Med1-Ex4-Esophageal Disorders

EXAMPLE-SCLERODERMA

DECREASED SALIVA + DECREASED/ABSENT PERISTALSIS + DECREASED OR ABSENT LES + DECREASED GASTRIC EMPTYING EQUALS INTRACTABLE GERD

Eosinophilic esophagitis Diagnosis

Diagnosis is based on Clinical and Histopathologic criteria: Symptoms of esophageal dysfunction > 15 Eo's/hpf on at least 1 biopsy Eosinophilia limited to esophagus Exclusion of GERD as cause (PPIR - EE)

DYSPHAGIA (DIFFICULT SWALLOWING)

-Definition -Always a worrisome symptom -Did it start Sudden vs. gradual. -Assoc w/ Solids vs. Liquids. -Intermittent vs. continuous-always trouble swallowing or once in a while

Esophageal motility disorders Achalasia

-Most easily recognized and defined motor disorder -Prevalence 1: 10,000 -Both sexes equally involved, all ages

Defense

-Mouth-saliv glands release bicarb and prostaglandin growth fact to maintain mucosal barrier -Esophagus-clearance -Stomach-empties normally-if not, inc intragast pressure=reflux

Boerhaaves Syndrome

-Usually precipitated by nausea and vomiting -Increased in ETOH abuse -Perforation usually occurs in the left distal esophagus -Acute onset of chest and abdominal pain -Fever, shock -Abnl CXR (pleural effusion, pneumomediastinum, pnthx, subcutaneous emphysema) -Treatment: usually surgery <24Hrs, occ conservative

Endoscopic appearance of Candida esophagitis

. Endoscopic appearance of Candida esophagitis. Raised white plaques that do not wash and are friable when brushed or biopsied. Both should be obtained to confirm Candida and rule out other diagnoses. (Courtesy of A. Tsuchida)

Pill induced esophageal injury

ANTIBIOTICS: Doxycycline, Tetracycline, Clindamycin, Erythromycin, Penicillin NSAIDS and ASPIRIN POTASSIUM CHLORIDE ASCORBIC ACID FERROUS SULFATE QUINIDINE THEOPHYLINE ALENDRONATE- classic for this... ANTIRETROVIRAL DRUGS

Achalasia radiography

All air fluid in a dilated esophagus- looks like a huge balloon

How to dx?

Almost looks like the trachea -Diagnoses is on biopsies and must be multiple

Esophageal Adenocarcinoma?

Almost tripling in the last 2-3 decades

Eosinophilic Esophagitis

An immune mediated disorder in which allergens in food or the environment stimulate a T-helper cell inflammatory response which recruits eosinophils within the esophageal mucosa.

MEDICATIONS

Anticholinergics / tricyclic antidepressants Antihistamines Theophylline Alpha antagonists Beta agonists-asthma inhaler Hormones Nitrates- relax smooth muscle Calcium channel blockers Sildenifil

Esophageal Dysmotility Upper esophageal dysphagia Oro-pharyngeal dysphagia What is the risk?

Aspiration

Esophageal Web/Rings Cervical Esophagus

Associated with Fe def. anemia epidermolysis bullosa, pemphigoid plummer vinson syndrome Lower Esophagus

ESOPHAGUS DIAGNOSTIC TESTS

Barium Esophagram- structural image Endoscopy- one of the gold standard CT Endoscopic Ultrasound (EUS) 24 hour pH probe Manometry - Impedance phlethesmography- look for reflux, not only acid, but also non-acid related stomach components (bile and ezymes)

Esohageal Diverticuli Dx

Barium swallow

Esophageal motility disorders Achalasia Dx

Barium swallow, esophageal manometry, EGD

Histopathology of reflux damage

Figure 6-22. The histopathologic changes of reflux damage to the esophageal epithelium most commonly noted on esophageal biopsy are basal cell hyperplasia and elongation of the rete pegs (arrows) [18]. These features have a high sensitivity but relatively low specificity for disease, the latter because of the presence of these features in 20% of healthy subjects in the lower 2.5 cm of esophagus [19]. (From Lewin [18]; with permission.) First thing seen histologically is sloughing off of tissue

