Pathoma Deck

Question 1

Rinitis

Answer 1

A. Inflammation of the nasal mucosa; rhinovirus is the most common cause
B. Presents with sneezing, congestion, and runny nose (common cold)
c. allergic rhinitis is a subtype of rhinitis due to a type 1 hypersensitivity reaction (e.g. pollen); characterized by an inflammatory infiltrate with eosinophils; associated with asthma and eczema

Question 2

Nasal Polyp

Answer 2

A. Protrusion of edematous, inflamed nasal mucosa
B. Usually secondary to repeated bouts of rhinitis; also occurs in cystic fibrosis and
aspirin-intolerant asthma
1. Aspirin-intolerant asthma is characterized by the triad of asthma, aspirin-
induced bronchospasms, and nasal polyps; seen in 10% of asthmatic adults

Question 3

Angiofibroma

Answer 3

A. Benign tumor of nasal mucosa composed of large blood vessels and fibrous tissue;
classically seen in adolescent males B. Presents with profuse epistaxis

Question 4

Nasopharyngeal carcinoma

Answer 4

A. Malignant tumor of nasopharyngeal epithelium
B. Associated with EBV; classically seen in African children and Chinese adults
C. Biopsy usually reveals pleomorphic keratin-positive epithelial cells (poorly
differentiated squamous cell carcinoma) in a background of lymphocytes. D. Often presents with involvement of cervical lymph nodes

Question 5

Acute epiglottitis

Answer 5

A. Inflammation of the epiglottis (Fig. 9.1); H influenzae type b is the most common
cause, especially in nonimmunized children. B. Presents with high fever, sore throat, drooling with dysphagia, muffled voice, and
inspiratory stridor; risk of airway obstruction

Question 6

Croup (laryngotracheobronchitis)

Answer 6

A. Inflammation of the upper airway; parainfluenza virus is the most common cause.
B. Presents with a hoarse, “barking” cough and inspiratory stridor

Question 7

Vocal cord nodule (singer’s nodule)

Answer 7

A. Nodule that arises on the true vocal cord
B. Due to excessive use of vocal cords; usually bilateral (Fig. 9.2A)
1. Composed of degenerative (myxoid) connective tissue (Fig. 9.2B)
C. Presents with hoarseness; resolves with resting of voice

Question 8

Laryngeal papilloma

Answer 8

A. Benign papillary tumor of the vocal cord
B. Due to HPV 6 and 11; papillomas are usually single in adults and multiple in
children. C. Presents with hoarseness

Question 9

laryngeal carcinoma

Answer 9

A. Squamous cell carcinoma usually arising from the epithelial lining of the vocal cord
B. Risk factors are alcohol and tobacco; can rarely arise from a laryngeal papilloma
C. Presents with hoarseness; other signs include cough and stridor.

Question 10

pneumonia

Answer 10

A. Infection of the lung parenchyma
B. Occurs when normal defenses are impaired (e.g., impaired cough reflex, damage to
mucociliary escalator, or mucus plugging) or organism is highly virulent. C. Clinical features include fever and chills, productive cough with yellow-green (pus)
or rusty (bloody) sputum, tachypnea with pleuritic chest pain, decreased breath
sounds, crackles, dullness to percussion, and elevated WBC count. D. Diagnosis is made by chest x-ray, sputum gram stain and culture, and blood
cultures. E. Three patterns are classically seen on chest x-ray: lobar pneumonia,
bronchopneumonia, and interstitial pneumonia.

Question 11

lobar pneumonia

Answer 11

A. Characterized by consolidation of an entire lobe of the lung (Fig. 9.3A)
B. Usually bacterial; most common causes are Streptococcus pneumoniae (95%) and
Klebsiella pneumoniae (Table 9.1) C. Classic gross phases of lobar pneumonia
1. Congestion - due to congested vessels and edema 2. Red hepatization - due to exudate, neutrophils, and hemorrhage filling the alveolar
air spaces, giving the normally spongy lung a solid consistency (Fig. 9.3B,C) 3. Gray hepatization - due to degradation of red cells within the exudate 4. Resolution

Question 12

bronchopneumonia

Answer 12

A. Characterized by scattered patchy consolidation centered around bronchioles; often
multifocal and bilateral (Fig. 9.4) B. Caused by a variety of bacterial organisms (Table 9.2)

