LO 1

Anatomy, Histology and Biochemicals from upper GI

ANATOMY

MOUTH

Esophagus• The largest part of thorax• Pars thoracalis (behind trachea)• Pars abdominalis : enter to the gastric cardia ventriculi• transition ostium cardiacum/ cardiac orificium/ junctio gastroesophagei• It has LES and its function for preventing reflux• The closing of spincter is controlled by vagal and amplified by gastrin , and

decreased by secretin response, cholecystokinin, glucacon• Vascularitation:

– a. gastrica sinistra– Branch of a. phrenica inferior– V. azygos– V. gastrica sinistra

• nerves : N. vagus (parasimpatis), N. splanchnici (simpatis)

Histology

Introduction

• The digestive system consists– Oral cavity, esophagus, stomach, small and large

intestines, rectum, and anus– Its associated glands—salivary glands, liver, and

pancreas

• Function– Obtain from ingested food the molecules

necessary for the maintenance, growth, and energy needs of the body

Introduction• The digestive system

consists– Oral cavity, esophagus,

stomach, small and large intestines, rectum, and anus

– Its associated glands—salivary glands, liver, and pancreas

• Function– Obtain from ingested

food the molecules necessary for the maintenance, growth, and energy needs of the body

General Structure• Mucosa

– Epithelial lining, underlying lamina propria (loose connective tissue rich in blood vessels, lymphatics, lymphocytes and smooth muscle cells, sometimes also containing glands)

– Thin layer of smooth muscle called the muscularis mucosae usually separating mucosa from submucosa

• Submucosa – Denser connective tissue with many blood and lymph vessels and the

submucosal plexus of autonomic nerves– Also contain glands and lymphoid tissue

• Muscularis – Smooth muscle cells that are spirally oriented and divided into two

sublayers (internal – circular; external – longitudinal)– Autonomic myenteric nerve plexus

• Serosa – Loose connective tissue, rich in blood vessels, lymphatics, and

adipose tissue, with a simple squamous covering epithelium (mesothelium).

Lips

• Has striated muscle & a transition from oral non keratinized epithelium to keratinized epithelium of the skin

Tongue

• Mass of striated muscle covered by a mucous membrane whose structure varies according to the region

• Tongue's dorsal surface is irregular, covered anteriorly by a great number of small eminences called papillae

• The posterior third of the tongue's dorsal surface is separated from the anterior two thirds by a V-shaped groove, the terminal sulcus

• Papillae– Filiform papillae

• Elongated conical shape, and are heavily keratinized, which gives their surface a gray or whitish appearance

• Lacks taste buds; mechanical in providing a rough surface that facilitates food movement during chewing

– Fungiform papillae• Lightly keratinized, and mushroom-shaped with connective

tissue cores and scattered taste buds on their upper surfaces– Foliate papillae – Vallate (or circumvallate) papillae

• Taste Buds

Teeth

• In the adult human there are normally 32 permanent teeth, arranged in two bilaterally symmetric arches in the maxillary and mandibular bones

• Each tooth has – Crown exposed above the gingiva– Constricted neck at the gum– One or more roots below the gingiva that hold the

teeth in bony sockets called alveoli, one for each tooth

• Dentin– Calcified tissue consisting of 70% calcium

hydroxyapatite, making it harder than bone– Organic matrix contains type I collagen fibers and

glycosaminoglycans secreted by odontoblasts– Mineralization of the predentin matrix involves

matrix vesicles in a process similar to that in osteoid – Slender apical odontoblast processes lie within

dentinal tubules which penetrate the full thickness of the dentin, gradually becoming longer as the dentin becomes thicker

• Enamel – The hardest component of the human body,

consisting of nearly 98% hydroxyapatite and the rest organic material (amelogenin and enamelin), but no collagen

– Containing fluorapatite is more resistant to acidic dissolution caused by microorganisms

– Consists of interlocking rods or columns, enamel rods (prisms), bound together by other enamel

– In developing teeth enamel matrix is secreted by a layer of cells called ameloblasts, each of which produces one enamel prism

