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Phase 2a - Introductory Clincal Sciences > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

List the 3 types of drug interactions.

A

1) physicochemical
2) pharmacodynamic
3) pharmacokinetic

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2
Q

Define physicochemical drug interactions.

A

Drugs directly reacting with each other.

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3
Q

List 4 types of physicochemical drug interactions.

A

1) adsorption
2) precipitation
3) chelation
4) neutralisation

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4
Q

Give an example of a physicochemical drug interaction.

A

Paracetamol binding to activated charcoal (paracetamol overdose). Adsorption.

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5
Q

Define pharmacodynamic drug interactions.

A

Physical effect of a drug on the body.

what the drug does to the body

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6
Q

List 4 types of pharmacodynamic drug interactions.

A

1) summative reactions
2) synergistic reactions
3) antagonistic reactions
4) potentiation reactions

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7
Q

Define summative reactions.

A

1+1=2

Addition of 2 drugs works in the same way.

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8
Q

Give an example of a summative reaction.

A

sevoflurane + isoflurane

anaesthetics

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9
Q

Define synergistic reactions.

A

1+1>2

Addition of 2 drugs works better than they would individually.

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10
Q

Give 2 examples of a synergistic reaction.

A

1) paracetamol + morphine

2) paracetamol + ibuprofen

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11
Q

Define antagonistic reactions.

A

1+1=0

Drugs work against each other.

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12
Q

Give an example of antagonistic reactions.

A

morphine + naloxone

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13
Q

Define potentiation reactions.

A

1+1=1+1.5

Drug A increases drug B potency. Drug B doesn’t increase drug A potency.

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14
Q

Give an example of potentiation reactions.

A

probenicid + penicillin

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15
Q

Define pharmacokinetic drug interactions.

A

Movement of drug in the body.

What the body does with the drug.

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16
Q

List 4 factors that affect pharmacokinetic drug interactions.

A

1) absorption
2) distribution
3) metabolism
4) excretion

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17
Q

Define bioavailability.

A

Proportion of administered drug that is in systemic circulation.

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18
Q

What is bioavailability expressed as? (2)

A

1) percentage

2) fraction

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19
Q

What route of administration has a bioavailability of 100%/1?

A

Intravenous.

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20
Q

List 3 reasons why the bioavailability of oral drugs varies.

A

1) gut surface area
2) gut pH
3) diarrhoea

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21
Q

What oral drug has a very high bioavailability?

A

Paracetamol.

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22
Q

List 2 factors that affect absorption.

A

1) gut motility

2) gut acidity

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23
Q

What are 2 forms a drug exists as?

A

1) unionised - can pass through membrane

2) ionised - cannot pass through membrane

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24
Q

How does change in gut pH affect absorption?

A

Changes concentration of unionised and ionised forms of drug, therefore affects passage across membranes.

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25
Q

List 3 ‘places’ a drug could be distributed from a blood vessel.

A

1) bind to plasma protein
2) effect site
3) other tissue

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26
Q

What is the effect of a drug binding to a plasma protein.

A

It exerts no clinical effect.

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27
Q

What organ is most important for drug metabolism?

A

Liver.

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28
Q

Describe alcohol and the metabolism of morphine. (5)

A

1) morphine is metabolised by cytochrome P450 enzymes in the liver into morphine-6-glucoronide
2) morphine-6-glucoronide is 10x more effective than morphine
3) alcohol increases efficacy of cytochrome P450 enzymes
4) concentration of morphine-6-glucoronide increases due to alcohol
5) analgesic effect increases due to alcohol

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29
Q

What is altered to improve excretion of a drug?

A

pH.

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30
Q

How do you increase excretion of an acidic drug? (3)

A

1) give an alkali
2) urine becomes more alkaline
3) increased renal excretion of drug

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31
Q

How do you increase excretion of an alkaline drug? (3)

A

1) give an acid
2) urine becomes more acidic
3) increased renal excretion of drug

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32
Q

Define druggability.

A

Ability of a protein to bind to small molecules (drugs) with high affinity.

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33
Q

List 2 things a drug target must be.

A

1) linked to disease

2) druggable

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34
Q

List 4 drug targets.

A

1) receptors
2) enzymes
3) transporters
4) ion channels

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35
Q

Define receptor.

A

Cell component that interacts with specific ligand to initiate a cellular response.

