Esophagus Pathophysiology Flashcards

(31 cards)

1
Q

What is the role of the upper esophageal sphincter? (3)

A

Barrier between pharynx and esophagus
Allows food in and belching/vomiting
Prevents air entry, reflux of gastric contents

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2
Q

What are the two sphincters of the gastroesophageal Junction?

A

Lower esophageal sphincter (LES)

Diaphragm

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3
Q

Describe the central control of the striated muscle portion of the esophagus

A

Nucleus ambiguous provides innervation

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4
Q

Describe the central control of peristalsis for the smooth muscle portion of the esophagus

A

Rostral Dorsal motor nuclei: excitatory pathways via ACh

Caudal dorsal motor nuclei: inhibitory pathways via NO

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5
Q

Which pathway is initiated first in swallowing

A

Inhibitory pathways are always initiated first followed by sequential activation

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6
Q

What is TLESR?

A

Transient lower esophageal sphincter relaxation: reflex arc that results in transient relaxation that can occur due to stomach distention

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7
Q

Describe symptoms of esophageal disorder (6)

A

Dysphagia: impediment of normal passage
Odynophagia: pain on swallowing
Globus: sensation of having something in throat
Regurgitation: return of gastric contents
Chest pain
Heartburn

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8
Q

Achalasia Presentation (4)

A

Dysphagia to solids/liquids
Regurgitation
Chest pain
Heartburn

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9
Q

Achalasia Epidemiology

A

M=W

Incidence is 1/100k with peak between 30-60yr

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10
Q

What is the etiology of achalasia

A

No lower esophageal sphincter relaxation!

Degeneration of myenteric plexus due to autoimmune, viral, neurodegenerative causes

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11
Q

Name some mimics of achalasia (4)

A

Pseudoachalsia: tumor at GEJ with myenteric plexus infiltration
Tight fundoplicatoin
Laporscopic gastric banding
Infection with trypanosoma cruzi

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12
Q

Describe the epidemiology of GERD

A

Western issue– don’t see it in East asia but up to 28% in North America

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13
Q

Describe possible etiologies of GERD

A

Too much food late at night–>distend fundus
Hiatal hernia
Decreased saliva
Poor gastric emptying (obesity!)

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14
Q

What is the role of obesity in GERD?

A

Increased intra-abdominal and intra-gastric pressure increases risk of hiatal hernia

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15
Q

Which patients with GERD do you test? What test (3)

A

Endoscopy– people with alarming symptoms or that don’t respond to PPIs
Manometry
pH testing

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16
Q

How does endoscopy usually look for patients with GERD?

A

Usually observe normal esophagus– it is diagnosed based on symptoms

17
Q

Treatment strategies for GERD (4)

A

Lifestyle
Antacids
Antisecretory therapy: Antihistamine, PPI
Antireflux surgery

18
Q

What happens with cessation of PPI?

19
Q

What are some of the safety concerns with PPI use? (6)

A
Metabolic bone disease/hip fracture
(BnC2Rebound):
Infection: C diff, pneumonia
B12 deficiency
Hypomagnesemia 
Interstitial nephritis
Microscopic colitis
20
Q

Barrett’s Esophagus: Epidemiology

A

1.5% population prevalence– more common in men, increasing with age, associated with obesity
15% prevalence in pts with chronic GER symptoms

21
Q

What is Barrett’s Esophagus? What is its clinical significance?

A

Metaplasia of cells in lower esophagus to goblet cells

It is a common precursor to esophageal adenocarcinoma

22
Q

Describe the process of carcinogenesis in Barrett’s

A

oxidative stress and inflammation lead to metaplasia–>clonal population then begins replicating–>clones lose its cell cycle control

23
Q

Treatment for Barrett’s Esophagus

A

Antisecretory therapy
Surgery
Chemoprevention?
Endoscopic ablation

24
Q

Describe findings of eosinophilic esophagitis:

A

Symptoms related to esophageal dysfunction
Histology: eosinophil predominant inflammation
Absence of GERD– no response to PPI, normal pH

25
Epidemiology of eosinophilic esophagitis:
M>W | young people
26
Pathogenesis of eosinophilic esophagitis
Presentation of allergens to esophagus Stimulation of Th2 cytokine response (IL13/IL5) Cytokines stimulate esophageal epithelium to produce eotaxin-3
27
Clinical presentation of eosinophilic esophagitis (6)
``` solid food dysphagia food impaction chest pain heartburn (despite therapy) upper abdominal pain esophageal perforation ```
28
Allergic phenotype of eosinophilic esophagitis
``` Food allergies Asthma Eczema Chronic rhinitis Environmental allergens ```
29
What is the therapy for EoE?
Diet Dilation PPI Topical steroids
30
What happens if treatment delayed in EoE?
Progressive fibrosis leads to increased symptoms/severity
31
What is presentation of scleroderma?
Absent peristalsis and LESp GERD Dysphagia