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Physiology 1 Semester 2 > Regulation and Disorders of Gastric Secretion > Flashcards

Regulation and Disorders of Gastric Secretion Flashcards

1
Q

State the content of normal gastric juice

A

Cations - Na+, K+, Mg2+, H+
Anions - Cl-, HPO4 2-, SO4 2-
Pepsinogen
Lipase
Mucus
Intrinsic - pH approx 1-3

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2
Q

Describe the stomach

A
  • Thin walled upper portion of the stomach (fundus and the body) - mucus, HCl and pepsinogen
  • Thick walled lower portion (antrum) - increased gastric secretion, gastrin mediates acid secretion (HCl secretion)
  • Body of the stomach has epithelial cells with tubular glands - wall of glands lined with parietal cells for HCL/intrinsic factor release
  • Exocrine of mucus, acid and pepsinogen from the stomach
  • Contains enterochromaffin like cells that secrete paracrine agents like histamine that can then act on parietal cells
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3
Q

Explain how gastric acid is made in the stomach lumen

A
  • CO2 diffuses into the epithelium of enterocyte and reacts with H2O via carbonic anhydrase to form H2CO3 (carbonic acid)
  • This then dissociates into H+ and HCO3- ions
  • The HCO3- ions diffuse out of the epithelium and is exchanged for Cl- which decreases acidity of venous blood from the stomach compared to blood serving it
  • Excess Cl- diffuses out through chloride channels into the gut lumen
  • K+/H+ ATPase pumps H+ ions out into the stomach lumen and K+ ions into the epithelium
  • The net effect is that there is a net flow of H+ and Cl- (forming HCl) out of parietal cell and into the stomach lumen (stomach secretes 2L of HCL a day at 150 mM)
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4
Q

Describe gastric secretions

A
  • Some amount of gastric juice is described as resting juice - similar to plasma, non parietal cells secrete HCO3- which brings the pH to 7.4
  • Mucus is alkaline, thick and sticky - forms a water insoluble gel on epithelial surface - increases HCO3- - protects against H+ secretion
  • Rennin produced at birth curdles milk into casein clot - production is replaced by pepsinogen
  • Lipase - triglycerides -> fatty acids and glycerol
  • Intrinsic factors for absorption of vitamin B12
  • Gastric acid - kills bacteria- acid denaturation of digested food, acidic pH of gastric acid activates pepsinogen to pepsin for protein digestion
  • Promotes the action of gastric lipase and the secretion of pancreatic HCO3-
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5
Q

State the 3 stages of gastric secretions

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
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6
Q

Briefly how is HCl secretion controlled?

A
  • HCl secretion is regulated by neuronal pathways and duodenal hormones
  • Done by direct pathway by acting on parietal cells to increase acid secretion
  • Also can be done by an indirect pathway by influencing the secretion of gastrin and histamine which increase acid secretion
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7
Q

Describe the cephalic phase of gastric acid secretion including how it is regulated

A
  • Acetylcholine stimulates histamine release from ECL cells
  • Acetylcholine acts directly on parietal cells to cause HCl secretion
  • Acetylcholine can also stimulate G cells to secrete gastrin which then causes ECL cells to secrete histamine
  • Gastrin stimulates histamine release from ECL cells
  • Gastrin acts directly on parietal cells to cause HCl secretion
  • Too much HCl can lead to damage so when HCl increases too much then it stimulates the D cells to release somatostatin which inhibits the pathways that lead to HCl secretion e.g. inhibits parietal cell activation, ECL activation and G cell activation
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8
Q

Describe the gastric phase

A
  • Distension of the stomach which increases peptide concentration
  • This increases the acidity as there is increased [H+]
  • Distension of the stomach stimulates enteric neurons to release acetylcholine which then stimulated parietal cells to release HCl
  • Food in the stomach also buffers the acidity however to increase pH so that somatostatin secretion isn’t stimulated to allow HCl levels to remain high
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9
Q

Explain how protein content in a meal effects H= secretion-

A
  • Acidity of the lumen of the stomach is increased before a meal
  • The food mass containing proteins increases the peptides in the stomach which increases gastrin secretion
  • H+ ions + proteins decrease [H+] proteins acts as a buffer - proteins remove the inhibitory powers of HCl on gastrin secretion so there is more gastrin mediated acid secretion
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10
Q

Describe the intestinal phase

A
  • Balances the secretory activity of the stomach and the digestive and absorptive capacities of small intestine because high acidity can denature important enzymes
  • There is 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
  • Thus inhibition of acid secretion in the small intestine depends on composition of chyme, volume of chyme, distension of duodenum
  • The intestinal phase also has the ability to stimulate enterogastrones like CCK and secretin
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11
Q

Explain how acid secretion is inhibited during the intestinal phase

A
  • Short and long neuronal reflexes and hormones (enterogastrones like secretin, CCK inhibit acid secretion)
  • They do this via parietal cells or gastrin secretion by G cells which is inhibited by somatostatin (stomach, intestine, delta cells of pancreas, hypothalamus, brainstem, hippocampus)
  • When the chyme in the duodenum has increased stomach distension, there is increased [H+], it is high [peptides] and high osmolarity then neural reflexes inhibit neural input to inhibit acetylcholine release
  • There is also enterogastrones that inhibit ECL cells to stop them secreting histamine so that parietal cells are not activated and do not release HCl
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12
Q

State some other factors that cause HCl secretion

A
  • Histamine, acetylcholine, gastrin
  • Caffeine, alcohol, NSAIDs, nicotine
  • Helicobacter pylori
  • Zollinger ellison syndrome
  • Hyperparathyroidism
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13
Q

[HCl] can reach 150mM depending on?

