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Non-neoplastic disorders of
esophagus
Dr. S. Kannan
Outline
● Epidemiology
● Embryology of esophagus
● Congenital lesions
● Histology
● Esophagitis
● Barrett’s esophagus
● Mechanical esophageal disorders
● Systemic disorders with esophageal involvement
● Recap
● Reference
Epidemiology - CMC statistics
Epidemiology
6,683 subjects - screening UGI scopy at Gyeongsang National University Hospital
(March, 2005 to May, 2006)
1,154 (17.26%) - prevalence of esophageal disorders.
1. GERD.
2. Erosive reflux esophagitis.
3. Barrett`s esophagus.
4. Hiatal hernia.
(Korean J Gastroenterol 2007;50:306-312)
Embryology and histology of esophagus
2-3 weeks: 17th day
embryo showing
Notochord formation
Non neoplastic disorders of esophagus
Folding of the embryo: 3-4 wk
Formation of tracheo-esophagial septum
Starts from end of 3rd
week.
Completed by 5-6 week.
Congenital lesions
Case 1
1 day old neonate presented with
H/o choking, respiratory distress on breast
feeding.
H/o drooling since birth.
Antenatally: Polyhydramnios.
.
Foetal Autopsy
1: 3000 live births.
Male predominance.
50% cases - VATER/VACTERL association
Occasional association with: foregut duplications & bronchopulmonary foregut
malformations.
Esophagial atresia and Tracheo-esophagial fistula
Gross and Swenson’s classification of EA and TEF
A. 90% MC: atresia with fistula
B. 4% - isolated atresia
C. 4% - H type fistula
D & E1% each
Associations
Etiology of Esophageal Atresia and Tracheoesophageal Fistula: “Mind the Gap”
Elisabeth M. de Jong,
Congenital esophageal stenosis
1 : 50,000 live births
● Gr I: Membranous diaphragm / web
● Gr II: Tracheobronchial remnants
cartilage nodules
● Gr III: Fibromuscular stenosis
● Pancreatic heterotopias
Non neoplastic disorders of esophagus
Rebelo et all
Non neoplastic disorders of esophagus
DUPLICATIONS - Congenital cystic abnormalities of GIT seen on mesenteric side
sharing a common blood supply with the native boweI.
39% - foregut, 61% - both mid- and hindgut. (Ann Surg 208: 184-189, 1988)
C /O: Vomiting, respiratory distress, dysphagia.
● Partial Twinning
● Split Notochord
● Embryonic Diverticula and Recanalization Defects - for ileal diverticula
● Environmental Factors (4 theories)
Esophageal Cysts and Duplications
Seminars in Pediatric Surgery Volume 9, Gastrointestinal Duplications
Dimmick Hardwick 1992, Developmental pathology and embryo and foetus
Duplication cyst
1. Attachment to the esophagus,
2. Enclosure by two muscle layers,
3. Lining by epithelium.
Tracheobronchial duplication cyst
1. Located anteriorly.
2. Ciliated columnar
epithelium.
3. Mucous glands and cartilage.
Neurenteric remnant
Aka: Split notochord syndrome → Spectrum.
Associated with spinal dysraphism, vertebral anamolies.
1. Dorsal
enteric cyst;
2 , dorsal
enteric sinus;
3 , dorsal enteric
diverticulum
4.dorsal enteric
fistula
1. Normal layers of the GIT.
2. Neuroglial & leptomeningeal tissues
found around.
3. Mucosa: Indigenous to any segment of
the GI.
Congenital lesions
Atresias, fistulas and stenosis.
Congenital esophageal stenosis
Duplication cyst
Congenital short esophagus (dd: CDH)
Histology of esophagus
Late 1 st trimester
Third trimester
Non neoplastic disorders of esophagus
Normal mucosa
Superfcial
Prickle
Basal cell,
Lymphocytes: Occasional and suprabasal.
Clear halo or
Intraepithelial cells with irregular nuclear contours: Sqiggle cell.
CD3: Suppressive /CD8 cytotoxic
Lamina propria
Submucosa
Submucosal glands:
Continuation of the minor
salivary glands of the
oropharynx. Acid mucin, HCO3
Ducts: Squamous epithelium.
Periductal inflammatory
aggregates are normal
Esophagitis
Reflux Infectious Pill / corrosives / toxins
Case 2
44 year old obese male software
engineer, ℅ heartburns, acid
regurgitation. H/o chronic cough when
he lies down. He even had a ecg
examination as he was complaining of
chest pain.
H/o smoking and alcoholism +
O/e: pharyngitis, laryngitis.
ECG normal.
Gastro-esophagial reflux disease GERD.
Prevalence rate: 20% to 40%.
Risk increases with 40 years of age.
Endoscopic classification:
50-70% Nonerosive reflux disease (NERD) - normal endocsopy or erosive
esophagitis.
Pathogenesis: I) Acid and pepsin reflux. II) Bile reflux.
Old concept: Reflux esophagitis as a caustic chemical injury - peptic esophagitis.
Los Angeles Classification of Gastroesophageal Reflux Disease
Refluxed gastric material did not damage esophageal epithelial cells directly.
They secrete cytokines (interleukin [IL]-8 and IL-1β) that attracted immune
cells.
Acute GERD was a T lymphocyte–predominant form of inflammation, with
minimal involvement by neutrophils and eosinophils.
Submucosal infiltration by lymphocytes that later progressed upward to the
epithelial surface.
[IL]-8 and IL-1β - proliferative effects: esophageal basal cell and papillary
hyperplasia observed in the absence of surface erosions.
