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Asthma Flashcards

1
Q

what is asthma (definition)

A

recurrent and reversible (in short term) obstruction to the airways in response to substance or stimuli
chronic inflammatory disorder

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2
Q

3 characteristics of asthma

A

airflow limitation
airway (bronchial hyper-responsiveness)
bronchial inflammation

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3
Q

what is airflow limitation

A

reversible spontaneously or with treatment

reversible airway obstruction - constriction

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4
Q

how is airflow limitation measured

A

lung function test

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5
Q

how does bronchial hyper responsiveness contribute to asthma

A

increased airway sensitivity = twitchy smooth muslce

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6
Q

what is bronchial hyperresponsiveness due to

A

epithelial damage exposes sensory nerve endings
c-fibres
irritant receptors

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7
Q

what does bronchial hyperresponsivenss lead to

A

neurogenic inflammation - sensory nerve endings release peptides

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8
Q

what is the most important factor leading to asthma

A

bronchial hyperresponsiveness

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9
Q

what cells cause bronchial inflammation

A

T cells + mast cless

EUSINOPHILIA

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10
Q

what causes asthma

A 
allergens (atopic)
fungal 
atmospheric pollutants
drugs 
genetic factors
occupational sensitisers
cold dry air + exercise
emotion
resp infections
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11
Q

give an example of an allergen that causes asthma

A

house dust mites

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12
Q

what happens during in immediate asthma attack in the early reaction

A

airflow limitation
max 15-20mins
1 hour subsides

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13
Q

why is a prolonged sustained asthma attack after the early reaction more dangerous

A

doesn’t respond well to inhalation of bronchodilator eg. salbutamol

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14
Q

what reaction occurs after occupational sensitisers inhalation (eg. isocyanates) in asthmatics

A

isolate late-phase reactions (no preceding immediate response)
BHR increases

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15
Q

what is the hygiene hypothesis

A

growing up in clean environment predisposes IgE response to allergens
growing up in dirtier environment allows immune response to avoid allergic response
Pathogens stimulate TLRs on immune/epithelial cells to direct an immune inflammatory response away from allergic TH2 towards protective TH1

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16
Q

give an example of a fugal that causes asthma

A

aspergillus fumigates
INTRINSIC
increases sensitivity

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17
Q

give examples of atmospheric pollutants that cause asthma

A

SO2
tobacco smoke
perfumes

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18
Q

what drugs can trigger an asthma attack

A

NSAIDS

B-adrenoceptor antagonists (beta blockers)

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19
Q

how do NSAIDS trigger an asthma attack in affected individuals

A

aspirin-intolerated asthma
reduced PGE2
causes overproduction of cysteine leukotrienes by eusinophils, mast cells and macrophages

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20
Q

what can partially reverse an asthma attack caused by NSAIDS

A

anti-leukotrine therapy

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21
Q

list 3 (NSAID) drugs that can induce asthma

A

asprin
propionic acid derivatives =
indomethacin
ibuprofen

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22
Q

what percentage of asthma does NSAIDS cause

A

trigger 5%

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23
Q

what type of people is NSAID intolerance common in

A

people with nasal polyps

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24
Q

how do NSAIDS cause asthma in some people

A

inhibit arachidonic acid metabolism via cycle-oxigenase (COX) pathway
preventing synthesis of PGs

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25
Q

how do beta-blockers trigger the onset of asthma in some individuals

A

parasympathetic NS causes bronchoconstricition in ASM

no direct sympathetic innervation of ASM and antagonists

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26
Q

what do asthmatics develop after exercising in cold dry air

A

exercise wheeze
release of histamine, PGs and LTs from mast cells + stimulation of neural reflexes when epithelial lining of bronchi becomes hyperosmolar due to dry, cold air

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27
Q

what test can be performed after asthmatics exercise in cold dry air

A

hypertonic (saline/mannitol) provocation test after exercise

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28
Q

give an example of occupational sensitisers that induce asthma in some individuals

A

isocyanates
acid anhydrides

high molecular weight compounds - flour, dust = IgE antibody reaction

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29
Q

how do occupational sensitisers cause asthma

A

chemicals bond to epithelial cells activating them and provide haptens recognised by T cells

