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BMS 250 test 2 > Week 5 Lecture 2 > Flashcards

Week 5 Lecture 2 Flashcards

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1
Q

What defines obstructive lung diseases?

A

Impaired ability of air to leave the alveoli during expiration, clinically defined by decreased FEV1/FVC ratio

The residual volume (RV) and functional residual capacity (FRC) are increased, while total lung capacity is normal.

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2
Q

What are examples of obstructive lung diseases?

A
  • Bronchial Asthma
  • Chronic Obstructive Pulmonary Disease (COPD)
  • Chronic Bronchitis
  • Emphysema
  • Bronchiectasis
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3
Q

What characterizes bronchial asthma?

A

Episodic airway obstruction, airway hyperresponsiveness, usually accompanied by airway inflammation

Most airway obstruction is reversible, though it may become irreversible in some cases.

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4
Q

What is the heritable predisposition for asthma?

A

25–80% degree of heritability, influenced by complex polygenic inheritance and environmental interactions

Genes related to asthma are associated with risk for atopy.

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5
Q

What are common triggers of bronchoconstriction?

A
  • Allergens (e.g., animal waste, dust mites)
  • Upper airway infections
  • Inhalatory irritants
  • Anxiety
  • Cold air
  • Physical activity
  • Gastroesophageal reflux
  • Nonsteroidal anti-inflammatory drugs (e.g., aspirin)
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6
Q

What are the two classifications of asthma?

A
  • Older classification: Extrinsic and intrinsic
  • Newer classification: Allergic asthma versus nonallergic asthma
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7
Q

What is the mechanism of allergic asthma?

A

Type I hypersensitivity reaction

Associated with causes like pollens, dust, and drugs.

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8
Q

What characterizes nonallergic asthma?

A

IgE levels are normal, not a Type I hypersensitivity reaction

Common triggers include exercise, cold air, drugs, and viral infections.

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9
Q

What are the two stages of asthma?

A
  • Early Stage: Mediators promoting bronchoconstriction (e.g., leukotrienes, histamine)
  • Late Stage: Release of enzymes by eosinophils and neutrophils
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10
Q

What are the mechanisms leading to acute and chronic airway obstruction?

A
  • Airway hyperresponsiveness
  • Inflammation
  • Structural changes (e.g., smooth muscle hypertrophy, airway edema)
  • Vascular proliferation
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11
Q

What is the classic triad of clinical symptoms in asthma?

A
  • Wheezing
  • Dyspnea
  • Night-time cough
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12
Q

What defines Chronic Obstructive Pulmonary Disease (COPD)?

A

Preventable and treatable disease characterized by airflow limitation that is not fully reversible

Usually progressive and associated with an abnormal inflammatory response to noxious particles or gases.

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13
Q

What are major risk factors for COPD?

A
  • Susceptibility genes (e.g., alpha-1 antitrypsin deficiency)
  • Tobacco smoke
  • Indoor air pollution
  • Occupational dusts
  • Outdoor air pollution
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14
Q

What is the pathogenesis of COPD?

A
  • Inflammatory and immune cell recruitment
  • Proteinases damage the extracellular matrix
  • Structural cell death through oxidant-induced damage
  • Disordered repair of elastin
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15
Q

What defines chronic bronchitis?

A

Productive cough for at least 3 months in 2 consecutive years

Pathogenesis involves cigarette smoking leading to airway irritation and increased mucus production.

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16
Q

What is the definition of bronchiectasis?

A

Irreversible airway dilation that can be focal or diffuse, categorized as cylindrical, varicose, or cystic

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17
Q

What are the components required for the pathogenesis of bronchiectasis?

A
  • Infection
  • Obstruction
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18
Q

What is the ‘vicious cycle hypothesis’ in infectious diffuse bronchiectasis?

A

Susceptibility to infection leads to microbial colonization and chronic inflammation, resulting in airway wall damage

Conditions like cystic fibrosis can impair mucociliary clearance.

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19
Q

What is the morphology of bronchiectasis?