• Pulp – Consists of connective tissue resembling mesenchyme– Main components are the layer of odontoblasts, many

fibroblasts, thin collagen fibrils, and ground substance – Highly innervated and vascularized tissue

• Periodontium – Maintaining the teeth in the maxillary and mandibular

bones– consists of the cementum, periodontal ligament, alveolar

bone, and gingiva• Cementum covers the dentin of the root and is similar in

composition to bone

Esophagus

• A muscular tube whose function is to transport food from the mouth to the stomach

• Lined by nonkeratinized stratified squamous epithelium with stem cells scattered throughout the basal layer

• In the submucosa are groups of small mucus-secreting glands, the esophageal glands, secretions of which facilitate the transport of foodstuffs and protect the mucosa

Biochemicals

Source Enzyme Activator Substrat Function or catalytic product

Saliva gland α-Amilase Saliva Cl- Flour essence Hidrolisis bond 1:4 @; produce dextrin @limit, maltotriosa, and maltosa

Lingual gland Lingual lipase Trigliserida Lipid acid plus 1,2 - diasilgliserol

Gaster Pepsin (pepsinogen)

Gaster lipase

HCl- Protein and polipeptida

Trigliserida

Decompose peptida chain which closer with aromatic amino acid

Lipid acid and gliserol

Digestive EnzymesENZYME SOURCE SUBTRATES PRODUCTS

SALIVA

Salivary amylase Salivary glands. Starches. Maltose, maltotriose, α-dextrins.

Lingual lipase Lingual glands. Triglycerides (fats & oils) and other lipids.

Fatty acids & diglycerides.

GASTRIC JUICE

Pepsin Stomach chief cells. Proteins. Peptides.

Gastric lipase Stomach chief cells. Triglycerides. Fatty acids & monoglycerides.

PANCREATIC JUICE

Pancreatic amylase Pancreatic acinar cells. Starches. Maltose, maltotriose, α-dextrins.

Trypsin Pancreatic acinar cells. Proteins. Peptides.

Chymotrypsin Pancreatic acinar cells. Proteins. Peptides.

Elastase Pancreatic acinar cells. Proteins. Peptides.

ENZYME SOURCE SUBSTRATES PRODUCTS

Carboxypeptidase. Pancreatic acinar cells. Amino acid at carboxyl end peptides.

Amino acids & peptides.

Pancreatic lipase Pancreatic acinar cells. Triglycerides that have been emulsified by bile salts.

Fatty acids & monoglycerides.

Ribonuclease Pancreatic acinar cells. RNA. Nucleotides.

Deoxyribonuclease Pancreatic acinar cells. DNA. Nucleotides.

BRUSH BORDERS

α-Dextrinase Small intestine. α-Dextrins. Glucose.

Maltase Small intestine. Maltose. Glucose.

Sucrase Small intestine. Sucrose. Glucose & fructose.

Lactase Small intestine. Lactose. Glucose & galactose.

Enterokinase Small intestine. Trypsinogen. Trypsin.

Aminopeptidase Small intestine. Amino acid at amino end of peptides.

Amino acids & peptides.

Dipeptidase Small intestine. Dipeptidases. Amino acids.

Nucleosidases & phosphatases

Small intestine. Nucleotides. Nitrogenous bases, pentoses & phosphates.

LO 2

Physiology of swallowing

Physiology

LO3. Describe Physiology • Food is the body's source of fuel energy• Proteins need to be broken down into amino acids,

starches into sugars, and fats into fatty acids and glycerol.• During digestion two main processes occur at the same

time:– Mechanical Digestion: larger pieces of food get broken down

into smaller pieces while being prepared for chemical digestion. Mechanical digestion starts in the mouth and continues in to the stomach.

– Chemical Digestion: several different enzymes break down macromolecules into smaller molecules that can be more efficiently absorbed. Chemical digestion starts with saliva and continues into the intestines.

Physiology

• There are four basic digestive processes:– Motility– Secretion– Digestion– Absorption

Motility• MOTILITY The term motility refers to the

muscular contractions that mix and move forward the contents of the digestive tract.

