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GI-II, Exam 1 > 11-19 Pathology of the GI Tract (Hertz) - SRS > Flashcards

11-19 Pathology of the GI Tract (Hertz) - SRS Flashcards

1
Q

Why is there off-white and reddish tan colors to these tissues?

A

Esophagus is tan due to it being squamous epithelium

Stomach is glandular epithelium

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2
Q

What anomoly is this?

A

Duplication of the esophagus

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3
Q

What can you discern from this image? Hx includes a neonate presenting with coughing and difficulty feeding.

A

Baby has a tracheoesophageal fistula

Catheter was inserted into the stomach and dye was injected, revealing connection between trachea and esophagus

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4
Q

Describe the structures of tracheoesophageal fistulas.

A

A - blind upper and lower esophagus with thin cord of CT linking the 2 segments

B - Blind upper segment with fistula between lower segment and trachea

C - Fistula without atresia between patient esophagus and trachea

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5
Q

Which is the most common, A, B or C?

A

B

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6
Q

Describe the patient presentations associated with A, B and C pictured below.

A

A - fussy baby with projectile vomiting

B - fussy baby that spits up food, will develop pneumonia a few days after birth due to aspirating stomach contents into trachea and lungs

C - baby that develops an aspiration pnuemonia

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7
Q

Name and describe the findings on this film:

A

Diaphragmatic hernia

  • congenital anomoly of the diaphragm that allows GI tract organs to go into thorax cavity and cause atelectasis of the lungs
  • can see intestines and mediastinal shift in the thorax on the right side of the film
  • infant will present with hypoxia
  • surgical emergency
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8
Q

What is this? How is it treated?

A

Omphalocele - developmental anomaly of the GI tract

  • GI organs did not retract properly through anterior body wall in development, still covered with peritoneum
  • surgical emergency, treat immediately
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9
Q

Name this condition, and describe the treatment method:

A

Gastroschisis

  • failure of part of GI tract to retract through anterior body wall during development
  • exposed GI tract is not covered with peritoneum
  • surgical emergency, treat immediately
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10
Q

What is ectopia in regards to tissue?

A

presence of normally formed tissues in an abnormal site

  • common in GI tract
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11
Q

Describe what you see in the attached image of an esophagus. What is your next step in making a Dx?

A

Ectopic gastric mucosa

Punctate lesions in upper third of esophagus

Denuded epithelium with ectopic gastric mucosa

Have to biopsy this lesion

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12
Q

What’s this? Where is it?

A

Gastric heterotopia in the small bowel

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13
Q

For a diverticulum to be considered a ‘true’ diverticulum, it has to contain what?

A

All 3 layers have to be present: mucosa, muscularis, and submucosa

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14
Q

What is the most common true diverticulum?

A

The most common true diverticulum is the Meckel diverticulum, which occurs in the ileum

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15
Q

What is the “Rule of 2s” in regards to Meckel Diverticulum?

A

Occur in approximately 2% of the population

Are generally present within 2 feet (60 cm) of the ileocecal valve

Are approximately 2 inches (5 cm) long

Are twice as common in males

Are most often symptomatic by age 2 (only approximately 4% are ever symptomatic)

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16
Q

What’s this?

A

Meckel diverticulum

The blind pouch is located on the antimesenteric side of the small bowel

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17
Q

A male patient presents to you with severe abdominal pain in the RLQ despite having an appendectomy several years ago. You note that he has a Hx of Meckel diverticulum that was discovered during the appendectomy. What do you suspect is causing the pain?

A

Ectopic pancreatic or gastric tissue frequently present in Meckel diverticulum

  • gastric tissue may secrete acid, cause peptic ulceration of adjacent small intestinal mucosa, and present with occult bleeding or abdominal pain resembling acute appendicitis or obstruction
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18
Q

Describe what you see in this image:

A

Meckel diverticulum

  • normal small intestine with ectopic gastric tissue
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19
Q

What population(s) are more at risk for developing pyloric stenosis?

A

Males (3-5x more common)

Turner Syndrome

Trisomy 18 (Edwards syndrome)

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20
Q

What associations should you make with Edwards Syndrome?

