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asthma
By laith albazooni
TSU
• Asthma is a chronic reactive airway disorder
causing episodic airway obstruction that results
from bronchospasms,
• increased mucus secretion, and mucosal edema.
It is a type of chronic obstructive pulmonary
disease (COPD), a
• long-term pulmonary disease characterized by
increased airflow resistance; other types of COPD
include chronic
• bronchitis and emphysema
• Although asthma strikes at any age, about 50% of
patients are younger than age 10; twice as many
boys as girls are
• affected in this age group. One-third of patients
develops asthma between ages 10 and 30, and
the incidence is the
• same in both sexes in this age group. Moreover,
approximately one-third of all patients share the
disease with at least
• one immediate family member
• Asthma may result from sensitivity to extrinsic
or intrinsic allergens. Extrinsic, or atopic,
asthma begins in childhood;
• typically, patients are sensitive to specific
external allergens.
• AGE ALERT Extrinsic asthma is commonly
accompanied by other hereditary allergies,
such as eczema and
• allergic rhinitis, in childhood populations
• Intrinsic, or nonatopic, asthmatics react to
internal, nonallergenic factors; external
substances cannot be implicated in
• patients with intrinsic asthma. Most episodes
occur after a severe respiratory tract infection,
especially in adults.
• However, many asthmatics, especially
children, have both intrinsic and extrinsic
asthma
Causes
• Extrinsic allergens include:
• pollen
• animal dander
• house dust or mold
• kapok or feather pillows
• food additives containing sulfites
• other sensitizing substances.
Intrinsic allergens include
• irritants
• emotional stress
• fatigue
• endocrine changes
• temperature variations
• humidity variations
• exposure to noxious fumes
• anxiety
• coughing or laughing
• genetic factors
Signs and symptoms
 Patients with mild asthma
• wheezing due to edema of the airways
• coughing due to stimulation of the cough reflex to
eliminate the lungs of excess mucus and irritants
• histamine-induced production of thick, clear, or yellow
mucus
• dyspnea on exertion due to narrowing of airways and
inability to take in the increased oxygen that is required
for
• exercise
Patients with moderate asthma
• respiratory distress at rest due to narrowed
airways and decreased oxygenation to the
tissues
• hyperpnea (abnormal increase in the depth
and rate of respiration) due to the body's
attempt to take in more oxygen
• barrel chest due to air trapping and retention
• diminished breath sounds due to air trapping.
Patients with severe asthma
• marked respiratory distress due to failure of
compensatory mechanisms and decreased
oxygenation levels
• marked wheezing due to increased edema and
increased mucus in the lower airways
• absent breath sounds due to severe
bronchoconstriction and edema
• pulsus paradoxus greater than 10 mm Hg
chest wall contractions due to use of accessory
muscles
Diagnosis
• Pulmonary function studies reveal signs of
airway obstructive disease, low-normal or
decreased vital capacity, and
• increased total lung and residual capacities.
Pulmonary function may be normal between
attacks. Pa O2 and PaCO2
• usually are decreased, except in severe
asthma, when PaCO2 may be normal or
increased
• Serum IgE levels may increase from an allergic reaction.
• Sputum analysis may indicate presence of Curschmann's spirals (casts of airways), Charcot-
Leyden crystals, and
• eosinophils.
• Complete blood count with differential reveals increased eosinophil count.
• Chest X-rays can be used to diagnose or monitor the progress of asthma and may show
hyperinflation with areas of
• atelectasis.
• Arterial blood gas analysis detects hypoxemia (decreased Pa O2; decreased, normal, or
increasing PaCO2) and
• guides treatment.
• Skin testing may identify specific allergens; results read in 1 or 2 days detect an early
reaction, and after 4 or 5
• days reveal a late reaction.
• Bronchial challenge testing evaluates the clinical significance of allergens identified by skin
testing.
• Electrocardiography shows sinus tachycardia during an attack; severe attack may show signs
of cor pulmonale
• (right axis deviation, peaked P wave) that resolve after the attack.
Treatment
• prevention, by identifying and avoiding precipitating factors
such as environmental allergens or irritants, which is the best
treatment
• desensitization to specific antigens — helpful if the stimuli
can't be removed entirely — which decreases the
• severity of attacks of asthma with future exposure
• bronchodilators (such as theophylline, aminophylline,
epinephrine, albuterol, metaproterenol, and terbutaline) to
• decrease bronchoconstriction, reduce bronchial airway
edema, and increase pulmonary ventilation
• corticosteroids (such as hydrocortisone and
methylprednisolone) to decrease bronchoconstriction, reduce
bronchial
• mast cell stabilizers (cromolyn sodium and nedocromil
sodium), effective in patients with atopic asthma who have
• seasonal disease. When given prophylactically, they block
the acute obstructive effects of antigen exposure by
• inhibiting the degranulation of mast cells, thereby
preventing the release of chemical mediators responsible
for
• anaphylaxis
• low-flow humidified oxygen, which may be needed to treat
dyspnea, cyanosis, and hypoxemia. However, the
• amount delivered should maintain PaO2 between 65 and
85 mm Hg, as determined by arterial blood gas analysis
• mechanical ventilation — necessary if the
patient doesn't respond to initial ventilatory
support and drugs, or
• develops respiratory failure
• relaxation exercises such as yoga to help
increase circulation and to help a patient
recover from an asthma attack
Complications
•status asthmaticus
•respiratory failure
Thank you

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Asthma

  • 2. • Asthma is a chronic reactive airway disorder causing episodic airway obstruction that results from bronchospasms, • increased mucus secretion, and mucosal edema. It is a type of chronic obstructive pulmonary disease (COPD), a • long-term pulmonary disease characterized by increased airflow resistance; other types of COPD include chronic • bronchitis and emphysema
  • 3. • Although asthma strikes at any age, about 50% of patients are younger than age 10; twice as many boys as girls are • affected in this age group. One-third of patients develops asthma between ages 10 and 30, and the incidence is the • same in both sexes in this age group. Moreover, approximately one-third of all patients share the disease with at least • one immediate family member
  • 4. • Asthma may result from sensitivity to extrinsic or intrinsic allergens. Extrinsic, or atopic, asthma begins in childhood; • typically, patients are sensitive to specific external allergens.