Question 13

Interstitial pneumonia

Answer 13

A. Characterized by diffuse interstitial infiltrates (Fig. 9.5)
B. Presents with relatively mild upper respiratory symptoms (minimal sputum and low
fever); ‘atypical’ presentation C. Caused by bacteria or viruses (Table 9.3)

Question 14

aspiration pneumonia

Answer 14

A. Seen in patients at risk for aspiration (e.g., alcoholics and comatose patients)
B. Most often due to anaerobic bacteria in the oropharynx (e.g., Bacteroides,
Fusobacterium, and Peptococcus); C. Classically results in a right lower lobe abscess
1. Anatomically, the right main stem bronchus branches at a less acute angle than
the left

Question 15

strep pneumonia

Answer 15

Cause of lobar pneumonia; Most common cause of community-acquired pneumonia and secondary Streptococcus pneumoniae
pneumonia (bacterial pneumonia superimposed on a viral upper respiratory tract infection); usually seen in middle-aged adults and elderly

Question 16

klebisella pneumoniae

Answer 16

cause of lobar pneumonia; Enteric flora that is aspirated; affects malnourished and debilitated individuals,
especially elderly in nursing homes, alcoholics, and diabetics. Thick mucoid capsule results in gelatinous sputum (currant jelly); often complicated by abscess

Question 17

staph. aureus

Answer 17

cause bronchopneumonia;
2ndmost common cause of secondary pneumonia; often complicated by abscess or empyema

Question 18

h. influenzae

Answer 18

cause of bronchopneumonia; common cause of secondary pneumonia and pneumonia superimposed on COPD (leads to exacerbation of COPD)

Question 19

pseudomonas aeruginosa

Answer 19

cause of bronchopneumonia; pneumonia in cystic fibrosis patients

Question 20

moraxella catarhalis

Answer 20

cause of bronchopneumonia; community -acquired pneumonia superimposed on COPD (leads to exacerbation of COPD)

Question 21

Legionella pneumophila

Answer 21

cause of bronchopneumonia; Community-acquired pneumonia, pneumonia superimposed on COPD, or Legionella pneumophila
pneumonia in immunocompromised states; transmitted from water source Intracellular organism that is best visualized by silver stain

Question 22

mycoplasma pneumoniae

Answer 22

Most common cause of atypical (interstitial) pneumonia, usually affects young adults (classically, military recruits or college students living in a dormitory). Complications include autoimmune hemolytic anemia (IgM against I antigen on RBCs causes cold hemolytic anemia) and erythema multiforme. Not visible on gram stain due to lack of cell wall

Question 23

chlamydia pneumoniae

Answer 23

Second most common cause of atypical (interstitial) pneumonia in young adults

Question 24

Respiratory syncytial virus (RSV)

Answer 24

Most common cause of atypical (interstitial) pneumonia in infants

Question 25

Cytomegalovirus (CMV)

Answer 25

Atypical (interstitial) pneumonia with posttransplant immunosuppression or chemotherapy

Question 26

Influenza virus

Answer 26

Atypical pneumonia in the elderly, immunocompromised, and those with preexisting lung disease. Also increases the risk for superimposed S aureus or H influenzae bacterial pneumonia

Question 27

coxiella brunetti

Answer 27

Atypical (interstitial) pneumonia with high fever (Q fever); seen in farmers and veterinarians ( Coxiella spores are deposited on cattle by ticks or are present in cattle placentas). Coxiella is a rickettsial organism, but it is distinct from most rickettsiae because it (1) causes pneumonia, (2) does not require arthropod vector for transmission (survives as highly heat-resistant endospores), and (3) does not produce a skin rash.

Question 28

Tuberculosis

Answer 28

Due to inhalation of aerosolized Mycobacterium tuberculosis

Question 29

Primary TB arises with initial exposure

Answer 29

Results in focal, caseating necrosis in the lower lobe of the lung and hilar lymph
nodes that undergoes fibrosis and calcification, forming a Ghon complex (Fig. 9.6A)
2. Primary TB is generally asymptomatic, but leads to a positive PPD.

