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Y2 - Path - Exam 4 > 9: Pulm 2 > Flashcards

9: Pulm 2 Flashcards

1
Q

define: diffuse interstitial lung disease

A
  • Heterogeneous group of disorders
  • Interstitial inflammation (alveolar septae)
  • _**Fibrosis_ – stiff or restricted lung morphology
  • Reduced compliance with more effort needed to expand the “stiff” lungs
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2
Q

diffuse interstitial lung disease:

pathogenesis

A
  1. Inhaled or blood-born toxins –> Epithelial/endothelial injury
  2. Recruitment/activation of inflammatory cells including macrophages, neutrophils and
  3. Fibroblasts (alveolar walls/spaces)
  4. Release of injurious (oxidants/ cytokines) and fibrogenic (FGF,IL-1, TGF-β1) mediators
  5. Interstitial fibrosis and chronic inflammation
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3
Q

What are the FIBROSING DISEASES w/in the Diffuse Interstitial Lung Disease

A
  • Idiopathic pulmonary fibrosis, older males.
  • Collagen vascular diseases (SLE, RA, systemic sclerosis)
  • Pneumoconioses: non-neoplastic lung reactions to inhaled mineral dusts (coal dust, silica, asbestos), organic particulates, chemical fumes/vapors.
  • Therapeutic drugs, therapeutic radiation
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4
Q

What are the GRANULOMATOUS DISEASES w/in the Diffuse Interstitial Lung Disease

A
  • sarcoidosis
  • hypersensitivity pneumonitis
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5
Q

4 categories of Diffuse Interstitial Lung Disease

A
  • FIBROSING disease
  • GRANULOMATOUS disease
  • PULMONARY EOSINOPHILIA
  • PULMONARY ALVEOLAR PROTEINOSIS (more rare)
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6
Q

which histologic pattern is associated with Idiopathic pulmonary fibrosis?

A

Usual interstitial pneumonitis (UIP): is a chronic fibrosing interstitial lung disease

  • Pathologic correlate of clinical syndrome of idiopathic pulmonary fibrosis.
  • UIP can be pathologic diagnosis, whereas IPF is clinical term (idiopathic pulmonary fibrosis)
  • End result is FIBROSIS OF THE LUNG (irreversible)
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7
Q

define: idiopathic pulmonary fibrosis (IPF)

A

Progressive interstitial fibrosis with hypoxemia

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8
Q

IDIOPATHIC PULMONARY FIBROSIS:

etiology and epidemiology

A
  • Etiology: UNKNOWN
    • theory is that it’s caused by repeated cycles of epithelial injury and activation by unknown antigen –>
    • chronic inflammation and fibroblastic/myofibroblastic proliferation
  • Epi:
    • OLDER adults of either gender (mostly >50 years)
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9
Q

USUAL INTERSTITIAL PNEUMONIA (UIP)

histopathology

A
  • histopath:
    • interstitial fibrosis in PATCHWORK PATTERN
    • FIBROBLASTIC FOCI
    • parenchymal scarring
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10
Q

USUAL INTERSTITIAL PNEUMONIA (UIP):

end stage

A

end stage: honeycomb lung

(characteristic appearance of variably sized cysts in a background of densely scarred lung tissue)

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11
Q

which histo pattern is associated w/ the following images?

A

Usual intersitial pneumonia

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12
Q

Since Idiopathic Pulmonary Fibrosis is a diagnosis of exclusion (50% of interstitial fibrosis), what are the other disease in which Usual Interstitial Pneumonia (UIP) pattern is seen?

A

Similar pattern can be seen in later/end stage of diseases :

  • Pneumoconioses
  • Hypersensitivity pneumonitis
  • Collagen vascular diseases
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13
Q

Non-specific interstitial pneumonia (NSIP):

how are subtypes classified?

A

on basis of histology – divided into:

  • cellular pattern
  • fibrosing pattern
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14
Q

define: Non-specific interstitial pneumonia (NSIP)

A

Uniform and diffuse alveolar septal expansion by lymphocytes or collagen or both

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15
Q

which condition was previously known as BOOP?

(bronchiolitis obliterans-organizing pneumonia)

A

organizing pneumona (OP): common pathologic finding in lung

  • characterized by the presence of polyp-like collections of fibroblasts within airspaces,
  • referred to as fibroblastic plugs or Masson bodies
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16
Q

what are the major causes of ORGANIZING PNEUMONIA

A
  • Infections (localized finding at the edge of another histologically obvious process such as fungal granuloma)
  • Minor part of the pathologic findings of another process
  • Connective tissue disease
  • Drug-related
  • Bronchial obstruction
  • Idiopathic (Cryptogenic organizing pneumonia)
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17
Q

what are the causes of PNEUMOCONIOSES?

A
  • Mineral dusts (e.g: coal, silica, asbestos, Beryllium)
  • Organic dusts (e.g: mold [aspergillus], bird droppings, cotton)
  • Fumes and Vapors (e.g: nitrous oxide, sulfur dioxide, ammonia, benzene)
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18
Q

what factors affect toxicity and fibrogenic activity in PNEUMOCONIOSES?

