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CIF > GIT > Flashcards

GIT Flashcards

1
Q

What is the gatric functions?

A
  • 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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2
Q

Describe the anatomy of the stomach.

A

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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3
Q

Describe the glands/pits in the oxyntic gland mucosa.

A

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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4
Q

What does parietal cells do?

A

Secrete HCl (acid)

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5
Q

What does cheif cells do?

A

Secrete pepsinogen

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6
Q

What is the function of HCl in the stomach?

A

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

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7
Q

Describe the channel composition of a parietal cell.

A

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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8
Q

How is protons produced in the parietal cells?

A

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

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9
Q

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

A

Acetylcholine, histamine, gastrin, and somatostatin (inhibit)

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10
Q

Describe the direct and indirect pathways of acid secretion stimulation.

A

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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11
Q

What is the gastric- and cephalic phase?

A

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

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12
Q

Describe the stimulation of acid secretion in the cephalic phase.

A

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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13
Q

Describe the stimulation of acid secretion in the gastric phase.

A

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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14
Q

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

A

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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15
Q

Describe the parallel pepsinogen secretion stimulation.

A

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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16
Q

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

A

True

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17
Q

How does the stomach protect itself from the acidic environment?

A

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

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18
Q

What can cause damage of the gastric mucosa?

A
  • 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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19
Q

How can gastic ulcers and gastroesophageal reflux disease be treated?

A

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

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20
Q

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

A

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

21
Q

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

A

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

22
Q

What is nutrient absorbtion coupled to?

A

Na+ transport (solute dragged after/with H2O)

23
Q

What is nutrient absorbtion coupled to?

A

Na+ transport (solute dragged after/with H2O)

24
Q

Describe the digestion of polysaccharides.

A

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

25
Q

Describe the digestion of proteins.

A

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

26
Q

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

A

10 %

27
Q

Describe the digestion of lipids.

A

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

28
Q

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

A

Neutralization of acid chyme (HCO3- secretion)

29
Q

Describe the channel composition of a duodenum epithelial cell.

A

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

30
Q

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

A

Making the intestinal contents fluid

31
Q

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

A

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

32
Q

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

A

Nutrient absorbtion

33
Q

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

A

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

34
Q

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

A

Salt and fluid absorption

35
Q

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

A

Lumen: Na+/H+ exchanger, Cl-/HCO3- exchanger

Basolateral: CCl2, Na+/K+ ATPase, K+ channel

H2O both intra- and paracellular transport

36
Q

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

A

Water and salt absorption

37
Q

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

A

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

38
Q

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

A

True.

39
Q

What are absorptagogues?

A

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

40
Q

What are secretagogeus?

A

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

41
Q

What are some distrubances of ion/fluid transport?

A

Osmotic-, secretory-, and congenital Cl- diarrhea

42
Q

What is osmotic diarrhea?

A

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

43
Q

What is secretory diarrhea?

A

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

44
Q

What is congenital Cl- diarrhea?

A

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

45
Q

How does the autonomic NS control GI regulation?

A

Via parasympaticus, sympaticus and enteric (ENS)

46
Q

What is the ENS, and what does it regulate?

A

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

47
Q

Describe the immune protection of the GI.

A

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

48
Q

Describe the non-immune protection of the GI.

A

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

CIF (11 decks)

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