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409 Cards in this Set

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  • Back
What is the Most common congenital disorder of oral cavity? What are genetics? Who does it occur more in? Does cleft lip or cleft palate and lip occur more?
1) cleft palate (∼1:800 live births)
2) Recurrence in subsequent siblings (3%)
3) More common in whites than blacks
4) Cleft lip and palate (50%)
5) Cleft lip alone (25%)
6) Male > female
What are complications of cleft lip and palate? What is pathogenesis?
(1) Malocclusion
(2) Eustachian tube dysfunction
a. Chronic otitis media
(3) Speech problems
(4) Failure of fusion of facial processes
What is the most common oral infection in HIV? What causes hairy leukoplakia and what is it?
1) candidiasis
2) Glossitis due to Epstein-Barr virus (EBV)
Examples of apthous ulcers are? What are possible causes? What are characteristics?
1) stomatitis
2) canker sores
Causes: relatively unknown
(1) Virus versus immunologic
(2) Often stress-induced
1) Painful ulcers covered by a shaggy gray membrane
What are the pre-AIDS lesions of the oral cavity?
1) thrush
2) hairy leukoplakia
3) apthous ulcers
Where in the mouth is kaposi sarcoma seen? What is cause?
1) Hard palate is the most common location.
2) Due to human herpesvirus 8
What is the main organism causing dental caries? How does it do this?
1) Streptococcus mutans produces acid from sucrose fermentation.
2) Acid erodes enamel and exposes underlying dentine.
What are 4 examples of noninfectious causes of ulcers in oral cavity?
1) Pemphigus vulgaris and mucous membrane pemphigoid
a. Both are immunologic skin disorders
2) Erythema multiforme
a. Hypersensitivity reaction against Mycoplasma or drugs (e.g., sulfonamides)
b. Called Stevens-Johnson syndrome when it involves the mouth
3) Apthous ulcers (stomatitis)
4) Behçet's syndrome
What is erythema multiforme called when it affects the mouth?
Called Stevens-Johnson syndrome when it involves the mouth
What are genetic factors that lead to Behçet's syndrome? What may precipitate an attack? Which group of people is it more common?
(1) Combination of environmental + genetic factors
a. HLA-B51, HLA-B27 associations
(2) May be precipitated by herpes simplex or parvovirus
(3) High incidence in Turkey and eastern Mediterranean
what is the pathology of Behcet's syndrome? What are clinical findings? How is it treated?
1. Pathophysiology
a) Immune complex small vessel vasculitis
3. Clinical findings
a) Recurrent aphthous ulcers, genital ulcerations
b) Uveitis, erythema nodosum
c) Attacks last 1 to 4 weeks
4. Treatment
a) Anti-inflammatory medications
b) Corticosteroids
c) Colchicine
d) Thalidomide
How does Peutz-Jeghers syndrome effect oral cavity? How does lead poisoning effect oral cavity?
1) Melanin pigmentation of the lips and oral mucosa
2) Lead deposits along the gingival margins in adults with gingivitis
How does addisons disease effect the oral cavity?
1. Increased adrenocorticotropic hormone (ACTH) stimulates melanocytes.
2. Melanin pigmentation of the buccal mucosa
Which drug can effect the color of teeth? Who is it not recommended in?
1. Tetracycline
a. Drug discolors newly formed teeth.
b. Drug not recommended in a child < 12 years of age.
How does flouride effect the presentation of teeth? What congenital disorder causes reddish brown discoloration of teeth?
1. Excess fluoride
a) Mottled, chalky white discoloration
2. Congenital erythropoietic porphyria
a) Porphyrins deposit in the teeth
b) Reddish brown discoloration
What are 5 conditions that can cause macroglossia?
1. Myxedema
* Severe primary hypothyroidism
2. Down syndrome
3. Acromegaly
4. Amyloidosis
5. Mucosal neuromas in multiple endocrine neoplasia (MEN) syndrome IIb (III)
how does glossitis present?
1) Sore
2) beefy red tongue
3) with or without papillary atrophy
What are 6 causes of glossitis?
1. Long-standing iron deficiency
2. Vitamin B12 or folate deficiency
3. Scurvy (vitamin C deficiency)
4. Pellagra (niacin deficiency)
5. Scarlet fever
6. EBV-associated hairy leukoplakia
Does leukoplakia or erythroplakia have a higher chance of progressing to oral cancer?
1) Leukoplakia literally means "white patch"
a. It has an ∼30% rate of progression to oral cancer.
2) Erythroplakia is a red patch
a. It has an ∼60% rate of progression to oral cancer
How are both leukoplakia and erythroplakia similar?
1) Lesion does not wipe off.
2) Both lesions are due to squamous hyperplasia of the epidermis.
3) Increased risk for squamous dysplasia or invasive squamous cancer
What are risk factors for leukoplakia and erythroplakia?
1. Chronic irritation (e.g., dentures)
2. All forms of tobacco use
3. Alcohol abuse
4. Human papillomavirus (HPV)
Where are locations for leukoplakia and erythroplakia? Which is most common? What should always be done when someone has one of these lesions?
1. Vermilion border lower lip (most common site)
2. Buccal mucosa
3. Hard and soft palates
4. Floor of the mouth
5. Always biopsy these lesions because of the high risk for progression to oral cancer
What is lichen planus associated with?
1. Often associated with Wickham's stria on buccal mucosa
a. Fine, white, lacy lesions
2. May be associated with squamous cell carcinoma
Where does a Dentigerous cyst derive from? What is tumor is it associated with? What tooth does it arise from?
1. Derives from epithelial elements of dental origin (odontogenic origin)
2. Associated with the crown of an unerupted or impacted third molar tooth
3. Association with ameloblastomas in 15% to 30% of cases
What is the most common benign tumor in oral cavity? What are features of tumor? On what structures do they commonly occur?
1) Squamous papillomas
2) Exophytic tumor with a fibrovascular core
3) May occur on the tongue, gingiva, palate, or lips
What is the most common odontogenic tumor? What do they arise from? What features do they have?
1) Ameloblastoma
2) Arise from enamel organ epithelium or a dentigerous cyst
3) Located in the mandible
a. Produces a radiolucency in bone that has a "soap bubble" appearance
b. Locally invasive but do not metastasize
What type of tumor is an odontoma?
1) haramtoma
2) composed of ondtogenic epithelium and odontoblastic tissue
What age group is effected by ameloblastomas? What does epulis refer to?
1) people <35
2) any benign growth of givgivae
What is the most Malignant tumor of the oral cavity (excluding salivary gland)? Who do they occur in?
1) Majority are well-differentiated squamous cell carcinomas
2) More common in men than women
What are risk factors for sqaumous cell carcinoma of the mouth?
(1) Smoking is the most common risk factor.
a. Pipe, cigarettes, chewing tobacco
(2) Alcohol abuse (synergistic with smoking)
(3) Synergism between smoking and alcohol excess
a. Increases relative risk 30-fold
(4) HPV
(5) Chronic irritation from dentures
(6) Lichen planus
Where are common sites for squamous cancer oral cancer?
(1) Lower lip (vermilion border) = most common site
(2) Floor of mouth
(3) Lateral border of tongue
What is a risk factor for malignant Verrucous carcinoma of oral cavity?
Associated with smokeless tobacco
What is basal cell carcinoma of oral cavity associated with? What is common site?
(1) Most common cancer of upper lip
(2) Associated with ultraviolet light B exposure
Who does sjogrens occur in? what is it associated with? What is pathogenesis to glands? What is there increased risk of developing?
1. Female dominant autoimmune disease associated with rheumatoid arthritis
2. Autoimmune destruction of minor salivary glands and lacrimal glands
3. malignant lymphoma
What are characteristics of sjogrens?
1) keratoconjunctivitis sicca
2) xerostomia
3) RA
Which oral salivary gland has higher rates of neoplasms? Are most salivary gland tumors in general benign or malignant?
(1) Parotid gland is the most common site.
(2) Major salivary gland tumors are more likely to be benign.
(3) Minor salivary gland tumors are more likely to be malignant
What is the Most common benign tumor of major and minor salivary glands? Which gland is most often involved? Who does it occur more in?
1) pleomorphic adenoma
2) Parotid gland is the most common site.
3) Female dominant (20-40)
How does a pleomorphic adenoma present? Histologically how does it appear? which nerve can determine if the tumor has become malignant?
1) Painless, moveable mass at the angle of the jaw
2) Epithelial cells intermixed with myxomatous and cartilaginous stroma
a. Tumor projections through capsule increase risk of recurrence
3) May transform into a malignant tumor
4) Facial nerve involvement is a sign of malignancy.
Is Warthins tumor benign or malignant? Which gland is involved? Who does it occur in? What are features?
1) Benign parotid gland tumor
2) Male dominant
3) Heterotopic salivary gland tissue trapped in a lymph node
a. Cystic glandular structures are located within benign lymphoid tissue.
What is the most common malignant salivary gland tumor? where is usually located? What are histologic features? What determines aggressiveness?
1) Mucoepidermoid carcinoma
2) Most commonly located in the parotid gland
3) Mixture of neoplastic squamous and mucus-secreting cells
4) greater number of epidermoid cells and nonparotid tumors tend to be more aggressive
what is a mucocele? Where do they develop? What is a ranula?
1) mucocele:
a. cyst-like pool of mucus lined by granulation tissue
b. develops near minor salivary gland
c. results from leakage caused by rupture of an obstructed or traumatized duct
2) ranula:
a. large mucocele of salivary gland origin usually on floor of mouth
What is sialadenitis?
1) inflammation of salivary glands
Where are adenoid cystic carcinomas located? What are features? are they malignant?
1) minor salivary glands
2) cribiform pattern with masses of small dark staining cells arrayed in cystic spaces
3) tend to infiltrate perineural spaces and cause pain
4) late metastisis
Where do oncocytomas occur? In who? How do they appear?
1) parotid gland
2) large, granular appearing eosinophilic staining epithelial cells
3) found in elderly
Is exudative tonsilitis caused primarily by viruses or bacteria?
1) viruses
2) Culture is necessary to differentiate bacterial versus viral infection
What causes hairy leukoplakia of mouth? How does it present?
1) EBV
2) Glossitis associated with bilateral white excrescences on lateral border of tongue
Herpes labialis is caused by which serotype? How does it present? What causes reactivation? How is it treated?
1) HSV type 1
2) Recurrent vesicular lesions on the lips (virus remains dormant in cranial sensory ganglia)
3) Reactivated by stress, sunlight, and menses
4) Treatment: oral acyclovir, valacyclovir, famciclovir; topical acyclovir, penciclovir
Mumps is caused by? is unilateral or B/L? Which serum marker is elevated? What are complications?
1) Paramyxovirus
2) Bilateral parotitis (70%) with increased serum amylase
3) Complications:
a. meningoencephalitis
b. unilateral orchitis or oophoritis
c. pancreatitis
Herpangina is caused by what? Who does it occur in? How does it present?
1) Coxsackievirus
2) Occurs in children
3) Multiple vesicles or ulcers on soft palate and pharynx surrounded by erythema
Hand-foot-mouth disease is caused by what? Is seen in who? How does it present?
1) Coxsackievirus
2) Occurs in young children
3) Vesicles located in mouth and distal extremities
Cervicofacial actinomycosis is caused by? What are features of this bacteria? What are features of disease? How is it treated?
1) Actinomyces israelii = gram-positive, branching filamentous bacteria; anaerobe
2) Draining sinus tract from facial or cervical area"Sulfur granules" in puss
a. granules contain bacteria
3) Often follows after extraction of an abscessed tooth
4) Treatment: ampicillin, penicillin G
Diphtheria is caused by? What is seen in disease? How is it treated?
1) Corynebacterium diphtheriae
2) Toxin produces "shaggy" gray pseudomembrane in posterior pharynx and upper airways
3) Treatment: erythromycin
Peritonsillar abscess is caused by? What are findings? How is it treated?
1) Peritonsillar abscess
2) Streptococcus pyogenes
3) Uvula deviates to contralateral side
4) "hot potato" voice
5) foul-smelling breath
6) Complication due to tonsillitis
7) Treatment:
a. surgical drainage of pus
b. penicillin G or V
c. add clindamycin for serious invasive infections
Ludwig's angina is caused by? How is it treated? How does it present and spread? what are causes?
1) a. Aerobic/anaerobic
b. Streptococcus
c. Eikenella corrodens
2) Treatment: surgical drainage; clindamycin + metronidazole
3) Cellulitis involving the submaxillary and sublingual space
a. follows fascial planes and may spread into pharynx, carotid sheath, superior mediastinum
4) Causes: dental extraction (most common), trauma to floor of mouth
Pharyngitis is typically caused by? What is it associated with? There is a potential to develop what? How is it treated?
1) S pyogenes
2) Associated with tonsillitis
3) Potential for acute rheumatic fever and glomerulonephritis
4) Treatment: penicillin V
Scarlet fever is caused by what? What are symptoms? what is there increased risk of developing? How is it treated?
1) S pyogenes
2) Pharyngitis, tonsillitis, glossitis
3) Erythrogenic toxin produces rash on skin and tongue (initially white and then strawberry colored)
4) Increased risk for glomerulonephritis
a. Nephritogenic strains pose no risk for acute rheumatic fever
5) Treatment: penicillin G or V
Sialadenitis is typically caused by? What is pathogenesis? How is it treated based on drug resistance?