A
  • Gross: Dilation of airways, especially in lower lobes
  • Microscopic: Inflammatory infiltrate and tissue destruction
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20
Q

What are common symptoms of bronchiectasis?

A
  • Dyspnea
  • Chronic cough (dry or with purulent sputum)
  • Hemoptysis
  • Clubbing of fingers
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21
Q

What is the spirometry finding for obstructive ventilatory impairment?

A

FEV1/FVC ratio < 0.7

FEV1 is reduced while FVC is normal or only slightly decreased.

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22
Q

What are the complications of COPD?

A
  • Pulmonary hypertension
  • Cor pulmonale
  • Mismatched ventilation-perfusion
  • Respiratory failure
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23
Q

What is the typical presentation of bronchiectasis?

A

Dilation of airways, usually involving lower lobes, right side more often than left, with airways almost extending to the pleural surface.

Microscopic appearance depends upon stage, inflammatory infiltrate, and tissue destruction.

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24
Q

What are common symptoms of bronchiectasis?

A
  • Dyspnea
  • Chronic cough (dry or with large amounts of purulent sputum production)
  • Hemoptysis

Signs include clubbing of the fingers, hypoxemia, and hypercapnia.

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25
What do chest radiographs of bronchiectasis typically show?
Parallel lines in peripheral lung fields, representing nontapering thickened bronchial walls. ## Footnote This finding is indicative of bronchial wall thickening.
26
What are common complications of bronchiectasis?
* Recurrent infections and microbial resistance to antibiotics * Hemoptysis, potentially life-threatening hemorrhage ## Footnote Rare complications include pulmonary hypertension, abscess formation, and amyloidosis.
27
What are the general characteristics of restrictive lung diseases?
Includes acute (e.g., ARDS) and chronic (e.g., idiopathic pulmonary fibrosis) conditions. ## Footnote Other examples include sarcoidosis and pneumoconioses.
28
What is the difference between extrapulmonary and intrapulmonary restrictive lung diseases?
* Extrapulmonary: obesity, chest deformities, kyphoscoliosis * Intrapulmonary: primary or secondary causes, acute or chronic conditions ## Footnote Intrapulmonary diseases can include up to 200 different disorders.
29
What characterizes the initial phase of pathogenesis for restrictive lung diseases?
Predominance of inflammation. ## Footnote This phase is crucial for the development of subsequent fibrosis.
30
What characterizes the late phase of pathogenesis for restrictive lung diseases?
Predominance of fibrosis. ## Footnote This phase leads to reduced lung function and gas exchange.
31
What defines acute restrictive lung disease?
Disease developing over a short time (minutes to days) secondary to a major systemic insult (e.g., sepsis, shock). ## Footnote It is characterized by diffuse pulmonary infiltrates and hypoxemic respiratory failure.
32
What is the clinical term for acute restrictive lung disease?
Acute respiratory distress syndrome (ARDS). ## Footnote The pathologic term is diffuse alveolar damage.
33
What are the stages of diffuse alveolar damage?
* Exudative stage * Proliferative stage * Fibrosis stage ## Footnote Each stage represents a different phase of lung injury and healing.
34
What are the main causes of diffuse alveolar damage?
* Severe pulmonary infection * Aspiration * Sepsis * Severe trauma with shock ## Footnote Other causes include acute pancreatitis, cardiopulmonary bypass, fat emboli, and viral infections.
35
What are the clinical symptoms of acute restrictive lung disease?
* Severe dyspnea * Pink frothy sputum within 72 hours of exposure * Diffuse crackles * Hypoxemia ## Footnote High mortality rate; survivors may develop chronic restrictive lung disease.
36
What characterizes chronic restrictive lung disease?
Chronic diffuse lung injury with inflammation and fibrosis, leading to impaired gas exchange. ## Footnote It is associated with low diffusing capacity of lung for carbon monoxide (DLCO).
37
What is the ground-glass appearance in interstitial lung disease indicative of?
