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

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2
Q

Congenital abnormalities

A
Atresia, Fistula, Duplications
Diaphragmatic hernia, Omphalocele, Gastroschisis
Ectopia
Meckel diverticulum
Pyloric stenosis
Hirschsprung dse
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3
Q

failure of organ development due to
absence of primordial tissues/cells; extremely
rare

A

Agenesis

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4
Q

○ Incomplete development or canalisation

A

Atresia

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5
Q

Atresia is commonly seen in the anatomical landmark of

A

tracheal bifurcation with the use of

barium swallow

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6
Q

a connection between the upper or lower pouch of the esophagus to a bronchus or the trachea

A

Fistula

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7
Q

T or F

Tubular structures are canals sometimes they
could be stenotic (usually absence of the
canal)

A

T

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8
Q

a thin, non canalized
cord replaces a segment of esophagus,
causing a mechanical obstruction

A

esophageal atresia

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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

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10
Q

T or F

Stenosis can result in either partial or complete obstruction

A

T

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11
Q

most commonly involved part in stenosis

A

esophagus or small intestines

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12
Q

The anus is not patent
most common example of congenital intestinal
atresia (duodenum)

A

Imperforate anus

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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

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14
Q

DIAPHRAGMATIC HERNIA

Most commonly occur on the

A

Left side

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15
Q

Diaphragmatic hernia, When severe, the space-filling effect of the displaced
viscera can cause

A

Pulmonary hypoplasia- incompatible with life

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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

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17
Q

There is an incomplete closure of abdominal
musculature. Your GI organs are protruding to a
membrane sac.

A

Omphalocele

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18
Q

Omphalocele: Usually to the _____side of your umbilicus

A

RIGHT

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19
Q

Herniates into the _______ can be

surgically repaired

A

ventral membranous sac

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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

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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

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22
Q

The incidence of gastroschisis is rising, possibly due

to environmental factors including

A

smoking and

exposure to agricultural chemicals.

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23
Q

Ectopia means normal cells in abnormal locations.

A

Ectopia

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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

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25
Q

While generally asymptomatic, acid released by gastric

mucosa within the esophagus can result in

A

dysphagia, esophagitis, Barrett esophagus, or,

rarely, adenocarcinoma

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26
Q

The most frequent site of ectopic gastric mucosa is

the upper third of the esophagus, where it is referred to as an

A

Inlet patch

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27
Q

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.

A

Gastric heterotopia

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28
Q

Gastric tissues may be seen in small intestines.

A

gastric ectopia

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29
Q

May be seen in proximal
and distal stomach; May produce symptoms
similar to gastritis because they are on a
different location

A

pancreatic ectopia

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30
Q

Outpouching of your GIT with a lumen and ends up

as a blind pouch

A

MECKEL DIVERTICULUM

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31
Q

Meckel diverticulum occurs in the

A

ileum

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32
Q

Meckel diverticulum occurs due to failed involution of the

A

vitelline duct

which connects the lumen of the developing gut to
the yolk sac.

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33
Q

MD rule of 2’s

A
○ 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
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34
Q

T or F

In MD, Histologically all layers are complete (mucosa, submucosa, muscularis, serosa)

A

T

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35
Q

Pyloric stenosis Can be congenital or acquired and are associated
with some genetic abnormalities such as your

A

Turner syndrome and Trisomy 18.

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36
Q

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

A

erythromycin or

azithromycin

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37
Q

The most common congenital form is _______pyloric stenosis.

A

congenital hypertrophic

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38
Q

PS
Presents between the_______ as new-onset regurgitation, projectile,
non-bilious vomiting after feeding

A

3rd - 6th week of

life

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39
Q

PS: PE

A

firm, ovoid, 1-2 cm
abdominal mass and
hyperperistalsis

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40
Q

PS diagnosis

A

Ultrasonography

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41
Q
○ 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
A

Pyloric stenosis

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42
Q

Aka Congenital Aganglionic Megacolon

A

HIRSCHSPRUNG DISEASE

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43
Q

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

A

HIRSCHSPRUNG DISEASE

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44
Q

10% of all cases occur in children with

A

Down syndrome

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45
Q

are present in 5% of infants with Hirschsprung

disease.

A

serious neurologic abnormalities

46
Q

Hirschsprung dse pathogenesis

A

The enteric neuronal plexus develops from neural crest cells that migrate into the bowel wall during
embryogenesis.

