SlideShare a Scribd company logo
1 of 28
GIT.Lec. 2
Dr.BASIM
The esophagus:
It is muscular tube of 25cm.
Functions:
 Conduct food & fluid from the pharynx to the stomach.
 Prevent reflux of gastric contents by the presence of two physiological
sphincters.
 Upper esophageal sphincter at the cricopharyngeal muscle.
 Lower esophageal sphincter proximal to the esophageo-gastric
junction.
Mic:
 Mucosa: non keratinizing Squamous epithelium.
 Lamina properia: connective tissue.
 Submucosa: containing glands.
 Muscularis properia: all consist of smooth muscle, except first 6-8cm
contains skeletal muscle.
 No serosal coat.
Congenital anomalies:
1. Esophageal atresia:
 Is congenital absence of normal esophageal canal (blind end of the
canal).
 Usually associated with tracheoesophageal fistula.
2. Tracheoesophageal fistula:
 It will lead to passage of food from the esophagus to the
trachea…….. Leading to aspiration pneumonia which leads to
suffocation.
Aquired lesions:
Stenosis:
 Is a fibrous thickening of the esophageal wall forming constrictions.
e.g. lower esophageal narrowing due to gastroesophageal reflux disease.
Webs:
 Protrusion of the esophageal mucosa into the esophageal lumen.
 Common in female > 40 years.
Etiology is unknown.
1. Upper esophageal Web: (web + iron deficiency anemia +
glossitis + chelosis), this is called plummer Vinson
syndrome……. Predispose to adenocarcinoma.
2. Lower esophageal Web (rings): called schtzki's ring
(pathological annular narrowing at the lower
esophagogastric junction; could be congenital or
inflammatory (reflux disease).
Lesions of motor dysfunctions:
Achalasia (FAILURE TO RELAX):
Incomplete relaxation of lower esophageal sphincter in response to
swallowing; result in functional obstruction of esophagus with
consequent dilation of more proximal esophagus.
By manometric studies, there are three abnormalities in achalasia:
1. Aperistalsis.
2. Partial or incomplete relaxation of lower esophageal sphincter
with swallowing.
3. Increased resting tone of lower esophageal sphincter.
Etiology:
Primary achalasia: mostly unknown causes (autoimmune, viral
infection??)
 There is loss of intrinsic inhibitory innervations of lower
esophageal sphincter & smooth muscles of body.
Secondary achalasia:
 Due to Chagas disease (due to Trypanosoma Cruzi…….. destruction
of myentric plexus of esophagus).
Gross: in primary disease
 Progressive dilation of the esophagus above the level of the lower
esophageal sphincter.
 Wall of esophagus either normal in thickness OR thicker than normal
because of hypertrophy of the muscular coat OR thinned & dilation.
MIC:
 Myentric plexus are usually absent from the body of esophagus.
 Myentric plexus are either normal or reduced in number in the
region of lower esophagus sphincter.
 Inflammation in the region of Myentric plexus (pathognomonic).
Complications:
 Squamous cell carcinoma in 5% of achalasia.
 Aspiration pneumonia.
 Candida esophagitis.
 Lower esophageal diverticuli.
Diverticuli:
 Is an outpouching of the alimentary tract containing all the
visceral layers.
Types:
1. Congenital Zenker 's diverticulum:
 Site: immediate above the upper esophageal sphincter.
 Cause: congenital weakness in the inferior constrictor muscle of
pharynx.
2. Traction diverticulum:
 Site: near the mid point of esophagus (lower third).
 Cause: T.B madiastinal lymphadenitis ……..pulling esophageal
wall….. sac like formation.
3. Pulsion diverticuli:
 Site: any part of esophagus.
 Cause: abnormal peristalsis of esophagus.
 Mic: lined by stratified Squamous epithelium.
Complications:
 Food regurgitation & aspiration.
 Mass in the neck.
Hiatus hernia:
 Separation & widening of diaphragmatic crura………. Protrusion
of dilated segment of stomach above the diaphragm.
Types:
1.Sliding hernia:
 Constitute 95% of cases.
 Associated with displacement of gastroesophageal junction above
