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74 Cards in this Set
- Front
- Back
PFTs in COPD:
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dec FEV1, inc FVC ==> dec FEV1/FVC ratio
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extent of ciliated mucosal epithelium in respiratory tract
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nose to terminal bronchioles
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what protects alveoli from inhaled particles?
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ciliated epithelium -> mucociliary clearance
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pathogenesis of centriacinar emphysema
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oxidative injury to resp bronchioles --> PMN recruitment --> elastase, proteinase, cathepsin, and MMPs released , along with oxygen free radicals which --| alpha1antitrypsin ==> protease-antiprotease imbalance --> acinar wall destruction
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clearance of differnt sized particles from resp tract
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10-15 um: trapped in URT; 2-10um: mucociliary xport; <2um (eg dust): phagocytosed by macrophages --> cytokine rleases --> tissue injury, inflammation --> fibrosis ==> PNEUMOCONIOSIS
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3 causes of pulmonary hypertension
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1) hypoxic vasocnstriction (eg following COPD); 2) volume overload (left heart, eg in decomensated cadiac disorder); 3) idiopathic dysfunction of the endothelium --> impaired apoptosis --> inc wall thickness
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most common cause of lung abscess
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aspiration of oropharyngeal contents (fusobacterium, peptostreptococcus, bacteroides); a/w LOC (EtOH, seizures, anesthesia)
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clinical triad of fat embolism syndrome
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1) hypoxemia (fat emoblus in lungs); 2) petechial rash (thrombocytopenia /petechiae from platelet adherence to and coating of fat microglobules; 3) neuro abnormalities (microinfarctions of brain tissue)
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role of type II pneumocytes
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1) secrete surfactant (dec alveolar surface tension); 2) presurcors of type I cells (proliferate during lung damage)
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which lung more common for inhaled foreing bodies?
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right lung (right main stem bronchus has less acute angle)
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lobes of each lung
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R: sup, middle, inf; L: sup, inf, Lingula, + space for heart
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relation of pulm artery to bronchus at each lung
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RALS (Right Anterior; Left Superior)
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where do structures perforate the diaphragm?
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"I 8 10 EGGS AT 12": T8: IVC; T10: EsophaGus + vaGus; T12: Aorta, Azygous, Thoracic duct
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muscles of forced inspiration (3)
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external intercostals, scalene muscles, SCM
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muscles of forced expiration
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"abs" + internal intercostals
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diffusion limited
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equilibrium not reached by the time blood reaches end of capillary -- seen in exercise, emphysema, fibrosis, and with CO
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calculating physiologic dead space
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V_D = V_T * (1 - PeCO2/PaCO2) = V_T * ( (PaCO2 - PeCO2)/PaCO2 )
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changes in v/q with exercise
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exercise --> vasodilation of apical arteries --> V/Q approaches 1
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three methods of CO2 transport from tissue to lungs
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1) as Bicarb (converted by CA) (90%); 2) bound to Hb as carbaminohemoglobin(5%); 3) dissolved CO2 (5%)
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how does Hb unload CO2 in lungs?
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Haldane effect: oxygenation of hemoglobin --> release of CO2
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how does O2 get unloaded in the tissues?
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tissues build up acid form metabolism; inc H+ --> shifts Hb curve to right --> unloading of O2 (Bohr effect)
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how to calc A-a gradient
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Aa gradient = PAO2 - PaO2; PAO2 = PiO2 - PACO2/R = 150 - PACO2/0.8
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causes of emphysema
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smoking (centriacinar) and alpha1-antitrypsin deficiency (panacinar + liver cirrhosis [accumulation of unreleased A1AT])
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emphysema vs bronchitis
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EMPHYSEMA: "pink puffer," decreased breath sounds, tachycardia, dec I/E ratio; BRONCHITIS: "blue bloater," wheezing, crackles, cyanosis
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findings in asthma
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wheezing, dec I/E ratio, pulsus paradoxus, Curschmann spirals, smooth muscle hypertrophy, mucous plugging
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what causes bronchiectasis?
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chronically infected/dilated bronchi/airways, often b/c of bronchial obstruction, CF, poor cilia motility, and Kartagener's syndrome
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PFTs in obstructive vs restrictive lung disease
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OBSTRUCTIVE: dec FEV1/FVC ratio; RESTRICTIVE: dec FEV1 and lung volumes (VC, TLC, FVC), but FEV1/FVC ratio > 80%
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causes of interstitial lung disease (8)
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ARDS, NRDS, IPF, Sarcoidosis, Pneumoconioses, Goodpasture, Wegener's, Eosinophilic Granuloma
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in what population do you see asbestosis?
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plumbers and shipbuilders
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pathologic findings in asbestosis
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Ferruginous bodies in lung (asbestos fibers coated in hemosiderin) + ivory-white plaques
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pathogenesis of NRDS
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surfactant deficiency --> inc surface tension --> atalectasis (alveolar collapse)
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tx for NRDS
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maternal steorids beore birth, artificial surfactant for infant
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central bronchogenic carcinomas
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squamos cell, small cell
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peripheral bronchogenic carcinomas
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1) ADENOCARCINOMA (most common); 2) BRONCHIOALVEOLAR (no smoking link); 3) LARGE CELL (undifferentiated)
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where do lung tumors met to?
