Lecture 28

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Esophageal Diseases
Objectives:
★ Describe the major components in the anatomy of the esophagus and
physiology of swallowing.
★ Explain the pathophysiology and etiology of common esophageal disorders.
★ Name the common presenting symptoms and complications of reflux
disease (GERD).
★ List the main points in the management of GERD.
★ Differentiate between oropharyngeal and esophageal dysphagia.
★ Explain the differences between anatomical and functional esophageal
disorders.
★ Explain the pathophysiology of common causes of dysphagia.
★ List the common presenting symptoms, appropriate investigations and
treatment options in different causes of dysphagia.

Color index:
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Original text Females slides Males slides
Doctor’s notes Text book Important Golden notes Extra
 Introduction 2

◄ Anatomy of the esophagus

● Muscular tube 20-25 cm long, located between the pharynx and the stomach.
● it has an UES & LES that help empty food between swallows while
preventing regurgitation of stomach contents
● The oesophagus is lined by stratified squamous epithelium, which extends
distally to the squamocolumnar junction where the oesophagus joins the
stomach.
● striated muscles make up the proximal ⅓.
● smooth muscles make up the distal ⅔.
● how long does it take a bolus to pass the entire esophagus?
○ about 7-10 seconds.

◄ Esophageal sphincters
Upper esophageal sphincter Lower esophageal sphincter
VS - A physiological sphincter comprised of
- Functions to prevent
regurgitation into oral cavity smooth muscles.
and larynx - Normally located within the
- Restricts airflow into the diaphragmatic hiatus with ⅔ in the
esophagus during inspiration. abdominal cavity and ⅓ in the thoracic
- Composed of striated muscles cavity. Can be displaced proximally
and are under conscious control, by hiatus hernia (discussed later)
used when breathing, eating, - It maintains a high pressure zone
belching, and vomiting. between stomach and esophagus
(barrier to reflux)

◄ Physiology of swallowing

UES opens and bolus is Primary peristalsis: Secondary peristalsis: LES open at the end of
introduced into the initiated in the pharynx initiated by esophageal swallowing to allow the
esophagus. esophagus by a swallow. the waves distention by food. food to pass to the
distends causing a are slow moving and these waves are stomach
contraction proximal to sweep the entire length important to remove all
distal. propagating of the esophagus. the food from the
sequence. esophagus if it has not
been totally cleared by
primary peristalsis
 GASTROESOPHAGEAL REFLUX DISEASE 3

(GERD)
◄ Introduction
● Symptoms or complications resulting from the reflux of gastric contents into esophagus or beyond, into
the oral cavity (including larynx) or lung
● Transient lower esophageal sphincter relaxations (TLESRs 1) are part of normal physiology, but occur
more frequently in patients with GERD, allowing gastric acid to flow back into the oesophagus.
● Prevalence in Saudi Arabia is 30%-40%.
● What causes GERD?
○ Hiatal hernia
○ Hypotensive LES
○ Increase Intra-abdominal pressure (eg: Pregnancy, obesity)

◄ Factors associated with GERD

Fat, chocolate, coffee or Cigarette smoking
1 Pregnancy or obesity 2 alcohol ingestion, Large 3
meals

Drugs – antimuscarinic, Hiatus hernia, Systemic Treatment for achalasia

4 5 6
calcium-channel blockers, sclerosis
nitrates

◄ SYMPTOMS OF GERD
● Heartburn is the major feature. This is a burning chest pain that is
aggravated by bending, stooping and lying down, all of which promote acid
exposure.
Typical ● Regurgitation of food and acid into the mouth occurs, particularly on bending
or lying flat. This can lead to excess salivation in the mouth, commonly known
as water-brash.

Atypical Chest pain, Early satiety, Nausea, Bloating, belching and Globus sensation3

Extra Cough, Asthma, Laryngitis, Sinusitis/recurrent otitis media, Dental erosions

Esophageal

◄ Classic features of GERD and cardiac ischaemic pain

● A cardiac cause should be excluded in patients with chest pain before starting GI evaluation 2.

