I. Esophagus:
A. Normal:
i. Function: Propel food from the oral pharynx [not mouth] to the stomach, lined with epithelia
a. No real digestive functions
b. Can swallow standing on your head because of peristalsis
c. Lower 2/3 smooth involuntary muscle
. d. Upper 1/3 striated voluntary muscle (only voluntary smooth mm. In body), gravity helps
e. Epiglottis keeps food from going into trachea
B. Primary Peristalsis (bolus propelled thru hollow viscera): voluntary most powerful
i. Initiated by swallowing (reflex)
ii. Propels food: less strength
C. Secondary Peristalsis (peristalsis in lower 2/3):
i. Not initiated by swallowing, done so by the food which is already in the esophagus
ii. Propels food through lower esophagus:
D. Tertiary Peristalsis (Curling phenomenon; Cork screw appearance)
i. Seen in the elderly - common
ii. No propulsion
a. Fibrillation of the esophagus; doesn’t cause any movement; is due to aging and breakdown of
myenteric plexus/ usually seen in elderly
E. Tumors: Malignant m/c- 90%
i. Leiomyoma is the most common benign tumor of the esophagus (Fibroid in the uterus)
ii. Sessile broad, wide base, no stalk: most common
iii. Pedunculated has a stalk
iv. Most in lower esophagus (because of reflux) (Barrett’s carcinoma/adenocarcinoma)
v. Squamous cell carcinoma is most common, squamous cells line the esophagus
vi. 7.6/100,000 cases in USA (per year): 130/100,000 cases in China
a. Because their diet is high of nitrites, smoked foods, preservatives
vii. M: F 3:1: Adenocarcinoma/Barrett’s carcinoma
a. Most patients greater than 60 years of age
viii. Most are asymptomatic because there is NO expansion in the lumen, No bleeding, not much pain,
hematemesis or melena.
F. Esophageal carcinoma:
i. Etiology:
a. Alcohol abuse (long-term) associated with 80-90% of cases: Cirrhosis Portal HTN
Esophageal Varices CA
1. Higher incidence of reflux (irritating to epithelium)
2. Alcoholics are usually smokers
3. Alcohol also irritates the esophagus itself
b. Cigarette Smoking: swallow nitrites [via salvia and swallowing air]CA
1. Nitrate Ingestion in lungs
2. Chronic Achalasia, poor relaxation of the proximal end caused by destruction: prestenotic
dilation reflux neoplasm: poor reflux sphincter
3. Esophageal spasm (stenosis):
a. Proximal end dilates; food gets stuck & irritates and ferments
b. Common sign is very bad breath especially when they belch
c. Swallow dysphagia regurgitation: Chronic GERD/Barrett’s Esophagus, CA
obstruction of hollow organregurgitation
c. Where food gets stuck
1. Thoracic inlet
2. Pharyngeal Esophageal Sphincter (Larynx)
3. Aortic Knob (because of aorta uncoiling leaves an indentation in the esophagus)
4. When the aorta uncoils due to aging and atherosclerotic Disease
5. Left Atrium
6. Cardiac Sphincter (lower esophageal)
7. Patients can usually with great accuracy point to the location where the bolus is
ii. S&S:
a. Dysphagia is a late symptom: Leads to these being unknown until metastasis
Patients don’t know they have usually until they become malignant
Adenomas, lipomas, angiomas all possible in the GI tract. Think of the structures in the GI tract and
the types of tumors associated with that type of tissue
b. 9 out of 10 esophageal tumors are malignant
iii. Physical Findings
a. Dysphagia mc symptom: usually asymptomatic until late stages of CA: vomiting frequent
b. motor problem – dysphagia with both solids 1st & then liquids
c. obstruction – dysphagia with solids early & progresses to dysphagia with fluids
d. CA cachexia occurs/wt loss just skin & fat (chronic disease wasting)
e. Weight Loss, suggestive that CA has metastasized: stage 3 or 4 usually
f. Cervical Adenopathy: Lymph nodes
g. Virchow’s nodes: Enlargement of supraclavicular lymph node: Common with GI malignancy-
Many times is first sign.
