Disorders of gastric acid secretion Flashcards

1
Q

What is the function of the GI tract?

What can the malformation of the GI tract cause?

A

storage, secretory, digestion, absorption of nutrients, salts, water, metabolism and elimination of (undigested) wastes

↓ nutrient status of the individual

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2
Q

What sites are affected by peptic ulcers?

What are the 3 effects of peptic ulcers?

A

Sites affected: Oesophagus, stomach and duodenum

Breakage of mucosal barrier
…imbalance between protective and damaging factors of GIT
…exposure of tissues to the erosive effects of gastric acids (HCl, bile acids) and pepsin

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3
Q

What factors are responsible for gastric acid secretion: damaging factors

A
Histamine
Acetylcholine
Gastrin
Food/protein, alcohol, smoking, caffeine, NSAIDs
Zollinger-Ellison syndrome
Hyperparathyroidism

Stress? - Can it aggravate it once ulcer is present?

Bile acids are irritants

Genetic?

Helicobacter pylori

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4
Q

Where can peptic ulcers form?

A

Duodenal cap/ampulla: first part of the duodenum; smooth walled; dilated; mesenteric
The stomach – junction of antrum and body
Distal oesophagus, especially in Barrett’s oesophagus
Meckel’s diverticulum – outpouching or bulge in the small intestine (congenital)
Weight loss surgery (gastroenterostomy) weight loss

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5
Q

What causes the formation of a peptic ulcer?

What is the outcome?

A

Hyperacidity; reflux of duodenal contents (oesophagus, stomach and duodenum)
Presence of H. pylori is a risk factor for gastric cancer – eradication → ↓ risk
NSAIDs; Genetic factors; Sex – being male?

Complete healing and replacement of tissue and some scarring

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6
Q

When are chronic peptic ulcers common?

A

Occurs in upper GIT (pepsin and HCl)
Asymptomatic in >80% of people
Low incidence in young; common in over 50s
90% incidence in developing countries
Inflammation plays a key role in the disease process

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7
Q

Where does an acute peptic ulcer form?

A

Develops from areas of corrosive gastritis (oesophagus, stomach, proximal duodenum), severe stress or shock (burns, trauma)

Acute hypoxia of surface epithelium (i.e., ischaemia of gastric mucosa)

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8
Q

What are the outcomes of an acute peptic ulcer? (3)

A

Severe bleeding
Heal with no scarring
Chronic peptic ulcer

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9
Q

H. pylori, Smoking, genetic factors, stress, NSAIDs

How do these cause a peptic ulcer

A

Acid pepsin

impaired mucosal defence

leads to peptic ulcer

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10
Q

What factors protect the stomach from digestion?

A

Gastric juices: 150mM HCl & pepsin in the stomach

Mucus layer protects the gastric mucosa from the low pH

Secretion of alkaline mucus and HCO3-

Somatostatin inhibits gastrin release (negative feedback control)

Protein content of food

Epithelial cells remove excess H+ via membrane transport systems; tight junctions of epithelial cells prevent back diffusion of H+ ions

Prostaglandins (E and I): inhibit acid secretion and enhance blood flow

  • Mucosal blood flow removes excess acid that has diffused across the epithelial layer
  • Maintenance of mucosal integrity and repair: growth factors (e.g., epidermal growth factor, insulin-like growth factor I) and PGs

Replacement of damaged cells within the gastric pits

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11
Q

Describe the H.Pylori bacteria

A

Gram negative; spiral shaped (can be coccoid too) aerobic bacterium

Penetrates gastric mucosa (able to survive under the harsh condition of the stomach)

Highly pathogenic, with many virulence factors

Peptic ulcer = ulcer in the digestive tract (in the stomach or duodenum)

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12
Q

What are the Virulence factors of H. pylori?

A
Motility: flagella; moves close to the epithelium (pH 7)
Produces urease (converts urea to ammonia, which buffers gastric acid and produces CO2)

Cytotoxin-associated antigen (CagA) – inserts pathogenicity islands and confers ulcer-forming potential

Vacuolating toxin A (VacA) – alters the trafficking of intracellular protein in gastric cells
A large number of outer membrane proteins: Adhesins (BabA), phospholipases, porins, iron transporters, and flagellum-associated proteins

H. Pylori is the commonest cause of peptic ulcer – ↑peptic ulcer risk by 10-20%

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13
Q

What tests can be used to identify ulcers?

How do we test for H. pylori?

A

Diagnostic tests
Endoscopy (oesophagogastroduodenoscopy, EGD)
Histological examination and staining of an EGD biopsy

Test for the presence of H. pylori
Stool antigen test
Evaluate urease activity
Urea breath test

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14
Q

What are the complications of peptic ulcer?

A

Haemorrhage (GI bleeding)

Perforation (peritonitis) and penetration (liver and pancreas may be affected); leakage of luminal contents

Narrowing of pyloric canal (stricture causing acquired pyloric stenosis in the stomach) or oesophageal stricture

Malignant change becomes 3-6 times likely with H. pylori infection

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