• maintains a constant low level of contraction known as tone

• Two basic types of phasic digestive motility are superimposedn on this ongoing tonic activity:– propulsive movements– mixing movements.

• Propulsive movements propel or push the contents forward through the digestive tract

• Mixing movements serve a twofold function. – First, by mixing food with the digestive juices, these

movements promote digestion of the food– Second, they facilitate absorption by exposing all parts of

the intestinal contents to the absorbing surfaces of the digestive tract

Secretion

• Exocrine glands • On appropriate neural or hormonal

stimulation, the secretions are released into the digestive tract lumen.

• Normally, the digestive secretions are reabsorbed in one form or another back into the blood after their participation in digestion.

Digestion

• Humans consume three diff erent biochemical categories of energy-rich foodstuffs: carbohydrates, proteins, and fats.

• Th e term digestion refers to the biochemical breakdown of the structurally complex foodstuff s of the diet into smaller, absorbable units by the enzymes produced within the digestive system as follows:

• The simplest carbohydrates are the simple sugars or monosaccharides (“one-sugar” molecules), such as glucose, fructose, and galactose

• Most ingested carbohydrate is in the form of polysaccharides (“many-sugar” molecules)

• starch derived from plant sources• meat contain glycogen• Cellulose, another dietary polysaccharide, found

in plant walls, (represents the indigestible fiber or “bulk” of our diets.)

• proteins consist of various combinations of amino acids held together by peptide bonds

• digestion, proteins are degraded primarily into their constituent amino acids as well as a few small polypeptides

• Most dietary fats are in the form of triglycerides, which are neutral fats, each consisting of a glycerol with three fatty acid molecules attached (tri means “three”)

• Triglycerides monoglycerides + free fatty acids

Absorption

• Through the process of absorption, the small absorbable units that result from digestion, along with water, vitamins, and electrolytes, are transferred from the digestive tract lumen into the blood or lymph

Accessory digestive organs

• The accessory digestive organs include the salivarynglands, the exocrine pancreas, and the biliary system, which is composed of the liver and gallbladder.

• Four factors are involved in regulating digestive system function1. Autonomous smooth muscle function 2. Intrinsic nerve plexuses 3. Extrinsic nerves4. Gastrointestinal hormones

Autonomous Smooth Muscle Function

• The prominent type of self-induced electrical activity in digestive smooth muscle is slow-wave potentials alternatively referred to as the digestive tract’s basic electrical rhythm (BER).

• Interstitial cells of Cajal are the pacemaker cells that instigate cyclic slow-wave activity

• These pacemaker cells lie at the boundary between the longitudinal and circular smooth muscle layers.

• At threshold, voltagegated Ca2 channels are activated resulting in Ca2 influx into the smooth muscle cell. The resultant Ca2 entry has two effects:– It is responsible for the rising phase of an action

potential, with the falling phase being brought about as usual by K efflux

– it triggers a contractile response• The greater the number of action potentials, the

higher the cytosolic Ca2 concentration, the greater the cross-bridge activity, and the stronger the contraction.

Intrinsic Nerve Plexus

• intrinsic nerve plexuses are the two major networks of nerve fibers—the submucosal plexus and the myenteric plexus

• Some of the output neurons are excitatory (acetylcholine), and some are inhibitory (nitric oxide, vasoactive intestinal peptide)

Extrinsic Nerve

• extrinsic nerves are the nerve fibers from both branches of the autonomic nervous system that originate outside the digestive tract and innervate the various digestive organs

• Th e sympathetic system, which dominates in “fight-or-flight” situations, tends to inhibit or slow down digestive tract contraction and secretion

• the autonomic nerves, especially the vagus nerve, can be discretely activated to modify only digestive activity

• To coordinate activity between different regions of the digestive system.

Gastrointestinal Hormones

• gastrointestinal hormones are carried through the blood to other areas of the digestive tract, where they exert either excitatory or inhibitory influences on smooth muscle and exocrine gland cells

Mastication • Digestion begins in the mouth• A brain reflex triggers the flow of saliva when we see or even think about

food moistens the food while the teeth chew it up and make it easier to swallow.