h. Hematemesis – vomiting of blood / Hemoptysis – spitting up blood (red or coffee grounds)
1. Direct extension into trachea or fistula- communicating tract aspiration pneumonia
a. Shouldering with barium swallow: squared off line across esophagus
i. Hoarseness: Due to compression or destruction of recurrent laryngeal in the mediastinum
j. Cough with clear sputum
k. Mets to liver m/c, pleura, lungs with associated signs and symptoms
l. Mc presentation if mets to lung is asymptomatic, depends on site
iv. Diagnostic Imaging
a. Double contrast esophagram: CO2 & Barium (barium swallow- “shoulder” sign- key 90° cutoff
Now we use endoscopy instead
b. Get lung & ab CT/MRI to check for mets
c. Esophagoscopy: EGD
d. Chest/abdominal CT: looking for mets
e. Abdominal MRI:
f. Mediastinum lymph nodes would be involved with esophageal cancer if metastasis has occurred
v. Laboratory Tests
a. Done also to check for mets
b. CBC, (WBC up, RBC down maybe), Blood Chemistries
1. Anemic male over 40 has GI cancer, unless proven otherwise
c. Liver Enzymes, metastasis to the liver is common
vi.. Differential Diagnosis
a. Achalasia: failure of sphincter to relax
b. Diffuse Esophageal Spasm (DES): cold ice cream chest pain that is never ending and 10x worse
Pain lasts min to hours
c. Esophageal Rings- (congenital): Fibrocartilaginous ring that narrow the esophagus
1. Schatzki’s Upper esophageal ring
2. Lower ring
d. Scleroderma (Progressive Systemic Sclerosis, newest term): Connective tissue disease: Hardening
of the interstitial tissues narrowing and lack of peristalsis dysphagia
vii. Treatment
a. Resection if no mets: En bloc Resection during surgery to see if they get all out
1. Take out CA in pieces till normal tissue seen in pathology & anastamose ends
2. Lab makes sure clean tissue is found around CA to ensure complete removal
3. Only done if no mets
4. Stomach/colon used for replacement of gut removed
5. Radiation Therapy: Targets rapidly changing/high turnover cells: CA cells, Hair, Gonads,
Bone marrow. Some divide too fast or too slow and are unaffected- renal cell = CA outpaces
chemo/radiation - Radiation not very effective with this cancer
6. Chemotherapy
viii. Prognosis: depends on stage at diagnosis: with -
a. Surgery 20-50% (all based on 5 year survival rate): stage 1 or 2 only usually
b. Radiation 6-20% (stage 2-3 usually)
1. Have a node involved (3-4)
2. Not very effective again, due to surrounding organs and tissues (4)
3. Squamos cell not radio-sensitive
c. Chemotherapy 15-80%: stage 1 best cure rate
1. Kills cells that are in the S1 phase (immature cells) that are rapidly dividing
Hair, gonads, bone marrow are all affected because they turn over very rapidly
G. Benign Tumors:
1. Tumor Types
a. Leiomyoma is most common: Found most commonly in the uterus
a. Broad based, smooth muscle & fibroid obstruction
b. Younger age than malignant: biopsy for diagnosis
b. Papilloma: unusual
c. Fibrovascular Polyps hamartoma - overgrowth of normal tissue, made up of normal and
fibrous tissue: Rare: can have occult blood- rare to bleed
H. Esophagitis: types
1. Reflux: Reflux of gastric contents with damage- stricture- Barrett’s = metaplasia
a. Contents reflux up through cardiac sphincter with force and through the lower esophageal
sphincter. Causing linear and nonlinear erosions of the esophageal lining
b. Progression of GERD
c. Incompetent LES (Lower esophageal sphincter)
d. Often associated with hiatus hernia: Protrusion of the stomach through the hiatus
e. 30-60’ (minutes) post-prandial/reclining heartburn
f. NOT GERD GERD damage is reversible: Is “GERD” gone wild:
g. More severe thus causes strictures
h. TX with Nexium
i. GERD tx: Prilosec & Prevacid
2. Acute Ulcerative:
a. Seen in patients with PUD: precursor
b. Associated with frequent vomiting: leads to inflammation of lower to mid-esophagus
ulceration if chronic contracted, inflexible lower esophagus,or can perforate into
mediastinum (heart-pericardial dilation leaks fluid around heart, trachea, great vessels)
c. Alcoholics, chemotherapy patients, bulimics, etc.
