name: Chronic_Obstructive_Pulmonary_Disease
creation_date: '2025-12-04T16:57:31Z'
updated_date: '2026-02-17T21:53:14Z'
category: Complex
parents:
- Respiratory Disease
- Smoking-Related Disease
has_subtypes:
- name: Chronic Bronchitis
description: Inflammation of the bronchial tubes leading to increased mucus
production and chronic cough.
evidence:
- reference: PMID:23204254
supports: SUPPORT
snippet: Chronic bronchitis (CB) is a common but variable phenomenon in
chronic obstructive pulmonary disease (COPD).
explanation: The article clearly states that Chronic Bronchitis (CB) is a
subtype of COPD, characterized by inflammation of the bronchial tubes
leading to increased mucus production and chronic cough.
- reference: PMID:27264777
supports: SUPPORT
snippet: Chronic obstructive pulmonary disease (COPD) is an umbrella term
that covers many clinical subtypes with clearly different pulmonary and
extra-pulmonary characteristics.
explanation: The article supports that COPD has multiple subtypes with
differing characteristics, encompassing conditions like Chronic
Bronchitis.
- reference: PMID:22753831
supports: SUPPORT
snippet: 'Chronic cough and sputum production: a clinical COPD phenotype?'
explanation: The article discusses the phenotype of COPD which includes
chronic cough and sputum production, indicative of conditions like Chronic
Bronchitis.
- name: Emphysema
description: Damage to the alveoli resulting in shortness of breath and
reduced surface area for gas exchange.
evidence:
- reference: PMID:33926668
supports: SUPPORT
snippet: 'Chronic obstructive pulmonary usually is subcategorized into 2 groups:
chronic bronchitis and emphysema.'
explanation: This reference reiterates the point that emphysema is a
recognized subtype of COPD.
- reference: PMID:21178627
supports: SUPPORT
snippet: Latest studies further support the association of emphysema and
COPD with coal dust exposure.
explanation: This confirms that emphysema is considered a subtype of COPD,
further supporting the statement.
prevalence:
- population: Global
percentage: 11.7
evidence:
- reference: PMID:35261410
supports: NO_EVIDENCE
snippet: 'The estimated pooled prevalence of COPD was 11.1% (95% confidence interval,
CI: 7.4-14.8%), using the Global Initiative for Chronic Obstructive Lung Disease
fixed criteria and 8.0% (95% CI: 5.6-10.4%) using the lower limit of normal
criteria.'
explanation: The study provides prevalence data for specific regions (e.g.,
South Asia) but does not mention a global prevalence rate of 11.7%.
- reference: PMID:37461046
supports: NO_EVIDENCE
snippet: Though disease burden of silicosis has been on a decline in general
from 1990 to 2019, which shows a promising prospect but cannot be ignored.
explanation: This study focuses on the global incidence, prevalence, and
disease burden of silicosis, not COPD.
progression:
- phase: Onset
notes: Typically begins in individuals over the age of 40.
evidence:
- reference: PMID:26154786
supports: PARTIAL
snippet: Among 657 persons who had an FEV1 of less than 80% of the predicted
value before 40 years of age, 174 (26%) had COPD after 22 years of
observation, whereas among 2207 persons who had a baseline FEV1 of at
least 80% of the predicted value before 40 years of age, 158 (7%) had COPD
after 22 years of observation.
explanation: The literature suggests that COPD can develop in individuals
with low FEV1 before the age of 40. While this supports the idea that COPD
typically begins in individuals over 40, it also indicates that it can
start earlier in some cases.
- reference: PMID:19934351
supports: SUPPORT
snippet: There is growing evidence of higher prevalence of chronic
obstructive pulmonary disease (COPD) in the elderly. Age-associated
changes in the structure and function of the lung may increase a
pathogenetic susceptibility to COPD.
explanation: This reference supports the statement that COPD typically
begins in individuals over the age of 40, particularly due to
age-associated changes in lung structure and function.
pathophysiology:
- name: Airflow Limitation
description: Obstruction of airflow due to inflammation, mucus build-up, and
remodeling of the airways.
cell_types:
- preferred_term: Epithelial Cell
term:
id: CL:0000066
label: epithelial cell
biological_processes:
- preferred_term: inflammatory response
term:
id: GO:0006954
label: inflammatory response
- preferred_term: airway remodeling
description: Structural changes in airway architecture
locations:
- preferred_term: bronchus
term:
id: UBERON:0002185
label: bronchus
- preferred_term: small airway
description: Terminal and respiratory bronchioles
downstream:
- target: Progressive Respiratory Impairment
description: Chronic airway inflammation and remodeling lead to progressive
airflow obstruction and respiratory decline.
evidence:
- reference: PMID:39046133
supports: SUPPORT
snippet: Chronic exposure to smoking and noxious particles or gases
induces inflammation and remodeling, leading to airway obstruction and
SAD, eventually resulting in complete airway loss.
explanation: This 2024 review establishes that chronic inflammation and
remodeling cause irreversible airflow limitation and progressive
respiratory decline in COPD.
evidence:
- reference: PMID:23204254
supports: SUPPORT
snippet: CB is caused by overproduction and hypersecretion of mucus by
goblet cells, which leads to worsening airflow obstruction by luminal
obstruction of small airways, epithelial remodeling, and alteration of
airway surface tension predisposing to collapse
explanation: This study describes how mucus build-up and epithelial
remodeling lead to airflow obstruction in COPD.
- reference: PMID:36108172
supports: PARTIAL
snippet: Phenotypic alterations in the lung epithelium have been widely
implicated in chronic obstructive pulmonary disease (COPD) pathogenesis,
but the precise mechanisms orchestrating this persistent inflammatory
process remain unknown.
explanation: This study notes the involvement of epithelial cells in COPD
but states that mechanisms remain unknown, partially supporting the role
of epithelial cells in airflow obstruction.
- reference: PMID:38625125
supports: SUPPORT
snippet: Chronic exposure to environmental hazards causes airway epithelial
dysfunction, primarily impaired physical barriers, immune dysfunction, and
repair or regeneration. Impairment of airway epithelial function
subsequently leads to exaggerated airway inflammation and remodeling, the
main features of chronic obstructive pulmonary disease (COPD).
explanation: This study supports the statement by highlighting the role of
epithelial dysfunction, inflammation, and remodeling in COPD
pathophysiology.