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30
Q

beta-blockers should/should not be used to treat hypertension or angina in asthmatics

A

SHOULD NOT

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31
Q

how does adrenaline cause bronchodilation

A

it is an antagonist of parasympathetic receptors

it acts on B2 receptors on ASM

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32
Q

how do beta-blockers eg. propranolol trigger an asthma attack

A

they inhibit B2 adrenoceptors preventing andrenaline from binding causing bronchoconstriction

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33
Q

what are the 2 types of beta blocker

A

B2 adrenoceptor blockers eg. propranolol

selective B1 adrenergic blockers eg. atenolol

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34
Q

what respiratory infections can cause asthma

A

viral inactions eg. rhinovirus, parainfluenza and RSV

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35
Q

are viral infections an intrinsic or extrinsic cause of asthma

A

EXTRINSIC

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36
Q

what are the extrinsic causes of asthma

A

external environmental factors
Allergens - IgE response
Chemicals in workplace

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37
Q

extrinsic causes of asthma are more common in children/adults

A

CHILDREN

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38
Q

what is intrinsic causes of asthma

A 
no external cause identified
adult onset asthma
non-atopic 
aspergillus fumigatus 
due to extrinsic causes
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39
Q

what does NSAIDS stand for

A

non-steroidal anti-inflammatory drugs

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40
Q

what extrinsic causes cause intrinsic asthama

A

sensitisation due to occupational agents (toluene isocyanate)
NSAIDS
b-adrenoceptor blocking agens

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41
Q

what is hay fever an example of

A

atopic asthma

usually runs in families

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42
Q

what happens during an acute asthma response (4 stages)

A
  1. airway narrowing, impeded airflow (reversible)
  2. airway hyper responsiveness + airway spasms = bronchoconstriction
  3. increased mucosal inflammation + recruitment of inflammatory cells (eosinophils, mast cells, neutrophils, T lymphocytes)
  4. hyper secretion of mucus = mucus plugs
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43
Q

what causes chronic asthma

A

long standing inflammation in bronchioles

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44
Q

what happens as a result of chronic asthma

A

changes in bronchioles

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45
Q

what happens as a result of long standing bronchial inflammation resulting in increased bronchial constriction

A

plasma exudation
accumulation of interstitial fluid = oedema
increased smooth muscle mass = hypertrophy + hyperplasia
matrix desposition
sub-epithelial fibrosis
increased mucus = mucus plugging
epithelial damage - sensory nerve endings exposed

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46
Q

how does exposure of sensory nerve endings increase bronchoconstriction

A

feed forward effect, inhaled allergens have direct access to blood and tissue causing more inflammation

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47
Q

chronic asthma results in decreased/increased FEV1 + PEFR

A

decreased

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48
Q

why is chronic asthma worse than acute asthma

A

IRREVERSIBLE airflow limitation due to inflammation

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49
Q

what happens to the airways as a result of chronic asthma

A

airway remodelling = excess narrowing & swelling outside the smooth muscle layer

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50
Q

what changes in the epithelium causes airway remodelling due to chronic asthma

A

conducting airway epithelium is stressed/damaged with loss of ciliated columnar cells
metaplasia - increased mucus-secreting goblet cells
lots of mediators
epithelium becomes hyperresponsive = increased sensitivity to bronchoconstrictors, more vulnerable to viruses

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51
Q

how does changes in the epithelium basement membrane cause airway remodelling

A

increased desposition of repair collagens + proteoglycans in laminal reticlaris beneath basement membrane
increased disposition of lamina, tenascin + fibronectin
increased disposition of matrix proteins
THICKENED BASEMENT MEMBRANE

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52
Q

what does collagen despostitions cause

A

activation of underlying fibroblast sheath

contractile myofibroblasts

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53
Q

how does changes to airway smooth muscle cause airway remodelling in chronic ashtma

A

hypertrophy
hyperplasia of helical bands of ASM
bands contract more easily, stay contracted due to change in actin-myosin cross-link cyclin
asthmatic airways contract too much and too easily

