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Y2S1 - Drug Action > Drug Action 2 > Flashcards

Drug Action 2 Flashcards

1
Q

What are the two most common NSAIDs?

A

Aspirin and paracetamol

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2
Q

What are the benefits of aspirin over paracetamol?

A

Anti-platelet action, reduced risk of colonic and rectal cancer, reduced risk of Alzheimer’s, it’s a weak acid - rapid and efficient absorption in the ileum

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3
Q

What are the disadvantages of aspirin over paracetamol?

A

Aspirin is an irreversible suicide inhibitor

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4
Q

What are the benefits of paracetamol over aspirin?

A

Weak anti-inflammatory, COX-2 selective, well absorbed and metabolised in the liver, fewer side effects long term

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5
Q

What are the disadvantages of paracetamol over aspirin?

A

Kidney damage in large acute doses, n-acetyl-p-benzoquinoneimine is hepatoxic, it’s a competitive inhibitor

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6
Q

What are the new NSAIDs?

A

Celecoxib and rofecoxib

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7
Q

Which type of COX is involved with inflammatory response?

A

COX-2

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8
Q

Which NSAID forms a metabolite that damages the liver?

A

Paracetamol

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9
Q

What is rheumatoid arthritis?

A

Incurable common chronic inflammatory and destructive arthropathy that typically affect synovial joints

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10
Q

What is the average onset and incidence of rheumatoid arthritis?

A

70 years, can be much younger, 1% of UK population

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11
Q

How much does RA cost the UK per year?

A

3.4-8.75 billion

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12
Q

What does RA stand for?

A

Rheumatoid arthritis

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13
Q

What is the prognosis for RA patients?

A

Poor - 80% disabled after 20 years, life expectancy reduced by 3-18 years

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14
Q

What disease presents with three or more warm, swollen joints, with stiffness in the morning?

A

RA

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15
Q

What nine symptoms can lead to a positive diagnosis of RA?

A

Three or more warm, swollen joints; stiffness in the mornings; arthritis of hand joints; symmetrical arthritis; presence of rheumatoid nodules; fatigue; fever; tiredness; presence of rheumatoid factor

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16
Q

What are rheumatoid nodules?

A

Firm tissue bumps under the skin on the arms

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17
Q

What occurs in synovial joints during early RA?

A

Synovial membrane becomes hyperplastic and synoviocytes become hypertrophic; an immune response is launched and neutrophils, T cells and B cells descend

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18
Q

What would hyperplastic synovial membranes and hypertrophic synoviocytes lead to?

A

RA

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19
Q

What do chondrocytes produce?

A

Cartilage

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20
Q

What do fibroblasts produce?

A

ECM components

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21
Q

What do osteoclasts produce?

A

Involved in bone absorption during growth

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22
Q

What two cytokines are involved in RA?

A

IL-1 and TNF-alpha

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23
Q

What condition are IL-1 and TNF-alpha involved in?

A

RA

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24
Q

Where is IL-1 produced?

A

Monocytes, macrophages and other cells

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25
Q

What three kinds of IL-1 exist?

A

Alpha, beta and ra

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26
Q

What response does IL-1 evoke?

A

Proinflamamtory

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27
Q

What does IL-1 stimulate the release of?

A

Matrix metalloproteinases from fibroblasts and chondrocytes

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28
Q

What stimulates the release of metalloproteinases?

A

IL-1

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29
Q

Where is TNF-alpha produced?

A

Macrophages, monocytes and mast cells

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30
Q

What response does TNF-alpha evoke?

A

Proinflammatory

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31
Q

Why does blocking TNF-alpha have more profound effects than blocking other cytokines?

A

It induces other pro-inflammatory cytokines so blocking TNF-alpha can simultaneously block many other cytokines

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32
Q

What does TNF-alpha stimulate the release of?

A

Metalloproteinases from chondrocytes

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33
Q

What are DMARDs?

A

Disease-modifying antirheumatic drugs

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34
Q

What are DMARDs used for?

A

May be useful in limiting the progression of disease

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35
Q

What is methotrexate?

A

DMARD - folic acid antagonist

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36
Q

What does methotrexate do?

A

Reduces antigen activated T-cell proliferation

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37
Q

What secondary function is methotrexate known to perform?

