Asthma Flashcards

1
Q

Asthma

Definition

A

Chronic inflammatory disorder of the airways.

  • Many cells and cellular elements involved
  • Airway hyper-responsiveness
  • Caused by reversible generalized narrowing of the airways
  • Periodic ↑ contraction of airway smooth muscle and hypersecretion of bronchial mucus in response to internal or external stimuli
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2
Q

Asthma

Epidemiology

A
  • 24 million people in USA
  • Most common chronic childhood disease ⇒ ~ 5 million kids
    • Boys > Girls
  • Women > men (over age 40)
  • Prevalence rate ↑ 1%/yr
  • Mortality rates ↑ in late-half of 20th century
  • Highest risk population ⇒ urban minorities living in poverty areas
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3
Q

Asthma

Risk Factors

A
  • Genetics
    • Atopy ⇒ genetic tendency to develop allergic diseases
      • Typically associated with heightened immune responses to common allergens, especially inhaled and food allergens
  • Environmental cigarette smoke exposure
  • House dust mite exposure
  • Cockroach allergen
  • RSV infection
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4
Q

Asthma

Bronchial Changes

A
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5
Q

Bronchial Wall

Comparison

A
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6
Q

Asthma

Histological Changes

A
  • Thickened basement membrane
  • Edema
  • Inflammatory infiltrates
  • Prominence of eosinophils in bronchial wall and sputum
  • Hypertrophy of bronchial wall smooth muscle
  • Mucus gland proliferation
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7
Q

Asthmatic Sputum

A

Sputum can include:

  • Curshmann spirals ⇒ dried out mucus
  • Charcot Leyden crystals ⇒ eosiniphil breakdown product
  • Bronchial casts
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8
Q

Mucus Histology

A
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9
Q

Airway Inflammation

A

Causes obstructive lung disease by four mechanisms:

  1. Acute bronchoconstriction
  2. Swelling and edema of the airway walls
  3. Airway remodeling
  4. Mucus plug formation
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10
Q

Asthma Phenotyping

A
  • Asthma is not one disease
  • Several pathologic phenotypes lead to same sx manifestations
  • Characterizing phenotype ⇒ more customized asthma threatment
  • Increasing importance w/ new biologic treatments
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11
Q

Airway

Hyper-responsiveness

A

Exposure to specific and nonspecific irritants cause airways to become narrow and obstructed.

Level of airway responsiveness correlates with severity of disease.

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12
Q

Airway

Inflammation

A
  • Asthmatics usually have increased leukocytes
    • Activated eosinophils
    • Mast Cells
    • T-cells
  • Cells may be present when pt clinically asymptomatic
  • E/O asthma phenotypes with similar disease manifestations
  • Many inflammatory mediators involved
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13
Q

Allergic Asthma

A

Asthma exacerbation precipitated by exposure to allergens in many patients.

Atopic mechanism.

Binding of Ag to cell-bound IgE stimulates mediator release from mast cells, MΦ, and basophils.

Preformed vs non-preformed mediators.

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14
Q

Preformed Mediators

A
  • Histamine and serotonin
    • Bronchoconstriction, swelling, edema
  • Proteolytic enzymes and histamine
    • Disrupt or destroy pulmonary lining
      • Allows fluid to leak in
        • Leads to swelling, edema, obstruction
      • Removes barrier to inhaled irritants
        • Easier to trigger another attack
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15
Q

Non-preformed Mediators

A

Formed at time of activation from arachidonic acid.

  • Lipoxygenase products
    • Leukotriene B4
      • Chemoattractant for inflammatory cells
    • Leukotriene C4
      • Bronchoconstriction
    • Leukotriene D4
      • Bronchoconstriction
  • Cycooxygenase products
    • Prostaglandin D2
      • Potent bronchoconstrictor
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16
Q

Non-allergic Asthma

A

Airway epithelial cells can respond to injury or irritants by releasing cytokines.

