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Chronic Obstructive Pulmonary Disease, Cigarette smoking - Coggle Diagram
Chronic Obstructive Pulmonary Disease
Clinical Manifestations
Shortness of breath (Dyspnea)
Especially during physical activities
Hypoxemia
Wheezing
Chest tightness
Chronic cough
May produce mucus(Sputum)
White
Clear
Yellow
Green
Lack of energy
Unintended weight loss
Swelling
Ankles
Feet
Legs
Respiratory infections
Make it much more difficult to breathe and could cause further damage to lung tissue
People with COPD are more likely to catch colds, the flu and pneumonia
Heart problems
COPD can increase the risk of heart disease, including heart attack
Reasons aren't fully understood
May be due to a constant lack of oxygen supply to the heart
Lung Cancer
High blood pressure (Cor pulmonale)
In the arteries that bring blood to your lungs (pulmonary hypertension)
Depression
Difficulty breathing can keep people from doing activities that they enjoy
Dealing with serious illness can contribute to the development of depression
Hypercapnia
Risk Factors
Exposure to:
Tobacco Smoke
The more years someone smokes and the more packs they smoke, the greater their risk
Pipe smokers, cigar smokers and marijuana smokers also may be at risk
Dusts and chemicals
Long-term exposure to chemical fumes, vapors and dusts in the workplace
Irritate and inflame lungs
Fumes from burning Fuel
Burning fuel for cooking and heating in poorly ventilated homes
Asthma
A chronic inflammatory airway disease
Genetics
Alpha-1-antitrypsin deficiency
Not enough of the protein causes the lungs to be more vulnerable
Age
40 and older
The cumulative effects of smoking, secondhand smoke, exposure to air pollutants, and recurrent infections can damage the lungs over the years.
Low Family Income
Poor nutrition, untreated lung infections, exposure to irritants, or the effects of smoking, which is now more common in lower socioeconomic groups.
Infections
Severe viral and bacterial lung infections in early childhood
Especially tuberculosis
Human immunodeficiency virus (HIV) can speed up the development
Female
More severe symptoms, longer years with the disease, and a higher risk of COPD-associated death than men
Even when they have lower pack-years of smoking
Deficient lung function
Complications or developmental issues during gestation, birth, or early childhood can affect lung size or function
Nutrition
Malnutrition can reduce respiratory muscle strength and endurance.
If a patient has COPD and a BMI is lower than 21, mortality increases
Diagnostics
Spirometry
Test Results:
Stage 1 COPD
Value greater or lesser than FEV1/FVC less than 70 percent
Stage 2 COPD
FEV1 will fall between 50 percent and 79 percent
Stage 3 COPD
FEV1 falls somewhere between 30 percent and 49 percent
Stage 4 COPD
FEV1is less than 30 percent
It will measure the total amount that you were able to exhale
Bronchodilator reversibility test
The patient will be asked to take a deep breath and then blow into the spirometer as hard as you can. The spirometer records the results.
The patient will be given a dose of bronchodilator medicine
Wait for about 15 minutes
The patient will take a deep breath and then blow into the spirometer as hard as they can.
