RRPathCh17GIdisorders1.txt

Card Set Information

Author:
mcaster24
ID:
73918
Filename:
RRPathCh17GIdisorders1.txt
Updated:
2011-03-28 19:52:01
Tags:
Rapid Review
Folders:

Description:
RR Path Ch 17 GI disorders 1
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user mcaster24 on FreezingBlue Flashcards. What would you like to do?


  1. Oral Cavity and Salivary gland disorders:
    Cleft Lip and Palate
    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
  2. Oral Manifestations of HIV
    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!
  3. Dental Caries
    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.
  4. Common Infections of Oral Cavity: Viral
    • 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
  5. Infections of Oral Cavity: Bacterial
    • 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
  6. Infections of Oral Cavity: Fungal
    • 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
  7. Non Infectious ulcerations in Oral Cavity
    • 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
  8. Pigmentation Abnomalites
    • 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
  9. Tooth discoloration
    • 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
  10. Macroglossia (enlarged tongue) causes:
    • Myxedema:
    • severe primary hypothyroidism

    Downs syn:

    Acromegaly

    Amyloidosis

    Mucosal neuroromas in MENIIb (MENIII)
  11. Glossitis (inflammation of tongue) causes:
    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
  12. Leukoplakia and Erythroplakia
    • 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.
  13. Lichen Planus and Dentigerous cyst
    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.
  14. Benign Tumors of Oral Cavity (excludes salivary gland)
    • 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
  15. Malignant Tumors of Oral Cavity (except salivary gland)
    • 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
  16. Salivary gland disorders
    • 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.
  17. Esophageal Disordes: Signs and symptoms of esophageal dz.
    • 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
  18. Esophageal disorders: Tracheoesophageal (TE) fistula
    • 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
  19. Esophageal disorders: Plummer Vinson syndrome
    • due to chronic iron deficiency
    • Leuloplakia in oral mucosa and esophagus
    • Intermittent dysphagia for solids. This b/c of an esophageal web or stricture
  20. Esophageal Disorders: Esophageal diverticulum
    • 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
  21. Esophageal disorders: Hiatal Hernia
    • 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.
  22. Gastroesophageal reflux dz (GERD)
    • 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.
  23. Barrett's esophagus
    • 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
  24. Infectious Esophagitis
    • 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)
  25. Corrosive esophagitis
    • Ingestion of strong alkali (e.g. lye) or acid (HCl, etc)
    • Complications:
    • stricture form
    • perforation
    • squamous cell carc
  26. Esophageal varices
    • 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
  27. Mallory-Weiss syndrome
    • 1. Mucosal tear in proximal stomach and distal esophagus. due to severe retching in alcoholics or bulimia
    • 2. Causes hematemesis
  28. Boerhaave's syndrome
    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
  29. Motor disorders
    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
  30. Esophageal tumors
    • 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%
  31. Stomach Disorders: Signs and sxs of stomach dz
    • 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.
  32. Stomach disorder: congenital pyloric stenosis (CPS)
    • 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
  33. Stomach disorder: Gastroparesis
    • 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
  34. Stomach Disorders: Acute hemorrhagic (erosive) gastritis
    • 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
  35. Stomach disorder: Chronic atrophic gastritis:
    • 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
  36. Stomach Disorders: Peptic ulcer dz (PUD)
    • 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
  37. Stomach Disorders: Zollinger Ellison syndrome
    • 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
  38. Stomach Disorder: Gastric Polyps
    • 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
  39. Stomach Disorders: Gastric Tumors part 1
    • 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
  40. Stomach disorders: gastric tumors part 2
    • 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.
  41. Small Bowel and Large Bowel disorders: Signs and symptoms of small bowel dz
    • 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
  42. Signs and Sxs of Large Bowel Dz
    • 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
  43. Diarrheal Dzs (excluding malabsorption)
    • 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
  44. Malabsorption 1
    • 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
  45. Malabsorption 2
    • 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!

What would you like to do?

Home > Flashcards > Print Preview