GIT [Guyton and Hall physiology] & [UW 2016]
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1. 21 years female+Nausea+
diarrhea+light headedness+
flatulence. After overnight fast, the
physicain administrates 50 gm of oral
lactose at time zero (indicated by the
arrow). Which combination is most
likely in the patient during the next 3
months?
2. patients with lactase deficiency can't
digest milk products that contains
lactose (milk sugar)
3. 43 years man+ eat a meal (protein
40%) +fat (10%) + CHO (50%). 30
minutes later the man feels urge to
defecate. Which reflex results in the
urge when the duodenum is
stretched?
4. 23 years man+ eat a meal (protein
30%) +fat (15%) + CHO (55%). At which
location are bile salts most likely to
be absorbed by active transport
process?
(1) Serum glucose 5.
(will not change)
(2) Breath Hydrogen
(will increase)
(3) Intestinal
6.
methane production
(will increase)
So the operons of
gut bacteria quickly
switch over to
lactose metabolism-
-> fermentation-->
large amount of gas
(mix of Hydrogen +
CO2 + Methane).
(1) This gas-->
abdominal cramps +
7.
bloating+ flatulence.
(2) This gas is
absorbed by blood
(in colon) and
exhaled by lungs.
(3) Blood glucpse
don't increase (as
lactose is not
digested to glucose
and galactose in
these patients.
Duodenocolic reflex.
Small intestine (distal
ileum); 95% of bile 8.
salts are reabsorbed
into the blood from
small intestine, with;
A- 1/2 of this by
diffusion (early part
9.
of S.I. mucosa).
B- The rest by active
transport in distal
ileum
The highest ion conc. in saliva
under the basal condition;
Experiment shows initial rise,
peak, and then decline in
gastric acid production during
and after meal. [Which helps
most to down regulate gastric
secretion after a meal?]
Gastric Acid secretion is
separated into 3 phases;
Receptive relaxation;
Postprandial alkaline tide
Bicarbonate (HCO3); 50-70
mEq/L in saliva whereas K
conc is 30 mEq/L, under
basal condition.
[Intestinal influences[; as are
effective in down regulating
gastric acid secretion.
-Ileum and colon release
peptide YY, which binds to
receptors on the endocrine,
histamine containing cells
described as
enterochromaffin like cell.
-This binding counteracts the
cephalic and gastric phases
of acid secretion by
inhibiting gastrin-stimulated
histamine release from ECLs
[1] The cephalic phase is
mediated by cholinergic and
vagal mechanisms, is
triggered by thought, sight,
smell, and taste of food.
[2]The gastric phase is
mediated by the presence of
gastrin (which stimulates
histamine secretion), is
triggered by chemical
stimulus of food and
distension of the stomach.
[3] The intestinal phase is
initiated when protein-
containing food enters the
duodenum, but this phase
plays only a minor role in
stimulating gastric acid
secretion.
reflex that shows the gastric
fundus to dilate in
anticipation of food passing
through the pharynx and
esophagus.
an increase in plasma HCO3
and decrease in plasma Cl
secondary to the surge of
acid within the gastric
lumen.
10. 34 years+ follow up+ Hx. of acute
calculous cholecystitis+ had
uncomplicated laproscopic
cholecystectomy+ No abdominal
pain nor nausea+ well healed
abdominal incisions+ The abdomen
is soft and non tender+ the patient
has been avoiding fatty acids since
surgery+ the physician assures her
that she can start adding fatty
foods back into her diet as
tolerated. In this ptn, dietary lipids
will most likely be absorbed from
which?
11. Loss of concentrating and storage
functions of the GB after
cholecystectomy
12. Proximal colon
13. Distal colon
14. Ileum
[Jejunum]; Dietary 15.
lipids (e.g TGs,
phospholipids,
cholesterol esters) are
digested in the
duodenum via the
action of pancreatic
enzymes.
Bile is also released
into the duodenum ,
16.
where the bile salts
emulsify the end
products of fat
digestion (FA ,
monoglyceride) and 17.
form water soluble
micelles.
In jejunum, these
micelles come into
close contact with the
gut epithelium , which
facilitates passive 18.
absorption of FA , MG,
and Cholesterol across
the brush border.
results in a constant
release of bile into the
duodenum, allowing
most patients to
tolerate a normal diet.
However, this
continous biliary
drainage can
overwhelm the
absorptive capacity of
the bile salts in the
ileum and may lead to
chronic, secretory
diarrhea in some
patients. [Post-
cholecystectomy
diarrhae]
responsible for water
and electrolytes
absorption
responsible for storage
of feces
responsible for
absorption of bile salts
and vitamins.
43 years obese women+
severe epi-gastric pain after
heavy meal+ had several
milder episodes before
related to fatty food
consumption. marked
tenderness in Rr subcostal
area+ [Hormone that
provoked the current attack]
In cholecystitis,
Vasoactive intestinal peptide
(VIP)
Animal pancreatic duct is
cannulated and different
secretory stimuli are applied
to the gland. The following
tracings are obtained by
measuring pancreatic fluid
constituents; [Substance X]
CCK; responsible for GB
contraction. Produced by I
cells of duodenum and
jejunum when fat-protein-
rich chyme enters the
duodenum. Also functions
to increase pancreatic
enzyme secretion by acinar
cells.
fatty foods increase CCk
production and pain occurs
when an inflamed and/or
obstructed GB contracts.
Produced by pancreas.
(1) Stimulates intestinal
water secretion.
(2) Counteracts gastrin in
the stomach
(3)promotes HCO3
secretion for the pancreas
[HCO3]; Pancreatic juice is
isotonic contains normally
Na and K conc. as plasma.
Higher HCO3 conc tham in
plasma and lower CL conc
than plasma.
-Secretin produced by
duodenal S cells in
response to H conc. ,
Secretin increases
pancreatic HCO3 secretion.
The cholride content of
pancreatic secretions
decreases in proportion to
bicarbonate conc. increase.
19. 32 years female+ 6 months persistent diarrhea+ had 8-10 episodes a day of tea [VIP]; the ptn has secretory diarrhea NOT
colored , odorless, watery stools. symptoms persisted despite a lactose free diet and inflammatory diarrhea distinguished by
a fasting trial. NO abdominal pain , fever, or vomiting. Temp. 36.7. Sampling of her absence of blood or pus and from
gastric contents shows a total lack of gastric acid secretion. SOmatostatin ttt osmotic diarrhea (e.g due to lactose
promptly relives the symptoms. An excess of which is most likely responsible for this intolerance) by its failure to improve with
patient's symptoms? dietary modification.

Excess VIP secretion due to pancreatic

islet cell tumor called VIPoma can result
in watery diarrhea, hypokalemia, and
achlorhydria (WDHA) syndrome.
(Pancreatic cholera).
20. VIPoma; VIP stimulate pancreatic HCO3 and Cl secretion Binds to intestinal epithelial cells leads
to adenylate cyclase activation and
increased cAMP production--> Na, Cl,
and water secretion into the bowel
(Secretory watery diarrhea. often >3
L/day)
21. Somatostatin (octreotide) decrease the production of many GIT hormones (e.g VIP, its inhibition of VIP production by this
gastrin, glucagon, CCK). VIPoma results in resolution of ptn's
symptoms