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64 Cards in this Set
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A 43-year-old African-American orthopedic surgeon is being evaluated because he is unable to complete his usual 18 holes of golf without gasping for air. He has no past medical history. He has never smoked. On physical exam his vital signs are normal and there are fine inspiratory rales in both lungs but no wheezing. Cardiac examination is normal. There is no clubbing or cyanosis but there is trace, pitting edema of both distal lower extremities
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Sarcoidosis
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What is the differential diagnosis for parenchymal diseases?
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SHITFACED IM
Sarcoidosis Histiocytosis-X (eosinophilic granuloma) Idiopathic pulmonary fibrosis (UIP) Tuberculosis Furadantoin (Nitrofurantoin) Asbestosis Collagen vascular disease Extrinsic Allergic Alveolitis (hypersensitivity pneumonitis) DIP (Desquamative interstitial pneumonitis) Infections Malignancy |
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What is sarcoidosis?
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multisystem granulomatous disorder of unknown etiology characterized by noncaseating granulomas in involved organs
Commonly affects young & middle-aged adults & frequently presents w/ bilateral hilar lymphadenopathy, pulmonary infiltrates & skin lesions (other organs can be involved) |
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Describe the epidemiology and clinical presentation of sarcoidosis
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A. epidemiology
more prevalent among African-Americans (black women have highest risk) Peaks in 4th decade Higher prevalence among nonsmokers B. Most common symptoms 1. Shortness of breath 2. Nonspecific chest pain 3. Nonproductive cough 4. Hemoptysis note-can present in acute, subacute or chronic forms; patients are often asymptomatic |
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Describe the staging of Sarcoidosis based on imaging
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A. Stage 1 (most common)-bilateral hilar adenopathy; normal lung parenchyma; usually asymptomatic; usually regresses on its own
B. Stage 2-bilateral hilar adenopathy and lung involvement; usually symptomatic; most (2/3) undergo spontaneous regression C. Stage 3-significant fibrosis without bilateral hilar adenopathy; no spontaneous regression D. Stage 4-characterized by reticular opacities w/ evidence of volume loss;pulmonary fibrosis w/ honeycombing, cysts & bullae; won't spontaneously regress |
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Describe the lab findings of Sarcoidosis
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Angiotension Converting enzyme (ACE)-lacks specificity; can't be used for definitive diagnosis
Hypercalcemia/Hypercalcuria Elevated liver function test Elevated creatinine |
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How do you make the diagnosis of sarcoidosis?
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1. clinical picture
2. histologic findings-epitheloid (noncaseating granuloma) w/ little or no necrosis is hallmark sign (not specific for sarcoidosis) 3. exclusion of other diseases note-potential biopsy sites lymph nodes, skin, lung parenchyma (higher prevalence in parenchymal disease) |
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Describe the treatment of sarcoidosis
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A. Asymptomatic-monitor
B. Steroids (6-12 months) Indications: Progressive pulmonary impairment or respiratory symptoms Ocular involvement Myocardial involvement CNS sarcoidosis Disfiguring cutaneous lesions Persistent hypercalcemia/hypercalicuria w/ renal insufficiency note-influence of steriods on natural history of disease unknown C. Steroid Sparing Agents (hydroxy)-chloroquine; zathiaprine; methotrexate (most common); cyclophosphamide D. Lung Transplantation (last resort) |
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23-year-old man presents to you with yet “another” respiratory infection. He tells you that he had 3 “viral illnesses” so far this year that are characterized by fever, dyspnea, and occasional wheezes. Each time he is given antibiotics the illness resolves. Lately, these episodes have become more frequent and he doesn’t think he fully recovers from them. He is a sales representative for a communication company. He has never smoked cigarettes and has had no exposures to irritant fumes or chemicals. He is working part-time in a pet store that specializes in birds.
His physical exam is unremarkable except for bilateral fine rales. His PaO is 59 mm Hg at rest |
hypersensitivity pneumonitis
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What is hypersensitivity pneumonitis(extrinsic allergic alveolitis)?
