Lecture 1- Control of the gut- hormones Flashcards

1
Q

Hormones

A

oPeptidesreleasedfromendocrinecells o Intoportalcirculation
o Passthroughliver
o Entersystemiccirculation
o Endupprettyclosetowheretheywere

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2
Q

paracrine hormones

A

o Relating to or denoting a hormone which has effect only in the vicinity of the gland secreting it.
o Peptides released by endocrine cells
o Act in local environment
o Diffuse short distances

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3
Q

neurocrine hormones

A

o Peptides released by neurones in the GI tract

o Released after action potential

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4
Q

how many categories of GI hormones

A

2

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5
Q

name the 2 broad categories of GI hormones

A

Gastrin family

Secretin family

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6
Q

Name the hormones of the gastrin family

A

gastrin

cholecytokinin (CCK)

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7
Q

gastrin is released from

A

G cells

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8
Q

where is gastrin released into

A

the antrum of the stomach

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9
Q

effect of gastrin

A
  • stimulates parietal cells to produce HCL
  • Increasing gastric acid secretion
  • increase motility
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10
Q

Cholecystokinin (CCK) released from

A

I cells in the duodenum and jejunum

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11
Q

effect of CCK

A
  • increase pancreatic/ gallbladder secretion (enzymes, bile, HCO2)
  • by increasing gall bladder contractions
  • relaxes sphincter of Oddi
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12
Q

CCK release stimulated by

A

fat and proteins

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13
Q

Name the hormones of the secretin family

A

secretin

gastric inhibitory polypeptide (GIP)

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14
Q

secretin is released by

A

S cells into the duodenum

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15
Q

what stimulates S cells to release secretin

A

H+ and fatty acids

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16
Q

effect of secretin

A

increase HCO3 from pancreas/gall bladder

decrease gastric acid secretion

17
Q

gastric inhibitory polypeptide (GIP) cells found

A

in the duodenum and jejunum

18
Q

gastric inhibitory polypeptide (GIP) release stimulated by

A

sugars, amino acids and fatty acids

19
Q

GIP effect

A
  • increase insulin
  • decrease gastric acid secretion
  • decreases intestinal motility
20
Q

motilin released from

A

ECL cell

21
Q

motilin effect

A
  • increase small bowel motility

- increase gastric emptying

22
Q

somatostatin released from D cells

A

decrease secretion and action of many hormones

23
Q

what do parietal cells release

A

HCL

24
Q

what triggers parietal cells to release HCL

A

Parietal cells bear receptors for three stimulators of acid secretion, reflecting a triumverate of neural, paracrine and endocrine control:

  • Acetylcholine (muscarinic type receptor)
  • Gastrin
  • Histamine (H2 type receptor)
25
Q

histamine released from

A

ECL cells

Histamine stimulates the parietal cells to secrete HCl.
- gastrin-ECL cell pathway

26
Q

acetylcholine produced by which type of neurone

A

parasympathetic

27
Q

which hormones reduced HCL PRODUCTION

A

secretin, gastric inhibitory peptide, glucagon and somatostatin.

28
Q

change in morphology of parietal cells during HCL secretion

A

When acid secretion is stimulated there is a dramatic change in the morphology of the membranes of the parietal cell. Cytoplasmic tubulovesicular membranes which are abundant in the resting cell virtually disappear in concert with a large increase in the cannalicular membrane. It appears that the proton pump as well as potassium and chloride conductance channels initially reside on intracellular membranes and are transported to and fused into the cannalicular membrane just prior to acid secretion.

29
Q

mechanism of acid secretion

A

The key player in acid secretion is a H+/K+ ATPase or “proton pump” located in the cannalicular membrane. This ATPase is magnesium-dependent, and not inhibitable by ouabain. The current model for explaining acid secretion is as follows:

Hydrogen ions are generated within the parietal cell from dissociation of water. The hydroxyl ions formed in this process rapidly combine with carbon dioxide to form bicarbonate ion, a reaction cataylzed by carbonic anhydrase.
Bicarbonate is transported out of the basolateral membrane in exchange for chloride. The outflow of bicarbonate into blood results in a slight elevation of blood pH known as the “alkaline tide”. This process serves to maintain intracellular pH in the parietal cell.
Chloride and potassium ions are transported into the lumen of the cannaliculus by conductance channels, and such is necessary for secretion of acid.
Hydrogen ion is pumped out of the cell, into the lumen, in exchange for potassium through the action of the proton pump; potassium is thus effectively recycled.
Accumulation of osmotically-active hydrogen ion in the cannaliculus generates an osmotic gradient across the membrane that results in outward diffusion of water - the resulting gastric juice is 155 mM HCl and 15 mM KCl with a small amount of NaCl.