Esophagus Pathophysiology Flashcards
What is the role of the upper esophageal sphincter? (3)
Barrier between pharynx and esophagus
Allows food in and belching/vomiting
Prevents air entry, reflux of gastric contents
What are the two sphincters of the gastroesophageal Junction?
Lower esophageal sphincter (LES)
Diaphragm
Describe the central control of the striated muscle portion of the esophagus
Nucleus ambiguous provides innervation
Describe the central control of peristalsis for the smooth muscle portion of the esophagus
Rostral Dorsal motor nuclei: excitatory pathways via ACh
Caudal dorsal motor nuclei: inhibitory pathways via NO
Which pathway is initiated first in swallowing
Inhibitory pathways are always initiated first followed by sequential activation
What is TLESR?
Transient lower esophageal sphincter relaxation: reflex arc that results in transient relaxation that can occur due to stomach distention
Describe symptoms of esophageal disorder (6)
Dysphagia: impediment of normal passage
Odynophagia: pain on swallowing
Globus: sensation of having something in throat
Regurgitation: return of gastric contents
Chest pain
Heartburn
Achalasia Presentation (4)
Dysphagia to solids/liquids
Regurgitation
Chest pain
Heartburn
Achalasia Epidemiology
M=W
Incidence is 1/100k with peak between 30-60yr
What is the etiology of achalasia
No lower esophageal sphincter relaxation!
Degeneration of myenteric plexus due to autoimmune, viral, neurodegenerative causes
Name some mimics of achalasia (4)
Pseudoachalsia: tumor at GEJ with myenteric plexus infiltration
Tight fundoplicatoin
Laporscopic gastric banding
Infection with trypanosoma cruzi
Describe the epidemiology of GERD
Western issue– don’t see it in East asia but up to 28% in North America
Describe possible etiologies of GERD
Too much food late at night–>distend fundus
Hiatal hernia
Decreased saliva
Poor gastric emptying (obesity!)
What is the role of obesity in GERD?
Increased intra-abdominal and intra-gastric pressure increases risk of hiatal hernia
Which patients with GERD do you test? What test (3)
Endoscopy– people with alarming symptoms or that don’t respond to PPIs
Manometry
pH testing
How does endoscopy usually look for patients with GERD?
Usually observe normal esophagus– it is diagnosed based on symptoms
Treatment strategies for GERD (4)
Lifestyle
Antacids
Antisecretory therapy: Antihistamine, PPI
Antireflux surgery
What happens with cessation of PPI?
Relapse
What are some of the safety concerns with PPI use? (6)
Metabolic bone disease/hip fracture (BnC2Rebound): Infection: C diff, pneumonia B12 deficiency Hypomagnesemia Interstitial nephritis Microscopic colitis
Barrett’s Esophagus: Epidemiology
1.5% population prevalence– more common in men, increasing with age, associated with obesity
15% prevalence in pts with chronic GER symptoms
What is Barrett’s Esophagus? What is its clinical significance?
Metaplasia of cells in lower esophagus to goblet cells
It is a common precursor to esophageal adenocarcinoma
Describe the process of carcinogenesis in Barrett’s
oxidative stress and inflammation lead to metaplasia–>clonal population then begins replicating–>clones lose its cell cycle control
Treatment for Barrett’s Esophagus
Antisecretory therapy
Surgery
Chemoprevention?
Endoscopic ablation
Describe findings of eosinophilic esophagitis:
Symptoms related to esophageal dysfunction
Histology: eosinophil predominant inflammation
Absence of GERD– no response to PPI, normal pH
Epidemiology of eosinophilic esophagitis:
M>W
young people
Pathogenesis of eosinophilic esophagitis
Presentation of allergens to esophagus
Stimulation of Th2 cytokine response (IL13/IL5)
Cytokines stimulate esophageal epithelium to produce eotaxin-3
Clinical presentation of eosinophilic esophagitis (6)
solid food dysphagia food impaction chest pain heartburn (despite therapy) upper abdominal pain esophageal perforation
Allergic phenotype of eosinophilic esophagitis
Food allergies Asthma Eczema Chronic rhinitis Environmental allergens
What is the therapy for EoE?
Diet
Dilation
PPI
Topical steroids
What happens if treatment delayed in EoE?
Progressive fibrosis leads to increased symptoms/severity
What is presentation of scleroderma?
Absent peristalsis and LESp
GERD
Dysphagia