Association of Acute Gastroesophageal Reflux Disease With Esophageal Histologic Changes Kerry B. Dunbar
Gastroesophageal Reflux Might Cause Esophagitis Through a Cytokine-Mediated Mechanism Rather Than Caustic Acid Injury
Rhonda F.Souza
Squamous hyperplasia: 1. Basal cell hyperplasia, without surface maturation
(nucleated cells at surface of epithelium)- >15%.
2. Elongation of the lamina propria papillae- >2/3. (1970, Ismail-Beigi)
Increased intraepithelial inflammation (lymphocytes, eosinophils, neutrophils)
Distended pale squamous “balloon” cells.
Intercellular edema (acantholysis)
Severe cases surface erosions or ulcerations
Histological features
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Cytoarchitectural uniformity cytoarchitectural pleomorphism
Reactive Changes in Ulcers and dense inflammatory lymphoid infiltrte
Case 2, Repeat endoscopy after few years due to
recurrence of symtoms.
Barrett’s esophagus
GERD is associated with a 10–15% risk of Barrett’s esophagus.
Risk factors: Advanced age>63, male sex, white race, hiatus hernia,
duodenal-gastric reflux, obesity, tobacco and alcohol.
Risk of cancer 30 to 125 times greater. Risk of cancer 30 to 125 times
greater.
Def: Endoscopically recognizable columnar metaplasia of the esophageal
mucosa - confirmed pathologically to contain intestinal metaplasia, the
latter defined by the presence of goblet cells. (Updated guidelines 2008).
Non neoplastic disorders of esophagus
Prague classification
Long-segment >3cm, short-
segment 1-3cm, and ultrashort-
segment <1cm.
11% increased risk of high-grade
dysplasia and EAC for every 1 cm
increase in BE length.
American college of gasteroenterology recommendation
2016 update
BE: only if salmon colored mucosa into the tubular esophagus extending ≥1 cm.
No Bx if normal Z line or a Z line with <1 cm of variability.
Prague classification. Report: Location of GEJ, Z line and diaphragmatic hiatus.
least 8 random biopsies. (harrison R, Perry. Am J Gastroenterol 2007;102:1154-61.)
In short segments Barrett’s: 4 biopsies/ cm of circumferential BE 1 biopsy/ cm in
tongues.
If histology negative for Barrett’s, repeat endoscopy 1–2 years of time to rule out
BE
Kenneth K. Wang, M.D. and Richard E. Sampliner, M.D. The Practice Parameters Committee of the American College of
Gastroenterology
New British Society of Gastroenterology (BSG)
guidelines
The presence of areas of intestinal metaplasia (IM), although often present, is not
a requirement for diagnosis.
Excludes “ultra‐short Barrett's.
BO but without dysplasia, the recommended surveillance protocols are two yearly,
four quadrant biopsies every 2 cm,
Persistant inflammation and ulceration.
squamous epithelium becomes columnar (cardiac
type with underlying mucinous glands)
intestinal phenotype (goblet cells)
transitional phase multilayered epithelium
strongly associated with GERD-induced
inflammation of the GEJ region,
associated with goblet cell metaplasia and
100% specific for BE
Pospective evaluation of multilayered epithelium in Barrett's esophagus. Shields HM
Recent advances in Barrett’s esophagusJohn Inadomi,
Non neoplastic disorders of esophagus
Burried Barrett’s esophagus
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
IHCs
MUC 2.
CDX2
Villin
Case 3
Endocsopies of esophagial ulcers in two different patients with immunosuppresion
both with ℅ odynophagia, nausea, substernal pain, and fever.
4A) Bone marrow transplantation on
immunosuppressants.
4B) HIV with CD4 <than
50 cells/µL)
v
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Case 4
15 year old male was
admitted with impacted
chicken bone.
H/o nausea, vomiting,
chest pain, dysphagia to
solid-food not responding to
response to PPI.
Patient has chronic h/o
allergy to certain foods and
allergic rhinitis.
Definition: “Chronic, immune/antigen-mediated esophageal
disease characterized clinically by symptoms related to
esophageal dysfunction and histologically by eosinophil-
predominant inflammation.
Children and adults with male preponderance.
H/o concurrent allergic diatheses: food allergy, asthma,
eczema, chronic rhinitis, and environmental allergies.
Peripheral blood eosinophilia +.
Disease of type 2 (Th2) helper T cells triggered by inhaled
and food allergens. Thymic stromal lymphopoietin (TSLP),
IL5, IL13, and eotaxin3 - Eosinophil activation.
Inflammatory response leads to the pathologic changes
observed in the mucosa, submucosal fibrosis, remodelling,
Allergic eosinophilic esophagitis: a primer for pathologists Donald A
Food Allergies and Eosinophilic Gastrointestinal Illness
lNirmalaGonsalvesMD
Furuta GT. Eosinophilic esophagitis: update on clinicopathological manifestations and pathophysiology. Curr Opin Gastroenterol. 2011
Eosinophilic esophagitis
ACG Clinical Guidelines 2013
Al least six biopsies should be taken
from different locations, focusing on
areas with endoscopic mucosal
abnormalities
Symptoms do not correlate
accurately with histologic disease
activity, so histology currently continues
to be necessary to monitor the disease.
2 – 4 biopsies should be obtained
from both the proximal and distal
esophagus.
Obtain biopsies from the antrum
and / or duodenum to rule out
other causes of esophageal
eosinophilia in all children and in
adults with gastric or small intestinal
symptoms or endoscopic
abnormalities.
