COPD

Question 1

What is COPD?

Answer 1

Chronic airflow obstruction due to chronic bronchitis and/or pulmonary edema

NOT ACUTE, doesn’t go away, not completely reversible

Airflow obstruction is FEV1/FVC ratio < 0.70

Also can be viewed as persistent post-bronchodilator FEV1/FVC < 0.70 not due to dz other than COPD)

Question 2

What is the definition of chronic bronchitis?

Answer 2

Persistent cough & sputum production for at least three months in at least two consecutive years

Leads to airflow obstruction vie intramural & intraluminal pathways

Question 3

What is the definition of emphysema?

Answer 3

Destructino of acinar walls –> loss of radial traction on airways & increased lung compliance –> hyperinflation, poor lung mechanics

Question 4

What are the risk factors for COPD?

Answer 4

Cigarette smoke

Occupational dust/chemicals

Environmental tobacco smoke

Air pollution

Genetic variation

Question 5

Can FEV1 change if you quit smoking? Even if you’re really old?

Answer 5

Yes!

If you quit smoking, FEV 1 improves over the years: improves based on how long ago you quit smoking

Question 6

What is alpha-1 antitrypsin deficiency?

Answer 6

Autosomal codominant disorder caused by mutation in the SERPINA1 gene

Mutations/deficiencies are correlated with emphysema risk

2% of COPD patients have sever A1A deficiency, esp younger patients with basilar emphysema

Can also cause liver dz

Treatment = IV pooled plasma alpha-1-antitrypsin

Question 7

What does alpha-1-antitrypsin do?

Answer 7

Inhibits neutrophil elastase; consequence is the break down of alveolar walls

Question 8

What happens to compliance in emphysema? Result?

Answer 8

Increased compliance

Leads to increased lung volume at lower pressures! Both for residual volume and inspiratory volume

Question 9

What happens to the alveolar walls in COPD?

Answer 9

Loss of A1A –> loss of alveolar walls –> loose structure of the lung –> change elastic properties of the lung = hyperinflation due to increased compliance

Question 10

Why does COPD/loss of alveolar walls lead to obstruction of the airway?

Answer 10

You also lose the radial traction that’s normally on your airways pulling it open –> airway collapses down (extraluminal cause of airway obstruction)

Question 11

What happens to airway during forced expiration in COPD?

Answer 11

Loss of radial traction –> airways start to collapse; leads to something that you have to overcome during forced expiration; can eventually close down all the way

Results in a lower overall pressure in alveoli during forced expiration

“floppy airways” = bronchomalatia

Question 12

What happens to the flow volume loop during COPD?

Answer 12

Lower flow at a given volume!

Question 13

What happens to gas exchange in COPD? What’s the mechanism?

Answer 13

Mild hypoxemia (severe is rare)

Due to areas of Low V/Q, Alveolar hypoventilation, but NOT R–>L shunt!

Question 14

What’s abnormal about ventilation in COPD?

Answer 14

Increased dead space ventilation (emphysemous regions are poorly perfused, increased work of breathing)

Alveolar hypoventilation

Question 15

What’s the clinical presentation of COPD?

Answer 15

Half are asymptomatic

Half are symptomatic: cough, sputum production, chronic bronchitis, exertional dyspnea, muscular wasting

During an exacerbation: change in sputum, wheezing, increased dyspnea

Question 16

What findings do you have on the physical exam in COPD?

Answer 16

Early dz=normal

Later dz = barrel chest, bilaterally diminished breath sounds, skeletal muscle atrophy

During exacerbation: wheezing, ronchi, cyanosis

Question 17

Chx in COPD?

Answer 17

Big dark lungs

Flat diaphragm (seen better in lateral xray)

Also in CT you can see the airspaces

Question 18

How do you diagnose COPD?

Answer 18

Clinical presentaiton

Airflow obstruction on spirometry that’s not reversible with bronchodilator

Exclude alternative cause

Question 19

Which test is used to diagnose and to stage COPD?

Answer 19

Spirometry

If FEV1/FVC is < 0.70 = COPD

Then use FEV1 for staging

You can further use ABG to stage: PaO2/PaCO2

Question 20

Why is staging important?

Answer 20

It determines how you manage COPD: each stage gets all the stages less severe than it

Stage 1: risk factor reduction, vaccination, short-acting inhalde beta 2 agonist

Stage 2: long acting inhaled bronchodilators, pulm rehab

Stage 3: inhaled corticosteroids

Stage 4: long term O2 therapy, surgical therapy

Question 21

What is Varenicline?

Answer 21

Chantix- smoking cessation drug; partial agonist of alpha4beta2 subumint of nicotinic acetylcholine receptor

Stimulats it (which reduces withdrawal) while blocking nicotine from binding (reduces reward)

33% 6 month quit rate

Take until you’ve quit for 12 weeks and then for 12 weeks after they quit

Poorly tolerated: nausea, HA, insomnia, weird dreams, depression, suicidal thoughts, CV events

Question 22

What are the 2 main classes of drugs used to treat COPD?

Answer 22

Symptom relief and controllers

Question 23

Which drug classes are for symptom relief?

Answer 23

Short acting beta2 agonist (SABA)

Short acting anti-cholinergic

They come in a combo formulation

Question 24

Which drug classes are controllers?

Answer 24

Long acting beta-2 agonist (LABA)

Long acting anti-cholinergic

Glucocorticoid (which can come in a formulation with LABA)

Question 25

What is the overall effect of these drugs

Answer 25

Better lung function

Reduced exacerbation

Patient feels better

No mortality benefit

Question 26

What are the side effects of beta-2 agonists?

Answer 26

tremor, tachycarida, hypokalemia, LABA: possibly death

Question 27

Anti-cholinergics SE:

Answer 27

dry mouth

CV events (maybe)

Question 28

Glucocorticoids SE?

Answer 28

Oral thrush

Cataracts

Osteoporosis

Pneumonia in COPD patients

Question 29

What is Roflumilast?

Answer 29

PDE-4 inhibitor: used in patients who can’t tolerate other treatments

SE= diarrhea, weight loss

Decreases airway inflammation/promotes smooth muscle relaxation

Improves FEV1, decreases exacerbation

Question 30

Which antibiotic is commonly used to treat COPD?

Answer 30

Azithromicin

Decreases exacerbations, improves quality of life

SE= hearing decrements, microbial resistance, CV risk

Question 31

What are the indications for long-term O2 therapy in COPD?

Answer 31

Chronic hypoxemia: PaO2 <55 mmHg, SpO2<88%

Or PaO2 56-59, SpO2 <89% with one of the following: hematocrit >55%, cor pulmonale, or dependent edema

Improves survival, pulm hemodynamics, exercise capacity

Question 32

Which 2 surgeries can you do to treat COPD?

Answer 32

(1) LVRS: lung volume reduction surgery

remove about 1/4 of each lung

Works for select patients: upper lobe predominant emphysema, low exercise capacity

Improves exercise capacity, quality of life, survival

(2) Lung transplant (possibly improved survival, improved quality of life, improved exercise capacity)

Question 33

What does an acute exacerbation of COPD look like?

Answer 33

Increased sputum quantity, thickness, change in color

Often with systemic signs of infection/dyspnea

Question 34

How do you manage acute exacerbation of COPD?

Answer 34

Short acting beta agonists & anti-cholinergics

O2 therapy (but avoid O2 induced hypercapnia)

Systemic antibiotics/corticosteroids

Noninvasive positive pressure ventilation (for acute alveolar hypoventilation/hypercapnia)

Question 35

COPD summary of therapies

Answer 35