Gastrointestinal Disorders

Chapter 17 Gastrointestinal Disorders

I. Oral Cavity and Salivary Gland Disorders

A. Cleft lip and palate

1. Epidemiology

a. Most common congenital disorder of oral cavity

Cleft lip/palate: most common congenital disorder of oral cavity

• ∼︀1:800 live births

b. Genetic factors involved

• Recurrence in subsequent siblings (3%)

c. More common in whites than blacks

d. Cleft lip and palate (50%)

e. Cleft lip alone (25%)

• Male > female

f. Cleft palate alone (25%; Fig. 17-1)

• Female > male

g. Complications

(1) Malocclusion

(2) Eustachian tube dysfunction

• Chronic otitis media

(3) Speech problems

17-1: Cleft palate. Note the defect in the palate (arrow).

(From Grieg JD: Color Atlas of Surgical Diagnosis. London, Mosby-Wolfe, 1996, p 68, Fig. 10-7.)

Cleft lip/palate: failure of fusion of facial processes

2. Pathogenesis

• Failure of fusion of facial processes

3. Treatment is surgery.

B. Common infections in the oral cavity (Table 17-1 and Fig. 17-2)

C. Oral manifestation of HIV

1. Candidiasis (see Fig. 17-2F)

• Most common oral infection

2. Apthous ulcers (stomatitis; canker sores)

a. Unknown origin

(1) Virus versus immunologic

(2) Often stress-induced

b. Painful ulcers covered by a shaggy gray membrane (Fig. 17-3)

3. Hairy leukoplakia (see Fig. 17-2B)

• Glossitis due to Epstein-Barr virus (EBV)

Table 17-1 Infections of the Oral Cavity

17-2: A, Exudative tonsillitis. Note the gray-white pus in the tonsillar crypts (arrow). B, Hairy leukoplakia along the lateral border of the tongue. It is a glossitis due to Epstein-Barr virus and is a pre-AIDS-defining lesion. C, Herpes simplex type 1. Note the clusters of vesicles around the vermilion border of the upper and lower lips. D, Actinomycosis. Note the colony of Actinomyces (sulfur granule) surrounded by an inflammatory infiltrate. E, Notched teeth in congenital syphilis. F, Oral thrush. Note the extensive white “curd-like” plaque that can be wiped off leaving an erythematous base.

(A courtesy of Edward L. Applebaum, MD, Department of Otolaryngology, University of Illinois, Urbana, Illinois; B from Lookingbill D, Marks J: Principles of Dermatology, 3rd ed. Philadelphia, WB Saunders, 2000, p 338, Fig. 23-7; C from Swartz MH: Textbook of Physical Diagnosis, 5th ed. Philadelphia, Saunders Elsevier, 2006, p 333, Fig. 12-10; D from Corrin B: Pathology of the Lungs. London, Churchill Livingstone, 2000, p 195, Fig. 5.3.15; E from Bouloux P: Self-Assessment Picture Tests: Medicine, Vol. 1. London, Mosby-Wolfe, 1997, p 11, Fig. 21; F from Grieg JD: Color Atlas of Surgical Diagnosis. London, Mosby-Wolfe, 1996, p 65, Fig. 10-1.)

17-3: Apthous ulcer. Note the ulcerated surface on the lip covered by a shaggy gray exudate.

(From Bouloux P: Self-Assessment Picture Tests: Medicine, Vol. 1. London, Mosby-Wolfe, 1997, p 35, Fig. 69.)

Pre-AIDS–defining lesions: thrush, hairy leukoplakia, apthous ulcers

4. Kaposi’s sarcoma

a. Hard palate is the most common location.

b. Due to human herpesvirus 8

Kaposi’s sarcoma: hard palate; HHV-8

D. Dental caries

1. Streptococcus mutans produces acid from sucrose fermentation.

Dental caries: caused by Streptococcus mutans

• Acid erodes enamel and exposes underlying dentine.