d. Eventually leading to strictures, thus dysphagia sets in depending on level of dysphagia as
to weather solids and or liquids are involved
e. Can lead to laryngitis
f. Contracted fibrotic lower esophagus results
3. Infective:
a. Infection of the esophagus is rather unusual
b. Immunosuppressed patient: not seen in healthy usually
1. AIDS most common group, cancer, DM, transplant
c. Long term corticosteroid treatment
d. Organisms: Herpes Simplex, Candida Albicans-Typically found in the vaginal region of
females and faces of children
e. Pic: Candida Esophagitis, occurs especially with immunocompromised patients
f. CMV (Cytomegalovirus), causes encephalitis in kids
g. S & S: Dysphagia, Odynophagia (Painful swallowing), Chest Pain – more of a burning
sensation instead of a crushing pain
h. Treated with Antibodies
4. Mechanical:
a. Swallowed object becomes lodged at narrowed portions
1. Laryngopharynx, Aorta, Gastroesophageal junction, Left Atrium (not very often
unless preexisting CHF)
b. Objects include coins, pills, bone pieces
c. 3 main groups that do this: Elderly, children, and insane
d. Leads to ulceration, maybe perforation- Which can lead to mediastinitis
e. Treated with an EGD, scope with surgical attachments on the end.
5. Esophageal Varicies: Enlarged tortuous veins in the esophagus, typically occurring in the lower 1/3
of the esophagus: Varicose veins of the esophagus
a. Alcohol is the most common cause portal hypertension (pressure increased in portal
venous system, blood backs up cirrhosis)
b. Lower 1/3 submucosal veins involved
c. 1/3 of patients bleed: Alcohol Cirrhosis Esophageal Varices Bleeding out
d. Highest mortality of any UGI bleed
1. Peptic Ulcer Disease most common reason for UGI bleed
e. Coffee ground emesis, hematemesis: Time depends on which you will see
f. Treated with sclerotherapy & Compression Bougie balloon down the lower esophagus
and the balloon flattens out the varices
g. Sclerotherapy inject hardening agent that hardens (sclerosis) the walls so they can no
longer extend also used in peripheral vascular disease
h. S/Sx : Pt has some pain and dysphagia: Symptoms are not extreme
6. Esophageal Diverticula: Localized outpouching of tubular viscus
a. Usually acquired (congenital forms are rare)
b. Two Types:
1. Traction (extraesophageal) : Mediastinal mass (inflamed lymph node next to
esophagus)that as it grows attaches to the esophagus as patient swallows and
breaths it pulls on the wall months to years creates a weak spot that allows the
outpouching: Something pulls on esophagus from the outside-Eg; an attached
neoplasm
a. Most common in middle esophagus. Adhesions outside tract
b. Because most lymph nodes are in mediastinum their enlargement can cause
them to become adherent to the esophagus
2. Pulsion: Weakness in the esophageal wall (where the vessels enter a lot of time)
that eventually becomes weak and forms a diverticula occurs from a pushing out of a
weak area of the esophageal wall where the small micro vascularity occurs to supply
blood to the esophagus
a. Most common lower/upper esophagus.
