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12. GI Test 2 > 4. Secretions of the Gastrointestinal Tract and the Pancreas > Flashcards

4. Secretions of the Gastrointestinal Tract and the Pancreas Flashcards

1
Q

What would be the effect of atropine on the salivary glands?

Which branch of the autonomic nervous system is affected?

A

Atropine decreases production of saliva, bicarbonate, enzymatic secretions, and constriction of myoepithelial cells.

Atropine is a muscarinic acetylcholine receptor antagonist, and therefore affects the parasympathetic nervous system.

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2
Q

Why might cystic fibrosis lead to pancreatitis?

A

Patients with cystic fibrosis may develop acute and chronic pancreatitis due to an absent/defective CFTR channel (cystic fibrosis transmembrane conductance regulator). When CFTR is absence/defective, chloride has difficulty reentering the lumen of the duct, which can inhibits bicarbonate secretion into the lumen. This may result in a diminished ability to “flush active enzymes out of the duct” and pancreatitis may develop.

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3
Q

A vagotomy abolishes which phase of HCl secretion?

A

The cephalic phase.

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4
Q

What controls the cephalic phase of gastric HCl secretion?

A

The vagus nerve.

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5
Q

What is the enzymatic target of omeprazole?

A

The H+-K+ ATPase on the luminal side of gastric parietal cells.

This is the “proton pump” we are talking about.

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6
Q

Which of the major salivary glands produces the enzymes for the early digestion of food?

What type of secretory cells predominate in this gland?

A

The parotid gland.

Serous cells.

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7
Q

Between parasympathetic and the sympathetic nervous system, which has the more significant control over the major salivary glands?

A

The parasympathetic nervous system.

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8
Q

What are the primary damaging factors of the gastric mucosa?

A

Acid.

Pepsin.

Bile.

NSAIDs.

Helicobacter pylori.

Alcohol.

Stress.

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9
Q

What component of gastric juice is required for the absorption of vitamin B12?

A

Intrinsic factor

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10
Q

What are the primary methods by which chief cells are stimulated to produce pepsinogen?

A

Vagal nerve stimulation during the cephalic and gastric phases of gastric HCl secretion.

Local reflexes responding to H+ directly.

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11
Q

Which secretory cells are unique to the oxyntic glands?

A

Enterochromaffin like cells.

Chief cells.

Parietal cells.

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12
Q

What cells do we find in the oxyntic glands?

A

Parietal cells.

Enterochromaffin like cells.

Chief cells.

D cells.

Enterochromaffin cells.

(As well as the mucous / mucous neck cells)

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13
Q

What are the differences between nonparietal gastric juice and parietal gastric juice?

A

Non-parietal gastric juice can be considered the “tone” of gastric juice. It is an alkaline solution of constant and low volume, is made of sodium, chloride, potassium, and bicarbonate.

Parietal gastric juice is slightly hyperosmotic, contains a great deal of hydrogen, less potassium, and a great deal of chloride. As this secretion rate of the parietal cells increases, the more the total gastric juice appears to become pure parietal cell secretion.

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14
Q

What is secreted by D cells?

A

Somatostatin.

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15
Q

What is of the optimal pH for pepsin?

A

1.8 to 3.5

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16
Q

What is unique about the interface of the parietal cell and the lumen it secretes its product into?

A

The lumen extends into the parietal cells as a structure called a canaliculus. That canaliculus is lined with microvilli which increase the surface area for HCl secretion.

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17
Q

Besides production of Gi, how do prostaglandins inhibit H+ secretion by H+-K+ ATPase?

A

Inhibition of enterochromaffin like cells.

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18
Q

What is the effect of histamine on H+ secretion?

What is the pathway used to affect the target enzyme?

What is the target enzyme?

A

Histamine increases H+ secretion.

Histamine activates the H2 receptor, which causes the production of Gs, which increases available cAMP, which upregulates H+-K+ ATPase.

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19
Q

What enzyme is key in the creation of bicarbonate in the pancreatic ductal cells?

A

Carbonic anhydrase.

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20
Q

How does the sympathetic nervous system produce an effect on the ductal cells of the salivary glands?

A

Sympathetic nerve fibers release norepinephrine, and activates Beta adrenergic receptors, which increases cAMP to produce an effect.

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21
Q

What controls the gastric phase of gastric HCl secretion?

A

Local nervous secretory reflexes.

Vagal reflexes.

Gastrin-histamine.

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22
Q

Which of the enzymatic secretions of the pancreatic acinar cells are secreted in their inactive forms?

A

Pancreatic proteases.

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23
Q

What hormone can inhibit both gastrin release and histamine release?

A

Somatostatin

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24
Q

What are the primary protective factors of the gastric mucosa?

A

HCO3-.

Mucus.

Prostaglandins.

Mucosal blood flow.

Gastrin (trophic effect).

Other growth factors.

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25
Q

What type of cell releases cholecystokinin?

A

I cells

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26
Q

What transporter is responsible for the “alkaline tide” in the bloodstream after eating?