A

Promote adenosine release and adenosine-mediated suppression of inflammation

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38
Q

What is the primary difference between methotrexate and other DMARDs?

A

Superior in terms of efficacy, unwanted effects and rapid onset

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39
Q

Why must methotrexate treatment be closely monitored?

A

High incidence of blood and liver toxicity

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40
Q

What is sulfasalazine used to treat?

A

RA

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41
Q

What effect does sulfasalazine have on active RA?

A

Remission

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42
Q

What is sulfasalazine a complex of?

A

Sulphonamide and salicylate

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43
Q

What does a complex of sulphonamide and salicylate form?

A

Sulfasalazine

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44
Q

What does MOA stand for?

A

Method of action

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45
Q

What is the MOA of sulfasalazine?

A

Scavenges toxic oxygen metabolites produced by neutrophils

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46
Q

What are the three main classes of immunosuppressant drugs for RA?

A

IL-2 production/action inhibitors, cytokine gene expression inhibitiors, purine/pyrimidine synthesis inhibitors

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47
Q

Describe ciclosporin’s structure.

A

Naturally occuring 11 a/a cyclic peptide found in fungus

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48
Q

What does ciclosporin do?

A

Decrease clonal proliferation of T cells by inhibitting IL-2 synthesis and decreasing expression of IL-2 receptors

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49
Q

Where is ciclosporin metabolised and excreted?

A

Liver and mainly excreted in bile

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50
Q

What are the side effects of ciclosporin?

A

Nephrotoxicity, hepatoxicity and hypertension

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51
Q

Name a drug that inhibits IL-2 production and action.

A

Ciclosporin

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52
Q

What is the primary function of glucocorticoids?

A

Anti-inflammatory and immune suppression

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53
Q

How do glucocorticoids work?

A

Transciptional inhibition of cytokines including - IL-1,2,6 and TNF

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54
Q

What other activities do glucocorticoids perform?

A

Inhibition of adhesion molecule expression, arachidonic acid metabolism, metalloproteinase production

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55
Q

Name a family of drugs that inhibits cytokine gene expression.

A

Glucocorticoids

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56
Q

What two drugs inhibit purine and pyrimidine synthesis in RA treatments?

A

Azathioprine, mycophenolate mofetil

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57
Q

What does azathioprine do?

A

Inhibits DNA synthesis through its active metabolite mercaptopurine

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58
Q

What is the active ingredient in azathioprine?

A

Mercaptopurine

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59
Q

What side effects are associated with azathioprine and mycophenolate mofetil?

A

GI side effects

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60
Q

What extra side effect does azathioprine have over mycophenolate mofetil?

A

Mild hepatotoxicity

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61
Q

What does mycophenolate mofetil do?

A

Inhibits DNA synthesis through inhibition of de novo urine synthesis

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62
Q

What are anticytokine drugs?

A

Engineered recombinant antibodies and other proteins that target specific aspects of RA and other inflammatory diseases

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63
Q

What are some anticytokine drugs co-administered with?

A

Methotrexate

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64
Q

What are the three mechanisms of anticytokine drugs?

A

Neutralisation of cytokines, receptor blockade and activation of antiinflammatory pathways

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65
Q

How do anticytokine drugs neutralise cytokines?

A

Cytokine is prevented from binding to cell-surface receptor by soluble receptor or monoclonal anti-body attachment to the cytokine

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66
Q

How do anticytokine drugs peform receptor blockade?

A

Antagonistic occupation of receptor or monoclonal antibody attachment to the receptor, blocking binding site

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67
Q

Name five anticytokine therapies.

A

Etanercept, infliximab, anakinra, abatacept, efalizumab

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68
Q

At what indication are anticytokine therapies prescribed to RA sufferers?

A

Moderate-severe

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69
Q

What type of anticytokine therapy is etanercept?

A

Fusion protein

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70
Q

What type of anticytokine therapy is infliximab?

A

Chimeric antibody

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71
Q

What type of anticytokine therapy is anakinra?

A

Recombinant protein

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72
Q

What type of anticytokine therapy is abatacept?

A

Fusion protein

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73
Q

What type of anticytokine therapy is efalizumab?