2. Fluoride prevents dental caries.

Fluoride: prevents dental caries

• Excess fluoride causes a chalky discoloration of the teeth.

E. Noninfectious ulcerations in the oral cavity

1. Pemphigus vulgaris and mucous membrane pemphigoid

• Both are immunologic skin disorders (refer to Chapter 24).

2. Erythema multiforme (refer to Chapter 24)

a. Hypersensitivity reaction against Mycoplasma or drugs (e.g., sulfonamides)

b. Called Stevens-Johnson syndrome when it involves the mouth

3. Apthous ulcers (stomatitis; see Fig. 17-3)

4. Behçet’s syndrome

a. Epidemiology

Behcet’s syndrome: recurrent apthous ulcers, uveitis, genital ulcers

(1) Combination of environmental + genetic factors

• HLA-B51, HLA-B27 associations

(2) May be precipitated by herpes simplex or parvovirus

(3) High incidence in Turkey and eastern Mediterranean

b. Pathophysiology

• Immune complex small vessel vasculitis

c. Clinical findings

(1) Recurrent aphthous ulcers, genital ulcerations

(2) Uveitis, erythema nodosum

(3) Attacks last 1 to 4 weeks

(1) Anti-inflammatory medications

(2) Corticosteroids

(4) Thalidomide

F. Pigmentation abnormalities

1. Peutz-Jeghers syndrome (see section IV)

• Melanin pigmentation of the lips and oral mucosa (Fig. 17-4)

2. Addison’s disease (see Fig. 22-21)

a. Increased adrenocorticotropic hormone (ACTH) stimulates melanocytes.

b. Melanin pigmentation of the buccal mucosa

17-4: Peutz-Jeghers syndrome. Note the melanin pigmentation on the lips.

(From Swartz MH: Textbook of Physical Diagnosis, 5th ed. Philadelphia, Saunders Elsevier, 2006, p 334, Fig. 12-12.)

Melanin pigmentation in oral mucosa: Addison’s disease, Peutz-Jeghers syndrome

3. Lead poisoning

• Lead deposits along the gingival margins in adults with gingivitis

G. Tooth discoloration

1. Tetracycline

Tooth discoloration: tetracycline, ↑ fluoride, erythropoietic porphyria

a. Drug discolors newly formed teeth.

b. Drug not recommended in a child < 12 years of age.

2. Excess fluoride

• Mottled, chalky white discoloration

3. Congenital erythropoietic porphyria

a. Porphyrins deposit in the teeth

b. Reddish brown discoloration

H. Macroglossia (enlarged tongue)

• Severe primary hypothyroidism

2. Down syndrome

5. Mucosal neuromas in multiple endocrine neoplasia (MEN) syndrome IIb (III)

Macroglossia: myxedema, Down syndrome, acromegaly, amyloidosis, MENIIb

I. Glossitis (inflammation of tongue)

1. Sore, beefy red tongue with or without papillary atrophy

Glossitis: deficiency of iron, B₁₂, folate, vitamin C, niacin; scarlet fever; hairy leukoplakia

a. Long-standing iron deficiency

b. Vitamin B₁₂ or folate deficiency

c. Scurvy (vitamin C deficiency)

d. Pellagra (niacin deficiency)

e. Scarlet fever

f. EBV-associated hairy leukoplakia

J. Leukoplakia and erythroplakia

1. Leukoplakia literally means “white patch” (Fig. 17-5).

• It has an ∼︀30% rate of progression to oral cancer.

2. Erythroplakia is a red patch (Fig. 17-6).

• It has an ∼︀60% rate of progression to oral cancer.

3. Lesion does not wipe off.

4. Both lesions are due to squamous hyperplasia of the epidermis.

• Increased risk for squamous dysplasia or invasive squamous cancer

a. Chronic irritation (e.g., dentures)

17-5: Leukoplakia of the tongue with invasive squamous cell carcinoma. Discrete raised white patches are evident on both sides of the tongue.

