Pathology: Respiratory Pathology
CONGENITAL CYSTIC LUNG LESIONS
The 2 most common malformations of the lung are congenital cystic adenomatoidmalformation (CCAM) and bronchopulmonary sequestration (BPS). CCAM is ahamartomatous lesion, and BPS is a nonfunctioning bronchopulmonary segment separate from the tracheobronchial tree.
These conditions are followed by serial ultrasonography. Some resolve spontane-ously, though minimally invasive surgery may be required.
ATELECTASIS
Atelectasis refers to an area of collapsed or nonexpanded lung. It is reversible, butareas of atelectasis predispose for infection due to decreased mucociliary clearance.
The major types are as follows:
· Obstruction/resorption atelectasis is collapse of lung due to resorption ofair distal to an obstruction; examples include aspiration of a foreign body, chronic obstructive pulmonary disease (COPD), and postoperative atelectasis.
· Compression atelectasis is atelectasis due to fluid, air, blood, or tumor in thepleural space.
· Contraction (scar) atelectasis is due to fibrosis and scarring of the lung.
· Patchy atelectasis is due to a lack of surfactant, as occurs in hyaline membranedisease of newborn or acute (adult) respiratory distress syndrome (ARDS).
PULMONARY INFECTIONS
In bacterial pneumonia, acute inflammation and consolidation (solidification) of the lung are due to a bacterial agent. Clinical signs and symptoms include fever and chills; productive cough with yellow-green (pus) or rusty (bloody) sputum; tachypnea; pleuritic chest pain; and decreased breath sounds, rales, and dullness to percussion.
Studies typically show elevated white blood cell count with a left shift (an increase in immature leukocytes). Chest x-ray for lobar pneumonia typically shows lobar or segmental consolidation (opacification), and for bronchopneumonia typically shows patchy opacification. Pleural effusion may also be picked up on chest x-ray.
In general, the keys to effective therapy are identification of the organism and early treatment with antibiotics.
Lobar pneumonia is characterized by consolidation of an entire lobe. The infect-ing organism is typically Streptococcus pneumoniae (95%) or Klebsiella . The lancet-shaped diplococcus Streptococcus pneumoniae is alpha-hemolytic, bile soluble, and optochin sensitive.
The 4 classic phases of lobar pneumonia are congestion (active hyperemia and edema); red hepatization (neutrophils and hemorrhage); grey hepatization (degra-dation of red blood cells); and resolution (healing). In today’s antibiotic era, these changes are not generally observed in practice.
Bronchopneumonia is characterized by scattered patchy consolidation centered onbronchioles; the inflammation tends to be bilateral, multilobar, and basilar, and particularly susceptible populations include the young, old, and terminally ill. Infecting organisms exhibit more variation than in lobar pneumonia, and include Staphylococci, Streptococci, Haemophilus influenzae, Pseudomonas aeruginosa, etc.Microscopic examination of tissue shows acute inflammation of bronchioles and surrounding alveoli. The diagnosis can often be established with sputum gram stain and sputum culture, but will sometimes require blood cultures.
Complications of pneumonia include fibrous scarring and pleural adhesions, lung abscess, empyema (pus in a body cavity), and sepsis.
Treatment of pneumonia is generally initial empiric antibiotic treatment, modified by the results of cultures and organism sensitivities.
Lung abscess is a localized collection of neutrophils (pus) and necrotic pulmonaryparenchyma. The etiology varies with the clinical setting. Aspiration is the most common cause. It tends to involve right lower lobe and typically has mixed oral flora (often both anaerobic and aerobic) for infecting organisms.
Lung abscess may also occur following a pneumonia, especially one due to S. aureus or Klebsiella . Lung abscesses may also occur following airway obstruction (postob-structive) or deposition of septic emboli in the lung.
Complications of lung abscess include empyema, pulmonary hemorrhage, and sec-ondary amyloidosis.
Atypical pneumonia is the term used for interstitial pneumonitis without consolida-tion. It is more common in children and young adults.