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54
Q

how do nerves cause airway remodelling

A

nerve reflexes cause airway irritability

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55
Q

4 factors that cause a change in the airways in asthmatics

A
  1. increased smooth muscle mass
  2. accumulation of interstitial fluid
  3. increased mucus secretion
  4. epithelial damage
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56
Q

in asthma what drives mild/moderate inflammation

A

Th-2 lymphocytes

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57
Q

what do Th-2 cells facillitate

A

produce IL-4 = IgE synthesis

produce IL-5 = eosinophilic inflammation

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58
Q

what drives sever/chronic asthma

A

loss of sensitivity to corticosteroids

Th1 + Th 2 response

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59
Q

what does a Th1 response do

A

Th1 cells release mediators eg. TNF-a

causes tissue damage, mucus metaplasia, aberrant epithelial + mesenchymal repair

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60
Q

where are mast cells increased in asthma inflammatory response

A

epithelium
smooth muscle
mucous glands

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61
Q

what mediators to mast cells release in the immediate asthma reation

A

histamine
tryptase
PGD2
cysteine leukotrines

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62
Q

what do mediators from mast cells act on

A

ASM
blood vessels
mucous secreting cells
sensory nerves

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63
Q

what do mast cells release in the late asthma response and in chronic asthma

A

cytokine
chemokines
growth factors

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64
Q

what are mast cells inhibited by

A

sodium cromoglycate

B2 agonsits

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65
Q

where is there large numbers of eosinophils in asthma

A

bronchial wall + secretions

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66
Q

what triggers eosinophilic recruitment of the airways

A

cytokines: IL-3, IL-5, GM-CSF
chemokine: act on type 3 C-C chemokine recepors (CCR-3)

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67
Q

what is the role of mediators

A

prime eosinophils for enhanced mediator secretions

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68
Q

what do activated eosinophils release

A

LTC4, MBP, ECP, EPX (all toxic to epithelia cells)

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69
Q

what effect does corticosteroids have on eosinophils

A

they decrease the number and activation of eosinophils

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70
Q

where is there lots of dendritic cells and lymphocytes in asthma response

A

in mucous membranes of airways and alveoli

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71
Q

what is the role of dendritic cells + lymphocytes in an asthma reaction

A

uptake of allergens

CD4+ cells show evidence of activation

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72
Q

what cytokines released by dendritic cells + lymphocytes cause migration and activation of mast cells

A

IL-3, IL-4, IL-9, IL-13

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73
Q

what cytokines released by dendritic cells + lymphocytes cause migration and activation of eosinophils

A

IL-3, Il-5, GM-CSF

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74
Q

what cytokine maintain pro allergic TH2

A

IL-3, IL-4

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75
Q

describe the helper T cell response during an immune response in atopic and nonatopic individuals

A

atopic: strong TH2 response

non-atopic: low-level TH1 response

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76
Q

what type of inflammatory response occurs in atopic and non-atopic

A

atopic: antibody mediated

non-atopic: cell-mediated

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77
Q

what antibodies and inflammatory cells are involved in atopic and non-atopic responses

A

atopic: IgE

non-atopic: IgG + macrophages

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78
Q

individuals who readily produce IgE to common antigens are more/less prone to allergic asthma

A

MORE

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79
Q

what type of reaction is an allergic asthma reaction

A

TYPE 1 Hypersensitivity reaction

caused by antigen/IgE induced mast cell degranulation

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80
Q

what do mast cells release in an allergic asthma reaction

A

spasmogens
histamine
leukotrienes (LTC4 + LTD+4)
chemotaxis + chemokine (prostaglandins D2 + platelet activating factors)

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81
Q

what do spasmogens + histamine + leukotrienes cause

A

increased mucus product. and therefore bronchoconstriction

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82
Q

what happens during the late asthma response

A

chmokines + chemotaxis infiltrate mast cells + Th2 lymphocytes
stimulating resale of cytokines which attracts eosinophils and neutrophils to area
causing: epithelial damage, airway limitation, hyper-reactivity, bronchospasm, wheeze, cough