1) S aureus
2) Bacterial inflammation of major salivary gland
3) Secondary to a calculus, which obstructs the duct in postoperative patients
4) Treatment:
a. oxacillin
b. nafcillin if methicillin susceptible
c. TMP/SMX if community-acquired methicillin resistant
d. vancomycin if methicillin resistant in hospital
Congenital syphilis is caused by? How is oral cavity affected? what is treatment?
1) Treponema pallidum (spirochete)
2) Abnormalities involving incisors (tapered like a peg) and molar teeth (resemble mulberries)
3) Treatment: aqueous crystalline penicillin G
Oral thrush is caused by? Who does it present in? How is it treated?
1) Candida albicans (yeast)
2) May occur in neonates, immunocompromised patients (common pre-AIDS-defining lesion), diabetes mellitus, and following antibiotic therapy
3) Treatment: fluconazole, itraconazole
A patient has extensive white "curd-like" plaque that can be wiped off leaving an erythematous base on tongue. what do they have?
oral thrush from candida
acute necrotizing ulcerative gingivitis is caused by?
usually a mixture of:
1) fusobacterium
2) borrelia vincentii
Note: this are symbiotic bacteria and infection occurs in immunocompromised
heartburn is usually from? Dysphagia of solids only usually results form?
1. Heartburn
a. Most commonly due to gastroesophageal reflux disease
2. Dysphagia (difficulty swallowing) for solids alone
a. Symptom of an obstructive lesion
b. Examples-esophageal cancer, esophageal web, stricture
Dysphagia of both solids and liquids can mean what? Break it down into upper and lower esophageal problems!
1. Symptom of a motility disorder
2. Oropharyngeal (upper esophageal) dysphagia
a) Striated muscle dysmotility
b) Examples-dermatomyositis, myasthenia gravis, stroke
3. Lower esophageal dysphagia
a) Smooth muscle dysmotility
b) Examples-systemic sclerosis, CREST syndrome, achalasia
What is the most common variant of tracheoesophageal fistula? What is 2nd most common variant? and 3rd kind? What is TE fistula associated with?
1) lower portion of esophagous communicates with trachea near bifurcation
2) fistulous connection between the upper esophagous and trachea, where the lower esophagous is not connected to upper esophagous
3) fistulous connection between trachea and a completely patent esophagous
4) Associated with VATER
how does apthous stomatitis present?
1) painful
2) recurrent
3) erosive oral lesion
What are clinical findings in a tracheoesophageal fistula?
1) Maternal polyhydramnios
a. Swallowed amniotic fluid cannot be reabsorbed in the small intestine.
2) Abdominal distention in newborn
a. Air in the stomach from tracheal fistula
3) Difficulty with feeding
4) Food regurgitates out of the mouth.
5) Chemical pneumonia from aspiration
6) VATER syndrome:
a. Vertebral abnormalities
b. Anal atresia
c. TE fistula
d. Renal disease and absent radius
What is VATER syndrome?
a. Vertebral abnormalities
b. Anal atresia
c. TE fistula
d. Renal disease and absent radius
Plummer-vinson syndrome is due to what? How does it present?
1. Due to chronic iron deficiency
2. Leukoplakia in oral mucosa and esophagus
3. Intermittent dysphagia for solids
a. Due to an esophageal web or stricture
4. glossitis
What are signs and symptoms of plummer-vinson syndrome?
1) Dysphagia (difficulty in swallowing)
2) Pain
3) Weakness
4) Odynophagia (Painful swallowing)
7) Angular stomatitis
8) increased risk of carcinoma
What is a true diverticulum? What is a false or propulsion diverticulum?
1) True = Outpouching lined by mucosa, submucosa, muscularis propria, and adventitia
2) False:
a. Weakness in underlying muscle wall
b. Outpouching of mucosa and submucosa into area of weakness
What is zenkers diverticulum?
1) Pulsion type located in upper esophagus
a. Area of weakness is cricopharyngeus muscle
How does zenkers diverticulum present?
(1) Painful swallowing
(2) Halitosis
a. Entrapped food
(3) Regurgitate food through mouth
(4) Diverticulitis
(5) laryngeal irritation resulting in changing voice
What is the Bochdalek hernia also known as? When does it present? What is pathology? What is seen on X-ray?
1) Pleuroperitoneal diaphragmatic hernias
2) present early in life
3) The visceral contents extend through the posterolateral part of the diaphragm on the left into the chest cavity causing respiratory distress at birth.
3) Loops of bowel are present in the left pleural cavity on radiograph.
What is the incidence of hiatal hernia? Who does it occur most in?
1) Found in 50% of persons over 50 years old
a. Increases with age
2) More common in women than men
What is a hiatal hernia associated with?
1) Sigmoid diverticulosis (25%)
2) Esophagitis (25%)
3) Duodenal ulcers (20%)
4) Gallstones (18%)
What is the Most common type of hiatal hernia? Where is hernia?
1) sliding hernia (99%)
2) Herniation of proximal stomach into thoracic cavity through the diaphragmatic esophageal hiatus
Clinically what is seen in someone with a sliding hernia?
(1) Heartburn
(2) Nocturnal epigastric distress from acid reflux
(3) Hematemesis (vomiting blood)
(4) Ulceration, stricture
(5) Bowel sounds heard over left lung base
how is a sliding hernia treated?
(1) Nonpharmacologic
a. Reduce intake of foods/drugs that decrease lower esophageal sphincter tone
o 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
Paraesophageal hernia is also known as? it is a type of?
1) rolling hernia
2) hiatal hernia
3) Gastroesophageal junction remains at the level of the diaphragm.
4) Part of the stomach bulges into the thoracic cavity.
A diverticulum immediately above the lower esophageal sphincter is known as?
epiphrenic diverticulum
How many adults have GERD daily? Who is GERD very common in? What commonly accompanies GERD?
1) Approximately 10% of adults have GERD daily.
2) Approximately 80% of pregnant women have GERD.
3) Hiatal hernia present in ∼70% of people with GERD
What are risk factors for GERD?
(1) Smoking, alcohol
(2) Caffeine, fatty foods, chocolate
(3) Pregnancy, obesity
(4) Hiatal hernia
What is the pathogenesis of GERD?
1. Transient relaxation of lower esophageal sphincter (LES)
a. Reflux of acid and bile into the distal esophagus
2. Ineffective esophageal clearance of reflux material
Clinically how does someone with GERD present?
1. Noncardiac chest pain
a. Heartburn, indigestion
2. Nocturnal cough, nocturnal asthma
3. Acid injury to enamel
4. Early satiety, abdominal fullness
5. Bloating with belching
6. Barrett's esophagus
What are diagnostic tests that can be used to determine atypical GERD?
1. Twenty-four-hour esophageal pH monitoring
a. Sensitivity/specificity 80% to 90%
2. Esophageal endoscopy
3. Manometry
b. LES pressure < 10 mm Hg
Barrets esophagous is due to what? What occurs? What are complications?
1. Complication of GERD
2. Glandular metaplasia in distal esophagus due to acid injury
a. Gastric-type columnar cells and small intestine-type cells (goblet cells)
3. Complications
a. Ulceration with stricture formation (most common)
b. Glandular dysplasia with increased risk for distal adenocarcinoma
What are pathogens that cause infectious esophagitis? Infections of the esophagous typically occur in who?
1. Herpes simplex virus (HSV)
a. See multinucleated squamous cells with intranuclear inclusions
2. Cytomegalovirus (CMV)
a. See basophilic intranuclear inclusions
3. Candida
a. See yeasts and pseudohyphae (extended yeast forms)
4. occurs in immunocompromised people
what causes corrosive esophagitis? What are complications?
1) Ingestion of strong alkali (e.g., lye) or acid (e.g., HCl)
2) Complications:
a. Stricture formation
b. Perforation
c. Squamous cell carcinoma
Left gastric vein drains blood from where into where?
from distal esophagus and proximal stomach into the portal vein.
What is the pathogenesis of esophageal varices? What is it most commonly due to?
1) Dilated submucosal left gastric veins
2) Complication of portal hypertension from cirrhosis
a. Alcohol abuse is the most common cause.
What are clinical findings of esophageal varices?
1. Rupture with massive hematemesis (vomiting blood)
2. Most common cause of death in cirrhosis
How are esophageal varices initially managed?
1. Endoscopy
a. Most important diagnostic procedure
b. Value in treatment of the bleed as well
2. Assess/maintain intravascular volume
3. Insert nasogastric tube for gastric aspirate/lavage.
a. Confirms upper gastrointestinal source of bleeding
b. Assesses rate of bleeding
How are esophageal varices treated and prevented?
1. β-Blockers and isosorbide
a. Decrease rate of recurrent bleeding
b. Increase survival by 5% to 10%
2. Transjugular intrahepatic portasystemic stent (TIPS)
a. Used for both treatment of bleeding and intractable ascites
3. Octreotide intravenous drip (somatostatin analogue) for bleeding
4. Endoscopic ligation
5. Endoscopic sclerotherapy
6. Open surgery with stapling
What is Mallory-Weiss syndrome? what is a symptom?
1. Mucosal tear in the proximal stomach and distal esophagus
a. Due to severe retching in alcoholics or bulimia
b. vertical and linear tears from mm to cm
2. Causes hematemesis
What is Boerhaave's syndrome? what are causes?
1) Rupture of the distal esophagus
2) Causes:
a. Endoscopy (∼75% of cases)
b. Retching
c. Bulimia
What are complications of Boerhaave's syndrome? what sound is heard?
1) Pneumomediastinum
a. Air dissects subcutaneously into the anterior mediastinum.
b. Crunching sound (Hamman's crunch) is heard on auscultation.
2) Pleural effusion contains food, acid, amylase
Who does achalasia occur in? what type of distribution does it have? What is there increased risk of?
(1) Bimodal
a. Occurs in those 20 to 40 years old
c. Occurs after 60 years of age
(2) Men and women affected equally
(3) Risk for esophageal cancer
Pathologically what is occurring in achalasia? what is genetic association?
(1) Incomplete relaxation of LES
(2) Destruction of ganglion cells in myenteric plexus (auerbachs)
a. Probable autoimmune destruction of myenteric plexus
b.+ HLA-DQw1 association and CREST association
c. Decreases proximal smooth muscle contraction
d. Loss of nitric oxide (NO) synthase producing neurons
e. Cause of incomplete relaxation
(3) Dilation of esophagus proximal to LES with absent peristalsis
What is an acquired cause of achalasia?
1) Acquired cause is Chagas' disease (trypanosoma cruzi)
a. Destruction of ganglion cells by amastigotes (lack flagella)
Clinically how does achalasia present?
(1) 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
How is achalasia diagnosed?
(1) Abnormal barium swallow
a. Dilated, aperistaltic esophagus with a beak-like tapering at distal end
(2) Abnormal esophageal manometry
a. Detects aperistalsis and failure of LES relaxation
How is achalasia treated?
1) Nonpharmacologic
a. Pneumatic dilation
b. Esophagomyotomy
2) Pharmacologic (short-term)
a. Long-acting nitrates
b. Calcium channel blockers
c. Botulinum toxin injection
What is the most common benign tumor of esophagus? What is the Most common primary cancer of the esophagus in the United States? What is a predisposing factor?
1) leiomyoma
2) adenocarinoma of distal esophagous
a. Barrett's esophagus is most common predisposing cause.
b. Prevention of GERD decreases risk for developing adenocarcinoma
Who is squamous cell carcinoma of the esophagous common in? which countries?
(1) Most common primary cancer in developing countries
a. Caspian Sea to Northern China
(2) More common in blacks than whites
(3) Occurs in men more often than women
What are risk factors for squamous carcinoma of the esophagous?
(a) Smoking most common cause
(b) Alcohol abuse, lye strictures
(c) Achalasia, Plummer-Vinson syndrome
Where are squamous carcinomas of the esophagous primarily located? Where does it metastisize to first then later?
(a) Upper third (∼15%)
(b) Middle third (∼50%)
(c) Lower third (∼35%)
(d) Spreads to local nodes first and then to liver and lungs
Clinically how can someone with squamous carcinoma of the esophagous present?
(1) Dysphagia for solids initially
(2) Weight loss of short duration
(3) Painless enlargement supraclavicular nodes
(4) Dry cough and hemoptysis
a. symptoms often relate to local invasion
b. Suggests tracheal invasion
(5) Hoarseness
a. Probable invasion of recurrent laryngeal nerve
(6) Odynophagia
(7) Hypercalcemia
a. Parathyroid harmone-related peptide similar to squamous cancer in lungs
Symptoms of squamous cell carcinoma relate to what a lot of the time? what paraneoplastic syndrome can be seen with it? what is the prognosis?
1) local invasion usually causes symptoms
2) hypercalcemia from Parathyroid harmone-related peptide similar to squamous cancer in lungs
3) Overall 5-year survival rate is 13%
is adenocarcinoma or squamous cell carcinoma of the esophagous more common in US? What about worldwide?
1) adenocarcinoma in US
2) squamous worldwide (decreasing in US)
What are some causes of hematemesis?
1. Most commonly due to peptic ulcer disease (PUD)
2. Other causes-esophageal varices, hemorrhagic gastritis
What does melena signify? How is it made?
1) dark, tarry stools
2) Hemoglobin (Hb) is converted into hematin (black pigment) by acid.
3) Signifies a bleed proximal to duodenojejunal junction (90%)
What does a gastric analysis entail?
1) measurement of basal acid output (BAO), maximal acid output (MAO), and the BAO:MAO ratio
How is basal acid output measured (BAO)? What is the normal value?
