Harrisons chapter 281 - Asthma

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Asthmatics harbor a special type of in-

flammation in the airways that makes
them more responsive than nonasthmat-
What is special abut the inflammation of
ics to a wide range of triggers, leading
asthmatics
to excessive narrowing with consequent
reduced airflow and symptomatic wheez-
ing and dyspnea.
Is the narrowing of the airways caused Usually reversible but it can also be irre-
by asthma reversible or irreversible versible in patients with chronic asthma
Astham can present at any age but has
3 years old
a peak age of how many years old
There are twice as many males then fe-
males that are asthmatic but by adult-
hood the sex ratio has equalised
In childhood who are more asthmatic fe-
males or males
Adults with asthma, including those with
onset during adulthood, rarely become
permanently asymptomatic
Atopy
What is the major risk factor for asthma
Non atopic individuals have a very low
risk of developing asthma
Atopy refers to the genetic tendency to
develop allergic diseases such as aller-
gic rhinitis, asthma and atopic dermatitis
(eczema).
What is atopy
Atopy is typically associated with height-
ened immune responses to common al-
lergens, especially inhaled allergens and
food allergens.
Allergic rhinitis (80% of asthmatic pa-
tients)

And atopic dermatitis (eczema)

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Atopy may be found in 40-50% of the
Patients with astham commonly suffer population in affluent countries but only a
from other atopic diseases what are they proportion of atopic individuals become
asthmatic
Early viral infections are endogenous not
environmental.. but respiraotry infection
are environmental

The allergens that lead to sensitisation

are usually proteins that have what spe- Protease activity
cific function
house dust mites,

cat and dog fur,

The most common allergens are derived
cockroaches (in inner cities),
from what
grass and tree pollens,

and rodents (in laboratory workers)

It is due to the genetically determined
production of specific IgE antibody with
What causes atopy
many patients showing a family history of
allergic diseases
The most consistent findings in genetics
5q (including the T helper 2 cells and
that lead to asthma have been in associ-
interleukins )
ation with polymorphism of what gene
What interleukins are associated with
4,5,9,13
atopy

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DNA methylation and his one modifica-

tion which may be inflicted by diet, ciga-
rette smoke exposure, and air pollution,
and may affect genes involved in the
What epigenetic mechanisms are in-
pathogenesis of asthma.
volved in asthma
These epigenetic changes may occur in
the fetus as a result of maternal environ-
mental exposure.
Rhinovirus
What viral infections is a common trigger
But it is uncertain whether these virus
of asthma exacerbations
play a role in etiology but they do play a
role in exacerbation
Atypical bacteria like MC
What bacteria have been implicated in
the mechanisms of SEVERE asthma Mycoplasma
Chlamydophilia
This "hygiene hypothesis" proposes that
lack of infections in early childhood pre-
serves the Th 2 cell bias at birth, where-
as exposure to infections and endotoxin
results in a shift toward a predominant
What is the hygiene hypothesis protective Th 1 immune response.

. Children brought up on farms who are

exposed to a high level of endotoxin are
less likely to develop allergic sensitiza-
tion than children raised on dairy farms.
Intestinal parasite infection like hook-
worm infections have been associated Reduced risk of asthma
with a higher or lower risk of asthma
Does obesity increase or decrease the
Increase the risk of asthma
risk for asthma

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Exposure to house dust mites in ear-

ly childhood is a risk factor for allergic
sensitization and asthma, but rigorous
allergen avoidance has not shown any
evidence for a reduced risk of developing
asthma.
Statement

Domestic pets, particularly cats, have

also been associated with allergic sen-
sitization, but early exposure to cats in
the home may be protective through the
induction of tolerance.
may also be linked to the pro-inflamma-
Why are patients with obesity frequently tory adipokines and reduced anti-inflam-
develop asthma matory adipokines that are released from
fat cells.
Asthma that occurs in patients that are
non-atopic and usually show a LATER
onset of disease (adult onset asthma)