Reflux Pain Cardiac Ischaemia Pain

Rarely radiates to the arms Gripping or crushing, Radiates to neck or left arm

Worse with spicy food, hot drinks or alcohol Worse with exercise

Relieved by antacids Accompanied by dyspnoea

1- In TLESR the LES sphincter relax 3-6 time every hour for 3-10 sec to allow gases to go out of the stomach, otherwise bloating will occur (Considered as a protective mechanism)
2- All patient with chest pain must undergo cardiac evaluation first (ECG) before doing any GI evaluation. Even if they present with very suggestive signs and symptoms of GERD
3- Very common, pt words “I feel something is stuck in my throat, and isn’t relieved by eating or drinking” . It’s a sensation caused by the irritation of the esophagus.
 GASTROESOPHAGEAL REFLUX DISEASE 4

(GERD)
◄ HOW TO DIAGNOSE
GERD?
● The clinical diagnosis can usually be made without investigation and is often made using mainly:
○ Typical symptom presentation.
○ Antisecretory responsiveness. (PPI responsive)

● In some cases you will need to go further with:

Endoscopy Ambulatory reflux

monitoring (PH study)
indications for endoscopy in suspected GERD:
1. Alarm symptoms, like? Indications for ambulatory PH
○ Dysphagia, Weight loss, Positive family or personal history monitoring:
of esophageal malignancy 1. Suspected GERD with normal
○ Hematemesis, Melena, Anemia.
Endoscopy (to confirm
2. Non-Cardiac chest pain GERD)
3. Screening high risk patients for Barrett’s: overweight, white 2. Persistent symptoms even with
males, older than 50, chronic GERD, smokers, Family history PPI1 (To R/o other causes)
4. Patients that are unresponsive to PPI

◄ MANAGEMENT OF GERD
● Weight loss, Head of bed elevation at night, Smoking Cessation
Lifestyle ● Avoidance of meals 2-3 hours before bedtime for patients with nocturnal GERD.
changes ● Culprits: fatty foods, caffeine, chocolate, ETOH, spicy foods, carbonated beverages,
peppermints

● Proton pump inhibitors (PPIs) are the most commonly used medications, usually
effective in resolving symptoms and healing esophagitis.
● domperidone, when dysmotility features are prominent, can be helpful.
Medical ● antacids and alginates can also provide symptomatic benefit.
● H2-receptor antagonist drugs, helpful in resolving symptoms without healing
esophagitis.

● Fundoplication2, which can treat both hiatal hernia and GERD, the Indications for
Fundoplication are:
Surgical ○ Persistence reflex even with PPI’s
○ Barrett’s esophagus

1- Patients with functional esophagitis: the esophagus is hypersensitive and gets irritated from anything, not necessarily acid. We monitor the
pH to know the nature of the reflux causing the irritation
2-Patients undergoing Fundoplication must be evaluated first by endoscopy to make sure they have a reflux. If normal, do PH monitoring.
 GASTROESOPHAGEAL REFLUX DISEASE 5

(GERD)
◄ Complications

01 Erosive Esophagitis:
● AKA Ulcerative esophagitis, if left untreated it will lead to Barrett’s
Esophagus.
● Treatment : proton pump inhibitors (PPIs)

02 Barrett’s Esophagus:
● Metaplastic columnar epithelium (gastric and intestinal) replaces the stratified squamous
epithelium in the distal esophagus, it’s More common in Men.
● Risk Factors for Barrett’s :
○ Chronic (>5 years) GERD symptoms, Advancing age (>50 years).
○ Male gender, Caucasian race, Family history
○ Tobacco usage, Central obesity.
○ Alcohol doesn’t increase risk of Barrett’s
● The risk of cancer seems to relate to the severity and duration of reflux rather than the
presence of Barrett’s oesophagus per se.
Metaplasia1
(Barrett’s) High Grade
dysplasia
(HGD)

01 02 03 04 05

GERD Adenocarcinoma 2
Low Grade
dysplasia (LGD)

03 Peptic Stricture:
● They usually occur in patients over the age of 60 and present with
intermittent dysphagia for solids, which worsens gradually over a
long period.
● Mild cases may respond to PPIs alone.
● More severe cases need endoscopic dilation and long-term PPI
therapy.
● Surgery is required if medical treatment fails.

