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1. See notes and text.
2. Contractions are initiated by intrinsic elec. activity of gastric & intestinal smooth muscle cells themselves. Frequency and amplitude are influenced by neural and hormonal events. Slow rhythmic depolarizations and repolarizations (slow waves) set the frequency, but do not necessarily lead to contraction unless there is sufficient depolarization — e.g., as caused by action potential(s) occurring at peak of slow wave. The number of action potentials, and hence degree of contractility, depends on neural and hormonal input, which in turn depends on the volume & nature of luminal contents and the digestive state of the individual. For striated muscle: excitation occurs at a defined synapse, usually 1:1, neuron to muscle cell; excit/contraction coupling is via Ca2+ entry (from a well-defined S.R.) which binds to troponin, making sterically feasible the ATP-powered interaction between myosin and actin; relaxation results from the removal of Ca2+ back into the S.R. Modification of myosin, e.g., by MLCK and ATP, does not occur in striated muscle.
3. See notes and text.
4. a & c
5. b & d
6. b & d
7. b
8. c
9. a
10. d
11. c
12. L, A, A
13. S, D
14. (a) F. Carbohydrate digestion starts in the mouth: salivary amylase (ptyalin) acts on starch: this amylase activity is inhibited by gastric acidity.
(b) T. Final breakdown occurs at the brush border of the epithelial cells, where the appropriate enzymes are located.
(c) F. Fats have more than twice the energy
15. (a) F. Three hours is about right, although there is variation with the nature of the food.
(b) F. There is 'receptive relaxation' as food enters, so that pressure is unchanged.
(c) T. This produces waves of contraction, every 20 seconds.
(d) F. Enterogastrone provides the hormonal link between duodenal filling and inhibition of gastric emptying, not acid secretion.
1. Keep mouth wet, facilitate speech, lubricate, inhibit dental caries, dilute noxious stimuli, neutralize acid, digest starches, bacteriocidal function (lysozyme). Parotid glands are serous and secrete enzyme and a watery secretion; sublingual glands have mucin-secreting cells and secrete a very scant watery component; submaxillary glands are a mixed histological type (mucin and serous cells). Parasympathetic innervation via the IX (glossopharyngeal) and VII (facial) cranial nerves; primary means for stimulation of aqueous flow. Sympathetic innervation via superior cervical ganglion leads to mucin and enzyme output, also decreases blood flow to glands.
2. Storage of food, milling of food, regulation of food reaching small intestine, "sterilizes" food, protein denaturation, protein hydrolysis, secretion of intrinsic factor, reduction of ferric ions. Cardiac glands: mucous cells only. Fundic and Body glands: mucous cells; oxyntic cells (HCl & IF); chief cells (pepsinogen). Antral glands: mucous cells (but also secrete some pepsinogen; G cells (gastrin).
3. Duodenal ulcer is frequently associated with more voluminous acid output. Damage to the integrity of the gastric epithelial layer will permit entry of HCl and pepsin into cells and tissue with subsequent degenerations, ulceration, and hemorrhage. While reduction of acid output will usually give time for an ulceration to heal, there is high probability for recurrence of the ulcer if the root cause of tissue suscesptibility, infection by the bacterium Helicobacter pylori, is not eliminated.
4. Rate of gastric emptying is dependent on volume and quality of chyme in stomach. Initial rate of emptying is more rapid with larger volume, and with a more fluid consistency. Duodenal factors are also very important: emptying decreased by high osmolarity and high acidity. Chemical composition reveals that emptying rate of CH2O > protein > fats.
5. a, c, e
6. F. Enterokinase, secreted by duodenal mucosal cells, serves to activate trypsinogen.
7. Gall bladder bile has increased concentrations of most organic constituents and decreased amounts of many of the inorganic constituents (except for Na+ and Ca2+). This is due to active salt and water absorption by the bladder epithelium.
