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Respiratory (Annie) > ASTHMA > Flashcards

ASTHMA Flashcards

1
Q

what is asthma?

A

Common condition inn which there is a HYPER-REACTIVITY of the airways and chronic inflammation

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2
Q

what are the symptoms of asthma

A
  • wheeze
  • tightness of chest
  • NON-PRODUCTIVE cough
  • shortness of breath, often worse at night
  • cough that is worse in the mornings or at night
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3
Q

when is asthma most commonly diagnosed?

A

between ages of 3-5 where it can either worsen or get better with age

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4
Q

what are the 3 characterises of asthma.

A

1) airflow limitation
- reversible airflow obstruction
2) airway hyper-responsiveness
3) bronchial inflammation

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5
Q

what can asthma be classified according to?

A

1) its trigger factors
- Atopic or Non-atopic
- extrinsic or intrinsic

2) by age of onset
- adult onset
- childhood onset

3) by inflammatory subtypes
- Type 2 (characterised by TH2 lymphocytes)
- Non-type 2

4) Response to therapy

5) chronic or acute asthma
- chronic = asthma requiring long term maintenance
- acute = short term exacerbation

6) brittle asthma
= asthma in patients whose PEFR variability is significant despite considerable medical therapy
or
= sudden acute attacks without an obvious trigger on a background of good control

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6
Q

what does atopy mean?

A
  • characteristic skin reactions to common allergens
  • have circulating allergen specific antibodies (IgE)
  • runs in families
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7
Q

what 2 factors affect serum total IgE levels?

A

1) genetic factors

2) environmental

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8
Q

airway hyper-responsiveness is a characteristic feature of asthma, so what 2 things could be done to demonstrate if you have it or not?

A

1) bronchial provocation tests
= inhale gradually increasing concentration of histamine or metha-choline

2) Exercise testing or inhalation of cold, dry air, mannitol or hypertonic saline.

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9
Q

How does inhaling gradually increasing concentrations of histamine and metha-choline work?

A
  • they induce transient airflow limitation in susceptible individuals
  • patients with asthma respond to very low doses of methacholine
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10
Q

how does exercise testing orinhalation of cold, dry air, mannitol or hypertonic saline work?

A

they are indirect tests that release endogenous mediators, e.g. histamine, prostaglandins and leukotrienes, which cause broncho-constriction.

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11
Q

what are the triggers for asthma?

A

1) allergens
- house dust mite
- pollen
- animal dander
- fungi

2) airborne irritants
- pollution
- tobacco smoke
- fumes
- cold air
- mould and damp

3) drugs
- NSAIDS = non-steroidal anti-inflammatory drugs
- beta blockers

4) infections
- upper respiratory tract infections
- acute bronchitis

5) foods
- eating lots of fruit and veg is meant to reduce your chances of getting asthma

6) physical activity
- exercise

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12
Q

why does exercise & cold, dry air cause asthma?

A
  • exercise induced asthma doesn’t occur when exercising, but occurs afterwards
  • during exercise, prostaglandins, histamine and leukotrienes are released and theres stimulation of neural reflexes when the epithelial lining flood of the bronchi becomes hyperosmolar owing to drying & cooling during exercise
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13
Q

what NSAID drugs trigger asthma?

A
  • aspiring and propionic acid derivatives, such as indometaciin and ibuprofen
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14
Q

Why do NSAIDs drugs trigger asthma?

A
  • the drugs BLOCK the COX-1 enzyme
  • therefore decreasing the production of thromboxane & some anti-inflammatory prostaglandins
  • this causes the over production of pro-inflammatory leukotriene
  • causing severe exacerbations of asthma
  • causing bronchoconstriction
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15
Q

does the inhibition of enzyme COX-2 trigger asthma?

A

no

- its only the inhibitors of COX-1 that triggers it

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16
Q

give an example of a beta blocker drug?

A

Pro-pranolol

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17
Q

do the airways have a direct parasympathetic or sympathetic interaction?

A

the airways have a direct PARASYMPATHETIC innervation, which causes bronchoCONSNTRICTION.
- there is no direct sympathetic innervation of bronchial smooth muscle

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18
Q

due to the airways having a direct parasympathetic innervation, what is the airway critically dependent upon circulating?

A

it is critically dependent upon circulating ADRENALINE, acting through BETA-2 RECEPTORS on the surface of smooth muscle cells.

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19
Q

therefore, what happens if there are beta-blockers?

A
  • then there is inhibition of this effect

- causing broncho-constriction and airflow limitation

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20
Q

in allergen induced asthma, what are the 2 phases of an asthma attack?