Infecting organisms that can cause atypical pneumonia includeMycoplasmapneumoniae, influenza virus, parainfluenza virus, respiratory syncytial virus (RSV)(which is especially important in young children), adenovirus, cytomegalovirus (CMV) (which is especially important in the immunocompromised), varicella virus, and many others.
Diagnosis.Chest x-ray typically shows diffuse interstitial infiltrates. An elevatedcold agglutinin titer specifically suggests Mycoplasma as a cause, which is important to identify since antibiotic therapy for Mycoplasma exists. Lung biopsy, if performed, typically shows lymphoplasmacytic inflammation within the alveolar septa.
Complications include superimposed bacterial infections and Reye syndrome (potentially triggered by viral illness [influenza/varicella] treated with aspirin).
Tuberculosis (TB).The number of cases of TB is declining in the United States, butthe proportion of cases in people born outside the country is rising. In this clinical setting, a positive PPD skin test may demonstrate that the person has been exposed to the mycobacterial antigens. Individuals who have received the BCG vaccine in some foreign countries may have a positive PPD test without being infected. In such cases chest x-ray and sputum smears and cultures are done.
Infection is usually acquired by inhalation of aerosolized bacilli.
The clinical presentation of Mycobacterium tuberculosis includes fevers and night sweats, weight loss, cough, and hemoptysis.
Primary pulmonary TB develops on initial exposure to the disease. The Ghonfocus of primary TB is characterized by subpleural caseous granuloma formation, either above or below the interlobar fissure. The term Ghon complex refers to the combination of the Ghon focus and secondarily-involved hilar lymph nodes with granulomas. Most primary pulmonary tuberculosis lesions (95%) will undergo fibro-sis and calcification.
Progressive pulmonary TB can take several forms, including cavitary tuberculosis,miliary pulmonary tuberculosis, and tuberculous bronchopneumonia.
Secondary pulmonary TB (also known as postprimary or reactivation TB) occurseither with reactivation of an old, previously quiescent infection or with reinfection secondary to a second exposure to the mycobacteria. In secondary pulmonary TB, the infection often produces a friable nodule at the lung apex (Simon focus) second-ary to the high oxygen concentration present at that site, since the upper parts of the lung typically ventilate more efficiently than the lower parts. Biopsy of affected tissues will typically show AFB-positive caseating granulomas.
Additionally, dissemination to other organ systems can occur in advanced TB via a hematogenous route that often results in a miliary pattern within each affected organ. Sites that may become involved include meninges; cervical lymph nodes (scrofula) and larynx; liver/spleen, kidneys, adrenals, and ileum; lumbar vertebrae bone marrow (Pott disease); and fallopian tubes and epididymis.
Nontuberculous mycobacteria.M. avium complex (MAC) typically occurs in AIDSpatients with CD4 counts <50 cells/mm3 and presents as disseminated disease.
The diagnosis of TB requires identification of the bacilli. Positive sputum smear necessitates culture for species identification. Adequate treatment requires drug susceptibility testing.
SARCOIDOSIS
Sarcoidosis is a systemic granulomatous disease of uncertain etiology. The diseaseaffects females more than males, with typical age 20–60. It is most common in African American women. Clinical presentation varies. It may be asymptomatic, or presenting symptoms may include cough and shortness of breath; fatigue and malaise; skin lesions; eye irritation or pain; and fever or night sweats. Most often, the disease is first detected on chest x-ray as bilateral hilar lymphadenopathy or parenchymal infiltrates.
The noncaseating granulomas that are characteristic of sarcoidosis may occur in anyorgan of the body. In the lung, they typically form diffuse scattered granulomas;lymph node involvement may cause hilar and mediastinal adenopathy. Skin, liver and/or spleen, heart, central nervous system, bone marrow, and gastrointestinal tract are also frequent targets of the disease. Eye involvement can be seen in Mikulicz syndrome (involvement of the uvea and parotid).
