Download Free Medical Esophagus and Disorders PowerPoint Presentation

Esophagus and Disorders PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : PPT ON OESOPHAGUS AND DISORDERS, EEPING IN VIEW OF FREE KNOWLEDGE TRANSFER, THANKS TO ALL WHOSE WORK HAS BEEN USED AND ALL FREE TO USE IT TOO

Tags : ESOPHAGUS,DISORDERS

Published on : Dec 15, 2021 | Views : 2123 | Downloads : 9

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

ESOPHAGUS & DISORDERS Dr Harjitpal Singh Assistant Professor(ENT), Dr RKGMC, Hamirpur
Slide 2-

ESOPHAGEAL ANATOMY Upper Esophageal Sphincter (UES) Lower Esophageal Sphincter (LES) Esophageal Body (cervical & thoracic) 18 to 25 cm
Slide 3-

ESOPHAGEAL ANATOMY Functionally the esophagus can be considered in three zones (UES, body, LES). The upper esophageal sphincter (UES) is tonically closed and contracts during inspiration, preventing air from entering into the gastrointestinal tract, and reflux. It relaxes during swallow, belching and vomiting. The lower esophageal sphincter (LES) maintains a steady baseline tone (~20 mm Hg) to prevent gastric contents from entering the esophagus. The LES also contracts during periods of increased intra-abdominal pressure, preventing reflux due to the pressure build up in the abdomen.
Slide 4-

ESOPHAGEAL ANATOMY The esophagus has 2 muscle layers: Inner circular layer Outer longitudinal layer. The longitudinal muscle shortens the esophagus, while the circular muscle forms lumen-occluding ring contractions. The combination of these localized contractions is responsible for peristalsis. The proximal esophagus contains striated muscle and the distal esophagus smooth muscle, with a long transition zone between. Striated muscle is “faster”. Lined by non keratinizing stratified squamous epithelium.
Slide 5-

ESOPHAGEAL ANATOMY Tubular structure about 25 cm long. Begins at the level of C6. Pierces the diaphragm atT10. It is divided into 3 parts: 1- Cervical. 2- Thoracic. 3- Abdominal. Cervical Thoracic Abdominal
Slide 6-

RELATIONS-CERVICAL PART Post: Vertebral column. Laterally: Lateral: Lobes of the thyroid gland. Anteriorly: Anterior: Trachea and the recurrent laryngeal nerves.
Slide 7-

RELATIONS-THORACIC PART In the thorax, it passes downward and to the left through superior then to posterior mediastinum At the level of the sternal angle, the aortic arch pushes the esophagus again to the midline.
Slide 8-

ANTERIOR RELATIONS-THORACIC PART Trachea Left recurrent laryngeal nerve Left principal bronchus Pericardium Left atrium
Slide 9-

POSTERIOR RELATIONS-THORACIC PART Bodies of the thoracic vertebrae Thoracic duct Azygos vein Right posterior intercostal arteries Descending thoracic aorta (at the lower end)
Slide 10-

LATERAL RELATIONS-THORACIC PART On the Right side: Right mediastinal pleura Terminal part of the azygos vein. On the Left side: Left mediastinal pleura Left subclavian artery Aortic arch Thoracic duct
Slide 11-

ESOPHAGEAL CONSTRICTIONS The esophagus has 3 anatomic constrictions. The first is at the junction with the pharynx(pharyngeoesophageal junction). The second is at the crossing with the aortic arch and the left main bronchus. The third is at the junction with the stomach.
Slide 12-

ESOPHAGEAL CONSTRICTIONS They may cause difficulties in passing an endoscope. In case of swallowing of caustic liquids (mostly in children), this is where the burning is the worst and strictures develop. The esophageal strictures are a common sites of the development of esophageal carcinoma
Slide 13-

ESOPHAGUS-ARTERIAL SUPPLY Upper third by the inferior thyroid artery. The middle third by the thoracic aorta. The lower third by the left gastric artery.
Slide 14-

ESOPHAGUS-VENOUS DRAINAGE The upper third drains in into the inferior thyroid veins. The middle third into the azygos veins. The lower third into the left gastric vein, which is a tributary of the portal vein.
Slide 15-