(From Forbes C, Jackson W: Color Atlas and Text of Clinical Medicine, 2nd ed. St. Louis, Mosby, 2003, p 362, Fig. 8-28.)

17-6: Erythroplakia. Note the raised erythematous area (arrow) on the palate.

(From Goldman L, Ausiello D: Cecil’s Textbook of Medicine, 23rd ed. Philadelphia, Saunders Elsevier, 2008, p 1451, Fig. 200-2.)

Leukoplakia/erythroplakia: smoking and alcohol are major risk factors

b. All forms of tobacco use

c. Alcohol abuse

d. Human papillomavirus (HPV)

a. Vermilion border lower lip (most common site)

b. Buccal mucosa

c. Hard and soft palates

d. Floor of the mouth

Leukoplakia/erythroplakia: biopsy to rule out squamous dysplasia or cancer

7. Always biopsy these lesions because of the high risk for progression to oral cancer.

K. Lichen planus (refer to Chapter 24)

1. Often associated with Wickham’s stria on buccal mucosa

• Fine, white, lacy lesions

Wickham’s stria: association with squamous dysplasia or cancer

2. May be associated with squamous cell carcinoma

L. Dentigerous cyst

1. Derives from epithelial elements of dental origin (odontogenic origin)

2. Associated with the crown of an unerupted or impacted third molar tooth

Dentigerous cyst: association with 3rd molar and ameloblastoma

3. Association with ameloblastomas in 15% to 30% of cases

M. Benign tumors of the oral cavity (excluding salivary gland)

Squamous papillomas: most common benign tumor in oral cavity

1. Squamous papillomas

a. Most common benign tumor in oral cavity

b. Exophytic tumor with a fibrovascular core

c. May occur on the tongue, gingiva, palate, or lips

2. Ameloblastoma

a. Arise from enamel organ epithelium or a dentigerous cyst

Ameloblastoma: most common odontogenic tumor; “soap bubble” appearance in mandible

b. Located in the mandible

(1) Produces a radiolucency in bone that has a “soap bubble” appearance

(2) Locally invasive but do not metastasize

N. Malignant tumors of the oral cavity (excluding salivary gland)

1. Epidemiology

a. Majority are well-differentiated squamous cell carcinomas

b. More common in men than women

c. Risk factors

Squamous cell carcinoma: smoking products most common risk factor

(1) Smoking is the most common risk factor.

• Pipe, cigarettes, chewing tobacco

(2) Alcohol abuse (synergistic with smoking)

(3) Synergism between smoking and alcohol excess

• Increases relative risk 30-fold

(5) Chronic irritation from dentures

(6) Lichen planus

d. Cancer sites in descending order

(1) Lower lip (vermilion border; Fig. 17-7)

17-7: Squamous cell carcinoma of the lower lip.

(From Grieg JD: Color Atlas of Surgical Diagnosis. London, Mosby-Wolfe, 1996, p 67, Fig. 10-5.)

Squamous cell carcinoma: most common site is lower lip

(2) Floor of mouth

(3) Lateral border of tongue

• “Tonsillar node” (superior jugular node)

f. Verrucous carcinoma

• Associated with smokeless tobacco

g. Basal cell carcinoma

(1) Most common cancer of upper lip

(2) Associated with ultraviolet light B exposure

Basal cell carcinoma: most common oral site is upper lip

2. Treatment for squamous cancer

• Surgery and radiation; chemotherapy in advanced cases

O. Salivary gland disorders

1. Sjögren’s syndrome (refer to Chapter 23)

a. Female dominant autoimmune disease associated with rheumatoid arthritis

b. Autoimmune destruction of minor salivary glands and lacrimal glands

2. Salivary gland tumors

Sjögren’s syndrome: dry eyes, dry mouth

a. Epidemiology

(1) Parotid gland is the most common site.