Exudation to alveoli. ## Footnote It may resemble lung edema in left ventricular failure.
38
What is the late (progressive) phase of interstitial lung disease characterized by?
Honeycomb lung appearance due to prominent fibrosis of the alveolar septae. ## Footnote It results in a cobblestone appearance of the pleural surface.
39
What are the seven histological categories of idiopathic interstitial pneumonia?
* Usual interstitial pneumonia (UIP) * Nonspecific interstitial pneumonia (NSIP) * Organising pneumonia (OP) * Diffuse alveolar damage (DAD) * Desquamative interstitial pneumonia (DIP) * Respiratory bronchiolitis (RB) * Lymphocytic interstitial pneumonia (LIP) ## Footnote Each category has distinct histological features.
40
What are common symptoms of interstitial lung disease?
* Insidious onset of dyspnea on exertion * Dry nonproductive cough * Tachypnea ## Footnote Signs may include fine bibasilar end-inspiratory crackles and clubbing of fingers.
41
What is the diagnosis for interstitial lung disease typically confirmed by?
Lung biopsy. ## Footnote Chest radiograph may show a reticular or reticulonodular pattern with diminished lung volumes.
42
What are pathogenetic implications for therapy in interstitial lung disease?
* Immunosuppressive therapy (Corticosteroids, Azathioprine, Cyclophosphamide, Colchicine) * Biological therapy (monoclonal antibodies) * Receptor tyrosine kinase inhibitors * Long term home oxygen therapy (LTOT) * Lung transplantation ## Footnote These therapies aim to manage symptoms and slow disease progression.
43
What defines obstructive lung diseases?
Impaired ability of air to leave the alveoli during expiration, clinically defined by decreased FEV1/FVC ratio. ## Footnote The residual volume (RV) and functional residual capacity (FRC) are increased, while total lung capacity remains normal.
44
What are common examples of obstructive lung diseases?
* Bronchial Asthma * Chronic Obstructive Pulmonary Disease * Chronic Bronchitis * Emphysema * Bronchiectasis ## Footnote Each of these diseases is characterized by specific pathophysiological mechanisms leading to obstructive impairment.
45
What defines restrictive lung diseases?
Characterized by reduced FEV1/FVC ratio, with reduced residual volume (RV) and functional residual capacity (FRC), and reduced total lung capacity. ## Footnote The physiological changes in restrictive diseases differ significantly from obstructive diseases.
46
What is the definition of bronchial asthma?
Episodic airway obstruction and airway hyperresponsiveness usually accompanied by airway inflammation. ## Footnote In many cases, the airway obstruction is reversible, but may become irreversible in some patients.
47
What is the heritable predisposition for bronchial asthma?
25–80% degree of heritability suggested by family and twin studies. ## Footnote Genetic studies indicate complex polygenic inheritance complicated by environmental exposures.
48
What are the symptoms of atopy?
* Allergic rhinitis * Allergic conjunctivitis * Eczema * Hay fever * Allergies (food, contact, inhalation) * Positive skin tests (prick tests) ## Footnote Atopy refers to a genetic tendency to develop allergic diseases.
49
What are common triggers of bronchoconstriction?
* Allergens (e.g., animal waste, dust mites) * Upper airway infections * Inhalatory irritants * Anxiety * Cold air * Physical activity * Gastroesophageal reflux * Drugs (e.g., aspirin) * Preservatives in food ## Footnote Frequently, the trigger remains unknown.
50
Fill in the blank: The older classification of asthma is categorized into _______ and _______.
[Extrinsic], [Intrinsic]
51
What are the newer classifications of asthma?
* Allergic asthma (Atopic) * Nonallergic asthma (Nonatopic) * Drug-induced asthma * Occupational asthma * Cardiac asthma ## Footnote This classification reflects a better understanding of asthma's diverse triggers and mechanisms.
52
What is the mechanism of allergic asthma?
Type I hypersensitivity reaction. ## Footnote Common causes include pollens, dust, and drugs.
53
What distinguishes nonallergic asthma from allergic asthma?
Occurs more frequently in adults, with normal IgE levels and not involving type I hypersensitivity. ## Footnote Common triggers include exercise, cold air, and viral infections.
54
