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Pharm 2A > Drugs Masterlist > Flashcards

Drugs Masterlist Flashcards

1
Q

What are MAOIs and how do they work

A

monoamine oxidase inhibitors - prevent the metabolism of common neurotransmitters (dopamine -> noradrenaline)

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2
Q

What is an example of a MAOI

A

iproniazid

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3
Q

What are TCAs and how do they work

A

Tricyclic antidepressants - block neurotransmitter uptake in the synapse (in particular noradrenaline and serotonin)

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4
Q

What is an example of a TCA

A

imipramine

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5
Q

How well does fluoxetine get into the brain

A

almost completely absorbed by oral administration and readily crosses the BBB

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6
Q

What is fluoxetine metabolised into

A

norfluoxetine (an active SSRI)

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7
Q

How was fluoxetine efficacy tested

A

Forced swim test

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8
Q

What did human clinical trials for fluoxetine show

A

more than 50% of clinical studies failed to show elevated 5-HT level - suggests that the mechanism of action for Fluoxetine cannot be attributed to an increase in 5-HT alone

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9
Q

What condition is CPPene developed for

A

Epilepsy and stroke

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10
Q

What receptor does CPPene act on

A

NMDA antagonist

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11
Q

How was selectivity of CPPene determined

A

22Na+ efflux assay - CPPene blocked the response of NMDARs but not of AMPARs or Kainate receptors

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12
Q

What type of antagonist is CPPene

A

competitive - could be overcome by large concentrations of NMDA agonist

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13
Q

How was the type of antagonism exhibited by CPPene determined

A

Rat cortical wedge preparations

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14
Q

What toxin induces excitotoxicity through activation of NMDA receptors

A

quinolinic acid (QUIN)

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15
Q

Why did CPPene fail in human clinical trials

A

Inhibition of normal NMDAR function
Patients were more sensitive to the side effects than healthy volunteers
NMDARs are not the only receptors involved in neuronal cell death

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16
Q

What drug affects ACh reuptake

A

hemicholinium

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17
Q

What drug affect ACh release into the synapse

A

botulinum toxin
tetanus toxin

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18
Q

What are non-depolarising blockers

A

competitive antagonists which act post-synaptically to inhibit neuromuscular transmission

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19
Q

What are some non-depolarising blockers

A

alpha-bungarotoxin
tubocurarine
gallamine

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20
Q

What is the onset and duration of action of tubocurarine

A

slow onset (>5min) and long duration of action (1-2h)

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21
Q

What are some adverse effects of tubocurarine

A

hypotension, bronchoconstriction

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22
Q

What are depolarising blockers

A

agonists which act post-synaptically

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23
Q

What is an example of a depolarising blocker

A

suxamethonium

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24
Q

How long is the onset of action for suxamethonium

A

fast (1-2min)

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25
Q

How long is the duration of action of suxamethonium

A

about 10min

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26
Q

How is suxamethonium cleared

A

hydrolysed by plasma cholinesterases

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27
Q

How is tubocurarine cleared

A

reversible by anticholinesterase drugs

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28
Q

What is the key difference between non-depolarising and depolarising blockers

A

depolarising blockers produce initial fasciculations and often postoperative pain

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29
Q

Are anticholinesterases depolarising or non-depolarising blockers

A

depolarising blockers

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30
Q

What drug is used in the diagnosis of myasthenia gravis

A

edrophonium

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31
Q

What drugs are used in the reversal of non-depolarising blocks

A

neostigmine

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32
Q

What drugs are used in the treatment of myasthenia gravis

A

pyridostigmine
physostigmine

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33
Q

What are some organophosphate compounds which act as anticholinesterases

A

insecticides (e.g. malathion), nerve gases (e.g. dysflos)

