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Pathology > Other Lung Path > Flashcards

Other Lung Path Flashcards

1
Q

Sarcoidosis

A

Multisystem disease of unknown etiology characterized by noncaseating granulomas in many tissues and organs
Bilateral hilar lymphadenopathy and/or lung involvement is the major presenting manifestation in most cases
Epidemiology
-Adults younger than 40
-Danish, Swedish, African Americans (10x)
-Higher prevalence even in non-smokers

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2
Q

Sarcoidosis path

A

Disordered immune regulation in genetically predisposed individuals exposed to certain environmental agents
Process is driven by TH1 cells

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3
Q

Sarcoidosis morphology

A

Noncaseating epithelioid granulomas
Many organs involved
-Lungs: involved at some point in 90% of patients; in 5-15% of patients granulomas are eventually replaced by diffuse interstitial fibrosis
-Hilar and paratracheal lymph nodes enlarged in 75-90%
-Skin, eye, lacrimal glands, salivary glands
-Spleen, liver, bone marrow

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4
Q

Sarcoidosis clinical

A

Many individuals are entirely asymptomatic
In symptomatic cases,
-2/3 have respiratory symptoms (shortness of breath, dry cough, substernal discomfort) or constitutional symptoms (fever, fatigue, weight loss, anorexia, night sweats)
Unpredictable course
-Progressive chronicity or periods of activity and remission
-65-70% recover with minimal to no residual effects
-20% develop permanent lung dysfunction or visual impairment
-15-20% die from progressive pulmonary fibrosis and cor pulmonale

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5
Q

Hypersensitivity Pneumonitis

A

Allergic alveolitis
Immunologically mediated inflammatory lung disease that primarily affects the alveoli
-Immune complex and delayed-type hypersensitivity reactions
-2/3 have interstitial noncaseating granulomas
Heightened sensitivity to inhaled antigens
-Most often an occupational disease

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6
Q

Hypersensitivity Pneumonitis clinical

A

Acute reaction
-Fever, cough, dyspnea, constitutional complaints 4-8 hours after exposure
-Complete remission, if antigen exposure is terminated
Chronic disease
-Insidious onset of cough, dyspnea, malaise, weight loss
-If antigen is not removed, chronic interstitial disease develops without the acute exasperations on antigen re-exposure

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7
Q

Pulmonary Eosinophilia

A

Entities characterized by an infiltration and activation of eosinophils
-Generally immunologic in origin, but poorly understood
Acute eosinophilic pneumonia with respiratory failure
-Rapid onset of fever, dyspnea, hypoxia, and diffuse pulmonary infiltrates
-Bronchioalveolar lavage fluid contains >25% eosinophils
-Prompt response to steroids

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8
Q

Pulmonary Eosinophilia

A

Simple pulmonary eosinophilia (Löffler syndrome)

  • Transient pulmonary lesions and blood eosinophilia
  • Alveolar septal infiltrate of eosinophils
  • Benign clinical course

Tropical eosinophilia
-Microfilariae infestation

Secondary eosinophilia
-Asthma, drug allergies, vasculitis

Idiopathic chronic eosinophilic pneumonia

  • Aggregates of lymphocytes and eosinophils in alveolar septa and airspaces
  • High fever, night sweats, dyspnea
  • Disease of exclusion
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9
Q

Smoking Related Interstitial Diseases

A

Desquamative interstitial pneumonia (DIP)

  • Accumulation of large numbers of macrophages in the airspaces
  • Good prognosis
  • Excellent response to steroids and smoking cessation

Respiratory bronchiolitis
-Similar histology to DIP but centered on respiratory bronchioles

Clinical

  • Gradual onset of dyspnea and dry cough
  • Symptoms recede with smoking cessation
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10
Q

Pulmonary Thromboembolism

A 
95% arise from thrombi within the deep veins of the legs
Risk factors
Prolonged bedrest
Surgery
Severe trauma
Congestive heart failure
Around childbirth
High estrogen birth control pills
Disseminated cancer
Primary hypercoagulability disorders
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11
Q