1) BAO is the acid output of gastric juice collected via a nasogastric tube over a 1-hour period on an empty stomach
2) It is normally less than 5 mEq/hour
How is the maximal acid output determined? What is the normal value?
1) MAO is the acid output of gastric juice that is collected over 1 hour after pentagastrin stimulation.
2) Normally, it is 5 to 20 mEq/hour
Gastric analysis determines the basal acid output to the maximal acid output. What is the normal ratio?
The normal BAO:MAO ratio is 0.20:1.
What are causes of congenital pyloric stenosis? Does it occur more in boys or girls? How can it be acquired?
1. Probable genetic basis
2. Occurs in males > females
3. Affected fathers or mothers
a. Increased for child with CPS
4. Acquired pyloric obstruction
a. Complication of chronic duodenal ulcer disease with pyloric scarring
What is the pathophysiology of congenital pyloric stenosis? When does it present?
1. Progressive hypertrophy of the circular muscles in the pyloric sphincter
a. Not present at birth but occurs over the ensuing 3 to 5 weeks
2. Deficiency of NO synthase precipitates the disease
Clinically how does congenital pyloric stenosis present? How is it treated?
1. Projectile vomiting of non-bile-stained fluid
2. Hypertrophied pylorus is palpated in the epigastrium (70%).
a. Called an "olive"
3. Visible hyperperistalsis
4. Myotomy if it does not resolve
What is gastroparesis? How can it occur?
1) Decreased stomach motility
a. Autonomic neuropathy (e.g., diabetes mellitus)
b. Previous vagotomy
Clinically how does gastroparesis present? How is it treated?
1. Early satiety and bloating
2. Vomiting of undigested food a few hours after eating
1. Small volume frequent feeding
2. Metoclopramide
Note: D2 antagonist and 5HT4 agonist
What is the difference between erosions and ulcers?
1. Erosions are a breach in the epithelium of the mucosa.
2. Ulcers are a breach in the mucosa with extension into the submucosa or deeper.
What are causes of Acute hemorrhagic (erosive) gastritis?
1. NSAIDs = most common
2. Alcohol, Helicobacter pylori
3. CMV (AIDS), smoking
4. Burns (called Curling's ulcers)
5. CNS injury (called Cushing's ulcers)
6. Uremia
7. Anisakis
* Worm associated with eating raw fish
What are clinical findings in acute erosive gastritis?
1. Hematemesis
2. Melena
3. Iron deficiency
If someone has acute erosive gastritis and an infection is not present, how can they be treated?
1. Nonpharmacologic
a. Avoid mucosal irritants (e.g., NSAIDs, alcohol)
b. Cessation of smoking
2. Pharmacologic
a. Misoprostol
b. Proton pump inhibitors
What part of stomach does Type A chronic atrophic gastritis involve? What are complications? What is it most often due to?
1. Involves the body and fundus
2. Most often due to pernicious anemia
3. Complications
a) Achlorhydria with hypergastrinemia (loss of negative feedback)
b) Macrocytic anemia due to vitamin B12 deficiency
c) Increased risk for gastric adenocarcinoma
Where in stomach does Type B chronic atrophic gastritis occur? What is most common cause? where in world does it occur?
1) Involves the antrum and pylorus
2) Epidemiology
a. Most common cause is Helicobacter pylori.
*** Gram-negative, curved rod
b. Present in 30% to 50% of population in United States
c. Prevalence increases with age.
d. Transmitted by fecal-oral/oral-oral route
e. Common in areas of poor sanitation
Pathologically how does H pylori damage mucosal lining? How does it colonize?
(1) Gram-negative, curved rod
(2) Produces urease, proteases, cytotoxins
a. Urease converts amino groups in proteins to ammonia
b. Secretion products produce chronic gastritis and PUD.
(3) Colonizes mucus layer lining
a. Attaches to blood group O receptors on mucosal cells
b. Not an invasive bacterium
What are microscopic findings of H pylori? What can with longterm infection?
(1) Chronic inflammatory infiltrate in the lamina propria
(2) Intestinal metaplasia
a. Precursor lesion for adenocarcinoma
A urea breath test is used for someone suspected of having H pylori. Is it sensitive or specific? Does it determine active or past infection?
(a) Documents active infection
(b) Sensitivity and specificity > 90%
Note: serology can't distinguish active from past
Is the stool test for H pylori sensitive or specific? Does it detect current or past infection?
(a) Positive when there is active infection
(b) Negative when infection has been eradicated
(c) Sensitivity and specificity > 90%
Note: excellent screen test
This test is Considered gold standard test albeit an invasive test for H pylori?
Tests to detect urease in a gastric biopsy
Are serologic tests useful for active or past infection with H pylori? Are they sensitive or specific?
(a) High sensitivity and specificity
(b) Do not distinguish current from past infection
How is H pylori treated? Which test is used to determine if infection has resolved?
(1) Bismuth, metronidazole, tetracycline, omeprazole
(2) Omeprazole, amoxicillin, clarithromycin
(3) Length of treatment varies from 7 to 14 days
(4) Test of cure is stool antigen test
a. If negative 8 weeks after therapy, infection is cured.
b. Does not imply that infection cannot recur
Menetrier's disease is also known as? What is pathology? What is there increased risk of?
1) hypertrophic gastropathy
2) Giant rugal folds
a. Due to hyperplasia of mucus-secreting cells
b. Causes hypoproteinemia (protein-losing enteropathy)
3) Atrophy of parietal cells (achlorhydria)
a. Increased risk for adenocarcinoma
4) increased risk of stomach cancer
What are diseases associated with H pylori infection?
(1) Duodenal and gastric ulcers
(2) Gastric adenocarcinoma
(3) Low-grade B-cell malignant lymphoma
(4) Chronic atrophic gastritis
What is the most common cause of PUD around world and in US? Where in GI are ulcers most common?
1. H. pylori (70%).
a. Other parts of the world > 90%
b. Eradication of H. pylori markedly reduces PUD recurrence.
2. Duodenal ulcers are more common than gastric ulcers.
3. Locations
a. Duodenal ulcer first portion of duodenum (>90%)
b. Gastric ulcer in lesser curvature near incisura angularis
4. Recurrence rate for untreated PUD ∼60% (>70% in smokers)
What are microscopic and gross features of ulcers?
1) Clean, sharply demarcated, and slightly elevated around the edges
2) Four layers in sequence are noted in histologic sections of ulcers.
a. Necrotic debris
b. Inflammation with a predominance of neutrophils
c. Granulation tissue (repair tissue)
d. Fibrosis
Should a duodenal ulcer or a stomach ulcer be biopsied for malignancy?
1) Most gastric ulcers are benign.
a. Small percentage may be malignant (reason for biopsy).
2) Duodenal ulcers are never malignant
What is the epidemiology and pathogenesis of ZE?
1) Majority (>60%) are malignant pancreatic islet cell tumors.
2) Secrete excess gastrin producing hyperacidity
3) Sporadic in two thirds of cases
4) Ulcers are usually single and in the usual locations; there may be multiple ulcers
5) ulcers in ileum or jejunum suggest ZE
Which multiple endocrine neoplasia is ZE associated with?
MEN type I association (20-30% of cases)
1) prolactinoma
2) Hyperparathyroidism
3) Pancreatic islet cell tumor (ZE note could also be insulinoma
What are clinical findings that would make you suspect ZE?
(1) Multiple ulcers in usual places (jejunum)
(2) Ulcers resistant to therapy
(3) Ulcers distal to first portion of duodenum
(4) PUD plus diarrhea
(5) Family history of parathyroid or pituitary tumors
(6) PUD without H. pylori or history of NSAIDs
Someone presents with signs of PUD and diarrhea with maldigestion of food. What should you suspect?
zollinger ellison syndrome
Clinically how does someone with ZE syndrome present?
1. Epigastric pain with weight loss
2. Heartburn from GERD (60%)
3. Peptic ulceration
a. Most are solitary duodenal ulcers rather than multiple ulcers.
4. Acid hypersecretion with diarrhea
5. Maldigestion of food
a. Acid interferes with pancreatic enzyme activity.
What are laboratory findings in ZE syndrome? How is it treated?
1. Increased BAO, MAO, and BAO:MAO ratio
2. Serum gastrin level > 1000 pg/mL
3. Chemotherapy and proton pump inhibitors
What are gastric polyps a complication of? What are the 2 types? Which is most common? Which is malignant?
1. Complication of chronic gastritis and achlorhydria
2. Hyperplastic polyp
a. Most common type
b. Hamartoma with no malignant potential
3. Adenomatous polyp
a. Neoplastic polyp
b. Potential for malignant transformation
What is the most common benign tumor in stomach? How do they present?
1) leiomyoma
2) May ulcerate or bleed
Where is primary adenocarcinoma decreasing? where and in who is it increasing?
(1) Decreasing incidence in United States
(2) Increasing incidence in Japan
(3) Increased incidence in blood group A people
(4) increased in men >50
What is the most common type of gastric carcinoma? What are risk factors?
1) Intestinal type of gastric adenocarcinoma
2) Risks:
(a) Intestinal metaplasia due to H. pylori (most important)
(b) Nitrosamines
(c) Smoked foods (Japan)
(d) Diets lacking fruits/vegetables
(e) Type A chronic atrophic gastritis
(f) Menetrier's disease
(g) achlorhydria
(e) chronic gastritis with or without pernicious anemia
At autopsy an irregular ulcer crater with piling up of the mucosa around the ulcer in the antrum. what was probable cause of death?
intestinal type gastric adenocarcinoma
Note: ulcers can be Polypoid or ulcerated
Where are common locations for intestinal type gastric adenocarcinomas?
(a) Lesser curvature of pylorus and antrum (50-60%)
(b) Cardia (25%), body and fundus
How has the incidence of diffuse gastric adenocarcinoma changed? Is H pylori a leading cause?
(1) Incidence has remained unchanged.
(2) Not associated with H. pylori
What are the two type of primary stomach adenocarcinomas?
1) Intestinal type of gastric adenocarcinoma
2) diffuse gastric carcinoma
Pathogenically what is seen and what occurs in diffuse gastric adenocarcinoma? What else is it called? Where does it metastisize and how?
1) Diffuse infiltration of malignant cells in the stomach wall
a. Sometimes called "linitis plastica"
b. Stomach does not peristalse.
c. Signet-ring cells infiltrate the stomach wall
d. Produces Krukenberg tumors of the ovaries
e. Hematogenous spread of signet-ring cells to both ovaries
Is linitis plastica associated with H pylori?
1) no association
2) diffuse gastric adenocarcinoma
How do Krukenberg tumors occur? What cell type is seen?
1) hematogenous metastisis to ovaries from stomach with diffuse gastric adenocarcinoma
2) signet ring cells
Clinically what is seen in someone with primary gastric adenocarcinoma?
(1) Cachexia and weight loss (most common; 60%)
(2) Epigastric pain (50%)
(3) Vomiting often with melena (20%)
(4) Metastasis to left supraclavicular node (Virchow's node)
(5) Paraneoplastic skin lesions
a. Acanthosis nigricans
b. Multiple outcroppings of seborrheic keratoses (Leser-Trélat sign)
(6) Metastasis to umbilicus (Sister Mary Joseph sign)
What are 4 unique signs that can occur with primary gastric adenocarcinoma?
1) Metastasis to umbilicus (Sister Mary Joseph sign)
2) Multiple outcroppings of seborrheic keratoses (Leser-Trélat sign)
3) Acanthosis nigricans
4) Metastasis to left supraclavicular node (Virchow's node)
Where do gastric adenocarcinomas metastisize? how are they treated? What is 5 year survival rate?
1) Liver
2) lung
3) ovaries
4) Treatment: Surgery, local radiation, and chemotherapy
5) Approximately 10% to 15% overall 5-year survival rate
What is the most common site for extranodal malignant lymphoma? What cell type are the low grade lymphomas composed of? What is associated with low grade? What cell type is high grade?
1) stomach
2) Low-grade B-cell lymphoma
a. H. pylori-related
b. MALToma (derives from mucosa-associated lymphoid tissue)
2) High-grade B- or T-cell lymphomas
3) Treatment for H. pylori produces 50% cure rate.
A polypoid solid mass is found projecting into the stomach. What is it and what is it associated with?
1) intestinal type gastric adenocarcinoma
2) H pylori
Note: polypoid = fungating
How can peptic ulcer and adenocarcinoma be distinguished?
1) PUD = smooth base with nonelevated, punched out margins
2) carcinoma = irregular necrotic base with firm raised margins
leather bottle neck stomach is also known as?
1) linitis plastica and diffuse adenocarcinoma
2) extensive fibrosis
3) not associated with H pylori
Is the prognosis better for Maltoma or adenocarcinoma?
What percentage of ulcers are gastric and duodenal? Which is the occurrence of each in men and women? What are the associations of each? What percentage of each is caused by H pylori?
Gastric ulcer:
1) 25%
2) Male/female ratio 1:1
3) Smoking does not cause PUD but delays healing
4) ∼ 80% of cases from H pylori
Duodenal ulcer:
1) 75%
2) Male/female ratio 2:1
3) Risk increased with MEN I
Increased risk in cirrhosis, COPD, renal failure, hyperparathyroidism
4) 90-95% of cases from H pylori
What is the pathogenesis of duodenal ulcer vs gastric ulcer? How are BAO and MAO affected in each?
Gastric ulcer:
1) Defective mucosal barrier due to H. pylori
2) Mucosal ischemia (reduced PGE), bile reflux, delayed gastric emptying
3) BAO and MAO normal to decreased
Duodenal ulcer:
1) Defective mucosal barrier due to H. pylori
2) Increased acid production (increased parietal cell mass)
3) BAO and MAO both increased
Where are duodenal vs gastric ulcers located?
