q

what factors affect the pharmacodynamics?

A

affinity
efficacy
potency

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3
Q

what are pharmacokinetics?

A

what the body does to the drug

i.e. what does the body do once the drug is in it?

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4
Q

what factors affect pharmacokinetics?

A
  • absorption - gut vs parenteral
  • distribution
  • metabolism - first pass metabolism
  • excretion - usually renal
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5
Q

what is affinity?

A

it is how well a drug will bind to a receptor
high affinity = binds well
low affinity = binds less well

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6
Q

what is efficacy?

A

it is the degree to how well a drug works on a specific receptor
it can be seen as the maximum effect a drug can have in the body

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7
Q

what is potency?

A

it is the amount of the drug needed to achieve a response

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8
Q

what is an agonist?

A

a molecule that attaches to a receptor, causing a reaction in the cell
- it stimulates the receptor

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9
Q

what is a partial agonist?

A

a molecule that attaches to a receptor, causing the same reaction as a full agonist, to a lesser extent

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10
Q

what are competitive inhibitors?

A

molecules that block other things from binding to the receptor by sitting in it’s action site

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11
Q

what are non-competitive inhibitors?

A
  • molecules that block other things from binding to the receptor but not by sitting in it’s action site
  • it may attach to a different part of the receptor and cause the action site to change shape
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12
Q

what factors affect distribution in pharmacokinetics?

A
  • blood flow
  • molecular weight/size
  • how lipophilic/phobic a drug is
  • blood brain barrier/blood testicle barrier
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13
Q

where does first pass metabolism occur?

A

in the liver

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14
Q

what is bioavailability?

A

the proportion of the drug given that enters circulation and so can exert an effect on the body

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15
Q

why are different doses of the same drug prescribed when given orally vs IV?

A
  • with oral medications, first pass metabolism via the liver will reduce how much enters circulation - reduces bioavailability
  • giving mediations IV means drug enters straight into circulation - bioavailability = 100%
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16
Q

what are the main routes of drug administration?

A
  • oral
  • IV
  • subcutaneous
  • intramuscular
  • topical
  • rectal
  • intrathecal
  • sublingual/buccal
  • inhalation
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17
Q

what does parenteral drug administration?

A

non-oral drug administration routes

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18
Q

what is intrathecal drug administration?

A

into the spinal column for anaesthesia, chemotherapy or pain management

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19
Q

what is oral drug administration?

A

drugs taken orally

undergoes first pass metabolism - reduced bioavailability

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20
Q

what is IV drug administration?

A

drugs enter directly into circulation

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21
Q

what is subcutaneous drug administration?

A

drugs have to diffuse through subcutaneous fat

- drug is absorbed more slowly

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22
Q

what is intramuscular drug administration?

A

muscle tissue is vascular so it is rapidly absorbed

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23
Q

what is topical drug administration?

A
  • directly onto skin/mucosa
  • avoids first pass metabolism
  • slowly absorbs into circulation
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24
Q

what is rectal drug administration?

A

can be used when patient is unable to tolerate oral route

highly vascular tissue so absorbs quickly

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25
Q

what is sublingual/buccal drug administration?

A

avoids first pass metabolism

rapidly enters circulation

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26
Q

what is inhalation drug administration?

A

passes through trachea into the lungs

good if target site is lungs

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27
Q

what is GFR used for?

A
  • glomerular filtration rate is a test used to check how well the kidneys are working
  • it estimates how much blood passes through the glomeruli each minute
  • used in staging CKD
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28
Q

what is creatinine clearance (CrCl)?

A

volume of blood plasma cleared of creatinine per unit of time

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29
Q

what is creatinine clearance used for?

A

used to estimate GFR since glomeruli freely filter creatinine
this is done by comparing serum creatinine with urine creatinine

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30
Q

why is it important to know kidney function when prescribing drugs?

A

most drugs are excreted by kidneys
if kidneys are not functioning well, this can lead to reduced renal excretion and a build up of drug = toxicity
this can lead to further renal impairment

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31
Q

which drugs should be avoided/adjusted in renal impairment?

A

NSAIDs
PPIs
antibiotics

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32
Q

which conditions should you look out for before prescribing?

A

CKD
diabetes
hypertension
polycystic kidney disease

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33
Q

what do preganglionic neurones release at the autonomic ganglion in the sympathetic nervous system?

A

ACh

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34
Q

what do postganglionic neurones release at effector organs in the sympathetic nervous system?

A

catecholamines

  • adrenaline
  • noradrenaline
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35
Q

what happens in the sympathetic nervous system?