A

Trisomy 18

congenital hypertrophic pyloric stenosis

heart defects - VSD and PDA

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21
Q

You have a patient brought to you by a distraught pair of new parents. Their 3 week old baby has recently started to projectile vomit, with emissions a milky (not green) color. The baby is fussy and appears hungry. During the exam, you note an unusual left to right hyperperistalsis when mom attempts to feed the baby, and baby then vomits and hits your attending in the face. What do you suspect for a Dx?

A

Baby has Dx of congenital hypertrophic pyloric stenosis

You probably have schadenfreude

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22
Q

What will congenital hypertrophic pyloric stenosis reveal on physical exam?

A

Physical examination reveals a firm, ovoid, 1 to 2 cm abdominal mass. In some cases abnormal left to right hyperperistalsis is evident during feeding and immediately before vomiting.

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23
Q

What is the presentation for congenital hypertrophic pyloric stenosis?

A

Congenital hypertrophic pyloric stenosis generally presents between the third and sixth weeks of life as new-onset regurgitation, projectile, nonbilious vomiting after feeding, and frequent demands for re-feeding. Physical examination reveals a firm, ovoid, 1 to 2 cm abdominal mass. In some cases abnormal left to right hyperperistalsis is evident during feeding and immediately before vomiting.

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24
Q

What does this US show?

A

again, congenital hypertrophic pyloric stenosis

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25
Q

What is another name for Hirschsprung Disease?

A

congenital aganglionic megacolon

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26
Q

What is the source of the defect in congenital aganglionic megacolon?

Also, what two things are missing?

A

results when the normal migration of neural crest cells from cecum to rectum is arrested prematurely or when the ganglion cells undergo premature death.

This produces a distal intestinal segment that lacks both the Meissner submucosal and the Auerbach myenteric plexus (“aganglionosis”)

(neuronal tracts fail to migrate full from proximal to distal, and stop befor reaching anus)

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27
Q

A distal portion of the colon lacks innervation in congenital aganglionic megacolon. Why does this result in pathology?

A

Coordinated peristaltic contractions are absent and functional obstruction occurs, resulting in dilation proximal to the affected segment

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28
Q

How is Hirschsprung disease visualized?

A

barium enema

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29
Q

What’s this?

A

Hirschsprung disease

A - preoperative barium enema study showing constricted rectum (bottom of the image) and dilated sigmoid colon

B - Corresponding intraoperative photograph showing contricted rectum and dilation of the sigmoid colon

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30
Q

What populations are more likely to have Hirschsprung disease?

A

10% of all cases occur in children with Down syndrome and serious neurologic abnormalities are present in another 5%

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31
Q

What is the typical presentation of Hirschsprung disease?

A

Hirschsprung disease typically presents with a failure to pass meconium in the immediate postnatal period. Obstruction or constipation follows, often with visible, ineffective peristalsis, and may progress to abdominal distention and bilious vomiting.

When only a few centimeters of rectum are involved occasional passage of stool may occur and obscure the diagnosis.

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32
Q

Why is Hirschsprung disease sometimes deadly?

A

The major threats to life are enterocolitis, fluid and electrolyte disturbances, perforation, and peritonitis.

33
Q

What is the treatment for Hirschsprung disease? Is it healed quickly?

A

The primary mode of treatment is surgical resection of the aganglionic segment followed by anastomosis of the normal proximal colon to the rectum. Even after successful surgery, it may take years to attain normal bowel function and continence

34
Q

What does “nutcracker esophagus” refer to?

A

Patients with high amplitude contractions of the distal esophagus that are, in part, d/t loss of normal coordination of the inner circular layer and outer longitudinal layer smooth muscle contractions.

35
Q

What does diffuse esophageal spasm refer to?

A

Repetitive simultaneous contractions of the distal esophageal smooth muscle.

36
Q

Lower esophageal sphincter dysfunction, such as high resting pressure or incomplete relaxation, are present in many patients with nutcracker esophagus or diffuse esophageal spasm. In the absence of altered patterns of esophageal contraction, these sphincter abnormalities are termed?

A

Hypertensive lower esophageal sphincter

37
Q

In esophageal obstruction, because wall stress is increased, esophageal dysmotility may result in development of small diverticulae. Where does this primarily happen?

A

primarily the epiphrenic diverticulum located immediately above the lower esophageal sphincter.

