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ASTHMA
Presented by
IMRAN ALI
M.PHILL(Pharmacy Practice)
Department of Pharmacy
Quaid i Azam University
Islamabad
Table of content
 INTRODUCTION
History
Brief discussion
 SYMPTOMS
 HISTOPATHOLOGY
 TESTS
 TREATMENT
Asthma
2
History
• Asthma : derived from the Greek aazein, meaning "sharp breath."
The word first appears in Homer's Iliad.
• In 450 BC. Hippocrates: more likely to occur in tailors, anglers, and
metalworkers.
• Six centuries later, Galen: caused by partial or complete bronchial
obstruction.
• 1190 AD, Moses Maimonides: wrote a treatise on asthma, describing
its prevention, diagnosis, and treatment
• 17th century, Bernardino Ramazzini: connection between asthma and
organic dust.
• 1901: The use of bronchodilators started.
• 1960s: inflammatory component of asthma was recognized and anti-
inflammatory medications were added to the regimens.
Asthma 3
SIMPLE DEFINITION
A reversible chronic inflammatory airway disease which is
characterized by bronchial hyper-responsiveness of the airways to
various stimuli, leading to widespread bronchoconstriction, airflow
limitation and inflammation of the bronchi causing symptoms of
cough, wheeze, chest tightness and dyspnoea.
ASTHMA 4
CLASSIFICATION
Extrinsic – implying a definite external cause
 more frequently in atopic inviduals
 (atopic – individual which tends to develop hypersensitivity by
contact with allergens)
 often starts in childhood - accompanied by eczema
Intrinsic/cryptogenic – no causative agent can be
identified
 starts in middle age
ASTHMA 5
TYPES OF ASTHMA
According to the severity:
helpful for treatment and
management.
Very mild
Mild
Moderate
Moderately
Severe
Severe
ASTHMA 6
TYPES OF ASTHMA
According to pathophysiology
Allergic asthma
Intrinsic (Non-Allergic)
Exercise-induced
Occupational (allergic)
Steroid-resistant
ABPA (allergic)
ASTHMA 7
BRONCHIAL ASTHMA
ETIOLOGY
ASTHMA 8
 SYMPTOMS
5 most common symptoms of asthma
Asthma 9
COUGHING
 A cough, especially when
it occurs at night, is a sign
that you may be suffering
from asthma. The cough
may or may not be
accompanied by phlegm.
 Often, the coughing
becomes worse when you
have any type of
respiratory virus. This
includes the cold and flu
among others.
ASTHMA 10
SHORTNESS OF BREATH
 Many who suffer from
asthma report that they
feel short of breath and
that they cannot get
enough air into their
lungs.
 In many cases, activity or
exercise can make this
asthma symptom more
noticeable.
ASTHMA 11
WHEEZING
 This symptom often comes and
goes and may be worse first thing
in the morning or at night. The
wheezing may go away on its own
or you may need to use a
bronchodilator or inhaler to open
the airways.
 The wheezing may get severe due
to breathing in cold air, heartburn
or even with exercise and the
symptoms may arise without any
warning. This symptom is
frequently seen in children.
ASTHMA 12
CHEST PAIN OR TIGHTNESS
 This symptom may also
appear as pressure in the
chest. Some notice that
when they are breathing,
the skin between the ribs
pulls in.
 Doctors refer to this as
intercostal retractions.
ASTHMA 13
INABILITY TO TAKE IN ENOUGH AIR
This is most commonly seen
with the other symptoms as
the airway become inflamed,
tighten or become mucus
filled.
If this asthma symptom is seen
without others, it may be a
sign of another condition such
as panic disorder.
ASTHMA 14
HISTOPATHOLOGY
Asthma 15
PATHOLOGIC FEATURES
OF ASTHMAi. Inflammatory cell infiltration of the airways
ii. Increased thickness of the bronchial smooth muscle
iii. Partial or full loss of the respiratory epithelium
iv. Subepithelial fibrosis
v. Hypertrophy and hyperplasia of the submucosal glands
and goblet cells
vi. Partial or full occlusion of the airway lumen by mucous
plugs
vii. Enlarged mucous glands and blood vessels
ASTHMA 16
PATHOPHYSIOLOGY
Smooth muscle contraction
Thickening of airway –cellular infiltration and
inflammation
Excessive secrection of mucus
Genetic factor
Cytokine gene complex (chromosome 5)-IL-4 gene
cluster control IL-3, IL-4 , IL-5 and IL-13
Environment factor
Childhood expose irritants or childhood infection
ASTHMA 17
PATHOPHYSIOLOGY
Extrinsic asthma: Atopic/allergic,
occupational, allergic bronchopulmoary
aspergillosis.