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caused by inhaled organic dust or chemicals producing an immunologically mediated inflammatory response of alveoli and terminal bronchioles
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Describe the clinical presentation of hypersensitivity pneumonitis (HP) and differentiate b/t acute, subacute, and chronic processes
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characterized based on frequency, length of exposure and duration of illness; occupational & environmental history are important for accurate diagnosis
a. acute-symptoms characteristically occur 4-6 hours after initial heavy exposure; removal of exposure results in subsiding symptoms w/in 12hrs to several days (complete resolution of physical signs w/in several weeks); may recur w/ re-exposure b. subacute-gradual development of symptoms (productive cough, dyspnea, fatigue, anorexia, weight loss) c. chronic-continuous or low intensity exposure for months-years; insidious onset of cough, dyspnea, fatigue & weight loss; fever/chills usually absent; may progress to severe pulmonary fibrosis |
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Describe the findings of imaging for HP
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A. CXR (not good diagnostic tool)
1. acute or subacute-fine reticular pattern w/ multiple small defined nodules; diffuse nodular shadows involving middle & lower lung zones 2. chronic-infiltrate will takes coarser interstitial pattern (honey-combing) B. high resolution CT (improved sensitivity) 1. Acute & subacute-bilateral air-space consolidation, ground glass opacity & small ill-defined centrilobular nodules 2. Chronic-often mirror pulmonary fibrosis w/ honeycombing, irregular reticular opacities, traction bronchiectasis |
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Describe the PFT and histopathological findings associated w/ HP
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A. PFT
acute-restrictive pattern (seen 4-6 hrs after exposure); PFT improvement occurs 12-18 hrs after removal of exposure(complete resolution occurs w/in 1-6 months) chronic-restrictive defect B. pathology-noncaseating granulomas; advanced cases may have interstitial fibrosis; organic dust & fungal spores may be seen |
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Describe the serum precipitins testing done in HP
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Antigenic material used to test for circulating Abs are contain up to 50 antigenic substances (lack standardization)
Sensitized patients to a specific Ag may not react due to the lack of antigen in test material (absence of serum precipitins does not rule out HP) |
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What is the diagnostic criteria for HP?
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1. Characteristic signs & symptoms
2. radiographic findings (HRCT best imaging) 3. PFT data 4. Evidence of exposure to relevant Ag w/ relationship to clinical findings 5. Exclusion of other illnesses |
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Describe Bird-Breeder's lung
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Most common to encounter chronic form of disease
Higher incidence of serum precipitins in bird-breeder’s than other forms of HP (responsible agents are avian proteins from urine & feces) Exposure to occur more continuously than w/ seasonal variations |
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What is the prognosis and treatment of HP?
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A. prognosis
majority of pts experience near total recovery (bird fancier’s HP has worse prognosis due to owner's refusal to get rid of birds) Repeated exposure increases risk for progressive impairment or continued symptoms Factors affecting prognosis include repeated episodes & presence of restrictive defect on spirometry note-smokers have less incidence than non-smokers B. treatment 1. avoidence of Ag 2. corticosteroids-judgment call |
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Differentiate b/t the different exposure types of HP
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Bird Fancier’s Lung–proteins from bird feathers & droppings
Farmer’s lung-xposure to saccharopolyspora rectivirgula (theromphilic atinomycetes) in moldy hay Silo filler’s disease-inhalation of gases (oxides of nitrogen) from plant material Byssinosis-ccurs in workers in textile factors; contact with cotton, linen, hemp products;workers feel better over the weekend (no exposure to Ags); depression occurs when returning to work (Monday morning blues) Office workers lung-similar presentation to byssinosis (monday morning blues) |
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72-year-old man is found to have an abnormal CXR during a pre-op evaluation for bilateral total knee replacement surgery. He denies any respiratory complaints. His O2 saturation is normal on room air. Spirometry is unremarkable. He is a retired after working 30 years in a shipbuilding yard
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Asbestosis
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What is asbestosis?
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slowly progressive diffuse interstitial fibrosis produced by inhalation of asbestos fibers
associated w/ magnitude & duration of exposure to inhaled particles (has been found many years after brief intense exposure) latent period b/t state of exposure & discovery of asbestosis usually >15 yrs 4 disease categories: Pulmonary fibrosis (asbestosis) Benign asbestos-related pleural response Bronchogenic carcinoma Mesothelioma |
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Describe the pathologic features of asbestos
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Inhaled asbestos in lung is coated w/ proteinaceous iron resulting in Feruginous body
Pulmonary fibrosis in asbestos in lower lobes (asbestos particles are heavy) advanced disease-lungs small & fibrotic Honeycombing may be prominent in lower lobes |
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What are some clinical features of asbestosis?
