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Asthma Flashcards

1
Q

.51

A

Activation of beta-adrenergic receptors leads to relaxation of smooth muscle in the lung, and dilation and opening of the airways.
Beta-adrenergic receptors are coupled to a stimulatory G protein ofadenylyl cyclase. This enzyme produces the second messenger cyclic adenosine monophosphate (cAMP). In the lung, cAMP decreases calcium concentrations within cells and activates protein kinase A. Both of these changes inactivate myosin light chain kinase and activate myosin light chain phosphatase. In addition, beta-2 agonists open large conductance calcium-activated potassium channels and thereby tend to hyperpolarize airway smooth muscle cells. The combination of decreased intracellular calcium, increased membrane potassium conductance, and decreased myosin light chain kinase activity leads to smooth muscle relaxation and bronchodilation.

Myosin light-chain kinasealso known asMYLKorMLCKis aserine/threonine-specific protein kinasethatphosphorylatesthe regulatory light chain ofmyosin II.[3] Theseenzymesare important in the mechanism of contraction inmuscle. Once there is an influx ofcalciumcations (Ca2+) into the muscle, either from thesarcoplasmic reticulumor from theextracellular space, contraction of smooth muscle fibres may begin. First, the calcium will bind tocalmodulin. This binding will activate MLCK, which will go on to phosphorylate themyosin light chainatserineresidue 19. This will enable the myosincrossbridgeto bind to theactin filamentand allow contraction to begin (through thecrossbridge cycle). Since smooth muscle does not contain atroponincomplex, asstriated muscledoes, this mechanism is the main pathway for regulating smooth muscle contraction. Reducing intracellular calcium concentration inactivates MLCK but does not stop smooth muscle contraction since the myosin light chain has been physically modified through phosphorylation. To stop smooth muscle contraction this change needs to be reversed. Dephosphorylation of the myosin light chain (and subsequent termination of muscle contraction) occurs through activity of a second enzyme known asmyosin light-chain phosphatase(MLCP).

Incell biology,Protein kinase A(PKA) is a family ofenzymeswhose activity is dependent on cellular levels ofcyclic AMP(cAMP). PKA is also known ascAMP-dependent protein kinase(EC2.7.11.11). Protein kinase A has several functions in the cell, including regulation ofglycogen,sugar, andlipidmetabolism.
It should not be confused withAMP-activated protein kinase- which, although being of similar nature, may have opposite effects -[1]nor be confused withcyclin-dependent kinases(Cdks), nor be confused with theacid dissociation constantpKa.

In the field ofmolecular biology, thecAMP-dependent pathway, also known as theadenylyl cyclasepathway, is aG protein-coupled receptor-triggeredsignaling cascadeused incell communication.[1]

G protein-coupled receptors(GPCRs) are a large family ofintegral membrane proteinsthat respond to a variety of extracellular stimuli. Each GPCR binds to and is activated by a specificligandstimulus that ranges in size from small moleculecatecholamines, lipids, orneurotransmittersto large protein hormones. When a GPCR is activated by its extracellular ligand, a conformational change is induced in the receptor that is transmitted to an attached intracellularheterotrimeric G proteincomplex. TheGsalpha subunitof the stimulated G protein complex exchangesGDPforGTPand is released from the complex.
In a cAMP-dependent pathway, the activated Gsalpha subunit binds to and activates an enzyme calledadenylyl cyclase, which, in turn, catalyzes the conversion ofATPintocyclic adenosine monophosphate(cAMP).[2]Increases in concentration of thesecond messengercAMP may lead to the activation of
cyclic nucleotide-gated ion channels[3]
exchange proteins activated by cAMP (EPAC)[4]such asRAPGEF3
popeye domain containing proteins (Popdc)[5]
an enzyme calledprotein kinase A(PKA).[6]
The PKA enzyme is also known as cAMP-dependent enzyme because it gets activated only if cAMP is present. Once PKA is activated, it phosphorylates a number of other proteins including:[7]
enzymes that convertglycogenintoglucose
enzymes that promote muscle contraction in the heart leading to an increase in heart rate
transcription factors, which regulate gene expression
Specificity of signaling between a GPCR and its ultimate molecular target through a cAMP-dependent pathway may be achieved through formation of a multiprotein complex that includes the GPCR, adenylyl cyclase, and the effector protein