Atopic or allergic
Dust, pollens, animal dander, food etc.
Family history of atopy.
↑ serum IgE.
Skin test with Ag  wheal, flare ( Classical
IgE mediated response)
Exposure of pre-sensitised mast cells to
the Ag stimulates chemical mediators from
these cells. Type 1 hypersensitivity.
ASTHMA 18
ASTHMA - HISTOPATHOLOGY
Patchy necrosis of epithelium
Sub-mucosal glandular hyperplasia
Hypertrophy of bronchial smooth muscle
Eosinophils, mast cells; lympho (TH2, CD4)
Mucous plugs, Curschmann spirals,
Charcot Layden crystals.
ASTHMA 19
ASTHMA HISTOPATHOLOGY
Obstructed
Inflamed
Bronchi
ASTHMA 20
HISTOPATHOLOGY OF A SMALL
AIRWAY IN FATAL ASTHMA.
ASTHMA 21
ASTHMA - BRONCHIAL MORPHOLOGY
inflammation
Eosinophil's
Gland hyperplasia
Mucous plug in
lumen
Hypertrophy of
muscle layer
ASTHMA
TESTS AND DIAGNOSIS
Asthma 23
DIAGNOSIS & TESTS
Initial exam (conducted by doctor):
Medical history
Asthma symptoms, how you feel, known asthma and allergy triggers,
your activity level and diet, your home and work environment, and
family history.
Then, some tests will be conducted to diagnose asthma
ASTHMA 24
PEAK FLOW TESTING
Peak Flow Meter
PEFR is used to assess the severity of wheezing in
those who have asthma. PEFR measures how quickly
a person can exhale air from the lungs
Peak expiratory flow rate (PEFR)
ASTHMA 25
SPIROMETERY (LUNG FUNCTION
TEST)
It measures how much air you can exhale.
FEV1(force expiratory volume) > 80% = normal
Confirms the presence of airway obstruction and measure the
degree of lung function impairment.
Monitor your response to asthma medications
ASTHMA 26
ALLERGY-SKIN TEST
A drop of liquid containing the allergen in placed on your skin
(generally forearms is used).
A small lance with a pinpoint is poked through the liquid into the
top layer of skin (prick test).
If you are allergic to the allergen, after about 2 minutes the skin
begins to form a reaction (red, slightly swollen, and itchy: it makes a
hive).
The size of the hive is measured and recorded.
The larger the hive, the more likely it is that you are allergic to the
allergen tested.
ASTHMA 27
Allergy-skin test
ASTHMA 28
CHEST X-RAY
If there are symptoms that may be caused by another condition such
as pneumonia, your doctor may want to do a chest X-ray.
It also may help to clarify the problem if there is problem with
asthma treatment.
ASTHMA 29
TREAMENT AND MANAGEMENT
Asthma 30
APPROACH OF CHRONIC ASTHMA
Education of patient and family
Avoidance of precipitating factors
Use of the lowest effective dose of convenient medications
minimizing short and long term side effects.
Assessment of severity and response to treatment.
ASTHMA 31
1) EDUCATION OF PATIENT
AND FAMILY
i. Nature of asthma
ii. Preventive
measures/avoidance of
triggers
iii. Drugs used and their side-
effects
iv. Proper use of inhaled
drugs
v. Proper use of peak flow
meter
vii. Knowledge of the difference
between relieving and
preventive medications
vii. Recognition of
features of worsening
asthma
 increase in
bronchodilator
requirement
 development of
nocturnal symptoms
 reducing peak flow
rates).
viii. Self management plan
for selected,
motivated patients or
parents.
ix. The danger of non
prescribed self
medication including ASTHMA 32
2) AVOIDANCE OF PRECIPITATING FACTORS
The following factors may precipitate
asthmatic attacks:
•Beta blockers  contraindicated in all
asthmatics
•Aspirin and nonsteroidal anti-inflammatory
drugs  if known to precipitate asthma,
these drugs should be avoided.
•Allergens  e.g. house dust mites,
domestic pets, pollen should be avoided
whenever possible.
•Occupation  should be considered as a
possible precipitating factor.
• Smoking  active or passive.
• Day to day triggers  such as exercise
and cold air. It is preferable to adjust
treatment if avoidance imposes
inappropriate restrictions on lifestyle.
