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gi 4th year > Pathology of esophageal diseases > Flashcards

Pathology of esophageal diseases Flashcards

1
Q

Non-neoplastic disorders of the esophagus:

Congenital and mechanical disorders:

A
  • Agenesis
  • Atresia
  • diverticulum: Traction, Pulsion
  • Hiatus hernia
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2
Q

Atresia

A

failure of canalization

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3
Q

Atresia: failure of canalization associated with

A

tracheo esophageal-fistula

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4
Q

Traction diverticulum:

A

external forces pulling on the wall

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5
Q

Pulsion diverticulum:

A

forcible distension

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6
Q

Pulsion diverticulum: e.g?

A

Zenker diverticulum

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7
Q

Hiatus hernia:

A

protrusion of upper part of stomach into thorax

via diaphragmatic orifice

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8
Q

Hiatus hernia:cause?

A

increased intra-abdominal pressure and loss of

diaphragmatic muscular tone with ageing

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9
Q

Hiatus hernia

Predisposing factors:

A

obesity, lifting heavy loads,

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10
Q

Sequnces of Hiatus hernia:

A

regurgitation of gastric contents and GERD

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11
Q

Ectopic gastric mucosa most commonly occurs in

A

upper third of

esophagus

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12
Q

Functional Esophageal obstruction

A

Abnormal contraction of esophageal muscle

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13
Q

Mechanical Abnormal contraction of esophageal muscle

A
  • webs

- rings/Schatzki ring

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14
Q

Diff btw webs/rings

A

Webs: thin mucosal membrane that grows across the lumen

Rings or Schatzki ring: a ring of tissue near the end of esophagus

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15
Q

Webs e.g?

A

Plummer-Vinson syndrome

(Paterson-Brown Kelly syndrome):

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16
Q

Symptoms of

Plummer-Vinson syndrome (Paterson-Brown Kelly syndrome):

A 
Dysphagia, 
Esophageal webs, 
Iron deficiency anemia,
Angular stomatitis, 
Atrophic tongue, 
Brittle nails, 
Increased incidence of post-cricoid carcinoma
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17
Q

Plummer-Vinson syndrome (Paterson-Brown Kelly syndrome)

Cause?

A

unclear

Probable mechanisms include iron and nutritional deficiencies,

genetic predisposition, and autoimmunity

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18
Q

Rings or Schatzki ring:

A

ring of tissue near the end of esophagus

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19
Q

Achalasia (megaesophagus)

A

LES fails to relax/open → stays contracted → food unable
to pass to stomach → accumulates in lower esophagus → esophagus dilates
(megaesophagus)]

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20
Q

Achalasia (megaesophagus)

Symptoms

A

triad
1-Incomplete LES relaxation (stays closed),
2-Increased LES tone( contracted),
3-esophageal aperistalsis (no peristalsis)

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21
Q

Primary

Achalasia (megaesophagus)

A

failure of distal esophageal inhibitory neurons, idiopathic

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22
Q

Secondary

Achalasia (megaesophagus)

A

Degenerative changes in neural innervation

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23
Q

Secondary

Achalasia (megaesophagus) e.g?

A

Chagas disease

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24
Q

How Chagas disease can cause achalasia??

A

Trypanosoma cruzi infection causes destruction of the

myenteric plexus, failure of LES relaxation, and esophageal dilatation

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25
Q

Achalasia-like disease may be caused by:

A

o diabetic autonomic neuropathy
o infiltrative disorders such as malignancy, amyloidosis, or sarcoidosis
o lesions of dorsal motor nuclei, which may be produced by polio or surgical
ablation

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26
Q

Esophageal varices

A

localized dilatations of veins

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27
Q

Esophageal varices

Cause

A

Portal hypertension → results in a porto-systemic shunt → esophageal veins
become congested and dilated →Protrude into esophageal lumen → easily traumatised
by passage of food → acute hemorrhage

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28
Q

Esophageal varices complication

A

Acute hemorrhage

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29
Q

Esophageal varices

Commonly detected during

A

Endoscopy

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30
Q

Esophageal lacerations / mucosal injury

A

Mallory-Weiss tears (most common)

