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Block 12 - Neurological, Neuromuscular and Musculoskeletal Disease > Block 12 Pharmacology DONE > Flashcards

Block 12 Pharmacology DONE Flashcards

1
Q

azathioprine is an (a____)

A

antagonist

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2
Q

azathioprine antagonises

A

purine metabolism

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3
Q

azathioprine inhibits

A

purine synthesis

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4
Q

because azathioprine inhibits purine synthesis it also inhibits…

A

DNA and RNA synthesis and so cell proliferation

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5
Q

azathioprine is used to treat

A

autoimmune diseases, transplant recipients

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6
Q

azathioprine MOA (2 steps)

A
  1. incorporates thiopurine analogues into DNA structure

2. causes chain termination and cytotoxicity

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7
Q

azathioprine’s most severe side effect is

A

bone marrow suppression

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8
Q

azathioprine should not be given in conjunction with

A

purine analogues, e.g. allopurinol

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9
Q

people with the enzyme _____ are most at risk of bone marrow deficiency side effect of azathioprine

A

TPMT (thiopurine s-methyltransferase)

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10
Q

(azathioprine) genetic polymorphisms of TPMT (thiopurine s-methyltransferase) can lead to

A

excessive drug toxicity

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11
Q

to avoid excessive azathioprine drug toxicity due to genetic polymorphisms of TPMT we can do an…

A

assay of serum TPMT

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12
Q

in long-term azathioprine treatment we must do…

A

blood tests and monitoring for signs of myelosuppression

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13
Q

diclofenac class

A

NSAID, COX inhibitor

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14
Q

diclofenac has an ______ effect (2)

A

analgesic and anti-pyretic

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15
Q

diclofenac’s analgesic effect is due to

A

inhibition of COX-1 and COX-2 enzymes

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16
Q

diclofenac’s anti-pyretic effect is due to (4 steps)

A
  1. effects hypothalamus
  2. peripheral dilation
  3. increased cutaneous blood flow
  4. heat dissipation
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17
Q

diclofenac is prescribed for (3 examples)

A

pain, dysmenorrhea, ocular inflammation

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18
Q

diclofenac is the least favoured non-COX specific NSAID because it…

A

targets COX-2 more than others

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19
Q

a better choice than diclofenac if we want a non-cos specific NSAID is…

A

naproxen

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20
Q

celecoxib class

A

NSAID, COX-2 specific inhibitor

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21
Q

celecoxib inhibits

A

COX-2

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22
Q

by inhibiting COX-2 celecoxib reduces

A

production of prostaglandins

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23
Q

celecoxib MOA (1 step)

A
  1. uses its polar sulfonamide side chain to bind to hydrophilic side region close to active COX-2 binding site
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24
Q

celecoxib only targets COX-2 so does not give _______ effects

A

anti-platelet

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25
Q

as celecoxib does not give anti-platelet effects it is not a substitute for…

A

aspirin for cardiovascular prophylaxis

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26
Q

celecoxib’s inhibition of prostaglandin synthesis can cause…. due to….

A

sodium and water retention in ascending loop of henle due to increased fluid reabsorption

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27
Q

in collecting duct, PGE2 (prostaglandin) inhibits..

A

water reabsorption by counteracting antidiuretic hormone

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28
Q

celecoxib is used to treat (3)

A

rheumatoid arthritis, osteoarthritis, familial adenomatous polyposis (FAP)

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29
Q

celecoxib is used sparingly due to it’s possible effects on the…

A

cardiovascular system

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30
Q

cyclophosphamide class

A

alkylating agent

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31
Q

cyclophosphamide is an _________ and ________ agent

A

antineoplastic, antiimmunosuppressive

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32
Q

cyclophosphamide is activated by the

A

cytochrome P450 isoforms (CYP2A6, 2B6, 3A4, 3A5, 2C9, 2C18, 2C19) in the liver

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33
Q

cyclophosphamide is used to treat (3)

A

multiple cancers including myelomas and leukaemias

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34
Q

cyclophosphamide has 3 MOAs, give them (3)

A
  • attaches alkyl group to DNA bases, so DNA is fragmented by repair enzymes, stopping DNA synthesis and RNA transcription
  • cross-linking of DNA to prevent DNA transcription
  • induction of DNA mispairing leading to mutations
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35
Q

alkylating agents are not specific to a certain part of the….