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Diagnosis usually based on
presence, extent & nature of disease; important to determine exposure history & duration Asymptomatic for at least 20-30yrs after initial exposure Earliest symptom is the gradual onset of dyspnea w/ exertion clubbing of digits; rales |
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Describe the findings on PFT associates with asbestosis
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1. Restrictive ventilatory defect
2. Hypoxemia may be present at rest or exercise 3. Diffusion capacity reduced note-if airflow obstruction is presnent-->reflects concomitant cigarette smoking |
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Describe imaging findings associated w/ asbestosis and treatment
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A. CXR
Interstitial pattern begins in lower lung zones & associated w/ mid-lung zone pleural plaques (diagnostic of asbestosis) Honeycombing develops in advance disease B. HRCT (more sensitive than CXR) Pulmonary Fibrosis Honey combing Pleural plaques (diagnostic) C. treatment Early detection & prompt removal of workers Smoking cessation (key!!) |
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Describe pleural diseases associated w/ asbestosis
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a. pleural plaques-smooth white raised lesions located on posterolateral aspect of parietal pleura or diaphragm; asymptomatic in pts w/out parenchymal disease
associated w/ likelihood of developing parenchymal disease; seen >20yrs after exposure b. pleural thickening (worsening of pleural plaque)-more diffuse; associated w/ parenchymal disease (symptomatic); asbestos bodies can be found in visceral pleura c. pleural effusions-may persist for months-years; may be bloody symptoms-chest tightness, pleuritic chest pain, fever, dyspnea may reoccur on same side or opposite side after yrs of exposure d. mesothelioma-arise in pleura & peritoneum; occurs in from exposure in workplace or living near mines (women living in shipyard or from husband's clothes) smoking does not enhance prevalence of disease |
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Describe the association of lung cancer w/ asbestos
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Average latency period: 20-30yrs
Association of lung cancer with smokers & asbestos exposure is multiplicative (Adenocarcinoma & squamous cell carcinoma) note-smoking increases chance of lung cancer in association w/ asbestosis, but decreases or doesn't affect risk of mesothelioma |
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56-year-old man is discovered to have abnormal densities on a pre-op CXR. He tells you that he has had “abnormal spots” on his CXR for years. He has no respiratory symptoms. He worked as a sandstone driller for over 20 years.
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silicosis
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What is silicosis?
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attributed to inhalation of silicon dioxide or silica; occurs in form of silicates such as asbestos, mica & talc
Most common occupational lung disease worldwide (coal mining, concrete making, dentists-grinding teeth molds) |
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Describe the clinical features and diagnostic criteria of silicosis
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A. clinical features
Dyspnea-initially w/ exercise Cough w/ or w/out sputum Wheezing or chest tightness which can lead to respiratory failure B. diagnostic criteria 1. Exposure history sufficient to cause degree of illness & appropriate latency period from time of 1st exposure 2. CXR-shows opacities consistent w/ silicosis 3. exclusion of other diseases |
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Describe the PFT of silicosis
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May provide early detection of disease before CXR findings
usually show restrictive defect a. simple silicosis-normal or reduced VC, TLC b. complicated silicosis-reduced lung volumes, diffusion capacity & arterial desaturation c. acute silicosis-restrictive defect w/ reduced diffusion capacity & arterial desaturation |
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Describe the chest x-rays (CXRs) of silicosis and differentiate between types)
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a. simple silicosis-enlargement of hilar nodes may precede parenchymal disease; small round opacities (egg-shell calcification of hilum)
b. complicated silicosis-mass lesions tend to contract in upper lobes (oalescence of small densities to form larger lesions); Opacities >1cm |
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Describe the treatment and complicatiions of silicosis
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A. treatment
Prevention rather than cure Corticosteroids may be helpful Supportive care Lung Transplantation B. complications 1. tuberculosis 2. malignancies 3. pneumothorax |
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A 65 year old male retired teacher presents with a dry cough and dyspnea on exertion that began 15months ago. It has gradually progressed to the point that he is unable to perform his usual activities. He has never smoked and has no known exposure to environmental respiratory hazards.
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interstitial lung disease (ILD)
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What is interstitial lung disease?
