COPD

Question 1

hypoxemia

Answer 1

decreased P O2 in blood, mismatch between perfusion and ventilation

Question 2

hypercapnia

Answer 2

increased P CO2 in blood

Question 3

emphysemia

Answer 3

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

Question 4

acute respiratory failure in COPD

Answer 4

acute drop in P O2 of 10-15mm Hg or any acute P CO2 increase that decreases blood ph to 7.3 or less

Question 5

what rank is COPD in deaths

Answer 5

4th and 2nd leading cause of disability

Question 6

Risk factors of developing COPD

Answer 6

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

Question 7

how does COPD obstruct airflow

Answer 7

narrows the lumen of lower airways causing increased resistance, loss of lung elasticity, chronic bronchitis, obsturction, emphysemia

Question 8

chronic bronchitis

Answer 8

long term inflammatory condition of lower respiratory airways resulting from inhalation of irritants, leads to chronic build up of mucous and thicking of airways

Question 9

important consequences of emphysema

Answer 9

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

Question 10

inflammatory cell role in COPD

Answer 10

macrophage, neutrophils, CD8 (macrophage and neutrohil induce release of proteases

Question 11

inflammatory mediators in COPD

Answer 11

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

Question 12

protease-antiprotease

Answer 12

anti-trypsen normally protects proteases from degrading lung tissue but in genetic deficencies of alph anti trypsen they are not stopped

Question 13

what is oxidative stress’s role in COPD

Answer 13

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

Question 14

why do people with COPD get lots of infections

Answer 14

excessive mucous production, stagnation and plugging, and reduced cilia,

Question 15

explain cor pulmonale

Answer 15

right sided heart failure that it caused by hypertension in the lungs due to vasoconstricion and remodeling

Question 16

systemic effects of COPD

Answer 16

osteoprosis, muscle wasting, depression

Question 17

what are the symptoms of COPD

Answer 17

dyspnea coughing, chronic sputum production, history of risks, family history

Question 18

diagnostic tests

Answer 18

spirometry

Question 19

pulse oxometry and arterial blood gasses

Answer 19

asses if patients needs supplemental oxygen

Question 20

when to do an alpha- antitripsen assay

Answer 20

when patient is younger than 45 with COPD

Question 21

how does the mMCR work

Answer 21

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

Question 22

CAT

Answer 22

broader assessment of COPD

Question 23

spirometry assessment

Answer 23

> 80 mild, 50-79 moderate, 30-49 severe, <30 very severe

Question 24

nonpharm treatment

Answer 24

oxygen and pulmonary rehabilitation

Question 25

when to use oxygen

Answer 25

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)

Question 26

what has been shown to decrease long term decline of FEV and slow progession of COPD

Answer 26

smoking cessation

Question 27

beta agonists

Answer 27

can be used as monotherapy, indactole is best

Question 28

anitcholinergic

Answer 28

need to be in combination with beta agonist

Question 29

when should rolfumalast be used

Answer 29

severe cases, with a bronchodilator

Question 30

rolfumalast vrs theophyllen

Answer 30

can use rolf. with smoking,less drug drug interation, larger therapuetic index, rolf has an antimfalmitory effect while theo has a bronchiodialator effect

Question 31

when to use theophyllen

Answer 31

with bronchiodilators, if other things failed

Question 32

when to use cortiocsteroids

Answer 32

only in severe cases, other wise avoid

Question 33

alternative therapy

Answer 33

N-acytle cystiene, panax ginsing, and beta caratonie seems like it would help but supplements do not

Question 34

monitoring

Answer 34

spirometry test once a year, CAT every 2-3 months

Question 35

therapy recommendations for category A

Answer 35

short acting anti cholingergic or short acting beta, can use long acting of both or combinations , can add theophylline

Question 36

recommendations for category B

Answer 36

mMCR of >2 CAT >10: long acting anti and beta, can add short acting or theophylline

Question 37

recommendations for C

Answer 37

mMCR 0-1, long acting beta and corticosteroid, or long acting anti and corticosteroid, can add short acting and thoephylline

Question 38

recommendations for D

Answer 38

mMCR >2. same as C but also all three options can be combined