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34
Q

What are some effects of anticholinesterase intoxication on the NMJ

A

convulsions, followed by flaccid paralysis

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35
Q

How is anticholinesterase intoxication at the NMJ treated

A

cholinesterase reactivation - pralidoxime

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36
Q

How do benzodiazepines bind to GABAA receptors

A

at the alpha-gamma interface

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37
Q

What condition is L-DOPA used in

A

Parkinson’s Disease

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38
Q

What does L-DOPA target

A

target synthesis

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39
Q

What condition is reserpine used in

A

hypertension - disruption of noradrenaline vesicular storage

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40
Q

What condition is amphetamine used in

A

ADHD

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41
Q

How does amphetamine work

A

re-uptake inhibitor

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42
Q

What receptors does mirtazapine work on

A

alpha2-adrenoceptor antagonist and 5-HT antagonist

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43
Q

What is mirtazapine

A

antidepressant

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44
Q

What condition is atomoxetine used in

A

ADHD

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45
Q

What is clonidine used for

A

antihypertensive, epidural anaesthetic

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46
Q

What receptor does clonidine act on

A

alpha2-adrenoceptor

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47
Q

How does L-DOPA work

A

bypasses rate limiting synthetic enzyme -> more dopamine produced

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48
Q

What is haloperidol

A

antipsychotic

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49
Q

What receptor does haloperidol act on

A

D2-receptor antagonist

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50
Q

What condition does amantadine treat and how does it work

A

Parkinson’s Disease - DA releasing agent

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51
Q

How does bupropion work

A

DA/NA re-uptake inhibitor

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52
Q

What receptor does aripiprazole act on

A

D2 partial agonist

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53
Q

What is risperidone

A

atypical antipsychotic

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54
Q

what receptors does risperidone act on

A

5-HT2 and D2 antagonist

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55
Q

What receptor does buspirone

A

5-HT1A partial agonist

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56
Q

What is scopolamine

A

muscarinic antagonist (amnesic)

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57
Q

What is morphine

A

selective (partial) agonist for mu receptors

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58
Q

What is naloxone

A

mu, delta and kappa antagonist - antidote to opiate overdose

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59
Q

What is pentazocine

A

mu antagonist and kappa agonist

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60
Q

What are some opioid drugs

A

morphine
heroin
codeine
oxycodone
methadone
fentanyl

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61
Q

What opioid drug is used in anaesthesia

A

fentanyl

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62
Q

What makes benzocaine different to other local anaesthetics

A

no use-dependence
ester group, no amine group (0% ionised)
works via hydrophobic pathways only

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63
Q

What makes QX-314 different from other local anaesthetics

A

100% ionised
blocks Na channels only if introduced into cells (experimental tool)

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64
Q

What is lidocaine

A

local anaesthetic

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65
Q

What is the half life of lidocaine

A

2h

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66
Q

How is lidocaine metabolised

A

metabolised in the liver by N-dealkylation

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67
Q

How long is the onset and duration of action of lidocaine

A

rapid onset (5-10min), moderate duration of action

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68
Q

What are the atypical local anaesthetics

A

benzocaine and QX-314

69
Q

How are ester-linked local anaesthetics metabolised

A

metabolised by plasma esterases

70
Q

How are amide-linked local anaesthetics metabolised

A

metabolised in the liver

71
Q

How do vasodilator properties of local anaesthetic affect their pharmacokinetics

A

leads to more rapid vascular uptake and shorter duration of activity

72
Q

How can vasodilator properties of local anaesthetics be overcome

A

give a vasoconstrictor to prolong anaesthesia (usually adrenaline)

73
Q

What are adverse effects of local anaesthetics

A

respiratory depression
decreased blood pressure
hypersensitivity reactions
toxic metabolites produced from pilocarpine, articaine, benzocaine

74
Q

What are the ways of general anaesthetic drug administration

A

inhalation, injection

75
Q

What general anaesthetics are administered by inhalation

A

nitrous oxide
halogenated ethers

76
Q

What general anaesthetics are administered by injection

A

propofol
thiopental
ketamine

77
Q

What are the pharmacokinetics of propofol (induction, distribution, metabolism)