Endoscopic therapy of reflux disease

Figure 6-46. The Food and Drug Administration has approved two novel endoscopic techniques for the treatment of gastroesophageal reflux disease (GERD), the EndoCinch (A) procedure and the Stretta procedure (B). The EndoCinch procedure permits the endoscopist to create a gastroplication just below the esophagogastric junction using an overtube and sewing attachment, and this plication serves as a barrier to reflux [43],[44]. The Stretta procedure, through the use of thermocouples attached to a balloon and catheter system positioned at the esophagogastric junction, permits the delivery of high-frequency energy to the lower esophageal sphincter and cardia of the stomach. This injury within the sphincter region controls reflux by producing collagen deposition, remodeling, and reduced compliance of the esophagogastric junction [45],[46]. Although these procedures have been met with initial enthusiasm and some success in reducing the reliance on chronic acid suppressant medications, neither one is free of serious side effects, and their data have not established their durability. These procedures are also not indicated in patients with hiatal hernias or erosive esophagitis, and they should currently be considered experimental. GERD—gastroesophageal reflux disease. You can suction in fold of esoph and stitch thru it or inject collagen in area and try to buff it up but these are not very successful

...

For solids - if young person with dysphagia

What is the most common GI dx to outpt clinics?

GERD

LIFESTYLE/FOOD

Gastric emptying Fat and volume of food Increased Acid Cigarettes *When senses more fat in duodenum, says empty slower so have time to break down-worse GERD

WHICH FORCES ARE KEY?

Gerd is a motility disorder! Most people with gerd have normal acid production, normal les baseline pressure and normal gastric emptying.

EFFECTS OF SLEEP: LESS...

Gravity Saliva Peristalsis Transient LES relaxation- pts with reflux have inc in # and length of time of these relaxations

Achalasia Tx Srugery

Heller Myotomy, laparoscopic 95% symptom resolution

Note two muscles of UES

Inferior constrictor Cricopharyngeus LES is also important

MEDICATIONS THAT ^ GERD

Inhibit peristalsis and lower sphincter pressure

Management of Barrett's

Initial bx After a year look and if good Every 3-5 years regardless of symptoms Only try to ablate in patients who has advance dysplasia

SWALLOWING

Initiation of swallow - voluntary Involuntary mechanisms follow

sophageal Dysmotility Upper esophageal dysphagia Oro-pharyngeal dysphagia What is the swallowing problem with?

Liquids

LIFESTYLE/FOOD

Lower LES pressure: Chocolate Fat Mint Alcohol Cigarettes-dec secretion of bicarb so system becomes more acidic

Esophagitis

Peptic-associated with GERD Infectious Caustic - chemical injury(lye,acid,pill induced injury) Radiation Eosinophilic esophagitis

Defense-Mouth

Saliva-sheer volume and basicity Volume Bicarbonate

Esophageal Perforation

Spontaneous Boerhaaves Syndrome- major vomiting External Trauma Iatrogenic, instrumentation

ESOPHAGEAL FUNCTION IS SWALLOWING

Starts in mouth. Upper esophageal sphincter Peristalsis delivers food to: Lower Esophageal Sphincter (LES)

MUCOSA

Stratified squamous. Only mildly acid resistant. Can change in response to insult. Results in scarring and metaplasia. **Like skin w/o keratin buildup and has sub mucosal and mucosal glands that sec bicarb and mucosa can change in response to acid-metaplasia=change in type of tissue in lower esoph Hyperplasia-hyperreprod cells Metaplasia-squamous to intes lining type Dysplasia-disarray of cells No dig begins here Not very acid resistant

GERD COMPLICATIONS

Stricture- presents w/dysphagia for solids Metaplasia (Barrett's)***-squamous replaced with intestinal like lining Ulceration Bleeding Cancer

Mechanical causes of Dysphagia

Strictures - peptic, neoplastic Rings, webs Diverticuli - Zenkers Foreign Body impaction

TREATMENT If do not want to take meds forever...