United European Gastroenterology
2017
Differential Diagnosis of Esophageal Eosinophilia
Eosophagial eosinophilia.
Lymphocytic Esophagitis A Histologic Subset of Chronic Esophagitis Carlos A. Rubio
0.1% of an endoscopic population (Haque S, and Genta RM Gut 2012)
1. High numbers of IELs in peripapillary fields.
2. Spongiosis
3. Absence of granulocytes (neutrophils and eosinophils).
Lymphocytic esophagitis.
Differentials:
1. Reflux,
2. Radiation, and
3. C albicans esophagitis
Interpapillary IELs more
than ones in peripapillary
Areas.
Neutrophils and eosinophils
present.
Non neoplastic disorders of esophagus
Case 5
White patches noted during UGI scopy in three individuals
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Non neoplastic disorders of esophagus
Case 6
40 year old rural areas Latin
American male from a poor
socioeconomic background with ℅
chronic dysphagia of solid and
liquid food, regurgitaion and heart
burn.
Non neoplastic disorders of esophagus
Chagasic Disease - megaesophagus
.
Pill esophagitis
Corrosive Esophagitis
Acid injury: Coagulative necrosis, with the
depth of injury limited by the eschar.
Alkaline injury: Liquefactive necrosis with
fat and protein digestion- risk of
perforation.
Mucosal edema, erythema, hemorrhage,
and necrosis ---->Ulcers.
Micro: dense neutrophilic infiltrate, vessel
thrombosis, bacterial invasion, and
abundant granulation tissue
Case 7
Patient with h/o coughing up an
esophagial cast.
Esophagitis dissecans superficialis
Mechanical disorders
Achalasia
Traumatic Esophageal Disorders
Esophageal Rings and Webs
Esophageal Diverticula
Achalasia cardia
Esophageal Involvement in Systemic Disease
Graft-versus-Host Disease
Eosinophilic Gastroenteritis
Collagen Vascular Disorders
(Including Scleroderma)
Dermatologic Diseases
Crohn's disease.
Amyloidosis
Reference
1. Odze and Goldblum Surgical Pathology of the GI Tract, Liver, Biliary Tract
and Pancreas 3e.
2. Morson and Dawson's Gastrointestinal Pathology, 5th Edition
3. Histology for Pathologists, Stacey E. Mills.
4. The Developing Human: Clinically Oriented Embryology, Moore.
5. Langman's Medical Embryology.
6. Articles.
Thank you

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Non neoplastic disorders of esophagus

  • 2. Outline ● Epidemiology ● Embryology of esophagus ● Congenital lesions ● Histology ● Esophagitis ● Barrett’s esophagus ● Mechanical esophageal disorders ● Systemic disorders with esophageal involvement ● Recap ● Reference
  • 3. Epidemiology - CMC statistics
  • 4. Epidemiology 6,683 subjects - screening UGI scopy at Gyeongsang National University Hospital (March, 2005 to May, 2006) 1,154 (17.26%) - prevalence of esophageal disorders. 1. GERD. 2. Erosive reflux esophagitis. 3. Barrett`s esophagus. 4. Hiatal hernia. (Korean J Gastroenterol 2007;50:306-312)
  • 5. Embryology and histology of esophagus 2-3 weeks: 17th day embryo showing Notochord formation
  • 7. Folding of the embryo: 3-4 wk
  • 8. Formation of tracheo-esophagial septum Starts from end of 3rd week. Completed by 5-6 week.
  • 10. Case 1 1 day old neonate presented with H/o choking, respiratory distress on breast feeding. H/o drooling since birth. Antenatally: Polyhydramnios. .
  • 12. 1: 3000 live births. Male predominance. 50% cases - VATER/VACTERL association Occasional association with: foregut duplications & bronchopulmonary foregut malformations. Esophagial atresia and Tracheo-esophagial fistula
  • 13. Gross and Swenson’s classification of EA and TEF A. 90% MC: atresia with fistula B. 4% - isolated atresia C. 4% - H type fistula D & E1% each
  • 14. Associations Etiology of Esophageal Atresia and Tracheoesophageal Fistula: “Mind the Gap” Elisabeth M. de Jong,
  • 15. Congenital esophageal stenosis 1 : 50,000 live births ● Gr I: Membranous diaphragm / web ● Gr II: Tracheobronchial remnants cartilage nodules ● Gr III: Fibromuscular stenosis ● Pancreatic heterotopias
  • 19. DUPLICATIONS - Congenital cystic abnormalities of GIT seen on mesenteric side sharing a common blood supply with the native boweI. 39% - foregut, 61% - both mid- and hindgut. (Ann Surg 208: 184-189, 1988) C /O: Vomiting, respiratory distress, dysphagia. ● Partial Twinning ● Split Notochord ● Embryonic Diverticula and Recanalization Defects - for ileal diverticula ● Environmental Factors (4 theories) Esophageal Cysts and Duplications Seminars in Pediatric Surgery Volume 9, Gastrointestinal Duplications
  • 20. Dimmick Hardwick 1992, Developmental pathology and embryo and foetus
  • 21. Duplication cyst 1. Attachment to the esophagus, 2. Enclosure by two muscle layers, 3. Lining by epithelium.
  • 22. Tracheobronchial duplication cyst 1. Located anteriorly. 2. Ciliated columnar epithelium. 3. Mucous glands and cartilage.
