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66 Cards in this Set

  • Front
  • Back
Upper Esophageal Sphincter
extends 3 to 4 cm in length

comprised of at least 3 groups of striated muscles:
- distal portion of the inferior pharyngeal constrictor muscle
- cricopharyngeus muscle
- muscle of the proximal esophagus

separates the pharynx from the esophagus

closed in basal state to prevent air from entering GI tract and exit of substances from esophagus
Lower Esophageal Sphincter
circular muscle of the esophagus (internal portion of sphincter)

phernoesophageal ligament

the crual part of the diaphragm (external portion of sphincter)

there is also a squamocolumnar junction intraluminally
Innervation of the esophagus
Proximal esophagus (striated muscle)
- supplied by the somatic efferent fibers carried in the vagus nerve (nucleus ambiguus, no intermediate neurons) through cholinergic, nicotinic receptors

Distal esophagus (smooth muscle)
- vagus nerves (dorsal motor nucleus) caries preganglionic fibers that release ACh on 2 types of postganglionic effector neurons within the wall of esophagus
1. effector neuron excites with ACh release
2. effector neuron inhibits with Nitric oxide (NO) and vasoactive intestinal polypeptide (VIP)
Pharyngeal Phase of Swallowing
1. Food reaches the pharynx
2. Swallowing center activated
3. Cranial nerves 5, 7, 9, 10, & 12
4. Tongue raises to hard palate (thrusting food posteriorly)
5. Nasal airway closes (soft palate and posterior pharyngeal wall come together)
6. Epiglottis closes (suprahyoid muscles pull the hyoid bone and .: larynx superiorly and anteriorly; contraction of the thyrohyoid, aryepiglottic and thyroepiglottic muscles)
7. UES relaxes
8. Pharyngeal muscles contract
Esophageal Phase of Swallowing
1. Food reaches the proximal esophagus
2. Vagal afferents are activated
3. Peristalsis begins by activation of the intrinsic esophageal nerves (MYENTERIC plexus)
4. LES relaxes
5. Peristalsis proceeds from proximal to distal esophagus
Which nerves activate peristalsis?
Myenteric Plexus (a.k.a. intrinsic esophageal nerves)
Esophageal Symptoms
Dysphagia

Odynophagia

Heartburn (“pyrosis”)

Regurgitation

Chest Pain (noncardiac)
Odynophagia
Painful swallowing
Regurgitation
Effortless movement of gastric contents into the back of the throat
Oropharyngeal Dysphagia
Transfer problem – inability to initiate the act of swallowing

OR

inability to transfer the bolus from the pharynx to the upper esophagus
Oropharyngeal Dysphagia

Associated Symptoms
Food sticking in throat (residual food in pharynx after swallowing)

Repetitive swallows

Nasal regurgitation

Coughing

Aspiration
Etiology

Oropharyngeal Dysphagia
Structural:
Zenker’s diverticulum, cricopharyngeal bar, webs, tumors

CNS:
Stroke, tumors, trauma

Other neurologic:
Parkinson’s, multiple sclerosis, amyotrophic lateral sclerosis

Myopathy:
Myasthenia gravis, polymyositis, mixed connective tissue disease
Zenker’s Diverticulum
Outpouching of top of esophagus
Esophageal Dysphagia

Symptoms
The patient feels that the FOOD BOLUS STOPS somewhere IN THE CHEST, from the suprasternal notch to the xiphoid process

If the food bolus is regurgitated, it consists of bland chewed food or swallowed liquids, and does not have a bitter or acidic taste, and does not contain the yellow or green fluid of gastric or biliary secretions.
Esophageal Dysphagia

Diagnostic Evaluation
Barium Esophagram
- modified barium swallow with videofluoroscopy
- single or double contrast

Esophagoscopy (EGD)

Esophageal Manometry
2 Categories that cause Esophageal Dysphagia
Mechanical causes

Motility disorders
ESOPHAGEAL DYSPHAGIA

Mechanical Causes - Etiology
Rings (muscular) and webs

Peptic stricture

Tumors

Infections

Caustic ingestion

Iatrogenic: Pill-induced esophagitis, radiation, sclerotherapy, NG tube
esophageal web
a congenital or acquired transverse fold of the mucous membrane and sometimes the deeper layers of the esophagus often causing dysphagia, usually in the lower half of the esophagus
Causes of Esophagitis
GERD

Eosinophilic esophagitis (EoE)

Infections

Medications
- tetracycline, KCl, quinidine, alendronate
- chemotherapy: 5-FU, daunorubicin, bleo

