Pharmacology Flashcards
(246 cards)
1
Q
List the 3 types of drug interactions.
A
1) physicochemical
2) pharmacodynamic
3) pharmacokinetic
2
Q
Define physicochemical drug interactions.
A
Drugs directly reacting with each other.
3
Q
List 4 types of physicochemical drug interactions.
A
1) adsorption
2) precipitation
3) chelation
4) neutralisation
4
Q
Give an example of a physicochemical drug interaction.
A
Paracetamol binding to activated charcoal (paracetamol overdose). Adsorption.
5
Q
Define pharmacodynamic drug interactions.
A
Physical effect of a drug on the body.
what the drug does to the body
6
Q
List 4 types of pharmacodynamic drug interactions.
A
1) summative reactions
2) synergistic reactions
3) antagonistic reactions
4) potentiation reactions
7
Q
Define summative reactions.
A
1+1=2
Addition of 2 drugs works in the same way.
8
Q
Give an example of a summative reaction.
A
sevoflurane + isoflurane
anaesthetics
9
Q
Define synergistic reactions.
A
1+1>2
Addition of 2 drugs works better than they would individually.
10
Q
Give 2 examples of a synergistic reaction.
A
1) paracetamol + morphine
2) paracetamol + ibuprofen
11
Q
Define antagonistic reactions.
A
1+1=0
Drugs work against each other.
12
Q
Give an example of antagonistic reactions.
A
morphine + naloxone
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.
14
Q
Give an example of potentiation reactions.
A
probenicid + penicillin
15
Q
Define pharmacokinetic drug interactions.
A
Movement of drug in the body.
What the body does with the drug.
16
Q
List 4 factors that affect pharmacokinetic drug interactions.
A
1) absorption
2) distribution
3) metabolism
4) excretion
17
Q
Define bioavailability.
A
Proportion of administered drug that is in systemic circulation.
18
Q
What is bioavailability expressed as? (2)
A
1) percentage
2) fraction
19
Q
What route of administration has a bioavailability of 100%/1?
A
Intravenous.
20
Q
List 3 reasons why the bioavailability of oral drugs varies.
A
1) gut surface area
2) gut pH
3) diarrhoea
21
Q
What oral drug has a very high bioavailability?
A
Paracetamol.
22
Q
List 2 factors that affect absorption.
A
1) gut motility
2) gut acidity
23
Q
What are 2 forms a drug exists as?
A
1) unionised - can pass through membrane
2) ionised - cannot pass through membrane
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.
25
List 3 ‘places’ a drug could be distributed from a blood vessel.
1) bind to plasma protein
2) effect site
3) other tissue
26
What is the effect of a drug binding to a plasma protein.
It exerts no clinical effect.
27
What organ is most important for drug metabolism?
Liver.
28
Describe alcohol and the metabolism of morphine. (5)
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
29
What is altered to improve excretion of a drug?
pH.
30
How do you increase excretion of an acidic drug? (3)
1) give an alkali
2) urine becomes more alkaline
3) increased renal excretion of drug
31
How do you increase excretion of an alkaline drug? (3)
1) give an acid
2) urine becomes more acidic
3) increased renal excretion of drug
32
Define druggability.
Ability of a protein to bind to small molecules (drugs) with high affinity.
33
List 2 things a drug target must be.
1) linked to disease
| 2) druggable
34
List 4 drug targets.
1) receptors
2) enzymes
3) transporters
4) ion channels
35
Define receptor.
Cell component that interacts with specific ligand to initiate a cellular response.
36
List 4 types of receptor.
1) G-protein coupled receptors (GPCRs)
2) kinase-linked receptors
3) cytosolic/nuclear receptors
4) ligand-gated ion channels
37
Give an example of a G-protein coupled receptor.
β-adrenoceptors.
38
Give an example of a kinase-linked receptor.
Growth factor receptors.
39
Give an example of a cytosolic/nuclear receptor.
Steroid receptors.
40
Give an example of a ligand-gated ion channel.
Nicotine ACh receptor.
41
What are G proteins?
GTPases. Enzymes that hydrolyse guanine triphosphate.
42
When is a GPCR ‘on’/‘off’?
On - bound to GDP
| Off - bound to GTP
43
List the 2 main enzymes that GPCRs interact with.