A

rapid

78
Q

What is propofol used for

A

maintaining anaesthesia

79
Q

What receptors does propofol act on

A

GABAA and Glycine receptor potentiation

80
Q

What are adverse effects of propofol

A

can cause burning pain at injection site
cardiovascular depressant

81
Q

What is thiopental

A

A bartbiturate (GABAA receptor potentiator)

82
Q

What are the pharmacokinetics of thiopental

A

rapid induction, rapid recovery from single dose and high lipid solubility (rapid distribution)

83
Q

What are adverse effects of thiopental

A

may depress respiratory centres of brain

84
Q

How long does it take for thiopental to clear

A

‘Hangover effect’ - drug remains in body for prolonged time

85
Q

What is an example of a dissociative anaesthetic

A

ketamine

86
Q

What are advantages of dissociative anaesthetics

A

high therapeutic index
no cardiovascular or respiratory depression
analgesic

87
Q

What are disadvantages of dissociative anaesthetics

A

psychic disturbances
involuntary movements

88
Q

What are advantages of injectable anaesthetics

A

easy to administer
rapid induction

89
Q

What are disadvantages of injectable anaesthetics

A

complex pharmacokinetics
slow elimination
side effects

90
Q

What is minimum alveolar concentration (MAC)

A

a measure of potency - alveolar concentration giving surgical anaesthesia in 50% of patients

91
Q

How is blood solubility related to induction speed

A

lower blood solubility -> faster induction

92
Q

Are nitrous oxides sedative or anaesthetic

A

sedative - they are unable to give surgical anaesthesia on their own

93
Q

What is nitrous oxides given with to become a good analgesic

A

O2 (entonox)

94
Q

What receptors to nitrous oxides act on

A

NMDA antagonist, potassium channel activator

95
Q

What are some halogenated ethers

A

desflurane, isoflurane, sevoflurane, enflurane

96
Q

What receptors do halogenated ethers act on

A

GABAA receptor potentiator, glycine receptor potentiator, potassium channel activator

97
Q

What are advantages of inhalation anaesthetics

A

quick introduction
rapid recovery
easily change depth of anaesthesia

98
Q

What are disadvantages of inhalation anaesthetics

A

need specialist equipment to administer

99
Q

What are the drug combinations for general anaesthesia

A

premedication
rapid induction
maintenance of anaesthesia
analgesic supplement
muscle relaxant
muscarinic antagonist
antiemetic

100
Q

What premedications are given in general anaesthetics

A

sedatives

101
Q

What rapid induction drugs are given in general anaesthetics

A

propofol
thiopental

102
Q

What drugs are given for maintenance of general anaesthesia

A

desflurane

103
Q

What analgesic supplements are given in general anaesthetics

A

opiate

104
Q

What muscle relaxants are given in general anaesthetics

A

NMJ blocking agent e.g. atracurium

105
Q

What antiemetics are given in general anaesthesia

A

ondasetron

106
Q

What is the mechanism of action of NSAIDS

A

competitively inhibit cyclooxygenase, inhibiting production of prostaglandins

107
Q

What are some examples of NSAIDS

A

ibuprofen, aspirin, naproxen, diclofenac, celecoxib

108
Q

What are side effects of NSAIDS

A

GI disturbances: abdominal pain, diarrhoea, damage to stomach lining, ulcers

109
Q

Is paracetamol a NSAID

A

no - no anti-inflammatory action and no GI disturbances

110
Q

What is paracetamol

A

weak cyclooxygenase inhibitor

111
Q

How does paracetamol reduce pain

A

metabolites activate TRPA1 receptor -> reduces voltage-gated sodium and calcium channels -> reduces action potential firing

112
Q

What is ziconotide

A

N-type calcium channel inhibitor - a synthetic derivative of snail toxin w-conotoxin MVIIA (from Conus Magnus)

