W5 ICS- RESP Flashcards
List FIVE main points that the GP pharmacist should address during an asthma
review
- Assess whether asthma is controlled.
- Review prescribed inhalers (right treatment, right dose)
- Check the lung function
- Check the inhaler technique
- Update the written asthma action plan.
Summarise the diagnostic tests in asthma: (6)
- Assess signs and symptoms: cough and wheeze and, in adults, shortness of breath
(SOB); Symptom variability; Combinations of symptoms – more important in children
(cough, wheeze, chest tightness, dyspnoea, exercise-induced symptoms). - History of atopy: Personal/family history of atopic/ allergic diseases.
- Spirometry (to demonstrate airway obstruction): Regard a FEV1/FVC ratio of less
than 70% as a positive test for obstructive airway disease. - Bronchodilator reversibility demonstrating variability in airway obstruction.
- Peak flow charting: Monitor peak flows for 2-4 weeks, calculate mean variability.
Regard ≥20% variability as a positive test. The number of days with diurnal variation
was found to be more accurate than calculating the mean variation. - Strategies for detecting eosinophilic inflammation or atopy: exhaled FeNO. Blood
eosinophils and IgE are poorly predictive
Summarise the tools that can be used to assess asthma
- Spirometry: Good for short and longer-term reversibility testing in adults with pre-
existing airflow obstruction. >400 ml increase in FEV1 post-bronchodilator highly
suggestive of asthma in adults. Values usually within normal range in adults and
children with asthma. - Peak expiratory flow (PEF): benefit in adult patients with more severe disease and in
those with poor perception of bronchoconstriction. - Asthma Control Questionnaire (ACQ).
- Asthma Control Test.
- Mini Asthma Quality of Life Questionnaire.
- Exhaled nitric oxide (FeNO): Raised FeNO 40 ppb or more is predictive of a positive
response to corticosteroids. - Eosinophil differential count in induced sputum: Close relationship between raised
sputum eosinophil count and corticosteroid responsiveness in adults.
Mrs B’s asthma is triggered by smoking. What other risk factors can exacerbate
asthma?
a. Viral infections
b. High pollen count
c. Lack of adherence
d. Suboptimal inhaler technique
e. Smoking (active or passive)
f. Occupational exposures
g. Psychosocial factors – dealing with Patient Z illness?
h. Seasonal or environmental factors
What are the aims of asthma management?
a. no daytime symptoms
b. no night-time awakening due to asthma
c. no need for rescue medication
d. no asthma attacks
e. no limitations on activity including exercise
f. normal lung function (in practical terms FEV1 and/or PEF>80% predicted or best) - cannot be reliably used to guide asthma management in children under five years of age.
g. minimal side effects from medication
Discuss the non-pharmacological interventions that you may suggest to manage asthma. (3)
- Smoking cessation.
- Weight-loss interventions (including dietary and exercise-based programmes).
- Breathing exercise programmes (including physiotherapist-taught methods) can be
offered to people with asthma as an adjuvant to pharmacological treatment to
improve quality of life and reduce symptoms.
There’s evidence that Mrs B wasn’t adherent to her treatment. Discuss the steps
that the GP pharmacist needs to take here before stepping up her treatment
- Mrs A is non-adherent
- She often reduces or stops her inhaled steroids
- Recheck adherence
- Re-check inhaler technique
What would the GP pharmacist prescribe to step up her treatment based on
SIGN/BTS guidelines
- Currently on SABA and low-dose ICS
- Addition of LABA to ICS alone improves lung function and symptoms and decreases asthma attacks in adults and children.
- Preferably used as fixed doses in a MART inhaler
What is a personalised asthma action plan (PAAP)
- A (written) PAAP reminds patients of their regular treatment, how to monitor and
recognise that control is deteriorating and the action they should take. As an adult, our
patient can choose whether she wishes to monitor her control with symptoms or by
recording peak flows (or a combination of both). Symptom-based monitoring is
generally better in children. - Plans should include action points including emergency doses of reliever medication;
increasing low dose (or recommencing) inhaled steroids; or starting a course of oral
steroids according to severity of the exacerbation. - Personalisation of the action plan is crucial. Focussing specifically on what actions she
could take to prevent a repetition of the recent attack is likely to engage her interest.
