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GIGU > Secretions of GI Tract and Pancreas > Flashcards

Secretions of GI Tract and Pancreas Flashcards

1
Q

Rate of salivary secretion

A

1L/day

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2
Q

Define secretion

A

addition of fluids, enzymes, mucus to lumen of GI tract

-saliva, gastric secretion, pancreatic secretion, bile

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3
Q

Fxn of saliva

A
  • initial digestion of starches and lipids by salivary enzymes
  • dilution and buffering of ingested foods
  • lubrication of ingested food with mucus to aid in movement through esophagus
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4
Q

3 salivary glands

A

parotid
submaxillary
sublingual

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5
Q

cells of parotid gland

A

serous that secrete aqueous fluid with amylase

25% saliva production

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6
Q

cells of sublingual and submaxillary glands

A

serous that secrete aqueous fluid, mucous that secrete mucin glycoprotein for lubrication

75% saliva production

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7
Q

Describe the structure of salivary glands

A

Acinar- blind end that produces inital saliva (water, ions, enzymes, mucus)

Intercalated duct connects acinar to striated duct and ductal cells (saliva here similar to plasma)

Striated duct has ductal cells that alter the ion concentration–> final saliva is HYPOTONIC

Myoepithelial calls line entire gland, contract and expel saliva through gland when + by neural input

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8
Q

What is the composition of saliva

A

water, electrolytes, alpha amylase, lingual lipase, kallikrein, mucus

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9
Q

What are the electrolyte concentrations in saliva

A

hypotonic to plasma
–> high K+ and HCO3-

–> low Na+ and Cl-

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10
Q

How does primary saliva become hypotonic as it travels through the salivary gland?

A

Acinar cells secrete isotonic saliva, travels to ductal cells where exchange ions to make saliva hypotonic

—> net absorption of NaCl back into plasma

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11
Q

Besides electrolyte concentration, how do ductal cells maintain salivary hypotonicity?

A

Ductal cells are impermeable to water

——-> as NaCl absorbed back into plasma, water can’t follow, so it stays in the duct and dilutes saliva

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12
Q

What exchangers are on the apical side of ductal cells?

A

Na+/H+ exchanger
Cl-/HCO3- exchanger
H+/K+ exchanger

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13
Q

What exchangers are on the basolateral side of ductal cells?

A

Na+/K+ ATPase

Cl- channels

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14
Q

What innervates salivary glands?

A

Parasympathetic: facial or glossopharyngeal–> ganglia–> ACh on muscarinic receptors (acinar and ductal)–> produce IP3 and Ca+

Sympathetic: T1-3–>cervial ganglion–> release NE on B adrenergic receptors (acinar and ductal)–> produce cAMP

both increase saliva secretion

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15
Q

Why are innervations to salivary glands special?

A

Both parasympathetic and sympathetic systems are excitatory—> stimulation produces saliva

para is dominant, though

Salivary glands exclusively under ANS control (not neural and hormonal like GI)

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16
Q

What stimulates parasympathetics in saliva production?

A

conditioning: food, smell, N

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17
Q

What inhibits parasympathetics in saliva production?

A

fear, sleep, dehydration

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18
Q

What occurs when salivary glands are stimulated by ANS?

A

Increased saliva secretion, HCO3- and enzyme secretions, contraction of myoepithelial cells

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19
Q

How do aldosterone and ADH alter saliva?

A

Decrease saliva Na+ concentrations, increase K+ concentrations

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20
Q

How does Atropine affect saliva production?

A

Prevents parasympathetic pathway–> inhibits production of saliva
—————> prevents ACh from binding muscarinic receptors on acinar or ductal cells

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21
Q

What secretes gastric juice

A

gastric mucosa cells

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22
Q

What are the components of gastric juice

A

HCl, pepsinogen, water, mucus, intrinsic factor

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23
Q

What is the only “essential” component of gastric juice

A

Intrinsic factor, how Vitamin B12 is absorbed in ileum

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24
Q

Fxn of mucus in gastric juice

A
  • lines stomach to protect from damage
  • lubrication
  • combines with HCO3- to neutralize acid and maintain neutral pH at mucosa
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25
Q

Fxn of HCl in gastric juice

A
  • initiates protein digestion with pepsinogen
  • required to convert pepsinogen to active pepsin
  • kills large number of bacteria that enter stomach
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26
Q

What glands are found in the gastric mucosa?