What is intrinsic asthma They have concomitant nasal polyps and

may be aspirin sensitive

They usually have more severe and per-

sistent asthma
What percentage of asthmatic patients
Around 10%
have intrinsic asthma
Intrinsic asthma? Because they have
If a patient with asthma has normal
negative skins tests to common aller-
serum concentrations of igE what do you
gens nad a normal serum concentration
suspect
of igE
Inhaled allergens activate mast cells with
bound IgE directly leading to the immedi-
What do inhaled allergens do that leads
ate release of bronchoconstrictor media-
to bronchoconstriction
tors, resulting in the early response that
is reversed by bronchodilators.
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Dermatophagoides species

And environmental exposure leads to

What is the most common allergen to
low grade chronic symptoms that are
trigger asthma
perennial

So these two are the most common

No they usually cause allergic rhinitis
rather than asthma but in thunderstorms
the pollen grains are disrupted and the
Do pollens usually cause asthma
particles that may be released can trig-
ger severe asthma exacerbations (thun-
derstorm asthma).
1. Rhinovirus

2. Respiratory syncytial virus

3. Coronavirus
What viruses are the most common trig-
Generally these are UPPER respiraotry
gers of acute exacerbations and may in-
tract viruses.
vade epithelial cells of the lower as well
as hte upper airways
Mechanisms not properly understood but
reduced production of type I interferons
by epithelial cells from asthmatic pa-
tients, r ing in increased susceptibility to
these viral infections and a greater in-
flammatory response.

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1. Beta- adrenergic blockers commonly

acutely worsen asthma, and their use
may be fatal. May be due to increased
cholinergic bronchoconstriction
What drugs may trigger asthma and
should be avoided 2. Angiotensin convertin enzyme in-
hibitors - inhibit breakdown of kin is which
are bronchoconstrictors

3. Aspirin
Mechanism is linked to HYPERventila-
tion which results in increased OSMO-
Why can exercise trigger asthma LALITY in airway lining fluid and triggers
mast cell mediator release , resulting in
bronchoconstriction
Exercise-induced asthma (EIA) typical-
When does exercise induced asthma be- ly begins after exercise has ended, and
gin and end recovers spontaneously within about 30
min.
Is exercise induced asthma worse in cold It is worse in cold, dry climates than in
,dry climates or hot, humid conditions hot , humid conditions
Prior administration of ²2-agonists and
antileukotrienes, but is best prevented by
regular treatment with ICS, which reduce
How do you prevent exercise induced
the population of surface mast cells re-
asthma
quired for this response.

Cold air can also trigger asthma

Occupational asthma is characteristical-
ly associated with symptoms at work with
relief on weekends and holidays. If re-
Within 6 months = complete recovery
moved from exposure within how many
months of symptoms, is there usually
complete recovery.

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Premenstrual worsening of asthma due

to a FALL IN PROGESTERONE and may
be improved by treatment with high dos-
es of progesterone or gonadotropin re-
What hormones can worsen asthma
leasing hormones

Thryotoxicosis and HYPOthyroidism can

worsen asthma
Why is Gastroesophageal reflux com-
It is increased by bronchodilators.
mon in asthmatic patients
Psychological factors can induce bron-
choconstriction through cholinergic re-
flex pathways.
How can stress lead to asthma
Paradoxically, very severe stress such as
bereavement usually does not worsen,
and may even improve, asthma symp-
toms.
The degree of inflammation is poorly re-
lated to disease severity and may even
Statement be found in atopic patients without asth-
ma symptoms. This inflammation is usu-
ally reduced by treatment with ICS.
Thickening of the basement membrane
due to subepithelial collagen deposition

What structural changes in the airways But this finding is found in eosinophilic
(remodelling) are seen in patients with bronchitis and even found in patients
asthma without asthma

So this I s actually a marker of

eosinophilic inflammation
Direct observation by bronchoscopy indi-
cates that the airways may be narrowed,
erythematous, and edematous.