38
Q

What leads to the development of a Zenker diverticulum?

A

Impaired relaxation and spasm of the cricopharyngeus muscle after swallowing leads to increased pressure in the distal pharynx and development of a Zenker diverticulum.

39
Q

Where is a Zenker diverticulum found?

A

AKA Pharyngoesophageal diverticulum.

Located immediately above the upper esophageal sphincter.

40
Q

Zenker diverticulae are uncommon, but typically develop after age 50 and may reach several centimeters in size.

What are some of the symptoms associated with this condition?

A

Small = asymptomatic

Larger = Food accumulation leading to a mass, regurgitation and halitosis.

41
Q

What is shown here?

A

Zenker’s Diverticulum

42
Q

What is this?

A

Schatzki rings

43
Q

What is the difference between A rings and B rings?

A
  • A rings are covered by squamous mucosa
  • B rings are located at the squamocolumnar junction of the lower esophagus and may have gastric cardia-type mucosa on their undersurface.
44
Q

What is shown here?

A

Characteristic “bird’s beak” finding associated with Achalasia.

45
Q

What is the triad that characterizes achalasia?

A
  1. incomplete LES relaxation
  2. Increased LES tone
  3. aperistalsis of the esophagus
46
Q

What are the main symptoms of achalasia? 3

A
  1. dysphagia for solids and liquids
  2. difficulty belching
  3. chest pain
47
Q

What do you see in the attached biopsy?

What can arise as a complication of this?

A

Trypanosoma cruzi infection - Chagas disease

Causes destruction of the myenteric plexus, failure of peristalsis and esophageal dilation.

A cause of secondary achalasia

48
Q

What happens in primary achalasia?

A

The result of distal esophageal inhibitory neuronal (i.e. ganglion cell) degeneration

49
Q

What is shown here?

What is this most often associated wtih?

A

Mallory-Weiss tears: longitudinal mucosal tears near the gastroesophageal junction.

Most often associated with vomiting secondary to acute alcohol intoxication.

50
Q

What is Boerhaave syndrome?

What causes it?

A

Esophageal perforation leading to severe medastinitis.

  1. Trauma
  2. SCC or adenocarcinoma that degrades the esophageal wall
51
Q

The attached image represents the results of chemical (or infectious) esophagitis.

What are some causes of this we should be aware of?

What is the main symptom this patient would complain of?

A

CC: Odynophagia - painful swallowing

  1. ETOH
  2. Heavy smoking
  3. Corrosive acids
  4. Alkalis
  5. Excessively hot fluids
52
Q

What caused this patients Esophagitis?

A

Viral esophagitis caused by HHV - note the multinucleate squamous cells containing herpes virus nuclear and cytoplasmic inclusions.

53
Q

What caused this patients esophagitis?

A

Viral esophagitis caused by CMV - note the present (but shittily depicted) owls eye inclusions.

54
Q

What is depicted here?

What is this?

A

Image shows esophageal pseudomembranes.

Candidiasis

55
Q

What organism should we associate with “punched out” esophageal lesions?

How about linear lesions?

A

Punched out = HHV

Linear = CMV

56
Q

This biopsy was taken from a young child with chest pain and odynophagia. What is this and what most likely caused it?

A

Eosinophilic esophagitis

Typically caused by a milk allergy in kids.

57
Q

What are the common clinical symptoms of GERD?

A

Heartburn

Dysphagia

Regurgitation of sour-tasting gastric contents

Rarely - attacks of severe chest pain

58
Q

Identify each type of hernia shown

A

Left: sliding hiatus hernia

Right: paraesophageal hiatus hernia

59
Q

What is a characteristic of the majority of individuals with eosinophilic esophagitis?

A

Majority of individuals are atopic and many have atopic dermatitis, allergic rhinitis, asthma or modest peripheral eosinophilia.

60
Q

How should the patient these images are from be treated?

A

Eosinophilic esophagitis

  1. Dietary restrictions to prevent exposure to food allergens such as cow’s milk and soy products
  2. Topical or systemic corticosteroids
61
Q

Gastroesophageal varices are present in nearly half of the patients with cirrhosis, and 25-40% of patients with cirrhosis develop variceal bleeding.

Approximately 12% of previously asymptomatic varices bleed each year. Variceal hemorrhage is an emergency that can be treated medically by doing what?

