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medicine 2 - 01 asthma > 3 Asthma: Diagnosis, Monitoring, Pathophysiology and Management > Flashcards

3 Asthma: Diagnosis, Monitoring, Pathophysiology and Management Flashcards

1
Q

Define asthma

A

It is an auto-immune chronic airway hyper-responsiveness and airway inflammation with a history of respiratory symptoms such as wheeze, SoB, chest tightness and cougj

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2
Q

What are the symptoms of asthma?

more than one of…

A
  • Wheeze
  • Chest tightness
  • Cough
    Variable airflow obstruction
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3
Q

What are the identifiable changes in the FEV1:FVC observed in asthma?

A
  • It is characterised by reversible decreases in FEV1:FVC

less than 70-80% suggests increases in airway resistance

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4
Q

Important features

e.g. to distinguish from COPD

A

The airflow obstruction is reversible, whereas in COPD it is irreversible

Variations in the PEF, which can be improved with B2 agonist

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5
Q

Clinical features of asthma

A
  • Wheezing
  • Breathlessness
  • Tight chest
  • Cough (worse at night/exercise)
  • Decreases in FEV1, reversed by a B2-agonist
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6
Q

What can provoke an asthmatic attack?

genetic predisposition

A
  • Allergens
  • Cold air
  • Viral infections
  • Smoking
  • Excercise
  • Drug-induced asthma
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7
Q

What are the observable differences in the FEV1 and a volume/time curve?

A
  • lower FEV1
  • the graph will have a less steep slope but will eventually reach TLC
    It is an obstructive deficit
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8
Q

What are the objective tests available for diagnosis of asthma (in adults, young people, and children aged 5 and over)

(and what to expect for a positive test for obstructive airway disease)

A
  • Offer a FeNO (fractional exhaled nitric oxide) test to adults (17 and over)
  • Blood test (eosinophil level), to look for eosinophilic airway inflammation or atopy
  • offer spirometry
    (regard FEV1/FVC ratio of less than 70% as a positive test for obstructive airway disease)
  • offer a BDR (bronchodilator reversibility) test to adults with obstructive spirometry.
    (regard an improvement in FEV1 of 12% or more, together with an increase in the volume of 200ml or more, as a positive test of obstructive airway disease
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9
Q

How do you use a peak flow meter to Monitor asthma

A

PEF is one’s maximum ability to breathe out air

  • Useful for monitoring disease than making an initial diagnosis
  • track the PEF over a few weeks (taking 2/3 times daily measurements, and asking patients to keep a record of the measurements)
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10
Q

What is the pathophysiology of Asthma

A
  • Immunoglobulin IgE likelihood of asthma increases with serum concentrations
  • Body first exposed to the allergen, leading to the production of allergen-specific IgE
  • Re-exposure occurs, where the allergen binds to IgE molecule on the surface of mast cells
  • Degranulation occurs, with the release of inflammatory mediators such as histamines, prostaglandins, and leukotrienes (from mast cells)
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11
Q

Describe the early phase of asthma

A
  • Infiltration by eosinophils, T-cells, and mast cells
  • Goblet cells produce mucus (causes wheeze, where the air is trying to push through constricted and mucus-filled airways
  • T cells release cytokines

(late phase airways become more responsive to triggers)

Asthma is steroid-responsive
- Long term damage is untreated

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12
Q

What are the aims of treatment for asthma?

A
  • No day-time symptoms
  • No night-time awakening due to asthma
  • No need for rescue medication
  • No asthma attacks
  • No limitations of activity, including exercise
  • Normal lung function (PEF>80%)
  • Minimum side-effects of medication
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13
Q

What 3 questions can you ask a patient to assess the control of their asthma (and the medications)

A

In the last week (month):

  • Have you had difficulty sleeping because of asthma symptoms (cough?)?
  • Have you had your usual daily activities?

Yes, to any, implies uncontrolled asthma

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14
Q

What is the approach to management for asthma?

A

-Start treatment at level most appropriate severity
-Achieve early control
-Maintain control by:
o Increasing treatment as necessary
o Decreasing treatment when control is good

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15
Q

What is the first-line treatment all asthmatics get?

A

B2-adrenoceptor agonists

(SABA as reliever therapy

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16
Q

Give examples of B2-adrenoceptor agonists, and how they are used

A

Short-acting beta-agonists (SABA) - used as a reliever
- e.g. Salbutamol, terabutaline

Long-acting beta-agonists (LABA) - stay on receptor longer
- LABAs are given as add-on therapy for long-term prevention and long-term control (overnight)

[long-term use, especially of LABA, may lead to receptor down-regulation]

17
Q

Describe how SABA’s work, and give features of it

A

Inhale short-acting beta-agonists as required

  • this step only manages symptoms and does not control the underlying inflammation
  • SABA works more quickly and/or with fewer side effects than the tablet/syrup alternatives
18
Q

Give the mechanism of action of Salbutamol (SABA)

A

Activation of Beta-2 adrenergic receptors on airway smooth muscle:

  • leads to the activation of Adenyl Cyclase (through the G-protein coupled receptor activation)
  • And leads to an increase in concentration in cAMP.
  • This increase in cAMP leads to relaxation of the smooth muscles in the airways

This causes bronchodilation

19
Q

How to give the LABA (salmeterol), and why?

