Conference Objectives Flashcards

1
Q

Generate a differential diagnosis for a patient presenting with upper GI tract symptoms: pyrosis, dysphagia, GI bleeding, wt. loss

A
  • 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
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2
Q

List all of the complications associated with GERD, PUD and esophageal cancer

A
  1. GERD –> Barrett Esophagus –> ulceration with stricture formation AND dysplasia with a risk of adenocarcinoma
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3
Q

List all of the complications associated with GERD, PUD and esophageal cancer

A
  1. GERD –> Barrett Esophagus –> ulceration with stricture formation AND dysplasia with a risk of adenocarcinoma
  2. 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.
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4
Q

Generate a management plan for a patient presenting with gastric ulcer

A

Pharmacologic: eradication of H. pylori via PPI-based triple therapy
Surgery for resistant cases is uncommon: ulcer removal with antrectomy or hemigastrectomy without vagotomy

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5
Q

Recognize and address psychological, societal and epidemiologic factors associated with GERD

A

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.

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6
Q

Recognize and address psychological, societal and epidemiologic factors associated with Gastrointestinal disorders

A

,

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7
Q

Describe the physical exam findings in a patient presenting with a perforated peptic ulcer

A

,

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8
Q

Clinical presentation of GERD

A

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

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9
Q

Clinical presentation of peptic ulcer disease

A

Duodenal: epigastric pain, better after eating, never malignant
Gastric: epigastric pain, worse with eating, small percentage are malignant

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10
Q

Discuss the pathophysiologic mechanisms leading to GERD

A
  • 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
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11
Q

Discuss the pathophysiologic mechanisms leading to Gastric Ulcers

A

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

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12
Q

Discuss the pathologic features of carcinoma of the esophagus

A

.

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13
Q

Discuss the pathologic features of carcinoma of the esophagus

A

.

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14
Q

Infective esophagitis

A

AIDS-related esophagitis
Pathogens:
HSV = multinucleated squamous cells with intranuclear inclusions
CMV = eosinophilic intranuclear inclusions
Candida = yeasts and pseudohyhae (extended yeast forms)

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15
Q

Corrosive Esophagitis

A

Ingestion of strong alkali (lye or acid)

Complications = stricture formation, Perforation, SCC

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16
Q

Clinical Presentation of Achalasia

A
Nocturnal regurgitation or undigested foods
Dysphagia for solids and liquids
Chest pain and heartburn
Frequent hiccups
Nocturnal cough from aspiration
Difficulty belching
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17
Q

Pathogenesis of Achalasia

A
  1. Normal relaxation of smooth muscle in the lES is due to NO and vasoactive peptide (VIP)
  2. 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
  3. dilation of esophagus occurs proximal to LES, but peristalsis is absent
  4. Acquires cause is chagas disease –> destruction of ganglion cells by amastigoses (lack flagella)
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18
Q

Diagnosis of achalasia

A
  • 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
19
Q

Treatment of achalasia

A
  1. Nonpharmacologic = pneumatic dilation and esophagomyotomy

2. Pharmacologic = long-acting nitrates, CEBs, botox injection

20
Q

Mallory Weiss Syndrome presentation

A

Mucosal tear in the proximal stomach and distal esophagus due to severe retching, most often associated with alcoholism or bulimia
Presents with hematemesis

21
Q

Mallory Weiss Syndrome

A

.

22
Q

Epidemiology of GERD, PUD and Esophageal Cancer

A

GERD: 10% of adults have GERD daily, 80% of pregnant women have GERD, hiatal hernia is present in 70% of people with GERD

23
Q

Treatment of GERD

A

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

24
Q

Treatment of GERD

A

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

25
Q

Discuss the pathophysiologic mechanisms leading to Gastric Ulcers

A

Defective mucosal barrier due to H. pylori infection,
Increased acid output (increased parietal cell mass)
BAO and MAO both increased

26
Q

Complications of gastric Ulcers

A

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.

27
Q

Complications of duodenal ulcers

A

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.

28
Q

Generate a management plan for a patient presenting with duodenal ulcer

A

Pharm: eradication of H. pylori via PPI- based triple therapy
Surgery for resistant cases is uncommon = highly selective vagotomy

29
Q

Generate a management plan for a patient presenting with esophageal cancer

A

.

30
Q

Generate a management plan for a patient presenting with esophageal cancer

A

.

31
Q

Gross appearance of ulcers

A
  • 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
32
Q

Epidemiology of Gastric and Duodenal Ulcers

A

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

33
Q

Risk factors for duodenal ulcers

A

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

34
Q

Risk factors for duodenal ulcers

A

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

35
Q

Symptomatic clinical condition/histopathologic alteration from reflux of irritant gastric juices from the stomach into the esophagus is…

A

GERD

36
Q

characteristic histopathologic changes in the esophageal mucosa that can often be seen endoscopically

A

Reflux esophagitis which occurs in a subset of GERD patients

37
Q

The most common presenting symptoms of GERD include

A

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.

38
Q

Recognize and address psychological, societal and epidemiologic factors associated with PUD

A

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)

39
Q

Regurgitation vs Nausea

A
  • 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.
40
Q

Less common presenting signs of GERD

A

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.

41
Q

How do hiatal hernias lead to GERD?

A

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.

42
Q

How do hiatal hernias lead to GERD?

A

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.

43
Q

Management of refractory GERD

A

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.

44
Q

Treatment of Nonerosive GERD and Functional GERD

A
  1. 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.
  2. Other NERD patients have abnormal acid but have not developed overt mucosal injury.
    –> 1 and 2 may respond to antisecretory therapy = PPIs
  3. Function Heartburn: those with heartburn not attributable to acid reflux