Respiratory III (COPD; Acute asthma) Flashcards
Define COPD [1]
Chronic obstructive pulmonary disease (COPD) involves a long-term, progressive condition involving airway obstruction, chronic bronchitis and emphysema. It is almost always the result of smoking and is largely preventable.While it is not reversible, it is treatable.
Define chronic bronchitis [1] and emphysema [1]
Chronic Bronchitis- the presence of chronic productive cough and sputum for at least 3 months in each of two successive years
Emphysema involves damage and dilatation of the alveolar sacs and alveoli,
Describe the typical presentation of a COPD patient
A typical presentation of COPD is a long-term smoker with persistent symptoms of:
- Shortness of breath
- Cough
- Sputum production
- Wheeze
- Recurrent respiratory infections, particularly in winter
- Barrel chested
Which symptoms does COPD not cause? [4]
Clubbing
Chest pain
Haemoptysis
Chest pain
If have these, investigate other diseases
Describe the pathophysiology of COPD [5]
Inflammation
- Inhalation of noxious particles or gases, such as cigarette smoke or occupational irritants, triggers an inflammatory response in the airways and lung parenchyma.
- Causes infiltration of neutrophils, macrophages, and lymphocytes, leading to the release of pro-inflammatory cytokines and chemokines.
Protease-Antiprotease Imbalance
- Causes an imbalance between proteases (e.g., neutrophil elastase, matrix metalloproteinases) and antiproteases (e.g., alpha-1 antitrypsin, tissue inhibitors of metalloproteinases)
- The excess protease activity degrades extracellular matrix components, leading to the destruction of lung parenchyma and the development of emphysema.
Oxidative Stress:
- Toxins induce ROS
- ROS causes direct cellular damage, impair antiprotease activity, and promote inflammation
Airway Remodeling
- thickening of the airway wall
- increased mucus production
- goblet cell hyperplasia
Alveolar Destruction
- destruction of alveolar walls, leading to the formation of larger, less efficient airspaces and a reduction in the surface area available for gas exchange.
Explain genetic disorder can lead to early onset COPD? [1]
Alpha-1 antitrypsin deficiency:
- reduced inhibition of neutrophil elastase, leading to uncontrolled protease activity and lung tissue destruction
What are the 5 grades of the MRC dyspnoea scale? [5]
- Grade 1: Breathless on strenuous exercise
- Grade 2: Breathless on walking uphill
- Grade 3:Breathlessness that slows walking on the flat
- Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
- Grade 5: Unable to leave the house due to breathlessness
mMRC ≥2
What investigations would you conduct for COPD? [7]
Spirometry:
- FEV1/FVC < 70%
Pulse ox:
- low oxygen saturation
- In patients with chronic disease, an oxygen saturation of 88% to 90% may be acceptable.
CXR:
- hyperinflation
- bullae
- flat hemidiaphragm
COPD Assessment Test (CAT) or Modified British Medical Research Council (mMRC)
- mMRC ≥2 or CAT score ≥10 indicates higher symptoms burden
FBC
- polycythaemia (raised haemoglobin due to chronic hypoxia),
- anaemia
- infection & WBC count
BMI:
- weight loss occurs in severe disease
Serum alpha-1 antitrypsin
- look for alpha-1 antitrypsin deficiency
What are common ECG changes might you see in COPD patients? [4]
- Rightward deviation of the P wave and QRS axis
- Low voltage QRS complexes, especially in the left precordial leads (V4-6)
- With development of cor pulmonale, right atrial enlargement (P pulmonale) and right ventricular hypertrophy
- Arrhythmias including multifocal atrial tachycardia
State how the different severity scores for COPD are calculated [4]
The severity can be graded using the forced expiratory volume in 1 second (FEV1):
Stage 1 (mild):
- FEV1 more than 80% of predicted
Stage 2 (moderate):
- FEV1 50-79% of predicted
Stage 3 (severe):
- FEV1 30-49% of predicted
Stage 4 (very severe):
- FEV1 less than 30% of predicted
If the FEV1 is greater than 80% predicted but the post-bronchodilator FEV1/FVC is < 0.7 then this is classified as Stage 1 - mild. Symptoms should be present to diagnose COPD in these patients
Describe the stepwise approach to treating COPD
First line treatment:
- SABA (salbutamol) or SAMA (e.g ipratropium bromide)
The next stage depends on whether the patient has asthmatic features / features suggesting steroid responsiveness
If NONE: use a combination:
- Add LABA AND LAMA regularly
If ASTHMATIC features:
- Add LABA & ICS regularly
Next stage for both:
- Use LABA AND LAMA AND ICS
What are the determinants that decide if COPD is asthmatic or steroid responsive? [4]
- Previous diagnosis of asthma or atopy
- Variation in FEV1 of more than 400mls
