GIT 1 Flashcards
1
Q
T or F
Congenital abnormalities, When present within esophagus, they are
discovered shortly after birth, usually due to
A
regurgitation during feeding; Without surgical intervention, these are incompatible with life
2
Q
Congenital abnormalities
A
Atresia, Fistula, Duplications Diaphragmatic hernia, Omphalocele, Gastroschisis Ectopia Meckel diverticulum Pyloric stenosis Hirschsprung dse
3
Q
failure of organ development due to
absence of primordial tissues/cells; extremely
rare
A
Agenesis
4
Q
○ Incomplete development or canalisation
A
Atresia
5
Q
Atresia is commonly seen in the anatomical landmark of
A
tracheal bifurcation with the use of
barium swallow
6
Q
a connection between the upper or lower pouch of the esophagus to a bronchus or the trachea
A
Fistula
7
Q
T or F
Tubular structures are canals sometimes they
could be stenotic (usually absence of the
canal)
A
T
8
Q
a thin, non canalized
cord replaces a segment of esophagus,
causing a mechanical obstruction
A
esophageal atresia
9
Q
Incomplete forms of atresia in which the lumen is
markedly reduced. In caliber, as a result of fibers
thickening of the wall.
A
STENOSIS
10
Q
T or F
Stenosis can result in either partial or complete obstruction
A
T
11
Q
most commonly involved part in stenosis
A
esophagus or small intestines
12
Q
The anus is not patent
most common example of congenital intestinal
atresia (duodenum)
A
Imperforate anus
13
Q
occurs when there’s
incomplete formation of the diaphragm and sections
of your GIT, allowing the abdominal viscera to
herniate into the thoracic cavity.
A
DIAPHRAGMATIC HERNIA
14
Q
DIAPHRAGMATIC HERNIA
Most commonly occur on the
A
Left side
15
Q
Diaphragmatic hernia, When severe, the space-filling effect of the displaced
viscera can cause
A
Pulmonary hypoplasia- incompatible with life
16
Q
There is a failure of your extra embryonic gut to
return to your abdominal cavity with your abdominal wall closed
A
OMPHALOCELE: Abdominal musculature;
membranous sac
17
Q
There is an incomplete closure of abdominal
musculature. Your GI organs are protruding to a
membrane sac.
A
Omphalocele
18
Q
Omphalocele: Usually to the _____side of your umbilicus
A
RIGHT
19
Q
Herniates into the _______ can be
surgically repaired
A
ventral membranous sac
20
Q
All layers of the abdominal wall are not perfectly
developed. Hence, we can see the protrusions of all
the peritoneal organs.
A
GASTROSCHISIS
21
Q
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
A
GASTROSCHISIS
22
Q
The incidence of gastroschisis is rising, possibly due
to environmental factors including
A
smoking and
exposure to agricultural chemicals.
23
Q
Ectopia means normal cells in abnormal locations.
A
Ectopia
24
Q
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
A
Gastric ectopia
25
While generally asymptomatic, acid released by gastric
| mucosa within the esophagus can result in
dysphagia, esophagitis, Barrett esophagus, or,
| rarely, adenocarcinoma
26
The most frequent site of ectopic gastric mucosa is
| the upper third of the esophagus, where it is referred to as an
Inlet patch
27
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
28
Gastric tissues may be seen in small intestines.
gastric ectopia
29
May be seen in proximal
and distal stomach; May produce symptoms
similar to gastritis because they are on a
different location
pancreatic ectopia
30
Outpouching of your GIT with a lumen and ends up
| as a blind pouch
MECKEL DIVERTICULUM
31
Meckel diverticulum occurs in the
ileum
32
Meckel diverticulum occurs due to failed involution of the
vitelline duct
which connects the lumen of the developing gut to
the yolk sac.
33
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
```
34
T or F
| In MD, Histologically all layers are complete (mucosa, submucosa, muscularis, serosa)
T
35
Pyloric stenosis Can be congenital or acquired and are associated
with some genetic abnormalities such as your
Turner syndrome and Trisomy 18.
36
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
37
The most common congenital form is _______pyloric stenosis.
congenital hypertrophic
38
PS
Presents between the_______ as new-onset regurgitation, projectile,
non-bilious vomiting after feeding
3rd - 6th week of
| life
39
PS: PE
firm, ovoid, 1-2 cm
abdominal mass and
hyperperistalsis
40
PS diagnosis
Ultrasonography
41
```
○ 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
42
Aka Congenital Aganglionic Megacolon
HIRSCHSPRUNG DISEASE
43
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
44
10% of all cases occur in children with
Down syndrome
45
are present in 5% of infants with Hirschsprung
| disease.
serious neurologic abnormalities
46
Hirschsprung dse pathogenesis
The enteric neuronal plexus develops from neural crest cells that migrate into the bowel wall during
embryogenesis.
47
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.
48
lacks
both the Meissner submucosal and the
Auerbach myenteric plexus
aganglionosis
49
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
50
The primary mode of treatment in Hirschsprung dse
surgical resection
| of the aganglionic segment.
51
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
52
Diagnosis of Hirschsprung disease requires
| histologic confirmation that
ganglion cells are
| absent within the affected segment.
53
Disease limited to the rectosigmoid is termed
short-segment Hirschsprung disease
54
e cases with
| more proximal extension are termed
long-segment
| Hirschsprung disease.
