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GI Exam II > Lecture 3: Secretions of the GI tract and Pancreas > Flashcards

Lecture 3: Secretions of the GI tract and Pancreas Flashcards

1
Q

What is the function of saliva?

A
  • Initial digestion of Starches and lipids
  • Dilution and buffering of ingested food
  • Lubrication of ingested food w/ mucus
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2
Q

What are Parotid glands?

A
  • Composed of serous cells
  • Secrete fluids composed of water, ions, enzymes (rich in amylase)
  • Secrete 25% of the daily output of saliva
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3
Q

What are submaxillary and Sublingual glands?

A
  • Composed of serous and mucous cells
  • Secrete aqueous fluid and mucin glycoprotein for lubrication
  • Secrete majority, 75%, of daily output of saliva
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4
Q

Describe the structure/function of a salivary gland (acinus, myoepithelial cells, intercalated duct, and striated ducts)

A

Acinus (blind end) - acinar cells secrete initial saliva

Myoepithelial cells - motile extensions, when stimulated by neural input, contract to eject saliva into the mouth

Intercalated duct - saliva here is similar in ionic composition to plasma

Striated duct - modify the initial saliva to produce the final saliva (hypotonic), alter the concentration of various electrolytes

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5
Q

What is saliva composed of?

A

H2O, electrolytes, α-amylase, lingual lipase, kallikrein, and mucus

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6
Q

What are the concentrations of electrolytes that make saliva hypotonic compared to plasma?

A

Increased K+ & HCO3 concentrations

Decreased Na+ & Cl- concentrations

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7
Q

What are the 2 main steps in the formation of saliva and the cells involved?

A

1) Formation of isotonoc, plasma-like, solution by acinar cells
2) Modification of the isotonic solution by the ductal cells

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8
Q

What are the transport mechanism occuring on the lumen/apical side of the salivary ductal cell?

A

Na+/H+ exchanger

Cl-/HCO3- exchanger

H+/K+ exchanger

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9
Q

What are the transport mechanism occurs on the blood/basolateral side of the salivary ductal cell?

A
  • Na+/K+ ATPase
  • Cl- channels
  • HCO3-/Na+ symporter
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10
Q

During salivary secretion what is the combined action of solute movement and what is the net effect; why does it become hypotonic?

A
  • Absorption of Na+ and Cl- (lower compared to plasma)
  • Secretion of K+ and HCO3- (higher compared to plasma)
  • Net absorbtion of solute (more NaCl is absorbed than KHCO3 secreted), and because ductal cells are impermeable to water the solution can become hypotonic
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11
Q

How does saliva become hypotonic as it flows through the ducts?

A

Ductal cells are impermeable to H2O

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12
Q

Discuss the ANS innervations of salivary glands, which is the dominant effect; why is this one of our exceptions?

A

PNS - presynaptic nerves originate at facial (CN VII) and glossopharyngeal (CN IX) nerves - PNS is DOMINANT effect

SNS - preganglionic nerves originate at the cervical ganglion, whose postganglionic fibers extend to gands in the periarterial space

*BOTH PNS and SNS stimulate salivary secretion - one of the exceptions

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13
Q

What stimulants activate and inhibit the PNS for salivary secretion, describe the pathway?

A
  • Conditioning, food, nausea, smell (activators)
  • Dehydration, fear, and sleep (inhibitors)
  • Presynaptic nerves of CN VII or IX will release ACh that binds to a mAChR –> Increases IP3 and Ca2+ in the acinar or ductal cells, which will increase the secretion of saliva
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14
Q

Decribe the SNS innervation pathway for secretion of saliva

A
  • Pre-ganglionic nerves from T1-T3 synapse at cervical ganglion.
  • Post-ganglionic sympathetic neurons release NE, which interacts w/ β-adrenergic receptors on acinar and ductal cells.
  • Activation of these receptors leads to stimulation of adenyly cyclase and production of cAMP, which leads to increased saliva production
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15
Q

Stimulation of salivary cells results in what 3 things?

A
  1. Increased saliva production
  2. Increased HCO3 and enzyme secretion
  3. Contraction of myoepithelial cells
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16
Q

What effects do Vasopressin and aldosterone have on the composition of saliva?