the diaphragm…………. Protrusion of stomach above the
diaphragm as bell- like dilation.
 Usually associated with reflux esophagitis.
2. Rolling (Paraesophageal hernia):
 Here separated portion of stomach (mainly fundus) enter the thorax
through a wide diaphragmatic foramen, without displacement of
gastroesophaageal junction.
 Not associated with reflux esophagitis.
Complications:
1. Mucosal ulceration.
2. Bleeding.
3. Perforation.
3. Mixed type.
Lacerations of esophagus (Mallory – Weiss Syndrome):
 Longitudinal tearing in the esophagus at the gastroesophageal
junction.
 Seen in alcoholic individuals after severe retching, & vomiting.
 Tear can extend through mucosa, submucosa……. Upper
gastrointestinal bleeding.
 It forms 10% of Upper gastrointestinal bleeding.
Esophagitis:
 Inflammation of esophagus with injury to mucosa.
 Types:
 Infective 2. Non infective.
Non infective causes:
 Acute esophagitis:
 Ingestion of mucosal irritants (alcohol, corrosive acids & alkali,
hot tea).
 Uremia.
 Drugs
 Irradiation.
 Reflux esophagitis:
Is reflux of gastric contents into the lower esophagus in which the
acid- peptic action of the gastric juice is the main cause of injury
leading to inflammation of the lower esophagus.
Predisposing factors:
1. Decrease of efficacy of esophageal anti reflux mechanisms (of LES).
2. Inadequate or slowed esophageal clearance of refluxed material.
3. Presence of sliding hernia.
4. Increased gastric volume.
5. Impaired reparative capacity of the esophageal mucosa by prolonged
exposure to gastric juices.
Mic:
Three characteristics features:
1. Eosinophils with or without neutrophils in epithelial layer.
2. Basal cells hyperplasia.
3. Intraepithelial neutrophils are marker of severe injury.
 Elongation of lamina propria papillae.
Symptoms:
 Age more than 40years, dysphagia, heartburn, regurgitation.
Complications:
 1. Bleeding 2. Stricture. 3. Barrett esophagus
4. Predisposing to malignancy.
Barrett esophagus:
Is a replacement of the normal distal stratified Squamous mucosa by
metaplastic columnar epithelium containing goblet cells.
 Is a complication of long standing gastroesophageal reflux disease.
Pathogenesis:
 Prolonged & recurrent reflux………. Inflammation & ulceration of
Squamous esophageal mucosa ……. Then healing by ingrowth of
stem cells & re-epithelialization……. Formation of metaplastic
columnar cells (resistant to gastric acid).
 Sex: male>female, white > than other races.
Complications:
1. Esophageal ulcer.
2. Stricture formation.
3. Develpement of adenocarcinoma (risk of 30 – 40 times than normal
population).
Tumors of Esophagus:
1. Benign tumors:
 Leiomyoma (commonest tumor).
 Squamous cell papilloma.
2. Malignant tumors:
 Squamous cell carcinoma 90% of cases.
 Adenocarcinoma, carcinoid, undifferentiated 10%
Squamous cell carcinoma:
 Age: >50years.
 Sex: male >female, black > white.
 Geographic differences: most common in iran, china, central asia.
Etiology:
1. Dietary causes:
 Deficiency of vitamins & trace minerals e.g. vita A,C,Zn.
 Fungal contamination of foodstaffs.
 High contents of nitrites/ nitrosamines.
3. Life style:
 Alcohol consumption.
 Tabacco abuse.
4. Esophageal disorders:
 Long standing esophagitis.
 Achalasia.
 Plummer Vinson syndrome.
5. Genetic predisposition.
Sites:
 50% occur in the middle third.
 30% occur in the lower third.
 20% occur in the upper third.
Gross:
 Polypoid mass protrude into the lumen (60%).
 Ulcerative (25%).
 Diffuse thickening of wall …… narrowing thelumen.
Mic:
 Early lesions are dysplasia…….. carcinoma in situ……… invasive
carcinoma (Squamous cell carcinoma).
Spread:
1. Local spread to the mediastinum, resp. tract, aorta.
2. Lymphatics……… regionallymph nodes.
3. Hematogenous ……… liver, lung.
Adenocarcinoma:
 Mainly at distal third.
 Commonest predisposing cause is Barrett esophagus.
 Mic: mucin producing malignant glands.
THANK YOU

