Regulation and disorders of gastric acid secretion Flashcards by Aina Ahmad

What are the contents of gastric juice in the fasting state

-cations (Na+, K+ etc)
-anions (Cl- etc)
-pepsinogen
-lipase
-mucus
-intrinsic factor

Gastric juice adds 2.5L a day to intestinal contents
-gastric juice is essential for digestion and absorption

How well did you know this?

Not at all

Perfectly

Explain the characteristics of the stomach

-thin walled upper portion of the stomach (fundus and body) contains mucus, HCL and pepsionogen
-thick walled lower portion (antrum): increased gastric secretion: gastrin mediates acid secretion

-Body has numerous epithelial cells with numerous tubular glands
-walls of the glands is lined with parietal cells —-> HCL and intrinsic factor

How well did you know this?

Not at all

Perfectly

How is gastric acid made in the stomach lumen

1) HCO3- is exchanged for Cl- in the blood—-> decreased acidity of venous blood from stomach compared to blood serving it

2) Excess Cl- diffuses out into the stomach through chloride channels

3) Net effect= net flow of H+ and Cl- out of the parietal cell and into the stomach lumen

How well did you know this?

Not at all

Perfectly

Explain gastric secretions

mucus: alkaline, thick and sticky (forms water insoluble gel on epithelial surface) —-> increased HCO3- protects against H+ secretion

Rennin: produced at birth; curdles milk into casein clot

Lipase: triglycerides—-> fatty acids and glycerol

-intrinsic factor: absorption of vitamin B12

How well did you know this?

Not at all

Perfectly

What does gastric acid (HCL) do?

-kills bacteria; acid denaturation of digested food
-promotes the action of gastric lipase and the secretion of pancreatic HCO3

How well did you know this?

Not at all

Perfectly

List the three phases of secretion of gastric juice

At meal times there is increased HCL secretion

The three phases are:
1) cephalic phase
2) gastric phase
3) intestinal phase

How well did you know this?

Not at all

Perfectly

What is HCL secretion regulated by

HCL secretion is regulated by neuronal pathways and duodenal hormones

How well did you know this?

Not at all

Perfectly

How does acid secretion occur through direct and indirect pathways

1) direct pathway, by acting on parietal cells —-> increased acid secretion

2) indirect pathway, by influencing the secretion of gastrin and histamine —-> increased acid secretion

How well did you know this?

Not at all

Perfectly

Explain what happens in the cephalic phase (regulation)

1) Ach stimulates histamine release from ECL cells

2) ACh acts directly on parietal cells—> HCL secretion

3) Gastrin stimulates histamine release from ECL cells

4) gastrin acts directly on parietal cells—-> HCl secretion

How well did you know this?

Not at all

Perfectly

Explain what happens in the gastric phase

Gastric phase (distension of stomach; increased peptide concentration): increased acidity

How well did you know this?

Not at all

Perfectly

What is the effect of protein content of a meal on gastrin secretion

-food mass containing proteins—> increased peptides in stomach so increased gastrin secretion

How well did you know this?

Not at all

Perfectly

What do proteins do to luminal acidity

-proteins act as buffers in the gastric lumen
-HCl secretion increases

How well did you know this?

Not at all

Perfectly

Explain this mechanism

1) H+ and proteins causes decreased concentration of H+

2) protein acts as a buffers

3) proteins remove the inhibitory powers of HCL on gastrin secretion

How well did you know this?

Not at all

Perfectly

What does a meal containing proteins elicit?

a meal containing proteins elicits feedback inhibitory and stimulatory signals which increases acid secretion via stimulation of gastrin secretion

How well did you know this?

Not at all

Perfectly

Explain 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 all inhibit acid secretion

How well did you know this?

Not at all

Perfectly

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

-composition of chyme
-volume of chyme
-distension of duodenum

How well did you know this?

Not at all

Perfectly

How is acid secretion inhibited during the intestinal phase

-short and long neuronal reflexes and hormones inhibit acid secretion via parietal cells or gastrin secretion by the G cells
-which is inhibited by somatostatin

How well did you know this?

Not at all

Perfectly

What are direct and indirect pathways of three acid secretagogues (Ach, gastrin and histamine)

direct pathway:
-Ach, gastrin and histamine stimulate the parietal cell—> triggering the secretion of H+ into the lumen

Indirect pathway:
-Ach and gastrin also stimulate the ECL cell, resulting in secretion of histamine

How well did you know this?