Surgery

Nutcracker esophagus

Very high pressure waves

Barium swallow

Zenker Diverticuli

GERD

a condition that develops when the reflux of stomach contents cause troublesome symptoms or complications." At least 2 episodes of heartburn per week

Pseudoachalasia

due to tumors involving the cardio-fundic area of the stomach

What is the concern of safety of drugs?

lower calcium metabolism?-hip fx, radial bone fx Increase risk of certain infx such as C.diff, aspiration pneumonia - etc.....

Esophageal Dysmotility Upper esophageal dysphagia Oro-pharyngeal dysphagia Motor Disorders

musc dystrophy, ALS, Parkinsons, cva affecting base of brain CNs

Innervated by

vagus branches

Esophageal Dysmotility Upper esophageal dysphagia Oro-pharyngeal dysphagia Dx

cine' esophagram- studies motor fxn, speech therapy assessment

Esophageal Motility disorders

-Disorders of deglutitive inhibition or propagative excitation -Peristaltic dysfunction is defined by manometric or radiographic methods usually -Oro-pharyngeal vs. Esophageal

DIAGNOSTIC APPROACH TO GERD PATIENTS

-For patients with occasional symptoms - therapeutic trial of acid suppression therapy/lifestyle changes -If alarm symptoms are present (dysphagia, odynophagia, GI blood loss, anemia, weight loss, atypical symptoms) - endoscopy -Chronic unremitting or atypical symptoms - consider endoscopy

Pathophysiology of GERDOffensive factors

-Gastric acid-primary irritant -Most GERD patients produce normal amounts of gastric acid -Pepsin,bile

Conclusion

-Gerd is primarily a motility disorder. -Its evolution can best be explained in terms of a breakdown in the balance between the normal digestive and defensive forces. -The spectrum of symptoms can be matched by tailored treatment. -Understanding the pathophysiology leads to effective and rational treatment.

VESSELS

-Good arterial supply. Rarely suffers ischemia. -Plexus represents potential anastomoses between -systemic and portal venous circulation. Esoph and stomach have great blood flow Portal venous system at distal esop where commun bw portal and reg venous system Portal sys-artery, arteriole, capillary in stomach, vein, capillary in liver, vein to heart Esoph has areas that drain to liver and also to heart-liver has dual supply of arterial O2 blood from heart and venous system from stomach high in nutrients but low in oxygen Aorta-Celiac a- gastrica, stomach, liver, vena cava

GERD SYMPTOMS-typical

-Heartburn-retrosternal burning -Chest pain-not distinguishable from esoph pain or CV disease -Dysphagia -Regurgitation -Waterbrash

How long do you leave on PPI?

-In this case, after 8 to 12 weeks of a standard dose of a proton-pump inhibitor, I would advise the patient to titrate the dose to find the lowest dose that provides satisfactory control of heartburn. -A reasonable target is 80% symptom relief; patients often continue to have symptoms triggered by overindulgence. -Occasional breakthrough symptoms can be treated with antacids as necessary. -Although proton-pump inhibitors are more effective in general than H₂-blockers, the latter will suffice for some patients, and some will find as-needed therapy to be sufficient. -Other patients will require twice-daily therapy with a proton-pump inhibitor; in such cases, medication should be taken 30 to 60 minutes before breakfast and dinner.

What about PPI and cardiac concerns?

-Might interfere with anti-platelet interaction, i.e. Plavix

PILL ESOPHAGITIS

-Presentation acute onset odynophagia+/- dysphagia -Associated with Left Atrial enlargement, often occurs in mid-esophagus -May see mid-esoph ulceration surrounded by NL mucosa -Can form strictures

Eosinophilic EsophagitisDifferential Diagnosis

-Proton Pump Inhibitor Responsive esophageal eosinophilia (PPIR-EE) -GERD -Systemic eosinophilic disorders

A 53-year-old man, who is otherwise healthy and has a 20-year history of occasional heartburn, reports having had worsening heartburn for the past 12 months, with daily symptoms that disturb his sleep. He reports having had no dysphagia, gastrointestinal bleeding, or weight loss and in fact has recently gained 20 lb (9 kg). What would you advise regarding his evaluation and treatment?