GM-CSF ⇒ stimulate eosinophils and mast cells

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17
Q

Neutrophilic Asthma

A

Some asthmatics have a predominantly Th1 type inflammation ⇒ neutrophils

  • High levels of PMNs can be found in pts with severe asthma or during acute exacerbations
  • Correlated with lower FEV1
  • Do not respond as well to therapy
    • Corticosteroids do not reduce PMNs
    • Most therapy targeted at eosinophils
  • Linked to fatal asthma
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18
Q

Bronchoconstriction

A

Caused by contraction of circular smooth muscle within bronchial walls.

  • Bronchoconstriction
    • Inflammatory mediators
    • PNS ⇒ irritant or cold air may trigger a parasympathetic vagal reflex ⇒ constriction
  • Bronchodilation
    • SNS
      • NE/Epi ⇒ cAMP ⇒ relaxation
    • Non-adrenergic, non-cholineric inhibitor nerves
      • Releases NO ⇒ potent bronchodilator
19
Q

Mucus Plugs

A
  • Produced by glands located below epithelial lining
  • Asthma↑ production
    • Inflammatory mediators
    • PNS stimulation
  • Can plug up airways causing further narrowing
20
Q

Airway Remodeling

A
  • Inflammation & cytokines (TGF-β) ⇒ myofibroblast activation
  • Myofibroblasts ⇒ collagen and fibronectin production
  • Results in airway remodeling ⇒ fixed obstruction
    • Not reversed by bronchodilators
    • Leads to residual obstructive lung disease despite max therapy
21
Q

Asthma

Etiologies

A
  • Environmental
  • Viral infection
  • Sinusitis
  • Exercise induced
  • GERD ⇒ vagal response
  • ASA induced
    • Sampter’s triad: a chronic condition defined by asthma, sinus inflammation with recurring nasal polyps, and aspirin sensitivity
  • Obesity
  • Occupational
    • Farmers ⇒ dust, hay, chemicals
    • Painters ⇒ isocyanite asthma
    • Cleaners ⇒ household products
22
Q

Aggrevating Factors

23
Q

Asthma

Presentation

A
  • Any age group
    • 75% dx prior to age 7
    • Some show remission during adolescence
  • Recurrent episodes
    • Wheezing
    • Breathlessness
    • Chest tightness/pain
    • Coughing
    • Sputum production
  • Particularly at night or early morning
  • Widespread and variable airflow obstruction
  • Often reversible either spontaneously or with treatment
24
Q