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diverse group of lung infiltrates cause disruption of alveolar structures & have common clinical, radiographic & physiological consequences
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Describe the etiology of ILD
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2/3 of cases have no known cause; classified based on clinical, radiographic & pathological features
Classification of ILD A. Occupational/Environmental B. Drugs & Poisons (most common cause of ILD)-know medications patient is currently taking and what they have taken in the past; amiodarone (heart medication-must common drug to cause ILD); Nitrofurantoin (decreasing frequency of use) C. Connective Tissue Disease (more common in women w/ exception of RA) D. Idiopathic ILD E. Infection F. Other Systemic Disease |
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Describe idiopathic interstitial pneumonia
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Initially thought to be same disease w/ different stages of idiopathic pulmonary fibrosis
reclassified into 4 categories: 1. Usual Interstitial Pneumonia (UIP) 2. Nonspecific interstitial pneumonia (NSIP) 3. Desquamative interstitial pneumonia 4. Acute interstitial pneumonia |
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Describe the pathogenesis of ILD
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repeated stimulus-->sequential lung injury-->inflammation and aberrant wound healing-->fibrosis
(genetic factors-->inflammation and Th1/Th2 balance-->aberrant wound healing) |
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Describe the history and physical exam findings of a patient w/ ILD
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A. history (most important initial evaluation tool!)
patients middle aged presenting w/ progressive dyspnea & nonproductive cough Smoking history Detailed & life-long occupational-long latency period from time of exposure to disease; environmental Ags & occupational exposure may lead to hypersensitivity pneumonitis current and prior Medication Use and Irradiation B. physical exam bibasilar rales clubbing of fingers common in idiopathic pulmonary fibrosis (rare in Sarcoidosis) signs of pulmonary HTN or right heart failure are seen only in advanced diseases |
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Describe the imaging findings of ILD
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A. CXR
suggests presence but not stage of ILD Most common radiographic pattern is reticular or reticulonodular pattern; honey-combing is a late finding Pleural disease uncommon in IPF-suggestive of CT disease B. HRCT (diagnostic test of choice) detects early ILD Patterns can suggest presence of specific ILD Directs biopsies |
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Describe PFT in ILD
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Can't distinguish inflammatory stage from fibrosis or honey-combing
Classic findings are restrictive ventilatory defect Diffusion capacity is reduced due to loss of capillary bed (precede abnormalities in lung volumes) |
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Describe bronchoscopy in ILD
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A. Bronchoscopy-initial procedure of choice:
Sarcoidosis Hypersensitivity pneumonitis Eosinophilic pneumonia Lymphangitic Carcinomatosis B. Video Assisted Thoroscopy (VATS)-usually yields specific diagnosis (85%) note-most cases don’t need biopsy (history is sufficient) |
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Describe the management of ILD
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note-many ILDs are not responsive to therapy
A. goals of therapy 1. identify & aggressively treat inflammatory process a. corticosteroids (drug of choice) b. Immunosuppressive agents-azathioprine, cytoxan, cyclosporin 2. removal of offending agent B. monitor w/ 1. PFT (less invasive) 2. HRCT (if PFT results are dropping) C. lung transplant |
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A thin, 18-year-old nonsmoking female presents to the clinic with complaints of increasing frequency and severity of wheezing, coughing, and sputum production over the past year. She states she has averaged 2-3 such episodes per year since the age of 10. In the past, she has been given ampicillin and bronchodilators without significant benefit.
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cystic fibrosis (CF)
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What is cystic fibrosis (CF)?
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most lethal genetic disease of white Americans (dramatic improvement in median survival over the years)
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What is the pathogenesis of CF?
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Autosomal recessive disease with a deletion of the delta F 508 locus on chromosome 7
Mutations on the CF gene affects Cystic Fibrosis transmembrane conductance regulator (CFTR) Disruption in Cl transport across epithelial membranes (airways, sweat ducts, pancreatic ducts, intestine) Thick & viscous mucus in lungs w/ excessive Na concentrations in sweat are clinical features of CF In lungs, abnormal conductance draws H2O away from airway into cells; thick sputum is lethal aspect of CF, trapping bacteria (P. aeruginosa most common), giving rise to fatal infections (bronchiolitis, bronchitis & bronchiectasis) & lung damage; neutrophils are attracted to area & will help destroy lung w/ proteases & elastases |
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What criteria is needed for the diagnosis of CF?
