ESOPHAGEAL OBSTRUCTION - rEMERGs

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MOTILITY DISORDERS ‣ Nutcracker Esophagus ‣ Normal propagation but high amplitude waves in distal esophagus and prolonged contraction, LES normal (pressure may be elevated) ‣ C/O angina-like CP not usu dysphagia ‣ Most common abnormal manometric finding in pts reffered for non-cardiac CP ‣ Tx: nitrates, CCBS, antireflux treatment ‣ Diffuse Esophageal Spasm ‣ Normal peristalsis w/ frequent high pressure nonpropagated or tertiary waves and multipeaked waves ‣ C/O CP + dysphagia ‣ Tx: nitrates, CCBs, esophageal myotomy ‣ Achalasia ‣ Aperistalsis in esphageal bd, elevated LES pressure, and inadequeate LES relaxation leading to prominent dilation of proximal esoph on XR; distal end narrows to a “beak” ‣ ‣ ‣ ‣ ‣ ‣ Vigorous achalasia: associated vigorous contractions in esph body Pathology: degeneration of inhibitory neurons w/i the esoph and LES myenteric plexus; nerve damage also occurs in vagal nerve trunks and the dorsal motor nuclei Trypanosoma cruzi (Chaga’s dz) can distroy myenteric neurons (BRAZIL) Neoplasm can also cause secondary achalasia Symptoms: dysphagia +/- CP and HB (due to degeneration of stagnant contents, not GER) Treatment: CCBs and nitrates, pneumatic balloon dilation of LES is usu required, Heller myotomy via laproscope if above fails, botulinum toxin injection effective but only lasts for 1yr
GASTRO<strong>ESOPHAGEAL</strong> REFLUX DISEASE Introduction ‣ MOST COMMON condition of the esoph: daily 7%, weekly 14%, monthly in 40% ‣ Spectrum from normal to severe symptoms, barret’s esoph, adenoCa Normal Barriers to GER ‣ Lower esophageal sphincter: most important barrier, near normal in pts w/ GERD ‣ Esophageal clearance: primary and secondary peristalsis, neutralization by saliva ‣ Mucosal resistance Pathophysiology ‣ Due to “Acid in the wrong place, NOT over acid production” ‣ Majority of reflux episodes due to transient LES relaxation ‣ GERD can occur w/o hiatus hernia and hiatus hernia can occur w/o GERD ‣ Aggravating factors - fat, caffeine, chocolate - salivation disorders - juices, pepermint - delayed gastric emptying - posture - obesity - hiatus hernia - inc abd pressure (pregnancy) - drugs (CCBs, NTG, - alcohol/cigarrettes ‣ Drugs that worsen GERD: CCB, NTG, BB, anticholinergics, etc) Clinical Features ‣ Onset usu following meals or postural maneuvers (lie flat, bending) ‣ Symptoms: HB, regurg, waterbrash, CP, dysphagia due to stricture or motility, resp s/s; odynophagia is rare and suggests infection ‣ Pregnancy: increased abd P and relaxed LES due to progesterone ‣ Atypical presentations ‣ non-cardiac CP ‣ respiratory s/s: laryngitis, pharyngitis, asthma, chronic cough, pneumonias ‣ globus hystericus: lump in throat (hypertonic LES in response to GER) Diagnosis ‣ pH reflux study (Gold standard for proving presence of GER) ‣ 24hr pH recording determines if symptoms are due to reflux ‣ Red Flags require endoscopy - dysphagia, new onset in elderly, anemia, hemetamesis, s/s refractory to tx, atypical CP, odynophagia, pharyngitis, laryngitis - once in a lifetime endoscopy to R/O barret’s - young, mild s/s ------- empiric tx w/o endoscopy Complications of GERD ‣ Ulcer (5%) ‣ Esophagitis ‣ Hemmorrhage (
Page 1 and 2: ESOPHAGEAL OBSTRUCTION ANATOMY ‣
Page 3 and 4: ESOPHAGEAL PERFORATION INTRODUCTION
Page 5 and 6: DYSPHAGIA DEFINITIONS ‣ Dysphagia
Page 7 and 8: INVESTIGATIONS ‣ Neck Xrays: look
Page 9: ‣ Resp Complications: recurrent c
Page 13 and 14: ABDO PAIN: GASTRIC OR DUODENAL ORIG
Page 15 and 16: ‣ ‣ May present w/ Complication
Page 17 and 18: NSAID INDUCED ULCERS EPIDEMIOLOGY
Page 19 and 20: MEDICATION OPTIONS ‣ Gastric Acid
Page 21 and 22: ‣ urease splits urea and produces

ESOPHAGEAL OBSTRUCTION - rEMERGs

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