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60 Cards in this Set
- Front
- Back
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non neplastic rxn of lungs to deposits of inorganic dusts, organic dustts, fumes & vapors, excluding asthma, bronchitis & emphysema
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pneumoconiosis
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tissue response from pneumoconiosis depends upon multiple factors including:
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chemical composition of dust
crystalline form of the dust quantity of the dust deposited host factors |
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how much dust is deposited in lungs varies with several factors:
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concentration of dust in the inspired air
duration of exposure ventilation pattern ofthe hostaswell as the size, shape, charge & solubility of the inspired dust more than 40 diff inhaled mineralscan produce lung lesions & radiographic abrnomalities; most are relatively innocuous; however, some can cause severe pulm dz |
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respirable particles
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generally < 5 microns aerodyynamic size
larger particles deposit on nasal, oropharyngeal & ciliatd resp mucosa & swallowed or expectorated as particle sizedropsbelow 1 micron, they start to act more like gases and do not deposit as effectively in the distal parenchyma |
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complicated pneumonoconiosis
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generrally refers to dust dz's that include consolidated (usually fibrotic) foci that are > 1 cm
assessment can be made pathologically or radiologically |
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progressive massive fibrosis: PMF
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generally refers to consolidated fibrotic foci that are > 1-2 cm
most are substantially > 2 cm |
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anthracosis
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accumulation of carbon pigment from inhaled smoke or dust in thelungs
small amount of dust is foten found in the lungs of almost all adults dust more prominent in urban populations and evne more so in smokers this level of dust accumulation is generally not associated with significanat functional deficits |
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coal workers pneumoconiosis: CWP
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no sharp cut off b/w anthracosis and CWP
pulm rxn due to inhaled coal dust may be seen in both simple & complicated forms coal miners with CWP have genreally been exposed to relatively high levels of respirable coal dust for > 20 yrs b4 clinical pic of CWP seen |
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simple CWP
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coal macules : 0.1-0.5 cm
coal nodules in centriacinar zones, involving resp bronchioles focal centrilobular emphysema (focal dust emphysema) may be associated with these lesions - lesions tend to be more prominent in upper zonesof lungs |
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simple CWP microscopically
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dust lesions consist of dust filled macs surrounding dilated resp bronchioles
coal nodule very similar to coal dustt macule, except coal nodule is palpable and may have small amount of delicate fibrosis centrally |
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functional deficit in simple CWP
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little that can be attributed to these lesions
minorfuncitonal abnormalities that have been reported are most likely relatedto industtrial bronchitis simple CWP usually does not progress in absence of further exposure |
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complicated CWP
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small % of ppl will have lesions that are > 1 cm
fibrosis prominent may develop sig functional defects progressive massive fibrosis: PMF: lesions > 2 cm - range from a few cm to large lesions that actually extend across lobar fissures & destroy sig portions of lung parenchyma |
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complicated CWP progression & disability
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progresses whether exposure ends or not
may be associatd with sig pulmonary disability & premature death many of cses are actually anthrosilicosis due to exposure to respirablesilic in addition to coal dust |
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silicon accounts for what % of earth's crust
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28%
so potential for exposure to oxides of silicon is ubiquitous (everywhere) |
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silica (silicon dioxide) occurs in
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amorphous or crystalline forms
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silicosis occurs as rxn to
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inhaled crystalline silic, of which quartz is one example
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silicosis 2 forms seen clinically
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classic/nodular/chronic silicosis: characterized by formation of hyalinized collagenous nodules
acute silicosis: lipoproteinosis |
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chronic (simple) silicosis
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generally not seen b4 20 yrs of exposure
although very high exposuremay result in disease after as little as 5-10 years of exposure (accelerated silicosis) |
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chronic silicosis classic lesions
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hyalinized, fibrotic silicotic nodules: each measuring 0.2-0.4 cm in diamter
