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Management of asthma and copd
1.
2.
A chronic inflammatory disorder of the
airway
Infiltration of mast cells, eosinophils
and lymphocytes
Airway hyperresponsiveness
Recurrent episodes of wheezing,
coughing and shortness of breath
Widespread, variable and often
reversible airflow limitation
6. 1.
Extrinsic or allergic:
1.
History of `atopy` in childhood
Family history of allergies
Positive skin test
Raised IgE level
Below 30 years of age
Less prone to status asthmaticus
Intrinsic or Idiosyncratic:
No family history of allergy
Negative skin test
No rise in IgE level
Middle age onset
Prone to status asthmaticus
7. CLASSIFY SEVERITY
STEP 4
Severe
Persistent
STEP 3
Moderate
Persistent
STEP 2
Mild
Persistent
STEP 1
Intermittent
Clinical Features Before Treatment
Nighttime
PEF
Symptoms
Symptoms
Continuous
<60% predicted
Limited physical Frequent
Variability >30%
activity
Daily
Use β2-agonist
daily
Attacks affect
activity a week
>1 time
but <1 time a
day
< 1 time a week
Asymptomatic
and normal PEF
between attacks
>1 time week
>2 times a month
<2 times a month
>60%-<80%
predicted
Variability >30%
>80% predicted
Variability 2030%
>80% predicted
Variability <20%
The presence of one of the features of severity is sufficient to place a patient in that
category.
Global Initiative for Asthma (GINA) WHO/NHLBI, 2002
8.
GINA Guideline clearly states that THERE
IS NO CURE FOR ASTHMA, But
appropriate management most often
leading to CONTROL of asthma
16.
Formoterol ( fast relief and sustained
relief ) +
Budesonide ( twice or even once
daily use )
Dose: 1- 4 puffs ( OD/BD )
Another combination
Salmeterol + Fluticasone
20.
Step I: When symptoms are less than once daily occasional inhalation of a short acting Beta-2 agonist –
salbutmol, terbutaline. If used more than once daily –
step II (Mild episodic asthma)
Step II: Regular inhalation of low-dose steroids.
Alternatively, cromoglycates. Beta-2 agonist as and
whenever required (Mild chronic asthma)
Step III: Inhalation of high dose of steroids (800 mcg) +
Beta-2 agonist. Sustained release theophylline may be
added. LT inhibitors may be tried instead of steroids
(Moderate asthma with frequent exacerbations) spacers
Step IV: Higher dose of steroid (800 to 200 mcg) +
regular beta-2 agonist (long acting salmeterol)
Additional treatment with oral drugs – LT antagonist
or SR theophylline or oral beat-2 agonist
23. Birth:TH2
Older siblings:
Many infections
[TH1 stimuli]
Allergen
Exposure
TH1
No allergies
Source: Busse WW, Lemanske RF. N Engl J Med 2001.
Only child:
Few infections
Still TH2
Allergies
24.
Patients diagnosed with
allergic asthma
Patients diagnosed with
allergies such as hay
fever
Patients diagnosed with
sinusitis that predisposes
them to asthma
Patients diagnosed with
insect sting allergy
25.
COPD is characterized by airflow limitation caused by
chronic bronchitis or emphysema often associated with
long term tobacco smoking
This is usually a slowly progressive and largely
irreversible process
Consists of increased resistance to airflow, loss of
elastic recoil, decreased expiratory flow rate, and
overinflation of the lung.
COPD is clinically defined by a low FEV1 value that
fails to respond acutely to bronchodilators, a
characteristic that differentiates it from asthma.
26.
Chronic Bronchitis is characterized by
Chronic inflammation and excess mucus production
Presence of chronic productive cough
Emphysema is characterized by
Damage to the small, sac-like units of the lung that
deliver oxygen into the lung and remove the carbon
dioxide
Chronic cough
*Source: Braman, S. Update on the ATS Guidelines for COPD. Medscape Pulmonary Medicine. 2005;9(1):1.
30.
Night time waking with breathlessness or
wheeze is common in asthma and uncommon in
COPD.
COPD is rare before the age of 35 whilst asthma
is common in under-35.
31. Classification of COPD Severity
by Spirometry
Stage I: Mild
FEV1/FVC < 0.70
FEV1 > 80% predicted
Stage II: Moderate
FEV1/FVC < 0.70
50% < FEV1 < 80% predicted
Stage III: Severe
FEV1/FVC < 0.70
30% < FEV1 < 50% predicted
Stage IV: Very Severe
FEV1/FVC < 0.70
FEV1 < 30% predicted or
FEV1 < 50% predicted plus
32. Physical examination
Signs of heavy smokers
Observe for clubbing
Distended neck vein on expiration
The presence of barrel chest
Observe for abdominal breathing
The use of pursed lips breathing and chest
movement
Auscultate the chest& listen for musical wheezes
characteristics of chronic bronchitis
35.