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36
Q

List 4 types of receptor.

A

1) G-protein coupled receptors (GPCRs)
2) kinase-linked receptors
3) cytosolic/nuclear receptors
4) ligand-gated ion channels

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37
Q

Give an example of a G-protein coupled receptor.

A

β-adrenoceptors.

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38
Q

Give an example of a kinase-linked receptor.

A

Growth factor receptors.

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39
Q

Give an example of a cytosolic/nuclear receptor.

A

Steroid receptors.

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40
Q

Give an example of a ligand-gated ion channel.

A

Nicotine ACh receptor.

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41
Q

What are G proteins?

A

GTPases. Enzymes that hydrolyse guanine triphosphate.

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42
Q

When is a GPCR ‘on’/‘off’?

A

On - bound to GDP

Off - bound to GTP

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43
Q

List the 2 main enzymes that GPCRs interact with.

A

1) phospholipase C

2) adenylyl cyclase

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44
Q

List 3 reasons characterising receptors is important therapeutically.

A

1) identify receptor involved in pathology
2) develop drugs that act at the receptor
3) quantify drug action at that receptor

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45
Q

Define agonist.

A

Molecule that binds to a receptor eliciting an up regulated response.

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46
Q

Define antagonist.

A

Molecule that reduces the effect of an agonist.

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47
Q

Define potency.

A

Dose required to produce a given response.

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48
Q

Define EC50.

A

Measure of potency. Dose that gives half the maximal response.

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49
Q

List 2 factors that affect potency.

A

1) drug-receptor affinity

2) no. of receptors available

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50
Q

Define efficacy.

A

How well a ligand activates a receptor. The maximal response.

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51
Q

List 2 types of efficacy.

A

1) Emax

2) intrinsic activity (IA)

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52
Q

Define Emax.

A

The maximal response achieved from a specific dose.

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53
Q

Define intrinsic activity.

A

The maximal response achieved by a drug-receptor complex.

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54
Q

What is the effect of a competitive antagonist?

A

Decreases potency.

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55
Q

What is the effect of a non-competitive antagonist?

A

Decreases potency and efficacy.

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56
Q

Define affinity.

A

How well a ligand binds to a receptor.

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57
Q

Define inverse agonist.

A

Molecule that binds to a receptor eliciting a down regulated response.

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58
Q

Define tolerance.

A

Reduction in drug efficacy. Due to repeated or high drug doses.

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59
Q

Describe selectivity using β adrenoceptors. (2)

A

1) isoprenaline - non-selective β adrenoceptor agonist —> activates β1 and β2
2) salbutamol - selective β2 adrenoceptor agonist —> activates only β2

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60
Q

Define enzyme inhibitor.

A

Molecule that binds to an enzyme decreasing its activity.

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61
Q

List the 2 types of enzyme inhibitor.

A

1) irreversible inhibitor

2) reversible inhibitor

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62
Q

How do irreversible inhibitors bind to enzymes.

A

Covalently.

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63
Q

How do reversible inhibitors bind to enzymes?

A

Non-covalently.

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64
Q

What is the advantage of a complex pathway?

A

Many therapeutic targets, e.g. treating Parkinson’s disease.

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65
Q

Define transport.

A

Movement of a molecule across a cell membrane.

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66
Q

List the 3 types of transporters.

A

1) uniporter
2) symporter
3) antiporter

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67
Q

How do uniporters work?

A

Use energy from ATP to transport a molecule against its concentration

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68
Q

How do symporters work?

A

Use the movement of one molecule to transport another molecule against its concentration gradient. (In the same direction).

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69
Q

How do antiporters work?

A

Use the movement of one molecule to transport another molecule against its concentration gradient. (In opposite directions).

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70
Q

Define absorption (pharmacokinetics).

A

Transfer of drugs from site of administration into general or system circulation.

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71
Q

List 12 routes of drug administration.

A

1) oral
2) intravenous
3) intraarterial
4) intramuscular
5) intrathecal
6) intranasal
7) inhalation
8) topical
9) transcutaneous
10) subcutaneous
11) sublingual
12) rectal

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72
Q

What is a key consideration of pharmacokinetic absorption?

A

Drug must pass through at least one membrane to pass from route of administration into circulation.

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73
Q

List 5 ways a drug may pass through a membrane.