Positive test can implicate COPD
An increase in FEV1 from baseline that is more than 200ml and more than 15% of the prebronchodilator value
Blood tests
Arterial blood gas test
Measures the acidity (pH), and the levels of oxygen and carbon dioxide in the blood from an artery
Results that are a sign of COPD
Normal PaCO2, PaO2 > 60 mmHg
PaCO2 > 45 mmHg, PaO2 < 60 mmHg
Genetic testing
Alpha-1 antitrypsin (AAT)
It helps protect the lungs from the damage caused by inflammation that can lead to emphysema and chronic obstructive pulmonary disease
Deficiency leads the lungs vulnerable to inflammation
Chest X-ray
Looking for signs of COPD:
Hyperinflated lungs
Diaphragm may look lower and flatter than usual
Heart may look longer than normal
CT Scan
Looking for signs of COPD:
Pockets of air in the lungs
Looking for signs of emphysema
Destroyed air sacs
Emphysema can cause COPD, so these signs may be present with COPD as well
Looking for signs of Chronic Bronchitis
Inflammation of the airway lining
Chronic Bronchitis can cause COPD, so these signs may be present with COPD as well
Sputum examination
Looking for the sputum to be:
Darker with either a yellow of green tinge
Evidence of an infection
Opaque (mucopurulent), slightly thicker, or cloudy
Evidence of COPD
Electrocardiogram(ECG or EKG)
Patients with COPD commonly have low voltage due to interposition of hyperexpanded lungs between the heart and ECG electrodes
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Vallerand, April Hazard, and Cynthia A. Sanoski. Davis's Drug Guide for Nurses. F.A. Davis Company, 2021.
Treatment
Quit Smoking
Bronchodilators
Short-Acting Beta Agonists
Ipratropium (Atrovent HFA)
Action: Inhalation= Inhibits cholinergic receptors in bronchial smooth muscle, resulting in decreased concentrations of cyclic guanosine monophosphate (cGMP).
Decreased levels of cGMP produce local bronchodilation
Action: Local application inhibits secretions from glands lining the nasal mucosa
Effects:
Bronchodilation without systemic anticholinergic effects
Decreased rhinorrhea
Levalbuterol (Xopenex)
Action: R-enantiomer of racemic albuterol. Binds to beta-2 adrenergic receptors in airway smooth muscle leading to activation of adenylcyclase and increased levels of cyclic-3′, 5′-adenosine monophosphate (cAMP)
Increases in cAMP activate kinases, which inhibit the phosphorylation of myosin and decrease intracellular calcium
Decreased intracellular calcium relaxes bronchial smooth muscle
Relatively selective for beta-2 (pulmonary) receptors
Effect: Relaxation of airway smooth muscle with subsequent bronchodilation
Albuterol (ProAir HFA, Ventolin HFA, others)
Action: Binds to beta-2 adrenergic receptors in airway smooth muscle leading to activation of adenylcyclase and increased levels of cyclic-3′, 5′-adenosine monophosphate (cAMP)
Increases in cAMP activate kinases, which inhibit the phosphorylation of myosin and decrease intracellular calcium
Decreased intracellular calcium relaxes bronchial smooth muscle
Relatively selective for beta-2 (pulmonary) receptors
Effect: Bronchodilation
Long-Acting Beta Agonists
Theophylline
Less expensive
Action: Inhibit phosphodiesterase, producing increased tissue concentrations of cyclic adenosine monophosphate (cAMP)
Effects:
Bronchodilation
CNS stimulation
Positive inotropic and chronotropic effects
Diuresis
Gastric acid secretion
Aclidinium (Tudorza Pressair)
Action: Acts as an anticholinergic by inhibiting the M3receptor in bronchial smooth muscle
Arformoterol (Brovana)
Action: Produces accumulation of cyclic adenosine monophosphate (cAMP) at beta-adrenergic receptors
Relatively specific for beta2(pulmonary) receptors
Effect: Relaxation of airway smooth muscle
Formoterol (Perforomist)
Action: Produces accumulation of cyclic adenosine monophosphate (cAMP) at beta-adrenergic receptors
Relatively specific for beta2(pulmonary) receptors
