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Body in Balance Midterm #2 > restrictive lung disease > Flashcards

restrictive lung disease Flashcards

1
Q

Using HRCT (High-resolution computed tomography) to Diagnose IPF

A
  • UIP RADIOGRAPHIC Pattern: Typical features of UIP need be present on HRCT and atypical features absent to make confident diagnosis of IPF/UIP [UIP = usual interstitial pneumonia]

Characteristic Features:

  • Irregular reticular lines (diffuse)
  • Subpleural, posterior, and lower-lobe predominance
  • Subpleural honeycombing
  • Minimal ground glass opacities
  • Traction bronchiectasis (occurs later in disease course)
  • Loss of normal lung architecture/distortion
  • Patchy involvement of the lung (heterogeneity)
  • Peripheral zones of chronic scar and honeycomb change predominate
  • Fibroblast foci present at junction of normal lung and fibrotic change
  • Interstitial inflammatory change is usually only mild and focal
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2
Q
A

Siliconic nodules x ray

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3
Q

Common Risk Factors for ARDS

A

Direct

  • Pneumonia
  • Aspiration
  • Inhalational Injury
  • Pulmonary Contusion
  • Pulmonary Vasculitis
  • Drowning

Indirect

  • Non-pulmonary sepsis
  • Major Trauma
  • Pancreatitis
  • Severe Burns
  • Non-cardiogenic shock
  • Drug Overdose
  • Transfusion related acute lung injury (TRALI)
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4
Q

Diagnosis of IPF

A
  • Gradual onset
  • Age 50+ (rarely seen in younger individuals)
  • Exclusion of other known causes of interstitial lung disease including drug toxicities, environmental exposures, and collagen vascular diseases
  • Exam usually shows inspiratory crackles (or rales) and clubbed digits
  • High-resolution computed tomography (HRCT) scans show Usual Interstitial Pneumonia (UIP) radiographic pattern
  • PFTs show restriction, reduction in DLCO, and exertional desaturation
  • Surgical Lung Biopsy showing Usual Interstitial Pneumonia (UIP) pathologic pattern
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5
Q

Pathophysiology of ARDS

A
  • Acute respiratory distress syndrome (ARDS) is an acute lung injury due to an inciting event causing complement activation and subsequent lung damage, leading to refractory hypoxemia.
  • Initial Injury to capillary Endothelium and/or alveolar epithelium
  • Results in leaky alveolar capillary units
  • Elaboration of protein-rich, cell-rich exudates into the alveolar space.
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6
Q

Pathology of Hypersensitivity Pneumonitis

A
  • Poorly formed (loose) granulomas that are centered around small airways (bronchioles)
  • Multinucleated Giant Cells
  • Diffuse mixed interstitial inflammation
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7
Q

What is Silicosis

A
  • a slowly progressing nodular, fibrosing pneumoconiosis that is caused by inhalation of pro-inflammatory silicon dioxide (a component of many types of stone). Silicosis is currently the most prevalent occupational disease worldwide
  • Chronic bouts of inflammation and resolution are the main cause of the slowly progressive nodular fibrosis
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8
Q

Pathogenesis of Fibrosis in Idiopathic Pulmonary Fibrosis

A
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9
Q

Pulmonary Edema triggered by:

A
  • Increased hydrostatic force (cardiogenic pulmonary edema)
  • Damage to the alveolar-capillary barrier (ARDS)
  • Lymphatic obstruction
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10
Q

Classification of Interstitial Lung Diseases (chart visualization)

A
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11
Q

Pulmonary function tests of hypersensitivity pneumonitis

A
  • Important to establish severity and progression
  • Mixed obstructive/restrictive pattern can be found
    • Isolated elevated RV
    • Disproportionately low flows (FVC and FEV1)
    • Low FEV1/FVC
  • Most common: isolated restriction
  • Summary: some patients just have restrictive patterns, some patients have both obstructive and restrictive
    • The mix of obstructive and restrictive indication is unique to HP
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12
Q

Etiologies of Restrictive Lung Disease: Extrapulmonary Causes and Pulmonary Causes