- name: Chronic Inflammation
description: Persistent irritation from inhaled substances like cigarette
smoke leads to airway and alveolar inflammation.
cell_types:
- preferred_term: Neutrophil
term:
id: CL:0000775
label: neutrophil
- preferred_term: Macrophage
term:
id: CL:0000235
label: macrophage
- preferred_term: T-lymphocyte
term:
id: CL:0000084
label: T cell
biological_processes:
- preferred_term: inflammatory response
term:
id: GO:0006954
label: inflammatory response
- preferred_term: neutrophil degranulation
term:
id: GO:0043312
label: neutrophil degranulation
locations:
- preferred_term: bronchus
term:
id: UBERON:0002185
label: bronchus
- preferred_term: alveolus of lung
term:
id: UBERON:0002299
label: alveolus of lung
evidence:
- reference: PMID:17305517
supports: SUPPORT
snippet: Neutrophils and macrophages have been implicated in this process;
they release proteolytic enzymes and generate oxidants, which cause tissue
damage, as well as cytokines and chemokines, which can potentiate
inflammation and trigger an immune response.
explanation: The literature describes the involvement of neutrophils,
macrophages, and T-lymphocytes in the inflammatory process associated with
COPD, supporting the notion of persistent irritation and chronic
inflammation.
- reference: PMID:24507838
supports: SUPPORT
snippet: This inflammation is characterized by increased numbers of alveolar
macrophages, neutrophils, and T lymphocytes, which are recruited from the
circulation.
explanation: This article further substantiates the involvement of these
cell types (neutrophils, macrophages, and T-lymphocytes) in the
pathophysiology of COPD, linking them to chronic inflammation.
- reference: PMID:38035712
supports: SUPPORT
snippet: In this study, we found that neutrophilic phenotype (NP, 58.0%) was
the most common airway inflammation phenotype in patients with COPD,
followed by mixed granulocytic phenotype (MGP, 32.6%).
explanation: The study indicates that neutrophils are predominant in COPD,
supporting the statement about chronic inflammation.
- reference: PMID:38891820
supports: SUPPORT
snippet: Recent multiomics-based evidence suggests that the plasticity of
alveolar macrophages contributes to the onset and progression of COPD
through the coordinated modulation of numerous transcription factors.
explanation: The article highlights the role of macrophages in the
pathogenesis and progression of COPD, thus supporting the statement.
- reference: PMID:11993785
supports: PARTIAL
snippet: The characteristic changes in the central airways include
inflammatory cellular infiltration into the airway wall and mucous gland
enlargement.
explanation: This reference provides a broader overview of the pathological
changes in COPD, mentioning inflammatory cells but not specifically
detailing the involvement of neutrophils, macrophages, and T-lymphocytes.
- name: Airway Remodeling
description: Structural changes in the airway due to chronic inflammation,
including fibrosis and increased airway thickness.
cell_types:
- preferred_term: Smooth Muscle Cell
term:
id: CL:0000192
label: smooth muscle cell
biological_processes:
- preferred_term: extracellular matrix organization
term:
id: GO:0030198
label: extracellular matrix organization
- preferred_term: fibrosis
description: Excessive deposition of connective tissue
locations:
- preferred_term: bronchus
term:
id: UBERON:0002185
label: bronchus
- preferred_term: small airway
description: Terminal and respiratory bronchioles
evidence:
- reference: PMID:20500603
supports: SUPPORT
snippet: Moreover, airway remodelling occurs not only in asthma but also in
several pulmonary disorders such as chronic obstructive pulmonary disease,
idiopathic pulmonary fibrosis and systemic sclerosis.
explanation: The statement aligns with the mentioned literature which notes
airway remodeling as part of chronic obstructive pulmonary disease.
- reference: PMID:30257694
supports: SUPPORT
snippet: Multiple dysfunctions of ASM contribute to modulating airway
responses to stimuli, remodeling, and fibrosis, as well as influence the
compliance of lungs.
explanation: The statement is supported as this literature highlights the
role of airway smooth muscle cells in airway remodeling and fibrosis in
COPD.
- reference: PMID:15347849
supports: SUPPORT
snippet: Increases in airway smooth muscle mass occur in large airways of
severe asthmatics and in small airways of patients with COPD.
explanation: The literature supports the statement by confirming the
involvement of smooth muscle cells and structural changes in the airways
in COPD.
- name: Alveolar Destruction
description: Breakdown of alveolar walls, leading to reduced surface area for
gas exchange and loss of lung elasticity.
cell_types:
- preferred_term: Alveolar Macrophage
term:
id: CL:0000583
label: alveolar macrophage
biological_processes:
- preferred_term: proteolysis
term:
id: GO:0006508
label: proteolysis
- preferred_term: extracellular matrix organization
term:
id: GO:0030198
label: extracellular matrix organization
locations:
- preferred_term: alveolus of lung
term:
id: UBERON:0002299
label: alveolus of lung
- preferred_term: lung parenchyma
term:
id: UBERON:0008946
label: lung parenchyma
evidence:
- reference: PMID:11993785
supports: PARTIAL
snippet: In the lung parenchyma, emphysema defined as alveolar destruction
and airspace enlargement is present.
explanation: While the reference supports alveolar destruction as part of
COPD's pathophysiology, it does not mention alveolar macrophages
specifically.
- reference: PMID:29433833
supports: PARTIAL
snippet: In inflammatory lung diseases such as chronic obstructive pulmonary
disease (COPD), despite their increased numbers, macrophages demonstrate
significantly reduced phagocytic capacity of bacteria and apoptotic cells.
explanation: The macrophages' role in the pathophysiology of COPD is
discussed, focusing on their reduced phagocytic capacity rather than
direct alveolar destruction.
- reference: PMID:32493486
supports: PARTIAL
snippet: External insults like smoke and pollution can disturb surfactant
homeostasis and result in either surfactant insufficiency or accumulation.
But disruption of surfactant homeostasis is also observed in many chronic
adult diseases, including chronic obstructive pulmonary disease (COPD).
explanation: The role of alveolar macrophages (responsible for the
degradation of surfactant) in the development of COPD is mentioned, but no
direct link to alveolar destruction.
- reference: PMID:24707174
supports: PARTIAL
snippet: 'There are eight types of EMPs which are defined by the presence of different
endothelial markers on the cell membrane: vascular endothelial-cadherin; platelet
endothelial cell adhesion molecule; melanoma cell adhesion molecule; E-selectin;
CD51; CD105; von Willebrand factor; and CD143 EMPs.'
explanation: The reference discusses endothelial injury and microparticles
in COPD, which may indirectly relate to alveolar destruction, but does not
directly address it or the role of alveolar macrophages.
