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Pulmonary Pathology > Pulmonary Pathology > Flashcards

Pulmonary Pathology Flashcards

1
Q

Rhinitis

A
  • inflammation of the nasal mucosa
  • most common cause is rhinovirus
  • common cold (sneezing, congestion, runny nose)
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2
Q

Allergic Rhinitis

A
  • subtype of rhinitis
  • due to a type I hypersensitivity reaction (e.g. pollen)
  • inflammatory infiltrate with eosinophils
  • associated with asthma and eczema
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3
Q

Nasal Polyp

A
  • protrusion of edematous, inflamed nasal mucosa
  • usually secondary to repeated bouts of rhinitis
  • also occurs in CF and aspirin-intolerant asthma
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4
Q

Aspirin-Intolerant Asthma

A
  • characterized by the triad of asthma, aspirin-induced bronchospasms, and nasal polyps
  • seen in 10% of asthmatic adults
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5
Q

Angiofibroma

A
  • benign tumor of nasal mucosa
  • composed of large blood vessels and fibrous tissue
  • classically seen in adolescent males
  • presents with profuse epistaxis
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6
Q

Nasopharyngeal Carcinoma

A
  • malignant tumor of nasopharyngeal epithelium
  • associated with EBV
  • classically seen in African children and Chinese adults
  • biopsy usually reveals pleomorphic keratin-positive epithelial cells (poorly differentiated squamous cell carcinoma) in a background of lymphocytes
  • often presents with involvement of cervical lymph nodes
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7
Q

Acute Epiglottitis

A
  • inflammation of the epiglottis
  • common cause is H. influenzae type B (esp. non-immunized children)
  • high fever, sore throat, drooling with dysphagia, muffled voice, and inspiratory stridor
  • risk of airway obstruction
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8
Q

Laryngotracheobronchitis (Croup)

A
  • inflammation of the upper airway
  • parainfluenza virus is most common cause
  • hoarse, “barking” cough and inspiratory stridor
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9
Q

Vocal Cord Nodule (Singer’s Nodule)

A
  • nodule that arises on the true vocal cord
  • due to excessive use of vocal cords; usually bilateral
  • composed of degenerative (myxoid) connective tissue
  • presents with hoarseness
  • resolves with resting of voice
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10
Q

Laryngeal Papilloma

A
  • benign papillary tumor of the vocal cord
  • due to HPV 6 and 11
  • papillomas are usually single in adults and multiple in children
  • presents with hoarseness
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11
Q

Laryngeal Carcinoma

A
  • squamous cell carcinoma usually arising from the epithelial lining of the vocal cord
  • risk factors are alcohol and tobacco
  • can rarely arise from a laryngeal papilloma
  • presents with hoarseness
  • other signs include cough and stridor
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12
Q

Pneumonia

A
  • infection of the lung parenchyma
  • when normal defenses are impaired (impaired cough reflex, damage to mucociliary escalator, or mucus plugging)
  • fever and chills, productive cough with yellow-green (pus) or rusty (bloody) sputum, tachypnea, pleuritic CP, dec breath sounds, dullness to percussion, elevated WBC count
  • diagnosed with CXR, sputum gram stain and culture, and blood cultures
  • 3 patterns on CXR: lobar pneumonia, bronchopneumonia, and interstitial pneumonia
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13
Q

Lobar Pneumonia

A
  • characterized by consolidation of an entire lung lobe
  • usually bacterial (S. pneumoniae (95%); Klebsiella pneumoniae are most common)
  • 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)
    3. gray hepatization (due to degradation of red cells within the exudate
    4. resolution
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14
Q

Bronchopneumonia

A
  • characterized by scattered patchy consolidation centered around bronchioles
  • often multifocal and bilateral
  • caused by a variety of bacterial organisms
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15
Q

Interstitial (Atypical) Pneumonia

A
  • characterized by diffuse interstitial infiltrates
  • presents with relatively mild upper respiratory sxs (minimal sputum and low fever)
  • “atypical” presentation
  • caused by bacteria or viruses
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16
Q