Give antibiotics to treat infection
Give bronchodilators to relieve bronchospasm, reduce
airway obstruction, mucosal edema and liquefy
secretions.
Chest physiotherapy and postural drainage to improve
pulmonary ventilation.
Proper hydration helps to cough up secretions or
tracheal suctioning when the patient is unable to cough.
Steroid therapy if the patient fails to respond to more
conservative treatment.
36.
Stop smoking
Oxygenation with low concentration during the acute episodes
In asthma adrenaline ( epinephrine) SC if the bronchospasm not
relieved.
Aminophylins IV if the above treatment does not help.
IV corticosteroids for patients with chronic asthma or frequent attack.
Sedative or tranquilizers to calm the patient.
Increase fluids intake to correct loss of diaphoresis and inaccessible
loss of hyperventilation.
Intubations and mechanical ventilation if there is respiratory failure .
37. Oxygen therapy
Used as long-term continuous therapy, during exercise,
or to relieve acute dyspnea
Improves survival in COPD patients with severe
hypoxemia (partial pressure of oxygen [pO2] < 55 mm
Hg or oxygen saturation [sO2] <88%) (Strength of
Recommendation [SOR]: A)
When used for >15 hours daily
Does not improve survival in patients with moderate
Cranston, 2008
hypoxemia or desaturation at night
GOLD, 2009
38.
Annual flu vaccine
Reduces risk of flu and its complications
Pneumonia vaccine
Reduces risk of common cause of pneumonia
39. G lobal Initiative for Chronic
bstructive
O ung
L isease
D
November 19, 2006
World COPD Day, Kyoto Japan
Environmental and genetic factors lead to atopic sensitization, which may be asymptomatic. Together with local tissue factors it can develop to clinical disease. The balance between these factors is responsible for the allergic phenotype
Atopy involves the capacity to produce IgE in response to common environmental proteins such as house dustmite, grass pollen, and food allergens. From the Greek atopos meaning out of place.
A hereditary disorder marked by the tendency to develop immediate allergic reactions to substances such as pollen, food, dander, and insect venoms and manifested by hay fever, asthma, or similar allergic conditions. Also called atopic allergy.
Atopy involves the capacity to produce IgE in response to common environmental proteins such as house dustmite, grass pollen, and food allergens. From the Greek atopos meaning out of place.
This combination is available today in both metered dose and dry powder inhalers (Rotacaps).
It is available in 3 different Rotacap strengths where the dose of formoterol remains constant but the budesonide dose varies according to the need (severity of asthma); i.e. 100, 200 and 400 mcg of budesonide in 3 different Rotacaps.
One theory that might explain why we seem to be more vulnerable than ever to allergic disease is called the hygiene hypothesis. We’re all born with an abundance of TH2 immune cells designed to fight internal parasites. Exposure to infections triggers the development of TH1 immune cells, designed to fight bacteria and viruses, shown here on the left.
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With no exposure to infections, the TH1 immune cells never take over, illustrated by the right arrow. Investigators theorize that with few parasites to conquer in the modernized West, TH2 immune cells might have turned on harmless allergens instead, resulting in more allergic disease. This hypothesis is based on studies showing lower asthma rates for children who live on farms, attend day care centers, have indoor pets or older siblings; all things that expose children to higher levels of bacteria and infection. Children who have delayed development of TH1 cells, possibly because they aren’t exposed to infections through contact with animals, dirt and other children, seem to have more allergies and might be more predisposed to asthma.
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SOURCE: Busse WW, Lemanske RF. Advances in Immunology. NEJM. 2001 Feb; 344(5):350-362.
So who can be helped by this treatment?
Patients diagnosed with allergic asthma.
Patients with allergies such as hay fever.
Patients diagnosed with sinusitis that predisposes them to asthma.
Patients diagnosed with an allergy to insect stings.
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When used for more than 15 hours per day in patients with severe COPD (pO2 < 60 mm Hg), oxygen has been shown to increase survival. It doesn’t improve survival in patients with only moderate COPD or nocturnal desaturation only. Benefits on quality of life are unclear, but oxygen may improve general alertness and psychological state in some patients. Oxygen therapy can be used as long-term with continuous delivery, only during exercise, or to relieve acute dyspnea.
GOLD, 2009; Rabe, 2007; Cranston, 2008