nitally located bout resp bronchioles hilar LN's may conain similar lesions with eggshell calcificaiton of the nodes freq visible radiographically upper lung involvement predominates often progressive, even if dust exposure ends |
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complicated chronic silicosis
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lesions > 1 cm
may include conglomerate nodules (fused hyalinized nodules), PMF or secondary infection with tb fibrotic changes may lead to severe functional defects |
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acute silicosis
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lipoproteinosis
relatively rare pulmonary rxn caused by heavy exposure over a relatively shortt period (1-3 yrs) to high levels of silic a of small particle size - sandblasting, boiler scaling |
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acute silicosis pathology
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alveolar proteinosis with varying degress of background fibrosis or chronic silicosis
die after relatively brief courses (multiple months to few years) compared to chronic nodular silicosis, which may progress over multiple years to decades |
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asbestos: family of
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natural fibrous silicate minerals with a crystalline structure
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2 major fibertypes of asbestos
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serpentine (chrysotile)
more pathogenic: amphiboles (crocidolite, amosite, tremolite, actinolite, anthophylite) |
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3 main areas of pulm path associated with exposure to respirable asbestos
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pulmonary fibrosis: asbestosis
tumors pleural disease |
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asbesttos induced dz accounts for how many deather per year in US alone
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>10,000
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latent period in asbestos dz
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long latent period b/w exposure & development of dz due to asbestos
freq on order of 20-30 yrs |
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asbestosis
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fibrotic lung dz due to asbestos
- latent period of 20-30 yrs - diffuse interstitial fibrosis more prominent in lower lung zone - fibrosis more prominent peripherally than centrally - asbestos fibers (amphibole) may be encrusted with an iron protein coating resultin in formation of ferruginous bodies (other respirable dust particles may also lead to formation of ferruginous bodies) ferruginous bodies with asbestos core = asbestos body - fibrotic process begins in resp bronchioles & proximal alveolar ducts |
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asbestosis progression
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often proressive even after exposure discontinued
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asbestos related tumors
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diffuse malignant mesothelioma
bronchogenic carcinoma |
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diffuse malignant mesothelioma
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relatively rare
highly fatal malignancy of the mesothelial lining of the pleural or peritoneal cavities not related to smoking incidence of tumor increased up to 1000 fold by exposure to respirable asbestos - amphiboles account for great majority of asbestos induced mesotheliomas |
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latent period of diffuse malignant mesothelioma
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b/w exposure & development of tumor usually > 20 yrs
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diffuse malig mesothelioma tumor diffusely involves
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pleura, ecasing lung
epithelial, sarcomatoid and mixed varinats |
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bronchogenic carcinoma
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exposure to respirableasbestos also associated with increased incidence of bronchogenic carcinoma of about 5 times backgroun, non smoking, non exposed pop
smoking has synergistic effect on asbestos exposure yielding 50 fold increased risk for it in individuals with asbestosis: not simply asbestos exposure alone |
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asbestos pleural disease
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often occurs in absence of parenchymal lesions (asbestosis)
pleural effusions: usually smmall, asymptomatic pleural plaques: bilateral, parietal pleura; diaphragms, marker of exposure to respirable asbestos difffuse pleural fibrosis: rare |
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systemic disease caussed by exposure to beryllium or beryllium compounds
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berylliosis
mining, computer, aerospace, and nuclear industries work with beryllium alloys |
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acute berylliosis
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symptoms within hours to days after inhalation of beryllium metal
essentially chemical pneumonitis with pathologyy of DAD +/- injuryy of upper airways - rhinitis, pharyngitis, ttracheobronchitis usually heavy exposure most recoverif they survive the DAD period |
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chronic berylliosis
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may develop in small # of ppl who have an acute episode or may develop without an acute phase
host factors are important as only 2% of thosse exposed develop dz |
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chronic berylliosis latent period
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may be as long as 15 yrs from exposure to some individuals