More Related Content

Similar to 2_2019_04_16!05_54_09_AM.ppt

Ulcerative intestine
Ulcerative  intestineUlcerative  intestine
Ulcerative intestineSaurav Singh
 
GIT & UGT 18.08.2012.ppt
GIT & UGT 18.08.2012.pptGIT & UGT 18.08.2012.ppt
GIT & UGT 18.08.2012.pptNazishIrfan3
 
The Oral Cavity And Gastrointestinal System June 08 Xition
The Oral Cavity And Gastrointestinal System   June 08 XitionThe Oral Cavity And Gastrointestinal System   June 08 Xition
The Oral Cavity And Gastrointestinal System June 08 XitionKarl Robstad
 
GASTROINTESTINAL PATHOLOGY
GASTROINTESTINAL PATHOLOGY GASTROINTESTINAL PATHOLOGY
GASTROINTESTINAL PATHOLOGY Dr Yaseen Khan
 
Gastrointestinal disorders 2
Gastrointestinal disorders 2Gastrointestinal disorders 2
Gastrointestinal disorders 2MD Specialclass
 
Gastrointestinal disorders 2
Gastrointestinal disorders 2Gastrointestinal disorders 2
Gastrointestinal disorders 2MD Specialclass
 
Seminar on genital Tuberculosis
Seminar on genital Tuberculosis Seminar on genital Tuberculosis
Seminar on genital Tuberculosis DR. AISHA ATEEQ
 
Lect.3.diseases of esophagus
Lect.3.diseases of  esophagusLect.3.diseases of  esophagus
Lect.3.diseases of esophagusMohanad Mohanad
 
Abdominal Tuberculosis
Abdominal TuberculosisAbdominal Tuberculosis
Abdominal TuberculosisPrateek Kumar
 
OESOPHAGUS PATHOLOGY
OESOPHAGUS PATHOLOGYOESOPHAGUS PATHOLOGY
OESOPHAGUS PATHOLOGYSuraj Dhara
 
ca gall bladder seminar.ppt
ca gall bladder seminar.pptca gall bladder seminar.ppt
ca gall bladder seminar.ppt9459654457
 
Peptic ulcer disease
Peptic ulcer diseasePeptic ulcer disease
Peptic ulcer diseaseLincyAsha
 
Lecture diseases of the git
Lecture diseases of the gitLecture diseases of the git
Lecture diseases of the gitluciferahamed
 

Similar to 2_2019_04_16!05_54_09_AM.ppt (20)

Ulcerative intestine
Ulcerative  intestineUlcerative  intestine
Ulcerative intestine
 
PEPTIC ULCERS.pptx
PEPTIC ULCERS.pptxPEPTIC ULCERS.pptx
PEPTIC ULCERS.pptx
 
GIT & UGT 18.08.2012.ppt
GIT & UGT 18.08.2012.pptGIT & UGT 18.08.2012.ppt
GIT & UGT 18.08.2012.ppt
 
Esophageal disorders
Esophageal disordersEsophageal disorders
Esophageal disorders
 
The Oral Cavity And Gastrointestinal System June 08 Xition
The Oral Cavity And Gastrointestinal System   June 08 XitionThe Oral Cavity And Gastrointestinal System   June 08 Xition
The Oral Cavity And Gastrointestinal System June 08 Xition
 
Tropical disease
Tropical diseaseTropical disease
Tropical disease
 
GASTROINTESTINAL PATHOLOGY
GASTROINTESTINAL PATHOLOGY GASTROINTESTINAL PATHOLOGY
GASTROINTESTINAL PATHOLOGY
 
Gastrointestinal disorders 2
Gastrointestinal disorders 2Gastrointestinal disorders 2
Gastrointestinal disorders 2
 
Gastrointestinal disorders 2
Gastrointestinal disorders 2Gastrointestinal disorders 2
Gastrointestinal disorders 2
 
Seminar on genital Tuberculosis
Seminar on genital Tuberculosis Seminar on genital Tuberculosis
Seminar on genital Tuberculosis
 
Lect.3.diseases of esophagus
Lect.3.diseases of  esophagusLect.3.diseases of  esophagus
Lect.3.diseases of esophagus
 
Abdominal Tuberculosis
Abdominal TuberculosisAbdominal Tuberculosis
Abdominal Tuberculosis
 
Peptic ulcer
Peptic ulcerPeptic ulcer
Peptic ulcer
 
Anat,ac,cancer
Anat,ac,cancerAnat,ac,cancer
Anat,ac,cancer
 
OESOPHAGUS PATHOLOGY
OESOPHAGUS PATHOLOGYOESOPHAGUS PATHOLOGY
OESOPHAGUS PATHOLOGY
 
ca gall bladder seminar.ppt
ca gall bladder seminar.pptca gall bladder seminar.ppt
ca gall bladder seminar.ppt
 
