Cough, Asthma & COPD

Question 1

What is Asthma

Answer 1

It is a common acute reversible obstructive pulmonary diseae that leads to acute attacks of coughing wheezing and feelings of breathlessness & a tight chest.

Question 2

Discuss the basic epidemiology & pathophysiology of asthma

Answer 2

Asthma is often associated with a family history of atopy, which includes the atopic triad of asthma, allergic rhinitis, and atopic eczema.
The disease involves a type 1 hypersensitivity reaction, with allergens stimulating Type 2 helper T cells to produce cytokines like IL-4, IL-5, and IL-13.
The inflammation of the respiratory airways results in bronchial hyperresponsiveness and reversible bronchoconstriction.

Question 3

Discuss the basic presentation of asthma

Answer 3

• Wheeze
• Dyspnoea
• Cough (may be nocturnal)
• Chest tightness
• Diurnal variation (symptoms worse in the morning)

Question 4

Discuss the basic investigation of an acute asthma attack

Answer 4

• Routine blood tests (including FBC, CRP) – to look for precipitating causes of an asthma attack (eg. infection)
• Chest X-ray – to exclude pneumothorax or consolidation
• Arterial bloods gas
  In a tachypnoeic patient respiratory alkalosis is expected – owing to hyperventilation causing low paCO2 & paO2 will likely be high
• a falling respiratory rate is a sign of patient fatigue
  paCO2 will return towards normal – this is a very concerning sign and the patient = requires urgent escalation
  type 2 respiratory failure (low paO2 and high paCO2) due to hypoventilation is a sign of a life-threatening attack

Question 5

Discuss the basic investigation of Chronic Asthma

Answer 5

• Peak flow diary – due to diurnal variation these readings will be lower in the mornings
• variability >20% is diagnostic
• Bloods – total IgE and eosinophils will be raised; can also test for specific allergens
• Chest X-ray to exclude other causes of wheeze
• Spirometry – FEV1/FVC <0.7 (obstructive spirometry)
• Performed before and after a bronchodilator – reversabilty is expected
• Fractional exhaled nitric oxide (FeNO) – >40 ppb in adults or >35 ppb in children

Question 6

What are the signs of a severe Asthma attack?

Answer 6

Signs of a severe attack:
* inability to speak in complete sentences
* respiratory rate >25 breaths per minute
* peak flow 33–50% predicted
* heart rate >110 bpm

Question 7

What are the signs of a Life Threatening Asthma Attack

Answer 7

Signs of a life-threatening attack:
* peak flow <33% of predicted
* silent chest
* altered consciousness: confusion or drowsiness
* bradycardia
* hypotension
* hypoxia
* cyanosis
* exhaustion
These patients should be urgently escalated to intensive care.

Question 8

What are high risk features for a severe asthma attack?

Answer 8

• Previous intensive care admission
• Those on step 3 or higher of the stepwise asthma treatment pathway
• Hospital admission in the last year

Question 9

Discuss the management of Acute Asthma

Answer 9

Acute Asthma
* ABCDE approach
* Ensure the patient is in a visible, monitored environment
* Ensure a patent airway
* Ensure oxygen saturations of 94–98%
* Nebulisers (eg. salbutamol, ipratropium)
* Steroids – oral prednisolone or IV hydrocortisone (if severe asthma or unable to swallow)

Question 10

Discuss the management of Chronic Asthma

Answer 10

Nonpharmacological
* Smoking cessation
* Avoidance of precipitating factors (eg. known allergens)
* Review inhaler technique

Pharmacological (stepwise approach based on BTS Guidelines)
* Step 1: short-acting inhaled β2 agonist (eg. salbutamol)
* Step 2: add low-dose inhaled corticosteroid steroid (ICS)
* Step 3: add long-acting β2 agonist (eg. salmeterol)
* if no benefit, stop this and increase ICS dose
* if benefit but inadequate control, continue and increase ICS dose
* Step 4: trial of oral leukotriene receptor antagonist, high-dose steroid, oral β2 agonist, oral theophylline
Patients escalated to steps 3 and 4 should be referred to a respiratory specialist.