-The patient in the vignette reports a history of frequent heartburn consistent with gastroesophageal reflux disease. -Clinical experience suggests that dietary changes may be beneficial if there are obvious dietary precipitants (coffee, chocolate, or fatty foods) and that lifestyle changes are warranted to reduce obesity, smoking, or excessive alcohol use if present. -However, lifestyle modification alone is unlikely to eliminate his symptoms. -I would also recommend therapy with a proton-pump inhibitor and would anticipate the need for maintenance therapy, given the patient's long history of symptoms.

Conclusion-continued

-There is no evidence that the risk of esophageal adenocarcinoma is reduced by any current medical or surgical therapy. -Patients whose heartburn has not adequately responded to twice-daily therapy with a proton-pump inhibitor should be referred for specialist evaluation. -If a patient has symptoms refractory to proton-pump inhibitors (especially those attributable to regurgitation) or cannot tolerate such therapy, antireflux surgery may be considered; patients should understand that there are associated risks and that medication is often still needed after surgery.

How long is the esophagus?

20-22cm in length Esophagus is split up anatomically with spinal column - cervical, upper thoracic, etc..

Achalasia Tx Mechanical Dilatation

51% sx resolution; 2-5% perforation rate - most clinicians not doing this anymore

Tissue resistance: altering esophageal

A number of factors that can alter the ability of the esophageal epithelium to defend itself against refluxed gastric acid are depicted here. Among the most common factors are smoking; alcohol; hot (temperature) beverages; foods such as pizza; salt and spices that produce hypertonic luminal environments; and medications that produce topical irritation, including tetracycline or doxycycline, potassium chloride, vitamin C, quinine, and nonsteroidal anti-inflammatory drugs.

Esophageal Dysmotility Upper esophageal dysphagia Oro-pharyngeal dysphagia

Cricopharyngeal dysphagia (UES)Parkinsons

Esohageal Diverticuli Tx

Cricopharyngeal myotomy with diverticulectomy, endoscopic stapling

Spastic esophageal motility disorders

Disorders of excitation and abnl peristalsis Diffuse esophageal spasm Nutcracker esophagus Vigorous Achalasia Hypertensive LES Nonspecific motility disorders

Esophageal motility disorders Achalasia Clinical presentation

Dysphagia, Chest pain, Regurg, aspiration pneumonia, weight loss, esophageal CA

Esophageal symptoms

Dysphagia- cannot swallow Odynophagia- Pain with swallowing Chest Pain (atypical) Regurgitation Waterbrash- Hypersalivation Pyrosis

Esophageal motility disorders Achalasia

Failure of the LES to relax with swallowing- motor component Aperistalsis of SM portion of the esophagus (distal 2/3)- propagative component

Cutaway view of anatomy of tubular esophagus

Figure 1-13. The esophagus is a muscular tube that is composed of longitudinal and circular muscle with extensive neural network in between. Auerbach's plexus (myenteric) lies between the longitudinal and circular muscle layers. Another nerve network, Meissner's plexus (submucosal), is situated between the muscularis mucosa and the circular muscle layer. Note that there is no serosa to the esophagus and that the lumen is collapsed and empty. In fact, activity of both esophageal sphincters preserves the vacuum of the esophagus; the upper esophageal sphincter acts to exclude air during respiration and the lower esophageal sphincter excludes gastric contents from refluxing back into the esophagus. (Adapted from Kahrilas [11].) Nerves run bw muscle layers in myenteric plexus No serosa to contain perforation or malignancy if cancer

Normal histology of the esophagus

Figure 1-14. The lining of the esophagus is a partially or non-keratinized stratified squamous epithelium that overlies the connective tissue of the submucosa and the thick circular and longitudinal muscle layers (not shown). (Courtesy of Dr. Sambastiva Rao, Northwestern University Medical School.)