Amebiasis
AmebiasisAmebiasis
Amebiasis
 
Peptic ulcer disease
Peptic ulcer diseasePeptic ulcer disease
Peptic ulcer disease
 
Lecture diseases of the git
Lecture diseases of the gitLecture diseases of the git
Lecture diseases of the git
 
Gall bladder
Gall bladderGall bladder
Gall bladder
 

More from Ytchechy

Chapter 30 Urinalysis.ppt
Chapter 30 Urinalysis.pptChapter 30 Urinalysis.ppt
Chapter 30 Urinalysis.pptYtchechy
 
varicjvivose veiuvug8ns 9.ppt
varicjvivose veiuvug8ns 9.pptvaricjvivose veiuvug8ns 9.ppt
varicjvivose veiuvug8ns 9.pptYtchechy
 
8159968.ppt
8159968.ppt8159968.ppt
8159968.pptYtchechy
 
Anatomy of oesophagus.ppt
Anatomy of oesophagus.pptAnatomy of oesophagus.ppt
Anatomy of oesophagus.pptYtchechy
 
esophagus.pptx
esophagus.pptxesophagus.pptx
esophagus.pptxYtchechy
 
66_15575_EC410_2014_1__2_1_LECTURE 9.ppt
66_15575_EC410_2014_1__2_1_LECTURE 9.ppt66_15575_EC410_2014_1__2_1_LECTURE 9.ppt
66_15575_EC410_2014_1__2_1_LECTURE 9.pptYtchechy
 
04usdoppler.ppt
04usdoppler.ppt04usdoppler.ppt
04usdoppler.pptYtchechy
 
1a_Sources_of_Radiation.ppt
1a_Sources_of_Radiation.ppt1a_Sources_of_Radiation.ppt
1a_Sources_of_Radiation.pptYtchechy
 

More from Ytchechy (8)

Chapter 30 Urinalysis.ppt
Chapter 30 Urinalysis.pptChapter 30 Urinalysis.ppt
Chapter 30 Urinalysis.ppt
 
varicjvivose veiuvug8ns 9.ppt
varicjvivose veiuvug8ns 9.pptvaricjvivose veiuvug8ns 9.ppt
varicjvivose veiuvug8ns 9.ppt
 
8159968.ppt
8159968.ppt8159968.ppt
8159968.ppt
 
Anatomy of oesophagus.ppt
Anatomy of oesophagus.pptAnatomy of oesophagus.ppt
Anatomy of oesophagus.ppt
 
esophagus.pptx
esophagus.pptxesophagus.pptx
esophagus.pptx
 
66_15575_EC410_2014_1__2_1_LECTURE 9.ppt
66_15575_EC410_2014_1__2_1_LECTURE 9.ppt66_15575_EC410_2014_1__2_1_LECTURE 9.ppt
66_15575_EC410_2014_1__2_1_LECTURE 9.ppt
 
04usdoppler.ppt
04usdoppler.ppt04usdoppler.ppt
04usdoppler.ppt
 
1a_Sources_of_Radiation.ppt
1a_Sources_of_Radiation.ppt1a_Sources_of_Radiation.ppt
1a_Sources_of_Radiation.ppt
 

Recently uploaded

Daily Lesson Plan in Mathematics Quarter 4
Daily Lesson Plan in Mathematics Quarter 4Daily Lesson Plan in Mathematics Quarter 4
Daily Lesson Plan in Mathematics Quarter 4JOYLYNSAMANIEGO
 
Visit to a blind student's school🧑‍🦯🧑‍🦯(community medicine)
Visit to a blind student's school🧑‍🦯🧑‍🦯(community medicine)Visit to a blind student's school🧑‍🦯🧑‍🦯(community medicine)
Visit to a blind student's school🧑‍🦯🧑‍🦯(community medicine)lakshayb543
 
Multi Domain Alias In the Odoo 17 ERP Module
Multi Domain Alias In the Odoo 17 ERP ModuleMulti Domain Alias In the Odoo 17 ERP Module
Multi Domain Alias In the Odoo 17 ERP ModuleCeline George
 
Q-Factor General Quiz-7th April 2024, Quiz Club NITW
Q-Factor General Quiz-7th April 2024, Quiz Club NITWQ-Factor General Quiz-7th April 2024, Quiz Club NITW
Q-Factor General Quiz-7th April 2024, Quiz Club NITWQuiz Club NITW
 