Effect: Relaxation of airway smooth muscle
Indacaterol (Arcapta Neoinhaler)
Produces accumulation of cyclic adenosine monophosphate (cAMP) at beta2-adrenergic receptors
Relatively specific for pulmonary receptors
Tiotropium (Spiriva)
Action: Acts as anticholinergic by selectively and reversibly inhibiting M3receptors in smooth muscle of airways
Effect: Decreased incidence and severity of bronchospasm
Salmeterol (Serevent)
Action: Produces accumulation of cyclic adenosine monophosphate (cAMP) at beta2-adrenergic receptors
Relatively specific for beta (pulmonary) receptors
Umeclidinium (Incruse Ellipta)
Action: Acts as an anticholinergic by inhibiting M3 muscarinic receptors in bronchial smooth muscle
Inhaled Steroids
Fluticasone (Flovent HFA)
Action: Potent, locally acting anti-inflammatory and immune modifier
Budesonide (Pulmicort Flexhaler)
Action: potent anti-inflammatory actions that reduces inflammation and hyper-reactivity (spasm) of the airways
Combination inhalers
Bronchodilators and inhaled steroids
Examples:
Fluticasone and vilanterol (Breo Ellipta)
Fluticasone = inhaled corticosteroid
Decreases airway inflammation
Vilanterol = long-acting beta2 agonist
Relaxes bronchial smooth muscle
Fluticasone, umeclidinium and vilanterol (Trelegy Ellipta)
Attaches to beta-2 receptors in some types of muscle cells. When inhaled, vilanterol activates the beta-2 receptors in the airways
The muscles of the airways to relax, helping to keep the airways open and allowing the patient to breathe more easily
Formoterol and budesonide (Symbicort)
Budesonide = works by reducing and preventing respiratory tract inflammation
Formoterol = a long-acting beta2-agonist bronchodilator (LABA) that decreases resistance in the respiratory airway and increases airflow to the lungs.
Salmeterol and fluticasone (Advair HFA, AirDuo Digihaler, others)
Fluticasone = inhaled corticosteroid
Decreases airway inflammation
Long-acting beta agonists
The muscles of the airways to relax, helping to keep the airways open and allowing the patient to breathe more easily
More than 1 type of bronchodilator Examples:
Aclidinium and formoterol (Duaklir Pressair)
Aclidinium = Acts as an anticholinergic by inhibiting the M3 receptor in bronchial smooth muscle
Formoterol = Beta2-adrenergic agonist that stimulates adenyl cyclase, resulting in accumulation of cyclic adenosine monophosphate and subsequent bronchodilation
Albuterol and ipratropium (Combivent Respimat)
Albuterol = Beta-2 agonists are medications that stimulate beta-2 receptors on the smooth muscle cells that line the airways, causing these muscle cells to relax and thereby opening airways
Ipratropium = blocks the effect of acetylcholine in airways and nasal passages
Formoterol and glycopyrrolate (Bevespi Aerosphere)
Glycopyrrolate = acts as an anticholinergic by inhibiting M3 muscarinic receptors in bronchial smooth muscle resulting in bronchodilation
Formoterol = a beta2-adrenergic agonist that stimulates adenyl cyclase, resulting in accumulation of cyclic adenosine monophosphate at beta2—adrenergic receptors resulting in bronchodilation
Glycopyrrolate and indacaterol (Utibron)
Indacaterol = a beta2-adrenergic agonist that stimulates adenyl cyclase, resulting in accumulation of cyclic adenosine monophosphate at beta2—adrenergic receptors resulting in bronchodilation
Glycopyrrolate = acts as an anticholinergic by inhibiting M3 muscarinic receptors in bronchial smooth muscle resulting in bronchodilation
Olodaterol and tiotropium (Stiolto Respimat)
Olodaterol = A long-acting beta2-adrenergic agonist (LABA) that stimulates adenyl cyclase, resulting in accumulation of cyclic adenosine monophosphate (cAMP) at beta2—adrenergic receptors resulting in bronchodilation
Tiotropium = Acts as anticholinergic by selectively and reversibly inhibiting M3receptors in smooth muscle of airways.
