GIT Flashcards by Sofie Sørensen

What is the gatric functions?

Secretory: secretes acid (and bicarbonate), pepsinogens, H2O and intrinstic factors (vitamin B)
Breakdown and digestion of proteins
Antimicrobial
Motor functions: receives food, mechanical breakdown of food, and propulsion
Endocrine: gastrin, somatostatin, histamine, ghrelin

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Describe the anatomy of the stomach.

Lower esophageal sphincter –> cardia (no acid secreting cells) –> fundus (ghrelin secreting cells, when stomach is empty) –> corpus (parietal, cheif, and mucus secreting cells, histamine secreting cells) –> antrum (cheif cells, G- and D cells (release gastrin and somatostatin))

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Describe the glands/pits in the oxyntic gland mucosa.

Mucosa found in the corpus of the stomach:
- Glands: superficial epithelial cells (HCO3-) –> mucous neck cells –> stem/regenerative cells –> parietal cells (H+, intrinsic factor) –> cheif cells (pepsinogen) –> endocrine cells

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What does parietal cells do?

Secrete HCl (acid)

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What does cheif cells do?

Secrete pepsinogen

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What is the function of HCl in the stomach?

HCl facilitates the conversion of pepsinogen into the active pepsin, which breakdown protein

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Describe the channel composition of a parietal cell.

Luminal side/secretory canaliculus: H+/K+-ATPase, Cl- channel, K+ channel
Basolateral side: HCO3-/Cl- exchanger, Na+/H+ exchanger, Na+/K+ ATPase, K+ channel

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How is protons produced in the parietal cells?

H2O + CO2 -(CA)-> HCO3- + H+

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What receptors are found on the interstitial side of parietal cells?

Acetylcholine, histamine, gastrin, and somatostatin (inhibit)

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Describe the direct and indirect pathways of acid secretion stimulation.

Direct: acetylcholine, histamine and gastrin stimulate the parietal cell to secrete HCl (rise in Ca2+)
Indirect: ACh and gastrin stimulate ECL cells –> secretion of histamine –> stimulates acid secretion by parietal cell

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What is the gastric- and cephalic phase?

Cephalic: the act of eating
Gastric: food arive in the stomach

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Describe the stimulation of acid secretion in the cephalic phase.

Ghrelin is secreted from fundus –> CNS –> ENS –> ACh on parietal cells, ECL cells (secretes histamine), and D-cells (inhibits) –> ENS also stimulates G-cells by release of GRP –> release of gastrin –> ECl cells –> histamine
Histamine, ACh and gastrin stimulates acid secretion by parietal cells (30 %)

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Describe the stimulation of acid secretion in the gastric phase.

Distension (swelling from eating) in fundus –> ENS –> ACh on parietal cells, ECL cells (secretes histamine), and D-cells (inhibits) –> ENS also stimulates G-cells by release of GRP –> release of gastrin –> ECl cells –> histamine
Histamine, ACh and gastrin stimulates acid secretion by parietal cells (50-60 %)
CNS (afferent) is also directly stimulates by the fundus –> –> –> acid secretion

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Describe the stimulation of acid secretion in the intestinal phase (food is passed to the intestines).

ENS –> D-cells in antrum –> somatostatin secretion by D-cells –> somatostatin inhibits parietal cells, ECL cells and G-cells –> inhibition of acid secretion (5-10 %)

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Describe the parallel pepsinogen secretion stimulation.

Afferent ENS/CNS –> ACh, gastrin, secretin, and PGE2 stimulates chief cells secretion of pepsinogen –> HCl facilitates the conversion of pepsinogen to pepsin –> preotein degradation in lower corpus/antrum

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True or false: gastric motility are facilitated by pacemaker cells in the stomach.

True

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How does the stomach protect itself from the acidic environment?

By a mucous gel layer and buffering with HCO3- (mucous cells)

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What can cause damage of the gastric mucosa?

If the acid and pepsinogen secretion overseeds HOCO3- and mucuos secertion
Pancreatic islet cell “gastrinoma” (Zollinger-Ellison syndrome)
Alcohol, caffeine, smoking
Non-steroidal anti-inflammatory drugs (asprin, iboporofen)
Helicobacter pylori infection

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How can gastic ulcers and gastroesophageal reflux disease be treated?

Proton pump inhibitors, antihistamines, antibiotics (kills helicobacter), lifestyle and dietary change

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Describe the anatomical differences between the small- and the large intestine.

Small: circular folds, villi –> crypts
Cells:
Villi: absorptive cells, goblet cells
Crypt: enteric endocrine cells, stem/progenitor cells, paneth cells

Large: semilunar folds, surface epithelium, crypts
Cells: absorptive cells, goblet cells, microvacuolated columnar cells, enteric endocrine cells, stem/progenitor cells,

Microvilli on all cells

Describe the functional differences between the small- and large intestine.