A
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13
Q

ARDS: Acute Respiratory Distress Syndrome

A
  • Referred to as the lower pressure pulmonary edema
  • Syndrome of acute respiratory failure characterized by:
    • Injury and disruption of the alveolar-capillary membrane
    • Alveolar flooding with protein-rich edema fluid (exudative)
    • Severe hypoxemia
    • Reduced lung compliance
  • Acute: Within one week of a known clinical insult or new or worsening respiratory sxs
  • Bilateral pulmonary infiltrates on CXR or CT
  • Non-cardiac: pulmonary edema not fully explained by cardiac failure or fluid overload
    • need objective assessment (echo) if no risk factor present
  • Hypoxemia
    • P:F ≤ 300 (where P=PaO2 and F=FiO2) on PEEP ≥5 cmH20
    • Mild (200-300); Moderate (100-200); Severe (<100)
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14
Q

Asbestos-Related Malignancy

A
  • Malignant Mesothelioma
    • Smoking does NOT increase the risk of mesothelioma in asbestos workers
    • malignant tumor of the visceral or parietal pleura that results from long term exposure to asbestos
  • Primary Lung Cancer
    • Smoking greatly increases the risk of lung cancer in patients exposed to asbestos
    • No preferential pathologic subtype
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15
Q

Acute Exacerbation of IPF

A
  • Acute shortness of breath
  • New radiographic infiltrate
  • Worsening gas exchange
  • No evidence of other cause: – Infection – Heart failure – Thromboembolism – Pneumothorax
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16
Q

Asbestosis

A
  • Asbestosis is a pneumoconiosis associated with the inhalation of asbestos particle
  • Asbestos fibers are persistent (not able to be cleared) and biologically active, and may lead to the generation of oxygen free radicals, which is injurious to the local tissue
  • Results in slowly progressive fibrosis of the lung.
  • Due to long latency between exposure and disease onset (>20 years), age-adjusted mortality of asbestosis continues to increase in US
  • Concomitant tobacco abuse is common.
  • The earliest symptom of asbestosis is typically dyspnea with exertion.
  • Bibasilar Fine Crackles on lung exam, clubbing
  • Restriction on PFTs
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17
Q

Imaging in Chronic Hypersensitivity Pneumonitis

A
  • Upper lobe predominance:
  • Diffuse bilateral reticulo-nodular pattern (lines and dots)
  • Ground-glass opacities
  • Areas of Air-trapping (mosaicism)
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18
Q

Lung Biopsy in Asbestosis

A
  • The presence of ferruginous bodies in lung tissue strongly suggests asbestos-related pulmonary disease. They arise from the coating of inorganic particulates with an iron-containing proteinaceous material. They microscopically appear as golden colored rods, because they have become coated with ferruginous (iron rich) protein rich material following phagocytosis by tissue macrophages.
  • strong indicator of abestos, but hard to find so not required for diagnosis
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19
Q

Chest CT in Asbestosis

A
  • Peripheral and basilar interstitial fibrosis and honeycombing
  • can be identical to UIP pattern of fibrosis
  • Pleural plaque – Calcification of the pleura as well as the domes of the diaphragm can occur, forming “pleural plaques.
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20
Q

the most common manifestation from asbestos exposure

A

Pleural plaques

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21
Q

How cardiogenic pulmonary edema causes restrictive lung disease

A
  • Decreased compliance:
    • Interstitial water
    • Flooded alveolar units (loss of participation in ventilation)
  • Hypoxemia
  • Activation of alveolar stretch receptors (J receptors)
    • Nerve endings in alveolar walls next to capillaries (Vagal nerve afferent)
    • Responsive to increases in interstitial fluid
    • Leads to simulation of ventilation (increased respiratory rate)
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22
Q

Common Clinical Findings in Interstitial Lung Diseases

A
  • Dyspnea on exertion (due to increased work of breathing)
  • Fatigue
  • Non-productive (paroxysmal) cough
  • Abnormal breath sounds to auscultation
  • Abnormal CXR/CT (interstitial opacities)
  • Hypoxemia (first with exercise/ambulation)
  • Clubbing
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23
Q

Common Interstitial Lung Diseases

A
  • Idiopathic pulmonary fibrosis
  • Asbestosis
  • Silicosis
  • Hypersensitivity Pneumonitis
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24
Q

Hypersensitivity Pneumonitis (HP) (Extrinsic Allergic Alveolitis)

A
  • Hypersensitivity pneumonitis is caused by chronic high-level exposure to inhaled irritants
  • Lung disease resulting from recurrent exposures to organic particles
  • Susceptible subjects are sensitized to the inciting antigen, and develop bronchiolocentric granulomatous lymphocytic infiltrates
    • Bronchiolocentric –inflammation centered around terminal bronchioles
  • Acute or chronic
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25
Q

