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Adult Years > Gastric Acid Secretion, H. pylori and Ulceration > Flashcards

Gastric Acid Secretion, H. pylori and Ulceration Flashcards

1
Q

Why is it necessary for gastric secretions to be acidic?

A
  • Acid necessary for:
    • Digestion of food
    • Iron absorption
    • Killing pathogens
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2
Q

What are the protective gastric secretions?

What are the consequences of disruption of this protective layer?

A
  • Mucous secreting cells:
    • ​Trap bicarbonate ions (alkaline)
    • Creates gel-like barrier
    • Important protective layer
  • Prostaglandins locally produced:
    • ​Stimulates secretion of mucous and bicarbonate
    • Dilate mucosal blood vessels
    • Cytoprotective
  • If disturbance in protective layer or secretions PLUS acid - risk of GORD and peptic ulcers.
  • Many NSAIDs disturb these protective functions (inhibit COX1 - enzyme responsible for synthesis of prostaglandins) therefore increase risk.
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3
Q

Which cells secrete HCl and intrinsic factor?

A

Parietal / oxyntic cells

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4
Q

Which cells secrete proenzymes e.g. prorenin and pepsinogen?

A

Chief / peptic cells

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5
Q

How much gastric juice is secreted per day?

A

2.5L

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6
Q

What are the 3 gastric endogenous secretagogues?

A
  • Gastrin
  • Acetylcholine
  • Histamine
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7
Q

Describe the secretion and action of gastrin.

A
  • Gastrin is a polypeptide hormone.
  • Gastrin is secreted by gastrin cells (G cells).
  • Located in the gastric antrum and duodenum.
  • Proteins in food have astrong effect on the gastrin cells.
  • Gastrin is released into the blood.
  • Stimulates secretion of acid by parietal cells (through the proton pump).
  • Also increases pepsinogen secretion - stimulates blood flow and increases gastric motility.
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8
Q

Describe the secretion and action of gastrin.

A
  • Released from neurons.
  • Stimulates muscarinic receptors on surface of parietal cells and histamine containing cells.
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9
Q

Describe the secretion and action of histamine in the stomach.

A
  • Mast cells lying close to parietal cells release histamine.
  • Histamine released increased by gastrin and acetylcholine.
  • Acts on parietal cell H2 receptors.
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10
Q

What is Helicobacter pylori?

What diseases is it associated with?

A
  • ~50% of the world population is infected with H. pylori.
  • Causative factor in gastric and duodenal ulcers.
  • Risk factor for gastric cancer (adenocarcinoma).
  • Strong link with MALT lymphoma.
  • Additional associations:
    • Dyspepsia
    • Atrophic gastritis
    • Iron deficiency anaemia
    • Idiopathic thrombocytopaenic purpura
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11
Q

By what mechanism can H. pylori colonise the gastric mucosa?

A
  • Urease produced by the organism raises the gastric pH, allowing it to colonise.
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12
Q

Describe acute infection with H. pylori.

A
  • Can cause acute infection with symptoms that include nausea, dyspepsia, malaisa and halitosis.
  • Acute infection tends to last ~2 weeks.
  • Gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration.
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13
Q

Describe chronic infection with H. pylori.

A
  • Local inflammation and gastritis.
  • Outcome depends on:
    • Pattern of inflammation
    • Host response
    • Bacterial virulence
    • Environmental factors
    • Patient age
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14
Q

Define dyspepsia.

A

Pain or discomfort centred in upper abdomen, exacerbated by food.

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15
Q

Define GORD.

A

Reflux of gastric contents into oesophagus, heartburn, regurgitation, odynophagia, cough, associated water-brash.

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16
Q

What advice would you offer a patient with dyspepsia or GORD?

A
  • Offer simple lifestyle advice:
    • Healthy eating
    • Weight reduction
    • Smoking cesation
  • Avoid known precipitants:
    • Alcohol
    • Coffee
    • Chocolate
    • Fatty foods
  • Raising the head of the bed and not eating directly before going to bed can also help.
17
Q

What medications can be considered when dealing with dyspepsia and GORD?

A
  • STOP NSAIDs where appropriate / applicable.
  • Consider over the counter remedies:
    • Antacids - directly neutralise acid and inhibit activity of peptic enzymes.
      • Salts of magnesium and aluminium
      • E.g. Maalox, Mucogel
    • Alginates - taken in combo with antacid (varying amounts), increases viscosity and adherence of mucus to oesophageal mucosa; some form a raft.
      • E.g. Gaviscon
    • Simeticone - antifoaming agent (helps bloating, flatulence).
      • E.g. Infacol
  • Consider H. pylori testing
18
Q

What are the common tests for diagnosis of H. pylori infection?

A
  • Proton pump inhibitors should be stopped 2 weeks, and ABx 4 weeks, before diagnostic tests are conducted.
19
Q

What should be done following treatment of H. pylori if eradication has been successful?

