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GI Secretions Flashcards

1
Q

What are the functions of saliva?

A
  • initial digestion
  • dilution and buffering
  • lubrication with mucus
  • oral hygiene
  • evaporative cooling in dogs
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2
Q

Higher salivary pH may increase susceptibility to what?

A

gingivitis due to more calculus

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3
Q

How does saliva function for intial digestion?

A
  • contains amylase for starch breakdown and lipase for lipid breakdown
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4
Q

The dilution and buffering function of saliva is important for what?

A

rumination

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5
Q

Saliva functioning to provide lubrication with mucus helps form what?

A

bolus

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6
Q

How does saliva help with oral hygiene?

A
  • flush oral cavity of food debris
  • lysozomes in saliva to lyse bacteria
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7
Q

What are the major salivary glands?

A
  • parotid glands
  • submandibular glands
  • sublingual glands
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8
Q

Initial saliva passes through which duct before the striated duct?

A

intercalated duct

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9
Q

What structure is lined with acinar cells?

A

acinus

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10
Q

What structure is responsible for producing initial saliva?

A

acinus

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11
Q

Which duct is lined with ductal cells to alter the ion concentration of saliva?

A

striated duct

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12
Q

What causes myoepithelial cells to contract and eject saliva?

A

neural stimulation

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13
Q

Acinar and ductal cells have what type of innervation?

A

SNS and PSNS, but usually PSNS dominates

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14
Q

Do salivary glands have high or low blood flow?

A

high

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15
Q

Blood flow of salivary glands increases when what is stimulated?

A

saliva production

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16
Q

What is saliva composed of?

A
  • water
  • electrolytes
  • amylase (some species)
  • lingual lipase
  • kallikrein
  • mucus
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17
Q

What enzyme regulates local vasodilation associated with secretions?

A

kallikrein

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18
Q

Saliva is _____ compared with plasma.

A

hypotonic

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19
Q

Saliva is formed in a two step process. What are they?

A
  • formation of isotonic solution by acinar cells
  • modification of solution by ductal cells to become hypotonic
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20
Q

Modification of saliva involves transporters where?

A

on the luminal and basolateral membranes

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21
Q

What are the luminal membrane transporters for saliva formation?

A
  • Na+/H+ exchange
  • Cl-/HCO3- exchange
  • H+/K+ exchange
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22
Q

What are the basolateral membrane transporters for saliva formation?

A

-Na+/K+ ATPase
- Cl- channels

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23
Q

Low concentrations in saliva mean what?

A
  • Absorption of Na+ and Cl- into blood
  • Secretion of K+ and HCO3- into saliva
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24
Q

How is saliva hypotonic?

A
  • ductal cells impermeable to water (not reabsorbing water)
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25
Q

Acing cells secrete what organic components?

A
  • alpha-amylase (pig and human only)
  • lingual lipase
  • mucin glycoproteins
  • IgA
  • Kallikrein
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26
Q

At high flow rates (4mL/min), final saliva resembles what?

A

plasma

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27
Q

At low flow rates (<1mL/min), final saliva is what?

A

hypotonic

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28
Q

Final composition of saliva depends on wha?

A

Contact time with ductal cells

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29
Q

What is the exception to final composition being contact dependent? Why?

A

HCO3- concentration lowest at low flow rates and highest at hgh flow rates because its secretion is selectively stimulated by PSNS when saliva production is stimulated

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30
Q

What are the two features of salivary secretion regulation?

A
  • salivary secretion is exclusively under neural control
  • Salivary secretion stimulated by BOTH PSNS and SNS (usually PSNS dominant)
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31
Q

What is the PSNS innervation of salivary secretion regulation?

A
  • carried on facial and glossopharyngeal nerves
  • postganglionic neurons release acetylcholine
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32
Q

Acetylcholine released by postganglionic neurons of the PSNS for salivary regulation does what?

A
  • acts on muscarinic receptors on acinar and ductal cells to increase volume and enzymes in saliva
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33
Q

What is the SNS innervation of salivary secretion regulation?

A
  • originates in T1 to T3, synapse on superior cervical ganglion
  • postganglionic neurons release NE
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34
Q

Norepinephrine released by postganglionic neurons of the SNS for salivary secretion regulation does what?

A
  • acts on beta adrenergic receptors to increase secretions
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35
Q

What are the components of gastric juice?

A
  • HCl
  • pepsinogen
  • intrinsic factor
  • mucus
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36
Q

What components of gastric juice initiate protein digestion?

A
  • HCl
    pepsinogen
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37
Q

What component of gastric juice is essential for absorption of vitamin B12 in ileum?

A

intrinsic factor

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38
Q

What component of gastric juice protects gastric mucosa from HCl and lubricates?

A

mucus

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39
Q

The body of the stomach contains what glands?

A

oxyntic glands

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40
Q

Oxyntic glands empty products via ducts into where?

A

stomach lumen

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41
Q

The openings (aka pits) of oxyntic glands are lined with?

A

epithelial cells

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42
Q

Mucous neck cells of oxyntic glands secrete what?

A

mucus

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43
Q

Parietal cells of oxyntic glands secrete what?

