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40 Cards in this Set
- Front
- Back
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What is Zenker's Diverticulum and how is it treated?
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Diverticula formed by protrusion of posterior hypopharyngeal mucosa between muscular layers
Treatment: surgical removal |
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What is the presentation for a patient with Zenker's and how is it diagnosed?
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After age 60, acute or chronic symptoms, dysphagia for liquids and solids, nausea, emesis of undigested foods, cough, halitosis
PE: bulge in neck Diagnosis: esophagram (barium swallow) |
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What is esophageal candidiasis and how is it treated?
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Caused by Candida albicans
Commonly seen in immunocompromised patients Treatment: antifungal therapy |
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What is the presentation for esophageal candidiasis and how is it diagnosed?
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Odynophagia (hallmark) - pain when swallowing
Retrosternal pain, nausea, weight loss PE: oral examination Diagnosis: EGD (white mucosal plaque like lesions) - with biopsy (yeast and pseudohyphae) |
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What is Herpetic Esphagitis and how is it treated?
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Infection of the esophagus with herpes simplex virus type I
Affects mucosa layer only More common in immunocompromised Treatment: antiviral agent |
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What is the presentation for herpetic esphagitis and how is it diagnosed?
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Odynophagia, retrosternal pain, nausea, fever
PE: oral examination Diagnosis: esophagram (suggstive) and EGD with biopsy (vesicles join to form ulcers) |
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What is achalasia and how is it treated?
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Loss of peristalsis in distal esophagus and failure of LES relaxation with swallowing
Treatment: Meds (nitrates and CCB), botulinum toxin injections, dilation of LES, surgical myotomy (cut fibers of LES) |
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What is the presentation for achalasia and how is it diagnosed?
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Progressive dysphagia for solids and liquids, vomit undigested food, weight loss, globus sensation
PE: weight loss Diagnosis: barium swallow (suggestive) - dilated esophagus terminates in beak-like narrowing; esophageal manometry (confirmatory) - tube through nose to esophagus that measures peristalsis |
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What is gastroesophageal reflux disease (GERD)?
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Abnormal movement of gastric contents from stomach into esophagus leading to troublesome symptoms or mucosal damage from inflammation
Applied to pts with symptoms suggestive of reflux , but not necessarily with esophageal inflammation Very common |
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What is physiologic and pathologic reflux?
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Physiologic: contents from stomach come up to esophagus then go back down; episodes occur postprandially, short-lived, asymptomatic, and rarely occur during sleep
Pathologic: associated with symptoms or mucosal injury, often including nocturnal episodes |
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What is the presentation for GERD?
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"Heartburn" (pyrosis) - can mimic angina
Precipitated by meals or laying down (can awaken pt from sleep) Odynophagia and/or dysphagia Regurgitation, nausea, globus sensation Water brash (acidic/sour taste in mouth) PE: mostly unremarkable, may have epigastric pain |
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How is GERD diagnosed?
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Not necessary or practical to initiate a diagnostic evaluation in every pt with heartburn
Can put them on meds and see if get better; see them back in a few weeks Potential studies: endoscopy, esophageal manometry, ambulatory esophageal pH monitoring |
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When do you do endoscopy for a case of GERD?
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Endoscopy with biopsy should be done at presentation for patients with troublesome dysphagia
Should also be done to evaluate pts with suspected GERD who have not responded to empiric trial of twice daily PPI therapy |
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When is esophageal manometry done in a case of GERD and why?
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Pts with suspected GERD, not responded to empiric trial of twice daily PPI therapy and have normal findings on endoscopy
Allows for evaluation of LES pressure and muscle contractions of esophagus |
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When is ambulatory esophageal pH monitoring done for GERD and what does it do?
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Pts with suspected GERD, not responded to PPI, normal endoscopy, no major abnormality on manometry
Trans-nasally placed catheter or wireless, capsule shaped device affixed to distal esophageal mucosa (trans-nasal 24 hrs, wireless 48-96 hrs) Monitors percentage of time esophageal pH is below 4 |
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What is the treatment for GERD?
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Mild symptomatic GERD managed empirically
Lifestyle modifications Antacids Histamine-2 receptor antagonists Proton pump inhibitor (PPI) - treat for 8-12 weeks Surgery (Nissen fundoplication) - tighten LES |
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What lifestyle modifications can be made for someone with GERD?
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Avoidance of foods that may precipitate reflux (coffee, alcohol, chocolate, fatty foods)
Avoidance of acidic foods may precipitate heartburn (citrus, carbonated drinks, spicy foods) Adoption of behaviors that may reduce esophageal acid exposure (weight loss, smoking cessation, elevating head of bed, avoid laying down 2-3 hrs after meals) |
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What is Barrett's esophagus?
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Complication of GERD
Columnar epithelium replaces stratified squamous epithelium that normally lines distal esophagus (more resistant to acid) Predisposes to development of adenocarcinoma of esophagus |
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What is the presentation of Barrett's?
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Most pts seen initially for GERD symptoms (columnar metaplasia causes no symptoms)
Ulceration, stricture formation, bleeding PE: similar to GERD |
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How is Barrett's diagnosed?
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EGD with biopsy
Squamocolumnar junction and gastroesophageal junction Columnar epithelium has reddish color and velvet-like texture on endoscopic exam, squamous has pale, glossy appearance |
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How is Barrett's managed?