• Atmospheric pollution.
• Food  if known to trigger asthma,
should be avoided.
ASTHMA 33
CLASSIFICATION OF DRUGS FOR
ASTHMABRONCHODILATORS:
1. β-Sympathomimetic: Salbutamol, Terbutaline, Bambuterol, Salmeterol,
Formoterol, Ephedrine
2. Methyl Xanthines: Theophylline, Aminophylline, Choline theophyllinate,
Hydroxyethyl theophylline, Doxophylline.
3. Anticholinergics: Ipratropium bromide, Tiotropium bromide
LEUKOTRIENE ANTAGONISTS: Montelukast, Zafirlukast
MAST CELL STABILIZERS: Sodium chromoglycate, Ketotifen
CORTICOSTEROIDS
1. Systemic: Hydrocortisone, Prednisolone
2. Inhalational: Beclomethasone, Budesonide, Fluticasone, Flunisolide
ANTI Ig-E ANTIBODY: Omalizumab
ASTHMA 34
SYMPATHOMIMETICS
Mechanism of action:
 β2 stimulation increased cAMP formation in bronchial muscle
cellrelaxation
 Also decreases mediator release
E.g. Salbutamol, Terbutaline, Bambuterol, Salmeterol,
Formoterol, Ephedrine
ASTHMA 35
SYMPATHOMIMETICS
Salbutamol
 Highly selective β2 agonist
 Inhaled Salbutamol produces bronchodilatation in 5 min and action lasts for 2-4 hrs
 Side effects: Palpitations, restlessness, nervousness, throat irritation, ankle edema
 Uses: Reserved for patients who cannot correctly use inhalers, Used as an adjuvant in
severe asthma
 Not suitable for round the clock prophylaxis
Terbutaline:
 Similar to Salbutamol
 Inhaled Salbutamol and Terbutaline are currently the most popular drugs for quick reversal
of bronchospasm
ASTHMA 36
SYMPATHOMIMETICS
Salmeterol:
It is the first long acting selective β2 agonist (LABA) with slow onset of
action
Used by inhalation on a twice daily schedule
Used for maintenance therapy and nocturnal asthma
Formeterol:
Another LABA
Acts for 12 hrs
Compared to Salmeterol it has faster onset of action
ASTHMA 37
METHYL XANTHINES
Naturally occuring Methyl Xanthine alkaloids are Caffein, Theophylline
and Theobromine
Mechanism of action:
 Inhibition of phosphodiesterase (PDE)  increased cAMP Bronchodilatation, cardiac
stimulation, vasodilation
 Blockade of adenosine receptorsrelaxes smooth muscles
 Release of Ca2+ from sarcoplasmic reticulum, especially in skeletal and cardiac
muscle (only at higher concentrations)
E.g: Theophylline, Aminophylline, Choline theophyllinate, Hydroxyethyl
theophylline, Doxophylline
ASTHMA 38
METHYL XANTHINES
Theophylline:
 Well absorbed orally
 T1/2 is 7-12 hrs
 Side effects: gastric pain (with oral), rectal inflammation (with
rectal suppositories), pain at site of injection (i.m), Rapid IV can
cause precordial pain, syncope and sudden death.
 Interactions:
 metabolism is induced by smoking, phenytoin, rifampicin,
phenobarbitone
 Metabolism is inhibited by erythromycin, ciprofloxacin,
cimetedine, OCPs, allopurinol
 Uses: Bronchial asthma and COPD, Apnoea in premature infant,
ASTHMA 39
ANTICHOLINERGICS
• Atropinic drugs cause bronchodilatation by blocking cholinergic
constrictor tone
• Act primarily in larger airways
• Produce slower response than inhaled sympathomimetics
• Better suited for regular prophylactic use
• Combination of inhaled Ipratropium with β2 agonists produce more
marked and longer lasting bronchodilatation.
