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179 Cards in this Set
- Front
- Back
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What are kulchitsky cells?
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neuroendocrine cells within bronchi and bronchioles
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What are the pores of Kohn?
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connections between alveoli that allow passage of exudates and bacteria
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What does the interstitium among alveoli contain?
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Elastic fibers
Collagen Fibroblasts Smooth muscle cells Occasionally inflammatory cells |
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What is hemodynamic edema most commonly due to?
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Increased hydrostatic pressure as occurs in left heart failure
Greater hydrostatic pressure causes fluid to initially accumulate in basal regions of lower lobes - first in interstitium then alveolar space |
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How does edema caused by microvascular injury arise?
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Primary injury to vascular endothelium OR to alveolar epithelial cells with secondary microvascular injury
Increased alveolar capillary permeability results in leakage of fluids and proteins into interstitial space and alveoli |
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What is a key difference between hemodynamic edema and edema caused by microvascular injury?
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hydrostatic pressure in pulmonary capillaries is NORMAL in edema caused by microvascular injury
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What are 2 disease processes that serve as examples of edema due to microvascular injury?
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Pneumonia - localized edema
Adult respiratory distress syndrome - diffuse edema |
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What are other common terms for acute lung injury?
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Acute respiratory distress syndrome
Non-cardiogenic pulmonary edema Adult respiratory failure Shock lung |
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How is ARDS characterized?
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Abrupt onset of significant hypoxemia and diffuse pulmonary infiltrates in the absence of cardiac failure
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What is DAD - diffuse alveolar damage?
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Term describing pathologic findings associated with ARDS
Called acute interstitial pneumonia when there is no etiologic assoc. |
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What is the clinical presentation of ARDS?
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Rapid onset of severe life threatening respiratory insufficiency
Tachypnea, dyspnea, cyanosis, hypoxemia Diffuse alveolar infiltrates on radiograph Hypoxemia often refractory to oxygen therapy - multiorgan failure |
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Which cell type plays a critical role in mediating ALI/DAD?
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Neutrophils - release variety of products that cause direct and indirect damage to endothelium and epithelium; ROS and reactive nitrogen species
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The expression of which factor is likely to be involved in tipping the balance to pro-inflammatory in ARDS?
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NF-KB - then results in increased IL-8, IL-1, TNF which leads to endothelial cell and neutrophil activation
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What contributes to the formation of hyaline membranes in ALI/DAD?
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Disturbed alveolar fibrin turnover
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What is the clinical course of ALI?
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Profound dyspnea and tachypnea at onset
Followed by increasing cyanosis, hypoxemia, and resp. acidosis |
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Why might hypoxemia become unresponsive to oxygen therapy in ALI?
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Due to V/Q mismatching - functional abnormalities in ALI not evenly distributed, poorly aerated (alveoli filled with junk) areas being perfused cause mismatch
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What are some complications associated with ALI?
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Interstitial fibrosis - irreversible scarring
Infection - bronchopneumonia |
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What is the prognosis of ALI?
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40% mortality due to sepsis, multi-organ failure, or direct lung injury
May resolve with restoration of normal lung architecture Approx. 50% of survivors develop fibrosis and end-stage honeycomb lung |
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What is the fundamental defect in neonatal RDS?
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Deficiency of pulmonary surfactant
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What are pre-disposing factors for neonatal RDS?
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Male gender
Maternal diabetes - high insulin level in infant depresses surfactant Birth by C-section - labor induces surfactant production |
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What are the clinical features of neonatal RDS?
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Dyspnea, tachypnea, cyanosis, fine rales - even though breathing and oxygenation may have been fine intially
On x-ray "ground-glass appearance" Lack of improvement with 80% oxygen |
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What is the ground-glass appearance characteristic of neonatal RDS indicative of'?
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Appearance comes from uniform minute reticulonodular densities
Indicates atelectatic terminal airspaces and retained alveolar fluid |
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What does surfactant deficiency result in?
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Stiff atelectatic lungs leading to hypoxemia, CO2 retention and acidosis which leads to pulmonary microvascular injury and hyaline membrane formation
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What is the most critical period in neonatal RDS?
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First 3-4 days because lack of responsiveness to oxygen therapy - of survive this period then good prognosis
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During pregnancy how is lung maturity estimated?
