Pharmacology GI Flashcards

1
Q

what class is orlistat

A

lipase inhibitor

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2
Q

what is usage orlistat

A

Used as an adjunct for obese patients with a BMI ≥ 30 to lose and maintain weight

cease treatment after 12 weeks if no more than 5% change.

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3
Q

what receptor does orlistat work on and is it anatgonist/agonist

A

lipase enzyme antagonist

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4
Q

what is MOA orlistat

A

Binds to lipases, therefore preventing the breakdown and absorption of fat (triglycerides) in the duodenum.

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5
Q

what are side effects orlistat

A

Oily spotting, flatus with discharge, faecal urgency, fatty/oily stool, increased defecation and faecal incontinence

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6
Q

what class is methylcellulose

A

antihypersensitive

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7
Q

what is methylcellulose usage

A

constipation, diarrhoe, obesity

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8
Q

what is methylcellulose MOA

A

Polysacharide polymer that forms a gel in the GIT and can’t be absorbed. This gel is formed in the SI and distends it. It stimulates peristaltic activity. Also thought to suppress appetite.

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9
Q

what is side effects methylcellulose

A

mild laxative effects. flatulence

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10
Q

what class is atrovastatin//simvastatin

A

HmG-coA reductase inhibitos (statins)

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11
Q

what is atrovastatin/simvastain usage

A

Lower LDL cholesterol
Familial and non-familial
Hypercholesteremia and mixed dyslipidemia
Hypertriglyceridaemia

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12
Q

what receptor is atrovastin/simvastatin and is it agonist/antagonist

A

HmG-coA reductase, competitive antagonist

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13
Q

what is atrovastatin/simvastatin MOA

A

HMG-CoA reductase is the rate limiting step in cholesterol biosynthesis. Statins competitively inhibit this enzyme, thereby lowering cholesterol levels.
Since cholesterol is essential for the prouction VLDL, we also see lower levels of triglycerides

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14
Q

what is atrovastatin/simvastatin side effects

A

Myalgia - common side effect of statin therapy

Diarrhoea, Joint pain, Nausea, Trouble sleeping, Stuffy nose, Sore throat

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15
Q

what class is cyclizine (no sedation)

A

anti-emetic, anti histamine

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16
Q

what is usage clyclizine (no sedation)

A

Nausea due to vertigo
Nausea due to motion sickness
Labrinythitis and menieres disease

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17
Q

where does cyclazine bind and its it antagonist/agonist

A

H1 receptor reverse agonist IT IS ANTAGONIST

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18
Q

what is cyclazine moa

A

H1 receptor has 2 states - active and inactive. The inverse agonist binds to the inactive form to reduce receptor activity

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19
Q

what is cyclazine side effects

A

drowsiness, prolong QT interval

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20
Q

what is promethazine(if sedation required) class

A

antihistamine, antipsychotic, sedative, and antiemetic

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21
Q

what is promethazine usage

A

Nausea due to vertigo
Nausea due to pregnancy
Nausea due to motion sickness. Labyrinthitis and meniere’s disease

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22
Q

what receptor is promaethezine and is it antagonistit/agonist

A

H1 receptor inverse agonist, H1 receptor anagonist

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23
Q

what is promoethazine moa

A

Bind to H1 receptors and so prevent the activation of the second messenger system stated on the left. This results in reduced hypersecretion, pruritis & sneezing

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24
Q

what is promethezine side effects

A

Drowsiness

Can’t see - blurred vision
Can’t pee - urinary retention
Can’t shit - constipation
Can’t spit - dry mouth

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25
Q

what class is Metoclopramide
Prochlorperazine
Domperidone

A

anti emetic prokinetic

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26
Q

what is usage of Metoclopramide
Prochlorperazine
Domperidone

A

Nausea due to pregnancy
Nausea due to migraine
Dysmotility dyspepsia
GORD

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27
Q

what receptor does Metoclopramide
Prochlorperazine
Domperidone work on and is it antagonist/agonist