1- PPi’s have the capability to stop the progression of Barretts’s metaplasia to dysplasia, But has no benefit once patients develop dysplasia
(even low grade).
2- A patient has cancer in the lower esophagus, what is the most likely type ? Adenocarcinoma
What is the most likely risk factor ? Barrett’s esophagus secondary to GERD
 6
DYSPHAGIA
◄ Introduction
● Subjective sensation of difficulty or abnormality of swallowing.
● Oropharyngeal vs Esophageal dysphagia1.

Oropharyngeal Dysphagia Esophageal Dysphagia 2

Recurrent Pneumonia (Aspiration)

Weight loss

Coughing or choking with swallowing. Usually no problem with initiation of swallowing.

Difficulty initiating swallowing. Sensation of food getting Stuck in the chest.

Change in Voice or Speech Can have Pain in the chest from food bolus.

Nasal regurgitation. Oral or Pharyngeal regurgitation.

Systemic Neurologic (Such as Stroke) or Myopathic (Such as Functional or Anatomical abnormalities in the esophagus
dermatomyositis) Syndromes.
Functional causes: Anatomical causes:
● Achalasia. ● Esophageal strictures
● Secondary dysphagia. ● Esophageal ring.
● Esophageal spasm. ● Esophageal web.
● Eosinophilic esophagitis. ● Malignancy.

◄ HISTORY TAKING IN DYSPHAGIA

01 03 05 07
Duration Stable vs Associated
Onset
(weeks/months progressive symptoms
02 04 06
vs years) (weight loss,
Intermittent vs anemia/blood
Solids vs Solids Regurgitation
persistent in stool …)
+ liquids

Oropharyngeal or Solid vs both solid

esophageal and liquid
CARDINAL SIGNS
FOR DYSPHAGIA
Persistent vs Important associated
intermittent symptoms

1- it’s very imp to differentiate between them.

2-In esophageal dysphagia, function refers to the “movement” While anatomy refers to obstruction caused by cancer/strictures
 Oropharyngeal Dysphagia 7

◄ Zenker’s diverticulum

● AKA cricopharyngeal diverticulum, Sac like, outpouching of the mucosa

and submucosa in the area of muscular weakness in the hypopharynx
Introduction between the inferior constrictor and cricopharyngeus muscle above the UES.
● An area of weakness known as Killian’s dehiscence allows a pulsion
diverticulum to form.

Cause ● Hypertensive / noncompliance of the Upper esophageal sphincter

● Oropharyngeal dysphagia symptoms.

● Food undigested on the pillow at night or after meals.
● Halitosis1.
● Weight Loss happens in late stages (the diverticulum becomes big & obstructs
Symptoms2 the esophagus)
● Occasionally, patients present with recurrent pneumonia following
aspiration of food into the trachea.
● They may also complain that a gurgling sound is heard in the neck following
a swallow as liquid and food collect in the pouch.

● Diagnosis:
○ Video swallow testing
○ Modified barium swallow.
○ Endoscopy may be hazardous, since the instrument may enter and perforate
the pouch.

● Treatment:
○ Surgical, either via an external approach through the neck where the pouch is excised or, more
commonly, via endoscopy with stapling of the party wall

1-Halitosis is considered as a “characteristic feature” of Zenker’s diverticulum that every physician must keep an eye on secondary to
retention of undigested food.
2- In late stages of zenker's diverticulum, Patients may present with symptoms of both oropharyngeal and esophageal dysphagia as it begins
to obstructs the esophagus.
 Esophageal Dysphagia 8

◄ 1- ESOPHAGEAL STRICTURE

Causes:
● Benign peptic stricture caused by GERD
● Malignant stricture
● Iatrogenic? eg: Suicidal ingestion of acids
Diagnosis:
● Done by endoscopy
Treatment:
● Depends on the cause: 3 months history of dysphagia? most likely secondary to GERD treat it with
PPI’s. Didn't work? then its either secondary to fibrosis > Dilation, or cancer > resection

◄ 2- ESOPHAGEAL RINGS AND WEBS

Esophageal ring Esophageal web

Common in the lower esophagus (above LES) Usually in upper esophagus (cervical)

Connective tissue + muscularis mucosa Thin membrane

Caused by ? GERD Unknown cause? Genetic

Schatzki’s ring Plummer vinson syndrome1 (triad2)

PVS has increased risk for squamous cell cancer

No cancer risk
in the esophagus, hypopharynx and oral mucosa.

