02 Esophageal disorders Flashcards
Secondary peristalsis
Contraction of esophagus just proximal to distention- continues in a wave
Primary peristalsis
Pharyngeal constriction and UES relaxation
400-600ms (.5 second relaxation)
Esophageal peristalsis coordination
- Wave of inhibition( VIP—>NO via cGMP blocks Ca and hyperpolarizes)
- Followed by a wave of excitation (Substance P —> Ca2+ influx)
Dysphagia
food “gets stuck” Shortly after swallowing (NOT 20 min later)
Peristalsis speed and duration
- 3-7 seconds in length, 3-5 cm/second
* LES relaxes 3-8 seconds for bolus
Achalasia
- Impaired LES relaxation, can have ^ LES tone (loss of No synthase activity)
- Loss of peristalsis in body- MEGA ESOPHAGUS/dilation, haphazard contraction
- “Birdbeak sign” on radiograph
- Ganglionic degeneration and inflammatory lymphocyte proliferation
70 year olds and 20-30 year olds
Acalasia like
Malignancy blocking sphinctor
Achalasia causes
Infiltrative cancers Amyloidosis- sarcoidosis Chagas Para neoplastic ANS damage- polio, dabetes, iatragenic
Achalasia treatments
NO donors
Anticholinergics
Botox/ ballooning
Operative
Esophageal spasm
Dis-coordinated esophageal movements with inefficient delivery of foods to stomach
Complete esophageal aperistalsis
Scleroderma esophagus
ENTIRE ESOPHAGUS RELAXED
muscle unable to contract
Submucosal esophageal glands
(also submucosal glands in duodenum)
Secrete mucin and bicarb to protect epithelium
Reflux pathophys
inflammation –> IL6 –> h202 —> ^ PGE2—> decreased LES tone
Most common reflux cause
Increased transient LES opening
Reflux morphology
- Basal zone >20% of epithelial thickness
- increase depth of lamina propria papillae
- Some eosinophils- lots of neurtophils
Alarm symptoms
Dysphagia Anemia Weightloss Abdominal mass Vomiting
Eosinophilic esophhagitis
*Most common cause of food impaction
*failure of acid suppressive for presumed GERD may point to it
*allergic related
*Eosinophils and IL5, IL13, and MBP
>15 eosinophils per HPF and symptoms
Biopsy helpful- Corregated esophagus, longitudinal furrows, white abscesses
Eosiophilic esophagitis treatment
- Elimination diet
- Topical Steroids
- Systemic steroids
- Endoscopic dilation
Infective esophagitis
- Most common in immunosuppressed
- Healthy people too
HSV- nuclear inclusions
CMV- cytoplasmic and nuclear inclusions
Candida- pseudomembranes
Bacterial- sometimes ulcer related, invasion of lamina propria
Barretts esophagus
Switch to duodenal mucosa- Goblet cells
Cdx gene association
Esophageal Adenocarcinoma
*White middle aged males
*Highest incidence in developed countries
*risk factors- tobbaco, BE dysplasia, obesity, radiation
*P53, cERB-B2, cyclin D1 and E
TNF and NFkB secreted nearby
*80% survival if superficial, overall 25% survival (late diag common)
Es. Adenocarcinoma morphology
- near Barrets
- Flat or raised patches
- distal 1/3 of Es. to cardia
- Mass, diffuse infiltration, ulcerate
- Mucinous glandular structure
Squamous cell carcinoma
AA adult males >45 years
Risk factors: alcohol and TOBACCO, poverty, caustic esoph inj, achalasia/plummer-vinson sndrome, Hot beverage consumption, radiation therapy
Asia, south america, africa
Es. SCC Morphology
*middle 1/3
*early are gray-white plaques
*obstructive masses
*invasion of wall and neighboring structures
75% survival if caught early, poor prognosis otherwise (most caught late)
