Week 19 Physiology - GI Flashcards

1
Q

Describe the process and mechanism of peristalsis in the GIT:

A

Reflex arc/response to stretch of gut wall.

Local stretch in smooth muscle layer of wall leads to release of serotonin, signalling neurons in myenteric plexus.

Reflex release from neurons of Acetycholine and Substance P proximal to contents cause smooth muscle contraction, cause increased pressured and move contents forward.

Distal to contents and initiation of stretch, there is nitric oxide and vasoactive peptide –> causing downstream smooth muscle relaxation

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2
Q

What is the enteric nervous system?

A

Intrinsic component of GI innervation that can exist without external innervation, communicating with autonomic nervous system.

Intrinsic component formed by myenteric (located between longitudinal and circular smooth muscle) and Submucosal plexus (as described)

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3
Q

What are the mechanisms which stimulate gastric acid secretion? (On parietal cells in gastric body)

A
  1. Histamine via H2 receptors
  2. Acetylcholine via M3 receptors
  3. Gastrin via enterochromaffin-like cells

Net effect of these mechanisms is to stimulate the action of H/K ATPase pumps on apical membrane of parietal cells –> H+ pumped into gastric lumen against concentration gradient.

H+ is liberated from H2O and CO2 via carbonic anhydrase and H+ combines with Cl- to form HCl in stomach lumen

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4
Q

What is the role of enterochromaffin-like cells in regulating stomach pH?

A

ECL cells are neuroendocrine cells located in stomach.

Role is secretion of histamine, which acts on parietal cells to increase H+ secretion into stomach contents.

This is stimulated by gastrin, a hormone secreted by G-cells in antrum/proximal duodenum –> feedback if undigested food, increased acid production

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5
Q

What is the role of somatostatin?

A

Acts to reduce secretion of other hormones, i.e. gastrin, digestive enzymes - as well as reducing splanchnic blood flow

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6
Q

What is the role of gastrin?

A

Acts on ECL cells to stimulate histamine release –> increased gastric acid.

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7
Q

What is the role of secretin?

A

Alkalinisation of duodenal contents by increasing pancreatic secretions, biliary bicarbonate –> stimulated by increased acidity of small bowel.

Also functions to decrease rate of gastric emptying.

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8
Q

What is the role of cholecystokinin?

A
  • Promotes delivery of food from stomach into duodenum
  • Stimulates gallbladder contraction
  • Increases pancreatic secretions
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9
Q

What stimulates CCK secretion?

A

Fatty acids
Amino acids

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10
Q

What makes up bile? How does bile from liver and gallbladder differ?

A

Water (97%)
Biles salts (0.7%)
Pigments (0.2%)
Cholesterol (0.06%)

Bile from GB is more concentrated, 89% is water

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11
Q

What are the different forms of bile salts?

A

(Synthesised from cholesterol, emulsifies fats in lumen, facilitating absorption. Without, 50% ingested fat appears in stool)

Cholic acid 50%
Chenodeoxycholic acid 30%
Deoxycholic acid 15%
Lithocholic acid 5%

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12
Q

Describe process of digestion from complex carbs:

A

Ingestion of carbs, no chemical digestion in stomach.

Chyme enters small bowel, and triggers pancreatic secretions of amylase, which breaks down glycosidic bonds, yielding mono/disaccharides.

Lactase, sucrase, maltase yields monosaccharides which are then absorbed across brush border via SGLT-2 contransporters. Basal membrane GLUT transporters facilitate transport to blood.

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13
Q

Describe process of digestion and absorption of proteins:

A

Pepsin enzyme active in stomach, which breaks down into smaller chains (oligopeptides, dipeptides, and amino acids).

Absorbed via facilitated diffusion in similar way to carbs, utilising sodium co-transport.

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14
Q

Describe process of digestion of lipids:

A

Small action of lipase in mouth and stomach, majority in small bowel.

Lipids hydrophobic, poorly soluble in aqueous digestive tract.

Bile aids in digestion by emulsifying the fats, breaking down and increasing surface area so that enzymes can break down into fatty acids (Pancreatic lipase, phospholipase A2 and cholesterol ester hydrolase action)

Then bile acids forms a amphiphilic molecule, with hydrophilic ends and lipophilic heads, encapsulating the lipid near apical membrane and allowing facilitated diffusion.

Packed into chylomicrons in cells of SI, and then transported into lymphatics, and then into circulation.

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15
Q

Where is the predominant site of water absorption in GIT?

A

Primarily small bowel, but some in colon also.

Water moves down concentration gradient depending on tonicity of the GI contents.

2L usually ingested per day, but bowel handles 9L of fluid/water from secretions from saliva, stomach, pancreas, bile, intestines.

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16
Q

Where are vitamins ADEK absorbed?

A

Small intestine, likely jejunum, ingested via diet and incorporated into micelles and absorbed as per lipid pathway

17
Q

Where is iron absorbed?

A

Duodenum

18
Q

How is iron absorbed?

A

Either in heme or non-heme form.

Heme form iron is directly absorbed into enterocytes via heme transported from intestinal lumen.

Non-heme either is Ferric (Fe3+) or Ferrous (Fe2+), but readily absorbed in ferrous state. Ferric reductase enzyme on enterocyte membrane assists with absorption. Ferroportin transfers Fe2+ into interstitial fluid, and can enter blood, attached to transferrin.