1) phospholipase C
| 2) adenylyl cyclase
44
List 3 reasons characterising receptors is important therapeutically.
1) identify receptor involved in pathology
2) develop drugs that act at the receptor
3) quantify drug action at that receptor
45
Define agonist.
Molecule that binds to a receptor eliciting an up regulated response.
46
Define antagonist.
Molecule that reduces the effect of an agonist.
47
Define potency.
Dose required to produce a given response.
48
Define EC50.
Measure of potency. Dose that gives half the maximal response.
49
List 2 factors that affect potency.
1) drug-receptor affinity
| 2) no. of receptors available
50
Define efficacy.
How well a ligand activates a receptor. The maximal response.
51
List 2 types of efficacy.
1) Emax
| 2) intrinsic activity (IA)
52
Define Emax.
The maximal response achieved from a specific dose.
53
Define intrinsic activity.
The maximal response achieved by a drug-receptor complex.
54
What is the effect of a competitive antagonist?
Decreases potency.
55
What is the effect of a non-competitive antagonist?
Decreases potency and efficacy.
56
Define affinity.
How well a ligand binds to a receptor.
57
Define inverse agonist.
Molecule that binds to a receptor eliciting a down regulated response.
58
Define tolerance.
Reduction in drug efficacy. Due to repeated or high drug doses.
59
Describe selectivity using β adrenoceptors. (2)
1) isoprenaline - non-selective β adrenoceptor agonist —> activates β1 and β2
2) salbutamol - selective β2 adrenoceptor agonist —> activates only β2
60
Define enzyme inhibitor.
Molecule that binds to an enzyme decreasing its activity.
61
List the 2 types of enzyme inhibitor.
1) irreversible inhibitor
| 2) reversible inhibitor
62
How do irreversible inhibitors bind to enzymes.
Covalently.
63
How do reversible inhibitors bind to enzymes?
Non-covalently.
64
What is the advantage of a complex pathway?
Many therapeutic targets, e.g. treating Parkinson’s disease.
65
Define transport.
Movement of a molecule across a cell membrane.
66
List the 3 types of transporters.
1) uniporter
2) symporter
3) antiporter
67
How do uniporters work?
Use energy from ATP to transport a molecule against its concentration
68
How do symporters work?
Use the movement of one molecule to transport another molecule against its concentration gradient. (In the same direction).
69
How do antiporters work?
Use the movement of one molecule to transport another molecule against its concentration gradient. (In opposite directions).
70
Define absorption (pharmacokinetics).
Transfer of drugs from site of administration into general or system circulation.
71
List 12 routes of drug administration.
1) oral
2) intravenous
3) intraarterial
4) intramuscular
5) intrathecal
6) intranasal
7) inhalation
8) topical
9) transcutaneous
10) subcutaneous
11) sublingual
12) rectal
72
What is a key consideration of pharmacokinetic absorption?
Drug must pass through at least one membrane to pass from route of administration into circulation.
73
List 5 ways a drug may pass through a membrane.
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
74
What property must a drug possess to passively diffuse through a membrane.
Lipid solubility.
75
List 4 factors that affect the rate of diffusion.
1) concentration gradient
2) membrane surface area
3) membrane permeability
4) membrane thickness
76
What molecules diffuse via an ion channel or pore?
Very small water soluble molecules.
77
Define pinocytosis.
Endocytosis of molecules suspended in extracellular matrix.
78
Describe ionisation of drugs in terms of solubility. (2)
1) ionised form - water soluble
| 2) unionised form - lipid soluble
79
List 2 factors that effect the extent of ionisation of a drug.
1) strength of ionisable group
| 2) pH
80
Define PKa.
Dissociation constant. The pH where half the drug is ionised and half is unionised.
81
Where are weak acid drugs best absorbed?
Stomach.
82
Where are weak base drugs best absorbed?
Intestines.
83
What route of administration is most convenient for most drugs and why? (2)
Oral.
1) large surface area of small intestine
2) high blood flow to small intestine
84
List 4 features that affect the absorption of oral drugs.
1) drug structure
2) drug formulation
3) gastric emptying
4) first pass metabolism
85
How does drug formulation affect drug absorption?
Rate of disintegration and dissolution affects the rate of absorption. Drugs can be modified to be fast or slow release.