1) Single ulcer on lesser curvature of antrum (same location for cancer)
1) Single ulcer on anterior portion of first part of duodenum followed by single ulcer on posterior portion (danger of perforation into pancreas and pancreatitis)
What is the danger of a duodenal ulcer?
danger of perforation into pancreas and pancreatitis
What are complications of gastric vs duodenal ulcers?
1) Bleeding (most commonly in left gastric artery)
1) Bleeding (most commonly in gastroduodenal artery)
Perforation (air under diaphragm, pain radiates to left or right shoulder)
Gastric outlet obstruction, pancreatitis
is epigastric pain of a duodenal ulcer or a gastric ulcer relieved by eating?
1) gastric = worse with eating
2) duodenal better with eating
Is a barium swallow or an endoscopy more accurate in identifying PUD?
1) endoscopy 90-95%
2) Barium 70-80%
How is a gastric ulcer treated?
1) Nonpharmacologic:
a. stop smoking
b. avoid NSAIDs and alcohol
c. avoid foods causing symptoms
2) Pharmacologic:
a. eradication of H. pylori
b. H2 receptor antagonists
c. proton pump inhibitors
d. antacids
3) Surgery for resistant cases uncommon:
a. ulcer removal with antrectomy or hemigastrectomy without vagotomy
How is a duodenal ulcer treated?
1) Nonpharmacologic:
a. stop smoking
b. avoid NSAIDs
c. alcohol
d. avoid foods causing
2) Pharmacologic:
a. eradication of H. pylori
b. H2 receptor antagonists
c. proton pump inhibitors
d. antacids
3) Surgery for resistant cases uncommon:
a. highly selective vagotomy
Colicky pain is a sign of what?
1. Pain followed by a pain-free interval
a. Accompanied by constipation and inability to pass gas
2. Symptom of bowel obstruction
a. Example-adhesions from previous surgery
bloody diarrhea may be a sign of what small intestinal problems?
(1) Infarction
(2) Volvulus
(3) Dysentery
What is dysentery?
1) Refers to bloody diarrhea with mucus
2) Infection
what is melanosis coli?
black bowel from laxatives
What are causes of pain if produced in the large intestine?
1. Inflammatory bowel disease
2. Ischemic colitis
3. Diverticulitis
4. Appendicitis
5. Peritonitis
What is tenesmus? What is it commonly seen with?
1. Painful, ineffective straining at stool
2. Commonly present in ulcerative colitis
If someone has iron deficiency from a colon problem, what could be differential?
1) polyps
2) colorectal cancer
What is Hematochezia? What causes it?
1. Massive loss of whole blood per rectum)
2. Causes
a. Sigmoid diverticulosis (most common)
b. Angiodysplasia
Who is lactase deficiency most common in? What is deficient?
1) common genetic defect in Native Americans, Asians, and blacks
2) disaccharidase deficiency in brush border
What happens in lactose deficiency?
Colon anaerobes degrade undigested lactose into lactic acid and H2 gas leading to abdominal distention with explosive diarrhea
How is diarrhea classified?
1) More than 250 g of stool per day
2) Acute diarrhea is defined as less than 3 weeks
3) chronic diarrhea over 4 weeks
4) Invasive, osmotic, secretory types
What are tests used to distinguish osmotic diarrhea from secretory diarrhea? Invasive from noninvasive organisms?
1) Fecal smear for leukocytes (e.g., invasive diarrhea)
2) Stool osmotic gap
a. 300 mOsm/kg (value used to represent normal POsm) - 2 × (random stool Na+ + random stool K+)
b. Gap < 50 mOsm/kg from POsm is a secretory diarrhea.
** Indicates that diarrheal fluid approximates POsm (isotonic loss)
c. Gap > 100 mOsm/kg from POsm is an osmotic diarrhea (hypotonic loss)
** Indicates a hypotonic loss of stool due to presence of osmotically active substances
What is the definition of malabsorption?
1) Increased fecal excretion of fat plus
2) Concurrent deficiencies of fat-soluble vitamins, minerals, carbohydrates, and proteins
Pancreatic insufficiency is most often caused by? How is it different in adults and children?
1) chronic pancreatitis
2) Most commonly due to alcohol in adults and cystic fibrosis in children
Pathologically how does malabsorption occur with pancreatic insufficiency? Which nutrient is not affected?
1) Maldigestion of fats
(a) Due to diminished lipase activity
(b) Undigested neutral fats and fat droplets are in stool.
(2) Maldigestion of proteins
(a) Due to diminished trypsin
(b) Undigested meat fibers are in stool.
(3) Carbohydrate digestion is not affected.
(a) Amylase is present in salivary glands.
(b) Disaccharidases are present in the brush border of intestinal epithelium
What are bile salts and acids needed for?
Bile salts/acid are required to micellarize monoglycerides and fatty acids
List 5 causes that lead to malaborption from having decreased bile salt or bile acids?
(1) Inadequate synthesis of bile salts/acids from cholesterol (e.g., cirrhosis)
(2) Intrahepatic/extrahepatic blockage of bile
a. Examples-primary biliary cirrhosis, stone in common bile duct
(3) Bacterial overgrowth in small bowel with destruction of bile salts/acids
a. Examples-small bowel diverticula, autonomic neuropathy
(4) Excess binding of bile salts
a. Example-cholestyramine
(5) Terminal ileal disease
a. Prevents recycling of bile salts/acids
b. Examples-Crohn's disease, resection of ileum
micelles are absorbed in the small bowel. What are several conditions that prevent this and in turn lead to malabsorption?
(1) Inability to reabsorb micelles
a. Due to loss of villous surface
b. Examples-celiac disease (see later), Whipple's disease
(2) Lymphatic obstruction

* Examples-Whipple's disease, abetalipoproteinemia
What are screening tests for fat malabsorption?
1. Quantitative stool for fat
a. Best screening test
b. 72-hour collection of stool
c. Positive test > 7 g of fat/24 hours.
2. Qualitative stool for fat
a. Stains are used to identify fat in stool.
b. Lacks sensitivity
3. Decreased serum beta carotene
a. Precursor for fat-soluble retinoic acid (vitamin A)
4. d-Xylose screening test
a. Xylose does not require pancreatic enzymes for absorption.
b. Lack of reabsorption of orally administered xylose
c. Indicates small bowel disease
What screening tests for pancreatic insuficiency?
1) Serum immunoreactive trypsin
a. Trypsin is specific for the pancreas.
b. Serum immunoreactive trypsin in chronic pancreatitis is decreased
c. Increased concentration = excellent for early cystic fibrosis
2) CT scan of pancreas shows dystrophic calcification.
a. Sign of chronic pancreatitis
3) Functional tests
a. Secretin stimulation test (requires instrumentation)
** Tests ability of pancreas to secrete fluids and electrolytes
b. Bentiromide test
** Tests ability of pancreatic chymotrypsin to cleave orally administered bentiromide to para-aminobenzoic acid (measured in urine)
Increased concentration of what pancreatic marker in serum is an excellent way to diagnose cystic fibrosis?
What are tests for bile acid/salt deficiency?
1. Total bile acids can be measured.
a. Decreased in liver disease (e.g., cirrhosis)
2. Bile breath test (oral radioactive test)
a. Decreased amount radioactive cholylglycine in breath indicates bacterial overgrowth or terminal ileal disease
What are tests to determine bacterial overgrowth leading to malabsorption?
1. 14C-xylose
a. Most sensitive/specific test
b. Measures 14CO2 in the breath
2. Lactulose-H2
a. Measures H2 in the breath
Clinically what is found in someone that has a malabsorption problem?
1. Steatorrhea
a. Excessive, large, sticky, stools that float
2. Fat-soluble vitamin deficiencies
a. Fat-soluble vitamins are A, D, E, K
3. Water-soluble vitamin deficiencies
a. Particularly folate and vitamin B12
4. Combined anemias
a. Example-folate and iron deficiency
5. Ascites and pitting edema
a. Due to hypoproteinemia
What is celiacs disease? Who and when does it occur?
(1) Inappropriate immune response to gluten in wheat products
a. Also related proteins in rye and barley
(2) Prevalence of 1% in North America
(3) Common in whites; uncommon in blacks and Asians
(4) Occurs at any age
a. Highest incidence in infancy
** First introduction to gluten products
b. Third decade
** Frequent association with pregnancy
c. Seventh decade
What is Celiacs disease associated with?
(a) Dermatitis herpetiformis
(b) Autoimmune disease
** Hashimoto's thyroiditis, primary biliary cirrhosis
(c) Type 1 diabetes mellitus
(d) IgA deficiency
(e) Down syndrome, Turner's syndrome
Where in body does Celiacs disease effect? What are genetic associations? What enzyme and immune cells are involved?
(1) Multiorgan autoimmune disease
(2) Inappropriate T-cell and IgA-mediated response against gluten in genetically predisposed persons
a. Association with HLA-DQ2 (95%) and HLA-DQ8 (5%)
(3) Timing and dose when gluten introduced in the diet is important.
(4) Tissue transglutaminase (tTG; deamidating enzyme) in the lamina propria has a pivotal role.
Pathologically once gluten is ingested what happens?
(a) It deaminates mucosally absorbed gluten to produce deaminated and negatively charged gluten peptides.
(b) It also enhances the immunostimulatory effect of the deaminated gluten peptides.
(c) These peptides are phagocytosed by antigen-processing cells in the lamina propria.
(d) They are presented in complex with HLA-DQ2 or -DQ8 to gluten-specific CD4 T-helper cells.
(e) CD4 T cells produce cytokines that release matrix proteases causing cell death and degradation in the epithelial cells in the villi
What are several important diagnostic antibodies in Celiacs disease?
(1) Anti-tissue transglutaminase IgA (most important), IgG antibodies
a. Sensitivity and specificity 98%
b. Excellent screening test
(2) Anti-endomysial (EMA) IgA antibodies
a. Sensitivity and specificity 100%
b. Excellent screening test
(3) Antigliadin IgA, IgG antibodies
a. Sensitivity 80%, specificity 85%
b. Moderately good screening test
Clinically how are people affected by Celiacs disease? What are systemic findings?
(1) Steatorrhea
(2) Weight loss
(3) Failure to thrive in infants and children
(4) Pallor due to anemia (often combined anemias)
(5) Dermatitis herpetiformis
(6) Findings related to water-soluble and fat-soluble vitamin deficiencies
(7) Other systemic findings
(a) Bone-osteoporosis, arthritis
(b) CNS-seizures, depression
(c) Reproductive-delayed puberty, miscarriages, infertility
What is dermatitis herpetaformis considered? What occurs in bowel? Are antibodies present?
a. Considered to be a form of celiac disease
b. Villous atrophy in 75% of cases with or without diarrhea
c. Low levels of above diagnostic antibodies
Note: pruitic papules and vesicles with deposits of IgA at tips of dermal papillae
How is Celiacs diagnosed?
(1) Anti-tissue transglutaminase IgA (most important), IgG antibodies
(2) Anti-endomysial (EMA) IgA antibodies
(3) Antigliadin IgA, IgG antibodies
(4) Endoscopic biopsy
a. Flattened villi, particularly in duodenum and jejunum
b. Hyperplastic glands with intense lymphocytic inflammation
How is Celiacs treated?
(1) Gluten-free diet
(2) Correct nutritional deficiencies
a. All fat-soluble vitamins; folate, vitamin B12; calcium
(3) Corticosteroids in refractory cases
Who does Whipples disease occur in? What causes it? How is it detected?
1) Occurs in men more commonly than women
2) Peak incidence in middle age
3) Caused by Tropheryma whippelii
a. Identified by polymerase chain reaction
What are microscopic features of Whipples disease?
(a) Blunting of villi
(b) Foamy PAS-positive macrophages in lamina propria
(c) Macrophages obstruct lymphatics and reabsorption of chylomicrons
(d) Malabsorption of fats
A child presents with weight loss, weakness, diarrhea and pale, bulky, frothy and foul smelling stools. He has growth retardation. Mother says that he eats normal things like cereal. What is suspected?
Clinically how does someone with Whipples disease present?
(a) Steatorrhea
(b) Fever
(c) Recurrent polyarthritis
(d) Generalized lymphadenopathy
(e) Increased skin pigmentation
(f) cardiac and neurologic symptoms
Note: gram +, PAS + macrophages in intestinal lamina propria and mesenteric nodes,
Note: occurs more in older men
Where in GI tract is the most common site for obstruction? What are radiographic findings?
1) small bowel
1) Bowel distention
2) Air-fluid levels with a step-ladder appearance
3) Absence of air distal to obstruction
What are clinical findings in bowel obstruction?
1. Colicky pain
a. Severe pain alternating with pain free intervals
2. Abdominal distention
3. No rebound tenderness
4. Tympanitic to percussion
5. High-pitched tinkling sounds
what is the most common cause of small bowel obstruction?
adhesions after surgery
What is the most common hernia?
indirect inguinal
Is the Small bowel or large bowel more likely to have ischemic damage? Most of the small bowel is supplied by what artery?
1) small bowel
2) SMA
What areas of GI does the SMA supply?
(1) Most of the small bowel
(2) Ascending and transverse colon
(3) SMA and inferior mesenteric artery (IMA) overlap at the splenic flexure.
Where is the point in the bowel where the SMA and IMA meet?