Endoscopic ultrasound of the esophagus

Figure 1-15. This endosonographic image of the esophageal wall demonstrates the five-layer structure that is seen throughout the gastrointestinal tract. These layers correspond to the mucosa (e, d), submucosa (c), muscularis (b), adventitia (a). Because of balloon filling, the layer structure is not recognizable in all parts of the circumference. (Courtesy of Dr. Arvydas Vanagunas, Northwestern University Medical School.)

Portal venous blood flow seen with esophageal and gastric varices

Figure 1-18. Portal venous blood flow observed with esophageal and gastric varices. (Adapted from Kitano et al.[13].)lower esoph and gastric v to portal v to liver to hepatic v to IVC to heart Plexus of veins can become distended and bleed in liver disease=varices

Esophageal varices

Figure 1-20. Esophageal varices seen endoscopically. The varices appear as slightly bluish dilated vessels (arrow).Submucosal distended veins

Lower esophageal mucosal ring

Figure 3-21. The presence of a lower esophageal mucosal ring is one of the most common causes of dysphagia. It has been proposed that these rings are related to gastroesophageal reflux, but a true ring is not associated with inflammation. A ring's upper surface is covered with esophageal (squamous) epithelium, and its lower surface by gastric (columnar) epithelium. Rings smaller than 13 mm are usually symptomatic and those over 20 mm rarely produce symptoms. Intermittent solid food dysphagia is the main presenting symptom. Treatment consists of dilation, which can be accomplished by passage of a single large-caliber dilator (i.e., 17 to 20 mm) through the esophagus to disrupt the ring.

Hiatal hernia x-ray

Figure 6-12. An example of a moderate-sized sliding hiatal hernia (arrows) is demonstrated on this barium esophagogram. This figure illustrates the distorted anatomy of the gastroesophageal junction in the presence of the hernia. (From Eisenberg [12]; with permission.)people used to think that reflux was caused by hiatal hernia but not true-just has potential to worsten reflux Here the top of the stomach is in the chest above the diaphragm and there is no assistance of diaphragm to create larger pressure area and keep acid in stomach and now acid is being stuck and not pushed thru

Characteristics of heartburn

Figure 6-20. Heartburn is a symptom complex characterized by substernal (burning) pain radiating toward the mouth, which is worsened by meals and recumbency, and ameliorated by antacid ingestion. When typical, recurrent heartburn is adequate for the diagnosis of gastroesophageal reflux disease (GERD). Acid regurgitation, the spontaneous eructation of bitter material in the esophagus and mouth, and water brash, the spontaneous appearance of a bland or salty fluid in the mouth, are also common symptoms of GERD. Odynophagia, however, is very uncommon in those with GERD and usually reflects mucosal destruction from pills (doxycycline or tetracycline, nonsteroidal antiinflammatory agents, vitamin C, quinine) or infectious agents (Herpes simplex virus, cytomegalovirus, Candida albicans, HIV). GERD—gastroesophageal reflux disease.

Endoscopic view of erosive esophagitis

Figure 6-25. The endoscopic hallmark of reflux esophagitis is the presence of one or more erosions within the distal esophagus [23]. Shown here is grade III esophagitis with confluent erosions involving the entire circumference of the distal esophagus. The endoscopic presence of erosions, however, is an insensitive indicator of reflux disease because the lesions are identified in fewer than 50% of subjects with heartburn severe enough to undergo the procedure. (From Tytgat et al.[23]; with permission.)