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2
Q

Aetiology

A

the cause, set of causes, or manner of causation of a disease or condition:

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3
Q

Asthma is an —— ——– disease

A

obstructive airway

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4
Q

In asthma the spirometry will show:

1 = Increased FVC > 70%
2 = Reduced FVC < 70%
3 = Increased FEV1 > 70%
4 = FEV1/FVC of > 70%
5 = FEV1/FVC of < 70% i

A

5
Its obstructive and hence FEV will reduce

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5
Q

Obstructive Airway Disease

A
  • conditions that cause narrowing of the large, medium sized and small airways (bronchi)
  • asthma, COPD, bronchiectasis
  • results in air-trapping and hyperinflation
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6
Q

Obstructive Airways Disease Spirometry

A

↓ FEV1
↔ FVC (unchanged)
↓ FEV1/FVC < 70%

FEV1 = forced expiratory volume in 1 second
FVC = forced vital capacity

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7
Q

Asthma definition

A
  • reversible, obstructive airways disease
  • caused by inflammation, hyper-responsiveness and narrowing of the bronchial tree
  • occurs in a susceptible individual secondary to a variety of stimuli
  • FEV1/FVC <70%
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8
Q

Asthma is characterised by (2):

A
  • recurrent attacks of breathlessness and wheezing
  • varies in severity and frequency from person to person
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9
Q

obstructive airways disease

A
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10
Q

Diagnosis of asthma

A
  • clinical diagnosis
  • no consistent gold standard diagnostic criteria
  • central to diagnosis is presence of symptoms:
    • more than one of wheeze, breathlessness, chest tightness, cough
    • variable airflow obstruction
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11
Q

Epidemiology of asthma:

  • incidence
  • prevalence
  • mortality in the UK
  • hospital admissions
  • money
  • deaths compared to EU
A
  • incidence is 2.6-4/1000 individuals year in UK (3-34% worldwide)
  • prevalence is 8% of adults and 20% of children: 5.4M people in UK
  • mortality is 4/100,00 in the UK with 1500 deaths every year
  • 185 hospital admissions every day
  • 1bn spent by NHS treating asthma
  • deaths from asthma in UK is 50%> in EU
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12
Q

Aetiology of Asthma

A
  • multifactorial; genetic factors(polygenic) and environmental
  • airway inflammation occurs when a genetically susceptible individual with atopy is exposed to certain environmental factors
  • atopy is the tendency to produce high amounts of IgE when exposed to small amounts of an antigen
  • atopic individuals have a high prevalence of asthma, allergic rhinitis, urticaria and eczema
  • atopic individuals will demonstrate positive reactions to antigens on skin prick testing

The genetic predisposition is actually disposition to atopy; hence will always ask patient about hayfever, eczema and family history of asthma

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13
Q

Genetics of asthma

A
  • atopy and asthma show polygenic inheritance and genetic heterogeneity, with gene linkages on chromosome 11q13
  • allergen exposure in early life may determine sensitisation foe example to HDM, pet allergens and viral infections
  • hygiene hypothesis postulates that LACK of infections in childhood results in alteration of T cell function and a predisposition to developing asthma
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14
Q

Atopy

A
  • atopic individuals produce IgE antibodies to specific allergens, which can be measured in the serum
  • atopic conditions include asthma, hayfever, allergic dermatitis, allergic rhinitis
  • always ask about family history of atopy
  • individuals with asthma are highly likely to have other atopic conditions
  • skin prick testing can be used to demonstrate allergy to a specific allergen
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15
Q

pathophysiology of asthma: airway inflammation:

A
  • sensitisation of atopic individuals
  • inhalation of allergen
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16
Q