A

Modify composition by decreasing its [Na+] and increasing its [K+]

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17
Q

What are the 2 unusual features in the regulation of salivary secretion?

A
  • Salivary is exclusively under the control of the ANS
  • Salivary secretion is increased by BOTH the PNS and SNS (generally these 2 have opposite actions in the GI tract)
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18
Q

What are the main components secreted in gastric juice?

A
  • HCL (H+)
  • Pepsinogen
  • Mucus
  • Intrinsic factor
  • H2O
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19
Q

What is the function of HCL (H+) in gastric juice?

A
  • Together w/ pepsin, it initiates protein digestion
  • Necessary for conversion of pepsinogen to pepsin
  • Kills a large # of bacteria that enter the stomach
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20
Q

Function of the mucus secreted in gastric juice?

A
  • Lines the wall of stomach and protects it from damage
  • Lubricant
  • Together w/ HCO3, it neutralizes acid and maintains the surface of mucosa at neutral pH
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21
Q

Function of Intrinsic Factor (IF) secreted in gastric juice?

A

Required for the absorption of vitamin B12 in the ileum

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22
Q

What are the 2 gland divisions of the gastric mucosa, where is each found, and what is the function of each?

A

Oxyntic gland - proximal 80% of stomach (body and fundus), secretes acid

Pylroic gland - distal 20% of stomach (antrum), synthesizes and releases gastrin

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23
Q

What cells types are found in the oxyntic gland and what does each secrete?

A
  • Mucous neck cell: mucus and pepsinogen
  • Parietal cells: HCL and IF
  • Enterochromaffin-like cell: Histamine
  • D cell: Somatostatin
  • Chief cell: Pepsinogen
  • Enterochromaffin cell (ANP): Serotonin
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24
Q

What cell types are found in the pyloric gland and what does each secrete?

A
  • Mucous neck cell: mucus and pepsinogen
  • G cell: gastrin
  • D cell: somatostatin
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25
Q

What does the # of parietal cells determine?

A

Maximal secretory rate

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26
Q

What is the function of the low gastric pH (1-2) and where is HCL formed?

A
  • Low pH converts pepsinogen to pepsin
  • HCL is formed at the villus-like membranes of the canaliculi
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27
Q

Atropine blocks what component of the ANS during salivarys secretion?

A

Blocks ACh binding to mAChR

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28
Q

Discuss the cellular mechanism of HCL secretion by gastric parietal cells

A
  • CO2 + H2O inside cells are converted to H2CO3 by carbonic anhydrase, which is then quickly converted to H+ and HCO3-
  • On the luminal/apical side: there is a K+/H+ ATPase, which moves H+ into the lumen and Cl- will follow H+ to form HCL
  • On the basolateral/blood side: there is an Na+/K+ ATPase moving Na+ out and K+ into the cell. There is also a HCO3/Cl- exchanger that moves Cl- into the cell and HCO3- out.
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29
Q

What effect does Omeprazole have on gastric parietal cells; used in the treatment of?

A
  • Inhibits the K+/H+ ATPase so that less H+ is secreted into the lumen which ultimately decreases HCL
  • Used in the treatment of ulcers
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30
Q

What is the net effect of the cellular mechanism of gastric parietal cells?

A

Net secretion of HCL and net absorption of HCO3-

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31
Q

What is Alkaline tide?

A

This occurs after a meal where during the production of HCL by parietal cells more HCO3- is entering the blood and raising the pH

32
Q

What are the agents that stimulate H+ secretion by gastric parietal cells?

A

Vagus n releases ACh to an mAChR –> Gq –> IP3/Ca2+

G cells release gastrin to CCKβ receptor –> Gq –> IP3/Ca2+

ECL cells release Histamin to H2 receptor –> Gs –> cAMP

*These pathways all lead to activation of H+/K+ ATPase and the secretion of H+

33
Q

What are the agents that inhibit H+ secretion by gastric parietal cells?