Esophageal stricture

Figure 6-28. A barium esophagogram demonstrates the presence of a high-grade, smooth-walled distal esophageal stricture that resulted from reflux esophagitis [6]. Patients with this complication of reflux disease usually note amelioration of heartburn as they develop the symptom of dysphagia. The dysphagia is for solids and not liquids (unless their is solid food impaction first), indicating the presence of a lumen-narrowing lesion. The absence of anorexia and weight loss and slow rate of progression of dysphagia are good indications that the lesion is a benign peptic process. The presence of anorexia and weight loss and rapid progression of dysphagia raises the likelihood that the lesion is malignant and most likely an adenocarcinoma arising in a Barrett's esophagus (seeFig. 6-29). (From Stewart et al.[27]; with permission.) Stricture can be malignant or benign-here shows no mass

Barrett's esophagus

Figure 6-29. The endoscopic appearance of a long segment (= 3 cm) of columnar-lined lower (Barrett's) esophagus is shown. The typical red coloration of the columnar epithelium is readly distinguished from the lighter pink or orange stratified squamous epithelium. Endoscopic biopsy, however, is essential for histologic confirmation. Barrett's esophagus is characterized by a specialized columnar epithelium with prominent goblet cells containing acidic mucin (seeFig. 6-30). Esophageal segments of less than 3 cm but with similar histopathologic features have been designated as "short segment" Barrett's esophagus. Short segment Barrett's esophagus has been reported in approximately 18% of subjects undergoing endoscopy irrespective of complaints or evidence for reflux disease [28]. In many instances, it is difficult to distinguish short segment Barrett's esophagus from metaplasia of the gastric cardia, which also exhibits the same histopathology (i.e., a lining containing specialized columnar epithelium). (From Tytgat [28]; with permission.)salmon colored tissue vs pink stomach-line seaprating 2 dif types of tissue should be smooth but here is is not-barretts

Pathophysiology and etiology of reflux esophagitis

Figure 6-4. The initial cause of reflux esophagitis is unknown. However, the key pathogenetic mechanisms involve the ability of noxious gastric contents, especially hydrochloric acid (HCl) and pepsin, to access the esophagus and remain within the lumen long enough to produce damage to the epithelial lining. Because gastric acid and pepsin secretion are normal in patients with gastroesophageal reflux disease (GERD) and bile salts are present in noncytotoxic amounts in gastric juice, the likely cause of GERD involves one or more defects in the esophageal defense against refluxed acid-pepsin. This may include defects in the antireflux barrier (lower esophageal sphincter [LES], diaphragm), which controls the frequency of gastric contents entering the esophagus; the luminal clearance mechanisms (esophageal peristalsis, salivary and esophageal submucosal gland bicarbonate secretion), which control the duration of contact between gastric contents and esophageal epithelium; and the esophageal epithelium, which determines whether the time of contact between epithelium and gastric contents results in injury. (Adapted from Orlando [6].)HCl—hydrochloric acid; GERD—gastroesophageal disease; LES—lower esophageal sphincter.

Antireflux surgical management (B)

Figure 6-45. Patients who are successfully controlled with acid suppressant therapy but do not desire to remain on medications lifelong are candidates for antireflux surgery. The most commonly performed surgical procedures for gastroesophageal reflux disease (GERD) are the Hill gastropexy (A), Belsey (partial) fundoplication (B), and Nissen (complete) fundoplication (C) [28]. The Nissen procedure is the most popular and can be performed either as an open procedure or using the laparoscopic approach. The laparoscopic Nissen procedure has an initial failure rate of approximately 10% and an approximate 1% breakdown of the wrap each year. The procedure itself carries little mortality risk, but morbidity rates, including esophageal perforations, wound infections, splenic tears, postoperative dysphagia, and gas bloat, occur in about 10% of patients. The cost of a successful Nissen procedure is estimated to be equivalent in cost to 10 years of chronic proton pump inhibitor (PPI) therapy, but this analysis will change in favor of PPI therapy after a generic version is available in 2002. (Adapted from Pope [42].) GERD—gastroesophageal reflux disease; PPI—proton pump inhibitor. Wrap stomach around esoph sphyncter to inc pressure

Herpes simplex esophagitis

Herpes simplex esophagitis. Biopsy and brushings should be at ulcer edge. Brushings should be obtained to help in diagnosis. (Courtesy of S. Kadakia.)don't need to endoscope everyone w/ HIV and dysphagia if have oral thrush, treat for candida

SYMPTOMS-atypical

Hoarseness Laryngitis Cough Asthma Dental decay

Esohageal Diverticuli Where is it located?

