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Pill Esophagitis

Extraesophageal manifestations: asthma (GERD exacerbates, does not cause asthma), chronic cough, nocturnal cough, sinusitis, pneumonitis, laryngitis, hoarseness, hiccups, dental disease

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  therapeutic trial of PPI (sensitivity ~80%); this is the more popular, cost-effective and easiest method
  
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  esophageal pH monitoring (sensitivity 60-100%); to evaluate equivocal endoscopic findings on patients refractory to PPI (i.e. to see why the PPI isn’t working, still sure of the diagnosis do while on PPI) or with atypical symptoms and need for diagnosis; when considering anti-reflux surgery with negative endoscopy (i.e. you want to do surgery but have to prove the pt really has GERD, do while off PPI x 1 wk)
  
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  double contrast barium swallow (sensitivity 25%)
  

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  antacids, H₂ blockers (50% effective), proton pump inhibitors (80% effective, BID dosing may make a difference, switching agents have been reported to make a difference)
  
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  can also try metoclopramide
  
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  surgery / post-op complications include perforation, acute gastric herniation (<1%)
  

Primary causes: idiopathic LES dysfunction, Chagas disease

Radiography: beak-like tapering over LES (bird’s beak)

Manometry: absence of peristalsis, elevated LES pressure, incomplete LES relaxation (although there is a rare form of vigorous achalasia with large-amplitude prolonged contractions

Treatment:

Drugs: nitrates, anticholinergics, ß-agonists, Ca channel blockers are 50% effective

prostaglandins under investigation

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  Pneumatic dilation – 70-90% effective (0.2% mortality, 2-3% perforation)
  
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  Endoscopic injection of botulinum toxin – helpful in 70-80%
  
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  Heller myotomy – 65-90% success rate (3-4% complications) / increased reflux years later in 25-30%
  
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  Endoscopic myotomy – under investigation
  

CVA (transient brainstem edema), myasthenia gravis, myotonic dystrophy, polymyositis, bulbar poliomyelitis, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, hypothyroidism

Primary idiopathic or secondary (collagen vascular disease, radiation, diabetes)

radiography corkscrew-shaped esophagus

esophageal manometry 30% of basal state with spastic contractions / nutcracker esophagus (contractions associated with chest pain)

30% with incomplete LES relaxation / some normal contractions present

balloon distension of lumen lower threshold of pain upon insufflation

Treatment: 50% success rate with anticholinergics, nitrates, calcium channel blockers, bougienage, hydralazine (decreases amplitude), surgery in severe cases (longitudinal myotomy)
Scleroderma (see connective tissue)

Pathology: early – neural degeneration / late – atrophy of circular smooth muscle

Clinical findings: dysphagia, severe reflux/heartburn (50%), stricture (25%)

Radiography – poor emptying

Manometry – decreased LES pressure / weak contractions in distal 2/3

Treatment: anti-reflux therapy
Esophageal Cancer (very bad prognosis)

Epidemiology: male 4:1 / blacks 4:1 / incidence in U.S. 1 in 25,000 whites (50-70 yrs) / 1 in 8,000 blacks / worst in China and Iran / almost always malignant / esophagus has NO serosa / currently, in US, 50% adenocarcinoma, 50% squamous cell

Risk Factors: alcohol, smoking, GERD (Barrett’s esophagitis; 10% risk, endoscopy q 2-3 yrs), hot liquids, burns, radiation, malnutrition (vitamin A and C deficiency), nitrosamines, burns (lye ingestion), achalasia (10% risk), Tylosis (hyperkeratosis of palms, soles; 80% develop squamous cell Ca of esophagus), celiac sprue, Plummer-Vinson syndrome

Presentation: progressive dysphagia (1.2 cm narrowing), pain (extension beyond esophagus), dysphagia for liquids, cough, hoarseness, weight loss signify advanced esophageal cancer

Diagnosis: barium swallow, endoscopy (90% sensitive; down to 1 cm), CT and bronchoscopy

Treatment: surgery for distal lesions 5 yrs survival only 5-10%, radiotherapy for proximal lesions, stent placement or bougienage, laser therapy, chemotherapy regimens under investigation (currently no strong evidence for using chemotherapy in esophageal cancer 5/00)

Complications: ruptured esophagus thoracotomy and repair / antibiotics

gastrograffin study later / 50% die if untreated / avoid mediastinitis, pneumomediastinum and pneumothorax

body – chief cells – pepsinogen

body - parietal – H+ ions / IF?

antrum - G-cells – gastrin

usually on the left

congenital hypertrophic pyloric stenosis - multifactorial / projectile vomiting / 1 in 300

acquired pyloric stenosis - gastritis, peptic ulcer, cancer
Gastritis
Acute gastritis

NSAIDS, alcohol, chemo, infection, smoking, uremia, ischemia, mech. injury, etc.

superficial erosion / may result in severe hemorrhage
Chronic gastritis
type A – uncommon

patchy autoimmune disease / occurs in body-fundus mucosa / 50% prevalence in elderly / associated with pernicious anemia, achlorhydria

H. pylori (antral mucosa) / not invasive, Giemsa or Warthin-Starry stain, serum Ab,

urease in biopsy, histology/culture, breath test
diffuse (DAG) only antrum / 50% over 60 population

multifocal (MAG) intestinal metaplasia / hypochlorhydria

antibodies directed against parietal cells / 10% get pernicious anemia / increased gastrin

Elective surgery for outlet obstruction, hypochloremia, hyponatremia

has not yet perforated muscularis / requires pepsin and acid secretion

Risk Factors: NSAID, smoking, alcohol, corticosteroids, stress, H. pylori (30-60% of non-NSAID-related gastric ulcers) (see below)
Acute gastric ulceration

penetration of muscularis / requires gastric acid / shock, burns (Curling’s), sepsis, trauma, acidosis, CNS-mediated from ICP and hypothalamic changes (Cushing’s) / more severe version of acute gastritis / multiple lesions in any location / scarring and vessel thickening absent / 5 - 10 % of all ICU patients / radiating mucosal folds, sloping distal margin (benign)

mostly fundus / bleed but do not penetrate

solitary, antral, deep / may perforate

5-10% lifetime incidence / DU more common, younger, (type O, nonsecretors, HLA B5), rapid gastric emptying, increased acid