A

1) immediate asthmatic reaction

2) dual & late phase reaction

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21
Q

what 2 factors play an important role in the severity of asthma?

A

1) airway inflammation

2) airway wall remodelling

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22
Q

what 4 cells are involved in airway inflammation?

A

1) mast clles
2) eosinophils
3) dendritic cells
4) lymphocytes

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23
Q

what do mast cells release that cause the asthmatic reaction?

A

They release mediators;

  • histamine
  • tryptase
  • PGD2
  • cysteinyl leukotrine
  • cytokines
  • chemokine
  • growth factors
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24
Q

what are the 3 hallmarks of asthma?

A

1) basement membrane THICKENS
2) COLLAGEN DEPOSITED in the sub-mucosa
3) smooth muscle undergoes HYPERTROPHY

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25
Q

what happens to the epithelium during asthma?

A
  • it is damaged and stressed
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26
Q

what is the epithelium a major source of?

A

its a major source of mediators, cytokines and growth factors that enhance inflammation and promote tissue remodelling

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27
Q

what does damage to the epithelium make it more vulnerable to?

A

more vulnerabel to infections bu common respiratory viruses and to the effects of air pollution

28
Q

what investigations could be done?

A

1) Lung function tests
= PEAK FLOW

2) exercise tests
3) Histamine or methacholine bronchial provocation test
4) trial of corticosteroids
5) exhaled nitric oxide
6) skin tests
7) allergen provocation tests

29
Q

what 2 lung function tests can be done?

A

1) peak expiratory flow rate (PEFR)

2) spirometer

30
Q

when should the peak flow be carried out?

A
  • when you wake up
  • before you go to bed
  • before you take your bronchodilator
  • after you take your bronchodilator
31
Q

what result in spirometry would you be able to diagnose asthma?

A
  • reduced forced expiratory ratio (FEV1/FVC < 75%)

- if there is a GREATER THAN 15% improvement in FEV1 or PEFR following the inhalation of a bronchodilator

32
Q

what does the test of histamine and methocholine bronchial provocation test indicate?

A

the presence of airway hyper-responsiveness

33
Q

describe the asthma treatment pyramid.

A

1) shorting acting B2 agonists

2) INHALED STEROIDS
e.g. cromoglicate
+ CysLT1 Rec antagonists
+ LABA/LAMA
+ theophyline
+ Anti IgE / IL5

3) oral steroids

34
Q

give examples of steroid sparing agents.

A
  • methotrexate
  • ciclosporin
  • intravenous immunoglobulins
  • anti-IgE monoclonal antibody
    = omalizumab
  • etanercept
    = infliximab
    = lebrikizumab
35
Q

if a patient has just occasional symptoms with 100% predicted PEFR, how would you treat them? STEP 1

A
  • as required short acting B2 agonists
36
Q

if the SABA is used more than once, theres daily symptoms of PEFR is <80% of predicted what would you do? STEP 2

A
  • regular inhaled preventer therapy

= anti-inflammatory drugs - inhaled low dose corticosteroids

= leukotriene receptor antagonists (LTRA), theophyllinee & sodium cromoglicate

37
Q

if that doesn’t control it, symptoms are severe or the PEFR is 50-80% of predicted what would you do?

STEP 3

A
  • inhaled corticosteroids & long acting inhaled B2 agonists

= continue inhaled corticosteroids

= add regular inhaled (long acting) LABA

= if still not controlled add either LTRA, modified release oral theophylline or B2 agonists

38
Q

if still not control, symptoms are uncontrolled even with high dose inhaled corticosteroid, what would you do?

STEP 4

A
  • high dose inhaled corticosteroid and regular bronchodilator

= increase high dose corticosteroids up to 200microrgam daily

= plus regular long acting B2 agonists

= plus either LTRA or modified release theophylline or B2 agonists

39
Q

is the symptoms deteriorate and PEFR is < 50% of predicted what would you do?

STEPS 5 & 6

A
  • regular oral corticosteroids

or

  • hospital admission
40
Q

what do beta-adrenoceptor agonists do?

A

1) relax bronchial smooth muscle
2) effective in relieving symptoms

  • but they DON’T AFFECT UNDERLYING AIRWAY INFLAMMATION
41
Q

what sort of asthmatics should be using bronchodilator treatment ALONE.

A

only people with the MILDEST ASTHMA with only occasional intermittent attacks.

42
Q

if an individual is using their B2-adrenoceptor agonists on a daily basis, what should they be started on?

A

they should be started onn inhaled corticosteroids.

43
Q

if an individual has poorly controlled asthma and is on a standard dose of inhaled steroid what else should they be given?

