RRPathCh17GIdisorders1.txt

Most common congenital disorder of oral cavity: 1:800 live births.

• Genetics: recur 3% in siblings
• morecommon in Whites than blacks

• Cleft lip and palate 50%
• Cleft lip alone 25% M>F
• Cleft palate alone 25% F>M

• Complications:
• 1. Malocclusion
• 2. Eustachian tube dysfxn: chronic otitis media
• 3. speech problems

• Path: failure of fusion of faciel processes
• Treat: Surgery

Candidiasis: most common oral infxn!!

• Apthous ulcers (stomatitis; canker sores)
• Unknown origin
• 1. virus vs immunogenic
• 2. Often stress induced
• painful ulcer covered by shaggy gray membrane

Hairy Leukoplakia: glossitis b/c of EBV

• Kaposi's sarcoma:
• Hard palate is most common locale
• Due to HPV8!

Dental Caries:

1. Strep mutans produces acid from sucrose fermentation. acid erodes enamel and expose underlying dentine

2. Flouride prevents dental caries: excess flouride causes chalky discolor teeth.

• Exudative tonsillitis:
• path: viruses most cases
• Features: culture necessary to diff bac vs virsl

• Hairy Leukoplakia:
• path: EBV
• Features: glossitis ass w/ bilat white excrescences on lateral tongue border. Pre aids defining lesion.

• Herpes labialis:
• path: HSV type 1
• Features: recurrent vesicular lesions on the lips (virus dormant in cranial sensory ganglia.) Reactivated by stress, sunlight, and menses.
• Treat: oral acyclovir, valacyclovir, famciclovir, topical acyclovir, penciclovir

• Mumps:
• path: Paramyxovirus
• Features: bilat parotitis (70% w/ up serum amylase.
• Complications: meningoencephalitis, unilat orchitis or oophoritis, pancreatitis.

• Herpangina
• path: Coxsackievirus
• Features: occurs in kids. multiple vesicles or ulcers on soft palate and pharynx surrounded by erythema

• Hand-foot-mouth dz: occurs in young kids.
• path: Coxsackievirus
• features: occurs in kids. vesicles located in mouth and distal extremities

• Cervicofacial actinomycosis:
• Path: Actinomyces israelii
• Features: draining sinus tract from facial or cervical area. "sulfer granuses" in pus; contain gram pos, branching filamentous bac; anaerobe. often follows after extracting abscesses tooth.
• Treat: Ampicillin, penicillin G

• Diptheria:
• Path: Corynebacterium diptheriae
• Features: produce "shaggy" gray pseudomembrane in post pharynx and upper airways.
• Treat: Erythromycin

• Peritonsillar Abscess:
• pATH: Strep pyogenes
• Features: Uvula deviates to contralat side, "hot potato" voice, foul breath b/c of tonsillitis
• Treat: Surg drainage of pus; pen G or V; add clindamycin for serious invasive infxns.

• Ludwig's angina:
• Path: Aerobic/anaerobic stres, Eikenella corrodens
• Features: Cellulitis involves submaxillary and sublingual space; follows fascial planes and may spread into pharynx, carotid sheath, superior mediastinum
• Causes: dental extract, trauma to floor of mouth
• Treat: surg drain; clindamycin + metronidazole

• Pharyngitis:
• Path: S. Pyogenes
• Features: Ass w/ tonsillitis. Potential for acute rheum fever and glomerulonephritis
• Treat: Pen V

• Scarlet fever:
• Path: S. Pyogenes
• Features: Pharyngitis, tonsillitis, glossitis. Erythrogenic toxin produces rash on skin and tongue (first white then strawberry colored.) Up risk for glomerulonephritis. Nephritogenic stains pose no risk for acute reeum fever.
• Treat: Penicillin G or V

• Sialadenitis:
• Path Staph aureus
• Features: Bac inflammation of major slivary gland. Secondary to a calculus, which obstructs the duct in postop pts.
• Treat: oxacillin, nafcillin if methicillin susceptible; TMP/SMX if comm acqu meth resistant; vanc if meth resistant in hospital

• Congenital Syphillis:
• Path Treponema Pallidum (spirochete)
• Features: Abnormal incisors (Tapered like a peg) and moral teeth (resemble mulberries)
• Treat: aqueous crystalline pen G

• Oral Thrush:
• Path: Candida albicans (yeast)
• Features: May occur in neonates, immunocomp pts (follows pre aids defining lesion), diabetes mellitus, and following antibio therapy
• Treat: Fluconazole, itraconazole