Splenic flexure is a watershed area
What are the types of infarctions in the small bowel? How does each occur?
1. Transmural
a. Full-thickness hemorrhagic infarction
b. Usually involves all or part of the small bowel
c. Usually due to occlusion of SMA
2. Mural and mucosal infarctions
a. Usually occur in hypoperfusion states (e.g., shock)
What are causes of acute mesenteric ischemia of small bowel? note this is 50% of mesenteric ischemia!
(1) Embolism from the left side of the heart to the SMA
a. Atrial fibrillation is the most common predisposing arrhythmia.
(2) Thrombosis of the SMA
What are causes of nonocclusive ischemia of the small bowel?
(1) Hypotension secondary to heart failure (most common)
(2) Hypovolemic shock
(3) Patient taking digitalis (? vasospasm)
What are causes of mesenteric vein thrombosis?
(1) Thrombosis states
a. Polycythemia vera
b. Antiphospholipid syndrome
(2) Extension of renal cell carcinoma into vena cava
Clinically what is seen with a small bowel infarct? Who does it usually occur in?
1) Sudden onset of diffuse abdominal pain
a. Pain disproportionate to physical findings
2) Bowel distention
3) Bloody diarrhea
4) Usually occurs in an elderly patient
5) Absent bowel sounds (ileus)
6) No rebound tenderness (peritonitis) early in infarction
7) Profound neutrophilic leukocytosis
8) Positive stool guaiac
What are radiographic findings with a small bowel infarct?
(1) "Thumbprint sign" due to edema in bowel wall
(2) Bowel distention with air-fluid levels similar to bowel obstruction
What is best diagnostic test for small bowel infarct? How is it treated?
1) Abdominal CT scan has 90% sensitivity.
2) Treatment
a. Surgery for embolic disease
b. Thrombotic disease = Anticoagulation and surgery if necessary
Where does ischemic colitis occur? What is pathogenesis? When does pain occur? What fear develops?
1) Involves the splenic flexure of the large bowel
a. Watershed area of SMA and IMA
2) Atherosclerotic narrowing of SMA causes mesenteric angina.
a. Severe pain occurs in splenic flexure shortly after eating.
b. Patient loses weight for fear of pain related to eating.
What are 2 major findings in ischemic colitis with infarction?
mesenteric angina + bloody diarrhea
What are clinical findings in ischemic colitis? What is diagnostic sign? what happens after it is repaired?
(1) History compatible with mesenteric angina
(2) Pain localized to the splenic flexure after eating
a. Accompanied by bloody diarrhea due to mucosal or mural infarction
(3) Barium study shows "thumb-printing" of the colonic mucosa
a. Due to edema of the mucosa
(4) Normal repair of infarction site may result in fibrosis.
a. Common cause of ischemic strictures and obstruction
Note: people develop weight loss
Where does angiodysplasia of GI occur? Who does it occur in?
1) Dilation of mucosal and submucosal venules in cecum and right colon
a. Usually occurs in elderly individuals
b. Vascular ectasias in the cecum increase with age.
2) Increased wall stress in the cecum stretches the venules
What is the main clinical finding in angiodysplasia of cecum? What is it associated with?
(1) Hematochezia
(2) Association with von Willebrand disease (vWD) and calcific aortic stenosis
How is angiodysplasia of cecum treated?
(1) Colonoscopy
a. Identifies lesions
b. Cautery of lesions
(2) Angiography localizes the disease
(3) Right hemicolectomy
(4) Correction of aortic stenosis (if present)
a. Bleeding often abates
Meckel diverticulum is a remnant of what? Is it a true or false diverticulum? Where is it located?
1) Vitelline (omphalomesenteric) duct remnant
a. True diverticulum
2) Mnemonic: 2 inches long, 2 feet proximal from ileocecal valve, 2% of population, 2% symptomatic
what does meckels diverticulum frequently have in it? What is there increased risk of?
1) Contains pancreatic rests and heterotopic gastric mucosa
a. Increase the risk for bleeding
Clinically how does Meckels diverticulum present? how can it be distinguished from an appendicitis?
(1) Newborn finding
a. Fecal material in umbilical area due to persistence of vitelline duct
(2) Bleeding (most common finding)
a. Common cause of iron deficiency in newborns and young children
(3) Diverticulitis
a. Clinically impossible to distinguish Meckel diverticulitis from appendicitis
How is Meckels diverticulum diagnosed? What can it be associated with?
1) 99mTc nuclear scan identifies parietal cells in ectopic gastric mucosa
Occasional associations:
1) intussusception = invagination of a proximal segment of bowel into more distal segment
2) volvulus = twisting of a portion of GI tract about itself
3) bleeding
4) obstruction near terminal ileum
Note: Meckels is persistence of vitelline duct or yolk stalk in contrast to omphalomesenteric cyst = cystic dilation of vitelline duct
A Newborn has fecal material in umbilical area. What do you suspect?
persistence of vitelline duct
Small bowel pulsion diverticula most often occur where? If it is wide-mouthed what does it suggest? What are complications?
1. Duodenum is most common site.
a. Wide-mouthed diverticula suggests systemic sclerosis.
2. Complications:
a. Diverticulitis (danger of perforation)
b. Bacterial overgrowth
** May produce bile salt deficiency and vitamin B12 deficiency
What is a Colovesical fistula? what is it associated with?
1) connection between large bowel and the bladder
a. is a common fistula in the gastrointestinal tract.
2) It is associated with pneumaturia (air in urine) and recurrent urinary tract infections
What is the Most common site for diverticula in entire gastrointestinal tract? Who does it occur in?
1) sigmoid colon
2) Incidence in general public is 35% to 50%
3) Incidence increases with age
What is pathogenesis of a colonic diverticulum? Where is area of weakness?
1) Due to a low-fiber diet with increased constipation
2) Sigmoid colon most common site
3) Area of weakness is where vasa recta penetrate the muscular propria.
a. Diverticulum is juxtaposed to a blood vessel.
Sigmoid diverticular disease is most often due to?
constipation most common cause
What are colonic diverticula associated with?
(1) Marfan syndrome
(2) Ehlers-Danlos syndrome
(3) Adult polycystic kidney disease
What is the most common complication sigmoid diverticulosis? How is it caused?
1) Diverticulitis
2) Caused by stool impacted (fecalith) in diverticulum sac
a. Produces ulceration and ischemia
Clinically how does diverticulitis present?
(a) Fever
(b) Diarrhea initially followed by constipation
(c) Left lower quadrant pain ("left-sided appendicitis")
(d) Tender mass can be palpated in some cases
Someone presents with left sided lower quadrant pain and history of constipation. What do you suspect?
How is diverticulitis diagnosed? What are risks?
1) Best diagnosed with CT scan or water-soluble barium study
2) Increased risk for perforation and abscess formation
How does diverticulosis present?
1) Painless bleeding
2) often massive (hematochezia)
Are hematochezia and fistulas associated with diverticulitis or diverticulosis? why?
(1) Refers to diverticulosis not diverticulitis
(2) Scarring of the vessel in diverticulitis prevents bleeding
How is a sigmoid diverticulum treated?
1. Nonpharmacologic
a. Increase fiber in diet to prevent constipation
2. Antibiotics for acute disease
3. Colonic resection in selected cases
a. Examples-repeated episodes diverticulitis; bleeding that does not stop; abscess/fistula formation; obstruction
What is intermediate colitis?
Features of ulcerative colitis and Crohn's disease
What are causes of IBS?
1) Intrinsic colonic motility disorder
a. Possible loss of tolerance to gastrointestinal flora
b. Possible genetic factors
c. Environmental triggers
What is the Most common functional bowel disorder that is responsible for 50% of gastroenterology visits? what are risk factors?
1) IBS
(1) History of childhood sexual abuse
(2) Domestic abuse in women
(3) Increased stress, depression, personality disorder
How is IBS characterized?
1) Alternating bouts of diarrhea and constipation
2) Abdominal pain and bloating relieved by defecation
3) Stools accompanied by mucus
4) Abnormal defecation
a. Straining
b. Sense of incomplete evacuation
What is seen in IBS with flexible sigmoidoscopy/colonoscopy
nothing it is normal
How is IBS treated pharmacologically and non-pharmacologically?
1. Nonpharmacologic
a. Mainstay is adequate fiber intake.
b. Eliminate foods that aggravate
c. Examples-coffee, fatty foods, dairy products
2. Pharmacologic:
a. Antispasmodics-anticholinergics
b. Example-dicyclomine
c. Loperamide is effective for diarrhea.
** Loperamide is an opioid-receptor agonist and acts on the μ-opioid receptors in the myenteric plexus of the large intestine
d. Lubiprostone (chloride channel activator) is effective for constipation.
e. Rifaximin is effective if small bowel bacterial overgrowth is documented.
Where is the least common site for a primary malignancy in GI tract? Where is the most common site for a primary adenocarcinoma of small bowel?
1) small bowel
2) Duodenum most common site
what is the Most common small bowel malignancy? What do tumor cells contain? They invade or metastisize depending on where they are found in GI tract. So which invade and which metastisize?
1) carcinoid tumor
2) Contains neurosecretory granules visible on electron microscopy
3) Carcinoid tumors are malignant.
4) Metastatic potential correlates with size and depth.
a. Size > 2 cm
b. Depth of invasion (∼50% of bowel thickness)
4) Foregut (e.g., stomach) and hindgut (e.g., rectum) carcinoid tumors
a. Invade but rarely metastasize
5) Midgut carcinoid tumors (e.g., terminal ileum)
a. Invade and metastasize
Where is the most common site for a carcinoid tumor in GI tract? Do they metastisize?
(1) Vermiform appendix
a. Most common site (40%)
b. Usually <2 cm, which is too small to metastasize to liver
Where in the small bowel is a carciniod tumor likely found? Do they metastisize?
(a) Majority in terminal ileum
(b) Commonly metastasize to liver
If a carcinoid tumor is present in the ileum how is the clinical presentation different than if it were in site outside of the GI tract? Why is it different?
1) Tumor produces bioactive compounds (e.g., serotonin)
a. Compounds are delivered to the liver by the portal vein.
2) Serotonin is metabolized to 5-hydroxyindoleacetic acid (5-HIAA).
a. 5-HIAA is excreted in the urine.
3) Serotonin is completely metabolized and does not enter the systemic circulation.
a. No signs or symptoms of carcinoid syndrome
4) if in another site carcinoid syndrome would be present
Where are main sites in GI tract of carcinoid tumor?
1) vermis appendix most common
2) ileum 2nd most common
3) esophagous
4) stomach
5) colon
On gross exam how does a carcinoid tumor look? For carcinoid syndrome to be seen from carcinoid tumor in ileum what has to happen?
1) Bright yellow tumor
2) For gut origins (e.g., terminal ileum) of the carcinoid tumor, liver metastasis must occur to produce the syndrome.
3) Serotonin is secreted by metastatic tumor nodules.
4) Serotonin entering hepatic vein tributaries gains access to the systemic circulation.
5) May occur without metastasis if located in the bronchus (rare)
Clinically what is the presentation of a carcinoid tumor? How is heart effected?
1) Due to serotonin and other bioactive compounds (e.g., histamine, bradykinin)
2) Flushing of the skin (75-90%)
a. Due to vasodilation; may be triggered by emotion, alcohol, other foods
3) Diarrhea (>70%)
a. Increased bowel motility
4) Intermittent wheezing and dyspnea (25%)
a. Due to bronchospasm
5) Facial telangiectasia
6) Tricuspid regurgitation and pulmonary stenosis
a. Serotonin increases collagen production in the valves.
How is carcinoid tumor diagnosed?
(a) Increase in urine 5-HIAA
(b) CT scan of liver to detect metastasis
(c) Scanning techniques to detect primary location and metastasis
How is a carcinoid tumor treated?
(a) Avoid alcohol
(b) Surgical resection of primary tumor
(c) Chemotherapy
(d) Somatostatin analogue
a. Effective in controlling diarrhea and flushing
Where does primary lymphoma predominately occur? What type of lymphoma is it usually?
1) usually in Peyer's patches in terminal ileum
2) Usually B-cell origin (e.g., Burkitt's lymphoma)
Where is the most common site for gastrointestinal polyps, diverticula, cancer?
sigmoid colon
What are examples of non-neoplastic polyps?
1) Hyperplastic polyp
2) Juvenile (retention) polyps
3) Peutz-Jeghers polyposis (PJP)
Who do hyperplastic polyps occur in? Where? What is histologic feature?
(1) Most common type in adults
(2) Majority are in the sigmoid colon.
(3) No malignant potential or polyposis syndromes
(4) Histologically have a "sawtooth" appearance
What is the most common polyp in children? where are they located? How do they present? What is cronkhite-canada syndrome?
(1) Juvenile (retention) polyps
(2) Located in the rectum
a. Sometimes prolapse out of the rectum and bleed
(3) Solitary polyp
a. Smooth surface with enlarged cystic spaces on cut section
(4) Juvenile polyposis
a. Autosomal dominant or nonhereditary
(5) Cronkhite-Canada syndrome
(a) Nonhereditary polyposis syndrome
(b) Polyps plus ectodermal abnormalities of the nails
What are genetics of Peutz-Jeghers polyposis? Where do they occur? What are clinical findings?
(1) Autosomal dominant
(2) Hamartomatous polyps predominate in the small bowel
a. Less common in stomach and colon
(3) Clinical findings:
a. Mucosal pigmentation of buccal mucosa, lips
b. Increased risk (>50%) for colorectal, breast, gynecologic cancers
** This is true even though the GI polyps are hamartomas
Neoplastic polyps are also called adenomas. What increases risk? Do they occur more in men or women?
