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Chronic Obstructive Pulmonary Disease, Cigarette smoking - Coggle Diagram

- - - - White
      - Clear
      - Yellow
      - Green
  - - - People with COPD are more likely to catch colds, the flu and pneumonia
  - - - Reasons aren't fully understood
        
        May be due to a constant lack of oxygen supply to the heart
- - - - 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
    - - Long-term exposure to chemical fumes, vapors and dusts in the workplace
        
        Irritate and inflame lungs
    - - Burning fuel for cooking and heating in poorly ventilated homes
  - - - Not enough of the protein causes the lungs to be more vulnerable
  - - - The cumulative effects of smoking, secondhand smoke, exposure to air pollutants, and recurrent infections can damage the lungs over the years.
  - - - Especially tuberculosis
      - Human immunodeficiency virus (HIV) can speed up the development
  - - - Even when they have lower pack-years of smoking
- - - - 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
  - - - 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.
    - - An increase in FEV1 from baseline that is more than 200ml and more than 15% of the prebronchodilator value
  - - - 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
  - - - 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
  - - - Hyperinflated lungs
      - Diaphragm may look lower and flatter than usual
      - Heart may look longer than normal
  - - - Pockets of air in the lungs
    - - Destroyed air sacs
        
        Emphysema can cause COPD, so these signs may be present with COPD as well
    - - Inflammation of the airway lining
        
        Chronic Bronchitis can cause COPD, so these signs may be present with COPD as well
  - - - Darker with either a yellow of green tinge
        
        Evidence of an infection
      - Opaque (mucopurulent), slightly thicker, or cloudy
        
        Evidence of COPD
- - - - 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
    - - 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
  - - - Action: Potent, locally acting anti-inflammatory and immune modifier
    - - Action: potent anti-inflammatory actions that reduces inflammation and hyper-reactivity (spasm) of the airways
  - - - 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
  - - - Decrease airway inflammation
        
        apremilast
        
        crisaborole
        
        roflumilast
        
        only PDE4 inhibitor approved for the treatment of a subset of patients with severe
  - - - 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
  - - - Respironics Simply Go
      - SeQual Eclipse 5
      - Oxlife Independence
      - GCE Group Zen-O
      - DeVilbiss iGo
    - - Lightweight, portable units
        
        AirSep® FreeStyle. ®
        
        AirSep® LifeStyle.
        
        Inogen One. ®
        
        Respironics EverGo™
        
        SeQual Eclipse. ®
  - - - 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
  - - - Improve breathing
      - Decrease retention of carbon dioxide (hypercapnia) that may lead to acute respiratory failure and hospitalization
  - - - 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
    - - 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
- - - - 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
- - - - 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
  - - - 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
  - - - 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.
  - - - 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.
- - - - 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
- - - - 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