ESOPHAGUS-LYMPH DRAINAGE The upper third is drained into the deep cervical nodes. The middle third is drained into the superior and inferior mediastinal nodes. The lower third is drained in the celiac lymph nodes in the abdomen.
Slide 16-

ESOPHAGUS-NERVE SUPPLY It is supplied by sympathetic fibers from the sympathetic trunks. The parasympathetic supply comes form the vagus nerves. Inferior to the roots of the lungs, the vagus nerves join the sympathetic nerves to form the esophageal plexus. The left vagus lies anterior to the esophagus. The right vagus lies posterior to it.
Slide 17-

NORMAL PHASES OF SWALLOWING Voluntary oropharyngeal phase – bolus is voluntarily moved into the pharynx Involuntary UES relaxation peristalsis (aboral movement) LES relaxation
Slide 18-

NORMAL PHASES OF SWALLOWING Between swallows UES prevents air entering the esophagus during inspiration and prevents esophagopharyngeal reflux LES prevents gastroesophageal reflux peristaltic and non-peristaltic contractions in response to stimuli capacity for retrograde movement (belch, vomiting) and decompression
Slide 19-

NORMAL PHASES OF SWALLOWING Primary peristalsis is a wave that strips the esophagus proximal to distal, pushing the food bolus aborally toward the stomach. In the body, the wave travels at 3-4 cm/s. Secondary peristalsis is induced by esophageal distension from retained bolus, reflux, or swallowed air. It’s role is to clear the esophagus of retained food. Tertiary contractions are simultaneous (nonperistaltic), dysfunctional contractions and have no known physiologic role and are seen more often in the elderly and can be induced by stimuli (stress, reflux, etc.)
Slide 20-

NORMAL SWALLOWING Cortical Swallowing Areas Swallowing Center Motor Nuclei Oropharynx & Esophagus Frontal cortex Brainstem
Slide 21-

NORMAL SWALLOWING Primary peristalsis is triggered by the swallowing center. Myogenic propagation occurs in the body of the esophagus.
Slide 22-

ESOPHAGEAL DISORDERS Motility Anatomic & Structural Reflux Infectious Neoplastic Miscellaneous
Slide 23-

ESOPHAGEAL MOTILITY DISORDERS
Slide 24-

ESOPHAGEAL MOTILITY DISORDERS These can be further divided into hypomotlity and hypermotlity disorders.
Slide 25-

ESOPHAGEAL MOTILITY DISORDERS UES UES disorders neuromuscular disorders Esophageal Body achalasia diffuse esophageal spasm nutcracker esophagus nonspecific esophageal dysmotility LES achalasia hypertensive LES Primary Disorders achalasia diffuse esophageal spasm nutcracker esophagus nonspecific esophageal dysmotility Secondary Disorders severe esophagitis scleroderma diabetes Parkinson’s stroke
Slide 26-

ESOPHAGEAL MOTILITY DISORDERS Achalasia – Inadequate LES relaxation Diffuse Esophageal Spasm – Uncoordinated contraction Nutcracker Esophagus – Hypercontraction Ineffective Esophageal Motility – Hypocontraction
Slide 27-

CARDIAC ACHALASIA First clinically recognized esophageal motility disorder Described in 1672, treated with whale bone bougie Term coined in 1929 Epidemiology 1-2 per 200,000 population usually presents between ages 25 to 60 male=female Caucasians > others average symptom duration at diagnosis: 2-5 years The characteristic features of this smooth muscle motility disorder are absence of peristalsis in the body of esophagus and high resting pressure in LES, which does not relax during swallowing.
Slide 28-

CARDIAC ACHALASIA Barium swallow study demonstrating characteristics of achalasia, including the bird's beak deformity and a dilated esophagus.
Slide 29-

CARDIAC ACHALASIA Etiology: Exact primary cause is not known but data suggest following factors: Hereditary Degenerative Autoimmune Infectious. The secondary causes may be following: Chagas disease: It consists of cardiomyopathy, megacolon and achalasia. Gastric carcinoma Lymphoma infiltrating lower esophagus Scleroderma.
Slide 30-

