Respiratory Medicine Flashcards
What is FEV1, what is a normal value?
FEV1= Forced expiratory volume in 1 second
- In which a person takes a maximal inspiration and then exhales maximally as fast as possible. The important value is the fraction of the total “forced” vital capacity expired in 1 second
- Healthy individuals can expire approximately 80% of the vital capacity in one second
What is FEF25?
Flow is greatest at the start of expiration, it declines linearly with volume. FEF25 = flow at point when 25% of total volume to be exhaled has been exhaled
What is does a low FVC suggest?
FVC—Forced vital capacity; the total volume of air that can be exhaled during a maximal forced expiration effort
A low FVC = airway restriction
FEV1/FVC is <0.7, what does this indicate?
If the ratio is below 0.7 = airway obstruction
FEV1/FVC is normal but FVC is low, what does this indicate?
If the ratio is high i.e. normal but the FVC is low = airway
What is the difference between type 1 and type 2 respiratory failure?
- TYPE 1 RESPIRATORY FAILURE:
• pO2 (partial O2 pressure) is low
• pCO2 (partial CO2 pressure) is low or normal
• With Type 1 = 1 change = low pO2 then normal/low CO2
• Pulmonary embolism (form of ventilation-perfusion mismatch) most commonly causes Type 1
- TYPE 2 RESPIRATORY FAILURE:
• pO2 is low
- pCO2 is high
- With Type2=2changes=lowpO2+highpCO2
• Alveolar Hypoventilation causes Type 2
What can cause respiratory failure?
Respiratory failure can occur as a result of:
• Impaired ventilation:
- Neural problems e.g. due to narcotics, encephalitis, a cerebral space-occupying lesion, motor neurone disease (resulting in neuromuscular weakness) etc
- Mechanical problems e.g. airway obstruction (type 1, if severe type 2, e.g. obstructive sleep apnoea (OSA) - relaxation of pharynx
- Impaired perfusion, if extensive e.g. cardiac failure or multiple pulmonary emboli
- Impaired gas exchange defects, if severe e.g. emphysema or diffuse pulmonary fibrosis
Give 5 signs of hypercapnia
Signs of hypercapnoea (high CO2):
- Bounding pulse
- Flapping tremor
- Confusion
- Drowsiness
- Reduced consciousness
How would you manage Type 1 Respiratory failure?
Management:
TYPE1 RESP FAILURE:
- Treat the underlying cause
- Give O2 (35-60%) by face mask to correct the hypoxia
- If PaO2 does not rise above 8kPa then give assisted ventilation
How would you manage type 2 respiratory failure?
TYPE2 RESP FAILURE:
In type II failure, the respiratory centre is likely to have become desensitised to CO2 levels, and hypoxia will now be its main driving force, thus oxygen therapy should be given with care!
- Give controlled oxygen therapy, starting at 24% O2
- Recheck the ABG after 20 minutes – if the PaCO2 is steady or lower, then you can increase the O2 to 28%.
- If the PaCO2 has risen >1.5kPa– then consider giving a respiratory stimulant such as doxapram (1.5-4mg/min IV) or assisted ventilation.
- You can also see CO2 retention as physical signs – the patient will become drowsy and confused
- If this fails consider intubation / ventilation
What is the difference between obstructive and restrictive respiratory disease?
Give examples of each
Restrictive vs. Obstructive Respiratory Disease:
- Obstructive:
• FEV1/FVC below 0.7 - FEV1 lower than FVC
- E.g.:
ASTHMA:
- Variable airflow obstruction
- Reversible
COPD:
- Relatively fixed airflow obstruction
- May be a mixture of restrictive and obstructive disease
- Restrictive:
- FEV1/FVC above 0.7
- FVC & FEV1 below 80% predicted value
- Due to restriction, lung volumes are small and most of breath is out in first second
- Interstitial lung disease:
- FIBROSING ALVEOLITIS
- SARCOID
What is transfer co efficent?
How does it change?
- Transfer Co-efficient:
- Measure of ability of oxygen to diffuse across the alveolar membrane
- Can calculate by inspiring a small amount of carbon monoxide (not too much since can kill) then hold breath for 10 seconds at total lung capacity (TLC) then the gas transferred is measured
- Low in:
- Severe emphysema
- Fibrosing alveolitis
- Anaemia
- Pulmonary hypertension
- Idiopathic pulmonary fibrosis
- COPD
- High in:
- Pulmonary haemorrhage - can absorb O2 very efficiently due to bleeding resulting in more red blood cells being available
What is asthma?
- Asthma is the most common chronic respiratory disorder encountered in clinical practice.
- It affects over 10% of children and around 5-10% of adults, with the prevalence of asthma increasing.
- Not only does asthma account for a significant morbidity burden it should be remembered that around 1,000 people die in a year from asthma in the UK, 30-40 of whom are children.
- Asthma may be defined as a chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity.
- The symptoms are variable and recurring and manifest as reversible bronchospasm resulting in airway obstruction.
- The immune response is CD4 mediated, and the lungs will show an eosinophil infiltrate
- asthma exists where the obstruction is reversible by >15%, and COPD exists where it is reversible by <15%.