• Amylasebreak down starch into simpler sugars before the food even leaves the mouth.

• The nervous salivary excretion stimulation of receptors in the mouth, sensory impulses to the brain stem, and parasympathetic impulses to salivary glands.

• Swallowing muscles in tongue and mouth move the food pharynx.• Epiglotiscloses over the pharynx prevent food trachea and thus choking.• For swallowing to happen correctly a combination of 25 muscles must all work

together at the same time.• Salivary glands also produce an estimated three liters of saliva per day.

Esophagus • Is the muscular tube in vertebrates through which ingested food

passes from the throat to the stomach. • The esophagus is continuous with the laryngeal part of the pharynx

at the level of the C6 vertebra. • Where the second stage of digestion is initiated (the first stage is in

the mouth with teeth and tongue masticating food and mixing it with saliva).

• After passing through the throat, the food moves into the esophagus and is pushed down into the stomach by the process of peristalsis (involuntary wavelike muscle contractions along the G.I. tract).

• At the end of the esophagus there is a sphincter that allows food into the stomach then closes back up so the food cannot travel back up into the esophagus.

Swallowing - harrison

• Swallowing begins with a voluntary (oral) phase (mastication and mixed with saliva) transfer phase pharynx bolus entry to hypopharynx pharyngeal swallow response food through the pharynx into the esophagus while preventing its entry into the airway the larynx is elevated and pulled forward, actions that also facilitate upper esophageal sphincter (UES) opening

• Lower esophageal sphincter (LES) relaxes as the food enters the esophagus remains relaxed bolus into the stomach (by peristaltic)

UES• consists of the cricopharyngeus muscle, the adjacent

inferior pharyngeal constrictor, and the proximal portion of the cervical esophagus.

• derived from the vagus nerve facilitate its opening during swallowing V,VII,XII cranial nerves.

• The UES remains closed inherent elastic properties and neurogenically mediated contraction of the cricopharyngeus muscle.

• UES opening during swallowing : – cessation of vagal excitation to the cricopharyngeus – simultaneous contraction of the suprahyoid and geniohyoid

muscles open UES with the upward and forward displacement of the larynx.

LES• Distal esophagus and LES are composedsmooth

musclecontrolled by excitatory and inhibitory neurons esophageal myenteric plexus.

• Medullary preganglionic neurons from the dorsal motor nucleus of the vagus trigger peristalsis primary peristalsis Neurotransmitters of the excitatory ganglionic neurons acetylcholine and substance P.

• LES relaxation : – onset of deglutitive inhibition– persists until the peristaltic sequence is complete.

• At rest, the LES is contracted because of excitatory ganglionic stimulation and its intrinsic myogenic tone1

• LES Function is supplemented by the surrounding muscle of the right diaphragmatic crus, which acts as an external sphincter during inspiration, cough, or abdominal straining.

LO 3

Explain various difficulty of swallowing

Dysphagia

• Dysphagia is defined as a sensation of "sticking" or obstruction of the passage of food through the mouth, pharynx, or esophagus. (Harrison's Internal Medicine)

• Aphagia: complete esophageal obstruction • Odynophagia: painful swallowing • Globus pharyngeus: the sensation of a lump

lodged in the throat (no difficulty is encountered when swallowing is performed)

• Phagophobia: fear of swallowing

Pathophysiology of Dysphagia

– Dysphagia caused by a large bolus or a narrow lumen is called mechanical dysphagia

– Dysphagia due to weakness of peristaltic contractions or to impaired deglutitive inhibition causing nonperistaltic contractions and impaired sphincter relaxation is called motor dysphagia.

Dysphagia may be divided into:1. Oral Pharyngeal Dysphagia

Associated with poor bolus formation and control.Pharyngeal stasis leads to nasal regurgitation and laryngeal aspiration during the process of swallowing.

2. Esophageal DysphagiaIn an adult, the esophageal lumen can distend up to 4 cm in diameter. When the esophagus cannot dilate beyond 2.5 cm in diameter, dysphagia to normal solid food can occur. Dysphagia is always present when the esophagus cannot distend beyond 1.3 cm.Results abnormalites in peristaltis and deglutitive inhibition due to diseases of the esophageal striated or smooth muscles.

