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Category Archives: Lung
Chronic Bronchitis
Chronic bronchitis
Chronic bronchitis definition
· Persistent cough with sputum production for at least 3 months in 2 consecutive years, in the absence of any other identifiable cause
Chronic bronchitis histology
· Chronic inflammation of the airways (predominantly lymphocytes)
· Enlargement of mucus-secreting glands of the trachea and bronchi
· Ratio of thickness of mucus gland layer to ratio of wall thickness between epithelium and cartilage (Reid index) is >0.4
· Squamous metaplasia and dysplasia of bronchial epithelium
· Marked narrowing of bronchioles due to goblet cell metaplasia, mucus plugging, chronic inflammation and fibrosis
· Clusters of pigmented alveolar macrophages may be seen
· Obliteration of the lumen due to fibrosis (bronchiolitis obliterans) may be seen in severe cases
Chronic bronchitis pathology
· Chronic irritation of bronchiolar and bronchial epithelium secondary to:
o Tobacco smoke
o Grain
o Cotton
o Silica dust
o Air pollutants (sulfur dioxide, nitrogen dioxide)
· Bacterial and viral infection are acute exacerbators of the disease
Longstanding severe chronic bronchitis changes
Hyperemia, edema, and swelling of mucous membranes
Excessive mucinous to mucopurulent layering of the epithelial surfaces
Heavy casts of secretions and pus filling bronchi and bronchioles
Evidence of cor pulmonale and cardiac failure with increase in right ventricular thickness, right atrial thickness and heart weight
Evidence of pulmonary hypertension with pulmonary artery atherosclerosis, thickening and luminal narrowing of pulmonary arterioles
Posted in Lung
Tagged , Bronchitis, Chronic bronchitis, Chronic bronchitis lung changes, Chronic bronchitis lung findings, Lung inflammation
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Malignant mesothelioma types
Malignant mesothelioma types
Malignant mesothelioma histologic classification
• Epithelioid
• Sarcomatoid
• Mixed
• Desmoplastic
• Lymphohistiocytoid
• Small cell variant
• Squamous differentiation
Malignant Mesothelioma Immunohistochemistry Electron Microscopy
Malignant Mesothelioma
Malignant mesothelioma histochemical, immunohistochemistry and electron microscopy ultrastructural features helpful in the differential diagnosis from metastatic adenocarcinoma
• Histochemical
o Mesothelioma: Alcian blue and colloidal iron positive; Alcian blue-hyaluronidase negative
o Metastatic adenocarcinoma: Mucicarmine, PAS positive
• Immunohistochemistry
o Mesothelioma: Calretinin, CK5/6, thrombomodulin, WT-1, vimentin
o Metastatic adenocarcinoma: CEA, BerEP4, B72.3, MOC-31, CD15, Bg8, TTF-1
• Electron microscopy
o Mesothelioma: Long numerous and slender microvilli (ratio:diameter of 15:1) with abundant tonofilaments, but absent microvillous rootlets and lamellar bodies
o Metastatic adenocarcinoma: Short, plump microvilli, less numerous
Posted in Lung
Tagged , malignant mesothelioma, Malignant mesothelioma electron miscroscopy, Malignant mesothelioma histochemistry, Malignant mesothelioma immunohistochemistry
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Diffuse Pulmonary Hemorrhage
Diffuse Pulmonary Hemorrhage
Associated conditions
• Goodpasture syndrome
• Wegener granulomatosis
• Hypersensitivity angiitis
• SLE
• Idiopathic pulmonary hemosiderosis
Microscopic findings
• Focal necrosis of alveolar walls
• Intra-alveolar hemorrhage
• Intra-alveolar hemosiderin-laden macrophages
• Fibrous thickening of septae, type II pneumocyte hypertrophy, organization of blood in alveolar spaces
• Capillaritis, scattered, poorly-formed granulomas
Prognosis
Idiopathic pulmonary hemosiderosis
o Clinical benefit from corticosteroid therapy has been reported, however long-term benefit is unlikely
o Mean length of survival is 3-5 years; adults have better prognosis than children
o 25% are free of disease after first episode; another 25% are free of active disease, but have persistent dyspnea and anemia; another 25% have persistent active disease that leads to fibrosis and severe restrictive lung disease; the remainder have unresponsive disease with repeated massive hemorrhage and early death from respiratory failure
Goodpasture syndrome
o Treatment with plasmapheresis, corticosteroids and cytotoxic drugs is effective
o Studies have shown 50% survival at 2 years (majority of deaths due to pulmonary hemorrhage with infection within the first year)
o Oligoanuric renal failure reduces survival to 50% at 6 months
Wegener granulomatosis
o Untreated, the disease course is malignant with 80% dying within first year; may be reduced to 37% with treatment
References: Robbins & Cotran Pathologic Basis of Disease, Seventh Edition
by: Vinay Kumar, Nelso Fausto, Abul Abbas
Posted in Lung
Tagged Diffuse Pulmonary Hemorrhage, Goodpasture syndrome, Hypersensitivity angiitis, Idiopathic pulmonary hemosiderosis, Pulmonary Hemorrhage, SLE, Wegener granulomatosis
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Acute Respiratory Distress Syndrome
Acute Respiratory Distress Syndrome (ARDS)
Causes
• Infection
o Sepsis
o Diffuse pulmonary infections (viral, Mycoplasma, Pneumocystis, military TB)
o Gastric aspiration?