Pulmonary Thromboembolism

A

Pathophysiologic consequences depend upon the size of the embolus and the cardiopulmonary status of the patient
-Increase in pulmonary artery pressure from occlusion and possibly vasospasm
-Ischemia of down-stream lung tissue
-Hypoxia
Infarct of lung occurs in only about 10% of cases
-Depends on size of vessel occluded, status of bronchial circulation and cardiac function, ventilation of effected lung region
Thromboemboli may cause virtually instantaneous death

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12
Q

Pulmonary Thromboembolism clinical course

A

Most emboli are clinically silent (60-80%)
-Embolus removed by fibrinolytic activity
-Lung viability is maintained
Sudden death, acute right-sided heart failure, or cardiovascular collapse (5%)
->60% of total pulmonary vasculature is obstructed
Obstruction of small to medium pulmonary branches (10-15%)
-Causes pulmonary infarction
Recurrent multiple emboli (<3%)
-Pulmonary hypertension, chronic right-sided heart failure, vascular sclerosis, worsening dyspnea
30% chance of having a second embolus after having a first

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13
Q

Pulmonary Thromboembolism Non-thrombotic emboli

A

Air, fat, amniotic fluid, foreign body, bone marrow
Talc in intravenous drug users
-Interstitial and vascular complications

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14
Q

Pulmonary Hypertension

A

Pulmonary hypertension occurs when mean pulmonary pressures reach ¼ systemic pressure
Most often a secondary disease
-Chronic obstructive or interstitial lung disease
*Reduction in alveolar capillaries results in increased resistance
-Recurrent pulmonary emboli
*Reduces functional cross-section of pulmonary vasculature
-Heart disease
*Mitral stenosis, congenital left to right shunt
Primary or idiopathic pulmonary hypertension
-Most cases are sporadic (6% familial form)

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15
Q

Pulmonary Hypertension path

A

Pulmonary endothelial cell and/or smooth muscle dysfunction
In secondary pulmonary hypertension, endothelial cell dysfunction
-Reduced vasodilatory agents
-Increase vasoconstrictive mediators
-Induce replication of vascular smooth muscle and extracellular matrix elaboration

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16
Q

Pulmonary Hypertension clinical

A

Secondary PH may develop at any age
-Accentuation of respiratory insufficiency and right-sided heart strain
Primary PH is almost always in young persons, more commonly women
-Fatigue, syncope (particularly on exercise), dyspnea on exertion, and sometimes chest pain
-Develop severe respiratory insufficiency and cyanosis
-Death usually results from right-sided heart failure
-Survival is 2-5 years from diagnosis

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17
Q

Diffuse Alveolar Hemorrhage Syndromes

A

Immune related diseases that present with the triad of hemoptysis, anemia, and diffuse pulmonary infiltrates
Goodpasture syndrome
Idiopathic pulmonary hemosiderosis

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18
Q

Goodpasture syndrome

A
  • Proliferative, usually rapidly progressive, glomerulonephritis and hemorrhagic interstitial pneumonitis
  • Caused by antibodies targeted against collagen IV
  • 90% have detectable serum antibodies
  • Diffuse alveolar hemorrhage
  • Linear pattern of immunoglobulin deposition along alveolar septa
  • Treat with plasmapheresis and immunosuppressives
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19
Q

Idiopathic pulmonary hemosiderosis

A

Diffuse alveolar hemorrhage similar to Goodpasture syndrome but no renal involvement or anti-basement membrane antibodies
Mild to moderate course with periods of activity followed by prolonged remissions
Most cases are seen in children

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20
Q

Pulmonary Angiitis and Granulomatosis

A

Wegner granulomatosis
>80% of WG patients develop upper respiratory or lung involvement
Lung lesions
-Necrotizing vasculitis and parenchymal necrotizing granulomatous inflammation
-Pulmonary vessels may show necrotizing granulomas but most often acute and chronic inflammation with fibrinoid necrosis