Asthma

Clinical Work-Up

A
  • H&P
  • PFTs
  • FENO
  • Bronchoprovocation testing
  • Peak flow monitoring
  • CBC and sputum for eosinophils
  • CXR
25
Asthmatic History
* **Recurrent episodes of cough, wheezing, or SOB** * **Return of function between episodes** * Atopic history? * Family history? * Symptoms triggered by usual asthma triggers * Exercise, allergens, airborne irritants, seasonal changes, after illness
26
Conditions That Mimic Asthma
27
Physical Findings
Varies with intensity of asthma. May have no signs between attacks. * Asthma exacerbations * Tachycardia * Tachypnea * Fragmented speech * Accessory muscle use * Diaphoresis * Mild asthmatics * Persistent cough * ± Wheezing * Severe asthmatics * **Quiet chest** ⇒ no wheezing and minmal breath sounds; implies minimal air flow * **± Larger chest volume** ⇒ hyperinflation d/t air trapping
28
Asthmatic Pulmonary Function Tests
* _Spirometry_ * Obstructive lung disease * **FEV-1% \< 70% or lower limit of normal** * May be normal between attacks * **Improvement after trial of bronchodilator therapy** * _Peak flow meters_ * Measures initial flow rate with forced expiratory effort * **Absolute reduction in peak flow** * **Variability in peak flow of more than 20%**
29
Bronchodilator Response
Defined as: **12% improvement in FEV-1 & at least 200 cc improvement** or **12% improvement in FVC & at least 200 cc improvement** or **30% improvement in FEF 25-75%**
30
Peak Flow Meters
* **May be 1st sign of worsening asthma** * Have pt do 3 times and take their best number * Pt should know their "personal best" * _Clinical relavence_ * Used with asthma action plan to improve health outcomes * Triage severity of asthma exacerbation * Used to determine triggers
31
FeNO
* **Marker of eosinophilic inflammation of the lungs** * **Measures exhaled NO** * Levels decrease with inhaled corticosteroids (ICS) * Can be used to assess compliance and predict exacerbations * Clinically practical
32
Bronchial Provocation Testing
**Inhaling an agent that provokes an asthmatic response to establish diagnosis.** * Non-specific agents * **Methacholine** * **Mannitol** * Histamine * Cold air challenge * Exercise challenge * Inhaled antigens * **20% drop in FEV-1 is significant** * **Excellent negative predictive value**
33
CXR
* Usually done during preliminary evaluation * Typically normal * Asthmatic CXR * Hyperinflation ⇒ see more ribs * Flattening of diaphragm
34
Asthma Evaluation
* **Assess severity** ⇒ intermittent or persistent; mild, moderate, or severe * **Assess likelihood for exacerbation in the future** * **Assess for degree of asthma control using a standard metric** * E.g. Asthma Control Test
35
Asthma Severity
Warrants daily therapy if experiencing sx: \> 2 days per week \> 2 nights per month
36
Asthma Control
**Asthma Control Test** 5 questions Score ≤ 19 means poorly controlled
37
Asthma Therapy Goals
Outlined by NAEPP and GINA: * Achieve and maintain symptom control * Prevent exacerbations * Maintain pulmonary function as close to normal as possible * Maintain normal activity levels, including exercise * Avoid adverse effects of asthma medications * Prevent development of irreversible airflow obstruction * Prevent asthma mortality
38
Asthma Therapy Components
Recommendations based on severity, control, and responsiveness. _Includes:_ * **Patient education** * **Asthma Action Plan** * How to monitor asthma on a daily basis * What to do if they have an exacerbation * **Avoidance of asthma triggers** * Allergens, irritants, respiratory viruses * **Pharmacotherapy** * Stepwise management ⇒ goal to limit sx or rescue inhaler use \< 2 days/wk or 2 nights/month * **Immunotherapy when appropriate**
39
Pharmacotherapy
40
Patient Education
Provide patients with the info needed to self-manage their own asthma in conjunction with physician guidance. * **Knowledge of avoidance measures** * Active & passive smoking * Beta-blockers * In patients who are sensitive: * ASA and NSAIDS * Occupational agents * Dust mites * Other common allergens * Foods and additives * **Knowledge of treatment modalities** * Diagnosis * Rescue inhalers vs controllers * Inhaler use training * Advice regarding prevention * Signs that might suggest asthma is worsening and actions to take * Training in monitoring asthma * How and when to seek medical attention * Written self-management plan
41
Asthma Management
* Intermittent * SABA only * Persistent * Inhaled corticosteroids * Add LABA * Consider LTRA * Biologics for appropriate patients * Consider LAMA
42
Acute Exacerbation Management
* **Short-acting** β-**agonists** * Albuterol ⇒ intermittent neb, continuous neb, MDI * MDI equivalent to nebulizers if proper technique used * **Inhaled anticholinergic** * Ipratropium bromide (Atrovent) * May be given with albuterol with additive effects (Duoneb) * **Steroids** * Prednisone, methylprednisolone, or prednisolone * PO or IV based on severity * Dose: 40-80 mg/day until PEF reaches 70% of predicted or personal best * Higher doses do not appear to offer added benefit * **Adjunctive treatments** * Oxygen if hypoxic * Goal: O2 sat ≥ 90% if not pregnant, ≥ 95% if pregnant * Magnesium ⇒ 2g IV over 20 minutes * Heliox: 70/30 mixture * Low viscosity gas ↓ WOB * May prevent intubation in severe asthmatics * CPAP/BiPAP * ↓ WOB and may prevent intubation
43
Indications for Intubation
Clinical judgement based on: * Rising or normal pCO2 * Progressive deterioration despite aggressive treatment * Deteriorating mental status * Refractory hypoxia * Hemodynamic instability
44
Asthma Summary
* Common disease * Diagnosis based on history and findings suggestive of inflammation and airway contriction * Treatment geared towards bronchodilation and decreasing inflammation