Pathophysiology of asthma: two phase response:

A
  • early reaction (20minutes) and late reaction (6-12 hours later)
  • T helper lymphocytes regulate the inflammatory response
  • Th2 cells secrete pro-inflammatory interleukins which lead to the release of IgE antibodies by plasma cells
  • Th1 cells down regulate the atopic response
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17
Q

Pathophysiology of asthma: IgE antibodies bind to receptors on mast cells and eosinophils and stimulate them to release:

A
  • histamine, prostaglandins, cysteinyl leukotrienes
  • these mediators cause bronchoconstriction of airways within minutes
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18
Q

What are targets for therapies for asthma?

A

Mediators: histamines prostaglandins, cysteinyl leukotrienes

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19
Q

What distinguishes asthma from COPD?

A

Reversibility of bronchoconstriction

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20
Q

Pathophysiology of asthma: Late phase response:

A
  • infiltration of the smooth muscle layer by eosinophils, basophils, neutrophils, monocytes and dendritic cells
  • results in patchy desquamation of epithelial cells
  • increase in number of mucous glands and goblet cell hyperplasia
  • hypertrophy and hyperplasia of airway smooth muscle
  • cytokines cause contraction of smooth muscle and narrowing of airways
  • increased permeability of blood vessels
  • increased mucous production and mucous plugging
  • acute inflammation results in oedema
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21
Q

Pathophysiology of asthma: dynamic hyperinflation:

A
  • polyphonic wheezing caused by narrowing of bronchi of different calibers
  • narrowing of bronchi <2cm leads to closure at low lung volumes leading to air trapping an increase in residual volume and increase in total lung capacity
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22
Q

What type of immune cells are associated with acute asthma?

A

Eosinophils

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23
Q

What are neutrophils associated with (asthma)?

A
  • persistent airway inflammation
  • steroid dependent asthma
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24
Q