What are the two stages of asthma?
* Early Stage: Mediators promoting bronchoconstriction (e.g., leukotrienes, histamine) * Late Stage: Release of enzymes by eosinophils and neutrophils ## Footnote The late phase leads to morphologic changes in asthma.
55
What are the mechanisms leading to acute and chronic airway obstruction?
* Airway hyperresponsiveness * Inflammation * Structural changes (smooth muscle hypertrophy, collagen deposition, edema) ## Footnote These mechanisms contribute to the severity and persistence of asthma symptoms.
56
What is airway hyperresponsiveness?
A hallmark of asthma characterized by excessive narrowing of the airways in response to non-trigger agents. ## Footnote It can be functional or structural in nature.
57
What are the morphological features of asthma?
* Hyperinflated lungs * Mucous plugging of airways * Hypertrophy of smooth muscle * Eosinophilic infiltrate ## Footnote Microscopic features include increased collagen and mucus glands.
58
What are Charcot-Leyden crystals?
Composed of major basic protein, found in the context of eosinophilic infiltrate in asthma. ## Footnote Their presence is indicative of eosinophilic inflammation.
59
What is the significance of mucous plugging in asthma?
Characteristic feature of status asthmaticus, leading to airway obstruction. ## Footnote It may contribute to respiratory distress and hypoxemia.
60
What is the impact of structural changes in the airway wall in asthma?
Associated with disease severity and duration, including smooth muscle hypertrophy and subepithelial collagen deposition. ## Footnote These changes can contribute to chronic airflow limitation.
61
What defines obstructive lung diseases?
Impaired ability of air to leave the alveoli during expiration, clinically defined by decreased FEV1/FVC ratio. ## Footnote The residual volume (RV) and functional residual capacity (FRC) are increased, while total lung capacity remains normal.
62
What are common examples of obstructive lung diseases?
* Bronchial Asthma * Chronic Obstructive Pulmonary Disease * Chronic Bronchitis * Emphysema * Bronchiectasis ## Footnote Each of these diseases is characterized by specific pathophysiological mechanisms leading to obstructive impairment.
63
What defines restrictive lung diseases?
Characterized by reduced FEV1/FVC ratio, with reduced residual volume (RV) and functional residual capacity (FRC), and reduced total lung capacity. ## Footnote The physiological changes in restrictive diseases differ significantly from obstructive diseases.
64
What is the definition of bronchial asthma?
Episodic airway obstruction and airway hyperresponsiveness usually accompanied by airway inflammation. ## Footnote In many cases, the airway obstruction is reversible, but may become irreversible in some patients.
65
What is the heritable predisposition for bronchial asthma?
25–80% degree of heritability suggested by family and twin studies. ## Footnote Genetic studies indicate complex polygenic inheritance complicated by environmental exposures.
66
What are the symptoms of atopy?
* Allergic rhinitis * Allergic conjunctivitis * Eczema * Hay fever * Allergies (food, contact, inhalation) * Positive skin tests (prick tests) ## Footnote Atopy refers to a genetic tendency to develop allergic diseases.
67
What are common triggers of bronchoconstriction?
* Allergens (e.g., animal waste, dust mites) * Upper airway infections * Inhalatory irritants * Anxiety * Cold air * Physical activity * Gastroesophageal reflux * Drugs (e.g., aspirin) * Preservatives in food ## Footnote Frequently, the trigger remains unknown.
68
Fill in the blank: The older classification of asthma is categorized into _______ and _______.
[Extrinsic], [Intrinsic]
69
What are the newer classifications of asthma?
* Allergic asthma (Atopic) * Nonallergic asthma (Nonatopic) * Drug-induced asthma * Occupational asthma * Cardiac asthma ## Footnote This classification reflects a better understanding of asthma's diverse triggers and mechanisms.
70
What is the mechanism of allergic asthma?
Type I hypersensitivity reaction. ## Footnote Common causes include pollens, dust, and drugs.
71
What distinguishes nonallergic asthma from allergic asthma?
