Gastric Flashcards
Gastric volvulus results when the stomach twists on itself, but
rarely occurs unless there is an associated
diaphragmatic hernia.
, the stomach folds on its
short axis, which runs across the stomach from the lesser curvature
to the greater curvature, with
the antrum twisting anteriorly and superiorly.
In mesenteroaxial volvulus
Mesenteroaxial volvulus
is often incomplete and intermittent, manifesting chronic symptoms.
organoaxial volvulus, the stomach twists along its long
axis, which passes through the esophagastric junction region to
the pylorus.
In most cases, the antrum rotates anteriorly and
superiorly and the fundus posteriorly and inferiorly, twisting the
greater curvature at some point along its length
Acute gastric volvulus causes sudden severe pain in the upper
abdomen or lower chest, associated with the inability to swallow.
Persistent unproductive retching is common.
The combination of pain, unproductive
retching, and inability to pass a nasogastric tube is called
Borchardt triad
If the volvulus is associated with a diaphragmatic
hernia, plain chest or abdominal films will show a large gas-filled
structure in the chest
Acute gastric volvulus is an emergency, with a mortality rate in
the vicinity of 30%.
signs of gastric infarction are not present,
acute endoscopic detorsion may be considered. Using fluoroscopy,
the endoscope is advanced to form an alpha loop in the
proximal stomach
The tip is passed through the area of torsion
into the antrum or duodenum if possible, avoiding excess
pressure. Torque may then reduce the gastric volvulus.
type 1 gastroesophageal
varices (GOV1) extend 2 to 5 cm below the gastroesophageal
junction and are in continuity with esophageal varices;
type 2 gastroesophageal varices (GOV2) are in the cardia and
fundus of the stomach and in continuity with esophageal varices
varices that occur in the fundus of the stomach in the absence of
esophageal varices are called isolated gastric varices type 1 (IGV1),
whereas varices that occur in the gastric body, antrum, or pylorus
are called isolated gastric varices type 2 (IGV2).
Approximately 25% of patients with portal hypertension have
gastric varices, most commonly GOV1, which comprise approximately
70% of all gastric varices. Intrahepatic causes of portal
hypertension may be associated with both GOV1 and GOV2.
Splenic vein thrombosis usually results in IGV1, but the most common
cause of fundal gastric varices may be cirrhosis
Gastric varices typically occur in association with advanced portal
hypertension. Bleeding is thought to be more common in patients
with GOV2 and IGV1 than in those with other types of gastric
varices; in other words, bleeding is more common from fundal varices
than from varices at the gastroesophageal junction
Gastric varices, however,
tend to be larger in diameter than esophageal varices.
Gastric
varices are supported by gastric mucosa, whereas esophageal varices
tend to be unsupported in the lower third of the esophagus
Although gastric varices
have been thought to bleed less frequently than esophageal varices,
the bleeding rates probably are comparable if patients are matched
for the severity of cirrhosis (Child-Turcotte-Pugh score
Large gastric varices (>20 mm diameter), especially in patients
with a MELD score above 17, are most likely to bleed.
Cyanoacrylate glue injection
may be more effective than beta blocker therapy in preventing
gastric variceal bleeding246 but is not currently recommended
until confirmed by larger studies. TIPS is also not recommended
for the primary prevention of gastric variceal bleeding. BRTO has
been used in uncontrolled studies to prevent bleeding from gastric
varices, with some success.
acute gastric variceal hemorrhage and includes volume
resuscitation, avoidance of overtransfusion, and antibiotic prophylaxis
with norfloxacin, 400 mg twice daily, or ciprofloxacin,
500 mg twice daily, for 7 days. EGD is carried out after patients
have been volume resuscitated and stabilized and often following
endotracheal intubation to protect the airway.
blood is found in the
stomach and gastric varices with a “white nipple sign” (indicating
a fibrin-platelet plug) are seen in the absence of other causes
of bleeding; or gastric varices are noted in the absence of other
lesions in the esophagus and stomach.
Medical
management with vasoactive agents should be started as early as
possible, preferably at least 30 minutes before endoscopic therapy
is carried out. The preferred endoscopic therapy for fundal gastric
variceal bleeding is injection of polymers of cyanoacrylate, usually
N-butyl-2-cyanoacrylate
Obliteration of the varices occurs
when the injected cyanoacrylate adhesive hardens on contact with
blood.
The endoscope may be damaged by the glue, but the risk is
minimized if silicone gel is used to cover the tip of the instrument
and suction is avoided for 15 to 20 seconds following injection
Cyanoacrylate injection has been
found to be superior to both variceal band ligation and sclerotherapy
using alcohol.251 Complications of cyanoacrylate injection
include bacteremia and variceal ulceration
For injection of GOV2 or IGV1, a retroflexed endoscopic
approach is recommended.
It is much easier to
obliterate GOV1 than GOV2 or IGV1. IGV1 are the most difficult
gastric varices to obliterate and, when present, should prompt
early consideration of definitive treatment such as portosystemic
shunting if cyanoacrylate is not available.