A
  • Somatostatin and Prostaglandins –> Gi —> inhibit cAMP
  • Somatostatin can also inhibit ECL cells and G cells
  • Prostaglandins can inhibit ECL cells
34
Q

What effect does Cimetidine have on the secretion of H+ by gastric parietal cells and what is it used to treat?

A
  • Antagonst of H2 receptors, which block histamines action
  • Used to treat duodenal/gastric ulcers, and GERD
35
Q

Why are prostaglandins important within the stomach and what effect does NSAIDs have on them?

A
  • Protect the lining of the GI by decreasing gastric acid production, decreasing blood flow, and producing mucous
  • NSAIDs will inhibit the actions of Prostaglandins
36
Q

What is the passive feedback mechanism for regulatng HCL secretion?

A

As the pH falls, gastrin release is inhibited, which will decrease the amount of HCL secreted

37
Q

Discuss how the role of the vagus nerve on HCL secretion from parietal cells is twofold; how does Atropine play a role here?

A
  • There is a direct and indirect pathway of vagus nerve stimulation
  • Direct: release of ACh to parietal cells (Atropine can block ACh)
  • Indirect: GRP is released from vagus to G cells, which increases gastrin secretion (Atopine will NOT block the vagal affects on gastrin secretion due to the NT being GRP)
38
Q

How is the rate of HCL secretion potentiated by histamine, ACh, and gastrin?

A
  • Histamine potentiates the action sof ACh and gastrin
  • ACh potentiates the actions of histamine and gastrin

*Potentiation is a combined response to 2 stimulants, which exceed the sum of their individual responses

39
Q

What are the pharmological implications due to the potentiation effect produced by histamine, ACh, and gastrin?

A
  • Antagonists of H2 receptors (i.e., Cimetidine) block the direct action of histamine and also block potentiated effects of ACh and gastrin
  • Antagonist of mAChRs (i.e., Atropine) blocl the direct effects of ACh and the ACh-potentiated effects of histamine and gastrin
40
Q

What are the 3 phases of gastric HCL secretion?

A
  1. Cephalic phase (30% total HCL secreted): via vagus
  2. Gastric phase (60% total HCL secreted): local nervous secretory reflexes, vagal reflexes, and gastrin-histamine stimulation
  3. Intestinal phase (10% total HCL secreted) - nervous mechanisms and hormonal mechanisms
41
Q

What are the stimuli and mechanism for the cephalic phase of gasrtic HCL secretion; what is the effect of vagotomy on this phase?

A

Stimuli: smelling, tasting, chewing, swallowing, and conditioning

  • Mechanisms:
  • Vagus releases ACh to parietal cell = HCL secretion
  • Vagus releases GRP to G cells = gastrin secretion, which is delivered back to the stomach to stimulate HCL secretion from parietal cells

*Vagotomy abolishes this phase*

42
Q

What are the stimuli for the gastric phase of gastric HCL secretions

A

Stimuli: distention of stomach and presence of broken down proteins, AA’s and small peptides

43
Q

What are the mechanisms involved in the gastric phase of gastric HCL secretion (4 of them)?

A

Mechanisms: Distention activates mechanoreceptors in the mucosa of oxyntic and pyloric glands

  • Vagus nerve releases ACh to parietal cells = stimulates HCL secretion
  • Vagus nerve releases GRP to G cells = secretion of gastrin, which travels to parietal cells and stimulates HCL secretion
  • Distention of antrum causes local pyloropyloric reflex –> gastrin –> parietal cells
  • AA’s and small peptides causes gastrin release to parietal cells
44
Q

What effect does coffee (caffeinated and decaffeinated) have on gastric HCL secretion?

A

Stimulates gastric HCL secretion

45
Q

What leads to the HCL secretion during the intestinal phase?

A
  • Distention of small intestine stimulates acid secretion
  • Digested protein stimulates acid secretion via direct effect on parietal cell: gastrin (intestinal G cells) –> parietal cell
46
Q

What is the non-parietal component of gastric juice composed of?

A
  • Basal alkaline secretion of constant and low volume
  • Primarly Na+, Cl+ and K+ at same concentration as plasma
  • HCO3 is secreted at a concentration of ~30 mEq/L
47
Q

Waht is the parietal component of gastric juice composed of?