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Analysis of amniotic fluid phospholipids (specific tests listed on page 259)
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What are 2 complications of prolonged oxygen therapy?
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Retrolental fibroplasia (retinopathy of prematurity)
Bronchopulmonary dysplasia |
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What is the pathogenesis of retinopathy of prematurity?
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Increased VEGF induced by hypoxia which causes angiogenesis and retinal vessel proliferation - can displace macula, cause retinal detachment
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What is bronchopulmonary dysplasia (BPD)?
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Potentially reversible impairment of alveolar septation at the saccular stage of lung development
Clinical definition: at least 28 days of O2 therapy in infant at least 36 weeks GA with dec alveolar septation & abnormal capillary distribution |
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Is the effect of interstitial lung diseases limited to the interstitium?
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No, most affect alll anatomic components of the lung
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What are the clinical classifications of interstitial lung diseases?
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Drug-induced
Collagen vascular disease and IBD Environmental and occupational exposures: hypersensitivity pneumonitis, pneumoconiosis Idiopathic interstitial pneumonias Diffuse alveolar damage Primary or unclassified: sarcoidosis, eosinophilic pneumonia, pulmonary alveolar proteinosis, langerhan's cell histiocytosis |
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What are the signs and symptoms of interstitial lung diseases?
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Dyspnea
Dry cough early on in course Crackles, usually basilar Clubbing of fingers Findings consistent with collagen vascular disease |
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Are wheezing and chest pain commonly present with interstitial lung disease?
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NO
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When is serologic testing useful for diagnosing interstitial lung disease?
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In suspected collagen vascular disease or environmental exposures
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What is idiopathic pulmonary fibrosis?
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Also referred to as usual interstitial pneumonia
A histologic pattern characterized by patchy, temporally heterogenous fibrosis seen with insidious onset of diffuse bilateral interstitial disease |
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Grossly, how do the lungs appear in a patient with idiopathic pulmonary fibrosis?
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Smaller overall size
Cobblestone appearance of pleural surface Patchy tan-white fibrous scarring in lower lobes, peripheral, and subpleural regions |
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What is the clinical course and treatment for idiopathic pulmonary fibrosis?
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Gradual deterioration of lung function with transplantation the only effective treatment
Respiratory failure most common cause of death Subgroup has accelerated disease with rapid decline |
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What 3 factors can influence the epithelium to promote lung fibrosis?
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Pulmonary surfactant protein C abnormalities
ABCA3 abnormalities Latent herpesvirus infection |
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What are the distinct characterisitcs of fibroblasts in a lung with active fibrosis?
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Increased proliferation
Anchorage-independent growth Enhanced migration Enhanced invasion of matrices |
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What is the induction of lung fibrosis dependent on?
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Amount and length of TGF-beta1 induced downstream cytokine signaling
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What is ABCA3?
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An ATP-binding cassette family member whose protein is normally localized to lamellar bodies (organelle of type 2 pneumocyte that stores surfactant)
Abnormalities in this protein associated with fibrotic diseases |
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What is non-specific interstitial pneumonia?
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Seen in the clinical setting similar to other IPFs but specifically show uniform temporally homogenous appearance of either interstitial inflammation or fibrosis
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What is the morphology of NSIP like?
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Grossly there is ground-glass attenuation
Histologically there are cellular and fibrosing patterns that lack areas of dense fibrosis and honeycombing |
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How does the clinical course differ between cellular NSIP pattern and fibrosing NSIP pattern?
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Patients with cellular NSIP tend to be younger and have a 100% 5 year survival rate
Fibrosing pattern older with 90% 5 year survival |
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How is NSIP treated?
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Corticosteroid therapy
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What is organizing pneumonia?
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Histologic pattern characterized by excessive proliferations of granulation tissue within small airways and alveolar ducts
Associated with mild interstitial chronic inflammation |
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What is the clinical course of cryptogenic organizing pneumonia?
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A better outcome than those who have secondary organizing pneumonia
COP responsive to corticosteroid therapy but 1/3 have persistent disease |
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What is the morphology like in organizing pneumonia?
