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BMS13 > Pharmacology of Gastric Acid Control > Flashcards

Pharmacology of Gastric Acid Control Flashcards

1
Q

What are ulcers?

A

Chronic, usually solitary lesions/sores in areas of the GI tract exposed to acids/peptic juices

Display spontaneous relapse and remission

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2
Q

Where are ulcers most commonly found?

A

Duodenum

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3
Q

How much more common are duodenal ulcers than gastric ulcers?

A

4 times

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4
Q

What are the symptoms of ulcers? (5)

A

Abdominal pain - typically an epigastric burning sensation

Usually nocturnal pain

Heartburn

Bloating

Duodenal ulcer pain relieved by eating

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5
Q

What are the three complications which can arise from ulcers?

A

Penetration

Perforation

Upper GI bleeding

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6
Q

Does acid hypersecretion cause ulcers?

A

Only in Zollinger-Ellison syndrome

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7
Q

What is Zollinger-Ellison syndrome?

A

Rare, gastrin-producing tumour of pancreas or duodenum causing oversecretion of acid

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8
Q

Does smoking cause ulcers?

A

No, risk factor - interferes with healing/blood flow

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9
Q

By how much does smoking increase the risk of getting ulcers?

A

50% increase

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10
Q

What is the main bacteria which is associated with ulcers?

A

Helicobacter pylori

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11
Q

Does Helicobacter pylori cause ulcers?

A

Causes chronic gastritis which weakens the mucosal barrier allowing ulcers to form

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12
Q

What drugs can cause ulcers?

A

Aspirin and NSAIDS

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13
Q

What is the main type of ulcer caused by NSAIDs?

A

Gastric

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14
Q

What percentage of ulcers are idiopathic?

A

20%

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15
Q

How do NSAIDs and aspirin cause ulcers?

A

Inhibit prostaglandin production which weakens the mucosal barrier allowing ulcers to form

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16
Q

What must be balanced to prevent ulcers?

A

Mucosal defense

Acid/pepsin secretion

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17
Q

What are the usual characteristics of gastric ulcers?

A

Helicobacter pylori infection of gastric corpus

Low-normal levels of acid with defect in gastric mucosal defense

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18
Q

What are the usual characteristics of duodenal ulcers?

A

Helicobacter pylori infection of pyloric antrum

Increased acid/pepsin secretion causing gastric metaplasia of duodenum which allows infection by H. pylori

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19
Q

What type of tissue can Helicobacter pylori infect?

A

Gastric

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20
Q

What affects the progression of acute gastritis to chronic gastritis?

A

Host factors

Strain of Helicobacter pylori

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21
Q

What does antral predominant gastritis lead to?

A

Duodenal ulcers

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22
Q

What does multifocal atrophic gastritis lead to?

A

Gastric ulcers

Gastric cancer

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23
Q

Why is there often low levels of acid production with gastric ulcers?

A

Multifocal atrophic gastritis - ongoing inflammation causes gastric mucosa to be replaced by intestinal and fibrous tissue

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24
Q

Are those in the age group 20-40yo more likely to get gastric ulcers or duodenal ulcers?

A

Duodenal ulcers

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25
Q

What is Helicobacter pylori?

A

Spiral-shaped bacterium which causes chronic gastritis

Incidence increases with age

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26
Q

What does Helicobacter pylori do?

A

Grows on enterocyte surface beneath mucus

Increases secretion of gastrin and pepsin

May produce toxins which damage the mucosa

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27
Q

What is the Cag pathogenicity island?

A

Collection of genes coding for CagA and a type IV secretion system

Makes some strains of H. pylori especially pathogenic

28
Q

What is CagA?

A

Cytoskeleton-disrupting protein

29
Q

What does a type IV secretion system do?

A

Injects CagA into epithelial cells

30
Q

How does Helicobacter pylori protect itself from acid?

A

Secretes a urease

Converts endogenous urea to HCO3 and CO2 = alkaline bubble

31
Q

How do we test for H. pylori?

A

Test for antigens in stool samples

Test for antibodies in blood samples

32
Q

How does histamine affect parietal cells?

A

Binds H2 receptors

Increase cAMP and phosphorylation

Increase acid production

33
Q

How do ACh and gastrin affect parietal cells?

A

Increase intracellular Ca to increase acid production

34
Q

Which prostaglandin is prominent in the mucosal defence system?

A

PGE2

35
Q

What does PGE2 do?

A

Bind to EP3 receptors

  • On mucus-producing cells to stimulate release of HCO3 and mucus
  • On parietal cells to suppress HCl secretion

Vasodilatation

36
Q

Give an example of a proton pump inhibitor.