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21
Q

Pulmonary Angiitis and Granulomatosis

A

Can have both upper respiratory and pulmonary symptoms
-Chronic sinusitis, epistaxis, nasal perforation
-Cough, hemoptysis, chest pain
Radiographically, multiple nodular densities (confluence of granulomas, some may cavitate)
While usually a multisystem disease, it may be restricted to the lung (“limited” WG)

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22
Q

Lung Tumors

A

Common site for metastatic disease
Primary lung cancer is also common
Primary lung tumors
-Bronchial epithelium; carcinomas (95%)
-Others (5%)
*Bronchial carcinoids, mesenchymal malignancies, lymphomas, benign lesions
*Hamartoma is the most common benign lesion
Spherical, small (3-4 cm), often appear as “coin” lesions

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23
Q

Carcinomas

A

1 cause of cancer related deaths in industrialized countries

-1/3 of cancer deaths in men in US
-Leading cause of cancer death in women since 1987
Causal link to cigarette smoking
Peak incidence: 50-70 years of age
At diagnosis,
-50% have distant metastatic disease
-25% have disease in regional lymph nodes
5 year survival rate
-All stages combined: 15%
-Localized to lung: 45%

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24
Q

Carcinomas Four major histological types

A

Squamous cell carcinoma
Adenocarcinoma
Small-cell carcinoma
Large-cell carcinoma
Combination patterns exist
Adenocarcinoma is now the most common type
Adenocarcinomas are by far the most common type in women, lifetime non-smokers, and younger than 45 years of age

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25
Q

For therapeutic purposes, lung carcinomas are divided into two broad groups

A

Small-cell lung cancer (SCLC)
Non-small-cell lung cancer (NSCLC)
Virtually all SCLC has metastasized at the time of diagnosis
Not curable by surgery
Treated by chemotherapy with or without radiation
NSCLC respond poorly to chemotherapy and are better treated by surgery

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26
Q

Genetic differences between SCLC and NSCLC

A

G1-S checkpoint is abrogated by different mechanisms
SCLC has high frequency of RB gene mutations
NSCLC commonly has inactivated p16/CDKN2A gene
Activating KRAS and EGFR mutations occur in adenocarcinomas

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27
Q

Carcinomas Etiology and pathogenesis

A

Arise by step-wise accumulation of genetic abnormalities that transform benign bronchial epithelium into neoplastic tissue
Predictable sequence that parallels histologic progression
-Inactivation of tumor suppressor genes on 3p is a very early event
-p53 mutations and KRAS activation occurs late
Subset of adenocarcinoma arising in non-smoking, Far-Eastern women has EGFR activation

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28
Q

Carcinomas

A

There is an impressive body of evidence that cigarette smoking causes lung cancer
-Squamous cell and small-cell carcinomas have the strongest association with tobacco exposure
Other environmental influences are associated with an increased incidence of lung cancer
-Miners of radioactive ores; asbestos workers; exposure to dusts containing arsenic, chromium, uranium, nickel, vinyl chloride, mustard gas

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29
Q

Carcinomas morphology

A

Usually begin as small mucosal lesions
May form intraluminal masses, invade the bronchial mucosa, or push into the lung parenchyma
Large masses may undergo central necrosis, hemorrhage, or cavitation
May extend to pleura and invade the pleural cavity, chest wall, or adjacent intrathoracic structures
May spread by lymphatic or hematogenous routes

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30
Q

Squamous Cell Carcinoma

A

M>F
Closely correlated with smoking history
Tend to arise centrally in major bronchi
Spread to local hilar lymph nodes eventually
Spreads outside the thorax later than other types
Large tumors may have central necrosis and may cavitate
Preneoplastic lesions are well characterized
-Squamous metaplasia
-Dysplasia
-Carcinoma in situ

31
Q

Adenocarcinoma

A

More peripherally located
Most common type in non-smokers and women
Slower growing and form smaller masses
Metastasize at an early stage
Precursor lesion is thought to be atypical adenomatous hyperplasia
Cell of origin is thought to be bronchioalveolar stem cells
-Multipotential cells at the bronchioalveolar junction