A
  1. Rate of secretion
  2. Amount of buffering provided by resting juice
  3. Composition of ingested food
  4. Gastric motility
  5. Rate of gastric emptying
  6. Amount of diffusion back into mucosa
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14
Q

Why is HCl essential?

A
  • Acts as a defence as it kills germs
  • Protein digestion - activates pepsinogen to pepsin which initiates protein digestion
  • Lack of HCl causes failure of protein digestion (achlorhydria/hypochlorhydria = absent or low gastric acid production)
  • Stimulates the flow of bile and pancreatic juice (HCO3- rich watery secretions)
  • Promotes the action of gastric lipase
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15
Q

How is pepsinogen secretion stimulated?

A
  • Inputs to chief cells from the nerve plexus
  • There are parallels between gastric acid secretion and pepsinogen secretion
  • Stimulators/inhibitors of acid secretion during the cephalic and intestinal phases exert the same effect on pepsinogen secretion
  • Secreted by chief cells as the inactive form zymogen - activated if [H+] is high - shape is altered by acidic conditions which exposes the active site
  • There is an autocatalytic feedback process which means that while HCl is needed for the initial pepsinogen -> pepsin conversion after that the pepsin made can carry out its own activation of the conversion
  • Inactivated upon entry of food into the small intestine as HCO3- and peptides neutralise the H+
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16
Q

What is the function of pepsin?

A

Initiates digestion of proteins - degrades food proteins in meats and seeds into peptides

17
Q

Describe how NSAIDs play a role in gastric acid secretion disorders - include both normal circumstances and the effects of NSAIDs

A

Normal circumstances -
- Gastric vagus nerve signals can cause acetylcholine release which then can act on histamine secreting cells to release histamine which binds to H2 receptors on parietal cells to cause secretion of acid
- The histamine secreting cells can also be activated by gastrin
- Acetylcholine can also act directly onto the parietal cells via muscarinic receptors
- Prostaglandins inhibit parietal cell activity and increases mucus cell activity as well as causing vasodilation - they can also promote bicarbonate secretion to neutralise stomach acid

NSAIDs -
- NSAIDs (non steroidal antiinflammatory drugs) inhibits prostaglandin E2 secretion so parietal cells are not inhibited from acid secretion and there is less mucus secretion
- It also blocks secretion of TXA which promotes healing so there is impaired healing

18
Q

State some factors that prevent infection of gastric mucosa

A
  • Mucus production
  • Peristalsis and fluid movement
  • Seamless epithelium with tight junctions
  • Fast cell turnover
  • IgA secretion at mucosal surfaces
  • HCl and pepsin secretion
19
Q

State and describe the protective factors that prevent autodigestion of the stomach by HCl and pepsin

A
  • Mucus layer protects the gastric mucosa from the low pH
  • Secretion of alkaline mucus and HCO3-
  • 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 between epithelial cells prevents back diffusion of H+ ions
  • Prostaglandins (E and I) inhibit acid secretion and enhance blood flow - mucosal blood flow removed excess acid that has diffused across the epithelial layer - maintenance of mucosal integrity and repair - growth factors e.g. epidermal growth factor
  • Replacement of damaged cells within gastric pits (crypt cells)
20
Q

State the factors needed for gastric acid secretion that are therefore damaging to the gut epithelium

A
  • Histamine, acetylcholine, gastrin
  • Food - protein, alcohol, smoking, caffeine, NSAIDs
  • Zollinger ellison syndrome
  • Hyperparathyroidism
  • Stress
  • Bile acids = irritants
  • Genetics
  • Helicobacter pylori
21
Q

What is the main major risk factor for ulcers?

A

H pylori infection

22
Q

When is H pylori acquired and what is the prevelence?

A

H pylori is acquired in childhood and is present in 10-15% of the population

Environmental and host factors can determine the distribution and colonisation of H pylori in the stomach

23
Q

Describe how NSAIDs play a role in gastric acid secretion disorders

A
  • NSAIDs are acidic and so cause topical irritation of the gut
  • They also inhibit the function of prostaglandins and thromboxane A2 which are both important in gut healing
  • This impairs the barrier properties of the mucosa which suppresses gastric prostaglandin synthesis
  • This then decreases gastric mucosal blood flow which interferes with the repair of superficial injury and inhibits platelet aggregation
  • Presence of acid in the stomach promotes NSAID mediated gastric disorders

How:
- It impairs the restitution process
- Inactivated FGF which interferes with the haemostasis process

24
Q

Where can ulcers occur and what can they cause?