• Pemphigus vulgaris and mucous membrane pemphigoid:
• both are immunologic skin disorders

• Erythema multiforme:
• Hypersensitivity rxn against Mycoplasma or drugs (sulfonamides
• Called Stevens-Johnson syndrome when involves mouth

• Apthous Ulcers (Stomatitis):
• In AIDS relates sxn

• Behcet's syn:
• Epi: combo of environment + genetic. HLA-B51, HLA-B27 associations. may be precipitated by herp simplex or parvovirus. High incidence in Turkey and mediterranean.
• Path: Immune complex small vessel vasculitis.
• Clinical findings:
• 1. recurrent apthous ulcers, genital ulcerations
• 2. Uveitis, erythema nodosum
• 3. Attacks last 1-4w
• Treat:
• 1. Anti inf meds
• 2. Corticosteroids
• 3. Colchicine
• 4. Thalidomide

• Peutz-Jeghers syn:
• melanin pigmentation of lips and oral mucosa

• Addison dz:
• increased ACTH stims melanocytes.
• melanin pigmentation of buccal mucosa

• Lead poisoning:
• lead deposits along gingival margins in adults w/ gingivitis

• Tetracycline:
• drug discolors newly formed teeth
• Not recomended in a child less than 12

• Excess flouride
• Mottled, chalky, white discoloration

• Congenital erythropoietic porphyria:
• porphyrins depo in teeth
• reddish brown discoloration

• Myxedema:
• severe primary hypothyroidism

Downs syn:

Acromegaly

Amyloidosis

Mucosal neuroromas in MENIIb (MENIII)

1. Sore, beefy red tongue w/ or w/out papillary atrophy

• Causes:
• 1. Long standing iron def
• 2. Vitamin B12 or folate def
• 3. Scurvy (vit c def)
• 4. Pellagra (niacin def)
• 5. Scarlet fever
• 6. EBV ass hairy leukoplakia

• Leukoplakia: AKA "white patch"
• has 30% rate of progression to oral Cancer

• Erythroplakia: "Red patch"
• has 60% rate of progression to oral cancer

• Lesion does not "wipe" off
• both lesions are due to squamous hyperplasia of epidermis. This ups risk of squamous dysplasia or invasive squamous cancer

• Causes:
• chronic irritation (dentures)
• all forms of tobacco use
• alcohol abuse
• HPV

• Locations:
• 1. Vermillion border lower lip (most common site)
• 2. Buccal mucosa
• 3. Hard and soft palates
• 4. Floor of mouth

ALWAYS BIOPSY THESE LESIONS b/c of high risk for progression to oral cancer.

Often ass w/ Wickham's stria on buccal mucosa. Fine white, lacy lesions.

may be ass w/ squamous cell carc

• Dentigerous cyst:
• derives from epi elements of dental origin (odontogenic origin
• Ass w/ crown of an unerupted or impacted 3rd molar
• Ass w/ ameloblastomas in 15-30% cases.

• Squamous Papillomas:
• most common benign tumor in oral cavity
• Exophytic tumor w/ fibrovbasc core
• May occur on tongue, gingiva, palate, or lips

• Ameloblastoma:
• Arise from enamel organ epi or dentigerous cyst
• Located in mandible: produces radiolucency in bone that has "soap bubble" appearance. It's locally invasive but does NOT mets

• Most are well differentiated squamous cell carc
• M>W
• Risk Factors:
• 1. smokins is most common
• 2. Alcohol abuse (synergy w/ smoking. up 30x w/ both)
• 3. HPV
• 4. Chronic irritation from dentures
• 5. Lichen planus

• Cancer sites in descending order:
• 1. Lower lip (vermillion border
• 2. mouth floor
• 3. Lateral border of tongue

• Mets:
• "Tonsillar node" (superior jugular node

• Verrucous carcinoma:
• Ass w/ smokeless tobacco

• Basal cell carc:
• most common cancer of upper lip
• Ass w/ UV light exposure

• Treat squamous cancer:
• surg and radiation, chemo if advanced

• Sjogren's syndrome:
• fem dominant autoimmune dz ass w/ rheum arthritis
• AI destruction of minor salivary glands and lacrimal glands.

• Salivary gland tumors:
• Epi:
• 1. Parotid gland is most common site. Major salivary gland tumors more likely to be benign, and minor likely malignant.

• Pleomorphic Adenoma (mixed tumor):
• Most common benign tumor of major and minor salivary glands. Parotid gland is most common site.
• Female dominant
• Painless, moveable mass at angle of jaw
• Epi cells intermix w/ myxomatois and cartilaginous stroma (tumor projections thru capsule up recur risk.)
• May transform into malig tumor (facial nerve involvement=sign of malignancy.