Pathophysiology of asthma

A
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25
Normal vs asthmatic patient airway diagram
26
With increased severity and chronicity of asthma (if untreated):
- remodelling of the airways - collagen deposition - fibrosis of the airway wall - fixed narrowing
27
Environmental triggers for acute asthma:
- animal dander - HDM - grass and tree pollen - mould - viral and bacterial infection - atmospheric pollution: ozone, SO2, NO, fumes, thunder storms - perfumes, hair sprays, plug-ins - cigarette smoking, passive smoking - indoor fire, chlorine, paints - cold air/change in temperatue
28
Drug triggers for acute asthma:
- aspirin - NSAIDS ( non-steroidal anti-inflammatory drugs) - beta blockers
29
Physiological triggers for acute asthma:
- pregnancy - premenstrual - exercise - occupational asthma
30
Symptoms of acute asthma during exacerbation (4):
- breathlessness - chest tightness - wheeze - cough
31
Symptoms of acute asthma between exacerbations(4):
- completely well - mild chest tightness - occasional wheeze - dry cough (cough-variant asthma)
32
Diurnal variability of asthma:
- worse at night and early morning - linked to circadian rhythm
33
Signs of acute asthma during exacerbation(4):
- tachypnoea (breathlessness with raised respiratory rate) - tachycardia - polyphonic wheeze during inspiration and expiration - signs of hyperinflation
34
Signs of severe asthma:
- cyanosis - silent chest = air can't go in and out, cant hear anything - bradycardia
35
An 18-year-old woman attends her GP surgery complaining of a dry cough and chest tightness. Her GP thinks she might have asthma. Which of the following investigations would be most helpful in making a diagnosis of asthma? 1 = blood test for neutrophil count 2 = chest X-ray 3 = CT thorax 4 = spirometry 5 = sputum analysis
4=spirometry
36
Investigation for suspected asthma:
- blood tests: full blood count; raised eosinophil count - raised IgE, radioallergosorbent test (RAST) if a specific allergy is suspected - skin prick test - chest x ray - peak flow/diary - spirometry - full lung function test with reversibility to bronchodilator If eosinophil count is normal, if spirometry/peak flow is normal, not reversible and a dry cough then: - HRCT if emphysema or bronchiectasis suspected - Methacholine or histamine provocation - Sputum (microbiological analysis, differential cell count)
37
Peak flow measurements
- diurnal variation: lower value in the morning compared to the evening - records of PEF measurements taken in the mornings and the evenings for several weeks can be helpful - 20% or greater variability between mornings and evenings
38
What is this? What does it show?
Shows diurnal variation; needs to be significant difference
39
Spirometry
- show obstruction: - reduced FEV1 - FEV1/FVC<70% - reversibility to bronchodilator 20 minutes after 200mcg inhaled salbutamol with the FEV1 - patient with COPD little to no reversibility
40
Lung Function Test for asthma:
- increase in TLC and RV due to air trapping (total lung capacity and residual volume) - normal transfer factor/diffusing capacity (TLCO/DLCO)
41
FENO
- fractional exhaled nitric oxide - measure of eosinophilic inflammation in the airways - a positive test (>40ppb) supports a diagnosis of asthma - can also be used to monitor treatments/ look at compliance
42
What test is this?
43
What is the control in a skin prick test?
Saline
44
Chest X-Ray in asthma:
- if mild may be normal - may show hyperinflation with increased lung volumes and flat diaphragms - > 6 anterior ribs or 10 posterior ribs in the mid-clavicular line - heart is vertical and narrow
45
HRCT in asthma:
- shows air trapping
46
Which of these statements about asthma is true? 1 = is an irreversible obstructive airways disease 2 = is a restrictive lung disease 3 = is associated with increased eosinophil count 4 = is rare in patients with atopy 5 = does not usually run in families
3
47
Management of asthma:
- avoid allergens if possible - inhaled therapy - oral therapy
48
Aims of pharmacological management of asthma:
- symptom control: minimal symptoms during day and night, minimal need for reliever, no limitation of physical activity - achieve best possible pulmonary function: FEV1, PEF>80% predicted or best - prevent exacerbations - reduce morbidity and mortality - minimal side effects
49
2 main receptors in bronchial mucosa are
- Beta 2 adrenoreceptors in the smooth muscle of the airways from the trachea to the terminal bronchioles - muscarinic cholinergic receptors: receive parasympathetic nerve supply
50
Route of Medication for Lung Diseases:
- Inhaled: inhaler, nebuliser (acute setting) - Oral - Intravenous - Intramuscular - Subcutaneous