A
  • intrinsic factor
  • HCl
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44
Q

Chief cells of oxyntic glands secrete what?

A

pepsinogen

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45
Q

What glands can be found in the antrum of the stomach?

A

pyloric glands

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46
Q

G cells of pyloric glands secrete what?

A

gastrin into circulation

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47
Q

Mucous neck cells of pyloric glands secrete what?

A
  • mucous
  • bicarbonate
  • pepsinogen
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48
Q

What is the brief general mechanism of HCl secretion?

A
  • by parietal cells
  • apical (luminal) membrane has H+/K+ ATPase and Cl- channels
  • basolateral membrane has Na+/K+ ATPase and Cl-/HCO3- exchangers
  • cells contain carbonic anhydrase
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49
Q

What is the detailed mechanism of HCl secretion?

A
  • CO2 combines with water to form H2CO3, which dissociates into H+ and HCO3-. Hydrogen goes to lumen of stomach via H+/K+ ATPase. Bicarb absorbed into blood via bicarbonate/Cl- exchanger.
  • Cl- follows H+ into lumen by diffusing through Cl- channels
  • Absorbed bicarbonate responsible for “alkaline tide” in gastric venous blood after meal. Alkaline tide eventually secreted back to GI tract via pancreatic secretions.
  • net secretion of HCl and net absorption of bicarbonate
50
Q

In order to alter HCl secretion, we can alter H+ secretion. What substances stimulate H+ secretion?

A
  • histamine (paracrine)
  • acetylcholine (neurocrine)
  • gastrin (hormone)
51
Q

Strong interaction of histamine with either acetylcholine or gastrin is called?

A

potentiation
- sum of two stimuli causes a greater response than individual responses alone

52
Q

What drug will block histamine action on parietal cells? How?

A

Cimetidine blocks H2 receptors to block histamine action

53
Q

Describe the action of histamine to stimulate H+ secretion.

A
  • released from ECL cells in gastric mucosa
  • binds to H2 receptors on parietal cells
  • cAMP is second messenger
54
Q

Describe the action of acetylcholine to stimulate H+ secretion.

A
  • released from vagus nerves innervating gastric mucosa
  • binds muscarinic receptors in parietal cells
  • IP3/Ca2+ are second messengers
  • Ach also stimulates ECL cells to release histamine
55
Q

Describe the action of gastrin to stimulate H+ secretion.

A
  • secreted by G cells in stomach antrum
  • binds CCKB receptors on parietal cells
  • IP3/Ca2+ are second messengers
  • gastrin also stimulates ECL cells to release histamine
56
Q

What drug mostly blocks H+ secretion, no matter the stimulus?

A

omeprazole

57
Q

What are the two direct paths of vagal stimulation for HCl secretion?

A
  1. vagus nerve –> parietal cells –> Ach –> HCl
  2. vagus nerve –> GRP –> G cells –> gastrin
58
Q

What is the indirect path of vagal stimulation for HCl secretion?

A

gastrin from G cells –> systemic circulation –> HCl from parietal cells

59
Q

Atropine will not block HCl secretion completely. Why?

A

Because it cannot affect the second direct pathway at all

60
Q

What are the phases of HCl secretion?

A
  • cephalic phase
  • gastric phase
  • intestinal phase
61
Q

The cephalic phase accounts for how much HCl secretion?

62
Q

The gastric phase accounts for how much HCl secretion?

63
Q

The intestinal phase accounts for how much HCl secretion?

64
Q

What are the two mechanisms to promote HCl secretion in cephalic phase?

A
  • direct stimulation of parietal cells by vagus nerve to relase Ach
  • indirect stimulation via gastrin
65
Q

What are the four mechanisms to promote HCl secretion in gastric phase?

A
  • distention –> vagal stimulation –> parietal cells
  • indirect via gastrin
  • distension of antrum –> gastrin
  • amino acids and peptides –> gastrin
66
Q

Alcohol and caffeine stimulate HCl in what phase?

A

gastric phase

67
Q

The intestinal phase is stimulated by what?

A

products of protein digestion

68
Q

The gastric phase is stimulated by what?

A

distension of stomach and presence of AA and peptides

69
Q

The cephalic phase is stimulated by what?

A
  • smelling
  • tasting
  • chewing
  • swallowing
  • conditioned reflexes
70
Q

When is HCl secretion inhibited?

A

When it is no longer needed for conversion of pepsinogen to pepsin

71
Q

What three things trigger inhibition of HCl secretion?

A
  • decreased pH of gastric contents
  • somatostatin (directly and indirectly)
  • prostaglandins antagonize histamine by reducing cAMP
72
Q

What is peptic ulcer disease?

A
  • ulcerative lesion of gastric or duodenal mucosa caused by loss of mucus, have excessive H+ and pepsin secretion, or ombination of both
  • can be classified as either gastric or duodenal ulcers
  • other damaging factors include H pylori infection and stress
73
Q

What are the barriers to acid and pepsin damage to mucosa?

A
  • bicarbonate
  • mucus
74
Q

How does bicarbonate provide a barrier to mucosa?

