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Pharmacology Semester II > Exam III Asthma COPD > Flashcards

Exam III Asthma COPD Flashcards

1
Q

Asthma VS COPD

A

Asthma

  • Allergen based irritation
  • Smooth muscle thickening-> bronchoconstriction
  • Episodic SOB, wheeze, cough, chest tightness
  • Often reversible lung fxn w/ meds

COPD

  • Inflammation-based irritation
  • Cellular damage by external irritants
  • Chronic cough, sputum production, Dyspnea on Exertion
  • Often irreversible lung fxn w/ meds
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2
Q

Treatment approaches for Asthma

A

Short-acting B agonists (SABA)

Long-acting B agonists (LABA)

Inhaled corticosteroids (ICS) – oral too

Mast cell stabilizers

Leukotriene antagonists

Methylxanthine derivatives

Immunotherapy

Long acting antimuscarinics (LAMA)

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3
Q

Treatment approaches for COPD

A

Smoking cessation

Short-acting B agonists (SABA)

Long-acting B agonists (LABA)

Short-acting antimuscarinics (SAMA)

Long-acting antimuscarinics (LAMA)

Inhaled corticosteroids (ICS) – oral too

Methylxanthine derivatives

Phosphodiesterase 4 (PDE-4) inhibitors

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4
Q

Notes on Delivery systems

A

Aerosolized delivery systems preferred

-+: small particles size, delivered directly to leading to reduced systemic exposure, doses usually lower, usually quicker onset

–: requires proper technique for effective therapy, expensive, variability in devices that require different techniques

Multiple delivery systems including metered dose inhaler (MDI), dry powder inhaler (DPI), soft mist inhaler, nebulizer.

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5
Q

Aerosolized delivery systems - Metered dose inhaler (MDI)

A

Advantages

  • Small, compact, portable, Easy to use (<1 minute)
  • Can be used with spacer
  • No drug prep

Disadvantages

  • Needs proper technique / coordination with breath (requires breath hold)
  • Expensive
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6
Q

Aerosolized delivery systems – Dry powder inhaler (DPI)

A

Advantages

  • Small, compact, portable
  • Easy to use (<1 minute)
  • Usually cheaper vs MDI
  • Less coordination needed

Disadvantages

  • PT must prepare the dose
  • Requires fast, deep inhalation (requires breath hold)
  • Moisture sensitive
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7
Q

Aerosolized delivery systems – Soft Mist inhaler

A

Advantages

  • Compact, portable
  • Multi-dose device
  • High lung deposition
  • Does not contain propellants

Disadvantages

  • Complicated process for first dose
  • Slow moving mist
  • Cannot use a spacer
  • Expensive
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8
Q

Aerosolized delivery systems – Nebulizer

A

Advantages

  • Minimal technique required
  • PT is not required to Hold breath

Disadvantage

  • Expensive, requires dose prep
  • Bulky (not portable)
  • Administration time 5-15 minutes
  • Needs a power source
  • Cleaning needed
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9
Q

Considerations for device selection

A

PT related factors

-Age, physical and cognitive abilities

PT preference

Availability of the drug

-Combination products

Convenience

-Portability, maintenance, cleaning

Cost / reimbursement

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10
Q

Bronchodilators

A

SABA

LABA

Muscarinic antagonists

Methylxanthine derivatives

PDE-4 inhibitors

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11
Q

Short-Acting B2 Agonists (SABA)

A

MOA: Stimulate adenylyl cyclase at B2. Inc cAMp. Dilation

Selective for B2

Drug of choice for Acute Asthma Attacks and exercise-induced Asthma

  • Onset 5 minutes
  • Duration 3-4 Hours

Route: Inhalation

Well tolerated for PRN use

ADR:

  • Mouth Irritation and Cough
  • At high doses

–Skeletal muscle tremor

– Tachycardia/palpations

–Arrhythmia

–Tolerance with excessive use

—Decreased responsiveness and decrease in number of B receptors

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12
Q

SABA Agents

A

Albuterol

-Racemic mixture of (S)-albuterol and (R)-albuterol

–(R)-albuterol (levalbuterol) is therapeutically active

–(S)-albuterol is clinically inert but has unwanted side effects

Levalbuterol

  • Developed to minimize side effects
  • In acute asthma (&COPD) attacks, no sig Diff in efficacy
  • No Diff in HR
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13
Q

Long Acting B2 Agonists (LABA)

A

MOA: Same as SABA

  • Slower onset (~30 min)
  • Longer duration (12-24 Hrs)

Not for rescue therapy

Cannot be used as MONOTHERAPY

-Ok in COPD

ADEs same as SABA

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14
Q

LABA Agents

A

Long-acting

  • Salmeterol
  • Formoterol

Ultra-long acting

  • Indacaterol
  • Olodaterol
  • Vilanterol
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15
Q

Antimuscarinics

A

MoA: Competitively block muscarinic receptors (M1, M2, M3) and the effects of ACh in airway-> Prevent vasoconstriction mediated by vagal discharge

No effects on Chronic inflammation

Bronchodilation effect last longer than B agonists

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16
Q

Antimuscarinic ADEs

A

Minimally absorbed, generally well tolerated

Potential for:

  • Dry mouth, eyes
  • Bitter, metallic taste
  • Constipation
  • Urinary retention

No tremors or arrhythmias

17
Q

Antimuscarinic Agents

A

Ipratropium

Tiotropium

Aclidinium

Umeclidinium

Glycopyrolate

18
Q

Methylxanthine derivative

A

Theophylline – oral

MoA: (1) Non-selectively inhibits phosphodiesterase (PDE)-> increases cAMP-> broncodilation (2) Block adenosine receptors-> bronchodilation

Duration: ~12 Hrs

Requires high concentration

Narrow therapeutic index

19
Q

Theophylline

A

Metabolized via CYP450, 1A2 enzyme system

-Many DDIs – febuxostat, bupropion, carbamazepine, macrolide antibiotics, etc.