• E.g: Ipratropium bromide, Tiotropium bromide
ASTHMA 40
LEUKOTRIENE ANTAGONISTS
Competitively antagonize cysLT1 receptor mediated
bronchoconstriction, increased vasodilatation and
recruitment of eisonophils
Indicated for prophylactic therapy of mild to moderate
asthma as alternative to inhaled glucocorticoids
May obviate need for inhaled glucocorticoids
Safe drugs
Side effetcs: headache, rashes
E.g: Montelukast, Zafirlukast
ASTHMA 41
MAST CELL STABILIZERS
Inhibits degranulation of mast cells
Release of mediators like Histamine, LTs, PAF, ILs, etc is
restricted
Not absorbed orally, administered as an aerosol through
metered dose inhaler (MDI)
Uses: Long term prophylaxis in mild to moderate Bronchial
asthma, Allergic rhinitis, Allergic conjunctivitis
Side effetcs: Bronchospasm, throat irritation, cough
E.g: Sodium chromoglycate, Ketotifen
ASTHMA 42
CORTICOSTEROIDS
These do not cause bronchodilatation,
Reduce bronchial hyper-reactivity, mucosal edema, by
supressing inflammatory response to AG:AB reaction
Two forms are used Systemic and Inhalational
1. Systemic/Oral Cortico Steroid (OCS)
 Used in severe chronic asthma and Status asthmaticus
 E.g: Hydrocortisone, Prednisolone
2. Inhalational Cortico Steroid (ICS)
 Step one for all asthma patients
 Safe during regnancy
 Side effetcs: mood changes, osteoporosis, bruising,
petechiae, hyperglycemia
 E.g: Beclomethasone, Budesonide, Fluticasone, Flunisolide
ASTHMA 43
GUIDELINES FOR THE TREATMENT OF
ASTHMA
ASTHMA 44
MANAGEMENT OF ACUTE SEVERE ASTHMA
•RR >50/min
•PEFR <50%
•Pulse >140 beats/min
•breathlessness
•10 puffs Bronchodilator
and Metered Dose Inhaler
•High flow 02, bronchoD
•MDI, nebulizer(1-2h)
•Oral prednisolone (3-5d)
•Monitore PEFR/O2
•B2 agonist / 02 if
required
•PEFR <33%
•Tiredness
•Cyanosis
•Decrease respiratory
effort
•Silent chest
•iv aminophylline
•Iv hydrocortisone
•Salbutamol
•Ipratropium bromide
•Adequate hydration
•antibiotic
•ICU
•Artificial ventilation•Wean iv
•Β2 Agonist
•Oxygen if required
•Oral prednisolone
•Monitor PEFR
•Patient’s education
•Review maintenance
medication
•Review inhaler
technique
•Follow up
•PEFR monitor
DISCHARGE PLAN
response
Give
treatment
improve
ASTHMA 45
MANAGEMENT OF ACUTE ASTHMA
Aims Of Management
i. To prevent death
ii. To relieve respiratory distress
iii. To restore the patient’s lung function to the best possible level
as soon as possible.
iv. To prevent early relapse
ASTHMA 46
MANAGEMENT: PREGNANCY IN ASTHMATICS
Treatment should be aggressive, with the aim of
eliminating symptoms and restoring and maintaining
normal lung function
Beta2 agonists: No evidence of a teratogenic risk with
the commonly used inhaled beta2 agonists
Ipratropium bromide: appears to be safe for use
during pregnancy
Salmeterol/formoterol: not been tested extensively in
pregnant women
ASTHMA 47
ACUTE SEVERE ASTHMA
Immediate Rx: O2 40-60% via mask or cannula + β2 agonist (salbutamol 5mg) via
nebulizer + Prednisone tab 30-60mg and/or hydrocortisone 200mg IV. With
lifethreatening features add 0.5mg ipratropium to nebulized β2 agonist + Aminophyllin
250mg IV over 20 min or salbutamol 250ug over 10 min.
Subsequent Rx: Nebulized β2 agonist 6 hourly + Prednisone 30-60mg daily or
hydrocortisone 200mg 6 hourly IV + 40-60% O2.
No improvement after 15-30 min: Nebulized β2 agonist every 15-30 min +
Ipratropium.
Still no improvement: Aminophyllin infusion 750mg/24H (small pt), 1 500mg/24H
(large pt), or alternatively salbutamol infusion.
Monitor Rx: Aminophyllin blood levels + PEF after 15-30 min + oxymetry (maintain
SaO2 > 90) + repeat blood gases after 2 hrs if initial PaO2 < 60, PaCO2 normal or
raised and patient deteriorates.
Deterioration: ICU, intubate, ventilate + muscle relaxant.
ASTHMA 48
MANAGEMENT: PREGNANCY IN
ASTHMATICS
Theophyllines: may aggravate the nausea and GERD and can
caause transient neonatal tachycardia and irritabilityTeratogenicity
has been shown in animals.