A

gets trapped in mucus and neutralizes acid/deactivates protein

75
Q

How does mucus provide a barrier to mucosa?

A

forms barriers between cells and luminal contents

76
Q

Why do gastric ulcers form?

A

because mucosal barrier is defective which allows H+ ions to penetrate and pepsin is able to digest mucosa

77
Q

How does H. pylori cause gastric ulcers?

A

colonizes gastric mucus and attaches to epithalial cells and releases cytotoxins which help breakdown the mucus barrier

78
Q

How does H pylori colonize gastric mucus?

A

because it has urease enzyme which allows it to survive the acidic environment

79
Q

Whaat syndrome has high rates of H+ secretion due to high gastrin, delivers high H+ to duodenum, and causes steatorrhea?

A

gastrinoma (Zollinger-Ellison syndrome)

80
Q

The aqueous component of the exocrine pancreas is high in what?

A

bicarbonate

81
Q

The enzymatic component of the exocrine pancreas digests what?

A
  • carbs
  • protein
  • fat
82
Q

The exocrine pancreas comprises ____% of the pancreas.

83
Q

What is the structure of exocrine glands?

A
  • acinus lined with acinar cells
  • ducts lined with ductal cells
  • centroacinar cells
84
Q

What cells of the exocrine pancreas are responsible for secreting the aqueous portion?

A
  • ducts lined with ductal cells
  • centroacinar cells
85
Q

What part of the exocrine pancreas secretes enzymes?

86
Q

Does the PSNS stimulate or inhibit the exocrine pancreas?

A

stimulates

87
Q

Does the SNS stimulate or inhibit the exocrine pancreas?

88
Q

Enzymes secreted from the pancreas are synthesized where?

A

rough er of acinar cells

89
Q

Amylase and lipase are secreted as what?

A

active enzymes

90
Q

Proteases are secreted in what form?

A

inactive known as zymogens

91
Q

The juice of the aqueous component of pancreatic secretions is what and contains what?

A
  • isotonic
  • contains Na+, Cl-, K+, HCO3-
92
Q

For the aqueous component of pancreatic secretions, what cells make the intiial secretion that is then modified by transport processes in ductal cells?

A

centroacinar and ductal cells

93
Q

What ions of pancreatic secretions have a constant flow rate?

94
Q

The bicarbonate concentration of pancreatic secretions increases with high or low flow rates?

95
Q

The The Cl- concentration of pancreatic secretions decreases with high or low flow rates?

96
Q

Why does bicarb secretion increase with high flow rates?

A

Because at high flow rates, secretions are mostly Na+, HCO3-, and water

97
Q

Why does Cl- secretion increase with low flow rates?

A

because at low flow rates, solution contains mostly Na+, Cl-, and water

98
Q

The aqueous portion of pancreatic secretion is stimulated by what?

A

H+ in duodenum

99
Q

The enzymatic portion of pancreatic secretion is stimulated by what?

A

products of digestion

100
Q

Acinar cells are receptors for what?

101
Q

Ductal cells are receptors for what?

A
  • CCK
  • Ach
  • secretin
102
Q

Bile secretion is needed for what?

A

digestion and absorption of lipids

103
Q

What is bile?

A

a mixture of bile salts, bile pigments, cholesterol, phospholipids, ions, water

104
Q

Why do we need bile salts?

A

to emulsify lipids for digestion which makes them water soluble

105
Q

The biliary system includes what?

A
  • liver
  • gallbladder
  • bile duct
  • duodenum
  • ileum
  • portal circulation
106
Q

What synthesizes the components of bile?

A

hepatocytes

107
Q

Bile flows out of the bile ducts and into where?

A

gallbladder

108
Q

What stimulates contraction of the gallbladder and relaxes the sphincter of Oddi?

109
Q

After lipid absorption, bile salts are recirculated to liver via?

A

reabsorption in ileum (enterohepatic circulation)

110
Q

Liver conjugates bile acids with amino acids to form what?

A

bile salts

111
Q

What are the two primary bile acids formed by hepatocytes?

A
  • cholic acid
  • chenodeoxycholic acid
112
Q

What are the two amino acids that can conjugate with bile acids?

A
  • glycine
  • taurine
113
Q

Bile salts have what charge?

114
Q

Bile salts bind products of lipid digestion to form what?

115
Q

Bile salts assist in absorption of what products?

A

lipid products

116
Q

What is the product of hemoglobin degradation?

117
Q

What is the function of the gallbladder?

A

stores, concentrates, and ejects bile

118
Q

Ejection of bile occurs how long after ingestion of a meal?

A

30 minutes

119
Q

Is bile constantly ejected or ejected in spurts?

120
Q

Is bile constantly made or only as it is needed?

A

constantly made and stored in gallbladder

121
Q

Describe the enterohepatic circulation of the ileum.

A
  • bile salts transported from small intestine lumen into portal blood by Na+/bile salt co-transporters
  • portal blood carries to liver
  • liver extracts bile salts and add to hepatic bile salt/bile acid pool
  • fecal loss of bile salts approximately 600mg / day

Physiology (18 decks)

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