CARDIAC ACHALASIA Pathophysiology: Patchy infiltration of T lymphocytes, eosinophils and mast cells. Loss of ganglion cells. Myenteric neural fibrosis. Selective loss of postganglionic inhibitory neurons (nitric oxide and vasoactive intestinal polypeptide) in LES results in insufficient LES relaxation. Postganglionic cholinergic neurons, which produces high basal LES pressure, are spared.
Slide 31-

CARDIAC ACHALASIA Clinical presentation: Most common symptoms, which persist and do not progress for years, include: Dysphagia for liquids and solids. Regurgitation of swallowed food especially in night. Choking and coughing awake the patient. Chest pain. History of compensatory measures: Lifting of neck and carbonated drinks. Weight loss: It is minimal. Physical examination: It is unremarkable.
Slide 32-

CARDIAC ACHALASIA Investigations: Plain film (air-fluid level, wide mediastinum, absent gastric bubble, pulmonary infiltrates) Barium swallow with fluoroscopy: (dilated esophagus with taper at LES) Bird peak (good screening test-95% accurate) Endoscopy (rule out GE junction tumors, esp. age>60) Esophageal manometry (absent peristalsis,  LES relaxation, & resting LES >45 mmHg)
Slide 33-

CARDIAC ACHALASIA Investigations: Barium swallow with fluoroscopy: In addition to the characteristic smooth tapering of lower esophagus leading to closed LES resembling rattail or bird’s beak, other findings include Loss of primary peristalsis in distal two-third esophagus Poor emptying of esophagus Retained food and saliva produce heterogeneous airfluid level at the top of barium column Esophagus may be dilated or tortuous like sigmoid Presence of epiphrenic diverticulum
Slide 34-

CARDIAC ACHALASIA Treatment Goals: Reduce LES pressure and Increase emptying Endoscopic pneumatic dilatation: It tears LES muscle fibers and thus reduces LES pressure. Perforation occurs in 5% of patients. Modified Heller’s operation: Myotomy (incision of circular muscle fibers) of narrowed lower portion of esophagus is the definitive treatment. Botulinum toxin injection in LES: It block’s cholinergic nerves and needs to be repeated every 2 years. Medical: Calcium channel blockers and nitrates.
Slide 35-

SPASTIC MOTILITY DISORDERS of the ESOPHAGUS Hypertensive LES Nonspecific Esophageal Dysmotility Nutcracker Esophagus Diffuse Esophageal Spasm
Slide 36-

HYPERTENSIVE LES NONSPECIFIC ESOPHAGEAL DYSMOTILITY High LES pressure >45 mm Hg Normal peristalsis Often overlaps with other motility disorders 1/3 of pts with non-specific dysmotility will have LES hypertension. Abnormal motility pattern Fits in no other category non-peristalsis in 20-30% of wet swallows low pressure waves (<30 mm Hg) prolonged contractions
Slide 37-

NUT CRACKER ESOPHAGUS • There occur strong and high amplitude peristaltic esophageal contractions, which can be seen in manometric studies. • There is high manometeric esophageal pressure of 180 mm of Hg • Patients present with dysphagia and substernal pain like diffuse esophageal spasm (DES). .
Slide 38-

SPASTIC MOTILITY DISORDERS of the ESOPHAGUS Manometry Barium Esophagram Endoscopy PH monitoring
Slide 39-

SPASTIC MOTILITY DISORDERS of the ESOPHAGUS Treatment: Reassurance Nitrates, anticholinergics, hydralazine - all unproven Calcium channel blockers - too few data with negative controlled studies in chest pain Psychotropic drugs – trazodone, imipramine and setraline effective in controlled studies Dilation - anecdotal reports, probable placebo effect
Slide 40-

DIFFUSE ESOPHAGEAL SPASM/ CORK SCREW ESOPHAGUS In this motility disorder of smooth muscle, there occur spontaneous strong nonperistaltic contractions of the body of esophagus. There occurs degeneration of nerve processes but sphincter relaxation is normal. Clinical Features: Sudden dysphagia and substernal chest pain simulating angina pectoris in adults. Symptom improves with sublingual nitroglycerin.
Slide 41-

DIFFUSE ESOPHAGEAL SPASM Diagnosis: Barium swallow: Shows segmented esophageal spasms, which appear like a rosary bead or a corkscrew. Manometry: Normal relaxation of the sphincter on swallowing and strong nonperistaltic uncoordinated esophageal contractions. Upper gastrointestinal endoscopy.
Slide 42-