A

D2 Gi receptor antagonist

(Dopamine Antagonist), dopamine receptor ANTAGONIST

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28
Q

what Metoclopramide
Prochlorperazine
Domperidone is MOA

A

Inhibit dopamine inhibition of ACh-induced contraction. Causes enhanced gastric emptying, reduction in the acid available to reflux and increased lower oesophageal sphincter basal tone

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29
Q

what is Metoclopramide
Prochlorperazine
Domperidone side effects

A

Parkinsonism
Tardive dyskinesia
Dystonia
Drowsiness, nervousness, agitation and anxiety
Increased pituitary prolactin release - impotence, galactorrhea, menstrual disorders

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30
Q

what class is metoclopramide

A

anti-ematic, prokinetic

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31
Q

what is metoclopramide usage

A

Nausea - migraine
Also used to treat GORD. DON’T USE REGULARLY. . Can also br used recreationally so be careful when prescribing

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32
Q

what is binding site of metoclopramide and is it antagonist/agonist

A

D2 receptor anatagonist , dopamine recepor antagonist

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33
Q

what is MOA of metoclopramide

A

Antiemetic action is due to its antagonist activity at D2 receptors in the chemoreceptor trigger zone (Ach induced contraction)

Agonist effect on peripheral 5HT3 and antagonist effect on muscarinic receptors to promote gastric emptying

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34
Q

what is side effects of metoclopramide

A

Tardive dyskinesia
Parkinsonism
Hyperprolactinaemia

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35
Q

what class is hydocine hydrobromide (can cross BBB) so

A

anti ematic, anti muscaranic, anti spasmotic

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36
Q

what is usage of hyoscine hydrobromide (can cross bbb)

A

H1 receptor antagonist (antimuscarinic)

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37
Q

what is hyoscine hydrobromide moa

A

Blocks muscarinic cholinergic M1 receptors in the vestibular nuclei, the nucleus of the solitary tract and the vomitting centre. (activation of these receptors required to trigger vomitting reflex)

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38
Q

what is hydoscine hydrobromide side effects

A

Can’t see - blurred vision
Can’t pee - difficulty passing urine
Can’t spit - Dry mouth
Can’t shit - constipation

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39
Q

what aprepitatnt (used before chemo) is usage

A

only used as prevention of nausea, not whilst patient has it. Usually in cancer chemo with moderate/hight emetogenic outcomes .

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40
Q

what receptor binds to aprepitant (used before chemo)

A

NK1 antagonist - supstance P (pain) can’t bind

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41
Q

what is dexamthesone class

A

Anti-emetic
Corticosteroid

Only antiemetic given IV. Used in combo with aprepitant

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42
Q

what is dexamethasone usage

A

Post-operative nausea
Nausea due to cancer chemotherpay and radiotherapy for those at low risk pre-treatment. Don’t use in diabetic patients as can induce glucose in blood

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43
Q

what is dexamethasone receptor and is it agonist/antagonist

A

minercorticoid- 5H3 receptor antagonist

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44
Q

what is dexamethasone MOA

A

unkown

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45
Q

what is prochloperazaine class

A

anti-emetic

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46
Q

what is prochloperazaine usage

A

post-operative nausea

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47
Q

what is prochloperazaine binding site and is it antaginist /agonist

A

D2 antagonist

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48
Q

what is prochloperazaine MOA

A

inhibit stimulation of the chemoreceptor trigger zone (CTZ)

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49
Q

what is graniestron/ondansetron

A

faecal softener

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50
Q

what is graniestron/ondansetron usage

A

Prevention and treatment of chemotherpay-induced nausea and vomitting . Some of the most effective at managing nausea and vomiting , really good at healping w acute phase, less w delayed phase . Also used in nausea and vomiting in opeates (ondansaterone first line w managmt of opiates)