Clearance mediated by age, smoking status, and other drugs

Requires monitor

-Therapeutic range 10-20 mcg/mL

–Levels correlate with efficacy

Smoking will reduce drug levels as smoking is a 1A2 inducer.

20
Q

Theophylline ADEs

A

GI distress (enhanced gastric acid secretion)

Tremor

Insomnia

In overdose, severe nausea and vomiting, hypotension, agitation, arrhythmias, cardiac arrest, seizures

21
Q

PDE-4 inhibitors

A

Roflumilast – oral

MoA: Not fully elucidates; selectively inhibits PDE-4-> increases cAMP-> bronchodilation

Used for severe or very severe COPD

-should be given in combination with at least 1 other long-acting bronchodilator for COPD

Given by mouth once daily

-Duration of action > 10-20 Hrs

22
Q

Roflumilast ADE/DDI

A

Partially metabolized by CYP450 3A4

-DDIs with rifampin, phenobarbital, phenytoin, carbamazepine

ADEs:

  • Diarrhea, nausea, vomiting, abdominal pain, HA, dyspepsia
  • Psychiatric events
  • Weight loss
23
Q

Corticosteroids

A

MoA: Binds glucocorticoid receptor to:

  • Inhibit inflammatory cell migration/activation
  • Inhibit cytokine and mediator release
  • Up regulate B2 receptors
  • Inhibit IgE synthesis

Drug of choice for persistent asthma

-Prophylaxis

May take 4-6 weeks for effect

Multiple dosing

Do not abruptly D/C – Taper

24
Q

Corticosteroid (inhaled) ADEs

A

Inhaled

Thrush (oral candidiasis)

-Counsel PTs to rinse mouth after use

Dysphonia

Sore throat

Cough

25
Q

Corticosteroid (oral/IV) ADEs

A

Adrenal suppression

Cushing Syndrome

Growth retardation

Osteoporosis

Glucose intolerance

Infection risk

Mood changes

Weight gain

Edema

26
Q

Corticosteroid agents

A

Inhaled

  • Beclomethasone
  • Budesonide
  • Fluticasone propionate
  • Fluticasone furoate
  • Mometasone
  • Flunisolide
  • Ciclesonide

Oral/IV

  • Prednisone
  • Prednisolone
  • Methylprednisolone
  • Hydrocortisone
27
Q

Corticosteroids in kids

A

Potential growth stunting in children

Still preferred DOC (drug of choice) in children

28
Q

Leukotriene antagonists – Lipoxygenase inhibitor

A

Zileuton – Oral

MoA: Inhibits actions of 5-lipoxygenase to inhibit the synthesis of Leukotrienes

ADEs:

HA

Insomnia

Somnolence

GI Upset

Hepatotoxicity

-Do not administer if LFTs >3x ULN

-Females > 65 Yrs of age and those with preexisting LFT elevations are highest-risk -> monitor!

29
Q

Leukotriene Receptor Antagonists

A

Montelukast - Oral

Zafirlukast - Oral

MOA: Competitively block actions of Leukotrienes at the LTD receptor

Can be used for asthma, allergic symptoms, exercise-induced bronchospasm, urticaria

30
Q

Leukotriene receptor antagonists

A

DDIs:

Zafirlukast + warfarin -> may increase risk of bleed

ADEs:

Generally well tolerated

HA

Hepatoxicity (Zafirlukast)

Neuropsychiatric events

-Abnormal Dreams, hostility, aggression, suicidality, agitation, hallucinations, etc.

–2008: Reports to FDA MedWatch

–2009: Labeling change on all leukotrienes

31
Q

Mast cell stabilizers

A

Indicated for mild asthma cases

-Not used much in clin practice

Not for rescue use

Require multiple daily doses

Clin improvement may take 2-6 weeks

Well tolerated

-Mild throat irritation, cough abnormal taste

No DDIs

32
Q

Immunotherapy - Anti IgE agents

A

Omalizumab

MOA: Monoclonal IgE antibody -> inhibits binding of IgE to surface of mast cells & basophils -> inhibits release of inflammatory mediators

Indicated for allergic asthma not relieved with corticosteroid therapy

-Must have evidence of allergic sensitization

Dose based on IgE levels and body weight

-Sub Q injection every 2-4 weeks

33
Q

Omalizumab - ADEs/DDIs

A

Indicated for > 12 Y/O

Clin improvement delayed - Takes up to 12 weeks

ADEs:

  • Injection site RXN (45%)
  • Anaphylaxis -> 1.5-2 hours post-dose (watch for RXN)
  • Arthralgia, HA
  • Pharyngitis, sinusitis
  • Malignancies?

DDI-None

34
Q

IL-5 Antagonists

A

Mepolizumab

Reslizumab

35
Q

IL-5 MOA

A

Humanized IL-5 monoclonal antibody antagonist to reduce the amount of circulating eosinophils

Used for the maintenance of severe asthma for PTs who continue to have attacks despite therapy

Admin:

SubQ (mepolizumab)

IV (reslizumab)

q4w by HCP

36
Q

IL-5 ADEs

A

Not recommended monotherapy

-Must be > 18 Y/O with eosinophilic phenotype

ADEs:

-Injection site RXN

-HA

-Hypersensitivity RXNs ->Anaphylaxis

-Malignancy?

-Muscle/Face pain

Pharmacology Semester II (21 decks)

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