The diagnosis of sarcoidosis can be suggested by clinical studies. In the laboratory, serum angiotensin converting enzyme (ACE), which is synthesized by endothelial cells and macrophages, may be elevated. X-ray studies frequently show bilateral hilar lymphadenopathy.
Sarcoidosis is considered to be a diagnosis of exclusion. In practice, this means that the diagnosis is considered when a biopsy shows features characteristic of sarcoidosis (such as noncaseating granulomas, Schaumann bodies [laminated dystrophic calci-fication], and asteroid bodies [stellate giant cell cytoplasmic inclusions]). There are no pathognomonic microscopic features though, and the diagnosis requires clini-copathologic correlation.
The prognosis is favorable with a variable clinical course. Most patients completely recover but some succumb to respiratory compromise.
OBSTRUCTIVE VERSUS RESTRICTIVE LUNG DISEASE
OBSTRUCTIVE PULMONARY DISEASE
Chronic obstructive pulmonary disease (COPD) is a general term used to indicatechronic decreased respiratory function due to chronic bronchitis or emphysema. Both diseases are associated with smoking.
Chronic bronchitis is a clinical diagnosis made when a patient has a persistent coughand copious sputum production for at least 3 months in 2 consecutive years. It is highly associated with smoking (90%). Clinical findings include cough, sputum production, dyspnea, frequent infections, hypoxia, cyanosis, and weight gain.
Microscopic examination demonstrates hypertrophy and hyperplasia of bronchial mucous glands (Reid index equals the submucosal gland thickness divided by the bronchial wall thickness between the pseudostratified columnar epithelium and the perichondrium; normal ratio is ≤0.4).
Complications include increased risk for recurrent infections; secondary pulmonary hypertension leading to right heart failure (cor pulmonale) and lung cancer.
Emphysema is the term used when destruction of alveolar septa results in enlargedair spaces and a loss of elastic recoil. The 4 types of emphysema are named for the anatomical distribution of the septal damage.
· In centrilobular emphysema, the damage is in the proximal portion of the acinus and the cause is cigarette smoking.
· In panacinar emphysema, the damage affects the entire acinus and the com-mon cause is alpha-1 antitrypsin deficiency.
· In distal acinar emphysema (unknown cause), extension to the pleura causes pneumothorax.
· In irregular emphysema, post-inflammatory scarring involves the acinus in an irregular distribution.
The etiology of emphysema involves a protease/antiprotease imbalance. On gross examination, the lungs are overinflated and enlarged, and have enlarged, grossly visible air spaces. Clinical findings include progressive dyspnea, pursing of lips and use of accessory respiratory muscles to breathe, barrel chest (increased anterior-posterior diameter), and weight loss.
Asthma is due to hyperreactive airways, which undergo episodic bronchospasmwhen triggered by certain stimuli.
· Atopic (type I IgE-mediated hypersensitivity reaction) asthma (most com-mon form) usually affects children and young adults. There is often a positive family history.
· Nonatopic asthma is triggered by processes including respiratory infections(usually viral), stress, exercise, or cold temperatures.
· Drug-induced asthma affects about 10% of adults with a diagnosis of asthma.Aspirin is a key example of a precipitating drug.
· Occupational asthma is caused by workplace triggers including fumes anddusts.
An asthma attack is characterized by wheezing, severe dyspnea, and coughing. Prob-lems with expiration cause lung overinflation. Status asthmaticus is a potentially fatal unrelenting attack of asthma.
Microscopic examination of sputum cytology may show Curschmann spirals (twisted mucus plugs admixed with sloughed epithelium), eosinophils, or Charcot-Leyden crystals (protein crystalloids from broken down eosinophils).
In patients dying from disease, autopsy findings include mucus plugs, increased mucous glands with goblet cell hyperplasia, inflammation (especially with eosino-phils), edema; hypertrophy and hyperplasia of bronchial wall smooth muscle, and thickened basement membranes.