51
Advantages of inhaled route of medication:
- direct deposition into lungs
52
Disadvantages of Inhaled route of medication:
- technique dependent
53
Advantages of Oral route of medication:
Not technique dependent
54
Disadvantages of Oral route of medication:
Dependent on absorption in the gut
55
Advantages of Intravenous route of medication:
- Systemic effects - Not technique dependent
56
Disadvantages of the intravenous route of medication:
- more systemic side effects
57
Principles of drug deposition into the lungs:
- inhaler/nebuliser directly deposits drug into lungs: rapid absorption - aerosol: suspension of fine particles of varying sizes, hence ensures small dose dispersed widely over airways and alveolar surfaces - systemic side effects from inhaled therapy less than with oral or intravenous treatment - however all inhaler systems are relatively inefficient, only 8-15% of the drug reaching the lungs, no matter how good the inhaler technique is
58
How can drug distribution into the lungs be measured?
- particle distribution within the lungs can be measured by radio-labelling the drug and using a gamma camera to quantify deposition.
59
Factors determining drug deposition in the lungs:
- size of the particle - inspiratory flow rate - distance needed for the particle to travel (determined by the method of inhalation)
60
Factors that favour distal particle sedimentation:
- small particle size - slow flow rate
61
What size particles are more likely to be deposited centrally?
- Large - >6 micrometers in diameter
62
What size particles reach the smaller airways?
- smaller particles - <5 micrometers in diameter
63
What size particles reach the alveoli?
- smaller particles - 2-3 micrometers in diameter
64
What happens to particles even smaller than 2-3 micrometers in terms of drug deposition?
- may not settle - expired
65
What does SABA stand for?
Short-acting Beta-2 agonist
66
What does LABA stand for?
Long-acting Beta-2 agonist
67
What does SAMA stand for?
Short-acting muscarinic antagonist
68
What does LAMA stand for?
long-acting muscarinic antagonist
69
What does ICS stand for?
Inhaled corticosteroids
70
How does SABA and LABA work?
- acts on Beta-2 receptors in the smooth muscle of the bronchial mucosa - activated enzyme adenylate cyclase, which increase concentration of cyclic AMP produced. Cyclic AMP activates pka, which phosphorylates several target proteins within the cell, leading to a decrease in intracellular calcium concentration by active removal of calcium from the cell into intracellular stores, which results in bronchodilation
71
Examples of SABA (2):
- salbutamol (ventolin) - terbutaline (bricanyl)
72
Examples of LABA (2):
- salmeterol - formoterol
73
Insert G protein card/diagram
insert
74
Stimulation of beta-2 adrenoreceptor results in relaxation of smooth muscle and (2):
- stabilisation of mast cells and inhibit inflammatory mediator release - enhanced mucociliary clearance and a decrease in vascular permeability
75
Core Drug: Salbutamol: - how does it work (brief)? - route of administration? - why? - how long for effects to be seen? - how long do the effects last?
- short acting bronchodilator - given via inhaler for asthma/copd for symptom control: - breathlessness, chest tightness, wheeze - rapid onset of action (usually within 10 minutes) - short acting: effects last 3-5 hours
76
Core Drug: Salbutamol: Adverse Effects:
- tachycardia (beta-1 receptors in the heart) - tremor (beta-2 receptors in the skeletal muscle) - agitation - side effects are dose-dependent - more side effects with an intravenous route
77
Core Drug: Salbutamol: Interactions:
complete later
78
Core Drug: Salmetarol: - treatment for? - how does it work (brief)? - route of administration? - how long for effects to be seen? - how long do the effects last? - extra?
- treatment for asthma and copd - Long-acting beta-2 agonist - inhaled only - onset of action 30 minutes - duration of effects 10-12 hours - always used in combination with ICS and or LAMA
79
Beta-2 agonist overuse can results in
fine tremors
80
Core Drug: Why are LABAs like salmeterol used in combination with ICS and or LAMA?
- combination of ICS and LAMA complement each other and gives optimal control of airways by suppressing chronic inflammation and reducing airways hyper-responsiveness
81
Core Drug: Salmeterol: Side Effects:
complete later
82
Core Drug: Salmeterol: Interactions:
complete later
83
How do SAMAs work?
- cholinergic reflex bronchoconstriction may be initiated by irritants such as cold air and stress - SAMA drugs block muscarinic receptors and INHIBIT cholinergic nerve-induced bronchoconstriction leading to bronchodilatation - normal airways have a resting vagal bronchomotor tone caused by tonic cholinergic nerve impulses, which release Ach near the airway smooth muscle