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Patchy consolidation without scarring or honeycombing
Intraluminal plugs of loose fibrous tissue occluding bronchioles, alveolar ducts, and alveoli Preserved lung architecture |
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What is respiratory bronchiolitis-interstitial lung disease?
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Mild form of ILD characterized by histologic pattern of chronic bronchiolitis with pigmented carbon macrophages in bronchioles and adjacent alveoli
Seen mostly in current or recent heavy smokers |
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Which ILD has a mean age of onset that is earlier than the others?
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Respiratory bronchiolitis-interstitial lung disease
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Which 2 ILDs are closely related?
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Respiratory bronchiolitis-interstitial lung disease and desquamative interstitial pneumonia
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What is the prognosis like for respiratory bronchiolitis-interstitial lung disease?
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Excellent, quitting of smoking usually leads to spontaneous regression
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What is the morphology like for respiratory bronchiolitis ILD?
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Patchy areas of ground-glass opacities with bronchial wall thickening
Pigmented macrophages in lumens of bronchioles, alveolar ducts, and adjacent alveoli Mild peribronchiolar chronic inflammation and fibrosis |
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What is the morphology like in desquamative interstitial pneumonia?
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Bilateral symmetric areas of ground-glass opacities
Diffuse intra-alveolar macrophage accumulation Uniform involvement of lung parenchyma with interstitial fibrosis and chronic inflammation |
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What is desquamative interstitial pneumonia?
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Almost exclusively seen in current or recent heavy smokers
Characteristic pattern of intra-alveolar mononuclear cell infiltration without prominent dense fibrosis or honeycombing |
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What is the clinical course like in DIP?
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More common in men, presents in 30s and 40s
Responsive to corticosteroids in severe cases Otherwise spontaneous regression with cessation of smoking |
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What is sarcoidosis?
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Systemic disease primarily involving lungs and is diagnosis of exclusion supported by pattern of noncaseating granulomatous inflammation
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Besides the lung what does sarcoidosis commonly involve?
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Lymph nodes
Eyes Skin Spleen Bone marrow Heart Liver |
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What is the role of genetics in sarcoidosis?
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Genes that influence susceptibility appear to be separate from genes that influence clinical phenotype
Strong association with HLA-DRB1 |
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What is the immune response like in sarcoidosis?
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Cell-mediated: T helper 1 response with cytokines - IL2, IFN-gamma, TNF
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What is the clinical course like for sarcoidosis?
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Occurs worldwide typically in young adults 20-40
Most patients present in winter or early spring In US mainly affects blacks, irish, scandinavians Corticosteroids effective but clinical course unpredictable |
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What is hypersensitivity pneumonitis?
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Represents a combo of type III (immune-complex mediated) and type IV (t-cell mediated) reactions
Characterized by diffuse interstitial granulomatous inflammatory pattern |
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What causes the inflammatory response in hypersensitivity pneumonitis?
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Immunologic reaction to prolonged exposure to inhaled organic antigens (classically moldy hay)
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How is the clinical course for hypersensitivity pneumonitis?
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Majority have slow but near-total recovery of lung function
But once dense fibrosis with honeycombing is present disease is not reversible Primary treatment is removal of antigen exposure, also corticosteroids |
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What is eosinophilic pneumonia?
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Diseases characterized by pattern of eosinophil accumulation in alveolar spaces and/or interstitium commonly assoc. with peripheral blood eosinophilia
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What are the different classifications of eosinophilic pneumonia?
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Acute eosinophilic pneumonia with respiratory failure
Simple pulmonary eosinophilia (Loffler syndrome) Tropical eosinophilia Secondary eosinophilia Idiopathic chronic eosinophilic pneumonia |
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In eosinophilic pneumonitis what is the clinical course?
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Has dramatic response to corticosteroids
Disease usually recurs or relapses but responds to re-treatment |
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Which eosinophilic pneumonia is peripheral blood eosinophilia with pulmonary radiographic infiltrates associated with?
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NONE
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What causes differentiation in the histologic pattern of eosinophilic pneumonia?
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The initiating cause:
inhaled - bronchiocentric bloodstream - angiocentric |
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Is asthma present in all cases of eosinophilic pnuemonia?
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NO
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In eosinophilic pneumonia how do blood esosinophils correlate with the extent of eosinophilic inflammation in involved organs or with total IgE levels?