1) Premalignant dysplastic colonic polyps
a) Increase with age
b) Equal sex incidence
What is the Most common polyp? How do they look? Where are they most common?
(1) Tubular adenoma (adenomatous polyps) (60% of polyps)
(2) Sigmoid colon is most common site.
(3) Stalked polyp
a. Looks like a mushroom
b. Sections show complex branching of glands (adenomatous change)
What are neoplastic polyps?
1) tubular adenoma = low malignancy potential
2) tubulovillous adenoma = intermediate malignancy potential
3) villous adenoma = high malignancy potential
How is tubulovillous adenoma characterized?
(1) Usually stalked polyp
(2) Adenomatous and villous change (similar to small bowel villi)
How are villous adenomas characterized? where are they located? what can they secrete?
(1) Sessile polyp (no stalk) with primarily a villous component
(2) Rectosigmoid location
(3) Secrete protein and potassium-rich mucus
a. Can produce hypoalbuminemia and hypokalemia
What are risk factors for malignancy of neoplastic polyps?
(1) Adenoma > 2 cm (40% risk of malignancy)
(2) Multiple polyps
(3) Polyps with increased villous component
a. Villous adenomas have a 30% to 40% risk for malignancy.
Peutz-jegher polyps have no malignant potential themselves but the syndrome is associated with what?
1) adenocarcinoma of colon
2) malignancy of stomach, ovaries and breasts
What are genetics of FAP?
(1) Autosomal dominant (AD) chromosome 5 APC gene
a. All patients develop tubular adenomas and cancer. (complete penetrance)
b. Polyps begin to develop between 10 and 20 years of age.
(2) Inactivation of adenomatous polyposis coli (APC) suppressor gene
When does malignant transformation occur in FAP? What is prophylaxis? What is it associated with?
1) Malignant transformation usually occurs between 35 and 40 years of age.
a. Prophylactic colectomy is recommended.
2) Associated with congenital hypertrophy of retinal pigment epithelium
What is gardners syndrome?
(a) AD polyposis syndrome
(b) Additional findings include benign osteomas and desmoid tumors.
(c) retinal hyperplasia
What are genetics of turcot's polyposis? What are findings?
(a) Autosomal recessive (AR) polyposis syndrome
(b) Additional finding of malignant brain tumors
** Astrocytoma and medulloblastoma
(c) FAP+
Who is ulcerative colitis vs crohns disease more common in? What ages?
1) More common in whites than blacks
2) No sex predilection
3) Occurs between 14 and 38 years of age
1) More common in whites than blacks, in Jews than non-Jews
2) No sex predilection
3) majority between 11 and 35
What lowers the incidence of UC but increases incidence of crohns?
1) Lower incidence in smokers and other nicotine users
2) Lower incidence if previous appendectomy <20 years old
1) Smoking is a risk factor
How are crohns and UC different in the depth of tissue affected?
1) Mucosal and submucosal
1) Transmural
How does the location differ between UC and Crohns?
1) Mainly rectum (usually begins in this location)
2) Extends continuously into left colon (may involve entire colon)
3) Does not involve other areas of GI tract
1) Terminal ileum alone (30% of cases), ileum and colon (50% of cases), colon alone (20% of cases)
2) Involves other areas of GI tract (mouth to anus)
How are UC and Crohns different on gross appearance?
1) Inflammatory pseudopolyps
2) Areas of friable, bloody residual mucosa
3) Ulceration and hemorrhage
4) lead pipe sign on barium swallow
1) Thick bowel wall and narrow lumen (leads to obstruction)
2) Aphthous ulcers in bowel (early sign)
3) Skip lesions, strictures, fistulas
4) Deep linear ulcers with cobblestone pattern
5) Fat creeping around serosa
6) discrete non-caseating granulomas in some cases
7) string sign on barium swallow
How does the microscopic appearance of Crohns differ from UC? Which has a higher risk of cancer?
1) Ulcers and crypt abscesses containing neutrophils
2) Dysplasia or cancer may be present
1) Noncaseating granulomas (60% of cases), lymphoid aggregates
2) Dysplasia or cancer less likely
What are clinical manifestations of ulcerative colitis? What are extragastroinestinal symptoms? What antibody is seen?
1) Recurrent left-sided abdominal cramping with bloody diarrhea and mucus
2) Fever, tenesmus, weight loss
3) Extragastrointestinal:
a. primary sclerosing cholangitis (UC > CD)
b. erythema nodosum = an inflammation of the fat cells under the skin (panniculitis) usually on shins
c. iritis/uveitis (CD > UC)
d. pyoderma gangrenosum HLA-B27 positive arthritis
e. p-ANCA antibodies > 45% of cases
Clinically how does Crohns present? What genetic association is there?
1) Recurrent right lower quadrant colicky pain (obstruction) with diarrhea
2) Bleeding occurs only with colon or anal involvement (fistulas; abscesses)
3) Apthous ulcers in mouth
4) Extragastrointestinal:
a. erythema nodosum
b. sacroiliitis (HLA-B27 association)
c. pyoderma gangrenosum
d. iritis (CD > UC)
e. primary sclerosing cholangitis (UC > CD)
f. migratory polyarthritis
g. ankylosing spondylitis
Does primary cholangitis occur more in Crohns or UC? Does iritis and uveitis occur more in Crohns or UC?
1) UC
2) Crohns
Radiography can distinguish UC and Crohns how?
1) "Lead pipe" appearance in chronic disease
1) "String" sign in terminal ileum from luminal narrowing by inflammation, fistulas
What are complications of UC vs Crohns? What is there increased risk of in UC?
1) Toxic megacolon (hypotonic and distended bowel)
2) Adenocarcinoma: greatest risks are pancolitis, early onset, duration of disease > 10 years)
1) Fistulas, obstruction, colon cancer (UC > CD)
2) Calcium oxalate renal calculi (increased reabsorption of oxalate through inflamed mucosa)
3) Malabsorption due to bile salt deficiency
4) Macrocytic anemia due to vitamin B12 deficiency
How is UC treated?
1) Sulfasalazine or mesalamine (5-ASA active metabolite; O2 free radical scavenger; inhibits lipoxygenase pathway in arachidonic acid metabolism)
2) Corticosteroids for severe disease (systemically or enemas)
3) Nicotine patch
4) Immunosuppressants:
a. azathioprine or cyclosporine
5) Surgery: colectomy with ileostomy usually cures
How is Crohns treated?
1) Sulfasalazine or mesalamine (5-ASA; oral salicylate)
2) Corticosteroids for moderate to severe disease
3) Steroid analogues that target areas of GI tract (e.g., budesonide)
4) Immunosuppressants:
a. azathioprine or cyclosporine
5) Metronidazole for colonic fistulas
6) TNF inhibitors for enterocutaneous fistulas
7) Surgery for obstruction, fistulas, toxic megacolon, refractory disease
Crohns disease is also known as? If Crohns is occurring in the colon what is one feature if absent that will make it indistinuishable from UC?
1) regional enteritis
2) lack of granulomas
What is the Third most common cancer-related death in adults? How is the incidence changing? What age is peak incidence?
1) colon cancer
2) Incidence rates have been decreasing.
a. Increase in screening (fecal occult blood test, colonoscopy)
3) Peak incidence is in the seventh decade.
How are rectal and colon cancers detected?
1) Rectal cancers
a. Approximately 50% are detected by digital rectal examination.
2) Colon cancers
a. Approximately 50% are detected by flexible sigmoidoscopy.
What are risk factors for colon cancer?
(1) Age > 50 years old
(2) Cigarette smoking
(3) Obesity, physical inactivity, heavy alcohol intake
(4) Hereditary polyposis syndromes
(5) Hereditary nonpolyposis colon cancer
(6) Family cancer syndrome
(7) First-degree relatives with colon cancer
(8) Inflammatory bowel disease
a. Ulcerative colitis > Crohn's disease
(9) Dietary factors
a. Low-fiber diet; increased saturated fats; reduced vegetable intake
How does the carcinogenesis of colon cancer occur?
1) Adenoma-carcinoma sequence
a. Sequential mutations of different genes
b. APC, RAS, TP53
c. Accounts for 80% of sporadic colon cancers
2) Inactivation of DNA mismatch genes
What are the most frequent sites of colon cancer?
1. Rectosigmoid (50% of cases)
2. Ascending colon (15% of cases)
3. Descending colon (15% of cases)
4. Transverse colon and cecum (each 10% of cases)
How does the fecal occult blood test work? Can it distinguish hemoglobin from myoglobin? Is it sensitive or specific for colon cancer?
(1) Not very sensitive or specific for colon cancer
a. Does not distinguish hemoglobin from myoglobin
(2) Tests are based on the peroxidase activity of heme in Hb.
a. Myoglobin also has peroxidase activity.
(3) Peroxidase catalyzes the oxidation of a reagent (guaiac) by peroxide.
a. Reaction produces a color change
Why is there a varying level of sensitivity and specificity with a fecal occult blood test?
(1) False positive results
a. Myoglobin in meat
b. Plant peroxidases (e.g., radishes)
(2) False negative results
(3) Newer tests detect hemoglobin
Colonoscopy is the gold standard for colon cancer. When should it begin? what about if 1st degree relative has polyps or colorectal cancer?
(1) Start at age 50 if no risk factors
(2) Every 3 to 5 years if history of polyp removal
(3) Begin at age 40 if first-degree relative has polyps or colorectal cancer
Clinically what are findings if colon cancer occurs on the left?
(1) Tend to obstruct
a. Bowel diameter is smaller than right colon.
b. Lesions have an annular, "napkin-ring" appearance
(2) Change in bowel habits
a. Constipation and diarrhea with or without bleeding
b. Bright red blood coats the stool
(3) Streptococcus bovis endocarditis
Clinically what are findings in right sided colon cancer?
(1) Tend to bleed
a. Bowel diameter is greater than left colon.
b. Tumors are more polypoid in appearance.
(2) Blood is mixed in with stool.
(3) Iron deficiency is more likely than in left-sided cancer.
Where does colon cancer metastisize?
1) Liver (most common)
2) lungs
3) bone
4) brain
how is colon cancer prevented?
1. Aspirin and other NSAIDs
a. Decreases incidence of colorectal adenomas
2. Annual fecal occult blood testing
3. Estrogens and progestins
a. May reduce colorectal cancer risk
4. Dietary alterations
a. Decrease fat intake to 30% of total caloric intake
b. Increase fiber
c. Increase intake of fruits and vegetables
5. ? Statins
a. May inhibit growth of colon cancer lines
6. Cessation of smoking
What is the 5 year prognosis of colon cancer? What is used to monitor recurrences?
1) Five-year relative survival rate ∼65%
2) Serum carcinoembryonic antigen (CEA) is used to detect recurrences
What is the most common abdominal surgical emergency?
1) acute appedicitis
2) Occurs in 10% of the population
What is the pathogenesis of appedicitis in children?
1. Lymphoid hyperplasia (60% of cases) often secondary to a viral infection
2. Examples-adenovirus, measles virus infection or immunization
What is the pathogenesis of appendicitis in adults? What are primary pathogens?
1. Fecalith obstructs the proximal lumen
a. Increased intraluminal pressure causes mucosal injury and bacterial invasion.
2. Other causes
a. Seeds (sunflower, persimmons), pinworm infection
3. Primary pathogens are Escherichia coli (most common) and Bacteroides fragilis.
Where does pain with an appendicitis initially present? Where does it shift? What nerve fibers are involved based on where pain is? Which fibers localize pain?
1) Initial colicky periumbilical pain (50%)
a. Irritation of unmyelinated afferent C fibers on visceral peritoneal surface
b. Refer pain to the midline
2) Pain shifts to right lower quadrant (RLQ) in 12 to 18 hours.
a. Irritation of Aδ fibers on parietal peritoneum
** Localizes pain to the exact location
b. Rebound tenderness at McBurney's point (Blumberg's sign)
c. Pain with right thigh extension (psoas sign)
d. RLQ pain with palpation of left lower quadrant (Rovsing's sign)
Clinically how does appendicitis present?
1) Initial colicky periumbilical pain (50%)
a. type c fibers localize to midline
2) fever
a. Very important sign for identifying appendicitis in children with abdominal pain
3) Nausea, vomiting, and fever
a. Pain precedes nausea and vomiting
4) Cutaneous hyperesthesia at level of T12
5) Pain shifts to right lower quadrant (RLQ) in 12 to 18 hours
a. localizes pain via delta nerves
6) Signs of a lower urinary tract infection may occur.
a. Increased frequency
b. Dysuria
What are special tests that and signs used to indicate appendicitis?
1) Rebound tenderness at McBurney's point (Blumberg's sign)
2) Pain with right thigh extension (psoas sign)
3) RLQ pain with palpation of left lower quadrant (Rovsing's sign)
What are laboratory findings with an appendicitis?
(1) Neutrophilic leukocytosis with left shift (90%)
(2) Abnormal urinalysis:
a. Increased protein, hematuria, pyuria
What radiologic sign is seen on with a retrocecal appendicitis? What is the disorder?
1. Radiograph shows a sentinel loop in the RLQ
2. Localized ileus (lack of motility) from subjacent appendicitis
What are complications of appendicitis?
1) Periappendiceal abscess with or without perforation
a. Most common complication
b. May develop subphrenic abscess
** Usually due to Bacteroides fragilis
2) Pyelophlebitis
a. Infection of the portal vein
b. Danger of portal vein thrombosis
c. Radiograph shows gas in the portal vein.
