GI 6 - The Stomach Flashcards Preview

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Flashcards in GI 6 - The Stomach Deck (31):

Which gastric cells secrete histamine?

Enterochromaffin-like cells


What acts to stimulate Gastrin secretion in the stomach?

- Peptides/ amino acids in lumen
- Vagally released Acetylcholine
- Vagally released Gastrin-releasing peptide (GRP)


What is the function of intrinsic factor? Which gastric cell produces it?

- Necessary for Vitamin B12 absorption in the ileum
- Parietal cells


Why do parietal cells change shape when stimulated to produce acid?

Tubulovesicular structure rearranges into a canicular structure = massively increases surface area for secretion


Describe the mechanism of HCl secretion:

- Carbonic anhydrase combines CO2 + OH- to form HCO3- + H+ in parietal cell
- Cl- moves into parietal cell via HCO3-/Cl- antiporter
- Cl- moves into stomach lumen via apical Cl- channel, down conc. grad.
- H+ is pumped into lumen via H+/K+-ATPase
- Basolateral Na+/K+-ATPase sets up Na+ conc. grad.
- Na+/H+-ATPase maintains pH of parietal cell
- Excess K+ leaves via apical/basolateral K+ channels


What is the alkaline tide that occurs after eating? What causes it?

- Temporary increase in pH after eating
- Caused by efflux of HCO3- by parietal cells during the secretion of acid into the stomach


Name the channels used in acid secretion on the basolateral parietal wall:

HCO3-/Cl- exchanger
K+ channel


Name the channels used in acid secretion on the apical parietal wall:

Cl- channel
K+ channel


What directly stimulates the production of gastric acid?

- Vagus nerve secretes Ach -> M3 on parietal cells
- Histamine
- Gastrin


How does the vagus nerve stimulate the production of acid both directly and indirectly?

Directly: stimulates parietal cells via Ach -> M3
- Stimulates enterochromaffin-like cells to secrete Histamine = stimulates parietal cells
- Stimulates G cells to secrete Gastrin = stimulates parietal cells


How is acid secretion from parietal cells inhibited?

Luminal acid stimulates D cells to secrete Somatostatin, which:
- Directly inhibits Parietal cells
- Inhibits Gastrin production from G cells, which indirectly inhibits parietal cells


Name the 3 phases of digestion, and the percentage of total HCl secretion caused by each stage:

1) Cephalic ~ 30% of total HCl production
2) Gastric ~ 60%
3) Intestinal ~ 10%


Describe the cephalic stage of digestion:

- Anticipation of food (sight, smell, taste, chewing) stimulates the parasympathetic fibres on the Vagus nerve
- This directly stimulates Parietal cells = acid secretion
- and G cells = gastrin production


Somatostatin is released when D cells detect luminal acid. Why is somatostatin release inhibited when food is present in the stomach?

Food acts as a buffer, causing pH to rise, inhibiting D cells


What is the Enterogastric reflex?

- Lipids and gastric acid in the duodenum reduces vagal stimulation
- Inhibition of gastrin secretion in the stomach
- This reduces stomach motility, reducing the rate of emptying from the stomach


Chyme in the duodenum stimulates the release of:

- Secretin
- Gastric Inhibitory Hormone


How does the duodenum control the rate of gastric emptying?

- Lipids and gastric acid in the duodenum reduces vagal stimulation
- Inhibition of gastrin secretion in the stomach
- This reduces stomach motility, reducing the rate of emptying from the stomach


How can gastric acid secretion be reduced via drugs?

- H2 blockers - prevent Histamine stimulating Parietal cells
- Proton-pump inhibitors - prevent H+ moving from the Parietal cell into the stomach lumen


Name some drugs which can reduce gastric acid secretion:

H2 blockers: Cimetidine, Ranitidine
PPI: Omeprazole


How do gastric epithelia survive the pepsins and low pH of the lumen?

Covered in an alkaline mucous layer, secreted by mucous neck cells and surface epithelial cells
= Diffusion barrier for H+ and pepsins


The peristaltic contractions of the stomach are stimulated by a pacemaker in which area of the stomach? How frequently do these contractions occur?




What are the common causes of acute gastritis?

- Alcohol
- Chemotherapy
- Bile reflux
- Stress


How does heavy NSAIDs use lead to gastritis?

- NSAIDs reduce the number of prostaglandins
- Decreases blood flow
- Less nutrients to cells
- Reduced mucous production
- Reduced protection of gastric epithelia


What can cause chronic gastritis?

- Helicobacter pylori
- Cytomegalovirus
- Some parasites
- Autoimmune
- Chronic bile reflux
- Chronic NSAIDs use
- Chronic alcohol intake
- Chronic radiation
- Crohn's
- Sarcoidosis
- Wegener granulomatosis
- Coeliac disease


Why can pernicious anaemia be caused by chronic gastritis?

- Damaged parietal cells = less intrinsic factor secreted
= Less vitamin B12 absorbed - vital for erythropoesis


What is the treatment for Helicobacter pylori?

Triple therapy:

1) PPI ie Omeprazole
2) Clarithromycin
3) Amoxicillin


Name the specific test used to diagnose Helicobacter pylori:
Explain how it works:

Urease breath test:

- Swallow radioactive urea
- If H. pylori present, will break this down into ammonia + CO2
- CO2 will be expired and detected


Is Helicobacter pylori gram positive or negative? Will it stain red or purple?

Gram negative



How is Helicobacter pylori infection spread between people?



How does Helicobacter pylori survive the acidic gastric conditions?

- Uses flagellum to burrow into the gastric epithelia
- Expresses Urease, which converts urea to ammonium, which increases the local pH


What are the key properties of chyme leaving the stomach?

- Acidic
- Hypertonic
- Partially digested

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