32
Q

Bronchioloalveolar Carcinoma

A

Subtype of adenocarcinoma
Key feature is growth along preexisting structures
preservation of alveolar architecture

33
Q

Small-cell Carcinomas

A

Centrally located masses with extension into the parenchyma
Early involvement of hilar and mediastinal lymph nodes
Necrosis is always present and may be extensive
Tumor cells are fragile
Derived from neuroendocrine cells
Associated with paraneoplastic syndromes

34
Q

Carcinomas clinical

A

Silent, insidious lesions
-Often unresectable before they produce symptoms
Chronic cough and expectoration may call attention to an early lesion
Hoarseness, superior vena cava syndrome, effusions, persistent segmental atelectasis, pneumonitis all tend to appear with advanced lesions
Often symptoms related to metastatic disease are the presenting symptoms
-Brain, liver, bone

35
Q

carciomas clinical contin

A

Overall, NSCLC has a better prognosis than SCLC
-NSCLC can be detected before metastasis or local spread
*Surgical cure possible
-SCLC has always spread at time of diagnosis
*While very sensitive to chemotherapy, they always recur
*Mean survival is 1 year
3-10% of people with lung cancer develop paraneoplastic syndromes
-Hypercalcemia (SCC), Cushing syndrome, SIADH, neuromuscular syndromes, clubbing of fingers, hematologic manifestations (adenoca)

36
Q

Bronchial Carcinoids

A

Arise from neuroendocrine cells of the bronchial mucosa
Appear at an early age (mean: 40 years)
About 5% of all pulmonary neoplasms
Often resectable and curable

37
Q

Bronchial Carcinoids growth pattern

A

Obstructing, polypoid, spherical intraluminal mass
Mucosal plaque penetrating the bronchial wall and fanning out into the peribronchial tissue
5-15% have metastasized to hilar lymph nodes
Distant metastasis is rare

38
Q

Bronchial Carcinoids Atypical carcinoids

A

More aggressive
Higher rates of lymph node and distant metastasis
p53 mutations in 20-40% of cases
Typical carcinoid, atypical carcinoid, and small-cell carcinoma represent increasing histologic aggressiveness and malignant potential among pulmonary neuroendocrine neoplasms

39
Q

Bronchial Carcinoids Clinical

A 
Most present with findings related to intraluminal growth
-Cough, hemoptysis, infections
Carcinoid syndrome is rare
-Intermittent attacks of diarrhea, flushing, and cyanosis
10 year survival rates
-Typical carcinoid: >85%
-Atypical carcinoid:  35%
-Small-cell carcinoma:  5%
40
Q

Pulmonary Infections

A

Pneumonia can be broadly defined as any infection in the lung
Pneumonia is responsible for 1/6 of all deaths in the US
-Epithelial surfaces are exposed to liters of contaminated air
-Nasopharyngeal flora are regularly aspirated during sleep
-Other lung diseases render the lung vulnerable

41
Q

Lung Defenses

A

Defects in innate or humoral immunity typically leads to infections with pyogenic bacteria
Defects in cell-mediated immunity typically leads to infection with intracellular microbes, viruses, low virulence organisms
Exogenous interferences
-Cigarette smoking (mucociliary clearance, macrophage activity), alcohol (impaired reflexes, neutrophil mobilization and chemotaxis)

42
Q

Pneumonia

A

Clinically, may present as an acute, fulminant disease or as chronic disease with a protracted course
Histologically
-Fibrinopurulent exudate in acute bacterial pneumonias
-Mononuclear interstitial infiltrates in viral and other atypical pneumonias
-Granulomas and cavitation in some chronic pneumonias

43
Q

Acute bacterial pneumonias

A

Acute bacterial pneumonias present with one of two anatomic and radiographic patterns