A

1) diffusion through lipid bilayer - passive diffusion
2) diffusion through ion channel or pore - facilitated diffusion
3) diffusion via carrier - facilitated diffusion
4) active transport
5) pinocytosis

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74
Q

What property must a drug possess to passively diffuse through a membrane.

A

Lipid solubility.

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75
Q

List 4 factors that affect the rate of diffusion.

A

1) concentration gradient
2) membrane surface area
3) membrane permeability
4) membrane thickness

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76
Q

What molecules diffuse via an ion channel or pore?

A

Very small water soluble molecules.

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77
Q

Define pinocytosis.

A

Endocytosis of molecules suspended in extracellular matrix.

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78
Q

Describe ionisation of drugs in terms of solubility. (2)

A

1) ionised form - water soluble

2) unionised form - lipid soluble

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79
Q

List 2 factors that effect the extent of ionisation of a drug.

A

1) strength of ionisable group

2) pH

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80
Q

Define PKa.

A

Dissociation constant. The pH where half the drug is ionised and half is unionised.

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81
Q

Where are weak acid drugs best absorbed?

A

Stomach.

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82
Q

Where are weak base drugs best absorbed?

A

Intestines.

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83
Q

What route of administration is most convenient for most drugs and why? (2)

A

Oral.

1) large surface area of small intestine
2) high blood flow to small intestine

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84
Q

List 4 features that affect the absorption of oral drugs.

A

1) drug structure
2) drug formulation
3) gastric emptying
4) first pass metabolism

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85
Q

How does drug formulation affect drug absorption?

A

Rate of disintegration and dissolution affects the rate of absorption. Drugs can be modified to be fast or slow release.

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86
Q

Why do some oral drugs have coatings?

A

To resist stomach acidity.

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87
Q

How does gastric emptying affect drug absorption?

A

Determines time taken for drug to be delivered to small intestine to be absorbed.

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88
Q

List 3 things that slow down gastric emptying.

A

1) food
2) drugs
3) trauma

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89
Q

What can speed up gastric emptying?

A

Gastric surgery, e.g. gastrectomy or pyloroplasty.

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90
Q

List the 4 major metabolic barriers an oral drug must pass to reach circulation.

A

1) intestinal lumen
2) intestinal wall
3) liver
4) lungs

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91
Q

Why is the intestinal lumen a metabolic barrier to oral drug absorption? (2)

A

1) luminal digestive enzymes —> split bonds

2) colonic bacteria —> hydrolyse and reduce drugs

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92
Q

Why is the intestinal wall a metabolic barrier to oral drug absorption? (2)

A

1) cellular digestive enzymes

2) enterocyte efflux transporters that transport drugs back into the lumen

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93
Q

Why is the liver a metabolic barrier to oral drug absorption?

A

Major site of drug metabolism.

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94
Q

How do you avoid hepatic first pass metabolism? (2)

A

Administer drug to a region of gut not drained by splanchnic circulation.

1) sublingual
2) rectal

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95
Q

What is the main disadvantage transcutaneous drug administration?

A

Limited absorption. Epidermis is an effective barrier to water soluble drugs. Rate and extent of absorption of lipid soluble drugs is limited.

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96
Q

List 2 features are necessary for transcutaneous drug administration.

A

1) potent

2) non-irritant

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97
Q

List 2 instances when subcutaneous drug administration is used.

A

1) for a local effect, e.g. local anaesthetic
2) to limit rate of absorption, e.g. long term contraceptive implants
Due to limited blood flow.

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98
Q

List 2 factors that affect intramuscular drug administration.

A

1) blood flow
2) water solubility
Increase in either enhances drug removal from site.

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99
Q

List 2 advantages of intranasal drug administration.

A

1) low level of enzymes

2) large surface area

100
Q

List 2 advantages of inhalation drug administration.

A

1) large surface area

2) extensive blood supply

101
Q

List 3 disadvantages of inhalation drug administration.

A

1) risk of alveoli toxicity
2) mainly restricted to volatile drugs
3) inefficient —> only 5% delivered to small airways

102
Q

Define distribution (pharmacokinetics).

A

Reversible transfer of drugs between general circulation and tissues.

103
Q

List 2 ways drugs can bind to plasma or tissue proteins.

A

1) reversibly

2) irreversibly

104
Q

What plasma protein do drugs most commonly reversibly bind to?

A

Albumin.