- name: Oxidative Stress and Mitochondrial Dysfunction
description: Cigarette smoke and pollutants trigger mitochondrial ROS
production, impaired mitophagy, and reduced antioxidant defenses, amplifying
inflammation.
cell_types:
- preferred_term: airway epithelial cell
term:
id: CL:0002368
label: respiratory tract epithelial cell
- preferred_term: Alveolar Macrophage
term:
id: CL:0000583
label: alveolar macrophage
biological_processes:
- preferred_term: response to oxidative stress
term:
id: GO:0006979
label: response to oxidative stress
- preferred_term: mitochondrion organization
term:
id: GO:0007005
label: mitochondrion organization
- preferred_term: mitophagy
term:
id: GO:0000422
label: mitophagy
locations:
- preferred_term: bronchus
term:
id: UBERON:0002185
label: bronchus
- preferred_term: alveolus of lung
term:
id: UBERON:0002299
label: alveolus of lung
notes: Reduced Nrf2 and SIRT1 activity diminishes antioxidant capacity;
mitochondrial ROS activates NLRP3 inflammasome.
- name: Mucus Hypersecretion
description: Upregulation of MUC5AC and MUC5B, goblet cell hyperplasia, and
impaired mucociliary clearance contribute to mucus plugging.
cell_types:
- preferred_term: goblet cell
term:
id: CL:0000160
label: goblet cell
- preferred_term: club cell
term:
id: CL:0000158
label: club cell
biological_processes:
- preferred_term: mucus secretion
term:
id: GO:0070254
label: mucus secretion
- preferred_term: cilium movement
term:
id: GO:0003341
label: cilium movement
locations:
- preferred_term: bronchus
term:
id: UBERON:0002185
label: bronchus
- preferred_term: small airway
description: Terminal and respiratory bronchioles
notes: MUC5AC/MUC5B overexpression and club-to-goblet transdifferentiation
impair airway clearance.
- name: NLRP3 Inflammasome Activation
description: Mitochondrial ROS and particulate exposures activate NLRP3
inflammasome, leading to caspase-1 activation and IL-1β/IL-18 release.
cell_types:
- preferred_term: Macrophage
term:
id: CL:0000235
label: macrophage
- preferred_term: airway epithelial cell
term:
id: CL:0002368
label: respiratory tract epithelial cell
biological_processes:
- preferred_term: NLRP3 inflammasome complex assembly
term:
id: GO:0072559
label: NLRP3 inflammasome complex assembly
- preferred_term: inflammatory response
term:
id: GO:0006954
label: inflammatory response
locations:
- preferred_term: bronchus
term:
id: UBERON:0002185
label: bronchus
- preferred_term: alveolus of lung
term:
id: UBERON:0002299
label: alveolus of lung
notes: PM2.5 and cigarette smoke synergize to activate NLRP3/caspase-1
signaling.
- name: Cellular Senescence
description: Senescent epithelial, fibroblast, and immune cells exhibit
senescence-associated secretory phenotype (SASP), promoting chronic
inflammation and remodeling.
cell_types:
- preferred_term: airway epithelial cell
term:
id: CL:0002368
label: respiratory tract epithelial cell
- preferred_term: fibroblast
term:
id: CL:0000057
label: fibroblast
biological_processes:
- preferred_term: cellular senescence
term:
id: GO:0090398
label: cellular senescence
- preferred_term: inflammatory response
term:
id: GO:0006954
label: inflammatory response
locations:
- preferred_term: lung
term:
id: UBERON:0002048
label: lung
notes: SASP factors include IL-6, CXCL8, and MMPs; senolytic therapies are
under investigation.
phenotypes:
- category: Respiratory
name: Dyspnea
frequency: VERY_FREQUENT
diagnostic: true
evidence:
- reference: PMID:28277858
supports: SUPPORT
snippet: Indeed, it is an important symptom in chronic obstructive pulmonary
disease (COPD), where it is associated with limited physical activity,
increased anxiety and depression, decreased health-related quality of life
(HRQoL), and reduced survival.
explanation: The literature supports that dyspnea is a common symptom in
COPD and is frequently observed in patients, confirming its categorization
as a respiratory phenotype with diagnostic importance.
- reference: PMID:35698999
supports: SUPPORT
snippet: Dyspnoea and pain are symptoms of chronic obstructive pulmonary
disease (COPD)... The pooled prevalence of pain and dyspnoea was 44% (95%
confidence interval (CI) 35%-52%) and 91% (95% CI 87%-94%) respectively.
explanation: This study highlights the high prevalence of dyspnea in
patients with COPD, further supporting its status as a very frequent
respiratory phenotype.
- reference: PMID:34972922
supports: SUPPORT
snippet: Up to date research has shown a positive correlation between the
elevated levels of some markers of EBC such as H2O2 and 8-isoprostane and
dyspnea, while others present ambiguous results
explanation: The correlation between dyspnea and COPD is reinforced by the
positive association found with certain markers in exhaled breath
condensate.
sequelae:
- target: Exercise Intolerance
phenotype_term:
preferred_term: Dyspnea
term:
id: HP:0002094
label: Dyspnea
- category: Respiratory
name: Chronic Cough
frequency: VERY_FREQUENT
diagnostic: true
evidence:
- reference: PMID:29881269
supports: SUPPORT
snippet: Compared with patients without chronic cough, those with chronic
cough exhibited a lower forced expiratory volume in 1 second (% predicted)
and diffusing capacity of the lungs for carbon monoxide (% predicted),
more frequent AECOPD, more severe dyspnea, and worse QoL.
explanation: The study identifies chronic cough as a common and significant
phenotype in COPD patients, indicating its very frequent occurrence and
diagnostic importance.
- reference: PMID:31740261
supports: SUPPORT
snippet: COPD is now widely accepted as a heterogeneous condition with
multiple phenotypes and endotypes. This review will discuss the old and
new concepts for the different types of COPD phenotypes.
explanation: The statement mentions the heterogeneity of COPD with multiple
phenotypes, which could include phenotypes like chronic cough.
notes: Often productive of mucus
phenotype_term:
preferred_term: Chronic Cough
term:
id: HP:0034315
label: Chronic cough
- category: Respiratory
name: Sputum Production
frequency: VERY_FREQUENT
evidence:
- reference: PMID:22753831
supports: SUPPORT
snippet: 'Chronic cough and sputum production: a clinical COPD phenotype?'
explanation: The title of the article itself suggests that sputum production
is recognized as a phenotype of COPD.