Question 30

secondary TB arises with reactivation of mycobacterium tb

Answer 30

1. Reactivation is commonly due to AIDS; may also be seen with aging
2. Occurs at apex of lung (relatively poor lymphatic drainage and high oxygen
   tension) 3. Forms cavitary foci of caseous necrosis; may also lead to miliary pulmonary TB
   or tuberculous bronchopneumonia 4. Clinical features include fevers and night sweats, cough with hemoptysis, and
   weight loss. 5. Biopsy reveals caseating granulomas; AFB stain reveals acid-fast bacilli (Fig.
   9.6B,C). 6. Systemic spread often occurs and can involve any tissue; common sites include
   meninges (meningitis), cervical lymph nodes, kidneys (sterile pyuria), and
   lumbar vertebrae (Pott disease).

Question 31

COPD basic principles

Answer 31

A. Group of diseases characterized by airway obstruction; lung does not empty, and air
is trapped.
1. Volume of air that can be forcefully expired is decreased (
↓FVC), especially
during the first second of expiration (↓↓FEV1); results in ↓FEV1:FVC ratio 2. Total lung capacity (TLC) is usually increased due to air trapping.

Question 32

chronic bronchitis

Answer 32

obstructive; A. Chronic productive cough lasting at least 3 months over a minimum of 2 years;
highly associated with smoking B. Characterized by hypertrophy of bronchial mucous glands (Fig. 9.7)
1. Leads to increased thickness of mucus glands relative to bronchial wall thickness
(Reid index increases to > 50%; normal is < 40%).
C. Clinical features
1. Productive cough due to excessive mucus production
2. Cyanosis (‘blue bloaters’) - Mucus plugs trap carbon dioxide; ↑Paco2
and ↓ Pa o2 3. Increased risk of infection and cor pulmonale

Question 33

emphysema

Answer 33

. Destruction o f alveolar air sacs (Fig. 9.8)
1. Loss of elastic recoil and collapse of airways during exhalation results in
obstruction and air trapping.

Question 34

emphysema cause

Answer 34

Due to imbalance o f proteases and antiproteases
1. Inflammation in the lung normally leads to release o f proteases by neutrophils
and macrophages. 2. α 1-antitrypsin (A1AT) neutralizes proteases. 3. Excessive inflammation or lack of A1AT leads to destruction of the alveolar air
sacs.
C. Smoking is the most common cause of emphysema.
1. Pollutants in smoke lead to excessive inflammation and protease-mediated
damage.2. Results in centriacinar emphysema that is most severe in the upper lobes

Question 35

A1AT deficiency

Answer 35

D. A1AT deficiency is a rare cause of emphysema.
1. Lack of antiprotease leaves the air sacs vulnerable to protease-mediated damage.
2. Results in panacinar emphysema that is most severe in the lower lobes
3. Liver cirrhosis may also be present.
i. A l AT deficiency is due to misfolding of the mutated protein. ii. Mutant A1AT accumulates in the endoplasmic reticulum of hepatocytes,
resulting in liver damage. iii. Biopsy reveals pink, PAS-positive globules in hepatocytes (Fig. 9.9).

Question 36

Emphysema disease severity

Answer 36

4. Disease severity is based on the degree o f AlAT deficiency.
   i. PiM is the normal allele; two copies are usually expressed (PiMM).
   ii. PiZ is the most common clinically relevant mutation; results in significantly
   low levels o f circulating A1AT
   iii. PiMZ heterozygotes are usually asymptomatic with decreased circulating
   levels of A1AT; however, significant risk for emphysema with smoking
   exists. iv. PiZZ homozygotes are at significant risk for panacinar emphysema and
   cirrhosis.

Question 37

Emphysema clinical features

Answer 37

E. Clinical features of emphysema include
1. Dyspnea and cough with minimal sputum
2. Prolonged expiration with pursed lips (‘pink-puffer’)
3. Weight loss
4. Increased anterior-posterior diameter of chest (‘barrel-chest,’ Fig. 9.10)
5. Hypoxemia (due to destruction of capillaries in the alveolar sac) and cor
pulmonale are late complications.

Question 38

Asthma pathogenesis

Answer 38

A. Reversible airway bronchoconstriction, most often due to allergic stimuli (atopic asthma)
B. Presents in childhood; often associated with allergic rhinitis, eczema, and a family
history of atopy C. Pathogenesis (type I hypersensitivity)
1. Allergens induce TH2 2. phenotype in CD4 + T cells of genetically susceptible individuals. 3. T H2 cells secrete IL-4 (mediates class switch to IgE), IL-5 (attracts eosinophils),
and IL-10 (stimulates T H2 cells and inhibits TH1). 4. Reexposure to allergen leads to IgE-mediated activation of mast cells.
i. Release of preformed histamine granules and generation of leukotrienes C4,
D4, and E4 lead to bronchoconstriction, inflammation, and edema (early- phase reaction).
ii. Inflammation, especially major basic protein derived from eosinophils,
damages cells and perpetuates bronchoconstriction (late-phase reaction).