Parotid gland: most common site for salivary gland tumors

• Major salivary gland tumors are more likely to be benign.

(2) Minor salivary gland tumors are more likely to be malignant.

b. Pleomorphic adenoma (mixed tumor)

(1) Most common benign tumor of major and minor salivary glands

Pleomorphic adenoma: most common salivary gland tumor

• Parotid gland is the most common site.

(2) Female dominant

(3) Painless, moveable mass at the angle of the jaw

(4) Epithelial cells intermixed with myxomatous and cartilaginous stroma

• Tumor projections through capsule increase risk of recurrence

(5) May transform into a malignant tumor

• Facial nerve involvement is a sign of malignancy.

c. Warthin’s tumor (papillary cystadenoma lymphomatosum)

(1) Benign parotid gland tumor

Warthin’s tumor: heterotopic salivary gland tissue in a lymph node

• Male dominant

(2) Heterotopic salivary gland tissue trapped in a lymph node

• Cystic glandular structures are located within benign lymphoid tissue.

d. Mucoepidermoid carcinoma

(1) Most common malignant salivary gland tumor

Mucoepidermoid carcinoma: most common malignant salivary gland tumor

(2) Most commonly located in the parotid gland

(3) Mixture of neoplastic squamous and mucus-secreting cells

II. Esophageal Disorders

A. Signs and symptoms of esophageal disease

• Most commonly due to gastroesophageal reflux disease

2. Dysphagia (difficulty swallowing) for solids alone

Dysphagia for solids: obstructive lesion

a. Symptom of an obstructive lesion

b. Examples—esophageal cancer, esophageal web, stricture

3. Dysphagia for solids and liquids

Dysphagia for solids and liquids: motor disorder

a. Symptom of a motility disorder

b. Oropharyngeal (upper esophageal) dysphagia

(1) Striated muscle dysmotility

(2) Examples—dermatomyositis, myasthenia gravis, stroke

c. Lower esophageal dysphagia

(1) Smooth muscle dysmotility

(2) Examples—systemic sclerosis, CREST syndrome (see page 47), achalasia

B. Tracheoesophageal (TE) fistula

1. Characteristics

a. Proximal esophagus ends blindly (Fig. 17-8).

17-8: Tracheoesophageal fistula. The proximal esophagus ends blindly, and the distal esophagus arises from the trachea. The stomach is distended with air owing to communication of the esophagus with the trachea.

TE fistula: proximal esophagus ends blindly; distal esophagus from trachea

b. Distal esophagus arises from the trachea.

2. Clinical findings

a. Maternal polyhydramnios (excess amniotic fluid)

• Swallowed amniotic fluid cannot be reabsorbed in the small intestine.

TE fistula: polyhydramnios

b. Abdominal distention in newborn

• Air in the stomach from tracheal fistula

c. Difficulty with feeding

(1) Food regurgitates out of the mouth.

(2) Chemical pneumonia from aspiration

d. VATER syndrome

VATER syndrome: vertebral abnormalities, anal atresia, TE fistula, renal disease, and absent radius

(1) Vertebral abnormalities

(2) Anal atresia

(4) Renal disease and absent radius

C. Plummer-Vinson syndrome (refer to Chapter 11)

1. Due to chronic iron deficiency

Plummer-Vinson syndrome: associated with chronic iron deficiency

2. Leukoplakia in oral mucosa and esophagus

3. Intermittent dysphagia for solids

• Due to an esophageal web or stricture

D. Esophageal diverticulum

1. Types of diverticulum

a. True diverticulum

• Outpouching lined by mucosa, submucosa, muscularis propria, and adventitia

b. False, or pulsion diverticulum

(1) Weakness in underlying muscle wall

(2) Outpouching of mucosa and submucosa into area of weakness

2. Zenker’s diverticulum

a. Pulsion type located in upper esophagus

Zenker’s diverticulum: most common esophageal diverticulum

• Area of weakness is cricopharyngeus muscle.

b. Clinical findings

(1) Painful swallowing

• Entrapped food

(3) Regurgitate food through mouth

(4) Diverticulitis

c. Treatment is surgery.