DIFFUSE ESOPHAGEAL SPASM Upper gastrointestinal endoscopy revealed typical corkscrew esophagus. A barium swallow examination showed a constricted and twisted lumen of the esophagus.
Slide 43-

DIFFUSE ESOPHAGEAL SPASM Treatment: Medical: Calcium channel blockers and nitrates usually give good response. Surgical: Dilatation of lower esophagus and myotomy of esophagus extending from the arch of aorta to lower sphincter is done in severe refractory cases.
Slide 44-

HYPOMOTILTY DISORDERS Primary (idiopathic) Aging produces gradual decrease in contraction strength Reflux patients have varying degrees of hypomotility More common in patients with atypical reflux symptoms Usually persists after reflux therapy Defined as Low contraction wave pressures (<30 mm Hg) Incomplete peristalsis in 30% or > of wet swallows
Slide 45-

HYPOMOTILTY DISORDERS Secondary Scleroderma in >75% of patients progressive, resulting in aperistalsis in smooth-muscle region incompetent LES with reflux Other “connective tissue diseases” CREST polymyositis & dermatomyositis Diabetes 60% with neuropathy have abnormal motility on testing (most asx) Other hypothyroidism, alcoholism, amyloidosis
Slide 46-

GASTROESOPHAGEAL REFLUX DISEASE Etiology: Inappropriate function of LES permits reflux of gastric contents into esophagus. The conditions, which decrease LES tone, are following: High levels of progesterone in pregnancy Sliding hiatus hernia Fatty foods, Chocolate and peppermints Tobacco smoking and alcohol Drugs, which relax the smooth muscle: Anticholinergic, beta-adrenergic drugs and calcium channel blockers
Slide 47-

GASTROESOPHAGEAL REFLUX DISEASE Clinical Features: Typical: Heartburn and acid regurgitation usually occur after meal when patient is recumbent. Dysphagia (peptic stricture in esophagus), odynophagia (esophagitis) and belching. Angina-like chest pain, which worsens after sublingual nitroglycerin, while lying in bed at night.
Slide 48-

GASTROESOPHAGEAL REFLUX DISEASE Clinical Features: Atypical GERD symptoms include nonproductive cough, hoarseness of voice and asthma-like symptoms and dental erosions. They indicate extra esophageal GERD. The diagnosis is confirmed when symptoms respond to GERD therapy. Nonproductive cough: GERD is among the most common causes of chronic cough. Other causes include postnasal drip, asthma and tuberculosis.
Slide 49-

GASTROESOPHAGEAL REFLUX DISEASE Reflux laryngitis or laryngoesophageal reflux : – Symptoms include hoarseness, throat clearing, dysphagia, increased phlegm and globus sensation. – Physical findings, which may be secondary to associated smoking, alcohol, allergies, asthma, viral illness and voice abuse, include laryngeal erythema, edema, vocal cord nodules and polyps, granulations, leukoplakia, cancer and pharyngeal ulcerations. – Other signs, which again may be secondary to associated nasal congestion and postnasal drip, include interarytenoid bar, arytenoids medial wall erythema.
Slide 50-

GASTROESOPHAGEAL REFLUX DISEASE Dental erosions: Repeated long time exposure. Asthma-like symptoms: About 70–80% asthma patients have GERD and treated with PPI. GERD-induced asthma is suspected in following cases – Adult onset of asthma – No family history of asthma or atopy – Heartburn precedes onset of asthma – Wheezing exacerbated with meals, exercise or supine position – Nocturnal wheezing.
Slide 51-

GASTROESOPHAGEAL REFLUX DISEASE Diagnosis: Clinical: History and response to therapy confirm the diagnosis. Esophagogastroduodenoscopy: Erosions and ulcerations at SCJ in reflux esophagitis and findings of Barrett’s esophagus. Ambulatory 24-hour pH monitoring: This gold standard test is done in refractory cases. Bernstein test: Infusion of 0.1 M HCl in esophagus reproduces chest pain.
Slide 52-