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1 or more clinical features
PLUS 2 CF mutations OR 2 positive quantative pilocarpine iontophoresis sweat Cl values >60mmol/L is positive test OR abnormal nasal transepithelial potential difference value |
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What is the clinical presentation of CF?
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chronic sinusitis
severe chronic bacterial infection of airways severe hepatobiliary disease pancreatic exocrine insufficiency meconium ileus at birth sweat Cl value >60 obstructive azoospermia |
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Describe some of the acute treatments for CF?
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note-lung disease accounts for >90% of the morbidity & mortality; treatment largely symptomatic & empiric
A. Control of Infections (S. aureus most common 0-10; P. aeruginosa most common >10) Antibiotics and vaccines B. Treatment of Airway Inflammation i. prednisone-reduces inflammation due to hyperimmune response (side effects precludes routine use) ii. azithromycin-improves FEV1 iii. Ibuprofen-reduces airway inflammation C. Treatment of Airflow Obstruction-central feature of CF due to bronchial plugging of secretions, inflammation & airway destruction; treat w/ bronchodilators D. removal of secretions i. postural drainage/chest percussion (improves clearance of secretions, but didn't improve long-term outcome ii. Inhalation 7% hypertonic saline-improves FEV1; doesn't improve overall lung function iii. Inhaled Dnase (pulmozyme)-breaks up long strands of DNA into smaller segments w/in sputum, allowing increased clearance note-hypertonic saline treatments are similar effectiveness to pulmenzyme treatments at a fraction of the cost; therapies are making the switch |
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Describe chronic treatments for CF and lung transplant
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A. Chronic treatments
i. Inhaled treatment Tobramycin (on-off cycles) Aztreonam hypertonic saline Dornase Albuterol or LABA ii.. Oral treatment Azithromycin Ibuprofen iii.. Chest Physiotherapy-(increase frequency when sick) B. Lung transplant (usually double lung)-improves quality of life; doesn't address non-pulmonary problems (cirrhosis, pancreatic insufficiency, DIOS, diabetes) |
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What are pulmonary complications of CF?
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Lobar Atelectasis-beat it out (postural emptying) or bronchoscopy
Pneumothorax-may require sclerotherapy (burn pleural space w/ chemical to prevent recurrance) Massive Hemoptysis-stop the bleeding!! Cor Pulmonale Hypoxemic/Hypercarbic Respiratory Failure |
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75y/o male with 80pack-year smoking history is evaluated for 3 month hx of night sweats, weight loss & progressive SOB. He has been complaining of a dull ache in the left chest for the past 3 months. He has occasional coughing with mucoid sputum. On physical exam he is afebrile, pulse 112/min, RR 26/min, BP 100/80. His trachea is shifted to right. There is dullness to percussion & decrease breath sounds throughout his right chest. His abdomen is scaphoid with no organomegaly & no peripheral edema.
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Pleural effusion
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Describe transudative and exudative pleural effusions and differentiate between them
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A. Transudative Effusion
Abnormalities in Starling law resulting in imbalance b/t hydrostatic and oncotic pressures w/in chest; fluid accumulates until pleural fluid formation is equal to absorption B. Exudative Effusion-from pleural & lung inflammation (leading to leakage of proteinaceous material into pleural space) or impaired lymphatic drainage of pleural space C. differentiation-exudative effusion meets at least 1 of the following criteria: i. pleural fluid protein/serum protein ratio >0.5 ii. Pleural fluid LDH/serum LDH ratio >0.6 iii. Pleural fluid LDH >2/3 upper limit for serum LDH (If none of criteria are met, patient has transudative effusion) |
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Describe how the appearance of pleural fluid can help narrow the diagnosis
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note-odor, color & character of fluid is helpful in diagnosis
a. bloody effusion (in absence of trauma) i.malignancy ii. asbestosis (elderly) iii. pulmonary embolism b. Whitish pleural fluid-chyle, cholesterol or empyema c. Brown fluid-ameobic liver abscess d. Black fluid-aspergillus e. Ammonia odor-urinothorax f. Putrid odor-empyema |
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Describe how the chemical analysis of pleural effusion helps narrow the diagnosis
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A. total protein count-transudates <3 (low); exudates >3 (high)