Small: digestion and absorbtion of nutrients, ion and water secretion/absorbtion by enterocytes, release of hormones (e.g., CCK and secretin), immunity (80 % IGs and other molecules by Paneth cells)

Large: storage and concentration, absorbtion/secretion of Na+, Cl- and water, sensitive to aldosterone, bacterial digestion of non-digestible CHO, and production of SCFA, immunity

What is nutrient absorbtion coupled to?

Na+ transport (solute dragged after/with H2O)

What is nutrient absorbtion coupled to?

Na+ transport (solute dragged after/with H2O)

Describe the digestion of polysaccharides.

Carbohydrates -salivary amylase-> -pancreatic amylase-> disaccharides -(small intestine)-> monosaccharides
Monosaccharides can then be transported ascross the small intestine and enter the blood

Describe the digestion of proteins.

Proteins -gastric pepsin-> -pancreatic endopeptidase exopeptidases-> oligopeptides -peptidases in small intestine-> amino acids Amino acids can then be transported across the small intestine and into the blood

Protein can also be transported directly across epithlia through the direct pathway by endocytosis. How much is app. transported this way?

10 %

Describe the digestion of lipids.

Lipids -pancreatic lipase + lingual and gastric lipases-> emulation/droplet formation (micelle) --> transported into the cell --> golgi --> exocytosis

What happens in the duodenum (first part of the small intestine)?

Neutralization of acid chyme (HCO3- secretion)

Describe the channel composition of a duodenum epithelial cell.

Luminal side: HCO3-/Cl-/anion exchanger, CFTR Basolateral side: nHCO3-/Na+ cotransporter, Na+/H+ exchanger, Na+/K+ ATPase, K+ channel

What is the Cl- dependent secretion in both the small and the large intestine important for?

Making the intestinal contents fluid

Describe the channel composition of cells in the small and large intestines responsible for the Cl- dependent secretion.

Luminal side: CaCC, CFTR, Cl-/HCO3- exchanger Basolateral side: Na+/K+/Cl- cotransporter, Na+/K+ ATPase, K+ channel Na+ and H2O transport paracellularly, H2O also intracellular

What is the Na+ dependent absorbtion 1 in the small intestine (jejunum>ileum) important for?

Nutrient absorbtion

Describe the channel composition of a cell responsible for the Na+ dependent absorbtion 1.

Lumen: SGLT1 (Na+/glucose cotransporter, not regulated), Na+/AA cotransporter, Cl- channel, AQP10 Basolateral: AQP3, Na+/K+ ATPase, K+ channel, AA transporter, glucose transporter Cl- and H2O is also transported paracellularly

What is the Na+ dependent absorbtion 2 in the small/large intestine (ileum and proximal colon) important for?

Salt and fluid absorption

Describe the channel composition of a cell responsible for the Na+ dependent absorbtion 2.

Lumen: Na+/H+ exchanger, Cl-/HCO3- exchanger Basolateral: CCl2, Na+/K+ ATPase, K+ channel H2O both intra- and paracellular transport

What is the Na+ dependent absorption 3 in the colon important for?

Water and salt absorption

Describe the aldosterone dependent K+ secretion and Na+ absorption in the colon.

Aldosterone binds intracellularly to MR receptor --> transcription and translocation of ENaC to luminal membrane --> Na+ transported to the blood via Na+/K+ ATPase Hormones on the interstitium side --> Ca2+ cAMP increase --> K+ efflux on luminal side

True or false: there are similarities in the Na+/K+ homeostasis between the colon and the kidney.

True.

What are absorptagogues?

Agonists that increase absorption, e.g., mineralcorticoids (e.g., aldosterone), glucocorticoids, somatostatin --> final effects on ENac, Cl-/HCO3-, and Na+/H+ transport on luminal membrane

What are secretagogeus?

Agonists that increase secretion, e.g., hormones and neurotransmitters, immune cell products, laxatives, bacterial enterotoxins --> final effects on luminal Cl- channels

What are some distrubances of ion/fluid transport?

Osmotic-, secretory-, and congenital Cl- diarrhea

What is osmotic diarrhea?

caused by dietary nutrient that is not absorbed, e.g., lactose, glucose etc.

What is secretory diarrhea?

1) caused by exogeneous agents, e.g., bacterial toxins (cholera) 2) caused by endogeneous provoked secretions induced by hormone-producing tumors --> stimulation of Cl- channels --> H2O follows

What is congenital Cl- diarrhea?

Defect in Cl-/HCO3- channels --> reduced Cl- reabsorption and reduced HCO3- secretion

How does the autonomic NS control GI regulation?

Via parasympaticus, sympaticus and enteric (ENS)

What is the ENS, and what does it regulate?

The ENS is part of the autonomic NS, and governs the functions of the GI (motility and ion/fluid transport)

Describe the immune protection of the GI.

Gut-associated lymphoid tissue (GALT) in Peyer's patches + single lymphocytes and mast cells Large contact with infections, toxic and immunogenic material --> large production of immunoglobulins

Describe the non-immune protection of the GI.

Acid secretion by stomach, mucuos secretion, peristalsis, epithelial permeability barrier