A

Oxyntic glands and Pyloric glands

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27
Q

What do parietal cells of stomach produce?

A

HCl and intrinsic factor

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28
Q

What do chief cells of stomach produce?

A

Pepsinogen

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29
Q

What do G cells of stomach produce?

A

Gastrin into circulation (not ducts)

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30
Q

What do mucous neck cells secrete?

A

mucus, HCO3-, pepsinogen

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31
Q

Where are oxyntic glands found?

A

proximal 80% of stomach (body and fundus)

secrete acid

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32
Q

Where are pyloric glands found?

A

distal 20% of stomach (antrum)

synthesize and release gastrin

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33
Q

What cells are in oxyntic glands?

A 
Mucous neck cells--> mucus, HCO3-, pepsinogen
Chief cell--> pepsinogen
Parietal cells--> HCl, intrinsic factor
Enterochromaffin-like cell-->Histamine
D cell--> somatostatin
Enterochromaffin cell--> ANP
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34
Q

What cells are in pyloric glands?

A

Mucous neck cells–> mucus, HCO3-, pepsinogen
G cell–>gastrin
D cell–>somatostatin

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35
Q

What majority of cells are in the body of the stomach?

A

Parietal, chief

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36
Q

What majority of cells are in the antrum of the stomach?

A

Mucous, G cell

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37
Q

What determines the maximal secretory rate of HCl?

A

number of parietal cells

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38
Q

What is the function of low gastric pH (1-2)

A

convert pepsinogen to pepsin

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39
Q

Where is HCl formed?

A

villus-like membranes of canaliculi of parietal cells

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40
Q

Overview of HCl formation/secretion in gastric parietal cell

A

CO2 from aerobic metabolism combines with water–> H2CO3 via CARBONIC ANHYDRASE

–> dissociates into H+ and HCO3-

–> H+ goes out into lumen and combines with Cl–>HCl

–>bicarbonate absorbed in blood

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41
Q

What exchangers are on the apical (lumen) side of gastric parietal cells?

A

H+/K+ ATPase (to get H+ into lumen)

Cl- channels

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42
Q

What drug inhibits the H+/K+ ATPase on the apical side of parietal cells?

A

Omeprazole

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43
Q

What is the function of omeprazole

A

Reduce H+ secretion, treat stomach ulcers

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44
Q

What exchangers are found on the basolateral (blood) side of gastric parietal cells?

A

Cl-/HCO3- exchanger (to absorb bicarb into blood)
—-> alkaline tide (high pH after meal)

Na+/K+ ATPase

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45
Q

What is the net absorption/secretion at gastric parietal cells?

A

Net secretion of HCl

Net absorption of HCO3-

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46
Q

What secretions make up gastric juice?

A

Non-parietal and parietal secretions

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47
Q

Why do you need to know the composition of gastric juice?

A

required to treat patients with vomiting or maintained with IV

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48
Q

Describe non-parietal secretions

A
  • basal alkaline of constant and low volume
  • primarily Na+, Cl—> K+ same concentration as in plasma
  • HCO3- secreted at 30 mEq/L
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49
Q

Describe parietal secretions

A
  • hyperosmotic
  • Cl- only anion
  • H+ (150-160 mEq)
  • K+ (10-20 mEq)

as secretion rate increases, electrolyte concentration appreaches that of pure parietal secretion

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50
Q

Describe passive feedback regulating HCl secretion

A

as pH falls, gastrin release is inhibited–> decreases HCl secretion

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51
Q

What stimulate H+ secretion by gastric parietal cells?

A

histamine, ACh, gastrin

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52
Q

What receptors does Cimetidine block?

A

H2 receptors, blocks histamine action

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53
Q

What parietal cell receptor does histamine bind to?