Bronchiectasis is an abnormal permanent airway dilatation due to chronic necro-tizing inflammation. Clinical findings include cough, fever, malodorous purulent sputum, and dyspnea. Causes are diverse, and include bronchial obstruction by for-eign body, mucus, or tumor, necrotizing pneumonias, cystic fibrosis, and Kartagener syndrome.
· Kartagener syndrome is an autosomal recessive condition caused by immotilecilia due to a defect of dynein arms (primary ciliary dyskinesia). It is character-ized clinically by bronchiectasis, chronic sinusitis, and situs inversus (a con-genital condition where the major visceral organs are anatomically reversed compared with their normal anatomical positions).
On gross examination, bronchiectasis shows dilated bronchi and bronchioles extend-ing out to the pleura. These changes may also be appreciated on chest x-ray. Compli-cations include abscess, septic emboli, cor pulmonale, and secondary amyloidosis.
INFILTRATIVE RESTRICTIVE LUNG DISEASES(DIFFUSE INTERSTITIAL DISEASES)
Acute respiratory distress syndrome (ARDS) refers to diffuse damage of alveolarepithelium and capillaries, resulting in progressive respiratory failure that is unre-sponsive to oxygen treatment. Clinicians use the term ARDS, while pathologists use the term diffuse alveolar damage (DAD) to describe the pathologic changes.
ARDS may be caused by shock, sepsis, trauma, gastric aspiration, radiation, oxygen toxicity, drugs, or pulmonary infection. Activated neutrophils mediate cell damage. Clinically, patients show dyspnea, tachypnea, hypoxemia, cyanosis, and use of acces-sory respiratory muscles. X-rays show bilateral lung opacity (“white out”).
On gross pathologic examination affected lungs are heavy, stiff, and noncompli-ant. Microscopically, there is intra-alveolar edema, and hyaline membranes line the alveolar spaces. In resolving cases there is proliferation of type II pneumocytes and interstitial inflammation and fibrosis.
Treatment is based on treating the underlying cause and on supporting respiration with mechanical ventilation. The prognosis is problematic even with good care, with overall mortality 40%.
Respiratory distress syndrome of the newborn (hyaline membrane disease of new-borns) is caused by a deficiency of surfactant. It is associated with prematurity (gestational age of <28 weeks has a 60% incidence), maternal diabetes, multiple births, male gender, and cesarean section delivery. Clinically, infants are normal at birth but within a few hours develop increasing respiratory effort, tachypnea, nasal flaring, use of accessory muscles of respiration, an expiratory grunt, and cyanosis. Chest radiograph may demonstrate bilateral “ground- glass” reticulogranular densi-ties. Autopsy findings include atelectasis and hyaline membranes.
Treatment is surfactant replacement, mechanical ventilation, and continuous posi-tive airway pressure (CPAP). Respiratory distress syndrome of the newborn can sometimes be prevented if labor can be delayed and if corticosteroids are used to mature the lung. With improved therapies, now >90% of babies survive.
Chronic interstitial lung disease is a term describing heterogeneous lung disorderswhich share similar symptomology but vary in prognosis. Patients present with dys-pnea and cough. Lung biopsy findings can be paired with clinical information to aid in therapeutic management/palliative care.
· Idiopathic pulmonary fibrosis (IPF) is a fatal disease. It shows patchy intersti-tial fibrosis and inflammation. “Honeycomb fibrosis” refers to dilated cystic spaces lined with type II pneumocytes; this histology is consistent with end-stage lung. Pathologists use the term usual interstitial pneumonia for IPF.
· Nonspecific interstitial pneumonia has a better prognosis than IPF. There is acellular pattern and a fibrosing pattern.
· Cryptogenic organizing pneumonia responds to steroids. Histologically, thereare plugs of connective tissue inside the alveolar spaces.
· Collagen vascular disease pneumonitis has varied patterns of parenchymaland pleural involvement. The prognosis is poor.