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chronic berylliosis pathology
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noncaseating granulomas (type IV hypersensitivity rxn) with interstitial fibrosis
clinical & path pic may ver closely mimic sarcoidosis clinical history & lab data (tissue analysis, urine beryllium analysis and/or lymphocyte blast transformation studies) necessary to make dx about 2 fold increase in bronchogenic CA with occupational beryllium exposure |
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numerous cases of eosinophilic pneumonia/pulmonary eosinohpilia
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acute eosinophilic pneumonia with resp failure
simple pulmonary eosinophilia tropical eosinophiia other parasites chronic eosinophilic pneumonia vasculitis allergic bronchopulmonary aspergilosis other causes |
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acute eosinohpilic pneumonia with resp failure
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rapid onset
fever hypoxxemia often steroid responsive DAD histology with eosinophils |
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simple pulmonary eosinohpilia
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Loffler's syndrome
transiet pulmonary infiltrates peripheral blood eosinohpilia benign clinical course |
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tropical eosinophilia
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filarial worms: Wuchereria, Brugia
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other parasites that cause eosinophilic pneumonia
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ascaris, toxocara, strongyloids: larval migration through lungs
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chronic eosinohpilic pneumonia
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idiopathic in majority of cases
clinical: asthmatic symptoms, atopy, cough, fever, sweats, wt loss, patchy subpleural lung infiltrates idiopathic form is steroid responsive |
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vasculitis causing eosinophilic pneumonia
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Churg-Strauss syndrome/asthma
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other causes of eosinohpilic pneumonia
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infection
CT diseases drug rxn crack cocain L-tryptophan |
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smoking relatd interstitial disorders include
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desquamative interstial pneumona: DIP
respiratory bronchiolitis associated interstital lung disease: RB-ILD |
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desquamative interstital pneumona: DIP
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IS lung dz characterized by airspace collections of smokers' macs (once though to be desquamated type 2 pneumocytes) and a chronic IS inflammatory infiltrate
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DIP clinical
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smokers
30-50 yrs old few months of dry cough clubbing in 50% mild restriction, mild to moderate drop in DLCO bibasilar ground glass changes (airspace filling) predominate on CT scans |
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DIP prognosis
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does not progress to sig honeycomb change
overall good prog with 10 yr survivals of 70-90% smoking cessation & steroids are effective |
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resp bronchiolitis associated interstitial lung disease: RB-ILD
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smokers' bronchiolitis characterized by smokers' macs accumulating about resp bronchioles
when smokers bronchiolitis associated with clinical symptoms, PFT changes, and radiologic infiltrates |
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RB-ILD clinical
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smokers (>30 pack-years)
30-40 yrs old several months of dyspnea, cough, no clubbing mild restriction,mild decrease in DLCO ground glass changes and centrilobularr nodules on CT scans |
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RB-ILD prognosis
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good if stop smoking
often do not requiure steroids |
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patchy bilateral accumulation of surfactant
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alveolar proteinosis
- defective clearance, increased production, or combo accumulation of homogenous PAS + granular surfactant rich material in alveolar spaces & bronchioles with almost no inflammatory response autoimmune, secondary, congenital |
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autoimmune alveolar proteinosis
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acquired
90% of cases thought to be autoimmune disorder related to anti-GM-CSF antibody wwhich functionally impairs GM-CSF clearance mechanisms for surfactant |
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secondary alveolar proteinosis
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uncommon
malignancy leukemias immunodeficiency acute silicosis others |
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congenital alveolar proteinosis
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rare: immediate onset of neonatal resp distress
ABCA3 lamellar body membrane; surfacant protein B, surfactant protein C, GM-CSF mutations plus others - interefere with transportation and clearance of surfactant |
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alveolar proteinosis clinical
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productive cough with gelatinous sputum, frequent secondar infections
autoimmune : vriable course = some resolve spontaneously while other progress to resp failure secondary forms: often prognonsis of underlying disorder congenital: almost always fatal |