3) Subphrenic abscess
a. Persistent fever postoperative
b. Diaphragm fixed on the right; right-sided pleural effusion
c. Tenderness over lateral seventh and eighth ribs
How is a subphrenic abscess from an appendicitis diagnosed and treated?
1) Diagnosis
a. Ultrasound, CT scan, gallium scan
2) Treatment
a. Extraperitoneal drainage and antibiotics
How is appendicitis diagnosed in addition to the PE?
1. Clinical examination
2. Spiral CT RLQ after Gastrografin enema
a. Sensitivity 90% and specificity 94%
3. Plain CT scan with rectal contrast agent
4. Ultrasonography
a. Sensitivity 75% and specificity 90%
How is an appendicitis treated?
1. Appendectomy
2. Cefoxitin
a. Given prophylactically perioperatively if perforation suspected
What are several disorders that mimic appendicitis?
1) viral gastroenteritis
2) ruptured follicular cyst
3) ruptured ectopic pregnancy
4) mesenteric lymphadenitis
5) Meckel's diverticulitis.
Shigella causes what type of diarrhea? how is it diagnosed?
1) invasive
2) invades in enterocytes
3) Fecal smear for leukocytes: positive in most cases
Campylobacter jejuni causes what type of diarrhea? How can it be diagnosed?
1) Invasive
2) low-volume
3) Fecal smear for leukocytes: positive in most cases
Entamoeba histolytica causes what type of diarrhea? How is it diagnosed?
1) invasive
2) Diarrhea with blood and leukocytes (i.e., dysentery)
3) Order stool culture and stool for O&P look for RBCs inside organism
Secretory diarrhea with a Loss of isotonic fluid and is High-volume diarrhea is caused by what?
1) Laxatives: danger of melanosis coli (black bowel syndrome) with use of phenanthracene laxatives
2) Production of enterotoxins:
a. Vibrio cholerae
b. Enterotoxigenic E. coli
c. Increased serotonin: carcinoid syndrome
What are several pathologic mechanisms that lead to secretory diarrhea? Is there inflammation of the bowel in secretory diarrhea?
1) Laxatives
2) Enterotoxins stimulate Cl- channels regulated by cAMP and cGMP
3) Serotonin increases bowel motility (carcinoid tumor)
4) No inflammation in bowel mucosa
In secretory diarrhea are there fecal leukocytes? If carcinoid tumor is present what metabolite is found? What is stool osmotic gap?
1) Fecal smear for leukocytes: negative
2) Increased 5-HIAA: carcinoid syndrome
3) Stool osmotic gap < 50 mOsm/kg
What is occurring with an osmotic diarrhea? Is it high or low volume? Is there inflammation?
1) Osmotically active substance is drawing hypotonic salt solution out of bowel
2) High-volume diarrhea
3) No inflammation in bowel mucosa
What are a few causes of osmotic diarrhea?
1) Disaccharidase deficiency
2) "Stunned gut" in giardiasis
3) Ingestion of poorly absorbable solutes (e.g., magnesium sulfate laxatives)
Will a fecal smear show leukocytes with osmotic diarrhea? What will stool osmotic gap be?
1) Fecal smear for leukocytes: negative
2) Stool osmotic gap > 100 mOsm/kg
In Who and when does CMV cause diarrhea? How is it treated?
1) Common cause of diarrhea in AIDS when CD4 TH cell count < 50-100 cells/mm3
3) Treatment: ganciclovir
What is the Most common cause of adult gastroenteritis? What are symptoms? When do they resolve? How is it transmitted? How is it treated?
1) Norwalk virus
2) Nausea, vomiting, diarrhea that resolves in 12-24 hours
3) Occasionally can be fatal
4) Fecal-oral transmission
5) Common infection on cruise ships
6) Treatment: supportive
What is the Most common cause of childhood diarrhea? How is it transmitted? What is pathogensis? How is it diagnosed and treated?
1)Rotavirus particularly occurs in winter months
2)Fecal-oral transmission
3) Damages ion transport pump in small intestine; secretory diarrhea
4) Rotazyme test on stool establishes diagnosis
5) Rotavirus vaccine highly effective in prevention; oral vaccine
6) Treatment: oral hydration; nitazoxanide
What type of bacteria is bacillus cereus? where is it found? what is it associated with? How is it treated?
1) Gram-positive rod
2) Food poisoning with preformed toxin
3) Associated with reheated fried rice or tacos
4) Self-limited
What is the Most common food-borne illness and invasive enterocolitis in United States? what are reservoirs? How is it transmitted? Treated?
1) campylobacter jejuni = Curved or S-shaped gram-negative rod
2) Animal reservoirs: cattle, chicken, puppies (common source for children)
3) Transmission fecal-oral via contaminated water, poultry, or unpasteurized milk
4) Treatment: azithromycin or erythromycin
Clinically how does campylobacter jejuni present?
1) Invasive and secretory enterocolitis:
a. dysentery (bloody diarrhea) with crypt abscesses and ulcers resembling ulcerative colitis
b. high fever and cramping abdominal pain
c. organisms in stool with blood and leukocytes
What are complication of a C jejuni infection?
1) Guillain-Barré syndrome (antibodies cross-react with neurons)
2) hemolytic uremic syndrome
3) HLA-B27 positive seronegative spondyloarthropathy
Clostridium botulinum is what type of bacteria? What is pathogenesis and findings if toxin eaten? how is it treated? What happens if it occurs in a baby?
1) Gram-positive rod
2) Adult food poisoning with preformed toxin (blocks release of acetylcholine release in presynaptic terminal of neuromuscular junction in autonomic nervous system
3) causes descending paralysis, mydriasis, dry mouth
4) Treatment: trivalent antitoxin
5) Infant food poisoning often contracted by eating spores in honey (lack protective bacteria); floppy baby with constipation
What is the the most common cause of nosocomial diarrhea? what is it associated with? What type of diarrhea? when does carrier rate increase?
1) C difficile = Gram-positive rod
2) Associated with pseudomembranous colitis
3) secretory type of diarrhea
4) Normally present in 3% of people
5) carrier rate increases to >20% in hospitalized patients (related to contact with spores in environment and fecal-oral contamination)
C difficile diarrhea is caused by what in the majority of cases? What is pathogenesis? What is end result?
1) Antibiotic-induced in 65-90% of cases
a. antibiotics (e.g., ampicillin, quinolones, clindamycin) cause overgrowth of toxin-producing C. difficile in colon
b. toxins A and B release proinflammatory mediators and cytokines that attract neutrophils and stimulate excess fluid secretion (watery diarrhea)
2) Pseudomembrane covers colon mucosa
a. composed of cellular debris, leukocytes, fibrin, and mucin
What are specific and nonspecific lab findings with C difficile? How is it treated?
1) Nonspecific lab findings:
a. neutrophilic leukocytosis with left shift
b. fecal leukocytes
c. decreased serum albumin
2) Cytotoxin assay of stool has greater specificity (75-100%) than culture of stool (75-80%) for securing the diagnosis
3) Treatment:
a. metronidazole
b. vancomycin produces resistant strains
Enterotoxic E coli causes diarrhea how? What other organisms do same? how is this type of E coli treated?
1) certain strains produce toxin that activate adenylate or guanylate cyclase, causing secretory diarrhea (traveler's diarrhea; accounts for 60% of cases)
2) other causes include Campylobacter, Salmonella, Shigella
3) levofloxacin
O157:H7 serotype E coli is contracted from where? What syndrome does it produce? Which antibiotics are recommended?
1) contracted by eating undercooked beef
2) Produces hemolytic uremic syndrome
3) Antibiotics not recommended; may enhance toxin release
Mycobacterium avium-intracellulare complex causes diarrhea in who? What disease does it resemble why?
1) Acid-fast rods
2) Causes diarrhea with malabsorption in AIDS (CD4 count < 50 cells/mm3)
3) Foamy macrophages in lamina propria simulate Whipple's disease
How does M tuberculosis get to GI tract? what do they invade and cause?
1) Acid-fast organisms swallowed from primary focus in lung
2) Invade Peyer's patches
3) Circumferential spread in lymphatics leads to stricture formation
What are pathogenic salmonella what are reservoirs?
1) Types:
a. S. typhi
b. S. paratyphi
c. S. enteritidis
2) Reservoirs:
a. turtles
b. hamsters
c. lizards
Salmonella enteritidis enterocolitis can be cause? How is it contracted?
1) Second most common food-borne illness in United States
2) contracted by eating raw or undercooked egg products, raw milk and milk products, and poultry or drinking contaminated water
3) Treatment: ciprofloxacin or levofloxacin
What is clinical course of S typhi? What is classic triad? How is it treated? What can result if not eliminated?
1) Week 1: invades Peyer's patches and produces sepsis (blood culture best for diagnosis)
2) Week 2: diarrhea (positive stool culture)
a. classic triad of bradycardia, neutropenia, splenomegaly
3) Treatment: treat if symptomatic with fluoroquinolone; antibiotics do not shorten the illness and may increase frequency of carrier states
4) Chronic carrier state due to gallbladder disease: cholecystectomy
Note: causes rose colored spots on abdomen
Shigella dysenteriae and Shigella sonnei are found where? What do they cause? what association is there? How are they treated?
1) Highly infectious in children in day care centers or in mental institutions
2) Symptoms:
a. Mucosal ulceration
b. pseudomembranous inflammation in rectosigmoid
c. dysentery
3) Association with HLA-B27 positive seronegative spondyloarthropathy
4) Treatment: treat if symptomatic with fluoroquinolone or azithromycin
when does gastroenteritis from s aureus present?
1) Gastroenteritis occurs in 1-6 hours after eating
2) preform toxin
what type of bacteria is V choleraie? What is pathogenesis? What is reservoir? How is it treated?
1) Gram-negative comma-shaped rod
2) Enterotoxin (AB) stimulates adenylate cyclase in small bowel
3) Contracted from drinking contaminated water or eating contaminated seafood, especially crustacea
4) Treatment:
a. fluid replacement; glucose and sodium required in oral supplements (cotransport system for reabsorption)
b. doxycycline or fluoroquinolone or tetracycline
What type of bacteria is Yersinia enterocolitica? What does it cause? What does it simulate? What is it associated with? how is it treated?
1) Gram-negative coccobacillus with bipolar staining
2) Enterocolitis in children and mesenteric lymphadenitis (granulomatous microabscesses) that simulates acute appendicitis (pseudoappendicitis)
3) Association with HLA-B27 positive seronegative spondyloarthropathy
4) Treatment: TMP-SMX
What type of organism is Balantidium coli? How is it transmitted? What does it produce? How is it treated?
1) Protozoan (ciliate)
a. largest protozoan
2) Transmitted by ingestion of cysts in food or water
3) Produces colonic ulcers with bloody diarrhea
4) Treatment: tetracycline
What type of organism is cryptosporidium parvum? How is it transmitted? Who is it most common in? How is it diagnosed and treated?
1) Protozoan (sporozoa) = acid fast cysts
2) Transmitted by ingestion of oocysts in food or water
3) Responsible for outbreaks of diarrhea in water supply (e.g., Milwaukee, Wisconsin)
4) Most common cause of diarrhea in AIDS
5) Diagnosis: stool antigen test (sensitivity/specificity 98%); oocysts partially acid-fast
6) Treatment if immunocompetent:
a. nitazoxanide (less responsive to drug if immunodeficient)
What are common features of Cyclospora, Microsporidia, Isospora belli?
1) Protozoa (sporozoa)
2) Fecal-oral transmission
3) All are common pathogens in AIDS diarrhea
Out of Cyclospora, Microsporidia, Isospora belli which contaminates raspberries? Which are partially acid-fast?
1) Cyclospora can contaminate raspberries
2) Microsporidia spores not partially acid-fast
3) Cyclospora oocysts partially acid-fast
4) Isospora oocysts partially acid-fast
How are Cyclospora, Microsporidia, Isospora belli treated?
1) Treatment:
a. Cyclospora: TMP-SMX double strength
b. Microsporidia: albendazole
c. Isospora: TMP-SMX double strength
What type of organism is Entamoeba histolytica? How is transmitted? Describe cysts and trophozoites? How is it diagnosed and treated?
1) Protozoa (amoeba)
2) Transmitted by ingestion of cysts in food and water
3) Cysts are nonmotile and are present in formed stool
a. trophozoites are motile and are present in diarrhea
b. Trophozoites characteristically phagocytose red blood cells
3) Diagnosis: stool antigen test (sensitivity/specificity 100%)
4) Treatment: metronidazole and iodoquinol
Describe pathogenic process of Entamoeba histolytica? What are characteristic findings when it invades?
1) Produces dysentery (bloody diarrhea)
2) cysts excyst in the cecum and become trophozoites in the cecum
3) trophozoites release powerful histolytic agents that produce flask-shaped ulcers
4) trophozoites can penetrate portal vein tributaries and drain to the liver to produce a liver abscess ("anchovy paste" abscess)
5) trophozoites can penetrate hepatic vein tributaries and produce systemic disease
what organism produces "anchovy paste" abscess in liver and flask shaped ulcers in GI?
Entamoeba histolytica
What is the Most common protozoal cause of diarrhea in United States? How is it transmitted? who and where is it common? What does it cause? How is it diagnosed and treated?