A
  • Physical properties of the particles (size/shape)
  • Physiochemical reactivity, solubility
  • Concentration
  • Duration of exposure
  • Effectiveness of clearance mechanisms
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19
Q

how do the physical properties of particles affect toxicity and fibrogenic activity in Pneumoconiosis?

A
  • Particles 1-5 µm are greatest danger as get lodged at bifurcation points in distal airways
  • Elicit macrophage (MO) phagocytosis → release of mediators/cytokines → inflammation and fibrosis
    • RECALL: MO should be in lung for protection
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20
Q

define, and epidemiology:

anthracosis

A
  • DEF: Accumulation of coal-dust in lungs, pleura, and lymph nodes
    • No significant reaction
    • Asymptomatic
  • Epi: Smokers & urban dwellers
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21
Q

define: Simple Coal Workers’ Pneumoconiosis (CWP)

and symptoms

A
  • Coal macules (coal-dust laden macrophages 1-2 mm, peribronchial) and coal nodules (> 2 mm) in a background of collagen deposition
  • Sxs:
    • Cough
    • Black sputum
    • No dysfunction
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22
Q

define: COMPLICATED Coal Workers’ Pneumoconiosis (CWP)

and effect on respiration

A
  • Complicated CWP (progressive massive fibrosis - PMF)
    • Progressive severe fibrosis in a background of simple CWP
  • RESPIRATORY INSUFFICIENCY results
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23
Q

COMPLICATED Coal Workers’ Pneumoconiosis (CWP):

histo features

A

Multiple nodules and black scars > 2cm (dense collagen and black pigment) with central necrosis

24
Q

define: Caplan’s Syndrome

A
  • a combination of rheumatoid arthritis (RA) and pneumoconiosis
25
Q

CAPLAN’S SYNDROME:

diagnosis, course, associated w/ which minerals/conditions?

A
  • dx: Nodular lesions with central necrosis and peripheral fibrohistiocytic inflammation
    • nodules are seen on xray
  • course: Faster progression/more severe
  • assoc: carbon, silicosis and asbestosis
26
Q

sources of exposure of Silicosis:

what is the most damaging/fibrogenic of these causes?

A
  • **Most damaging/fibrogenic to the lung: crystalline forms such as QUARTZ
  • Other causes (occupational):
    • Mining (gold, tin, copper, coal)
    • Quarrying
    • Sandblasting, stone cutting
    • Metal grinding
    • Manufacture of ceramics
27
Q

what specific disease does SILICOSIS increase the susceptiblity of?

A

silicosis –> increased susceptibility to TUBERCULOSIS

(bc it interferes w/ immune function –> macrophage clearance is decreased)

28
Q

SILICOSIS:

histopathology

A
  • Nodular fibrosis
  • Hyalinized whorls of collagen
  • Scant inflammation
  • Birefringent silica particles
  • Coalescence of nodules/large areas of dense scars (progression even after cessation of exposure)
  • Concomitant anthracosis
29
Q

SILICOSIS:

radiology

A
  • Eggshell calcification on chest x-ray
30
Q

ASBESTOSIS:

histology

A
  • Mineral fibers containing crystalline hydrated silicates
    • curled flexible serpentines
    • straight stiff amphiboles (more pathogenic)
    • ferruginous bodies (iron coating)** important clue on histology
  • Diffuse interstitial fibrosis
  • Pleural effusions/fibrous adhesions
  • Hyalinized fibrocalcific pleural-plaques
31
Q

what is the KEY histological finding to confirm ASBESTOSIS?

A

FERRUGINOUS BODIES (iron coating)

32
Q

ASBESTOSIS:

pathogenesis

A
  • Fibers ingested by macrophages leads to:
    • activation of macrophages and neutrophils
    • release of enzymes and fibrogenic cytokines
    • deposition in interstitium and lymphatics
    • direct stimulation of fibroblast collagen
  • Progressive fibrosis even after cessation of exposure
33
Q

what are occupational exposure causes of asbestosis?

A
  • Mining
  • Pipefitters and plumbers
  • Textile industry
  • Shipbuilding
  • Constructions
  • Insulations
34
Q

asbestosis acts synergistically with what to increase risk of carcinoma (but not mesothelioma)

A

cigarette smoking

(act synergistically to inc risk of carcinoma)

35
Q

asbestosis has strong association with which tumors?

A
  • Strong association with malignant mesothelioma and bronchogenic carcinoma
  • (Generates free radicals and adsorbs toxic chemicals, affecting nearby mesothelium or bronchial epithelium)
36
Q

what condition is this gross anatomical image of?