A

Humanised monoclonal antibody

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74
Q

What is the target cytokine for etanercept?

A

TNF - by decoy receptor

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75
Q

What is the target cytokine for infliximab?

A

TNF - by neutralisation

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76
Q

What is the target cytokine for anakinra?

A

IL-1 - by receptor agonism

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77
Q

What is the target cytokine for abatacept?

A

B7 - by antigen presentation in cells

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78
Q

What is the target cytokine for efalizumab?

A

CD11a - neutralises leukocytes

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79
Q

What drug therapies can nausea and vomiting be side-effects of?

A

Cytotoxic chemotherapy, opioids, general anaesthetics and digoxin

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80
Q

What endogenous stimuli can cause nausea and vomiting?

A

Motion sickness, morning sickness, numerous disease states, migraine, ingestion of toxins, fear, pain and olfactory stimuli

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81
Q

What antagonists can block emetic effects?

A

5-HT-3 anatagonists

82
Q

What can 5-HT-3 antagonists do?

A

Block the emetic effects of cytotoxic drugs used during cancer chemotherapy

83
Q

What two main pathways supply visceral sensation?

A

Vagal and spinal

84
Q

Which of the two pathways of visceral sensation supplies mainly physiological stimuli?

A

Vagal

85
Q

Which of the two pathways of visceral sensation supplies mainly noxious stimuli?

A

Spinal

86
Q

Where do vagal cell bodies of the visceral sensation pathway reside?

A

Nodose ganglia

87
Q

Which visceral sensatory cell bodies lie in the nodose ganglia?

A

Vagal

88
Q

Where do spinal cell bodies of the visceral sensation pathway reside?

A

Dorsal root ganglia

89
Q

Which visceral sensatory cell bodies lie in the dorsal root ganglia?

A

Spinal

90
Q

What two systems does the spinal visceral sensatory pathway split into?

A

Splanchnic and pelvic

91
Q

Describe the vagal 5HT-3 receptor.

A

Pentameric ligand gated ion channel - subunits 5HT-3A to 5HT-3E

92
Q

Can 5HT-3 form a homomeric complex? If so, of which subunit?

A

Yes - 5HT-3A

93
Q

What are the most studied 5HT-3 receptors?

A

Heteromeric 5HT-3A/B

94
Q

What is the ionic activity about a 5HT-3 receptor?

A

K out, Na and Ca in

95
Q

What are EC cells?

A

Enterochromaffin cells

96
Q

What cells are responsible for sensory transduction in the gut?

A

Enterochromaffin cells

97
Q

What proportion of the body’s serotonin is found in the gut?

A

95%

98
Q

Where is 95% of the body’s serotonin found?

A

The gut

99
Q

In what cells is serotonin found in the gut?

A

EC cells, enteric neurons and mast cells

100
Q

What are the setron family of drugs?

A

Antiemetics - 5HT-3 receptor antagonists

101
Q

Name three first generation setron family drugs.

A

Granisetron, ondansetron and tropisetron

102
Q

What kind of drug is gransetron?

A

Anti-emetic - setron family - 1st generation 5HT-3 receptor antagonists

103
Q

What kind of drug is ondansetron?

A

Anti-emetic - setron family - 1st generation 5HT-3 receptor antagonists

104
Q

What kind of drug is tropisetron?

A

Anti-emetic - setron family - 1st generation 5HT-3 receptor antagonists

105
Q

How do 1st generation setron family drugs function?

A

Competitive antagonists at both peripheral and central 5HT-3 receptors

106
Q

What are 1st generation setron family drugs usually used to treat?

A

Acute chemotherapy-induced emesis; not very good at treating delayed emesis

107
Q

Name one second generation setron family drug.

A

Palonosetron

108
Q

What is different about second generation setron family drugs?

A

Effective in preventing both acute and delayed emesis; believed to act through allosteric mechanisms causing receptor internalisation

109
Q

What are NK-1 receptors, and what are they activated by?

A

Neurokinin receptors - tachykinin peptides

110
Q

What is the order of potency of tachykinin peptides?

A

Substance P > NK A > NK B

111
Q

What is a strong alternative to the setron family anti-emetics?

A

NK-1 receptor antagonism

112
Q

Name one NK-1 receptor antagonist.