There are also now biologic therapies in the form of monoclonal antibodies
* these aim to suppress overactivity of the immune system by either directly targeting eosinophils or allergy processes
* they are highly specialised, expensive treatments and strict criteria must be met to access them

Patients will often be educated that their treatment consists of:
* reliever inhalers (salbutamol) and
* preventer inhalers (long-acting β2 agonist or ICS)

Question 11

Discuss the prognosis of Asthma

Answer 11

Asthma commonly develops in children but can present for the first time in adults
those who had childhood asthma can ‘grow out’ of mild symptoms but may find symptoms recur with certain triggers
eg. weather changes, pollen, and viral infections

Question 12

Discuss the basic epidemiology & pathophysiology of Chronic Bronchitis

Answer 12

Smoke, pollution or occupational dust particles are inhaled and over time lead to Hypertrophy and hyperplasia of Goblet and Bronchial mucinous gland cells. This leads to Hypermucous production in the Large and small airways. As a result Air becomes trapped in the Alveoli which increases the partial pressure of C02 and decreases the partial pressure of 02. As a result the
diffusion gradient to the bloodstream is affected leading to acidosis of the blood, this can cause vasoconstriction to reduce to the effected alveoli, however as many alevoli are affected this increases the workload of the pulmonary vascular supply and therefore the right side of the
heart. Leading to right sided heart failure.

Question 13

Discuss the “difficult-to-manage asthma”, non-concordance with treatment

Answer 13

Asthma often gets worse for a short period of time, this could be because of a cold, stress or hay fever but if the patient is having asthma symptoms 3 times or more a week whilst on Step 3 or 4 of the treatment ladder then they have “difficult to manage” asthma.
This is not the same as severe asthma – severe asthma is asthma that does not respond to treatment but with difficult to treat asthma it is possible to get good control with the right support
Why might asthma be harder to control?
* Smoking
* Related Health conditions such as GERD
* Hormones around the menopause & periods
* Being overweight
* Non-compliance – not taking the preventative inhaler everyday
What to recommend that might help?
* Taking the preventative inhaler everyday
* Using a written asthma action plan agreed with your GP
* Keep a peak flow diary along with a record of triggers & symptoms
* Get support to quit smoking

Question 14

Discuss the link between Asthma & GERD

Answer 14

Reflux may induce asthma directly or indirectly
* Directly by affects on the airway through an aspiration-induced response
* Indirectly by neurologically induced inflammation
Reflux may induce bronchoconstriction through a vagus-mediated reflex, or through neurally bronchial reactivity or directly through microaspiration
Asthma may predispose to GERD by a variety of mechanisms including;
* Increased intrathoracic pressure
* Vagus nerve dysfunction
* Altered diaphragmatic crural function
* Decreased lower oesophageal sphincter pressure due to asthma medicines
Hyperinflation common is asthma may also lead to changed pressure between the lungs and oesophagus that leads to an impaired barrier to reflux
Changing asthma medication may lower GERD symptoms. Medications such as Theophylline may lower oesophageal sphincter tone causing GERD symptoms so avoiding these asthma medications will help to reduce GERD.

Question 15

Discuss the link between Asthma & Rhinitis

Answer 15

The mucous membranes of both the upper & lower respiratory system is covered in pseudostratified columnar ciliated epithelium and so both are susceptible to inhaled allergens. Exposure to allergen triggers an immediate reaction by mast cells and histamines, leukotrienes and prostaglandins. In rhinitis this leads to nasal congestion and runny nose from an increase in vascular permeability and in asthma it results in bronchospasm. The late phase reaction of both is triggered by CD₄⁺T cells. This shows a common cellular inflammation pattern however this is only initially as the long term structural consequences differ which the epithelium being disrupted in asthma but not rhinitis.

