3 Stomach Flashcards

1
Q

Q: What’s the purpose of epithelial transition? Stomach?

A

A: match function to a particular region

has huge excretory role

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2
Q

Q: What are the 3 key functions of the stomach?

A

A: -Digestion of macronutrients: this can be chemical (acid and enzymes) and mechanical (mixing and churning)

  • Storage reservoir for food: until downstream organs are ready to receive the stomach contents
  • Immunological protection: Strong acid helps to destroy ingested pathogens
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3
Q

Q: What’s specific about the stomach wall? (2)

A

A: extra oblique layer of smooth muscle inside the circular layer, which aids in performance of complex grinding motions (mechanical digestion).

In the empty state, the stomach is contracted and its mucosa and submucosa are thrown up into folds called rugae. Following consumption of food and fluids, as the volume of the stomach increases, the rugae are stretched and become flat.
-The stomach only has a minor role in absorption, so the presence of rugae (instead of villi) allows the stomach to undertake its reservoir function.

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4
Q

Q: How is the stomach split up? Name the parts? Diagram. What do they produce? In terms of acid?

A

A: 5 anatomical parts

(duodenum)
-pyloric canal MUCUS ONLY
-pyloric antrum GASTRIN
-body MUCUS, HCL, PEPSINOGEN
-fundus MUCUS, HCL, PEPSINOGEN
-cardia MUCUS ONLY 
(oesophagus)

2L per day, up to 150mM H+

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5
Q

Q: What are the 5 cell types within the stomach? How are they distributed? (3)

A

A: in tubular gastric glands in gastric pits

  • mucous cells
  • Parietal cells- secretes HCl and intrinsic factor
  • chief cells- secretes pepsinogen and gastric lipase
  • G cells- secretes gastric hormone
  • other
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6
Q

Q: What provides considerable protection against the corrosive acid in the stomach? What else? What’s the pH in the lumen? epithelial surface? Which cell contributes?

A

A: mucous gel lining which has trapped HCO3- in it
-protect the stomach lining from active lipase and proteases, which may interfere with the lipid bilayer and its membranous transporters

6-7
1-2

mucous cells-secrete a bicarbonate-rich mucous

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7
Q

Q: What lines the stomach? Which structures can form? (2) What do they contain?

A

A: stomach mucosa is lined with simple columnar epithelia and it invaginate into gastric pits

= are deep pores within the stomach mucosa, which lead to multiple tubular gastric glands, which house the functional secretory cells of stomach- endo and exocrine

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8
Q

Q: In the stomach, what are the 5 products cells can make and what are the cell shapes? Distribution? (3)

A

A: -gastrin- droplet/round shape (endocrine)

  • pepsinogen- triangle
  • HCl- fat orange segment
  • mucus- goblet
  • HCO3- / mucus= common to all cell types- rectangle

antrum= find most endocrine cells (gastrin)
body and fundus= heavy secreting capacity- lots of pepsinogens and acids and mucus
cardia and pyloric= few are for acid secretion but lots of mucus

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9
Q

Q: What are the 2 functions that stomach contractions result in? Percentage? Describe. Control?

A

A: peristalsis:

  • 20% of stomach contractions
  • propels chyme towards colon- more powerful as moves from LOS to pyloric sphincter
  • ANS essential

segmentation

  • 80%
  • weaker. fluid chyme towards pyloric sphincter and solid pushed back to body => mixes stomach contents to get more effective digestion
  • stretching activates enteric NS
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10
Q

Q: What do chief cells produce? (2) role? Method of production? Structure? (3)

A

A: -protease zymogen (pepsinogen) -> breaks dietary proteins into smaller peptide chains
-lipase (gastric lipase) -> digests fats by removing a fatty acid from a triglyceride molecule (triglycerides -> fatty acid and a diglyceride)

EXOCRINE ROLE

high volume and store them in granules until they are stimulated to exocytose them into the stomach lumen

abundant rER, masses of apical granules, lots of GA

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11
Q

Q: What’s the relationship between pepsinogen and pepsin?

A

A: Pepsinogen is activated to pepsin in the presence of HCl in the gastric lumen; it is secreted as a precursor to prevent it auto digesting the chief cells

pepsin can also cleave pepsinogen = positive feedback

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12
Q

Q: What are parietal cells? How do they exist? What can happen? What do they contain? (3)

A

A: acid-secreting cells of the stomach (export H+ to lumen)

in a quiescent (sleeping) state until activated
-tubovesicles in the cytoplasm fuse with the small invaginations on the apical surface (between microvilli) to make complicated canalicular surface, with a large surface area for acid secretion=> become open to lumen when activated

  • rich in mitochondria to provide energy for membrane transport
  • high number of cytoplasmic tubulovesicles (contain H+/K+ ATPase)
  • internal caniculi (extend to apical surface)=> not connected to lumen in resting state
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13
Q

Q: What’s the function of strong HCl? (3)

A

A: 1) to kill ingested pathogens; 2) activate protease zymogens; 3) alter protein structure to help digestion

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14
Q

Q: What do parietal cells secrete? Deficiency?

A

A: -H+
-intrinsic factor, a glycoprotein essential for the absorption of vitamin B12. Deficiency in this substance will lead to pernicious anaemia.

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15
Q

Q: What are G cells? where? Release? in response to? (3) Where are they predominately?

A

A: These are enteroendocrine cells found at the bottom of the gastric pits.