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Brain (seizures), Bone (fractures), Liver (jaundice, hepatomegaly)
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complications from lung cancer
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SPHERE (SVC compression/invasion, Pancoast tumor, causes Horner syndrome (cervical sympathetic plexus dysfunction), Endocrine (paraneoplastic), Recurrent laryngeal symptoms (hoarseness), Effusions (pleural or pericardial)
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lobar pneumonia: bugs and characteristics
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pneumococcus; lobar consolidation (can be of whole lung)
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bronchopneumonia: bugs and characteristics
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S. aureus, H.flu, Klebsiella, S.pyogenes; patchy distribution, acute inflam infiltrates from bronchioles to alveoli
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interstitial (atypical) pneumo: bugs and characteristics
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viruses (RSV, adeno), mycoplasma, legionella, chlamydia; diffuse patchy inflam, localized to interstitla areas at alveolar walls
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PFTs in asthma vs emphysema
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both COPD so both have dec FEV1/FVC, inc TLC; however, EMPHYSEMA causes destruction of alveoli and adjoining capillary beds --> DECREASED DLCO, while ASTHMA INCREASE DLCO due to increased pulmonary blood volumes
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how to rule out asthma?
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METHACHOLINE: muscarinic agonist --> causes bronchioconstriction (sensitive but not specific)
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extrinsic vs intrinsic asthma
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extrinsic (atopic, allergic) asthma caused by Type I hypersensitivity to inhaled / ingested allergens, begins in childhood; INTRINSIC asthma is a/w chronic bronchitis, exercise, and cold-induced asthma; occurs in ADULT life, no a/w allergy
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pathogenesis of ARDS
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diffuse alveolar damage --> NEUTROPHILS --> leaky alveolar capillaries --> protein-rick fluid in alveoli ==> intra-alveolar hyaline membrane
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chronic lung rejection
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causes bronchiolitis obliterans -- lyphocytic inflam, necrosis, and fibrosis of small airways ==> eventual occlusion of bronchiolar lumen
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MCC meconium ileus
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CF
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MCC death in CF
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cardiorespiratory complications (pneumonia, bronchiectasis, cor pulmonale) -- 80%
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embryologic origin of diaphragm
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Some Parts Build Diaphragm (Septum Transversum, Pleuroperitoneal folds, Body Wall, Dorsal mesentary of the esophagus)
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cheyne-stokes breathing
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caused by pontine dysfunction, a/w drug OD, hypoxia, CNS depression, CHF, inc intracranial pressure
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hyaline membranes
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eosinophlic membranous structures lining alveolar wall; characteristic of both ARDS and NRDS
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common description of pt with spontaneous PTX
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tall, slender men 20-40 yo
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bronchial obstruction vs pneumothorax: tracheal deviation
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both have tracheal deviation; in PTX, trachecial deviation AWAY from lesion; in bronchial OBSTRUCTION, tracheal devation TOWARD lesion
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increased Reid index
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chronic BRONCHITIS (persistent irritation --> hyperplasia of goblet cells and submucosal glands)
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what does "blue bloater" mean
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BRONCHITIS: blue = cyanosis, bloater = peripheral edema from pulmHTN and RV overload (cor pulmonale)
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what does "pink puffer" mean
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EMPHYSEMA: pink = not cyanotic (PaO2 ~ nl); puffer = hypervent
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3 MCC hemoptysis
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TB, malignancy, Goodpasture
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honeycomb lung
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idiopathic pulmonary fibrosis
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silicosis seen in what occupations?
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mining, stone cutting, glass production (inhaled silica dust --> macrophages -> alveolar damage, scarring)
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immune response in typical vs atypical pneumo
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TYPICAL: PMNs, fibrin, RBCs (sputum = bac + PMNs); ATYPICAL: T cells and macrophages (intracellular orgs --> no sputum)
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pneumo in dairy workers
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coxiella burnetti
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fungal ball of hyphae in preexisting lung cavity
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aspergilloma (aspergillus)
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most common location of TB
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PRIMARY: upper lower lobe or lower upper lobe; SECONDARY: apical
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rifampin interactions with other drugs
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rifampin INDUCES p450, so it REDUCES HALF LIFE of: {oral contraceptives, warfarin, digitoxin, ketoconazole, propanalol, prednsione}
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causes of viral rhinitis
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Rhinovirus, coronavirus, adenovirus, parainfluenza virus
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mech of action of streptomycin
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same as aminoglycosides (--| initiation of ribosomal complex)
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reid index
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(thickness of mucous gland layer) / (thickness of bronchial wall between resp epithelium and bronchial cartilage) ==> measure of MUCOUS GLAND ENLARGEMENT, increased in CHRONIC BRONCHITIS
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MCC cause and site of lung abscess
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cause: aspiration; site: right lung (right bronchus is straighter than left), lower lobe if standing during aspiration, posterior if supine
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immune response to TB
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macrophage phagocytosis --> Ag presentation to CD4+ TH1 cells --> stim macrophages --> kill M.TB, form Langerhans giant cells
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most common side effect of inhaled steroids
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oral candidiasis (risne mouth to prevent)
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epithelium of respiratory tree
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pseudostratified ciliated columnar until respiratory bronchioles --> simple cuboidal ciliated until alveoli --> no cilia in alveolar sacs / terminal alveolar ducts
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chronic obstructive disease with recurrent resp infections
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chronic bronchitis
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sweating in CF vs normal person
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in normal people, CFTR makes sweat hypotonic (pulls Na/Cl back from isotonic sweat); this creates hypertonic volume loss in which ECF loss is compensated for by redistribution from ICF; in pts with CF, lack of CFTR causes secretion of isotonic sweat --> exclusively extracellular volume contraction --> hypovolemia, severe hypotension
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minute ventilation vs alveolar ventilation
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minute ventilation includes dead space, alveolar ventilation does not
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source of gastrin, location
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G cells in stomach/duodeneum
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common locations of gastrinoma (zollinger-ellison syndrome)
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pancreas (MEN I), duodenum
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