GIT 1 Flashcards
T or F
Congenital abnormalities, When present within esophagus, they are
discovered shortly after birth, usually due to
regurgitation during feeding; Without surgical intervention, these are incompatible with life
Congenital abnormalities
Atresia, Fistula, Duplications Diaphragmatic hernia, Omphalocele, Gastroschisis Ectopia Meckel diverticulum Pyloric stenosis Hirschsprung dse
failure of organ development due to
absence of primordial tissues/cells; extremely
rare
Agenesis
○ Incomplete development or canalisation
Atresia
Atresia is commonly seen in the anatomical landmark of
tracheal bifurcation with the use of
barium swallow
a connection between the upper or lower pouch of the esophagus to a bronchus or the trachea
Fistula
T or F
Tubular structures are canals sometimes they
could be stenotic (usually absence of the
canal)
T
a thin, non canalized
cord replaces a segment of esophagus,
causing a mechanical obstruction
esophageal atresia
Incomplete forms of atresia in which the lumen is
markedly reduced. In caliber, as a result of fibers
thickening of the wall.
STENOSIS
T or F
Stenosis can result in either partial or complete obstruction
T
most commonly involved part in stenosis
esophagus or small intestines
The anus is not patent
most common example of congenital intestinal
atresia (duodenum)
Imperforate anus
occurs when there’s
incomplete formation of the diaphragm and sections
of your GIT, allowing the abdominal viscera to
herniate into the thoracic cavity.
DIAPHRAGMATIC HERNIA
DIAPHRAGMATIC HERNIA
Most commonly occur on the
Left side
Diaphragmatic hernia, When severe, the space-filling effect of the displaced
viscera can cause
Pulmonary hypoplasia- incompatible with life
There is a failure of your extra embryonic gut to
return to your abdominal cavity with your abdominal wall closed
OMPHALOCELE: Abdominal musculature;
membranous sac
There is an incomplete closure of abdominal
musculature. Your GI organs are protruding to a
membrane sac.
Omphalocele
Omphalocele: Usually to the _____side of your umbilicus
RIGHT
Herniates into the _______ can be
surgically repaired
ventral membranous sac
All layers of the abdominal wall are not perfectly
developed. Hence, we can see the protrusions of all
the peritoneal organs.
GASTROSCHISIS
similar to omphalocele except that it
involves all the layers of the abdominal wall, from the
peritoneum to the skin, is usually limited to the
intestine, and occurs as an isolated defect without
other abnormalities
GASTROSCHISIS
The incidence of gastroschisis is rising, possibly due
to environmental factors including
smoking and
exposure to agricultural chemicals.
Ectopia means normal cells in abnormal locations.
Ectopia
involves your gastric secreting cells
that are seen in your distal esophagus and proximal
duodenum and may cause ulcerations and disorders
due to their presence in an abnormal location
Gastric ectopia
While generally asymptomatic, acid released by gastric
mucosa within the esophagus can result in
dysphagia, esophagitis, Barrett esophagus, or,
rarely, adenocarcinoma
The most frequent site of ectopic gastric mucosa is
the upper third of the esophagus, where it is referred to as an
Inlet patch
small patches of ectopic gastric mucosa in the small bowel or colon, may present with occult blood loss due to peptic ulceration of
adjacent mucosa.
Gastric heterotopia
Gastric tissues may be seen in small intestines.
gastric ectopia
May be seen in proximal
and distal stomach; May produce symptoms
similar to gastritis because they are on a
different location
pancreatic ectopia
Outpouching of your GIT with a lumen and ends up
as a blind pouch
MECKEL DIVERTICULUM
Meckel diverticulum occurs in the
ileum
Meckel diverticulum occurs due to failed involution of the
vitelline duct
which connects the lumen of the developing gut to
the yolk sac.
MD rule of 2’s
○ Presentation before the age of 2 ○ 2x more common in males ○ 2% of the population ○ 2 feet of the ileocecal valve (60 cm) ○ 2 inches in length (5 cm) ○ 2 types of mucosa
T or F
In MD, Histologically all layers are complete (mucosa, submucosa, muscularis, serosa)
T
Pyloric stenosis Can be congenital or acquired and are associated
with some genetic abnormalities such as your
Turner syndrome and Trisomy 18.
studies have
shown that mothers who have ___________ exposure, either orally or via
mother’s milk, in the first 2 weeks of life are
associated with pyloric stenosis
erythromycin or
azithromycin
The most common congenital form is _______pyloric stenosis.
congenital hypertrophic
PS
Presents between the_______ as new-onset regurgitation, projectile,
non-bilious vomiting after feeding
3rd - 6th week of
life
PS: PE
firm, ovoid, 1-2 cm
abdominal mass and
hyperperistalsis
PS diagnosis
Ultrasonography
○ Occurs in adults as a consequence of antral gastritis or peptic ulcers close to the pylorus. ○ Carcinomas of the distal stomach and pancreas may also narrow the pyloric channel due to fibrosis or malignant infiltration
Pyloric stenosis
Aka Congenital Aganglionic Megacolon
HIRSCHSPRUNG DISEASE
causes functional obstruction
of the colon due to failure of ganglion cells to migrate to the wall of the colon resulting from a mutation in the receptor tyrosine kinase
HIRSCHSPRUNG DISEASE
10% of all cases occur in children with
Down syndrome
are present in 5% of infants with Hirschsprung
disease.
serious neurologic abnormalities
Hirschsprung dse pathogenesis
The enteric neuronal plexus develops from neural crest cells that migrate into the bowel wall during
embryogenesis.