E. Hiatal hernia

1. Epidemiology

a. Found in 50% of persons over 50 years old

• Increases with age

Hiatal hernia: increases with age

b. More common in women than men

c. Associations

(1) Sigmoid diverticulosis (25%)

(2) Esophagitis (25%)

(3) Duodenal ulcers (20%)

(4) Gallstones (18%)

2. Sliding hernia

a. Most common type of hiatal hernia (99%)

Hiatal hernia: sliding type most common; proximal stomach in thoracic cavity

b. Herniation of proximal stomach into thoracic cavity through the diaphragmatic esophageal hiatus

c. Clinical findings

Hiatal hernia: acid reflux most common symptom

(2) Nocturnal epigastric distress from acid reflux

(3) Hematemesis (vomiting blood)

(4) Ulceration, stricture

(5) Bowel sounds heard over left lung base

(1) Nonpharmacologic

(a) Reduce intake of foods/drugs that decrease lower esophageal sphincter tone

• Examples—coffee, chocolate, calcium channel blockers

(b) Avoid large quantities of food

(c) Sleep with head of the bed elevated

(2) Pharmacologic

(a) H₂ antagonists

(b) Proton pump inhibitors

(c) Prokinetic agents

(3) Surgery if indicated

Paraesophageal hernia: gastroesophageal junction at level of diaphragm

3. Paraesophageal (rolling) hernia (1%)

a. Gastroesophageal junction remains at the level of the diaphragm.

b. Part of the stomach bulges into the thoracic cavity.

Pleuroperitoneal diaphragmatic hernias (Bochdalek hernia) are present early in life. The visceral contents extend through the posterolateral part of the diaphragm on the left into the chest cavity causing respiratory distress at birth. Loops of bowel are present in the left pleural cavity on radiograph.

F. Gastroesophageal reflux disease (GERD)

1. Epidemiology

a. Approximately 10% of adults have GERD daily.

b. Approximately 80% of pregnant women have GERD.

c. Hiatal hernia present in ∼︀70% of people with GERD.

d. Risk factors

(1) Smoking, alcohol

(2) Caffeine, fatty foods, chocolate

(3) Pregnancy, obesity

(4) Hiatal hernia

GERD: relaxed LES causes acid reflux

2. Pathogenesis

a. Transient relaxation of lower esophageal sphincter (LES)

• Reflux of acid and bile into the distal esophagus

b. Ineffective esophageal clearance of reflux material

3. Clinical findings

a. Noncardiac chest pain

• Heartburn, indigestion

b. Nocturnal cough, nocturnal asthma

GERD: nocturnal cough/asthma; acid injury to enamel; Barrett’s esophagus

c. Acid injury to enamel

d. Early satiety, abdominal fullness

e. Bloating with belching

f. Barrett’s esophagus

4. Diagnostic tests with atypical presentation

GERD atypical presentation: esophageal pH monitoring, endoscopy, manometry

a. Twenty-four–hour esophageal pH monitoring

• Sensitivity/specificity 80% to 90%

b. Esophageal endoscopy

• LES pressure < 10 mm Hg

a. Nonpharmacologic

• Similar to hiatal hernia (see earlier)

b. Pharmacologic

• Similar to hiatal hernia (see earlier)

c. Surgery if indicated

(1) Fundoplication procedure

(2) Involves putting a gastric wrap around the gastroesophageal junction

G. Barrett’s esophagus

1. Complication of GERD

2. Glandular metaplasia in distal esophagus due to acid injury (see Fig. 1-10E)

• Gastric-type columnar cells and small intestine–type cells (goblet cells)