These pathologic changes are found in

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all airways, but do not extend to the lung
parenchyma!!
On bronchoscopy what can be seen in
patients with asthma peripheral airway inflammation is found
particularly in patients with severe asth-
ma
In patients with asthma is there vasodila- Vasodilation and increase number of
tion or vasoconstriction blood vessels
There is inflammation in the respirato-
ry mucosa from the trachea to termi-
In the BRONCHI (cartilaginous airways)
nal bronchioles, but with a predominance
where
What is the physiologic abnormality of
Airway hyperresponsiveness
asthma

Although the common pattern of inflam-

mation in asthma is characterized by
eosinophil infiltration, some patients with
severe asthma show a neutrophilic pat-
Statement
tern of inflammation that is less sensi-
tive to corticosteroids. However, many in-
flammatory cells are involved in asthma
with no key cell that is predominant
They are activated by allergens through
an IgE-dependent mechanism, and bind-
How are mast cells activated leading to
ing of specific IgE to mast cells ren-
bronchoconstriction
ders them more sensitive to activation by
physical stimuli such as osmolality
Mast cells release several b chocon-
What do mast cells release strictor mediators, including hista-
mine, prostaglandin D2 , and cys-
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teinyl-leukotrienes, but also several cy-
tokines, chemokines, growth factors, and
neurotrophins.
Dendritic cells which are specialised
macrophage - like cells

Dendritic cells take up allergens, process

them to peptides, and migrate to local
lymph nodes where they present the al-
What are the major antigen presenting lergenic peptides to uncommitted T lym-
cells in the airway epithelium phocytes to program the production of
allergen-specific T cells.

Immature dendritic cells in the respirato-

ry tract promote Th 2 cell differentiation
and require cytokines such as IL-12 and
tumor necrosis factor ±TNF-±),
( to promote
the normally preponderant Th1 response
They release basic proteins and oxygen
derived FREE radicals
What do eosinophils do that links them to
the development of airway hyperrespon- Eosinophils may be important in release
siveness of growth factors involved in airway re-
modelling and in exacerbations but prob-
ably not in AHR
The naïve immune system and the im-
What is the difference between the naive mune system of asthmatics are skewed
immune system vs normal immune sys- to express the Th 2 phenotype, whereas
tem in regards to the T lymphocytes in normal airways Th 1 cells predomi-
nate.
TH2 cells through the release of what
1. IL-5
interleukins are associated with
1. Eosinophilic inflammation
2. IL-4and 13
2. Increased IgE formation
Give examples of structural cells of the
airways
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Statement
What cytokines mediate allergic inflam- IL4,5, 9 and 13
mation and what cytokines mediate a
more severe disease
What cytokines are anti inflammatory
and may be deficient in asthma
What cells produce reactive oxygen
species
Statement
1. Epithelial cells
2. Fibroblasts
3. Airway smooth muscle cells
Mast cell-derived mediators, such as
histamine, p taglandin D2 , and
cysteinyl-leukotrienes, contract airway
smooth muscle, increase microvascular
leakage, increase airway mucus secre-
tion, and attract other inflammatory cells.
Allergic inflammation = TH2 cytokines ,
More severe disease = IL-1B and TNF-a
(pro inflammatory cytokines)
IL-10 and 12
Activated inflammatory cells such
as macrophages, eosinophils, and
neutrophils produce reactive oxygen
species
So cytokines dont produce ROS
Nitric oxide (NO) is produced by NO
synthases in several cells in the airway,
particularly airway epithelial cells and
macrophages.
The level of NO in the expired air of pa-
tients with asthma is higher than normal
and is related to the eosinophilic inflam-
mation. Increased NO may contribute to
the bronchial vasodilation observed in
asthma.
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loss of its barrier function to allow pene-

tration of allergens;

loss of enzymes (such as neutral en-

dopeptidase/ neprilysin) that degrade
certain peptide inflammatory mediators
How does epithelial damage affect and like bradykinin;
lead to airway hyperresponsiveness
loss of a relaxant factor (so-called epithe-
lial-derived relaxant factor);

and exposure of sensory nerves, which

may lead to reflex neural effects on the
airway.
a ently thickened due to subepithelial fi-
brosis with deposition of types III and V
collagen below the true basement mem-
brane and is associated with eosinophil
In all asthmatic patients what happens to
infiltration, presumably through the re-
the basement membrane
lease of profibrotic mediators such as
transforming growth factor-².