G-cells release the hormone gastrin into the bloodstream in response to vagus nerve stimulation, the presence of peptides in the stomach, and stomach distension

pyloric antrum of stomach

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16
Q

Q: What’s the role of gastrin? (3)

A

A: -Stimulation of smooth muscles by gastrin leads to stronger contractions of the stomach and the opening of the pyloric sphincter to move food into the duodenum.

  • Gastrin also binds to receptors on cells in the pancreas and gallbladder where it increases the secretion of pancreatic juice and bile.
  • stimulate histamine release from chromaffin cells (lamina propia)
17
Q

Q: Name 2 strong stimuli for acid secretion.

A

A: histamine, gastrin

18
Q

Q: How do parietal cells release acid? (4)

A

A: 1. Carbon dioxide diffuses down its concentration gradient from the blood into the parietal cell and, in the presence of carbonic anhydrase, is combined with water to form carbonic acid, which dissociates into bicarbonate and a proton

  1. The bicarbonate is exchanged with a chloride ion in the interstitial space. This causes chloride ions to move down their concentration gradient into the stomach lumen via chloride channels.
  2. To pump the protons into the lumen the cell needs to move potassium from the interstitial space to the lumen. This is achieved via a sodium potassium exchanger in the basolateral membrane, and chloride channels in the apical membrane.
  3. Now, potassium can be pumped into the cell in exchange for protons. The potassium then re-enters the lumen through the potassium channels and the secreted proton combines with chloride to form hydrochloric acid.
19
Q

Q: What are Enterochromaffin-like cells (ECL)? where? Role?

A

A: type of neuroendocrine cell found deep in the gastric glands, usually in the vicinity of parietal cells

They secrete histamine which stimulates the secretion of acid from the parietal cells.

20
Q

Q: What are D-cells? Produce? effect? (2)

A

A: enteroendocrine cells secrete somatostatin, which has a generally inhibitory effect on gastrointestinal function

Within the gastric gland somatostatin inhibits ECL production of histamine and parietal cell activity, both of which inhibit the secretion of hydrochloric acid.

21
Q

Q: What are Gastric stem cells?

A

A: pluripotent cells are capable of differentiating into all of the different cells of the stomach, under the influence of different factors

22
Q

Q: What are the 2 exocrine cells of the stomach?

A

A: parietal and chief

23
Q

Q: What are the 3 phases of gastric secretion and motility?

A

A: cephalic, gastric, intestinal

24
Q

Q: What is stage 1 of gastric secretion and motility called? Summarise. Afferents? (4) Efferents? (3) Effect? Mechanism?

A

A: cephalic
-anticipatory, preparitory phase

Afferents: Sight, smell, taste and thought of food.

Efferents: Vagus nerve (neurons secreting ACh) stimulate secretion from mucous cells, chief cells, parietal cells and G-cells via the submucosal plexus. Gatsrin (from G-cells) and histamine (from ECL cells) also stimulate parietal cell secretion.

Effects: Small secretion for a few minutes

3 pronged acid secretion stimulus

  • acetycholine delivered by vagus nerve
  • (ECL produced) histamine
  • gastrin
25
Q

Q: What is stage 2 of gastric secretion and motility called? Afferents? (3) Efferents? (4) Effect? (2) ENS?

A

A: gastric phase

Afferents: Distension of stomach (stretch) and chemoreception of nutrients and a reduced pH.
-stomach stretch receptors= afferent signals to brain-> parasympathetic effect

Efferents: Vagus nerve (neurons secreting ACh) stimulate secretion from mucous cells, chief cells, parietal cells and G-cells via the submucosal plexus and increase motility (mixing waves) via the myenteric plexus. Gatsrin (from G-cells) and histamine (from ECL cells) also stimulate parietal cell secretion.

Effect: 3-4 hours of gastric activity (secretion of acid, enzymes and hormones) and mechanical digestion.

has a role- senses stretch and certain chemicals and activates local NT= more acid

26
Q

Q: What is stage 3 of gastric secretion and motility called? Afferents? (3) Efferents? (5) Effect?

A

A: intestinal phase

Afferents: Duodenal stretch and chemodetection of reduced pH and duodenal distension

Efferents: I-cells secrete cholecystokinin (CCK) and S-cells secrete secretin into the blood. This decreases parietal cell secretion and inhibits gastric motility and emptying. Stretch receptors input into the enteric nervous system, which reduces activation of the stomach.

Effect: Gastric emptying slows down to allow downstream organs to deal with current content
=> largely inhibitory effect

27
Q

Q: What’s the process of stage 3 of gastric secretion and motility? (3)

A

A: CENTRAL EFFECT 1. chyme enters small intestine = chyme has low pH and high fat content -> low pH means that afferent nerves signal to brain -> sends inhibitory signal to stomach to cease acid etc production
ENDOCRINE 2. cells of small intestine (enterocytes) produce high number of inhibitory hormones
LOCAL ENS MEDIATED 3. another local effect-> as food passes out through pyloric sphincter-> ENS mediated

3 armed response of inhibition phase

28
Q

Q: How might you produce a useful drug to decrease acid secretion? Why?

A

A: 4 options- any of the 3 receptors (ACh, histamine, gastrin) or ATPase

acid reflux is a big problem

29
Q

Q: Name 2 actively used drugs to decrease acid secretion.

A

A: -omeprazole (blocks ATPase)

-ranitidine (anti histamine that blocks histamine receptor)