A

myelinated preganglionic neurones synapse with unmyelinated postganglionic neurones at the autonomic ganglia

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36
Q

what does the autonomic ganglia contain?

A

cell body clusters

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37
Q

what is a ganglion?

A

collection of neurone cell bodies in the PNS

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38
Q

which receptors does the sympathetic nervous system act on?

A 
alpha 1
alpha 2
beta 1
beta 2
beta 3
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39
Q

what are the effects of stimulation of the sympathetic nervous system?

A
  • fight or flight
  • increased HR, increased CO
  • vasoconstriction
  • bronchodilation
  • reduced GI motility and secretions
  • reduced bladder detrusor activity
  • increased sweating
  • reduced salivation
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40
Q

where are beta 1 receptors found?

A

heart

kidneys

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41
Q

what is the effect of beta 1 receptor stimulation?

A

increased CO

increased renin production

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42
Q

where are beta 2 receptors found?

A 
lungs
blood vessels
GI tract
bladder
uterus
liver
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43
Q

what are the effects of beta 2 receptor stimulation?

A
  • bronchodilation
  • vasodilation
  • decreased peristalsis and digestion
  • decreased urination
  • conversion to glucose in liver
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44
Q

where are beta 3 receptors found?

A

adipose tissue

bladder

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45
Q

what are the effects of beta 3 receptor stimulation?

A

increased lipolysis

decreased urination

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46
Q

how do you remember where beta 1 and beta 2 receptors are found?

A

beta 1 = heart ( 1 x heart)

beta 2 = lungs ( 2 x lungs)

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47
Q

where are alpha 1 receptors found?

A 
blood vessels
pupils
pylorus
urinary sphincter
prostate
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48
Q

what are the effects of alpha 1 receptor stimulation?

A
  • vasoconstriction
  • pupil dilation
  • urinary sphincter constriction
  • pyloric sphincter constriction
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49
Q

where are alpha 2 receptors found?

A

presynaptic nerve terminals

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50
Q

what are the effects of alpha 2 receptor stimulation?

A

inhibitory

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51
Q

what do preganglionic neurones release at the autonomic ganglion in the parasympathetic nervous system?

A

ACh

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52
Q

what do postganglionic neurones release at effector organs in the parasympathetic nervous system?

A

ACh

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53
Q

which receptors does the parasympathetic nervous system act on?

A

muscarinic

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54
Q

what are the effects of parasympathetic nervous system stimulation?

A
  • decreased HR
  • decreased CO
  • vasodilation
  • bronchoconstriction
  • increased bladder detrusor activity
  • reduced sweating
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55
Q

how do ACE-inhibitors work?

A
  • they block the action of ACE
  • this prevents angiotensin I being converted to angiotensin II
  • therefore no aldosterone is secreted so there is no vasodilation etc.
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56
Q

what do loop diuretics act on?

A

the ascending limb of the loop of henle

Na+/K+/Cl- co-transporter

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57
Q

what is the effect of loop diuretics?

A
  • inhibits Na+/K+/Cl- co-transporter
  • usually all three get absorbed and water follows
  • transportation blocked = less water reabsorbed and more excreted
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58
Q

what do thiazide diuretics act on?

A

distal convoluted tubule

Na+/Cl- co-transporter

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59
Q

how do loop diuretics cause hypokalaemia?

A

less K+ is absorbed

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60
Q

what is the effect of thiazide diuretics?

A

less Na+ is reabsorbed, therefore less water follows

- more water is excreted

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61
Q

how do thiazide diuretics cause hypokalaemia?

A

there is more Na+ in DCT where it can be exchanged for K+

therefore more K+ is lost in urine

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62
Q

what do K+ sparing diuretics act on?

A

distal convoluted tubule

ENaC channels

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63
Q

what are the effects of K+ sparing diuretics?

A

inhibits the reabsorption of Na+ and water in ENaC channels in DCT
this leads to Na+ and water excretion and K+ retention

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64
Q

what is the mechanism of action of NSAIDs?

A
  • COX inhibitors - prevents the production of prostaglandins

- COX-2 inhibition is useful but COX-1 inhibition causes adverse effects

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65
Q

what is the mechanism of action of antihistamines?

A
  • H1 receptor antagonist

- prevents the release of histamine from storage granules in mast cells which cause allergic reaction symptoms

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66
Q

what is the mechanism of action of proton pump inhibitors (PPIs)?