51
Q

what is granisetron/ondansetron receptor and is it agonist/antagonist

A

5HT3 antagonists

52
Q

what is granisetron/odansetron MOA

A

Selective blockade of peripheral 5HT3 receptors on intestinal vagal afferents.
CNS actions at both the CTZ (chemoreceptor trigger zone) and vomitting centre (VC) also involved

Have peripheral and central effects

53
Q

what is granisetron/ondansetron side effects

A

Transient, mild headache
Dizziness
Constipation
Small prolongation of QT interval

54
Q

what is cisplatin usage

A

most likely to cause emertic episodes in 24 hours after administration in cancer chemo and radiotherapy

55
Q

what is cisplatin MOA

A

What is the mechanism of cisplatin?
The mechanism of action of cisplatin has been associated with ability to crosslink with the urine bases on the DNA to form DNA adducts, preventing repair of the DNA leading to DNA damage and subsequently induces apoptosis within cancer cells.

56
Q

what receptor does cisplatin bind to

A

N7 receptor on purine residues

57
Q

what is cisplatin side effects

A

Anaemia; arrhythmias; bone marrow failure; electrolyte imbalance; extravasation necrosis; fever; leucopenia; nephrotoxicity (dose-related and potentially cumulative); sepsis; thrombocytopenia

58
Q

what is arepitant class

A

antiematic

59
Q

what is aripitent usage

A

Prevent nausea and vomitting caused by cancer chemotherapy with moderate or high emetogenic outcomes (PREVENTATIVE ONLY)

60
Q

what is binding site of arepitant and is it antagonist/agonist

A

NK! receptor antagonist

61
Q

what is arepitant moa

A

Binds to NK1 receptor in the brain at the CTZ and VC and antagonise them. It blocks the actions of substance P (neurokinin).

62
Q

what is arepitant side effects

A

Fatigue
Constipation
Induces CYP3A4 - can shorten warfarin half life

63
Q

effetcs of aspirin

A

inhibition of cyclose-oxigenase by aspirin leads to decreased production of thrombaxin A2

64
Q

what do nsaids inhibit

A

clycloxygenase

65
Q

what classes is Aluminium Hydroxide/ Magnesium carbonate/ Magnesium trisilicate

A

antacid and alginate

66
Q

what is the usage of Aluminium Hydroxide/ Magnesium carbonate/ Magnesium trisilicate

A

provide GORD symtom relief

67
Q

what is the 2 MOA of Aluminium Hydroxide/ Magnesium carbonate/ Magnesium trisilicate

A

Antacids are weak bases that react with gastric acid to neutralise the acid to water and a metal salt (also indirectly reduce pepsin activity)

Alginates form strong gels with divalent cations such as Ca2+ giving it strength and flexibility. Mode of action is physical rather than pharmalogical - gel physically keeps gastric acid down therefore supressing reflux and relieving GORD

68
Q

what are Aluminium Hydroxide/ Magnesium carbonate/ Magnesium trisilicate side effect

A

Aluminium compounds - constipation
Magnesium Compounds - Diarrhoea

69
Q

what are contraindications of Aluminium compounds - constipation
Magnesium Compounds - Diarrhoea

A

Diabetes - could affect glycemi control
Tetracycline antibiotics - react with 2+ ions antacids and inactivate antibiotic - leave at least 2 hours between adminsitration
Renal impairment - Mg and Ca accumulation could affect electrolyte balance. can contribute to bone disease and encephlopthy
Hypertension and congestive heart failure - Na could be in antacids- affect electrolyte balance. constipation w aluminium salts diarrhoea with magnesium salts so usually given in combination to counter the effects systemic alkolosis can occur with very large doses drug interactions: aluminium salts can bind to NSAIDs and tetracyclines in gut reducing absorption