A

The HCO3- / Cl- exchanger on the basolateral side of gastric parietal cells, which releases bicarbonate into the bloodstream.

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27
Q

What controls of the intestinal phase of gastric HCl secretion?

A

Nervous and hormonal mechanisms.

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28
Q

Ulcers typically form due to either a defective mucosal barrier or increased acid secretion. Which of those two causes is more common in the case of the gastric ulcer?

A

Defective gastric mucosal barrier.

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29
Q

In general, what is absorbed by the ductal cells of the salivary gland, and what is secreted?

A

The ductal cells of the salivary glands secrete K+ and HCO3-.

The ductal cells of the salivary glands absorb Na+ and Cl-.

(There is also a net absorption of solutes here, leading to an overall hypotonic solution.)

30
Q

Where do the sympathetic nerves which innervate the major salivary glands originate?​

A

T1-T3

31
Q

What is the primary active process which transports H+ out of gastric parietal cells?

A

The action of H+-K+ ATPase on the luminal side of gastric parietal cells.

32
Q

What are the results of stimulation to the acinar ductal cells of the salivary glands?

A

Increased saliva production.

Increased HCO3- and enzyme secretions.

Increased contraction of myoepithelial cells.

33
Q

What is the contribution of the surface epithelial cells of the stomach to the mucus barrier?

A

Bicarbonate.

Mucus from mucous cells mixes with bicarbonate from surface epithelial cells to form a neutralizing and protecting barrier.

34
Q

How are H+ and HCO3- produced in the gastric parietal cells?

A

By the action of carbonic anhydrase on CO2 and H2O.

35
Q

Are gastric or duodenal ulcers more common?

A

Duodenal ulcers are more common.

36
Q

Where does the osmolarity of the saliva within the salivary gland change?

A

Initial saliva is isotonic, it passes through the intercalated duct as isotonic, but the ductal cells of the striated duct change it to hypotonic.

37
Q

What is the effect of acetylcholine and gastrin on H+ secretion?

What pathway is used to affect the target enzyme?

What is the target enzyme?

A

Acetylcholine and gastrin increase H+ secretion.

Acetylcholine activates the M3 receptor – gastrin activates the CCK(b) receptor. Both cause the production of Gq, which activates IP3, which upregulates H+-K+ ATPase

38
Q

What four ways can the vagus nerve stimulate H+ secretion?

A

Direct: activation of Gq -> H+-K+ ATPase via the muscarinic acetylcholine receptor.

Indirect: gastrin releasing peptide on the G cells causes gastrin to be released AND acetylcholine from the vagus nerve inhibits somatostatin release, which down regulates Gi, thereby up regulating H+-K+ ATPase AND that same inhibition of somatostatin further increases gastrin release, because somatostatin inhibits G cells.

39
Q

What are the mechanisms of the cephalic phase of HCl secretion?

A

The vagus nerve either stimulates parietal cells directly, or stimulates G cells to release gastrin by releasing gastrin releasing peptide.

40
Q

What is the basic pathophysiology of Zollinger-Ellison syndrome?

A

A tumor, typically in the pancreas, which secretes a great deal of gastrin. This sees and increased H+ secretion by parietal cells, and an increase in parietal cell mass due to a trophic effect.

Secretin cannot compensate, and as a result, pancreatic lipases are ineffective. This leads to steatorrhea.

41
Q

What 2 nerves supply the parasympathetic innervation to the major salivary glands?

Which glands are supplied by which nerves?

A

The facial and glossopharyngeal nerves provide parasympathetic innervation to the major salivary glands.

The facial nerve supplies the sublingual and submandibular glands, whereas the glossopharyngeal nerve supplies the parotid gland.

42
Q

What is the basic pathophysiology of pernicious anemia?

What conditions commonly lead to pernicious anemia?

A

The basic pathophysiology is a loss or inactivation of intrinsic factor leading to B12 insufficiency.

Pernicious anemia can be caused by a loss of parietal cells due to chronic inflammation (e.g. atrophic gastritis).

Pernicious anemia can also be caused by autoimmune disorders which attack the gastric parietal cells are intrinsic factor itself (autoimmune metaplastic atrophic gastritis).

43
Q

What transporters are used in the salivary ductal cells to increase luminal K+?

A

Luminal K+ / H+ exchanger releases potassium in exchange for H+.

Luminal H+ / Na+ exchanger releases that hydrogen in exchange for sodium.

Basolateral Na/K ATPase pulls another potassium from the blood into the cell in exchange for that sodium.

44
Q

What secretory cells are located within pyloric glands?

A

Enterochromaffin cells.

G cells.

D cells.

(As well as of the mucus / mucus next cells)

45
Q

What determines the maximal secretory rate of HCl?

A

Number of parietal cells

46
Q

In which ganglion do the sympathetic nerves synapse before enervating the major salivary glands?

A

The superior cervical ganglion.

47
Q

What are the effects of somatostatin and prostaglandins on hydrogen ion secretion?