And if eradication has been unsuccessful?

A
20
Q

What is the first-line treatment for H. pylori?

A
  • Offer patients who test positive for H. pylori a 7-day, twice-daily course of treatment with:
    • PPI
    • Amoxicillin
    • Either clarithromycin or metronidazole
  • Offer patients who are allergic to penicillin a 7-day, twice-daily course of treatment with:
    • PPI
    • Clarithromycin and metronidazole
  • Offer people who are allergic to penecillin and who have had previous exposure to Clarithromycin a 7-day, twice-daily course of treatment with:
    • PPI
    • Bismuth
    • Metronidazole
    • Tetracycline
21
Q

What are PPIs used to treat?

A
  • Peptic ulcer disease
  • Reflux oesophagitis
  • One component of H pylori eradication and Zollinger-Ellison syndrome
22
Q

Describe the action of a PPI.

A
  • Block K+H+ATPase (proton pump) of gastric parietal cells, reducing gastric acid secretion.
  • The first was Omeprazole - inhibits K+H+ATPase irreversibly.
  • Drug is weak base and accumulated in acid environment of the canaliculi of the stimulated parietal cell.
  • Usually oral administration.
23
Q

What are the adverse effects of PPIs?

In which conditions is PPI use cautioned?

A
  • Relatively uncommon:
    • Headache
    • Diarrhoea
    • Rashes
    • Dizziness
    • Somnolence
    • Confusion
    • Abdominal pain
    • Constipation
    • Dry mouth
    • GI disorder
    • Gynaecomastia
  • Caution in liver disease, severe renal insufficiency, pregnancy, breast feeding, risk of osteoporosis.
  • May mask the symptoms of gastric cancer, may increase risk of GI infections.
24
Q

What is depicted in this endoscopy photograph?

A

Ulcer of the mucosa on / adjacent to acid environment. Most common in stomach or proximal duodenum.

25
Q

How are peptic ulcers formed?

A
  • Can be associated with infection of gastric mucosa with H. pylori.
  • Imbalance between mucosal-damaging and mucosal-protecting factors:
    • Acid
    • Pepsin
    • Mucus
    • Bicarbonate
    • Prostaglandins
    • Nitric oxide
26
Q

What are the symptoms of peptic ulcer disease?

A
  • Burning epigastric pain
  • May be partially relieved by antacids and related to meal times
  • DU pain - worse at night and when hungry
  • Nausea
  • Heartburn
  • Flatulence
  • Perforation / haemorrhage / bleeding
27
Q

Describe the appropriate management of peptic ulcer disease in adults.

A
28
Q

What is the initial treatment for peptic ulcer disease?

A
  • H. pylori positive
    • ​Offer H. pylori eradication if peptic ulcer disease and H. pylori positive.
  • NSAID-associated ulcers
    • ​Stop the use of NSAIDs where possible.
    • Offer full-dose PPI or H2RA therapy for 8 weeks and, if H. pylori is present, subsequently offer eradication therapy.
  • H. pylori negative; no NSAID use
    • ​Offer full dose PPI or H2RA therapy for 4-8 weeks.
29
Q

What are Histamine H2 receptor antagonists used to treat?

State their mechanism of action.

A
  • Clinically used for peptic ulcers and reflux oesophagitis.
  • Competitively inhibit histamine actions at all H2 receptors.
  • Inhibit histamine-, gastrin- and acetylcholine- stimulated acid production.
  • Pepsin secretion also falls with reduction in volume of gastric juice.
30
Q

Give examples of H2 receptor antagonists.

A
  • Ranitidine (approximately 50% bioavailability, half life 2-2.5 hours, renal excretion).
  • Cimetidine (>60% bioavailablilty, half life 2 hours, renal excretion).
  • Usually given orally
  • Low dose available over the counter
31
Q

What are the adverse effects of H2RA?

More specifically, of Cimetidine?

A
  • Side effects are rare
    • ​Diarrhoea
    • Constipation
    • Dizziness
    • Muscle pains
    • Alopecia
    • Transient rashes
    • Hypergastrinaemia
  • Ranitidine is the better tolerated of the two
  • Cimetidine
    • ​Can interact with androgen receptors
      • Gynaecomastia in men
      • Decreased sexual function
    • Inhibits cytochrome P450
      • Slows the metabolism (and potentiates action) of range of drugs e.g. oral anticoagulants and tricyclics
    • Confusion in the elderly
32
Q

What should you do with a patient who has undergone treatment but still has an unhealed peptic ulcer?

A
  • Exclude non-adherence, malignancy, failure to detect H. pylori, inadvertent NSAID use, other ulcer-inducing medication and rare causes such as Zollinger-Ellison syndrome or Crohn’s disease.

Adult Years (27 decks)

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