COPD Flashcards
Define: COPD
Progressive, chronic disorder characterised by airway obstruction
FEV1 < 80% predicted
FEV1/FVC <0.7
An umbrella term encompassing chronic bronchitis and emphysema
Chronic bronchitis - what is it, how is it diagnosed?
Clinical diagnosis
Cough/sputum for most days for 3 months, 2 years in a row
Emphysema - what is it, how is it diagnosed
Histological diagnosis
Enlarged airspaces in acinus*, alveolar wall destruction. This causes elastic recoil problems :. difficulty exhaling
*we can talk about peri-acinar enlargements and all the different types of airspace enlargement. Or just get a life
HISTOLOGY TIME
The airways are covered by what type of epithelium
Ciliated, pseudostratified, columnar epithelium.
Along with goblet cells here and there. Underneath is the lamina propria. These layers together are the muscosa.
The submucosa (under this) has smooth muscle and mucus glands - the latter which hypertrophy when they get upset (by smoking etc)
PATHOPHYSIOHISTOPATHOIMMUNOLOGICAL…
Whats the eventual result of upset mucus glands in the context of COPD?
Irritant - caused hypertrophy of mucus glands and overproduction of sputum.
These block airways.
They trap air INSIDE the lungs.
(Think hyperinflated chest, bullae and the boys)
Bullae? Are they important?
Focal regions of empysema in the lungs
If they rupture then they can cause pneumothorax.
Kind of a big deal (Anchorman 2004)
Can you have asthma and COPD?
With God all things are possible (Mat 19:26)
But it’s unlikely to have both together - though they share some similarities they can be confused
What makes a COPD diagnosis more likely than Asthma?
Onset after 35 Smoker/lives in pollution Chronic dyspnoea Sputum Little diurnal/day to day variation FHx of COPD - a1 antitrypsin deficiency
a1 anti-trypsin
Talk to me
Produced in liver. A deficiency doesn’t mean you don’t make it - it means it can’t escape the liver.
It inhibits proteases in the lungs, so in its absence these proteases go wild to the detriment of the lungs. in 10% - liver cirrhosis occurs too, which isn’t ideal.
A genetic cause of COPD
Symptoms
Cough
Sputum
Dyspnoea
Wheeze
Signs
RR up Use of respiratory muscles Hyperinflated chest Resonant to percussion Wheeze Cyanosis Cor pulmonale (R-HF)
Pink puffers (emphysematous)
Breathless (increased alveolar ventilation)
Normal Pa02
Normal or low PaCO2
NOT cyanosed (they are compensating)
Exhale through pursed lips
Weight loss from the effort of breathing
Barrel chest
Can lead to type 1 resp failure
Blue bloaters
Not breathless (decreased alveolar ventilation)
Low PaO2
High PaO2
Cyanosed - not compensating
Rely on hypoxic drive, relatively insensitive to CO2 - so don’t be too generous with the O2 (88-92% target sats)
Tests
FBC - raised PVC (haemocrit) CXR - hyperinflation ECG - RA, RV hypertrophy ABG - PaO2 / PaCO2 - as described LFTs - obstructive pattern, increased TLC and RV, DLCO down
Grade COPD severity (in terms of FEV1)
FEV1 - Severity >80% - mild 50-79% - moderate 30-49% - severe <30% - very severe
Treatment of all COPD
Smoking cessation
More exercise
Lose weight, sort out diet
Flu jabs
Treatment of mild/moderate COPD
Tiotropium or salmeterol
Treatment of severe COPD
Combination LAMA/inhaled steroid inhaler
Treatment of very severe COPD
Tiotropium, LAMA, inhaled steroid
Plus steroid trial, theophylline
See specialist
Treatment of COPD - despite Rx. patients PaO2 is still less than 7.3. Shall shall we do?
Long term oxygen therapy (LTOT)
Tiotropium
Long acting anti muscarinic LAMA
- Prevent breathless exacerbation of COPD
Competitive inhibitor of ACh.
Normally the ACh stimulates the muscarinic receptor to activate parasympathetic effects.
So blocking this causes:
increase HR/conduction
Reduce smooth muscle contraction
Reduce secretions from glands (in resp/gastro tract)
Pupils dilate
Ipratropium
Short acting anti muscarinic
Can be used as a reliever