113
Q

How is ziconotide administered

A

intrathecal pump (large molecule - not orally active)

114
Q

What are examples of endogenous cannabinoids

A

anandamine and 2-AG

115
Q

What receptor does bradykinin act on

A

B2 receptor -> stimulates prostaglandin synthesis

116
Q

What drug is licensed to treat ALS

A

Riluzole

117
Q

What is the mechanism of action of Riluzole

A

Activates potassium channels and blocks VG Na+ channels
Inhibits glutamate release and may inhibit non-NMDA glutamate receptors
Enhances activity of GLT1

118
Q

What are drugs which potentiate GABA action at GABAA receptors

A

benzodiazepines
valproate
phenobarbitone
felbamate

119
Q

What are drugs which inhibit GABA-transaminase

A

vigabatrin

120
Q

What are drugs which inhibit SSA dehydrogenase

A

valproate

121
Q

What are drugs which inhibit GABA transporter

A

tiagabine

122
Q

What are some uses of benzodiazepines

A

emergency/rescue medication
acute/short-term medication
adjunctive therapy

123
Q

When are benzodiazepines used as emergency medication

A

tonic-clonic seizures lasting >5mins

124
Q

What are examples of benzodiazepines used in emergency medications

A

diazepam, midazolam (paediatric)

125
Q

What is acute/short-term medication in epilepsy

A

reducing the effects of a cycle of seizures

126
Q

What are examples of benzodiazepines used as acute/short-term medication

A

clonazepam, clobazam

127
Q

When is adjunctive therapy used in epilepsy

A

Adjunctive therapy is the principal mode of drug treatment for refactory epilepsy

128
Q

What drugs are used in adjunctive therapy in epilepsy

A

clonazepam, clobazam

129
Q

What AMPAR antagonist is licensed for epilepsy

A

perampanel - negative allosteric modulator (licensed for the treatment of partial seizures)

130
Q

What NMDA receptor antagonist is used to treat epilepsy

A

felbamate (is also a GABAA receptor potentiator)

131
Q

How is glutamate release reduced

A

metabotropic glutamate receptor agonists

132
Q

What are examples of drugs used to block voltage-gated sodium channels in epilepsy

A

carbamazepine, valproate, phenytoin, lamotrigine

133
Q

How does gabapentin and pregabalin work

A

bind to alpha2-delta (P/Q) subunit and prevents trafficking to plasma membrane

134
Q

How does levetiracetam work

A

binds to the synaptic vesicle glycoprotein SV2A
also inhibits presynaptic VGCC -> reduction in transmitter release

135
Q

How does retigabine work

A

activates K+ channels -> hyperpolarises neurons -> reduces seizure activity
licensed for partial seizures

136
Q

How does valproate work

A

increases brain GABA concentration
- potentiates GABAA receptors
- inhibits Na+ channels
- inhibits T-type Ca2+ channels

137
Q

What is topiramate

A

a broad spectrum convulsant

138
Q

What is Epidyolex licensed to treat

A

Dravet syndrome and Lennox-Gastaut Syndrome

139
Q

How does epidyolex work

A

Potentiator of GABAA receptor activity
Antagonism of G-protein-coupled receptor 55 (GPR55)
Activation of TRPV1 channels
Inhibition of the equilibrium nucleoside transporter (ENT-1)

140
Q

How are biologics used in epilepsy therapy

A

mAbs disrupt signalling pathways
Anti-HMGB1 shown to prevent/reduce status epilepticus and epileptogenesis

141
Q

What are some cholinesterase inhibitors used in treating Alzheimer’s disease

A

donepezil
galantamine
rivastigmine

142
Q

What are some partial NMDA antagonists used in treating Alzheimer’s Disease

A

memantine

143
Q

How does memantine work in Alzheimer’s Disease

A

Low affinity uncompetitive NMDA receptor antagonist - enhances depolarisation-mediated glutamate release; inhibits glial glutamate uptake