Band ligation of varices greater than
10 mm in diameter is usually unsafe. Ligation is safest if the varices
are in the cardia of the stomach
If endoscopic and pharmacologic therapies fail to control gastric
variceal bleeding, then a Linton-Nachlas tube may be passed
as a temporizing measure. Most patients in whom endoscopic and
pharmacologic treatment fails to control gastric variceal bleeding
will require a TIPS, which can control bleeding in greater than
90% of patients—
Patients require an average of 2 or 3 sessions for obturation of
gastric varices with cyanoacrylate polymers
Comparison of Portal Hypertensive Gastropathy (PHG) and
GAVE
Feature
PHG
Proximal stomach
Mosaic pattern Present
Red color signs Present
GAVE
Distal stomach
Mosaic pattern Absent
Red color signs Present
The stomach volume
ranges from approximately 30 mL in a neonate to 1.5 to 2 L in
adulthood.
The stomach is recognizable in the fourth week of gestation
as a dilation of the distal foregut
As the stomach
enlarges, the dorsal aspect grows more rapidly than the ventral
aspect, therefore forming the greater curvature. Additionally,
during the enlargement process the stomach rotates 90 degrees orienting the greater curvature (the
dorsal aspect) to the left and the lesser curvature (ventral aspect)
to the right.
right vagus nerve innervating
the posterior stomach wall (the primordial right side) and
the left vagus nerve innervating the anterior wall (the primordial
left side).
The esophagogastric
junction generally lies to the left of the T10 vertebral body,
1 to 2 cm below the diaphragmatic hiatus. The gastroduodenal
junction lies at L1 and generally to the right of the midline in
the recumbent fasted individual
The esophagogastric
junction generally lies to the left of the T10 vertebral body,
1 to 2 cm below the diaphragmatic hiatus. The gastroduodenal
junction lies at L1 and generally to the right of the midline in
the recumbent fasted individual
The greater curvature forms the left lower stomach border,
whereas the lesser curvature forms the right upper border. Posteriorly,
portions of the pancreas, transverse colon, diaphragm,
spleen, and apex of the left kidney and adrenal gland bound the
stomach.
The posterior wall of the stomach actually comprises
the anterior wall of the omental bursa, or lesser peritoneal sac.
Anteriorly, the liver bounds the stomach, whereas the inner
aspect of the anterior abdominal wall bounds the anterior left
lower aspect.
The stomach is completely invested by peritoneum,
except for a small bare area at the esophagogastric junction.
This peritoneum passes as a double layer from the lesser curvature
to the liver as the gastrohepatic portion of the lesser
omentum and then hangs down from the fundus and greater
curvature as the greater omentum, extending to the transverse
colon (as the gastrocolic ligament), spleen (as the gastrosplenic
ligament), and diaphragm (as the gastrophrenic
ligament).
The arterial blood supply to the stomach is derived from branches
of the celiac artery—common hepatic, left gastric, and splenic
arteries
that form 2 arterial arcades situated along the lesser
curvature and the lower two thirds of the greater curvature
The
lesser curvature is supplied from above by the left gastric artery
and from below by the right gastric artery, a branch of the common
hepatic artery or gastroduodenal artery (which is a branch
of the common hepatic artery).
The greater curvature below the
fundus is supplied from above by the left gastroepiploic artery (a
branch of the splenic artery) and from below by the right gastroepiploic
artery (a branch of the gastroduodenal artery). The right
and left gastroepiploic arteries usually terminate by anastomosing,
therefore completing the greater curvature arterial arcade;
occasionally they end without anastomosis
The greater curvature below the
fundus is supplied from above by the left gastroepiploic artery (a
branch of the splenic artery) and from below by the right gastroepiploic
artery (a branch of the gastroduodenal artery
The arterial supply to
the gastric fundus and left upper aspect of the greater curvature is
via the short gastric arteries, which arise from the splenic artery
the short gastric arteries, which arise from the splenic artery.
The venous drainage of the stomach generally accompanies
the arterial supply, emptying into the portal vein or 1 of its tributaries,
the splenic or superior mesenteric veins
The left gastroepiploic vein becomes the
splenic vein and later receives the short gastric veins, therefore
draining the fundus and upper great curvature of the stomach.
The inferior gastric region drains into subpyloric
and omental nodes, then the hepatic nodes, terminating in the
celiac nodes
The superior gastric or lesser curvature region
lymph drains into the left and right gastric nodes adjacent to their
respective vessels and terminates in the celiac nodes.
The gastric sympathetic innervation is derived from preganglionic
fibers arising predominantly from T6 to T8 spinal nerves,
The parasympathetic innervation is via the right and left vagus
nerves, which form the distal esophageal plexus, and gives rise to
the posterior and anterior vagal trunks near the gastric cardia.
The luminal surface of the gastric wall forms thick, longitudinally
oriented folds, or rugae, that flatten with distention. Four layers
make up the gastric wall: mucosa, submucosa, muscularis propria,
and serosa
The mucosa of the cardia, antrum,
and pylorus is somewhat paler than that of the fundus and body.