Sodium cromoglycate: no adverse foetal effects
Inhaled corticosteroids: mainstay of tx in persistent asthma,good
safety profile in pregnancy
Oral corticosteroids: necessary for severe asthma in pregnancy
but usually only for short periods.Increased risk of cleft palate in
animals given huge doses of oral steroids
Anti-leukotrienes: no data available
ASTHMA 49
REFRENCES
 Davidson’s Principle and Practice of Medicine (20th Ed)
 kumar & Clark’s., Clinical Medicine(7th Ed)
 Harison’s .,Principles of Internal medicine(17th )
 http://emedicine.medscape.com/
Asthma
50
THANK YOU
Asthma

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ASTHMA SYMPTOMS AND TREATMENT

  • 1. ASTHMA Presented by IMRAN ALI M.PHILL(Pharmacy Practice) Department of Pharmacy Quaid i Azam University Islamabad
  • 2. Table of content  INTRODUCTION History Brief discussion  SYMPTOMS  HISTOPATHOLOGY  TESTS  TREATMENT Asthma 2
  • 3. History • Asthma : derived from the Greek aazein, meaning "sharp breath." The word first appears in Homer's Iliad. • In 450 BC. Hippocrates: more likely to occur in tailors, anglers, and metalworkers. • Six centuries later, Galen: caused by partial or complete bronchial obstruction. • 1190 AD, Moses Maimonides: wrote a treatise on asthma, describing its prevention, diagnosis, and treatment • 17th century, Bernardino Ramazzini: connection between asthma and organic dust. • 1901: The use of bronchodilators started. • 1960s: inflammatory component of asthma was recognized and anti- inflammatory medications were added to the regimens. Asthma 3
  • 4. SIMPLE DEFINITION A reversible chronic inflammatory airway disease which is characterized by bronchial hyper-responsiveness of the airways to various stimuli, leading to widespread bronchoconstriction, airflow limitation and inflammation of the bronchi causing symptoms of cough, wheeze, chest tightness and dyspnoea. ASTHMA 4
  • 5. CLASSIFICATION Extrinsic – implying a definite external cause  more frequently in atopic inviduals  (atopic – individual which tends to develop hypersensitivity by contact with allergens)  often starts in childhood - accompanied by eczema Intrinsic/cryptogenic – no causative agent can be identified  starts in middle age ASTHMA 5
  • 6. TYPES OF ASTHMA According to the severity: helpful for treatment and management. Very mild Mild Moderate Moderately Severe Severe ASTHMA 6
  • 7. TYPES OF ASTHMA According to pathophysiology Allergic asthma Intrinsic (Non-Allergic) Exercise-induced Occupational (allergic) Steroid-resistant ABPA (allergic) ASTHMA 7
  • 9.  SYMPTOMS 5 most common symptoms of asthma Asthma 9
  • 10. COUGHING  A cough, especially when it occurs at night, is a sign that you may be suffering from asthma. The cough may or may not be accompanied by phlegm.  Often, the coughing becomes worse when you have any type of respiratory virus. This includes the cold and flu among others. ASTHMA 10
  • 11. SHORTNESS OF BREATH  Many who suffer from asthma report that they feel short of breath and that they cannot get enough air into their lungs.  In many cases, activity or exercise can make this asthma symptom more noticeable. ASTHMA 11
  • 12. WHEEZING  This symptom often comes and goes and may be worse first thing in the morning or at night. The wheezing may go away on its own or you may need to use a bronchodilator or inhaler to open the airways.  The wheezing may get severe due to breathing in cold air, heartburn or even with exercise and the symptoms may arise without any warning. This symptom is frequently seen in children. ASTHMA 12
  • 13. CHEST PAIN OR TIGHTNESS  This symptom may also appear as pressure in the chest. Some notice that when they are breathing, the skin between the ribs pulls in.  Doctors refer to this as intercostal retractions. ASTHMA 13
  • 14. INABILITY TO TAKE IN ENOUGH AIR This is most commonly seen with the other symptoms as the airway become inflamed, tighten or become mucus filled. If this asthma symptom is seen without others, it may be a sign of another condition such as panic disorder. ASTHMA 14