A

cell cycle so induce cell death

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36
Q

vitamin d class

A

coenzyme

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37
Q

vitamin d itself has little

A

biological activity

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38
Q

vitamin d is metabolised to

A

1,25-dihydroxycholecalciferol

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39
Q

1,25-dihydroxycholecalciferol is

A

hormonally active

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40
Q

vitamin d to 1,25-dihydroxycholecalciferol is 2 steps, the first step is in the

A

liver

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41
Q

the first step of vitamin d to 1,25-dihydroxycholecalciferol (in the liver) is…

A

cholecalciferal is hydroxylated to 25-hydroxycholecalciferol by 25-hydroxylase

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42
Q

vitamin d to 1,25-dihydroxycholecalciferol is 2 steps, the second step is in the

A

kidney

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43
Q

the second step of vitamin d to 1,25-dihydroxycholecalciferol( in the kidney) is…

A

25-hydroxycholecalciferol is metabolised to 1,25-dihydroxycholecalciferol,
due to action of 1-hydroxylase

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44
Q

25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol are

A

hydrophobic

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45
Q

as 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol are hydrophobic, they are transported in the blood bound to

A

vitamin-D binding protein

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46
Q

25-hydroxycholecalciferol half life

A

several weeks

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47
Q

1,25-dihydroxycholecalciferol half life

A

few hours

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48
Q

1,25- dihydroxycholecalciferol has a much ______ ______ for the vitamin D receptor than 25- hydroxycholecalciferol.

A

higher affinity

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49
Q

ciclosporin class

A

immunosuppressant, cyclophilin binder

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50
Q

ciclosporin use

A

prophylaxis of graft rejection in organ and tissue transplantation

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51
Q

ciclosporin MOA (4 steps)

A
  1. binds to cyclophilin
  2. inhibits calcineurin
  3. stops transcription of IL-2
  4. reversible inhibits immunocompetent lymphocytes in G0 or G1 phase of cell cycle
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52
Q

ciclosporin preferentially inhibits…

A

T-lymphocytes, T-1 helper and T1-suppressor

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53
Q

ciclosporin’s main target is

A

T1-helper lymphocyte

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54
Q

aurothiomalate class

A

gold based anti-inflammatory, cytokine inhibitor

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55
Q

MOA of sodium aurothiomalate

A

unknown, free thiols play a role

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56
Q

aurothiomalate is given as an

A

IM injection

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57
Q

aurothiomalate benefit is not expected till…

A

300-500mg given

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58
Q

important to avoid ______ _____ of aurothiomalate as….

A

complete relapse, as second gold course not effective

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59
Q

aurothiomalate is not

A

widely used

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60
Q

aurothiomalate has been superceded by

A

other DMARDs

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61
Q

chloroquine class

A

anti-inflammatory, DNA/RNA synthesis inhibitor

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62
Q

chloroquine is more widely known as an

A

anti-malarial

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63
Q

chloroquine MOA for malaria (2 steps)

A
  1. inhibit parasitic enzyme heme polymerase

2. toxic build up of heme in parasite

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64
Q

chloroquine MOA for rheumatoid arthritis

A

unknown, reduces levels of inflammatory agents (IL-6, IL-1b, TNF-alpha) by blocking release or reducing transcription

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65
Q

methotrexate class

A

folate antagonist, anti-metabolite

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66
Q

anti-metabolites are…

A

synthetic versions of purine or pyrimidines

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67
Q

purines/pyrimidines are the

A

building blocks of DNA

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68
Q

anti-metabolites prevent purines or pyrimidines becoming incorporated into DNA during…

A

S phase (of cell cycle)

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69
Q

methotrexate inhibits

A

folic acid reductase

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70
Q

folic acid reductase converts

A

folic acid to tetrahydrofolic acid

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71
Q

tetrahydrofolic acid is needed for

A

purine and pyrimidine synthesis

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72
Q

methotrexate MOA (4 steps)

A
  1. inhibits folic acid reductase
  2. lack of tetrahydrofolic acid
  3. purines/pyrimidines can’t be made
  4. DNA synthesis stops
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73
Q

methotrexate affects the

A

most rapidly dividing cells

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74
Q

methotrexate uses

A

low dose for RA

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75
Q

sulfasalazine class

A

immunomodulatory, anti-inflammatory

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76
Q

sulfasalazine uses

A

ulcerative colitis, RA

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77
Q

sulfasalazine MOA

A

unknown

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78
Q

sulfasalazine is broken down into

A

5-aminosalicyclic acid (5-ASA) and sulfapyridine (SP)

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79
Q

in ulcerative colitis, sulfasalazine action is mainly via

A

5-ASA

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80
Q

sulfasalazine has been replaced to an extent by

A

mesalazine

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81
Q

mesalazine is better than sulfasalazine as it has

A

same active metabolite, no sulphur, better tolerated

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82
Q

calcitonin is a

A

hormone

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83
Q

calcitonin is produced by the

A

thyroid gland

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84
Q

calcitonin is important in

A

control of calcium conc in blood

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85
Q

calcitonin _____ action of parathyroid hormone

A

antagonises

86
Q

calcitonin antagonises the action of

A

parathyroid hormone

87
Q

calcitonin MOA (7 steps)