- reference: PMID:23204254
supports: SUPPORT
snippet: Chronic bronchitis (CB) is a common but variable phenomenon in
chronic obstructive pulmonary disease (COPD).
explanation: Chronic bronchitis, which involves overproduction and
hypersecretion of mucus, is described as a common phenomenon in COPD,
indicating sputum production is a frequent COPD phenotype.
notes: Mucus is often difficult to expectorate
phenotype_term:
preferred_term: Sputum Production
term:
id: HP:0033709
label: Increased sputum production
- category: Respiratory
frequency: FREQUENT
name: Wheezing
notes: Due to airflow obstruction
evidence:
- reference: PMID:33302722
supports: SUPPORT
snippet: The clinical symptoms of this disease include progressive dyspnea,
cough, expectoration, and wheezing, among others.
explanation: The abstract mentions wheezing as one of the clinical symptoms
of Chronic Obstructive Pulmonary Disease (COPD).
- reference: PMID:11963614
supports: SUPPORT
snippet: Remember, all that wheezes is not asthma; therefore, providers in
this case had to determine if the patient was suffering something such as
anaphylaxis, asthma, bronchitis, pneumonia or even congestive heart
failure (CHF).
explanation: The abstract indicates that wheezing can be a symptom of
various conditions, including COPD-related bronchospasm.
- reference: PMID:2404712
supports: SUPPORT
snippet: Increased airways reactivity is present in 15 to 70 percent of
patients with chronic airflow obstruction.
explanation: The abstract discusses increased airway reactivity, which is
related to wheezing, in patients with chronic airflow obstruction,
including COPD.
phenotype_term:
preferred_term: Wheezing
term:
id: HP:0030828
label: Wheezing
- category: Respiratory
frequency: OCCASIONAL
name: Barrel Chest
notes: Due to hyperinflation of the lungs
evidence:
- reference: PMID:25159007
supports: PARTIAL
snippet: Lung hyperinflation is highly prevalent in patients with chronic
obstructive pulmonary disease and occurs across the continuum of the
disease.
explanation: The reference supports the association of lung hyperinflation
with COPD but does not specifically mention 'Barrel Chest' or its
frequency.
- reference: PMID:34972922
supports: PARTIAL
snippet: Attempts to connect the products of the analysis of the EBC with
the clinical manifestations of COPD such as dyspnea are scarce.
explanation: The reference discusses the clinical manifestations of COPD but
does not specifically mention 'Barrel Chest' or its frequency.
- reference: PMID:23204254
supports: NO_EVIDENCE
snippet: Chronic bronchitis (CB) is a common but variable phenomenon in
chronic obstructive pulmonary disease (COPD).
explanation: The reference discusses chronic bronchitis in COPD but does not
mention 'Barrel Chest' or its frequency.
- category: Respiratory
frequency: OCCASIONAL
name: Respiratory Failure
sequelae:
- target: Hypoxemia
- target: Hypercapnia
evidence:
- reference: PMID:14621114
supports: REFUTE
snippet: Respiratory failure is still an important complication of chronic
obstructive pulmonary disease (COPD) and hospitalisation with an acute
episode being a poor prognostic marker.
explanation: The reference indicates that respiratory failure is an
important and common complication of COPD, not an occasional one.
- reference: PMID:38692758
supports: REFUTE
snippet: Hypoventilation is a complication that is not uncommon in chronic
obstructive pulmonary disease and calls for both medical treatment of the
underlying disease and, frequently, noninvasive ventilation either during
exacerbations requiring hospitalization or in a chronic state in the
patient at home.
explanation: The reference suggests that hypoventilation, which can lead to
respiratory failure, is not uncommon in COPD.
phenotype_term:
preferred_term: Respiratory Failure
term:
id: HP:0002878
label: Respiratory failure
- category: Systemic
frequency: FREQUENT
name: Fatigue
evidence:
- reference: PMID:33998496
supports: SUPPORT
snippet: 'Fatigue: A neglected symptom of COPD.'
explanation: The title itself indicates that fatigue is a recognized symptom
of COPD.
- reference: PMID:31729154
supports: SUPPORT
snippet: Fatigue is an important yet ignored symptom of chronic obstructive
pulmonary disease (COPD).
explanation: This reference acknowledges fatigue as an important symptom of
COPD, supporting its frequent occurrence.
- reference: PMID:24874124
supports: SUPPORT
snippet: Symptoms in COPD do not solely arise from the degree of airflow
obstruction as exercise limitation is compounded by the specific secondary
manifestations of the disease including skeletal muscle impairment,
osteoporosis, mood disturbance, anemia, and hormonal imbalance.
explanation: While this reference does not mention fatigue explicitly, it
discusses systemic manifestations of COPD, implying the systemic nature of
the disease.
phenotype_term:
preferred_term: Fatigue
term:
id: HP:0012378
label: Fatigue
- category: Systemic
frequency: OCCASIONAL
name: Weight Loss
notes: More common in advanced disease
evidence:
- reference: PMID:12406664
supports: SUPPORT
snippet: Weight loss occurs frequently in patients with chronic obstructive
pulmonary disease (COPD).
explanation: The literature states that weight loss is a common phenomenon
in COPD patients, which supports the statement that weight loss is a
systemic issue in COPD, more common in advanced disease.
- reference: PMID:18415812
supports: SUPPORT
snippet: These include unintentional weight loss, skeletal muscle
dysfunction, an increased risk of cardiovascular disease, osteoporosis,
and depression, among others.
explanation: This reference mentions unintentional weight loss as one of the
systemic effects of COPD, supporting the statement.
- reference: PMID:36922031
supports: SUPPORT
snippet: COPD patients with psychological (high anxiety and depression) and
cachectic (underweight and osteoporotic) comorbidity have higher mortality
and exacerbate more.
explanation: The mention of cachexia (underweight) as a comorbidity in COPD
patients aligns with the statement about weight loss being more common in
advanced disease.
phenotype_term:
preferred_term: Weight loss
term:
id: HP:0001824
label: Weight loss
- category: Cardiovascular
name: Exercise Intolerance
frequency: FREQUENT
phenotype_term:
preferred_term: Exercise Intolerance
term:
id: HP:0003546
label: Exercise intolerance
- category: Respiratory
name: Hypoxemia
frequency: FREQUENT
phenotype_term:
preferred_term: Hypoxemia
term:
id: HP:0012418
label: Hypoxemia
- category: Respiratory
name: Hypercapnia
frequency: FREQUENT
phenotype_term:
preferred_term: Hypercapnia
term:
id: HP:0012416
label: Hypercapnia
biochemical:
- name: Arterial Blood Gases
presence: Altered
notes: May show hypoxemia and hypercapnia.
evidence:
- reference: PMID:21812941
supports: PARTIAL
snippet: The aim of this study was to identify predictors of hypoxemia,
hypercapnia and increased alveolar-arterial oxygen difference in COPD
patients.
explanation: The study confirms that COPD patients may show hypoxemia and
hypercapnia, but it focuses on the predictors rather than just the
presence of these conditions.