Aspiration Pneumonia

A
  • seen in pts at risk for aspiration (alcoholics and comatose pts)
  • most often due to anaerobic bacteria in the oropharynx (e.g. Bacteroides, Fusobacterium, and Peptococcus)
  • classically results in a right lower lobe abscess
  • anatomically, the right main stem bronchus branches at a less acute angle than the left
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17
Q

Primary Tuberculosis (TB)

A
  • inhalation of aerosolized Mycobacterium tuberculosis
  • primary TB arises with initial exposure
  • 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
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18
Q

Secondary TB

A
  • arises with reactivation of Mycobacterium tuberculosis
  • reactivation is commonly due to AIDS; may also be seen with aging
  • occurs at apex of lung (relatively poor lymphatic drainage and high oxygen tension)
  • forms cavitary foci of caseous necrosis; may also lead to miliary pulmonary TB or TB bronchopneumonia
  • fevers, night sweats, cough with hemoptysis, weight loss
  • biopsy reveals caseating granulomas
  • AFB stain reveals acid-fast bacilli
  • 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)
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19
Q

Basic Principles of COPD

A
  • group of diseases characterized by airway obstruction
  • lung does not empty; air trapping
  • decreased FVC
  • extremely decreased FEV1
  • decreased FEV1/FVC ratio
  • TLC is usually increased due to air trapping
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20
Q

Chronic Bronchitis

A
  • chronic productive cough lasting at least 3 months over a minimum of 2 yrs; highly associated with smoking
  • hypertrophy of bronchial mucinous glands
  • leads to increased thickness of mucus glands relative to bronchial wall thickness
  • productive cough due to excessive mucus production
  • cyanosis (“blue bloaters”) due to mucus plugs trapping carbon dioxide and increased PaCO2 and dec PaO2
  • increased risk of infection and cor pulmonale
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21
Q

Emphysema

A
  • destruction of alveolar sacs
  • loss of elastic recoil and collapse of airways during exhalation results in obstruction and air trapping
  • due to imbalance of proteases and antiproteases (excessive inflammation or lack of A1AT leads to destruction of the alveolar air sacs)
  • alpha-1 antitrypsin (A1AT) neutralizes proteases
  • smoking is most common cause (smoke pollutants lead to inflamm. and protease-mediated damage)
  • smoking results in centriacinar emphysema that is most severe in upper lobes
  • A1AT deficiency is a rare cause
  • disease severity is based on the degree of A1AT deficiency
  • dyspnea and cough with minimal sputum
  • prolonged expiration with pursed lips (“pink puffer”)
  • weight loss
  • inc anterior-posterior diameter of chest (“barrel chest”)
  • hypoxemia and cor pulmonale are late complications
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22
Q

A1AT Deficiency

A
  • lack of antiprotease leaves the air sacs vulnerable to protease-mediated damage
  • results in panacinar emphysema that is most severe in the lower lobes
  • liver cirrhosis may also be present (A1AT def. due to misfolding of the mutated protein; accumulates in the ER of hepatocytes, resulting in liver damage; biopsy reveals pink, PAS-positive globules in hepatocytes)
  • PiM is the normal allele
  • PiZ is the most common clinically relevant mutation (significantly low levels of A1AT)
  • PiMZ heterozygotes are usually azymptomatic with dec circulating levels of A1AT (significant risk for emphysema when smoking exists)
  • PiZZ homozygotes are at significant risk for panacinar emphysema and cirrhosis
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23
Q

Asthma

A
  • reversible airway bronchoconstriction
  • most often due to allergic stimuli (atopic asthma)
  • presents in childhood; often associated with allergic rhinitis, eczema, and a family history of atopy
  • type I hypersensitivity
  • clinical features are episodic and related to allergen exposure
  • dyspnea and wheezing
  • productive cough, classically with spiral-shaped mucus plugs (Curschmann spirals) and Eosinophil-derived crystals (Charcot-Leyden crystals)
  • severe, unrelenting attack can result in status asthmaticus and death
  • may also arise from nonallergic causes (non-atopic asthma) such as exercise, viral infection, aspirin, and occupational exposures
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24
Q