• Physical/Trauma
o Mechanical trauma (including head injuries)
o Pulmonary contusions
o Near-drowning
o Fractures with fat embolism
o Burns
o Ionizing radiation
• Inhaled irritants
o Oxygen toxicity
o Smoke
o Irritant gases and chemicals
• Chemical injury
o Heroin/methadone overdose
o ASA
o Barbiturate overdose
o Paraquat
• Haematologic conditions
o Multiple transfusions
o DIC
• Pancreatitis
• Uremia
• Cardiopulmonary bypass
• Hypersensitivity reactions
• Organic solvents
• Drugs
Pathogenesis
• Due to diffuse damage to the alveolar capillary walls
• Initial injury is to capillary endothelium (usually) or alveolar epithelium (less often)
• Leads to increased vascular permeability, alveolar flooding and loss of diffusion capacity and widespread surfactant abnormalities secondary to damage of type II pneumocytes
• The exudate and diffuse tissue destruction that occurs cannot be resolved and organization with scarring results in chronic disease
• As early as 30 minutes after the initial insult, IL-8 synthesis by macrophages increases. This, with IL-1 and TNF leads to pulmonary microvascular sequestration and activation of neutrophils which are thought to play an important role in ARDS
• Activated neutrophils release oxidants, proteases, PAF, and leukotrienes that damage tissue and maintain the inflammatory cascade. Release of macrophage inhibitory factor sustains the inflammatory response.
Histological features
• Congestion, interstitial and intra-alveolar edema, fibrin deposition and inflammation
• The alveoli are lined by hyaline membranes (consisting of fibrin-rich edema mixed with cytoplasmic and lipid remnants of necrotic cells).
• Proliferation of type II pneumocytes seen in organizing stage
• Organization of fibrin exudate with intra-alveolar fibrosis; alveolar septal thickening secondary to deposition of collagen and proliferation of interstitial cells
• May see superimposed bronchopneumonia
References: Robbins & Cotran Pathologic Basis of Disease, Seventh Edition
by: Vinay Kumar, Nelso Fausto, Abul Abbas
Posted in Lung
Tagged , Acute Respiratory Distress Syndrome, ARDS, ARDS Causes, ARDS Pathogenesis
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Wegeners Granulomatosis
Wegener’s Granulomatosis
Clinical features
• Persistent pneumonitis with bilateral nodular and cavitary infiltrates
• Chronic sinusitis
• Mucosal ulcerations of the nasopharynx
• Evidence of renal disease
• Skin rashes
• Myalgias
• Articular involvement
• Mononeuritis/polyneuritis
• Fever
Findings in kidney
• Focal necrotizing glomerulonephritis
• Crescentic glomerulonephritis (diffuse)
Other organs that can be involved
• Lungs
• Upper respiratory tract (ear, nose, sinuses and throat)
• (Eye, skin, heart)
Positive blood test
• c-ANCA
Posted in Lung
Tagged , c-ANCA, Crescentic glomerulonephritis, Focal necrotizing glomerulonephritis, Vasculitis, Wegener’s granulomatosis
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Lung Carcinoma
Lung Carcinoma
Lung Cancer
Most common lung cancer histologic types
• Squamous cell carcinoma
• Adenocarcinoma
• Small cell carcinoma
• Large cell carcinoma
Electron microscopy features for lung cancers
• Squamous cell carcinoma
o Desmosomes seen
o Cytoplasmic tonofilaments also seen
• Adenocarcinoma
o May exhibit mucin granules
o Luminal microvilli
• Small cell carcinoma
o Dense neurosecretory granules (100 nm diameter)
o Scant cytoplasm, sparse organelles
Prognostic factors
• Tumour size
• Tumour histological type
• Invasion of visceral and or parietal pleura
• Presence of obstructive pneumonitis
• Lymph node involvement
• Involvement of main bronchus
• Presence/absence of malignant effusion
• Involvement of chest wall, diaphragm, pericardium, mediastinal pleura, mediastinum, heart, great vessels
• Vascular invasion (arteries, veins)
• Involvement of margins
• Presence of separate tumour nodules
Immunohistochemistry stains that differentiate lung carcinoma from metastatic colon carcinoma
• TTF-1
• CK20
Posted in Lung
Tagged , CK20, electron microscopy, Large cell carcinoma, lung adenocarcinoma, lung cancer, Lung carcinoma, Lung small cell carcinoma, Lung squamous cell carcinoma, ttf-1
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Emphysema
Emphysema
1. Disruption in balance between proteases (elastase) and anti-proteases in favour of the former (protease-anti-protease theory).