Question 16

What is COPD

Answer 16

COPD (Chronic obstructive pulmonary disease) is an umberlla term for the irreverisble reduction
in airflow in the lungs, importantly, caused by the inhalation of toxic dust or smoke particles
which cause damage to the lungs. It includes the conditions of Chronic Bronchitis, Emphysema
and Recurrent or irreversible asthma

Question 17

Discuss the basic epidemiology & pathophysiology of Emphysema

Answer 17

Ciggarrete smoke, Pollution and dust particles lead to an inflammatory response within the alveoli, this draws in macrophages and other inflammatory cells which secrete proteases such as collagenase and elastase. This breaks down the elastin fibres of the alveoli reducing structural integrity. This has multiple effects, firstly during expiration the air moves through the airways at a high velocity leading to a decreased pressure in the airway. Because of the loss of structure this causes the airway to collapse, as a result patients will use pursed lip breathing to reduce airflow and airway collapse. Secondly the disstention force of the Alveoli decreases meaning less volume is require to expand the alveoli due to the loss of elastin, increasing
compliance. This leads to the alveoli expanding more than they should and causing the breakdown of septa leading to alveoli coalescence. This reduces the area of gas exchange in the alveoli leading to a similar build up of C02 in the bloodstream as in Chronic bronchitis. In severe Emphysema the alveoli expand to such an extent that they can burst though the visceral pleura leading to a pneumothorax.
There are 2 patterns of Emphysema.
1. Centriacinar - Caused by cigarette smoke depositing mostly in the proximal alveoli, this primarily affects the upper lobes of the lungs
2. Panicar - Caused by a congenital deficiency in Alpha1-Antitrypsin which neutralises elastase. As a result there is a continued breakdown of elastin across the whole of the acinus / small airways

Question 18

Discuss the basic presentation of Emphysema/COPD

Answer 18

Signs and Symptoms of Chronic Bronchitis
* Wheeze - Caused by a restricted airway
* Crackles - Caused by popping open of the airway
* Productive cough - Clearing of the mucous
* Recurrent infections - Increased mucous and decreased cillia size leads to trapping of bacteria
* Cyanosis - Blue lips, Increased C02 concentration in the blood
* COR pulmonale - Right sided heart failure as previously mentioned
Signs and symptoms of pure Emphysema
* Pursed lip breathing
* Non-productive cough
* Weight loss due to increased energy breathing
* Cor pulmonale
* Shortness of breath

Question 19

Discuss the basic investigation of Emphysema/COPD

Answer 19

Spirometry
In a healthy patient you Divide the FEV1/FVC and you get a figure of 0.8. In COPD patients this number is decreased. To determine the severity of the disease you can look at this figure using the GOLD staging measurement.
● stage I: mild, FEV1 > 80% of normal
● stage II: moderate, FEV1 = 50-79% of normal
● stage III: severe, FEV1 = 30-49% of normal
● stage IV: very severe, FEV1 <30% of normal or <50% of normal with presence of chronic respiratory failure present
* Arterial Blood gas - Raised C02 partial pressure and reduced 02, Decreased pH
* ECG - Atrial fibrillation in acute cases due to overuse of salbutamol
* P-pulmonale (right atrial hypertrophy) Right ventricular hypertrophy
* Chest X-ray - Commonly non specific signs however in severe emphysema you may
* see a hyperinflated chest in a lateral view, and a flattened diaphragm.
* Use a COPD assessment tool (CAT)
* Aswell as a mMRC Dysepnea scale

Question 20

Discuss the basic management of Emphysema/COPD

Answer 20

Non-Pharmacological
* Smoking cessation - There is evidence that Electronic cigarettes reduce Changes in COPD, however patches and nicotine gum should be offered first.
* Nutrional supplementation - Some weak evidence that Vitamin D can help, but increasing calorie consumption is also advisable due to weight loss in emphysema
* Pulmonary rehabilitation
Pharmacological
* First line - Inhaled short acting Beta 2 agonists such as salbutamol
* Second Line - Long acting Beta 2 agonists such as Salmeterol and formoterol
* Third line - Long acting muscarinics antagonists such as tiotropium
* Fourth line with many exacerbations - LAMA & LABA and consider using ICS if there is repeated exacerbations, high levels of eosinophillic infiltration or asthma overlap.
* Oral prednisolone may be used for a severe exacerbation
* Consider Non-Invasive ventilation, however getting patients off ventilation is hard. Always do a chest x-ray before giving oxygen or ventilation due to possible pneumothorax leading to a tension pneumothorax.
Indications for Surgery
A younger patient with upper lobe predominant emphysema may undergo a lung volume reduction surgery to decrease compliance

Question 21

What is Atopy?