Etiologies of Lung Inflammation

A
  • Autoimmune (lupus, scleroderma, rheumatoid arthritis)
  • Injury (aspiration, noxious inhalation, trauma)
  • Medications (methotrexate, bleomycin, nitrofurantoin, amioadarone, etc)
  • Hypersensitivity pneumonitis (moldy hay, hot tubs, birds, water damage/molds)
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26
Q

Management of ARDS

A
  • Protecting lung from further injury – “Lung protective ventilator strategy”
  • Addressing shunt
  • Deliver positive and re
  • Low tidal volumes (4-6cc/kg ideal BW)
  • Permissive hypercapnea (pH ≥ 7.20)
  • Limit alveolar distending pressure (≤30 cmH2O)
  • Non-toxic FiO2 (≤0.60)
  • Positive end-expiratory pressure to recruit (open-up) flooded/collapsed alveolar units
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27
Q

Pneumoconioses

A
  • Definition: “the accumulation of dust in the lungs and the tissue reactions to its presence”
  • Tissue reactions (severity is related to total dust burden): Nodular fibrosis and Diffuse fibrosis
  • Dusts of concern:
    • Asbestos
    • Silica
    • Coal
    • Dust
    • Talc
    • Mica
    • Hard Metal (Silicon Carbide)
    • Beryllium
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28
Q
A

Asbestos induced pleural plaques

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29
Q

Pathophysiology of Silicosis

A
  • Inhaled crystalline particles are engulfed by alveolar macrophages. Phagocytosed silica causes activation of those macrophages, and promotes the release of inflammatory mediators such as IL-1, TNF, and the formation of free radicals.
  • Inside those macrophages, engulfed silica also impairs phagolysosome formation, leading to an increased risk of infection/exacerbation of infection with intracellular bacteria.
  • An increased susceptibility to M. tuberculosis (an intracellular bacteria) infection or exacerbation of an ongoing or latent M. tuberculosisinfection is an especially feared complication of silicosis
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30
Q
A

Progressive Massive Fibrosis

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31
Q

Asbestos-related (benign) pleural diseases

A

Benign asbestos pleural effusion (BAPE)

  • Shortest latency period to disease presentation
  • Termed benign, as it occurs in the absence of mesothelioma
  • Usually unilateral, and often bloody and eosinophilic
  • Thought to be a reaction to asbestos fibers in pleural space • Typically resolves
  • Tends to go away on its own

Hyaline pleural plaques

  • Most common CXR abnormality in asbestos-exposed pts
  • (in 20-60% of patients with significant exposure)
  • Usually asymptomatic
  • Discrete areas of fibrosis/thickening of parietal pleura
  • Does not progress to malignant melanoma

Rounded atelectasis secondary to pleural adhesions

  • Usually asymptomatic
  • “Comet-tail” sign on chest CT
32
Q

Resolution phase of ARDS

A
  • Full re-epithelialization (differentiation into type I AECs)
  • Endothelial restoration
  • (partial) resolution of scar formation
33
Q
A

Hypersensitivity Pneumonitis

34
Q

Cardiogenic pulmonary edema

A
  • Cardiogenic (hydrostatic or high pressure) pulmonary edema
  • Rising capillary hydrostatic forces:
    • Increase in interstitial edema
    • Overwhelms lymphatic drainage
    • Development of alveolar edema
  • Fluid is transudative (low protein, low cells)
35
Q

ARDS leading to restrictive lung disease

A

Reduced lung compliance

  • flooded alveolar units
  • collapsed alveolar units
  • Surfactant dysfunction from inactivation from plasma protein leak and decreased production (type II cell injury)
  • interstitial edema/inflammation

Acutely, leads to severe restrictive lung disease

  • Difficult to inflate/ventilate
  • Loss of ventilated alveoli leads to risk of over-distension and barotrauma
36
Q

Idiopathic Pulmonary Fibrosis (IPF)