  • 16. PATHOLOGIC FEATURES OF ASTHMAi. Inflammatory cell infiltration of the airways ii. Increased thickness of the bronchial smooth muscle iii. Partial or full loss of the respiratory epithelium iv. Subepithelial fibrosis v. Hypertrophy and hyperplasia of the submucosal glands and goblet cells vi. Partial or full occlusion of the airway lumen by mucous plugs vii. Enlarged mucous glands and blood vessels ASTHMA 16
  • 17. PATHOPHYSIOLOGY Smooth muscle contraction Thickening of airway –cellular infiltration and inflammation Excessive secrection of mucus Genetic factor Cytokine gene complex (chromosome 5)-IL-4 gene cluster control IL-3, IL-4 , IL-5 and IL-13 Environment factor Childhood expose irritants or childhood infection ASTHMA 17
  • 18. PATHOPHYSIOLOGY Extrinsic asthma: Atopic/allergic, occupational, allergic bronchopulmoary aspergillosis. Atopic or allergic Dust, pollens, animal dander, food etc. Family history of atopy. ↑ serum IgE. Skin test with Ag  wheal, flare ( Classical IgE mediated response) Exposure of pre-sensitised mast cells to the Ag stimulates chemical mediators from these cells. Type 1 hypersensitivity. ASTHMA 18
  • 19. ASTHMA - HISTOPATHOLOGY Patchy necrosis of epithelium Sub-mucosal glandular hyperplasia Hypertrophy of bronchial smooth muscle Eosinophils, mast cells; lympho (TH2, CD4) Mucous plugs, Curschmann spirals, Charcot Layden crystals. ASTHMA 19
  • 21. HISTOPATHOLOGY OF A SMALL AIRWAY IN FATAL ASTHMA. ASTHMA 21
  • 22. ASTHMA - BRONCHIAL MORPHOLOGY inflammation Eosinophil's Gland hyperplasia Mucous plug in lumen Hypertrophy of muscle layer ASTHMA
  • 24. DIAGNOSIS & TESTS Initial exam (conducted by doctor): Medical history Asthma symptoms, how you feel, known asthma and allergy triggers, your activity level and diet, your home and work environment, and family history. Then, some tests will be conducted to diagnose asthma ASTHMA 24
  • 25. PEAK FLOW TESTING Peak Flow Meter PEFR is used to assess the severity of wheezing in those who have asthma. PEFR measures how quickly a person can exhale air from the lungs Peak expiratory flow rate (PEFR) ASTHMA 25
  • 26. SPIROMETERY (LUNG FUNCTION TEST) It measures how much air you can exhale. FEV1(force expiratory volume) > 80% = normal Confirms the presence of airway obstruction and measure the degree of lung function impairment. Monitor your response to asthma medications ASTHMA 26
  • 27. ALLERGY-SKIN TEST A drop of liquid containing the allergen in placed on your skin (generally forearms is used). A small lance with a pinpoint is poked through the liquid into the top layer of skin (prick test). If you are allergic to the allergen, after about 2 minutes the skin begins to form a reaction (red, slightly swollen, and itchy: it makes a hive). The size of the hive is measured and recorded. The larger the hive, the more likely it is that you are allergic to the allergen tested. ASTHMA 27
  • 29. CHEST X-RAY If there are symptoms that may be caused by another condition such as pneumonia, your doctor may want to do a chest X-ray. It also may help to clarify the problem if there is problem with asthma treatment. ASTHMA 29
  • 31. APPROACH OF CHRONIC ASTHMA Education of patient and family Avoidance of precipitating factors Use of the lowest effective dose of convenient medications minimizing short and long term side effects. Assessment of severity and response to treatment. ASTHMA 31
  • 32. 1) EDUCATION OF PATIENT AND FAMILY i. Nature of asthma ii. Preventive measures/avoidance of triggers iii. Drugs used and their side- effects iv. Proper use of inhaled drugs v. Proper use of peak flow meter vii. Knowledge of the difference between relieving and preventive medications vii. Recognition of features of worsening asthma  increase in bronchodilator requirement  development of nocturnal symptoms  reducing peak flow rates). viii. Self management plan for selected, motivated patients or parents. ix. The danger of non prescribed self medication including ASTHMA 32