  • 23. Neurenteric remnant Aka: Split notochord syndrome → Spectrum. Associated with spinal dysraphism, vertebral anamolies. 1. Dorsal enteric cyst; 2 , dorsal enteric sinus; 3 , dorsal enteric diverticulum 4.dorsal enteric fistula
  • 24. 1. Normal layers of the GIT. 2. Neuroglial & leptomeningeal tissues found around. 3. Mucosa: Indigenous to any segment of the GI.
  • 25. Congenital lesions Atresias, fistulas and stenosis. Congenital esophageal stenosis Duplication cyst Congenital short esophagus (dd: CDH)
  • 27. Late 1 st trimester
  • 31. Lymphocytes: Occasional and suprabasal. Clear halo or Intraepithelial cells with irregular nuclear contours: Sqiggle cell. CD3: Suppressive /CD8 cytotoxic
  • 33. Submucosa Submucosal glands: Continuation of the minor salivary glands of the oropharynx. Acid mucin, HCO3 Ducts: Squamous epithelium. Periductal inflammatory aggregates are normal
  • 34. Esophagitis Reflux Infectious Pill / corrosives / toxins
  • 35. Case 2 44 year old obese male software engineer, ℅ heartburns, acid regurgitation. H/o chronic cough when he lies down. He even had a ecg examination as he was complaining of chest pain. H/o smoking and alcoholism + O/e: pharyngitis, laryngitis. ECG normal.
  • 36. Gastro-esophagial reflux disease GERD. Prevalence rate: 20% to 40%. Risk increases with 40 years of age. Endoscopic classification: 50-70% Nonerosive reflux disease (NERD) - normal endocsopy or erosive esophagitis. Pathogenesis: I) Acid and pepsin reflux. II) Bile reflux. Old concept: Reflux esophagitis as a caustic chemical injury - peptic esophagitis.
  • 37. Los Angeles Classification of Gastroesophageal Reflux Disease
  • 38. Refluxed gastric material did not damage esophageal epithelial cells directly. They secrete cytokines (interleukin [IL]-8 and IL-1β) that attracted immune cells. Acute GERD was a T lymphocyte–predominant form of inflammation, with minimal involvement by neutrophils and eosinophils. Submucosal infiltration by lymphocytes that later progressed upward to the epithelial surface. [IL]-8 and IL-1β - proliferative effects: esophageal basal cell and papillary hyperplasia observed in the absence of surface erosions. Association of Acute Gastroesophageal Reflux Disease With Esophageal Histologic Changes Kerry B. Dunbar Gastroesophageal Reflux Might Cause Esophagitis Through a Cytokine-Mediated Mechanism Rather Than Caustic Acid Injury Rhonda F.Souza
  • 39. Squamous hyperplasia: 1. Basal cell hyperplasia, without surface maturation (nucleated cells at surface of epithelium)- >15%. 2. Elongation of the lamina propria papillae- >2/3. (1970, Ismail-Beigi) Increased intraepithelial inflammation (lymphocytes, eosinophils, neutrophils) Distended pale squamous “balloon” cells. Intercellular edema (acantholysis) Severe cases surface erosions or ulcerations Histological features
  • 46. Reactive Changes in Ulcers and dense inflammatory lymphoid infiltrte
  • 47. Case 2, Repeat endoscopy after few years due to recurrence of symtoms.
  • 48. Barrett’s esophagus GERD is associated with a 10–15% risk of Barrett’s esophagus. Risk factors: Advanced age>63, male sex, white race, hiatus hernia, duodenal-gastric reflux, obesity, tobacco and alcohol. Risk of cancer 30 to 125 times greater. Risk of cancer 30 to 125 times greater. Def: Endoscopically recognizable columnar metaplasia of the esophageal mucosa - confirmed pathologically to contain intestinal metaplasia, the latter defined by the presence of goblet cells. (Updated guidelines 2008).
  • 50. Prague classification Long-segment >3cm, short- segment 1-3cm, and ultrashort- segment <1cm. 11% increased risk of high-grade dysplasia and EAC for every 1 cm increase in BE length.
  • 51. American college of gasteroenterology recommendation 2016 update BE: only if salmon colored mucosa into the tubular esophagus extending ≥1 cm. No Bx if normal Z line or a Z line with <1 cm of variability. Prague classification. Report: Location of GEJ, Z line and diaphragmatic hiatus. least 8 random biopsies. (harrison R, Perry. Am J Gastroenterol 2007;102:1154-61.) In short segments Barrett’s: 4 biopsies/ cm of circumferential BE 1 biopsy/ cm in tongues. If histology negative for Barrett’s, repeat endoscopy 1–2 years of time to rule out BE Kenneth K. Wang, M.D. and Richard E. Sampliner, M.D. The Practice Parameters Committee of the American College of Gastroenterology
  • 52. New British Society of Gastroenterology (BSG) guidelines The presence of areas of intestinal metaplasia (IM), although often present, is not a requirement for diagnosis. Excludes “ultra‐short Barrett's. BO but without dysplasia, the recommended surveillance protocols are two yearly, four quadrant biopsies every 2 cm,
  • 53. Persistant inflammation and ulceration. squamous epithelium becomes columnar (cardiac type with underlying mucinous glands) intestinal phenotype (goblet cells) transitional phase multilayered epithelium strongly associated with GERD-induced inflammation of the GEJ region, associated with goblet cell metaplasia and 100% specific for BE Pospective evaluation of multilayered epithelium in Barrett's esophagus. Shields HM
  • 54. Recent advances in Barrett’s esophagusJohn Inadomi,
  • 60. Case 3 Endocsopies of esophagial ulcers in two different patients with immunosuppresion both with ℅ odynophagia, nausea, substernal pain, and fever. 4A) Bone marrow transplantation on immunosuppressants. 4B) HIV with CD4 <than 50 cells/µL)
  • 61. v
  • 66. Case 4 15 year old male was admitted with impacted chicken bone. H/o nausea, vomiting, chest pain, dysphagia to solid-food not responding to response to PPI. Patient has chronic h/o allergy to certain foods and allergic rhinitis.