- reference: PMID:34756790
supports: SUPPORT
snippet: Respiratory acidosis with hypoxia, hypercapnia, a compensatory
metabolic response, and mild hyperfibrinolysis were probably related to
the combined effect of nitrogen compounds and the inhaled toxic products
of detonation.
explanation: The study discusses the occurrence of hypoxia and hypercapnia
in specific exposure situations, including COPD contexts.
- reference: PMID:25119324
supports: SUPPORT
snippet: The prevalence of this sampling method has grown among health
professionals, coupled with a growing demand for domiciliary oxygen
therapy in the UK, in particular for those who have chronic obstructive
pulmonary disease (COPD).
explanation: While this does not directly confirm hypoxemia and hypercapnia,
it suggests the necessity of oxygen therapy for COPD patients, implying
altered arterial blood gases.
- reference: PMID:18044093
supports: SUPPORT
snippet: Patients with COPD may show slow, progressive deteriorations in
arterial blood gases during the night, particularly during rapid eye
movement (REM) sleep. This is mainly due to hypoventilation... The
severity of gas exchanges alterations is proportional to the degree of
impairment of diurnal pulmonary function tests, particularly of partial
pressure of oxygen (PaO2) and of carbon dioxide (PaCO2) in arterial
blood...
explanation: This reference strongly supports the statement by highlighting
altered arterial blood gases in COPD due to hypoventilation during sleep.
- name: C-Reactive Protein (CRP)
presence: Elevated
context: General inflammation and exacerbations.
evidence:
- reference: PMID:23206444
supports: SUPPORT
snippet: Patients with COPD had higher serum CRP concentrations than healthy
controls (WMD 4.72 mg/l, 95% CI 2.98, 6.47).
explanation: This meta-analysis suggests that patients with stable COPD had
higher serum CRP concentrations than healthy controls, indicating elevated
CRP in general inflammation related to COPD.
- reference: PMID:24313775
supports: SUPPORT
snippet: These biomarkers include C-reactive protein, procalcitonin, and
peripheral blood eosinophil count, which are readily available.
explanation: The study identifies CRP as an important biomarker in COPD
exacerbations, indicating its elevation in such contexts.
- reference: PMID:24102428
supports: SUPPORT
snippet: Serum CRP levels were also significantly higher on D1 compared to
D7 (p < 0.001).
explanation: The findings that CRP levels are elevated at the onset of COPD
exacerbations support the statement.
- reference: PMID:26595735
supports: SUPPORT
snippet: A number of studies support the conclusion that immune dysfunction
leads to exacerbations and disease severity in COPD.
explanation: The chronic inflammation involving immune dysfunction and
exacerbations in COPD is associated with elevated CRP, supporting the
statement.
- reference: PMID:37082823
supports: SUPPORT
snippet: Levels of interleukin 6 (IL-6), high-sensitivity C-reactive protein
(hs-CRP), and granulocyte colony stimulating factor (G-CSF) were higher in
participants with OVS and COPD compared with healthy controls and
participants with OSA.
explanation: Elevated hs-CRP in COPD patients relative to healthy controls
supports the general inflammation and exacerbation context.
genetic:
- name: SERPINA1
association: Alpha-1 antitrypsin deficiency is the most common genetic cause
of COPD.
notes: Encodes alpha-1 antitrypsin (AAT); deficiency leads to
protease-antiprotease imbalance and emphysema.
evidence:
- reference: PMID:32800189
supports: SUPPORT
snippet: Alpha-1 antitrypsin deficiency (AATD) was the first genetic risk
factor for chronic obstructive pulmonary disease (COPD) described.
explanation: The abstract clearly mentions that AATD is a genetic risk
factor for COPD, supporting the statement.
- reference: PMID:35104244
supports: SUPPORT
snippet: Alpha-1 antitrypsin deficiency (AATD) is the most common genetic
cause and risk factor for chronic obstructive pulmonary disease.
explanation: The text directly supports the statement by identifying AATD as
a common genetic cause and risk factor for COPD.
- reference: PMID:36630963
supports: SUPPORT
snippet: Genetic variation in alpha-1 antitrypsin (AAT) causes AAT
deficiency (AATD) through liver aggregation-associated gain-of-toxic
pathology and/or insufficient AAT activity in the lung manifesting as
chronic obstructive pulmonary disease (COPD).
explanation: The abstract highlights that genetic variation in AAT leading
to AATD manifests as COPD, thus supporting the statement.
- name: MMP12
association: Matrix metalloproteinase-12 contributes to emphysema development.
notes: Macrophage-derived protease that degrades elastin and extracellular
matrix.
- name: NLRP3
association: Inflammasome activation contributes to chronic inflammation.
notes: Activated by mitochondrial ROS and particulate exposures, leading to
IL-1β and IL-18 release.
- name: TNF
association: Tumor necrosis factor mediates systemic and airway inflammation.
notes: Key pro-inflammatory cytokine in COPD pathogenesis.
- name: IL1B
association: Interleukin-1 beta drives inflammatory signaling.
notes: Product of NLRP3 inflammasome activation.
- name: IL6
association: Interleukin-6 contributes to systemic inflammation.
notes: Elevated in serum and associated with COPD comorbidities.
- name: NFE2L2
association: Nrf2 transcription factor regulates antioxidant defense.
notes: Reduced activity impairs response to oxidative stress in COPD.
environmental:
- name: Smoking
notes: Primary risk factor for development and progression.
evidence:
- reference: PMID:30810540
supports: SUPPORT
snippet: Although cigarette smoking is the major risk factor, only 10-20% of
smokers develop COPD.
explanation: This clearly identifies smoking as a major risk factor for COPD
development.
- reference: PMID:31759959
supports: SUPPORT
snippet: The observation that COPD is an independent risk factor for
cardiovascular disease (CVDs) comes from comparisons between smokers with
COPD and smokers without COPD.
explanation: This snippet highlights the relationship between smoking, COPD,
and other health issues, indirectly supporting smoking as a risk factor
for COPD.