Diagnosis: barium, endoscopy

Treatment: endoscopic dilation if needed (persistent symptoms)

PPI daily for GERD Iron replacement therapy if PVS

1-Supplementing PVS patients with iron will make esophageal web disappear,however they need continuous surveillance as they have an
increased risk of esophageal squamous cell carcinoma
2- the triad of Plummer vinson syndrome are: Dysphagia, Iron deficiency anemia, and esophageal web. Very common in young females
 ESOPHAGEAL DYSPHAGIA 9

ESOPHAGEAL MOTILITY
DISORDERS CAUSING
DYSPHAGIA

Aperistalsis in
esophagus (connective
Esophageal spasms Achalasia
tissue disease)
(Scleroderma)

◄ 3-Achalasia
Achalasia
● Pathophysiology: Failure of lower esophageal sphincter to relax (lacking
ganglion cells in the myenteric plexus in the distal esophagus).
● Males = Females
Characterised by:
● A hypertonic lower esophageal sphincter, which fails to relax in response to
Primary
swallowing waves.
Achalasia1 ● Failure of propagated esophageal contraction, leading to progressive dilatation of
the gullet.
Etiology:
● Immune mediated.
● Genetic predisposition.

● Chagas disease, Parasitic Infection by Trypanosoma cruzi (common in latin

America), Result in achalasia with features of diffuse enteric myenteric
destruction, including megacolon, heart disease (cardiomyopathy), and
Secondary neurologic disorders.
Achalasia2 ● Diagnosis: serology testing.
● Treatment: Anti trypanosoma like Benznidazole (GI symptoms managed
symptomatically3)

● Achalasia symptoms and similar diagnostic findings.

● Due to Malignancy (tumors in the gastric cardia or those infiltrating the
myenteric plexus like adenocarcinoma of gastroesophageal junction, pancreatic,
Pseudoachalasia5 breast, lung, or hepatocellular cancers)
● When to suspect (rapid onset over weeks-months4, elderly and risk factors for
cancer)
● Need to get CT scan or endoscopic US for further workup.

1-Primary achalasia is the comments, Patients present with history of esophageal dysphagia that persist for years ( 2-3 years history)
2- The main feature of secondary achalasia is that it is multi-system (unlike primary) and not restricted to the esophagus only. It is Important to look for and
ask about travel history in secondary achalasia
3- Symptoms are reversible following anti trypanosoma treatments except for the esophagus(irreversible damage), thats why its managed symptomatically
4- Keep in mind that even 8 Months in Pseudo-achalasia is considered as rapid onset in comparison to primary achalasia (which usually takes 2-3 years)
5- in pseudo achalasia, CT scan or endoscopic US is a MUST to roll-out carcinoma specially in high risk group (but it has to be done after the usually workup
approach: (barium, endoscopy, and manometry to diagnose and confirm achalasia first)
 ESOPHAGEAL DYSPHAGIA 10

◄ 3-Achalasia (Cont.)
● Symptoms of Achalasia:

Dysphagia to solids and liquids Regurgitation of undigested food

Heartburn1 Chest pain6 Weight loss

● Diagnosis of Achalasia:
○ Esophageal Manometry:
01 ○ Barium swallow (First Step): 03 ■ Shows aperistalsis of the
■ Dilated esophagus
esophagus and failure of
■ Tight LES relaxation of the LOS.
■ BIRD BEAK APPEARANCE ■ Confirmatory test

02 ○ Endoscopy
■ Normal with some resistance at the LES
■ Dilated esophagus.
■ Retained saliva, liquid, and food in the esophagus without mechanical
obstruction from stricture or mass

● Management of achalasia:
○ Medical therapy3:
■ Calcium channel blocker
■ Nitrate
■ Antimuscarinic agents.

○ Endoscopic therapy:
■ Pneumatic dilatation4 (effective/ longer term/ more complications)
■ Botox injection at LES. (effective/ short term 3-6 months)
■ Peroral endoscopic myotomy (POEM)

○ Surgical (Heller’s myotomy):

■ performed laparoscopically or as opened surgery, accompanied by a partial fundoplication
anti-reflux surgery.
❖ Higher risk for Esophageal squamous cell cancer.