  • 67. Definition: “Chronic, immune/antigen-mediated esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil- predominant inflammation. Children and adults with male preponderance. H/o concurrent allergic diatheses: food allergy, asthma, eczema, chronic rhinitis, and environmental allergies. Peripheral blood eosinophilia +. Disease of type 2 (Th2) helper T cells triggered by inhaled and food allergens. Thymic stromal lymphopoietin (TSLP), IL5, IL13, and eotaxin3 - Eosinophil activation. Inflammatory response leads to the pathologic changes observed in the mucosa, submucosal fibrosis, remodelling,
  • 68. Allergic eosinophilic esophagitis: a primer for pathologists Donald A Food Allergies and Eosinophilic Gastrointestinal Illness lNirmalaGonsalvesMD
  • 69. Furuta GT. Eosinophilic esophagitis: update on clinicopathological manifestations and pathophysiology. Curr Opin Gastroenterol. 2011
  • 71. ACG Clinical Guidelines 2013 Al least six biopsies should be taken from different locations, focusing on areas with endoscopic mucosal abnormalities Symptoms do not correlate accurately with histologic disease activity, so histology currently continues to be necessary to monitor the disease. 2 – 4 biopsies should be obtained from both the proximal and distal esophagus. Obtain biopsies from the antrum and / or duodenum to rule out other causes of esophageal eosinophilia in all children and in adults with gastric or small intestinal symptoms or endoscopic abnormalities. United European Gastroenterology 2017
  • 72. Differential Diagnosis of Esophageal Eosinophilia
  • 74. Lymphocytic Esophagitis A Histologic Subset of Chronic Esophagitis Carlos A. Rubio 0.1% of an endoscopic population (Haque S, and Genta RM Gut 2012) 1. High numbers of IELs in peripapillary fields. 2. Spongiosis 3. Absence of granulocytes (neutrophils and eosinophils). Lymphocytic esophagitis. Differentials: 1. Reflux, 2. Radiation, and 3. C albicans esophagitis Interpapillary IELs more than ones in peripapillary Areas. Neutrophils and eosinophils present.
  • 76. Case 5 White patches noted during UGI scopy in three individuals
  • 80. Case 6 40 year old rural areas Latin American male from a poor socioeconomic background with ℅ chronic dysphagia of solid and liquid food, regurgitaion and heart burn.
  • 82. Chagasic Disease - megaesophagus .
  • 84. Corrosive Esophagitis Acid injury: Coagulative necrosis, with the depth of injury limited by the eschar. Alkaline injury: Liquefactive necrosis with fat and protein digestion- risk of perforation. Mucosal edema, erythema, hemorrhage, and necrosis ---->Ulcers. Micro: dense neutrophilic infiltrate, vessel thrombosis, bacterial invasion, and abundant granulation tissue
  • 85. Case 7 Patient with h/o coughing up an esophagial cast.
  • 87. Mechanical disorders Achalasia Traumatic Esophageal Disorders Esophageal Rings and Webs Esophageal Diverticula
  • 89. Esophageal Involvement in Systemic Disease Graft-versus-Host Disease Eosinophilic Gastroenteritis Collagen Vascular Disorders (Including Scleroderma) Dermatologic Diseases
  • 91. Reference 1. Odze and Goldblum Surgical Pathology of the GI Tract, Liver, Biliary Tract and Pancreas 3e. 2. Morson and Dawson's Gastrointestinal Pathology, 5th Edition 3. Histology for Pathologists, Stacey E. Mills. 4. The Developing Human: Clinically Oriented Embryology, Moore. 5. Langman's Medical Embryology. 6. Articles.

Editor's Notes

  1. dlondz@gmail.com
  2. 9,52,887
  3. GERD - 14.66%. Erosive reflux esophagitis - 8.45%. Barrett`s esophagus - 1.12%, Hiatal hernia - 2% Others with >0.1% prevelance. esophageal varices (0.37%), esophageal squamous papilloma (0.31%), esophageal candidiasis (0.25%), heterotopic gastric mucosa (0.16%),
  4. One tube on top and the other tube below. Establishment of fore gut - primer of esophagus
  5. http://whittakersembryology.co.uk/keyevents/gastrulation.html http://anatomy.cgu.edu.tw/ezfiles/71/1071/img/1622/E02.pdf https://wrhhs.org/chapter-15-digestive-system/
  6. EA- curved ng tube. Gas pattern.
  7. The tracheal ostium of a fistula to the distal esophageal segment is often at the carina
  8. Defective septation Vertebral anomalies, Anal atresia, cardiac defect, tracheo esophageal fistula, r enal and limb anomalies
  9. mutations and deletions of the FOX gene cluster on chromosome 16q24 appear to be the most signficant.
  10. Conginital membranous diverticulum: Epithelium of the edoderm proliferates and obliterates the lumen. Incomplete esophageal recanalization during the 8 week of human embryologic development
  11. Congenital esophageal stenosis owing to tracheobronchial remnants. Rebelo et all Congenital esophageal stenosis (CES) was attributed to Frey and Duschl, in 1936.