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83
Q

what happens if inflammation in late reaction isn’t treated

A

collagen lays down
fibrosis
formation of scar tissue
DOES NOT RESPOND TO BRONCHODILATORS

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84
Q

what treatment should be given if there is no bronchodilator response due to fibrosis and collagen deposition

A

CORTICOSTEROIDS

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85
Q

in an early asthma attack what occurs during the early (immediate phase)

A 
alveolar hyperventilation
increased resp drive
decreased PaO2
decreased PaCO2
Bronchoconstriction
normally subsides in 2 hours
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86
Q

in the late phase asthma attack what occurs

A 
alveolar hypoventilation
decreased resp drive
decreased PaO2
Increased PaCO2
hypercapnic drive
= high conc of O2 (60%)
mechanical venitaltion
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87
Q

what is asthmaticus

A

acute severe asthma = medical emergency

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88
Q

who gets asthma

A 
5-10% industrialised countries
childhood (3-5)
more common in UK, Australia, NZ
less common in Far East + africa
Genetics + Environment
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89
Q

what symptoms do asthmatics present with

A

episodic: intermittent attacks of bronchoconstriction
- tight chest
- wheezing (increased resistance + turbulence)
- creating difficulty (worse night + morning)
cough (worse at night)

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90
Q

what other symptom are children with atopic asthma likely to have

A

eczema (dermatitis)

91
Q

what clinical signs do people which asthma present with

A

increased IgE: rhinitis, conjunctivitis, eczema
blood eosinophilia > 4%
steroid/b-agonist responsive
family history

92
Q

what genes can predispose people to asthma

A

genes controlling cytokine production (IL-)
affects mast cells + eosinophil development
genes encode neuropeptide S receptor

93
Q

what gene defect predisposed people to atopic asthma

A

polymorphic variation in proteins in Il-4/IL-13 pathway

94
Q

what gene defect can affect airway hyper-responsiveness and tissue remodelling

A

ADAM 33 (diintegin + metalloproteinase) on chromosome 20p13

95
Q

what are the 4 hallmarks during examination of someone with asthma

A

WHEEZE
tight chest
breathlessness
cough

96
Q

what do we look for in the blood/sputum of asthmatics

A 
high eosinophils (more significant in sputum)
asthmatics don't usually produce sputum
97
Q

what lung function tests can be used to assess asthma

A

PEFR (peak expiratory flow rate)

spirometry = reduced forced expiratory ratio

98
Q

how is peak flow (PEFR) measured

A

measured on walking prior to taking bronchodilator + before bed after bronchodilator
diurnal variation of peak flow to see if asthma symptoms at night
keep diary

99
Q

what does spirometry asssess

A

reversibility

100
Q

how does spirometry diagnose asthma

A

demonstrating > 15% improvement in FEV1 or PEFR after inhalation of bronchodilator
FVC = normal
FEV1 = decreased

101
Q

what FEV1/FEV ratio indicates asthma (obstructive airway disease)

102
Q

how does spirometry assess asthma severity

A

as the conc of bronchoconstrictor increases the % fall in FEV1 increased
> severity = > FEV1 fall

103
Q

what is FEV1

A

forced expiratory volume (in litres) in 1 second

104
Q

mild asthma shows hypersensitivity/hyper-reactivity and a moderate/large fall in FEV1

A

hypersensitivity

moderate

105
Q

severe asthma shows hypersensitivity/hyper-reactivity and a moderate/large fall in FEV1

A

hyper-reactivity

large

106
Q

how does expiration differ in asthmatics to healthy people

A

asthmatics have slower gas flow, harder to breath out, exhalation declines

107
Q

how can exercise be used to test asthma in children

A

child - 6 min treadmill run

HR > 160 bpm

108
Q

what is bronchial provocation testing

A

inhaled bronchonstictors eg. spasmogens cause bronchospasm

109
Q

give examples of bronchoconstrictors

A

mannitol
histamine - activates ASM H1 receptor
methalcholine - activates ASM M3 receptor

110
Q

what people will react only to higher dose of methalcholine in bronchial provocation tests