- Asthma often ‘flares up’ with viral infections – which often cause a loud wheeze.
- Asthma may present at any age although it typically develops in childhood
It should be remembered that it is common for young children to wheeze when they develop a virus (‘viral-induced wheeze’). This makes the diagnosis of asthma in younger children difficult.
What are the three characteristics of asthma?
Three main characteristics of asthma (very important this got asked many times in exams):
- Airflow limitation – this is usually reversible, either spontaneously, or with treatment
- Airway hyper-responsiveness – this occurs to a wide range of stimuli
- Inflammation of the bronchi – with infiltration by eosinophils, T cells and mast cells. there is associated plasma exudate, oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage.
How can you test for airway hyper responsiveness?
You can test for airway hyper-responsiveness by asking the patient to inhale gradually increasing amounts of methacholine or histamine. This is known as a bronchial provocation test. This will induce transient airflow limitation in 20% of the population – and these are the patients that exhibit airway hyper-responsiveness.
What are the two types of asthma?

What are the two types of allergic asthma?
The disease can either be intrinsic (aka cryptogenic); where no causatory factor can be found, or extrinsic, where there is a definite external cause.
- Intrinsic – this often starts in middle age, and is sometimes called late onset asthma. No trigger can be identified.
-
Extrinsic – this usually occurs in atopic individuals who have positive skin prick test results. This type of asthma causes 90% of childhood cases, and 50% of adults with chronic asthma. It is often accompanied by eczema.
- Non-atopic individuals can develop asthma in later life via sensitisation to e.g. occupational agents, aspirin, or as a result of taking β-blockers for hypertension or angina.
Extrinsic asthma involves a type I hypersensitivity reaction to inhaled allergens (there is also a delayed phase reaction, type IV hypersensitivity which occurs hours-days after
What are the risk factors for asthma?
A number of factors can increase the risk of a person developing asthma:
- personal or family history of atopy
- antenatal factors: maternal smoking, viral infection during pregnancy (especially RSV)
- low birth weight
- not being breastfed
- maternal smoking around child
- exposure to high concentrations of allergens (e.g. house dust mite)
- air pollution
- ‘hygiene hypothesis’: studies show an increased risk of asthma and other allergic conditions in developed countries. Reduced exposure to infectious agents in childhood prevents normal development of the immune system resulting in a Th2 predominant response
What is atopy?
In which families does it run in?
How does it present?
What are people with asthma also commonly allergic to?
ATOPY:
- individuals who readily develop IgE (produced by B cells) against common environmental antigens
- There is a strong correlation between the levels of IgE and the severity of asthma and airway hyper-responsiveness
- Serum IgE levels are affects by several genetic and environmental factors
- The trait runs in families (i.e. genetic component)
- The ADAM33 gene is associated with airway hyper-responsiveness, and airway remodelling
- The PHF11 gene is associated with increased IgE production
- Environmental factors:
- Early childhood exposure to allergens and maternal smoking has a major influence on IgE production
- Hygiene hypothesis
- Focusing on atopy, patients with asthma also suffer from other IgE-mediated atopic conditions such as:
- atopic dermatitis (eczema)
- allergic rhinitis (hay fever)
Notes:
- A number of patients with asthma are sensitive to aspirin.
- Patients who are most sensitive to asthma often suffer from nasal polyps. (N.B. the nose is part of the respiratory tract from a histological point of view)
- The allergens for asthma are very similar to those that cause rhinitis. Rhinitis is inflammation of the mucosal lining of the upper respiratory tract, particularly affecting areas near the nose; thus causing a constant runny nose.
What is occupational asthma?
Give some common triggers?
When does it present?
Occupational asthma
- Around 10-15% of adult asthma cases are related to allergens in the workplace.
- Patients may either present with concerns that chemicals at work are worsening their asthma or you may notice in the history that symptoms seem better at weekends / when away from work
- It is usually diagnosed by observing reduced peak flows during the working week with normal readings when not at work.
- Diagnosis: serial measurements if PEF at work and away from work
- Exposure to the following chemicals is associated with occupational asthma:
- isocyanates - the most common cause. Example occupations include spray painting and foam moulding using adhesives
- flour
- platinum salts
- soldering flux resin
- glutaraldehyde
- epoxy resins
- proteolytic enzymes
- Typically the onset is 3-6 months after you start working at the place, although it can take years to develop.
- Check for possible occupational asthma by asking employed people with suspected new-onset asthma, or established asthma that is poorly controlled:
- Are symptoms better on days away from work?
- Are symptoms better when on holiday?
What is the pathophysiology of asthma?
Pathophysiology:
- Primary abnormality in asthma is narrowing of the airway which is due to smooth muscle contraction, thickening of the airway wall by cellular infiltration and inflammation and the presence of secretions within the airway lumen
- Exposure to the antigen will make CD4 T cells differentiate into T helper cells (Th2 type, as opposed to Th1), and they will begin to secrete IL-4 and IL-5.
- IL-4 will cause B cells to become plasma cells and being secreting IgE.
- IL-5 will act on eosinophils and mast cells, making them reactive to the new antigen. Other factors are also released that are chemotaxic for eosinophils.