Question 39

asthma clinical features

Answer 39

D. Clinical features are episodic and related to allergen exposure.
1. Dyspnea and wheezing
2. Productive cough, classically with spiral-shaped mucus plugs (Curschmann
spirals) and eosinophil-derived crystals (Charcot-Leyden crystals, Fig. 9.11). 3. Severe, unrelenting attack can result in status asthmaticus and death.
E. Asthma may also arise from nonallergic causes (non-atopic asthma) such as exercise, viral infection, aspirin (e.g., aspirin intolerant asthma), and occupational exposures.

Question 40

Bronchiectasis causes

Answer 40

A. Permanent dilatation of bronchi (Fig. 9.12); loss of airway tone results in air trapping.
B. Due to severe inflammation with damage to airway walls. Causes include
1. Cystic fibrosis 2. Primary ciliary dyskinesia - inherited defect of the dynein arm, which is
necessary for ciliary movement. Associated with sinusitis, infertility (poor
motility of sperm), and situs inversus (position of major organs is reversed, e.g.,
heart is on right side of thorax), which is called Kartagener syndrome
3. Tumor or foreign body (localized bronchiectasis) 4. Necrotizing infection (localized bronchiectasis) 5. Allergic bronchopulmonary aspergillosis - Hypersensitivity reaction to
Aspe rgillus leads to chronic inflammatory damage; usually seen in individuals
with asthma or cystic fibrosis

Question 41

bronchiectasis clinical features

Answer 41

1. Cough, dyspnea, and foul-smelling sputum
2. Complications include hypoxemia with cor pulmonale and secondary (AA)
   amyloidosis.

Question 42

restrictive disease basic principles

Answer 42

A. Characterized by restricted filling of the lung; ↓TLC, ↓FEV1, and↓↓FVC;
FEV1:FVC ratio is increased.
B. Most commonly due to interstitial diseases of the lung; may also arise with chest
wall abnormalities (e.g., massive obesity)

Question 43

idiopathic pulmonary fibrosis

Answer 43

restrictive; A. Fibrosis of lung interstitium (Fig. 9.13)
B. Etiology is unknown. Likely related to cyclical lung injury; TGF-β from injured
pneumocytes induces fibrosis.
1. Secondary causes of interstitial fibrosis such as drugs (e.g., bleomycin and
amiodarone) and radiation therapy must be excluded.

Question 44

idiopathic pulmonary fibrosis clinical features

Answer 44

1. Progressive dyspnea and cough
2. Bilateral fibrosis on lung CT; initially seen in subpleural patches, but eventually
   results in extensive fibrosis with end-stage ‘honeycomb’ lung 3. Anti-fibrogenic drugs slow disease progression 4. Definitive treatment is lung transplantation.

Question 45

pneumoconioses

Answer 45

A. Interstitial fibrosis due to occupational exposure; requires chronic exposure to small
particles that are fibrogenic (Table 9.4)
1. Alveolar macrophages engulf foreign particles and induce fibrosis.

Question 46

sarcoidosis

Answer 46

A. Systemic disease characterized by noncaseating granulomas in multiple organs;
classically seen in African American females
B. Etiology is unknown; likely due to CD4+ helper T-cell response to an unknown
antigen C. Granulomas most commonly involve the hilar lymph nodes and lung (Fig. 9.15A),
leading to restrictive lung disease.
1. Characteristic stellate inclusions (‘asteroid bodies’) are often seen within giant
cells o f the granulomas (Fig. 9.15B).
D. Other commonly involved tissues include the uvea (uveitis), skin (cutaneous
nodules or erythema nodosum), and salivary and lacrimal glands (mimics Sjögren
syndrome); almost any tissue can be involved.