1- Heartburn in achalasia is due to acids in foods which accumulate in the esophagus

3- Medical therapy for achalasia almost never work, however we can describe it for elderly patients with comorbidities that prevent them from doing any
endoscopic or surgical procedure
4- pneumatic dilation is associated with risk of perforation
6- some patients experience severe chest pain due to esophageal spasm; it might be misdiagnosed as cardiac pain.
 11
ESOPHAGEAL
DYSPHAGIA
◄ 4- Diffuse esophageal spasm (DES)

Diffuse esophageal spasm (DES) (corkscrew esophagus)

❖ A severe form of esophageal dysmotility that presents in late middle age with episodic retrosternal
chest pain (that can mimic angina) and transient dysphagia.
❖ Could occur as a response to gastroesophageal reflux.
❖ Can be precipitated by drinking cold liquids.
❖ On barium swallow, the appearance may be that of a corkscrew esophagus.
❖ Nutcracker, a variant of diffuse esophageal spasm, is characterized by very high-amplitude
peristalsis within the esophagus.
❖ Treatment is based on PPI when gastroesophageal reflux is present, antispasmodics, nitrates,
calcium channel blocker (nifedipine) and GABA agonists (baclofen) are also used.
❖ Occasionally, balloon dilatation or longitudinal esophageal myotomy is necessary.
❖ DES and nutcracker can be distinguished only by manometry.

◄ 5- Eosinophilic Esophagitis
Eosinophilic Esophagitis1
● Chronic inflammation due to immune-mediated disease resulting in
eosinophilic infiltration of esophagus
● No malignancy Potential.
Overview ● Commonly present with food impaction. Main symptom is dysphagia.
● History of allergies is seen in >50% of these patients.

Endoscopy:
● Can be normal.
● Strictures.
Diagnosis ● linear furrows.
● Trachealization of the esophagus.
● BIOPSY shows 15 or more eosinophils/hpf on microscopy (from proximal
and distal esophagus2)

● PPI first for 8 weeks then repeat Endoscopy if Eosinophils is still 15 or more:
○ Corticosteroids3 (swallowed fluticasone/
budesonide/betamethasone)for 8-12 weeks.
Treatment ● If symptoms persists repeat endoscopy if there’s a ring try dilation.
● Leukotriene inhibitor (montelukast) for refractory symptoms.
● Elimination diets for children.

1- Patients with Eosinophilic esophagitis may present with history of allergies eg: Asthma, allergic rhinitis, food allergies
2- Biopsy MUST be taken from both ends of the esophagus as refluxes may also cause eosinophilia
3- Corticosteroids are initiated if PPI didn’t work, it has to be swallowed (the patient has to use corticosteroid inhaler(not tablets!) but instead of
inhaling the substances he swallows them)
 ODYNOPHAGIA+/- 12

DYSPHAGIA
◄ Acute Esophagitis
1 2

Pill-induced1
Antibiotics: (Tetracycline/Doxycycline)
● A patient taking tetracycline for his acne present complaining of
acute odynophagia for one week, what is the most likely the
diagnosis and the cause?
Bisphosphonate (alendronate)
● A 50 years old post menopausal woman present with odynophagia
following bisphosphonate therapy for her osteoporosis, what is
mostly likely the diagnosis and the cause ?
Potassium
● A HF patient on lasix and diuretics with hypokalemia using
potassium supplements
Treatment :
● Stop the medication and give them PPI

1 2

Infections

● Immunocompromised patients
○ Patients on corticosteroid therapy are at risk of “Infection
induced” acute esophagitis
● Viral (CMV, HSV)
○ Treatment: antiviral
● Candida
○ Treatment: anti fungal

1- The comments site for pill induced acute esophagitis is at the aortic constriction of the esophagus as it is considered as the tightest area of the
esophagus where pills can get stuck (produce kissing ulcer appearance), for that when you prescribe these medications, advise the pt to drink a lot
of water and stay in upright position at least for 30 min after taking the pill.
 Summary

GERD

● Typical: heartburn (the major feature), regurgitation

Sx ● Atypical: nausea, chest pain, bloating and belching, globus sensation, early satiety.
● extra-esophageal: sinusitis / recurrent otitis media, cough, asthma, dental erosions, laryngitis.