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They do not correlate
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What is pulmonary langerhans cell histiocytosis?
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Chronic, progressive, systemic disease characterized by proliferation of langerhans cell infiltrates which form multiple bilateral interstitial nodules
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What are langerhans cells?
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Terminally differentiated cells of monocyte-macrophage lineage; function as antigen-presenting cells
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What is pulmonary langerhans cell histiocytosis associated with?
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Smoking!
Presents in young adults 20-40, more common in men, rarely seen in blacks |
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What is characteristic of pulmonary langerhans cell histiocytosis morphology?
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Nodules with peribronchial distribution mainly affecting the upper lobes
Nodules have stellate borders and varying degrees of central cavitation |
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What is pulmonary alveolar proteinosis?
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Histologic pattern associated with variety of clinical conditions but characterized by intra-alveolar accumulation of granular eosinophilic surfactant-derived lipid rich material
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What is the "crazy paving" pattern seen on HRCT associated with?
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Pulmonary alveolar proteinosis; caused by interlobular septal thickening
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What is the clinical course of pulmonary alveolar proteinosis?
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Rare, presents in adults 30-50
More common in men Most commonly idiopathic |
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The deficiency of which factor is associated with acquired pulmonary alveolar proteinosis?
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Granulocyte-macrophage colony-stimulating factor (GM-CSF)
Patients identified with mutations in GM-CSF and GM-CSF receptor genes Also people with GM-CSF autoantibodies which causes functional deficiency Result: impaired clearing of surfactant by alveolar macrophages |
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How is pulmonary alveolar proteinosis treated?
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By whole lung lavage to wash it out
GM-CSF replacement therapy useful for some BUT NO corticosteroid or cytotoxic therapy because not inflammatory! |
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What are the most common patterns of lung involvement in collagen vascular diseases?
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NSIP
UIP vasculitis OP bronchiolitis |
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What lung patterns are associated with rheumatoid arthritis?
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Chronic pleuritis
Diffuse ILD with fibrosis Rheumatoid nodules Pulmonary hypertension |
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Which fibrotic lung patterns are seen with scleroderma?
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NSIP
UIP |
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What lung patterns are seen with SLE?
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Patchy, transient infiltrates
Lupus pneumonitis |
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What is acute radiation pneumonitis?
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Occurs 1-6 months after treatment in about 10-20% of patients
Symptoms may improve after steroid treatment but may also progress |
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What is chronic radiation pneumonitis?
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Diffuse alveolar damage with marked atypia of type 2 pneumocytes and fibroblasts
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What are some pulmonary defense mechanisms?
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Cough reflex
Mucociliary clearance - mucus contains antioxidants, lysozyme, IgA, IgG Pulmonary macrophages Alveolar epithelium - secretes surfactant |
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What is pneumonia?
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Infection of lung parenchyma resulting in exudation and consolidation
Classified according to specific etiologic agent and clinical syndrome |
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What are the modes of infection for pneumonia?
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Inhalation
Hematogenous From adjacent structures Nosocomial |
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What are community acquired acute pneumonias?
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Most often bacterial or viral (viral pneumonias called atypical)
Bacterial pneumonias often follow viral infection |
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What are predisposing conditions for community acquired acute pneumonia?
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Extremes of age
Chronic disease Immune deficiencies Splenic dysfunction (sickle cell) |
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What are the common organisms responsible for nosocomial pneumonia?
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Gram-negative rods (enterobacteriaceae and pseudomonas)
Staph aureus - especially resistant strains |
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What are complications of bacterial pneumonia?
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Abscess formation
Empyema Organization into solid tissue/scar Bacterial dissemination |
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What are the major symptoms of pneumonia?
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Fever, chills, cough with mucopurulent sputum
Pleuritic pain and pleural friction rub |
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What is the most common cause of community acquired pneumonia?
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Strep pneumoniae - most common pneumonia to follow influenza epidemic also
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What kind of pneumonia pattern does Strep pneumoniae cause?
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Lobar
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What is the treatment for pneumonia caused by strep pneumoniae?
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Penicillin
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What bacteria is a major cause of community pneumonia in children?
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H. influenzae, usually type B
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What is the most common bacterial cause of acute exacerbation of COPD?