Smoking-related pneumonitis.Several entities have been identified.
o Desquamative interstitial pneumonia features alveolar macrophages.
o Respiratory bronchiolitis features bronchiolocentric macrophages.
o Smoking-related interstitial fibrosis shows septal collagen deposition without significant associated inflammation.
· Hypersensitivity pneumonitis.After exposure to a sensitizing agent such asmoldy hay, patients present with a febrile acute reaction or a chronic disease with weight loss. Biopsy shows peribronchiolar acute and chronic interstitial inflam-mation +/- noncaseating granulomas. The disease is immunologically mediated.
Eosinophilic pneumonia describes a group of diseases with varying clinicalfeatures but a common histologic finding of a mixed septal inflammatory infiltrate and eosinophils within alveolar spaces. Loeffler’s syndrome is a self-limiting type of eosinophilic pneumonia with peripheral blood eosinophilia.
Occupation-associated pneumoconiosis is a common cause of chronic interstitiallung disease. It is considered separately here to show the full spectrum of disease since neoplasia may occur during its course.
· Pneumoconioses are fibrosing pulmonary diseases caused by inhalation of anaerosol (mineral dusts, particles, vapors, or fumes). Key factors affecting their development include the type of aerosol and its ability to stimulate fibrosis; the dose and duration of exposure; and the size of the particle, with only particles <10 microns entering the alveolar sac.
Coal worker’s pneumoconiosis is an important pneumoconiosis that isdue to anthracosis, in which carbon pigment (anthracotic pigment) fromcoal mining accumulates in macrophages along the pleural lymphaticsand interstitium. Clinically, the disease may progress through severalstages. The earliest stage is asymptomatic.
Simple coal worker’s pneumoconiosis (black lung disease) is character- ized by coal-dust macules and nodules in the upper lobes that producelittle pulmonary dysfunction.
Complicated coal worker’s pneumoconiosis is characterized by progres-sive massive fibrosis that is accompanied by increasing respiratory dis- tress, secondary pulmonary hypertension, and cor pulmonale.
Caplan syndrome is the term when pneumoconiosis (of any type) accom- panies rheumatoid arthritis.
· Asbestosis is caused by members of a family of crystalline silicates. Occupa-tions in which asbestos exposure may occur include shipyard work, insulation and construction industries, brake-lining manufacture.
Serpentine asbestos is composed of curved, flexible fibers, with the most common type of serpentine asbestos being chrysotile.
Amphibole asbestos is composed of straight, brittle fibers. Important types include crocidolite, tremolite, and amosite. Amphibole asbestos is more pathogenic than serpentine asbestos, and is highly associated with mesotheliomas.
The pulmonary pathology of asbestosis is a diffuse interstitial fibrosis that begins in the lower lobes; it causes slowly progressive dyspnea which may eventually be complicated by secondary pulmonary hypertension and cor pulmonale. Pulmonary biopsy may demonstrate asbestos bodies that have become coated with iron (ferruginous bodies). Otherwise, the findings are the same as usual interstitial pneumonia.
Pleural involvement may take the form of parietal pleural plaques (acel- lular type I collagen deposition) in a symmetrical distribution involving the domes of the diaphragm and posterolateral chest walls on chest x-ray.
The apices and costophrenic angles are spared. Plaques on the anterior chest wall may be seen on CT. Fibrous pleural adhesions may occur on the visceral pleura.
Lung cancer is the most common tumor in asbestos-exposed individu- als; there is a strong synergistic effect between smoking and asbestos exposure.
Malignant mesothelioma is a rare, highly malignant neoplasm associ- ated with occupational exposure to asbestos in 90% of cases. It presents with recurrent pleural effusions, dyspnea, and chest pain. The tumor grossly encases and compresses the lung; microscopic exam exhibits car- cinomatous and sarcomatous elements (biphasic pattern), while electron microscopy shows long, thin microvilli on some tumor cells. The prog- nosis of mesothelioma is poor. Other problems include increased risk of laryngeal, stomach, and colon cancers. Family members also have increased risk of cancer due to the worker bringing home clothing cov- ered with asbestos fibers.
