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Asthma and COPD Flashcards

1
Q

Differences between Asthma and COPD

  • Disease of?
  • Reduced airway via?
  • Inflammatory mediators?
  • Symptoms?
  • Reversible or Irreversible?
A
  • Asthma
    • inflammation + allergen exposure
    • reduced airway via smooth muscle thickening that → bronchoconstriction
    • Inflamm mediators: Eosinophils, basophils, mast cells, CD4 cells, IL-5
    • symptoms: episodic SOB, wheeze, cough, chest tightness
    • Reversible
  • COPD
    • ​inflammation + irritation
    • reduced airway via cellular damage by external irritants
    • Inflamm mediators: neutrophils, macropages, CD8 cells
    • Symptoms: chronic cough, excessive sputum, production
    • Irreversible
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2
Q

Pathophysiology of Asthma

A
  • IgE production in response to trigger
  • Binds to mast cells
  • Upon next exposure mast cells degranulate and leake things like leukotrienes and histamine
  • 3-6 hrs later more sustained bronchoconstriction mediated by cytokines
    • late reponse= increased sensitivity to stimuli
      • inhaled GC’s
      • for early phase=SABA’s
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3
Q

Pathophysiology of COPD

A
  • irritants cause inflammatory cells to accumulate in the lungs
  • triggers release of inflammatory mediators
    • TNF-alpha, IL-6, IL-8 and fibrinogen (airway inflammation)
  • tissue damage and systemic effects
    • chronic inflammation leads to fibrosis, alveolar damage, and mucus hypersecretion (structural remodeling + mucociliary dysfunction)
      • loss of alveolar elasticity =poor O2 exhange
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4
Q

What is the number one cause of COPD and what is the # 1 treatment for COPD?

What does COPD meds cure the disease?

A
  • smoking
    • smoking cessation leads to increase lung function
  • No they only treat symptoms
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5
Q

What is the preferred method of treatment for Asthma and COPD? Pros and Cons

A
  • aeroslized delivery system pro’s
    • medication gets delivered directly to site (reduces systemic exposure)
    • lower dose & quicker onset
  • con’s
    • requires proper technique (variability in diff. device techniques)
    • exspensive
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6
Q

Aerosilzed Delivery Systems

  • What devices do we have available?
  • Advantages/ Disadvantages
A

Examples

  • Metered dose inhaler (MDI)
    • Small, easy to use, can be used with spacer
      • Needs proper technique/coordination with breath being held
  • Dry powder inhalers (DPI)
    • small, compact, cheaper, less coordination needed
      • patient must prepare the dose, fast deep inhalation, moisture sensitive
  • Soft mist inhalers
    • high lung depostion-does not contain propellants
      • Complicated process for first dose , no spacer
  • Nebulizer
    • minimal technique, pt doesn’t need to hold breath
      • $$$, requires dose preparation, bulky (not portable), 5-15 min administration, power source
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7
Q

What Considerations should you keep in mind when selecting a device for your patient? (5 things)

A
  • Patient-related factors
    • age, physical and cognitive abilities
  • patient preference
  • availability of the drug
  • convience
    • portability
  • cost/ reimburstment
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8
Q

Short Acting Beta-2 Agonists (SABA)

  1. MOA?
  2. Selective for what receptor?
  3. DOC for?
  4. Onset of action and duration of action?
  5. Administered?
A
  1. MOA: stimulate adenylyl cyclase at beta-2 receptor →increase in cAMP in bronchial smooth muscle→bronchodilation
  2. Selective for beta-2 receptor
  3. DOC for ACUTE ASTHMA ATTACKS and exercise induced asthma
  4. Onset: 5 min – Duration: 3-4 hrs
  5. administered via inhalation
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9
Q
  1. What SABA agents do we have available?
  2. ADR’s with PRN use and long term?
A
  1. Albuterol and Levalbuterol
  2. )
  • PRN use
    • well tolerated maybe mouth irritation or cough
  • Long term
    • muscle tremor
    • tachycardia
    • build up a tolerance to medication ( due to downregulation of beta receptors)
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10
Q

Albuterol vs. levalbuterol

A
  • albuterol is mixutre of (s)- albuterol and (r)-albuterol (levalbuterol)
    • (r)-albuterol is theraputically active
      • developed to minimize side effects
    • (s) is clinically inert w/ cardiac side effects
  • in acute asthma and COPD attacks no sig difference b/w two- and no difference in HR
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11
Q
  1. What longacting and ultra long acting agents (LABA’s) do we have available?
  2. MOA?
  3. Indication?
  4. Always use LABA w/ ?
  5. ADR’s?
A

1.)

