What is it? - failure to relax the LES/aperistalsis during swallowing - degeneration of myenteric (Auerbach) plexus - dysphagia for solids AND liquids, SLOWLY progressive

Lecture 4: Upper GI Complaints Flashcards by fluffy bunny

Where does oropharyngeal (Transfer) dysphagia occur?

throat ABOVE suprasternal notch or substernally

-rarely epigastric, location where sticking is perceived does not predict level of lesion

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How does oropharyngeal (Transfer) dysphagia present?

1) immediate onset of symptoms-seconds
2) difficulty INITIATING SWALLOW
3) cough
4) choke
5) drool
6) nasal regurgitation

*often worse with liquids than solids

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What causes oropharyngeal dysphagia?

1) poor dentition
2) reduced saliva production=xerostomia (dry mouth) (sjogrens), meds (anti-cholinergics, anti-histamines)
3) NEUROMUSCULAR DISORDERS (stroke, parkinsons, myasthenia gravis, neuropathies, myopathies, botulism)
4) structural lesions (tumor, zenker diverticulum, inflammation)

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What problem do you have in esophageal dysphagia if symptoms are worse with solids?

mechanical obstruction

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What problem do you have in esophageal dysphagia if symptoms are the same with solids and liquids?

motility disorder

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Is your problem with food sticking for several seconds after swallow?

esophageal problem

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Are your problems swallowing intermittently?

Schatzki’s ring (narrowing of lower esophagus)

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How do you test for oropharyngeal dysphagia?

1) videofluoroscopy
2) barium radiography (both)
3) nasopharyngeal laryngoscopy

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How do you test for esophageal dysphagia?

1) upper endoscopy
2) barium radiography (both)
3) esophageal manometry

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What causes odynophagia (painful swallowing)?

less common than dysphagia
1) Infectious Esophagitis
Herpes, CMV
unusual except immunocompromised

2) Pill Esophagitis
- Doxy, tetracycline, Alendronate, ASSA, NSAIDS, potassium chloride, direct caustic effect of agent on esophageal mucosa, prevented by taking meds upright with water

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What is Achalasia?

What is it?

failure to relax the LES/aperistalsis during swallowing
degeneration of myenteric (Auerbach) plexus
dysphagia for solids AND liquids, SLOWLY progressive

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Who does achalasia effect?

Who does it effect?

-middle aged males and females equally

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What causes Achalasia?

What causes it?

mostly idiopathic
pseudochalasia, paraneoplastic, Chagas disease

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What are the consequences of Achalasia?

What are its consequences?

increased risk to develop esophageal cancer
can cause pulmonary problems due to chronic aspiration

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How do you diagnose achalasia?

1) Barium study
- dilated esophagus
- impaired emptying
- distal tapering
2) manometry-test that measures f(x) of LES
3) EGD-aka upper endoscopy

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How do you treat achalasia?

1) pneumatic balloon dilatation
2) surgical myotomy-muscles of LES are cut so foods can pass nice and smooth baby
3) endoscopic injection of botulinum toxin (botox)-helps relax LES

What is the pathophysiology behind GERD?

1) incompetent antireflux barrier
- transient relaxations of LES
- altered anatomy (hiatal hernia)
- decreased LES pressure (scleroderma)
2) aggressive refluxate (gastric acid +/- bile acids)
3) reduced clearance of acid from the esophagus
4) increased abdominal pressure
- prego

What are the symptoms of regurgitation?

1) heartburn (pyrosis)-hot/burning sensation
2) regurg- return of gastric contents into pharynx
3) water brash-mouth fills with saliva, sour/salty taste
4) dysphagia-inflammation can cause dysmotility, stricture

*odynophagia is uncommon in GERD, if present it can indicate an ulcer

What are some extra-esophageal symptoms?

1) hoarseness-reflux laryngitis
2) globus sensation-lump in throat
3) chronic cough
4) asthma-intermittent microaspiration
5) chest pain-discomfort can mimic angina pectoris

How to diagnose GERD?

1) therapeutic trial with acid suppressing meds

2) diagnostic eval is indicated for
- doubt about diagnosis-atypical symptoms
- chronic/refractory symptoms
- warning symptoms-dysphagia, bleeding, weight loss

3) endoscopy

4) ambulatory pH monitoring if
- atypical symptoms and negative endoscopy
- symptoms refractory (don’t respond) to standard therapy

What are some complications of GERD?

Barrett’s esophagus

squamous epithelium in distal esophagus is replaced by specialized columnar epithelium
can be complicated by dysplasia—>adenocarcinoma

How do you treat GERD?

1) lifestyle mods-elevate bed, avoid fatty foods, chocolate, peppermint, alcohol, lose weight, avoid late meals
2) meds-PPI, H2 blockers, antacids
3) surgery-fundoplication

Eosinophilic Esophagitis

symptoms
associations
histology
treatment

1) Symptoms-dysphagia, food impaction
2) Associations-allergic rhinitis, asthma, food allergies
3) Endoscopy-trachealization, furrows, strictures, diffuse narrowing, eosinophilic abscesses
4) Histology-eosinophils (overlap with GERD)
5) Treatment: PPI, topical steroids, elimination diet

What are some alarm symptoms/signs to watch out for?

