COPD

Question 1

COPD

Answer 1

• persistent, widespread inflmtn of the airway, parenchyma, and vasculature
• leading cause of death

Question 2

what is parenchyma and vasculature?

Answer 2

parenchyma is the epithelial cells involved in gas exchange at the alveolar level

vasculature is the vessels involved in gas exchange

Question 3

what does COPD involve?

Answer 3

chronic bronchitis and emphysema

• neither are fully reversible and usually coexist
• may coexist with asthma

Question 4

is it acute or chronic?

Answer 4

• acute, chronic and recurrent

- when it recurs, a/w obstruction is acute

Question 5

etiology and risks

Answer 5

• smoking (80-90%)
• ageing (risk factor)
• recurring infections
• genetic deficiency of alpha-1 antitrypsin

Question 6

explain what happens when the resp tract gets irritated by smoking

Answer 6

goblet cells in epithelial lining increase mucus prod as a natural defense mechanism to protect the a/w lining

• impedes gas exchange
• mucociliary blanket is also a defense mechanism; hypersecretion of mucus overwhelms cilia and they aren’t able to sweep up harmful debris

Question 7

irritants in smoke causes damage to…

Answer 7

cilia, capillaries and alveoli

- increased mucus secretion occupies lumen of a/w = obstruction

Question 8

what do irritants induce?

Answer 8

coughing, which is a defense mechanism for expectoration of harmful debris

• if chronic or recurring, can damage a/w and irritate inflamed surface causing increased damage to tissues
• also damages walls between alveoli, decreasing fx

Question 9

explain the relationship between smoking and cancer

Answer 9

some compounds in irritants are organ-specific carcinogens that are absorbed into circulation and make contact with target organs, causing cancer

Question 10

why is ageing a risk factor?

Answer 10

as one ages, there’s degenerative changes to tissue causing decreased compliance and elasticity

Question 11

how does recurring infections affect the lungs?

Answer 11

infection -> inflmtn -> tissue damage -> l/o elasticity and compliance

Question 12

what does excess compliance cause?

Answer 12

floppy lungs and less elasticity, causing a problem inflating the lungs

Question 13

manifestations

Answer 13

• onset is insiduous, mnftns become more pronounced later in life (late 40-60s)
• dyspnea OE initially then at rest w/ progression of disease
• pronounced hypoxemia and hypercapnia
• cough (productive in bronchitis)
• activity intolerance
• increased sputum (copious amounts)
• wheezing and wet crackles d/t fluid buildup
• barrel chest (emphysema)
• pursed lip breathing and nasal flaring
• prolonged exhalation

Question 14

hypercapnia

Answer 14

increased CO2 levels in blood

Question 15

explain barrel chest in emphysema

Answer 15

• increased resp effort of accessory muscles
• chest becomes fixed in an inspiratory position b/c air is trapped between alveoli
• ratio of APD:TD is usually 1:2, but with barrel chest is 1:1 or even 2:1

Question 16

diagnosis

Answer 16

• Hx, Px
• CXR -> to find consolidation, damage and decreased vol of lungs
• pulmonary function tests
  ~spirometry
  ~FVC: total vol maximally, forcefully exhaled
  ~FVE1: vol of air forcefully exhaled in 1s
  ~total long volume, TV
• labs (ABGs)

Question 17

treatment

Answer 17

• manage progression (smoking cessation, avoid airway irritants like strong odours, smoke from fires)
• vaccinations d/t increased risk for infection
• drugs (stage based)

Question 18

early stage treatment

Answer 18

1st line therapy = short-acting beta agonist + anticholinergics

Question 19

function of beta-adrenergic agonists

Answer 19

bronchodilators that stimulate B2 adrenergic recpetors in the lings, activating adenylate cyclase to prod cAMP, triggering relaxation of smooth muscle

Question 20

what happens when adrenaline binds with smooth muscle?

Answer 20

it binds to the beta receptor, relaxing the smooth muscle. Agonists bind and relax smooth muscle, causing bronchodilation

Question 21

function of anticholinergics

Answer 21

bronchodilators that act by blocking Ach receptors on the bronchial tree so that the PNS isn’t activated to release Ach -> causes bronchodilation

Question 22

more advanced COPD-stage treatment

Answer 22

add inhaled steroids
~decrease inflmtn by decreasing release of
mediators and limiting WBC activity and increasing
responsiveness of bronchial smooth muscle to
beta-agonists

Question 23

late stage treatment

Answer 23

• long acting B-agonists

- theophylline

Question 24

theophylline

Answer 24

• causes bronchodilation by increasing levels of cAMP to trigger smooth muscle relaxation
• has short and long-acting forms
• can reduce inflmtn