● clinical: typical symptom presentation, antisecretory responsiveness.

● endoscopy: in case of alarm symptoms, non cardiac chest pain, screening high risk patients for Barrett’s, Pts
Dx unresponsive to PPI.
● 24h pH monitoring and motility: suspected GERD with normal endoscopy, Persistent symptoms even with PPI.

MG
● PPI, antacids and alginates, domperidone, H2 receptor antagonist.
T
● peptic strictures: >60, intermittent dysphagia for solids which worsens gradually.
● erosive esophagitis.
Cx ● Barrett’s esophagus: white men >50, chronic GERD symptoms, Fx history, tobacco, central obesity, Risk for
adenocarcinoma.

Zenker’s diverticulum

● oropharyngeal dysphagia symptoms, undigested food on the pillow at night or after meals, Halitosis, Weight loss in late
Sx stage

Dx ● modified barium swallow, video swallowing testing

● surgical Either via external

approach (through the neck) or
Tx endoscopy (more commonly) with
stapling of the party wall. eosinophilic esophagitis

● dysphagia or food bolus obstruction

Sx ● chest pain and heartburn caused by the eosinophil induced esophageal inflammation
● History of allergy seen in >50% of patients.

Dx ● endoscopy: can be normal / strictures / linear furrows / trachealization of the esophagus

● PPI: used first for 8 weeks then repeat endoscopy.

Tx ● corticosteroids: swallowed fluticasone / budesonide / betamethasone
● montelukast: for refractory symptoms

Esophageal webs and rings

Esophageal ring Esophageal web

Common in the lower esophagus (above LES) Usually in upper esophagus (cervical)

Connective tissue + muscularis mucosa Thin membrane

Caused by ? GERD Unknown cause ?genetic

Schatzki’s ring Plummer vinson syndrome (triad)

No cancer risk PVS has increased risk for squamous cell cancer in the esophagus,
hypopharynx and oral mucosa.

Diagnosis: barium, endoscopy

Treatment: endoscopic dilation if needed (persistent symptoms)

PPI daily for GERD Iron replacement therapy if PVS

 Diffuse esophageal spasm
Achalasia
(corkscrew esophagus)

Sx● Primary
● Episodic
achalasia:
retrosternal
Hypertonicchest
LESpain
which
andfails
Summary
(cantomimic
relax angina),
in response
dysphagia,
to swallowing
precipitated
waves,byand
drinking
failurecold
of propagated
liquids. esophageal
contraction leading to progressive dilation of the gullet.
● Immune mediated and genetic predisposition.

Dx ● Barium swallow: appearance maybe that of a corkscrew esophagus.

Esophageal strictures
Tx ● PPI when GER is present.
causes ● Benign peptic strictures, malignant strictures, iatrogenic.
● dysphagia (develops slowly,initially intermittent, solids and liquids), chest pain( due to esophageal spasm), regurgitation
Sx and pulmonary aspiration, heartburn and weight loss.

Dx ● ●
barium Endoscopy.
esophagography shows dilatation of the esophagus narrowing into a “beak-like” pattern at the lower end.
● esophageal manometry shows increased LES resting pressure + no/partial relaxation, low amplitude contraction, no
Dx propagation.
● Depends on the cause: 3 months history of dysphagia? most likely
Tx ● endoscopy normaltowith
secondary GERDsome resistance
treat at the LES,
it with PPI’s. Didn'tdilates
work?esophagus and retained saliva, liquid and food in the
then its either
esophagus.
secondary to fibrosis > Dilation, or cancer > resection

functional -achalasia
-secondary dysphagia
esophageal
-esophageal spasm
anatomical
dysphagia

-eosinophilic esophagitis

-esophageal stricture
Zenker’s -esophageal ring
diverticulum -esophageal web
oropharyngeal -malignancy
neurologic

myopathic
 Lecture Quiz (Dr’s slides)

Q1: A 42 y/o male presents for evaluation of heartburn. He denies any dysphagia or weight loss. He has no other medical
conditions and is currently not taking any medications. You suspect that he may have GERD. Which of the following
describes the role of upper endoscopy in the evaluation of this patient?
A- He should undergo an Esophagogastroduodenoscopy with biopsy to ensure a more serious condition is not missed
B- He should undergo an Esophagogastroduodenoscopy only if he has no improvement in his symptoms after an empiric trial of twice daily PPI therapy.
C- He should undergo ambulatory PH monitoring while on PPI therapy to ensure the medication is working
D- He should undergo both an Esophagogastroduodenoscopy and ambulatory PH monitoring prior to the initiation of any therapy.