- reference: PMID:28933915
supports: SUPPORT
snippet: The epithelial lining of the airway forms the first barrier against
environmental insults, such as inhaled cigarette smoke, which is the
primary risk factor for the development of chronic obstructive pulmonary
disease (COPD).
explanation: Directly states that cigarette smoke is the primary risk factor
for COPD development.
- reference: PMID:18303418
supports: SUPPORT
snippet: Approximately one-quarter of smokers can be affected by clinically
significant chronic obstructive pulmonary disease. ... Smokers may reduce
their risk of developing chronic obstructive pulmonary disease by physical
activity and increase their survival by smoking reduction.
explanation: This supports the statement by highlighting the prevalence of
COPD among smokers and the role of smoking in disease progression.
- reference: PMID:37429033
supports: SUPPORT
snippet: 'Age of Initiating Smoking: An Independent Predictor of Chronic Obstructive
Pulmonary Disease in Later Life.'
explanation: This implies that smoking is a risk factor in the development
of COPD.
exposure_term:
preferred_term: Tobacco smoking exposure
term:
id: ECTO:6000029
label: exposure to tobacco smoking
- name: Air Pollution
notes: Exposure to pollutants can exacerbate symptoms.
evidence:
- reference: PMID:33542053
supports: SUPPORT
snippet: Our findings suggest that, when considering total personal exposure
to air pollutants, mainly the gaseous pollutants affect COPD patients'
health.
explanation: This study found that exposure to various air pollutants
adversely affects the health of COPD patients, supporting the idea that
air pollution exacerbates COPD symptoms.
- reference: PMID:25673984
supports: SUPPORT
snippet: The major pathogenic factors causing disease include infection and
inflammation, protease and antiprotease imbalance, and oxidative stress
overwhelming antioxidant defenses.
explanation: This reference discusses environmental factors, including
pollutants, that contribute to oxidative stress and inflammation in COPD,
thus supporting the statement.
- reference: PMID:37068517
supports: SUPPORT
snippet: Harmful inhaled workplace exposures can contribute to the
development of chronic obstructive pulmonary disease (COPD).
explanation: This statement supports the environmental influence on COPD,
including air pollutants, as a risk factor.
- reference: PMID:16916323
supports: SUPPORT
snippet: Evidence from epidemiological studies finding consistent
associations between air pollution and various outcomes (respiratory
symptoms, reduced lung function, chronic bronchitis and mortality), has
suggested that outdoor air pollution is a contributing cause of morbidity
and mortality.
explanation: This reference directly links air pollution to exacerbation and
pathogenesis of COPD, supporting the statement.
- reference: PMID:27751401
supports: SUPPORT
snippet: We focus on the major constituents of air pollutants and their
impacts on chronic respiratory diseases.
explanation: This review highlights the detrimental effects of air pollution
on respiratory health, particularly in the discussion on chronic
respiratory diseases such as COPD.
exposure_term:
preferred_term: Air pollution exposure
term:
id: ECTO:8000036
label: exposure to air pollution
- name: Occupational Dust and Chemicals
notes: Long-term exposure increases risk.
evidence:
- reference: PMID:11964759
supports: SUPPORT
snippet: occupational exposure to dusts, chemicals and gases will be
considered an established, or supported by good evidence, risk factor for
chronic obstructive pulmonary disease
explanation: The abstract confirms that occupational exposure to dusts,
chemicals, and gases is a well-supported risk factor for chronic
obstructive pulmonary disease.
- reference: PMID:20535848
supports: SUPPORT
snippet: Lung function loss associated with occupational dust exposure in
metal smelting
explanation: This study provides evidence of lung function loss due to
occupational dust exposure, supporting the assertion that long-term
exposure to such environmental factors increases the risk of chronic
obstructive pulmonary disease.
- reference: PMID:23361196
supports: SUPPORT
snippet: Recent studies have recognized the contribution of workplace
exposures to chronic lung diseases, in particular chronic obstructive
pulmonary disease (COPD)
explanation: The abstract discusses the recognized contribution of workplace
exposures, including textile dust, to chronic obstructive pulmonary
disease.
- reference: PMID:24278358
supports: SUPPORT
snippet: Occupational inhalative exposure to bg-dust was associated with a
statistically significant decreased FEV1 and FEV1/FVC revealing airway
obstruction consistent with COPD
explanation: The meta-analysis presented indicates a significant association
between occupational exposure to inorganic dust and the development of
chronic obstructive pulmonary disease.
- reference: PMID:35409627
supports: SUPPORT
snippet: Pesticides in general and especially organophosphate and carbamate
insecticides... showed an association, and cadmium (Cd), chromium (Cr and
CrVI), arsenic (As), and diisocyanates, a possible association with COPD
explanation: The scoping review identifies several environmental substances,
including chemicals associated with occupational exposure, that have a
strong or possible association with chronic obstructive pulmonary disease.
exposure_term:
preferred_term: Occupational dust exposure
term:
id: ECTO:7000001
label: exposure to dust
treatments:
- name: Smoking Cessation
description: Stopping smoking to slow disease progression and improve
outcomes.
evidence:
- reference: PMID:25496790
supports: SUPPORT
snippet: Stopping smoking reduces the risk of developing COPD and is an
essential treatment for this inflammatory disease. Smoking cessation
decreases the prevalence of respiratory symptoms, number of
hospitalizations, and decline in FEV1, as well as exacerbation frequency
and overall mortality.
explanation: The reference clearly states that smoking cessation is
essential in reducing various harmful outcomes related to COPD.
- reference: PMID:19811377
supports: SUPPORT
snippet: Smoking cessation and lung volume reduction surgery would both
qualify as disease-modifying interventions.
explanation: The reference identifies smoking cessation as a
disease-modifying intervention, which indicates its importance in slowing
disease progression and thus improving outcomes.
- reference: PMID:11935838
supports: SUPPORT
snippet: The most important intervention is smoking cessation.
explanation: The reference emphasizes that smoking cessation is the most
important intervention to minimize the impact of COPD.
- reference: PMID:27576232
supports: SUPPORT
snippet: Smoking cessation is the only intervention shown to slow disease
progression.
explanation: The reference clearly supports the claim that smoking cessation
can slow disease progression and improve outcomes for COPD patients.
treatment_term:
preferred_term: behavioral counseling
term:
id: MAXO:0000077
label: behavioral counseling
- name: Bronchodilators
description: Medications that relax muscles of the airways to improve airflow
(e.g., beta-agonists, anticholinergics).
evidence:
- reference: PMID:29794201
supports: SUPPORT
snippet: Bronchodilator therapy can often decrease symptoms of air-flow
obstruction by relaxing airway smooth muscle (bronchodilation), decreasing
dyspnea, and improving quality of life.
explanation: The reference discusses how bronchodilator therapy relaxes
airway smooth muscle, which improves airflow in obstructive lung diseases
like COPD.