  • long acting (LABA)
    • salmeterol
    • formoterol
  • ultra long acting (LABA)
    • indacaterol
    • olodaterol
    • vilanterol

2.) same as SABA- MOA: stimulate adenylyl cyclaseat beta-2 receptor →increase in cAMPin bronchial smooth muscle→bronchodilation

3&4.)

  • used in COPD-always use LABA with inhaled corticosteroid
    • NOT USED as monotherapy in asthma
    • Not for rescue therapy

5.) same as SABA

  • PRN use
    • well tolerated maybe mouth irritation or cough
  • Long term
    • muscle tremor
    • tachycardia
    • build up a tolerance to medication ( due to downregulation of beta receptors)
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12
Q
  1. What antimuscarinic agents are appropiate to use? WHAT IS IT THE DOC FOR?
  2. Which one is short acting?
  3. MOA?
  4. anti-muscarinic and chronic inflammation effects
  5. How long does the bronchodialating effects last?
A

1.) DOC for COPD

  • Ipratropium
    • short acting (2.)
  • Tiotropium
  • Aclidinium
  • Umeclidinium
  • Glycopyrolate
  1. ) blocks muscarinic receptors in airway- ACh cant bind- prevents vasoconstriction
  2. ) no effects on chronic inflammation
  3. ) bronchodilating effects last longer than beta-agonists
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13
Q
  • ADR’s for Antimuscarinics?
    • these drugs are good for what patients?
A
  • dry mouth/eyes
  • bitter, metallic taste
  • constipation
  • uriniary retention
  • NO tremors or arrhythmias
    • DOC for elderly- b/c med is minimally absorbed, generally well tolerated
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14
Q

Methylxanthine derivative

  1. Agent available?
  2. MOA?
  3. Duration of action?
A
  1. Theophylline-oral
  2. Dual MOA:
    • non selectively inhibits PDE→ increase in cAMP→bronchodilation
    • blocks adenosine receptors →bronchodilation
  3. Duration of action 12 hours
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15
Q

Methylxanthine derivative

  1. Agent available?
  2. DDI’s?
  3. Clearence mediated by what three things
  4. Monitoring?
A
  1. Theophylline
  2. Many DDI’s via CYP 1A2
  3. clearance mediated by age, smoking status, and other drugs
  4. yes need to monitor due to narrow theraputic index
    • if you make the slightest dose change you are at risk for toxicity
    • requires higher conc. esp in adults
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16
Q

What woud happen if Theophylline is given to a smoker?

What would happen overtime if patient stopped smoking and remained on theophylline?

A
  • Theophylline is a CYP 1A2 substrate
    • smoking is an inducer of CYP 1A2
      • will cause theophylline to be metabolized faster
        • dose will be ineffective and u need to increase it
  • If patient stopped smoking but stayed on theophylline then..
    • dose of drug needs to be REDUCED
17
Q

What are the ADR’s of Theophylline?

What are the ADR’s of Theophylline overdose?

A
  • GI distress
    • due to enhanced gastric secretion (b/c of increase in cAMP)
  • Tremor
  • Insomnia
  • In overdose
    • severe n/v
    • hypotension
    • cardiac arrest
18
Q

Roflumilast

  1. Class?
  2. MOA?
  3. Indication?
  4. Administration?
A

Roflumilast

  1. PDE-4 inhibitors
  2. MOA: selectively inhibits PDE-4 → increase cAMP → bronchodilation
  3. Indication: severe COPD (used last-roflumiLAST)
  4. Should be given with at least one LABA-oral once daily
    • duration of action > 10-20 hours
19
Q

Roflumilast (PDE-4 inhibitor)

  • ADR’s?
  • DDI’s?
A

Roflumilast (PDE-4 inhibitor)

  • ADR’s
    • psychiatric events- need to screen prior to use
    • weight loss
  • DDI’s with CYP 3A4
20
Q

Corticosteriods?