31 ĐỀ THI THỬ VÀO LỚP 10 - TIẾNG ANH - FORM MỚI 2025 - 40 CÂU HỎI - BÙI VĂN V...
31 ĐỀ THI THỬ VÀO LỚP 10 - TIẾNG ANH - FORM MỚI 2025 - 40 CÂU HỎI - BÙI VĂN V...31 ĐỀ THI THỬ VÀO LỚP 10 - TIẾNG ANH - FORM MỚI 2025 - 40 CÂU HỎI - BÙI VĂN V...
31 ĐỀ THI THỬ VÀO LỚP 10 - TIẾNG ANH - FORM MỚI 2025 - 40 CÂU HỎI - BÙI VĂN V...Nguyen Thanh Tu Collection
 
How to Make a Duplicate of Your Odoo 17 Database
How to Make a Duplicate of Your Odoo 17 DatabaseHow to Make a Duplicate of Your Odoo 17 Database
How to Make a Duplicate of Your Odoo 17 DatabaseCeline George
 
week 1 cookery 8 fourth - quarter .pptx
week 1 cookery 8  fourth  -  quarter .pptxweek 1 cookery 8  fourth  -  quarter .pptx
week 1 cookery 8 fourth - quarter .pptxJonalynLegaspi2
 
Influencing policy (training slides from Fast Track Impact)
Influencing policy (training slides from Fast Track Impact)Influencing policy (training slides from Fast Track Impact)
Influencing policy (training slides from Fast Track Impact)Mark Reed
 
ANG SEKTOR NG agrikultura.pptx QUARTER 4
ANG SEKTOR NG agrikultura.pptx QUARTER 4ANG SEKTOR NG agrikultura.pptx QUARTER 4
ANG SEKTOR NG agrikultura.pptx QUARTER 4MiaBumagat1
 
How to Manage Engineering to Order in Odoo 17
How to Manage Engineering to Order in Odoo 17How to Manage Engineering to Order in Odoo 17
How to Manage Engineering to Order in Odoo 17Celine George
 
DIFFERENT BASKETRY IN THE PHILIPPINES PPT.pptx
DIFFERENT BASKETRY IN THE PHILIPPINES PPT.pptxDIFFERENT BASKETRY IN THE PHILIPPINES PPT.pptx
DIFFERENT BASKETRY IN THE PHILIPPINES PPT.pptxMichelleTuguinay1
 
Mental Health Awareness - a toolkit for supporting young minds
Mental Health Awareness - a toolkit for supporting young mindsMental Health Awareness - a toolkit for supporting young minds
Mental Health Awareness - a toolkit for supporting young mindsPooky Knightsmith
 
Congestive Cardiac Failure..presentation
Congestive Cardiac Failure..presentationCongestive Cardiac Failure..presentation
Congestive Cardiac Failure..presentationdeepaannamalai16
 
INTRODUCTION TO CATHOLIC CHRISTOLOGY.pptx
INTRODUCTION TO CATHOLIC CHRISTOLOGY.pptxINTRODUCTION TO CATHOLIC CHRISTOLOGY.pptx
INTRODUCTION TO CATHOLIC CHRISTOLOGY.pptxHumphrey A Beña
 
ESP 4-EDITED.pdfmmcncncncmcmmnmnmncnmncmnnjvnnv
ESP 4-EDITED.pdfmmcncncncmcmmnmnmncnmncmnnjvnnvESP 4-EDITED.pdfmmcncncncmcmmnmnmncnmncmnnjvnnv
ESP 4-EDITED.pdfmmcncncncmcmmnmnmncnmncmnnjvnnvRicaMaeCastro1
 
Concurrency Control in Database Management system
Concurrency Control in Database Management systemConcurrency Control in Database Management system
Concurrency Control in Database Management systemChristalin Nelson
 

Recently uploaded (20)

Daily Lesson Plan in Mathematics Quarter 4
Daily Lesson Plan in Mathematics Quarter 4Daily Lesson Plan in Mathematics Quarter 4
Daily Lesson Plan in Mathematics Quarter 4
 
Visit to a blind student's school🧑‍🦯🧑‍🦯(community medicine)
Visit to a blind student's school🧑‍🦯🧑‍🦯(community medicine)Visit to a blind student's school🧑‍🦯🧑‍🦯(community medicine)
Visit to a blind student's school🧑‍🦯🧑‍🦯(community medicine)
 
Multi Domain Alias In the Odoo 17 ERP Module
Multi Domain Alias In the Odoo 17 ERP ModuleMulti Domain Alias In the Odoo 17 ERP Module
Multi Domain Alias In the Odoo 17 ERP Module
 