With her busy lifestyle and travel, our patient is likely to be keen to have an emergency
supply of prednisolone. - Identification and avoidance of her triggers is important. As pollen seems to be a
trigger, management of allergic rhinitis needs to be discussed: she may benefit from
regular use of a nasal steroid spray during the season
What counselling points would you provide when handing out the dispensed
prescription of MART and SABA?
Consult SPC/PIL of the selected LABA (Formoterol)
Adherence to MART
Keep a peak flow diary
Recognise symptoms of when asthma is poorly controlled
Describe the early events responsible for the pathogenesis of asthma in
general, paying particular attention to likely causes in this patient. How does
this result in chronic airway inflammation and airway hyperresponsiveness?
The earliest events in asthma are the activation of local inflammatory cells,
primarily mast cells and eosinophils, by the causative agents (what do you think
they may be in this case?). This can occur by specific IgE-dependent mechanisms
or indirectly by chemical irritant exposure or osmotic stimuli. In this case the
patient shows evidence of atopy (eczema etc) therefore IgE dependant
mechanisms are likely, however smoke seems to bring about the symptoms. Acute-
acting mediators, including leukotrienes, prostaglandins, and histamine, induce
smooth muscle contraction, mucus hypersecretion, and vasodilation with
endothelial leakage and local edema formation. Epithelial cells also participate,
releasing leukotrienes, prostaglandins, and inflammatory cytokines. Additional
inflammatory cells, including neutrophils and eosinophils, are recruited to the
airway. In addition, the cell cytokines released promote growth of mast cells and
eosinophils, the influx and proliferation of T cells, and the differentiation of B
lymphocytes into IgE- producing plasma cells. Over time this ongoing inflammation
results in injury to epithelial cells, denudation of the airway, greater exposure of
afferent sensory nerves, and subsequent smooth muscle hyperresponsiveness,
chronic inflammation, mucosal hypersecretion from glands and increased mucus volume.
This patient has also been prescribed Beclomethasone. What class of drug is this? Describe how it may be beneficial in asthma- linking your answer to the molecular mechanisms of this drug.
This is an inhaled Glucocorticoid (corticosteroid). It acts via a number of mechanisms. It acts as an immunosuppressor by increasing IL 10, decreasing cytokine formation and recruitment and activation of T cells and reducing eosinophils (this links with tests suggested). It has anti-inflammatory effects by inhibiting COX-2 inhibiting other inflammatory mediators (prostaglandins,
eicosanoids). Some evidence that this might reduce the severity of the early asthma response and prevent the late phase response
This patient has been prescribed salbutamol. This is a short-acting beta-agonist (SABA). Thinking about the physiology and pharmacology of the lungs state what effect drugs such as these bring about in the airways.
Explain their mode of action (tip- state the exact name of the receptor).
Salbutamol is a SABA, a short acting Beta-2 adrenoreceptor agonist. It stabilises this
receptor in its active form (ie it activates it). This leads to increased cAMP generation by Adenylyl cyclase and activation of PKA. This inhibits MLCK (myosin light chain kinase, therefore myosin is not phosphorylated – phosphorylation of myosin is required for muscle tone/ contraction, therefore, the airways relax.
What is the most common side effect when SABA is given in asthma. Why
does this occur?
Tremor: Unwanted effects arise from systemic absorption. The most common is fine skeletal muscle tremor from stimulation of beta 2 adrenoreceptors in these muscles
(causes twitches)
Considering the mode of action of salbutamol, why might high doses lead to
hypokalaemia? Define hypokalaemia. What side effects might this cause?
Salbutamol=SABA, a Beta 2 adrenoreceptor agonist. It stabilises the receptor in its active
form (ie activates). This leads to increased cAMP generation by Adenylyl cyclase and
activation of PKA. PKA phosphorylates proteins responsible for muscle tone/contraction. It also increases cellular uptake of K+, particularly by skeletal smooth muscle. This can lead to reduced serum levels of K+ (hypokalemia). This can lead to cardiac
arhythmias. Note: Tachycardia and arrhythmias result from both beta1 and beta2
adrenoreceptor stimulation in the heart with high doses of inhaled (or after oral/parenteral) administration.
(See Cardiac refresher lecture from Mel Healy hypokalaemia can lead to long qt
syndrome/ torsade de pointes).
