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