Pathogenesis of Asthma

A
  • type I hypersensitivity
  • allergens induce Th2 phenotype in CD4+ T cells of genetically susceptible individuals
  • Th2 cells secrete IL-4 (mediates class switch to IgE), IL-5 (attracts eosinophils), and IL-10 (stimulates Th2 cells and inhibits Th1)
  • reexposure to allergen leads to IgE-mediated activation of mast cells
  • release of preformed histamine granules and generation of leukotrienes C4, D4, and E4 lead to bronchoconstriction, inflammation, and edema (early-phase reaction)
  • inflammation, especially major basic protein derived from eosinophils, damages cells and perpetuates bronchoconstriction (late-phase reaction)
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25
Q

Bronchiectasis

A
  • permanent dilation of bronchioles and bronchi
  • loss of airway tone results in air trapping
  • due to necrotizing inflammation with damage to airway cells
  • caused by CF, Kartagener syndrome, tumor or foreign body, necrotizing infection, and allergic bronchopulmonary aspergillosis
  • cough, dyspnea, foul-smelling sputum
  • complications include hypoxemia with cor pulmonale and secondary (AA) amyloidosis
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26
Q

Kartagener Syndrome

A
  • 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)
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27
Q

Allergic Bronchopulmonary Aspergillosis

A
  • hypersensitivity reaction to Aspergillus leads to chronic inflammatory damage
  • usually seen in individuals with asthma or CF
28
Q

Basic Principles of Restrictive Diseases

A
  • restricted filling of the lungs
  • decreased TLC
  • decreased FEV1
  • extremely decreased FVC
  • FEV1:FVC ratio is increased
  • most commonly due to interstitial diseases of the lung
  • may also arise with chest wall abnormalities (e.g. massive obesity)
29
Q

Idiopathic Pulmonary Fibrosis

A
  • fibrosis of lung interstitium
  • likely related to cyclical lung injury
  • TGF-beta from injured pneumocytes induces fibrosis
  • secondary causes of interstitial fibrosis such as drugs (e.g. bleomycin and amiodarone) and radiation therapy
  • progressive dyspnea and cough
  • fibrosis on lung CT; initially seen in subpleural patches, but eventually results in diffuse fibrosis with end-stage “honeycomb” lung
  • treatment: lung transplantation
30
Q

Pneumoconioses

A
  • interstitial fibrosis due to occupational exposure
  • requires chronic exposure to small particles that are fibrogenic
  • alveolar macrophages engulf foreign particles and induce fibrosis
31
Q

Coal Workers’ Pneumoconiosis

A
  • type of pneumoconioses
  • carbon dust exposure
  • massive exposure leads to diffuse fibrosis (“black lung”)
  • associated with rheumatoid arthritis (Caplan syndrome)
  • mild exposure to carbon (e.g. pollution) results in anthracosis (collections of carbon-laden macrophages); not clinically significant
32
Q

Silicosis

A
  • type of pneumoconioses
  • silica exposure
  • seen in sandblasters and silica miners
  • fibrotic nodules in upper lobes of the lung
  • increased risk for TB
  • silica impairs phagolysosome formation by macrophages
33
Q

Berylliosis

A
  • type of pneumoconioses
  • beryllium exposure
  • seen in beryllium miners and workers in the aerospace industry
  • non-caseating granulomas in the lung, hilar lymph nodes, and systemic organs
  • increased risk for lung cancer
  • very similar to sarcoidosis
34
Q

Asbestosis

A
  • type of pneumoconioses
  • asbestos fiber exposure
  • seen in construction workers, plumbers, and shipyard workers
  • fibrosis of lung and pleura (plaques) with increased risk for lung carcinoma and mesothelioma
  • lung carcinoma is more common than mesothelioma in exposed individuals
  • lesions may contain long, golden-brown fibers with associated iron (asbestos bodies), which confirm exposure to asbestos
35
Q

Sarcoidosis

A
  • systemic disease characterized by non-caseating granulomas in multiple organs
  • likely due to CD4+ helper T-cell response to an unknown antigen
  • granulomas most commonly involve the hilar lymph nodes and lung leading to restrictive lung disease
  • characteristic stellate inclusions (“asteroid bodies”) are often seen within giant cells of the granulomas
  • other commonly involved tissues include the uvea (uveitis), skin (cutaneous nodules or erythema nodosum), and salivary and lacrimal glands (mimics Sjogren syndrome); almost any tissue can be involved
36
Q