• Warthin's tumor (papillary cystadenoma lymphomatosum):
• Benign parotid gland tumor. Male dominant
• Heterotopic salivary gland tissue trapped in a lymph node. Cystic glandular structures located w/in benign lymphoid tissue.

• Mucoepidermoid carcinoma:
• most common malignant salivary gland tumor
• Most commonly located in parotid gland
• mix of neoplastic squmous and mucus secreting cells.

• 1. Heartburn: most commonly due to gastroesophageal reflux dz
• 2. Dysphagia (hard to swallow) for only solids. Sxs of obstructive lesion. example: esophageal cancer, esophageal web, stricture.
• 3. Dysphagia for solids and liquids: Sxs Symptom of a motility disorder.
• a. oropharyngeal (upper esophageal) dysphagia. Striated muscle dysmotility. Ex: dermatomyositis, myasthenia gravis, stroke.
• b. Lower esophageal dysphagia: smooth muscle dysmotility. Ex: systemic sclerosis, CREST syn, achalasia

• Characteristics:
• proximal esophagus ends blindly
• distal esophagus arises from trachea

• Clinical findings:
• a. maternal polyhydramnios (excess amnio fluid). swallowed amnio fluid cannot be reabsorbed in sm int.
• b. Abdominal distend in newborn. Air in stomach from tracheal fistula
• c. Difficult feeding. food regurgitates out of mouth. Chem pneumonia from aspiration.
• d. VATER syndrome
• 1. Vertebral abnormal
• 2. Anal atresia
• 3. TE fistula
• 4. Renal dz and absent Radius

• due to chronic iron deficiency
• Leuloplakia in oral mucosa and esophagus
• Intermittent dysphagia for solids. This b/c of an esophageal web or stricture

• Types:
• 1. True diverticulum: outpouching lined by mucosa, submucosa, muscularis propria, and acventitia
• 2. False, or pulsion diverticulum: weakness in underlying muscle wall. Outpouchings of mucosa nad submucosa into area of weakness.

• Zenkers diverticulum:
• Pulsion type located in upper esophagus.
• Area of weakness is cricopharyngeus muscle
• Clinical:
• 1. painful swallow
• 2. Halitosis: entrapped food
• 3. Regurg food thru mouth
• 4. diverticulitis
• Treat: surgery

• Epi:
• found in 50% of people over 50 and ups w/ age.
• W>M
• Associations:
• 1. sigmoid diverticulosis (25%)
• 2. Esophagitis (25%)
• 3. Duodenal ulcers (20%)
• 4. Gallstones (18%)

• Sliding Hernia: most common type of hiatal (99%)
• Herniation of prox stomach into thoracic cavity thru the diaphragmatic esophageal hiatus.
• Clinical:
• 1. heartburn
• 2. Nocturnal epigastric distress form acid reflux
• 3. Hematemesis (vomit blood)
• 4. Ulceration, stricture
• 5. Bowel sounds heard over left lung base.
• Treat:
• 1. Non pharm: reduce intake of foods/drugs that down LES tone. Ex: coffee, chocolate, calcium channel blockers. avoid big portions of food. Sleep elevated.
• 2. Pharm:
• a. H2 antagonists
• b. PPI's
• c. Prokinetic agents
• 3. Surg if needed

• Paraesophageal (rolling) hernia (1%)
• Gastroesophageal jxn remains at level of diaphragm
• Parf of stomach bulges into thoracic cavity.

• Epi:
• 10% adults have GERD daily
• 80% of preg women have GERD
• Hiatal hernia present in 70% of people with GERD

• Risk factors:
• 1. Smoking, alcohol
• 2. Caffeine, fatty foods, chocolate
• 3. Pregnancy, obesity
• 4. Hiatal hernia

• Path:
• Transient relaxation of LES. reflux of acide and bile into distal esophagus.
• Inefective esophageal clearance of reflux material

• Clinical findings:
• Non cardiac chest pain (Heartburn, digestion)
• Nocturnal cough, nocturnal asthma
• Acid injury to enamel
• Early satiety, abdominal fullness
• Bloating w/ belch
• barrett's esophagus.

• Diag tests w/ atypical presentation:
• 24 hr esophageal pH monitoring (Sensitivity/Specificity 80%-90%)
• Esophageal endoscopy
• Manometry (LES pressure<10mm Hg)

• Treat:
• Non pharm : similar to hiatal hernia (earlier)
• Pharm: similar to hiatal (earlier)
• Surg if indicated:
• 1. Fundoplication procedure
• 2. Involves putting gastric wrap around gastroesophageal jxn.