Boerhaave’s syndrome

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31
Q

Mallory-Weiss tears often induced by

A

severe retching or vomiting or violent coughing

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32
Q

Mallory-Weiss tears

pathophysiology

A

reflex relaxation of the gastroesophageal musculature
fail during prolonged vomiting, with the result that refluxing
gastric contents cause the esophageal wall to stretch and tear

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33
Q

Mallory-Weiss tears Patients usually present with

A

hematemesis

34
Q

Mallory-Weiss tears result in

A 
linear lacerations (superficial and heal quickly without surgical intervention)
→ longitudinally oriented and usually cross the gastroesophageal junction (lower
esophagus)
35
Q

Boerhaave’s syndrome

Results in

A

severe transmural esophageal tears (catastrophic and require surgical
intervention)

36
Q

Boerhaave’s syndrome lead to

A

Mediastinitis ,

Subcutaneous emphysemia

37
Q

Boerhaave’s syndrome

Symptoms

A

Mack let’s triad

  • vomiting
  • chest pain
  • SC emphysemia
38
Q

Esophagitis

Non-infectious:

A 
▪  Reflux 
▪  Barret’s 
▪  Eosinophilic 
▪  Extremely hot drinks
▪  Chemical (pill, chemotherapy, radiation, acids, alkali, alcohol):
39
Q

Non-infectious:
▪ Chemical
generally causes

A

only self-

limited pain, particularly odynophagia (pain with swallowing)

40
Q

Pill induced esophagitis

Most commonly pills

A
  • doxycycline

- bisphosphates

41
Q

Esophagitis
Infectious
common in——,

can be primary or———-

A

immunocompromised

complicate a preexisting ulcer

42
Q

Infectious esophagitis
Viral?
Fungal?
Others?

A
  • HSV ,CMV
  • candida, mucormycosis, aspergillosis
  • Tuberculosis, Crohn’s disease
43
Q

Candidiasis

A

adherent, gray-white pseudo membranes composed of densely matted
fungal hyphae and inflammatory cells covering the mucosa

44
Q

Reflux esophagitis aka

A

gastroesophageal reflux disease (GERD) → (reflux of gastric juices)

45
Q

gastroesophageal reflux disease (GERD)

Causes

A 
Decreased LES tone, 
increased abdominal pressure, 
Delayed gastric emptying and increased gastric volume ,
Alcohol and tobacco use,
Chocolate / fatty foods, 
Obesity, 
CNS depressants, 
Pregnancy, 
Hiatal hernia,
46
Q

GERD Pathogenesis:

A

gastric acid + pepsin+ refluxed bile

47
Q

GERD

Morphology (histo):

A

hyperaemia,
linear streaks (erosions, ulcers),
hyperplasia of epithelium and thickened basal layer,
elongated sub-epithelial papillae,
mixed inflammatory cells with scattered eosinophils (few)

48
Q

GERD common at — yrs

A

40

49
Q

GERD symptoms

A

Heartburn, dysphagia, sour-tasting gastric contents

Rarely: attacks of severe chest pain (may be mistaken by heart disease)

50
Q

GERD treatment

A

proton pump inhibitors (reduces gastric acidity for symptomatic relief)

51
Q

GERD complications

A 
esophageal ulceration, 
hematemesis, 
melena (bloody/black stool),
stricture development, 
Barrett esophagus
52
Q 
Barret esophagus (complication of chronic GERD)
Characterized by
A

1-Intestinal metaplasia : change of normal esophageal epithelium [strat squamous] to intestinal [simple
columnar w/ goblet cells]

2-epithelial dysplasia

53
Q

change of normal esophageal epithelium [strat squamous] to intestinal [simple
columnar w/ goblet cells] especially in

A

distal esophagus

54
Q

Barret esophagus affect

A

White males; 40 and 60 years

55
Q

Barret esophagus increases risk of

A

esophageal adenocarcinoma

56
Q

Barret esophagus

Gross:

A

Tongues or patches of red,
velvety mucosa extending upward from the
gastroesophageal junction (indicates change to intestinal epithelium)

57
Q

Barret esophagus

histology:

A

presence of goblet cells in esophageal mucosa

58
Q

Goblet stain

A

Alcian blue stain shows the

blue- staining intestinal goblet cells) → DIAGNOSTIC

59
Q

Barret esophagus

diagnosis:

A
  • abnormal mucosa above the GE junction (endoscopy) and
  • histologically documented gastric or intestinal metaplasia (biopsy) needed for diagnosis
    • symptoms of GERD
60
Q

epithelial dysplasia

A

preinvasive lesion that develops in 0.2% to 1% of individuals with Barrett esophagus

➢ low grade or high grade or Intramucosal carcinoma

61
Q

What is recommended to do with patients w/ barret esophagus

A

screening for dysplasia
high-grade dysplasia and intramucosal carcinoma, always require therapeutic
intervention

62
Q

Eosinophilic esophagitis

A

➢ Chronic immunologically mediated disorder

63
Q

Eosinophilic esophagitis

Symptoms

A

Food impaction, dysphagia, feeding intolerance
➢ Patients also have atopy, atopic dermatitis, allergic rhinitis, asthma, peripheral
eosinophilia

64
Q

Eosinophilic esophagitis

Gross: Endoscopy reveals

A

circumferential rings

65
Q

Eosinophilic esophagitis

Histology:

A

Infiltration by numerous eosinophils in proximal esophagus (much more
than GERD)

66
Q

Eosinophilic esophagitis

Treatment

A

Poor response to proton pump inhibitors (treated w/ dietary restrictions)

67
Q

Most common Benign esophageal tumors:

A

Leiomyomas (smooth muscle)

68
Q

Rarer Benign esophageal tumors:

A

lipomas, hemangiomas, fibromas

69
Q

Benign esophageal tumors:

Squamous papilloma: linked to

A

human papilloma virus (HPV)

70
Q

Malignant esophageal tumors (cancers)

A
  • Esophageal squamous cell carcinoma (SCC) (most common)
  • Esophageal adenocarcinoma (AC)
  • Keratosis palmoplantaris (tylosis) / esophageal cancer syndrome
  • Metastatic neoplasms to esophagus
71
Q

Esophageal squamous cell carcinoma (SCC)

More common in:
Affects:

A

Asia and Africa

adults older than 45 years, M:F=4:1, six times more in African Americans than whites

72
Q

Esophageal squamous cell carcinoma (SCC)

risk factors:

A

alcohol, tobacco,
poverty,
caustic esophageal injury,
achalasia,
Plummer-Vinson syndrome,
frequent consumption of very hot beverages,
radiation therapy, Vitamin and mineral deficiencies, Lye strictures, Viruses (HPV 16, 18),
Genetic factors (Palmoplantar keratoderma /Tylosis)

73
Q

Esophageal squamous cell carcinoma (SCC) mostly occurs in

A

middle third of esophagus

74
Q

Esophageal squamous cell carcinoma (SCC)

gross
❖ Early lesions

A

: small, gray-white plaque like thickenings (superficial)

75
Q

Esophageal squamous cell carcinoma (SCC)

gross
❖ Later:

A

polypoid,
ulcerated or diffusely infiltrative lesions that
spread within esophageal wall, where they can cause thickening, rigidity, and
luminal narrowing

76
Q

Esophageal squamous cell carcinoma (SCC)

histology

A

normal squamous epithelium and mild, moderate, or severe esophageal
squamous dysplasia

77
Q

Esophageal squamous cell carcinoma (SCC)

symptoms

A

dysphagia to solids [80%], odynophagia (pain on swallowing), obstruction,
extreme weight loss (as consequences of both impaired nutrition and tumor-associated
cachexia), hemorrhage and sepsis (due to tumor ulceration)

78
Q 
Esophageal adenocarcinoma (AC)
Seen in
A

In the western world (USA, UK, Canada, Australia), incidence of SCC has reduced and AC
is higher

79
Q
  • Esophageal adenocarcinoma (AC)

Arises in a background of

A

Barrett esophagus and long-standing GERD

80
Q

Esophageal adenocarcinoma (AC)

➢ risk factors:
Affect?

A

documented dysplasia, tobacco, obese, radiation therapy

➢ whites; M:F = 7:1

81
Q

Esophageal adenocarcinoma (AC)

➢ pathogenesis

A

Barret esophagus progresses to AC
through the stepwise acquisition of genetic and
epigenetic changes (chromosomal abnormalities and
TP53 mutation are often present in early stages)

gi 4th year (11 decks)

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