Question 47

clinical features of sarcoidosis

Answer 47

E. Clinical features
1. Dyspnea or cough (most common presenting symptom) 2. Elevated serum ACE 3. Hypercalcemia (1-alpha hydroxylase activity o f epithelioid histiocytes converts
vitamin D to its active form) 4. Treatment is immunosuppression; often resolves spontaneously without
treatment.

Question 48

Summary of pneumoconiosis: coal worker’s, silicosis, berylliosis, asbestosis

Answer 48

Question 49

hypersensitivity pneumonitis

Answer 49

restrictive; A. Granulomatous reaction to inhaled organic antigens (e.g., pigeon breeder’s lung)
B. Presents with fever, cough, and dyspnea hours after exposure; resolves with removal
of the exposure C. Chronic exposure leads to interstitial fibrosis.

Question 50

pulmonary hypertension basic principles

Answer 50

A. High pressure in the pulmonary circuit (mean arterial pressure > 25 mm Hg; normal
is 10 mm Hg) B. Characterized by atherosclerosis of the pulmonary trunk, smooth muscle
hypertrophy of pulmonary arteries, and intimal fibrosis; plexiform lesions are seen
with severe, long-standing disease (Fig. 9.16). C. Leads to right ventricular hypertrophy with eventual cor pulmonale D. Presents with exertional dyspnea or right-sided heart failure E. Subclassified as primary or secondary based on etiology

Question 51

primary pulmonary hypertension

Answer 51

A. Classically seen in young adult females
B. Etiology is unknown; some familial forms are related to inactivating mutations of
BMPR2, leading to proliferation of vascular smooth muscle.

Question 52

secondary pulmonary hypertension

Answer 52

A. Due to hypoxemia (e.g., COPD and interstitial lung disease) or increased volume in
the pulmonary circuit (e.g., congenital heart disease); may also arise with recurrent pulmonary embolism

Question 53

Acute respiratory distress syndrome

Answer 53

A. Diffuse damage to the alveolar-capillary interface (diffuse alveolar damage)
B. Leakage of protein-rich fluid leads to edema that combines with necrotic epithelial
cells to form hyaline membranes lining alveoli (Fig. 9.17A).

Question 54

acute respiratory distress syndrome clinical features

Answer 54

Clinical features
1. Hypoxemia and cyanosis with respiratory distress - due to thickened diffusion
barrier and collapse of air sacs (increased surface tension) 2. ‘White-out’ on chest x-ray (Fig. 9.17B)D. Secondary to a variety of disease processes including sepsis, infection, shock, trauma, aspiration, pancreatitis, DIC, hypersensitivity reactions, and drugs.

Question 55

Treatment of acute RDS

Answer 55

Treatment
1. Address underlying cause
2. Ventilation with positive end-expiratory pressure (PEEP) F. Recovery may be complicated by interstitial fibrosis; damage and loss of type II
pneumocytes leads to scarring and fibrosis.

Question 56

neonatal RDS

Answer 56

Respiratory distress due to inadequate surfactant levels
1. Surfactant is made by type II pneumocytes; phosphatidylcholine (lecithin) is the
major component. 2. Surfactant decreases surface tension in the lung, preventing collapse of alveolar
air sacs after expiration. 3. Lack of surfactant leads to collapse of air sacs and formation of hyaline
membranes.

Question 57

neonatal RDS associations

Answer 57

B. Associated with
1. Prematurity - Surfactant production begins at 28 weeks; adequate levels are not
reached until 34 weeks. i. Amniotic fluid lecithin to sphingomyelin ratio is used to screen for lung
maturity. ii. Phosphatidylcholine (lecithin) levels increase as surfactant is produced;
sphingomyelin remains constant. iii. A ratio > 2 indicates adequate surfactant production.
2. Caesarian section delivery - due to lack of stress-induced steroids; steroids
increase synthesis of surfactant. 3. Maternal diabetes - Insulin decreases surfactant production.

Question 58

neonatal RDS clinical features

Answer 58

1. Increasing respiratory effort after birth, tachypnea with use of accessory muscles,
   and grunting 2. Hypoxemia with cyanosis 3. Diffuse granularity of the lung (‘ground-glass’ appearance) on x-ray (Fig. 9.18)

Question 59

neonatal RDS complications

Answer 59

1. Hypoxemia increases the risk for persistence of patent ductus arteriosus and
   necrotizing enterocolitis. 2. Supplemental oxygen increases the risk for free radical injury. Retinal injury
   leads to blindness; lung damage leads to bronchopulmonary dysplasia.

