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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
how do beta-blockers trigger the onset of asthma in some individuals
parasympathetic NS causes bronchoconstricition in ASM | no direct sympathetic innervation of ASM and antagonists
26
what do asthmatics develop after exercising in cold dry air
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
27
what test can be performed after asthmatics exercise in cold dry air
hypertonic (saline/mannitol) provocation test after exercise
28
give an example of occupational sensitisers that induce asthma in some individuals
isocyanates acid anhydrides high molecular weight compounds - flour, dust = IgE antibody reaction
29
how do occupational sensitisers cause asthma
chemicals bond to epithelial cells activating them and provide haptens recognised by T cells
30
beta-blockers should/should not be used to treat hypertension or angina in asthmatics
SHOULD NOT
31
how does adrenaline cause bronchodilation
it is an antagonist of parasympathetic receptors | it acts on B2 receptors on ASM
32
how do beta-blockers eg. propranolol trigger an asthma attack
they inhibit B2 adrenoceptors preventing andrenaline from binding causing bronchoconstriction
33
what are the 2 types of beta blocker
B2 adrenoceptor blockers eg. propranolol | selective B1 adrenergic blockers eg. atenolol
34
what respiratory infections can cause asthma
viral inactions eg. rhinovirus, parainfluenza and RSV
35
are viral infections an intrinsic or extrinsic cause of asthma
EXTRINSIC
36
what are the extrinsic causes of asthma
external environmental factors Allergens - IgE response Chemicals in workplace
37
extrinsic causes of asthma are more common in children/adults
CHILDREN
38
what is intrinsic causes of asthma
``` no external cause identified adult onset asthma non-atopic aspergillus fumigatus due to extrinsic causes ```
39
what does NSAIDS stand for
non-steroidal anti-inflammatory drugs
40
what extrinsic causes cause intrinsic asthama
sensitisation due to occupational agents (toluene isocyanate) NSAIDS b-adrenoceptor blocking agens
41
what is hay fever an example of
atopic asthma | usually runs in families
42
what happens during an acute asthma response (4 stages)
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
43
what causes chronic asthma
long standing inflammation in bronchioles
44
what happens as a result of chronic asthma
changes in bronchioles
45
what happens as a result of long standing bronchial inflammation resulting in increased bronchial constriction
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
46
how does exposure of sensory nerve endings increase bronchoconstriction
feed forward effect, inhaled allergens have direct access to blood and tissue causing more inflammation
47
chronic asthma results in decreased/increased FEV1 + PEFR
decreased
48
why is chronic asthma worse than acute asthma
IRREVERSIBLE airflow limitation due to inflammation
49
what happens to the airways as a result of chronic asthma
airway remodelling = excess narrowing & swelling outside the smooth muscle layer
50
what changes in the epithelium causes airway remodelling due to chronic asthma
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
51
how does changes in the epithelium basement membrane cause airway remodelling
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
52
what does collagen despostitions cause
activation of underlying fibroblast sheath | contractile myofibroblasts
53
how does changes to airway smooth muscle cause airway remodelling in chronic ashtma
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
54
how do nerves cause airway remodelling
nerve reflexes cause airway irritability
55
4 factors that cause a change in the airways in asthmatics
1. increased smooth muscle mass 2. accumulation of interstitial fluid 3. increased mucus secretion 4. epithelial damage
56
in asthma what drives mild/moderate inflammation
Th-2 lymphocytes
57
what do Th-2 cells facillitate
produce IL-4 = IgE synthesis | produce IL-5 = eosinophilic inflammation
58
what drives sever/chronic asthma
loss of sensitivity to corticosteroids | Th1 + Th 2 response
59
what does a Th1 response do
Th1 cells release mediators eg. TNF-a | causes tissue damage, mucus metaplasia, aberrant epithelial + mesenchymal repair
60
where are mast cells increased in asthma inflammatory response
epithelium smooth muscle mucous glands
61
what mediators to mast cells release in the immediate asthma reation
histamine tryptase PGD2 cysteine leukotrines
62
what do mediators from mast cells act on
ASM blood vessels mucous secreting cells sensory nerves
63