What pathway do they use to affect their target enzyme?

What is their target enzyme?

A

Somatostatin and prostaglandins inhibit hydrogen ion secretion.

They both cause the production of Gi, which decreases available cAMP, thus decreasing H+ secretion by H+-K+ ATPase.

48
Q

What is secreted by enterochromaffin like cells?

What is secreted by enterochromaffin cells?

A

Enterochromaffin like cells secrete histamine.

Enterochromaffin cells secrete serotonin..

49
Q

How do NSAIDs damage to the gastric mucosa?

A

They inhibit the production of prostaglandins, which protect the gastric mucosa by decreasing H+ secretion.

50
Q

How does the parasympathetic nervous system cause an effect on the ductal cells of the salivary glands?

A

Parasympathetic nerve fibers release acetylcholine, and activates muscarinic acetylcholine receptors, which increases IP3, which increases intracellular calcium to produce the effect.

51
Q

What all is saliva composed of? (6 things)

A

Water.
Mucus.
Electrolytes.
Alpha amylase.
Lingual lipase.
Kallikrein.

52
Q

With Zollinger-Ellison syndrome, what do we see regarding the levels of H+ secretion and gastrin?

A

Both are high due to a gastrin secreting tumor. (Typically pancreatic.)

53
Q

What receptors are used by the parasympathetic and sympathetic nervous system to stimulate the acinar or ductal cells of the salivary glands?

A

Parasympathetic: muscarinic acetylcholine receptor.

Sympathetic: Beta adrenergic receptor.

54
Q

Do we typically see increased or decreased gastrin levels in patients with a gastric ulcer?

A

Gastrin levels are typically increased due to the decreased H+ secretion in gastric ulcers.

55
Q

What is the function of cimetidine?

A

Blocks H2 receptors to decrease H+ secretion to the stomach.

56
Q

Distention of the gastric wall stimulates HCl secretion in the gastric phase by what two mechanisms?

A

Stimulation of the vagovagal reflex.

Stimulation of local enteric nervous systems.

57
Q

What secretory cells are unique to the pyloric glands?

A

G cells only.

58
Q

What are the four mechanisms to increase H+ secretion in the gastric phase?

A

Distention of the stomach causes the vagovagal reflex to release acetylcholine and stimulates G cells and parietal cells.

Distention of the stomach causes the local enteric reflexes to release acetylcholine and stimulates G cells and parietal cells.

Amino acids and small peptides trigger the release of gastrin from G cells.

59
Q

Besides production of Gi, how does somatostatin inhibit H+-K+ ATPase?

A

Inhibition of enterochromaffin like cells and G cells.

60
Q

What transporters are used in the salivary ductal cells to increase luminal HCO3-?

A

Luminal HCO3- / Cl- exchanger takes in chloride and releases bicarbonate.

Basolateral Cl- leak channels release chloride.

Basolateral HCO3- / Na+ symporter brings both bicarbonate and sodium into the cell.

61
Q

What secretory cells are common between oxyntic and pyloric glands?

A

Mucus / mucus neck cells.

Enterochromaffin cells.

D cells.

62
Q

If a patient is taking atropine, how could the vagus nerve still increase H+ secretion?

A

By releasing gastrin releasing peptide, which causes gastrin to be released, which uses the CCK(b) receptor to increase H+ secretion, which atropine does not affect.

(Atropine is an antagonist for muscarinic acetylcholine receptors)

63
Q

What receptor is shared by cholecystokinin and gastrin?

A

The CCK(b) receptor.

64
Q

What enzyme allows Helicobacter pylori to damage the gastric mucosa?

A

Urease.

65
Q

What is the function of misoprostol?

A

Misoprostol functions like a prostaglandin, increasing Gi, decreasing cAMP, and thereby decreasing H+ secretion into the stomach.

66
Q

With a gastric ulcer, do we typically see increased or decreased H+ secretion?

What about with a duodenal ulcer?

A

We typically see decreased H+ secretion with a gastric ulcer, probably as a protective mechanism.

With duodenal ulcers, patients typically have an increased number of parietal cells, which results in increased H+ secretion.

67
Q

What is the basis for the secretin stimulation test?

A

Typically injection of secretin should decrease gastrin release – but in the case that secretin administration paradoxically increases gastrin release, there is an indication of a gastrin releasing tumor.

68
Q

External stimuli such as smell, nausea, fear, or dehydration affect which branch of the autonomic nervous system to affect the acinar or ductal cells of the salivary glands?

A

The parasympathetic branch.

69
Q

Of the three pro-H+ signaling molecules – histamine, acetylcholine, and gastrin – which of the three does not potentiate the other two?

A

Gastrin does not potentiate acetylcholine or histamine.

Acetylcholine does potentiate histamine and gastrin, and histamine potentiates acetylcholine and gastrin.

70
Q

Where is most vitamin B12 absorbed?

A

In the ileum.

12. GI Test 2 (20 decks)

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