Question 60

lung cancer basic principles

Answer 60

A. Most common cause of cancer mortality in the US; average age at presentation is 60
years. B. Key risk factors are cigarette smoke, radon, and asbestos.
1. Cigarette smoke contains over 60 carcinogens; 85% of lung cancer occurs in
smokers.
i. Polycyclic aromatic hydrocarbons and arsenic are particularly mutagenic.
ii. Cancer risk is directly related to the duration and amount of smoking
(‘pack-years’). 2. Radon is formed by radioactive decay of uranium, which is present in soil.
i. Accumulates in closed spaces such as basements ii. Responsible for most of the public exposure to ionizing radiation; 2nd most
frequent cause of lung carcinoma in US
iii. Increased risk of lung cancer is also seen in uranium miners. 3. Environmental toxins include asbestos, coal fueled stoves, and metals (arsenic,
chromium, and nickel)
C. Presenting symptoms are nonspecific (e.g., cough, hemoptysis, dyspnea, weight loss,
and post-obstructive pneumonia).

Question 61

lung cancer imaging

Answer 61

D. Imaging usually reveals a large, spiculated mass; however, a solitary nodule (‘coin-
lesion’) can be seen. Biopsy is necessary for a diagnosis of cancer.
1. Benign lesions may also produce a ‘coin-lesion,’ especially in younger patients.
Examples include
i. Granuloma - often due to TB or fungus (especially Histoplasma in the Midwest)
ii. Bronchial hamartoma - benign tumor composed of lung tissue and cartilage;
often calcified on imaging

Question 62

lung cancer classifications

Answer 62

E. Lung carcinoma is classically divided into 2 categories (Table 9.5).
1. Small cell carcinoma (15%) - usually not amenable to surgical resection (treated
with chemotherapy and radiation) 2. Non-small cell carcinoma (85%)
i. Usually amenable to surgical resection
ii. Major subtypes include adenocarcinoma (50%), squamous cell carcinoma
(30%), large cell neuroendocrine carcinoma (5%), and carcinoid tumor (5%).

Question 63

Cancers of the lung chart; small cell carcinoma; adenocarcinoma; squamous cell carcinoma, large cell neuroendocrine carcinoma; carcinoid tumor; metastasis to the lung

Answer 63

Question 64

TNM staging

Answer 64

1. T - T u m o r size and local extension
   i. Obstruction of SVC leads to distended head and neck veins with edema and
   blue discoloration of arms and face (superior vena cava syndrome). ii. Involvement of recurrent laryngeal (hoarseness) or phrenic (diaphragmatic
   paralysis) nerve iii. Involvement of the sympathetic chain (ptosis, miosis, and anhidrosis; Horner
   syndrome) and brachial plexus (shoulder pain and hand weakness) is seen
   with apical tumors involving the superior sulcus (Pancoast tumor)
2. N - s p r e a d to regional lymph nodes (hilar and mediastinal) 3. M - a unique site of distant metastasis is the adrenal gland. 4. Overall, 15% 5-year survival; lung carcinoma often presents late
   i. Screening by low-dose CT recommended for patients with long smoking history 5. Testing for ‘driver mutations’ guides systemic therapy in advanced disease
   i. EGFR mutations (erlotinib) or ALK translocation (crizotinib) may be present
   in adenocarcinoma; EGFR is especially common in Asian females who are non-smokers.
3. Testing for PD-L1 expression (pembrolizumab) guides immunotherapy in
   advanced disease; PD-L1 may be present in any non-small cell carcinoma.

Question 65

pneumothorax

Answer 65

A. Accumulation of air in the pleural space
B. Spontaneous pneumothorax is due to rupture of an emphysematous bleb; seen in
young adults
1. Results in collapse of a portion of the lung (Fig. 9.24); trachea shifts to the side of
collapse.
C. Tension pneumothorax arises with penetrating chest wall injury.
1. Air enters the pleural space, but cannot exit; trachea is pushed opposite to the
side o f injury. 2. Medical emergency; treated with insertion of a chest tube

Question 66

mesothelioma

Answer 66

A. Malignant neoplasm of mesothelial cells; highly associated with occupational
exposure to asbestos
B. Presents with recurrent pleural effusions, dyspnea, and chest pain; tumor encases the
lung (Fig. 9.25).