144
Q

What is tarenflurbil

A

gamma-secretase modulator - favours the production of smaller less toxic beta-amyloid fragments (over beta-amyloid42)

145
Q

What is aducanumab

A

a high-affinity, fully human lgG1 monoclonal antibody against a conformational epitope found on beta-amyloid

146
Q

How does Lithium help treat Alzheimer’s

A

inhibitor of GSK-3b (one of the key enzymes which hyperphosphorylates tau)

147
Q

What is an example of a microtubule modifier used in Alzheimer’s Disease treatment

A

paclitaxel - chemical stabiliser of microtubules to compensate for the loss of function

148
Q

What is an example of a tau aggregation inhibitors

A

Rember (TauRx)

149
Q

How does TauRx work

A

Inhibits the formation of Tau oligomers and their conversion to paired helical filaments, also can dissolve tau aggregates in vitro

150
Q

What are some examples of monoclonal Antibodies against amyloid-beta

A

aducanumab, lecanamab, donanemab

151
Q

What is lecanamab

A

humanised lgG1 version of mouse monoclonal antibody (mAb158) against beta-amyloid protofibrils (which are soluble)
acts to stop formation/growth of plaques or breaks them down

152
Q

What is donanemab

A

humanised lgG1 mAb development based on targeting plaques specifically
- amyloid plaques reduced to sub-clinical levels

153
Q

What are the drug classes used in treating Parkinson’s Disease

A

dopaminergic agents
catechol-o-methyl transferase (COMT)
monoamine oxidase-B (MAO-B) inhibitors
anticholinergics
amantadine
memantine

154
Q

What are some dopaminergic agents used in the treatment of Parkinson’s Disease

A

L-DOPA
bromocriptine
pergolide
pramipexole
ropinirole

155
Q

how is levodopa transported across the gut-blood and BBB

A

Large neutral amino acid; requires active transport

156
Q

How does L-DOPA work

A

L-DOPA is a precursor which is metabolised by DOPA decarboxylase into dopamine

157
Q

Why does L-DOPA cause dyskinesias

A

result of excessive dopaminergic simulation

158
Q

What are advantages of direct dopamine receptor agonists

A

no metabolic conversion; bypasses nigrostriatal neurons
longer half-life than L-DOPA
monotherapy or adjunct therapy
may delay or reduce motor fluctuations and dyskinesias associated with L-DOPA
may be neuroprotective

159
Q

What are adverse side effects of direct dopamine receptor agonists

A

nausea, vomiting - activation of peripheral dopamine receptors
dizziness, postural hypotension
headache
drowsiness and somnolence
dyskinesias
confusion, hallucinations, paranoia
pulmonary and retroperitoneal fibrosis; pleural effusion and pleural thickening; Raynaud’s phenomenon

160
Q

What is selegiline

A

irreversible MAO-B inhibitor

161
Q

What are some side notes of selegiline

A

potential interactions with tricyclics and SSRI antidepressants
low tyramine diet necessary

162
Q

What are anticholinergics used for in the treatment of Parkinson’s Disease

A

effective mainly for tremor and to lesser degree, rigidity

163
Q

What are the side effects of using anticholinergics in Parkinson’s Disease

A

dry mouth, sedation, delirium, confusion, hallucinations, constipation, urinary retention

164
Q

When is amantadine used

A

Parkinson’s Disease - last resort if dyskinesias cannot be controlled

165
Q

What are the possible mechanisms of amantadine

A
  • enhancing release of stored dopamine
  • inhibiting presynaptic reuptake of catecholamines
  • dopamine receptor agonism
  • NMDA receptor blockade
166
Q

What is memantine

A

NMDA receptor antagonist

167
Q

What is memantine used for

A

used to treat cognitive defects in Alzheimer’s Disease and is beneficial for Parkinson’s related dementia

168
Q
A

Pharm 2A (10 decks)

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