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ASTHMA Flashcards

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1
Q

What is asthma?

A

Reversible, often intermittent, obstructive disease of the small airways.

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2
Q

Asthma

Restrictive or obstructive

A

Obstructive disease of the small airways.

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3
Q

Asthma

Upper or lower airway?

A

Lower airway disease.

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4
Q

Asthma

Large or small airways

A

Obstructive disease of the small airways.

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5
Q

Asthma

Reversible or irreversible?

A

Reversible, often intermittent, obstructive disease of the small airways.

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6
Q

Asthma

Constant or intermittent?

A

Reversible, often intermittent, obstructive disease of the small airways.

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7
Q

What are the 3 components to asthma?

A

• 3 components

  • airway hyperreactivity
  • bronchoconstriction
  • inflammation
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8
Q

What is the process of inflammation in asthma?

A

Increased IgE binds to mast cells, initiating an inflammatory response, including increased Leukotrienes.

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9
Q

What age does asthma present?

A

• Can present at any age but initial occurrence most common in childhood.

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10
Q

Asthma

What does IgE bind to?

A

Mast cells

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11
Q

Asthma

What happens after IgE binds to Mast cells?

A

An inflammatory response is initiated.

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12
Q

Asthma

When an inflammatory response is initiated due to IgE binding with Mast cells, what else increases?

A

Leukotrienes

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13
Q

Asthma

Risk factors associated with asthma?

A 
Atopy strongest risk factor
family history
air pollution
obesity
environmental tobacco smoke
male gender
  • Samter’s triad Asthma + chronic rhinosinusitis with nasal polyps + sensitivity to Aspirin and/or NSAlDs
  • Atopic triad - Asthma, Atopic dermatitis (Eczema), & Allergic rhinitis
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14
Q

What is Atopy?

A

Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema).

Atopy is typically associated with heightened immune responses to common allergens, especially inhaled allergens and food allergens.

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15
Q

What is Samter’s triad?

A

• Samter’s triad (Aspirin-exacerbated respiratory disease)

consists of

+ Asthma
+ Chronic rhinosinusitis with nasal polyps
+ Sensitivity to Aspirin and/or NSAlDs

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16
Q

What is the Atopic triad?

A

• Atopic triad (patients with one condition are likely to develop one or two of the other)

  • Asthma
  • Atopic dermatitis (Eczema)
  • Allergic rhinitis
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17
Q

Asthma Triggers

3 types

A
  • Intrinsic (non-allergic): anxiety, stress, exercise, cold air, dry air, hyperventilation, & viral infections.
  • Extrinsic (allergic): animal dander, pollen, mold, dust mites, cockroaches etc. Associated with increased IgE.
  • Other: medications (eg, Aspirin, NSAIDs, Beta blocker, histamine), GERD.
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18
Q

Asthma Triggers

Intrinsic

A

• Intrinsic (non-allergic):

anxiety, 
stress, 
exercise, 
cold air, 
dry air, 
hyperventilation, 
viral infections.
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19
Q

Asthma Triggers

Extrinsic

A

• Extrinsic (allergic):

animal dander, 
pollen, 
mold, 
dust mites, 
cockroaches etc.

Associated with increased IgE.

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20
Q

Asthma Triggers

Other

Study These Flashcards
A

• Other:

medications
(eg, Aspirin, NSAIDs, Beta blocker, histamine),

GERD.

21
Q

Clinical manifestations of Asthma

Study These Flashcards
A

• Classic triad:

dyspnea,
wheezing and cough (especially at night).
May have chest tightness & fatigue.

22
Q

What are some clues to severity of asthma?

Study These Flashcards
A

previous intubations,
hospital admissions
ICU admission.

23
Q

Asthma Physical exam findings

Study These Flashcards
A

Prolonged expiration with wheezing,

hyper-resonance to percussion

decreased breath sounds

tachycardia

tachypnea

use of accessory muscles.

24
Q

Asthma Physical exam findings

• Severe Asthma and Status asthmaticus:

Study These Flashcards
A

inability to speak in full sentences

“tripod” positioning

silent chest (no air movement)

altered mental status (ominous)

pulsus paradoxes (inspiratory blood pressure drop > 10 mmHg),

PEFR < 40% predicted

• Findings of longstanding disease: Nasal polyps or Atopic dermatitis may be seen.