84
Core Drug: Ipratropium Bromide (atrovent): SABA,LABA,SAMA,LAMA?
SAMA short-acting muscarinic antagonist
85
Core Drug: Ipratropium Bromide: When is SAMA used for asthma?
Only in acute exacerbation of asthma
86
Corticosteroids: - most common treatment for - effects - how does it work - used to
- most commonly used drugs for the treatment of lung disease apart from antibiotics - potent anti-inflammatory drugs, which have a variety of different systemic effects - Glucocorticosteroid receptors (GCS receptors) are found in most cells in the body - GCS is taken in to the cells - the GCS receptor-complex binds to the target genes and changes transcription of inflammatory/anti-inflammatory components - prevents inflammation
87
Corticosteroid mechanism
88
Why can corticosteroids work on many different parts of the body?
Most cells contain GCS receptor
89
Corticosteroids: Name a drug for each route of administration: - Oral - inhaled corticosteroids (ICS) - Intravenous - Intranasal
- prednisolone, dexamethasone - beclomethosone, fluticasone, budesonide - methylprednisolone, hydrocortisone - Beclomethasone (beconase), fluticasone (flixonase)
90
Core Drug: Prednisolone: Side effects and route of administration: - short term (days)(4)
- indigestion - skin bruising - insomnia - psychosis
91
Core Drug: Prednisolone: Side effects and route of administration: - medium term (weeks)(5)
- gastric ulcers - skin bruising - insomnia - psychosis - weight gain
92
Core Drug: Prednisolone: Side effects and route of administration: - long term (months) and some explanation(7)
- Osteoporosis (thin bones caused by decreases calcium absorption and increased bone turnover) - growth retardation in children - weight gain as steroids increase appetite - Cushingoid appearance: moon face, central obesity due to too much steroids - adrenal suppression: taking steroids reduces body's normal steroid production - hypertension (corticosteroids stimulate mineralocorticoid receptors leading to retention of Na+, which increases blood volume. - diabetes: steroids make liver less sensitive to insulin, leading to an increase in blood glucose
93
Advantages of systemic routes (IV/Oral) of steroids administration(4):
- stronger effects as higher doses available - action unaffected by inspiratory effort/inhaler technique - better route in the ill and in emergency
94
Disadvantages of systemic routes (IV/oral) of steroids administration (1):
- more side effects, especially with long term therapy
95
Advantages of inhaled route of steroid adminstration (2):
- localised action - fewer side effects
96
Disadvantages of inhaled route of steroid administration (2):
- ineffective - disease may prevent penetration of drug to affected areas
97
Why are ICS used in asthma?
ICS are the most effective preventer drugs for adults and children
98
How often should ICS be prescribed a day for asthma prevention?
Twice a day
99
Core Drug: Beclomethasone Diproprionate (BDP): - what type? - for what? - route of administration? - advice - use with
- ICS - effective preventer drug for asthma - pressurised metered dose inhaler (pMDI) or dry powder inhaler (DPI) - advise to gargle after use of ICS - use ICS with spacer for MDI or DPI
100
Core Drug: Beclomethasone Dipropionate: ICS: Side Effects:
- steroids reduce the body's ability to fight infection because they are anti-inflammatory, so fungal infections occur - oral candidiasis - dysphonia
101
Three main types of inhaler devices:
- pMDI (pressurised metered dose inhalers) - DPI (dry powder inhalers) - SMI (soft mist inhalers)
102
Which of the three inhaler types?
Despite the differences in drug delivery to the lung with these various devices, no significant difference in bronchodilator effect has been found.
103
104
Proportion of patients making no mistakes with a DPI.
53-59%
105
Proportion or patients making no mistakes with pMDI.
23-43%
106
Proportion of patients making no mistakes with a pMDI+spacer.
55-57%
107
Chronic asthma is treated with
LAMA tiotropium
108
Combination Therapy: Why do we use them?
- increases efficacy because they act synergistically - maximise bronchodilation - combinations improve symptoms and Quality of life and reduce exacerbations in asthma and COPD
109
Combination Therapy: Why would we adding a drug to an existing therapy?
Reduces the risk of adverse even as opposed to increasing the dose of an existing therapy may reduce the risk of adverse events.
110
Three logistical reasons combination therapies:
- more convenient - increases compliance - cost-effective
111