A

H2 receptor

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54
Q

What parietal cell receptor does ACh bind to directly?

A

M3 receptor

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55
Q

Describe direct ACh action on parietal cells

A

M3 receptor–>Gq—> IP3 and Ca++–> H+/K+ ATPase–> increase H+ secretion

56
Q

Describe histamine action on parietal cells

A

H2–> Gs–> cAMP–> increase H+ secretion via H+/K+ ATPase

57
Q

What receptor does atropine inhibit?

A

M3 receptor and ACh action

58
Q

How does ACh and gastrin increase H+ secretion indirectly?

A

stimulate release of histamine

59
Q

What parietal cell receptor does gastrin bind?

A

CCKb receptor

60
Q

Describe action of gastrin on parietal cells

A

IN CIRCULATION–> CCKb receptor–>Gq–> IP3 and Ca++–> gastrin secretion from G cells and H+/K+ ATPase–> H+ secretion

61
Q

Describe direct vagal stimulation of parietal cells

A

releases ACh on parietal cells–> H+ secretion

62
Q

Describe indirect vagal stimulation of parietal cells

A

releases GRP to + G cells–> releases gastrin –> circulation–> acts on parietal cells to secrete H+ (via IP3, Ca++ pathway= same as ACh)

—> indirect pathway also INHIBITS somatostatin so it can’t prevent gastrin release

63
Q

What vagal pathway does atropine block?

A

Direct pathway (ACh)

64
Q

Why does atropine not block indirect vagal pathway?

A

it won’t affect neurotransmitter GRP that activates gastrin release from G cells
——–> only affects M3 receptor activated by ACh

65
Q

How does somatostatin begin working again after indirect vagal stimulation of parietal cells?

A

Indirect vagal inhibits somatostatin

–> gastrin itself has negative feedback on somatostatin, so it increases somatostatin release along with H+ in gastric lumen

66
Q

Describe HCl potentiation

A

Histamine potentiates actions of ACh and gastrin

ACh potentiates actions of histamine and gastrin

67
Q

Define potentiation

A

sum of 2 stimulants exceeds the sum of their individual responses
—–> requires separate receptors on target cell

68
Q

How does cimetidine affect HCl potentiation?

A

Since it is an antagonist of H2 receptor, it blocks DIRECT action of histamine and POTENTIATION effects of ACh and gastrin

69
Q

How does atropine affect HCl potentiation?

A

since it is an antagonist of M3, it blocks DIRECT effects of ACh and POTENTIATION effects of histamine and gastrin

70
Q

What is cimetidine used to treat?

A

duodenal and gastric ulcers, GERD

71
Q

What is omeprazole used to treat?

A

ulcers via reduced H+ secretion

72
Q

What are the 3 phases of gastric HCl secretion?

A

Cephalic
Gastric
Intestinal

73
Q

What controls cephalic phase of gastric HCl secretion?

A

Vagus N

74
Q

What controls gastric phase of HCl secretion?

A
  • Local nervous secretory reflexes
  • Vagal reflexes
  • Gastrin-histamine stimulation
75
Q

What controls intestinal phase of HCl secretion?

A

Nervous mechanisms

Hormonal mechanisms

76
Q

What HCl secretion phase does a vagotomy abolish?

A

cephalic phase

77
Q

What stimuli activate the cephalic phase?

A

smelling, tasting, chewing, swallowing, conditioned reflexes

78
Q

What phase accounts for 30% of total HCl secretion in response to a meal?

A

cephalic phase

79
Q

What are the mechanisms behind the cephalic phase?

A

Vagus nerve releases ACh on parietal cells

Vagus nerve releases GRP–>gastrin–> circulation–> parietal cell

BOTH direct and indirect vagal mechanisms

80
Q

What phase accounts for 60% of total HCl secretion in response to a meal?

A

Gastric phase

81
Q

What stimuli activate the gastric phase?

A

distension of stomach, presence of breakdown of proteins, AA and small peptides

82
Q

What are the mechanisms of the gastric phase?