25
Asthma Physical exam findings | Findings of longstanding disease:
Nasal polyps or Atopic dermatitis may be seen.
26
DIAGNOSIS OF ASTHMA IN THE OFFICE
•Pulmonary function tests: - gold standard in making the diagnosis of Asthma. - Reversible obstruction (decreased FEV1, decreased FEV1/FVC; increased RV, TLC, and RV/TLC) •Bronchoprovocation: Methacholine challenge (>20% decrease on FEV1) followed by bronchodilator challenge (increase of FEV1 Sl2 % is expected).
27
Asthma | •Pulmonary function tests:
- gold standard in making the diagnosis of Asthma. - Reversible obstruction decreased FEV1, decreased FEV1/FVC; increased RV, TLC, and RV/TLC ***In Office
28
Asthma | •Bronchoprovocation:
Methacholine challenge (>20% decrease on FEV1) followed by bronchodilator challenge (increase of FEV1 Sl2 % is expected).
29
DIAGNOSIS OF AN ACUTE ASTHMA EXACERBATION
• Peak expiratory flow rate: best & most objective way to assess exacerbation severity & patient response to treatment.
30
Asthma Discharge criteria
- Discharge criteria: PEFR >70% predicted or PEFR > 15% initial attempt, subjective improvement. • Pulse oximetry: Sa02 <90% indicative of respiratory distress
31
Asthma | ABG's
• ABG: not usually ordered in most exacerbations. Respiratory alkalosis is expected (from tachypnea). Pseudo normalization (normal C02) or respiratory acidosis may indicate impending respiratory failure.
32
Asthma | Chest X ray
• Chest radiograph: usually normal. Generally, not helpful in the diagnosis of Asthma but may be used to rule out other causes of symptoms (eg, Pneumonia).
33
Asthma | Quick Relief for acute exacerbation (Rescue Drugs)
B2 agonists short acting SABA * Albuterol, Levalbuterol, Terbutaline, Epinephrine * Indications: first-line treatment for acute exacerbation - most effective & fastest (2-5 minutes). * MOA: bronchodilator (especially peripherally), decreases bronchospasm, inhibits the release of bronchospastic mediators, increases ciliary movement, Decreases airway edema & resistance.
34
Asthma Quick Relief for acute exacerbation (Rescue Drugs) B2 agonists short acting SABA: MOA
• MOA: bronchodilator (especially peripherally), decreases bronchospasm inhibits the release of bronchospastic mediators increases ciliary movement decreases airway edema & resistance.
35
Asthma Quick Relief for acute exacerbation (Rescue Drugs) B2 agonists short acting SABA: Administration
• Administration: MDI, nebulizer. Nebulizers most common used in ED (MDI ±slightly more efficacious). Generally given every 20 minutes x 3 doses (or continuous) + revaluation after 3 doses (at least q 1-2 hours).
36
Asthma Quick Relief for acute exacerbation (Rescue Drugs) B2 agonists short acting SABA: Side effects
``` • S/E: B-1 cross reaction: tachycardia/arrhythmias, muscle tremors, CNS stimulation, hypokalemia. ```
37
Asthma Quick Relief for acute exacerbation (Rescue Drugs) Anticholinergics (antimuscarinics) MOA
• MOA: central bronchodilator (inhibits vagal-mediated bronchoconstriction) & inhibits nasal mucosal secretions. positive synergy between p2 agonists & anticholinergics. Most useful in the first hour.
38
Asthma Quick Relief for acute exacerbation (Rescue Drugs) Anticholinergics (antimuscarinics)
Anticholinergics (antimuscarinics) | Ipratropium
39
Asthma Quick Relief for acute exacerbation (Rescue Drugs) Anticholinergics (antimuscarinics) Side Effects
• S/E: thirst, blurred vision, dry mouth, urinary retention, dysphagia, acute glaucoma, BPH.
40
Asthma Quick Relief for acute exacerbation (Rescue Drugs) Corticosteroids
Corticosteroids Prednisone , Methylprednisolone , Prednisolone
41
Asthma Quick Relief for acute exacerbation (Rescue Drugs) Corticosteroids MOA
• MOA: anti-inflammatory. All but the mildest exacerbations should be discharged on a short course of oral corticosteroids (eg 3-5 days) unless contraindicated. Steroids decrease relapse & reverse the late pathophysiology. Short courses don't need tapering (unless on chronic steroids, or recent treatment with repeated short courses in a short period). Onset of action 4-8 hours for both oral & IV. *
42
Asthma Quick Relief for acute exacerbation (Rescue Drugs) Corticosteroids Side Effects
• S/E: immunosuppression, catabolic, hyperglycemia, fluid retention, osteoporosis, growth delays
43
Asthma Long Term (Chronic, Control) Maintenance Meds (ICS)
``` INHALED CORTICOSTEROIDS (ICS) Beclomethasone, Flunisolide, Triamcinolone ```
44
Asthma Long Term (Chronic, Control) Maintenance Indications
• Indications: first-line long term, persistent (chronic maintenance). Effective long-term control with very low incidence of systemic side effects. MOA: cytokine & inflammation inhibition.
45
Asthma Long Term (Chronic, Control) Maintenance Side effects
• S/E: oral candidiasis (using spacer & rinsing mouth after inhaler use decreases risk), dysphonia.
46
Asthma Long Term (Chronic, Control) Maintenance Meds (LABA)
LONG-ACTING P z AGONISTS (LABA) Salmeterol, ICS/LABA: Budesonide/Formoterol, Fluticasone/Salmeterol * Mechanism: bronchodilator that prevents symptoms (especially nocturnal asthma). * Indications: long-acting p2 agonists added to steroids (or other long term asthma medications) ONLY if persistent asthma is not controlled with ICS alone (the option of increasing the ICS dose = addition of LABA). Once asthma control maintained (>3 months), step down off LABA is recommended.
47
Asthma Long Term (Chronic, Control) Maintenance LABA MOA
• Mechanism: bronchodilator that prevents symptoms (especially nocturnal asthma).
48
Asthma Long Term (Chronic, Control) Maintenance LABA Indications
• Indications: long-acting p2 agonists added to steroids (or other long term asthma medications) ONLY if persistent asthma is not controlled with ICS alone (the option of increasing the ICS dose = addition of LABA). Once asthma control maintained (>3 months), step down off LABA is recommended.
49
Asthma Long Term (Chronic, Control) Maintenance LABA Contra-Indications
• CI NOT used as a rescue drug in acute exacerbations or as monotherapy for long-term Asthma.

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