COPD

Question 1

what is COPD

Answer 1

chronic obstructive pulmonary disorder
- common, preventable, treatable disase of the lower airway
- its a CHRONIC (persistant) airflow obstrutive disease

• noxious particles (smoke) enter the airway, triggering lung inflammation which impacts the alveoli

Question 2

what is the pathogenesis of COPD

Answer 2

cigarette smoke, biomass fumes etc. + individual host factors (succeptibility) = inflammation in the lung

chronic exposure

the lung inflammation triggers oxidative stress and releases proteinases (these damage the wall, increase mucus, etc.)

these proteinases and the oxidative stress create the COPD pathology

Question 3

A1A deficiency
what is it
who does it affected
when
patients at higher risk for what
treatment

Answer 3

creates COPD (a genetic condtion)

genetic condition in which the body produces mutate A1A – which gets stuck in the liver
- normally –> A1A is released when there is immune response (neutrophil elastase) to prevent that from breaking apart the lungs – its a protector

this enzyme is noramlly produced in the hepatocytes – gets stuck – increased risk for hepatocellular cancer (15% devleop cirrhois)

symptoms: develop between 25-50

treament: COPD treatment (bronchodialators) + plasma A1AT (pro-lastin C)

high clincial sucpicsion in those who are young, few pack years and have COPD and liver signs

Question 4

what is the continuum of COPD
- Chronic bronchitis
- emphysema

Answer 4

COPD pts. can have chronic bronchitis and emphysema (w dont’ necessarily dictate which they have – just COPD)

Chronic Bronchitis
- chronic PRODUCTIVE cough for longer than 3 months in each of 2 consecutive years
- airway inflammation which results in mucus gland hyperplasia, narrowing and reducion in the number of the small airways
- can have CB before COPD diagnosis — can be seen prior to its inhibition of the airflow limiation aspect

Emphysema
- perminent enlargement of the airspaces as a result of increase compliance
- this perminent enlargement damages the walls of the alveoli –> therefore impacting gas exchange (loss of surface area)
- think overinflamtion and hyperaeration

Question 5

symptoms of COPD

Answer 5

symptoms
- the cardinal signs: chronic cough, prodution of sputum, dyspnea (on exercition especially)
- increased AP diameter (chronic retion of air within the destoryed alveoli)
- can also have weight loss/gain and anxiety
- ** always ask about hx.**

Question 6

signs of COPD on exam

Answer 6

signs
- “pink puffer” = emphysema (exhale through pursed lips,
- “blue bloater” = chornic bronchitis (cyanosis, overweight/edema, mucus production)
- crackles/rales (fluid), coarse rhoni, wheezing
- hyperresonance on percussion
- decreased breath sounds
- posture, accessory muscle use
- + Hoovers Sign == paradoxical retraction of the lower airspaces on inspiration – suckingin so much
- muscle jerks due to high CO2
- JVD
- RHF

Question 7

how do you diagnose COPD
- gold standard

• additional tests

Answer 7

spirometry!!! needed for the dx.
FEV1/FVC = < 0.7

the GOLD criteria just helps you decide severity (that is just looking at FEV1)

additional test
- CXR: hyperinflation, luecency and flattened diaphragm
- CT: airspace enlargement and destroyed alveoli
- labs: ABG/AVG, serum bicarb, AAT (A1A)

Question 8

What is the BODE score for COPD? what is is used for?

Answer 8

staging COPD – not for treatment or diagnosis
just lets us know how bad it is

B: Body mass index
O: airflow Obstruction (FEV1 %)
D: Dyspena (via mmrc score)
E: Exercise capactiy walking distance

Question 9

what are MMR and CAT scores for COPD?

Answer 9

staging the COPD – but CAN be used in treatment decisions (used in the ABCD algorithm)

Question 10

what is some non-pharm COPD treatmetn

Answer 10

SMOKING CESSATION!!!!!
- vaccinations to decrease risk of infections (pneumococcal, flu, covid)
- ensure proper inhaler technique
- activity and pulomary rehard
- ocygen therapy if chronic hypoxemia

Question 11

pharm treatment of COPD
groups of meds, some names

Answer 11

• SABA: albuterol (resuce & exacerbation) –> short onset to action
• LABA (maitnence) : formoteral, salmeterol, etc. (all = efficacy)
• LAMA: atrovent
• ICS: fluticosone (for reducing inflammatory)
• theophylline: minimal efficacy, narrow therapeduic index

** combo ICS/SABA, LAMA/LABA, ICS/LAMA/LABA exist**

Question 12

staging of COPD and correltaion to treatment

Answer 12

symptoms: MMRC or CAT score
severity: determiend by # of hospital stays

group A: minimal score of symptoms & no hostpial stays
group B: more symptoms but still no hospital stays
group C: minial symptoms but more hospital stays
group D: lots of symptoms and lots of stays

Question 13

medication treatment of COPD based on the Group GOLD score (initial treatment regimen)

Answer 13

Group A: any bronchodilator
Group B: LAMA OR LABA
Group C: LAMA
Group D: LAMA+ LABA ( LAMA/LABA/ICS for blood eos. >300)

** steroid use is not indicated in COPD pts. except during acute exacerbations or for severe disease in which a triple therapy is most effectice approach or for those with concominant asthma**

Question 14

treatment goals and approachs for an acute exacerpation of COPD (in the hospital/ED you would see this)

Answer 14

• respiratory care –> O2 if needed, intubation, NIV (get ABG to find out)
• steroids: oral prednisone or IV methylpred.
• nebulized bronchodialotrs: SABA or LAMA
• ## antibiotics: azithromycin has anti -inflammatory properties

Question 15

surgical options for extreme cases of severe COPD

Answer 15

lung reduction surgery
- improves elastic recoil and gas exchange (getting rid of the not working areas)

endobronchial valves
- one-way air values let air exit but does not let air in

advanced disease
- lung transplant
- for those GOLD stage 4 disease (FEV1 <25%) BODE 5-6 and resting hypercapnia