A

extreme exertion - winter sports enthusiast
wheeze/lots of coughing after viral infection
seasonal wheeze in pollen season
allergic rhinitis

111
Q

what do some x-rays of asthmatic patients show

A

over-inflation

x-ray can exclude pneumothorax as similar symptoms

112
Q

if a patient has suspected asthma due to severe airflow limitation what can be used to see if they are asthmatic

A

trail of corticosteroids
prednisolone 30 mg orally for 2 weeks
lung function measured before and after
FEV improvement > 15%

113
Q

how are bronchial provocation tests carried out

A

ask patient to inhale gradually increasing conc of histamine or methalcholine
induces transient airflow limitation
OR
inhalation of cold dry air, mannitol/hypertonic saline causes release of endogenous mediators eg. histamine, prostaglandins

114
Q

asthmatics respond to very low/high does of methalcholine

A

Low PD20FEV1

115
Q

how do bronchial provocation tests assess asthma severity

A

severity of BHR graded according to provocation dose of conc of agonise that produces a 20% fall in FEV1 (PD20 FEV1)

116
Q

how does inhaled NO indicate asthma

A

measures airway limitation + index corticosteroid response

117
Q

If high NO is exhaled what does this suggest

118
Q

how does a skin prick test test for asthma

A

identifies allergic/extrinsic asthma

119
Q

if SPT is not available how can allergen-specific IgE be measured

A

in serum

patient must be taking antihistamines

120
Q

what are the adverse effects of SABAs

A 
fine tremor
tachycardia 
cardiac dysrhythmia
hypokalaemia
increased BP
palpitations
121
Q

how do short-acting B2 adrenoceptors agonists (SABAs) treat asthma

A

stimulate bronchial smooth muscle B2 receptors - increased cAMP
relax bronchial smooth muscle 3-5 hours
mucus clearance
decrease mast cell/monocyte mediatory release

122
Q

examples of SABAs

A

salbutamol
albuterol
terbutaline

123
Q

what is the first line treatment for mild and intermittent asthma

124
Q

when are SABAs taken

A

when needed

125
Q

what route are SABAs taken by

A

inhalation - metered dose. dry powder (lessens systemic effect)
IV in emergency

126
Q

how do SABAs act

A

rapidly - 5 mins

max effect 30 mins

127
Q

what are LABAs

A

long acting B2 adrenoceptor agonists

128
Q

give examples of LABAs

A

salmeterol

formoterol

129
Q

why are LABAs used over SABAs sometimes

A

NOCTURNAL use
8 hours
long half life

130
Q

why are SABAs used over LABAs sometimes

A

LABAs are NOT for acute bronchospasm relief

salmeterol over formoterol = slow to act

131
Q

are LABAs used as monotherapy, what are they co-administered with

A

NO
add on asthma therapy
ALWAYS co-adminsitered with glucorticoids

132
Q

what are the adverse affects of LABAs

A

can increase asthmatic deaths

use of non-selective B-adrenoceptor antagonist eg. propranolol in asthmatics = contrainicated - bronchospasm

133
Q

what is the advantage of using selective B2 adrenoceptor agonists

A

they reduce harmful stimulation of cardiac B1 adrenoceptors

non-selective agonists eg isoprenaline = redundant

134
Q

what do combination inhalers consist of

A

ICS (glucocorteroid) + LABA

eg. Beclometasone, Formorterol

135
Q

why are combination inhalers safe

A

high therapeutic ratio

B2 down regulation + tachyphylaxis with chronic LABA

136
Q

how do CysLT1 receptor antagonists (leukotrienes) treat asthma

A

anti-inflammatory
act competitively at CysLT1 receptor, blocking the receptor
derived from mast cells
infiltrate inflammatory cells causing: smooth muscle contraction, mucus secretion + oedema

137
Q

Give examples of CysLT1s

A

LTC4
LTD4
LTE4

138
Q

when are cysLT1s used

A

second line therapy

139
Q

what is a 2nd line complimentary non-steroidal anti-inflammatory that is add on to inhaled steroid against bronchospasm in mild and persistent asthma