So collagen 3 and 5 are deposited.

In patients with asthma is there an in-
creased or decreased response to con-
strictors
How about responsiveness to the B-ag-
onists
In patients with asthma is there in-
creased or decreased blood flow
To constrictors (B- antagonists??) there
is NO INCREASED RESPONSIVNESS
But to the B agonists = there are RE-
DUCED responsiveness
In the asthmatic airways there are hyper-
trophy and hyerplasia
There is increased airway mucosal blood
flow which may contribute to airway nar-
rowing!!
There is an increase in the number of
blood vessels in asthmatic airways as
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 Harrisons chapter 281 - Asthma
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a result of angiogenesis in response to
growth factors, particularly vascular-en-
dothelial growth factor.
What interleukin contributes to mucus
IL-13
hypersecretion
Cholinergic pathways, through the re-
lease of acetylcholine acting on mus-
Does cholinergic pathways lead to bron-
carinic receptors, cause bronchocon-
chodilation or constriction
striction and may be activated reflexly in
asthma.
The characteristic structural changes are
What are the characteristic structural
increased airway smooth muscle, fibro-
changes in the airway of asthmatic pa-
sis, angiogenesis, and mucus hyperpla-
tients
sia.
Bronchoconstriction from mast cell medi-
ators

This results in a reduction in forced expi-

ratory volume in 1 second (FEV1), FEV1/
forced vital capacity (FVC) ratio, and
peak expiratory flow (PEF), as well as an
increase in airway resistance.
Limitation of airflow is due mainly to
bronchoconstriction, airway edema, vas-
Early closure of peripheral a way results
cular congestion or luminal occlusion?
in lung hyperinflation (air trapping) and
(Choose one)
increased residual volume, particularly
during acute exacerbations and in se-
vere persistent asthma.

in more severe asthma, reduced ventila-

tion and increased pulmonary blood flow
result in mismatching of ventilation and
perfusion and in bronchial hyperemia

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Direct = histamine and methacholine,

which CONTRACT airway smooth mus-
cle

Differentiate direct from indirect stimuli Indirect = indirect stimuli, which release
causing bronchoconstriction bronchoconstrictors from mast cells or
activate sensory nerves.

So indirect = release
While direct = directly contacts?
Indirectly including allergens, exercise,
Most of the triggers for asthma symp- hyperventilation , irritant dusts and sulfur
toms appear to act directly or indirectly dioxide (via cholinergic reflex), and fog
(via mast cell activation )
1. Wheezing
What are the characteristic symptoms of
2. Dyspnea
asthma
3. Cough
Are symptoms of asthma worse in the
Night
morning or night
Reversibility is demonstrated by a >12%
and 200-mL increase in FEV 1 15 min
after an inhaled short-acting ²2 -agonist
How can you tell if the asthma damage is
(SABA; such as inhaled albuterol 400 ¼ g)
REVERSIBLE
or in some patients by a 2-4 week trial of
oral corticosteroids (OCS) (prednisone
or prednisolone 30-40 mg daily).
Further lung function tests are rarely nec-
essary, but whole body plethysmography
shows increased airway resistance and
may show increased total lung capacity
and residual volume.
Statement
That is because its an obstructive dis-
ease?