what do mast cells release in the late asthma response and in chronic asthma
cytokine chemokines growth factors
64
what are mast cells inhibited by
sodium cromoglycate | B2 agonsits
65
where is there large numbers of eosinophils in asthma
bronchial wall + secretions
66
what triggers eosinophilic recruitment of the airways
cytokines: IL-3, IL-5, GM-CSF chemokine: act on type 3 C-C chemokine recepors (CCR-3)
67
what is the role of mediators
prime eosinophils for enhanced mediator secretions
68
what do activated eosinophils release
LTC4, MBP, ECP, EPX (all toxic to epithelia cells)
69
what effect does corticosteroids have on eosinophils
they decrease the number and activation of eosinophils
70
where is there lots of dendritic cells and lymphocytes in asthma response
in mucous membranes of airways and alveoli
71
what is the role of dendritic cells + lymphocytes in an asthma reaction
uptake of allergens | CD4+ cells show evidence of activation
72
what cytokines released by dendritic cells + lymphocytes cause migration and activation of mast cells
IL-3, IL-4, IL-9, IL-13
73
what cytokines released by dendritic cells + lymphocytes cause migration and activation of eosinophils
IL-3, Il-5, GM-CSF
74
what cytokine maintain pro allergic TH2
IL-3, IL-4
75
describe the helper T cell response during an immune response in atopic and nonatopic individuals
atopic: strong TH2 response | non-atopic: low-level TH1 response
76
what type of inflammatory response occurs in atopic and non-atopic
atopic: antibody mediated | non-atopic: cell-mediated
77
what antibodies and inflammatory cells are involved in atopic and non-atopic responses
atopic: IgE | non-atopic: IgG + macrophages
78
individuals who readily produce IgE to common antigens are more/less prone to allergic asthma
MORE
79
what type of reaction is an allergic asthma reaction
TYPE 1 Hypersensitivity reaction | caused by antigen/IgE induced mast cell degranulation
80
what do mast cells release in an allergic asthma reaction
spasmogens histamine leukotrienes (LTC4 + LTD+4) chemotaxis + chemokine (prostaglandins D2 + platelet activating factors)
81
what do spasmogens + histamine + leukotrienes cause
increased mucus product. and therefore bronchoconstriction
82
what happens during the late asthma response
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
83
what happens if inflammation in late reaction isn't treated
collagen lays down fibrosis formation of scar tissue DOES NOT RESPOND TO BRONCHODILATORS
84
what treatment should be given if there is no bronchodilator response due to fibrosis and collagen deposition
CORTICOSTEROIDS
85
in an early asthma attack what occurs during the early (immediate phase)
``` alveolar hyperventilation increased resp drive decreased PaO2 decreased PaCO2 Bronchoconstriction normally subsides in 2 hours ```
86
in the late phase asthma attack what occurs
``` alveolar hypoventilation decreased resp drive decreased PaO2 Increased PaCO2 hypercapnic drive = high conc of O2 (60%) mechanical venitaltion ```
87
what is asthmaticus
acute severe asthma = medical emergency
88
who gets asthma
``` 5-10% industrialised countries childhood (3-5) more common in UK, Australia, NZ less common in Far East + africa Genetics + Environment ```
89
what symptoms do asthmatics present with
episodic: intermittent attacks of bronchoconstriction - tight chest - wheezing (increased resistance + turbulence) - creating difficulty (worse night + morning) cough (worse at night)
90
what other symptom are children with atopic asthma likely to have
eczema (dermatitis)
91
what clinical signs do people which asthma present with
increased IgE: rhinitis, conjunctivitis, eczema blood eosinophilia > 4% steroid/b-agonist responsive family history
92
what genes can predispose people to asthma
genes controlling cytokine production (IL-) affects mast cells + eosinophil development genes encode neuropeptide S receptor
93
what gene defect predisposed people to atopic asthma
polymorphic variation in proteins in Il-4/IL-13 pathway
94
what gene defect can affect airway hyper-responsiveness and tissue remodelling
ADAM 33 (diintegin + metalloproteinase) on chromosome 20p13
95
what are the 4 hallmarks during examination of someone with asthma
WHEEZE tight chest breathlessness cough
96
what do we look for in the blood/sputum of asthmatics
``` high eosinophils (more significant in sputum) asthmatics don't usually produce sputum ```
97
what lung function tests can be used to assess asthma
PEFR (peak expiratory flow rate) | spirometry = reduced forced expiratory ratio
98
how is peak flow (PEFR) measured
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