70
Q

what class is ranitidine

A

H2 receptor antagonist

71
Q

what is ranitidine usage

A

Reduce gastric acid secretions
Heal ulcers. Dyspepsida . GORD

72
Q

what receptor does ranitidine bind to and is it antagonist/agonist

A

Gs H2 receptor competitive antagonist

73
Q

what is MOA of ranitidine

A

Ranitidine blocks the Gs H2 receptors on parietal cells lining the lumen of the stomach which reduces gastric acid secretion by 70% by preventing the following - normally H2 receptor actiation results in ↑ adenyl cyclase - ↑ cAMP - PKA activation - increased proton pump activity (K+ into parietal cell in exchange for H+;gastric acid out)

74
Q

what are side effects ranitidine

A

Cimitidine, Gyneacomastia and/or galactorrhea
Confusion - primarily in elderly
CYP450 enzyme inhibition - interferes with metabolism of clopidogrel and warfarin

75
Q

what class is Omeprazole
Clarithromycin
Amoxicillin
Metronidazole

A

quadruple therapy

76
Q

what is usage of Omeprazole
Clarithromycin
Amoxicillin
Metronidazole

A

H.pylori infection that can’t be eradicated

77
Q

what is MOA of Omeprazole
Clarithromycin
Amoxicillin
Metronidazole

A

MOA first 3 agents see below
metronidazole - T\his agent is reduced to an intermediate by receiving an electron from ferredoxin or flavadoxin, this activates the drug. The activated drug damages cells by forming protein and DNA adducts, inhibiting bacterial DNA synthesis and degrading existing DNA. The intermediate toxic metabolite is not produced in mammalian cells, ensuring antimicrobial selectivity.

78
Q

what is Omeprazole
Clarithromycin
Amoxicillin usage

A

H.pylori infection

79
Q

what is MOA of Omeprazole
Clarithromycin
Amoxicillin

A

Omeprazole see above
Clarithromycin MOA
Amoxicillin
This agent inhibits the final transpeptidation of N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) by forming covalent bonds with penicillin-binding proteins that have transpeptidase and carboxypeptidase activities thus preventing formation of the cross links between the peptidoglycan matrix.

80
Q

what class is Omeprazole
Clarithromycin
Amoxicillin

A

triple therapy

81
Q

what c lass is omeprazole

A

PPI

82
Q

what is usage of omeprazole

A

Reduce gastric acid secretions. Dyspepsia
Gastro-oesophageal reflux disease
NSAID-induced peptic ulcer (either gastric or duodenal)
Zollinger -Ellison syndrome

83
Q

what is receptor omeprazole

A

bind to H+/K+ ATPase to irriversibly inhibit

84
Q

what is MOA omeprazole

A

PPIs cause irreversible blockade of H+/K+ ATPase

Inhibit H+/K+ ATPase on parietal cells. Enterically coated omeprazoe is a weak base. At a physiological pH of 7.4, it is in its neutral form and passes freely into the cytoplasm of the parietal cell. Omeprazole passes into the acidic canaliculus where it is converted to its active form - sulfenamide.

Sulfenamide forms a covalent disulphide bond with H+/K+ ATPase, therefore inhibiting its activity, which results in prolonged supression (90-95%) of gastric acid secretion.

85
Q

what is omeprazole side effects

A

Nausea
Diarrhoea
Headache
GI disturbance
Bone fractures - increased risk with long term use: hip, wrist and spine

86
Q

what is loperamide class

A

Opiod
Anti-motility drug. Acts on myenteric plexus

87
Q

what is loperamide usage

A

diarrhoea

88
Q

what receptor is loperamide and is it antagonist/agonist

A

μ opioid receptor agonist

89
Q

what is MOA of loperamide

A

Act on μ opiod receptors in myenteric plexus of the large intestine to inhibit acetylcholine release and reduce motility

90
Q

what is bismuth subsalcylate class

A

Agent that modifies fluid transport

91
Q

what is bismuth subsalcylate usage

A

diarrhoea

92
Q

what is bismuth subsalcylate MOA

A

Stimulates absorption of fluids and electrolytes by the intestinal wall (anti-secretory action)
Reduces hypermotility of the stomach. Stimulates absorption of fluids + electrolytes by intestinal wall. Reduces hypermotility of stomach

93
Q

what is ispaghula husk class

A

bulk forming laxative

94
Q

what is isphalghula usage

A

constipation 1st line for short duration constipation

95
Q

what is ispaghula husk MOA

A

Bulk-forming laxatives relieve constipation by increasing faecal mass which stimulates peristalsis.