  • Bronchopneumonia
  • Patchy distribution of inflammation that generally involves more than one lobe
  • Lobar
  • Part or all of a lobe is filled homogenously with an exudate
  • 90% are due to S. pneumoniae
  • Distinction can be blurry
  • Many organisms can present with either pattern
  • Confluent bronchopneumonia can be hard to distinguish from lobar pneumonia
44
Q

Community-Acquired Acute Pneumonias

A

Most are bacterial
Frequently follows a viral upper respiratory tract infection
Onset is usually abrupt with high fever, shaking chills, pleuritic chest pain, productive mucopurulent cough, sometimes hemoptysis
S. pneumoniae (pneumococcus) is the most common cause

45
Q

Pneumoncoccal Pneumonia

A

Pneumococcal infections are more frequent in those with:
-Underlying chronic disease like CHF, COPD, or diabetes
-Congenital or acquired immunoglobulin defects
-Decreased or absent splenic function
Lobar or bronchopneumonia
Lower or middle lobes are most frequently involved

46
Q

Before antibiotics, lobar pneumococcal pneumonia had 4 classic pathologic stages

A

Congestion
Red hepatization
Gray hepatization
Resolution

47
Q

Congestion

A

Affected lobe is heavy, red, and boggy

Vascular congestion with proteinaceous fluid, scattered neutrophils, and many bacteria in the alveoli

48
Q

Red hepatization

A

A few days later
Lung as a liver-like consistency
Alveoli packed with neutrophils, red cells, and fibrin

49
Q

Gray hepatization

A

Lung is gray, dry, and firm (red cells have lysed)

Fibrinosuppurative exudate persists in the alveoli

50
Q

Resolution

A

Exudates are digested by enzymes producing a granular semi-fluid debris that is resorbed, ingested by macrophages, or coughed up
Alternatively, exudates are organized by fibroblasts growing into them

51
Q

Pneumoncoccal Pneumonia complications

A

The pleural reaction may resolve or undergo organization leaving fibrous thickening or permanent adhesions
Early antibiotic treatment alters this classic progression
Complications
-Abscess
-Empyema
-Organized areas of solid fibrosis
-Bacteremic dissemination (meningitis, arthritis, infective endocarditis)

52
Q

Community-Acquired Acute Pneumonias

A 
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Klebsiella pneumoniae
Pseudomonas aeruginosa
Legionella pneumophila
53
Q

Haemophilus influenzae

A

Most common bacterial cause of acute exacerbation of COPD in adults

54
Q

Moraxella catarrhalis

A

Second most common bacterial cause of acute exacerbation of COPD in adults

55
Q

Staphylococcus aureus

A

Post-viral secondary pneumonia
Abscess and empyema
IV drug use

56
Q

Klebsiella pneumoniae

A

Most frequent cause of gram-negative bacterial pneumonia
Debilitated and malnourished persons (chronic alcoholics)
Thick, gelatinous sputum

57
Q

Pseudomonas aeruginosa

A

Cystic fibrosis, neutropenic, burns, ventilators

58
Q

Legionella pneumophila

A

Cardiac, renal, immunologic, hematologic disease

Organ transplant recipients

59
Q

Community-Acquired Atypical Pneumonia

A 
Acute febrile respiratory disease characterized by patchy inflammation in the lungs, largely confined to the alveolar septa and interstitium
Moderate amounts of sputum, absence of consolidation, moderately elevated WBC, lack of alveolar exudates
Causative organisms
-Mycoplasma pneumoniae
*Most common
-Viruses
*Influenza, RSV, adenovirus
-Chlamydia pneumoniae
60
Q

Community-Acquired Atypical Pneumonia clinical

A

Acute, non-specific febrile illness
-Fever, headache, malaise, and later, cough without sputum
May have respiratory distress out of proportion to the physical and radiographic findings

61
Q

Nosocomial Pneumonia

A

Infections acquired in the course of a hospital stay
Most common in persons with severe underlying disease, immunosuppression, prolonged antibiotic therapy, and on ventilators
Organisms
-Gram-negative rods
*Enterobacteriaceae, Pseudomonas spp.
-S. aureus usually MRSA

