Small Bowel
Small Bowel
Small Bowel
Enterocytes, or absorptive cells, are found in the mucosa of the small and large bowel.
The normal enterocyte lives for a little more than 2 days. They are columnar and are the
principal cells of the villus. Enterocytes absorb a variety of nutrients including Ca, Fe and
H2O.
The primary fuel source of enterocytes is glutamine. Principles and Practice of Surgical
Pathology, 2nd Edition, Vol II, pgs 1121-23
Secretin/Gastrin Relationship
Secretin is produced by specialized cells in the small bowel mucosa and its release is
stimulated by acidification of the duodenum or by contact with bile and perhaps fat. It
stimulates the release of water and bicarbonate from pancreatic ductal cells, which
neutralizes gastric acid. Secretin also acts to stimulate the flow of bile and inhibits gastrin
release and therefore gastric acid secretion and gastrointestinal motility. Schwartz 6th pg.
1128, 1161-62
Activation of Trypsinogen
Trypsinogen is the inactive precursor of trypsin. It is produced by pancreatic acinar cells
along with other inactive proteolytic enzymes, chymotrypsinogen and
procarboxypolypeptidase. These inactivated enzymes are delivered to the duodenum in
an alkaline environment.
Enterokinase, an enzyme secreted by intestinal mucosa, lyses trypsinogen converting it
into the active enzyme. Trypsin is then able to lyse more trypsinogen into trypsin
(autocatalytic activation). Chymotrypsinogen is lysed into its active form chymotrypsin,
and procarboxypolypeptidase - activated form of trypsin also. Trypsinogen is protected
from activation prior to entering the intestinal lumen by trypsin inhibitor. This substance
is also secreted by the same pancreatic acini cells that secrete the proteolytic enzymes.
Guyton, Medical Physiology, pg 779
Physiology of Enteroglucagon
Enteroglucagon is released from the enteroglucagon cells, occurring predominately in the
distal small intestine. This peptide occurs in two forms - one small and one large form.
Release of this hormone is stimulated by carbohydrate and long-chain fatty acid. Its
primary action is to inhibit intestinal motility. Sabiston, Textbook of Surgery, 14th ed.,
pg. 834
Care, pp 350-351
Diagnosis of Gastrinoma
Fasting hypergastrinemia (>200 pg/ml) in the face of gastric acid hypersecretion defined
as basal acid output >15mEq/h with intact stomach or >5mEq/h after ulcer surgery. Most
patients with gastrinoma have serum gastrin levels >500 pg/ml. A secretin provocative
test is usually done to confirm diagnosis when serum gastrin is in the range of 200-500
pg/ml.
Secretin Provocative Test:
Following 2 u/kg secretin IV bolus, a rise in serum gastrin level of 200 pg/ml within 15
min or doubling of the fasting gastrin level is diagnostic of gastrinoma.
Additional Studies: Upper GI or endoscopy will show ulcers often in unusual locations,
i.e. 2nd & 3rd portions of duodenum or jejunum. The stomach may have prominent rugal
folds along with excessive luminal secretions. CT scan may show tumor in the pancreas
or paraduodenal areas. Angiography with portal venous sampling may show "hot spots"
of gastrin secretion. Schwartz, 6th ed, pp 1427-28
Duodenal Hematoma
Intramural hematoma of the duodenum is usually due to blunt abdominal trauma. This
causes rupture of intramural duodenal blood vessels with formation of a dark, sausage-
shaped mass in the submucosal layer of the duodenal wall. It can also occur
spontaneously in patients on anticoagulants. The hematoma may cause partial or
complete duodenal obstruction. The patient has signs of a high small bowel obstruction,
with nausea and vomiting associated with upper abdominal pain and tenderness, and
sometimes a suggestion of a right upper quadrant mass on palpation of the abdomen.
Plain films of the abdomen may show an ill-defined right upper quadrant mass and
obliteration of the right psoas shadow. An upper GI is usually diagnostic with filling of
the duodenal lumen and the appearance of a "coiled spring" in the second and third
portions due to crowding of the valvulae conniventes. The serum amylase may be
elevated. Most infants and children may be successfully treated without surgical
intervention. Nonsurgical treatment of these patients consists of cessation of oral intake,
nasogastric suction, and intravenous replacement of fluids and electrolytes. Schwartz, 6th
Edition. O'Leary, 2nd Edition, Physiologic Basis of Surgery