A

PLEURAL PLAQUES;

common manifestation of asbestos exposure

37
Q

key word associations of:

  • anthracosis
  • silicosis
  • asbestosis
A
  • Anthracosis: complicated coal workers pneumoconiosis
  • Silicosis: occupations exposed to silica; large collagenized nodules in lungs; seen under microscope
  • Asbestos: can cause pleural plaques, fibrosis (asbestosis), mesothelioma, lung cancer
38
Q

SARCOIDOSIS:

define

A
  • Non-caseating granulomas (many tissues and organs)
  • Disordered immune regulation in genetically predisposed individuals when exposed to certain environmental agents
    • CD4+ TH1 cells play a big role in formation of granulomas
39
Q

SARCOIDOSIS:

epidemiology

A
  • Common disease, with unknown etiology
  • Young adults (females)
  • Geographic/ethnic variations (African-americans)
40
Q

SARCOIDOSIS:

clinical presentation

A
  • bilateral, symmetrical, enlargement of lymph nodes (aka “potato lymph nodes”)
    • Peripheral lymphadenopathy/hepatosplenomegaly
  • may be asymptomatic (incidental on chest xray)
    • Usually lung involvement with hilar adenopathy (characteristic chest x-ray)
  • Insidious onset with respiratory and constitutional symptoms (fever, night sweats, weight loss)
  • Acute onset with fever, erythema nodosum, polyarthritis
    • isolated cutaneous or ocular lesions
  • Usually lung involvement with hilar adenopathy (characteristic chest x-ray)
41
Q

SARCOIDOSIS:

key histopathological findings

A
  • non-caseating granulomas
  • Pulmonary granulomas increase and eventually replaced by diffuse interstitial fibrosis of the lung
42
Q

Sarcoidosis is a DIAGNOSIS OF EXCLUSION;

how do you get a definitive diagnosis?

A

you need a transbronchial biopsy for a definitive diagnosis

(granuloma is circled)

43
Q

SARCOIDOSIS:

clinical course

A
  • 70% - recover w/ minimal or no residual disease
  • 20% - permanent lung or ocular dysfunction
  • 10% progress w/ severe interstitial pulmonary fibrosis and cor-pulmonale and death
44
Q

HYPERSENSITIVITY PNEUMONITIS:

define

A
  • Intense, prolonged exposure to inhaled organic antigen
    • Type III/IV hypersensitivity reactions
    • Inflammation w/ gradual fibrosis
45
Q

HYPERSENSITIVITY PNEUMONITIS:

causes

A
  • Farmer’s lung: thermophnilic actinomycetes in hay
  • Pigeon breeder’s lung: proteins from bird feathers and excreta
    • mold at home, or bird droppings
  • Humidifier/air-conditioner lung: thermo-philic bacteria
    • hot tub lung
46
Q

HYPERSENSITIVITY PNEUMONITIS:

histopathology;

what is key feature?

A
  • Non-caseating poorly formed interstitial granulomas - (key feature)
  • Interstitial pneumonitis
  • Fibrosis
  • Organizing pneumonia reaction
  • May progress to severe interstitial fibrosis
47
Q

PULMONARY ALVEOLAR PROTEINOSIS (PAP):

very rare disease; what is the clinical manifestation?

A
  • Sputum (chunks of gelatinous material)
  • Cough
  • Progressive respiratory difficulty
48
Q

PULMONARY ALVEOLAR PROTEINOSIS (PAP):

histopathology

A
  • Alveolar spaces filled with dense, amorphous, PAS-positive, lipid containing, surfactant-like material
  • autoimmune disease (whole lung undergoes lavalge in the patient)
49
Q

pulmonary alveolar proteinosis:

two common forms of the disease?

A
  1. autoimmune
  2. secondary (associated with hematopoietic disorders, malignancies and immunodeficiency
    states)
50
Q

lung disease can result from several causes:

what are the drug-induced lung diseases?

A
  • Bronchospasm (Aspirin, Beta-antagonists)
  • Pulmonary edema
  • Chronic pneumonitis/fibrosis (amiodarone/bleomycin)
  • Hypersensitivity pneumonitis (methotrexate)
51
Q

lung disease can result from several causes:

what are the radiation-induced lung diseases?

(acute and chronic)

A
  • Acute radiation pneumonitis (1-6 months.)
    • fever, dyspnea, radiologic infiltrates
    • Lymphocytic alveolitis, hypersensitivity pneumonitis
    • Respond to steroids
  • Chronic radiation pneumonitis
    • DAD and atypical type II pneumocytes
    • Progression to interstitial fibrosis
52
Q

what does CHRONIC radiation-induced lung diseases look like on histology?

A

can look like fibrotic lung disease

53
Q

lung disease can result from several causes:

what are complications of therapy following LUNG TRANSPLANT?

A
  • Infections (immunocompromised host)
  • Acute rejection - we want to recognize and tx this as early as possible
  • Chronic rejection
  • Lymphoproliferative diseases
54
Q

ACUTE rejection of lung transplant:

timing, sxs, tx

A
  • Timing: early weeks to months post transplant
  • Sxs: fever, dyspnea, cough, infiltrates on CXR
    • perivascular and peribronchiolar mononuclear cell infiltrates
  • Tx: increased immunosuppression
55
Q

CHRONIC rejection of lung transplant:

timing, sxs, tx

A
  • Timing: 6 - 12 months post transplant
  • Sxs: dyspnea, cough, –> bronchiolitis obliterans (BO, aka popcorn lung)
    • Chronic rejection –> total occlusion of bronchiole by fibrous tissue (BO)
    • BO is key histological finding
  • Tx: of BO disappointing

Y2 - Path - Exam 4 (13 decks)

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