b. Occur anywhere in esophagus
c. Lower just above the diaphragm Epiphrenic diverticula (just above
diaphragm)
7. Zenker’s diverticulum: pulsion type:
a. Occurs at pharyngoesophageal junction
b. Can be very large in size
c. Loss of upper esophageal sphincter laxity
d. Retains food
e. Signs/Symptoms
1. Halitosis – bad breath
2. Spontaneous Regurgitation
3. “Verp” – ½ vomit/ ½ burp
4. Nocturnal choking – position- elevate head of bed
5. Recommended not to eat within a few hours
6. Neck mass: pain & dysphagia
7. Can sometimes see peristalsis in the mass
f. Complications – Aspiration (inhaling something that wasn’t there Aspiration pneumonia
– which has a high mortality rate), abscess (walled off chronic infection), bronchiectasis
(chronic obstruction of the air flow that results in fluid build up infection; 3 layered
mucous, foul smelling sputum),
1. Aspiration, abscess, bronchiectasis – dilation = easier for bacteria
2. AM coughing: spit layered: surfactant, serous, pus
8. Epiphrenic diverticulum: weakened area in lower esophagus: usually asymptomatic & small
9. Middle esophageal diverticulum: usually traction type
a. From mediastinal lymphadenitis: lymphadenopathy
I. GERD reflux esophagitisBarrett’s esophagusEsophageal. CA always rule out cardiac Disease 1st
1. Cough & bronchospasm or laryngitis from aspiration
2. Early satiety GERD get “full” quickly
3. Chocolate fat & caffeine contents cause GERD episode
4. Tobacco when chemicals are swallowed
5. Commonly assoc. with hiatal hernia (>70%)
6. Nitroglycerin will make anginal chest pain better & Makes GERD chest pain worse
7. Gastroesophageal Reflux Disease: Reflux of gastric contents into lower esophagus
8. Incompetent lower esophageal sphincter: Stuff from your stomach comes back up into the lower
esophagus because the esophageal sphincter is not functioning correctly-Believes because of aging
9. Reflux Esophagitis Barrett’s Esophagus Squamous cell carcinoma
10. Heavier a person is the more chance they can have because increase in intra-abdominal pressure
11. Incidence: 60% of adults have heartburn: 80% of pregnant women have GERD
12. S/Sx: Heartburn (pyrosis) most common, Dysphagia, Regurgitation, Sour taste in the mouth
a. Can be confused with angina pectoris
b. Chronic cough- Bronchospasm, due to irritation of the bronchi airway
c. Laryngitis
d. Early Satiety (Getting full fast)
e. Belching/Bloating
13. Contributing Factors:
1. Chocolate (caffeine and fat), Yellow Onions, Peppermint, Garlic
2. Tobacco (nicotine and causes sphincter to relax), Alcohol (fat and causes sphincter to
relax), 3. Caffeine
4. 70% of GERD suffers have a hiatal hernia
5. Beta Blockers (control BP and angina), Ca++ Channel Blockers, nitroglycerin Causes
dilation of lower esophageal sphincter
6. Gastric Acid Hypersecretion
14. Diagnosis: 24 esophageal pH monitoring
a. E.G.D. – final dx for GERD
b. U.G.I (upper GI series, with barium swallowed)
c. Manometry, to rule out diffuse esophageal spasms (pressure test)
15. Treatment
a. Avoid triggers (diet modification)
b. Proton pump inhibitors
c. H2-blockers (cimetidine – Prilosec )
d. Antacids
e. Fundoplication: fundus of stomach wrapped around esophagus
1. Reserved for pts with daily reflux
2. Three types
a. Nissen (complete)
b. Posterior (partial)
c. Anterior (partial)
f. Drink excessive amount of water, water helps to dilute the acid and provide weight to the
stomach to pull the hiatal hernia down.
