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2. HDS Pulmonary > Asthma > Flashcards

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
    • MΦ
    • 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

A
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
Q

Asthmatic History

A
  • 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
Q

Conditions That Mimic Asthma

A
27
Q

Physical Findings

A

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
Q

Asthmatic

Pulmonary Function Tests

A
  • 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
Q

Bronchodilator Response

A

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
Q

Peak Flow Meters

A
  • 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
Q

FeNO

A
  • 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
Q

Bronchial Provocation Testing

A

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
Q

CXR

A
  • Usually done during preliminary evaluation
  • Typically normal
  • Asthmatic CXR
    • Hyperinflation ⇒ see more ribs
    • Flattening of diaphragm
34
Q

Asthma

Evaluation

A
  • 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
Q

Asthma

Severity

A

Warrants daily therapy if experiencing sx:

> 2 days per week

> 2 nights per month

36
Q

Asthma Control

A

Asthma Control Test

5 questions

Score ≤ 19 means poorly controlled

37
Q

Asthma Therapy

Goals

A

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
Q

Asthma Therapy

Components

A

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
Q

Pharmacotherapy

A
40
Q

Patient Education

A

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
Q

Asthma

Management

A
  • Intermittent
    • SABA only
  • Persistent
    • Inhaled corticosteroids
    • Add LABA
    • Consider LTRA
    • Biologics for appropriate patients
    • Consider LAMA
42
Q

Acute Exacerbation

Management

A
  • 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
Q

Indications for Intubation

A

Clinical judgement based on:

  • Rising or normal pCO2
  • Progressive deterioration despite aggressive treatment
  • Deteriorating mental status
  • Refractory hypoxia
  • Hemodynamic instability
44
Q

Asthma

Summary

A
  • Common disease
  • Diagnosis based on history and findings suggestive of inflammation and airway contriction
  • Treatment geared towards bronchodilation and decreasing inflammation

2. HDS Pulmonary (28 decks)

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