GASTROESOPHAGEAL REFLUX DISEASE Subgroups: The subgroups of GERD include: Non erosive reflux disease: Nonerosive reflux disease patients have typical GERD symptoms but do not show endoscopic findings of GERD. Reflux esophagitis: In reflux esophagitis, mucosal changes are confirmed histopathologically. Barrett’s esophagus: This potentially serious GERD complication predisposes to development of adenocarcinoma of esophagus. Normal stratified squamous epithelium of distal esophagus is replaced by intestinal columnar metaplasia.
Slide 53-

GASTROESOPHAGEAL REFLUX DISEASE Treatment: The aims of the treatment include decreasing reflux, improving esophageal clearance and protecting esophageal mucosa. Lifestyle modifications: Weight loss Small and frequent meals Avoid fats, sweets, chocolate, tomatoes, onions, alcohol and caffeine at bedtime Finish dinner 3 hours before going to bed Elevation of head end of bed during sleep
Slide 54-

GASTROESOPHAGEAL REFLUX DISEASE Medical treatment: It includes Antacids. H2 receptor antagonists: H2 receptor antagonist (ranitidine) heals 50% cases of reflux esophagitis. Proton pump inhibitors. Prokinetic drugs: Metoclopramide, Domperidone).
Slide 55-

GASTROESOPHAGEAL REFLUX DISEASE Antireflux surgery: In Nissen’s fundoplication, fundus of stomach is wrapped around LES. Indication: Patients who do not respond to medical treatment and have normal esophageal peristalsis, otherwise postoperative achalasia can occur. Recent developments: Endoscopic suturing Injection of biopolymers in LES Radiofrequency delivery to GEJ
Slide 56-

GASTROESOPHAGEAL REFLUX DISEASE Complications: Esophagitis Ulcers in esophagus Hemorrhage Peptic stricture in esophagus Aspiration Barrett’s esophagus
Slide 57-

BARRETT’S ESOPHAGUS Pathogenesis: In Barrett’s esophagus, the normal stratified squamous epithelium of distal esophagus is replaced by intestinal columnar metaplasia. This potentially serious complication occurs in 10–20% of GERD patients. It predisposes to the development of esophageal adenocarcinoma which is more likely in following conditions: Barrett is > 8 cm long Presence of dysplasia, Smoking.
Slide 58-

BARRETT’S ESOPHAGUS Diagnosis: Endoscopy: Pale pink mucosa of distal esophagus is replaced to salmon pink and SCJ is displaced proximal to GEJ. It can be divided into two types: short segment (< 3 cm) and long segment (> 3 cm). Biopsy: Intestinal columnar metaplasia shows mucin containing goblet cells.
Slide 59-

BARRETT’S ESOPHAGUS Treatment: Antireflux therapy: As mentioned in GERD. Enoscopic surveillance: To detect dysplasia and adenocarcinoma at an earlier and curable stage. Current guidelines suggest four quadrant biopsies at 2 cm intervals along the entire length of Barrett’s esophagus. No dysplasia: Every 3 years. Low-grade dysplasia: Every 1 year until no dysplasia. High-grade dysplasia: – Focal: Every 3 months. – Multifocal: Esophagectomy, ablation therapy, or esophageal mucosal resection.
Slide 60-

12/17/2021 60 Thank You

User Presentation
Related Presentations

Physiology of Hearing and Equilibrium

By: HarjitpalSingh
Views: 250

Esophagus and Disorders

By: HarjitpalSingh
Views: 2123

ANATOMY OF PHARYNX

By: HarjitpalSingh
Views: 6561

Tumours of Nose and PNS

By: HarjitpalSingh
Views: 2900

TUMORS OF NASOPHARYNX

By: HarjitpalSingh
Views: 3593

Benign Laryngeal Lesions

By: medhelp
Views: 1123

The Cochlear Implant

By: KhushbuSG
Views: 681

BASIC EAR ANATOMY

By: JenniferDwayne
Views: 2845

Esophageal Disorders

By: yourdoctors
Views: 730

Unilateral Vocal Cord Paralysis

By: FrankMarco
Views: 840

HarjitpalSingh

About : Associate Professor (ENT) at Dr Radhakrishnan Govt Medical College, Hamirpur(H P)
Occupation : Medical Professional
Specialty : MD
Country : India
Website :

HEALTH A TO Z