SSN SBPM WORKSHOP #5
Short Answer Questions & Answers
1. What happens in the parietal cells when a person who has fasted begins to eat?
After a couple minutes, there is activation of the Hydrogen, potassium ATPase, carbonic
anhydrase, and an increase in the production of ATP.
2. Acidification of the duodenal mucosa results in:
The main response to acidic fluid in the duodenum is the stimulation of secretin, which
stimulates the aqueous component of the pancreas (HC03). It also stimulates pepsinogen
secretion as well as release of gastrin. There is some release of CCK which stimulates
bile production and contributes to the inhibition of gastric emptying.
3. In the total absence of parietal cells, what would happen to a person?
The parietal cells secrete both H+ and intrinsic factor, which is required for the
reabsorption of vitamin B12. Without them, there is an elevated level of gastrin, since the
normal feedback inhibition of gastric acid secretion has been interrupted. Even though
the acidification helps in the digestion of proteins, it is not essential and the proteases
within the small intestine will compensate.
4. What metabolic changes would you find in a patient with severe diarrhea?
Since diarrheal discharge contains large amounts of HCO3, Na, and K, the patient loses
a significant amount of fluid, causing a depletion of the extracellular volume that leads to
a decrease in circulatory pressure. The loss of fluid will cause activation of the volume
receptors, which leads to an increase in heart rate and activation of the sympathetic
nervous system. The loss of potassium causes the patient to become hypokalemic (low
potassium). The loss of alkalotic fluid, will lead to metabolic acidosis leading to
compensatory hyperventilation to lower the H+ in the blood.
5. Do all seretonin antagonists have the same effect on the GI tract? Why or why
not?
No they do not. There are a number of different types of 5-HT receptors,and various
drugs are selective for one or another type of receptor. Forexample, a 5-HT3 blocker
alone will not inhibit the peristaltic reflexes;but this can be accomplished by blocking
both 5-HT3 and 5-HT3 receptors simultaneously. The other seretonin receptor involved
in GI response is5-HT1P.
6. Describe the process of signal transduction that results in the initiationof the
peristaltic reflex.
EC cells, the primary sensory cells of the gut, respond to increased pressure or chemical
stimulation in the gut lumen by secreting 5HT, aneurotransmitter. 5HT is picked up by
submucosal IPAN which are cholinergicneurons with CGRP activity. ACh and CGRP
are responsible for fast and slow EPSPs, respectively, in the subsequent neuron.
Submucosal IPANs activatethe enteric microsircuits that result in peristaltic and
secretory reflexes.
7. How is the existence of receptor subtypes taken advantage of in medications?
Mention 5-HT3 and 5-HT4 receptors, specifically.
5-HT receptor antagonists that are specific for 5-HT3 are used to stopsensations of
nausea and vomiting from reaching the CNS without affectingperistalsis or secretions
because 5-HT3 receptors are not involved ininitiating peristalsis or secretion. Also, 5HT4 receptor agonists are usedto increase peristalsis without causing nausea because
there are no 5-HT4 receptors on extrinsic sensory neurons of the gut.
8. A 15 year old diabetic girl is non-compliant with her insulin injections and loves
to splurge on sweets. At lunch time she eats a half pound of pure sugar. Which
gastro-intestinal hormone will be affected and what effect, if any, will this have on
her blood sugar? How would this compare to a normal person's physiology after
eating this much sugar?
GIP, the only GI hormone released in response to dietary carbs, will be released into the
circulation but insulin secretion will not follow. Normally, the secretion of GIP results in
the secretion of insulin by the pancreas, lowering blood glucose. In the type I diabetic,
however, the beta cells of the pancreas are non-functional or absent. So, elevated blood
sugar levels are unopposed by the pancreas (or by the effects of GIP on the pancreas).
9. In a normal individual, how would peak glucose levels differ after injection of
glucose compared to drinking soda pop (assuming only glucose in the pop and equal
grams of carbs)?
The blood glucose curve for injected glucose will be steeper and have a higher peak
because it hasn't been processed by the gut (so no GIP secretion occurs). Another reason,
although not directly relevant to GI phsyiology, is simply that injection is a faster mode
of administration.
10. Describe swallowing:
Swallowing is a reflex response that is triggered by afferent impulses in the trigeminal,
glossopharyngeal, and vagus nerves; these impulses are then integrated in the nucleus
tractus solitarius and nucleus ambiguus. Efferent fibers pass to the tongue and
pharyngeal musculature via the trigeminal, facial, and hypoglossal nerves.
11. What can cause a decrease in gastric motility by way of the enterogastric reflex?
-products of protein digestion and H+ ions bathing the duodenal mucosa
-distension of the duodenum
-peptide YY
-severing the vagus
-fear?
12. CCK exhibits some overlap of function with secretin. How do these GI
hormones interact and what might be the purpose of this interaction?