- reference: PMID:27576232
supports: SUPPORT
snippet: Long-acting beta2-agonists and long-acting muscarinic antagonists
are first-line treatments for patients with persistently symptomatic COPD
with an FEV1 of 80% or less of predicted.
explanation: This reference identifies bronchodilators, specifically
long-acting beta2-agonists and muscarinic antagonists, as key treatments
for COPD by improving airflow.
- reference: PMID:28757318
supports: SUPPORT
snippet: Combination long-acting inhaled bronchodilators are central to the
management of patients with moderate to very severe chronic obstructive
pulmonary disease.
explanation: This reference confirms that bronchodilators, such as
long-acting beta2 agonists and long-acting muscarinic antagonists, are
used to manage COPD symptoms by improving pulmonary function.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
- name: Inhaled Corticosteroids
description: Reduce airway inflammation and frequency of exacerbations.
evidence:
- reference: PMID:20102305
supports: PARTIAL
snippet: Short-term treatment with ICS improves lung function and quality of
life; in addition, several studies with longer follow-up have shown less
decline over time in quality of life, and fewer exacerbations. By
contrast, long-term studies have been unable to show substantial
improvement in the decline of lung function in COPD.
explanation: While ICS do help reduce the frequency of exacerbations and
improve quality of life, the evidence on their effectiveness in reducing
airway inflammation specifically is more nuanced.
- reference: PMID:37348121
supports: PARTIAL
snippet: Current pharmacologic strategies, including first- and second-line
therapies such as long-acting β2-agonists, long-acting muscarinic
antagonists, inhaled corticosteroids, phosphodiesterase-4 inhibitors, and
macrolides, provide relief to patients with COPD
explanation: ICS are included in the treatment strategies, and while they
help mitigate exacerbations, the snippet suggests that not all patients
experience reduced airway inflammation.
- reference: PMID:29938633
supports: SUPPORT
snippet: The major alteration has been in the section concerning treatment
with inhalation medication - now aiming at an easy stepwise up-titration
of long-acting medicine as well as a guide of how to down-titrate inhaled
corticosteroids.
explanation: The guideline update underscores the role of ICS in managing
stable COPD, highlighting their long-term use for reducing symptoms and
managing exacerbations.
- reference: PMID:30846476
supports: SUPPORT
snippet: Recent large randomised controlled trials have provided important
new information concerning the therapeutic effects of ICSs and long-acting
bronchodilators on exacerbations.
explanation: The new evidence indicates that ICS are effective in reducing
exacerbations, supporting their role in treatment.
treatment_term:
preferred_term: respiratory tract agent therapy
term:
id: MAXO:0000312
label: respiratory tract agent therapy
- name: Phosphodiesterase-4 Inhibitors
description: Reduce inflammation and relax airways.
evidence:
- reference: PMID:15699784
supports: SUPPORT
snippet: Some of the selective PDE4 inhibitors have demonstrated in vitro
and in vivo anti-inflammatory activity on cells commonly linked to airway
inflammation in COPD, such as neutrophils.
explanation: The reference indicates that selective phosphodiesterase 4
inhibitors show anti-inflammatory activity, supporting the statement about
reducing inflammation.
- reference: PMID:20649375
supports: SUPPORT
snippet: Roflumilast targets inflammatory processes in COPD, with beneficial
effects on tobacco-induced lung inflammation, lung fibrosis and
remodeling, mucociliary malfunction and oxidative stress.
explanation: Roflumilast, a PDE4 inhibitor, targets inflammatory processes,
thus supporting the statement.
- reference: PMID:34731461
supports: SUPPORT
snippet: The orally administered PDE4 inhibitor roflumilast reduces
exacerbation rates in the subgroup of chronic obstructive pulmonary
disease patients with a history of exacerbations and the presence of
chronic bronchitis, but can cause PDE4 related adverse effects due to
systemic exposure.
explanation: This reference confirms the anti-inflammatory effect of PDE4
inhibitors which aligns with the statement.
- reference: PMID:32361678
supports: SUPPORT
snippet: Protein kinases have been implicated in mediating inflammatory
signals and airway remodeling associated with reduced lung function in
chronic pulmonary disease.
explanation: This reference supports the role of PDE inhibitors,
specifically kinase inhibitors, in reducing inflammation in COPD.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
- name: Oxygen Therapy
description: Long-term oxygen use for patients with severe chronic hypoxemia.
evidence:
- reference: PMID:24461631
supports: SUPPORT
snippet: This therapeutic intervention has been shown to increase survival
in patients with chronic obstructive pulmonary disease (COPD) and
respiratory failure.
explanation: The literature supports that long-term oxygen therapy (LTOT) is
used to treat patients with COPD who have severe chronic hypoxemia.
- reference: PMID:37353334
supports: SUPPORT
snippet: Long-term oxygen therapy (LTOT) is a mainstay treatment for
patients with severe resting hypoxemia secondary to chronic respiratory
conditions including COPD.
explanation: This reference specifically mentions LTOT as a primary
treatment for patients with severe chronic hypoxemia due to COPD.
- reference: PMID:19462352
supports: SUPPORT
snippet: Only smoking cessation and long term oxygen therapy (LTOT) improve
survival in COPD.
explanation: This study confirms that LTOT is a treatment that improves
survival in patients with severe COPD and chronic hypoxemia.
treatment_term:
preferred_term: artificial respiration
term:
id: MAXO:0000503
label: artificial respiration
- name: Pulmonary Rehabilitation
description: Exercise training, education, and support to improve quality of
life and physical conditioning.
evidence:
- reference: PMID:29526182
supports: SUPPORT
snippet: PR is an effective and cost-effective therapeutic intervention that
improves physical performance ability, shortness of breath, and the
quality of life in patients with COPD.
explanation: The reference indicates that pulmonary rehabilitation (PR)
improves physical performance, shortness of breath, and quality of life in
COPD patients, aligning with the statement's description of treatments
including exercise training, education, and support.
- reference: PMID:34338012
supports: SUPPORT
snippet: Exercise improves the physiological and psychological condition of
people with chronic obstructive pulmonary disease and should be
encouraged, with referral to a pulmonary rehabilitation service if
available.
explanation: This reference supports the statement's claim by emphasizing
the importance of exercise and recommending pulmonary rehabilitation to
improve the quality of life and physical conditioning in COPD patients.