105
Q

Describe drugs reversibly binding to proteins. (3)

A

1) decreases free concentration of drug
2) acts as store of drug
3) increase free concentration of drug when plasma concentration drops due to redistribution or elimination

106
Q

What is a drug binding irreversibly to a protein equivalent to?

A

Elimination.

107
Q

List 4 features of the blood brain barrier that limit drug distribution to the brain.

A

1) tight junctions
2) small pore sizes
3) small pore number
4) efflux transporters

108
Q

What feature must drugs possess to pass through the blood brain barrier?

A

Lipid soluble.

109
Q

List 3 considerations when prescribing a pregnant mother.

A

1) lipid soluble drugs readily cross the placenta
2) large drugs do not cross the placenta
3) foetal liver has low levels of drug metabolising enzymes

110
Q

What occurs during drug metabolism and why?

A

Drug is converted to a less biologically active water soluble product.
To stop the drugs effects and remove the drug via urine.

111
Q

What occurs in phase 1 drug metabolism

A

Drug is made more polar by unmasking or adding polar functional groups, e.g. -OH.

112
Q

What occurs in phase 2 drug metabolism?

A

Drug is covalently bonded to an endogenous substrate to render it less active - conjugation.

113
Q

List 3 states of drug excretion.

A

1) fluid - urine, bile, sweat, tears
2) solid - faeces
3) gas - air

114
Q

List 3 factors affecting drug urine excretion.

A

1) glomerular filtration
2) tubular secretion
3) reabsorption

total excretion = glomerular filtration + tubular secretion - reabsorption

115
Q

Define zero order kinetics.

A

Change in drug concentration per time is a fixed amount.

116
Q

What are zero order kinetic systems independent of?

A

Drug concentration.

117
Q

When does zero order kinetics take place?

A

Enzyme system that removes the drug is saturated.

118
Q

Define first order kinetics.

A

Change in concentration per time is proportional to the concentration.

119
Q

Define bioavailability.

A

F.

Proportion of administered drug that reaches systemic circulation unaltered.

120
Q

What route of drug administration has F=1?

A

IV.

121
Q

List 2 reasons why oral drug administration has F<1.

A

1) first pass metabolism

2) incomplete absorption

122
Q

Formula of bioavailability.

A

F = AUC Oral ÷ AUC IV

123
Q

Define dose.

A

D.

Quantity of drug administered.

124
Q

Define plasma concentration.

A

C.

Concentration of drug in blood.

125
Q

What affects water soluble drugs rate of distribution?

A

Rate of passage across membranes.

126
Q

What affects lipid soluble drugs rate of distribution?

A

Blood flow to tissues.

127
Q

Define apparent volume of distribution.

A

Vd.
Theoretical volume necessary to contain total amount of administered drug at the same concentration observed in blood plasma.

128
Q

Formula of apparent volume of distribution.

A

Vd = D ÷ C

129
Q

What does a low Vd suggest?

A

Drug is confined to circulation.

130
Q

What does a high Vd suggest?

A

Drugs has distributed to total body water.

131
Q

Define clearance.

A

CL.

Volume of plasma completely cleared of drug per unit time.

132
Q

List 5 factors that affect clearance.

A

1) renal clearance
2) hepatic clearance
3) respiratory clearance
4) faecal clearance
5) salivary clearance

133
Q

Formula for CL.

A

CL = D x F ÷ AUC

134
Q

Define half-life.

A

T1/2.

Time taken for plasma drug concentration to halve.

135
Q

Define elimination rate constant.

A

K.

Rate drug is removed from the body.

136
Q

Formula relating T1/2 and K.

A

ln2 = T1/2 x K

137
Q

Formula relating Vd, CL and K.

A

CL = K x Vd

138
Q

Define steady state.

A

Css.

Equilibrium between drug administration and elimination.

139
Q

How long does an IV infusion take to reach 95% of steady state?

A

Approx 4-5 half-lives.

140
Q

List 2 features that increase time to reach steady state.

A

1) slow elimination

2) high apparent volume of distribution

141
Q

What is true when steady state is reached in an IV infusion?

A

Rate of elimination equal rate of infusion.

142
Q

Formula relating CL, Css and K.

A

K = CL x Css

143
Q

Formula relating Css, F, D, CL and t. When does this formula apply?

A

Css = (F x D) ÷ (CL x t)

Oral drug administration.