A
  • Slightly hyperosmotic
  • Contains 150-160 mEq H+/L and 10-20 mEq K+/L
  • Cl- is the only anion present
  • As the secretion rate increases, the concentration of electrolytes begins to approach those of pure parietal juices
48
Q

How is the release of gastrin regulated by somatostatin, gastrin, H+ and vagus stimulation?

A
  • Somatostatin acts on G cells to inhibit gastrin release
  • Vagal activation stimulates gastrin release through GRP and inhbits the release of somatostatin
  • Negative feedback by gastrin causes increased somatostatin
  • H+ in gastric lumen stimulates the release of somatostatin
49
Q

What is the most important stimuli for pepsinogen release, where is it released from, and what is the pH requirement?

A
  • Secreted by Chief and Mucus cells in the oxyntic glands
  • Requires H+ secretion from parietal cells to lower pH <5
  • Vagus is the most important stimulus
  • H+ triggers local cholinergic reflexes that stimulate chief cells to secrete pepsinogen
50
Q

What effect does pepsin have on pepsinogen?

A

Pepsin converts more pepinogen to pepsin

51
Q

What is the function of pepsin and what is its optimal pH, when is it reversibl activated, and irreversibly activated?

A
  • Proteolytic enzyme, splits interior peptide linkages
  • Optimal pH: 1.8 -5.5
  • Reversibly inactivated: pH >5.0
  • Irreversibly inactivated: pH >7-8
52
Q

What is intrinsic factor and why is it so important?

A
  • Mucoprotein secreted by parietal cells
  • Binds to and protects B12 for absorption in the Ileum
  • ONLY secretion by the stomach that is required (essential)
53
Q

What does failure to secrete IF by parietal cells lead to?

A
  • Pernicious anemia
54
Q

What are common underlying causes of pernicious anemia?

A
  • Atrophic gastritis: chronic inflammation of the stomach mucosa that leads to loss of parietal cells
  • Autoimmune metaplastic atrophic gastritis: immune system attacks IF protein or gastric parietal cells
55
Q

How does the gastric mucosal barrier protect the gastric mucosal epithelium against the HCL and pepsin?

A
  • Mucous neck cells secrete mucus
  • Gastric epithelial cells secrete HCO3
56
Q

What substances protect the gastric mucosa?

A

Mucous, HCO3, prostaglandins (i.e., Misoprostol), mucosal blood flow, gastrin, and growth factors

57
Q

What substances damage the gastric mucosa?

A

Acid, pepsin, NSAIDs, H. pylori, alcohol, smoking, bile, and stress

58
Q

What is Zollinger-Ellison syndrome, causes, and mechanism of the disease?

A
  • Tumor, usually in the pancreas, secretes large quanities of gastrin, which increases H+ secretion by parietal cells and increases parietal cell mass (trophic effect)
  • Excessvie H+ arrives to duodenum and overwhelms the buffer capacity of HCO3, creating an ulcer
  • Low duodenal pH inactivates pancreatic lipase –> steatorrhea
59
Q

What is the Secretin stimulation test?

A
  • Used in the dx of gastrin-secreting tumors (i.e., Zollinger-Ellison)
  • Under normal conditions, secretin administration inhibits gastrin release
  • In gastrinomas, injection of secretin causes a paradoxical increase in gastrin release
60
Q

What are the predominate causes of peptic ulcer disease, and what are the two types?

A
  • H. pylori infection and the use of NSAIDs
  • Gastric and duodenal ulcers
61
Q

How is H. pylori able to damage the gastric mucosa; what is a common diagnostic test based on?

A
  • Releases cytotoxins that break down the barrier and underlying cells
  • Release urease which converts urea –> NH3, which alkalinizes the local enviornment. The NH3 reacts w/ H+ –> NH4+ (ammonium).
  • Common diagnostic test based on urease activity
62
Q

Where do gastric ulcers form, major cause, and how do they differ from duodenal ulcers?

A
  • Form on lining of stomach
  • Gastric mucosal barrier is defective, as opposed to increased H+ secretion seen in duodenal ulcers
  • Major causative agent = H. pylori
63
Q

Where do duodenal ulcers form, major cause, and difference from gastric ulcers?