A
  • Distension + mechanoreceptors in mucosa of oxyntic and pyloric glands
  • –> vagus nerve releases ACh on parietal cell
  • —> vagus nerve releases gastrin–circulation–parietal cell
  • Distension of antrum
  • —> local reflexes release ACh on parietal and G cells (GASTRIN)
  • Amino acids and small peptides
  • —–> activate GASTRIN–circulation–parietal cell and chief cell (pepsin)
83
Q

What food/drink can also stimulate gastric HCl secretion?

A

coffee

alcohol

84
Q

What phase accounts for 5-10% of total HCl secreted in response to a meal?

A

Intestinal phase

85
Q

What are the mechanisms behind the intestinal phase?

A

Distention of small intestine + acid secretion

Digested protein + acid secretion via DIRECT effect on parietal cells and GASTRIN on parietal cells

86
Q

What stimulus activate the intestinal phase?

A

products of protein digestion

87
Q

When is pepsinogen secreted?

A

Only when gastric pH is acidic enough to convert it to pepsin (<5)

88
Q

What secretes pepsinogen?

A

chief cells and mucus cells in oxyntic glands

——> needs H+ secretion from parietal cells to lower pH in stomach

89
Q

What is the most important stimulus for pepsinogen secretion?

A

Vagus N

90
Q

What role does H+ play in pepsinogen secretion?

A

triggers local cholinergic reflexes–> stimulate chief cells to secrete pepsinogen

91
Q

What allows more conversion of pepsinogen to pepsin?

A

Pepsin

92
Q

What is the fxn of pepsin?

A

converts more pepsinogen to pepsin

degrades food proteins into peptides

93
Q

What is the optimal pH for pepsin?

A

1.8-3.5

94
Q

What pH makes irreversible inactivation of pepsin?

A

over 7-8

–>reversible if between 3.5 and 5

95
Q

Where is intrinsic factor synthesized?

A

parietal cells

96
Q

What is the fxn of intrinsic factor?

A

binds to vitamin B12 for absorption in ileum

97
Q

What is the only secretion required in the stomach?

A

intrinsic factor

98
Q

What is associated with failure to secrete intrinsic factor?

A

achlorhydria, absence of parietal cells

99
Q

What occurs when stomach does not produce enough intrinsic factor?

A

decreased absorption of vitamin B12

100
Q

What occurs when there is a failure to secrete intrinsic factor?

A

pernicious anemia

101
Q

Causes of pernicious anemia

A

atrophic gastritis (chronic inflammation of stomach mucosa–> loss of parietal cells)

autoimmune metaplastic atrophic gastritis (immune system attacks intrinsic factor protein or gastric parietal cells)

102
Q

What is a consequence of gastrectomy?

A

loss of parietal cells, therefore instrinsic factor

103
Q

What occurs with a gastric bypass

A

exclusion of the stomach, duodenum and proximal jejunum—> alters absorption of vitamin B12

104
Q

What is the fxn of the gastric mucosal barrier?

A

protect mucosal epithelium against HCl and pepsin

105
Q

What is the gastric mucosal barrier composed of?

A

HCO3- (surface epithelial cells)

Mucus (mucous cells)

Both form gel-like barrier over gastric mucosa

106
Q

What protects the gastric mucosa?

A
  • HCO3-
  • mucus
  • prostaglandins (misoprostol)
  • mucosal blood flow
  • gastrin
  • growth factors
107
Q

What damages the gastric mucosa?

A
  • acid
  • pepsin
  • NSAIDs
  • Helicobacter pylori
  • alcohol
  • bile
  • stress
  • smoking
108
Q

Describe Zollinger-Ellison syndrome

A

large secretion of gastrin by duodenal or pancreatic gastrinomas

  • –> increases parietal cell mass
  • –> H+ secretory rate high

** inhibits absorption of Na+ and H20 by SI= secretory diarrhea

109
Q

How do you get an ulcer with Zollinger-Ellison syndrome?