Answer 21

Atopy is the tendency to develop IgE antibodies to commonly encountered environmental allergens by natural exposure where route of entry is mucosal surfaces.

Question 22

Discuss the immune mechanisms of atopic disease and our current understanding of environmental and dietary causes

Answer 22

• The central mechanism of atopic allergy is** type I hypersensitivity**, mucosal contact with allergen results in APC uptake where the allergen is held on MHC II for a helper T cell to identify. A previously committed B cell interacts with this T cell and makes an IgE antibody. Nature of APC could be important in determining whether IgE antibody is made over IgG, in eczema and allergic rhinitis, Langerhans cells which are HLA-DR positive and bear high affinity IgE receptors have been observed. Class switching to IgE is promoted by cytokines IL-4 and IL-13 and is inhibited by interferon gamma, in atopics, increased levels of TH2 producing IL-4 have been described.
• Class switching with production of mRNA for IgE has been described within 30 mins of allergen contact, this probably takes place in the local lymphoid tissues. Its then rapidly bound to its Fc receptors on mast cells and basophils thus sensitising them. Subsequent contact with this allergen results in cross linking between IgE and Fab portion of the cells causing calcium influx, cell degranulation and mediator release.
• Certain mediators are preformed in granules whereas others are formed after phospholipase A2 breakdown of cell membrane releasing arachidonic acid, this goes on to produce prostaglandins, thromboxanes or leukotrienes.

Question 23

Discuss our current understanding of environmental and dietary causes of Atopy

Answer 23

• Over 250 materials encountered in the workplace can cause occupational asthma, which accounts for up to 15% of all asthma cases.
• Smoking increases this risk.
• Most asthmatics wheeze after prolonged exercise or inhalation of cold, dry air.
• Exercise-induced wheeze is driven by release of histamine, prostaglandins (PGs) and leukotrienes (LTs) from mast cells, as well as stimulation of neural reflexes.
• Increased intake of fresh fruit and vegetables has been shown to be protective, possibly owing to the greater consumption of antioxidants or other protective molecules such as flavonoids, genetic variation in antioxidant enzymes is associated with more severe asthma.

Question 24

What are the 2 theorys associated with Atopy? Describe them

Answer 24

The ‘hygiene hypothesis’ suggests growing up in a clean environment may predispose you towards an IgE response to allergens, early exposure to inhaled and ingested products of microorganisms as occurs in livestock farming communities may reduce risk of allergies/asthma
The dual allergen exposure hypothesis suggests that when peanut exposure occurs through the skin T cell proliferation is skewed to the Th2 cell phenotype which will lead to IgE production, whereas early oral exposure causes T-cell skewing towards Th1 cell subtypes which is more in line with tolerance rather than sensitisation.

Question 25

Discuss the presentation & key differential diagnosis of acute breathlessness

Answer 25

Acute dyspnea is classified as breathlessness that onset hours to days ago with previously normal breathing

DDX
* Obstuctive Lunch Disease; Asthma, Anaphylaxis, COPD
* Filling of alveolar spaces; Pneumonia, ARDS, haemorrhage
* Compression of the lung; Pleural effusion, Pneumothorax
* Impairment of Resp Muscles; Ascities, pregnancy, NMDs
* Decrease of O2 capacity; Anaemia, CO poisoning
* Panic Attack

