Lecture 12 Flashcards

1
Q

What is asthma?

A
  • Asthma is a chronic inflammatory disease of the airways, characterized by airflow obstruction, and bronchospasm
  • It is episodic
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2
Q

What are the symptoms of asthma?

A
  • wheezing, cough, sputum production, chest tightness, and shortness of breath associated with airway hyperresponsiveness
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3
Q

Epidemiology of asthma?

A
  • 1 in 6 adults and 1 in 4 kids in nz
  • NZ has growing asthma prevalence, NZ one of worst nations
  • Developed countries more than undeveloped
  • In children males > females, in adults females > males
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4
Q

How is asthma diagnosed?

A
  • Physical Examination: Wheezing, high‐ pitched whistling sounds, (But, wheezing is not specific for asthma)
    1. History of any of the following: Cough, Recurrent wheeze, Recurrent dyspnea, Recurrent chest tightness, Reversible airflow limitation and diurnal variation
    1. Lung function test: evidence of variable airflow obstruction
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5
Q

What are some atypical presentations of asthma?

A
  • Dyspnea without wheezing
  • Chronic cough
  • Increased shortness of breath at nighttime
  • Allergic rhinitis with wheezing
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6
Q

What lab studies can be done to help diagnose asthma?

A
  • Lung function tests
    • Peak expiratory flow (PEF)
    • Spirometry: FEV1 (a better measure for asthma)
  • Skin allergy test and serologic studies
  • Radiographic studies
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7
Q

How will an asthma patient’s spirometry test differ from a normal patients?

A
  • For asthma:
    • FEV1 ↓↓
    • FVC ↓
    • FEV1/FVC ↓
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8
Q

What blood tests are done to help diagnose asthma?

A
  • Eosinophil count: >4 % or 300 ‐ 400/mm3 (> 800 /mm3 suggests the presence of other disorders)
  • Increased Serum IgE leve
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9
Q

What allergy tests are done?

A
  • Tree, grass, weed and flower pollens
  • Dust mites
  • Mold and mold spores
  • Animal Dander
  • Insect allergens
  • Smoking
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10
Q

What are the pathogenisis models for asthma?

A
  • allergy pathway model
  • non‐ allergy pathway model
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11
Q

What is atopic asthma?

A
  • The most common type of asthma
  • Usually begins in childhood, early-onset
  • Trigged by environmental antigens
  • A positive family history
  • Often preceded by allergic rhinitis, urticaria or eczema.
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12
Q

How does the histology of the airway differ in asthma pateints?

A
  • Epithelium broken down
  • More inflammatory cells:
    • Eosinophils
    • Mast cells
    • Macrophages
    • T cells
    • Neutrophils
    • Basophils
    • Dendritic cells
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13
Q

What are the 2 responses to allergens in asthma?

A
  • The Acute-Phase Response
    • In the acute-phase response (APR), inhalation of allergen causes an immediate fall in lung function (as short as 5-10 min).
  • Late-phase response (LPR)
    • beginning about 4 to 6 hours after allergen challenge.
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14
Q

What mechanism –> acute phase response?

A
  • Allergens causing mast cells to secrete histamines etc –> SM constriction
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15
Q

What mechanism –> late-phase response?

A
  • Allergen –> dendritic cells which recruits inflammatory cells
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16
Q

Which cell type is usually mutated in asthma?

A
  • T-helper 2 cells
  • These are the TH cells that secrete cytokines
  • Causes type 1 hypersensitivity/atopy: such as eczema (atopic dermatitis), hay fever (allergic rhinitis), asthma,Chronic airway inflammation,Bronchial hyper responsiveness.
17
Q

What is nonatopic asthma?

A
  • late‐onset asthma usually nonatopic
  • It may be associated with respiratory tract infections, such as Mycoplasma pneumoniae and Chlamydia pneumoniae
  • Other risk factors: medications induced asthma (eg. NSAIDs, beta blockers and aspirin).
18
Q

What are the key mediators of asthma?

A
  • Leukotrienes (synthesised by mast cells, eosinophils.)
    • Cause prolonged broncho constriction
  • Ach
    • SM contraction
  • Chemokines
    • Recruits inflammatory cells
  • Prostanoids
    • SM contrtaction
  • IgE
    • Triggers mast cell causing airway inflammation
  • NO
    • reflects levels of airway inflammaiton
  • Granular proteins
    • Major basic protein (MBP) and Eosinophil cationic protein (ECP) which can cause membrane dammage
  • Adhesion molecules of inflammation
    • Integrins are the primary mediators of cellextracellular matrix adhesion
19
Q
A