A
  • irreversibly inhibits H+/K+ATPase pump in gastric parietal cells to reduce H+ (acid) secretion
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67
Q

what is the mechanism of action of opioids?

A

activation of mu receptors in CNS

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68
Q

what are the common side effects of NSAIDs?

A

GI upset
GI bleeding
renal impairment

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69
Q

what are the side effects of anti-histmines?

A
  • older ones can corss BBB and cause sedation

- there are many H1 receptors in vomiting centre - can act as anti-emetics

70
Q

what are the side effects of ACE-inhibitors?

A

dry cough due to bradykinin!!!

dilates afferent arteriole so worsens kidney function

71
Q

what are the side effects of PPIs?

A

prolonged use in elderly can increase risk of fracture

72
Q

what are the side effects of opioids?

A
  • respiratory depression - give naloxone
  • nausea and vomiting
  • constipation
  • tolerance and withdrawal
73
Q

what are the side effects of diuretics?

A

can cause hyperkalaemia
increased urinary frequency
dehydration

74
Q

what is a side-effect?

A

a known, secondary and typically undesirable effect of a drug

75
Q

what are adverse drug reactions?

A

unexpected

76
Q

what are type A ADRs?

A 
augmented
• Commonest
• An extension of the clinical effect
• Predictable
• Dose related
• Self-limiting
77
Q

what are type B ADRs?

A 
bizarre
• Unexpected
• Unrelated to dosage and not expected from known pharmacological
action
• Unpredictable
• Mostly immunological mechanisms
• Hypersensitivity
78
Q

what is a type C ADR?

A

chronic
• Occurs after long term therapy
• May not be immediately obvious with new medicines

79
Q

what is a type D ADR?

A

delayed

• Also occurs after a long period of time after treatment - many years

80
Q

what is a type E ADR?

A

end of use
• Relatively long term use (days/weeks)
• Withdrawal reactions
• Serious complication of stopping related to clinical effect

81
Q

what are the different types of ADR according to Rawlins-Thompson classification

A
  • A - Augmented
  • B - Bizarre
  • C - Chronic
  • D - Delayed
  • E - End of Use
82
Q

what factors increase susceptibility of ADRs?

A
  • Age - elderly
  • Gender - more common in females
  • Pregnancy - negative effect on baby etc.
  • Disease - liver or renal in particular
  • Drug interactions
  • Diet or alcohol intake changes
  • Genetics
  • Hypersensitivity
83
Q

how are ADRs reported?

A

using yellow card system

84
Q

what is the equation for renal clearance?

A

clearance = rate of appearance in urine / plasma concentration

85
Q

what is used as a marker substance in the kidney?

A

creatinine

86
Q

what are the adult renal clearance values?

A
  • Renal blood flow is 18% of cardiac output = 1L/min
  • Renal plasma flow is 60% of blood flow = 600mls/min
  • Glomerular filtration is 12% of renal blood flow = 130mls/min
87
Q

what is the hepatic extraction ratio (HER)?

A

The proportion of drug removed by one passage through the liver

88
Q

what is a high HER limited by?

A

hepatic blood flow - perfusion

89
Q

what is a low HER limited by?

A

diffusion

90
Q

what is pain?

A

Unpleasant sensory and emotional experience associated with actual or
potential tissue damage

91
Q

what are c fibres, what information do they convey?

A
  • Unmyelinated

- Characterised by diffuse dull intense pain

92
Q

what are a delta fibres and what information do they convey?

A
  • Small and myelinated

- Conduct localised sharp sensation

93
Q

what is 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.

94
Q

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

A

pH.

95
Q

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

A

Henderson Hasselbach.

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

96
Q

What can enhance non ionic diffusion?

A

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

97
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.

98
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.

99
Q

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

A

The weak acid will become more ionised.

100
Q

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

A

The weak base will become less ionised.

101
Q

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

A

The weak acid will become less ionised.

102
Q

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

A

The weak base will become more ionised.

103
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.

104
Q

Give 3 factors that can increase gastric pH.

A
  1. Ingesting alkaline foods.
  2. Antacids.
  3. Omeprazole (PPI).
105
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.

106
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.

107
Q

Where do phase 1 hepatic metabolism reactions occur?

A

liver

108
Q

What enzyme usually catalyses phase 1 reactions?

A

CYP450

109
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.

110
Q

Briefly describe catecholamine synthesis.

A

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

111
Q

Which enzymes inactivate catecholamines?

A

MAO and COMPT.