Clinical Features of Sarcoidosis

A
  • dyspnea or cough (most common presenting symptom)
  • elevated serum ACE
  • hypercalcemia (1-alpha hydroxylase activity of epithelioid histiocytes converts vit. D to its active form)
  • treatment is steroids; often resolves spontaneously without treatment
37
Q

Hypersensitivity Pneumonitis

A
  • granulomatous rxn to inhaled organic antigens (e.g. pigeon breeder’s lung)
  • presents with fever, cough, and dyspnea hours after exposure
  • resolves with removal of the exposure
  • chronic exposure leads to interstitial fibrosis
38
Q

Pulmonary Hypertension (Basic Principles)

A
  • high pressure in the pulmonary circuit (mean arterial pressure > 25 mmHg; normal is 10 mmHg)
  • 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
  • leads to RVH with eventual cor pulmonale
  • presents with exertional dyspnea or right-sided heart failure
  • subclassified as primary or secondary based on etiology
39
Q

Primary Pulmonary Hypertension

A
  • classically seen in young adult females
  • etiology is unknown
  • some familial forms are related to inactivating mutations of BMPR2, leading to proliferation of vascular smooth muscle
40
Q

Secondary Pulmonary Hypertension

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
41
Q

Acute Respiratory Distress Syndrome

A
  • diffuse damage to the alveolar-capillary interface (diffuse alveolar damage)
  • leakage of protein-rich fluid leads to edema that combines with necrotic epithelial cells to form hyaline membranes in alveoli
  • secondary to a variety of disease processes including sepsis, infection, shock, trauma, aspiration, pancreatitis, DIC, hypersensitivity rxns, and drugs
  • activation of neutrophils induces protease- and free radical-mediated damage of type I and II pneumocytes
  • recovery may be complicated by interstitial fibrosis; damage and loss of type II pneumocytes leads to scarring and fibrosis
42
Q

Clinical Features of ARDS

A
  • hypoxemia and cyanosis with respiratory distress - due to thickened diffusion barrier and collapse of air sacs (increased surface tension)
  • “white out” on CXR
43
Q

Treatment of ARDS

A
  • address underlying cause

- ventilation with positive end-expiratory pressure (PEEP)

44
Q

Neonatal Respiratory Distress Syndrome

A
  • due to inadequate surfactant levels
  • surfactant is made by type II pneumocytes
  • phosphatidylchoine (lecthin) is the major component
  • lack of surfactant leads to collapse of air sacs and formation of hyaline membranes
45
Q

Prematurity and Neonatal Respiratory Distress Syndrome

A
  • surfactant production begins at 28 wks; adequate levels are not reached until 34 wks
  • amniotic fluid lecithin to sphingomyelin ratio is used to screen for lung maturity
  • phosphatidylcholine (lecithin) levels increase as surfactant is produced; sphingomyelin remains constant
  • a ratio >2 indicates adequate surfactant production
46
Q

Caesarian Section Delivery and Neonatal Respiratory Distress Syndrome

A

-due to lack of stress-induced steroids; steroids increase synthesis of surfactant

47
Q

Maternal Diabetes and Neonatal Respiratory Distress Syndrome

A

-insulin decreases surfactant production

48
Q

Clinical Features of Neonatal Respiratory Distress Syndrome

A
  • increasing respiratory effort after birth, tachypnea with use of accessory muscles, and grunting
  • hypoxemia with cyanosis
  • diffuse granularity of the lung (“ground-glass” appearance) on CXR
49
Q

Complications of Neonatal Respiratory Distress Syndrome

A
  • hypoxemia increases the risk for persistence of patent ductus arteriosus and necrotizing enterocolitis
  • supplemental oxygen increases the risk for free radial injury
  • retinal injury leads to blindness
  • lung damage leads to bronchopulmonary dysplasia
50
Q