A
  • Form on lining of the duodenum
  • More common than gastric ulcers and H+ secretion rates are higher than normal
  • H. pylori is a major etiologic factor
64
Q

What are the secretory cells of the exocrine pancreas and what does each secrete?

A
  • Acinus: lined by acinar cells that secrete enzymes
  • Ducts: lined by ductal epithelial cells; extends to the region in the acinus containing centroacinar cells. Ductal and centroacinar cells secrete the aqueous solution containing HCO3
65
Q

What are the enzymes secreted by acinar cells of the pancreas?

A
  • Amylases and lipases are secreted as active enzymes
  • Proteases are secreted in inactive forms and converted to their active forms in the lumen of the duodenum
66
Q

What is produced by pancreatic centroacinar and ductal cells; what happens to the initial secretion?

A
  • Produce initial aqueous solution which is isotonic and contains Na+, K+, Cl-, and HCO3-
  • Initial secretion is modified by transport processes in the ductal epithelial cells
67
Q

What are the transport mechanism inside the pancreatic ductal cell, on the luminal/apical side, and on the basolateral/blood side?

A
  • Inside ductal cell CO2 + H2O is converted to H2CO3 by carbonic anhydrase, which quickly dissociates into HCO3 and H+
  • Luminal side: HCO3 is sent to lumen in exhchange for Cl-
  • Basolateral side: Na+/K+ ATPase brings K+ in and a Na+/H+ exhanger gets H+ out of the cell into the blood

*Na+ is free to travel between pancreatic ductal cells to be used by the Na+/H+ exchanger

68
Q

What is the net result of tranport mechanisms by the pancreatic ductal cells?

A

Secretion of HCO3 into pancreatic ductal juice and net absorption of H+ into blood

69
Q

How does cystic fibrosis affect the pancreas?

A
  • One of the 1st organs to fail in CF patients
  • Mutations in the CFTR, a regulated Cl- channel in the apical surface of the duct cells, leads to a decrease in HCO3 secretion
  • Pancreas loses ability to flush active enzymes out of the duct
  • May lead to recurrent acute and chronic pancreatitis
70
Q

What is the cephalic phase of pancreatic secretion, stimuli, mediated by, and what does it produce?

A

Stimuli: smell, taste, and conditioning

Mediated: by Vagus nerve

Produces: mainy an enzymatic secretion

71
Q

What is the gastric phase of pancreatic secretion, stimuli, mediated by, and what does it produce?

A

Stimuli: distention of stomach

Mediated: by Vagus nerve

Produces: mainly an enzymatic secretion

72
Q

The intestinal phase of pancreatic secreton accounts for what percentage of the pancreatic secretion and what does it produce?

A
  • Accounts for 80% of pancreatic secretion
  • Enzymatic and aqueous secretions are stimulated
73
Q

How does the SNS innervate the pancreas and what are its effects?

A
  • Post-ganglionic nerves from celiac and superior mesenteric plexus
  • Inhibits secretions
74
Q

How does the PNS innervate the pancreas and what are its effects?

A
  • Pre-ganglionic fibers synapse in the ENS
  • Post-ganglionic fibers synapse on the exocrine pancreas
  • Stimulates pancreatic secretions
75
Q

Explain why CCK is an important hormonal regulator of pancreatic secretion during the intestinal phase, what stimulates it, where is it released from, and what potentiates its effect?

A
  • Phe, Met, Trp, small peptides, and FA’s stimulate I-cells of the duodenum to release CCK.
  • CCK leads to the contraction of the gallbladder and release of the enzymatic secretion from the pancreas into the duodenum
  • ACh can potentiate this effect
76
Q

Explain why Secretin is an important hormonal regulator of pancreatic secretions during the intestinal phase, where is it released from, what stimulates it, and what potentiates its effects?

A
  • H+ stimulates S cells of the duodenum to release Secretin, which acts on ductal cell increasing their release of the aqueous secretion containing Na+ and HCO3
  • ACh and CCK potentiate the effects of Secretin

GI Exam II (12 decks)

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