1) Giardia lamblia = Protozoa (flagellate)
2) Transmitted by ingestion of cysts in food and water
a. Common in day care centers, mental hospitals, hikers, water supplies (chlorination does not kill the cysts), men who have sex with men (anal-oral contact), IgA deficiency, common variable immunodeficiency
3) Produces acute and chronic diarrhea with malabsorption (cysts in formed stool; trophozoites in loose stools)
4) Diagnosis: stool antigen test (sensitivity/specificity 100%)
5) Treatment: tinidazole or nitazoxanide
What is Anisakis simplex? How is it transmitted? what is pathogenesis? how is it diagnosed and treated?
1) Intestinal nematode (helminth)
2) Transmission: eating raw fish dishes (i.e., sushi, sashimi); eating pickled herring
3) Larvae penetrate gastric and intestinal mucosa
4) Produce cramping abdominal pain; epigastric distress with nausea, vomiting, and diarrhea within a few hours after eating
5) Diagnosis: endoscopy; IgE antibody test
6) Treatment: removal by endoscope or surgery
What is the Most common helminth in the United States? How is it transmitted? What does it cause? Why is there not eosinophilia? How is it treated?
1) Enterobius vermicularis = Intestinal nematode (helminth)
2) Transmission: ingestion of eggs
3) Eggs deposited in anus by adult worms cause pruritus ani
4) Other infections: urethritis in girls; acute appendicitis
5) No eosinophilia because adult worms are not invasive
6) Treatment: albendazole or mebendazole
What type of organism is Trichuris trichiura? How is it transmitted? What does it cause? How is it diagnosed? How is it treated?
1) Intestinal nematode (whipworm)... helminth
2) Transmitted by ingestion of eggs
3) Produces diarrhea
a. can produce rectal prolapse in children
4) Diagnosis: stool for ova and parasites; eosinophilia
5) Treatment: albendazole
Ascaris lumbricoides is what type of organism? How is it transmitted? What is pathogenesis? Why is eosinophilia not seen in adult phase? How is it treated?
1) Intestinal nematode (helminth)
2) Largest intestinal nematode
3) Transmitted by ingestion of eggs
4) Larval phase through lungs: cough, pneumonitis, eosinophilia (invasion of tissue)
5) Bowel obstruction in adult phase
a. no eosinophilia (no invasion of tissue)
6) Treatment: albendazole and mebendazole
Necator americanus is what type of organism? what does it cause? How is it treated?
1) Intestinal nematode (hookworm) = helminth
2) Adults attach to villi, resulting in blood loss and iron deficiency
3) Treatment: albendazole or mebendazole
Note: penetrate skin and suck blood from intestinal wall resulting in anemia
What type of organism is Strongyloides stercoralis? Autoinfection can occur. What does this mean? What are symptoms of infection? How is it treated?
1) Intestinal nematode (helminth)
2) Autoinfection may occur if filariform larvae in the intestine penetrate the mucosa and migrate to the lungs to repeat the cycle
3) In immunocompromised patients (e.g., AIDS), massive reinfection occurs with dissemination throughout the body
4) Produces abdominal pain and diarrhea and anemia
5) Treatment: ivermectin
What is lifecycle of Strongyloides stercoralis in body?
1) Transmission:
a. filariform larvae in soil penetrate the feet → larval phase through the lungs → swallowed and molt into adults that enter the intestinal mucosa and lay eggs → eggs hatch into rhabditiform larvae which enter the intestinal lumen and are passed in the stool → develop into filariform larvae (infective form) in the soil
Diphyllobothrium latum is what type of organism? How is it transmitted? What does it produce? how is it diagnosed and treated?
1) Intestinal cestode (tapeworm) = helminth
2) Transmission: ingest larvae in lake trout (Great Lakes)
3) Produce diarrhea with or without vitamin B12 deficiency
a. preferential uptake of vitamin B12 by the worm
4) Diagnosis: eggs in the stool
5) Treatment: praziquantel
What is the Most common cause of small bowel obstruction? How does crohns cause obstruction?
1) adhesions
2) Crohns:
a. Lumen in terminal ileum is narrow due to full-thickness inflammation of bowel wall
b. Serosal adhesions from bowel-to-bowel also cause obstruction
Where does duodenal atresia occur? What is it associated with? How does it present at birth? What sign is seen?
1) Atresia is distal to entry of the common bile duct
2) Association with Down syndrome
3) History of maternal polyhydramnios (cannot reabsorb amniotic fluid)
4) Vomiting of bile-stained fluid at birth
5) "Double bubble sign": air in stomach and air in proximal duodenum
who does gastric ileus occur in? what is pathogenesis? What does a radiograph show?
1) Occurs in elderly women with chronic cholecystitis and cholelithiasis
2) Fistula develops between gallbladder and small bowel.
3) Stone passes into small bowel and lodges at the ileocecal valve causing obstruction.
4) Radiograph shows air in biliary tree
what is congenital hirschprungs disease due to? pathologically what occurs?
1) Absence of ganglion cells in Meissner's submucosal plexus and Auerbach's myenteric plexus causes localized aperistalsis
2) no sympathetic neurons in aganglionic segment
3) constant contraction without relaxation, which is necessary for peristalsis, resulting in obstruction
What is cause of acquired Hirschprungs?
1) due to Chagas' disease and destruction of ganglion cells by amastigotes
What segments are involved in hircshsprungs disease? What is it associated with? What is a complication?
1) Involves distal sigmoid and rectum; may involve entire rectum and descending colon; proximal uninvolved bowel is dilated but has peristalsis
2) Association with Down syndrome
3) Complication: enterocolitis of dilated bowel (danger of perforation), which is the most common cause of death
Note: failure of neural crest cell migration
Clinically how does Hirschsprungs present? How is it diagnosed and treated?
1) Abdominal pain
2) chronic constipation without large stools of retentive encopresis
3) physical exam reveals absent stool on the examining finger, because there is no stool in the rectal vault (very important differential point from other causes of chronic constipation)
4) Alternating signs of obstruction with diarrhea
5) Diagnose with rectal biopsy
6) Treatment: surgical resection of affected segment
Where does an indirect inguinal hernia become trapped?
Bowel becomes trapped in the inguinal canal
When does intussusception occur usually? If it occurs later what is cause?
1) Peak incidence ages 1-5
2) In adults, a polyp or cancer is the nidus for intussusception
How does intussusception occur in children?
1) In children, the terminal ileum invaginates into the cecum
2) mound of hyperplastic lymphoid tissue in Peyer's patches serves as the nidus for the intussusception (may be from adenovirus infection)
3) combination of obstruction and ischemia
4) telescoping sign
how does intussusception present? What sign is seen? How is it treated?
1) colicky pain with bloody diarrhea
2) oblong mass palpated in midepigastrium (Dance's sign)
3) usually self-reduces
4) may require air reduction under fluoroscopy or ultrasound
5) may occur with rotavirus oral vaccine
What is meconium ileus a complication of? why?
1) Complication of newborn with cystic fibrosis
2) Meconium lacks NaCl and obstructs the bowel lumen
what is volvulus? Where does it occur in elderly? in young adults? what are risk factors?
1) Bowel twists around mesenteric root producing obstruction and strangulation
2) Sigmoid colon is most common site in elderly
3) Cecum is the most common site in young adults
4) Risk factors: chronic constipation (most common), pregnancy, laxative abuse
what layers of abdomen go through hesselbachs triangle in a direct hernia? What are borders of triangle? can it go to scrotum?
1) Single layer of transversalis fascia is stretched in the floor of the triangle of Hesselbach
2) Medial border of triangle is rectus sheath, lateral border is inferior epigastric artery, inferior border is inguinal ligament
3) Hernia bulges through floor of triangle of Hesselbach
a. bulge disappears when patient reclines.
4) Small bowel cannot enter scrotal sac; therefore, there is no obstruction or incarceration
5) Treatment: sutured mesh covering inguinal canal and Hesselbach's triangle
What is pathogenesis in adults for developing inguinal hernia? in children?
1) Pathogenesis in children:
a. persistence of peritoneal connection between inguinal canal and tunica vaginalis
2) Pathogenesis in adults:
a. protrusion of new peritoneal process into inguinal canal
with an indirect hernia can the bowel enter scrotum? what are complications?
1) Small bowel passes through internal inguinal ring and may enter scrotal sac
2) Bowel directly hits the examining finger within the inguinal canal
3) Complications: entrapped in inguinal canal (incarceration) or strangulated obstruction (hemorrhagic infarction)
How are indirect hernias treated in children? adults?
1) In children: high ligation of hernia sac at the level of the internal inguinal ring + tightening of the internal inguinal ring
2) In adults: sutured mesh covering inguinal canal and Hesselbach's triangle
Who does a femoral herniation occur more in? Where is bulge located? How is it treated?
1) Most common in women
2) Bulge located below inguinal ligament
3) Highest rate of incarceration of small bowel
4) Treatment: transversalis fascia and conjoined tendon are sutured to Cooper's ligament
Who do umbilical hernias occur more in?
1) Most common hernia in adults with ascites, pregnancy, or obesity
2) Most common hernia in black newborns
What happens in an umbilical herniation?
1) Peritoneal protrusion extends into a fascial defect containing remnants of umbilical cord
2) Majority close spontaneously by the second year
3) Incarceration more likely in adults than children
barium enema shows "thumb-printing" of the colonic mucosa in the region of the splenic flexure. What is cause?
ischemic colitis.
A barium swallow shows "apple core" lesion in rectum. What is suspected?
adenocarcinoma causing circumferential narrowing of the lumen
What are signs of anorectal disease?
1. Internal hemorrhoids (painless)
2. Anorectal cancer
3. Infection
4. Fissure
What anorectal disorders produce pain? which cause pruritus? which causes fistulas?
1) Pain:
a. Anal fissure
b. Thrombosed external hemorrhoids
2) Pruritus (e.g., pinworms)
3) Anal fistula (e.g., Crohn's disease)
Where do internal hemorrhoids occur?
1) Dilated superior hemorrhoidal veins in mucosa and submucosa
2) Located above the pectinate line (superior plexus)
What are causes of internal hemorrhoids?
(1) Straining at stool (most common)
a. Often associated with constipation, low-fiber diet
(2) Pregnancy
(3) Obesity
(4) Anal intercourse
(5) Portal hypertension
Clinically what is seen with internal hemorrhoids?
(1) Often prolapse out of the rectum
(2) Commonly pass bright red blood with stool
a. Blood coats the stool.
b. Painless bleeding
(3) Anal pruritus and soiling of underwear
How are internal hemorrhoids treated?
(1) Nonpharmacologic
a. High-fiber diet; warm soaks/sitz baths; avoid prolonged sitting or stooling
(2) Pharmacologic
a. Topical hydrocortisone
b. Stool softeners
Where do external hemorrhoids occur?
1) Dilated inferior hemorrhoidal veins
a. Located below the pectinate line (inferior plexus)
2) Painful thrombosis
What is rectal prolapse?
1) Intussusception of the rectum through the anus
a. Due to weak rectal support mechanisms
What are causes of rectal prolapse in children less than 2?
(1) Whooping cough
(2) Trichuriasis
(3) Common sign of cystic fibrosis
What is a pilonidal sinus or abscess? How is it treated?
1. Excess hair in a deep gluteal fold Becomes traumatically buried into a sinus
2. Painful sacrococcygeal mass with purulent drainage
3. Treatment
a. Incision and drainage first episode
b. Chronic disease
** Marsupialization-wide excision and wound left open
What are some causes of pruitus ani?
(1) Anorectal diseases
a. Internal hemorrhoids (common), fissures, anal incontinence, diarrhea, cancer
(2) Infections
a. Pinworm, Candida, venereal diseases
(3) Local irritants
a. Soap, underwear, obesity, coffee, beer, acidic foods
(4) Dermatologic disease
a. Psoriasis, atopic dermatitis
(5) Diabetes mellitus
Who anorectal fistulas common in? what are they associated with?
(1) Common in all ages
(2) Associated with constipation
(3) Pediatric population
a. More common in infants
b. Boys > girls
What are a few causes of anorectal fistulas?
1) Nonspecific cryptoglandular infection most common
2) Inflammatory bowel disease
a. Crohn's disease > ulcerative colitis
3) Trauma
a. Episiotomy, prostatectomy, anal intercourse
4) Malignancy
a. Anal carcinoma, treatment for anal carcinoma
What is pathology behind anal fissures?
(1) Firm bowel movements
a. Once formed, perpetuated by bowel movements
(2) Associated and perpetuated by spasm of the internal sphincter
Where do anal fissures typically occur? if they are else where what should be considered?
(1) Posterior (90%) fissure and/or ulcer between anal verge and dentate line
a. Consider Crohn's disease if not in this location
(2) Anal tag at anal verge marks its location.
(3) Prominent proximal papilla
What is the most common type of anal cancer? Where is it located? Who does it occur in?
1) Basaloid (epidermoid or cloacogenic) carcinoma
2) Located in the transitional zone above the dentate line
3) Female dominant
4) Treatment is surgery
squamous cancer in the anal area is due to what? Where is it located?
(1) Located in the anal canal
(2) Majority occur in men who have sex with men.
a. HPV 16 and 18 association
(3) Treatment is surgery
abeta-lipoproteinemia is what type of genetic deficiency? what protein is missing? What results? What is seen on blood smear?
1) autosomal recessive
2) can't synthesize apolipoprotein B needed for lipoprotein export from mucosal cells
3) presents in infancy with failure to thrive
4) blood smear shows acanthocytes (burr cells)
blood group A is associated with? blood group O with?
1) A = carcinoma of stomach
2) O = peptic ulcers