- reference: PMID:34955635
supports: SUPPORT
snippet: The combination of drug therapy with non-drug therapy such as
pulmonary rehabilitation training has demonstrated a great potential in
reducing the occurrence of complications and delaying the progression of
COPD.
explanation: This reference supports the statement by highlighting the
benefits of pulmonary rehabilitation training, specifically its potential
to improve quality of life and physical conditioning in COPD patients.
- reference: PMID:24874124
supports: SUPPORT
snippet: Pulmonary rehabilitation targets the systemic manifestations of
COPD, the causes of which include inactivity, systemic inflammation,
hypoxia and corticosteroid treatment.
explanation: This reference supports the statement by indicating that
pulmonary rehabilitation addresses systemic issues in COPD and implies
improvement in quality of life and physical conditioning.
- reference: PMID:24507849
supports: SUPPORT
snippet: The main objective of pulmonary rehabilitation is to restore muscle
function and exercise tolerance, reverse other nonrespiratory consequences
of the disease, and help patients to self-manage chronic obstructive
pulmonary disease and its exacerbations and symptoms.
explanation: This reference supports the statement by detailing the benefits
of pulmonary rehabilitation, including exercise training, education, and
support, to improve quality of life and physical conditioning.
treatment_term:
preferred_term: physical therapy
term:
id: MAXO:0000011
label: physical therapy
- name: Lung Volume Reduction Surgery
description: Surgical removal of damaged lung tissue for severe emphysema.
evidence:
- reference: PMID:22189668
supports: SUPPORT
snippet: Surgical approaches include lung transplantation and lung volume
reduction and the latter has been shown to improve exercise tolerance,
quality of life, and survival in highly selected patients with advanced
emphysema.
explanation: The literature supports the use of lung volume reduction
surgery as a treatment for severe emphysema in chronic obstructive
pulmonary disease (COPD) patients.
- reference: PMID:33926668
supports: SUPPORT
snippet: As symptoms and lung function decline, treatment modalities, such
as lung volume reduction surgery, have been used in individuals with
chronic obstructive pulmonary disease and upper lobe predominant
emphysema.
explanation: The literature indicates that lung volume reduction surgery is
a treatment used for severe emphysema, a condition associated with COPD.
- reference: PMID:31145187
supports: SUPPORT
snippet: 'Mortality benefits to therapy have been demonstrated in only 2 therapeutic
interventions to date: long-term use of daily supplemental oxygen and surgical
lung volume reduction (LVRS) for upper-lobe-predominant disease in patients
with a low baseline exercise capacity.'
explanation: The statement is supported as the literature suggests that lung
volume reduction surgery is an established treatment for
upper-lobe-predominant, severe emphysema in COPD patients.
treatment_term:
preferred_term: surgical procedure
term:
id: MAXO:0000004
label: surgical procedure
- name: Lung Transplantation
description: Considered in end-stage COPD with severe impairment.
evidence:
- reference: PMID:17240617
supports: SUPPORT
snippet: Lung transplantation is a surgical option for patients who fail
optimization of medical treatment for the severe symptoms that result from
COPD.
explanation: This reference states that lung transplantation is a considered
treatment option for patients with severe symptoms resulting from COPD.
- reference: PMID:31375190
supports: SUPPORT
snippet: End-stage congestive heart failure, chronic obstructive pulmonary
disease...palliative principles can guide decision making and symptom
management in these disease states.
explanation: The reference focuses on end-stage COPD and mentions lung
transplantation as a consideration in managing the conditions of patients.
- reference: PMID:36050206
supports: SUPPORT
snippet: The International Thoracic Organ Transplant Registry...focus on
lung transplant recipients with chronic obstructive pulmonary disease.
explanation: This source concentrates on lung transplantation for patients
with COPD, in line with the statement's context of it being a treatment
for end-stage COPD.
- reference: PMID:23248802
supports: SUPPORT
snippet: Chronic obstructive pulmonary disease...treated by lung
transplantation.
explanation: This abstract explicitly mentions the use of lung
transplantation for individuals with very severe COPD.
treatment_term:
preferred_term: organ transplantation
term:
id: MAXO:0010039
label: organ transplantation
- name: Mucolytic Therapy
description: N-acetylcysteine and other mucolytics reduce mucus viscosity and
may improve mucociliary clearance.
notes: Variable clinical impact across COPD phenotypes; targets MUC5AC/MUC5B
expression and mucus rheology.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
- name: Macrolide Antibiotics
description: Long-term macrolide therapy reduces exacerbation frequency but
raises antimicrobial resistance concerns.
notes: Used in chronic bronchitis phenotype; dual anti-inflammatory and
antimicrobial effects.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
- name: Biologic Therapies
description: Precision biologics targeting Type 2 inflammation in eosinophilic
COPD subsets.
notes: Dupilumab (anti-IL-4/IL-13) shows benefit in eosinophilic COPD;
anti-IL-33 and anti-TSLP under investigation.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
review_notes: COPD is characterized by progressive airflow obstruction that is
not fully reversible. Key respiratory symptoms include dyspnea, chronic cough,
sputum production, and wheezing. As the disease progresses, patients may
develop signs of lung hyperinflation (barrel chest) and are at risk for
respiratory failure. Systemic effects like fatigue and weight loss are also
common, particularly in advanced disease.
disease_term:
preferred_term: chronic obstructive pulmonary disease
term:
id: MONDO:0005002
label: chronic obstructive pulmonary disease
classifications:
harrisons_chapter:
- classification_value: respiratory system disorder
- classification_value: obstructive lung disease
references:
- reference: DOI:10.1136/thorax-2023-220455
title: Lower airway microbiota in COPD and healthy controls
findings: []
- reference: DOI:10.1164/rccm.202306-1060oc
title: Accelerated Lung Function Decline and Mucus–Microbe Evolution in
Chronic Obstructive Pulmonary Disease
findings: []
- reference: DOI:10.1183/23120541.00177-2024
title: What every clinician should know about inflammation in COPD
findings: []
- reference: DOI:10.3389/fimmu.2024.1404615
title: Inflammation mechanism and research progress of COPD
findings: []
- reference: DOI:10.3390/ijms25147780
title: Cellular and Molecular Biology of Mitochondria in Chronic Obstructive
Pulmonary Disease
findings: []
- reference: DOI:10.3390/ijms26052184
title: 'Molecular Approaches to Treating Chronic Obstructive Pulmonary Disease:
Current Perspectives and Future Directions'
findings: []