A
  1. binds to calcitonin receptor (osteoclasts)
  2. activates cAMP and calcium signalling
  3. more production of vitamin D producing enzymes
  4. greater calcium retention
  5. more bone density
  6. more bone mass
  7. reduction in plasma calcium
88
Q

calcitonin also promotes

A

renal excretion of Ca, Na, Mg, K, phosphate ions by decreasing tubular reabsorption

89
Q

calcitonin is not

A

commonly used as treatment

90
Q

prednisolone class

A

glucocorticoid receptor agonist, corticosteroid

91
Q

prednisone is derived from

A

cortisone

92
Q

prednisone is metabolised in the (organ)

A

liver

93
Q

prednisone is metabolised in the liver to (thing)

A

active form, prednisolone

94
Q

prednisolone can cross

A

cell membrane

95
Q

prednisolone MOA (3 steps)

A
  1. binds to corticosteroid receptor
  2. changes DNA transcription
  3. reduced inflammatory proteins
96
Q

prednisolone specific example

A

reduction of phospholipase A2 reduces arachidonic acid production

97
Q

raloxifene class

A

selective estrogen receptor modulator

98
Q

raloxifene effect on bone and lipid metabolism

A

oestrogen-like (promotes)

99
Q

raloxifene effect on breast and uterine tissue

A

antagonises oestrogen (inhibits)

100
Q

raloxifene in bone (4 steps)

A
  1. binds to oestrogen receptors
  2. reduces bone resorption
  3. increases bone mineral density
  4. slows rate of bone loss
101
Q

raloxifene antagonises the effects of oestrogen on mammary and uterine tissue by (1 step)

A
  1. prevents transcription of genes with oestrogen response
102
Q

raloxifene use

A

less common as post-menopausal symptoms being treated with hormones decreases

103
Q

alendronic acid class

A

nitrogen-containing, second generation bisphosphonate

104
Q

alendronic acid used to treat

A

corticosteroid-induced osteoporosis, Paget’s disease, prevent osteoporosis in post-menopausal women

105
Q

nitrogen containing bisphosphonates inhibit

A

farnesyl pyrophosphate (FPP) synthase

106
Q

nitrogen containing bisphosphonates inhibit farnesyl pyrophosphate (FPP) synthase by acting as

A

analogues of isoprenoid diphosphate lipids

107
Q

inhibition of FPP (by nitrogen containing bisphosphonates) in osteoclasts prevents

A

post-translational farnesylation and geranylgeranylation of small GTPase signalling proteins, such as Rac and Rho

108
Q

alendronic acid basically ruins

A

osteoclast activity, reducing bone resorption

109
Q

in post-menopausal women alendronic acid causes

A

net gain in bone mass

110
Q

digoxin class

A

cardiac glycoside, sodium-potassium ATPas inhibitor

111
Q

digoxin uses

A

congestive heart failure, supraventricular arrhythmias, AF

112
Q

digoxin MOA (4 steps)

A
  1. inhibits Na-K-ATPase pump
  2. increase in intracellular sodium
  3. sodium-calcium exchanger (NCX) extrudes sodium and brings in calcium
  4. more Ca promotes contractile proteins, myosin and actin
113
Q

digoxin also acts on the

A

electrical activity of heart

114
Q

digoxin MOA on electrical activity of heart (4 steps)

A
  1. increases slope of phase 4 depolarisation
  2. shortens action potential duration
  3. decreases maximal diastolic potential
115
Q

digoxin is a 3rd line treatment for

A

AF

116
Q

digoxin is rarely involved in

A

heart failure

117
Q

betaxolol class

A

beta-adrenergic receptor

118
Q

betaxolol is a

A

competitive antagonist

119
Q

betaxolol competitively antagonises

A

beta-1 selective adrenergic receptor

120
Q

beta-1 blockers are mainly in the

A

heart

121
Q

beta-1 blockers bind

A

epinephrine, norepinephrine

122
Q

activation of beta-1 blockers leads to

A

G activation and cAMP signalling

123
Q

cAMP signalling results in a

A

reduction in heart rate, cardiac output, blood pressure

124
Q

betaxolol (beta-1 blockers) are routinely prescribed in patients with

A

ischaemic heart disease

125
Q

betaxolol can also competitively block (2 steps)

A
  1. release of renin (can cause vasoconstriction)

