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PHYSIOLOGY GIS > LEC 1 (Regulatory Substances in the GIT) > Flashcards

LEC 1 (Regulatory Substances in the GIT) Flashcards

1
Q

GI hormone classification

A
  1. depending on structure

2. depending on function t

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2
Q

GI endocrine (hormones)

A

released from endocrine cells in the GI mucosa ►portal circulation, ►general circulation ►physiologic actions on target cell

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3
Q

D Cell

A

somatostatin

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4
Q

G Cell

A

Gastrin

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5
Q

H Cell

A

VIP

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6
Q

S Cell

A

Secretin

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7
Q

I Cell

A

chole-cysto-kinin(CCK)

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8
Q

K Cell

A

gastric inhibitory peptide (GIP).

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9
Q

G Cell location

A

in the lateral walls of gastric glands in the antral portion of the gastric mucosa

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10
Q

Gastrin found in

A

stomach, pituitary gland, hypothalamus, medulla oblongata, vagus and sciatic nerve.

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11
Q

Gastrin contains

A

17 amino acids (“little gastrin”)

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12
Q

Gastrin form

A
  1. Little gastrin

2. Big gastrin

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13
Q

Little Gastrin is secreted in

A

response to a meal

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14
Q

Gastrin all biologic activity resides in the

A

four C-terminal amino acids.

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15
Q

G17 have half-life of

A

2 to 3 minutes in the circulation,

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16
Q

G34 has a half-life of

A

15 min

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17
Q

Actions of gastrin

A

↑ gastric acid and pepsin secretion
↑growth of mucosa of the stomach, and small and large intestines (trophic action
↑gastric motility.
↑insulin secretion

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18
Q

trophic action

A

gastrin ↑growth of mucosa of the stomach, and small and large intestines

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19
Q

Patients with gastrin secreting tumors

A

hypertrophy (size of cells) and hyperplasia (number of cells) of the gastric mucosa.

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20
Q

insulin secretion ؟

A

only after a protein meal, and not carbohydrate meal

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21
Q

Stimuli for secretion of gastrin

A
  1. Luminal
  2. Neural
  3. Blood borne
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22
Q

Luminal stimuli

A
  1. Stimuli for secretion of gastrin
  2. Distention of the stomach.
  3. Small peptides and amino acids,
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23
Q

Zollinger-Ellison syndrome (gastrinoma)

A

gastrin is secreted by non-β-cell tumors of the pancreas

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24
Q

Neural stimuli

A

Vagal stimulation, mediated by gastrin-releasing peptide (GRP)
.Stimuli for secretion of gastrin

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25
Q

(GRP)

A

is not acetylcholine (Ach).→Atropine DOSE NOT block vagally mediated gastrin secretion

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26
Q

Blood borne stimuli for secretion of gastrin

A

Calcium (hypercalcemia),

Epinephrine

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27
Q

Inhibition of gastrin secretion

A

Luminal

2.Blood borne

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28
Q

Inhibition of gastrin secretion Blood borne

A

Secretin, somatostatin, GIP (Gastric inhibitory polypeptide also known as the glucosedependent insulin-tropic peptide), VIP (vasoactive intestinal peptide), glucagon

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29
Q

Inhibition of gastrin secretion Luminal

A

↑acid →direct action on G cells
→release of somatostatin.
→ no gastrin

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30
Q

acid located

A

in the antrum

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31
Q

pernicious anemia

A

acid-secreting cells of the stomach are damaged, gastrin secretion
is chronically elevated

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32
Q

CCK half-life of circulating

A

5 minute

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33
Q

CCK is secreted from

A

I cells in duodenum and jejunum

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34
Q

The biologic activity of CCK resides in the

A

C-terminal heptapeptide (7).

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35
Q

CCK location

A

In the brain, especially the cerebral cortex

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36
Q

CCK function

A

regulation of food intake

the production of anxiety and analgesia

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37
Q

CCK structure

A

33 amino acids

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38
Q

CCK form

A

CCK58, CCK33, CCK22 and
CCK8
2.Big gast
small gastrin.

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39
Q

Big gastrin

A

The 7 C-terminal amino acids are the same

40
Q

small gastrin

A

The 4 C-terminal amino acids are the same

41
Q

the tetra-peptide (4) CCK

A

homologous to small gastrin

2.has gastrin activity as well as CCK activity

42
Q

Actions of CCK

A

↑contraction of the gallbladder →relaxation of the sphincter of Oddi for secretion of bile

  1. ↑ pancreatic enzyme secretion.
  2. ↑ trophic effect) of the exocrine pancreas
  3. كلي الباقي من سلايد 27
43
Q

Stimuli for the release of CCK

A

Small peptides and amino acids

(2) Fatty acids containing more than 10 carbon atoms and monoglycerides

44
Q

CCK receptors

45
Q

CCK-A recepter found in

A

the periphery

46
Q

CCK-b recepter found in

47
Q

Effect of TAG on CCK

A

DO NOT stimulate the release of CCK because they

cannot cross intestinal cell membranes.

48
Q

Secretin structure

A

contains 27 amino acids,(All of the amino acids are required for biologic activity)
2.homologous to glucagon; 12 of the 27 amino acids

49
Q

The secretin synthesized by

A

S cells, → duodenum and the jejunum

50
Q

The secretin half-life

51
Q

Actions of secretin

A
  1. ↑secretion of bicarbonate by the duct cells of the pancreas and biliary tract.
  2. ↓H+ secretion by gastric parietal cells.
  3. ↑growth of the exocrine pancreas.
  4. augments the action of CCK in producing pancreatic secretion of digestive enzyme
  5. has a mild effect on motility of the gastrointestinal tract
52
Q

increase secretion of bicarbonate causes

A

Pancreases watery, alkaline pancreatic juice.
Pancreatic HCO3
- neutralizes H+ in the intestinal lumen.
B. Liver HCO3- and H2O secretion
increases bile production.