2. Can occur in smoking due to influx of neutrophils and macrophages within terminal bronchioles and subsequent release of proteases (neutrophil elastase, cathepsin G, proteinase 3, macrophage elastase, matrix metalloproteinases). Release of ROS from neutrophils inhibits alpha-1-antitrypsin, thus swaying balance in favour of proteases.
3. Smoking also thought to disrupt oxidant-anti-oxidant balance. Smoke contains ROS which depletes natural anti-oxidants (superoxide dismutase, glutathione) and recruits neutrophils that also release ROS. AAT is also inhibited by ROS, which increases tissue damage)
4. AAT deficiency also leads to emphysema since the protease-anti-protease balance is shifted towards the proteases.
Emphysema Types
1. Centriacinar
2. Panacinar
3. Irregular
4. Distal acinar/Paraseptal
5. Bullous
6. Interstitial
Eosinophils in pleural effusion causes
1. Pneumothorax
2. Parasites
3. Hypersensitivity/Allergic reaction
4. Drugs
Mesothelioma
Mesothelioma
Cytological features
1. Clusters of cells with “scalloped” edges
2. Cells are larger than non-neoplastic mesothelial cells, but still demonstrate “windows”, and dense perinuclear cytoplasm with peripheral “halo”
3. Prominent nucleoli
Electron microscopy findings
1. Long, thin, branching microvilli with a length:diameter ratio of 15:1
2. Numerous bundles of tonofilaments
Carcinoma versus Mesothelioma Immunohistochemistry
Antibody Mesothelioma Adenocarcinoma
Calretinin + -
CK 5/6 + -
Thrombomodulin (?) + -
CEA - +
TTF (for lung adenoca.) - +
BerEP4 - +
CD15 - +
Cystic fibrosis
Cystic fibrosis
Cystic fibrosis pathogenesis
Mutation of CFTR (most often ΔF508)
In sweat duct epithelium, dysfunction of the Cystic fibrosis transmembrane conductance regulator (CFTR) causes decrease in reabsorption of sodium chloride via ENaC (epithelial sodium channel), resulting in hypertonic sweat (“salty sweat”) as normally, ENaC absorbs chloride ions in sweat duct epithelium.
In respiratory and intestinal epithelium, dysfunction of CFTR causes loss or decreased chloride release into the lumen. Sodium absorption is increased via ENac and results in net water absorption from the lumina of these systems, causing defective mucociliary function in the lungs and the accumulation of viscous secretions in the lungs and the intestines.
CFTR also mediates bicarbonate transport, so some mutations of CFTR can cause a decreased luminal pH, due to absence of bicarbonate ions. This can result in increased mucin precipitation and plugging of ducts, increased bacterial adherence to plugged mucin and pancreatic insufficiency.
Gross lung findings
Distension of bronchioles with thick mucus (mucus plugging)
Bronchiectasis
Lung abscesses
Pneumonia (consolidation)
Cystic Fibrosis Extrapulmonary Lesions
Chronic sinusitis
Nasal polyps
Salivary gland abnormalities (plugging of ducts, squamous metaplasia, gland atrophy, fibrosis)
Pancreatic insufficiency (malabsorption, steatorrhea), acute/chronic pancreatitis
Meconium ileus
Biliary cirrhosis
Absent vas deferens, azoospermia
Organisms that cause lung infections in Cystic Fibrosis patients
Staphylococcus aureus
Pseudomonas aeruginosa
Haemophilus influenzae
Burkholderia cepaciae
Posted in Lung
Tagged , cftr, cystic fibrosis, Cystic fibrosis transmembrane conductance regulator, lung infection
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