62
Q

Aspiration Pneumonia

A

Aspiration of gastric contents, typically while unconscious or vomiting
Partly chemical, partly bacterial
Aerobes and anaerobes
Often necrotizing with a fulminant course
Frequent cause of death in people predisposed to aspiration
Abscess formation is a common complication

63
Q

Lung Abscess

A

An lung abscess is a localized area of suppurative necrosis within the pulmonary parenchyma, resulting in the formation of one or more large cavities
Necrotizing pneumonia is a similar process resulting in multiple small cavities
How
-Aspiration of infective material
-Aspiration of gastric contents
-Complication of necrotizing pneumonia
*S. aureus, S. pyogenes, K. pneumoniae, Pseudomonas ssp.
*Mycotic infection and bronchiectasis
-Bronchial obstruction
*Especially by tumor
-Septic embolism
*Septic thrombophlebitis, infective endocarditis
-Hematogenous spread of bacteria
*Multiple abscesses

64
Q

Lung Abscess info

A

Anaerobic bacteria are present in almost all lung abscesses
-1/3 to 2/3 of the time only anaerobes are present
-Oral cavity organisms
More common on the right side
May rupture into airway or pleural cavity

65
Q

Lung Abscess clinical

A

Prominent cough that usually yields copious amounts of foul-smelling, purulent, or sanguineous sputum; occasionally hemoptysis
Spiking fever and malaise are common
Clubbing of fingers, weight loss, and anemia may occur
Infective abscesses occur in 10-15% of persons with bronchogenic carcinoma
Secondary amyloidosis may develop in chronic cases
Antibiotics and surgical drainage, if needed
Mortality rate: 10%

66
Q

Chronic Pneumonia

A

In the immunocompetent patient, chronic pneumonia is often a localized lesion that may or may not have regional lymph node involvement
Typically granulomatous inflammation due to bacteria or fungi
In the immunocompromised patient, there is often systemic dissemination and widespread disease
Tuberculosis is the most important chronic pneumonia

67
Q

Chronic Pneumonia organisms

A 
Mycobacterium tuberculosis
Nontuberculous mycobacteria
Histoplasma capsulatum
Coccidioides immitis
Blastomyces dermatitidis
68
Q

Pneumonia in the Immunocompromised Host

A 
Cytomegalovirus pneumonitis
Pneumocystis pneumonia
Candida albicans
Cryptococcus neoformans
Invasive aspergillosis and zygomycosis (Rhizopus and Mucor)
69
Q

Cytomegalovirus pneumonitis

A 
Most common groups
-Recipients of organ transplants 
-Recipients of allogeneic bone marrow transplant
-AIDS
Viral pneumonia with foci of necrosis
-Can progress to full-blown ARDS
70
Q

Pneumocystis pneumonia

A

Pneumocystis jiroveci
Common infection in AIDS
-Risk increases in proportion to decreasing CD4 count

71
Q

Candida albicans

A

Invasive candidiasis of the lung is most common in profoundly neutropenic acute leukemia patients
Bilateral nodular infiltrates; mimics pneumocystis

72
Q

Cryptococcus neoformans

A

AIDS and hematolymphoid malignancies
Localizes in the lungs then disseminates
Minimal inflammation to granulomas depending on degree of immunodeficiency

73
Q

Invasive aspergillosis and zygomycosis (Rhizopus and Mucor)

A

Predilection for vascular invasion, causing vascular necrosis and infarction
Hematolymphoid malignancies, allogeneic bone marrow transplant

74
Q

Pulmonary Disease and HIV

A

Not every infection is “opportunistic”
-Think of “usual” pathogens too
Not all pulmonary infiltrates are infections
-Kaposi sarcoma, non-Hodgkin lymphoma, and primary lung cancer are all more common with HIV
CD4 counts can help narrow the differential diagnosis
->200 cells/mm3: bacterial and tubercular more common
-<50 cells/mm3 : CMV and MAI complex
Multiple causes and atypical presentations

Pathology (16 decks)

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