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)
Diagnosis of achalasia
- abnormal finding with barium swallow = dilated aperistaltic esophagus with a beak-like tapering at distal end
- abnormal findings with esophageal manometry –> detects aperistalsis and failure of LES relaxation
Treatment of achalasia
- Nonpharmacologic = pneumatic dilation and esophagomyotomy
2. Pharmacologic = long-acting nitrates, CEBs, botox injection
Mallory Weiss Syndrome presentation
Mucosal tear in the proximal stomach and distal esophagus due to severe retching, most often associated with alcoholism or bulimia
Presents with hematemesis
Mallory Weiss Syndrome
.
Epidemiology of GERD, PUD and Esophageal Cancer
GERD: 10% of adults have GERD daily, 80% of pregnant women have GERD, hiatal hernia is present in 70% of people with GERD
Treatment of GERD
Nonpharamcologic: Lifestyle = Reduce intake of foods/drugs that decrease LES tone (coffee, CEBs); avoid eating large quantities of food; Sleep with head of the bed elevated; avoid meals at least 2hours before bed
Pharmacologic: Step UP or STEP Down approach.
H2 antagonists, PPIs, Prokinetic agents
Surgery: Fundoplication procedure which involves putting a gastric wrap around the GEJ junction
Treatment of GERD
Nonpharamcologic: Reduce intake of foods/drugs that decrease LES tone (coffee, CEBs); avoid eating large quantities of food; Sleep with head of the bed elevated
Pharmacologic: H2 antagonists, PPIs, Prokinetic agents
Surgery: Fundoplication procedure which involves putting a gastric wrap around the GEJ junction
Discuss the pathophysiologic mechanisms leading to Gastric Ulcers
Defective mucosal barrier due to H. pylori infection,
Increased acid output (increased parietal cell mass)
BAO and MAO both increased
Complications of gastric Ulcers
Gastric –> Ulceration of left gastric artery leading to bleeding, Perforation (air under diaphragm, pain radiates to left or right shoulder)
Bleeding spontaneously ceases in 80% of cases.
Complications of duodenal ulcers
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 duodenal ulcer
Pharm: eradication of H. pylori via PPI- based triple therapy
Surgery for resistant cases is uncommon = highly selective vagotomy
Generate a management plan for a patient presenting with esophageal cancer
.
Generate a management plan for a patient presenting with esophageal cancer
.
Gross appearance of ulcers
- clean, sharply demarcated and slightly elevated around the edges
Four layers noted in histologic sequence:
1. Necrotic debris, 2. inflammation with predominance of PMNs, 3. granulation tissue (repair tissue), 4. fibrosis
Epidemiology of Gastric and Duodenal Ulcers
Gastric: Male = female; smoking may delay healing; risk for developing gastric cancer is increased with blood group A individuals.
Duodenal: Male = female; smoking may delay healing; increased risk in MEN 1
Risk factors for duodenal ulcers
H. pylori (MC), chronic intake of NSAIDs, type O blood group (lack of blood group antigens that are protective to the mucosal surface),
Risk increased in MEN 1
Risk factors for duodenal ulcers
H. pylori (MC), chronic intake of NSAIDs, type O blood group (lack of blood group antigens that are protective to the mucosal surface),
Risk increased in MEN 1
Symptomatic clinical condition/histopathologic alteration from reflux of irritant gastric juices from the stomach into the esophagus is…
GERD
characteristic histopathologic changes in the esophageal mucosa that can often be seen endoscopically
Reflux esophagitis which occurs in a subset of GERD patients
The most common presenting symptoms of GERD include
pyrosis or the retrosternal sensation of burning and discomfort, acid regurgitation, and dysphagia.
Pyrosis = experienced by half of GERD patients = caused by acid stimulation of sensory nerve endings in the deeper layers of the esophageal epithelium.
Recognize and address psychological, societal and epidemiologic factors associated with PUD
PUD: MC cause is H.pylori (70%), other parts of the world its 90%; eradication of H.pylori reduces PUD recurrence; Duodenal MC than gastric; Duodenal has a higher association with H. pylori; incidence of bleeding is the same. Recurrence rate for untreated PUD is about 60% (>70% in smokers)
Regurgitation vs Nausea
- effortless return of gastric or esophageal contents into the mouth.
- Different from vomiting by the lack of nausea, retching and abdominal contractions. Patients often describe a sour
taste in their mouths, at times accompanied by small amounts of undigested food.
Less common presenting signs of GERD
Atypical chest pain; water brash, globus sensation; odynophagia; extra-esophageal manifestations like chronic cough, asthma, sore throat and posterior laryngitis. Some also suspect eosinophilic esophagitis.
How do hiatal hernias lead to GERD?
The crural fibers of the diaphragm in addition to the LES, maintain gastroesophageal competence, esp. when stressed by sudden increases in intraabdominal pressure. The HH serves as a reservoir for gastric contents and a transient relaxation of the LES is more likely to be followed by an episode of reflux if there is a hiatal pouch with retained acid, than in the absence of such a pouch.
How do hiatal hernias lead to GERD?
The crural fibers of the diaphragm in addition to the LES, maintain gastroesophageal competence, esp. when stressed by sudden increases in intraabdominal pressure. The HH serves as a reservoir for gastric contents and a transient relaxation of the LES is more likely to be followed by an episode of reflux if there is a hiatal pouch with retained acid, than in the absence of such a pouch.
Management of refractory GERD
When heartburn proves refractory to treatment, or is accompanied by dysphagia, odynophagia, or gastrointestinal bleeding, endoscopy should be done to detect other possible causes, such as eosinophilic esophagitis, infectious esophagitis, pill esophagitis, or malignancy.
Treatment of Nonerosive GERD and Functional GERD
- majority of patients with typical symptoms of GERD do not have esophagitis;
have symptoms despite having normal levels of esophageal acid on 24hrr pH study
= They have esophageal hypersensitivity to physiologic degrees of acid reflux. - Other NERD patients have abnormal acid but have not developed overt mucosal injury.
–> 1 and 2 may respond to antisecretory therapy = PPIs - Function Heartburn: those with heartburn not attributable to acid reflux
