Conference Objectives Flashcards
Generate a differential diagnosis for a patient presenting with upper GI tract symptoms: pyrosis, dysphagia, GI bleeding, wt. loss
- infectious esophagitis - presents with odynophagia
- pill esophagitis
- peptic ulcer disease
- non-ulcer dyspepsia - Mallory Weiss, achalasia, boerhaave syndrome
- biliary tract disease
- coronary artery disease
- esophageal motility disorders
- eosinophilic esophagitis
List all of the complications associated with GERD, PUD and esophageal cancer
- GERD –> Barrett Esophagus –> ulceration with stricture formation AND dysplasia with a risk of adenocarcinoma
List all of the complications associated with GERD, PUD and esophageal cancer
- GERD –> Barrett Esophagus –> ulceration with stricture formation AND dysplasia with a risk of adenocarcinoma
- PUD:
Gastric –> Ulceration of left gastric artery leading to bleeding, Perforation (air under diaphragm, pain radiates to left or right shoulder)
Duodenal –> Bleeding (anterior ulcer; MC ulceration of duodenal artery). Perforation (anterior ulcer = air under diaphragm, pain radiated to R/L shoulder). Gastric outlet obstruction, pancreatitis (posterior ulcer)
Bleeding spontaneously ceases in 80% of cases.
Generate a management plan for a patient presenting with gastric ulcer
Pharmacologic: eradication of H. pylori via PPI-based triple therapy
Surgery for resistant cases is uncommon: ulcer removal with antrectomy or hemigastrectomy without vagotomy
Recognize and address psychological, societal and epidemiologic factors associated with GERD
GERD: 10% of adults have GERD daily, 80% of pregnant women have GERD, hiatal hernia is present in 70% of people with GERD. Studies show that 33-44% of Americans experience heartburn at least monthly and 7-13% do so daily. It reaches a maximum prevalence in
pregnant woman where 25% of patients experience daily symptoms.
Recognize and address psychological, societal and epidemiologic factors associated with Gastrointestinal disorders
,
Describe the physical exam findings in a patient presenting with a perforated peptic ulcer
,
Clinical presentation of GERD
Noncardiac chest pain (heartburn, indigestion)
Worse when lying down, relieved by antacids
Nocturnal cough and asthma, Acid destruction of enamel
Early satiety and abdominal fullness
Bloating and Belching
Clinical presentation of peptic ulcer disease
Duodenal: epigastric pain, better after eating, never malignant
Gastric: epigastric pain, worse with eating, small percentage are malignant
Discuss the pathophysiologic mechanisms leading to GERD
- Transient relaxation of lower esophageal sphincter not associated with swallowing or distension of the esophageal body –> reflux of acid and bile into the distal esophagus
- ineffective esophageal clearance of reflux material
- hiatal hernia and the diaphragmatic sphincter
Discuss the pathophysiologic mechanisms leading to Gastric Ulcers
Gastric = defective mucosal barrier due to H. pylori.
Mucosal ischemia (reduced PGE, vasodilator)
Bile reflux, Delayed gastric emptying
BAO (basal acid output) and MAO (maximal acid output) are normal to decreased
Discuss the pathologic features of carcinoma of the esophagus
.
Discuss the pathologic features of carcinoma of the esophagus
.
Infective esophagitis
AIDS-related esophagitis
Pathogens:
HSV = multinucleated squamous cells with intranuclear inclusions
CMV = eosinophilic intranuclear inclusions
Candida = yeasts and pseudohyhae (extended yeast forms)
Corrosive Esophagitis
Ingestion of strong alkali (lye or acid)
Complications = stricture formation, Perforation, SCC
Clinical Presentation of Achalasia
Nocturnal regurgitation or undigested foods Dysphagia for solids and liquids Chest pain and heartburn Frequent hiccups Nocturnal cough from aspiration Difficulty belching
Pathogenesis of Achalasia
- Normal relaxation of smooth muscle in the lES is due to NO and vasoactive peptide (VIP)
- In achalasia, there is incomplete relaxation of the LES
- probably autoimmune process –> loss of myenteric nerve fibers and inhibitory neurons which produce NO synthase
- decrease in both NO and VIP - dilation of esophagus occurs proximal to LES, but peristalsis is absent
- Acquires cause is chagas disease –> destruction of ganglion cells by amastigoses (lack flagella)