A

The most common form of idiopathic interstitial pneumonia

  • Idiopathic Pulmonary Fibrosis = Clinical Condition
  • Usual Interstitial Pneumonia = Pathologic (or radiologic) pattern seen in IPF
  • Increasing incidence and prevalence (34K new dx/yr, 89k total US)
  • Disease of aging; Usually occurs after fifth decade of life (highest in the elderly)
  • Dismal prognosis; Median survival is approximately 3-4 years post-diagnosis
  • Immunosuppressive medications are harmful
  • Pirfenidone (anti-TGF-β) and Nintedanib (small molecule inhibitor of VEGF-R, EGFR, and FGF-R tyrosine kinases) now approved for use in this condition
37
Q

Asbestos

A
  • Fibrous, naturally occurring mineral, which possesses qualities of heat resistance, and can be spun.
  • Used in pottery and clothing (fire resistant) dating back to 2500 B.C.
  • In the industrial age, asbestos was used for in a wide variety of applications with the most common insulation, fire-proofing, and friction materials
  • Asbestos-related lung disease is directly caused by inhalation of the fibers
    • Phagocytosis of fibers
    • direct cell cytotoxic effects
38
Q

pathogenesis of asbestosis

A

mediated by macrophages within the lung tissue

  1. Pulmonary macrophages attempt phagocytosis of asbestos fibers.
  2. Within macrophages, asbestos fibers induce the release of chemotactic factors and inflammatory mediators, ultimately leading to pulmonary inflammation and fibrosis
39
Q

Disease Manifestations of Acute vs. Chronic Silicosis

A

Acute – Dyspnea, cough, fatigue Alveolar filling with protein/cell rich exudate (similar to pulmonary alveolar proteinosis)

Chronic – Upper lobe nodules; Egg-shell calcifications of mediastinal lymph nodes

40
Q

Treatment of silicosis

A
  • No proven therapies to prevent progression
  • Avoidance of further exposure
  • Tobacco cessation
41
Q

[P:F Ratio]

A
  • Ratio of arterial oxygen tension to the concentration of inspired oxygen (PaO2/FiO2)
  • FiO2 is expressed as a fraction of 1 (i.e. 60% = 0.6)
  • PaO2 112 in patient receiving FiO2 40% is a P:F ratio of 280 (112/0.4)
  • Lower P:F means worse oxygenation
42
Q

Diagnosis of Asbestosis

A
  • Take and document a reliable exposure history to asbestosis fibers
    • Need appropriate latency period (>20 yrs)
  • Evidence of interstitial lung fibrosis
    • Crackles on lung exam
  • Typical chest radiograph or chest CT
    • For legal cases a certified B-reader is required to score a chest radiograph
  • Absence of other causes
  • Histology – Sub-pleural pulmonary fibrosis is the primary gross histopathologic finding in asbestosis
43
Q

What is Pneumonia

A
  • Infection in the pulmonary parenchyma.
  • Initiates an inflammatory response
  • Neutrophilic infiltration into alveolar airspaces
  • Localized capillary leak and the formation of intraalveolar exudates
44
Q

Symptoms of ARDS include:

A
  • acute dyspnea
  • cyanosis
  • tachypnea
  • wheezing
  • rales and rhonchi
45
Q

Hypersensitivity Pneumonitis – Chronic HP

A
  • Chronic, repetitive small exposures
  • Indolent presentation, with dyspnea on exertion (indolent – causing little or no pain)
  • Cough, crackles, inspiratory squeaks
  • Some pts have evidence of fibrosis on chest CT
  • Poorer prognosis; some have progressive, irreversible disease; Can have stabilization
46
Q
A

Calcified lymph nodes (egg-shell calcification)

47
Q

Diagnosis of Hypersensitivity Pneumonitis

A
  1. Known exposure to inciting antigen: – History – Environmental investigation – Serologic evidence (IgG against antigen – indicates sensitization)
  2. Compatible clinical findings – Crackles, cough, SOB, wheeze, fatigue, fever, weight loss associated with antigen exposure – Chest radiograph/CT – reticular/nodular/ground-glass opacities
  3. Bronchoalveolar lavage with lymphocytosis (>20%) or biopsy
  4. Positive inhalation challenge – Improvement with removal from environment, worsening with re-exposure to the environment – Inhalation challenge (PFT) to the suspected antigen
  5. Histopathology: – Most often requires a surgical lung biopsy – Poorly formed, non-caseating granulomas – Mononuclear cell infiltrate

Definite HP = 1,2,3 OR 1,2,4 OR 2,3,5

48
Q

In silicosis, chronic exposure results in a local-tissue reaction in:

A
  • Lung (upper lung nodules)
  • mediastinal lymph nodes (egg-shell calcifications)
49
Q

Management of Idiopathic pulmonary fibrosis

A
  • Establish an accurate diagnosis (usually requires referral to a tertiary care center specializing in ILD
  • Pirfenidone and Nintedanib-Inhibit fibrogenic pathways
  • Pulmonary rehabilitation
  • Supplemental oxygen
  • Clinical trials of investigational agents for willing and eligible patients
  • Lung transplantation for eligible patients
  • Relief of dyspnea/palliative care/hospice
50
Q

Treatment of Hypersensitivity Pneumonitis

A
  • Identification and avoidance of exposure
  • Corticosteroids for subacute or severe acute
  • Consideration of steroid-sparing agents (mycophenolate mofetil, azathioprine, rituximab) for progressive disease
  • Lung transplant evaluation
51
Q
A

Rounded Atelectasis

52
Q

Dyspnea in silicosis

A

only seen late in the progression of the disease and after substantial fibrosis has occurred. Long term morbidity is due to progressive respiratory impairment

53
Q

Remember causes of ARDS with the mnemonic ARDS (AAAARDDDSSS):

A
  • Aspiration
  • Acute pancreatitis
  • Air or Amniotic embolism
  • Radiation
  • Drug overdose
  • DIC
  • Drowning
  • Shock
  • Sepsis
  • Smoke inhalation
54
Q
A

Silicotic Nodules

55
Q

gross pathological examination of silicosis

A
  • silicosis appears as tiny pale nodules commonly seen in the upper zones of the lung. As the disease progresses, the nodules turn into hard collagen-dense scars.
56
Q

Often first clinical presentation of prior asbestos exposure

A

Benign Asbestos Pleural effusion (BAPE)

57
Q

Compliance curves of restrictive lung disease

A

Restriction due to lung disease (lungs are more stiff)

  • Compliance curve of lung compliance will drop
  • The sum of the chest and lung compliances will also then drop
  • This means that at any given pressure the lung volume will be less

Restriction due to chest wall

  • If chest wall is less compliant then the sum compliance curve will more to the run
  • At any given pressure the lung volumes will be less

Restriction due to weakness

  • Has to do with how much strength we can generate
  • Patient has a maximal inspiratory pressure that they can reach that’s lower than a healthy person – compliance curve only goes up to a max pressure (maximum on x-axis) that leads to a max volume that can be reached following on the curve
58
Q

Arterial Blood Gas in ARDS

A
  • Low arterial oxygen tension (i.e low Pa02)
  • Much higher alveolar oxygen tension (PAO2) than arterial oxygen tension(PaO2) – high A-a gradient
  • Slight respiratory alkalosis (low PCO2, high pH) due to stimulation of ventilation by hypoxemia and stimulation of J receptors
59
Q

Restrictive lung disease

A
  • disruption in balance of elastic forces and transpulmonary pressures leading to smaller volumes
  • A reduction in total lung capacity (TLC) on PFTs is required to make the diagnosis

Caused by:

  • Lung diseases that result in decreased compliance, resulting in decreased lung volumes
  • Extrapulmonary restriction (chest wall, respiratory muscle strength, pleura) that limits the ability to generate negative pleural pressure
60
Q

Acute Hypoxemic Respiratory Failure

A
  • severe arterial hypoxemia that is refractory to supplemental O2. It is caused by intrapulmonary shunting of blood resulting from airspace filling or collapse. Findings include dyspnea and tachypnea.
  • Physiology
    • airspace flooding: edema, pus, blood in alveoli
    • Intrapulmonary shunt physiology (Qs/Qt)
    • Hypoxia is refractory to oxygen supplementation – oxygen supplementation doesn’t help much
61
Q

Interstitial Lung Diseases: overview and common pathophysiology

A

Overview

  • Disorders predominately affecting the interstitial space of the lung
  • Primarily (but not exclusively) affects the lung parenchyma (alveolar/capillary units) with variable patterns and degrees of inflammation, fibrosis, architectural distortion

Common Pathophysiology

  • Accumulation of inflammation and connective tissue in the alveolar interstitial spaces of the lung leading to:
  • Increased elastic recoil of the lung -> Restrictive lung physiology (low TLC, FRC, RV)
  • Increases work of breathing
  • Destruction of alveolar/capillary gas exchanging surfaces and resultant low DLCO, high A-a gradient
  • Thickening of the alveolar/capillary interface -> diffusion limitation
  • exercise-induced hypoxemia
62
Q