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H. influenzae
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Which type of pneumonia pattern does H. influenzae cause?
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lobar or lobular
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Which bacterial cause of community acquired pneumonia produces a toxin which paralyzes mucosal cilia and a protease that degrades IgA?
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H. influenzae
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What is the secondary bacterial pneumonia in children and healthy adults following viral respiratory illnesses?
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Staph aureus
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What is an important cause of nosocomial pneumonia?
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Staph aureus with high incidence of MRSA
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Which bacterial pneumonia is associated with endocarditis in IV drug abusers?
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Staph aureus
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What is the most frequent cause of a gram negative bacterial pneumonia?
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Klebsiella pneumoniae
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Is klebsiella a common cause of community acquired or nosocomial pneumonia?
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Less frequently a cause of community-acquired pneumonia than nosocomial
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Who is most susceptible to klebsiella pneumonia?
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Debilitated and malnourished people like chronic alcoholics because it is normal flora of the GI tract and acquired by aspiration
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A lung with klebsiella pneumonia looks like what?
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Has mucoid yellow consolidation
Thick, gelatinous sputum |
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What is a gram negative bacilli that is most commonly a nosocomial infection?
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Pseudmonas aeruginosa
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Which people are most susceptible to pneumonia by pseudomonas aeruginosa?
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Cystic fibrosis patients
Patients with neutropenia Other debilitated patients: burn patients, steroid treatment, cardiac disease, COPD |
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What are virulence factors produced by pseudomonas aeruginosa?
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Ciliostatic substance
Exotoxins and endotoxins Elastase which degrades blood vessel walls leading to extrapulmonary spread Pili and mucoid proteins for adherence |
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What is Pontiac fever?
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self-limited upper respiratory tract infection caused by legionella pneumophilia
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What are predisposing conditions for infection by legionella pneumophilia?
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Cardiac and renal disease
Organ transplant recipients |
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Abscess formation is common in pneumonia caused by which bacteria?
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Klebsiella
Staph aureus |
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In bacterial dissemination from pneumonia where are common sites the bugs end up?
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Heart valves
Pericardium Brain Kidneys Spleen Joints |
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Which pattern of pneumonia is characterized by fibrinosuppurative consolidation of large portion of lobe or entire lung?
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Lobar pneumonia
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Which pattern of pneumonia is characterized by patchy consolidation that is mulitlobar, bilateral, and basal?
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Bronchopneumonia
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What is primary typical pneumonia?
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Acute febrile respiratory disease characterized by patchy inflammatory changes involving alveoli and interstitium
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What are the causative agents of atypical pneumonia?
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Viruses - influenza, RSV, adenovirus
Mycoplasma pneumoniae - most common cause Chlamydia pneumoniae Coxiella burnetti (Q fever) |
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Why is atypical pneumonia considered atypical?
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Moderate sputum
No evidence of consolidation on physical exam Moderate elevation of white count No alveolar exudate |
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What are predisposing factors for atypical pneumonia?
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Most common in children and young adults in closed communities
Malnutrition Alcoholism Debilitating illnesses |
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What is the pathogenetic mechanism of atypical pneumonia?
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Organisms attach to upper respiratory tract epithelium followed by necrosis of cells and inflammatory reponse
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What is the histology like for atypical pneumonia?
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Interstitial inflammatory reaction localized to alveolar walls
Alveolar spaces are free of exudate - may have acellular exudate and hyaline membranes Alveolar septae are widened and edematous, usually have mononuclear inflammatory infiltrate |
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What is the clinical course for atypical pneumonia?
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Fever, headache, and muscle pains
Presents like a sever upper respiratory infection or chest cold |
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What is a lung abscess?
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Local suppurative process within lung characterized by necrosis of lung tissue
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What causes lung abscesses?
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Aspiration of infective material most frequent cause
Septic embolism Antecedent primary bacterial infection, pneumonia, bronchiectasis Obstruction by neoplasm Trauma Spread from neighboring organ Hematogenous seeding |
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What are common organisms causing lung abscesses?
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Aerobic and anaerobic streptococci - usually mixed
Staph aureus - usually from previous pneumonia Gram negative bacteria - usually from hematogenous dissemination Most of infections causes by anaerobes from oral cavity: bacteroides, fusobacterium, peptococcus |
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What is the clinical course like with lung abscesses?
