GIT - Lecture 7 Flashcards

1
Q

Where is mucin secreted in the GIT?

A

everywhere

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2
Q

What secretes mucin?

A

surface epithelial cells

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3
Q

Why is there an increase in production of mucin at the level of the stomach?

A

because we have an tubular glands in the cardiac and pyloric regions that fill with mucin producing cells

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4
Q

Which part of the stomach are mucous neck cells present?

A

fundus and corpus

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5
Q

What is the pH of the mucous gel below the mucous layer?

A

2

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6
Q

What is the pH of the mucous gel above the mucous layer

A

around 7

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7
Q

Why does the mucous layer have some degree of protection?

A

because surface epithelial cells also release bicarbonate-rich fluid in addition to mucin

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8
Q

Where do the bicarbonate ions get adsorbed?

A

into the mucous gel layer

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9
Q

What is the mucous gel layer also known as?

A

muci-bicarb layer

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10
Q

What happens when H+ enter the muci-bicarb layer?

A

they combine with the bicarbonate to produce water and CO2

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11
Q

What prevents a change in the pH below the mucosal layer?

A

the muci-bicarb layer

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12
Q

What is the main thing that protects the gastric mucosa?

A

gastric mucosal barrier (GMB)

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13
Q

Where is the gastric mucosal barrier (GMB) found?

A

apical surfaces and tight junctions

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14
Q

What are the 3 things that protect gastric mucosa?

A
  1. muci-bicarb layer
  2. gastric mucosal barrier
  3. rapid cell turnover
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15
Q

What happens during rapid cell turnover?

A

re-epitheliazation

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16
Q

People with a normal ___ output can have a ___ barrier, which causes ulceration of the gastric mucosa.

A

normal, weak

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17
Q

Which 2 drugs can weaken the barrier and cause ulcers?

A

aspirin and NSAIDS

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18
Q

Which bacteria weakens the barrier and causes ulcers?

A

helicobacter pylori

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19
Q

Where does helicobacter pylori go to release its toxin?

A

between the mucous and the top of the surface epithelial cells

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20
Q

People with a ___ barrier can have an ___ HCl output, which causes ulceration of the gastric mucosa.

A

normal, excessive

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21
Q

What is produced when there is excessive HCl output?

A

gastrin-producing tumors

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22
Q

Regulation of gastric secretions happen via which 2 systems?

A

nervous and hormonal

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23
Q

What division and nerve contributes to the nervous regulation of gastric secretions?

A

sympathetic and vagus nerve

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24
Q

What are the 3 phases of gastric secretion?

A
  1. cephalic
  2. gastric
  3. intestinal
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25
Q

What are the 2 parts of the cephalic phase of gastric secretion?

A

psychic and gustatory

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26
Q

What is the neural regulation of secretion?

A

ENS neurons synapse on the smooth muscle of the GIT and then synapse on the secretory cell

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27
Q

The ENS sends excitatory input (ACh) onto which 3 secretory cells to increase their secretion?

A
  • parietal
  • peptic
  • mucous
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28
Q

The cephalic phase is ___-mediated.

A

vagally

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29
Q

Activating secretory cells to produce secretions also causes…

A

vasodilation

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30
Q

What does sympathetic system do to secretion? What else does it cause?

A

inhibits secretion, causes vasoconstriction

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31
Q

What activates sensory neurons that leads to ACh secretion on secretory cells

A

distention and vago-vagal inputs

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32
Q

What do proteins produce when they get broken down into the stomach?

A

secretagogues

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33
Q

What are secretagogues?

A

amino acids or partially digested proteins?

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34
Q

What do secretagogues act on?

A

Gastrin-Releasing Cells (G-cells)

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35
Q

What do secretagogues lead to the release of when they act on G-cells?

A

gastrin

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36
Q

When secretagogues cause gastrin to be released from G-cells, what increases?

A

the parietal cell release of HCl

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37
Q

Gastrin released by endocrine cells in the antrum (G-cells) in response:

A
  1. secretagogues
  2. local enteric reflexes
  3. vagally-mediated reflexes
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38
Q

Which phase does vagally-mediated release of gastrin happen?

A

cephalic phase

39
Q

How is gastrin regulated?

A

it is self-regulated

40
Q

Where do secretagogues get excreted?

A

atrum

41
Q

What happens to secretagogues when HCl released by parietal cells increases?

A

it increases since it converts pepsinogen to pepsin

42
Q

What kind of feedback is the gastrin regulation?

A

positive

43
Q

What is gastrin release inhibited by? (2)

A

low pH in the stomach and somatostatin

44
Q

What do inhibitions contribute to the negative feedback on gastrin secretion?

A

low pH and somatostatin

45
Q

What are the 2 physiological roles of gastrin?

A
  • stimulates HCl secretion
  • stimulates production of more parietal cells
46
Q

What kind of effect does gastrin have on parietal cells?

A

trophic effect

47
Q

When is somatostatin released?

A

at low pH in the stomach

48
Q

What does somatostatin inhibit?

