Regulation And Disorders Of Gastruc Secretion Flashcards by amina Abbaci

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What are the contents of gastric juice fasting state

Cations: Na+, K+, Mg2+, H+ • Anions: Cl-, HPO42+, SO 42- • Pepsinogen • Lipase • Mucus • Intrinsic factor
– pH ~1-3.0

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What does the body of the stomach secrete

Mucus , pepsinogen and hcl

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Describe thick and thin walled elements of stomach

Thin-walled upper portion of the stomach (fundus and body): mucus, HCl
and pepsinogen • Thick-walled lower portion (antrum): ↑ gastrin secretion; gastrin
mediates acid secretion (HCl secretion)

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How is gastric acid made in the stomach

HCO3- is exchanged for Cl - in the blood → ↓ acidity of venous blood from stomach
compared to blood serving it
• Excess Cl - diffuses out into the stomach through chloride channels; K+/H+-ATPase
pumps H+ out into stomach lumen

 • Net effect = net flow of H + and Cl  – (forming HCl) out of the parietal cell and into
stomach lumen (-stomach secretes ~2L of HCl/day at 150mM)

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What contains resting juice

Non parietal secretions contain resting juice - Hugh hco3- conc

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Wage ads rage three phases of gastric juice secretion

The 3 phases involved: 1. Cephalic phase 2. Gastric phase 3. Intestinal phase

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How is hcl secretion regulated

HCl secretion is regulated by neuronal pathways and duodenal hormones

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Gastric acid secretion: regulation

Cephalic phase  (meal times-  smell, sight, taste, chewing)
• ACh stimulates histamine release from ECL cells • ACh acts directly on parietal cells → HCl secretion • Gastrin stimulates histamine release from ECL cells • Gastrin acts directly on parietal cells → HCl secretion

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Describe the cephalic phase

ACh stimulates histamine release from ECL cells • ACh acts directly on parietal cells → HCl secretion • Gastrin stimulates histamine release from ECL cells • Gastrin acts directly on parietal cells → HCl secretion

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What happens in the gastric phase

Gastric phase: effects of protein content of a meal on H + secretion
• Acidity of lumen of stomach is ↑ before a meal (no buffers) • Food mass containing proteins → ↑ peptides in stomach (↑ gastrin
secretion)

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What do proteins do to luminal acidity?

Proteins act as buffers in the gastric lumen And so what? HCl secretion increases

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How is gastrin secretion increased

• H+ + proteins → ↓ [H +]; protein acts as a buffer; proteins remove the
inhibitory powers of HCl on gastrin secretion
This then increases gastrin-mediated acid secretion

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Summary of gastric phase

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Describe the intestinal phase

Intestinal phase: balances the secretory activity of the stomach and the digestive and absorptive capacities of small intestine • High acidity of duodenal contents reflexly inhibits acid secretion
– Increased acidity inhibits the activity of digestive enzymes, bicarbonate
and bile salts
• Distension of duodenum, hypertonic solution, amino acids, fatty acids,
monosaccharides all inhibit acid secretion

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What does inhibition of acid secretion in the small intestine depend on

Composition of chyme • Volume of chyme • Distension of duodenum

How is acid secretion inhibited during the intestinal phase?

Short and long neuronal reflexes and hormones (enterogastrones, e.g.
secretin, CCK) inhibit acid secretion by the parietal cells or gastrin
secretion by the G cells, which is inhibited by somatostatin (stomach,
intestine, delta cells of pancreas, hypothalamus, brainstem,
hippocampus)

What does somatostatin do

Inhibits h+ , histamine and gastrin secretion

Factors that cause hcl secretion

Histamine, acetylcholine, gastrin, • Caffeine, alcohol, NSAIDs, nicotine • Helicobacter pylori • Zollinger-Ellison syndrome • Hyperparathyroidism (8-30%) *Avoid these drugs if you have peptic ulcer

What effects hcl reaching ideal hcl conc 150mM

Rate of secretion 2. Amount of buffering provided by the resting juice 3. Composition of ingested food 4. Gastric motility 5. Rate of gastric emptying 6. Amount of diffusion back into mucosa

Functions of hcl

Defence – kills germs • Protein digestion: activates pepsinogen to pepsin • Lack of HCl causes failure of protein digestion (achlorhydria or
hypochlorhydria = production of gastric acid in the stomach is absent or low ) • Stimulates flow of bile and pancreatic juice (HCO 3–rich watery secretions) • Promotes the action of gastric lipase

What stimulates the secretion of pepsinogen?

Inputs to chief cells from nerve plexus • There are parallels between gastric acid secretion and pepsinogen
secretion • Stimulators/inhibitors of acid secretion during the cephalic and intestinal
phases exert same effect on pepsinogen secretion

What stimulates the secretion of pepsinogen?

Secreted by chief cells in firm of pepsinogen. ( inactive = zygotes )
Activated if h+ is high - shape altered by acidity , exposing active site

What is the h+ pepsinogen mechanism called

Autocatalytic feedback process

Functions of pepsin

Initiates digestion of proteins - degrades food proteins in meats and seeds into peptides • But pepsin is not the only enzyme required for food digestion

What are the Protective factors that prevent autodigestion of the stomach by HCl and pepsin

Mucus layer protects the gastric mucosa from the low pH • Secretion of alkaline mucus and HCO 3- • Somatostatin inhibits gastrin release (negative feedback control) • Protein buffers- protein content of food is important • 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 • Replacement of damaged cells within the gastric pits (crypt cells)  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)

Factors responsible for gastric acid secretion: damaging factors

Histamine, acetylcholine, gastrin • Food/protein, alcohol, smoking, caffeine, NSAIDs • Zollinger-Ellison syndrome • Hyperparathyroidism

What Areas of the alimentary tract where peptic ulcers are common

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

What are causes of peptic ulcer

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?

Where do acute peptic ulcers occur symptoms

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 ) Severe bleeding • Heal with no scarring • Chronic peptic ulce

H. How does Pylori (Campylobacter pyloridis) cause peptic ulcer

Gram negative; spiral shaped (can be coccoid too) aerobic bacterium • Penetrates gastric mucosa (able to survive under the harsh condition of the stomach – pH 1-3) • Highly pathogenic, with many virulence factors Coccus (round) Bacillus (rod shaped) Spirochetes (spiral) The flagella enable its ‘corkscrew’ motility towards the gut epithelium Causes peptic ulcer = ulcer in the digestive tract (in the stomach or duodenum)

What are the Virulence factors of H. pylori

Motility: flagella; helps move it closer 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%

How are suspected ulcers investigated

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

What are the complications of peptic ulcer

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