02 Esophageal disorders

Question 0

Secondary peristalsis

Answer 0

Contraction of esophagus just proximal to distention- continues in a wave

Question 1

Primary peristalsis

Answer 1

Pharyngeal constriction and UES relaxation

400-600ms (.5 second relaxation)

Question 2

Esophageal peristalsis coordination

Answer 2

• Wave of inhibition( VIP—>NO via cGMP blocks Ca and hyperpolarizes)
• Followed by a wave of excitation (Substance P —> Ca2+ influx)

Question 3

Dysphagia

Answer 3

food “gets stuck” Shortly after swallowing (NOT 20 min later)

Question 4

Peristalsis speed and duration

Answer 4

• 3-7 seconds in length, 3-5 cm/second

* LES relaxes 3-8 seconds for bolus

Question 5

Achalasia

Answer 5

• 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

Question 6

Acalasia like

Answer 6

Malignancy blocking sphinctor

Question 7

Achalasia causes

Answer 7

Infiltrative cancers
Amyloidosis- sarcoidosis
Chagas
Para  neoplastic
ANS damage- polio, dabetes, iatragenic

Question 8

Achalasia treatments

Answer 8

NO donors
Anticholinergics

Botox/ ballooning

Operative

Question 9

Esophageal spasm

Answer 9

Dis-coordinated esophageal movements with inefficient delivery of foods to stomach

Question 10

Complete esophageal aperistalsis

Answer 10

Scleroderma esophagus
ENTIRE ESOPHAGUS RELAXED
muscle unable to contract

Question 11

Submucosal esophageal glands

Answer 11

(also submucosal glands in duodenum)

Secrete mucin and bicarb to protect epithelium

Question 12

Reflux pathophys

Answer 12

inflammation –> IL6 –> h202 —> ^ PGE2—> decreased LES tone

Question 13

Most common reflux cause

Answer 13

Increased transient LES opening

Question 14

Reflux morphology

Answer 14

• Basal zone >20% of epithelial thickness
• increase depth of lamina propria papillae
• Some eosinophils- lots of neurtophils

Question 15

Alarm symptoms

Answer 15

Dysphagia
Anemia
Weightloss
Abdominal mass
Vomiting

Question 16

Eosinophilic esophhagitis

Answer 16

*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

Question 17

Eosiophilic esophagitis treatment

Answer 17

1. Elimination diet
2. Topical Steroids
3. Systemic steroids
4. Endoscopic dilation

Question 18

Infective esophagitis

Answer 18

• 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

Question 19

Barretts esophagus

Answer 19

Switch to duodenal mucosa- Goblet cells

Cdx gene association

Question 20

Esophageal Adenocarcinoma

Answer 20

*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)

Question 21

Es. Adenocarcinoma morphology

Answer 21

• near Barrets
• Flat or raised patches
• distal 1/3 of Es. to cardia
• Mass, diffuse infiltration, ulcerate
• Mucinous glandular structure

Question 22

Squamous cell carcinoma

Answer 22

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

Question 23

Es. SCC Morphology

Answer 23

*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)