96
Q

what is lactulose class

A

Osmotic laxative. A non absorbable compund

97
Q

what is lactulose usage

A

Constipation - 2nd line for short duration constipation

98
Q

what is lactulose MOA

A

Absorbs water and increases stool bulk - this increases intestinal distension which increases peristaltic activity
Colonic bacteria use the hydrated material as a metabolic substrate - causes softening of the faeces. More water remains in gut.

99
Q

what class is liquid paraffin

A

faecal softener

100
Q

what is liquid paraffin usage

A

constipation

101
Q

what si liquid paraffin MOA

A

Becomes emulsified with the stool and soften/lubricate it for easier passage out

102
Q

what class is senna

A

Stimulant laxative - DON’T USE IN IBS

103
Q

what is usage of senna

A

Constipation - 3rd line for short-duration constipation

104
Q

what is senna MOA

A

Converted to active form by bacteria in the colon. Here they irritate the mucosa, causing low grade inflammation - this stimulates peristalsis and promotes the accumulation of water and electrolytes. Promotes accumulation of water and electrolytes

105
Q

what is senna side effects

A

Excessive use can cause diarrhoea

Prolonged use increases risk of hypokalemia - this presents with non-specific symptoms such as tiredness and fatigue. Other symptoms include weakness of muscles, constipation and rhabdomyolysis.. CAN CAUSE LOW GRADE INFLAMMATION BY IRRITATING MUCOSA

106
Q

what is hyoscine butylbromide class

A

Antispasmodic
Anti-muscarinic.

107
Q

what is usage of hyoscine butylbromide

A

helps prevent cramping in IBS

108
Q

what is hyooscine butylbromide receptor and is it antagonist or agonist

A

M3 receptor antagonist is the main one. Competitive H1 antagonist of M4 receptor

109
Q

what is MOA of hyoscine butylbromide

A

Competetively antagonise action of ACh in enteric plexus - prevents ACh binding to M3 receptors - results in smooth muscle relaxation and relieves cramping and spasms of the gut. The relaxation improves normal gut functioning and peristaltic activity and relieves pain caused by trapped wind.

110
Q

what is hyoscine hydrobromide side effects

A

Dry Mouth
Blurred vision
Cardiac arrhythmia

111
Q

what is ppepermint oil/meberverine usage

A

IBS

112
Q

how doe speppermint oil/meberverine work

A

Directly act on smooth muscle to relax it

113
Q

what mesalazine class

A

Aminosalicylates
(anti-inflammatory)

114
Q

what mesalazine usage

A

Mild to moderate UC and maintain remission

115
Q

what is mesalazine MOA

A

Absorbed in LI - unknown MOA - thought to inhibit inflammatory mediators e.g. prostaglandins & cytokines

116
Q

what class is prednisolone

A

Corticosteroid
(anti-inflammatory & immunosupressive)

117
Q

what usage is prednisolone

A

Moderate to severe attacks of UC and Crohn’s disease

118
Q

what recepto is prednistolone

A

glucocorticosteroid receptor
(nuclear receptor)

119
Q

what MOA of prednisolone

A

Inhibits synthesis of inflammatory mediators

120
Q

what class is infliximab

A

Antibodies to TNFα

121
Q

what is usage of infliximab

A

Patients with Crohns who are resistant to conventional therapy

122
Q

what moa of infliximab

A

TNFα causes activation of immune cells & release of inflammatory mediators - infliximab inhibits TNFα and induces remission in 1/3 of patients with Crohns who are resistant to conventional therapy

123
Q

cimetidine

A

Gi block binds to H2 receptors