144
Q

Define loading dose.

A

High initial dose that loads the system, shortening time to steady state.

145
Q

When is a loading dose administered?

A

If a drug has a long half-life.

146
Q

Formula relating Vd, CL and T1/2.

A

T1/2 = ln2 x Vd ÷ CL

147
Q

Define dependence.

A

Physical and physiological condition where the body has adapted to the presence of a drug.

148
Q

List 2 naturally occurring opioids.

A

1) morphine

2) codeine

149
Q

List 3 chemically modified opioids.

A

1) diamorphine
2) oxcycodone
3) dihydrocodeine

150
Q

List 4 synthetic opioids.

A

1) pethidine
2) fentanyl
3) alfentanil
4) remifentanil

151
Q

List 3 ways in which opioids work.

A

1) inhibit release of pain transmitters at spinal cord and midbrain
2) modulate pain perception in higher centres
3) change emotional perceptions of pain

152
Q

Why do opioids have side effects.

A

Opioid receptors exist outside the pain system.

153
Q

List 7 opioid side effects.

A

1) respiratory depression
2) sedation
3) nausea and vomiting
4) constipation
5) itching
6) immune suppression
7) endocrine effects

154
Q

How could you avoid opioid side effects?

A

Epidural drug administration.

155
Q

What is CYP2D6?

A

Cytochrome enzymes found in the liver important in xenobiotic metabolism.

156
Q

List 4 opioids metabolised by CYP2D6.

A

1) codiene
2) oxycodone
3) hydrocodone
4) tramadol

157
Q

Describe CYP2D6 activity in the Caucasian population. (4)

A

1) normal activity - 70-75%
2) under activity - 10-15%
3) absent - 10%
4) over activity - 5%

158
Q

What is the side effect of an overactive CYP2D6 enzyme?

A

Increased risk of respiratory depression.

159
Q

What is the side effect of an under active/absent CYP2D6?

A

Reduced or absent effect of codeine, tramadol, oxycodone and hydrocodone.

160
Q

Name an opioid antagonist.

A

Naloxone.

161
Q

What is tramadol metabolised into?

A

O-desmethyl tramadol.

162
Q

What is the secondary analgesic effect of tramadol?

A

Serotonin and noradrenaline reputable inhibitor.

163
Q

What percentage of orally administered morphine is metabolised by first pass metabolism?

A

50%.

164
Q

How long does a single dose of morphine last?

A

3-4 hours.

165
Q

How is morphine-6-glucuronide excreted.

A

Renal excretion.

166
Q

What does morphine administered to a patient with renal failure cause?

A

Respiratory depression.

167
Q

List 2 features of diamorphine in relation to morphine.

A

1) more potent

2) faster acting - crosses BBB faster

168
Q

What is the relative potency of morphine and diamorphine?

A

1) morphine - 10mg

2) diamorphine - 5mg

169
Q

What is diamorphine also known as?

A

Heroin

170
Q

What is morphine metabolised into?

A

Morphine-6-glucuronide.

171
Q

List 6 general uses of cholinergic and adrenergic pharmacology.

A

1) blood pressure control
2) heart rate control
3) anaesthetic agents - muscle relaxants
4) airway tone regulation - bronchospasm
5) GI function control - diarrhoea and constipation
6) eye pressure regulation - glaucoma

172
Q

What output from the central nervous system isn’t conveyed by the autonomic nervous system?

A

Skeletal muscle control.

173
Q

What is the general function of the parasympathetic nervous system?

A

Rest and digest.

174
Q

What is the parasympathetic outflow?

A

CN III, CN VII, CN IX, CN X and S2-S4.

175
Q

List 3 features of parasympathetic post-synaptic nerve fibres.

A

1) short post-synaptic nerve fibres
2) post-synaptic nerve fibres release ACh
3) act on muscarinic receptors

176
Q

What is the general function of the sympathetic nervous system?

A

Fight or flight.

177
Q

What is the sympathetic nervous system outflow?

A

T1 - L2/3.

178
Q

List 3 features of sympathetic post-synaptic nerve fibres.

A

1) long post-synaptic nerve fibres
2) post-synaptic nerve fibres release NA
3) act on adrenergic receptors

179
Q

List 3 ‘organs’ with opposing dual parasympathetic and sympathetic innervation.

