Salivary/ Gastric Function

Question 1

Hormones are released from endocrine cells. Where do they go before they get to their target cells?

Answer 1

Release from endocrine cell, to portal circulation, through the liver, to the systemic circulation, to the target cell

Question 2

What are neurocrines? What are some examples?

Answer 2

Molecules synthesized in neurons and released following an action potential. Includes ACh, VIP, NE, and substance P

Question 3

What are paracrines?

Answer 3

Molecules released from endocrine cells of the GI tract that act on the same tissue that secretes them

Question 4

What cells release gastrin? What is the function of gastrin?

Answer 4

Released by antral mucosal cells (G cells) in response to distension
Causes an increase in HCl secretion from the stomach

Question 5

What part of the GI tract releases CCK? What is the function of CCK?

Answer 5

Intestinal cells release

Inhibits gastric emptying and increases the gallbladder contractions and increases pancreatic enzymes into the duodenum

Question 6

What part of the GI tract secretes secretin? What is the function of secretin?

Answer 6

Intestines release
Increase of HCO3 release from pancreas
Decreases HCl secretion from the stomach

Question 7

What part of the GI tract secretes motilin? What is the function?

Answer 7

Intestines release during fasting

Increases the contractions of the distal stomach to try and clear the contents (sweep)

Question 8

What part of the GI tract secretes glucose-dependent insulinomic peptide (GIP)?

Answer 8

Intestines release in response to fat and carbs

Stimulates pancreas insulin secretion, inhibits HCl secretion from parietal cells

Question 9

Where in the GI tract do carbohydrates get digested?

Answer 9

Mouth (amylase), small intestine (pancreatic enzymes), brush border (disaccharidoses)

Question 10

Where in the GI tract are lipids digested?

Answer 10

Mouth (lingual lipase), stomach (gastric lipase), small intestine (pancreatic lipase)

Question 11

Where in the GI tract are proteins digested?

Answer 11

Stomach (gastrin), small intestine (pancreatic chymotrypsin), brush border (dipeptidases)

Question 12

What are the three functions of saliva?

Answer 12

Lubricate (moisten food/aid in swallowing), digest (amylase/lipase), protect (clear bacteria)

Question 13

Of the three salivary glands, 2 produce mucus-like saliva and one produces watery saliva? What are these glands?

Answer 13

Mucus: sublingual and submandibular
Water: parotid

Question 14

What is Sjogren syndrome?

Answer 14

Chronic and progressive autoimmune disease that destroys the salivary and lacrimal glands. Difficulty swallowing/speaking/dental cavities

Question 15

What is xerostomia?

Answer 15

Dry mouth- from inadequate saliva production

Question 16

At low rates of saliva secretion, how does the composition of saliva compare to plasma?

Answer 16

Saliva has more potassium and is more hypotonic

Question 17

At high rates of saliva secretion, what happens to the composition of the secretion?

Answer 17

Becomes more similar to plasma- have more sodium and less potassium (this is because the transporters can’t keep up)

Question 18

What are some factors that can cause an increase in salivation?

Answer 18

1. ANS- PNS strongly stimulates the salivary glands, SNS causes a smaller stimulus for salivation
2. Higher brain stimulation (CNS)- see/smell something and because PNS is close to the appetite centers in the brain get stimulation
3. Reflexive- when eat something that irritates the stomach/intestine start to increase salivation to try and clear the irritant

Question 19

What are the two types of glands in the stomach? Where are they found? What are the main types of cells in these two glands?

Answer 19

1. Oxyntic glands- proximal 80% of stomach- have peptic (chief cells) and parietal cells
2. Pyloric glands- distal 20% of stomach- have mucus cells, G cells, and D cells

Question 20

What causes achlorydia? What are the symptoms?

Answer 20

Gastric enteritis causes achlorydia (lack of stomach secretion) destroying the parietal cells and can result in decreased HCl and pernicious anemia (because lose intrinsic factor and can’t absorb Vit B12)

Question 21

What cells secrete: pepsinogen, gastric lipase, HCl, intrinsic factor, gastrin, somatostatin?

Answer 21

Peptic cells (chief): pepsinogen/gastric lipase
Parietal cells: HCl and Intrinsic factor
G cells: Gastrin
D cells: somatostatin

Question 22

What stimulates pepsinogen release?

Answer 22

Vagus stimulates the initial pepsinogen to release going to the stomach where it gets cleaved into pepsin. Pepsin then can cleave other pepsinogens into pepsin

Question 23

How does the stomach mucosal cells prevent itself from the acidic environment?

Answer 23

Has a mucus layer that has HCO3

Question 24

How does chronic NSAID use lead to gastric enteritis?

Answer 24

NSAIDs inhibit prostaglandins and prostaglandins function to stimulate the secretion of mucus and HCO3

Question 25

Is the venous blood from the GI tract acidic or alkaline?

Answer 25

Alkaline - because the parietal cell exchanges Cl- for HCO3 at the basolateral surface

Question 26

What is the primary target for GERD/ gastric ulcer patients?

Answer 26

The H+/K+ ATPase- this pump leads to the release of H+ into the GI tract

Question 27

What factors can cause vomiting?

Answer 27

Head trauma (concussion), intestinal/stomach irritant, systemic irritant (sensed in the 4th ventricle of the brain), virus/bacterial

Question 28

What happens to the serum after prolonged vomiting?

Answer 28

Alkalosis, hypokalemia, dehydration

Question 29

How does the vagus nerve stimulate HCl secretion from parietal cells? Name both the direct and indirect pathways.

Answer 29

Direct: ACh is released, binds to the M3 receptor, get Gq pathway with an increase of Ca and increased activity of the H/K ATPase Indirect: Vagus stimulates enterochromaffin-like cells (ECL) which causes histamine release which binds to H2 receptor, get Gs pathway, activation of cAMP, increased H/K ATPase. Vagus also causes release of gastrin releasing peptide which acts on G cells to release gastrin, which binds to CCKb receptors and activation of Gq pathway and increase Ca

Question 30

How does somatostatin inhibit HCl secretion?

Answer 30

D cells are stimulated with increased H+ which causes increased somatostatin release and activates the Gi pathway causing decreased cAMP and decreased H/K ATPase function

Question 31

What are the three phases of HCl secretion? What is the primary cause of secretion in each phase?

Answer 31

1. Cephalic phase- smelling/tasting- from vagus 2. Gastric phase-distention of stomach- from vagus and directly from the G cells in antrum 3. Intestinal phase-sense protein products