Umeclidinium and vilanterol (Anoro Ellipta)
Umeclidinium = acts as an anticholinergic by inhibiting M3 muscarinic receptors in bronchial smooth muscle resulting in bronchodilation
Vilanterol = a beta2-adrergic agonist stimulates adenyl cyclase, resulting in accumulation of cyclic adenosine monophosphate at beta2—adrenergic receptors resulting in bronchodilation
Phosphodiesterase-4 inhibitors
Blocking the breakdown of cyclic adenosine monophosphate
Decrease airway inflammation
apremilast
crisaborole
roflumilast
only PDE4 inhibitor approved for the treatment of a subset of patients with severe
Antibiotics
Treat episodes of worsening COPD
Amoxicillin-clavulanate potassium
Action: Clavulanic acid synergistically expands activity of amoxicillin against β-lactamase-producing bacteria by irreversibly and competitively inhibiting β-lactamases.
Severe exacerbations
Augmented penicillins
Action: Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes
Fluoroquinolones
Action: Act by inhibiting two enzymes involved in bacterial DNA synthesis, both of which are DNA topoisomerases that human cells lack and that are essential for bacterial DNA replication,
Enabling these agents to be both specific and bactericidal
Third-generation cephalosporins
Examples:
Ceftriaxone
Ceftibuten
Cefotaxime
Ceftazidime
Cefpodoxime
Cefixime
Action: The beta-lactam ring structure of third-generation cephalosporins mimics the “D-Ala-D-Ala” moiety of the natural substrate of PBPs.
Structural binding of cephalosporin antibiotics to the active site of PBPs in bacterial cell walls leads to inhibition of their enzymatic activity and leads to defective peptidoglycan synthesis
Inability to construct a functional cell wall and subsequent death of the bacterial cells by osmotic lysis
Aminoglycosides
Action: inhibit protein synthesis in bacteria by binding irreversibly to the 30S ribosomal subunit
This inhibits transfer of aminoacyl-tRNA to the peptidyl site, causing premature termination of the peptide chain; it also increases the frequency of misreading of mRNA.
Reasoning: The exacerbation may be due to a virus
Trimethoprim-sulfamethoxazole
Action: Combination inhibits the metabolism of folic acid in bacteria at two different points
Effect: Bactericidal action against susceptible bacteria
Doxycycline
Action: Inhibits bacterial protein synthesis at the level of the 30S bacterial ribosome
Low-dose products used in the management of periodontitis inhibit collagenase
Effect: Bacteriostatic action against susceptible bacteria
Not recommended for preventing COPD
Oxygen therapy
Constant oxygen
Respironics Simply Go
SeQual Eclipse 5
Oxlife Independence
GCE Group Zen-O
DeVilbiss iGo
Oxygen when sleeping or doing other activities
Lightweight, portable units
AirSep® FreeStyle. ®
AirSep® LifeStyle.
Inogen One. ®
Respironics EverGo™
SeQual Eclipse. ®
Improve quality of life and is the ONLY COPD therapy proved to extend life
Pulmonary rehabilitation program
Combination of:
Education
The role and correct use of medications.
Breathing techniques / managing breathlessness.