53
Q

Stimuli for the release of secreti

A

(1) H+
(2) Protein
in the lumen of the duodenum

54
Q

GIP

A

Glucose-dependent insulin-tropic peptide

Gastro-inhibitory peptide)

55
Q

GIP contains

A

42 amino acids.

56
Q

GIP is produced by

A

K cells in the mucosa of the duodenum and jejunum

57
Q

GIP is homologous to

A

secretin and glucagon.

58
Q

Actions of GIP

A
  1. Stimulates insulin release.
  2. inhibits gastric secretion (large dose )
  3. inhibits gastric motility ( large dose )
59
Q

Stimuli for the release of GIP

A

fatty acids, amino acids, and orally administered glucose

60
Q

only GI hormone

61
Q

GIP named

A

gastric inhibitory peptide

62
Q

Motilin is secreted by the

A

stomach and upper duodenum during fasting

63
Q

Motilin function

A

increase gastrointestinal motility

64
Q

↓Motilin secretion

A

ingestion of food

65
Q

inter-digestive myoelectric complexes (or migrating myoelectric complexes: MMC)

A

Motilin stimulates waves of gastrointestinal motility that move through the stomach and small intestine every 90 minutes in a person who has fasted and MMC contraction stop when you eat مهم

66
Q

The migrating myoelectric complex functions

A

to move undigested food into the colon and keep the upper parts of the GIT (small intestine and stomach) clear

67
Q

digestive myoelectric complexes (or MMC) is divided into four phases

A

(1) basal (Phase I)
(2) pre-burst (Phase II)
(3) burst (Phase III)
(4) Phase IV

68
Q

(1) basal (Phase I) is a

A
  1. quiescent هامدperiod
  2. no contractions
  3. lasts from 40–60 min
69
Q

(2) pre-burst (Phase II) consists of

A
  1. intermittenti
  2. rregular
  3. low-amplitude contractions
  4. lasts for 40–60 min
70
Q

parts of the GIT can have an active migrating myoelectric complex

A

The mid stomach to the terminal ileum

71
Q

(3) burst (Phase III) consists of

A
  1. intense
  2. short burst
  3. regular
  4. high-amplitude contractions
  5. for short periods (4–6 min).
72
Q

Phase III contractions periodically occur

A

every 90-120 minutes in humans.

73
Q

Motilin administration causes

A

gastric phase III contractions in humans.

74
Q

Plasma motilin level is highly associated with

A

the appearance of gastric phase III in humans

75
Q

(4) Phase IV

A
  1. short transition period back to the quiescence الهدوءof phase I
  2. lasts for 0–5 min
  3. with very little or no contractions
76
Q

housekeeper wave.

A

all the undigested material is swept out of the stomach down to the small intestine

77
Q

GI Paracrines are

A

Somatostatin

2.Histamine

78
Q

GI Paracrines are released from

A

endocrine cells in the GI mucosa.

79
Q

GI Paracrines diffuse

A

over short distances to act on target cells located in the GI tract.

80
Q

Histamine is secreted

A

by mast cells of the gastric mucosa.

81
Q

. Histamine function

A

increases gastric H+ secretion directly and by potentiating the effects of gastrin and vagal stimulation

82
Q

Somatostatin is secreted in response to

A

H+ in the lumen.

83
Q

Somatostatin secretion is inhibited by

A

vagal stimulation.

84
Q

Somatostatin inhibits

A
  1. the release of all GI hormones مهم
  2. pancreatic exocrine secretion;
  3. gastric acid secretion and motility;
  4. gallbladder contraction
  5. the absorption of glucose, amino acid, and triglycerides.
85
Q

GI Neurocrines

A
  1. Vasoactive intestinal peptide (VIP)
  2. GRP (Gastrin Releasing peptide or bombesin)
  3. Enkephalins (met-enkephalin and leu-enkephalin)
86
Q

GRP (Gastrin Releasing peptide or bombesin) is released from

A

vagus nerves that innervate the G cells.

87
Q

Enkephalins (met-enkephalin and leu-enkephalin) stimulate

A

contraction of GI smooth muscle,in
lower esophageal,
pyloric, and
ileocecal sphincters

88
Q

GRP stimulates

A

gastrin release from G cells.

89
Q

Enkephalins inhibit

A

intestinal secretion of fluid and electrolytes

90
Q

opiates in the treatment of diarrhea

A

Enkephalins inhibit intestinal secretion of fluid and electrolytes

91
Q

Neurocrines are synthesized in

A

neurons of the GI tract→ moved by axonal transport down the axon→ released by action potentials in the nerves→ then diffuse across the synaptic cleft to a target cell.

92
Q

VIP contains

A

28 amino acids and is homologous to secretin

93
Q

VIP is released from

A
  1. neurons in the mucosa

2. smooth muscle of the GI tract

94
Q

VIP has a half-life

95
Q

Functions of VIP

A
  1. relaxation of GI smooth muscle
  2. ↑pancreatic HCO3- secretion and ↓ gastric H+ secretion
  3. ↑intestinal secretion of electrolytes and hence of water
  4. potentates the action of acetylcholine in salivary glands
96
Q

VIP relaxation of GI smooth muscle, including the

A

a. relaxation lower esophageal sphincter

b. dilation of peripheral blood vessels

97
Q

VIP actions resembles secretin.

A

Stimulates pancreatic HCO3- secretion and inhibits gastric H+ secretion.

PHYSIOLOGY GIS (17 decks)

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