Question 26

Discuss the key differential diagnosis of acute respiratory distress

Answer 26

• Congestive heart failure
• Cariogenic oedema
• Exacerbation of interstitial lung disease
• Diffuse alveolar haemorrhage
• Pulmonary vasculitis
• Disseminated malignancy
• Pneumonia

Question 27

Discuss the presentation & initial investigation diagnosis of acute respiratory distress

Answer 27

ARDS presents as;
* SOB to severe difficulty breathing
* Short fast breaths
* Chest pain
* Tachycardia
* Diaphoresis
* Cyanosis - due to low blood oxygenation
Investigations;
* Clinical presentation and history; diffuse crackles on lung auscultation
* Chest xrays; Bilateral alveolar infiltrate/Pulmonary oedema with no cardiovascular cause
* CT scan; Bilateral airspace opacities
* Ultrasound; Sub pleural consolidations/Pleural line irregularities/No lung gliding
* Arterial blood gases

Question 28

Discuss the initial management of acute respiratory distress

Answer 28

• Antibiotics
• Diuretics
• Oxygen Therapy
• Mechanical Ventilation

Question 29

What is Acute Respiratory Distress (ARDS) & what causes it?

Answer 29

ARDS is a life threatening illness that happens when the lunghs aren’t working properly.
It usually occurs as a complication of other serious conditions;
* Sepsis
* Acute lung injury
* Gastric contents aspiration
* Infections e.g pneumonia
* Aspiration; Accidentally inhaling vomit or food; Drowning
* Smoke inhalation
* Serious burns
* Having blood transfusions
* Having lung transplant

Question 30

Discuss the presentation & initial investigation of chronic breathlessness/ dyspnoea

Answer 30

The patient may describe the symptom of breathlessness in a variety of ways. Common terms used are ‘puffed’, ‘can’t get enough air’, and ‘feeling suffocated’.
Key points to establish from the history include:
* Speed of onset
* Progression and variability
* Exacerbating and relieving factors
* Response to any treatment
The level of breathlessness should be quanitifed using a grade system that considers impact on quality of life.

Initial testing should include:
* Pulse oximetry
* FBC
* Basic Metabolic Panel
* Chest Radiography
* Spirometry
If the diagnosis remains unclear after these tests, anxiety or hyperventilation, deconditioning, or neuromuscular disease should be considered in the patient.

• Chest Radiography
• Electrocardiography
• Spirometry
• Computed Tomography
• Diagnostic bronchoscopy

Question 31

Discuss the initial management of chronic breathlessness/ dyspnoea

Answer 31

Hypoxia is the only indication for LTOT.
Smoking Cessation
Occupational Therapy
Respiratory Physiotherapy
Weight Management

Question 32

Discuss the key differential diagnosis of chronic breathlessness/ dyspnoea

Answer 32

Breathlessness may be episodic, and the situations under which the breathlessness arises can be characteristic of certain conditions:
* Diurnal variation is characteristic of Asthma
* Orthopnoea is a common feature of pulmonary oedema (and seen in any severe resp disease)
* Paroxysmal Nocturnal Dyspnoea is also classic of both pulmonary oedema and of asthma

Non-respiratory causes of breathlessness include anaemia, heart failure, cardiac arrhythmias, anxiety or even a sign of respiratory compensation in diabetic ketoacidosis.

Question 33

Describe the physiology of the cough mechanism

Answer 33

The cough reflex arc is made up of three main pathways:

1. Sensory Afferent Pathway
   The cough reflex arc is initiated by irritation of cough receptors, for example, mechanoreceptors or chemoreceptors. Irritants are detected by these receptors and they send sensory information to afferent nerves.
2. Central Pathway
   Sensory information travels to the nucleus tractus solitarius (NTS) of the medulla. The vagus nerve then synapses with motor neurones, delivering information to effector muscles which triggers the cough reflex to occur.
3. Motor Efferent Pathway
   Various respiratory muscles contract to allow initiation of the cough reflex.