3. Complications

Barrett’s esophagus complications: distal adenocarcinoma, stricture

a. Ulceration with stricture formation (most common)

b. Glandular dysplasia with increased risk for distal adenocarcinoma

H. Infectious esophagitis

1. Usually a complication of AIDS

AIDS-related esophagitis: HSV, CMV, Candida

a. Herpes simplex virus (HSV)

• See multinucleated squamous cells with intranuclear inclusions

b. Cytomegalovirus (CMV)

• See basophilic intranuclear inclusions

• See yeasts and pseudohyphae (extended yeast forms)

3. Presents with painful swallowing (i.e., odynophagia)

I. Corrosive esophagitis

1. Ingestion of strong alkali (e.g., lye) or acid (e.g., HCl)

2. Complications

Corrosive esophagitis: strictures, perforation, squamous cancer

a. Stricture formation

c. Squamous cell carcinoma

J. Esophageal varices

1. Epidemiology and pathogenesis

a. Dilated submucosal left gastric veins (Fig. 17-9)

17-9: Esophageal varices, showing many linear-oriented dilated and tortuous veins in the submucosa of the distal esophagus.

(From Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, p 110, Fig. 6-23A.)

Left gastric vein drains blood from distal esophagus and proximal stomach into the portal vein.

b. Complication of portal hypertension from cirrhosis

Esophageal varices: portal hypertension dilates left gastric veins

• Alcohol abuse is the most common cause.

2. Clinical findings

a. Rupture with massive hematemesis (vomiting blood)

b. Most common cause of death in cirrhosis

Ruptured esophageal varices: most common cause of death in cirrhosis

4. Initial management

Ruptured esophageal varices: endoscopy most important diagnostic procedure

(1) Most important diagnostic procedure

(2) Value in treatment of the bleed as well

b. Assess/maintain intravascular volume

c. Insert nasogastric tube for gastric aspirate/lavage.

(1) Confirms upper gastrointestinal source of bleeding

(2) Assesses rate of bleeding

5. Prevention/treatment of bleeds

a. β-Blockers and isosorbide

(1) Decrease rate of recurrent bleeding

(2) Increase survival by 5% to 10%

b. Transjugular intrahepatic portasystemic stent (TIPS)

• Used for both treatment of bleeding and intractable ascites

c. Octreotide intravenous drip (somatostatin analogue) for bleeding

d. Endoscopic ligation

e. Endoscopic sclerotherapy

f. Open surgery with stapling

K. Mallory-Weiss syndrome

1. Mucosal tear in the proximal stomach and distal esophagus

Mallory-Weiss syndrome: mucosal tear of distal esophagus

• Due to severe retching in alcoholics or bulimia

2. Causes hematemesis

L. Boerhaave’s syndrome

1. Rupture of the distal esophagus

Boerhaave’s syndrome: rupture of distal esophagus

a. Endoscopy (∼︀75% of cases)

3. Complications

a. Pneumomediastinum

(1) Air dissects subcutaneously into the anterior mediastinum.

Pneumomediastinum: air in subcutaneous tissue; crunching sound on physical exam

(2) Crunching sound (Hamman’s crunch) is heard on auscultation.

b. Pleural effusion contains food, acid, amylase.

M. Motor disorders

1. Systemic sclerosis and CREST syndrome (refer to Chapter 3)

Achalasia: most common neuromuscular disorder of the esophagus

a. Epidemiology

(a) Occurs in those 20 to 40 years old

(b) Occurs after 60 years of age

(2) Men and women affected equally

(3) Risk for esophageal cancer

b. Pathogenesis

(1) Incomplete relaxation of LES

(2) Destruction of ganglion cells in myenteric plexus

(a) Probable autoimmune destruction of myenteric plexus

• HLA-DQw1 association

Achalasia: autoimmune destruction ganglion cells myenteric plexus; loss smooth muscle motility

(b) Decreases proximal smooth muscle contraction

(c) Loss of nitric oxide (NO) synthase producing neurons

• Cause of incomplete relaxation

Achalasia: destruction NO synthase producing neurons causes incomplete relaxation LES

(3) Dilation of esophagus proximal to LES with absent peristalsis

(4) Acquired cause is Chagas’ disease.

