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notes to flashcards year 2 - LCRS1 > anti-ulcer drugs > Flashcards

anti-ulcer drugs Flashcards

1
Q

what is a peptic ulcer?

A

area of damage to inner lining of stomach (gastric ulcer) or upper part of the duodenum (duodenal ulcer)

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2
Q

how can these ulcers be distinguished?

A
  • based on timing of symptoms
  • gastric ulcer: pain at mealtimes when acid secreted
  • duodenal ulcer: pain relieved by a meal as pyloric sphincter closes (pain starts after 2 hours)
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3
Q

which ulcers are more common?

A

duodenal: gastric = 4:1

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4
Q

what are the protective factors of GI barrier? What do they do?

A
  • lubricate food and protect mucosal surfaces
  • mucus from gastric mucosa creates GI mucosal barrier
  • HCO3- ions are trapped in mucous, generate protective pH at 7 at mucosal surface
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5
Q

what do locally produced prostaglandins do?

A
  • stimulate mucus and bicarbonate production
  • inhibit gastric acid secretion
  • facilitate a good blood supply to stomach
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6
Q

what are some factors that convert the food into chyme and damage the mucosal barrier?

A
  • parietal cells: acid secretion from parietal cells of oxyntic glands in gastric mucosa
  • chief cells: pesinogens which erode mucous layer
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7
Q

what are the factors that contribute to mucosal damage?

A
  • inc. acid or dec. HCO3-
  • dec. thickness of mucosal layer
  • inc. in pepsin type 1
  • dec. mucosal blood flow
  • infections w/ H. pylori
  • risk factors: genetic, stress, diet
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8
Q

what are the 5 classes if drugs used to treat ulcers? what do each of them do?

A
  • antibiotics: eradicate H. pylori
  • inhibitors of gastric acid scretion: prevent gastric acid production
  • cytoprotective drugs: promote healing
  • antacids: neutralize gastric acid
  • triple therapy
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9
Q

how many ulcers are infected with H. pylori?

A
  • 100% of duodenal

- 80-90% gastric

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10
Q

what are the risk factors for acquiring H. pylori?

A
  • socioeconomic conditions

- contact w/ animals and contaminated faeces

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11
Q

what is the triple therapy treatment?

A
  • clarithromycin, amoxicillin, proton pump inhibitor
    1. antibiotics: more than 1 type as there is some small resistance
    2. drugs that reduce gastric acid secretion
    3. drugs that promote healing
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12
Q

what are the 3 inhibitors of gastric acid secretion?

A
  • proton pump inhibitors e.g. Omeprazole
  • H2 receptor antagonists e.g. Rantidine
  • Anti-muscarinics
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13
Q

describe the production of gastric acid

A
  • presence/ smell of food can trigger acid production
  • in fundus, there are acid secreting parietal cells
  • PNS can act on H-cells to stimulate histamine production
  • in antrum, amino acids can trigger g-cells to secrete gastrin
  • gastrin triggers more histamine release/ more acid production
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14
Q

how do inhibitors of gastric acid secretion work?

A
  • acid is produced by H/K exchanger
  • histamine then acts on H2 receptors on parietal cells
  • triggers activation of these exchangers via cAMP pathway
  • superficial epithelial cells provide protective bicarbonate secretion
  • mixes with mucus to protect
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15
Q

what is the MoA of proton pump inhibitors?

A
  • inhibits basal and stimulates gastric acid secretion
  • irreversible inhibitor of H/K ATPase exchanger
  • becomes inactive at neutral pH
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16
Q

where do proton pump inhibitors accumulate? Why?

A

at canaliculi as it is a weak base

17
Q

give an example of a proton pump inhibitor

A

omeprazole

18
Q

what are the uses of PPIs?

A
  • peptic ulcers resistant to H2-receptor antagonists
  • triple therapy component
  • GERD and oesophagitis
  • prophylaxis of peptic ulcers in intensive care
19
Q

what are the pharmacokinetics of PPIs?

A
  • oral

- administered in an enteric coating

20
Q

what are the side effects of PPIs?

A
  • side effects rare due to short term use

- long term + high dose –> enteric infections (C. diff), community acquired pneumonia

21
Q

what is the MoA of H2 receptor antagonists?

A
  • inhibits gastric acid secretion by parietal cells by around 60%
  • less effective than PPIs
  • competitive H2 receptor antagonists
22
Q

what are the pharmacokinetics and side effects of these?

A
  • oral, well absorbed

- rare side effects = headaches, dizziness

23
Q

are anti-muscarinic drugs used?

A
  • little use as anti-ulcer drug

- more effective in combo therapies

24
Q

what do cytoprotective drugs do? name examples

A
  • enhance mucosal protection
  • build physical barrier over ulcer
    e. g. Sucralfate, Misoprostol
25
Q

what is the MoA of sucralfate?

A
  • in an acid environment, needs a strong -ve charge
  • binds to +ve groups in large molecules
  • forms gel-like complexes
  • this coats and protects ulcer
  • limits H+ diffusion and pepsin degradation pf mucus
  • inc. prostaglandin, mucus and HCO3- production
  • dec. number of H pylori
26
Q

what is the structure of Sucralfate?

A
  • polymer containing Al(OH)3 and sucrose octa-sulphate
27
Q

what are the side effects of sucrafate?

A
  • most orally administered
  • sucralfate remains in GIT
  • causes constipation or reduced absorption of other drugs e.g. digoxin, antibiotics
28
Q

what is bismuth chelate/ pepto-bismol?

A

acts like sucralfate

used in triple therapy

29
Q

what is misoprostal?

A
  • prostaglandin analogue
  • orally active
  • mimics action of prostaglandins to maintain mucosal barrier
30
Q

why is misoprostal co-prescribed with NSAIDs when used chronically?

A
  • NSAIDs block COX enzymes needed for prostaglandin synthesis from arachidonic acid
31
Q

what are the side effects of misoprostol?

A
  • diarrhoea
  • abdo cramps
  • uterine contractions
32
Q

what are ant acids? what is the speed of action?

A
  • salts of Na, Al, Mg
  • sodium bicarbonate has rapid effects
  • aluminium hydroxide and magnesium trisilicate have slower actions
33
Q

what is the MoA of antacids?

A
  • neutralise acid
  • raise gastric pH
  • reduce pepsin activity
  • oral admin
34
Q

what are the problems with triple therapy?

A
  • compliance
  • antibiotic resistance
  • adverse response to alcohol (metronidazole)
35
Q

what drugs are included in the triple therapy?

A
  • antibiotics
  • inhibitors of gastric acid secretion
  • cyto-protective agents
  • reduces rate of peptic ulcer relapse rate
36
Q

what OTC medication can be used for GORD?

A

antacids

H2 antagonists

37
Q

what do patients experience with GORD?

A

heart burn

38
Q

what does chronic GORD lead to?

A
  • barrett’s oesophagus
39
Q

what drugs can be used to treat chronic GORD?

A

PPIs

H2 antagonists

notes to flashcards year 2 - LCRS1 (58 decks)

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