COPD Flashcards
hypoxemia
decreased P O2 in blood, mismatch between perfusion and ventilation
hypercapnia
increased P CO2 in blood
emphysemia
destruction of the gas exchanging surfaces of the lungs, permanent enlargment of alveola, loss of elasticity, and collapse of small airways. Results form excessive release of degrading enzymes
acute respiratory failure in COPD
acute drop in P O2 of 10-15mm Hg or any acute P CO2 increase that decreases blood ph to 7.3 or less
what rank is COPD in deaths
4th and 2nd leading cause of disability
Risk factors of developing COPD
smoking (most common cause), genetics (alpha antitripsen deficiency), occupational dust and chemicals, impaired lung growth, asthma and airway hyperresponsivness, history of severe childhood respiratory infections, lower socioeconimic status
how does COPD obstruct airflow
narrows the lumen of lower airways causing increased resistance, loss of lung elasticity, chronic bronchitis, obsturction, emphysemia
chronic bronchitis
long term inflammatory condition of lower respiratory airways resulting from inhalation of irritants, leads to chronic build up of mucous and thicking of airways
important consequences of emphysema
accessory muscles are enlisted which causes patient to tire, smaller bronchials collapse during exhalation trapping large amount of air in alveoli (hyperinlfation, barrel chest) reduces ventilations efficiency, pulmonary capillaries are damaged as alveoli walls destigrate, causing increased resistance so right ventricle has to over work and can become hypertrophic
inflammatory cell role in COPD
macrophage, neutrophils, CD8 (macrophage and neutrohil induce release of proteases
inflammatory mediators in COPD
TNF alpha, LTB4 (neutrophils and T cells), IL-8 (neutrophils and monocytes), IFN gama augments inflammation, IL-1beta and IL-6 amplify inflammatory response, TGF beta induce fibrosis in airways
protease-antiprotease
anti-trypsen normally protects proteases from degrading lung tissue but in genetic deficencies of alph anti trypsen they are not stopped
what is oxidative stress’s role in COPD
from cigarette smoking and inflammation, generates highly reactive oxygen species (ROS) like O2, H2O2, OH, ONOO-, these exacterbate COPD by reacting with lipids, proteins leading to damage and activate NFKB resulting in production of proinflammatory genes, also decrease antiproteases
why do people with COPD get lots of infections
excessive mucous production, stagnation and plugging, and reduced cilia,
explain cor pulmonale
right sided heart failure that it caused by hypertension in the lungs due to vasoconstricion and remodeling
systemic effects of COPD
osteoprosis, muscle wasting, depression
what are the symptoms of COPD
dyspnea coughing, chronic sputum production, history of risks, family history
diagnostic tests
spirometry
pulse oxometry and arterial blood gasses
asses if patients needs supplemental oxygen
when to do an alpha- antitripsen assay
when patient is younger than 45 with COPD
how does the mMCR work
classifies based off breathlessness, 0-only when working out, 1- fast walking or up hill, 2- on level ground i walk slower than pl my own age, stop for breath, 3- have to stop every 100 feet or every few mins, 4- can’t go anywhere
CAT
broader assessment of COPD
spirometry assessment
> 80 mild, 50-79 moderate, 30-49 severe, <30 very severe
nonpharm treatment
oxygen and pulmonary rehabilitation
when to use oxygen
when: PO2 resting is less than 55 mmHG or Sa is less than 88%, or if resting is 55-60 but there is pulmonary hypertension, edema, heart failure, or polychthemia (repeat test for levels twice over three weeks to confirm)
what has been shown to decrease long term decline of FEV and slow progession of COPD
smoking cessation
beta agonists
can be used as monotherapy, indactole is best
anitcholinergic
need to be in combination with beta agonist
when should rolfumalast be used
severe cases, with a bronchodilator
rolfumalast vrs theophyllen
can use rolf. with smoking,less drug drug interation, larger therapuetic index, rolf has an antimfalmitory effect while theo has a bronchiodialator effect
when to use theophyllen
with bronchiodilators, if other things failed
when to use cortiocsteroids
only in severe cases, other wise avoid
alternative therapy
N-acytle cystiene, panax ginsing, and beta caratonie seems like it would help but supplements do not
monitoring
spirometry test once a year, CAT every 2-3 months
therapy recommendations for category A
short acting anti cholingergic or short acting beta, can use long acting of both or combinations , can add theophylline
recommendations for category B
mMCR of >2 CAT >10: long acting anti and beta, can add short acting or theophylline
recommendations for C
mMCR 0-1, long acting beta and corticosteroid, or long acting anti and corticosteroid, can add short acting and thoephylline
recommendations for D
mMCR >2. same as C but also all three options can be combined