Not at all

Perfectly

Which factors promote the secretion of HCl

-histamine, acetylcholine and gastrin
-caffeine, alcohol, NSAIDs and nicotine
-helicobactor pylori
-Zollinger-Ellison syndrome
-Hyperparathyroidism

Which factors can cause HCl to reach 150mM

1) rate of gastric secretion, motility and rate of gastric emptying

2) amount of diffusion back into mucosa

3) amount of buffering provided by the non parietal cells

4) composition of ingested food

What are functions of HCL

1) defence
2)protein digestion —-> activates pepsionogen to pepsin
3) lack of Hcl causes failure of protein digestion
4) stimulates flow of bile and pancreatic juice
5) 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 of acid secretion during the cephalic and intestinal phases

What stimulates the secretion of pepsinogen

-secreted by chief cells in the form of pepsinogen
-activated if H+ is high
-auto catalytic feedback process
-inactivated upon entry of food in the small intestine and peptides neutralise the H+

What are 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

How does NSAIDs play a role in gastric acid secretion disorders

NSAIDs block the production of PGE₂ Without PGE₂: Less mucus is made → stomach lining is less protected Less blood flow → slower healing Acid keeps being produced → damaging the unprotected stomach lining

What are other factors that prevent infection of gastric mucosa

-mucus production -peristalsis and fluid movement -seamless epithelium with tight junctions -fast cell turnover -IgA secretion at mucosal surfaces

List protective factors that prevent auto digestion of the stomach by HCl and pepsin

-mucus layer protects the gastric mucosa from low pH -secretion of alkaline mucus and HCO3- -somatostatin inhibits gastrin release -protein buffers -epithelial cells remove excess H+ via membrane transport systems -prostaglandins: inhibit acid secretion -mucosal blood flow removes excess acid -maintenance of mucosal integrity and repair

What are predisposing factors to peptic ulcer formation

-gastric and duodenal infection with H.pylori is a major risk factor -environmental and host factors can determine the distribution and colonisation of H.pylori in the stomach

How do NSAIDs (aspirin) play a role in gastric acid secretion disorders

NSAIDs are acidic and causes topical irritation of the gut: -impair the barrier properties of mucosa -suppress gastric prostaglandin synthesis -decreases gastric mucosal blood flow -interfere with the repair of superficial injury -inhibit platelet aggregation

What is the GIT function

GIT function: -storage, secretory, digestion, absorption of nutrients, salts, water -metabolism and elimination of wastes

Describe what happens in malformation of GIT

-decrease nutrient status of the individual

Explain peptic ulcer and mechanism of peptic ulcer formation

-10% of population affected by ulcers -sites affected: oesophagus, stomach and duodenum Mechanism: -breakage of mucosal barrier -imbalance between protective and damaging factors of GIT -exposure of tissues to the erosive effects of gastric acids

What are areas of the alimentary tract where peptic ulcers are common

-distal oesophagus -the stomach (junction of antrum and body) -duodenal ampulla -meckel diverticulum

What are causes of peptic ulcer

-hyperacidity: reflux of duodenal contents -presence of H.pylori is a risk factor for gastric cancer -NSAIDs: genetic factors, sex?

What is an outcome of a peptic ulcer

-complete healing and replacement of tissue and some scarring

Explain characteristics of a peptic ulcer

-occurs in upper GIT -asymptomatic in >80% of people -common in over 50s -90% incidence in developing countries

Discuss an acute peptic ulcer

-less frequent -develops from areas of corrosive gastritis, severe stress or shock -acute hypoxia of surface epithelium

What are outcomes of a peptic ulcer

-severe bleeding -heal with no scarring -chronic peptic ulcer

What are virulence factors of H.pylori

-motility: flagella; helps it move closer to epithelium -produces urease (converts urea into ammonia) -cytotoxin associated antigen- inserts pathogenicity islands and confers ulcer forming potential -vacuolating toxin A- alters trafficking of intracellular protein in gastric cells -a large number of outer membrane proteins: adhesins, phospholipases, porins, iron transporters

What does H.pylori do to gastrin secretion

-H.pylori infection disregulates gastrin secretion—-> increased gastrin secretions

Explain the role of H. pylori in mucosal damage and ulceration

This bacteria lives in the stomach. It: Releases harmful substances (like cytokines, lipopolysaccharides, enzymes) Triggers the body’s inflammatory response (involving white blood cells and chemicals) Increases acid (H⁺) and pepsin (a stomach enzyme) All of this causes damage to the stomach lining and can lead to ulcers.

Explain the role of NSAIDs in mucosal damage and ulceration

Drugs like aspirin or ibuprofen They: Have topical effects (they can irritate the stomach lining directly) Have systemic effects (they block protective prostaglandins) This leads to: Less mucus Less blood flow More inflammation Less bicarbonate (which neutralizes acid) Poor healing of the stomach lining Result: Mucosal damage and ulcers

What are diagnostic tests for a suspected peptic ulcer

-endoscopy -histological examination and staining of an EDD biopsy

What is a test for the presence of H.pylori

-stool antigen test -evaluate urease activity -urea breath test

What are complications of a peptic ulcer

-haemorrhage -perforation and penetration -narrowing of pyloric canal or oesophageal stricture -malignant change becomes 3-6 times likely with H.pylori infection