  12. Pancreatic heterotopia
  13. Non communicating ones cause obstruction due to expanding intramural mass. Twinning: doubling of other body parts: 2 heads, colons, legs and Notoc : through the (neurenteric canal) the yolk sac herniates and adheres to the dorsal ectoderm> Rupture of the hernia> fistula>closure. GOOD FOR SPINAL ANOMOLY ASSO and DORSAL LOCATION. Eviron: Trauma or hypoxia, vascular insuff > > could induce duplications
  14. Cysts containing various epithelial types Gastric heterotopias are most common in esophageal and small intestinal duplications Similar to any where GIT: inner and outer layers of muscularis propria and myenteric and submucosal plexuses
  15. DD: Bronchogenic cysts --- are attached to bronchial tree, The wall lacks esophageal muscularis propria with myenteric and submucosal plexuses. Esophageal duplications to have extensive stratified squamous, gastric, or intestinal mucosa.
  16. notochord can induce the formation of the neural tube, gastrointestinal tract, and other organs- Multiple anomolies chemical meningitis due to perforation of an intraspinal cyst.
  17. In summary
  18. stratifed columnar epithelium. Note the lack of muscularis mucosae.
  19. stratifed squamous epithelium with occasional ciliated cells Note the individual smooth muscle cells of developing muscularis mucosae. Srt squ epi appears in the middle one-third of the esophagus and extends cephalad and caudally, replacing the ciliated epithelium “inlet patch”- upper esophagus progress to gastric differentiation if cialted columnar persists.
  20. Muscles: Skeletal muscle in the upper ⅓ No serosa.
  21. Basal zone: 5-15% thickness. - 1-3 cell thick -basophilic cells with dark nuclei Papillae: upto ⅓ to ½ thickness- Never into the upper ⅓. Distal esophagus: Normal to see >15% basal cells and papillae upto upper 1/3 (Farhad Ismail-Beigi) https://www.gastrojournal.org/article/S0016-5085(70)80004-X/pdf
  22. Others: Merkel cells - CK 20, Cam5.2. Melanocytes
  23. scattered inflammatory cells, and mucus(neutral mucin) secreting glands cardiac-type glands- distal and proximal regions
  24. Primary Eosinophilic Esophagitis Lymphocytic Esophagitis Esophagitis Dissecans Superficialis Radiation induced esophagitis
  25. Yellow base with red magins
  26. NERD to erosive esophagitis occurs in as much as 30% of patients annually hiatal hernia, a defective or weak lower esophageal sphincter (LES), impaired esophageal peristalsis with transient LES relaxation, delayed gastric emptying,
  27. Grade A One (or more) mucosal break no longer than 5 mm that does not extend between the tops of two mucosal folds Grade B One (or more) mucosal break more than 5 mm long that does not extend between the tops of two mucosal folds Grade C One (or more) mucosal break that is continuous between the tops of two or more mucosal folds but which involve less than 75% of the circumference Grade D One (or more) mucosal break which involves at least 75% of the esophageal circumference
  28. Initial theory: Once inside esophageal cells, acid was thought to kill them by denaturing vital proteins, by activating phospholipases and endonucleases, and by interfering with cell respiration.22,23 This lethal acid injury was assumed to start at the esophageal luminal surface, inducing an acute inflammatory response characterized by epithelial infiltration with granulocytes. The acid-induced death of surface cells was assumed to stimulate hyperplasia of squamous basal progenitor cells and to be associated with elongated and hyperplastic papillae.
  29. Nonendoscopically evident mucosal damage. Endoscopic/pathologic discrepancies - biopsies are always warranted in in symptomatic patients if empiric reflux therapy (4-8weeks) has failed. Demester etall: Twenty-four hour pH monitoring correlated better with papillary length
  30. Well-oriented tissue sections that include at least three consecutive papillae Increased mitoses, slight enlargement of basal and suprabasal nuclei, and prominent nucleoli and hyperchromatism. Esophagitis can be established even in the absence of inflammation if there is squamous hyperplasia - due to rx.
  31. Intraepithelial neutrophils - not sensitive only in 30%. Increased in erosions. Dd: viral or fungal ( Candida ) infection. IntraE lymphocytes: normal intraepithelial component - suprabasal perpapillary squiggly CD8+ and TIA-1+ T lymphocytes 10 to 12 lymphocytes per high-power field (HPF) Wang HH 1994 In isolation has no independent diagnostic significance, because normal control subjects may also have increased numbers Eosinophils: Adults normaly in distal 1 to 2 cm of the esophagus. Child: absent- useful in dx. S Mueller 2006- MBP ihc helped in picking up degranulated ones. Better dx eosinophilic esophagitis.
  32. ballooning degeneration of squamous cells, intercellular edema (acantholysis) Acid-induced increase in epithelial permeability that enables chloride anion and water in the esophageal lumen to enter and expand the intercellular space.
  33. lamina propria: K.Gebeos 1980: , vascular changes were observed in the top of the stromal papillae widening them. Ingrowth of capillaries into the epithelial layers Fibrosis and inflammation.