A

Omeprazole

Esomeprazole

37
Q

What do proton pump inhibitors do?

A

Irreversibly block parietal cell H/K-ATPase

38
Q

What is the mechanism of proton pump inhibitors? (4)

A

Inactive pro-drugs at neutral pH

Absorbed in SI and move via blood to accumulate in oxyntic glands

Converted to sulfenamides at pH<3

React covalently with sulfhydryl groups on ATPase

39
Q

Why is only one pill of omeprazole required per day?

A

Proton pump inhibitors irreversibly block H/K-ATPase

Cells must make more H/K-ATPase to secrete acid

40
Q

What are the adverse effects of PPIs?

A

Uncommon but long-term use can cause osteoporosis and increased risk of serious cardiac events

Withdrawal can cause rebound acid hypersecretion

41
Q

Give an example of a H2 receptor blocker.

A

Famotidine

Ranitidine

Cimetidine

42
Q

What do H2 receptor blockers do?

A

Selectively block parietal cell H2 receptors to decrease acid production

43
Q

What is the adverse effect associated with cimetidine?

A

Inhibits multiple cytochrome P450s

Retards metabolism of a large number of widely used drugs such as nifedipine and warfarin

44
Q

Why was ranitidine withdrawn in October 2019?

A

NDMA contamination (potential carcinogen)

45
Q

Which drugs enhance mucosal protection? (3)

A

Bismuth chelate

Sucralfate

Misoprostil

46
Q

What does bismuth chelate do? (3)

A

Coats ulcer to protect from gastric juices and promotes healing

Stimulates secretion of mucus, PG, HCO3

Chemotherapeutic effects against H. pylori

47
Q

What is sucralfate?

A

Aluminium hydroxide/sulfated sucrose complex

48
Q

What type of ulcers is sucralfate used for?

A

Duodenal ulcers not related to NSAID use

Stress ulcers

49
Q

What is the mechanism of sucralfate?

A

Negative sulfated sucrose (dissociated from complex) binds HCl to form a viscous adhesive which binds positive groups in the ulcer crater

This buffers acid and stimulates secretion of mucus, PG and HCO3

Decreases number and adherence of H. pylori

50
Q

How does sucralfate affect other drugs?

A

Decreases absorption of some drugs like antibiotics

51
Q

What is misoprostil?

A

Stable PGE1 analogue which heals and prevents NSAID-induced damage (when taken with NSAID)

52
Q

What are the adverse effects of misoprostil?

A

Diarrhoea

Abdominal cramps

Uterine contractions - avoid in pregnancy

53
Q

Why is antimicrobial therapy sometimes used when treating ulcers?

A

Eradicate H. pylori and prevent ulcer relapse

54
Q

How is antimicrobial therapy often used in ulcer treatment?

A

In combination with H2 blocker or PPI (increased pH to stabilise antibiotic)

2 weeks typically

55
Q

What is gastro-oesophageal reflux disease?

A

Reflux of stomach acid back into oesophagus

56
Q

What are the symptoms of GORD?

A

Pain (oesophageal)

Oesophagitis

Heartburn

Bad taste in mouth

57
Q

What is heartburn?

A

Retrosternal burning pain brought on by meals or lying flat

58
Q

What can increase the risk of developing GORD?

A

Transient lower oesophageal sphincter relaxation or atonic LOS

Increased intra-abdominal pressure due to obesity/pregnancy/heavy meals

59
Q

Why does GORD often worsen during sleep?

A

Normal defence mechanisms less active (salivation and swallowing)

60
Q

How can GORD affect the oral cavity?

A

Tooth erosion

61
Q

How does GORD cause tooth erosion?

A

Acid removes pellicle protection and can easily get beneath saliva due to lower surface tension

Dished-out lesions

62
Q

What lifestyle modifications might be advised for a GORD patient?

A

Leave at least 2 hours between meals and bedtime

Reduce fat, alcohol, coffee, chocolate intake

Elevate head during sleep

63
Q

What drugs may cause GORD?

A

Birth control pill

Hormone replacement therapy

Ca channel blockers

64
Q

What can be used to treat less severe GORD cases and how?

A

Antacids/alginic acid

Neutralise stomach acid

65
Q

How does alginic acid work?

A

Detergent which forms a foam ‘raft’ on top of stomach contents

Acts as a physical barrier to reduce reflux

66
Q

Why might gastric motility-stimulation agents be used with a PPI? Why don’t we use this?

A

Increase tone of lower oesophageal sphincter

Side effects

(Metoclopromide and domperidone)

BMS13 (7 decks)

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