  • 33. 2) AVOIDANCE OF PRECIPITATING FACTORS The following factors may precipitate asthmatic attacks: •Beta blockers  contraindicated in all asthmatics •Aspirin and nonsteroidal anti-inflammatory drugs  if known to precipitate asthma, these drugs should be avoided. •Allergens  e.g. house dust mites, domestic pets, pollen should be avoided whenever possible. •Occupation  should be considered as a possible precipitating factor. • Smoking  active or passive. • Day to day triggers  such as exercise and cold air. It is preferable to adjust treatment if avoidance imposes inappropriate restrictions on lifestyle. • Atmospheric pollution. • Food  if known to trigger asthma, should be avoided. ASTHMA 33
  • 34. CLASSIFICATION OF DRUGS FOR ASTHMABRONCHODILATORS: 1. β-Sympathomimetic: Salbutamol, Terbutaline, Bambuterol, Salmeterol, Formoterol, Ephedrine 2. Methyl Xanthines: Theophylline, Aminophylline, Choline theophyllinate, Hydroxyethyl theophylline, Doxophylline. 3. Anticholinergics: Ipratropium bromide, Tiotropium bromide LEUKOTRIENE ANTAGONISTS: Montelukast, Zafirlukast MAST CELL STABILIZERS: Sodium chromoglycate, Ketotifen CORTICOSTEROIDS 1. Systemic: Hydrocortisone, Prednisolone 2. Inhalational: Beclomethasone, Budesonide, Fluticasone, Flunisolide ANTI Ig-E ANTIBODY: Omalizumab ASTHMA 34
  • 35. SYMPATHOMIMETICS Mechanism of action:  β2 stimulation increased cAMP formation in bronchial muscle cellrelaxation  Also decreases mediator release E.g. Salbutamol, Terbutaline, Bambuterol, Salmeterol, Formoterol, Ephedrine ASTHMA 35
  • 36. SYMPATHOMIMETICS Salbutamol  Highly selective β2 agonist  Inhaled Salbutamol produces bronchodilatation in 5 min and action lasts for 2-4 hrs  Side effects: Palpitations, restlessness, nervousness, throat irritation, ankle edema  Uses: Reserved for patients who cannot correctly use inhalers, Used as an adjuvant in severe asthma  Not suitable for round the clock prophylaxis Terbutaline:  Similar to Salbutamol  Inhaled Salbutamol and Terbutaline are currently the most popular drugs for quick reversal of bronchospasm ASTHMA 36
  • 37. SYMPATHOMIMETICS Salmeterol: It is the first long acting selective β2 agonist (LABA) with slow onset of action Used by inhalation on a twice daily schedule Used for maintenance therapy and nocturnal asthma Formeterol: Another LABA Acts for 12 hrs Compared to Salmeterol it has faster onset of action ASTHMA 37
  • 38. METHYL XANTHINES Naturally occuring Methyl Xanthine alkaloids are Caffein, Theophylline and Theobromine Mechanism of action:  Inhibition of phosphodiesterase (PDE)  increased cAMP Bronchodilatation, cardiac stimulation, vasodilation  Blockade of adenosine receptorsrelaxes smooth muscles  Release of Ca2+ from sarcoplasmic reticulum, especially in skeletal and cardiac muscle (only at higher concentrations) E.g: Theophylline, Aminophylline, Choline theophyllinate, Hydroxyethyl theophylline, Doxophylline ASTHMA 38
  • 39. METHYL XANTHINES Theophylline:  Well absorbed orally  T1/2 is 7-12 hrs  Side effects: gastric pain (with oral), rectal inflammation (with rectal suppositories), pain at site of injection (i.m), Rapid IV can cause precordial pain, syncope and sudden death.  Interactions:  metabolism is induced by smoking, phenytoin, rifampicin, phenobarbitone  Metabolism is inhibited by erythromycin, ciprofloxacin, cimetedine, OCPs, allopurinol  Uses: Bronchial asthma and COPD, Apnoea in premature infant, ASTHMA 39
  • 40. ANTICHOLINERGICS • Atropinic drugs cause bronchodilatation by blocking cholinergic constrictor tone • Act primarily in larger airways • Produce slower response than inhaled sympathomimetics • Better suited for regular prophylactic use • Combination of inhaled Ipratropium with β2 agonists produce more marked and longer lasting bronchodilatation. • E.g: Ipratropium bromide, Tiotropium bromide ASTHMA 40
  • 41. LEUKOTRIENE ANTAGONISTS Competitively antagonize cysLT1 receptor mediated bronchoconstriction, increased vasodilatation and recruitment of eisonophils Indicated for prophylactic therapy of mild to moderate asthma as alternative to inhaled glucocorticoids May obviate need for inhaled glucocorticoids Safe drugs Side effetcs: headache, rashes E.g: Montelukast, Zafirlukast ASTHMA 41