Simple spirometry confirms airflow limi-

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tation with a reduced FEV1, FEV1/FVC
ratio, and PEF
measured by methacholine or hista-
How do you test for airway hyperrespon- mine challenge with calculation of the
siveness provocative concentration that reduces
FEV 1by 20% (PC20).
Positive in allergic asthma ( extrinsic)
Are skin prick tests positive in allergic
astham or intrinsic asthma
And negative in intrinsic asthma
1. Bronchodilators = rapid relief of symp-
toms mainly through relaxatio of airway
What are the two main divisions of drugs smooth muscle
for asthma
2. Controllers = inhibit the underlying in-
flammatory process
What are the most effective bronchodila-
B2 agonists
tor
1. B2 adrenergic agonists
What are the three classes of bron-
2. Anti cholinergics
chodilators in current use
3. Theophylline
Are bronchodilators sufficient to control No because it only affords rapid relief but
asthma in patients with persistent symp- has little or no effect on the underlying
toms inflammatory process
²22-Receptors are coupled through a
stimulatory G protein to adenylyl cy-
clase, resulting in INCREASED intracel-
How do B2 agonists cause bronchodila-
lular cyclic adenosine monophosphate
tion
(AMP), which relaxes smooth muscle
cells and inhibits certain inflammatory
cells, particularly mast cells.

The only "no's" are

No emergency visits
And NO limitations on activities including
exercise

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relax a way smooth-muscle cells of all

airways, where they act as functional an-
What is the primary action of B2 agonists tagonists, reversing and preventing con-
traction of airway smooth-muscle cells by
all known bronchoconstrictors
1. Inhibition of mast cell release
What are the non-bronchodilator effects
2. Reduction in plasma exudation
of B2 agonists
3. Inhibition of sensory nerve activation
Inflammatory cells express small num-
bers of ²2 r-eceptors, but these are rapidly
down-regulated with ²2 -agonist activa-
tion so that, in contrast to corticosteroids,
there are no effects on inflammatory cells
What are the effects of B2 agonists on in the airways and there is no reduction
inflammatory cells in AHR.

So basically they only down regulate the

RECEPTORS but do nothing against the
inflammatory cells and they DO NOT re-
duce airway hyperresponsiveness
SABA = salbutamol and terbutaline

Give the examples of SABA , LABA and LABA = Salmeterol and formoterol
the LABA's that can be used once daily
LABA 1x daily = Indacaterol, olodaterol
and vilanterol
How long is the effect duration of SABA 3-6 hours
How long is the effect duration of LABA
12 hours
(not the 1x daily LABA)
No it cannot because they do not control
Can LABA be given alone
the underlying inflammation
ICS because this combination have
proved to be highly effective in the control
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of astham and prevention of exacerba-
What should be given with LABA
tions
Muscle tremor and palpitations

What are the most common side effects There is a small fall in plasma potassium
of B2 agonists due to increased uptake of skeletal mus-
cle cells but this effect does not usually
cause any clinical problems
What is a potential problem with any ag-
Tolerance
onist given chronically
How do you prevent tolerance of B2 ag-
Concomitant administration of ICS
onists
What does increase use of SABA indi-
That the astham is not controlled
cate
Ipratropium bromide

LAMA = (long acting muscarinic antago-

Give an example of anticholinergics
nists) = tiotropium bromide

Basta BROMIDe = anticholinergics

Prevents cholinergic nerve induced
BRONCHOCONSTRICTION and MU-
CUS SECRETION
What does muscarinic receptor antago-
Less effective than B2 agonists as they
nists prevent
inhibit only the cholinergic reflex compo-
nent of bronchoconstriction, whereas ²2
-agonists prevent all bronchoconstrictor
mechanisms

Long-acting muscarinic antagonists

(LAMA), including tiotropium bromide or
glycopyrronium bromide, may be used as
Statement
an additional bronchodilator in patients
with asthma that is not controlled by max-
imal doses of ICS-LABA combinations,

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and improve lung function and further
reduce exacerbations
What is the most common side effect of
anticholinergics or muscarinic receptor Dry mouth
antagonists
It INHIBITS phosphodiesterase in airway
smooth muscle cells, which INCREAS-
ES cyclic AMP

How does theophylline cause bronchodi-

Theophylline activates the key nu-
lation
clear enzyme histone deacetylase-2
(HDAC2), which is a critical mechanism
for switching off activated inflammatory
genes and may therefore reduce corti-
costeroid insensitivity in severe asthma
Orally given as a slow release prepara-
How should you give theophylline
tion once or twice daily
Low doses of 5-10mg/L because doses
Should you give theophylline in high dos-
that are high (10-20mg/L) have a lot of
es or low doses
side effects
Nausea, vomiting and HEADACHES due
to phosphodiesterase inhibition

It is well absorbed and largely inactivated

What are the most common side effects
of theophylline
in the liver.
Theophylline side effects are related to
plasma concentration and are rarely ob-
served at plasma concentrations <10
mg/L.