• GERD complication
• Glandular metaplasia in distal esophagus due to acid injury. Gastric type columnar cells and sm int type cells (goblet)
• Complications:
• Ulceration w/ stricture formation (most common)
• Glandular dysplasia w/ upped risk for distal adenocarc

• Usually complication of AIDS
• Presents with painful swallowing (i.e. odynophagia)
• Pathogens:
• 1. Herp simplex virus (HSV). See multinucleated squamous cells w/ untranuc inclusions
• 2. Cytomegalovirus (CMV). See basophilic nuclear inclusions
• 3. Candida. See yeasts and pseudohyphae (extended yeast forms)

• Ingestion of strong alkali (e.g. lye) or acid (HCl, etc)
• Complications:
• stricture form
• perforation
• squamous cell carc

• Epi and Path:
• Dilated submucosal left gastric veins
• Complication of portal hypertension from cirrhosis. Alcohol abuse is most common cause.

• Clinical Findings:
• Rupture w/ massive hematemesis (blood vomit)
• Most common cause of death in cirrhosis

• Diag:
• Endoscopy

• Initial management:
• 1. Endoscopy
• most important diag procedure. Value in treat of bleed as well
• 2. Assess/ maintain intravasc volume
• 3. Insert nasogastric tube for gastric aspirate/lavage
• 1. confirms upper GI bleed source
• 2. Assess bleed rate

• Prevention/treat bleeds:
• B blockers and isosorbide
• 1. decrease rate of recurrent bleed
• 2. up survival 5-10%
• Transjugular intrahepatic portasystemic stent (TIPS)
• 1. Used for both bleeding and intractable ascites
• Octreotide IB drip (somatostatin analogue) for bleeding
• Endoscopic ligation
• Endoscopic sclerotherapy
• open surgery and stapling

• 1. Mucosal tear in proximal stomach and distal esophagus. due to severe retching in alcoholics or bulimia
• 2. Causes hematemesis

Rupture of distal esophagus

• Causes:
• endoscopy (75% of cases)
• Retching
• Bulimia

• Complications:
• 1. Pneumomediastinum
• a. Air dissects subcutaneously into anterior mediastinum
• b. crunching sound (Hamman's crunch) heard on auscultation
• 2. Pleural effusion contains food, acid, amylase

Systemic sclerosis aqnd CREST syn

• Achalasia:
• Epi:
• 1. bimodal: occurs in those 20-40yrs and occurs after 60
• 2. Mand W affected equal
• Risk for esophageal cancer

• Path:
• incomplete relax of LES
• Destruction of ganglion cells in myenteric plexus
• 1. probable AI destruction. HLADQw1 association
• 2. decrease proximal smooth musc contract
• 3. lose NO synthase producing neurons. cause incomplete relaxation.
• Dilation of esoph proximal to LES w/ absent peristalsis
• Acquired cause is Chagas' Dz
• 1. destruction of ganglion cells by amastigotes (lack flagella)

• Clinical findings:
• Nocturnal regurg of undigested food
• dysphagia for solids and liquids
• chest pain and heeartburn
• frequent hiccups
• nocturnal cough from aspiration
• difficulty belching

• Diag:
• Abnormal barium swallow
• 1. dilated, aperistaltic esoph w/ beak like tapering at distal end
• Abnormal esoph manometry
• 1. detects aperistalsis and fail of LES relaxation.

• Treat:
• Nonpharm
• 1. pneumatic dilation
• 2. esophagomyotomy
• Pharm (short term)
• 1. long acting nitrates
• Ca channel blockers
• botulinum toxin inject

• Leiomyoma
• 1. most common benign tumor of esophagus

• Adenocarcinoma of distal esophagus
• 1. most common primary cancer of esophagus in US
• 2. Barrets esoph is most common predisposing cause. prevention of GERD downs risk

• Squamous cell carcinoma
• Epi:
• most common primary cancer in developing countries
• 1. caspian sea to northern china
• More common in blacks
• Occurs in M more than W

• Risk facters:
• smoking most common cause
• Alcohol abuse, lye strictures
• Achalasia, plumer vinson syn

• Locations:
• Upper third (15%)
• Middle third (50%
• lower third (35%)
• spreads to local nodes first then to liver and lungs