what does spirometry asssess
reversibility
100
how does spirometry diagnose asthma
demonstrating > 15% improvement in FEV1 or PEFR after inhalation of bronchodilator FVC = normal FEV1 = decreased
101
what FEV1/FEV ratio indicates asthma (obstructive airway disease)
< 75%
102
how does spirometry assess asthma severity
as the conc of bronchoconstrictor increases the % fall in FEV1 increased > severity = > FEV1 fall
103
what is FEV1
forced expiratory volume (in litres) in 1 second
104
mild asthma shows hypersensitivity/hyper-reactivity and a moderate/large fall in FEV1
hypersensitivity | moderate
105
severe asthma shows hypersensitivity/hyper-reactivity and a moderate/large fall in FEV1
hyper-reactivity | large
106
how does expiration differ in asthmatics to healthy people
asthmatics have slower gas flow, harder to breath out, exhalation declines
107
how can exercise be used to test asthma in children
child - 6 min treadmill run | HR > 160 bpm
108
what is bronchial provocation testing
inhaled bronchonstictors eg. spasmogens cause bronchospasm
109
give examples of bronchoconstrictors
mannitol histamine - activates ASM H1 receptor methalcholine - activates ASM M3 receptor
110
what people will react only to higher dose of methalcholine in bronchial provocation tests
extreme exertion - winter sports enthusiast wheeze/lots of coughing after viral infection seasonal wheeze in pollen season allergic rhinitis
111
what do some x-rays of asthmatic patients show
over-inflation | x-ray can exclude pneumothorax as similar symptoms
112
if a patient has suspected asthma due to severe airflow limitation what can be used to see if they are asthmatic
trail of corticosteroids prednisolone 30 mg orally for 2 weeks lung function measured before and after FEV improvement > 15%
113
how are bronchial provocation tests carried out
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
asthmatics respond to very low/high does of methalcholine
Low PD20FEV1
115
how do bronchial provocation tests assess asthma severity
severity of BHR graded according to provocation dose of conc of agonise that produces a 20% fall in FEV1 (PD20 FEV1)
116
how does inhaled NO indicate asthma
measures airway limitation + index corticosteroid response
117
If high NO is exhaled what does this suggest
asthma
118
how does a skin prick test test for asthma
identifies allergic/extrinsic asthma
119
if SPT is not available how can allergen-specific IgE be measured
in serum | patient must be taking antihistamines
120
what are the adverse effects of SABAs
``` fine tremor tachycardia cardiac dysrhythmia hypokalaemia increased BP palpitations ```
121
how do short-acting B2 adrenoceptors agonists (SABAs) treat asthma
stimulate bronchial smooth muscle B2 receptors - increased cAMP relax bronchial smooth muscle 3-5 hours mucus clearance decrease mast cell/monocyte mediatory release
122
examples of SABAs
salbutamol albuterol terbutaline
123
what is the first line treatment for mild and intermittent asthma
SABAs
124
when are SABAs taken
when needed
125
what route are SABAs taken by
inhalation - metered dose. dry powder (lessens systemic effect) IV in emergency
126
how do SABAs act
rapidly - 5 mins | max effect 30 mins
127
what are LABAs
long acting B2 adrenoceptor agonists
128
give examples of LABAs
salmeterol | formoterol
129
why are LABAs used over SABAs sometimes
NOCTURNAL use 8 hours long half life
130
why are SABAs used over LABAs sometimes
LABAs are NOT for acute bronchospasm relief | salmeterol over formoterol = slow to act
131
are LABAs used as monotherapy, what are they co-administered with
NO add on asthma therapy ALWAYS co-adminsitered with glucorticoids
132
what are the adverse affects of LABAs
can increase asthmatic deaths | use of non-selective B-adrenoceptor antagonist eg. propranolol in asthmatics = contrainicated - bronchospasm
133
what is the advantage of using selective B2 adrenoceptor agonists
they reduce harmful stimulation of cardiac B1 adrenoceptors | non-selective agonists eg isoprenaline = redundant
134
what do combination inhalers consist of
ICS (glucocorteroid) + LABA | eg. Beclometasone, Formorterol
135
why are combination inhalers safe
high therapeutic ratio | B2 down regulation + tachyphylaxis with chronic LABA
136
how do CysLT1 receptor antagonists (leukotrienes) treat asthma
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
Give examples of CysLT1s
LTC4 LTD4 LTE4
138
when are cysLT1s used
second line therapy
139
what is a 2nd line complimentary non-steroidal anti-inflammatory that is add on to inhaled steroid against bronchospasm in mild and persistent asthma
CysLT1 receptor antagonists (leukotrienes)