• Destruction of ganglion cells by amastigotes (lack flagella)

c. Clinical findings

(1) Nocturnal regurgitation of undigested food

Achalasia: nocturnal regurgitation of undigested food

(2) Dysphagia for solids and liquids

(3) Chest pain and heartburn

(4) Frequent hiccups

(5) Nocturnal cough from aspiration

(6) Difficulty belching

(1) Abnormal barium swallow

• Dilated, aperistaltic esophagus with a beak-like tapering at distal end (Fig. 17-10)

17-10: Barium study of the esophagus in achalasia. Note dilated esophagus ending in a narrowed esophagogastric junction (“birds-beak” appearance) (arrow).

(From Grieg JD: Color Atlas of Surgical Diagnosis. London, Mosby-Wolfe, 1996, p 106, Fig. 16-6.)

Achalasia barium swallow: dilated, aperistaltic esophagus; beak-like tapering distal end

(2) Abnormal esophageal manometry

• Detects aperistalsis and failure of LES relaxation

(1) Nonpharmacologic

(a) Pneumatic dilation

(b) Esophagomyotomy

(2) Pharmacologic (short-term)

(a) Long-acting nitrates

(b) Calcium channel blockers

(c) Botulinum toxin injection

N. Esophageal tumors

Leiomyoma: most common benign tumor of esophagus

• Most common benign tumor of esophagus

2. Adenocarcinoma of distal esophagus (Fig. 17-11)

a. Most common primary cancer of the esophagus in the United States

17-11: Distal adenocarcinoma of the esophagus. Note the raised lesion at the junction of the distal esophagus and proximal stomach (arrow).

(From Grieg JD: Color Atlas of Surgical Diagnosis. London, Mosby-Wolfe, 1996, p 109, Fig. 16-12 [right].)

Distal adenocarcinoma of esophagus: most common esophageal cancer

b. Barrett’s esophagus is most common predisposing cause.

• Prevention of GERD decreases risk for developing adenocarcinoma.

3. Squamous cell carcinoma

a. Epidemiology

(1) Most common primary cancer in developing countries

• Caspian Sea to Northern China

(2) More common in blacks than whites

(3) Occurs in men more often than women

(4) Risk factors

Squamous cell carcinoma: smoking cigarettes most common cause

(a) Smoking most common cause

(b) Alcohol abuse, lye strictures

(c) Achalasia, Plummer-Vinson syndrome

(a) Upper third (∼︀15%)

(b) Middle third (∼︀50%) (Fig. 17-12)

(c) Lower third (∼︀35%)

(6) Spreads to local nodes first and then to liver and lungs

b. Clinical findings

(1) Dysphagia for solids initially

17-12: Midesophagus squamous cell carcinoma. Note the elevated round nodular mass with a central area of ulceration.

(From Rosai J, Ackerman LV: Surgical Pathology, 9th ed. St. Louis, Mosby, 2004, p 626, Fig. 11-14C.)

Squamous cell carcinoma: dysphagia for solids + weight loss

(2) Weight loss of short duration

(3) Painless enlargement supraclavicular nodes

Squamous cell carcinoma: symptoms often relate to local invasion

(4) Dry cough and hemoptysis

• Suggests tracheal invasion

• Probable invasion of recurrent laryngeal nerve

(6) Odynophagia

(7) Hypercalcemia

• Parathyroid harmone–related peptide similar to squamous cancer in lungs

(1) Esophagogram

• Surgery, radiation therapy, chemotherapy

• Overall 5-year survival rate is 13%.