That's why you give low doses of 5-10

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Inhaled corticosteroids

ICS are the most effective anti-inflam-

matory agents used in asthma therapy,
reducing inflammatory cell numbers and
their activation in the airways. ICS reduce
eosinophils in the airways and sputum,
What are hte most effective CON-
and numbers of activated T lymphocytes
TROLLERS of asthma
and surface mast cells in the airway mu-
cosa. These effects may account for the
reduction in AHR that is seen with chron-
ic ICS therapy.

Remember that ICS = reduce airway hy-

perresponsiveness while B2 agonists do
not
The major effect of corticosteroids is to
switch off the transcription of multiple ac-
tivated genes that encode inflammatory
proteins such as cytokines, chemokines,
adhesion molecules, and inflammatory
enzymes.
Statement
An important mechanism is recruitment
of HDAC2 to the inflammatory gene com-
plex, which reverses the histone acetyla-
tion associated with increased gene tran-
scription.
Twice daily (that's why together with
ICS are usually given how many times a
LABA with duration of action for 12
day
hours?)

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ICS rapidly improve the symptoms of

asthma, and lung function improves over
several days. They are effective in pre-
venting asthma symptoms, such as EIA
and nocturnal exacerbations, but also
prevent severe exacerbations.

ICS reduce AHR, but maximal improve-

ment may take several months of ther-
Statement
apy. Early treatment with ICS appears
to prevent irreversible changes in airway
function that occur with chronic asthma.

Withdrawal of ICS results in slow deteri-

oration of asthma control, indicating that
they suppress inflammation and symp-
toms, but do not cure the underlying con-
dition.
What is the first line for patients with
ICS
persistent asthma
If ICS cannot control the persistent asth-
LABA with ICS
ma what do you add
Hoarseness (dysphona) and oral can-
didiasis

Urine cortisol concentrations decrease.

What are the side effects of ICS
There is no convincing evidence that
long term treatment leads to impaired
growth in children or osteoporosis in
adults
Give oral corticosteroids (prednisone or
predinoslone 30-45mg once daily for
How do you treat acute severe asthma
5-10 days) or IV corticosteroids (hydro-
cortisone or methylpredinosolone)
Bone density

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So that preventive treatment with bis-
If patients require maintenance treat-
phosphonates or estrogen in POST-
ment with OCS it is important to monitor
MENOPAUSAL women may be initiated
what
if bone density is low
Mast cells
What releases cysteinyl leukotrienes
that are potent bronchoconstrictors
Lesser extent eosinophils release them
What drugs are anti leukotrienes Montelukast and zafirlukast
They are less effective than ICS in con-
trolling asthma and have less effect on
airway inflammation,

but are useful as an add-on therapy in

When are anti leukotrienes given some patients not controlled with low
doses of ICS, although less effective
than a LABA

They are given orally once or twice daily

and are well tolerated
Small child eating barbecue and smok-
ing = increased clearance

Omalizumab given subcutaneously

What is an example of an anti IgE
every 2-4 weeks

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For patients with mild, intermittent asth-
ma what is required
When is regular controller therapy re-
quired
What is the treatment of choice for pa-
tients required regular controller therpa- It is usual to start with an intermediate
py , how much to give, and when to step dose (e.g., 200 [¼
down or decrease the dose
What does ABG of a patient in acute
severe asthma show
What oxygen concentration should be
maintained in patients with acute severe
asthma
What is the mainstay of treatment for
acute severe asthma
In severely ill patients with impending
respiraotry failure what may be given
If B2 agonists alone is not satisfactory
what can be given in severe acute asth-
ma
SABA
When use of a reliever medication
MORE THAN TWICE A WEEK
The treatment of choice for all patients is
an ICS given twice daily.
g] bid of [beclometha-
sone dipropionate] BDP) or equivalent
and to decrease the dose if symptoms
are controlled after THREE months.
Arterial blood gases on air show hypox-
emia, and P CO2 is usually low due to
hyperventilation. A normal or rising P CO
2 is an indication of impending respirato-
ry failure and requires immediate moni-
toring and therapy
>90% so not 90 but 91!! But >!!
High doses of SABA given either by neb-
uliser or via a MDI with a spacer
IV B2 agonists
Nebulized anticholinergic
Intubate and institute ventilation