B. high pleural fluid LDH count (>1000 IU/L)-exudative effusion C. high pleural cholesterol (>45)-exudative pleural effusion D. low pleural glucose (<60)-exudative effusion (TB); esophageal rupture E. pleural pH-measured in blood gas machine (ABG); normal pleural pH is 7.60 Pleural pH <7.30-exudative effusion Low pleural pH-poor prognosis for malignant pleural effusion; in parapneumonic effusion indicates high likelihood of pleural space drainage F. Elevated Pleural Fluid Amylase (pleural fluid/serum amylase ratio >1)-pancreatic disorder; esophageal rupture (high mortality w/out early repair); malignancy; ruptured ectopic pregnancy G. WBC counts-not very diagnostic H. high PMN count-pneumonia; pulmonary embolus; pancreatitis; intraabdominal abscess I. pleural fluid eosinophilia (>10%)-exudative effusion |
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Describe chylous pleural effusion and pleural fluid cytology
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A. chylous effusion-high triglyceride count (>110); caused by lymphoma, trauma to thoracic duct
B. pleural fluid cytology Cell type-high yield w/ adenocarcinoma; low w/ Hodgkin’s lymphoma (yield increases w/ additional specimens due to exfoliation of fresh cells) |
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Describe the symptoms of pleural effusion
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Symptoms often related to underlying disease
1. pleuritic chest pain (most common symptom) 2. Inflammation of diaphragmatic portion of pleura causes ipsilateral shoulder pain 3. Nonproductive cough 4. Dyspnea |
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Describe the imaging diagnostic tests done in pleural effusion
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A. CXR
Effusions appear as homogeneous density through which lung markings are seen; upper margins of fluid form meniscus at lateral chest wall 200cc of fluid needed to blunt costophrenic angle Lateral decubitus chest xray may show less fluid if layering on CXR, ok to tap (thoracentesis) B. utrasound-best way to document & localize loculated pleural fluid; provides appropriate site for biopsy or thoracentesis C. CT scan-best for demonstrating parenchymal abnormalities in patients w/ extensive pleural disease Should be performed on all undiagnosed exudative effusions; distinguishes lung abscess from empyema |
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Describe thoracentesis and other invasive diagnostic tests of pleural effusion
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A. thracentesis-usually diagnostic (75%); sometimes useful in management (20%)
Should be performed in all newly discovered pleural effusion (exceptions-secure diagnosis or small effusion where risks outweigh benefits) 35-50cc pleural fluid needed for analysis Test requested should be based on clinical presentation i. pleural total protein, glucose, LDH, total cell count ii. Serum glucose, LDH & total protein iii. Amylase for bloody effusion iv. supspected infection-Gram, KOH, AFB stains & cultures of pleural fluid C. invasive testing (if exdudative cause is undiagnosed-20% of time) i. Thoracoscopy ii. Open Lung Biopsy |
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Transudative effusion Effusions are usually bilateral
pH in normal ranges Low protein count |
congestive heart failure
due to both left and right sided heart failure |
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Transudate effusion
Usually on right side Fluid moves from peritoneal to pleural cavity via defects in diaphragm (follow pressure gradient) |
cirrhosis of liver
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Exudative effusion
Associated w/ bacterial pneumonia or lung abscess May resolve w/out sequelae w/ antibiotic treatment Low glucose Low pH High proteins |
Parapneumonic Effusion or Empyema
Empyema-signs of infection-smells bad (purulent infection); positive gram stain empyema treatment-drainage Parapneumonic Effusion-no signs of infection |
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Exudative effusion (low pH, low glucose)
involves mediastinum moderate to massive effusions & frequently hemorrhagic with low WBC |
carcinomatous effusion
Most common primary tumors metastasis to the pleura are lung, breast, stomach & ovary note-cytology can show cancer cells |
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Exudative effusion w/ lymphocyte predominance and low mesothelial count
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TB effusion
often occurs in absence of CXR evidence of active TB and negative skin test (30%) Effusion due to hypersensitivity to TB protein mesothelial count distinguishes TB from malignancy-high in malignancy; low in cancer |
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Exudative effusion
more common in men may not produce symptoms Low glucose (very low) & pH Mechansism for low glucose may be transport block from blood to pleural space |
rheumatoid effusion
commonly found in men w/ rheumatoid nodules, disfigured joints, active articular disease & high serum rheumatoid factors (RF) |
