W10 ASTHMA COPD

Question 1

What are the 5 phenotypes of asthma

Answer 1

-allergic, often eosinophilic
-non allergic, can be neutrophillic or eosinophillic (less responsive to corticosteriods)
-adult onset / late onset, often non allergic and less responsive to corticosteroids
-asthma with persistant airflow limitation, this is common in long standing asthma who develop airflow limitation that is not reversible due to airway remodelling
-asthma with obesity

Question 2

describe pathophysiology of copd

Answer 2

a modification of normal inflammatory response to chronic irritants

characterised by an increased number of macrophages in peripheral airways, lung parenchyma and pulmonary vessels

with increased neutrophils and lymphocytes = increased release of inflammatory mediators = induction of structural changes secondary to growth factors

Question 3

How does airflow limitation and gas trapping occur in COPD

Answer 3

airflow obstruction caused by mixture of small airway disease and parenchymal destruction, these changes diminish the ability of the airways to remain open during expiration

loss of small airway also constribute to airflow obstruction and mucocillary dysfunction

these changes cause limited ability to empty the lungs during forced expiration and contribute to gas trapping and hyperinflation

Question 4

Why do we see pulmonary HTN in COPD patients

Answer 4

secondary to endothelial cell dysfunction
combo of loss of pulmonary capillary bed due to emphysema and/or hypoxic vasoconstriction of the small pulmonary arteries

Question 5

how do pulmonary gas exchange abnormalities occur in COPD

Answer 5

structural abnormalities in the airways/alveoli and pulmonary circulation alter normal VQ distributions

results in different degrees of arterial hypoxaemia with or without hypercapnia

worsens with disease progression

Question 6

inflammatory cells and mediators asthma

Answer 6

Airway epithelium secretes -> interleukins and TSLP

this attracts / activates-> eosinophils, basophils, mast cells and t helper cells

which causes bronchospasm, mucous hyper-secretion and airway oedema

Question 7

What is FEV1 and FVC

Answer 7

FEV1 = forced expiratory volume 1. the forced expiration volume over one second

FVC= forced vital capacity. the amount of air a person can quickly and forcefully exhale after deep inspiration

Question 8

what is the FEV1:FVC ratio

Answer 8

ratio that assissts in determining obstructuve vs restrictive lung pathologies
<70% = obstructive pattern

Question 9

SABA LABA ICS OCS LTRA LAMA

Answer 9

SABA short acting beta agonist
LABA long acting beta agonist
ICS inhaled
OCS oral
LTRA leukotriene receptor antagonist
LAMA long acting muscarinic antagonist
last two more common in COPD cohort

Question 10

Mechanism of corticosteroids

Answer 10

modulates gene expression, increases anti inflammatory genes, decreases pro inflammatory genes, increases resolution speed and decreases relapse of severities of asthma presentation

Question 11

Magnesium mechanism in use for asthma

Answer 11

leads to smooth muscle relaxation
transient block of NMDA gate Ca channels = muscle relaxation and bronchodilation

Question 12

GOLD (COPD) indications for NIV

Answer 12

resp acidosis with paco2>45mmhg and arterial pH <7.35

severe dyspnoea with clinical signs suggestive of resp muscle fatigue

persistent hypoxemis depsite supplemental oxygen therapy

Question 13

GOLD (COPD) indications for invasive mechanical ventilation

Answer 13

unable to tolerate NIV or NIV failure
post respiratory arrest or cardiac arrest
diminished consciousness, agitatiation that cannot be controlled with sedation
aspiration or persistent vomitting
persistant inability to remove airway secretions
severe haemodynamic instability without response to fluids and pressors
arrthymias
life threatening hypoxaemia in patients unable to tolerate NIV

Question 14

Indications for application of MV in severe asthma

Answer 14

cyanosis
paco2 <60 despite high flow oxygen
rising PaCO2
bradycardia
persistant acidosis
diminishing levels of consciousness

Question 15

normal pip for asthmatics

Answer 15

> 80-100

Question 16

Why would you expect your pplat to be relatively normal is asthmatics

Answer 16

the patho of asthma does not directly involve the alveoli

the pplat reflect lung compliance or alveolar pressure. an increase in pplat would suggest presence of either worsening bronchospasm with associated gas trapping or an expanding pneumothorax

Question 17

How to identify dynamic hyperinflation on MV for asthmatics

Answer 17

Look for an increase in both PIP and Pplat with no change to the pip to pplat gradient

Question 18

What is ACOS and who does it affect

Answer 18

= persistant airflow limitation in pts older than 40 with either asthma hx or large bronchodilator reversibility

tend to be younger, female, high BMI, low socio economic status and lower education levels

exacerbations 4-5 times higher

Question 19

How might asthma become ACOS

Answer 19

smoking - higher risk, shift from eosinphillic to neutrophillic pattern , remodelling of airways

air pollution

loss of elastic recoul and development of emphysema due to ongoing severe asthma

Question 20

how might COPD become ACOS

Answer 20

less compelling

requires 3 pathological traits
- allergen sensitisation,
-airway hyper-responsiveness and
-eosinophillic and type 2 mediated airway inflammation

Question 21

What is end expiratory lung volume and how does it relate to COPD

Answer 21

this is the stasis between tension of the lung walls wanting to collapse and the chest wall wanting to keep them out

ie tension between compliance and recoil

this increases in COPD patients = increase deadspace = increase in non functional space

this means a reduction in respiratory reserve volume = static hyperinflation

Question 22

Why use muscarinic inhalers for copd

Answer 22

promotes lung remodelling
reduces goblet cell secretion of mucous
reduces inflammatory mediators
reduces inappropiate cell proliferation

Question 23

moderate exacerbations/disease process mx for copd

Answer 23

LAMA and LABA
also preventers = corticosteroids
need to have eosinophilic testing done prior though

Question 24

moderate to severe COPD mx
(community)

Answer 24

seretide and symbicort
LAMA, SAMA, LABA and SABAS
+ongoing antibiotics
+PDE4 inhibitors (increase cAMP and promote bronchial smooth muscle relaxation and decrease pro-inflammatory mediators)