Physical exercise
Nutrition/healthy eating
Information on diseases (e.g. what the lungs do)
Coping with chronic lung disease and management of depression, anxiety and panic attacks
Exercise training
Improves circulation and helps the body better use oxygen
Examples: Walking, jogging, jumping rope, bicycling, skating, low-impact aerobics, swimming, and resistance training (hand weights or bands)
Nutrition advice
Eat protein at least twice a day
Maintain strong respiratory muscles
Examples: milk, eggs, cheese, meat, fish, poultry, nuts and dried beans or peas
Limit simple carbohydrates
Eat 20 to 30 grams of fiber each day
Limit foods with trans fats and saturated fats
Counseling
COPD Basics:
The common symptoms include shortness of breath, cough and/or sputum production
Tobacco smoking is the most common exposure that causes COPD
A patient with COPD must have a Forced Expiratory Volume during the first second (FEV1) to Forced Vital Capacity (FVC) ratio less than 0.70 measured by spirometry
Action Plan:
Green days: normal day, continue normal activity and medications
Yellow days: bad day, ask how many puffs of rescue medicine a day does patient use, call provider for possible steroids and/or antibiotics if needed
Red days: urgent medical attention needed; call 911
Medications
Vaccination Schedules
Smoking Cessation
Screenings
Patient Advocacy groups
Energy conservation
Airway clearance techniques
May reduce readmission to the hospital
Increase the ability to participate in everyday activities
Improve the quality of life
Managing exacerbations
Medications (such as antibiotics, steroids or both), supplemental oxygen or treatment in the hospital
In-home noninvasive ventilation therapy
bilevel positive airway pressure (BiPAP)
Improve breathing
Decrease retention of carbon dioxide (hypercapnia) that may lead to acute respiratory failure and hospitalization
Surgeries
Lung Volume Reduction Surgery
A tiny one-way endobronchial valve is placed in the lung, allowing the most damaged lobe to shrink so that the healthier part of the lung has more space to expand and function
removes small wedges of damaged lung tissue from the upper lungs
Creates extra space in your chest cavity so that the remaining healthier lung tissue can expand and the diaphragm can work more efficiently
Lung transplant
Bullectomy
Removing bullae, which are enlarged, damaged air sacs in the lungs
Healthier sections of the lungs to re-expand
The diaphragm move back into a better position that will make breathing easier
Incidence/Prevalence
U.S.
In 2008 7.2% of adults aged 40 years or older reported a diagnosis of COPD
In 2009 6.4% of adults aged 40 years or older reported a diagnosis of COPD
In 2014 and 2015 6% of adults aged 40 years or older reported a diagnosis of COPD
Age
4.6% are 40-64 years old
10.2% are older than 65
Smoker Status
15.1% of current smokers
9.8% of former smokers
3% of never smokers
Family Income
13.6% are poor or near poor
9.9% are low income
6.0% are Middle income
3.7% are High income
Health Insurance
4.3% have private
14.0% have Medicare
11.1% have other public
4.1% have no insurance
Health Status
4.7% are excellent to good
23.4% are fair to poor
Other Chronic conditions with COPD
64.1% of Cholesterol patients
61.4% of High Blood Pressure patients
46.0% of Heart Disease patients
40.9% of Asthma patients
27.3$ of Cancer patients
26.4% of Diabetes patients
Overall has decreased
World Wide
Europe = 12.4% (8.8–16.0%)
Africa = 13.9% (12.0–15.9%)
America = 13.2% (10.5–15.9%)
Asia = 13.5% (10.0–16.0%)
Oceania = 11.6% (9.8–13.1%.
Mean of the whole world = 13.1% (10.2–15.6%)
Pathogenesis
NLRP3 inflammasome
Alveolar macrophages play a central role in airway inflammation
These cells secrete multiple chemokines and cytokines, such as tumor necrosis factor-α (TNF-α), that induce the expression of adhesion molecules on endothelial cells, facilitating the migration of a variety of inflammatory cells
Inflammasome-dependent cytokines
An endogenous protective mechanism against oxidative stress via Nrf2, altered immune response of the airway inflammatory cells, exaggerated cellular senescence of the lung structural cells, and cell death with expanded inflammation. Recently, CS-induced mitochondria autophagy is reported to initiate programmed necrosis (necroptosis).