These patients may benefit from general

For patients with respiratory failure what anaesthetic like halothane, if they have
should be done not responded to conventional bron-
chodilators

Maybe since they're already incubated...

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They are NEVER given as they may de-

press ventilation..
Can sedatives be given to these patients
with acute severe asthma
So you can give general anaesthetics but
NOT SEDATIVES
Patients that are refractory to inhaler
technique require maintenance with Oral corticosteroids
what treatment
What is the most common reason for Poor adherence with medication particu-
poor control of asthma larly Inhaled corticosteroids
Unlike monitoring of ICS compliance Suppression of plasma cortisol levels
(which has no useful plasma measure- and the expected concentration of pred-
ment) how can you monitor OCS nisone/ prednisone in the plasma
Drugs such as betaadrenergic block-
What drugs can worsen asthma ers, aspirin, and other cyclooxygenase
(COX) inhibitors may worsen asthma.
Complete resistance to corticosteroids is
extremely uncommon and affects <1 in
1000 patients.
How can you say a patient is resistant to
It is defined by a failure to respond to
corticosteroids treatment for asthma
a high dose of oral prednisone/pred-
nisolone (40 mg once daily over 2
weeks), ideally with a 2-week run-in with
matched placebo.
Some show a persistent pattern of vari-
ability and may require OCS or, at times,
continuous infusion of ²2 a
- gonists (type I
brittle asthma),
What is the difference with type I brittle
asthma and type II brittle asthma whereas others have generally normal
or near-normal lung function but precip-
itous, unpredictable falls in lung function
that may result in death (type 2 brittle
asthma)

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 Harrisons chapter 281 - Asthma
Study online at https://quizlet.com/_7uqv9p
Subcutaneous epinephrine
Type II brittle asthma is difficult to treat
because they do not respond well to cor-
This suggests that the worsening is likely
ticosteroids what are the most effective
to be a localized airway anaphylactic re-
therapy for these patients
action with edema
What % of asthmatics become worse
1-5%
with aspirin and other COX inhibitors
Approximately one-third of asthmatic pa-
tients who are pregnant improve during SABA, ICS and theophylline
the course of a pregnancy, one-third de-
teriorate, and one-third are unchanged. LABA , antileukotrienes and IgE are new-
WHAT DRUGS HAVE BEEN SHOW TO er so less safety information
BE SAFE without teratogenic potential
better to use PREDNISONE rather than
In pregnant patients if OCS is required prednisolone as it cannot be converted to
what should be given predinosone or the active prednisolone by the fetal liver,
prednisone thus protecting the fetus from systemic
effects of the corticosteroid
There is evidence that smoking inter-
feres with the anti-inflammatory actions
What is smoking effect on corticos-
of corticosteroids by reducing HDAC2,
teroids
necessitating higher doses for asthma
control.
If asthma is well controlled, there is no
contraindication to general anesthesia
and intubation.

Patients who are treated with OCS will

have adrenal suppression and should be
treated with an increased dose of OCS
Statement
immediately prior to surgery.

Patients with FEV1 <80% of their normal

levels should also be given a boost of
OCS prior to surgery.

High Maintenance doses of corticos-

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 Harrisons chapter 281 - Asthma
Study online at https://quizlet.com/_7uqv9p
teroids may be a contraindication to
surgery because of increased risks of
infection and delayed wound healing.
Triple therapy
Asthma COPD overlap patients tend to
ICS
have more symptoms and exacerbations
LABA
and may benefit from what therapy
LAMA

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