  • 5. • AGE ALERT Extrinsic asthma is commonly accompanied by other hereditary allergies, such as eczema and • allergic rhinitis, in childhood populations
  • 6. • Intrinsic, or nonatopic, asthmatics react to internal, nonallergenic factors; external substances cannot be implicated in • patients with intrinsic asthma. Most episodes occur after a severe respiratory tract infection, especially in adults. • However, many asthmatics, especially children, have both intrinsic and extrinsic asthma
  • 7. Causes • Extrinsic allergens include: • pollen • animal dander • house dust or mold • kapok or feather pillows • food additives containing sulfites • other sensitizing substances.
  • 8. Intrinsic allergens include • irritants • emotional stress • fatigue • endocrine changes • temperature variations • humidity variations • exposure to noxious fumes • anxiety • coughing or laughing • genetic factors
  • 9. Signs and symptoms  Patients with mild asthma • wheezing due to edema of the airways • coughing due to stimulation of the cough reflex to eliminate the lungs of excess mucus and irritants • histamine-induced production of thick, clear, or yellow mucus • dyspnea on exertion due to narrowing of airways and inability to take in the increased oxygen that is required for • exercise
  • 10. Patients with moderate asthma • respiratory distress at rest due to narrowed airways and decreased oxygenation to the tissues • hyperpnea (abnormal increase in the depth and rate of respiration) due to the body's attempt to take in more oxygen • barrel chest due to air trapping and retention • diminished breath sounds due to air trapping.
  • 11. Patients with severe asthma • marked respiratory distress due to failure of compensatory mechanisms and decreased oxygenation levels • marked wheezing due to increased edema and increased mucus in the lower airways • absent breath sounds due to severe bronchoconstriction and edema • pulsus paradoxus greater than 10 mm Hg chest wall contractions due to use of accessory muscles
  • 12. Diagnosis • Pulmonary function studies reveal signs of airway obstructive disease, low-normal or decreased vital capacity, and • increased total lung and residual capacities. Pulmonary function may be normal between attacks. Pa O2 and PaCO2 • usually are decreased, except in severe asthma, when PaCO2 may be normal or increased
  • 13. • Serum IgE levels may increase from an allergic reaction. • Sputum analysis may indicate presence of Curschmann's spirals (casts of airways), Charcot- Leyden crystals, and • eosinophils. • Complete blood count with differential reveals increased eosinophil count. • Chest X-rays can be used to diagnose or monitor the progress of asthma and may show hyperinflation with areas of • atelectasis. • Arterial blood gas analysis detects hypoxemia (decreased Pa O2; decreased, normal, or increasing PaCO2) and • guides treatment. • Skin testing may identify specific allergens; results read in 1 or 2 days detect an early reaction, and after 4 or 5 • days reveal a late reaction. • Bronchial challenge testing evaluates the clinical significance of allergens identified by skin testing. • Electrocardiography shows sinus tachycardia during an attack; severe attack may show signs of cor pulmonale • (right axis deviation, peaked P wave) that resolve after the attack.
  • 14. Treatment • prevention, by identifying and avoiding precipitating factors such as environmental allergens or irritants, which is the best treatment • desensitization to specific antigens — helpful if the stimuli can't be removed entirely — which decreases the • severity of attacks of asthma with future exposure • bronchodilators (such as theophylline, aminophylline, epinephrine, albuterol, metaproterenol, and terbutaline) to • decrease bronchoconstriction, reduce bronchial airway edema, and increase pulmonary ventilation • corticosteroids (such as hydrocortisone and methylprednisolone) to decrease bronchoconstriction, reduce bronchial
  • 15. • mast cell stabilizers (cromolyn sodium and nedocromil sodium), effective in patients with atopic asthma who have • seasonal disease. When given prophylactically, they block the acute obstructive effects of antigen exposure by • inhibiting the degranulation of mast cells, thereby preventing the release of chemical mediators responsible for • anaphylaxis • low-flow humidified oxygen, which may be needed to treat dyspnea, cyanosis, and hypoxemia. However, the • amount delivered should maintain PaO2 between 65 and 85 mm Hg, as determined by arterial blood gas analysis
  • 16. • mechanical ventilation — necessary if the patient doesn't respond to initial ventilatory support and drugs, or • develops respiratory failure • relaxation exercises such as yoga to help increase circulation and to help a patient recover from an asthma attack