A

Aprepitant

113
Q

What family of drugs does aprepitant belong to?

A

NK-1 receptor antagonists - anti-emetics

114
Q

What is hyoscine also known as?

A

Scopolamine

115
Q

What type of drug in hyoscine?

A

Anti-emetic

116
Q

What receptors does hyoscine act upon?

A

mAChR

117
Q

What is the indication for hyoscine?

A

Motion sickness

118
Q

What are the side effects of hyoscine?

A

Drowsiness, dry mouth, blurred vision

119
Q

What type of drug is chlopromazine?

A

Anti-emetic

120
Q

What type of drug is perphenazine?

A

Anti-emetic

121
Q

What type of drug is prochlorpenazine?

A

Anti-emetic

122
Q

What type of drug is trifluoperzine?

A

Anti-emetic

123
Q

What receptor does chlopromazine act upon?

A

Dopamine antagonists (D2)

124
Q

What receptor does perphernazine act upon?

A

Dopamine antagonists (D2)

125
Q

What receptor does prochlorpenazine act upon?

A

Dopamine antagonists (D2)

126
Q

What receptor does trifluoperzine act upon?

A

Dopamine antagonists (D2)

127
Q

What is the indication for chlopromazine?

A

Severe cases of chemo/radio therapy or pharmacologicaly induced emesis

128
Q

What is the indication for perphenazine?

A

Severe cases of chemo/radio therapy or pharmacologicaly induced emesis

129
Q

What is the indication for prochlorpenazine?

A

Severe cases of chemo/radio therapy or pharmacologicaly induced emesis

130
Q

What is the indication for trifluoperzine?

A

Severe cases of chemo/radio therapy or pharmacologicaly induced emesis

131
Q

What are the side effects of chlopromazine?

A

Sedation, hypotension, dystonias, tardive dyskinesia

132
Q

What are the side effects of perphenazine?

A

Sedation, hypotension, dystonias, tardive dyskinesia

133
Q

What are the side effects of prochlorpenazine?

A

Sedation, hypotension, dystonias, tardive dyskinesia

134
Q

What are the side effects of trifluoperzine?

A

Sedation, hypotension, dystonias, tardive dyskinesia

135
Q

What type of drug is metaclopromide?

A

Anti-emetic

136
Q

What receptor does metaclopromide act upon?

A

Dopamine antagonists (D2)

137
Q

What is the indication for metaclopromide?

A

Increases gut motility and acts on CTZ

138
Q

What does CTZ stand for?

A

Chemoreceptor trigger zone

139
Q

What type of drug is domperidone?

A

Anti-emetic

140
Q

What type of drug is cinnarizine?

A

Anti-emetic

141
Q

What type of drug is cyclizine?

A

Anti-emetic

142
Q

What type of drug is promethazine?

A

Anti-emetic

143
Q

What receptor does domperidone act on?

A

Dopamine antagonists (D2)

144
Q

What receptor does cinnarizine act on?

A

Histmamine antagonists (H1)

145
Q

What receptor does promethazine act on?

A

Histmamine antagonists (H1)

146
Q

What receptor does cyclizine act on?

A

Histmamine antagonists (H1)

147
Q

What is the indication for domperidone?

A

Cytotoxic therapies

148
Q

What is the indication for cinnarizine?

A

Motion sickness

149
Q

What is the indication for cyclizine?

A

Motion sickness

150
Q

What is the indication for promethazine?

A

Motion sickness

151
Q

What are the side effects of cinnarizine?

A

Drowsiness, fatigue

152
Q

What are the side effects of cyclizine?

A

Drowsiness, fatigue

153
Q

What are the side effects of promethazine?

A

Drowsiness, fatigue

154
Q

Name six D2 antagonistic anti-emetics.

A

Chlopromazine, perphenazine, prochlorpenazine, trifluoperzine, metaclopromide, domperidone

155
Q

Name three H1 antagonistic anti-emetics.

A

Cinnarizine, cyclizine, promethazine

156
Q

What family of drugs is gathering evidence as anti-emetic?

A

Cannabinoids

157
Q

What family does the CB1 receptor belong to?

A

Endocannabinoid family

158
Q

What does CB1 agonism prevent?

A

Emesis

159
Q

What is emesis?