Q-Factor General Quiz-7th April 2024, Quiz Club NITW
Q-Factor General Quiz-7th April 2024, Quiz Club NITWQ-Factor General Quiz-7th April 2024, Quiz Club NITW
Q-Factor General Quiz-7th April 2024, Quiz Club NITW
 
31 ĐỀ THI THỬ VÀO LỚP 10 - TIẾNG ANH - FORM MỚI 2025 - 40 CÂU HỎI - BÙI VĂN V...
31 ĐỀ THI THỬ VÀO LỚP 10 - TIẾNG ANH - FORM MỚI 2025 - 40 CÂU HỎI - BÙI VĂN V...31 ĐỀ THI THỬ VÀO LỚP 10 - TIẾNG ANH - FORM MỚI 2025 - 40 CÂU HỎI - BÙI VĂN V...
31 ĐỀ THI THỬ VÀO LỚP 10 - TIẾNG ANH - FORM MỚI 2025 - 40 CÂU HỎI - BÙI VĂN V...
 
How to Make a Duplicate of Your Odoo 17 Database
How to Make a Duplicate of Your Odoo 17 DatabaseHow to Make a Duplicate of Your Odoo 17 Database
How to Make a Duplicate of Your Odoo 17 Database
 
week 1 cookery 8 fourth - quarter .pptx
week 1 cookery 8  fourth  -  quarter .pptxweek 1 cookery 8  fourth  -  quarter .pptx
week 1 cookery 8 fourth - quarter .pptx
 
Influencing policy (training slides from Fast Track Impact)
Influencing policy (training slides from Fast Track Impact)Influencing policy (training slides from Fast Track Impact)
Influencing policy (training slides from Fast Track Impact)
 
ANG SEKTOR NG agrikultura.pptx QUARTER 4
ANG SEKTOR NG agrikultura.pptx QUARTER 4ANG SEKTOR NG agrikultura.pptx QUARTER 4
ANG SEKTOR NG agrikultura.pptx QUARTER 4
 
How to Manage Engineering to Order in Odoo 17
How to Manage Engineering to Order in Odoo 17How to Manage Engineering to Order in Odoo 17
How to Manage Engineering to Order in Odoo 17
 
DIFFERENT BASKETRY IN THE PHILIPPINES PPT.pptx
DIFFERENT BASKETRY IN THE PHILIPPINES PPT.pptxDIFFERENT BASKETRY IN THE PHILIPPINES PPT.pptx
DIFFERENT BASKETRY IN THE PHILIPPINES PPT.pptx
 
Mental Health Awareness - a toolkit for supporting young minds
Mental Health Awareness - a toolkit for supporting young mindsMental Health Awareness - a toolkit for supporting young minds
Mental Health Awareness - a toolkit for supporting young minds
 
Congestive Cardiac Failure..presentation
Congestive Cardiac Failure..presentationCongestive Cardiac Failure..presentation
Congestive Cardiac Failure..presentation
 
INCLUSIVE EDUCATION PRACTICES FOR TEACHERS AND TRAINERS.pptx
INCLUSIVE EDUCATION PRACTICES FOR TEACHERS AND TRAINERS.pptxINCLUSIVE EDUCATION PRACTICES FOR TEACHERS AND TRAINERS.pptx
INCLUSIVE EDUCATION PRACTICES FOR TEACHERS AND TRAINERS.pptx
 
Faculty Profile prashantha K EEE dept Sri Sairam college of Engineering
Faculty Profile prashantha K EEE dept Sri Sairam college of EngineeringFaculty Profile prashantha K EEE dept Sri Sairam college of Engineering
Faculty Profile prashantha K EEE dept Sri Sairam college of Engineering
 
INTRODUCTION TO CATHOLIC CHRISTOLOGY.pptx
INTRODUCTION TO CATHOLIC CHRISTOLOGY.pptxINTRODUCTION TO CATHOLIC CHRISTOLOGY.pptx
INTRODUCTION TO CATHOLIC CHRISTOLOGY.pptx
 
Mattingly "AI & Prompt Design: Large Language Models"
Mattingly "AI & Prompt Design: Large Language Models"Mattingly "AI & Prompt Design: Large Language Models"
Mattingly "AI & Prompt Design: Large Language Models"
 