A

In asthma, LABA needs to be given with a corticosteroid
- Salmeterol (LABA) do not have any anti-inflammatory properties
(it control the symptoms, but doesn’t affect the inflammation)

20
Q

Give an example of a corticosteroid used to treatment in Asthma (as well as a feature)

A

e. g. Beclomethasone (inhaled corticosteroid - ICS)

- or prednisolone (oral)

21
Q

What is the mechanism of action of the corticosteroids?

A

Anti-inflammatory actions by:

  • activation of intracellular receptors, leading to altered gene transcription (decrease in cytokine production) and production of lipocortin
  • They decrease the production of prostaglandins (which trigger the release of inflammatory mediators), by inhibiting the arachidonic acid pathway
22
Q

What is the appropriate dosage for ICS?

A

Lower does give a higher response (whereas, the increasing dose does not give additional clinical benefit, whilst increasing adverse effects)

23
Q

What are the side effects of Inhaled Corticosteroids?

A
  • Hoarseness, dysphonia, throat infections, oral candidiasis
  • Higher doses reduce bone density, skin thinning, bruising
  • Increased risk of pneumonia

High dose of ICS - increased risk of diabetes

24
Q

What is the procedure to follow in a patient whose asthma is uncontrolled whilst on a low dose of ICS as maintenance therapy?

A

Offer the patient a Leukotriene-receptor antagonist (LTRA), in addition to the ICS, and review the response to treatment in 4-8 weeks

25
Q

What is a leukotriene receptor antagonist, and give features and examples of it

A

e. g. Montelukast, zafirlukast
- Oral option for adults (10mg), children (5mg), who do not respond to a LABA, and have poor control with a steroid + LABA

26
Q

After an LTRA, what is the next choice treatment available for asthma?

A

Exchange and MART (SMART)

- Maintenance and reliever therapy

27
Q

What is MART?

A

Maintenance and reliever therapy (MART) is a form of combined ICS and LABA treatment in a single inhaler, containing both ICS + fast-acting LABA (formoterol)

  • used for both daily maintenance therapy
  • and relief of symptoms as required
28
Q

What is the 5th line treatment for asthma?

A

Methylxanthines

29
Q

Give features of methylxanthines, with an example too

A

It is hardly used in Asthma

  • Need to be careful in dosage - as it has a narrow therapeutic range
  • It also has lots of interactions with other drugs
  • If prescribed to a patient who smokes, the dosage of theophylline (methylxanthine) needs to be halved
30
Q

What are the signs of toxicity of methylxanthine

A
  • Cardiac dysrhythmia
  • seizure
  • GI disturbances
31
Q

What is the mechanism of action of theophylline (methylxanthines)

A
  • Theophylline works to stop the breakdown of cAMP

- It inhibits the enzyme phosphodiesterase (PDE - which breaks down cAMP to AMP)

32
Q

Describe the use of monoclonal antibodies in the treatment of asthma

A
  • IgE antibodies - only prescribed by top consultants

e.g. Omalizumab (mAb)
It is used in the management of allergic asthma

e.g. Benralizumab is another mAb used for treating severe eosinophilic asthma

33
Q

What is the mechanism of action of monoclonal antibodies?

A
  • They are directed against free IgE, but not bound to IgE
  • They prevent IgE from binding to immune cells and basophils
  • Hence, decreases the release of allergic mediators
34
Q

Describe the use of mast cell stabilisers in the treatment of asthma

A

It used to be used, but not anymore (due to its side effects)

e.g. Cromoglycate (sodium cromoglicate) is given by inhalation

It is used as a prophylactic anti-inflammatory drug

35
Q

What is the mechanism of action of a cromone (like cromoglycate)?

A
  • Their effect is on the mast cells that are rich in histamine and other inflammatory mediators by preventing their activation to initiate inflammatory responses
36
Q

What is the contraindication between NSAIDs and asthma

A
  • Non-steroidal inflammatory drugs (NSAIDs) are good at treating pain and inflammation from prostaglandins (as they inhibit the production of prostaglandins)
    e. g. aspirin, ibuprofen
  • BUT, NSAID’s may provoke asthma by increasing leukotriene production

medicine 2 - 01 asthma (3 decks)

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