Asbestos Enviromental Exposure

A
  • Plumbing, insulators, Sheet metal
  • Shipbuilding
  • Brake workers
  • Dockworkers
  • Remodeling, demolition
  • Milling, mining
  • Soils, Turkey, Albania
63
Q

Presentation of lung inflammation (restrictive lung disease)

A
  • Widened alveolar septa
  • Increased elastic recoil forces
  • Increased work of breathing
  • Loss of alveolar/capillary units
  • Hypoxemia
64
Q

Environmental exposures of silicosis

A

mining, sand blasting, ceramics, metal casting

65
Q

Chronic Phase of ARDS

A
  • “Fibroproliferative Phase”
  • Fibroblast proliferation and collagen deposition in areas of injury (scarring)
  • Type II epithelial cell proliferation (re-epithelialization)
  • Initiation of resorption of the exudate
66
Q

Diffuse Alveolar Damage (DAD) in ARDS

A
  • Alveolar septal thickening (edema/inflammatory cells)
  • Hyaline membranes
    • Proteinacious deposits in alveolar spaces
    • Results from fibrin-rich exudative edema fluid and remnants of necrotic epithelial cells
  • Type II cell hyperplasia
    • Attempt at repair
67
Q

Hypersensitivity Pneumonitis – Acute HP

A
  • Relatively rare presentation
  • Associated with a large exposure to antigen
  • Mediated by immune complex deposition
  • Fevers, chills, muscle aches, cough, dyspnea a few hours after exposure
  • Occasionally fine crackles
68
Q

Pulmonary function tests of silicosis

A

will be normal or only slightly impaired in the early and middle stages of disease

69
Q

Common examples of hypersensitivity pneumonitis and associated exposures include

A
  • Farmer’s lung: exposure to inhaled mold dusts containing thermophilic actinomycetes spores
  • Pigeon breeders lung exposure to antigenic bird feathers, droppings, sera
  • Humidifier (“air conditioner”) lung: exposure to thermophilic bacteria in heated water
70
Q

Clubbing in ILD

A
  • Commonly seen in IPF, asbestosis, along with lung cancer, cystic fibrosis
  • Can be seen, but less common in COPD and other lung conditions
  • Likely develops in response to growth factors such as VEGF, PDGF
71
Q

Malignant Mesothelioma: overview, symptoms, requirement for diagnosis, chest xray, prognosis

A
  • Mesothelioma is a malignant tumor of the visceral or parietal pleura that results from long term exposure to asbestos
  • Smoking does NOT increase the risk of mesothelioma in asbestos workers. This is in contrast to the synergistic effect of smoking and asbestos exposure on developing primary bronchogenic lung carcinoma.
  • Rare tumor arising from pleural or parietal mesothelium
  • Forms a pleural mass or “rind”, often with associated effusion
  • The most common presenting symptoms of mesothelioma are chest pain, dyspnea, and recurrent idiopathic pleural effusions.
  • Diagnosis of malignant mesothelioma requires tissue biopsy.
  • Chest x-ray will show pleural thickening and possibly pleural effusion.
  • Malignant mesothelioma has a poor prognosis. Mean survival time is approximately 12 months.
72
Q

Lab findings consistent with ARDS include:

A
  • Respiratory alkalosis
  • Decreased O2
  • Decreased CO2
73
Q

How pneumonia causes restrictive lung disease

A

Lower compliance of the lung due to:

  • Loss of aerated lung (cellular and protein-rich exudate)
  • Atelectatic units
  • Flooded alveolar units means fewer alveolar units participate in ventilation
  • Also leads to hypoxemia
74
Q

Asbestos-Related Thoracic Disease

A
  • Asbestosis = ILD from asbestos exposure
  • Pleural Disease (often first manifestation of asbestos-related lung disease)
    • Pleural Plaques (most common 20-60% of exposed workers)
    • Benign Asbestos Pleural Effusion (BAPE)
    • Rounded Atelectasis
  • Malignant mesothelioma
  • Bronchogenic carcinoma
    • Asbestosis + Smoking
75
Q

Restrictive Lung Disease: results of TLC, RV, and DLCO for reduced compliance in chest wall, lung parenchyma, and muscle weakness

A

Body in Balance Midterm #2 (26 decks)

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