- Inflammation:
- Mast cells:
- Are increased in the epithelium, smooth muscle and mucous glands in asthma
- Become sensitised when IgE binds to mast cell receptor - mast cell will then respond to allergen if it binds to IgE
- When an allergen binds to IgE bound to the mast cell
- Mast cells releases:
- Histamine (seconds) - results in bronchoconstriction (via H1 receptor) and inflammation
- Tryptase (good indicator of mast cell activity since only found in mast cells)
- Prostaglandin 2 (minutes) - type of eicosanoid
- Cysteine leukotrienes (cys-LTs) (minutes) and more potent than histamine - results in bronchoconstriction (via cys-LT1 receptor) and inflammation
- Cytokines; TNF-alpha, IL-3 (increases number of mast cells), -4 (causes IgE synthesis) & -5 - synthesised in hours - results in inflammation and airway remodelling
- All of which act on smooth muscle, small blood vessels, mucus-secreting cells and sensory nerves causing the immediate asthmatic reaction
- Eosinophils:
- Found in large numbers in the bronchial wall and secretions of asthmatics
- Attracted to the airway by cytokines IL-3 & IL-5, these mediators also prime eosinophils for enhance mediator secretion
- When activated, eosinophils release LTC4 and basic proteins such as major basic protein (MBP), eosinophilic cationic protein (ECP) and eosinophilic peroxidase (EPX) that are toxic to epithelial cells
- Both the number and activation of eosinophils are rapidly decreased by corticosteroids
• Dendritic cells & lymphocytes:
- Abundant in mucous membranes of the airways and the alveoli
- Dendritic cells play a role in the initial uptake and presentation of allergens to lymphocytes
- T helper lymphocytes show activation and release of their cytokines is a key part in the activation of mast cells
Changes in the lung after allergen challenge:
- 30 mins after challenge; there is bronchoconstriction
- 3 hours after; the initial bronchoconstriction decreases, then inflammation occurs due to the vasodilation which decreases blood flow and thus leads to a build up of white blood cells, increased vascular permeability and unregulated adhesion molecules
- 6 hours after; There is worsening inflammation resulting in eosinophils (who are attracted to the site by chemotaxis due to IL-5) releasing their mediators that result in a second wave of bronchoconstriction
- Bronchodilators (the β-adrenergics) are good at treating the initial phase reaction; the late phase reaction tends not to respond well.
- Steroids (and other anti-inflammatories) are good for preventing the inflammation that causes the late phase reaction.
- The late phase reaction is more likely in poorly controlled / chronic asthma, where there is already a reasonable aggregation of eosinophils in the mucosa.
Effects of the bronchoconstriction and inflammation on lung function:
- Distal airway hyperinflation and collapse (and obviously reduced gaseous transfer to these regions)
- Mucus plugging of the bronchi – due to increased number of goblet cells – and these also secrete more than normal goblet cells
- Bronchial inflammation
- Curschmann’s spirals – these are bits of epithelium that have been shed, and can be seen on histology of the mucous plugs
- Charcot-Layden crystals – crystals that are formed as a result of eosinophil aggregation
- Thickening of the bronchial basement membrane – this is particularly important, and occurs via the process of remodelling (more on this below lolz). The submucosa becomes thickened, and this means that when the smooth muscle does contract, there is excessive narrowing of the airway in response to the contraction.
- Effects on the epithelium – the epithelium loses many of its columnar ciliated cells, and these are replaced with over-active mucous secreting cells. The mucosa also releases lots of inflammatory proteins. It is also likely to get damaged in the inflammatory processes, and this (along with the excess mucous production) increases the risk of infection.
- Effects on smooth muscle – the smooth muscle is hypertrophied, and also undergoes changes which make it more likely to contract, and more likely to stay contracted for longer.
List 4 symptoms and 4 clinical signs of asthma
Symptoms
- Diurnal variability(symptoms worse at night or early in the morning)
- cough: often worse at night
- periodic dyspnoea/SOB
- wheeze
- chest tightness
- attacks are due to triggers/Provoking factors; allergens, infections, exercise, cold air
Signs
- polyphonic expiratory wheeze on auscultation
- reduced peak expiratory flow rate (PEFR)
Acute asthma features (more on this below):
- worsening dyspnoea, wheeze and cough that is not responding to salbutamol
- tachypnoea
- prolonged expiratory time
- reduced chest expansion
- bilateral expiratory polyphonic wheeze
- maybe triggered by a respiratory tract infection
Define uncontrolled asthma
Uncontrolled asthma:
This describes asthma that has an impact on a person’s lifestyle or restricts their normal activities
This guideline uses the following pragmatic thresholds to define uncontrolled asthma:
- 3 or more days a week with symptoms or
- 3 or more days a week with required use of a SABA for symptomatic relief or
- 1 or more nights a week with awakening due to asthma.
list 4 Differential diagnoses of asthma
Differential diagnosis:
- COPD
- GORD
- Large airway obstruction by foreign body/tumour
- Pneumothorax
- Pulmonary fibrosis
- Bronchiolitis, croup (children)
- bronchiectasis