A

CysLT1 receptor antagonists (leukotrienes)

140
Q

when is CysLT1 receptor antagonists combined inhaled with corticosteroids

A

in severe asthma

141
Q

what is montelukask

A

taken orally, once daily, high therapeutic ration drug that is a non-steroidal anti-inflammatory that can be added to a corticosteroid

142
Q

adverse effects of montelukask

A

headache

gastrointestinal upset

143
Q

what is montelukask (a CysLT) effective against

A

antigen-induced + exercise induced bronchospasm

allergic rhinitis + anti-histamine

144
Q

what do cysLTs eg montelukask NOT treat

A

relief of acute severe asthma

145
Q

what are methylxanthines

A

bronchodilators + anti-inflammatory
increase diaphragmatic contractibility, improves ventilation and reduces fatigue
added to inhaled steroid as complimentary non steroidal anti-inflammatory
inhibit mediator release from mast cells
increase mucus clearing

146
Q

give an example of methylxanthines

A

theophylline

aminophylline

147
Q

what drug that can be used to treat asthma is present in

A

coffees, tea, chocolate beverages

148
Q

when is theophylline used to treat asthma

A

oral maintanence

149
Q

what does theophylline activate

A

histone deacetylase HDAC
anti-inflammatory action of glucocorticoids
add on therapy

150
Q

why must theophylline be monitored

A

due to drug interactions CYP450 drug interactions eg. antibitiotics inhibit erythromycin

151
Q

what drug is given as an add on during an acute asthma attack via IV

A

aminophylline

152
Q

what is the disadvantages of methylxanthine

A 
low therapeutic ratio - drug interactions 
narrow therapeutic window 
dysrhythmia
seizures
hypotension 
nausea 
vomiting 
abdominal discomfort
headache 
MUST GIVE ACCURATE DOSAGE
153
Q

advantage of using methylxanthines

A

oral route = sustained effect

154
Q

what type of drugs are methylxanthines

A

second line combined with B2 adrenoceptor agonists and glucocorticoids

155
Q

what is the action of methylxanthines

A

inhibitor of phosphodiserases isoforms (PDE3 + 4) that activates cAMP and cGMP (second messengers Thant relax smooth muscle

156
Q

what is ibruprofen

A

anti-inflammatory that can trigger bronchospasm in sensitive individuals

157
Q

what is a first line preventer inhaler that is an anti-inflammatory agent (surpasses inflammation)

158
Q

what synthesises corticosteroids on demand

A

adrenal cortex

released from zona fasciculata

159
Q

why are corticosteroids given to a patient

A

reduce exacerbations in eosinophilic COPD (ACOS- asthma COPD overlap syndrome)
optimises lung delivery (extra fine solution HFA/Spacer)

160
Q

what is the most important glucocorticoid

A

cortisol (hydrocortisone)

161
Q

what is the first line treatment for asthma where there is inflammation

A

glucocorticoids = CORTISOL

162
Q

what effect does cortisol have in the body

A

decreases inflammation, immunological response, glucose utilisation
increases liver deposition, gluconeogenesis, liver glucose output, protein catabolism, bone catabolism, gastric acid + peptide secretions

163
Q

do glucocorticoids have direct bronchodilator action

164
Q

does cortisol relive bronchospasms

165
Q

why is cortisol inhaled

A

to minimise adverse effects

166
Q

describe the 4 stages of the mechanism of action of cortisol

A
  1. lipophilic (enter by diffusion)
  2. combine with GRa causing dissociation of inhibitory heart shock proteins (HPS90) the activated receptor translocates to the nucleus by importins
  3. in nucleus receptor monomers become homodimers which bind to GRE (glucocorticoid response elements ) in the promotor region of specific genes
  4. transcription of specific genes: switched on (transactivated)/switched off (trans repressed) to alter mRNA levels and mediate protein synthesis
167
Q

in inflammation of bronchial asthma what are genes regulated by

A

glucocorticoid response elements

modifying chromatin structure (deacetylation of histones)

168
Q

what effect does cortisol have on genes

A

increases gene transcription encoding anti-inflammatory proteins
decreases gene transcription for genes encoding inflammatory proteins