Approach to the patient with dysphagia. ENT, ear, nose, and throat; VFSS, videofluoroscopic swallowing study.

History – Associated Clinical features

• Nasal regurgitation and tracheobronchial aspiration pharyngeal paralysis or a tracheoesophageal fistula (TEF)

• Hoarseness of voice:– Hoarseness precedes dysphagia (before) larynx– Hoarseness following dysphagia (after) involvement of the recurrent

laryngeal nerve by extension of esophageal carcinoma• Hiccups rarely occur with a lesion in the distal portion of the

esophagus.• Unilateral wheezing mediastinal mass involving the esophagus

and a large bronchus.• Transient dysphagia inflammatory• Progressive dysphagia lasting a few weeks to a few months, severe

weight loss suggestive of carcinoma of the esophagus.• Episodic dysphagia to solids lasting several years benign disease

characteristic of a lower esophageal ring.

• Only to solid mechanical dysphagia• Liquid + solid advanced obstruction• Chest pain DES and related motor disorders, large bolus

obstruction.• A prolonged history of heartburn and reflux preceding dysphagia

indicates peptic stricture.• A history of prolonged nasogastric intubation, ingestion of

caustic agents, ingestion of pills without water, previous radiation therapy, or associated mucocutaneous diseases esophageal stricture. If odynophagia is present, candidal, herpes, or pill-induced esophagitis should be suspected.

• In patients with AIDS or other immunocompromised states, esophagitis due to opportunistic infections such as Candida, herpes simplex virus, or cytomegalovirus and to tumors such as Kaposi's sarcoma and lymphoma should be considered.

Diagnostic Procedures• Dysphagia is usually a symptom of organic disease rather than a

functional complaint. If oral or pharyngeal dysphagia is suspected, VFSS by both a radiologist and a swallow therapist is the procedure of choice. Videoendoscopy is currently performed only in specialized centers. Otolaryngoscopic and neurologic evaluation are also usually required.

• If esophageal mechanical dysphagia is suspected on clinical history, barium swallow and esophagogastroscopy with or without mucosal biopsies are the diagnostic procedures of choice. In some cases, CT examination and endoscopic ultrasound may be useful. For motor esophageal dysphagia, barium swallow, esophageal manometry, esophageal pH, and impedance testing are useful diagnostic tests. Esophagogastroscopy is also often performed in patients with motor dysphagia to exclude an associated structural abnormality.

- ACHALASIA -

• Achalasia is a motor disorder of the esophageal smooth muscle and involves thoracic and abdominal parts of the esophagus.

• In achalasia, the esophageal body loses peristaltic contractions and the LES does not relax normally in response to swallowing.

Pathophysiology

• The underlying abnormality is the loss of intramural neurons

• The histopathology of achalasia involves inflammation of the myenteric plexus of the esophagus with diminution of ganglion cells.

Clinical features• Dysphagia, chest pain, and regurgitation are the main symptoms.

• Dysphagia occurs early with both liquids and solids and is worsened by emotional stress and hurried eating.

• Difficulty belching (sendawa).• The presence of gastroesophageal reflux argues against

achalasia; in patients with long-standing heartburn, cessation of heartburn and appearance of dysphagia may suggest development of achalasia, peptic stricture, or carcinoma on top of reflux esophagitis. The course is usually chronic, with progressive dysphagia and weight loss over months to years.

• Achalasia associated with carcinoma is characterized by severe weight loss and a rapid downhill course.

Diagnosis

• On fluoroscopy with barium swallow, normal peristalsis is lost in the lower two-thirds of the esophagus. The terminal part of the esophagus shows a persistent beaklike narrowing representing the nonrelaxing LES.

• Endoscopy is helpful in excluding the secondary causes of achalasia, particularly gastric carcinoma.

Treatment

• Laparoscopic myotomy is currently the procedure of choice

• Balloon dilatation reduces the basal LES pressure by tearing muscle fibers

- DES -

• Diffuse Esophageal Spasm and Hypertensive Motor Disorders

• In nutcracker esophagus, esophageal contractions are normally peristaltic but hypertensive.