How does a volumatic spacer device improve drug deliver?
increases distance from actuator to the mouth, allows particles time to evaporate and slow down before inhalation results in a larger proportion of particles deposited in the lungs and minimises oropharyngeal drug deposition, decreasing incidence of oropharyngeal candidasis
112
Why should patients inhaled using tidal breathing when using the spacer device as soon as possible after a single actuation?
- the drug aerosol is very short lived
113
Why and When do we use a nebuliser?
- nebulisers delivers a higher dose of drug to airways than an inhaler - solution containing the drug is turned inot an aerosol for inhalation - nebulised SABA and anticholinergic medication are used to treat patients with exacerbation of asthma or COPD - nebulised SABA can also be used to assess airway reversibility in patients with asthma and COPD
114
Core Drug: Theophylline: - what type of drug? - what does it do? - used to treat?
- methylxanthines = caffeine - non-selective phosphodiesterase inhibitor - has minimal effect on bronchomotor tone in normal airways - reverses bronchoconstriction asthmatic patients: - increases intracellular cyclic AMP concentration (G-alpha-s) - blocks adenosine receptor - decreases bronchoconstriction - used to treat asthma and COPD
115
Core Drug: Theophylline: Adverse Effects:
116
Core Drug: Theophylline: Drug Interactions:
117
Other treatments for asthma: Leukotriene Antagonist (montelukast):
- inhibit production of leukotrienes - for allergic and exercise induced asthma - unlikely to be used alone; generally with ICS (if not well controlled with ICS)
118
Other treatments for asthma: antihistamines and decongestants:
- hayfever - not lungs
119
Other treatments for asthma: Monoclonal Antibody:
- severe eosinophilic asthma
120
BTS guidelines for management of asthma:
- avoid allergens - smoking cessation - inhaled therapy - self-management plan - regular review by trained HCP to check compliance, technique and prescription - stepwise approach, up and down the asthma treatment ladder according to symptoms
121
122
Drugs for asthma can be categorised into preventers and relievers.
- Preventer inhalers reduce inflammation in the bronchi by blocking the inflammatory pathway: - ICS first line treatment - LABA with ICS if still symptomatic - Reliever inhalers cause bronchodilation of the airways for a few hours and improve symptoms: SABA
123
Patients should be on salbutamol alone. True or False?
False ICS too
124
Acute Asthma Summary Management:
- oxygen - nebulised bronchodilator: SABA (salbutamol) and SAMA (ipratropium bromide) - systemic corticosteroids - Mg sulphate (IV) if severe - Aminophylline (IV) - Antibiotics - ICU: intubation/ventilation
125
Summary of asthma management:
- smoking cessation - avoid known triggers - preventer inhalers: ICS+LABA - Leukotriene inhibitor - Oral theophylline - Stepwise approach (BTS)
126
A 19 year old woman is diagnosed with asthma by her GP. She has a persistent dry cough and breathlessness on exertion. What medication should she be started on according to BTS guidelines? 1 = aminophylline 2 = ICS 3 = SABA 4 = LAMA 5 = Oral Prednisolone
2
127
What is a PAAP?
personalised asthma action plan improves asthma control, reduces emergency contacts with GP, reduces hospital admissions
128
Discharge of asthma patients after admission
patient should have stopped nebulised therapy and been on discharge medication for at least 24hrs prior - reduce dose of oral steroids - review in 2 weeks
129
In Asthma the spirometry will show: 1 = Increased FVC > 70% 2 = Reduced FVC < 70% 3 = Increased FEV1 > 70% 4 = FEV1/FVC of > 70% 5 = FEV1/FVC of < 70%
5
130
An 18-year-old woman attends her GP surgery complaining of a dry cough and chest tightness. Her GP thinks she might have asthma. Which of the following investigations would be most helpful in making a diagnosis of asthma? 1 = blood test for neutrophil count 2 = chest X-ray 3 = CT thorax 4 = spirometry 5 = sputum analysis
4
131
Which of these statements about Asthma is true? 1 = is an irreversible obstructive airways disease 2 = is a restrictive lung disease 3 = is associated with increased eosinophil count 4 = is rare in patients with atopy 5 = does not usually run in families
3
132
A 24 year old woman attends the ED with severe breathlessness and wheeze. She has asthma. The FY1 doctor who admits her starts her on treatment but the patient does not improve quickly. Which of the following treatments is indicated for management of severe asthma? 1 = beclomethasone inhaler 2 = leukotriene antagonist 3 = magnesium sulphate 4 = montelukast 5 = nitric oxide
3

HLB (49 decks)

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