55
- you cannot
anymore see the ganglion cells. Ganglion cells
can be identified using immunohistochemical
stains for acetylcholinesterase.
Congenital Hypoganglionosis
56
- previously normal
ganglion cells but somehow there is destruction
such as in Chagas disease or Inflammatory bowel
disease
Acquired Hypoganglionosis
57
typically presents with a
failure to pass meconium in the immediate postnatal
period.
Hirschsprung disease
58
HD The major threats to life are
enterocolitis, fluid and
| electrolyte disturbances, perforation, and peritonitis.
59
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.
60
● 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)
```
61
● The esophagus develops from the
cranial portion of the foregut
62
Esophagus is recognizable by the
3rd week of gestation
63
Functional obstruction of the esophagus by
intense, high amplitude, uncoordinated
contractions of inner circular and outer
longitudinal smooth muscle
● Nutcracker Esophagus
64
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
65
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
66
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
67
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,
68
Generally caused by fibrous thickening of the
submucosa and is associated with atrophy of
the muscularis propria and secondary
epithelial damage
● Benign esophageal stenosis
69
Uncommon ledge-like mucosal protrusions.
mucosal weebs
70
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
71
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
72
Similar to webs but are circumferential, are
thicker, and include mucosa, submucosa, and
occasionally hypertrophic muscularis propria.
● Schatzki rings or Esophageal rings
73
a rings
squamous above GEJ
74
B rings
squamo-columnar, gastric glands
| below GEJ
75
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
76
Increased tone of the lower esophageal sphincter
(LES), as a result of impaired smooth muscle
relaxation, is an important cause of esophageal
obstruction.
ACHALASIA
77
achalasia triad
○ Incomplete LES relaxation
○ Increased LES tone
○ Aperistalsis
78
achalasia symptoms
dysphagia, difficulty in belching, chestpain
79
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
80
- idiopathic, failure of distal
esophageal inhibitory neurons (ganglion cell
degeneration).
Primary Achalasia
81
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
```
82
No produced nitrous oxide =
Increase
sphincter tone, and hence that causes
the triad.
83
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
84
ESOPHAGEAL OBSTRUCTION
```
Nutcracker esophagus
Diffuse Esophageal Spasm
Hypertensive Lower Esophageal Sphincter
Zenker Diverticulum:
Mucosal webs
Schatzki rings or Esophageal rings
```
85
Longitudinal mucosal tears near the gastroesophageal junction, called
● Mallory-Weiss tears/ Lacerations
86
most often associated with
severe retching or vomiting secondary to acute
alcohol intoxication
● Mallory-Weiss tears/ Lacerations
87
The roughly linear lacerations of Mallory-Weiss syndrome are oriented
longitudinally
88
is much less common
but far more serious and is characterized by
transmural tearing and rupture of the distal
esophagus
Boerhaave syndrome
89
diff diagnosis boerhaave syndrome
Myocardial infarction
90
Chemical injury
| Symptoms range from self-limited pain, particularly on swallowing,
called odynophagia
91
Less severe chemical injury to the esophageal
mucosa can occur when medicinal pills lodge
and dissolve in the esophagus.
● Pill-induced esophagitis
92
■ More common
■ Pediatric or ICH patients
■ Other fungi – Aspergillus and Mucor spp. (fatter hyphae, larger angulations)
○ Candida albicans
93
● Reflux (backflow) of gastric contents into the lower esophagus.
REFLUX ESOPHAGITIS
94
occurs because the esophageal
epithelium is sensitive to acid despite
being resistant to abrasive injury.
● GERD
95
This relaxation is mediated via vagal pathways and can be triggered by gastric distention
transient LES relaxation
96
Other conditions associated with GERD:
```
■ alcohol and tobacco use
■ obesity
■ CNS depressants
■ pregnancy
■ hiatal hernia
■ delayed gastric emptying
■ increased gastric volume
```
97
is a form of acute eosinophil- dominated
esophageal inflammation associated with atopic
disease.
EOSINOPHILIC ESOPHAGITIS
98
dilated veins within the
| lower esophagus. Although most small varices never bleed, rupture of large varices can result in exsanguination
Esophageal varices
99
○ Esophageal varices are caused by portal
hypertension, which is due to impaired
blood flow through the
portal venous
| system and liver.
100
common in patients with cirrhosis
VARICES
101
is the second most common
| cause of varices.
● Hepatic schistosomiasis (infection of
| Schistosoma)
102
is an emergency that can be treated medically by inducing splanchnic
vasoconstriction or endoscopically by sclerotherapy,
balloon tamponade, or variceal ligation.
Variceal hemorrhage
103
● Risk factors for hemorrhage include
e large or tortuous
varices, elevated hepatic venous pressure gradient,
previous bleeding, and advanced liver disease.
104
A complication of chronic GERD characterized by
intestinal metaplasia with esophageal squamous
mucosa. (more common)
BARRETT ESOPHAGUS
105
Increased risk for esophageal adenocarcinoma.
BARRETT ESOPHAGUS
106
● From Stratified squamous lining (lower esophagus)
| to Columnar epithelium.
barrett esophagus
107
● Precursor lesion to Esophageal Adenocarcinoma
BARRETT ESOPHAGUS
108
The vast majority of esophageal cancers fall into one of
| two types:
● Adenocarcinoma
| ● Squamous Cell Carcinoma
109
Benign tumors of the esophagus are generally
mesenchymal
110
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
111
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