Occurs more frequently in adults, with normal IgE levels and not involving type I hypersensitivity. ## Footnote Common triggers include exercise, cold air, and viral infections.
72
What are the two stages of asthma?
* Early Stage: Mediators promoting bronchoconstriction (e.g., leukotrienes, histamine) * Late Stage: Release of enzymes by eosinophils and neutrophils ## Footnote The late phase leads to morphologic changes in asthma.
73
What are the mechanisms leading to acute and chronic airway obstruction?
* Airway hyperresponsiveness * Inflammation * Structural changes (smooth muscle hypertrophy, collagen deposition, edema) ## Footnote These mechanisms contribute to the severity and persistence of asthma symptoms.
74
What is airway hyperresponsiveness?
A hallmark of asthma characterized by excessive narrowing of the airways in response to non-trigger agents. ## Footnote It can be functional or structural in nature.
75
What are the morphological features of asthma?
* Hyperinflated lungs * Mucous plugging of airways * Hypertrophy of smooth muscle * Eosinophilic infiltrate ## Footnote Microscopic features include increased collagen and mucus glands.
76
What are Charcot-Leyden crystals?
Composed of major basic protein, found in the context of eosinophilic infiltrate in asthma. ## Footnote Their presence is indicative of eosinophilic inflammation.
77
What is the significance of mucous plugging in asthma?
Characteristic feature of status asthmaticus, leading to airway obstruction. ## Footnote It may contribute to respiratory distress and hypoxemia.
78
What is the impact of structural changes in the airway wall in asthma?
Associated with disease severity and duration, including smooth muscle hypertrophy and subepithelial collagen deposition. ## Footnote These changes can contribute to chronic airflow limitation.
79
What is the classic triad of clinical symptoms in asthma?
Wheezing, Dyspnea, Cough (night-time) ## Footnote Symptoms are worse or only present at night due to the physiologic drop in cortisol secretion.
80
What are the key findings in spirometry for early asthma?
Findings are normal ## Footnote Late asthma shows low peak expiratory flow, decreased FEV1/FVC, and increased residual volume.
81
What characterizes the arterial blood gases during an exacerbation of asthma?
CO2 is low secondary to hyperventilation ## Footnote Rising CO2 indicates respiratory failure, which is a life-threatening asthmatic attack.
82
What is the definition of COPD according to GOLD?
Preventable and treatable disease with airflow limitation that is not fully reversible ## Footnote The airflow limitation is usually progressive and associated with an abnormal inflammatory response to noxious particles or gases.
83
What are the major risk factors for COPD?
* Susceptibility genes (e.g., alpha-1 antitrypsin deficiency) * Tobacco smoke (active and passive) * Indoor air pollution * Occupational dusts * Outdoor air pollution ## Footnote Smoking is the single most important risk factor for COPD.
84
What are the four interrelated events in the pathogenesis of COPD?
* Inflammatory and immune cell recruitment * Proteinases damage the extracellular matrix * Structural cell death through oxidant-induced damage * Disordered repair of elastin (emphysema) ## Footnote These events contribute to the progressive nature of COPD.
85
What defines chronic bronchitis?
Productive cough for at least 3 months in 2 consecutive years ## Footnote Pathogenesis involves cigarette smoking leading to increased mucus production and hyperplasia of mucous-secreting glands.
86
What are the types of emphysema?
* Centriacinar emphysema (smoking) * Panacinar emphysema (α1-antitrypsin deficiency) ## Footnote Centriacinar affects respiratory bronchioles in upper lobes, while panacinar affects alveoli and lower lobes.
87
What is the spirometry finding characteristic of obstructive ventilatory impairment?
FEV1/FVC < 0.7 ## Footnote FVC may be normal or only slightly decreased, while FEV1 is reduced.
88
What are common complications of COPD?
* Pulmonary hypertension * Cor pulmonale * Mismatched ventilation-perfusion * Respiratory failure ## Footnote These complications arise due to the severe effects of COPD on lung function.
89
What is bronchiectasis?
An irreversible airway dilation that can be focal or diffuse ## Footnote It can be categorized as cylindrical, varicose, or cystic.