A

they should also be on a LONG ACTING B2 ADRENOCEPTOR AGONISTS (LABA).

e.g. salmeterol or formoterrol

44
Q

describe how LABAs should be taken, how often and how they work.

A
  • taken by inhalation and are effective for up to 12 hours
  • given once or twice a day
  • they improve symptoms and lung function and reduce exacerbations in patients
45
Q

can LABAs be taken on their own?

A

LABA CANNOT be taken on their own, but always in combination with an inhaled corticosteroid

46
Q

give examples of non-selective anti-muscarinic bronchodilator drugs and what do they do in asthma treatment?

A
  • non-selective muscarinic antagonists;
    = ipratropium bromide
    = oxitropium bromide
  • useful in asthma exacerbations
  • less helpful in stable asthma
47
Q

what do the drugs sodium cormoglicate and nedocromil sodium do?

A

they are anti-inflammatory cells, preventing activation of inflammatory cells by blocking a specific chloride channel, which in turn prevents chloride influx

48
Q

what sorts of patients are anti-inflammatory drugs used in?

A

patients with milder asthma

  • used in step 2
49
Q

in what sorts of asthmatics should an inhaled corticosteroid be used?

A
  • used in people with regular persistent symptoms (even mild symptoms)
50
Q

what are tithe most commonly used inhaled steroids?

A

= BECLOMETASONE

  • budesonide
  • fluticasone propionate
  • fluticasone furcate
  • mometasone furcate
  • triamcinolone
51
Q

up to what dose do beclometasonne and budesonide not seem to present a risk?

A

up to 800micrograms/days

52
Q

what are some unwanted side effects of corticosteroids?

how could you reduce these side effects?

A
  • oral candidiasis
  • hoarseness
  • osteoporosis is less likely than with oral steroids but can occur with high dose inhaled corticosteroids (beclometasone and budesonide > 800 micrograms).
  • candidiasis and GI absorption minimised by using a spacer, mouth washing and teeth cleaning after use
53
Q

when should oral corticosteroids be used?

A

they should be used for individuals who are not controlled by inhaled corticosteroids.

STEP 5.

  • dose should be kept as low as possible to minimise side effects.
54
Q

what do the leukotriene receptor antagonists target?

A

they target the cysteinyl LT1 receptor.

55
Q

give examples of the types of drugs in the leukotriene receptor antagonists category and state how they are given?

A
  • montelukast
  • pranklukast
  • zafirlukast

= they are given orally.

56
Q

when should leukotriene receptor antagonist theory be tried?

A

in patients who is NOT controlled on low to medium dose of inhaled steroids.

57
Q

do they work along with LABAs or by themselves?

A

LTRAs action is additive to LABAs.

58
Q

when is LTRA therapy useful?

A
  • patents requiring high dose inhaled or oral corticosteroids
  • people with aspirin intolerant asthma
  • asthmatic smokers
59
Q

give 2 examples of monoclonal antibodies that could be used?

A
  • omalizumab

- lebrikizumab

60
Q

what does omalizumab do?

A
  • it is directed against IgE, chelates free IgE and down-regulates the number & activity of mast cells and basophils.
61
Q

when is omalizumab useful?

A

useful in patents with frequent exacerbations & hospital admissions.

62
Q

what does lebrikizumab target?

A

targets IL13

63
Q

why are asthma attacks most commonly caused?

A
  • by lack of treatment adherence
  • respiratory virus infection associated with the common cold
  • exposure to allergen or triggering drug e.g. NSAIDS
64
Q

what are the 4 things that indicate someone is having an acute severe asthma attack?

A

1) inability to complete a sentence in one breath
2) a respiratory rate of >25 breaths/min
3) tachycardia of > 110 bpm
4) PEFR < 50% of predicted normal or best

65
Q

features of life threatening attacks?

A

1) a silent chest, cyanosis or feeble respiratory effort
2) exhaustion, confusion, coma
3) bradycardia or hypotension
4) PEFR < 30% or predicted normal or best

66
Q

what stats suggest a life-threatening attack?

A
  • high PaCO2 > 6kPa
  • severe hyperaemia < 8kPa despite treatment with oxygen
  • low and or falling arterial pH
67
Q

how would you manage a severe or life threatening asthma attack?

A
  • nebuliser Short acting bronchodilators
  • oxygen 40%-60%
  • prednisolone (40-60mg daily) given orally
  • nebuliser anti-muscarinics (e.g. ipratropium)
  • magnesium sulfate are given IV
  • ventilation for patients whoa deteriorate

Respiratory (Annie) (47 decks)

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