• Clinical findings:
• dysphagia for solids initially
• weight loss of short duration
• painless enlargement supraclavicular nodes
• dry cough and hemoptysis
• 1. suggests tracheal invade
• Hoarseness
• 1. probable invasion of recurrent laryngeal nerve
• Odynophagia
• Hypercalcemia
• 1. PTH related peptide similar to squamous cancer in lungs

• Diag:
• Esophagogram
• Endoscopy

• Treat:
• Surg, rads, chemo

• Prognosis
• overall 5 yr survival rate is 13%

• Hematemesis (blood vomit)
• 1. most commonly due to peptic ulcer dz (PUD
• 2. Other causes, esophageal verices, hemorrhagic gastritis
• Melena (dark, tarry stools)
• 1. Hemoglobin is converted into hematin (black pigment) by acid
• 2. signifies bleed proximal do duodenojejunal jxn (90%)
• Gastric analysis.
• 1. measures basal acid output (BAO) and maximal acid output (MAO) and the ratio of the 2.

• Epi:
• probable genetic basis
• M>F
• Affected father or mothers
• 1. upped for child with CPS
• Acquired pyloric obstruction
• 1. complication of chronic duodenal ulcer dz w/ pyloric scarring

• Path:
• progressive hypertrophy of circular muscles in pyloric sphincter
• 1. NOT present at birth but occurs over ensuing 3-5 wks
• Deficiency of NO synthase precipitates the dz

• Clinical findings:
• projectile vomit of non biloe stained fluid
• Hypertrophied pylorus is palpated in epigastrium (70%)
• 1. Called an "olive"
• Visible hyperperistalsis

• Treat:
• Myotomy if it does NOT resolve

• Decreased stomach motility
• 1. Autonomic neuropathy (diabetes mellitus)
• 2. previous vagotomy

• Clinical Findings:
• Early satiety and bloating
• vomiting of undigested food a few hrs after eating

• Treat:
• small volume frequent feeding
• metoclopramide

• Terms:
• Erosions are a breach in epithelium of mucosa
• Ulcers are breach in mucosa w/ estension into submucosa or deeper

• Causes
• NSAIDS
• Alcohol, Helicobacter pylori
• CMV (AIDS), smoking
• Burns (called curlings ulcers)
• CNS injury (called cushings ulcers)
• Uremia
• Anisakis
• 1. worm associated w/ eating raw fish

• Clinical findings:
• hematemesis
• Melena
• Iron def

• Treat (excluding H. pylori):
• Non pharm:
• Avoid mucosal irritants (NSAISDS, alcohol
• Cesation of smoking
• Pharm:
• Misoprostol
• PPI's

• Type A chronic atrophic gastritis:
• Involves body and fundus
• Most often due o pernicious anemia
• Complications:
• Achlorhydria w/ hypergastrinemia (lose neg feedback)
• Macrocyti anemia b/c of vit B12 deficiency
• Upped risk for gastric adenocarcinoma

• Type B chronic atrophic gastritis
• Involves antrum and pylorus
• Epi:
• most common cause is H. pylori
• 1. gram neg, curved rod
• Present in 30-50% of pop in US
• Prevalence ups w/ age
• Pransmitted bby fecal oral/oral oral route
• 1. common in areas of poor sanitation

• Path:
• Gram neg, curved rod
• Produces urease, proteases, cytotoxins
• 1. Urease converts amino groups in proteins to ammonia
• 2. secretion products produce chronic gastritis and PUD
• Colonize mucus layer lining
• 1. Attaches to blood group O receptors on mucosal cells
• 2. NOT an invasive bacterium

• Micro:
• Chronic inflammatory infiltrate in lamina propria
• Intestinal metaplasia
• 1. precursor lesion for adenocarc

• Tests to ID H. pylori are highly sens and specific:
• Urea breath test:
• 1. Documents active infection
• 2. Sensitivity and spec>90%
• Stool antigen test (excellent screen):
• Pos when there is active infxn
• Neg when infxn is eradicated
• Sens and spec>90%
• Tests to detect urease in gastric biopsy:
• Considered gold standard test albeit invasive
• Serologic Tests:
• High sens and spec
• Do NOT distinguish current from past infxn

• Treat:
• Sequential therapy
• First Rabeprazole + amoxicillin
• Followed by Rabeprazole + clarithromycin + tinidazole

• Test of cure is stool antigen test
• If neg 8 wks ofter therapy, infxn is cured
• Does not imply infxn cannot recur

• Other dz associations w/ H. pylori:
• Duodenal and gastric ulcers (later)
• gastric adenocarc (later)
• low grade B cell malignant lymphoma (later)