A
  1. Splanchnic vasoconstriction
  2. Endoscopically by sclerotherapy
  3. Balloon tamponade
  4. Variceal ligation
62
Q

What is the general prognosis for esophageal varices?

A

30% or more will die as a direct consequence of hemorrhage such as hypovolemic shock, hepatic coma or other complications.

Further, more than 50% with one episode will have recurrent hemorrhages within a year, each with the same risk of death.

63
Q

What is barret’s esophagus?

What is the big deal with this?

A

Complication of chronic GERD that is characterized by intestinal metaplasia within the esophageal squamous mucosa.

Big deal = Increased risk of esophageal adenocarcinoma

64
Q

What is shown here?

A

Barret’s esophagus - note on gross examination the presence of small islands of residual pale squamous mucosa within the Barrett mucosa

On microscopy there is normal squamous mucosa on the left, and on the right Barrett metaplasia with abundant metaplastic goblet cells.

65
Q

How can a dx of Barret esophagus be made?

A

Only through endoscopy and biopsy.

66
Q

Intramucosal or invasive carcinoma requires therapeutic intervention. What do the treatment options include?

A
  1. Surgical resection
  2. Esophagectomy
  3. Photodynamic therapy
  4. laser ablation
  5. endoscopic mucosectomy
67
Q

How should multifocal high grade dysplasia be treated?

A

Same as intamucosal carcinoma.

If low grade, can get away with frequent monitoring.

If not, then same approaches to this as to intramucosal carcinoma.

68
Q

Identify the two esophageal tumors depicted below.

A

Left: Adenocarcinoma

Right: Squamous cell carcinoma

69
Q

What are the majority of esophageal cancers?

A

Either adenocarcinoma or squamous cell carcinoma

70
Q

Is H. pylori associated with Barretts and adenocarcinoma?

A

No, not really.

71
Q

What are the major chromosomal abnormalities that drive cells to adenocarcinoma?

A

Early Stages - down regulation

  1. TP53
  2. CDKN2A (p16/INK4a)

Late - amplification

  1. EGFR
  2. ERBB2
  3. MET
  4. cyclin D1
  5. Cyclin E
72
Q

Which of these samples stained positive for p53?

What does that tell us about our patients esophageal lesion?

A

Bottom left midly positive

bottom right strongly positive

Accumulation of mutant p53 indicates likelie adenocarcinoma

73
Q

Where is squamous cell carcinoma most frequently found?

A

Mid esophagus - where it commonly causes strictures

74
Q

Though esophageal adenocarcinomas are occasionally discovered in evaluation of GERD or surveillance of Barrett esophagus, what do they more commonly present with?

5

A
  1. Pain
  2. Dysphagia
  3. Weight loss
  4. hematemesis
  5. Vomiting
75
Q

What is the overall prognosis for esophageal adenocarcinoma?

Are there any situations in which this changes?

A

Typically by the time symptoms appear, the tumor has usually spread to submucosal and lymphatic vessels. Consequently, the 5 year survival rate is less than 25%.

In contrast if the adenocarcinoma is limited to the mucosa or submucosa, 5 year survival rates approach 80%.

76
Q

What are some main risk factors for SCC of the esophagus?

A

ETOH

Tobacco

poverty

caustic esophageal injury

achalasia

tylosis

Plummer-Vinson Syndrome

Diets deficient in fruit and vegetables

frequent consumption of very hot beverages

77
Q

The onset of esophageal squamous cell carcinoma is insidious and it most commonly presents with dysphagia, odynophagia (pain on swallowing), or obstruction.

How do patients respond to this?

What are the consequences?

A
  • Patients subconsciously adjust to the progressively increasing obstruction by altering their diet from solid to liquid foods.
  • Prominent weight loss and debilitation result from both impaired nutrition and effects of the tumor itself
78
Q

What prognosis is associated with SCC of the esophagus?

A

5 year survival rates are ~75% in those cases that are superficial only.

If more advanced, the survival rate drops substantially.

L. node metastases, which are common are associated with poor prognosis and the overall 5 year survival rate is under 20%

79
Q

What is the most prevalent cause of esophagitis?

A

GERD

GI-II, Exam 1 (8 decks)

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