A

the release of gastrin from G-cells and HCl secretion from parietal cells

49
Q

What is present in large quantities in the gastric mucosa?

A

histamine

50
Q

What does histamine elicit?

A

large volumes of gastric juice with lots of HCl

51
Q

What is the common mediator hypothesis?

A

Gastrin and ACh cause Histamine release. Histamine is the
FINAL local COMMON
CHEMOSTIMULATOR of the parietal cell.

52
Q

Parietal cells have receptors for what 3 things on their surface?

A
  • ACh
  • gastrin
  • histamine
53
Q

What receptor is found on the parietal cell that binds histamine?

A

H2 receptor

54
Q

What happens when one receptor binds to the parietal cell?

A

it sensitizes it from the stimulation of the other two

55
Q

What kind of effect is between the 3 different stimulators of the parietal cell?

A

cooperative effect

56
Q

Which substance is normally the one that activates the parietal cell since it is always present in the mucosa?

A

histamine

57
Q

What is the permissive hypothesis?

A

histamine is constantly released in the gastric mucosa and presented to the Parietal Cells as a tonic background, sensitizing them to other stimuli

58
Q

What happens to acid secretion in response to ACh and gastrin when the release of histamine is blocked or when there is an H2-receptor antagonist present?

A

it is inhibited

59
Q

When are H2 receptor blockers used?

A

during ulcer disease

60
Q

H2-receptor blockers are used to decrease ___ secretion.

A

HCl

61
Q

In addition to H2-receptor blockers, what other blocker is used to decrease HCl secretion?

A

H+/K+ ATPase blockers

62
Q

What is the feedback during intestinal phase of secretion?

A

inhibitory

63
Q

When is there a small burst of excitation during the intestinal phase?

A

when the secretagogues come in and activate cells in the duodenum

64
Q

What factors produce a negative feedback on secretion at the level of the stomach?

A
  • distension
  • pH<3.5
  • osmolarity
  • chemical composition
65
Q

Both motor and secretory activities of the stomach reflect a balance between what 2 influences on the muscular and glandular cells in the gastric wall?

A

excitatory and inhibitory

66
Q

Optimal secretory activity is the result of an interplay between which 2 mechanisms?

A

neural and hormonal

67
Q

Gastric secretion at any moment in time reflects a balances between what 2 influences?

A

stimulatory and inhibitory influences

68
Q

What are the pre-intestinal changes before digestion?

A
  • meal reduced to semi-liquid consistency
  • acidified, osmotic pressure is unchanged
  • limited digestion
69
Q

What are the pre-intestinal changes to some polysaccharides, some proteins and lipids?

A

-> Disaccharides
-> Polypeptides
-> Di-, monoglycerides, fatty acids

70
Q

What are the 4 upper intestine functions?

A
  • chyme neutralization
  • osmotic equilibration
  • digestion continues
  • absorption begins
71
Q

By the time the chyme leaves the small intestine, it will be ___.

A

isotonic

72
Q

What are the accessory organs that secrete substances into the small intestine?

A
  • liver
  • gallbladder
  • pancreas
73
Q

How do the accessory organs send their excretions to the duodenum?

A

through the sphincter of Oddi into the ampulla of Vater

74
Q

What is the swelling of the duodenum called?

A

ampulla of Vater

75
Q

Which ducts merge to drain into the sphincter of Oddi?

A

right and left hepatic ducts
cystic duct
common bile duct
pancreatic dut

76
Q

Where are all the pancreatic enzymes produced?

A

the head of the pancreas

77
Q

What is the volume of pancreatic juice in the body?

A

0.5-1.5L/day

78
Q

What kind of solution is pancreatic juice?

A

isotonic (300 mOsm)

79
Q

What are the 4 main electrolytes of pancreatic juice?

A

Na+, K+, Cl-, HCO3-

80
Q

What is the main electrolyte of pancreatic juice?

A

HCO3-

81
Q

What is the pH of pancreatic juice?

A

7.2-8.2

82
Q

Pancreas produces the largest quantities and the most powerful digestive ___.

A

enzymes

83
Q

How many g% of enzymes present in the pancreatic juice?

A

3 g %

84
Q

What are the 3 enzymes found in pancreatic juice?

A

amylases, proteases, lipases

85
Q

For absorption, disaccharides must be converted to ___.

A

monosaccharides

86
Q

All the proteases released at the level of the pancreas are in what kind of form?

A

inactive form

87
Q

Where do inactive pancreative proteases become active?

A

when they get cleaves in the small intestine

88
Q

What enzyme is produced in the small intestine to convert the inactive trypsinogen into trypsin?

A

enterokinase

89
Q

Why are enzymes inactive when they are released by the pancreas?

A

because they are very strong so they might damage the pancreas if they are released active

90
Q

What does trypsin convert chymotrypsinogen into?

A

chymotrypsin

91
Q

What does trypsin convert proelastase into?

A

elastase

92
Q

What does trypsin convert procarboxypeptidase into?

A

carboxypeptidase

93
Q

What is secreted by the pancreas to inactivate trypsin?

A

trypsin inhibitor