• Menetier's dz (hypertrophic gastropathy):
• Giant rugal folds
• 1. due to hyperplasia of mucus secreting cells
• 2. causes hypoproteinemia (protein losing enteropathy)
• Atrophy of parietal cells (acholhydria)
• 1. Ups risk for adenocarc

• Epi:
• PUD is most often caused by H. pylori (70%)
• 1. other parts of world higher percentage
• Eradication of H. pylori markedly reduces PUD recurrence
• Duodenal ulcers are more common than gastric ulcers
• Locations:
• 1. duodenal ulcer first portion of duodenum (90%)
• 2. Gastric ulcer in lesser curvature near incisure angularis
• Recurrence rate for untreated PUD 60% (70 in smokers)

• Gross appearance of ulcers:
• Clean, sharply demarcated, slightly elevated around edges
• Most Gastric ulcers are benign
• 1. small percent may be malig (reason for biopsy)
• Duodenal clcers are NEVER malignant
• Four layers in sequence are noted in histologic sections of ulcers
• 1.Necrotic debris
• 2. Inflammation w/ a predominance of neutrophils
• 3. Granulation tissue (repair tissue)
• 4. Fibrosis

• Epi and Path:
• Majority (60%) are malig pancreatic islet cell tumors
• Secreate excess gasrin producing hyperacidity
• Sporadic in two thirds of cases
• Ulcers are usualy single and in usual locales, there may be multiple ulcers
• MEN type 1 association (20-30% cases)
• Fam hx of parathyroid or pituitary tumors
• PUD without H. pylori or history of NSAIDS

• Clinical findings:
• Epigastric pain with weight loss
• Heartburn from GERD (60%)
• Peptic ulceration
• 1. Most are solitary duodenal ulcers rather than multiple ulcers
• Acid hypersecretion w/ diarrhea
• Malgestion of food
• 1. Acid interferes w/ pancreatic enzyme activity

• Lab Findings:
• Increased BAO, MAO, and BAO, MAO, and BAO:MAO ratio
• Serum gastrin level>100pg/mL

• Treat:
• Chemo and PPI's

• Complication of chronic gastritis and achlorhydria
• Hyperplastic polyp
• 1. most common type
• 2. Hamartoma w/ no malignant potential
• Adenomatous polyp
• 1. Neoplastic polyp
• 2. potential for malignant transformation

• Leiomyoma:
• Stomach is most common site
• May ulcerate or bleed

• Primary Stomach adenocarcinomas:
• Epi:
• decreasing incidence in US
• Increasing incidence in Japan
• Increased incidence in blood group A people
• Intestinal type of gastric adenocarcinoma:
• 1. most common gastric carcinoma
• 2. Risk factors:
• a. Intestinal metaplasia due to H. Pylori (most impt)
• b. Nitrosamines
• c. Smoked foods (japan)
• d. Diets lacking fruits/veggies
• e. Type A chronic atrophic gastritis
• f. Menetrier's dz
• 3. Polypoid or culerated
• 4. Locations:
• a. lesser curvature of pylorus and antrum (50-60%)
• b. Cardia (25%), body and fundus

• Diffuse type of gastric adenocarc:
• Incidence has remained unchanged
• Not associated w/ H. pylori
• Diffuse infiltration of malignant cells in stomach wall
• 1. sometimes called "linitus plastica"
• 2. Stomach does NOT peristalse
• 3. Signet ring cells infiltrate the stomach wall
• 4. Produces krukenberg tumors of overies
• a. hematogenous spread of signet ring cells to both ovaries

• Clinical findings of gastric adenocarc:
• Cachexia and weight loss (most common60%)
• Epigastric pain (50)
• vomiting often w/ melena (20)
• Metastasis to L supraclavicular node (Virchow's node)
• Paraneoplastic skin lesions
• 1. Acanthosis nigricans
• 2. Multiple outcroppings of seborrheic keratosis (Leser Trelat sign)
• Metastasis to umbilicus (sister mary joseph sign)

• Common Metastatic sites:
• Liver, lung, overies

• Treat:
• Surg, local rads, and chemo
• About 10-15% 5 yr survival rate

• Primary gastric malignant lymphoma:
• Stomach is most common site for extranodal malignant lymphoma
• Low grade B cell lymphoma
• 1. H. pylori related
• 2. MALToma (derives from mucosa associated lymph tissue.)
• High grade B or T cell lymphoma
• Treatment for J. pylori produces 50% cure rate.