Hirschsprung disease results when the migration
of neural crest cells from cecum to rectum is
arrested
prematurely or when the ganglion cells undergo
premature death.
lacks
both the Meissner submucosal and the
Auerbach myenteric plexus
aganglionosis
Heterozygous loss-of-function mutations in the
_________ account for the
majority of familial and approximately 15% of
sporadic Hirschsprung disease cases
receptor tyrosine kinase RET
The primary mode of treatment in Hirschsprung dse
surgical resection
of the aganglionic segment.
T or F
If meconium does not pass, confirmed through
biopsy by getting a portion of the segment and is
examined histologically if there is loss of meissner’s
plexus or auerbach’s plexus.
T
Diagnosis of Hirschsprung disease requires
histologic confirmation that
ganglion cells are
absent within the affected segment.
Disease limited to the rectosigmoid is termed
short-segment Hirschsprung disease
e cases with
more proximal extension are termed
long-segment
Hirschsprung disease.
- you cannot
anymore see the ganglion cells. Ganglion cells
can be identified using immunohistochemical
stains for acetylcholinesterase.
Congenital Hypoganglionosis
- previously normal
ganglion cells but somehow there is destruction
such as in Chagas disease or Inflammatory bowel
disease
Acquired Hypoganglionosis
typically presents with a
failure to pass meconium in the immediate postnatal
period.
Hirschsprung disease
HD The major threats to life are
enterocolitis, fluid and
electrolyte disturbances, perforation, and peritonitis.
In contrast to the congenital megacolon of
Hirschsprung disease, acquired megacolon may
occur at any age as a result of
Chagas disease,
obstruction by a neoplasm or inflammatory stricture,
a complication of ulcerative colitis, visceral
myopathy, or in association with psychosomatic
disorders.
● Signs and symptoms of esophageal pathology:
○ Heartburn- most common, (GERD) ○ Dysphagia is usually progressive from solid to liquid ○ Dysphagia for solids (Obstructive lesion) ○ Lower esophageal dysphagia (Smooth muscle dysmotility or problems with sphincters)
● The esophagus develops from the
cranial portion of the foregut
Esophagus is recognizable by the
3rd week of gestation
Functional obstruction of the esophagus by
intense, high amplitude, uncoordinated
contractions of inner circular and outer
longitudinal smooth muscle
● Nutcracker Esophagus
Also known as corkscrew esophagus due to
the appearance of barium swallow, it is
characterized by repetitive, simultaneous
contractions of the distal esophageal smooth
muscle.
● Diffuse Esophageal Spasm
Unlike nutcracker esophagus, these
contractions are of normal amplitude
include high resting pressure or incomplete
relaxation, may be present as an isolated
anomaly or accompany nutcracker esophagus
or diffuse esophageal spasm.
● Hypertensive Lower Esophageal Sphincter
Because wall stress is increased, esophageal
dysmotility may result in development of small
diverticula, particularly in the epiphrenic region
immediately above the lower esophageal
sphincter.
Zenker Diverticulum: cricopharyngeus muscle;
upper esophageal sphincter
Similarly, impaired relaxation and spasm of the
cricopharyngeus muscle after swallowing can
result in increased pressure within the distal
pharynx and development of a
Zenker
(pharyngoesophageal) diverticulum,
Generally caused by fibrous thickening of the
submucosa and is associated with atrophy of
the muscularis propria and secondary
epithelial damage
● Benign esophageal stenosis
Uncommon ledge-like mucosal protrusions.
mucosal weebs
mucosal weebs usually occur in
women older than age
40 and may be associated with
gastroesophageal reflux, chronic graft-versushost disease, or blistering skin diseases
In the upper esophagus, webs may be
accompanied by
iron-deficiency anemia,
glossitis, and cheilosis as part of the PatersonBrown-Kelly or Plummer-Vinson syndrome
Similar to webs but are circumferential, are
thicker, and include mucosa, submucosa, and
occasionally hypertrophic muscularis propria.
● Schatzki rings or Esophageal rings
a rings
squamous above GEJ
B rings
squamo-columnar, gastric glands
below GEJ
these are
outpouchings that involve all three layers of the
esophagus. The location is in the upper esophagus,
and the complication includes the halitosis as well
and this can be corrected through surgical
interventions
Zenker’s diverticulum
Increased tone of the lower esophageal sphincter
(LES), as a result of impaired smooth muscle
relaxation, is an important cause of esophageal
obstruction.