140
when is CysLT1 receptor antagonists combined inhaled with corticosteroids
in severe asthma
141
what is montelukask
taken orally, once daily, high therapeutic ration drug that is a non-steroidal anti-inflammatory that can be added to a corticosteroid
142
adverse effects of montelukask
headache | gastrointestinal upset
143
what is montelukask (a CysLT) effective against
antigen-induced + exercise induced bronchospasm | allergic rhinitis + anti-histamine
144
what do cysLTs eg montelukask NOT treat
relief of acute severe asthma
145
what are methylxanthines
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
give an example of methylxanthines
theophylline | aminophylline
147
what drug that can be used to treat asthma is present in
coffees, tea, chocolate beverages
148
when is theophylline used to treat asthma
oral maintanence
149
what does theophylline activate
histone deacetylase HDAC anti-inflammatory action of glucocorticoids add on therapy
150
why must theophylline be monitored
due to drug interactions CYP450 drug interactions eg. antibitiotics inhibit erythromycin
151
what drug is given as an add on during an acute asthma attack via IV
aminophylline
152
what is the disadvantages of methylxanthine
``` low therapeutic ratio - drug interactions narrow therapeutic window dysrhythmia seizures hypotension nausea vomiting abdominal discomfort headache MUST GIVE ACCURATE DOSAGE ```
153
advantage of using methylxanthines
oral route = sustained effect
154
what type of drugs are methylxanthines
second line combined with B2 adrenoceptor agonists and glucocorticoids
155
what is the action of methylxanthines
inhibitor of phosphodiserases isoforms (PDE3 + 4) that activates cAMP and cGMP (second messengers Thant relax smooth muscle
156
what is ibruprofen
anti-inflammatory that can trigger bronchospasm in sensitive individuals
157
what is a first line preventer inhaler that is an anti-inflammatory agent (surpasses inflammation)
QVAR
158
what synthesises corticosteroids on demand
adrenal cortex | released from zona fasciculata
159
why are corticosteroids given to a patient
reduce exacerbations in eosinophilic COPD (ACOS- asthma COPD overlap syndrome) optimises lung delivery (extra fine solution HFA/Spacer)
160
what is the most important glucocorticoid
cortisol (hydrocortisone)
161
what is the first line treatment for asthma where there is inflammation
glucocorticoids = CORTISOL
162
what effect does cortisol have in the body
decreases inflammation, immunological response, glucose utilisation increases liver deposition, gluconeogenesis, liver glucose output, protein catabolism, bone catabolism, gastric acid + peptide secretions
163
do glucocorticoids have direct bronchodilator action
NO
164
does cortisol relive bronchospasms
NO
165
why is cortisol inhaled
to minimise adverse effects
166
describe the 4 stages of the mechanism of action of cortisol
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
in inflammation of bronchial asthma what are genes regulated by
glucocorticoid response elements | modifying chromatin structure (deacetylation of histones)
168
what effect does cortisol have on genes
increases gene transcription encoding anti-inflammatory proteins decreases gene transcription for genes encoding inflammatory proteins
169
how does cortisol prevent inflammatory gene expression
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
how does cortisol switching off gene transcription of inflammatory proteins stop the inflammatory response
``` 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
what effect does glucocorticoid have on eosinophils
decrease number by apoptosis
172
what effect does glucocorticoid have on T cells
decrease cytokines
173
what effect does glucocorticoid have on mast cells
decrease numbers
174
what effect does glucocorticoid have on macrophages
decrease their release of cytokines
175
what effect does glucocorticoid have on dendritic cells
decrease number
176
what effect does glucocorticoid have on epithelial cells
decrease cytokine mediators
177
what effect does glucocorticoid have on endothelial cells
decrease leakiness
178
what effect does glucocorticoid have on ASM
increased B2 adrenoceptors | decrease cytokines
179
what effect does glucocorticoid have on mucus glands
decrease mucus secretions
180
why are glucocorticoids used
prevent inflammation and resolves established inflammation
181
do glucocorticoids have a short or long term effect and what is this effect
long term effect against allergens
182
what should glucocorticoids be combined with
LABAs
183
adverse effects of cortisol
``` dysphonia (weak/horse voice) oropharyngeal candidiasis (thrush) ```