A

excessive H+ arrives in duodenum and overwhelmes capacity of HCO3- in pancreatic juice

110
Q

Describe the consequences of low intestinal pH in Zollinger-Ellison syndrome

A
  • inactivation of pancreatic digestive enzymes
  • interferes with emulsification of fat via bile acid
  • damages intestinal epithelial cells and villi
  • leads to maldigestion and malabsorption–> steatorrhea
111
Q

Describe the secretin stimulation test

A

Injection of secritin causes paradoxical increase in gastrin release in gastrinomas

–> secretin used to dx gastrin-secreting tumors given the fact that it inhibits gastrin release normally

112
Q

Mechanical causes of Peptic ulcer disease

A

H. pylori infection and NSAIDs

113
Q

Functional causes of peptic ulcer disease

A
  • loss of protective mucosal barrier
  • excessive H+ and pepsin secretions

OR combination

114
Q

What are the types of peptic ulcer disease?

A

duodenal ulcers

gastric ulcers

115
Q

How does H pylori damage the gastric mucosa?

A

H pylori releases cytotoxins that breakdown mucosal barrier and damage the underlying epithelial cells

116
Q

What enzyme allows bacteria (H pylori) to colonize gastric mucosa?

A

urease

117
Q

What is the major cause of cytotoxicity in ulcer disease?

A

Ammonium

urease converts urea–> ammonia–> ammonium (damages epithelial cells after breaks barrier)

118
Q

Why do gastric ulcers form?

A

defective gastric mucosal barrier–> form ulcers that line stomach

119
Q

Why do duodenal ulcers form?

A

more common than gastric due to high H+ secretion rates

–>usually not malignant

120
Q

What ulcesr have increased gastrin levels?

A
  • gastric ulcer due to decreased H+ secretion
  • duodenal ulcer due to gastrin response to ingestion of food
  • zollinger-ellison syndrome (way higher gastrin c/t others)
121
Q

What ulcer has increased parietal cell mass due to increased gastrin levels?

A

duodenal ulcer

122
Q

What sympathetics innervate the exocrine pancreas?

A

postganglionic nerves via celiac and superior mesenteric plexuses

123
Q

What is the exocrine pancreas organized like?

A

salivary glands

124
Q

What cells of the exocrine pancreas secrete aqueous solution containing HCO3-?

A

ductal and centroacinar cells

125
Q

What are the two components of pancreatic secretions?

A
  • enzymatic secretion by acinar cells
  • ——> amylases and lipases
  • ——> proteases secreted in inactive form, converted to active in lumen of DUODENUM
  • aqueous secretion by centroacinar and ductal cells
  • ———> secrete HCO3- rich fluid (alkalinizes and hydrates acinar cell)
  • ———-> initial secretion modified by transport processes in ductal epithelial cells
126
Q

What is the net result of pancreatic secretions by ductal cells?

A

Secretion of HCO3- into ductal lumen

Absorption of H+ into blood

127
Q

Cystic fibrosis and the pancreas

A

mutations in transmembrane conductance regulator (CFTR)

128
Q

What organ is the first to fail in cystic fibrosis?

A

pancreas

129
Q

What is the function of CFTR in cystic fibrosis

A

regulated Cl- channel in the apical surface of ductal cell

130
Q

What is associated with CFTR mutations?

A

loss of HCO3- secretion, chronic or acute pancreatitis

131
Q

What phases are pancreatic secretions divided into?

A

cephalic
gastric
intestinal

132
Q

What is the different between gastric and pancreatic phases?

A

pancreas secretes mainly enzymatic secretions (aqueous in intestinal)

**intestinal is majority of secretion

133
Q

What induces pancreatic enzyme release into duodenal lumen?

A

CCK

134
Q

What induces secretion of HCO3- from pancreatic cells into duodenum?

A

Secretin

135
Q

What stimulates pancreatic intestinal phase?

A

Phe, Met, Trp, small peptides, fatty acids

–> I cells–> CCK–> IP3 and Ca++–> enzyme release

H+–> S cells–> Secretin–> cAMP–> aqueous secretion (Na+, HCO3-)

136
Q

What potentiates the pancreatic intestinal phase?

A

ACh and CCK

GIGU (37 decks)

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