8. Enterohepatic circulation; also see notes and text.
9. Bile salts: synthesized from cholesterol within the hepatocyte to form cholic and chenodeoxycholic acids — these are usually found in a form conjugated with either taurine or glycine. Dehydroxylations that occur by intestinal bacteria also serve to change forms, e.g., forming deoxycholic and lithocholic acids. Bile salts are constantly being secreted by the hepatocyte into the bile canaliculus; they are stored and concentrated in the gall bladder. Their function is almost entirely devoted to fat digestion which bile salts facilitate by promoting emulsification and micellar formation (see notes and text). Bile pigments: "synthesized" as a breakdown product of hemoglobin. Opening of porphyrin ring, and the elimination of methylene carbons and Fe2+ formation, leads to biliverdin formation; dehydrogenation leads to bilirubin formation. Principal sites are the spleen and liver. Bilirubin is enzymatically conjugated with UDP-glucuronic acid in the liver to form bilirubin-glucuronide which is a more soluble form, and the form for secretion by the hepatocyte. The bile pigments (and their bacterial breakdown products) give the stool its color — no other function, except to serve as the excretory pathway for the Hb catabolic products. Alteration in any of the steps of Hb breakdown, conversion, conjugation, or secretion could lead to hyperbilirubinemia or jaundice.
10. a, b, c & d
11. a & c
12. d (bilirubin is present but not synthsized by hepatocyte).
13. P, I, C
14. W, F
15. b
16. U, B
17. C, HCO3
18. C, S
19. (a) T. This is the 'alkaline tide': extrusion of H+ into the lumen raises HCO3− concentration in cells: this moves out into plasma.
(b) F. Gastric acidity aids digestion and kills most ingested bacteria, but is not essential to life.
(c) T. Pepsin is split off only as pH falls (acidity increases) below about 5
(d) F. Intrinsic factor is a necessary adjunct to the Vitamin B12 which comes from the diet. Without intrinsic factor, B12 is very poorly absorbed and pernicious anaemia ensues
(e) T. In the cephalic phase, vagal stimulation accounts for pepsinogen and acid secretion, both directly by stimulation of secretory cells, and indirectly by causing release of gastrin.
20. (a) T. The gastric receptors are H2 receptors. The standard histamine blockers, such as anthisan, block pulmonary histamine receptors but not the receptors in the stomach.
(b) T. This is the standard means of eliciting a maximal secretion of acid and thus assessing the 'parietal cell mass'.
(c) F. Gastrin is secreted by G cells located in the antrum.
21. (a) F. They are polypeptides.
(b) T.
(c) T. About 1.5 liters in 24 hours.
22. (a) F. Secretin is the important hormone in this case.
(b) T.
(c) F. This would be true of bile salts but not of bile pigments, only a tiny proportion of which are reabsorbed.
23. (a) T.
(b) F. It contains no iron.
24. (a) T. But bile remains isosmotic with plasma because of micelle formation.
(b) F. The reverse is true since bile salts render cholesterol soluble.
(c) T. This is also the route of elimination when plasma cholesterol is elevated.
(d) T.
(e) F. 10% indicates malabsorption; the figure for a healthy human is about 1%.
1. See notes and text.
2. (a) T, blocks Ach; (b) F, stimulant; (c) F, stimulant; (d) T, competes away the stronger agonist gastrin; (e) F, relatively ineffective on gastric receptors; (f) T, blocks histamine; (g) T, inhibits gastrin release; (h) T, releases secretin; (i) T, removes parasympathetic innervation (Ach); (j) T, reduces gastrin source.
3. See notes and text.
4. See notes and text.
5. a, c & d
6. a, b, c & d
7. c
8. a
9. b
10. d
11. d
12. b
13. b
14. c
15. c
16. d
17. b
18. a
19. C, T
20. I, N, C
21. (a) T. Copious water and electrolyte-rich secretion is the response to secretin.
(b) T.
(c) F.
22. (a) F. Protein digestion products stimulate gastrin release.
(b) F. Low antral pH inhibits gastric output (somatotstatin).
(c) F. Low duodenal pH stimulates HCO3− output via secretin.
(d) F. Much of the activity of the vagus is afferent, bringing information from receptors to the CNS.
1. S, S, S
2. BB, G
3. Passive diffusion: Process fits characteristics described by Fick's laws. Flux linear with respect to conc. gradient. Carrier-mediated transport: Implies involvement of some membrane component to catalyze translocation. Shows saturation kinetics. Competition. Stereospecificity. Effects of specific inhibitors. Counter-transport can be demonstrated. (This need not be active and should show equivalent transport in both directions.) Primary active transport: Would show many characteristics of carrier- mediated transfer, but also shows net transport against an electrochemical gradient and directly dependent upon a membrane enzyme system which uses metabolic energy to drive the net transport. Secondary active transport: The transporter does not directly use an energy-supplying molecule like ATP. Transport is driven by one or more electrochemical gradients which had to be established by a direct energy consumer, such as the Na/K-ATPase.