1) early satiety
2) dysphagia
3) hematemesis
4) anemia
5) occult blood in stool
6) melena
7) unintentional weight loss (>5% TBW)
8) onset at age >45 indicates potential serious disease

*majority of cancer or ulcer patients do not present initially with alarm symptoms!

What disease is characterized by: 1) stomach pain REDUCED by food/antacids - burning, gnawing, hunger pain - worse at night or in between meals - relief more common with duodenal ulcer - acute severe pain-->perforation 2) Nausea/vomiting - pre-pyloric or pyloric channel-gastric outlet obstruction 3) Hematemesis/Melena-bleeding ulcer 4) commonly asymptomatic until catastrophy - NSAID induced - old peoplez

Peptic Ulcer Disease

What are some causes of Peptic Ulcer Disease?

1) Heliobacter pylori infection 2) NSAIDS 3) hypersecretory states-gastrinoma-->more HCl in duodenum 4) severe physiological stress (Cushing's/Curling's ulcers)

H. pylori

1) motile gram - spiral shaped rod bacteria 2) most common infection in the world 3) associated with poor peoples 4) prevalence varies depending on age and ethnicity 5) mechanism of transmission unknown (fecal-oral, water?) 6) most infections asymptomatic 7) Causes both acute and chronic gastritis but NOT all persons infected with H. pylori develop ulcers 8) eradication of H. pylori reduces ulcer recurrence from 90% to 10%

H. pylori pathophysiology

1) H. pylori is NOT invasive-lives in gastric mucus layer at the surface of the gastric epithelium-disrupts mucus layer and makes it vulnerable to acid and bacterial enzymes and toxins 2) ALL strains make UREASE - splits urea into bicarb and NH3 - buffers acid - basis of several diagnostic tests 3) some strains express CagA - required for expression of VacA (vacuolating cytotoxin) - strains with CagA and VacA associated with greater tissue inflammation and cytokine production 4) CagA expressing strains more frequently associated with duodenal ulcer than non-CagA

Malignancy associated with H. pylori

1) Gastric Adenocarcinoma - H. pylori classified as type 1 (definite) carcinogen - major cause of GASTRIC CANCER 2) MALT lymphoma-98% cases associated with H. pylori - B-cell tumor infiltrating gastric mucosa - 80% regress with H. pylori eradicated

How do you diagnose H. pylori infection?

1) urease breath test 2) stool antigen test 3) serology (IgA Anti-Hp antibody)-does NOT distinguish past and present infection, remains positive even after eradication 4) gastric biopsy (If EDG (upper endoscopy) performed to evaluate symptoms) *all tests EXCEPT serology can be false with recent or ongoing antibiotic/PPI use

How do you treat H. pylori infections?

1) antibiotic resistance is common 2) triple therapy (PPI + 2 antibiotics for 2 weeks) - ex. Clarithromycin + Ampicillin or Metronidazole - eradication of 75% 3) confirmation of eradication recommended in cases with documented PUD, MALT lymphoma, persistent symptoms - urea breath test - stool antigen *NSAIDS CAUSE ULCERS!

How do NSAIDS cause ulcers?

1) direct damage to epithelial cells-not as imp 2) inhibit Cox-1 - prevents local prostaglandins production which protect intestinal mucosa 3) risk of PUD lower but NOT 0 with Cox-2 drugs 4) GI protective meds sometimes used - PPIs help, misoprostol gastroprotective

What am I describing? 1) gastrin producing neuroendrocine tumor 2) majority located in gastronome triangle 3) high blood gastrin level - stimulates gastric acid hyper production - increased basal acid output-ulcers, diarrhea - other causes of high gastrin level are more common (PPI, renal failure, atrophy gastritis) * oversecretion of gastric acid causes peptic ulcers

Zollinger-Ellison Syndrome-Gastrinoma

What condition am I describing? 1) postprandial bloating, early satiety 2) delayed vomiting partially digested contents 3) refractory (unmanageable) gastroesophageal reflux

Gastroparesis (delayed gastric emptying)

How do you diagnose Gastroparesis (Delayed Gastric Emptying)?

Diagnose: 1) succussion splash-showed obstruction 2) UGI (upper GI series) showing dilated stomach-uses barium and x-ray 3) Scintigraphy for rate of gastric emptying-2D imaging with radioisotopes

How do you treat Gastroparesis?

Treat: 1) improve underlying condition (control sugar-diabetes) 2) promotility agents-partially useful - metoclopramide side effects dyskinesia - erythromycin-tachphylaxis (lower drug response) 3) placement of PEG/PEJ tubes (feeding tube)