47
Q

Hirschsprung disease results when the migration

of neural crest cells from cecum to rectum is

A

arrested
prematurely or when the ganglion cells undergo
premature death.

48
Q

lacks
both the Meissner submucosal and the
Auerbach myenteric plexus

A

aganglionosis

49
Q

Heterozygous loss-of-function mutations in the
_________ account for the
majority of familial and approximately 15% of
sporadic Hirschsprung disease cases

A

receptor tyrosine kinase RET

50
Q

The primary mode of treatment in Hirschsprung dse

A

surgical resection

of the aganglionic segment.

51
Q

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.

A

T

52
Q

Diagnosis of Hirschsprung disease requires

histologic confirmation that

A

ganglion cells are

absent within the affected segment.

53
Q

Disease limited to the rectosigmoid is termed

A

short-segment Hirschsprung disease

54
Q

e cases with

more proximal extension are termed

A

long-segment

Hirschsprung disease.

55
Q
  • you cannot
    anymore see the ganglion cells. Ganglion cells
    can be identified using immunohistochemical
    stains for acetylcholinesterase.
A

Congenital Hypoganglionosis

56
Q
  • previously normal
    ganglion cells but somehow there is destruction
    such as in Chagas disease or Inflammatory bowel
    disease
A

Acquired Hypoganglionosis

57
Q

typically presents with a
failure to pass meconium in the immediate postnatal
period.

A

Hirschsprung disease

58
Q

HD The major threats to life are

A

enterocolitis, fluid and

electrolyte disturbances, perforation, and peritonitis.

59
Q

In contrast to the congenital megacolon of
Hirschsprung disease, acquired megacolon may
occur at any age as a result of

A

Chagas disease,
obstruction by a neoplasm or inflammatory stricture,
a complication of ulcerative colitis, visceral
myopathy, or in association with psychosomatic
disorders.

60
Q

● Signs and symptoms of esophageal pathology:

A
○ 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
Q

● The esophagus develops from the

A

cranial portion of the foregut

62
Q

Esophagus is recognizable by the

A

3rd week of gestation

63
Q

Functional obstruction of the esophagus by
intense, high amplitude, uncoordinated
contractions of inner circular and outer
longitudinal smooth muscle

A

● Nutcracker Esophagus

64
Q

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.

A

● Diffuse Esophageal Spasm

Unlike nutcracker esophagus, these
contractions are of normal amplitude

65
Q

include high resting pressure or incomplete
relaxation, may be present as an isolated
anomaly or accompany nutcracker esophagus
or diffuse esophageal spasm.

A

● Hypertensive Lower Esophageal Sphincter

66
Q

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.

A

Zenker Diverticulum: cricopharyngeus muscle;

upper esophageal sphincter

67
Q

Similarly, impaired relaxation and spasm of the
cricopharyngeus muscle after swallowing can
result in increased pressure within the distal
pharynx and development of a

A

Zenker

(pharyngoesophageal) diverticulum,

68
Q

Generally caused by fibrous thickening of the
submucosa and is associated with atrophy of
the muscularis propria and secondary
epithelial damage

A

● Benign esophageal stenosis

69
Q

Uncommon ledge-like mucosal protrusions.

A

mucosal weebs

70
Q

mucosal weebs usually occur in

A

women older than age
40 and may be associated with
gastroesophageal reflux, chronic graft-versushost disease, or blistering skin diseases

71
Q

In the upper esophagus, webs may be

accompanied by

A

iron-deficiency anemia,

glossitis, and cheilosis as part of the PatersonBrown-Kelly or Plummer-Vinson syndrome

72
Q

Similar to webs but are circumferential, are
thicker, and include mucosa, submucosa, and
occasionally hypertrophic muscularis propria.

A

● Schatzki rings or Esophageal rings

73
Q

a rings

A

squamous above GEJ

74
Q

B rings

A

squamo-columnar, gastric glands

below GEJ

75
Q

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

A

Zenker’s diverticulum

76
Q

Increased tone of the lower esophageal sphincter
(LES), as a result of impaired smooth muscle
relaxation, is an important cause of esophageal
obstruction.

A

ACHALASIA

77
Q

achalasia triad

A

○ Incomplete LES relaxation
○ Increased LES tone
○ Aperistalsis

78
Q

achalasia symptoms

A

dysphagia, difficulty in belching, chestpain

79
Q

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

A

Achalasia

manometric studies

80
Q
  • idiopathic, failure of distal
    esophageal inhibitory neurons (ganglion cell
    degeneration).
A

Primary Achalasia

81
Q

What chemical causes relaxation of your
muscles? /What is not produced by your
neuronal cells?