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Cough, fever, foul smelling purulent sputum, chest pain, weightloss
Clubbing of fingers and toes Most resolve with antibiotics |
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What are some complications associated with lung abscesses?
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Extension of infection into pleural cavity
Hemorrhage Septic emoboli can lead to brain abscess or meningitis Secondary amyloidosis |
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What are the types of lung neoplasms?
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Carcinomas - most common
Carcinoids Non-epithelial neoplasms - mostly mesoderm type |
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There are statistical associations between frequency of lung cancer and which aspects of smoking?
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Number of cigarettes per day
Tendency to inhale Pack-years duration of smoking habit |
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Are heavy smokers more likely to develop lung cancer?
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11% of heavy smokers develop lung cancer
Whereas 90% of lung cancers found in people with smoking history of any kind |
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What other cancers are associated with smoking?
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Mouth, larynx, oropharynx, esophagus
Pancreas Uterine cervix Kidney and urinary bladder |
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What are the clinical presentations of lung cancer?
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Cough
Weight loss Chest pain Dyspnea Symptoms from local effects of tumor Systemic symptoms from paraneoplastic syndrome |
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What are the two major classes of lung carcinomas?
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Small cell
Non-small cell |
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What are the classifications of non-small cell lung carinoma?
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Squamous cell carcinoma
Adenocarcinoma - papillary or mucinous Bronchioalveolar carcinoma - mucinous or non Large cell carcinoma |
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Where do the majority of lung carcinomas originate?
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From first-, second-, or third-order bronchi
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What are the invasive growth patterns of non-small cell lung carcinoma?
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Endobronchial
Intraparenchymal |
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Where do NSCLC frequently metastasize to?
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Intrapulmonary, bronchial, and/or mediastinal lymph nodes
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What are frequent sites of distant metastases for NSCLC?
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Adrenal glands most commonly
Liver Brain Bone |
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What is the most common type of lung cancer seen in the US?
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NSCLC adenocarcinoma
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What is the most common type of lung cancer seen in non-smokers?
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NSCLC adenocarcinoma
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Where are NSCLC adenocarcinomas most frequently located?
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Peripherally
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What are the common genetic changes associated with adenocarcinomas?
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Gain of chromosome 5p most common
Amplification of EGFR, KRAS, HER2 proto-oncogenes |
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What are some important characteristics of bronchioloalveolar carcinoma?
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Peripheral location but multivariate gross appearance
Grows along alveolar septae with lepidic growth NO signs of invasion 2 major subtypes: mucinous, non-mucinous |
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What are the variant gross appearances of bronchioloalveolar carcinoma?
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Small nodule
Multiple nodules Pneumonia-like infiltrate |
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What is the morphology of mucinous bronchioloalveolar carcinoma?
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Tall, columnar cells with cytoplasmic mucin
Tend to form a solitary peripheral nodule |
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What is the morphology of non-mucinous bronchioloalveolar carcinoma?
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Columnar, peg-shaped, or cuboidal
Tend to form multiple nodules or a pneumonia-like infiltrate |
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What are morphologic features of squamous cell carcinoma?
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Located centrally - larger than adenocarcinoma
Squamous differentiation: planar, polygonal cells with keratinization &/or intercellular bridging |
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What are the most common genetic alterations found with squamous cell carcinoma?
|
Losses of 9p and 3p
Amplification of proto-oncogenes: PIK3CA, BCL11A, MYC, KRAS |
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What is large cell carcinoma?
|
Heterogeneous category of "undifferentiated" malignant carcinomas lacking conventional cytologic features of adenocarcinoma, squamous or small cell carcinoma
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What are the cells of large cell carcinoma like?
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Arranged in solid sheets
Large nuclei Prominent nuceoli Abundant cytoplasm |
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What is neuroendocrine neoplasia?
|
Malignant tumors with range of aggressiveness but common morphological, ultrastructural, immunohistochemical, and molecular features
"Neuroendocrine" differentiation common to all |
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What is the neuroendocrine differentiation associated with neuroendocrine neoplasia?
|
NE markers: chromogranin, synaptophysin, CD57
Neurosecretory hormones: serotonin, bombesin, calcitonin |
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Which lung carcinoma has a very strong association with smoking?
|
Small cell carcinoma
|
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What is the difference between typical and atypical carcinoids?
|
Typical have NO p53, BCL2, or BAX mutations/abnormalities
Atypical DO show mutations/abnormalities in these genes |
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What genetic mutations are small cell carcinomas associated with?
