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45 Cards in this Set

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EGU/upper endoscopy
-passing an endocope with a light and video camera on one end through the mouth to examine the esophagus, stomach and duodenum
BRAVO/Esophageal pH testing
-capsule is passed through your mouth and suctioned to the wall of your esophagus
-the capsule transmits data every 12 sec to a pager that is worn for 48hrs
Manometry
-procedure to measure the tone within the esophagus and also the esophageal sphincter
muscular anatomy of the esophagus
-upper third is striated muscle
-middle third is a combination of striated and smooth muscle
-lower third - smooth m
Nerve innervation of esophagus
1. Parasym: motor innervation
2. Sympath: regulates blood vessel constriction, esophageal sphincters contractions, relaxation of the muscular wall, and increases in glandular and peristaltic activity
-peristalsis - vagus n
-spinal afferent act as nociceptors
layers of the esophagus
-mucosa
-lamina propria
-muscularis mucosae
-submucosa
-muscularis externa
upper esophageal sphincter anatomy
-prevent esophageal air insufflation
-Prevent esophagopharyngeal & laryngeal reflux
-contracted at rest
lower esophageal sphincter
-Composed of thickened circular smooth muscle
The Z-line marks the boundary between the esophageal squamos epithelium and the gastric columnar epithelium.
The phrenoesophageal ligament helps fix the LES within the diaphragm
Is contracted at rest
types of peristalsis
Primary peristalsis- a reflex associated with swallowing, involves all phases of the swallowing reflex including the oral phase, pharyngeal peristalsis, UES relaxation, esophageal peristalsis, and LES relaxation.
Secondary peristalsis- restricted to the esophagus, not accompanied by pharyngeal contraction or UES relaxation
Tertiary Contractions- not normally seen, nonperistaltic
odynophagia
globus
pyrosis
-pain with swallowing
-nonpainful sensation of a lump/foreign body in throat
-heartburn
dyspepsia
one or more of the following: postprandial fullness
Early satiety
and/or epigastric pain or burning
Oropharyngeal dysphagia
-disease arising from the cranial nerves or skeletal muscle
-Arise from disorders that affect the function of the oropharynx, larynx, and upper esophageal sphincte, such as:
poor dentition, decrease in salivary, neurologic disorders, disruption of the oropharyngeal mucosa, neuromuscular discoordination, zenkers diverticulum
Zenker's diverticulum
-outpouching of the mucosa through killan's triangle
-above the UES, at midpoint of esophagus, or just above the LES.
-older adults
-can retain contents
-sx:dysphagia, gurgling in throat, regurgitations
-tx: surgical or endoscopic resection
Esophageal dysphagia
-arises within the body of the esophagus, the lower esophageal sphincter, or cardia, and is most commonly due to mechanical causes (obstruction) or a motility disturbance.
-If related to solids only-likely caused by obstruction: stricture, ring, or lesion.
-If related to liquids and solids like due to motor dysfunction like esophageal spasm or achalasia.
Esophageal rings/webs
-web: thin mucosal fold that protrudes into the lumen; related to bullous conditions, iron def, graft vs. host dz
-ring: related to damage from GERD
-cause solid food dysphagia
-tx: EGD with dilatation, PPI
->50% recoccur w/in 5 yrs
Esophagitis
-inflamm/irritation of esophagus
-causes: GERD,meds, chemical ingestion, radiation, infx
-sx: pyrosis/dyspepsia, dysphagia, odynophagia
-rx: identify cause, reverse if possible, protect mucosa
Squmous cell cancer risks
1. familial
2. smoking
3. alcohol
4.foods containin N-nitroso liked pickled foods and mets
5. Betel nut chewing
6. Zinc def
7. HPV
adenocarcinoma risks
1. GERD
2. smoking
3. obesity
4. H. pylori infx
5. foods containing N-nitroso
Esophageal spasm
-sx: dyspepsia, dysphagia. chest pain
-dx with manometry
-mgmt: Calcium Channel Blockers diltiazem tid before meals, tricyclic antidepressants like imipramine , nitro 0.3mg 4-5 min before meals
Achalasia
-loss of peristalsis in the distal esophagus and failure of LES relaxation
-sx:dysphagia to solids >liquids, difficulty belching, wt loss, regurgitation, chest pain
-increases risk of developing squamoua cell cancer
Achalsais tx
Dilatation of LES-temporary relief, can increase reflux symptoms afterward
Surgical myotomy-70% have improvement still at 10 years, increase GERD symptoms along with risk of Barretts and squamos cell CA
Botox of LES-inhibits release of acetylhcoline and relaxes LES, mild to moderate improvement, no long term studies regarding efficacy or safety.