112
Q

what is specificity

A

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

113
Q

what is selectivity

A

the ability of the receptor to distinguish between drugs

114
Q

give an example of a local anaesthetic

A

lidocaine

115
Q

what is the mechanism of action for local anaesthetics?

A
  • interrupt axonal neurotransmission in sensory nerves

- block voltage dependent Na channels -> this prevents depolarisation so no action potential

116
Q

Give an example of a proton pump inhibitor.

A

Omeprazole.

117
Q

Give an example of a statin.

A

Simvastatin.

118
Q

Give an example of an ACE inhibitor.

A

ramipril

119
Q

Give an example of a COX inhibitor.

A

Aspirin and paracetamol.

120
Q

Give an example of a β2 adrenoceptor agonist.

A

Salbutamol.

121
Q

Give an example of a β1 adrenoceptor blocker.

A

Atenolol.

122
Q

Give an example of a Ca2+ channel blocker.

A

Amlodipine.

123
Q

Give an example of a broad spectrum antibiotic.

A

Amoxicillin.

124
Q

Give an example of an opiate analgesic.

A

Tramadol.

125
Q

What do most drugs target?

A

Proteins!

126
Q

Name 4 receptors that drugs target.

A
  1. Ligand gated ion channels.
  2. GPCR.
  3. Kinase linked.
  4. Cytosolic/nuclear.
127
Q

Give an example of a ligand gated ion channel.

A

Nicotinic Ach receptor.

128
Q

Give an example of a GPCR.

A

Muscarinic and β2 adrenoceptor.

GPCR’s usually interact with adenylate cyclase or phospholipase C

129
Q

Give an example of a kinase linked receptor.

A

Receptors for growth factors.

130
Q

Give an example of a cytosolic/nuclear receptor.

A

Steroid receptors; steroids affect transcription.

131
Q

Describe the shape of a log dose-response curve.

A

Sigmoidal.

132
Q

What does EC50 tell us about a drug?

A

Its potency!

133
Q

What is EC50?

A

The concentration of drug that gives half the maximal response.

134
Q

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

A

Greater potency.

135
Q

What does Emax tell us about a drug?

A

Efficacy.

136
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.

137
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.

138
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).

139
Q

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

A

Less signal amplification gives a reduced drug response.

140
Q

Describe allosteric modulation.

A

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

141
Q

What is inverse agonism?

A

Where an agonist has a negative effect at a receptor.

142
Q

Does an antagonist show efficacy?

A

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

143
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.
144
Q

Can aspirin be described as a selective drug?

A

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

145
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.

146
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.
147
Q

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

A

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

148
Q

Where do phase 1 hepatic metabolism reactions occur?

A

In the smooth endoplasmic reticulum.

149
Q

What enzyme usually catalyses phase 1 reactions?

A

CYP450.

150
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.
151
Q

Give 3 disadvantages of IV infusion.

A
  1. Expensive.
  2. Needs constant checking.
  3. Calculation error likely.
152
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.
153
Q

What type of receptor are muscarinic receptors?

A

GPCR.

154
Q

Give examples of adverse muscarinic agonist effects.

A
  1. Diarrhoea.
  2. Urination.
  3. Miosis.
  4. Brachycardia.
  5. Emesis (vomiting).
  6. Lacrimation.
  7. Salivation.
155
Q

What would an α1 adrenergic antagonist do?

A
  1. Vasodilation.

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

156
Q

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

A

Benign prostatic hyperplasia.

157
Q

What would a β1 adrenergic antagonist do?

A
  1. Reduce CO.

2. Reduce renin secretion

158
Q

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

A

Hypertension, angina and arrhythmia.

159
Q

Give 5 patient risk factors for drug interactions.

A
  1. Old age.
  2. Polypharmacy.
  3. Renal disease.
  4. Hepatic disease.
  5. Genetics.
160
Q

Give 3 drug related risk factors for drug interactions.

A
  1. Narrow therapeutic index.
  2. Steep dose/response curve.
  3. Saturable metabolism.
161
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.
162
Q

How might drug interactions affect drug metabolism?

A

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

163
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.

164
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.

165
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.

166
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.

167
Q

What drug acts as an antagonist at the μ receptor?

A

Naloxone.

168
Q

What is the bioavailability of morphine taken orally?

A

50%.

169
Q

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

A

5mg.

170
Q

What is morphine metabolised to?

A

Morphine 6 glucuronide.

171
Q

Give 5 side effects of opioid use.

A
  1. Respiratory depression.
  2. Sedation.
  3. Nausea.
  4. Vomiting.
  5. Constipation.
172
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.

Phase 2A revision (38 decks)

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