Module 2: Asthma & COPD Flashcards

1
Q

Asthma

A

Chronic inflammatory lung disorder

Characterized by:

  1. Reversible airway obstruction
  2. Airway inflammation
  3. Hypersensitivity (increased airway responsiveness to stimuli)

S/S: Coughing, wheezing, difficulty breathing, and chest tightness

One-half of pts that experience asthmatic symptoms are due to allergens (other half is idiopathic)

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2
Q

COPD

A

Chronic, progressive, and largely irreversible lung disorder

Underlying pathologic processes:

  1. Emphysema: destruction of alveolar septa and loss of elastic recoil of bronchial walls
  2. Chronic bronchitis: bronchial edema, hypersecretion of mucus, and bacterial colonization of airways
  3. Alpha-1 antitrypsin deficiency (3%)

Characterized by:

  1. Airflow restrictions
  2. Inflammation

S/S: Chronic cough, sputum, SOB, and poor exercise tolerance

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3
Q

Asthma Goals of Therapy

A

Asthma therapy goals:
1. Prevent symptoms/exacerbations

  1. Decrease use of short-acting beta-2 agonist rescue meds.
  2. Maintain normal lung function and limit reduction of lung function over time
  3. Decrease ED visits/hospitalizations
  4. Minimize AEs of therapy
  5. Smoking cessation (for COPD in particular)
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4
Q

Inhalation Dosage Forms

A

4 types of dosage forms:

  1. Metered-dose inhaler (MDI)
  2. Respimat
  3. Dry-powder inhaler (DPI)
  4. Nebulizer

Advantages of inhaled drug therapy:
1. Therapeutic effects are delivered to site of action

  1. Systemic effects are minimized
  2. Rapid relief of acute attacks
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5
Q

Metered-dose inhaler (MDI)

A

Consists of a pressurized canister of propellant with drug suspension that delivers a measured amount of med.

MDI with spacers are ideal for those with impaired coordination to actuate the device and breathe

Only about 10% of the drug reaches the lungs without a spacer (90% of the dose is either swallowed or stays in the oropharynx)

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6
Q

Respimat

A

Delivers the drug in a fine mist (smaller particles allow for greater deposition into the lungs)

They do NOT use propellant (like MDIs); the device is actuated by the user — thus, requires some coordination, but not to the same degree of MDIs

Issue: Strength and dexterity are required to assemble new cartridges

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7
Q

Dry-Powder Inhaler (DPI)

A

The med. is in a dry, micronized powder form; and the device is activated when pts inhale from the device (thus, there is no need for hand-breath coordination)

Issue: Difficult for pts who do not have the ability to deeply inspire (i.e. children <4 yrs. of old)

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8
Q

Nebulizer

A

Not ambulatory; drug solution is converted into a mist (the droplets are much finer than other dosage forms)

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9
Q

Asthma Drugs

A

Anti-inflammatory drugs:

  1. Corticosteroids
  2. Leukotriene modifiers

Bronchodilators:

  1. Beta-2 agonists
  2. Methylxanthines
  3. Anticholinergic drugs
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10
Q

Anti-inflammatory Drug #1: Corticosteroids

A

AEs (Inhaled):

  1. Adrenal suppression (most serious) — prolonged, high doses decrease the ability of the adrenal cortex to produce its own glucocorticoids
  2. Oral candidiasis
  3. Dysphonia (difficulty speaking; hoarseness) — drug can deposit in the oropharynx
  4. Growth suppression
  5. Bone loss
  6. Cataracts/glaucoma

AEs (Oral):

  1. Adrenal suppression
  2. Osteoporosis
  3. Hyperglycemia
  4. PUD
  5. Growth suppression
  6. Fluid retention

Med. safety concerns:

  1. IV or PO for acute exacerbation — delayed anti-inflammatory action (6-8 hours)
  2. Inhaled for chronic management — full response after 2-4 weeks of treatment

RN implications:

  1. Educate — PREVENTATIVE (does NOT abort acute attack); not PRN
  2. Proper ICS technique with spacer — inhale beta-2 agonist 5 min. before use to increase drug delivery; and rinse with water and gargle after use to prevent thrush
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11
Q

Anti-inflammatory Drug #2: Leukotriene Modifiers

A

Prototype: Monteleukast

MOA: Antagonist at leukotriene receptors; blocks activation by leukotrienes (enhance inflammatory response)

Therapeutic use:

  1. Chronic asthma
  2. COPD with reactive component

AEs (Generally well tolerated):

  1. Churg-Strauss syndrome: vasculitis commonly associated with skin and lung problems — when steroid dose is reduced
  2. Neuropsychiatric effects (rare)

RN implications:

  1. Give once daily, with or without food
  2. Ideal for pts that cannot use glucocorticoids
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12
Q

Bronchodilator #1: Short-Acting Beta-2 Agonist (SABA)

A

Prototype: Albuterol

MOA: Activates beta-2 receptors on smooth muscle cells of bronchial tree, causing muscular relaxation and bronchodilation (minimal beta-1 activity)

Therapeutic use:

  1. PRN to abort asthmatic exacerbation
  2. Prevent exercise-induced asthma attack
  3. COPD

AEs:

  1. Beta-1 (inhaler overuse): Tachycardia, arrhythmia, hyperglycemia
  2. Beta-2 (high doses): Tremors, hypokalemia (insulin shifts potassium into cells)
  3. Tolerance development with frequent use

RN implications (Education on MDI technique):

  1. Shake canister thoroughly
  2. Breathe out
  3. Place mouthpiece between lips
  4. Tilt head back
  5. Actuate inhaler and breathe slowly
  6. Hold for full breath (count to 10)
  7. Repeat after 1-5 min. if needed
  8. Clean mouthpiece
  9. Discard after used pre-specific number of doses
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13
Q

Bronchodilator #1: Long-Acting Beta-2 Agonist (LABA)

A

Prototype: Salmeterol; with Fluticasone

Therapeutic use: Long-term control (should not be used as mono-therapy)

AEs (same as SABAs):

  1. May increase risk of death when used as mono-therapy (refutable)
  2. Not used to stop an acute asthma attack

RN implications: Educate difference between use of rescue and controller inhalers

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14
Q

Bronchodilators #2: Methylxanthines

A

Prototype: Theophylline

MOA: Inhibits phosphodiesterase, and indirectly stimulates beta-1 and beta-2 receptors; bronchodilation and decreased inflammation

Therapeutic use:

  1. Aminophylline (more soluble) usually used IV in severe exacerbations
  2. Chronic asthma

Narrow therapeutic index — monitored by drug levels (5-15 mcg/ml is normal, >20 is associated with toxicity)

AEs:

  1. N/V and anorexia
  2. HA and dizziness
  3. CNS stimulation — caffeine-like symptoms (seizures, dysrhythmias, tachycardia in overdose >30)

Overdose management:

  1. Discontinue use
  2. Oral charcoal
  3. Treat dysrhythmias with verapamil or lidocaine

Individual variation: Liver disease and HF

DDIs:

  1. Decrease metabolism: Erythromycin & fluoroquinolone (antibiotics)
  2. Increase metabolism: Smoking & inducers

RN implications:

  1. Do not double following dose if missed
  2. Do not crush/chew ECT or SR formulation
  3. Report early S/S of toxicity — N/V/D, HA, and dizziness

**Older drug not used as frequently (ICS are much safer and effective); and not recommended at all for COPD

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15
Q

Bronchodilator #3: Short-Acting Anticholinergics (SAMAs)

A

Prototype: Ipratropium

MOA: Blocks muscarinic receptors on bronchial smooth muscle leading to bronchodilation

Therapeutic use:

  1. COPD
  2. Acute asthma exacerbation — SAMA added in conjunction with SABA (if severe)
  3. Onset: 15 min. (SABA onset is 2-5 min.), Duration: 4-6 hours

AEs:

  1. Dry mouth
  2. Pharynx irritation
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16
Q

Bronchodilator #3: Long-Acting Anticholinergics (LAMA)

A

Prototype: Tiotropium

MOA: Block muscarinic receptors on bronchial smooth muscle leading to bronchodilation

Therapeutic use:

  1. COPD
  2. Asthma (not first line)
  3. Onset: 30 min., Duration: 24 hours

AEs:

  1. Dry mouth
  2. Pharynx irritation

RN implication: Education on proper use

Safety issues: Capsules for inhalation device mistakenly admin. orally

17
Q

Pt Education

A

Meds.: Difference between long-term “controller” meds. and exacerbation “reliever” meds.

Pt factors:
1. Inhaler technique

  1. Identify and avoid trigger factors
  2. Monitor symptoms & PEFs
  3. Action plan for acute attacks