· Silicosis is due to exposure to silicon dioxide (silica). It is seen most frequentlywith occupational exposure (sandblasters, metal grinders, miners). The pul-monary pathology shows dense nodular fibrosis of the upper lobes whichmay progress to massive fibrosis; birefringent silica particles can be seen with polarized light.
Patients present with insidious onset of dyspnea that is slowly progressive despite cessation of exposure. X-ray shows fibrotic nodules in the upper zones of the lungs. There is an increased risk of TB.
· Berylliosis is an allergic granulomatous reaction due to workplace exposureto beryllium in the nuclear, electronics, and aerospace industries. Genetic susceptibility appears to play a role, as does a type IV hypersensitivity reac-tion, resulting in granuloma formation. Clinically, acute exposure causes acute pneumonitis, while chronic exposure causes pulmonary noncaseating granu-lomas and fibrosis, hilar lymph node granulomas, and systemic granulomas
VASCULAR DISORDERS
Pulmonary edema is fluid accumulation within the lungs, usually due to imbalanceof Starling forces or endothelial injury.
· Pulmonary edema due to increased hydrostatic pressure can be seen in left-sided heart failure, mitral valve stenosis, high altitude pulmonary edema, and fluid overload.
· Pulmonary edema due to decreased oncotic pressure can be seen in nephrotic syndrome and liver disease.
· Pulmonary edema due to increased capillary permeability can be due to infections, drugs (bleomycin, heroin), shock, and radiation.
The pathology grossly shows wet, heavy lungs (usually worse in lower lobes), while microscopic examination shows intra-alveolar fluid, engorged capillaries, and hemosiderin-laden macrophages (heart-failure cells).
Pulmonary hypertension is increased pulmonary artery pressure, usually due toincreased vascular resistance or blood flow.
The etiology varies and can include chronic obstructive pulmonary disease and interstitial disease (hypoxic vasoconstriction); multiple ongoing pulmonary emboli; mitral stenosis and left heart failure; congenital heart disease with left to right shunts (atrial septal defect, ventricular septal defect, patent ductus arteriosus); and primary (idiopathic) pulmonary hypertension, typically in young women.
The pathology includes pulmonary artery atherosclerosis, small artery medial hyper-trophy and intimal fibrosis, and plexogenic pulmonary arteriopathy. Pulmonary hypertension may also damage the heart, leading to right ventricular hypertrophy and then failure (cor pulmonale).
PULMONARY NEOPLASIA
Lung cancer is the leading cause of cancer death among both men and women; it hasbeen increasing in women (increased smoking) in the past few decades. It occurs most commonly age 50–80. Major risk factors include cigarette smoking, occu-pational exposure (asbestosis, uranium mining, radiation, etc.), passive smoking, and air pollution. Clinical features include cough, sputum production, weight loss, anorexia, fatigue, dyspnea, hemoptysis, and chest pain. Obstruction may produce focal emphysema, atelectasis, bronchiectasis, or pneumonia.
Common genetic mutations in lung cancer involve the oncogenes MYCL (small cell carcinomas) and KRAS (adenocarcinomas); tumor suppressor genes: TP53 and RB1.
Adenocarcinoma is more commonly seen in women and nonsmokers. Grossly, itcauses a peripheral gray-white mass, and the tumor may develop in areas of paren-chymal scarring (scar carcinoma). Microscopically, common patterns include acinar, papillary, mucinous, and solid. The precursor lesion—atypical adenomatous hyper-plasia—progresses to adenocarcinoma in situ (noninvasive well- differentiated tumor <3 cm) and to minimally invasive tumor (invasion no more than 5 mm) before progressing to invasive adenocarcinoma.