90
What are the two components required for the pathogenesis of bronchiectasis?
* Infection * Obstruction ## Footnote Each component can occur first and initiate the disease process.
91
What are the symptoms of bronchiectasis?
* Dyspnea * Chronic cough (dry or with purulent sputum) * Hemoptysis ## Footnote Signs may include clubbing of fingers and hypoxemia.
92
What defines restrictive lung disease?
Characterized by reduced lung volume and impaired ventilation ## Footnote Includes acute conditions like ARDS and chronic conditions such as idiopathic pulmonary fibrosis.
93
What is the pathogenesis of acute restrictive lung disease?
Develops over a short time period due to a major systemic insult ## Footnote Results in hypoxemic respiratory failure not attributable to left-sided heart failure.
94
What is the primary consequence of damage to the epithelium or endothelium in ARDS?
Increased vascular permeability allowing protein to enter the alveoli ## Footnote This leads to the formation of hyaline membranes.
95
What occurs during the exudative stage of diffuse alveolar damage?
Formation of hyaline membranes from protein and necrotic cells layering out on the alveolar septae ## Footnote This is the initial response to injury.
96
What happens during the proliferative stage of diffuse alveolar damage?
Type II pneumocytes undergo hyperplasia ## Footnote This is a response to the damage in the alveoli.
97
List the four main causes of diffuse alveolar damage.
* Severe pulmonary infection * Aspiration * Sepsis * Severe trauma with shock ## Footnote Other causes include acute pancreatitis, cardiopulmonary bypass, fat emboli, and viral infections.
98
What are the clinical symptoms of acute respiratory distress syndrome (ARDS)?
Severe dyspnea and pink frothy sputum within 72 hours of exposure to an inciting agent ## Footnote Symptoms indicate acute lung injury.
99
What signs are commonly observed in ARDS?
Diffuse crackles, hypoxemia, and diffuse alveolar infiltrates seen on chest radiograph ## Footnote These signs help in the diagnosis of ARDS.
100
What is the mortality rate associated with ARDS?
High mortality rate ## Footnote This indicates the severity of the condition.
101
What might patients develop if they survive ARDS?
Fibrosis leading to chronic restrictive lung disease and pulmonary hypertension ## Footnote This can significantly affect long-term health.
102
What characterizes chronic restrictive lung disease?
* Chronic diffuse lung injury * Inflammation and fibrosis * Impaired gas exchange * Obstructive ventilatory impairments ## Footnote Low DLCO is a key indicator.
103
What is the initial phase of interstitial lung disease characterized by?
Inflammation – Alveolitis ## Footnote This phase is crucial for the progression of the disease.
104
What does a ground-glass appearance on X-ray indicate?
Exudation to alveoli ## Footnote It may resemble lung edema in left ventricular failure.
105
What is the late (progressive) phase of lung disease often referred to as?
Honeycomb lung ## Footnote This phase is characterized by prominent fibrosis of the alveolar septae.
106
What are the histological categories of idiopathic interstitial pneumonia?
* Usual interstitial pneumonia (UIP) * Nonspecific interstitial pneumonia (NSIP) * Organising pneumonia (OP) * Diffuse alveolar damage (DAD) * Desquamative interstitial pneumonia (DIP) * Respiratory bronchiolitis (RB) * Lymphocytic interstitial pneumonia (LIP) ## Footnote These categories help classify the types of lung injury.
107
What is a common symptom of interstitial lung disease?
Insidious onset of dyspnea on exertion ## Footnote This symptom often progresses as the disease advances.
108
What diagnostic procedure is crucial for confirming interstitial lung disease?
Lung biopsy ## Footnote This procedure provides definitive histological evidence.
109
What therapies are considered for the treatment of interstitial lung disease?
* Immunosuppressive therapy (Corticosteroids, Azathioprine, Cyclophosphamide, Colchicine) * Biological therapy (monoclonal antibodies) * Long term home oxygen therapy (LTOT) * Lung transplantation ## Footnote These therapies target inflammation and fibrosis.

BMS 250 test 2 (11 decks)

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