BSI: GI Case Studies
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What is the role of esophageal peristalsis in normal swallowing?
The upper esophageal sphincter (UES)
and upper one third of the esophagus
are comprised of skeletal muscle
The lower two-thirds of the esophagus
and the lower esophageal sphincter (LES)
are comprised of smooth muscle
, which starts in the mouth is voluntary
, but then becomes a reflex
coordinated in the swallowing center of the medulla
Peristalsis of the esophagus
- There are three phases in swallowing:
- 1) oral phase: bolus of food is pushed back to pharynx and activates receptors that initiate swallowing reflex
- 2) pharyngeal phase: due to relaxation of the UES, food bolus is propelled from mouth to pharynx to esophagus
- 3) esophageal phase: food is propelled caudally along the esophagus to the stomach via peristalsis that is mediated by the swallowing reflex
works by creating a positive pressure
behind the bolus by contracting behind the bolus.
the esophagus is at zero pressure
, or atmospheric pressure
If primary peristalsis does not clear the bolus into the stomach, then a secondary peristaltic wave
is initiated by distention of the esophagus
. The enteric nervous system (ENS)
mediates the peristaltic contractions that start behind the bolus.
In a normal swallow, what events occur in the lower esophageal sphincter (LES), and what is the timing of these events? What is the innervation of the LES, and what transmitters are involved in its function?
, the LES is contracted
and has a positive pressure
to ensure the gastric contents do not reflux
into the esophagus.
, the LES must relax and dilate
in a timely fashion so the bolus of food can enter stomach
When peristaltic wave
of esophagus is initiated, the LES simultaneously relaxes
, its pressure decreases to zero (atmospheric)
, and the LES opens. The LES remains open until the peristaltic wave reaches the terminal portion of the esophagus.
of the LES is mediated by inhibitory neurons
in the vagus nerve
that release the neurotransmitters vasoactive peptide (VIP)
and nitric oxide (NO)
How are dietary carbohydrates absorbed from the lumen of the GI tract into the blood?
are the only absorbable
form of carbohydrates.
- The apical membrane is in contact with the lumen of the small intestine. It contains:
- Na+-glucose cotransporter
- Na+-galactose cotransporter
- The basolateral membrane is in contact with the circulating blood stream. It contains:
- Na+ -K+ ATPase
- Absorption of monosaccharides is a two-step process for each type of monosaccharide:
- 1) Glucose and galactose enter the apical membrane via secondary active transport, which is energized or driven by the Na+ gradient. Note that the Na+ gradient is maintained by the Na+-K+ ATPase in the basolateral membrane. Fructose, in contrast, simply diffuses right through the apical membrane.
- 2) Glucose, galactose and fructose all exit the cell via facilitated diffusion across the basolateral membrane into the blood.
What may cause lactose intolerance?
Lactose is a disaccharide
and therefore cannot be absorbed into the GI tract without first being converted to a monosaccharide
- Lactose intolerance can be caused by:
- 1) inability to convert lactose to a monosaccharides (e.g. lack of lactase enzyme)
- 2) defect in one of the monosaccharide transporters (i.e. not allowing absorption of monosaccharides) Note that a defect in transporter would be not discriminate against just lactose not being tolerated.
Why would lactose intolerance cause diarrhea? How does a lactose-H2 breath test work?
- When lactose cannot be absorbed, some of the lactose is fermented by colonic bacteria to:
- 1) lactic acid
- 2) methane
- 3) H2 gas
Undigested lactose and lactic acid
behave as osmotically active solutes
in the lumen of the GI tract. They draw water isosmotically into the intestinal lumen and produce osmotic diarrhea
gas is absorbed into the bloodstream and expired by the lungs
. Therefore, a breath test can detect higher H2
levels than normal in lactose intolerance.
Peptic ulcer disease is caused by digestion of the gastrointestinal mucosa by H+ and pepsin.
- Some causative factors of peptic ulcers include:
- increased H+ secretion by gastric parietal cells
- Helicobacter pylori infection
- use of NSAIDs (e.g. aspirin)
The common factor in each of the causes is they all digest the gastrointestinal mucosa by H+
; hence the dictum, "no acid, no ulcer."
The typical location of an ulcer is in the duodenum of the small intestine
because the excess H+
from the stomach travels with the chyme to the intestine and exceeds the neutralizing capacity
of pancreatic & intestinal secretions.
What is the mechanism of H+ secretion by gastric parietal cells?
Gastric parietal cells
are responsible for the secretion of H+
into the lumen of the stomach. Gastric parietal cells are stimulated by Gastrin
, which is released from G cells
The apical membrane
of the cell, which faces the lumen of the stomach
, contains an H+-K+ ATPase
The basolateral membrane
, which faces the blood
, contains the Na+-K+ ATPase
and a Cl--HCO3- exchanger
Inside the gastric parietal cell, the CO2 + H20
combine to form H2CO3 (carbonic acid)
, which dissociates into H+
is secreted into the lumen of the stomach by the H+-K+ ATPase
, acidifying the stomach contents to help with digestion of dietary proteins
Acid gastric pH
is required to convert inactive pepsinogen
to its active form, pepsin
(a proteolytic, or protein-degrading enzyme
is exchanged for Cl-
across the basolateral membrane
and thus is absorbed into gastric venous blood
. Eventually the HCO3-
is secreted into the lumen of the small intestine (via pancreatic secretions), where it neutralizes the acidic chyme
delivered from the stomach.
What are the major factors
that regulate H+ secretion
- Three major factors that stimulate H+ secretion by gastric parietal cells are:
- 1) parasympathetic nervous system (via vagus nerve): Postganglionic parasympathetic nerve fibers (PNS) via the vagus nerve stimulates H+ secretion both directly and indirectly. The parietal cells are directly innervated by postganglionic neurons that release acetylcholine (ACh) which activates muscarinic M3 receptors and stimulates H+ secretion. The G (gastrin-secreting) cells also have parasympathetic innervation. They release bombesin or gastrin releasing peptide, thus indirectly stimulating H+ secretion by increasing gastrin secretion.
- 2) gastrin (via G cells): G cells in the gastric antrum release gastrin, which enters the circulation and stimulates H+ secretion by the gastric parietal cells through the cholecystokinin-B (CCKB) receptor.
- 3) histamine (via ECL cells): Histamine is released from enterochromaffin-like cells (ECL) located near the parietal cells. Histamine diffuses to the parietal cells and activates H2 receptors, stimulating H+ secretion.
- Two major factors that inhibit H+ secretion by gastric parietal cells:
- 1) somatostatin (via D cells): somatostatin which is released from D cells of the GI tract inhibits H+ secretion in three ways...first, it directly inhibits H+ secretion by parietal cells via a G-protein (decreasing cAMP); second, somatostatin inhibits the release of gastrin from G cells, thus diminishing the stimulatory effect of gastrin; third, somatostatin inhibits the release of histamine from enterochromaffin-like cells (ECL), thus diminishing the stimulatory effect of histamine.
- 2) Prostaglandins: also inhibit H+ secretion via a G protein.
How does Zollinger-Ellison syndrome (a tumor, often located in the pancreas) cause excess H+ secretion?
Normally, the physiologic secretion of H+ is regulated by negative feedback. In other words, the low gastric pH inhibits further gastrin secretion.
However, in the case of Zollinger-Ellison syndrome (aka a gastrinoma), the secretion of gastrin by the gastrinoma is NOT feedback regulated; therefore even when the stomach contents are very acidic, gastrin secretion continues.
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