Squamous cell carcinoma (SCC) is strongly related to smoking and affects malesmore than females. Squamous cell carcinoma arises from bronchial epithelium after a progression:
metaplasia → dysplasia → carcinoma in situ → invasive carcinoma
Pathologically, the tumor grossly causes a gray-white bronchial mass, usually cen-trally located. Microscopically, well-differentiated tumors show invasive nests of squamous cells with intercellular bridges (desmosomes) and keratin production (“squamous pearls”).
Small cell carcinoma has a strong association with smoking, and affects males morethan females. This neuroendocrine tumor is very aggressive, with rapid growth and early dissemination. Small cell carcinoma is commonly associated with paraneo-plastic syndromes.
Large cell carcinoma has large anaplastic cells without evidence of differentiation.
Intrathoracic spread of lung cancer is to lymph nodes, particularly hilar, bronchial,tracheal, and mediastinal; pleura (adenocarcinoma); and lung apex causing Horner syndrome (Pancoast tumor).
· Obstruction of the superior vena cava by tumor causes superior vena cavasyndrome, characterized by distended head and neck veins, plethora, andfacial and upper arm edema.
· Esophageal obstruction can cause dysphagia.
· Recurrent laryngeal nerve involvement causes hoarseness, while phrenic nerve damage causes diaphragmatic paralysis.
Extrathoracic sites of metastasis include adrenal (>50%), liver, brain, and bone.
Paraneoplastic syndromes
· Endocrine/metabolic syndromes include Cushing syndrome secondary to ACTH production, SIADH secondary to ADH production, and hypercalcemia secondary to PTH production (squamous cell carcinoma).
· Eaton-Lambert syndrome
· Acanthosis nigricans
· Hypertrophic pulmonary osteoarthropathy is characterized by periosteal new bone formation with clubbing and arthritis.
Treatment of non–small cell lung cancer is with surgery, and treatment of small cell lung cancer is with chemotherapy and radiation. Despite treatment, the prognosis is poor, with overall 5-year survival 16%.
Bronchial carcinoids occur in a younger age group (mean age 40 years) and typi-cally produce a polypoid intrabronchial mass or plaque; it is characterized on light microscopy by small, round, uniform cells growing in nests (organoid pattern), and on electron microscopy by cytoplasmic dense-core neurosecretory granules. Atypi-cal carcinoid is more aggressive than typical carcinoid.
Metastatic carcinoma is the most common malignant neoplasm in the lung. It typi-cally causes multiple, bilateral, scattered nodules; common primary sites include breast, stomach, pancreas, and colon.
Hamartomas are benign tumors; they occur more commonly in middle-aged adultsbut also occur in children. They can appear as coin lesions on chest x-ray. Micro-scopically, they are comprised of nonencapsulated fibromyxoid tissue. Carney triad is the finding of a hamartoma with a predominantly cartilaginous component (pul-monary chondroma), an extra-adrenal paraganglioma and a gastric gastrointestinal stromal tumor.
LARYNGEAL CANCER
Laryngeal squamous cell carcinoma causes hoarseness, difficulty swallowing, pain,hemoptysis, and eventual respiratory compromise. Risk factors include smoking, alcohol, and frequent cord irritation (professional singing or lecturing). Complica-tions include direct extension, metastases, and infection.
DISEASES OF THE PLEURAL CAVITY
Pleural effusion is the accumulation of fluid in the pleural cavity.
· Empyema refers to pus in pleural space.
· Chylothorax refers to chylous fluid in the pleural space secondary to obstruc-tion of the thoracic duct, usually by tumor.
Pneumothorax is the term used for air in the pleural cavity. It can be due to traumaticpenetrating chest wall injuries or spontaneous rupture of apical blebs in typically tall young adults (spontaneous pneumothorax). The term tension pneumothorax is used if a life-threatening shift of thoracic organs across midline occurs.
Hemothorax is the presence of blood in the pleural cavity. Trauma is a commoncause. There may be hypotension and shift of the trachea to the unaffected side.
Chylothorax is lymphatic fluid in the pleural cavity. Malignancy is a common cause.
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