A
  • The oesophagus, stomach and duodenum can be affected
  • There is a breakage of the mucosal barrier and an imbalance between the protective and damaging factors in the GI tract
  • There is then an exposure of tissues to the erosive effects of gastric acids (HCl/bile acids and pepsin)
25
Q

State specially the areas where ulcers are common

A
  • Distal oesophagus especially when someone has barrett’s oesophagus
  • The stomach - the junction between the antrum and the body
  • Duodenal cap/ampulla - first part of duodenum - smooth walled, dilated, mesenteric
  • Meckel’s diverticulum - outpouching or bulge in the small intestine
  • Weight loss surgery (gastroenterostomy), weight loss
26
Q

State the 3 main causes of peptic ulcers

A
  • Hyperacidity - reflux of the duodenal contents (oesophagus, stomach and duodenum)
  • Presence of H pylori is a risk factor for gastric cancer - eradication decreases the risk
  • NSAIDs, genetic factors, sex - male
27
Q

Describe chronic and acute peptic ulcers

A

Chronic peptic ulcers -
- Common especially in over 50s, low incidence in the young
- Occurs in the upper GI tract
- Asymptomatic in over 80% of people
- 90% incidence in developing countries
- Inflammation plays a key role in the disease process
- Eventually will completely heal and there will be tissue replacement with some scarring

Acute peptic ulcers -
- Less common
- Develops from an area of corrosive gastritis (in the oesophagus, stomach of proximal duodenum)
- Or can develop due to severe stress or shock like burns or trauma
- There is acute hypoxia of the surface epithelium
- Leads to severe bleeding, heals with no scarring and can become a chronic peptic ulcer

28
Q

Describe the H pylori bacterium

A
  • Gram negative bacterium that is spiral shaped - Aerobic bacterium
  • Penetrates the gastric mucosa and so is able to survive under the harsh condition of the stomach (pH 1-3)
  • Highly pathogenic with many virulence factors
  • Causes peptic ulcer in stomach or duodenum
29
Q

Virulence factors of H pylori - state these

A
  • Motility - flagella - helps it to move closer to the epithelium
  • Produces urease - converts urea to ammonia which buffers gastric acids and produces carbon dioxide
  • Cytotoxin associated antigen - inserts pathogenicity islands and confers ulcer forming potential - can lead to actin remodelling, IL-8 induction , host cell growth and apoptosis inhibition - severe gastritis/ ulcers/ carcinoma
  • Vacuolating toxin A - alters the trafficking of intracellular proteins in gastric cells - presence of these exotoxins can increase someones risk for gastritis/ulcers/cancer
  • A large number of outer membrane proteins - adhesins, phospholipases, porins, iron transporters, and flagellum associated proteins
  • H pylori infection dysregulates gastrin secretion and increases it - it does this by increasing g cell numbers which are cells that secretion gastrin and reducing the number of d cells that secrete somatostatin which inhibited g cell activity
30
Q

Describe how H pylori gets to the epithelium and causes damage

A
  • Due to its corkscrew shape the bacteria can easily infiltrate the mucus layer from the gastric fluid and get close to the epithelial layer
  • They then produce urease to convert urea + water into ammonia and CO2 to neutralise the gastric acid
  • The bacterium then multiply and damage to the epithelium increases as the mucus layer has been disrupted so acid secreted now damages the stomach epithelium
  • This causes inflammation of the area by gastric acid, proteases and effector molecules
  • There is also mucosal cell death by cytotoxins and ammonia and white blood cells move to the area in an attempt to remove the bacterium - inflammation continues
31
Q

Summarise how H.pylori and NSAIDs

A

H. pylori - makes the stomach more acidic so there is higher [H+] and pepsin which causes mucosal damage directly
It also causes release of cytokines, liposaccharides, heat shock proteins, enzymes etc which initiates the inflammatory cascade (neutrophils, lymphocytes etc) which causes mucosal damage

NSAIDs - also increases [H+] and pepsin and has topical and systemic effects - decreases mucus production, decreases blood flow, increases neutrophils, decreases bicarbonate and decreases cell restitution - mucosal damage and ulceration

32
Q

State the tests for a peptic ulcer

A
  • Endoscopy
  • Histological examination and staining of an EGD biopsy
  • Test for the presence of H pylori - stool antigen test, evaluate the urease activity, urea breath test
  • Give someone a urea tablet with C14
  • If there is H pylori it is converted into ammonia and bicarbonate and the bicarbonate enters circulation
  • Then can be collected in the breath as 14 CO2 is now in the breath
  • 2L of breath is collected in a mylar balloon and Co2 is transferred to a counting vial
  • 10ml of scintillation fluid is added and it is put into a scintillation counter
  • Identifies if a person has urease activity and therefore has H pylori present
33
Q

State the potential complications of a peptic ulcer

A
  • Haemorrhage - GI bleeding
  • Perforation (peritonitis) and penetration (liver and pancreas may be affected) - leakage of luminal contents
  • Narrowing of the pyloric canal (stricture causing acquired pyloric stenosis in the stomach) or oesophageal stricture
  • Malignant change becomes 3-6 x more likely with H pylori infection

Physiology 1 Semester 2 (50 decks)

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