• Colicky pain
• 1. pain followed by pain free intervald
• a. accompanied by constipation and inability to pass gas
• 2. Symptom of bowel obstruct
• b. Example: adhesions form previous surgery

• Diarrhea:
• Sign of
• 1. infxn
• 2. malabsorption
• 3. osmotic diarrhea
• If bloody, may be sign of
• 1. Infarction
• 2. Volvulus
• 3. Dysentery

• Anemia: malaborption of...
• Iron
• Folate
• Vit B12

• Diarrhea
• 1. Sign of
• a. infxn
• b. laxative abuse
• c. inflammatory bowel dz
• 2. If blody, may be sign of infarction or dysentery

• Dysentery:
• Refers to bloody diarrhea w/ mucus
• Infection

• Pain:
• Inflammatory bowel dz
• Ischemic colitis
• diverticulitis
• Apendicitis
• peritonitis

• Tenesmus:
• Painful, ineffective straining at stool
• Commonly present in ulcerative colitis

• Iron deficiency:
• Consider polyps, colorectal cancer

• Hematochezia:
• massive loss of whole blood per rectum
• Causes:
• 1. sigmoid diverticulosis (most common)
• 2. Angiodysplasia

• Diarrhea:
• More than 250g of stool a day
• Acute diarrhea is defined as less than 3wks , chronic diarrhea over 4 weeks
• Invasive, osmotic, secretory types
• Important screening tests:
• 1. Fecal smear for leukocytes (eg, invasive diarrhea
• 2. Stool osmotic gap
• a. 300 mOsm/kg-2x(random stool Na + random stool K)
• b. Gap<50 from POsm is secretory diarrhea. indicates that diarrheal fluid approximates POsm
• c. Gap>100 from POsm is an osmotic diarrhea. indicates a hypotonic loss of stool due to presence of osmotically active substances.

• Lactase deficiency:
• most common gen defect in native americans, asians, and blacks.
• Colon anaerobes degrade undigested lactose into lactic acid and H2 gas leading to abdominal distention w/ explosive diarrhea.
• Treat: avoid dairy products

• Definition:
• 1. increased fecal excretion of fat plus
• 2. concurrent deficiencies of fat soluble vitamins, mineralsk, carbs, proteins.

• Path:
• Pancreatic insufficiency, bile salt/acid deficiency, small bwel dz.

• Pancreatic insufficiency:
• Most often caused by chronic pancreatitis
• 1. most commonly due to alcohol in adults and cytstic fibrosis in kids
• Path:
• 1. maldigestion of fats
• a. due to diminished lipase activity
• b. undigested neutral fats and fat droplets are in stool
• 2. maldigestion of progeins
• a. due to diminished trypsin
• b. undigested meat fibers are in stool
• 3. Carb digestion is NOT AFFECTED
• a. Amylase is present in salivary glands
• b. disaccharidases are present in the brush border of intestinal epithelium.

• Bile salt/adic deficiency:
• Bile salts/acid are required to micellarize monoglycerides anf FA's
• Etiology and path:
• 1. inadequate synth of bile salts/acids from cholesterol (cirrhosis)
• 2. Intrehepatic/extrahepatic blockage of bile
• a. Ex: primary biliary cirrhosis, stone in common bile duct
• 3. Bac overgrowth in sm bowel w/ destruction of bile salts/acids
• a. Ex: small bowel diverticula, autonomic neuropathy
• 4. Excess binding of bile salts
• a. Ex: cholestyramine
• 5. Terminal ileal dz
• a. prevents recycling of bile salts/acids
• b. Ex: Crohn's dz, resection of ileum.

• Small bowel Dz:
• Villi are required to reaborb micelle sinto enterocytes
• 1. villi increase the absorptive surface of sm int
• Etiology and Path:
• 1. inability to reabsorb micelles
• a. due to loss of villous surface
• b. Ex: celiac dz, whipples dz
• 2. Lymphatic obstruction
• a. Ex: whipples dz, abetalipoproteinimia

• General screening tests for fat malabsorptino
• Quantitative stool for fat
• 1. stains are used to ID fat in stool
• 2. Lacks sensitivity
• Decreased serum beta carotene
• 1. precursor for fat soluble retinoic acid (vit A)
• D-xyloxse screening test
• 1. Xylose does NOT require pancreativ enzymes for absorption
• 2. Lack of reabsorption of orally administered xylose
• a. indicates sm bowel dz

• Tests to eval pancreatic insufficiency:
• Serum immunoreactive trypsin
• 1. trypsin is specific for the pancrease
• 2. Serum immunoreactive trypsin in chronic panccreatititrs
• a. Decreased concentration; excellent serum for cystic fibrosis
• CT scan of pancrease shows dystrophic calcification
• 1. Sighn of chronic pancreatitis
• Functional Tests:
• 1. Secretin stim test
• a. tests ability of pancrease to secrete fluids and electrolytes
• 2. Bentiromide test
• a. Tests ability of panc chymotrypsin to cleave orally administered bentiromide to para aminobenzoic acid (measure in urine)

• Test for bile salt/acid deficiency:
• Total bile acids can be measured
• 1. decreased in liver dz (cirrhosis)
• Bile Breath test (oral radioactive test)
• 1. decreased amount fradioactive chlylglycine in breath indicates bac overgrowth or terminal ileal dz.

