GIT Flashcards
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
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))
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
What does parietal cells do?
Secrete HCl (acid)
What does cheif cells do?
Secrete pepsinogen
What is the function of HCl in the stomach?
HCl facilitates the conversion of pepsinogen into the active pepsin, which breakdown protein
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
How is protons produced in the parietal cells?
H2O + CO2 -(CA)-> HCO3- + H+
What receptors are found on the interstitial side of parietal cells?
Acetylcholine, histamine, gastrin, and somatostatin (inhibit)
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
What is the gastric- and cephalic phase?
Cephalic: the act of eating
Gastric: food arive in the stomach
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 %)
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
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 %)
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
True or false: gastric motility are facilitated by pacemaker cells in the stomach.
True
How does the stomach protect itself from the acidic environment?
By a mucous gel layer and buffering with HCO3- (mucous cells)
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
How can gastic ulcers and gastroesophageal reflux disease be treated?
Proton pump inhibitors, antihistamines, antibiotics (kills helicobacter), lifestyle and dietary change
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