• In hypercontracting LES, the normal sphincter relaxation is followed by hypertensive contraction.

• In hypertensive LES, basal LES pressure is elevated, but sphincter relaxation and contraction are normal.

Pathophysiology

• Nonperistaltic contractions are due to dysfunction of inhibitory nerves

• Histopathology shows patchy neural degeneration localized to nerve processes, rather than the prominent degeneration of nerve cell bodies seen in achalasia

Clinical features

• Chest pain (in patients with esophageal contractions of large amplitude with long duration)

• Dysphagia with solids and liquids may occur with or without chest pain and is correlated with simultaneous contractions.

• The presence of dysphagia in association with pain should point to the esophagus as the origin

Diagnosis

• Diffuse esophageal spasm (Fig. 286-3) is best diagnosed by manometry

• the "corkscrew" esophagus

Treatment

• Agents that relax smooth muscle, such as sublingual nitroglycerin (0.3–0.6 mg) or longer-acting agents such as isosorbide dinitrate (10–30 mg orally before meals) or nifedipine (10–20 mg orally before meals) may be helpful

- Scleroderma Esophagus -

• The esophageal lesions in systemic sclerosis consist of atrophy of smooth muscle, manifested by weakness in the lower two-thirds of the esophagus and incompetence of the LES.

Clinical features

• Patients usually present with dysphagia to solids

• Liquids may cause dysphagia when the patient is recumbent

• These patients usually also complain of heartburn, regurgitation, and other symptoms of GERD

Diagnosis

• Barium swallow shows dilation and loss of peristaltic contractions in the middle and distal portions of the esophagus

• Motility studies show a marked reduction in the amplitude of smooth-muscle contractions, which is usually peristaltic but may be nonperistaltic.

• The resting pressure of the LES is subnormal, but sphincter relaxation is normal

- GERD -

• Gastroesophageal reflux disease• Backflow of gastric acid and other gastric

contents into the esophagus due to incompetent barriers at the gastroesophageal junction.

Etiology

• Lifestyle - Use of alcohol or cigarettes, obesity, poor posture (slouching)

• Medications - Calcium channel blockers, theophylline, nitrates, antihistamines

• Diet - Fatty and fried foods, chocolate, garlic and onions, drinks with caffeine, acid foods such as citrus fruits and tomatoes, spicy foods, mint flavorings

• Eating habits - Eating large meals, eating soon before bedtime

• Other medical conditions - Hiatal hernia, pregnancy, diabetes, rapid weight gain

GERD

Pathophysiology

• The normal antireflux mechanisms consist of the LES, the crural diaphragm, and the anatomical location of the gastroesophageal junction below the diaphragmatic hiatus.

• Reflux occurs only when the gradient of pressure between the LES and the stomach is lost.

Gastric contents are most likely to reflux :• (1) when gastric volume is increased (after

meals, in pyloric obstruction, in gastric stasis, during acid hypersecretion states),

• (2) when gastric contents are near the gastroesophageal junction (in recumbency, bending down, hiatal hernia),

• (3) when gastric pressure is increased (obesity, pregnancy, ascites, tight clothes).

Clinical features

• Heartburn and regurgitation of sour material into the mouth are the characteristic symptoms of GERD

• Persistent dysphagia suggests development of a peptic stricture

• Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma in Barrett's esophagus

• Bleeding occurs due to mucosal erosions or Barrett's ulcer

GERD imbalance between defensive factor of esophagus and offensive factor from reflux agent

GERD

DEFENSIVE FACTORS :

• Antireflux separator

• Acid clearance from

esophageal luminal

• Esophagus epithelial

barrier

DEFENSIVE FACTORS :

• Antireflux separator

• Acid clearance from

esophageal luminal

• Esophagus epithelial

barrier

OFFENSIVE FACTORS :• HCl• Pepsin

Defensive Factors of Esophagus

• 1st Line : Antireflux separator LES tone– LES tone (↓) retrograd reflux during the

increase of intra abdominal pressure– Factors that cause LES tone (↓) :

