COPD/dyspnea readings Flashcards
COPD how is it characterized
• A common preventable and treatable disease, characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gasses
patho of COPD
-• progressive airflow limitation assoc w abn inflm response airways, parenchyma, and pulmonary vasculatureto noxious particles or gases.
• small a/w narrowing
• narrowing and scar formation
• Obstruction may be d/t parenchymal destruction
• Protineases and antiprotineases are released and damage the parenchyma of the lung–>a/w limitation
• Cigarette smoke or tobacco use may cause thickening of the vessel wall.
chronic bronchitis what must you have for dx
• Presence of cough and sputum production for at least 3 months in each 2 consecutive years
chronic bronchitis what are the patho issues
- irritants–>hypersec of mucus (d/t inc number and size of glands), dec ciliary fx and inflm
- thickened bronchial walls
- alveolia adjacent to bronchioles may get damaged and fibrosed
- alt fx of alveolar macrophages
- susceptible to infection
when is pt susceptible to chronic bronchitis exacerbation
winter
emphysema patho
- destr of walls of over distended alveoli byond terminal bronchioles
- dec alveolar SA–>inc dead space–> which dec pulm capillaries–>hypoxemia.
- once co2 elim is impaired–>hypercapnia–>resp acidosis
how does destr of pulm capillaries affect CV system
- Consequently, pulm blood flow is inc forcing the R. ventricle to maintain a higher bp in the pulm artery.
- R. sided heart failure- complication
mnfts of emphysema
• hyperinflated chest (barrel chest), - marked dyspnea on exertion - wt loss -Pt is SOB, chest is rigid, and ribs are fixed at joints • Derangement of ventilation-perfusion ratios, producing -chronic hypoxemia, -hypercapnia (inc co2 in arterial blood), -polycythemia, -episodes of r. sided heart failure. • Leads to central cyanosis, - peripheral edema - resp failure
outcome!! et/risk factors for COPD
- Env’t exposures
- Cigarette smoking, pipe, cigar, tobacco use. Second hand
- Smoking depresses activity of scavenger cells and affects ciliary cleansing mechanism, which keeps breathing passages free of inhaled irritants, bacteria, and other foreign matter. Airflow is then obstructed and alveoli are trapped and are greatly distended)
- Smoking irritates the goblet cells and mucous glands- inc accum of mucus- more irriation, infection, and damage to the lung
- Carbon monoxide also damaging
- Prolonged and intense exposure to occupational dusts and chemicals, indoor air pollution and
- A host risk factor- def of alpha1 antitrypsin (enzyme that protects the lung parenchyma from injury)
what can be offered to pt with A1 antitrypsin deficiency
how might their disease course present
tx
genetic counselling
- they will be v susceptible to a/w irritants
- may be given alpha protease replacement therapy which is $$$
3 classic mnfts of COPD
other mnfts
• Cough, sputum, dyspnea
- Wt loss- dyspnea interferes with eating
- Barrel chest- chronic hyperinflation d/t fixation of the ribs in the inspiratory position and loss of lung elasticity.
- Retraction of the supraclavicular fossae occurs on inspiration, causing the shoulders to heave upward
how is obstructive lung disease defined
post bronchodilator FEV1/FVC ratio of less than 70%
how is airflow obstr evaluated
• Spirometry- evaluate airflow obstruction by comparing FEV1 to FVC
how are spirometric results expressed
theyre given as absolute volume and as percent predicted using appropriate normal values for gender, age, and height
how is asthma ruled out
• Bronchodilator reversibility testing to rule out asthma and guide early tx
pts spirometry is obtained. pt is then given bronchodilator and spirometry is repeated .
who would get Alpha 1 antitrypsin testing
pts under 45 or those w strong famhx of COPD
which disease can COPD get confused with easily
• Rule out asthma which has key characteristics of: early onset in life, variation in daily symptoms, day to day occurrence or timing of symptoms, family hx, allergy, rhinitis or eczema
complications of COPD
- Resp insuff and failure
- Acuity of the onset of symptoms and severity depend on baseline pulm function, spo2, ABGs, comorbid conditions
- Pneumonia, atelectasis, pneumothorax, and cop pulmonae
headings of medical mgmt of COPD
- risk reduction
- pharm therapy: bronchodilators, corticosteroids
- mgmt of exacerbation
- oxygen
- surgical mgmt
- pulm rehabilitation
risk reduction how to quit smoking how else to mitigate risk of smoking
- smoke cessation (promoting and encourage to quit)–this is important to start in teen years as early age use is assoc w higher levels of dependence
- factors associated with continued smoking- strength of nicotine addiction, continued exposure to smoking, stress, depression, habit. Prevelant – low incomes, low education, and psychosocial problems
- psychosocial support and pharmacotherapy for smoking cessation for patients with COPD
- Explain risks. Set a “quit date” follow up 3-5 days after date.
- Refer to a program
- Emphasize success over failures
- First line pharmacotherapy that reliable increases long-term smoking abstinence rates is nicotine replacement (gum, inhaler, nasal spray, transdermal patch, SL tablet)
- Second line include antihypertensive agents such as clonidine (pregnancy and adolescents and light smokers are not recomm)
- Smoking cessation can begin anywhere- clinic, pulmonary rehab, community, hospital, home
surgical mgmt of COPD (name of sx and reason)
bullectomy (if have bullous emphysema)
lung volume reduction sx (if its isolated to one area of lung)
lung transplant
what is a bullae and how does it impact pt
. Bullae are enlarged airspaces in the thorax- may be surgically excised.
• Bullae compress areas of the lung that have adequate gas exchange.
