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CASE SUMMARY
• 20 yrs old male ,nonsmoker, normotensive, euglycemic presented with
• Chief c/o : Acute onset of dyspnea and cough with scanty sputum production X 2 d
• No H/o fever but however h/o wheezing and chest tightness is present.
• No H/o PND, chest pain, hemoptysis
CASE SUMMARY
• Symptoms appeared after he went to visit his friend ,while playing with his dog.
• Similar episodes was present 1 year back. Running nose ,sneezing and rashes were
accompanied features.
• Family history present .
• Patient became asymptomatic after use of some inhalers.
Pratap Sagar Tiwari
MD, Lecturer, NMC
AN INTRODUCTION TO ASTHMA
DEFINITION
• Asthma is a syndrome characterized by airflow limitation/obstruction that varies markedly
, both spontaneously and with treatment.
• There is a hyperresponsiveness to a wide range of triggers leading to excessive
narrowing with consequent decrease in airflow and symptomatic wheezing and dyspnea.
• Note: Airway hyper-reactivity (AHR)-the tendency for airways to contract too easily and
too much in response to triggers that have little or no effect in normal individuals.
Reference: Davidson
• The "classic" signs and symptoms of asthma are intermittent dyspnea, cough, and
wheezing.
ETIOLOGY/TRIGGERS/RISK FACTORS
• Atopy
• Hygiene hypothesis
• Infections
• Genetics: ADAM33, GPRA
• Occupational: bakers and chemical factory
• Diet: vit a/c/d def, Mg/Se def, obesity
• Hormonal: premenstrual period, thyroidal illness
ATOPY
It is the genetic predisposition to develop specific IgE antibodies directed against
environmental allergies.
It is the strongest identifiable risk factor for asthma.
Trigger includes pollen, fungal spores, food containing nuts, air pollution, cold air, laughter,
perfumes etc.
HYGIENE HYPOTHESIS
• Lower level of infection in childhood may be a factor related to increase risk of asthma.
• The HH proposes that lack of infection in early childhood preserves the TH2 bias.
• Exposure to infection result in shift towards predominant protective Th1 immune
response.
INFECTIONS
• Viral: rhinovirus, corona virus, RSV
• Bacterial: mycoplasma, chlamydia etc
ETIOLOGY/TRIGGERS/RISK FACTORS
Other risk factor includes,
• Low birth weight, prematurity, low maternal age
Other trigger includes b blockers, ACE inhibitors
Others: Exercise, Acid reflux, Stress
Note:
ACE inhibitors inhibits degradation of Bradykinin  Increase bradykinin  Vasodilation,
bronchoconstriction and increase vascular permeability.
B blockers  bronchospasms
PATHOPHYSIOLOGY
• Airway inflammation
• Airway obstruction
• Bronchial hyperresponsiveness
MAKING A DIAGNOSIS
• Compatible clinical features
• Precipitating factors
• Family history
• Reversibility of symptoms/response to bronchodilators
ASTHMA VS COPD
Asthma
• -- Not always productive cough
• -- Usually reversible
• -- Often associated with allergies
• -- Cough at night and early mornings
• -Family history
• --Variability
COPD
• -- Cough is usually productive
• -- Symptoms not reversible
• -- Common history of smoking
• -- Cough in morning and throughout the day.
• -- Age
Note: The diagnosis of asthma is predominantly clinical and based on a characteristic history.
A trial of corticosteroids: e.g. 30 mg daily for 2 weeks
Ref: GINA guideline
Pic taken from: http://upload.wikimedia.org/wikipedia/commons/f/f7/Peak_flow_meter_horiz.jpg
ASSESSMENT OF SEVERITY
DRUGS USED IN ASTHMA
Controller Reliever
ICS :Glucocorticosteroids
Beclomethasone/ budesonide/ fluticasone
SAB2A: Salbutamol/ Levalbuterol/
Terbutaline /Pirbuterol
LAB2A: Salmeterol/ formeterol Anticholinergics: Ipratropium /Oxitropium B
Antileukotrienes: montelukast/ zafirlukast Short acting Theophylline: Aminophylline
Cromones: Cromolyn /nedocromil sodium Epineprine/Adrenaline
Anti-IgE: Omalizumab
Controller medication: taken daily to prevent symptoms, improve lung function and prevent attacks.
Reliever: Occasionally required to treat acute symptoms such as wheezing, chest tightness and cough.
TREATMENT STRATEGY
1 2 3 4 5
Leukotriene modifier Anti IgE
Theophylline SR
LEVEL OF ASTHMA CONTROL
Notes:
• COPD affects both the airways and the parenchyma, whilst asthma affects only the
airways.
• The nature of inflammation in Asthma is primarily eosinophilic and CD4-driven .In COPD it
is neutrophilic and CD8-driven .
• For asthma, severity is based on symptom frequency and severity, lung function but for
COPD, the stages of severity are defined by lung function.
• Homework: Management of Acute severe Asthma
References:
• Harrison 18th ed .
• Davidsons.