86
Why do some oral drugs have coatings?
To resist stomach acidity.
87
How does gastric emptying affect drug absorption?
Determines time taken for drug to be delivered to small intestine to be absorbed.
88
List 3 things that slow down gastric emptying.
1) food
2) drugs
3) trauma
89
What can speed up gastric emptying?
Gastric surgery, e.g. gastrectomy or pyloroplasty.
90
List the 4 major metabolic barriers an oral drug must pass to reach circulation.
1) intestinal lumen
2) intestinal wall
3) liver
4) lungs
91
Why is the intestinal lumen a metabolic barrier to oral drug absorption? (2)
1) luminal digestive enzymes —> split bonds
| 2) colonic bacteria —> hydrolyse and reduce drugs
92
Why is the intestinal wall a metabolic barrier to oral drug absorption? (2)
1) cellular digestive enzymes
| 2) enterocyte efflux transporters that transport drugs back into the lumen
93
Why is the liver a metabolic barrier to oral drug absorption?
Major site of drug metabolism.
94
How do you avoid hepatic first pass metabolism? (2)
Administer drug to a region of gut not drained by splanchnic circulation.
1) sublingual
2) rectal
95
What is the main disadvantage transcutaneous drug administration?
Limited absorption. Epidermis is an effective barrier to water soluble drugs. Rate and extent of absorption of lipid soluble drugs is limited.
96
List 2 features are necessary for transcutaneous drug administration.
1) potent
| 2) non-irritant
97
List 2 instances when subcutaneous drug administration is used.
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.
98
List 2 factors that affect intramuscular drug administration.
1) blood flow
2) water solubility
Increase in either enhances drug removal from site.
99
List 2 advantages of intranasal drug administration.
1) low level of enzymes
| 2) large surface area
100
List 2 advantages of inhalation drug administration.
1) large surface area
| 2) extensive blood supply
101
List 3 disadvantages of inhalation drug administration.
1) risk of alveoli toxicity
2) mainly restricted to volatile drugs
3) inefficient —> only 5% delivered to small airways
102
Define distribution (pharmacokinetics).
Reversible transfer of drugs between general circulation and tissues.
103
List 2 ways drugs can bind to plasma or tissue proteins.
1) reversibly
| 2) irreversibly
104
What plasma protein do drugs most commonly reversibly bind to?
Albumin.
105
Describe drugs reversibly binding to proteins. (3)
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
What is a drug binding irreversibly to a protein equivalent to?
Elimination.
107
List 4 features of the blood brain barrier that limit drug distribution to the brain.
1) tight junctions
2) small pore sizes
3) small pore number
4) efflux transporters
108
What feature must drugs possess to pass through the blood brain barrier?
Lipid soluble.
109
List 3 considerations when prescribing a pregnant mother.
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
What occurs during drug metabolism and why?
Drug is converted to a less biologically active water soluble product.
To stop the drugs effects and remove the drug via urine.
111
What occurs in phase 1 drug metabolism
Drug is made more polar by unmasking or adding polar functional groups, e.g. -OH.
112
What occurs in phase 2 drug metabolism?
Drug is covalently bonded to an endogenous substrate to render it less active - conjugation.
113
List 3 states of drug excretion.
1) fluid - urine, bile, sweat, tears
2) solid - faeces
3) gas - air
114
List 3 factors affecting drug urine excretion.
1) glomerular filtration
2) tubular secretion
3) reabsorption
total excretion = glomerular filtration + tubular secretion - reabsorption
115
Define zero order kinetics.
Change in drug concentration per time is a fixed amount.
116
What are zero order kinetic systems independent of?
Drug concentration.
117
When does zero order kinetics take place?
Enzyme system that removes the drug is saturated.
118
Define first order kinetics.
Change in concentration per time is proportional to the concentration.
119
Define bioavailability.
F.
| Proportion of administered drug that reaches systemic circulation unaltered.
120
What route of drug administration has F=1?
IV.
121
List 2 reasons why oral drug administration has F<1.
1) first pass metabolism
| 2) incomplete absorption
122
Formula of bioavailability.
F = AUC Oral ÷ AUC IV
123
Define dose.
D.
| Quantity of drug administered.
124
Define plasma concentration.