169
Q

how does cortisol prevent inflammatory gene expression

A

acetylation of histones by HATs (histone acetyltransferase)
acetylation unwinds DNA from histones causing transcription
glucocorticoids recruit deacetylase HDAC activating genes and switches off gene transcription

170
Q

how does cortisol switching off gene transcription of inflammatory proteins stop the inflammatory response

A 
decreased Th2 cytokines (IL-4, IL-5)
Th2 apoptosis
eosinophils don't enter lungs
eosinophils apoptosis
mast cells reduced 
decrease Fc receptors on mast cells
prevent IgE production
restoration
171
Q

what effect does glucocorticoid have on eosinophils

A

decrease number by apoptosis

172
Q

what effect does glucocorticoid have on T cells

A

decrease cytokines

173
Q

what effect does glucocorticoid have on mast cells

A

decrease numbers

174
Q

what effect does glucocorticoid have on macrophages

A

decrease their release of cytokines

175
Q

what effect does glucocorticoid have on dendritic cells

A

decrease number

176
Q

what effect does glucocorticoid have on epithelial cells

A

decrease cytokine mediators

177
Q

what effect does glucocorticoid have on endothelial cells

A

decrease leakiness

178
Q

what effect does glucocorticoid have on ASM

A

increased B2 adrenoceptors

decrease cytokines

179
Q

what effect does glucocorticoid have on mucus glands

A

decrease mucus secretions

180
Q

why are glucocorticoids used

A

prevent inflammation and resolves established inflammation

181
Q

do glucocorticoids have a short or long term effect and what is this effect

A

long term effect against allergens

182
Q

what should glucocorticoids be combined with

183
Q

adverse effects of cortisol

A 
dysphonia (weak/horse voice)
oropharyngeal candidiasis (thrush)
184
Q

3 examples of glucocorticoid + LABA used to treat mild asthma

A

becolmetasone
budesonide
fluticasone

185
Q

how longs does becolmetasone have effect for

A

efficacy develops over days

186
Q

why is becolmetasone inhaled by metered dose

A

to minimise unwanted systemic effects

187
Q

what steroid is administered by IV

A

Hydrocortisone

188
Q

what is an oral steroid with a low therapeutic ratio that is administered for acute exacerbations NOT maintenace

A

Prednisolone

189
Q

side effects of prednisolone

A

retarded growth
water retention
hypertension
weight gain

190
Q

what is an inhaled steroid that has a high therapeutic ration and is used to treat chronic asthma, its maintenance can be given as mono therapy

A

becolmethasone

191
Q

where are mineralocorticoids released from in the adrenals

A

zona gomerulosa

192
Q

give an example fo a mineralocorticoid and its function

A

aldosterone

regulates salt and water retention by kidneys

193
Q

what should be given to patients with poor inhaler technique

A

SPACER
avoids coordination problems with pMDI (metered dose)
improves lung deposition

194
Q

what does a spacer device reduce

A

oropharyngeal + laryngeal side effects
systemic absorption from swallowed fraction
particle size + velocity

195
Q

what people usually require a spacer

196
Q

what anti-inflammatory preventer is a second line drug that is a mast cell stabiliser therefore surpasses histamine release from mast cells

197
Q

what method are croons administered by

A

inhaled only

198
Q

why are croons infrequently used

A

poor efficacy

weak effect

199
Q

how do cromones prevent inflammation

A

decreases sensitivity of sensory c-fibres that trigger exaggerated reflex
reduces cytokines

200
Q

give an example of a cromone

A

sodium cromoglicate

- inhaled (little systemic absorption)

201
Q

why is sodium cromoglicate given

A

reduces asthma attack in early + late phase

it takes several weeks to block late phase using frequent dosing

202
Q

why is sodium cromoglicate not completely useful against asthma attack

A

it takes several weeks to block late phase using frequent dosing

203
Q

what patients are commonly given sodium cromoglicate

204
Q

what anti-IgE drug is given to people with severe persisting allergic asthma to reduce exacerbations and is given via IV every 2-4 weeks