Tissue damage is not reversible; increases in severity, and eventually leads to respiratory failure
Pathway of COPD
Exposure to tobacco smoke air pollution
Inflammation of the airway epithelium
Infiltration of inflammatory cells and release cytokines
Which can cause increased protease activity with breakdown of elastin in connective tissue of lungs
Causing EMPHYSEMA
Pathophysiology: Destruction of alveolar septa and loss of elastic recoil of bronchial wall
Abnormal permanent enlargement of the gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis
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Which can cause Continuous bronchial irritation and inflammation
Causing CHRONIC BRONCITIS
Airway obstruction, Airway trapping, Loss of surface area for gas exchange, and frequent exacerbations
Symptoms
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Pathophysiology: Bronchial edema, hypersecretion of mucus, bacterial colonization of airways
Hypersecretion of mucus and chronic productive cough that lasts for at least 3 months of the year and for at least 2 consecutive years
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This can possibly lead to the inhiation of normal endogenous antiproteases
In the bronchial mucosa in patients with COPD, T lymphocytes predominate, mainly CD8+ cells and macrophages
The presence of increased CD8+ T lymphocytes differentiates between smokers who do and do not develop COPD and that there is a correlation between T-cell numbers, the amount of alveolar destruction, and the severity of airflow limitation
T cells in peripheral airways in patients with COPD show increased expression of CXCR3, a receptor activated by interferon-inducible protein 10, and expression of interferon-inducible protein 10 itself is increased in bronchiolar epithelial cells. This could contribute to the accumulation of CD8+ cells, which preferentially express CXCR3.
CD8+ cells have the potential to release tumor necrosis factor α, perforins, and granzymes, in addition to activating the Fas–Fas ligand apoptotic pathway. An association has been shown between CD8+ cells and apoptosis of alveolar epithelial cells in subjects with emphysema.
Increased numbers of activated neutrophils are found in sputum from patients with COPD
The lack of significant increased neutrophil numbers in the lung parenchyma may be due to the fact that these cells make a rapid transit through the airways and the lung parenchyma
Neutrophils have the potential to secrete serum proteinases, including neutrophil elastase, cathepsin G, and proteinase 3, as well as matrix metalloproteinase 8 (MMP-8) and MMP-9.
These proteases may contribute to alveolar destruction and are also potent stimuli of mucus secretion.
Cigarette smoking
Cigarette smoke activates macrophages to release inflammatory mediators, including tumor necrosis facto α, IL-8 and other CXC chemokines, monocyte chemotactic peptide-1, leukotriene B4, and reactive oxygen species.
Macrophages also secrete proteases, including MMP-2, MMP-9, and MMP-12; cathepsins K, L, and S; and neutrophil elastase, taken up from neutrophils
Result from increased recruitment of monocytes from the circulation in response to monocyte chemotactic chemokines such as monocyte chemotactic peptide-1, which has been shown to be increased in sputum and BALF in patients with COPD.
The concentration of growth-related oncogene-α is increased markedly in sputum and BALF from patients with COPD.
Monocytes from patients with COPD show a greater chemotactic response to growth-related oncogene-α than do cells from normal smokers and nonsmokers
CXC chemokines also act as chemoattractants to monocytes
Compared with macrophages from normal smokers, those from patients with COPD are more activated, secrete more inflammatory proteins, and have greater elastolytic activity, which is further enhanced by exposure to cigarette smoke
Cigarette smoke also has a direct stimulatory effect on granulocyte production in the bone marrow, possibly mediated by granulocyte-macrophage colony–stimulating factor and granulocyte colony–stimulating factor released from macrophages.
It is possible that neutrophils are activated within the pulmonary microcirculation to release reactive oxidant species and proteases that may have a direct injurious effect.
Once sequestered, neutrophils adhere to endothelial cells, and the adhesion molecule E-selectin has been shown to be upregulated in the airway epithelial cells of patients with COPD
Neutrophils can then migrate to the respiratory tract under the control of chemotactic factors, such as leukotriene B4, interleukin 8 (IL-8), and related CXC chemokines, including growth-related oncogene-α and epithelial cell−derived neutrophil attractant 78.
These chemotactic factors have been shown to be increased in the airways in patients with COPD
Airway epithelial cells can be activated by cigarette smoke to produce inflammatory mediators, including tumor necrosis factor α, IL-1β, granulocyte-macrophage colony–stimulating factor, and IL-8.
Epithelial cells can also secrete antioxidants, secrete antiproteases, and transport immunoglobulin-α, so they may be involved in adaptive immunity.
Cigarette smoke may impair these innate and adaptive immune responses of the airway epithelium and increase the likelihood of infection.