GERD
-sx: heartburn, "agita", bloating, early satiety, N/V
-caused by acid from the stomach entering esophagus from: transient lower esophageal sphincter, hypotensive lower esophageal sphincter, anatomic disruption of gastroesophageal junction
-esophageal acid clearance is altered
-esophageal emptying is impaired
Hiatal hernia
-a condition in which a portion of the stomach protrudes upward into the chest, through an opening in the diaphragm
GERD-hx
1. ulcer-like complaints: burning, epigastric hunger pain with food
2. Dysmotility-like complaints: chest pain/pressure, N, bloating
3. Unspecific dyspepsia-vague epigastric discomfort or burning, not necessarily related to meals, increased with lying down, c/o bloating, burping, sour taste in mouth, possible hiccups
GERD-PE
-usually nml except for epigastric tenderness
-evaluate with the Carnett test: increased local tenderness during muscle tensing
GERD-diagnostic strategies
1. trial of PPI or H2 blockers
2. noninvasive testing for H.pylori infx
3. Endoscopy
4. upper GI series (May demonstrate active ulcers and reflux when occurring, limited by technique and interpretation)
Gastric malgnancy-Alarms
Unintended weight loss
Persistent vomiting
Progressive dysphagia
Odynophagia
Anemia
Hematemesis
Palpable abdominal mass or lymphadenopathy
Unexplained iron deficiency anemia
Family history of upper gastrointestinal cancer
Previous gastric surgery
Jaundice
EGD
-Gold standard for dx of PUD, GERD, and malignancy
-Diagnostic yield of EGD for dyspepsia increases with age
mgmt of GERD
1. elevate head of bed
2. avoid exacerbating foods, acidic beverages, mint, caffeine, alcohol
3. avoid tight fitting garments
4. stop smoking
5. chew gum or inc salivation
6. PPI (prazoles) or H2 blocker (cimetidine, famotidine)
7. Metocloprimide:Increase LES tone, enhance gastric emptying, and improve peristalsis; used in refractory GERd; many SE
problems with long term acid suppresion
Atrophic Gastritis
Enteric Infections
Vitamin B12 Malabsorption
Decreased Calcium absorption and Osteopenia/porosis
Barrett's esophagus
-abnormal, intestinal-type epithelium called specialized intestinal metaplasia replaces the normal stratified squamous epithelium of the distal esophagus
-develops as a consequence of chronic GERD
-predisposes to adenocarcinoma
tx: esophagectomy, ablation, palliative (chemo, radiation)
Peptic ulcer disease
-Defects in the gastrointestinal mucosa that extend through the muscularis mucosae
-causes: H. pylori and NSAIDs
also...infx, drugs, hormonal or mediator induced, vascular
gastric and duodenal ulcers
-gastric- more likely to be NSAID related; higher rate of cancer
-duodenal- morel likely H.pylori related
presentation of PUD
-asymptomatic
-upper or lower GI bleed
-dyspepsia: burning, epigastric hunger pain with food, antacid and antisecretory agent relief
-anorexia, wt loss, early satiety
-classic of duodenal ulcer: pain 2-5 hrs after meals
-gastric ulcer-more severe pain occuring soon after meals
-dx: EGD
Complications of PUD
1. bleeding
2. perforation
3. penetration
4. obstruction
perforation
-ulcer erodes through all layers of the stomach or duodenum
-NSAID use
-sudden onset of severe diffuse abd pain and possibly altered VS/signs of shock
Penetration
-Penetration of the ulcer through the superficial layers of stomach wall without free perforation and leakage of luminal contents into the peritoneal cavity
-Pain with meals, and loss of food and antacid relief
CLO test
-A tissue sample is inoculated into a medium containing urea and phenol red, a dye that turns pink in a pH of 6.0 or greater. The pH will rise above 6.0 when H. pylori, the Campylobacter-like organism, metabolizes urea to ammonia by way of its urease activity
Urea breath test
-For the test, patients swallow a capsule containing urea made from an isotope of carbon
-If H. pylori is present in the stomach, the urea is broken up into nitrogen and carbon
-The carbon dioxide is absorbed across the lining of the stomach and into the blood. It then is excreted from the lungs in the breath. Samples of exhaled breath are collected, and the isotopic carbon in the exhaled carbon dioxide is measured.
treatment of H.pylori
-Standard dose PPI twice daily (or esomeprazole once daily) plus clarithromycin 500 mg twice daily, and amoxicillin 1000 mg twice daily for 10-14 days*
-metronidazole if allergic to PCN
-bismuth, metronidazole, tetracycline, rantidine
treatment of PUD not related to H.pylori
1. antisecretory med: H2 blockers, PPIs
2. Sucralfate
3. Misoprostol
treatment of refractory ulcers
-most respond to oral therapies
-Must differentiate between continued symptoms and continued disease
-surgery last resort: vagotomy,gastric resection, vagotomy with antrectomy
-r/o hypersecretory cause and tx
Gastrectomy complications
1. post vagatomy dirrhea
2. dumping-post prandial discomfort, nausea, vommitting, diarrhea, cramps, diaphoresis, palpitations
3. alkaline reflux
4. early satiety
NSAID induced PUD
-Risk increased with: prior h/o ulcer, length of use, increased age, cotherapy, and ? Dose/strength
-Most subtle change is disruption of mucosal barrier
-More sever problems include: edema, erythema, subepithelial hemorrhage, erosions, and ulcers
prevention of NSAID induced PUD
1. misoprostol
2. PPIs