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GI-1 - Exam One > Choudhury - Secretory Function of GI Tract: Salivary and Gastric > Flashcards

Choudhury - Secretory Function of GI Tract: Salivary and Gastric Flashcards

1
Q

List the constituents of saliva

A

0.5 % proteins, mucus, amylase, lysozyme

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2
Q

Functional significance of saliva?

A

Functions of Saliva:

Taste
Lubrication
Protection
Digestion
Speech
Not essential for life

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3
Q

Describe regulatory pathways for saliva production

A

•Parasymp ns stimulate secretion -Dominant

  • increases IP3 (major), increase fluid secretion
    - vasodilation to surrounding blood vessels
    - activation of both acinar & duct cells transporter
    - releases kallikrein
    - greater influence than symp ns

•Symp ns stimulates secretion:

 - increases cAMP (major), increase amylase secretion
 - increases IP3 (minor), increase fluid secretion
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4
Q

Describe ion transport pathways that modify saliva composition

A
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5
Q

List conditions where saliva production may be abnormal (long ass list, be familiar for vinettes)

A

Printed.

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6
Q

List common disorders of esophageal function

A
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7
Q

Physiologic role of gastric acid secretion?

A
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8
Q

Acetylcholine, gastrin, and histamine (function on parietal cells)

A

All stimulate release of HCl (activates pepsin, kills bacteria) and intrinsic factor (complexes with VB12 to permit absorption)

All three agonists (Acetylcholine, gastrin, and histamine) synergistically stimulate and potentiate acid secretion from parietal cell

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9
Q

Parietal cell agonists:

A

All three agonists synergistically stimulate and

potentiate acid secretion from parietal cell

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10
Q

Parietal cell receptors:

A

M3 receptors (ACh receptors)

H2 receptors (histamine receptors)

CCKB receptors (gastrin receptors)

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11
Q

Secretagogues involved in gastric acid secretion:

A
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12
Q

Describe the cephalic phase of the secretory response

A

30% of total gastric acid secretion -conditioned reflexes (thought, smell, taste, hypoglycemia

chewing, swallowing, hypoglycemia) send impulses to medulla oblangata which stimulates vagus nerve: -ACh acts on parietal cells to release acid -ACh acts on ECL cells to release histamine -ENS stimulate G cells to release gastrin -Chief cells release pepsinogen -Inhibits D cells, reduce release of somatostatin (somatostatin inhibits gastrin release)

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13
Q

Describe the gastric phase of the secretory response

A

50-60% of total gastric acid secretion -food distends gastric mucosa -vagus & ENS reflexes activated -increase in acid and pepsinogen secretion –peptides (peptones) & a.a stimulate gastrin release

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14
Q

Describe the intestinal phase of the secretory response

A
  • peptides in duodenum stimulates gastrin secretion -chyme containing lipids or acid (pH 2) inhibits impulses from medulla oblangata and decrease vagal nerve stimulation, decrease acid secretion -duodenum releases 3 hormones-inhibits acid secretion
  • Secretin
    • GIP (gastric inhibitory peptide) -

CCK (cholecystokinin)

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15
Q

What controls saliva release?

A

Saliva is under neuronal control

not hormonal

(hormones modify)

Salivary acinar & ductal cells have both Symp and

** Parasymp innervation**

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16
Q

Role of bicarbonate (HCO3-) in saliva?

A

minimizes tooth decay (neutralizes bacterial acid)

neutralizes refluxed gastric acid into lower esophagus (heartburn)

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17
Q

Which cells of the salivary glands allow for a hypotonic secretion?

A

Ductal cells are water impermeable, water is not

absorbed along with the solute, water remains

in lumen and saliva is secreted hypotonic relative

to plasma

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18
Q

Salivary secretion - rate and composition

A

Ionic composition of saliva changes as salivary flow rate changes

Duct cells modifies the composition of saliva

Faster flow rate = less hypotonic (less chance for the ductal cells to take the solutes back up, * except for K+ and HCO3-)

19
Q

Which side of the ductal cells require energy for pumps?

A

Basolateral membrane contains:

  • Na +/K + ATPase and Cl channels
20
Q

What we need to know for neuronal regulation of salivary secretion:

A

Both Symp and Parasymp stimulates secretion
Parasymp stimulates more than Symp
Symp: major beta receptors: protein secretion, minor alpha receptors fluid secretion
Parasymp: major M3 receptors: fluid secretion

21
Q

Salivary secretion and composition are controlled solely by the autonomic nervous system, in contrast, other parts of the GI tract include local reflexes and hormonal mechanisms as well

A

Salivary secretion and composition are controlled solely by the autonomic nervous system, in contrast, other parts of the GI tract include local reflexes and hormonal mechanisms as well

22
Q

Gastric secretion - rate and composition

A

Inverse relationship between luminal concentration of H+ and Na+ as a function of the rate of gastric secretion

23
Q

pH of blood leaving the stomach?