• Tests for bac overgrowth:
• C-xylose
• 1. most sensitise/spec test
• 2. measures CO2 in breath
• Lactulose H2:
• 1. measures H2 in breath

• Clinical findings in malabsorption:
• Steatorrhea
• 1. excessive, loarge, sticky, stools that float
• Fat soluble vit def
• Water soluble vit def
• 1. particularly folate and B12
• Combined anemias
• 1. Ex: folate and iron def
• Ascites and pitting edema
• 1. due to hypoproteinemia

• Celiac Dz:
• Epi:
• 1. Inappropriate immune response to gluten in wheat products. also related proteins in rye and barley
• 2. prevalence of 1% in N. america
• 3. Common in whites; uncommon in blacks and asians
• 4. Occurs at any age
• a. highest incidency in infancy. first intro to gluten products
• b. 3rd decade. frequent ass/ w/ pregnancy
• c. 7th decade.
• Associations:
• a. Dermatitis herpetiformis
• b. AI dz: Hashimotos thyroiditis, primary bliary cirrhosis
• c. type 1 diabetes mellitus
• d. IgA deficiency
• e. Down syn, Turner's syn
• Path:
• 1. multiorgan AI disease
• 2. Inappropriate Tcell and IgA mediated response against gluten in genetically predisposed persons. Ass with HLA-DQ2(90%) and HLA-DQ8 (5%)
• 3. Timing and dose when gluten introduced in diet is mimportant
• 4. Tissue transglutaminase (tTG; deamidating enzyme) in lamina propria has a pivotal role.
• a. it deaminates mucosally absorbed gluten to produce deaminated and negatively charged gluten peptides.
• b. It also enhances the immunostimulatory effect of deaminated gluten progpia.
• d. They are presented in complex w/ HLA-DQ2 or DQ8 to gluten specific CD4 Thelper cells
• e. CD4 Thelper produce cytokines that release matrix proteases causing cell death and degredation in epi cells in vili
• Impt Diag antibodies:
• 1. Anti-tissue transglutaminase IgA (most impt), IgA AB's
• a. Sensisivity and spec 98%
• b. excellent screening test
• 2. Anti endomysial (EMA) IgA AB's
• a. Sensitivity 80% and spec 100%
• b. moderately good screen test
• Clinical Findings:
• 1. Steatorrhea
• 2. Weigh6 loss
• 3. Fail to thrive in infants and children
• 4. Pallor due to anemia (often combined anemias)
• 5. Dermatitis herpetiformis
• a. considered to be a form of celiac dz
• b. villous atrophy in 75% of cases w/ or w/out diarrhea
• c. low levels of above diag AB's
• Findings related to water soluble and fat-soluble vit deficiencies (chapter 7):
• Other systemic Findings:
• a. Bone- osteoporosis, arthritis
• b. CNS- seizures, depression
• c. Reproductive- dela puberty, miscarriage, infertility
• Diagnosis:
• 1. Above diagnostic AB's
• 2. Endoscopic biopsy
• a. Flatened villi, particularly in duodenum and jejunum
• b. Hyperplastic glands w/ intense lymphocytic inf.
• Treatment:
• 1. gluten free diet
• 2. correct nutritional deficiencies
• a. all fat soluble vitiamins; folate, vit B12; Calcium
• 3. Corticosteroids in refractory cases.

• Whipples Dz:
• Epi:
• 1. M>W
• 2. Peak incidence in middle age
• 3. caused by Tropheryma whippelii
• a. IDed by PCR
• 4. Microscopic
• a. Blunting villi
• b. foamy PAS positive mcrophages in lamina propria
• c. Mac's obstruct lymphatics and reabsorption of chylomicrons. Leads to MALABSORTION OF FATS.
• 5. Clinical findings
• a. Steatorrhea
• b. fever
• c. precurrent polyarthritis
• d. generalized lymphadenopathy
• e. Upped skin pigmentation
• 6. Treat with Antibiotics!