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p53 and RB1
BCL2 overexpression BAX underexpression |
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At which sites is LOH found with increasing frequency from typical carcinoid/atypical to SCLC/LCNEC?
|
3p
13q14 (RB1) 9p 5q22 |
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What are tumorlets?
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Microscopic incidental hyperplastic proliferations of neuroendocrine cells typically seen in areas of scarring &/or chronic inflammation
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What is the difference between central and peripheral carcinoid tumors?
|
Central: digitate or spherical endobronchial polypoid masses
Peripheral: solid, circumscribed nodules |
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What is the morphologic difference between typical and atypical carcinoid?
|
Typical have <2 mitoses per high power field and lack necrosis
Atypical have 2-10 mitoses per hpf and have foci of necrosis; increased pleomorphism, more prominent nucleoli, invasive growth, and lymphovascular invasion |
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Which lung carcinoma is associated with salt and pepper chromatin?
|
Carcinoid
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What are some morphologic features of small cell carcinoma?
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High mitotic count
Individual cell necrosis and zonal necrosis |
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What can superior sulcus tumors of the lung cause?
|
Horner syndrome after invasion of the cervical sympathetic plexus
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What is responsible for paraneoplastic syndrome?
|
Systemic effects of humoral or immunologic factors produced by tumor cells
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What is cushing syndrome?
|
Paraneoplastic assoc with small cell lung carcinoma
Due to ACTH or ACTH-like substance - POMC POMC not found in people with inc ACTH from pituitary with Cushing disease |
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What is the most common paraneoplastic?
|
Hypercalcemia - assoc with squamous cell carcinoma of lung (production of parathyroid hormone-related protein PTHRP)
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What is SIADH?
|
Paraneoplastic assoc. with small cell lung carcinoma
Antidiuretic or atrial natriuretic hormones |
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What produces parathyroid hormone-related protein?
|
Squamous cell carcinoma of lung
Small amounts made by NORMAL epithelial and mesenchymal tissue |
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What is carcinoid syndrome?
|
Paraneoplastic assoc. with carcinoid tumors, rarely with small cell lung carcinoma
Dry flushing Watery diarrhea Wheezing |
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What is responsible for the symptoms seen in carcinoid syndrome?
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Release of enzyme kallikrein from tumor cells
Converts kininogen to vasoactive amines like bradykinin Serotonin also plays a role |
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Lambert-eaton myasthenic syndrome is associated with what?
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Small cell lung carcinoma
Autoantibodies against voltage-gated calcium channels |
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What are neuromuscular paraneoplastic syndromes?
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Lambert-eaton myasthenic syndrome
Sensory neuropathies Encephalomyelitis |
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What is acanthosis nigricans associated with?
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NSCLC
Possibly caused by TGF-alpha from tumor cells |
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What is dermatomyositis-like syndrome associated with?
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NSCLC
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What are osteroarticular and soft tissue paraneoplastic manifestations?
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Hypertrophic pulmonary osteoarthropathy - NSCLC
Vascular manifestations Hematologic changes |
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What is hypertrophic pulmonary osteoarthropathy?
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Assoc with NSCLC
Arthralgias &/or aching bone pain with or without clubbing "onion-skin periostitis" symmetrical periosteal new bone along diaphyses |
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What is a pulmonary hamartoma?
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Tumor consisting of mesenchymal elements - most frequently cartilage and epithelial components
Usually clefts lined by bronchial-type (ciliated columnar) epithelium |
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What are some reasons the lung is the most common site of metastatic neoplasms?
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Receives entire right heart output
Densest capillary bed in the body High tissue oxygen Molecular expression in local microvascular or stromal environment |
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What is the difference in treatement approach between NSCLC and SCLC?
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For NSCLC primary surgical approach (up to stage 3)
For SCLC primary chemotherapy approach |