  • 42. MAST CELL STABILIZERS Inhibits degranulation of mast cells Release of mediators like Histamine, LTs, PAF, ILs, etc is restricted Not absorbed orally, administered as an aerosol through metered dose inhaler (MDI) Uses: Long term prophylaxis in mild to moderate Bronchial asthma, Allergic rhinitis, Allergic conjunctivitis Side effetcs: Bronchospasm, throat irritation, cough E.g: Sodium chromoglycate, Ketotifen ASTHMA 42
  • 43. CORTICOSTEROIDS These do not cause bronchodilatation, Reduce bronchial hyper-reactivity, mucosal edema, by supressing inflammatory response to AG:AB reaction Two forms are used Systemic and Inhalational 1. Systemic/Oral Cortico Steroid (OCS)  Used in severe chronic asthma and Status asthmaticus  E.g: Hydrocortisone, Prednisolone 2. Inhalational Cortico Steroid (ICS)  Step one for all asthma patients  Safe during regnancy  Side effetcs: mood changes, osteoporosis, bruising, petechiae, hyperglycemia  E.g: Beclomethasone, Budesonide, Fluticasone, Flunisolide ASTHMA 43
  • 44. GUIDELINES FOR THE TREATMENT OF ASTHMA ASTHMA 44
  • 45. MANAGEMENT OF ACUTE SEVERE ASTHMA •RR >50/min •PEFR <50% •Pulse >140 beats/min •breathlessness •10 puffs Bronchodilator and Metered Dose Inhaler •High flow 02, bronchoD •MDI, nebulizer(1-2h) •Oral prednisolone (3-5d) •Monitore PEFR/O2 •B2 agonist / 02 if required •PEFR <33% •Tiredness •Cyanosis •Decrease respiratory effort •Silent chest •iv aminophylline •Iv hydrocortisone •Salbutamol •Ipratropium bromide •Adequate hydration •antibiotic •ICU •Artificial ventilation•Wean iv •Β2 Agonist •Oxygen if required •Oral prednisolone •Monitor PEFR •Patient’s education •Review maintenance medication •Review inhaler technique •Follow up •PEFR monitor DISCHARGE PLAN response Give treatment improve ASTHMA 45
  • 46. MANAGEMENT OF ACUTE ASTHMA Aims Of Management i. To prevent death ii. To relieve respiratory distress iii. To restore the patient’s lung function to the best possible level as soon as possible. iv. To prevent early relapse ASTHMA 46
  • 47. MANAGEMENT: PREGNANCY IN ASTHMATICS Treatment should be aggressive, with the aim of eliminating symptoms and restoring and maintaining normal lung function Beta2 agonists: No evidence of a teratogenic risk with the commonly used inhaled beta2 agonists Ipratropium bromide: appears to be safe for use during pregnancy Salmeterol/formoterol: not been tested extensively in pregnant women ASTHMA 47
  • 48. ACUTE SEVERE ASTHMA Immediate Rx: O2 40-60% via mask or cannula + β2 agonist (salbutamol 5mg) via nebulizer + Prednisone tab 30-60mg and/or hydrocortisone 200mg IV. With lifethreatening features add 0.5mg ipratropium to nebulized β2 agonist + Aminophyllin 250mg IV over 20 min or salbutamol 250ug over 10 min. Subsequent Rx: Nebulized β2 agonist 6 hourly + Prednisone 30-60mg daily or hydrocortisone 200mg 6 hourly IV + 40-60% O2. No improvement after 15-30 min: Nebulized β2 agonist every 15-30 min + Ipratropium. Still no improvement: Aminophyllin infusion 750mg/24H (small pt), 1 500mg/24H (large pt), or alternatively salbutamol infusion. Monitor Rx: Aminophyllin blood levels + PEF after 15-30 min + oxymetry (maintain SaO2 > 90) + repeat blood gases after 2 hrs if initial PaO2 < 60, PaCO2 normal or raised and patient deteriorates. Deterioration: ICU, intubate, ventilate + muscle relaxant. ASTHMA 48
  • 49. MANAGEMENT: PREGNANCY IN ASTHMATICS Theophyllines: may aggravate the nausea and GERD and can caause transient neonatal tachycardia and irritabilityTeratogenicity has been shown in animals. Sodium cromoglycate: no adverse foetal effects Inhaled corticosteroids: mainstay of tx in persistent asthma,good safety profile in pregnancy Oral corticosteroids: necessary for severe asthma in pregnancy but usually only for short periods.Increased risk of cleft palate in animals given huge doses of oral steroids Anti-leukotrienes: no data available ASTHMA 49
  • 50. REFRENCES  Davidson’s Principle and Practice of Medicine (20th Ed)  kumar & Clark’s., Clinical Medicine(7th Ed)  Harison’s .,Principles of Internal medicine(17th )  http://emedicine.medscape.com/ Asthma 50