It is within the fundic and body mucosa that most of the functional
secretory elements of the stomach are located
submucosa, immediately deep to the mucosa, provides
the dense connective tissue skeleton of collagen and elastin fibers.
Lymphocytes, plasma cells, arterioles, venules, lymphatics, and
the submucosal plexus are also contained within the submucosa
The third tissue layer, the muscularis propria, is a combination of
3 muscle layers: inner oblique, middle circular, and outer longitudinal.
The inner oblique muscle fibers course over the gastric
fundus, covering the anterior and posterior aspects of the stomach
wall; the middle circular fibers encircle the body of the stomach,
thickening distally to become the pyloric sphincter; and the outer
longitudinal muscle fibers course primarily along the greater and
lesser curvatures of the stomach
inner oblique, middle circular, and outer longitudinal.
The inner oblique muscle fibers course over the gastric
fundus, covering the anterior and posterior aspects of the stomach
wall; the middle circular fibers encircle the body of the stomach,
thickening distally to become the pyloric sphincter; and the outer
longitudinal muscle fibers course primarily along the greater and
lesser curvatures of the stomach
typical gland is subdivided into 3
areas: the isthmus (where surface mucous cells predominate), the
neck (where parietal and mucous neck cells predominate), and the
base (where chief cells predominate, along with some parietal and
mucous neck cells).
Chief cells, also known as zymogen cells, predominate in deeper
layers of the oxyntic glands. These pyramid-shaped cells play
a role in synthesis and secretion of pepsinogens I and II.
Those cells containing
granules that reduce silver without pretreatment are called argentaffin
cells. Argentaffin cells that stain with potassium dichromate
are enterochromaffin (EC) cells; most ECs contain serotonin
weeks 5
and 6 of embryologic development, the duodenal lumen is temporarily
obliterated owing to proliferation of its mucosal lining
patients with gastric
erosion(s) or ulcer(s), thick gastric fold(s), gastric polyp(s) or
mass(es), and for diagnosis of Hp infection (discussed later). Two
biopsies should be taken from the antrum (lesser and greater curvatures),
one from the incisura angularis, and 2 more from the
gastric body (lesser and greater curvatures)
Acute gastritis, characterized by dense infiltration of the stomach
with neutrophilic leukocytes
Phlegmonous (suppurative) gastritis is an infection of the gastric
submucosa and muscularis propria, often sparing the mucosa
The mortality rate of phlegmonous gastritis is close to 70%, Vancomycin and piperacillin/tazobactam is one empiric
regimen that can be used
Chronic gastritis is much more common than acute gastritis,
although it may be clinically silent
are risk factors for other diseases such as PUD and gastric neoplasms,
including adenocarcinoma and lymphoma (MALToma),
Three types of chronic gastritis are recognized: diffuse antral
gastritis which is usually due to Hp infection, environmental
metaplastic atrophic gastritis (EMAG), and autoimmune metaplastic
atrophic gastritis
Hp is a gram-negative helical- or spiral-shaped flagellated bacterium.
A form of Hp gastritis characterized by mucosal infiltration
by plasma cells that contain Russell bodies (Russell body gastritis)
has been described
A form of Hp gastritis that can be
recognized endoscopically is nodular gastritis, which can resolve
following eradication of the organism from the
Nodular gastritis/gastropathy is recognized by its chicken-skin
appearance and can be seen in other conditions, including Crohn
disease, syphilitic gastritis, lymphocytic (varioliform) gastritis,
collagenous gastritis (all discussed later), and in AA-amyloidosis
Hp infection is the most common chronic bacterial infection in
humans. Estimates suggest that over 50% of the world’s population
is infected with the bacterium, including 70% to 80% of
populations in developing nations.
key risk factor for infection is socioeconomic status during
childhood. Infection is commonly acquired at an early age, particularly in developing countries where the majority of children
become infected before the age of 10.
serologic
evidence of Hp infection is uncommon in children before
age 10, but rises to 10% in adults between 18 and 30 years of
age, and further increases to 50% in those age 60 or older
Organism loads are 100-fold higher in vomitus
when compared with stool and saliva; organisms are also present
in aerosolized vomitus out to 1.2 m during the act of vomiting.
Hp contain 6 to 8 flagella at one end of their bodies and flagella-
mediated motility is one of the few characteristics shown
to be required for successful Hp colonization of the host
Exposure of Hp to low gastric pH levels increases expression
of bacterial genes encoding urease.55 Urease helps Hp adapt to
the acidic gastric milieu, allowing a more neutral pH to occur
near the bacteria as its urease splits urea into CO2 and ammonia
(NH3), with the NH3 reacting with H+ to produce ammonium
ion (NH4
+)
Hp show strict tropism for gastric-type mucosa, including in
nongastric regions of the GI tract where there is gastric metaplasia
Metaplasia may also be associated with hypochlorhydria/
achlorhydria, encouraging overgrowth of the stomach with other
(non-Hp) species of bacteri