C.
| Concentration of drug in blood.
125
What affects water soluble drugs rate of distribution?
Rate of passage across membranes.
126
What affects lipid soluble drugs rate of distribution?
Blood flow to tissues.
127
Define apparent volume of distribution.
Vd.
Theoretical volume necessary to contain total amount of administered drug at the same concentration observed in blood plasma.
128
Formula of apparent volume of distribution.
Vd = D ÷ C
129
What does a low Vd suggest?
Drug is confined to circulation.
130
What does a high Vd suggest?
Drugs has distributed to total body water.
131
Define clearance.
CL.
| Volume of plasma completely cleared of drug per unit time.
132
List 5 factors that affect clearance.
1) renal clearance
2) hepatic clearance
3) respiratory clearance
4) faecal clearance
5) salivary clearance
133
Formula for CL.
CL = D x F ÷ AUC
134
Define half-life.
T1/2.
| Time taken for plasma drug concentration to halve.
135
Define elimination rate constant.
K.
| Rate drug is removed from the body.
136
Formula relating T1/2 and K.
ln2 = T1/2 x K
137
Formula relating Vd, CL and K.
CL = K x Vd
138
Define steady state.
Css.
| Equilibrium between drug administration and elimination.
139
How long does an IV infusion take to reach 95% of steady state?
Approx 4-5 half-lives.
140
List 2 features that increase time to reach steady state.
1) slow elimination
| 2) high apparent volume of distribution
141
What is true when steady state is reached in an IV infusion?
Rate of elimination equal rate of infusion.
142
Formula relating CL, Css and K.
K = CL x Css
143
Formula relating Css, F, D, CL and t. When does this formula apply?
Css = (F x D) ÷ (CL x t)
Oral drug administration.
144
Define loading dose.
High initial dose that loads the system, shortening time to steady state.
145
When is a loading dose administered?
If a drug has a long half-life.
146
Formula relating Vd, CL and T1/2.
T1/2 = ln2 x Vd ÷ CL
147
Define dependence.
Physical and physiological condition where the body has adapted to the presence of a drug.
148
List 2 naturally occurring opioids.
1) morphine
| 2) codeine
149
List 3 chemically modified opioids.
1) diamorphine
2) oxcycodone
3) dihydrocodeine
150
List 4 synthetic opioids.
1) pethidine
2) fentanyl
3) alfentanil
4) remifentanil
151
List 3 ways in which opioids work.
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
Why do opioids have side effects.
Opioid receptors exist outside the pain system.
153
List 7 opioid side effects.
1) respiratory depression
2) sedation
3) nausea and vomiting
4) constipation
5) itching
6) immune suppression
7) endocrine effects
154
How could you avoid opioid side effects?
Epidural drug administration.
155
What is CYP2D6?
Cytochrome enzymes found in the liver important in xenobiotic metabolism.
156
List 4 opioids metabolised by CYP2D6.
1) codiene
2) oxycodone
3) hydrocodone
4) tramadol
157
Describe CYP2D6 activity in the Caucasian population. (4)
1) normal activity - 70-75%
2) under activity - 10-15%
3) absent - 10%
4) over activity - 5%
158
What is the side effect of an overactive CYP2D6 enzyme?
Increased risk of respiratory depression.
159
What is the side effect of an under active/absent CYP2D6?
Reduced or absent effect of codeine, tramadol, oxycodone and hydrocodone.
160
Name an opioid antagonist.
Naloxone.
161
What is tramadol metabolised into?
O-desmethyl tramadol.
162
What is the secondary analgesic effect of tramadol?
Serotonin and noradrenaline reputable inhibitor.
163
What percentage of orally administered morphine is metabolised by first pass metabolism?
50%.
164
How long does a single dose of morphine last?
3-4 hours.
165
How is morphine-6-glucuronide excreted.
Renal excretion.
166
What does morphine administered to a patient with renal failure cause?
Respiratory depression.
167
List 2 features of diamorphine in relation to morphine.
1) more potent
| 2) faster acting - crosses BBB faster
168
What is the relative potency of morphine and diamorphine?
1) morphine - 10mg
| 2) diamorphine - 5mg
169
What is diamorphine also known as?
Heroin
170
What is morphine metabolised into?
Morphine-6-glucuronide.