2. beta(2)-adrenergic responses in bronchial and vascular smooth muscles, causing bronchospasm

126
Q

betaxolol is less commonly used than

A

bisoprolol

127
Q

diazepam class

A

benzodiazepine, GABA receptor agonist

128
Q

benzodiazepines (diazepam) bind non-specifically to

A

benzodiazepine receptors

129
Q

benzodiazepine receptors mediate (5)

A

sleep, muscle relaxation, anticonvulsant activity, motor co-ordination, memory

130
Q

diazepam causes GABA to bind to its receptor and open the chloride channel. causing

A

hyperpolarisation preventing further cell excitation

131
Q

diazepam is still used for

A

anxiety, muscle relaxant

132
Q

propofol class

A

anaesthetic, GABA receptor modulator

133
Q

propofol is given

A

IV

134
Q

propofol used for

A

induction and maintenance of general anaesthesia

135
Q

propofol MOA (1 step)

A
  1. makes GABA bind more to GABA-A receptors
136
Q

propofol IV produces

A

hypnosis rapidly, in 40 secs

137
Q

recovery from propofol-induced anaesthesia is generally

A

rapid and has less frequent side effects than thiopental, methohexital and etomidate

138
Q

lamotrigine class

A

anti-convulsant, sodium channel inhibitor

139
Q

lamotrigine uses

A

epilepsy, bipolar disorder

140
Q

lamotrigine MOA

A

unknown, could be inhibition of Na/Ca channels, stabilises neuronal membranes, modulates release of glutamate and aspartate

141
Q

carbamazepine class

A

anti-convulsant, sodium channel inhibitor

142
Q

carbamazepine is used to control

A

grand mal, psychomotor or focal seizures

143
Q

carbamazepine MOA

A

unknown, inhibits repetitive firing by blocking Na channels

144
Q

carbamazepine pain relief MOA

A

blocks synaptic transmission in trigeminal nucleus

145
Q

response to carbamazepine is

A

variable, may be resistant due to RALBP1

146
Q

carbamazepine is less commonly used as

A

anti-epileptic

147
Q

carbamazepine is still commonly used as a

A

mood stabiliser in bipolar, trigeminal neuralgia

148
Q

phenytoin class

A

anticonvulsant, sodium channel inhibitor

149
Q

phenytoin is an anticonvulsant that lacks the _____ effect of ______

A

sedation, phenobarbital

150
Q

phenytoin MOA

A

unclear, but in motor cortex to prevent spread of seizure

151
Q

phenytoin is not used a lot as it has a lot of

A

adverse effects and interactions with other drugs

152
Q

phenytoin rarely used as chronic therapy as there are better

A

anti-epileptic drugs

153
Q

phenytoin is still first line in

A

status epilepticus

154
Q

sodium valproate class

A

anti-convulsant, sodium channel inhibitor, GABA receptor agonist

155
Q

sodium valproate is a

A

fatty acid

156
Q

sodium valproate use

A

epilepsy, mood stabiliser

157
Q

sodium valproate possible MOA (3)

A
  1. increase GABA levels by inhibiting enzymes that catabolise GABA
  2. alter properties of voltage dependent Na channels
  3. histone deacetylase inhibitor
158
Q

sodium valproate therapeutic range in epilepsy

A

50-100mcg/mL of total valproate

159
Q

donepezil class

A

reversible acetyl cholinesterase inhibitor

160
Q

donepezil is relatively specific for

A

brain acetylcholinesterase

161
Q

donepezil leads to an increase in

A

aceylcholine at cholinergic synapses, enhancing cholinergic function

162
Q

donepezil use

A

dementia, alzheimer’s

163
Q

suxamethonium class

A

depolarising nicotinic cholinergic receptor antagonist

164
Q

suxamethonium MOA (5 steps)

A
  1. mimics acetylcholine at NMJ
  2. hydrolysed slower than acetylcholine
  3. prolonged depolarisation
  4. desensitisation
  5. muscle relaxation
165
Q

suxamethonium cannot be

A

reversed

166
Q

suxamethonium recovery is

A

spontaneous

167
Q

suxamethonium use

A

after general anaesthetic as muscle relaxation can be preceded by painful muscle fasciculations

168
Q

anticholinesterases such as neostigmine given alongside suxamethonium can potentiate

