B1. Where is the swallowing reflex controlled? What is the role of afferent nerves in both primary and secondary peristalsis?

B2. What happens to the size of the lumen when the circular layer contracts? When the longitudinal layer contracts? Do they usually contract at the same time? Why?

B3. How does the mechanical movement (contraction) of the stomach during the gastric cycle relate to emptying and mixing? Which comes first - emptying or mixing? How does the emptying of liquids differ from that of solids?

B4. When is more of the small intestines active - during fasting or after a meal?

Is propulsive velocity faster during fasting (i.e., Phase III) or after feeding? What is the significance of this?

B5. Know the seven gut reflexes on page B-25. There is some logic to each of the seven; try to understand them rather than just memorize them.

B6. Of the following sphincters, which are tonically contracted at rest? Upper esophageal (UES), lower esophageal (LES), pyloric, ileocecal (ICS), internal anal (IAS) and external anal (EAS). What does each of the sphincters contribute? When does each relax?

C1. List 3 endogenous stimuli for the oxyntic cell. Tell whether they are acting as neurocrine, paracrine or humoral transmitters.

Which have pharmacologic agonists and antagonists available (i.e., given in the notes or lecture).

After a meal, how are these stimulated?

Identify 3 factors which shut off gastric acid secretion when it is no longer needed - list 2 endogenous inhibitors.

C2. The pancreas is both an exocrine and an endocrine organ. List 2 hormones secreted by the pancreas.

C3. As an exocrine gland, the pancreas secretes 2 general types of secretions.

What are they and how is the secretion of each stimulated following a meal.

Enzymes and bicarbonate.

C4. Sodium bicarbonate and bile salts are both secreted in the bile. What is the role of each and what causes their secretion during a meal?

C5. What is the enterohepatic cycle? Why is it significant in terms of bile salts and certain drugs?

Conservation of B.S. and exposure to and modification by the enteric bacteria.

D1. What are the final digestion products of amylopectin digestion by pancreatic amylase? What form is required for carbohydrate absorption? How is CHO digestion completed?

D2. What is cotransported with glucose?

What is the clinical significance of this system in secretory diarrhea?

The administration of glucose and certain amino acids to stimulate sodium (and fluid) absorption from the lumen which decreases or reverses the net fluid movement into the lumen during a secretory diarrhea.

D3. What do pancreatic enzymes contribution to the digestion of lactose?

D4. List 2 contributions of HCl to protein digestion. Define endo- and exopeptidases. In general, what is the pH optimum for pepsin activity?

Acid (pH: 1.6 — 3.2)

What does gastric HCl contribute in terms of bacterial ingestion and iron absorption. How does the stomach facilitate Vitamin B₁₂ absorption?

D5. Amino acids sometimes appear in the blood faster when they are given as an acid hydrolysate of protein (i.e., peptides) vs an equimolar amount of free amino acids. How would you explain this?

Since the peptide carriers are different from the amino acid carriers, they may have different (sometimes faster) rates of transport. Similarly, peptides don’t have to compete with amino acids for absorption. Also, as the peptide is cleaved it may utilize both the peptide carrier plus the amino acid carrier(s).

What form(s) is required for protein to be absorbed?

D6. Mammals possess several lipases; what is the source of the primary lipase that digests long chain triglycerides (LCTG)? Why is it that exocrine pancreatic function is nearly gone by the time there are clinical signs (e.g., steatorrhea)?

D7. How do bile salts facilitate fat digestion? How do bile salts facilitate fat absorption? What do the enterocytes contribute to fat absorption? What is the route of absorption for fat?

D8. You are presented with a thin, 3-year-old german shepherd. The owners report that the dog appeared normal up until 6 months ago. At that time they noticed that he started losing weight and began to develop the disgusting habit of eating his own feces. Recently, the weight loss has become more severe, even though he has had a good appetite and seems normal otherwise. Lately they have noted that he seems to pass a large amount of feces, and the fecal material is soft, grey, and has a clay-like consistency. (from Cunnungham's Textbook of Veterinary Physiology).

Assume his xylose absorption test was low but within the normal range and his trypsin-like immunoreactivity (TLI) was below normal. What is your diagnosis?