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Treatment of associated GERD - initial therapy with PPI
Endoscopic surveillance to detect dysplasia - suggested in pts with multiple risk factors associated with esophageal adenocarcinoma (50 years or older, male, white, chronic GERD, hiatal hernia, elevated BMI, or intra-abdominal distribution of body fat) |
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How often should endoscopic surveillance be done to detect dysplasia in Barrett's?
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No dysplasia: 3-5 years
Low-grade dysplasia: 6-12 months High-grade dysplasia: 3 months |
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What is peptic ulcer disease?
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General term for defects in GI mucosa caused by HCl and pepsin in gastric juice (esophagus, stomach, or duodenum)
Associated with H. pylori infection and ingestion of NSAIDS including aspirin Risk factors: alcohol abuse, stress (physical or emotional), smoking, radiation therapy |
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What is the presentation for peptic ulcer disease?
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Can be asymptomatic until complications occur
Nausea Early satiety Abdominal pain - burning hunger-like empty feeling; immediately with meals (gastric); 2-5 hrs after meals (duodenal); nocturnal symptoms b/w 11-2 that wake pt; relieved with alkali, food, or antisecretory agent PE: wight loss, epigastric abdominal pain |
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How is peptic ulcer disease diagnosed?
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Endoscopy (most accurate) - biopsy urease testing, histology, bacteria culture
Urease breath testing Stool antigen testing Serology |
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How is peptic ulcer disease treated?
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Antisecretory therapy for all PUD pts (H2 blockers, PPI)
Eradicate H. pylori (PPI, amoxicillin, clarithromycin for 7-14 days) Avoidance (remove aggravants) Confirm eradication of infection in all pts 4-6 weeks after treatment (urea breath testing, stool antigen, endoscopy) |
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What is Zollinger-Ellison syndrome?
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Ulceration of upper jejunum, hypersecretion of gastric acid, and non-beta islet cell tumors of pancreas "gastrinomas"
Gastrin identified as agent responsible for syndrome 90% of pts with ZES develop peptic ulcers - solitary ulcers less than 1cm, frequently recurrent, 1st part of duodenum most common (also distal duodenum and 1st part jejunum) |
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What is the presentation for ZES and how is it diagnosed?
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Similar to PUD or GERD - nausea, abdominal pain
Diarrhea and/or steatorrhea may be prominent symptom PE: weight loss, abdominal pain Diagnosis: fasting serum gastrin conc. (off PPI 1 week prior), secretin stimulation test |
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What is done for ZES?
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Surgery for sporadic gastrinoma without metastasis - exploratory laparotomy with resection
Medical therapy to control gastric acid hypersecretion - PPI, high doses |
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What are risk factors for gastric malignancy?
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Diet (salt and salt preserved, nitroso compounds), obesity, smoking, H. pylori
Most pts symptomatic and have advanced disease Incidence highest in East Asia, East Europe, and S. America |
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What is the presentation for gastric malignancy?
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Nausea, persistent epigastric abdominal pain
Anorexia, early satiety, dysphagia PE: weight loss, abdominal pain |
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How is gastric malignancy diagnosed and treated?
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Diagnosis: endoscopy with biopsy (adenocarcinoma)
Treatment: endoscopic resection, gastrectomy, antibiotic treatment for eradication of H. pylori |
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What is acute pancreatitis?
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Inflammatory condition of pancreas characterized by abdominal pain and elevation of pancreatic enzymes
Etiology can be established in at least 70% of pts |
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What is the etiology for acute pancreatitis?
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BADHITS:
Biliary Alcohol Drugs Hypertriglyceridemia (levels > 1000) Idiopathic Trauma Scorpion bites |
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What is the presentation for acute pancreatitis?
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Abdominal pain (epigastric or umbilical) - deep, writhing pain radiates to the back
Nausea, vomiting Jaundice (gallstones) Fever (low grade - moderate) PE: relief of pain with bending forward, abdominal pain, jaundice, ecchymotic discoloration of flank or periumbilical region (Gray-Turner and Cullen's sign) |
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How is acute pancreatitis diagnosed?
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History and PE
Lab studies: amylase, lipase (levels stay elevated for longer periods than amylase) Ultrasonography: evaluate for gallstones, dilation of biliary duct, pancreatic inflammation CT scan - most important imaging test |
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What is the purpose for Ranson's criteria?
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Predicts prognosis in acute pancreatitis
Used to determine chance of pt dying from current episode of pancreatitis Pt gets one point for each criteria they are positive for |
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What are the risk factors in Ranson's criteria?
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Admission: over 55, blood glucose >200, serum LDH >350, AST >250, WBC >16,000
At 48 hours: hematocrit falls >10%, BUN increased >5mg/dl, serum calcium <0.8, arterial PO2 <60, base deficit >4, estimated fluid sequestration >6L |
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How are Ranson's criteria interpreted?
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Risk factors <3: 1% mortality
Risk factors 3-4: 15% mortality Risk factors 5-6: 40% mortality Risk factors >7: 100% mortality |
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How is acute pancreatitis treated?
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Treatment of associated condition
Fluid and electrolyte replacement Control hyperglycemia Keep pt NPO Adequate analgesia with narcotics NG suction? H2 blockers? Antibiotics: not given traditionally unless necrosis present |