The main purposes of CCK are to stimulate the gall bladder to contract, to stimulate the
pancreas to secrete its digestive enzymes (trypsin, chymotrypsin, carboxypeptidase,
amylase, lipase, etc.), and to stop the stomach from emptying, enabling the small intestine
to properly deal with the fats and proteins that are already in its lumen. However, it also
potentiates the effect of secretin on inducing bicarbonate secretion by the pancreatic
extralobular ductal cells. This synergy between CCK and secretin makes sense because
the enzymes that CCK causes to be released require an alkaline environment for their
optimal activity.
13. The exocrine pancreas secretes a fluid that is isotonic with plasma. The
concentration of bicarbonate in the pancreatic juice, however, is much higher than
it is in the plasma. Explain the cellular mechanism in the pancreatic ductal cells
responsible for both the increased bicarbonate and the maintenance of isotonicity.
The pancreatic ductal cell contains both luminal and basolateral exchangers that allow it
to increase the bicarbonate concentration in the pancreatic secretions. On the apical
(luminal) surface is a Cl-/HCO3- exchanger that secretes one bicarbonate ion into the
lumen for every Cl- ion it brings into the cell (this is thus a non-electrogenic exchanger).
On the opposite, basolateral, surface, both H+-ATPase and Na+/H+ exchangers exist to
secrete a proton out the other end of the cell, ensuring that acid does not build up inside
the cell. There are also apical Cl- and basolateral K+ channels that function in
maintaining osmotic balance. Remember, too, that the pancreatic ducts are permeable to
water, allowing isotonicity to be maintained between pancreatic secretions and plasma.
14. Trace the fate of dietary triglycerides from ingestion through their storage in
adipose tissue. Then trace the fate of triglycerides synthesized in the liver through
their storage in adipose tissue.
Fatty acids – triglycerides in chylomicrons (small intestine) – lacteals – lymphatic
vessels – bloodstream – peripheral tissue capillaries w/ extracellular lipoprotein lipase
(LPL) – free fatty acids (adipose tissue). Triglycerides (liver) – Very Low Density
Lipoprotein (VLDL) in bloodstream – peripheral tissue capillaries w/ extracellular
lipoprotein lipase (LPL) – free fatty acids (adipose tissue).
15 . What happens in reverse cholesterol transport?
In short, cholesterol is removed from tissues. Circulating High density lipoprotein
(HDL) probably extracts its cholesterol from cell surface membranes and converts it to
cholesterol esters via the enzyme lecitin-cholsterol acyl transferase (LCAT). The
cholesterol esters are then transferred to Low Density Lipoprotein (LDL) via cholesterol
ester transfer protein (CETP). LDL is removed from the plasma by the liver, which
excretes the cholesterol in bile.
16. What genetic and epidemiological evidence supports the idea that body weight is
regulated? What is the proposed model for this regulation?
In twin studies, comparing monozygous versus dizygous twins, the heritability of body
fatness is found to be between 65 and 85%.
Single gene mutations have been found that produce obesity.
Long-term constancy of body weight, and the lack of success of people in maintaining
lower body weight.
The quantity of stored energy (in adipose) is sensed by afferent systems that feed into the
central nervous system, whose efferents act on energy intake systems (feeding behavior)
and output to return body weight to its usual level.
17. Why is it so difficult for an obese person to maintain a reduced weight?
The body defends a particular weight. An obese person trying to maintain a weight
below usual will require a significantly smaller number of calories than predicted solely
on the basis of weight loss. Metabolic changes, such as an increase in skeletal muscle
efficiency and a decrease in resting energy expenditure, act to oppose the maintenance of
the altered weight.
18. What is the final mechanical event of sound transduction in the ear prior to the
electrical conduction of sound? What is the series of events of electrical conduction?
The movement of the hairs by the basilar membrane in the organ of corti is the final
mechanical event, and is absolutely critical to sound transduction. Once the hairs are
bent, energy is released in the form of ‘bioelectric potentials’ which leads to excitation of
the auditory nerve fibers in the middle ear. These fibers are simply composed of one
cytoplasmic process of a bipolar nerve cell. The other pole transmits the electrical
impulses to the CNS (as you learned in anatomy) where sound is processed. This
pathway proceeds through the cochlear nerve through the spiral ganglion to the brain.
19. Explain how the eye manipulates the lens to focus on near objects and why this
ability is diminished with ‘normal’ aging.
In order to focus on a near object, the lens must increase in both thickness and in
curvature. When your brain decides to look at something close to your eye, the ciliary
muscle is contracted, leading to tension on the ciliary body and suspensory ligaments
which attach directly to the lens and change its shape. The major age-related change
related to loss of near vision is presbyopia. As your parents put on their bifocals to read
the map, remember that this is due to hardening of the lens over time, and thus a loss of
flexibility, which leads to an inability to change lens shape to see near objects. Other
age-related changes include yellowing of the sclera and senile cataracts, which are a
result of focal opacities in the lens.