Key Risk Factors of Lung Cancer

A
  • cigarette smoke, radon, and asbestos
  • cigarette smoke contains over 60 carcinogens; 85% of lung cancer occurs in smokers
  • polycyclic aromatic hydrocarbons and arsenic are particularly mutagenic
  • cancer risk is directly related to the duration and amount of smoking (“pack years”)
  • radon is formed by radioactive decay of uranium, which is present in soil
  • radon accumulates in closed spaces such as basements
  • responsible for most of the public exposure to ionizing radiation; 2nd most frequent cause of lung carcinoma in US
  • increased risk of lung cancer is also seen in uranium miners
51
Q

Presenting Symptoms of Lung Cancer

A
  • nonspecific

- cough, weight loss, hemoptysis, and postobstructive pneumonia

52
Q

Imaging in Lung Cancer

A
  • reveals solitary nodule (“coin-lesion”); biopsy is necessary for a diagnosis of cancer
  • benign lesions, which often occur in younger patients, can also produce a “coin-lesion”
  • granuloma - often due to TB or fungus (especially Histoplasma in the Midwest)
  • bronchial hamartoma - benign tumor composed of lung tissue and cartilage; often calcified on imaging
53
Q

Small Cell Carcinoma

A
  • poorly differentiated small cells; arises from neuroendocrine (Kulchitsky) cells
  • associated with male smokers
  • location is central
  • rapid growth and early metastasis; may produce ADH or ACTH or cause Eaton-Lambert syndrome (paraneoplastic syndromes)
54
Q

Squamous Cell Carcinoma

A
  • non-small cell carcinoma
  • keratin pearls or intercellular bridges
  • most common tumor in male smokers
  • central in location
  • may produce PTHrP
55
Q

Adenocarcinoma

A
  • non-small cell carcinoma
  • characterized by glands or mucin
  • most common tumor in nonsmokers and female smokers
  • peripheral in location
56
Q

Large Cell Carcinoma

A
  • poorly differentiated large cells (no keratin pearls, intercellular bridges, glands, or mucin)
  • associated with smoking
  • central or peripheral in location
  • poor prognosis
57
Q

Bronchioloalveolar Carcinoma

A
  • columnar cells that grow along preexisting bronchioles and alveoli; arises from Clara cells
  • not related to smoking
  • peripheral in location
  • may present with pneumonia-like consolidation on imaging; excellent prognosis
58
Q

Carcinoid Tumor

A
  • non-small cell carcinoma
  • well differentiated neuroendocrine cells; chromogranin positive
  • not related to smoking
  • central or peripheral; when central, classically forms a polyp-like mass in the bronchus
  • low-grade malignancy; rarely, can cause carcinoid syndrome
59
Q

Metastasis to Lung

A
  • most common sources are breast and colon carcinoma
  • multiple “cannon-ball” nodules on imaging
  • more common than primary tumors
60
Q

TNM Staging (T) - Tumor Size and Local Extension

A
  • pleural involvement is classically seen with adenocarcinoma
  • obstruction of SVC leads to distended head and neck veins with edema and blue disoloration of arms and face (SVC syndrome)
  • involvement of recurrent laryngeal (hoarseness) or phrenic (diaphragmatic paralysis) nerve
  • compression of sympathetic chain leads to Horner syndrome and anhidrosis; usually due to an apical (Pancoast) tumor)
61
Q

TNM Staging (N)

A

-spread to regional lymph nodes (hilar and mediastinal)

62
Q

TNM Staging (M)

A

-unique site of distant metastasis is the adrenal gland

63
Q

Pneumothorax

A

-accumulation of air in the pleural space

64
Q

Spontaneous Pneumothorax

A
  • due to rupture of an emphysematous bleb; seen in young adults
  • results in collapse of a portion of the lung; trachea shifts to the side of collapse
65
Q

Tension Pneumothorax

A
  • arises when penetrating chest wall injury
  • air enter the pleural space, but cannot exit
  • trachea is pushe dopposite to the side of injury
  • medical emergency; treated with insertion of a chest tube
66
Q

Mesothelioma

A
  • malignant neoplasm of mesothelial cells
  • highly associated with occupational exposure to asbestos
  • presents with recurrent pleural effusions, dyspnea, and CP
  • tumor encases the lung

Pulmonary Pathology (1 decks)

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