  34. Multinucleated regenerative squamous cells at base/suprabasal. DD: Herpes: nuclear inclusions And surface cells.
  35. Reactive Squamous Hyperplasia versus Dysplasia Papillae Regular Absent or irregular Nuclear enlargement Nuclear pleomorphism Nuclear overlapping Nuclear hyperchromasia Irreg Nuclear membrane
  36. large atypical endothelial cells and fibroblasts scattered fashion not form solid clusters cytokeratins neg Activated and atypical lymphocytes that can simulate lymphoma. confined to the surface exudate Never involves underlying tissue dense, confluent, and homogeneous manner
  37. salmon-colored mucosa in the tubular esophagus that may show focal areas of surface erosion or ulceration. PPI Rx causes sq re-epitheli. Bx buried metaplastic epithelium is identified in biopsy specimens from these squamous islands
  38. By definition, this disease does not include patients who have intestinal metaplasia (goblet cells) of the gastric cardia intestinalized glands in the GEJ region of patients without endoscopically apparent columnar metaplasia does not qualify for barrett’s
  39. In 1950, Norman Barrett defined the esophagus as that part of the foregut lined by squamous epithelium. Barrett had called a tubular stomach was seen distal to the squamocolumnar junction but was actually CLE. diagnosis requires careful documentation of the anatomic landmarks and often requires the use of large-sized biopsies. Endoscopically: GEJ defined as the proximal margin of the gastric mucosal folds.
  40. measuring (in centimeters) the most proximal extent of circumferential columnar mucosa (C value) and the maximal extent of noncircumferential columnar mucosa (M value) above the GEJ
  41. Further improvement is not achieved unless 16 biopsies are taken Endoscopic surveillance should employ four-quadrant biopsies at 2 cm intervals in patients without dysplasia and 1 cm intervals in patients with prior dysplasia (strong recommendation, low level of evidence).
  42. the rationale behind this decision is that sampling errors at the initial endoscopy may miss an area(s) of IM If a sufficient number of biopsies are taken over an adequate period of time, IM can usually be demonstrated (in the majority of these patients)
  43. There is similar risk of progression to dysplasia or cancer in patients with and without goblets cells in columnar-lined eso­phagus columnar-lined eso­phagus shows physiologic properties of “intestinal” differentiation, such as expression of CDX2, HepPar-1, villin, DAS-1, and MUC3. Bile acids (deoxycholic acid) upregulate both the intestinal differentiation factor, CDX2, and the goblet cell–specific gene, MUC2 background nongoblet columnar epithelium in BE shows physiologic properties of “intestinal” differentiation, such as expression of CDX2, HepPar-1, villin, DAS-1, and MUC3.
  44. CellularoriginsofBarrett’sesophagus.PotentialtheoriesthatgiverisetoBarrett’sepitheliuminclude(1)reprogrammingof native squamous stem cells, (2) repopulation from submucosal gland stem cells, and (3) migration of gastric stem cells includingcells at the squamocolumnar junction (
  45. similar to the incomplete (type II or III) intestinal metaplasia that occurs in the stomach of patients with chronic gastritis
  46. However, with procedures other than RFA, a significant proportion of patients with apparent reversal of their Barrett's segment to squamous mucosa are shown to have buried intestinalized crypts or dysplasia, both of which make continued endoscopic surveillance more difficult.
  47. Herpes: Vesicles ----->Multiple shallow, sharply punched-out lesions and are often surrounded by relatively normal-appearing mucosa. CMV: Deep linear ulcers and shallow ulcers, erythema, diffuse erosive esophagitis,
  48. shallow, sharply punched-out lesions and are often surrounded by relatively normal-appearing mucosa. virus infects esophageal squamous epithelium. ------ >inclusion bodies are limited to the squamous epithelial cells, typically accentuated at the superficial lateral margin of ulcers and erosions.---> Biopsy from the the edge Herpes simplex type I is the most common cause
  49. Cowdry A intranuclear viral inclusion bodies: Cowdry A inclusions are eosinophilic to amphophilic round bodies separated by a clear zone from a thickened nuclear membrane with marginated chromatin. Ground-glass nuclei have a smooth, homogeneous chromatin pattern with a pale basophilic quality.
  50. Clue: Characteristic Cowdry A inclusions with a clear halo and ground-glass nuclei allows their distinction.
  51. Infects mesenchymal and columnar cells. Not the squamous cell: biopsy or brush the base of esophageal ulcers H&E: cytomegaly and nucleomegaly with large ovoid intranuclear inclusions and thick marginated chromatin Nuclear Eosinophilic or deeply basophilic and are usually separated from the nuclear membrane by a halo Cytoplasmic inclusions typically appear within minute vacuoles IHC: Immunohistochemistry may highlight infected cells without typical CMV morphology on routine stained sections and can be more sensitive than light microscopy.
  52. transient esophageal rings (also known as feline folds or felinization), with impacted food material In young children it presents as: Feeding intolerance.
  53. Esophageal eosinophilia remains a histologic finding that must be interpreted within the clinical context of each patient.
  54. not pathognomonic of EOE. Fixed esophageal rings, also referred to astrachealization or ringed esophagus diffuse esophageal narrowing, narrow-caliber esophagus, and mucosal tears readily induced by passage of the endoscope White exudates and plaques seen in some patients, which correspond to areas of eosinophilic abscess eruption through the esophageal mucosa.
  55. EOE is best evaluated in biopsy specimens obtained after 2 months of anti-GERD therapy to exclude PPI responsive EoE.