A

Vomiting

160
Q

What does CB1 inverse agonism cause?

A

Emesis

161
Q

Name two excitatory a/a NTs.

A

Glutamate, aspartate

162
Q

Name two inhibitory a/a NTs.

A

GABA, glycine

163
Q

What does GABA stand for?

A

Gamma-aminobutyric acid

164
Q

What seven characteristics define glutamate receptors?

A

Subunit, composition, pharmacology, time course, Ca permeability, distribution and neuronal function

165
Q

Characterise AMPA receptor Ca permability, and why they have evolved.

A

Low Ca permability, evolved for rapid depolarisation of cells

166
Q

Characterise GABA-A receptors.

A

Post-synaptic, choride selective ionotropic receptors

167
Q

What do GABA-A receptors do?

A

Mediate fast inhibitory transmission

168
Q

How many units comprise GABA-A receptors?

A

5

169
Q

What is the orthosteric GABA-A agonist?

A

Muscimol

170
Q

What are the orthosteric GABA-A antagonists?

A

Bicuculline, picrotoxin

171
Q

What is the allosteric GABA-A agonist?

A

Diazepam

172
Q

What is the allosteric GABA-A antagonist?

A

Flumazenil

173
Q

What does the allosteric GABA-A site do?

A

Increases or decreases strength of response

174
Q

Which GABA-A site does muscimol bind to? Agonist or antagonist?

A

Orthosteric agonist

175
Q

Which GABA-A site does bicuculline bind to? Agonist or antagonist?

A

Orthosteric antagonist

176
Q

Which GABA-A site does picrotoxin bind to? Agonist or antagonist?

A

Orthosteric antagonist

177
Q

Which GABA-A site does diazepam bind to? Agonist or antagonist?

A

Allosteric agonist

178
Q

Which GABA-A site does flumazenil bind to? Agonist or antagonist?

A

Allosteric antagonist

179
Q

Characterise GABA-B receptors.

A

Pre and post-synaptic G-i/o protein coupled receptor

180
Q

What do GABA-B receptors do?

A

Mediate slow transmission

181
Q

Inhibiton of which channels causes pre-synaptic inhibition?

A

Ca-v channels

182
Q

Activation of which channels causes post-synaptic inhibition?

A

K channels (GIRK)

183
Q

Name a GABA-B agonist.

A

Beclofen

184
Q

Name a GABA-B antagonist.

A

Phaclofen

185
Q

What is baclofen?

A

GABA-B agonist

186
Q

What is phaclofen?

A

GABA-B antagonist

187
Q

What does GIRK stand for?

A

G-protein-coupled inwardly-rectifying K channel

188
Q

What six drug types target GABA-A receptors?

A

Sedatives, anxiolytics, hypnotics, anti-convulsants, neurosteroids and some general anaesthetics

189
Q

What is the general structure of GABA-A receptors?

A

2 alpha, 2 beta and 1 ‘other’ subunit (usually gamma)

190
Q

Which superfamily does the GABA-A receptor belong to?

A

Nicotinic

191
Q

What are the five physiological effects of benzodizepine agonists?

A

Sedation, hypnosis, anterograde amnesia, anti-convulsant, reduction of muscle tone

192
Q

What determines the use of benzodiazepine agonists?

A

Pharmacokinetics

193
Q

Which benzodiazepines are used mainly as sleeping tablets?

A

Short acting

194
Q

What can intravenous diazepam be used to treat?

A

Status epilepticus

195
Q

Why have some benzodiazepines have such long half lives?

A

Metabolized in the liver to produce active intermediates

196
Q

What five key adverse effects can benzodiazepine agonists cause?

A

Sleepiness, impaired psychomotor function, amnesia, additive effects, tolerance, misuse, dependence

197
Q

What ‘additive effects’ can occur with benzodiazepine agonists?

A

Combinative effects with other CNS depressants - can be fatal

198
Q

Define drug tolerance.

A

Decreased responsiveness to a drug following continuous exposure

199
Q

What must physical dependence be characterised by?

A

Withdrawal - increased anxiety, insomnia, CNS excitability, convulsions

200
Q

How would you alleviate physical withdrawal?

A

Use a slower acting drug

Y2S1 - Drug Action (4 decks)

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