Q2: A 45-year-old man is evaluated for a 2-month history of a burning sensation starting in his stomach and radiating into
his chest, usually occurring 4 to 5 times weekly. He says that he usually eats dinner late and then goes to sleep. He often
wakes up with a sour taste in his mouth. He reports no dysphagia or unintentional weight loss. He takes no medication. On
physical examination, vital signs are normal; BMI is 34. The remainder of the examination, including abdominal
examination, is unremarkable. What would be the next step in his management?
A- PH testing
B- Barium esophagography
C- Empiric trial of proton pump inhibitor
D- Esophagogastroduodenoscopy

Q3: - A 56-year-old woman is evaluated for chest discomfort after meals occurring intermittently over the preceding
month. She describes a sensation of heaviness on her chest, and says that she also notices this pain sometimes while walking
up stairs. She reports no nausea, dysphagia, or reflux. She has been taking ranitidine with minimal relief of symptoms. She
also takes atorvastatin for hyperlipidemia. She smokes half a pack of cigarettes daily. On physical examination, her blood
pressure is 140/90 mm Hg and other vital signs are normal; BMI is 34. The remainder of the examination, including
abdominal examination, is unremarkable. What is your next step?
A- Barium esophagography
B- Electrocardiography
C- Empiric trial of a proton pump inhibitor
D- Esophagogastroduodenoscopy

Q4: - A 75-year-old man is evaluated for progressive dysphagia of 8 months' duration for both solids and liquids and the
necessity to induce vomiting several times each month to relieve his symptoms. He also has experienced chest pain and
heartburn symptoms. He has lost approximately 6 kg (13 lb) of weight over the preceding 3 months and a total of 9 kg (20
lb) since his symptoms began. He has a long history of cigarette and alcohol use. His medical history and review of systems
is otherwise negative. He has no travel history outside the northeastern United States. He takes no medication. On physical
examination, vital signs are normal; BMI is 23. He appears thin and tired. The remainder of the physical examination is
unremarkable. Esophagogastroduodenoscopy findings reveal retained saliva, liquid, and food in the esophagus without
mechanical obstruction. Manometry demonstrates incomplete lower esophageal relaxation and aperistalsis. What is the
most likely diagnosis?
A- Achalasia
B- Pseudoachalasia
C- EOE
D- Chagas disease

Q5: A 52-year-old man is evaluated for dysphagia of 3 months' duration. He reports regurgitating undigested food soon
after eating solid food, occasional coughing and choking after swallowing, and chronic halitosis. He reports no weight loss
or chest pain. He drinks two beers weekly and does not smoke. On physical examination, vital signs are normal; BMI is 25.
The remainder of the examination, including abdominal examination, is unremarkable. What is your next step?
A- Barium esophagram
B- Esophagogastroduodenoscopy
C- Manometry
D- PH study

Q6: A 25 year old man is evaluated for a sensation of solid food "sticking" several times per week. He reports that he
sometimes forces himself to vomit when he feels food "stuck" in the esophagus, but he has never gone to the emergency
department. He takes a multivitamin and is generally healthy.On physical examination, vital signs and other findings,
including those of an abdominal examination, are unremarkable. Esophagogastroduodenoscopy findings are shown.
Biopsies of the esophagus show more than 18 eosinophils/hpf. Which of the following is the most likely diagnosis?
A- Achalasia
B-Eosinophilic esophagitis
C- Gastroesophageal disease
D- Pill induced esophagitis

Answers: Q1:B | Q2:C | Q3:B | Q4:B | Q5:A | Q6:B

 THANKS!!
This lecture was done by:
- Faisal G Al-Zahrani
- Nawaf Albhijan
Quiz and summary maker:
- Faisal G Al-Zahrani

Note taker:
- Khaled Al-harbi

Females co-leaders: Males co-leaders:

Raghad AlKhashan Mashal AbaAlkhail
Amirah Aldakhilallah Nawaf Albhijan

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