3. Asthma is a chronic inflammatory disorder of the air way
characterized by inflammatory hyperreactivity of the
respiratory tree to various stimuli, resulting in reversible
airway obstruction
Clinically : by recurrent episodes of wheezing, breathlessness, chest
tightness, and cough, particularly at night/early morning.
Physiologically: A combination of mucosal inflammation, bronchial
musculature constriction, and excessive secretion of viscous mucus-causing mucous
plugs will produce bronchial obstruction. The bronchial hyperreactivity occurs in an
episodic pattern with interspersed normal airway tone.
4. Asthma can occur at any age but is usually seen in young
persons, 50% of whom “outgrow” their asthma by adulthood.
5. Classifications
Non-atopic/ intrinsic /non-allergic (%50) : A bronchial
reaction occurs secondary to nonimmunologic stimuli,
ETIOLOGY : infection, irritating inhalant, cold air, exercise, and emotional
upset. The asthma attacks are severe, and prognosis is less favorable.
Extrinsic (allergic, atopic) asthma (%20) :
ETIOLOGY : results from1- sensitization lead to elevate Specific immunoglobulins
(IgE ) 2- Allergens
6. Other symptoms include allergic rhinitis, urticaria, and eczema. Prognosis
is good and
RESPIRATORY INFECTION : (RSV -respiratory syncytial virus in young
children, rhinoviruses indults) are the major causes.
Pharmacological : coloring agents such as TARTRAZINE , and also B-
ADRENERGIC ANTAAGONIST , AND ASPRIN but why Asprin ??????
7. The mechanism by which aspirin and similar drugs
cause asthma appears to be chronic over-excretion of
leukotrienes, which activate the mast cells. This is the
reason why leukotriene inhibitors are considered to
be so effective.
8. Signs and Symptoms :
whizzing ,Dyspnea ,cough
During Mild attack : diffuse whizzing , tachypnea , tachycardia(increase Respiratory Rate )
,prolong expirations
During sever attack : use of accessory muscles of respiration, diminished breath sounds, loud
wheezing, hyper-resonance (increased vocal fremitus), and intercostal retraction are noted.
# ABG (Arteal blood gases)
in Acute phase : decrese PCO2, increase PH
In Sever phase : decrease PCO2 , increase PACO2 ,decrease PH
Note : Poor prognostic factors include fatigue, diaphoresis, pulsus paradoxus (>20 mm Hg),
inaudible breath sounds, decreased wheezing, cyanosis, and bradycardia.
11. Pathophysiology:
There is a narrowing of large and small airways caused by hypertrophy and
spasm of bronchial smooth muscle, edema and inflammation of the
bronchial mucosa, and production of viscous mucus and
The mediators released by the lung during an acute asthmatic attack are
histamine, bradykinin, leukotrienes (LTs) C, D, and E, and prostaglandins (PGs)
E2, F2α, and D2, which cause an intense inflammatory process leading to
bronchoconstriction and vascular congestion.
(The cells thought to play an important role in the inflammatory response
are the mast cells, lymphocytes, and eosinophils.)
12.
13.
14. Diagnosis:
Pulmonary function tests Spirometry+spiutom ex to slect AB
– estimate degree of obstruction , vital ex, blood ,skin , blood gases , physical ex , if you
don’t know history urin test cbc blood biochemistry(imuuno globulin) wbc rbc platlet
,glucose in urin for blood d-dimer important
– ↓FEV1, ↓FEV1/FVC, ↓PEF.
– >12% increase in FEV1, 15 minutes after β2 agonist inhalation.
– Morning dipping in PEF(chronic bronchitis)
AHR – histamine / methacholine provocation test > 20% fall in
FEV1
CXR+U/S – hyperinflation, pneumothorax, emphysema
Arterial blood-gas analysis +bronchioscopy hypoxia & hypocarbia(severe acute Asthma
hypercarbia)
Skin hypersensitivity test
Sputum & blood eosinophilia
Elevated serum IgE levels
15. TREATMENT
Clinical guidelines have classified asthma in 4 categories, based on frequency, severity of
symptoms, and requirements for medication. This classification provides general guidelines
for therapy.
• Mild intermittent
• Mild persistent
• Moderate
• Severe
Treatment of asthma : The treatment of choice is bronchodilator (albuterol); systemic
corticosteroids (usually start IV), and oxygen. (Long-acting bronchodilators are
contraindicated in the acute setting.) SO ( salbutamol +systemic GC iv +O2 )
Note : For an acute exacerbation of asthma, a long-acting beta agonist plus inhaled
corticosteroids is more effective.
-If, 3 days after hospitalization the patient is improving and you decide to send her home, her
drug regimen would likely be oral prednisone taper, albuterol inhaler, steroid inhaler.
16. • Mild Intermittent Asthma (SABA) albuterol
–– Symptoms of cough, wheeze, chest tightness, or difficulty breathing <2x/week
–– Flare-ups-brief, but intensity may vary
–– Nighttime symptoms <2x/month
–– No symptoms between flare-ups
–– Lung function test FEV1 that is ≥80 percent of normal values
–– Treatment: inhaled short-acting bronchodilators as needed
• Mild Persistent Asthma (SABA +ICS low dose ( albuterol +ICS low dose )
–– Symptoms of cough, wheeze, chest tightness or difficulty breathing 3−6x/week
–– Flare-ups-may affect activity level
–– Nighttime symptoms 3−4x/month
–– Lung function test FEV1 that is ≥80 percent of normal values
–– Treatment: start with inhaled corticosteroid and SABA; if not enough improvement,
add leukotriene inhibitor and possible LABA
17. • Moderate Persistent Asthma(SABA+LABA+ICS low dose )
–– Symptoms of cough, wheeze, chest tightness, or difficulty breathing daily
–– Flare-ups-may affect activity level
–– Nighttime symptoms ≥5x/month
–– Lung function test FEV1 that is >60 percent but <80 percent of normal values
–– Treatment: start with inhaled corticosteroid and SABA; leukotriene inhibitor and
LABA will likely be needed to improve nighttime symptoms
• Severe Persistent Asthma(SABA+LABA+ICS high dose )
–– Symptoms of cough, wheeze, chest tightness or difficulty breathing continually
–– Nighttime symptoms frequently
–– Lung function test FEV1 that is ≤60 percent of normal values
–– Treatment: inhaled corticosteroid, SABA (as needed), leukotriene inhibitor, and LABA
will likely be needed, as well as oral steroids (prednisone) at lowest possible dose
–– Do not stop leukotriene inhibitors and LABA once oral corticosteroids have been startedNRespiratory
acidosis or ’normalization’ of pH in patients with acute asthma exacerbation may be an indication for
intubation.
18.
19. References:
USMEL STEP 2 CK
Davidson's Principles & Practice of Medicine
23 Edition
harrison's principles of internal medicine