ESP 4-EDITED.pdfmmcncncncmcmmnmnmncnmncmnnjvnnv
ESP 4-EDITED.pdfmmcncncncmcmmnmnmncnmncmnnjvnnvESP 4-EDITED.pdfmmcncncncmcmmnmnmncnmncmnnjvnnv
ESP 4-EDITED.pdfmmcncncncmcmmnmnmncnmncmnnjvnnv
 
prashanth updated resume 2024 for Teaching Profession
prashanth updated resume 2024 for Teaching Professionprashanth updated resume 2024 for Teaching Profession
prashanth updated resume 2024 for Teaching Profession
 
Concurrency Control in Database Management system
Concurrency Control in Database Management systemConcurrency Control in Database Management system
Concurrency Control in Database Management system
 

2_2019_04_16!05_54_09_AM.ppt

  • 2. The esophagus: It is muscular tube of 25cm. Functions:  Conduct food & fluid from the pharynx to the stomach.  Prevent reflux of gastric contents by the presence of two physiological sphincters.  Upper esophageal sphincter at the cricopharyngeal muscle.  Lower esophageal sphincter proximal to the esophageo-gastric junction. Mic:  Mucosa: non keratinizing Squamous epithelium.  Lamina properia: connective tissue.  Submucosa: containing glands.  Muscularis properia: all consist of smooth muscle, except first 6-8cm contains skeletal muscle.  No serosal coat.
  • 3. Congenital anomalies: 1. Esophageal atresia:  Is congenital absence of normal esophageal canal (blind end of the canal).  Usually associated with tracheoesophageal fistula. 2. Tracheoesophageal fistula:  It will lead to passage of food from the esophagus to the trachea…….. Leading to aspiration pneumonia which leads to suffocation. Aquired lesions: Stenosis:  Is a fibrous thickening of the esophageal wall forming constrictions. e.g. lower esophageal narrowing due to gastroesophageal reflux disease. Webs:  Protrusion of the esophageal mucosa into the esophageal lumen.  Common in female > 40 years.
  • 4. Etiology is unknown. 1. Upper esophageal Web: (web + iron deficiency anemia + glossitis + chelosis), this is called plummer Vinson syndrome……. Predispose to adenocarcinoma. 2. Lower esophageal Web (rings): called schtzki's ring (pathological annular narrowing at the lower esophagogastric junction; could be congenital or inflammatory (reflux disease). Lesions of motor dysfunctions: Achalasia (FAILURE TO RELAX): Incomplete relaxation of lower esophageal sphincter in response to swallowing; result in functional obstruction of esophagus with consequent dilation of more proximal esophagus.
  • 5.
  • 6.
  • 7.
  • 8. By manometric studies, there are three abnormalities in achalasia: 1. Aperistalsis. 2. Partial or incomplete relaxation of lower esophageal sphincter with swallowing. 3. Increased resting tone of lower esophageal sphincter. Etiology: Primary achalasia: mostly unknown causes (autoimmune, viral infection??)  There is loss of intrinsic inhibitory innervations of lower esophageal sphincter & smooth muscles of body. Secondary achalasia:  Due to Chagas disease (due to Trypanosoma Cruzi…….. destruction of myentric plexus of esophagus).
  • 9. Gross: in primary disease  Progressive dilation of the esophagus above the level of the lower esophageal sphincter.  Wall of esophagus either normal in thickness OR thicker than normal because of hypertrophy of the muscular coat OR thinned & dilation. MIC:  Myentric plexus are usually absent from the body of esophagus.  Myentric plexus are either normal or reduced in number in the region of lower esophagus sphincter.  Inflammation in the region of Myentric plexus (pathognomonic). Complications:  Squamous cell carcinoma in 5% of achalasia.  Aspiration pneumonia.  Candida esophagitis.  Lower esophageal diverticuli.
  • 10.
  • 11. Diverticuli:  Is an outpouching of the alimentary tract containing all the visceral layers. Types: 1. Congenital Zenker 's diverticulum:  Site: immediate above the upper esophageal sphincter.  Cause: congenital weakness in the inferior constrictor muscle of pharynx. 2. Traction diverticulum:  Site: near the mid point of esophagus (lower third).  Cause: T.B madiastinal lymphadenitis ……..pulling esophageal wall….. sac like formation. 3. Pulsion diverticuli:  Site: any part of esophagus.  Cause: abnormal peristalsis of esophagus.  Mic: lined by stratified Squamous epithelium. Complications:  Food regurgitation & aspiration.  Mass in the neck.