171
List 6 general uses of cholinergic and adrenergic pharmacology.
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
What output from the central nervous system isn’t conveyed by the autonomic nervous system?
Skeletal muscle control.
173
What is the general function of the parasympathetic nervous system?
Rest and digest.
174
What is the parasympathetic outflow?
CN III, CN VII, CN IX, CN X and S2-S4.
175
List 3 features of parasympathetic post-synaptic nerve fibres.
1) short post-synaptic nerve fibres
2) post-synaptic nerve fibres release ACh
3) act on muscarinic receptors
176
What is the general function of the sympathetic nervous system?
Fight or flight.
177
What is the sympathetic nervous system outflow?
T1 - L2/3.
178
List 3 features of sympathetic post-synaptic nerve fibres.
1) long post-synaptic nerve fibres
2) post-synaptic nerve fibres release NA
3) act on adrenergic receptors
179
List 3 ‘organs’ with opposing dual parasympathetic and sympathetic innervation.
1) heart
2) bladder
3) gastrointestinal tract
180
List 2 ‘organs’ with only sympathetic innervation.
1) blood vessels
| 2) sweat glands
181
What ‘organ’ only has parasympathetic innervation?
Bronchial smooth muscle.
182
What is unique about sympathetic innervation of sweat glands?
Post-synaptic nerve fibres release ACh to stimulate muscarinic receptors.
183
What are NANCs?
Non-adrenergic, non-cholinergic transmitters.
184
List 2 parasympathetic NANCs.
1) nitric oxide
| 2) vasoactive intestinal peptide
185
List 2 sympathetic NANCs.
1) ATP
| 2) neuropeptide Y
186
What type of receptor are muscarinic receptors.
GPCR.
187
List the 5 subtypes of muscarinic receptors.
1) M1
2) M2
3) M3
4) M4
5) M5
188
Where are M1 receptors generally found? (2)
1) brain
| 2) exocrine glands
189
Where are M2 receptors generally found?
Heart.
190
Where are M3 receptors generally found? (3)
1) vascular smooth muscle
2) airway smooth muscle
3) exocrine glands
191
Where are M4 receptors generally found?
Brain.
192
Where are M5 receptors generally found?
Brain.
193
What is pilocarpine? (2)
Muscarinic agonist:
1) stimulates salivation
2) contracts iris smooth muscle
194
List 6 conditions muscarinic antagonists treat.
1) bradycardia
2) hypotension
3) bronchoconstriction
4) dry secretions
5) overactive bladder
6) intestinal and colonic spasm (IBS)
195
What muscarinic antagonistics prevent bronchoconstriction?
M3 receptor antagonists (SAMA and LAMA).
196
Describe ACh pharmacology’s effect on memory. (2)
1) anticholinergics - worsen memory
| 2) acetylcholinesterase inhibitors - dementia treatment
197
List 4 pharmacological uses of ACh outside of the autonomic nervous system.
1) anti-emetic
2) cosmetic and anti-spasmodic
3) inhibit muscle activity and induce muscle relaxation - for surgery
4) myasthenia gravis
198
Describe cosmetic and anti-spasmodic uses of ACh.
Botulinum toxin (Botox) prevents ACh release - muscle relaxant.
199
Describe ACh role in treatment of myasthenia gravis. (3)
1) autoimmune destruction of nicotine ACh receptors
2) anti-acetylcholinesterases given
3) increases acetylcholine available for signalling
200
List 6 anti-cholinergic side effects.
1) worsen memory
2) confusion
3) constipation
4) dry mouth
5) blurry vision
6) glaucoma
201
List 4 cholinergic side effects.
1) muscle paralysis
2) twitching
3) salivation
4) confusion
202
What is the catecholamine pathway?
DA —> NA —> A.
203
List 5 the subtypes of adrenergic receptors.
1) α1
2) α2
3) β1
4) β2
5) β3
204
What type of receptor are adrenergic receptors?
GCPR.
205
List 3 features that determine the outcome of adrenergic signalling.
1) receptor
2) cell
3) G protein
206
Define chronotropic effects.
Effects that change heart rate.
| Chrono - time.
207
Define ionotropic effects.
Effects that change force of muscle contractions.
| Ionos - fibre.
