Treatment Of Peptic Ulceration And Inflammatory Bowel Disease Flashcards

1
Q

Why do we need Gastric Acid?

A

Digestion of food, iron absorption and killing pathogens.

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2
Q

Gastrin

A
  • polypeptide hormone secreted by G cells located in the gastric antrum and duodenum.
  • Proteins in food have a strong effect on G cells and stimulates release of gastrin into blood.
  • Gastrin stimulates secretion of acid by Parietal Cells (through the proton pump) and increases Pepsinogen secretion stimulating blood flow and increasing gastric motility.
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3
Q

Acetylcholine

A
  • Released from neurons.

- Stimulates muscarinic receptors on surface of Parietal cells and histamine containing cells.

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4
Q

Histamine

A
  • Mast cells lying close to Parietal cell release Histamine.
  • Histamine release increased by gastrin and acetylcholine.
  • Acts on Parietal cell H2 receptors.
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5
Q

Treatment of Helicobacter Pylori

A

-First Line - Offer non-penicillin-allergic people who test positive for H. Pylori a 7-day, twice-daily course of treatment with a PPI and Amoxicillin and either Clarithromycin or Metronidazole.

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6
Q

Proton Pump Inhibitors

A
  • Esomeprazole, Lansoprazole, Omeprazole, Pantoprazole, Rabeprazole
  • Can treat H.Pylori infection, Peptic Ulcers, Dyspepsia, GORD, NSAID-associated ulcers, Reflux oesophagitis, Zollinger-Ellison Syndrome.
  • Inhibits K+H+ATPase irreversibly. Basal and stimulated gastric acid secretion reduced. Drug is weak base and accumulates in acid environment of the canaliculi of the stimulated parietal cells.
  • Usually oral administration.
  • Side-effects are relatively uncommon but include headache, diarrhoea, rashes, dizziness, somnolence, confusion, impotence, gynaecomastia, myalgia and arthalgia.
  • Caution in liver disease, pregnancy and breast feeding.
  • May mask the symptoms of gastric cancer.
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7
Q

Histamine H2 Receptor Antagonists

A
  • Used for peptic ulcers and reflux oesophagitis.
  • Competitively inhibits 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.
  • Usually given orally.
  • Low dose available OTC.
  • RANITIDINE - approx. 50% bioavailability, half life 2.5hrs, renal excretion. Tolerated better than Cimetidine.
  • CIMETIDINE- above 60% bioavailability, half life 2 hours, renal excretion. Can interact woth androgen receptors (gynaecomastia in men and decreased sexual function), cause confusion in elderly, and inhibits cytochrome P450 (slows metabolism (and potentiates action) of range of drugs e.g. oral anticoagulants and tricyclics).
  • Side-effects - rare but possible are diarrhoea, dizziness, myalgia, alopecia, transient rashes, hypergastrinemia.
  • Can mask signs and symptoms of gastric cancer.
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8
Q

Dyspepsia & Gastro-oesophageal Reflux Disease Treatment

A
  • Lifestyle advice - healthy eating, weight reduction, smoking cessation, avoid known precipitants (alcohol, coffee, chocolate, fatty foods), raise the head of bed and have main meal well before going to bed.
  • Stop NSAIDs where you can.
  • Consider OTC remedies: Antacids (directly neutralise acid and inhibit activity of peptic enzymes (salts of Mg or Al)), Alignates (increases viscosity and adherence of mucus to oesophageal mucosa), & Simeticone (antifoaming agent to help bloating and flatulence).
  • Consider PPI for symptomatic treatment.
  • H2 Receptor Antagonist potential alternative
  • Consider H. Pylori testing > treat if positive.
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9
Q

Peptic Ulceration Treatment

A
  • H.Pylori +ve - H.Pylori eradication
  • NSAID associated - stop use of NSAIDs where possible. Offer full dose PPI or H2RA therapy for 8 weeks and, if H. pylori is present, subsequently offer eradicaton therapy.
  • H. pylori -ve and no NSAIDs - offer full dose PPI or H2RA therapy for 4-8 weeks.
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10
Q

Inflammatory Bowel Disease Complications

A
  • Stoma
  • Anaemia
  • Perforation
  • Obstruction/Stricture
  • Fistulae
  • Toxic Megacolon
  • Malnutrition
  • Increased risk of bowel cancer
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11
Q

Investigations for IBD

A
  • FBC, CRP
  • Stool Microscopy
  • Faecal Calprotectin
  • CT Scan/MRI
  • Endoscopy (sigmoidoscopy, colonoscopy) and biopsies.
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12
Q

Treatment for IBD

A
  • Aminosalicylates e.g. Mesalazine
  • DMARDs e.g. Azathioprine, Methotrexate
  • Biologics e.g. Infliximab
  • Corticosteroids
  • Sympathetic relievers e.g. analgesics, laxatives, “constipators”
  • Surgery
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13
Q

Why do we need mucous secreting cells?

A

To create important protective mucous layer.

Do this by trapping bicarbonate ions (alkaline) and creating gel-like barrier.

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14
Q

What do Prostaglandins do in terms of protection?

A

Stimulates secretion of mucus and bicarbonate, dilate mucosal blood vessels and tehy are cytoprotective.

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15
Q

Oxyntic/Parietal Cells

A

Secrete HCl and intrinsic factor.

HCl is formed using a proton pump (K+H+ATPase).

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16
Q

Chief/Peptic Cells

A

Secrete proenzymes e.g. prorennin and pepsinogen