A
■ NITROUS OXIDE (Laughing 
gas) 
● Produced by your 
neuronal cells on the 
Primary Achalasia
● Causes relaxation of the 
sphincter tone
82
Q

No produced nitrous oxide =

A

Increase
sphincter tone, and hence that causes
the triad.

83
Q

may arise from Chagas
disease caused by Trypanosoma cruzi
leading to destruction or myenteric plexus.
Duodenal, colonic, and ureteric plexus can
also be affected

A

Secondary Achalasia

84
Q

ESOPHAGEAL OBSTRUCTION

A
Nutcracker esophagus
Diffuse Esophageal Spasm 
Hypertensive Lower Esophageal Sphincter
Zenker Diverticulum:
Mucosal webs
Schatzki rings or Esophageal rings
85
Q

Longitudinal mucosal tears near the gastroesophageal junction, called

A

● Mallory-Weiss tears/ Lacerations

86
Q

most often associated with
severe retching or vomiting secondary to acute
alcohol intoxication

A

● Mallory-Weiss tears/ Lacerations

87
Q

The roughly linear lacerations of Mallory-Weiss syndrome are oriented

A

longitudinally

88
Q

is much less common
but far more serious and is characterized by
transmural tearing and rupture of the distal
esophagus

A

Boerhaave syndrome

89
Q

diff diagnosis boerhaave syndrome

A

Myocardial infarction

90
Q

Chemical injury

Symptoms range from self-limited pain, particularly on swallowing,

A

called odynophagia

91
Q

Less severe chemical injury to the esophageal
mucosa can occur when medicinal pills lodge
and dissolve in the esophagus.

A

● Pill-induced esophagitis

92
Q

■ More common
■ Pediatric or ICH patients
■ Other fungi – Aspergillus and Mucor spp. (fatter hyphae, larger angulations)

A

○ Candida albicans

93
Q

● Reflux (backflow) of gastric contents into the lower esophagus.

A

REFLUX ESOPHAGITIS

94
Q

occurs because the esophageal
epithelium is sensitive to acid despite
being resistant to abrasive injury.

A

● GERD

95
Q

This relaxation is mediated via vagal pathways and can be triggered by gastric distention

A

transient LES relaxation

96
Q

Other conditions associated with GERD:

A
■ alcohol and tobacco use
■ obesity
■ CNS depressants 
■ pregnancy
■ hiatal hernia
■ delayed gastric emptying
■ increased gastric volume
97
Q

is a form of acute eosinophil- dominated
esophageal inflammation associated with atopic
disease.

A

EOSINOPHILIC ESOPHAGITIS

98
Q

dilated veins within the

lower esophagus. Although most small varices never bleed, rupture of large varices can result in exsanguination

A

Esophageal varices

99
Q

○ Esophageal varices are caused by portal
hypertension, which is due to impaired
blood flow through the

A

portal venous

system and liver.

100
Q

common in patients with cirrhosis

A

VARICES

101
Q

is the second most common

cause of varices.

A

● Hepatic schistosomiasis (infection of

Schistosoma)

102
Q

is an emergency that can be treated medically by inducing splanchnic
vasoconstriction or endoscopically by sclerotherapy,
balloon tamponade, or variceal ligation.

A

Variceal hemorrhage

103
Q

● Risk factors for hemorrhage include

A

e large or tortuous
varices, elevated hepatic venous pressure gradient,
previous bleeding, and advanced liver disease.

104
Q

A complication of chronic GERD characterized by
intestinal metaplasia with esophageal squamous
mucosa. (more common)

A

BARRETT ESOPHAGUS

105
Q

Increased risk for esophageal adenocarcinoma.

A

BARRETT ESOPHAGUS

106
Q

● From Stratified squamous lining (lower esophagus)

to Columnar epithelium.

A

barrett esophagus

107
Q

● Precursor lesion to Esophageal Adenocarcinoma

A

BARRETT ESOPHAGUS

108
Q

The vast majority of esophageal cancers fall into one of

two types:

A

● Adenocarcinoma

● Squamous Cell Carcinoma

109
Q

Benign tumors of the esophagus are generally

A

mesenchymal

110
Q

pathogenesis barrett esophagus

A

● 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
Q

ADENOCARCINOMA

CLINICAL FEATURES

A

● 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