• Hiatal hernia• LES lenght• Drugs• Hormonal Factor

• 2nd Line :Acid clearance from esophageal luminalAssociated factors:

• Gravitation• Peristaltic• Saliva and bicarbonate excretion

• 3rd Line : Esophageal epithelium barrierConsist of:– Cell Membrane – Intracelular junction – Esophageal blood flow– Ability of esophageal cells to transport the

ion

Offensive Factors of Esophagus

• Initially :– HCl – Pepsin

• The lower the pH esophagus mucosal damage >>

INTRAESOPHAGEAL

• Heartburn• Regurgitation of sour material into the mouth• Angina-like• Persistent dysphagia• Rapidly progressive dysphagia & weight loss• Bleeding

EXTRAESOPHAGEAL

• Chronic cough• Laryngitis• Pharyngitis• Morning

hoarseness• Reccurent

pulmonary aspiration

• Chronic sinusitis• Dental decay

ALARM SYMPTOMS :• Odynophagia• Unexplained weight loss• Recurrent vomiting• Occult or gross GI bleeding• Jaundice• Palpable mass or adenopathy• Family history of GI malignancy

Complication

• Reflux esophagitis is a complication of reflux develops when mucosal defenses are unable to counteract the damage caused by acid, pepsin, and bile

• Mild esophagitis microscopic changes of mucosal infiltration with granulocytes or small numbers of eosinophils, hyperplasia of basal cells, and elongation of dermal pegs

• In nonerosive reflux disease (NERD), the mucosa may be normal or mildly erythematous

• Erosive esophagitis reveals clear mucosal damage with redness, friability, superficial linear ulcers, and exudates

• Peptic stricture results from fibrosis that causes luminal constriction

Extraesophageal manifestations

• Morning hoarseness • Recurrent pulmonary aspiration

Diagnosis

• A therapeutic trial with a PPI such as omeprazole, 40 mg bid for 1 week, provides support for the diagnosis of GERD.

• The diagnostic approach :1. documentation of mucosal injury2. documentation and quantitation of reflux3. definition of the pathophysiology

• Mucosal damage is documented by the use of barium swallow, esophagoscopy, and mucosal biopsy– Barium swallow is usually normal but may reveal an ulcer or a stricture.

A high esophageal peptic stricture, a deep ulcer, or adenocarcinoma suggests Barrett's esophagus

– Esophagoscopy may reveal the presence of erosions, ulcers, peptic strictures, or Barrett's metaplasia with or without ulcer, peptic stricture, or adenocarcinoma

– The mucosal biopsies should be performed at least 5 cm above the LES, as the esophageal mucosal changes of chronic esophagitis are quite frequent in the most distal esophagus in otherwise normal individuals.

• Documentation and quantitation of reflux, when necessary, can be done by ambulatory long-term (24–48 h) esophageal pH recording

• Reflux of nonacid contents can be documented by the use of an impedance test.

Diagnostic for Infant

Treatment

• The goals of treatment are to provide symptom relief, heal erosive esophagitis, and prevent complications

• The PPIs are comparably effective, for 8 weeks can heal erosive esophagitis in up to 90% of patients.

• The PPI should be taken 30 min before breakfast• Vitamin B12 and calcium absorption may be

compromised by the treatment.

- Barret’s Esophagus -

• The metaplasia of esophageal squamous epithelium to columnar epithelium (Barrett's esophagus) is a complication of severe reflux esophagitis and it is a risk factor for esophageal adenocarcinoma

• Metaplastic columnar epithelium develops during healing of erosive esophagitis with continued acid reflux because columnar epithelium is more resistant to acid-pepsin damage than is squamous epithelium

Diagnostic

• A one-time esophagoscopy is recommended in patients with persistent GERD symptoms at age 50, particularly in white males

• Barrett's intestinal metaplasia progresses to adenocarcinoma through dysplastic stages, including low-grade dysplasia (LGD) and high-grade dysplasia (HGD).