184
3 examples of glucocorticoid + LABA used to treat mild asthma
becolmetasone budesonide fluticasone
185
how longs does becolmetasone have effect for
efficacy develops over days
186
why is becolmetasone inhaled by metered dose
to minimise unwanted systemic effects
187
what steroid is administered by IV
Hydrocortisone
188
what is an oral steroid with a low therapeutic ratio that is administered for acute exacerbations NOT maintenace
Prednisolone
189
side effects of prednisolone
retarded growth water retention hypertension weight gain
190
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
becolmethasone
191
where are mineralocorticoids released from in the adrenals
zona gomerulosa
192
give an example fo a mineralocorticoid and its function
aldosterone | regulates salt and water retention by kidneys
193
what should be given to patients with poor inhaler technique
SPACER avoids coordination problems with pMDI (metered dose) improves lung deposition
194
what does a spacer device reduce
oropharyngeal + laryngeal side effects systemic absorption from swallowed fraction particle size + velocity
195
what people usually require a spacer
children
196
what anti-inflammatory preventer is a second line drug that is a mast cell stabiliser therefore surpasses histamine release from mast cells
Cromones
197
what method are croons administered by
inhaled only
198
why are croons infrequently used
poor efficacy | weak effect
199
how do cromones prevent inflammation
decreases sensitivity of sensory c-fibres that trigger exaggerated reflex reduces cytokines
200
give an example of a cromone
sodium cromoglicate | - inhaled (little systemic absorption)
201
why is sodium cromoglicate given
reduces asthma attack in early + late phase | it takes several weeks to block late phase using frequent dosing
202
why is sodium cromoglicate not completely useful against asthma attack
it takes several weeks to block late phase using frequent dosing
203
what patients are commonly given sodium cromoglicate
children
204
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
Omalizumab
205
what is the action of omalzumab
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
what drug is a monoclonal anti-IL5 antibody used to treat severe refectory eosinophilia ( >300 ul eosinophils) and reduce exacerbations
mepolizumab | reslizumab
207
how does mepolizumab work
blocks effect of TH2 cytokine IL-5 release (reducing eosinophilic inflammation)
208
what is the treatment of chronic asthma
- 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
if an asthma is atopic what should be prescribed
anti-IgE eg Omalizub
210
what is the treatment given to acute asthma
- 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
in asthma hat alliterates decline in lung function
airway remodelling
212
what is the stepwise therapy of asthma
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
what is a QVAR inhaler
ICS + LABA + LAMA
214
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
Acute severe asthma
215
list the features of an acute severe asthma attack
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
what treatment should be given to a patient with severe asthma attack
- nebulised SA bronchodilators - nebulised antimuscarinics = IPRATROPIUM BROMIDE - IV hydrocortisone - SABA/magnesium sulphate (IV) - oral prednisolone - ventilation
217
what happens to FEV1 during an asthma attack in the immediate phase then in the late phase
sudden fall then begins to increase then a large slower fall in FEV1 and a longer increase back to normal
218
in an asthma attack what type of reaction occurs in the early phase
Type I hypersensitivity reactio
219
in asthma attack what type of reaction occurs in the late phase
Type IV hypersensitivity reaction, delayed inflammation
220
in early phase of an asthma attack what causes bronchospasm
spasmogens CysLTs Histamine RELEASED FROM MAST CELLS
221
in early phase of an asthma attack what causes the late phase and exacerbates the immune response
chemotaxis and chemokines | FROM MAST CELLS
222
what happens during the late phase of an asthma attack
infiltration of cytokines releasing Th2 cells + monocytes | activation of inflammatory cells - eosinophils
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what does CysLTs cause in an acute asthma attack
``` airway hyper-responsiveness + airway inflammation bronchospasm wheeze mucus over-production cough ```
224
what does an infiltration of eosinophils cause in an asthma attack
``` epithelial damage airway hyper-responsiveness bronchospasm wheeze mucus over-production cough ```

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