ACHALASIA
achalasia triad
○ Incomplete LES relaxation
○ Increased LES tone
○ Aperistalsis
achalasia symptoms
dysphagia, difficulty in belching, chestpain
These involve manometric studies of the esophagus.
The cause of this condition might be Primary which
is the result from degeneration of neurons that produce relaxation
Achalasia
manometric studies
- idiopathic, failure of distal
esophageal inhibitory neurons (ganglion cell
degeneration).
Primary Achalasia
What chemical causes relaxation of your
muscles? /What is not produced by your
neuronal cells?
■ NITROUS OXIDE (Laughing gas) ● Produced by your neuronal cells on the Primary Achalasia ● Causes relaxation of the sphincter tone
No produced nitrous oxide =
Increase
sphincter tone, and hence that causes
the triad.
may arise from Chagas
disease caused by Trypanosoma cruzi
leading to destruction or myenteric plexus.
Duodenal, colonic, and ureteric plexus can
also be affected
Secondary Achalasia
ESOPHAGEAL OBSTRUCTION
Nutcracker esophagus Diffuse Esophageal Spasm Hypertensive Lower Esophageal Sphincter Zenker Diverticulum: Mucosal webs Schatzki rings or Esophageal rings
Longitudinal mucosal tears near the gastroesophageal junction, called
● Mallory-Weiss tears/ Lacerations
most often associated with
severe retching or vomiting secondary to acute
alcohol intoxication
● Mallory-Weiss tears/ Lacerations
The roughly linear lacerations of Mallory-Weiss syndrome are oriented
longitudinally
is much less common
but far more serious and is characterized by
transmural tearing and rupture of the distal
esophagus
Boerhaave syndrome
diff diagnosis boerhaave syndrome
Myocardial infarction
Chemical injury
Symptoms range from self-limited pain, particularly on swallowing,
called odynophagia
Less severe chemical injury to the esophageal
mucosa can occur when medicinal pills lodge
and dissolve in the esophagus.
● Pill-induced esophagitis
■ More common
■ Pediatric or ICH patients
■ Other fungi – Aspergillus and Mucor spp. (fatter hyphae, larger angulations)
○ Candida albicans
● Reflux (backflow) of gastric contents into the lower esophagus.
REFLUX ESOPHAGITIS
occurs because the esophageal
epithelium is sensitive to acid despite
being resistant to abrasive injury.
● GERD
This relaxation is mediated via vagal pathways and can be triggered by gastric distention
transient LES relaxation
Other conditions associated with GERD:
■ alcohol and tobacco use ■ obesity ■ CNS depressants ■ pregnancy ■ hiatal hernia ■ delayed gastric emptying ■ increased gastric volume
is a form of acute eosinophil- dominated
esophageal inflammation associated with atopic
disease.
EOSINOPHILIC ESOPHAGITIS
dilated veins within the
lower esophagus. Although most small varices never bleed, rupture of large varices can result in exsanguination
Esophageal varices
○ Esophageal varices are caused by portal
hypertension, which is due to impaired
blood flow through the
portal venous
system and liver.
common in patients with cirrhosis
VARICES
is the second most common
cause of varices.
● Hepatic schistosomiasis (infection of
Schistosoma)
is an emergency that can be treated medically by inducing splanchnic
vasoconstriction or endoscopically by sclerotherapy,
balloon tamponade, or variceal ligation.
Variceal hemorrhage
● Risk factors for hemorrhage include
e large or tortuous
varices, elevated hepatic venous pressure gradient,
previous bleeding, and advanced liver disease.
A complication of chronic GERD characterized by
intestinal metaplasia with esophageal squamous
mucosa. (more common)
BARRETT ESOPHAGUS
Increased risk for esophageal adenocarcinoma.
BARRETT ESOPHAGUS
● From Stratified squamous lining (lower esophagus)
to Columnar epithelium.
barrett esophagus
● Precursor lesion to Esophageal Adenocarcinoma
BARRETT ESOPHAGUS
The vast majority of esophageal cancers fall into one of
two types:
● Adenocarcinoma
● Squamous Cell Carcinoma
Benign tumors of the esophagus are generally
mesenchymal
pathogenesis barrett esophagus
● Molecular studies suggest that the progression of
Barrett esophagus to adenocarcinoma occurs over an extended period through the stepwise acquisition of genetic and epigenetic changes
ADENOCARCINOMA
CLINICAL FEATURES
● Pain or difficulty in swallowing
● Progressive weight loss from your solids then they
progress to having difficulty swallowing even liquids
because of mass effect that is seen in lower
esophagus
● Hematemesis
● Chest pain
● Vomiting
● Overall survival rate: <5% in 5 years (high mortality
rate).
● By the time symptoms appear, the tumor has usually
spread to submucosal lymphatic vessels