208
What is the agonist of α1 adrenergic receptors?
NA>A.
209
What is the agonist of α2 adrenergic receptors?
A=NA
210
What is the agonist of β1 adrenergic receptors?
A=NA
211
What is the agonist of β2 adrenergic receptors?
A>>NA.
212
What is the agonist of β3 adrenergic receptors?
NA>A.
213
What is the action of α1 adrenergic receptors?
Smooth muscle contraction.
214
What is the action of α2 adrenergic receptors?
Smooth muscle contraction/relaxation.
215
What is the action of β1 adrenergic receptors?
Chronotropic and ionotropic effects on the heart.
216
What is the action of β2 adrenergic receptors?
Smooth muscle relaxation.
217
What is the action of β3 adrenergic receptors? (2)
1) relaxes detrusor muscle (bladder)
| 2) enhances lipolysis
218
List 2 functions of α1 agonists.
1) raise blood pressure
| 2) vasoconstriction
219
What is the function of α2 agonists?
Lowers blood pressure.
220
What is the function of α1 blockers?
Lowers blood pressure.
221
What is the function of α2 blockers?
No useful α2 blockers.
222
What is the function of β1 agonists?
Increase heart rate.
223
List 2 functions of β2 agonists.
1) bronchodilation - asthma
| 2) delay onset of premature labour
224
What is the function of β3 agonists?
Reduce over-active bladder symptoms.
226
List 6 conditions treated by β blockers.
1) hypertension
2) arrhythmia
3) angina
4) MI prevention
5) heart failure
6) anxiety
227
List 6 side effects of β blockers.
1) bradycardia
2) cardiac depression
3) bronchoconstriction
4) hypoglycaemia
5) tiredness
6) cold extremities
229
List 4 side effects of β agonists.
1) tachycardia
2) arrhythmia
3) affect glucose metabolism in liver
4) affect carbohydrate and lipid metabolism (β1 and β3 only)
230
Define adverse drug reactions.
Unwanted or harmful reaction following administration of a drug.
231
List 4 statistics related to adverse drug reactions.
1) 5% of hospital admissions
2) 10-20% of hospital inpatients
3) 5th most common cause of hospital death
4) 60% preventable
232
List 6 types of adverse drug reactions in the Rawlins Thompson classification.
1) type A
2) type B
3) type C
4) type D
5) type E
6) type F
233
Define type A adverse drug reactions. (3)
Augmented reactions.
1) predictable
2) dose dependant
3) common
234
Define type B adverse drug reactions. (2)
Bizarre reactions.
1) not predictable
2) not dose dependant
235
Define type C adverse drug reactions.
Chronic reactions, e.g. steroids and osteoporosis
236
Define type D adverse drug reactions.
Delayed reactions. Malignancies after immunosuppression.
237
Define type E adverse drug reactions.
End of treatment reactions. Abrupt drug withdrawal.
238
Define type F adverse drug reactions.
Failure of therapy reactions.
239
List 3 factors of DoTS classification.
1) dose
2) timing
3) susceptibility
240
List 8 risk factors for adverse drug reactions.
1) genetic predisposition
2) allergies
3) female gender
4) elderly
5) neonate
6) polypharmacy
7) adherence problems
8) hepatic/renal impairment
241
List 7 causes of adverse drug reactions.
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
List 4 times you would suspect an adverse drug reaction.
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
List 6 types of drugs that commonly cause adverse drug reactions.
1) antibiotics
2) antineoplastics
3) NSAIDs
4) cardiovascular drugs
5) hypoglycaemic drugs
6) CNS drugs
244
List 6 common adverse drug reactions.
1) confusion
2) nausea
3) balance problems
4) diarrhoea
5) constipation
6) hypotension
245
List 7 reasons why adverse drug reporting is low.
1) ignorance
2) diffidence
3) fear
4) lethargy
5) guilt
6) ambition
7) complacency
246
Define gene therapy.
Treatment of disorder by altering patients genes.
247
List 3 gene therapy approaches.
1) replacing mutated gene with health gene
2) inactivating mutated gene
3) introducing new gene to fight disease
248
What is the nomenclature for therapeutic monoclonal antibodies? (4)
1) -omab - murine
2) -ximab - chimeric
3) -zumab - humanised
4) -umab - human