  • 12.
  • 13. Hiatus hernia:  Separation & widening of diaphragmatic crura………. Protrusion of dilated segment of stomach above the diaphragm. Types: 1.Sliding hernia:  Constitute 95% of cases.  Associated with displacement of gastroesophageal junction above the diaphragm…………. Protrusion of stomach above the diaphragm as bell- like dilation.  Usually associated with reflux esophagitis. 2. Rolling (Paraesophageal hernia):  Here separated portion of stomach (mainly fundus) enter the thorax through a wide diaphragmatic foramen, without displacement of gastroesophaageal junction.  Not associated with reflux esophagitis.
  • 14. Complications: 1. Mucosal ulceration. 2. Bleeding. 3. Perforation. 3. Mixed type. Lacerations of esophagus (Mallory – Weiss Syndrome):  Longitudinal tearing in the esophagus at the gastroesophageal junction.  Seen in alcoholic individuals after severe retching, & vomiting.  Tear can extend through mucosa, submucosa……. Upper gastrointestinal bleeding.  It forms 10% of Upper gastrointestinal bleeding. Esophagitis:  Inflammation of esophagus with injury to mucosa.  Types:  Infective 2. Non infective.
  • 15.
  • 16.
  • 17. Non infective causes:  Acute esophagitis:  Ingestion of mucosal irritants (alcohol, corrosive acids & alkali, hot tea).  Uremia.  Drugs  Irradiation.  Reflux esophagitis: Is reflux of gastric contents into the lower esophagus in which the acid- peptic action of the gastric juice is the main cause of injury leading to inflammation of the lower esophagus. Predisposing factors: 1. Decrease of efficacy of esophageal anti reflux mechanisms (of LES). 2. Inadequate or slowed esophageal clearance of refluxed material. 3. Presence of sliding hernia. 4. Increased gastric volume. 5. Impaired reparative capacity of the esophageal mucosa by prolonged exposure to gastric juices.
  • 18. Mic: Three characteristics features: 1. Eosinophils with or without neutrophils in epithelial layer. 2. Basal cells hyperplasia. 3. Intraepithelial neutrophils are marker of severe injury.  Elongation of lamina propria papillae. Symptoms:  Age more than 40years, dysphagia, heartburn, regurgitation.
  • 19. Complications:  1. Bleeding 2. Stricture. 3. Barrett esophagus 4. Predisposing to malignancy. Barrett esophagus: Is a replacement of the normal distal stratified Squamous mucosa by metaplastic columnar epithelium containing goblet cells.  Is a complication of long standing gastroesophageal reflux disease. Pathogenesis:  Prolonged & recurrent reflux………. Inflammation & ulceration of Squamous esophageal mucosa ……. Then healing by ingrowth of stem cells & re-epithelialization……. Formation of metaplastic columnar cells (resistant to gastric acid).  Sex: male>female, white > than other races. Complications: 1. Esophageal ulcer. 2. Stricture formation. 3. Develpement of adenocarcinoma (risk of 30 – 40 times than normal population).
  • 20.
  • 21.
  • 22. Tumors of Esophagus: 1. Benign tumors:  Leiomyoma (commonest tumor).  Squamous cell papilloma. 2. Malignant tumors:  Squamous cell carcinoma 90% of cases.  Adenocarcinoma, carcinoid, undifferentiated 10% Squamous cell carcinoma:  Age: >50years.  Sex: male >female, black > white.  Geographic differences: most common in iran, china, central asia. Etiology: 1. Dietary causes:  Deficiency of vitamins & trace minerals e.g. vita A,C,Zn.  Fungal contamination of foodstaffs.  High contents of nitrites/ nitrosamines.
  • 23. 3. Life style:  Alcohol consumption.  Tabacco abuse. 4. Esophageal disorders:  Long standing esophagitis.  Achalasia.  Plummer Vinson syndrome. 5. Genetic predisposition. Sites:  50% occur in the middle third.  30% occur in the lower third.  20% occur in the upper third. Gross:  Polypoid mass protrude into the lumen (60%).  Ulcerative (25%).  Diffuse thickening of wall …… narrowing thelumen.
  • 24. Mic:  Early lesions are dysplasia…….. carcinoma in situ……… invasive carcinoma (Squamous cell carcinoma). Spread: 1. Local spread to the mediastinum, resp. tract, aorta. 2. Lymphatics……… regionallymph nodes. 3. Hematogenous ……… liver, lung. Adenocarcinoma:  Mainly at distal third.  Commonest predisposing cause is Barrett esophagus.  Mic: mucin producing malignant glands.
  • 25.
  • 26.
  • 27.