A

NMJ block

169
Q

levodopa class

A

dopamine replacement therapy

170
Q

levodopa is a natural form of

A

dihydroxyphenylalanine

171
Q

levodopa is an immediate precursor of

A

dopamine

172
Q

levodopa can be taken

A

orally

173
Q

levodopa can readily cross

A

blood brain barrier

174
Q

levodopa within the brain is taken up by

A

dopaminergic neurons and converted to dopamine

175
Q

levodopa use

A

replace dopamine lost in Parkinson’s

176
Q

bromocriptine class

A

dopamine agonist

177
Q

bromocriptine mesylate is an

A

ergot alkaloid derivative

178
Q

bromocriptine stimulates

A

dopamine activity

179
Q

bromocriptine stimulates dopamine activity through the

A

D2 receptor

180
Q

bromocriptine MOA

A
  1. binds D2 receptor
  2. Gi signalling cascade
  3. inhibits adenyl cyclase
  4. reduction in cAMPL
  5. blockage of calcium release
181
Q

bromocriptine improves

A

muscle activity and coordination

182
Q

bromocriptine uses

A

Parkinson’s, hyperprolactinaemia, acromegaly, pulmonary fibrosis

183
Q

bromocriptine is less commonly used due to concerns about

A

fibrotic reactions

184
Q

in Parkinson’s, it is more common to use _____ or ______ than bromocriptine

A

pramipexole, ropinirole

185
Q

gabapentin class

A

anticonvulsant, GABA analogue

186
Q

gabapentin increases

A

synaptic conc of GABA

187
Q

gabapentin is (3)

A
  • high lipid solubility
  • not metabolised by liver
  • no protein binding
188
Q

gabapentin MOA (2)

A
  1. reduce mono-amine neurotransmitters

2. reduces axon excitability

189
Q

gabapentin use

A

epilepsy, neuropathic pain, adjunct in chronic pain

190
Q

selegiline class

A

dopamine therapy, monoamine oxidase B inhibitor

191
Q

selegiline uses

A

Parkinson’s, depression

192
Q

selegiline MOA (3 steps)

A
  1. irreversibly inhibit monoamine oxidase type B
  2. inhibits deamination of dopamine in brain
  3. enhances dopaminergic activity
193
Q

selegiline at higher doses can also inhibit

A

monoamine oxidase type A (depression treatment)

194
Q

isoflurane class

A

general anaesthetic, neuronal ion channel modulator

195
Q

isoflurane induces

A

muscle relaxation

196
Q

isoflurane reduces

A

pain sensitivity

197
Q

isoflurane MOA (5 steps)

A
  1. reduces gap junction channel opening times
  2. increases gap junction channel closing times
  3. activates calcium dependent ATPase in sarcoplasmic reticulum
  4. increases fluidity of lipid membrane
  5. binds to the GABA, glutamate, glycine receptors
198
Q

atracurium class

A

competitive cholinergic receptor antagonist, non-depolarising skeletal muscle relaxant

199
Q

atracurium MOA (3 steps)

A
  1. antagonises neurostransmitter action of acetylcholine
  2. by binding competitively with cholinergic receptors on motor end plate
  3. muscle relaxation
200
Q

repeat doses of atracurium can be administered at

A

regular intervals with predictable results

201
Q

action of atracurium is reversed by

A

acetylcholinesterase inhibitors, e.g. neostigmine, edrophonium, pyridostigmine

202
Q

repeated administration of maintenance doses of Atracurium has no cumulative effect on the duration of neuromuscular block if

A

recovery is allowed to begin prior to repeat dosing

203
Q

memantine class

A

NMDA receptor antagonist

204
Q

memantine use

A

dementia

205
Q

memantine MOA (4 steps)

A
  1. binds to NDMA receptor-operated cation channels
  2. increased glutamate in brain of dementia patients usually allows Mg2+ to bind to NDMA channels so lots of Ca2+ comes in so neuronal degeneration
  3. memantine binds better than Mg2+ so stops lots of Ca2+
  4. protects against elevated gutamata
206
Q

fentanyl class

A

opioid analgesic, opioid receptor agonist

207
Q

fentanyl interacts with

A

opioid mu, kappa, and delta opioid receptors

208
Q

opioid receptors are coupled with

A

G-protein receptors

209
Q

opioid receptors function as

A

regulators of synaptic transmission

210
Q

fentanyl MOA (3 steps)

A
  1. binds to opioid receptor
  2. stimulates exchange of GTP for GDP on G-protein complex
  3. inhibition of adenylate cyclase and so less cAMP
  4. decreased nociceptive neurotransmitter release
  5. fentanyl converted to morphine
  6. closure of N-type voltage calcium channels, opening of calcium-dependent potassium channels
  7. hypopolarisation, reduced excitability
211
Q

fentanyl use

A

IV analgesic, epidural, spinals (regional anaesthesia), transdermal patches (chronic pain)

Block 12 - Neurological, Neuromuscular and Musculoskeletal Disease (28 decks)

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