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ESA3 > GI 6 - The Stomach > Flashcards

GI 6 - The Stomach Flashcards

1
Q

Which gastric cells secrete histamine?

A

Enterochromaffin-like cells

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2
Q

What acts to stimulate Gastrin secretion in the stomach?

A
  • Peptides/ amino acids in lumen
  • Vagally released Acetylcholine
  • Vagally released Gastrin-releasing peptide (GRP)
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3
Q

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

A
  • Necessary for Vitamin B12 absorption in the ileum

- Parietal cells

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4
Q

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

A

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

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5
Q

Describe the mechanism of HCl secretion:

A
  • 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
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6
Q

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

A
  • Temporary increase in pH after eating

- Caused by efflux of HCO3- by parietal cells during the secretion of acid into the stomach

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7
Q

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

A

HCO3-/Cl- exchanger
Na+/K+-ATPase
Na+/H+-ATPase
K+ channel

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8
Q

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

A

H+/K+-ATPase
Cl- channel
K+ channel

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9
Q

What directly stimulates the production of gastric acid?

A
  • Vagus nerve secretes Ach -> M3 on parietal cells
  • Histamine
  • Gastrin
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10
Q

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

A

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

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11
Q

How is acid secretion from parietal cells inhibited?

A

Luminal acid stimulates D cells to secrete Somatostatin, which:

  • Directly inhibits Parietal cells
  • Inhibits Gastrin production from G cells, which indirectly inhibits parietal cells
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12
Q

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

A

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

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13
Q

Describe the cephalic stage of digestion:

A
  • 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
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14
Q

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

A

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

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15
Q

What is the Enterogastric reflex?

A
  • 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
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16
Q

Chyme in the duodenum stimulates the release of:

A
  • CCK
  • Secretin
  • Gastric Inhibitory Hormone
17
Q

How does the duodenum control the rate of gastric emptying?

A
  • 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
18
Q

How can gastric acid secretion be reduced via drugs?

A
  • H2 blockers - prevent Histamine stimulating Parietal cells

- Proton-pump inhibitors - prevent H+ moving from the Parietal cell into the stomach lumen

19
Q

Name some drugs which can reduce gastric acid secretion:

A

H2 blockers: Cimetidine, Ranitidine

PPI: Omeprazole

20
Q

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

A

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

21
Q

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

A

Cardia

3x/min

22
Q

What are the common causes of acute gastritis?

A
  • NSAIDs
  • Alcohol
  • Chemotherapy
  • Bile reflux
  • Stress
23
Q

How does heavy NSAIDs use lead to gastritis?

A
  • NSAIDs reduce the number of prostaglandins
  • Decreases blood flow
  • Less nutrients to cells
  • Reduced mucous production
  • Reduced protection of gastric epithelia
24
Q

What can cause chronic gastritis?

A
  • Helicobacter pylori
  • Cytomegalovirus
  • Some parasites
  • Autoimmune
  • Chronic bile reflux
  • Chronic NSAIDs use
  • Chronic alcohol intake
  • Chronic radiation
  • Crohn’s
  • Sarcoidosis
  • Wegener granulomatosis
  • Coeliac disease
25
Q

Why can pernicious anaemia be caused by chronic gastritis?

A
  • Damaged parietal cells = less intrinsic factor secreted

= Less vitamin B12 absorbed - vital for erythropoesis

26
Q

What is the treatment for Helicobacter pylori?

A

Triple therapy:

1) PPI ie Omeprazole
2) Clarithromycin
3) Amoxicillin

27
Q

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

A

Urease breath test:

  • Swallow radioactive urea
  • If H. pylori present, will break this down into ammonia + CO2
  • CO2 will be expired and detected
28
Q

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

A

Gram negative

Red

29
Q

How is Helicobacter pylori infection spread between people?

A

Oral-oral

Faecal-oral

30
Q

How does Helicobacter pylori survive the acidic gastric conditions?

A
  • Uses flagellum to burrow into the gastric epithelia

- Expresses Urease, which converts urea to ammonium, which increases the local pH

31
Q

What are the key properties of chyme leaving the stomach?

A
  • Acidic
  • Hypertonic
  • Partially digested

ESA3 (48 decks)

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