A

1) heart
2) bladder
3) gastrointestinal tract

180
Q

List 2 ‘organs’ with only sympathetic innervation.

A

1) blood vessels

2) sweat glands

181
Q

What ‘organ’ only has parasympathetic innervation?

A

Bronchial smooth muscle.

182
Q

What is unique about sympathetic innervation of sweat glands?

A

Post-synaptic nerve fibres release ACh to stimulate muscarinic receptors.

183
Q

What are NANCs?

A

Non-adrenergic, non-cholinergic transmitters.

184
Q

List 2 parasympathetic NANCs.

A

1) nitric oxide

2) vasoactive intestinal peptide

185
Q

List 2 sympathetic NANCs.

A

1) ATP

2) neuropeptide Y

186
Q

What type of receptor are muscarinic receptors.

A

GPCR.

187
Q

List the 5 subtypes of muscarinic receptors.

A

1) M1
2) M2
3) M3
4) M4
5) M5

188
Q

Where are M1 receptors generally found? (2)

A

1) brain

2) exocrine glands

189
Q

Where are M2 receptors generally found?

A

Heart.

190
Q

Where are M3 receptors generally found? (3)

A

1) vascular smooth muscle
2) airway smooth muscle
3) exocrine glands

191
Q

Where are M4 receptors generally found?

A

Brain.

192
Q

Where are M5 receptors generally found?

A

Brain.

193
Q

What is pilocarpine? (2)

A

Muscarinic agonist:

1) stimulates salivation
2) contracts iris smooth muscle

194
Q

List 6 conditions muscarinic antagonists treat.

A

1) bradycardia
2) hypotension
3) bronchoconstriction
4) dry secretions
5) overactive bladder
6) intestinal and colonic spasm (IBS)

195
Q

What muscarinic antagonistics prevent bronchoconstriction?

A

M3 receptor antagonists (SAMA and LAMA).

196
Q

Describe ACh pharmacology’s effect on memory. (2)

A

1) anticholinergics - worsen memory

2) acetylcholinesterase inhibitors - dementia treatment

197
Q

List 4 pharmacological uses of ACh outside of the autonomic nervous system.

A

1) anti-emetic
2) cosmetic and anti-spasmodic
3) inhibit muscle activity and induce muscle relaxation - for surgery
4) myasthenia gravis

198
Q

Describe cosmetic and anti-spasmodic uses of ACh.

A

Botulinum toxin (Botox) prevents ACh release - muscle relaxant.

199
Q

Describe ACh role in treatment of myasthenia gravis. (3)

A

1) autoimmune destruction of nicotine ACh receptors
2) anti-acetylcholinesterases given
3) increases acetylcholine available for signalling

200
Q

List 6 anti-cholinergic side effects.

A

1) worsen memory
2) confusion
3) constipation
4) dry mouth
5) blurry vision
6) glaucoma

201
Q

List 4 cholinergic side effects.

A

1) muscle paralysis
2) twitching
3) salivation
4) confusion

202
Q

What is the catecholamine pathway?

A

DA —> NA —> A.

203
Q

List 5 the subtypes of adrenergic receptors.

A

1) α1
2) α2
3) β1
4) β2
5) β3

204
Q

What type of receptor are adrenergic receptors?

A

GCPR.

205
Q

List 3 features that determine the outcome of adrenergic signalling.

A

1) receptor
2) cell
3) G protein

206
Q

Define chronotropic effects.

A

Effects that change heart rate.

Chrono - time.

207
Q

Define ionotropic effects.

A

Effects that change force of muscle contractions.

Ionos - fibre.

208
Q

What is the agonist of α1 adrenergic receptors?

A

NA>A.

209
Q

What is the agonist of α2 adrenergic receptors?

A

A=NA

210
Q

What is the agonist of β1 adrenergic receptors?

A

A=NA

211
Q

What is the agonist of β2 adrenergic receptors?

A

A»NA.

212
Q

What is the agonist of β3 adrenergic receptors?

A

NA>A.

213
Q

What is the action of α1 adrenergic receptors?

A

Smooth muscle contraction.

214
Q

What is the action of α2 adrenergic receptors?

A

Smooth muscle contraction/relaxation.

215
Q

What is the action of β1 adrenergic receptors?

A

Chronotropic and ionotropic effects on the heart.

216
Q

What is the action of β2 adrenergic receptors?

A

Smooth muscle relaxation.