Radiation

Caustic ingestion
Eosinophilic esophagitis

Clinically
Clinical symptoms of esophageal dysfunction – usually solid-food dysphagia and food impactions

Normal 24-hour pH monitoring

No response to high-dose PPI therapy
Eosinophilic esophagitis

Epidemiology
First case report in 1977

Initially described in children

In adults, 75 % are males

In adults, mean age = 38

50-80 % are atopic – atopic dermatitis, allergic rhinitis, asthma

Most likely food allergens, possibly aeroallergens
Eosinophilic esophagitis

Radiographic Appearance
Proximal Stenosis

OR

Corrugated (multiple) rings
Eosinophilic esophagitis

Endoscopic Signs
Concentric rings

Linear furrows

White plaques
(eosinophilic microabscesses)

Food impaction
Esophageal Dysphagia

Symptoms
The patient feels that the FOOD BOLUS STOPS somewhere IN THE CHEST, from the suprasternal notch to the xiphoid process

If the food bolus is regurgitated, it consists of bland chewed food or swallowed liquids, and does not have a bitter or acidic taste, and does not contain the yellow or green fluid of gastric or biliary secretions.
Esophageal Dysphagia

Diagnostic Evaluation
Barium Esophagram
- modified barium swallow with videofluoroscopy
- single or double contrast

Esophagoscopy (EGD)

Esophageal Manometry
2 Categories that cause Esophageal Dysphagia
Mechanical causes

Motility disorders
ESOPHAGEAL DYSPHAGIA

Mechanical Causes - Etiology
Rings (muscular) and webs

Peptic stricture

Tumors

Infections

Caustic ingestion

Iatrogenic: Pill-induced esophagitis, radiation, sclerotherapy, NG tube
esophageal web
a congenital or acquired transverse fold of the mucous membrane and sometimes the deeper layers of the esophagus often causing dysphagia, usually in the lower half of the esophagus
Eosinophilic Esophagitis

Histologic Findings
> 15 eosinophils/ high-power field
Eosinophilic Esophagitis

Therapy
Acid suppression

Diet – elimination, elemental

Topical steroids – swallowed fluticasone or budesonide (be careful... you can get yeast)

Systemic steroids

Cromolyn, Montelukast

Biologics
Etiology of Odynophagia
Infectious esophagitis
- Fungal (Candida)
- Viral – CMV, HSV
- Idiopathic

Corrosive esophagitis

Pill-induced esophagitis
Candida Esophagitis
Yeast Pseudohyphae and Budding Yeast

typically these patients are immunosuppressed or have an immune disorder

this is an AIDs defining disease
Esophageal Dysphagia

Motility Disorders
Achalasia

Other spastic motor disorders
- Diffuse esophageal spasm
- Nutcracker esophagus
- Hypertensive LES

Scleroderma

Other hypocontractile motor disorders
Achalasia

Epidemiology
Age range: 25 – 60 years

Gender: Male = Female

Incidence: 0.4 – 0.6/100,000/year

Prevalence: 8/100,000
Achalasia
“Does not relax”

Failure of LES relaxation + loss of peristalsis in distal esophagus
Typical Symptoms of Achalasia
Dysphagia (90%)

Regurgitation (70%)

Chest Pain (60 %)
- b/c dilated esophagus

Weight Loss (60 %)
Atypical Symptoms of Achalasia
Heartburn (40 %)

Difficulty belching

Globus

Hiccups
Globus
is a sensation of fullness or lump in throat
Pathophysiology of Achalasia
Selective loss of Inhibitory neurons (NO and VIP) in the postganglionic myenteric (located b/w longitudinal & circular muscle layers of the esophagus) plexus leads to unopposed cholinergic excitation which then produces hypertonic LES with failure to relax. The etiology of neural damage is unknown.
Aperistalsis
is not well understood, but could be due to the loss of latency gradient along the esophageal body mediated by NO.

associated with Achalasia
How does Achalasia look radiographically?
Dilated proximal esophagus, might see air-fluid level

extremely constricted distal esophagus
Achalasia

Definition
Aperistalsis: 100% of cases

Abnormal LES relaxation (absent, incomplete, insufficient duration): 100 % of cases

Elevated LES pressure: 50 % of cases
Treatment for Achalasia
1. Myotomy... cut the esophagus... best option

2. Nitrates, Calcium Channel Blockers, Botulinum toxin injection

3. Pneumatic Dilation ... insert ballon... risk of perforation
GER
gastroesophageal reflux, which is the effortless movement of stomach contents into the esophagus