  56. Major histologic features: biopsy frn the upper 1/3 1. increased intraepithelial eosinophils (≥15/HPF) (standard size of 0.3 mm2 ) obtained from the most densely populated areas 2. eosinophilic microabscesses (defined as a collection of four or more eosinophils within the epithelium) 3. Surface layering of eosinophils (i.e., affiliation of eosinophils to occupy the outer layer of the squamous epithelium), 4. surface sloughing of squamous cells mixed with abundant eosinophils, and 5 extracellular eosinophilic granules (deposition of these proteins, including eosinophil peroxidase and eosinophil derived neurotoxin, indicates degranulation). Minor histologic features: (nonspecific ) (1) marked basal zone hyperplasia (usually >20% of the epithelial thickness), (2) lengthening of the lamina propria papillae (often > two thirds of the epithelial thickness), (3) increased lamina propria fibrosis and chronic inflammation, (4) increased intercellular edema, and (5) increased intraepithelial lymphocytes and mast cells. Influx of neutrophils and the development of ulcers or erosions are unusual in EOE
  57. EoE is clinicopathologic disorder diagnosed by clinicians taking into consideration both clinical and pathologic information
  58. Biopsy sampling of the proximal, middle, and distal esophagus is important to differentiate the diorders.
  59. RX TOPICAL STEROIDS. COMPLICATION: fIBROSIS STRICTURE.
  60. Reached the epithelium through the basement membrane of papillary areas. Resemble allrgic contact dermatitis of skin. Association with : H. pylori gastritis, celiac disease, duodenal lymphocytosis, and Crohn's diseasespects of an emerging condition. Gut 2012
  61. Lymphocytic esophagitis. The esophageal mucosa shows peripapillary intraepithelial lymphocytosis with basal zone hyperplasia. No significant numbers of eosinophils or neutrophils are identified . H. pylori gastritis, celiac disease, duodenal lymphocytosis, and Crohn's disease. Probable autoimmune etiology has been postulated
  62. Candida- white plaques of fibrinopurulent exudate with focal or confluent, overlying erythematous mucosa, plaques can be scraped away to reveal ulceration underneath. Glycogenic acanthosis- occurs as white mucosal plaques that measure 2 to 5 mm. Diffuse esophageal glycogenic acanthosis -- Cowden syndrome. Ectopic sebaceous glands- small, pale yellow or white, punctate elevations of the mucosa.
  63. pseudohyphaeare identified within the ulcer slough and fibrinopurulent exudate. Pseudohyphae linear or ribbon-like appearance in which small indentations, Yeast forms have a slight ovoid contour immunosuppressed patients, who occasionally reveal only minimal inflammation
  64. 25% of the population. primarily in the distal one-third of the esophagus. distention of squamous epithelial cells with glycogen, which is evident as pale-staining material that is PAS positive and diastase digestible
  65. Resemblance to normal dermal sebaceous glands
  66. Humans are accidental hosts for T. cruzi. They are usually infected at night via contact with feces of blood-sucking triatomine insects(reduviidbugs, “kissing” bugs) Esophagial involvement: 7% to 10% of people with chronic T. cruzi infection.
  67. Pathology is dysperistalsis of the esophagus gradual narrowing of the distal esophagus with luminal enlargement of the proximal esophagus
  68. The submucosal and myenteric plexuses: Destruction of neuron plexuses in the esophagus by the inflammatory reaction induced by T. cruz distal muscular hypertrophy and mononuclear inflammatory infiltrates occur in the muscle layers.
  69. Antibiotics (tetracyclines and clindamycin), NSAIDs, Iron supplements Bisphosphonates- polarizable crystalline material in bx .Quinidine, Potassium chloride, ascorbic acid, Ulcers may be shallow or, more commonly, deep with extension into the muscularis mucosaeproximal and middle thirds of the esophagus, the area where the aortic arch compresses the esophagus and peristaltic amplitude is relatively low eosinophilic infiltration, spongiosis, and necrosis of squamous epithelium from biopsy from upper esophagus.
  70. multiple white patches of peeling mucosa, extending from the middle to the distal esophagus, association with: hot beverages, chemical irritants, collagen vascular disorders, and autoimmune bullous dermatoses (pemphigus and pemphigoid), heavy smoking, physical trauma, celiac disease, 140
  71. long, detached fragments of superficial squamous epithelium with intraepithelial splitting at varying levels above the basal layer of the squamous epithelium, prominent parakeratosis, orthokeratosis, and fragments of necrotic epithelium. DD: echanical trauma related to esophagoscopy, infectious esophagitis (fungal or herpetic), and chronic bullous diseases that involve the esophagus
  72. GI neuromuscular system begins at 4 wk with neural crest cells entering foregut rostrocaudally. Myenteric plexus develops 1st and submucosal plexus 2 to 3 wks. inability of the LES to relax after swallowing -→ esophageal obstruction marked reduction, or complete absence, of myenteric ganglion cells. T lymphocytes, and myenteric neural fibrosis Radiology: “bird's beak” sign.
  73. Apoptosis and individual cell damage, manifested in squamous mucosa as dyskeratotic keratinocytes, are typically prominent features in combination with a lichenoid interface inflammatory infiltrate eosinophilic gastroenteritis have increased serum total and food-specific IgE levels and positive skin test responses to a variety of food antigens - differentiate form EoE. Scleroderma: Myoneuroenteric dysmotility: esophageal hypomotility and aperistalsis, with incompetence of the LES. Derm: Stevens-Johnson syndrome 236 and bullous diseases such as bullous pemphigoid, benign mucous membrane pemphigoid, epidermolysis bullosa acquisita, pemphigus vulgaris, and lichen planus
  74. Granulomatous lesions are observed in 7% to 9% of patients with esophageal Crohn's disease.. reason: biopsies are superficial. definite diagnosis is established only when characteristic histologic features (strictures, deep ulcers, transmural inflammation, granulomas, mural fibrosis) are identified in the esophagus of a patient who is known to have Crohn's disease elsewhere in the GI tract 72% of patients with GI amyloidosis were shown to have esophageal involvement