GIT: (hormonal) regulation of GIT functions Flashcards

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1
Q

Enumerate all hormones affecting GIT

A
  • Gastrin
  • Cholecystokinin (CKK)
  • Secretin
  • Glucose dependent insulino-tropic peptid (GIP)
  • Vasoactive intestine Peptide (VIP)
  • Motilin
  • Somatostatin
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2
Q

Cells releasing Gastrin

A

G cells

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3
Q

Site of Gastrin Release

A
  • mainly in pyroic Antrum of stomach
  • duodenum & pancreas
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4
Q

Stimuli facilitating the release of gastrin

A

Mechanical:
* Distension caused by food

Chemical:
* basic pH
* Protein digestive products (phenyalanine, tryptophan, peptides)

Nervous:
* Post ganglionic vagal innervation (by release of GRP)

(pathologically)=Pernicious anemia

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5
Q

Explain why Atropine doesn’t block gastrin secretion

A

post ganglionic Vagal innervation of gastrin secretion occurs by release of GRP (gastrin-releasing peptide) & not Acetylcholine

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6
Q

Explain why pernicious anemia causes pathological secretion of gastrin hormone

A
  1. It destroys Acid secreting cells
  2. Less acid means no inhibition of gastrin secretion (negative feedback inhibition)
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7
Q

Stimuli inhibiting the secretion of Gastrin

A

Acid (HCL) :
* Directly: by acting on G cells (releasing gastrin)
* Indirectly: by acting on D cells, causing it to release Somatostatin, which inhibits Gastrin secretion

  • VIP (vasoactive Intestinal Peptide)
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8
Q

Actions of Gastrin

A
  1. Facilitates HCL secretion:
    * Directly: acting on parietal cells
    * Indirectly: stimulating Histamine secretion from ECL cells, histamine causes further acid secretion
  2. Trophic Action on stomach: stomach increases in size
  3. Stimulates insulin secretion
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9
Q

Cells releasing CCK (cholecysetokinin)

A

I Cells

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10
Q

Site of release of CCK

A

Mucous of Duodenum & jejunum (upper small intestine)

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11
Q

Stimuli faciliting release of CCK

A

presence of digestive products of peptides, amino acids & fats

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12
Q

Action of CCK on pancreas

A
  1. Stimulate pancreatic Acinar cells to secrete enzymes
  2. Trophic effect on pancreas (increase in size)
  3. Enhances effect of Secretin hormone on pancreas
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13
Q

Action of CCK on Stomach

A
  1. prevents motility of stomach
  2. (along with secretin) contraction of pyloric sphincter to prevent reflux from duodenum to stomach
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14
Q

Action of CCK on gall bladder

A
  1. relaxation of sphincter of oddi
  2. Contraction of walls of gall bladder —> secretion of bile
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15
Q

Describe positive feedback mechanism linked to gall bladder & CCK hormone

A
  1. CCK faciltates secretion of bile from gall bladder
  2. resulting in more digestion of proteins & fats
  3. Therefore, there is more Digestive product
  4. More CCK secreted
  5. More Bile secreted

It stops when food moves on from duodenum

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16
Q

Action of CCK on small intestine

A

it augemnts motility of small intestine

17
Q

Action of CCK on the brain

A

causes Satiety & decrease food intake

This is linked to anxiety & panic disorders

18
Q

Cells releasing Secretin

A

S cells

19
Q

Site of release of Secretin

A

glands of mucosa of upper part of small intestine (duodenum & jejunum)

20
Q

Stimuli facilitating release of Secretin

A
  • Decrease in Duodenal pH (increase in Acidity)
  • Protein digestive products
21
Q

Action of Secretin

A
  1. Augments action of CCK
  2. Decrease HCL secretion by parietal cells
  3. Neutralize Acidic pH by Secretion of bicarb (from pancreatic duct) & water

Secretin job is to prevent acidity

22
Q

Cells Releasing GIP

A

K cells

23
Q

Site of release of GIP

A

(like CCK) mucosa of Deudenum & jejunum

24
Q

Stimuli facilitating secretion of GIP

A

presence of Glucose & Fat inside the duodenum

25
Q

Action of GIP

A
  1. Stimulate insulin secretion by acting on pancreatic B cells
  2. increase B cell synthesis
  3. prevent B cell apoptosis
  4. Along with GLP, play a major role in Postprandial (after meal) insulin response

its job is glucose utilisation

26
Q

Mention the link between GIP & obesity

A

GIP is present in high level in obese people, along with hyperplasia (increase in cell size) of K cells (cells secreting GIP)

27
Q

Site of release VIP

A

Myenteric & submucosal Nervous Plexuses (along with acetylcholine)

28
Q

Stimuli facilitating release of VIP

A

presence of (substances causing VD):
* Acetylcholine
* ATP
* Serotonin
* Substance P

29
Q

Action of VIP

A
  1. VD of blood vessels of GIT
  2. Inhibition of Gastrin, to decrease HCL secretion
  3. Secretion of water, electrolytes & bicarbonate
30
Q

Cells releasing Motilin

A
  • Mo cells
  • Enterochrouffin cells
31
Q

Site of release of motilin

A

(all except eosophagus):
* Stomach
* small intestine
* Colon

32
Q

Stimuli facilitating secretion of Motilin

A

Binding to G protein coupled receptors (found mainly in pyloric Antrum)

33
Q

Stimuli inhibiting secretion of Motilin

A
  • Ingestion of glucose & fat
  • Pregnency
34
Q

Action of Motilin

A
  • Stimulate Contraction of GIT smooth muscles in between meals
  • Regulate Migrating motor complex (MMC)
35
Q

Explain why pregnent women have reoccuring constipation

A

Pregnency causes inhibition of Motilin hormone secretion, leading to decreased GIT movement in between meals

36
Q

Site of release & cells secreting somatostatin

A

D cells:
* 65% from mucosa
* 35% from pancreas

37
Q

Stimuli facilitiating secretion of Somatostatin

A

Food in Gut:
* Glucose
* Amino acids
* HCL in duodenum & pyloric antrum

38
Q

Action of Somatostatin

A

provide continuous supply of nutrients in the GIT by inhibiting all GIT (pausing it)