J. Barrett’s: usually asymptomatic
1. Pre-malignant
2. Associated with chronic reflux (5-10% incidence)
3. Stratified squamous manifests to columnar epithelium, a pre cancer action
4. Increased risk of adenocarcinoma
a. 30-50 times increased risk to develop adenocarcinoma of the esophagus
b. 500/100,000 people with Barrett’s esophagus who have GERD
5. Dx: EGD, biopsy almost always accompanies an EGD
6. Treatment:
1. Laser Ablation
2. Fundoplication
3. Surgical Resection (En Bloc if area is large enough)
K. Esophageal Achalasia:
1. Spasm (shut tight) of lower esophagus sphincter with pre-stenotic dilation which makes peristalsis
ineffective
2. Chest pain can occur when peristalsis is attempted: Pain usually colicky
3. Functional esophageal obstruction
4. Inadequate relaxation of the LES
5. Ineffective Peristalsis
6. 1/100,000 incidence; 30-50 y/o
7. S/Sx: Both Solid/liquid dysphagia-immediately, patient indicates they can feel the food sticking
usually in the lower chest = Chest pain- May be confused with angina (after meals)
a. Vomiting of undigested food with lying down- Aspiration, can develop pneumonia and die
b. Crescendo/decrescendo type pain like Stone in Ureter
c. Progressive dysphagia with classic “beck: at junction with stomach
8. Etiology
a. Degeneration of myenteric plexus
b. Viral
1. Herpes Zoster, Measles Virus
c. Autoimmune
d. Not completely understood, true etiology not know
9. Diagnosis: EGD with manometry, UGI
a. Tests to rule out other causes (eg: EKG), Especially with age group one wants to R/O MI
10. Treatment
a. Medical: Smooth muscle relaxants (70% effective)
1. Nitrates
2. Calcium channel blockers: relax LES
3. Botulinum toxins injection
4. mechanical dilation (90& effective): Bouginage: some GERD after
5. Esophagomyotomy (90% effective), incise into the muscle (sphincter – draw back,
reflux)
b. Prognosis: Excellent with appropriate RX
1. Long standing Disease increases risk of CA
L. Scleroderma: (PSS-) non-inflammatory arthritis
1. Aka: progressive systemic sclerosis (PSS): Means hardening of the skin
2. Primarily effects the skin, but is not limited to the skin: Tissue thickens and hardens
3. Severe hardening of lips to point must be tube feed: Sometimes must replace the esophagus
4. Parastasis is affected, thus difficulty in swallowing, reflux
5. Kidneys are often affected as well
6. Vessels become calcified, thickened and hardened
7. Female>Male Early teens to 20’s
8. Smooth mm relaxants used if esophagus does not need replacing, patient receives temporary relief,
usually do not work
9. Multisystem disorder often affecting the esophagus
10. Lose ability to have peristalsis
11. Become very narrow and can develop strictures
12. EGD used to diagnose
13. 75% have esophageal involvement
14. Fibrosis and inelasticity results
15. Signs & Symptoms
a. Dysphagia
b. Esophageal reflux/regurgitation
16. Diagnosis: EGD, UGI
17. Reaction with smooth muscle relaxants
18. Etiology – unknown
M. Diffuse Esophageal Spasm:
1. Ice cream eating too fast is the same pain, “brain freeze”
2. Pain lasts minutes to hours
3. Usually end up in the ER thinking they are having a cardiac problem
4. Diffuse sustained contraction (spasm) of esophagus
5. Etiology unknown
6. Can be confused with angina pectoris: vaso-vagal reaction
7. S/sx:
a. Substernal chest pain
b. Dysphagia with pain, worsened by swallowing, key differentiating feature
c. Regurgitation
8. Dx:
a. EGD (Esophagogastroduodenoscopy) & mamometer- pressure balloon
b. UGI: With barium swallow on x-ray appears as a cork screw
c. Reaction with Ca++ channel blockers/nitrates- muscle relaxant: Causes reflux
II. Stomach Diseases:
A. Anatomy:
1. Stomach B12 absorption (intrinsic factor), storage, mixing, mineral absorption
a. Decreased intrinsic factor low B12 pernious anemia malabsorption neuropathy -
hematopoetic
- 2. Rugae increases surface area inside the stomach for production of HCl and pepsin
3. GE Junction
4. Gastroesophageal Reflux Disease
5. Fundus- Usually holds gas
6. Magenblase air in the stomach
7. Antrum
8. Pylorus -Narrowed portion of the distal most aspect of the stomach
9. Pyloric Sphincter b/w stomach and duodenum help prevent outflow of gastric juices that
could lead to PUD
10. Pyloric stenosis prevents outflow, causes regurgitation
11. Curvatures: Lesser (top) & Greater curvature (bottom) - More metabolically active (because of
where food sits)
12. Estimated that 3 – 5 cc of blood is lost with each aspirin taken that is not buffered
B. Gastric digestion is mostly protein
1. HCL & pepsin secreted
2. HCO3- buffer
3. G astrin – stimulates muscle to “churn” food
C. Tampanade: fluid build up around organ: Heart – cannot work: Gastric = plug at sphincter
D. Cancer: occurs anywhere in stomach
1. Incidence is increasing in proximal CA (in Asia): Body & fundus
2. 2 - 4X more common in 1st degree relatives (mom, dad, siblings)
3. Male: Female 1.6:1: > 55 y/o: 7/100,000/year
4. Most common in blood group A
5. No symptom complex presented early in the Disease
6. Aggressive, Infiltrated carcinoma invades entire organ and cause thickening of entire organ -
rarely found before stage 3 or 4
7. S/SX: Cramps (colicky pain) unrelieved by antacids: S&S of ulcer
a. Loss of appetite- food may make pain worse: better with fasting: early satiety = not ulcer
b. Very low bleeding, No ulceration, Poor intrinsic factor production
c. Dysphasia: High in GES; n/v, constipation
8. Risk factors: Diet rich in additives (smoked, pickled); Atrophic gastritis
a. Inflammatory disease of the stomach where there is atrophy of the rugae Sequela : B12
deficiency pernicious anemia
b. Tobacco use: decreases blood flow & swallows air & tar
c. Hispanic, Japanese
d. Polyps - Growth into lumen Sessile and pedunculated. Usually premalignant mass (some
benign)
e. H. pylori infection (PUD associated wipatith H. pylori)
f. Barrett’s Esophagus
9. DX: Stool guaiac test test for blood
a. Any male > 40 with anemia, has GI malignancy until proven otherwise
b. Positive stool guaiac (blood to stool content): FOB, fecal occult blood test
c. Will have black tarry stool if blood occurs in the stool
d. Hemoglobin <12g/dl: Hematocrit <35
e. EGD: UGI (not done very often anymore): CT/MRI for nodes mets
f. Adenocarcinoma 90%, due to the abundance of glandular tissue, {adeno-, glandular}
g. Lymphoma 6%, malignancy of lymphocytes {mediastinum area is the most common area
for a lymphoma}
h. Gastric Sarcoma < 4%
i. Leiomyosarcoma < 1 %
10. Treatment: surgical resection, quit often an en bloc gastrectomy (resect until healthy tissue is
found)
a. node resection (when larger then 1cm)
b. radiation non-beneficial (tumors are non-sensitivity to radiation)
c. Chemotherapy non beneficial, research has shown this treatment has very low benefit for
gastric cancer. Chemotherapy is designed to “attack” fast growing tissue.
11. GASTRIC CA PROGNOSIS
a. No s/sx until late in course, primarily due to the size of the hollow organ. It takes a rather
large amount before it interferes with the function of the stomach
b.18% 5 year survival rate
c. 57% with local Disease (stage I)
d. 19% with regional spread (stage II)
e. 2% with distal mets (staged III)
12. BENIGN GASTRIC TUMORS
a. Leiomyoma – fibroid tissue usually found in the uterus, of smooth muscle
1. Common tumor
2. Rarely symptomatic- Only with obstruction