• Uptodate 19.2
• GINA guidelines

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Asthma

  • 1. CASE SUMMARY • 20 yrs old male ,nonsmoker, normotensive, euglycemic presented with • Chief c/o : Acute onset of dyspnea and cough with scanty sputum production X 2 d • No H/o fever but however h/o wheezing and chest tightness is present. • No H/o PND, chest pain, hemoptysis
  • 2. CASE SUMMARY • Symptoms appeared after he went to visit his friend ,while playing with his dog. • Similar episodes was present 1 year back. Running nose ,sneezing and rashes were accompanied features. • Family history present . • Patient became asymptomatic after use of some inhalers.
  • 3. Pratap Sagar Tiwari MD, Lecturer, NMC AN INTRODUCTION TO ASTHMA
  • 4. DEFINITION • Asthma is a syndrome characterized by airflow limitation/obstruction that varies markedly , both spontaneously and with treatment. • There is a hyperresponsiveness to a wide range of triggers leading to excessive narrowing with consequent decrease in airflow and symptomatic wheezing and dyspnea. • Note: Airway hyper-reactivity (AHR)-the tendency for airways to contract too easily and too much in response to triggers that have little or no effect in normal individuals. Reference: Davidson
  • 5. • The "classic" signs and symptoms of asthma are intermittent dyspnea, cough, and wheezing.
  • 6. ETIOLOGY/TRIGGERS/RISK FACTORS • Atopy • Hygiene hypothesis • Infections • Genetics: ADAM33, GPRA • Occupational: bakers and chemical factory • Diet: vit a/c/d def, Mg/Se def, obesity • Hormonal: premenstrual period, thyroidal illness
  • 7. ATOPY It is the genetic predisposition to develop specific IgE antibodies directed against environmental allergies. It is the strongest identifiable risk factor for asthma. Trigger includes pollen, fungal spores, food containing nuts, air pollution, cold air, laughter, perfumes etc.
  • 8. HYGIENE HYPOTHESIS • Lower level of infection in childhood may be a factor related to increase risk of asthma. • The HH proposes that lack of infection in early childhood preserves the TH2 bias. • Exposure to infection result in shift towards predominant protective Th1 immune response.
  • 9. INFECTIONS • Viral: rhinovirus, corona virus, RSV • Bacterial: mycoplasma, chlamydia etc
  • 10. ETIOLOGY/TRIGGERS/RISK FACTORS Other risk factor includes, • Low birth weight, prematurity, low maternal age Other trigger includes b blockers, ACE inhibitors Others: Exercise, Acid reflux, Stress Note: ACE inhibitors inhibits degradation of Bradykinin  Increase bradykinin  Vasodilation, bronchoconstriction and increase vascular permeability. B blockers  bronchospasms
  • 11. PATHOPHYSIOLOGY • Airway inflammation • Airway obstruction • Bronchial hyperresponsiveness
  • 12. MAKING A DIAGNOSIS • Compatible clinical features • Precipitating factors • Family history • Reversibility of symptoms/response to bronchodilators
  • 13. ASTHMA VS COPD Asthma • -- Not always productive cough • -- Usually reversible • -- Often associated with allergies • -- Cough at night and early mornings • -Family history • --Variability COPD • -- Cough is usually productive • -- Symptoms not reversible • -- Common history of smoking • -- Cough in morning and throughout the day. • -- Age
  • 14. Note: The diagnosis of asthma is predominantly clinical and based on a characteristic history. A trial of corticosteroids: e.g. 30 mg daily for 2 weeks Ref: GINA guideline Pic taken from: http://upload.wikimedia.org/wikipedia/commons/f/f7/Peak_flow_meter_horiz.jpg
  • 16. DRUGS USED IN ASTHMA Controller Reliever ICS :Glucocorticosteroids Beclomethasone/ budesonide/ fluticasone SAB2A: Salbutamol/ Levalbuterol/ Terbutaline /Pirbuterol LAB2A: Salmeterol/ formeterol Anticholinergics: Ipratropium /Oxitropium B Antileukotrienes: montelukast/ zafirlukast Short acting Theophylline: Aminophylline Cromones: Cromolyn /nedocromil sodium Epineprine/Adrenaline Anti-IgE: Omalizumab Controller medication: taken daily to prevent symptoms, improve lung function and prevent attacks. Reliever: Occasionally required to treat acute symptoms such as wheezing, chest tightness and cough.
  • 17. TREATMENT STRATEGY 1 2 3 4 5 Leukotriene modifier Anti IgE Theophylline SR
  • 18. LEVEL OF ASTHMA CONTROL
  • 19.
  • 20. Notes: • COPD affects both the airways and the parenchyma, whilst asthma affects only the airways. • The nature of inflammation in Asthma is primarily eosinophilic and CD4-driven .In COPD it is neutrophilic and CD8-driven . • For asthma, severity is based on symptom frequency and severity, lung function but for COPD, the stages of severity are defined by lung function.
  • 21. • Homework: Management of Acute severe Asthma References: • Harrison 18th ed . • Davidsons. • Uptodate 19.2 • GINA guidelines