Treatment

• Currently, patients with HGD can be treated with esophagectomy, endoscopic mucosal resection, or photodynamic therapy with HGD. Close endoscopic follow-up (every 3 months) is recommended in all patients with HGD. In LGD, follow-up endoscopy is recommended at 6 and 12 months initially and yearly thereafter, as long as LGD persists

- Infectious Esophagitis -

• Infectious esophagitis can be due to viral, bacterial, fungal, or parasitic organisms. In severely immunocompromised patients, multiple organisms may coexist.

*Viral Esophagitis

• Herpes simplex virus (HSV) type 1 occasionally causes esophagitis in immunocompetent individuals

Clinical features

• Patients may complain of an acute onset of chest pain, odynophagia, and dysphagia. Bleeding may occur in severe cases

• Systemic manifestations such as nausea, vomiting, fever, chills, and mild leukocytosis may be present

• Herpetic vesicles on the nose and lips may provide a clue to the diagnosis

Diagnosis

• Culture for HSV becomes positive within days and is helpful in diagnosis and to identify acyclovir-resistant strains

• PCR assays are more sensitive than viral cultures

Treatment

• Spontaneous resolution may occur in 1–2 weeks.

• Acyclovir (400 mg PO 5 times a day for 14–21 days) causes early resolution of symptoms

• Valacyclovir (1 g PO tid for 7 days) may be more convenient and have better patient adherence

*Bacterial Esophagitis

• Bacterial esophagitis is unusual, but Lactobacillus and b-hemolytic streptococci can cause esophagitis in immunocompromised patients

*Fungal Esophagitis

• Candida species are normal commensals in the throat but become pathogenic and produce esophagitis in a compromised host

• Patients may be asymptomatic or complain of odynophagia and dysphagia. Oral thrush or other evidence of mucocutaneous candidiasis may be absent

Diagnosis

• Barium swallow may be normal or show multiple nodular filling defects of various sizes

• Large nodular defects may resemble grape clusters. Endoscopy shows small, yellow-white raised plaques with surrounding erythema in mild disease.

• Diagnosis is made by demonstration of yeast or hyphal forms in plaque smears and exudate stained with periodic acid–Schiff or Gomori silver stains.

Treatment

• Oral fluconazole (200 mg on the first day, followed by 100 mg daily) for 7–14 days is the preferred treatment. Patients refractory to fluconazole often respond to itraconazole.

• Amphotericin B (10–15 mg IV infusion for 6 h daily to a total dose of 300–500 mg) is used in severe cases.

- Diverticula -

• Diverticula are outpouchings of the esophagus wall

• When it becomes large and filled with food, it can compress the esophagus and cause dysphagia or complete obstruction

- Webs and Rings -

• Weblike constrictions of the esophagus are usually congenital or inflammatory in origin

• When concentric, they cause intermittent dysphagia to solids

• The combination of symptomatic hypopharyngeal webs and iron-deficiency anemia in middle-aged women constitutes Plummer-Vinson syndrome.

• A lower esophageal mucosal ring (Schatzki ring) is a thin, weblike constriction located at the squamocolumnar mucosal junction at or near the border of the LES

• Dysphagia to solids is the only symptom, and it is usually episodic• Symptomatic rings and webs are easily

treated by dilatation

• A lower esophageal muscular ring (contractile ring) is located proximal to the site of mucosal rings and may represent an abnormal uppermost segment of the LES

• These rings can be recognized by the fact that they are not constant in size and shape

• Muscular rings do not respond well to dilatation

- Hiatal Hernia -

• A hiatal hernia is a herniation of part of the stomach into the thoracic cavity through the esophageal hiatus in the diaphragm.

• A sliding hiatal hernia is one in which the gastroesophageal junction and fundus of the stomach slide upward.

• Small sliding hiatal hernias alone probably produce no symptoms but can contribute to reflux esophagitis.

Bibliography

• Sherwood, Human Physiology• Fauci, Braunwald, Kasper, dkk. Harrison’s

Principles of Internal Medicine. 17 th edition . USA: Mc Graw Hill, 2008.

• A. Despopoulos et al - Color Atlas of Physiology 5th Ed Thieme 2003