Hypopharyngeal location due to crico-pharyngeal dysfunction Protrusion of mucosa between inferior pharyngeal constrictor muscle + cricopharyngeus muscle

LIFESTYLE/FOOD

Intraabdominal pressure Obesity, position

Esophageal Dysmotility Upper esophageal dysphagia Oro-pharyngeal dysphagia What type of neurons are dysfunction?

Involve UMN dysfunction

ANTIREFLUX MECHANISM

LES Diaphragm (crura) Ligaments (sling fibers) Angle of His All maintain LES and prevent inapporpriate reflux

What is classic way to diagnose achalasia besides imaging?

Manometry

Achalasia Tx Lower LES

Medications- Nitrates, Calcium channel blockers, Botulinum injection

SO WHAT'S THE PROBLEM?

More LES relaxations and poor acid clearance.-no peristalsis to remove acid and can be from hiatal hernia w/acid pool

Esophageal Web/Rings LES Schatski Ring

Most common cause of intermitant solid food dysphagia Seen in up to 14% of UGI series ? Pathogenesis Always symptomatic if lumen <13mm on Xray Treatment- esophageal dilation

Esohageal Diverticuli Zenkers diverticuli

Most common esophageal diverticulum

Stomach

Motility Relaxation Emptying

TREATMENT

Much harder to treat than peptic ulcers. Use higher doses and longer Rx Taylor treatment to severity Avoid offending foods and medicine, lifestyle modification Use gravity to advantage Decrease acid Antacids, H2Blkers, Proton pump inhibitors Improve motility **Recurrent episodes of reflux-lifelong tx necessary Strong connection bw obesity and reflux-wt loss Raise head of bed

...

Mucosa, Muscularis Longitudnal folds Submucosa Adventitia NOTE- No serosa in esophagus and is very important.

Dysphagia and Esophageal Symptoms Etiologies:

Mucosal disease Mechanical disorders Motility disorders

Schematic of manometry in achalasia

No pressure spike you usually see. LES pressure, there is a failure to relax properly

Achalasia Tx Neuropathology

Not reversible

NO SEROSA

Nothing to limit cancer spread Nothing to contain a rupture *Can spread to structures in mediastinum If have auto accident and rupture esoph, nothing there to contain output

Esohageal Diverticuli Presentation

Often Asx, dysphagia/regurgitation of old food, halitosis, aspiration, palpable mass

What is a disease process that can increase GERD?

Often have very serious esophageal disease, major GERD

Hiatal hernia

Often presents with GERD

MUSCLE

Oropharynx and top third of esoph striated or "voluntary muscle." Mid third mixed Lower third smooth muscle, involuntary *You can voluntarily start a swallow but you cannot stop it Esoph can initiate peristalsys w/o vol force

MAINTENANCE THERAPY FOR GERD

Patients often will have recurrant symptoms once initial course of therapy is completed. Many will need long term acid inhibition Rx at dose which suppresses symptoms

Vagus nerve

Peristalsis - Primary Secondary Highly coordinated and poorly understood *Motor control and sensation from vagus

INFECTIONS

Presentation=Odynophagia.(painful swallowing) Underlying causes: Bacteria, Candida, cmv, herpes, HIV associated

DEFENSE-Esophagus

Pressure barrier -LES Gravity Peristalsis-secondary peristalsis to clean out normal regurg Secretion mucus,bicarb Tight junctions Cell restitution Pge

GERD

Primarily motility disorder Requires acid to produce symptoms and potentially damage to the esophageal mucosal lining. "Non acid Reflux" - gastric enzymes, bile in refluxate

Achalasia- endoscopy

Referred to as bird beak sign

Clinical approach to Eosinophilic esophagitis

Trial of PPI Rx BID for 8 weeks. Repeat EGD and Bx. If Eo's resolved continue PPI Rx. If persistant Eo's: Topical po steroid Rx, Allergy assessment, etc.

What is the most important factor you can do to reduce reflux?

Weight loss