Exam 3 (Lecture 8) - Motility Patterns of LI and Stomach Secretory Activities

Question 1

Describe the three motility patterns of the colon.

Answer 1

1) Segmentation
- Multiple segments of inner circular smooth muscle contract and longitudinal muscle relaxes (decreases
lumen size).
- mixes and circulates colon contents over the absorptive mucosal surfaces for maximal contact
- important for both absorptive and fermentative functions
- no net forward movement

2) Tonic Contraction (Retropulsion)
- Non-propulsive motility (impedes the movement of ingest); due to a sphincter or colon pacemaker
- Pacemakers of colon:
- retropulsion is strong near the pacemakers
- sites of high resistance to the flow of colonic ingests
- colonic ENS can influence the ICC
- colonic slow wave activity originates in the ICC

3) Peristalsis
- Periods of intense propulsive activity that involve parts of the colon or the entire colon (mass peristalsis)

Question 2

Describe the rectosphincteric reflex.

Answer 2

1) Afferent impulses stimulated by movement of feces into rectum

2) Parasympathetic efferent impulses (via pelvic nerves) stimulate peristaltic contractions of rectum and relaxation of internal anal sphincter.

3) Diaphragm and abdominal muscles contract to increase intra-abdominal pressure

4) Striated muscles of the anal canal relax during defecation

5) Can be blocked by voluntary constriction of the external anal sphincter
- rectum soon relaxes to accommodate the fecal bolus, the internal anal sphincter regains tone

Question 3

Digestion can only take place in an ______________ environment provided by the digestive secretions.

Answer 3

Aqueous

Question 4

Digestive secretions are regulated by which systems or signaling pathways?

Answer 4

1) ENS
2) ANS
3) Endocrine signaling
4) Paracrine signaling
5) Enteric immune system

Question 5

Gastric glands include which cell types?

Answer 5

1) Surface mucous cells
2) Mucous neck cells
3) Chief cells
4) Parietal cells

Question 6

List the two general types of gastric mucosa.

Answer 6

1) Glandular
- most animals

2) Non-glandular and glandular region
- horse

Question 7

Describe the location, structure, and function of the gastric glands.

Answer 7

1) Gastric glands are located in the mucosa.

2) Structure and Function:
- Surface epithelium and the lining of the gastric pits are covered with surface mucous cells that produce
thick mucus that coats and protects the mucosa from the acidic conditions

  - Mucous Neck cells located in the neck of the gastric glands; they secrete thin mucus; they are progenitor
    cells for the gastric mucosa; only cells of the stomach lining capable of division; differentiate into any of the 
    several types of mature cells of the gastric glands. 

  - CHIEF cells located at the base of the gastric glands; secrete pepsinogen (HCl catalyzes pepsinogen to
     pepsin); pepsin starts protein digestion

Question 8

How is HCl secretion stimulated?

Answer 8

Stimulated by the cephalic phase of digestion and the presence of undigested food in the stomach.

Parasympathetic (vagal) impulses stimulate ENS
- Releases ACh into the vicinity of G cells (gastrin) and parietal cells (HCl)
- Secretory cells have ACh receptors on their surfaces and respond by secreting gastrin and HCl
- Gastrin circulates in the bloodstream and stimulates parietal cells with gastrin receptors
- Combined actions of gastrin and ACh on the parietal cells result in high rates of HCl flow
- Histamine is an amplifying substance in HCl secretion (stimulated by gastrin and ACh)

• When all three receptors are occupied (gastrin, ACh, and histamine) = maximal output of HCl secretion

Question 9

Describe how HCl secretion and gastric motility are regulated.

Answer 9

Stimulation of gastrin and HCl secretion:
- Food acts as a buffer, increasing the stomach pH
- Stimulates the production of gastrin
- Positive feedback (stimulate) loop staring with sensory receptors in the stomach mucosa
- Gastrin stimulates secretion of HCl and pepsin, and increases gastric motility

Inhibition of gastrin secretion:
- Negative feedback (inhibit) loop when gastric pH decreases
- Inhibits secretion of HCl and pepsin, and gastric motility

Gastric pH influences the secretion of HCl
- Acidic stomach contents flow into the duodenum and duodenal pH decreases stimulating:
- secretin, CCK, and GIP (gastric inhibitory peptide)
- stimulates the release of bile from gall bladder, digestive enzymes and HCO3- from pancreas
- decreases gastric HCl secretion and motility; increases pH in duodenum
-required for further protein and fat digestion of chyme in the duodenum

Question 10

What is an ulcer? How does chronic NSAID usage cause ulceration? How do the different drugs work to treat gastric ulceration?

Answer 10

1) An ulcer is a hole in the stomach; through the mucosa and into the submucosa.

2) Chronic NSAID use causes ulcerations by inhibiting prostaglandin synthesis. If your body can’t make prostaglandins, these cells cannot make mucus).

3) Proton Pump Inhibitors:
- Only given once daily
- Inhibits the proton K+/H+ ATPase pump
- Parietal cells secrete H+ through the K+/H+ ATPase pump
- Ex: Omeprazole

 H2 Blockers:
  - Have to give twice daily
  - Histamine type 2 receptor antagonist
  -Block histamine attachment to stimulatory receptors on the surface of parietal cells
  - Ex: Famotidine, Ranitidine, and Cimetidine

  Sucralfate:
  - Proteinaceous Band-aid
  - Forms a viscous paste-like complex with a strong negative charge that binds electrostatically to positively 
    charged proteins in the base of ulcers or erosions for up to 6 hours. 
  - Insoluble complex forms a barrier that protects the ulcer from further damage by preventing back diffusion
    of hydrogen ions, inactivating pepsin, and absorbing gastric-damaging bile acids refluxed from the 
    duodenum.