III. Stomach Disorders

A. Signs and symptoms of stomach disease

1. Hematemesis (vomiting blood)

a. Most commonly due to peptic ulcer disease (PUD)

PUD: most common cause of hematemesis and melena

b. Other causes—esophageal varices, hemorrhagic gastritis

2. Melena (dark, tarry stools)

a. Hemoglobin (Hb) is converted into hematin (black pigment) by acid.

Melena: hematin; sign of upper gastrointestinal bleed

b. Signifies a bleed proximal to duodenojejunal junction (90%)

3. Gastric analysis

B. Congenital pyloric stenosis (CPS)

1. Epidemiology

Gastric analysis includes measurement of basal acid output (BAO), maximal acid output (MAO), and the BAO:MAO ratio. BAO is the acid output of gastric juice collected via a nasogastric tube over a 1-hour period on an empty stomach. It is normally less than 5 mEq/hour. MAO is the acid output of gastric juice that is collected over 1 hour after pentagastrin stimulation. Normally, it is 5 to 20 mEq/hour. The normal BAO:MAO ratio is 0.20:1.

Gastric analysis: measures BAO and MAO

a. Probable genetic basis

b. Occurs in males > females

c. Affected fathers or mothers

• Increased for child with CPS

d. Acquired pyloric obstruction

• Complication of chronic duodenal ulcer disease with pyloric scarring

2. Pathophysiology

CPS: hypertrophy of pyloric sphincter muscles

a. Progressive hypertrophy of the circular muscles in the pyloric sphincter

• Not present at birth but occurs over the ensuing 3 to 5 weeks

b. Deficiency of NO synthase precipitates the disease

3. Clinical findings

a. Projectile vomiting of non–bile-stained fluid

CPS: vomiting of non–bile-stained fluid

b. Hypertrophied pylorus is palpated in the epigastrium (70%).

• Called an “olive”

c. Visible hyperperistalsis

• Myotomy if it does not resolve

C. Gastroparesis

1. Decreased stomach motility

Gastroparesis: sign of autonomic neuropathy; e.g., diabetes mellitus

a. Autonomic neuropathy (e.g., diabetes mellitus)

b. Previous vagotomy

2. Clinical findings

a. Early satiety and bloating

b. Vomiting of undigested food a few hours after eating

Gastroparesis: early satiety; vomiting of undigested food

a. Small volume frequent feeding

b. Metoclopramide

D. Acute hemorrhagic (erosive) gastritis

a. Erosions are a breach in the epithelium of the mucosa.

b. Ulcers are a breach in the mucosa with extension into the submucosa or deeper.

Hemorrhagic gastritis: NSAIDs most common cause; alcohol second

b. Alcohol, Helicobacter pylori (see below)

c. CMV (AIDS), smoking

d. Burns (called Curling’s ulcers)

e. CNS injury (called Cushing’s ulcers)

• Worm associated with eating raw fish

3. Clinical findings

c. Iron deficiency

4. Treatment (excluding H. pylori)

a. Nonpharmacologic

(1) Avoid mucosal irritants (e.g., NSAIDs, alcohol)

(2) Cessation of smoking

b. Pharmacologic

(1) Misoprostol

(2) Proton pump inhibitors

E. Chronic atrophic gastritis

a. Involves the body and fundus

Type A chronic atrophic gastritis: body and fundus; pernicious anemia

b. Most often due to pernicious anemia (refer to Chapter 11)

c. Complications

(1) Achlorhydria with hypergastrinemia (loss of negative feedback)

(2) Macrocytic anemia due to vitamin B₁₂ deficiency

(3) Increased risk for gastric adenocarcinoma

2. Type B chronic atrophic gastritis

a. Involves the antrum and pylorus

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Tags: Rapid Review Pathology Revised Reprint

Jun 25, 2017 | Posted by admin in PATHOLOGY & LABORATORY MEDICINE | Comments Off

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