A

Omalizumab

205
Q

what is the action of omalzumab

A

inhibits binding to high-affinity IgE receptor (prevents Fce attachment) so inhibits Th2 response and suppresses mediators from mast cells/basophil release
also reduces Fee receptor expression on inflammatory cells

206
Q

what drug is a monoclonal anti-IL5 antibody used to treat severe refectory eosinophilia ( >300 ul eosinophils) and reduce exacerbations

A

mepolizumab

reslizumab

207
Q

how does mepolizumab work

A

blocks effect of TH2 cytokine IL-5 release (reducing eosinophilic inflammation)

208
Q

what is the treatment of chronic asthma

A
  • inhaled steroid suppresses inflammatory cascade
  • anti-IL-5 (mepolizumab)
  • inhaled becolmethasone
  • LABA/LAMA to stabilise ASM
  • (+/-) non steroid anti-inflammatory eg. theophylline, anti-leyukotrine, cromoglicate
209
Q

if an asthma is atopic what should be prescribed

A

anti-IgE eg Omalizub

210
Q

what is the treatment given to acute asthma

A
  • oral prednisolone (or IV hydrocortisone) if rapidly deteriorating
  • nebulised high dose salbutamol (+/- nebulised ipratoropium) (+/- aminophylline/magnesium)
  • at least 60% oxygen
  • if falling PaO2 and rising PAO2 ITU assisted mechanical intubated ventilation
211
Q

in asthma hat alliterates decline in lung function

A

airway remodelling

212
Q

what is the stepwise therapy of asthma

A
  1. inhaled SABA (blue inhaler)
  2. addition of inhaled low dose steroid (brown inhaler)
  3. addition of LABA + increased dose of inhaled steroid
  4. increased dose of inhaled steroid + leukotrienes receptor antagonists (MONTELUKAST = for atopic asthma)
  5. ADD low dose oral steroid eg. ozmilzub + refer to specialist
213
Q

what is a QVAR inhaler

A

ICS + LABA + LAMA

214
Q

a patient presents to you with inability to complete sentences in 1 breath, resp rate >25, tachycardia > 110 bpm + pulse paradox and a PEFR < 50% predicted normal/best what is wrong with them

A

Acute severe asthma

215
Q

list the features of an acute severe asthma attack

A

silent chest, cyanosis, feeble resp effort
exhaustion, confusion, coma
bradycardia or hypotension
PEFR < 30%
High PaCO2 > 6 kPa
severe hyperaemia PaO2 < 8 kPa with O2 treatment
low arterial pH

216
Q

what treatment should be given to a patient with severe asthma attack

A
  • nebulised SA bronchodilators
  • nebulised antimuscarinics = IPRATROPIUM BROMIDE
  • IV hydrocortisone
  • SABA/magnesium sulphate (IV)
  • oral prednisolone
  • ventilation
217
Q

what happens to FEV1 during an asthma attack in the immediate phase then in the late phase

A

sudden fall then begins to increase then a large slower fall in FEV1 and a longer increase back to normal

218
Q

in an asthma attack what type of reaction occurs in the early phase

A

Type I hypersensitivity reactio

219
Q

in asthma attack what type of reaction occurs in the late phase

A

Type IV hypersensitivity reaction, delayed inflammation

220
Q

in early phase of an asthma attack what causes bronchospasm

A

spasmogens
CysLTs
Histamine
RELEASED FROM MAST CELLS

221
Q

in early phase of an asthma attack what causes the late phase and exacerbates the immune response

A

chemotaxis and chemokines

FROM MAST CELLS

222
Q

what happens during the late phase of an asthma attack

A

infiltration of cytokines releasing Th2 cells + monocytes

activation of inflammatory cells - eosinophils

223
Q

what does CysLTs cause in an acute asthma attack

A 
airway hyper-responsiveness + airway inflammation
bronchospasm
wheeze
mucus over-production 
cough
224
Q

what does an infiltration of eosinophils cause in an asthma attack

A 
epithelial damage
airway hyper-responsiveness
bronchospasm
wheeze
mucus over-production 
cough

RESPIRATORY (12 decks)

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