  1. MOA?
  2. DOC?
  3. Onset of action?
  4. Taper?
A
  1. MOA: binds to glucocorticoid receptor to
    • inhibits cell inflammation/migration
    • inhibits cytokine and inflammatory mediators release
    • up-regulate Beta-2 receptors
    • Inhibit IgE
  2. DOC for persistent asthma-prophylaxsis
  3. Onset of action: 4-6 weeks
  4. need taper don’t abruptly stop
21
Q

Corticosteroids

  • Inhaled vs. IV/ORAL
    • agents available
A
  • Inhaled
    • Beclomethasone
    • Budesonide
    • Fluticasone propionate (flovent)
    • Fluticasone furoate
    • Mometasone
    • Flunisolide
    • Ciclesonide
  • Oral/IV
    • Prednisone
    • Prednisolone
    • Methylprenisolone
    • Hydrocortisone
22
Q

Corticosteroids

  • Inhaled vs. IV/ORAL
    • ADR’s?
A
  • Inhaled
    • Thrush
      • counsel patients to rinse mouth after use
  • Oral
    • chronic use
      • cushings syndrome
      • infection risk
      • adrenal suppression
    • short term
      • mood changes
      • weight gain
      • edema
23
Q
  1. What can you do for a patient that no longer uses advair b/c of recurrent thrush and nystatin is giving her no relief?
  2. What inhaler causes thrush the most? examples?
A
  • Ensure she is using proper technique of her advair
    • rinsing mouth after each use
  • Mouth piece is cleaned
  • consider swtiching to a spacer
    • reduces medication deposited in mouth
  • Consider risning with alcohol based mouthwash
  • Try different steroid

2.)

  • DPI inhaler- dry powder inhaler
    • Diskus -advair
    • Handihaler
    • Twisthaler
    • Ellipta
    • Pressair
    • Flexhaler
24
Q
  1. Example of Soft mist inhaler?
  2. What cortico-steroid is the safest in pregnancy?
A
  1. Respimat
  2. Inhaled corticosteroid-Budesonide
25
Q
  1. What is the DOC in children for asthma?
  2. What are the potentional harms of this drug?
A
  1. Corticosteroids
  2. Potentional growth stunting in children
26
Q

Zileuton

  1. Class?
  2. MOA?
  3. ADR?
  4. C/I’s?
A
  1. Lipoxygenase inhibitor-adjunct asthma treatment
  2. MOA: Inhibits actions of 5-lipooxygenase to inhibit the synthesis of leukotrienes
  3. ADR:Hepatotoxicity
  4. C/I:
  • ​don’t give if LFT’s greater than 3x ULN
  • Females >65
    • those with pre-exsiting LFT elevation
27
Q
  1. What Leukotriene receptor antagonist do we have?
  2. MOA?
  3. Indication?
  4. DDI’s?
  5. ADR’s?
A
  1. Montelukast and Zafirlukast
  2. MOA: blocks actions of leukotrienes at the LTD4 receptor
  3. used for asthma, allergic symptoms (urticaria)
    • esp for allergic symptoms with no relief for antihistamine
  4. Zafirlukast + warfarin → increase risk of bleed
    • Generally well tolerated
    • Neuropsychiatric events
    • Hepatoxicity (Zafirlukast)
28
Q

Mast Cell Stabilizers

  1. Agents available?
  2. MOA?
  3. Indicaiton?
  4. Onset of action
A
  1. Cromolyn sodium and Nedocromil sodium
  2. MOA: block influx of Ca → prevents mast cell degranulation (stabilized)
  3. Mild cases of asthma but not DOC-NOT FOR RESCUSE SYMPTOMS
  4. 2-6 weeks
29
Q

Omalizumab

  1. Class?
  2. MOA?
  3. Indication? how old do you have to be?
  4. formulation? onset of action?
  5. ADR’s? why is this ADR important
A
  1. Anti-IgE agents
  2. Monoclonal IgE antibody- inhibits fusion of IgE to mast cell → no release of inflamm mediators
  3. Allergic asthma not relieved with corticosteriod therapy-MUST BE GREATER THAN 12 years of age
  4. subcutaneous injection (based on IgE and weight)- takes up to 12 weeks to work
  5. ADR’s -anaphylaxsis (1.5-2 hrs post dose) so you need to monitor in office
30
Q
  1. What IL-5 agents do we have?
  2. MOA?
  3. Indication? requirments?
  4. ADR?
A

1.)

  • Mepolizumab
  • Reslizumab

2.) MOA: antagonize IL-5 to reduce circulating eosinophils

3.) maintenance of severe asthma- MUST BE GREATER THAN 18 with eosinophilic phenotype

4.) Hypersensitivity rxn- can cause anaphylaxsis

***pt needs to stay for first dose

Pharm II (12 decks)

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