- Diurnal variability in peak flow of more than 20%
- Raised blood eosinophil count
Label A-E
When is oral theophylline indicated for COPD treatment? [1]
NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy
Polypharmacy of which drug classes with oral theophylline would cause the dose of theophylline to decrease [2]
the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed
Which antibiotic is given as oral prophylactic antibiotic therapy in some COPD patients? [1]
azithromycin prophylaxis is recommended in select patients
Explain which further tests would you need to conduct if giving azithromycin prophylaxis? [4]
ECG:
- can cause QT prolongation
LFTs:
- Can cause liver injury
CT scan:
- to exclude bronchiectasis
Sputum culture:
- exclude atypical infections and tuberculosis
Name a long-term risk of azithromycin use [1]
Long-term azithromycin use is associated with clinically significant hearing loss
What need to consider before prescribig azithromycin in COPD patients? [1]
. Little evidence of treatment benefit is seen in
current smokers
When are mucolytics indicated in COPD patients? [1]
Consider if have a chronic productive cough
Name an example and describe the MoA of phosphodiesterase-4 (PDE-4) inhibitors in COPD
roflumilast:
- antiinflammatory and immunomodulatory effects in the pulmonary system due to increased levels of intracellular cyclic AMP
When are roflumilast / PDE-4 inhibitors indicated in COPD treatment? [2]
FEV1 < 50%
AND
Ptx has two or more exacerbations in previous twelve months despitre triple therapy (LAMA; LABA & ICS)
A 62-year-old man presents to his general practitioner (GP) with symptoms of exertional breathlessness, wheeze and cough. He has a 30 pack-year smoking history.
As part of the patient’s work-up, spirometry is requested:
FEV1/FVC ratio 0.61
Given the likely diagnosis, which of the following would be an appropriate first-line treatment?
Ipratropium
Formoterol
Salmeterol
Tiotropium
Beclometasone
Ipratropium
SAMA or SABA is first line COPD
Describe what is meant by the term cor pulmonale [2]
RIght-sided heart failure caused by respiratory disease:
- The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) limits the right ventricle pumping blood into the pulmonary arteries.
- This causes back-pressure into the right atrium, vena cava and systemic venous system.
What are the most common causes of cor pulmonale? [5]
COPD (the most common cause)
Pulmonary embolism
Interstitial lung disease
Cystic fibrosis
Primary pulmonary hypertension
State 6 examination findings of cor pulmonale [6]
- Hypoxia
- Cyanosis
- Raised JVP
- Peripheral oedema
- Loud second heart sound
- systolic parasternal heave
- Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
Describe how you treat cor pulmonale? [2]
Which drugs are not recommended? [3]
Loop diuretics for oedema
LTOT
ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE
Explain the physiological reasons of what can happen to CO2 levels when treated with oxygen in COPD patients? [2]
Many patients retain CO2 when treated with oxygen (oxygen induced hypercapnia)
Due to:
Increased V/Q mismatch (most important)
- COPD ptx optimise gas exchange by hypoxic vasoconstriction leading to altered Va/Q ratios
- Excessive oxygen administration overcomes this, leading to increased blood flow to poorly ventilated alveoli, and thus increased Va/Q mismatch and increased physiological deadspace
The Haldane effect:
- deoxygenated Hb binds CO2 with greater affinity than oxygenated Hb
- Thus: oxygen induces a rightward shift of the CO2 dissociation curve (Haldane effect)
Describe the pathophysiological changes that occur in acute exacerbations of COPD [5]
- Increased inflammation, mucosal oedema and bronchospasm further limit expiratory flow
- Gas trapping worsens, increasing ventilation-perfusion mismatch
- The resulting hypoxia and hypercapnia trigger the neural drive to increase ventilation
- Respiratory muscles fatigue, leading to a ‘neuromechanical decoupling’ that reduces the ventilatory drive
- Existing cardiac dysfunction worsens due to increasing pulmonary vascular resistance
What PEF can you discharge if other needs are met? [1]
State some reasons why might not be discharged [5]
> 75% after 1hr
A 35-year-old lady with a history of asthma is brought to the Emergency Department with an acute asthma attack. She has previously been admitted to the intensive therapy unit (ITU) with the same problem. Treatment is commenced with high-flow oxygen and regular nebulisers.
Which of the following is a feature of life-threatening asthma?
Normal PaCO2
Peak expiratory flow rate < 50% of predicted or best
Pulse rate 105 bpm
Respiratory alkalosis
Unable to complete full sentences
Normal PaCO2