The diaphragm contracts to become flattened which increases the thoracic cavity space
The laryngeal muscles contract to close the vocal cords
The external intercostal muscles contract to change the space available in the thoracic cavity
Rectus abdominis contracts to depress the rib cage and decrease space in the thoracic cavity

Question 34

Describe the 3 main types of sesnory nerves in the afferent pathway

Answer 34

There are three main types of sensory nerve fibres involved in the afferent pathway:

Rapidly Adapting Stretch Receptors (RARs)
These are myelinated fibres found mostly in the pharynx and trachea which rapidly respond to mechanical stimuli, e.g. changes in lung volumes
Slowly Adapting Stretch Receptors (SARs)
These are myelinated fibres which respond more slowly to mechanical stimuli and are involved in the Hering-Breuer reflex
C-fibres
These are non-myelinated nerve fibres which respond to mechanical and chemical stimuli
Sensory information travels from these fibres through the afferent pathway via the vagus nerve to the medulla oblongata.

Question 35

Describe the 3 Phases of the cough reflex

Answer 35

Phases of the Cough Reflex
There are three main phases to the cough reflex:

Inspiratory Phase
Irritation of cough receptors causes the vocal cords to open more widely, allowing more air to enter the lungs. The external intercostal muscles and diaphragm then contract causing expansion of the chest cavity, facilitating movement of air into the lungs, and increasing intra-thoracic pressure.

Compression Phase
The epiglottis and vocal cords close, trapping the air within the lungs. There is expiration against the closed epiglottis, causing a further increase in intra-thoracic pressure.

Expiratory Phase
The internal intercostal muscles and abdominal muscles contract to depress the thoracic cavity. The vocal cords relax, and the epiglottis opens. This releases the pressure from the lungs and causes air and the irritant to be rapidly expelled.

Question 36

Discuss the basic epidemiology & pathophysiology of bronchiectasis

Answer 36

It is a less common obstructive airway disease
Irreversibly damaged bronchi often colonised with bacteria that lead to pus formation and mucus hypersecretion.
Causes;
* Respiratory infections can lead to bronchiectasis - bacterial, viral & mycobacteria.
* Direct damage- GORD & foreign body inhalation
* Allergic/inflammatory - Allergic BronchoPulmonary Aspergillosis (ABPA) where there is an IgE & IgG response to aspergillus. Often occuring in Asthmatics & CF
* Immune defects - Primary humoral defects like common variable immunodeficiency or secondary defects like lymphoid malignancy or HIV
* Mucociliary disorders - CF & ciliary dyskinesia
* Connective tissue disease - RA or systemic sclerosis

Question 37

Discuss the basic presentation & investigation of bronchiectasis

Answer 37

PC
* Persistent productive cough
* Long term HX - years
* abscence of smoking HX
* haemoptysis
* Purulent sputum
* Unexplained non-productive cough
IX
* Crackles over affected area
* Confirm diagnosis by High Res CT.
* missed in 50% of CXR
* Sputum microbiology - repeated & regular
* Lung Function tests - Spirometry
Test for underlying causes
* Immunoglobulins
* IgE & IgG - aspergillus specific
* RA & ANA Factor
* CF sweat test

Question 38

Discuss the basic management & prognosis of bronchiectasis

Answer 38

Tx of Underlying disorder
Respiratory Physiotherapy - BD airway techniques
Careful & appropriate use of antibiotics when exacerbated
Prognosis - between COPD & Asthma

Question 39

What is Bronchiectasis?

Answer 39

Bronchiectasis is irreversibly damaged bronchi that a dilated and thickened. They are often colonised with bacteria that lead to pus formation and mucus hypersecretion.

Question 40

Discuss the presentation, initial investigations, key differential diagnosis & initial management of cough

Answer 40

Chronic Cough is >6 weeks
is it productive?
IX - CXR, Sputum culture
Infection markers e.g. CRP
FBC for general wellness&raquo_space; any red flags?
DDX
* COPD
* Pneumonia
* GORD/ Nasal drip syndrome
* Asthma
* Bronchiectasis
* Malignancy
Manage in terms of underlying condition
Respiratory physio & occupation health
> consider psychological aspect of cough, esp after COVID