217
Q

What is the action of β3 adrenergic receptors? (2)

A

1) relaxes detrusor muscle (bladder)

2) enhances lipolysis

218
Q

List 2 functions of α1 agonists.

A

1) raise blood pressure

2) vasoconstriction

219
Q

What is the function of α2 agonists?

A

Lowers blood pressure.

220
Q

What is the function of α1 blockers?

A

Lowers blood pressure.

221
Q

What is the function of α2 blockers?

A

No useful α2 blockers.

222
Q

What is the function of β1 agonists?

A

Increase heart rate.

223
Q

List 2 functions of β2 agonists.

A

1) bronchodilation - asthma

2) delay onset of premature labour

224
Q

What is the function of β3 agonists?

A

Reduce over-active bladder symptoms.

226
Q

List 6 conditions treated by β blockers.

A

1) hypertension
2) arrhythmia
3) angina
4) MI prevention
5) heart failure
6) anxiety

227
Q

List 6 side effects of β blockers.

A

1) bradycardia
2) cardiac depression
3) bronchoconstriction
4) hypoglycaemia
5) tiredness
6) cold extremities

229
Q

List 4 side effects of β agonists.

A

1) tachycardia
2) arrhythmia
3) affect glucose metabolism in liver
4) affect carbohydrate and lipid metabolism (β1 and β3 only)

230
Q

Define adverse drug reactions.

A

Unwanted or harmful reaction following administration of a drug.

231
Q

List 4 statistics related to adverse drug reactions.

A

1) 5% of hospital admissions
2) 10-20% of hospital inpatients
3) 5th most common cause of hospital death
4) 60% preventable

232
Q

List 6 types of adverse drug reactions in the Rawlins Thompson classification.

A

1) type A
2) type B
3) type C
4) type D
5) type E
6) type F

233
Q

Define type A adverse drug reactions. (3)

A

Augmented reactions.

1) predictable
2) dose dependant
3) common

234
Q

Define type B adverse drug reactions. (2)

A

Bizarre reactions.

1) not predictable
2) not dose dependant

235
Q

Define type C adverse drug reactions.

A

Chronic reactions, e.g. steroids and osteoporosis

236
Q

Define type D adverse drug reactions.

A

Delayed reactions. Malignancies after immunosuppression.

237
Q

Define type E adverse drug reactions.

A

End of treatment reactions. Abrupt drug withdrawal.

238
Q

Define type F adverse drug reactions.

A

Failure of therapy reactions.

239
Q

List 3 factors of DoTS classification.

A

1) dose
2) timing
3) susceptibility

240
Q

List 8 risk factors for adverse drug reactions.

A

1) genetic predisposition
2) allergies
3) female gender
4) elderly
5) neonate
6) polypharmacy
7) adherence problems
8) hepatic/renal impairment

241
Q

List 7 causes of adverse drug reactions.

A

1) pharmaceutical variation
2) abnormal receptor
3) abnormal drug metabolism
4) abnormal biological system unmasked by drug
5) drug-drug reaction
6) immunological
7) multifactorial

242
Q

List 4 times you would suspect an adverse drug reaction.

A

1) symptoms appear when starting drug
2) symptoms appear when increasing drug dosage
3) symptoms disappear when stopping drug
4) symptoms reappear when restarting drug

243
Q

List 6 types of drugs that commonly cause adverse drug reactions.

A

1) antibiotics
2) antineoplastics
3) NSAIDs
4) cardiovascular drugs
5) hypoglycaemic drugs
6) CNS drugs

244
Q

List 6 common adverse drug reactions.

A

1) confusion
2) nausea
3) balance problems
4) diarrhoea
5) constipation
6) hypotension

245
Q

List 7 reasons why adverse drug reporting is low.

A

1) ignorance
2) diffidence
3) fear
4) lethargy
5) guilt
6) ambition
7) complacency

246
Q

Define gene therapy.

A

Treatment of disorder by altering patients genes.

247
Q

List 3 gene therapy approaches.

A

1) replacing mutated gene with health gene
2) inactivating mutated gene
3) introducing new gene to fight disease

248
Q

What is the nomenclature for therapeutic monoclonal antibodies? (4)

A

1) -omab - murine
2) -ximab - chimeric
3) -zumab - humanised
4) -umab - human

Phase 2a - Introductory Clincal Sciences (8 decks)

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