4. See notes and text.
5. (a) Abolish Na+ pump, also inhibits solute transfer. (b) Abolish Na+ gradient, also abolishes solute transport. (c) Artificially re-establish Na+ gradient, transport of solute recommences. (d) Reversed Na+ gradients will reverse direction of solute transport. (e) Gradients of solute will drive Na+ transport. (f) Measured electrochemical driving force of Na+ is sufficient to account for accumulation ratios of solute. (g) Studies with isolated brush border membrane vesicles have demonstrated the Na+-solute interdependencies in the membrane exclusive of cellular energy or ATPases.
6. (a) Decreased luminal hydrolysis of fats due to lowered lipase levels. (b) Decreased lipid esterification within the enterocyte. (c) Inability to form effective chylomicra (cells will tend to fill up with fat droplets). (d) Decreased luminal hydrolysis of fats due to poor micellar formation. (e) Primary observed effect is same as (c), i.e., lack of appropriate lipoprotein synthesis. (f) Same as (d) due to decreased synthesis of bile salts. (g) Same as (d) due to loss of bile salts in the stool. (h) Poor return of chylomicra from intestinal lacteals.
7. Normal intestinal function is one of absorption. A Na+ pump from intestinal enterocyte to blood is the principal driving force for absorption of other ions, e.g., Cl− (electrically coupled), H2O (osmotic force) and many sugars and amino acids (carrier co-transport or symport). The process ordinarily operates efficiently to absorb not only ingested salts, water and nutrients (~1.5 L/day), but in addition almost all of the 5-10 L/day of body fluids secreted into the digestive tract. Cholera toxin is particularly potent in severely reducing the net absorption process. The principal insult is the activation of a process of Cl− secretion. The net effect is to offer an opposing force to the Na+ transport process, thus reducing the efficiency of absorption and even causing net fluid loss across intestine.
8. Poorly absorbed solutes (e.g., MgSO4) represent an osmotic equivalent which would retain water in the intestinal lumen even in the presence of a relatively efficient Na+ pump. The increased volume will serve to "irritate" intestinal motility and provides the large volumes of excretion associated with the kind of laxative or catharsis. Lactose, a disaccharide, is the dominant carbohydrate of milk and is very poorly absorbed. However, the presence of an intestinal brush border membrane enzyme, lactase, catalyzes the hydrolysis of lactose to two readily absorbed monosaccharides, glucose and galactose. In the absence (or very low level) of intestinal lactase, the milk sugar will cause a certain amount of diarrhea, since it then represents a poorly absorbed solute. There would also be a tendency toward bloating and flatulence due to bacterial action on the lactose that reaches the colon.
9. (a) For every mole of HCl secreted by the stomach, there is an equivalent amount of HCO3− that flows into the plasma. (b) Intestinal absorption of sugars would lead to temporary elevation of blood glucose, before incorporation into cells for use or storage. (c) Ideal absorption of bile salts, which had previously been "sequestered" in the gall bladder then secreted in response to a meal, would account for an elevated plasma level. (d) Intestinal absorption of lipid ultimately results in an increased level of chylomicrons (lipoprotein) in the lymph which are then carried to the plasma. With such elevated plasma lipoprotein levels, after removal of RBC's by centrifugation, the plasma has a turbid, milky appearance.
10. S, E, E
11. b > c > a > d > e. For all solutions, at equilibrium [glucose]in = [glucose]out.
12. A glucose gradient would tend to give some net Na+ and Cl− movement in the direction of the gradient.
13. F. Much more water and salt is absorbed by small intestine.
14. F.
15. (a) T. Most of this is from gut secretions
(b) F. The products of protein digestion are absorbed as amino acids.
(c) T. Amino acids are absorbed by a carrier mediated mechanism linked to the sodium pump.
16. (a) F. Glucose is absorbed mostly in the proximal small gut.
(b) F. The jejunum is the principal site for the absorption of the products of fat digestion.
(c) T.
(d) F. Most vitamin K is absorbed in the large bowel after bacteria synthesize it in the lumen of that region.
(e) F. Most iron is absorbed in the jejunum.
17. (a) T.
(b) T. This causes inadequate bile salt secretion and hence deficient fat absorption.
(c) T. as (b)
(d) T. Inadequate lipase secretion results in deficient fat digestion.
(e) F. The stomach does not contribute significantly to fat digestion and absorption.
18. (a) T. Secretion is essentially mucous.
(b) F. Sympathetic stimulation decreases colonic motility.
(c) T. Water is absorbed consequent on active sodium reabsorption.
(d) T. Dietary intake is normally insufficient.