GER occurs in almost all people
GERD
GER disease, which is when reflux results in symptoms and/or injury to the esophagus

Key event is reflux of gastroduodenal contents (acid, pepsin, bile) into the esophagus

Acid is the primary mediator of symptoms and damage

Mucosal defenses are overwhelmed
GERD Symptoms
Heartburn (pyrosis) 83 %
Regurgitation 70 %
Dysphagia (from esophagitis or restriction) 37 %
Respiratory symptoms 30 %
Chest pain 10 %
Abdominal pain 10 %
Nausea 8 %
Belching 7 %
Mechanisms of Reflux
Transient lower esophageal sphincter relaxations (TLESRs) ... occurs in everyone

A hypotensive lower esophageal sphincter (LES)

Anatomic disruption of the gastroesophageal junction, usually associated with a hiatal hernia (MOST SEVERE)
When during breathing does the diaphragm increase the pressure at the lower esophageal sphincter?
during inspiration

... this is an non-LES anti-reflux mechanism
What is the normal pressure at the lower esophageal sphincter?
25 mmHg
Lower Esophageal Sphincter Incompetence
when there is a decline in basal resting pressure of the LES

if there is an increase in abdominal pressure, then the LES will not be enough to stop regurgitation
Hiatal Hernia and Reflux
LES - pressure often low

Gastric pouch - intra-thoracic reservoir ... esophageal sphinter is displaced upward with some of the stomach

Diaphragm - no esophageal pinch
How do we naturally clear acid from the esophagus?
Salivation (saliva contains bicarb)

Peristalsis (empties substances into stomach)

Gravity (empties substances into stomach, if standing)
GERD Diagnosis
Symptoms

Response to empirical trial of acid suppression therapy (PPI)

Endoscopy

24-hour pH monitoring
What are complications of GERD?
Ulcer

Stricture

Barrett's esophagus

Adenocarcinoma
Barrett's Esophagus
defined as a change in the lining of the esophageal mucosa from normal squamous epithelium to columnar with INTESTINAL METAPLASIA

occurs in 10-15% of patients with chronic GERD

a pre-malignant condition which may eventually lead to dysplasia and adenocarcinoma of the esophagus
What is the rate of Barrett's Esophagus to cancer?
The rate of progression is estimated to be 0.5% per year.
Barrett's Esophagus

Therapy
No Therapy is proven effective

Consider screening patients over the age of 50 with chronic GERD symptoms

Once identified, routine surveillance is indicated

Esophagectomy for high grade dysplasia or Cancer
What is the progression of Barrett's Esophagus
Chronic inflammation -->

metaplasia -->

dysplasia -->

carcinoma
GERD Treatment Goals
Reduce or eliminate symptoms

Heal esophagitis

Prevent complications

Improve quality of life
GERD Treatment Options
Lifestyle modifications
Antacids
H2-receptor antagonists
Proton pump inhibitors
Antireflux surgery
Prokinetic agents
New endoscopic therapies
What Lifestyle modifications can be made for GERD?
SLEEP
- Raise head of bed several inches
- Avoid meals 3 hours before bedtime

DIET
- avoid fatty and spicy foods
- avoid citrus and tomato-based foods
- avoid chocolate, peppermint

HABITS
- stop smoking
- reduce alcohol intake

BODY WEIGHT
- lose weight
Antacids
Generally contain ingredients such as aluminum hydroxide, magnesium hydroxide, magnesium trisilicate

Neutralize stomach acid

Work only on a short-term basis

Examples: Maalox, Mylanta, Gaviscon, Gelusil
H2 Receptor Antagonists
Are all over the counter and presciption

Tagamet (cimetidine)
Zantac (ranitidine)
Axid (nizatidine)
Pepcid (famotidine)
What works better PPI or H2RA?
PPIs are better at relieving heart burn and healing esophagus
Proton Pump Inhibitors
The only one that is over the counter is Prilosec

Prilosec (omeprazole)
Prevacid (lansoprazole)
Aciphex (rabeprazole)
Protonix (pantoprazole)
Nexium (esomeprazol)

Zegerid (omeprazole + bicarb)... combination drug
Anti-Reflux Surgery
Reduce Hiatal hernia

Restore Intra-abdominal esophagus

Approximate diaphragmatic crurae (tighten diaphragm)

Perform Fundoplication
- mobilize the fundus, remove blood vessels and attachments, wrap it around the esophagus, suture it together... restores esophageal pressure