A

Increased pH of venous blood leaving stomach following a meal is alkaline & referred to as alkaline tide

24
Q

Parietal cell agonists, agaaaaain:

A

Agonists: ACh, Gastrin and Histamine

all stimulate parietal cell to secrete acid

ACh binds to M3 receptors

Gastrin binds to CCKB receptors

      (gastrin 1500 X potent than

      histamine in releasing HCl)

Histamine binds to H2 receptors

25
Q

Inhibitors of parietal cells:

A

Inhibitors: Somatostatin and PGs directly

binds to parietal cell and inhibits Histamine

§Somatostatin binds to SST receptors
§PGs binds to PGs receptors

Both are linked to G protein (Gai) and

oppose action of histamine and Gs

26
Q

Vagotomy details (cutting of vagus nerve):

A
  • inhibits gastric acid secretion
    • used to treat peptic ulcers
    • side effects: delay in gastric emptying, diarrhea

Selective vagotomy:

-cutting vagal nerves supplying parietal cells only

27
Q

Secretin is referred to as what? Why?

A

Secretin is referred to as nature’s antacid

Release by S cells of duodenum

Stimulated by lower pH in duodenal lumen and by fatty acids

Actions: increase pancreatic HCO3- sectretion (neutralizes H+); trophic effect on exocrine pancreas; increases bile production; decreases gastric acid production

28
Q

What is a selective vagotomy?

A

cutting vagal nerve fibers supplying parietal cells only

29
Q

Pernicious anemia

A

Absence of IF –> decreased Vit B12 (not absorbed) –> leads to anemia and even neurological symptoms (weakness, numbness)

This produces macrocytic

anemia (megablastic anemia)

as B12 is required for DNA

synthesis in RBC progenitor cell

in bone marrow.

Inflammation destroys

parietal cells and chief cells,

reducing acid secretion causing

hypochloremic metabolic alkalosis

Loss of feedback mechanism,

gastrin levels rises sharply.

Prolong B12 deficiency causes

neurological symptoms

30
Q

Another name for Vit B12

A

Cobalamin

31
Q

Vit B12 deficiency caused by:

A

Decreased dietary intake (vegan)

Decreased absorption

- gastric resection

  (decreased IF)

- autoimmune disease

  (antibody against parietal

   cells and IF)
32
Q

“1-2 questions on peptic ulcer disease”

A

damage to the mucosa can cause ulcers

33
Q

ASA and ulcers

A

•NSAIDS (aspirin) inhibits COX-1

  • COX-1 forms PGs
  • PGs protects gastric mucosa

ØAspirin (a weak acid) is easily

  absorbed in low pH of the stomach

ØOnce absorbed it acts by acid

  stimulating histamine release and

  disruption of local mucosa

ØAspirin suppresses protective

  mucosal barrier production
34
Q

Zollinger-Ellison syndrome

A

Tumor

  that causes excessive secretion of

  gastrin, which stimulates acid

  hyper-secretion
35
Q

Other causes of ulcers?

A

H. Pylori ( > 80%)

  • Alcohol
  • Bile acid

Stressful situations

  • physical
  • emotional
36
Q

Gastric ulcer disease’s “vicious cycle”

A
  • Acid and pepsin break through mucosal barrier
  • Acid stimulates histamine release
  • Histamine stimulates parietal cells to release acid
  • Acid diffuses through broken barrier
  • Vicious cycle continues
37
Q

Gastric Ulcer Disease

A

Gastrinoma or Zollinger-Ellison syndrome (increases gastrin secretion)

38
Q

Duodenal ulcer disease

A
  • Occurs in the duodenum
  • Increase acid secretion in the gastric region
  • Pepsin remains active for too long
  • Decrease bicarbonate secretion from pancreas (pancreatitis)
39
Q

KNOW THIS

A

Gastric ulcers: H+, pepsin; less mucosal protection

Peptic ulcers: H+, pepsin; less mucosal protection

Duodenal ulcers: H+ and pepsin, 2-3 X more parietal cells than normal

40
Q

Gastric acid determination

A
  • Serum gastrin levels and gastric acid secretion used to evaluate gastric function
  • Pentagastrin is used to stimulate acid secretion
41
Q

Gastrinoma or Zollinger-Ellison syndrome:

A

VINETTE: Serum gastrin “will be very highhhh”

Pancreatic islet cell adenoma results - gastrin secretion stimulates parietal cells HCl secretion

       gastric acid secretion both at rest and after meal.

    Gastric and/or duodenal ulceration due to    acid and     pepsin activity
42
Q

Bacterium causing peptic ulcer disease?

A

Helicobacter pylori

43
Q

Things to know about increased H+ in the stomach (causes/tx’s)

A

uHistamine potentiates effects of gastrin & ACh on parietal cells via H2 to release acid
Inhibiting H2 will decrease H+ release in the stomach
PPIs inhibits proton pump and decreases H+ release, increases gastric pH

Long term side effects of PPIs usage are:
Pneumonia
Clostridium difficle growth in gut
Osteoporosis

44
Q

READ SUMMARY

A

READ SUMMARY

GI-1 - Exam One (9 decks)

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