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Pharmacology Test 2 > Asthma & COPD > Flashcards

Asthma & COPD Flashcards

1
Q

What are the therapeutic targets?

A
  • smooth muscle dysfunction

- airway inflammation

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2
Q

2 broad categories for the treatment of asthma

A
  • bronchodilators

- anti-inflammatory agents

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3
Q

Bronchodilators

A

used to relieve acute symptoms and for control therapy; asthma attacks

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4
Q

Anti-inflammatory Agents

A

used to control or prevent symptoms

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5
Q

B2AR Agonists

2 kinds

A

SABAs: short-acting B2-selective agonists
LABAs: long-acting B2-selective agonists

Mainly treats SMOOTH MUSCLE DYSFUNCTION

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6
Q

Bronchodilators

3 types

A
  • epinephrine
  • ephedrine
  • isoproterenol
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7
Q

Epinephrine

A
  • bronchodilator

- non-selective adrenergic agonist

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8
Q

Ephedrine

A
  • bronchodilator
  • non-selective adrenergic agonist
  • releases NE
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9
Q

Isoproterenol

A
  • bronchodilator
  • non-selective beta agonist
  • not used as much anymore
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10
Q

SABAs

Short-Acting B2-Selective Agonists

A
  • little rationale for choice among SABAs
  • maximal bronchodilation is achieved in 15-30 minutes; persists 3-4 hours
  • used for relief of acute asthma symptoms and brochospasms

FAST

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11
Q

LABAs

Long-Acting B2-Selective Agonists

A
  • potent selective B2-agonists that are delivered by metered-dose or dry powder inhalers
  • duration of action is >_ 12 hours, due to high lipid solubility
  • NOT RECOMMEND AS MONOTHERAPY
  • – lack any anti-inflammatory actions
  • –WORK WELL WITH inhaled corticosteroids to improve asthma control

SLOW

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12
Q

Catch with LABAs

A

CAN NEVER BE GIVEN BY ITSELF

  • continued use causes airways to be refractory/non-responsive
  • NEED to pair with INHALED CORTICOSTEROIDS
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13
Q

Methylxanthines
(PDE inhibitors)
Mechanism

A
  • catalyze breakdown of PDE and blunt response

- relax smooth muscle b/c keep cAMP around by preventing breakdown

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14
Q

Methylxanthines

PDE inhibitors

A
  • relax bronchial smooth muscle
  • anti-inflammatory properties
  • reduce release of inflammatory mediators and cytokines
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15
Q

Theophylline

in treatment of asthma

A
  • Methylxanthines
  • effective for treatment of asthma
  • – must be CAREFULLY regulated
  • not widely used because of narrow TI; used when asthma is unresponsive to other drugs
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16
Q

Theophylline TI

A

Narrow TI

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17
Q

Which drug has a narrow TI

A

Theophylline

mathylxanthine

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18
Q

Muscarinic Receptor Antagonists
(SAMRA, LAMRA)
Mechanism

A
  • block M2R/M3R receptors
  • inhibits contraction from occurring
    (rather than inducing dilation)
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19
Q

Anti-muscarinics

A
  • not used much anymore
  • – B2-selective agonists preferred
  • has role in parasympathetic pathways
  • many times COMBINED with B2-agonist to enhance dilatory effects
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20
Q

Smooth Muscle Dysfunction

- leads to (4 things)

A

leads to:

  • bronchoconstriction
  • bronchial hyperreactivity
  • hyperplasia/hypertrophy
  • inflammatory mediator release
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21
Q

Airway Inflammation

A

leads to:

  • inflammatory cell infiltration/activation
  • mucosal edema
  • cellular proliferation
  • epithelial damage
  • basement membrane thickening
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22
Q

Anti-inflammatory agents

3 Types

A
  • leukotriene modifiers
  • corticosteroids
  • biologics
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23
Q

Leukotrienes in Asthma

A

potent bronchoconstrictors and are associated with

  • mucus hypersecretion
  • increased bronchial reactivity
  • mucosal edema
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24
Q

Leukotriene Modifiers

Strategy for Therapeutic Use

A
  • inhibit 5-lipoxygenase (first step)
  • – Zileuton
  • block binding of LTD4 to CysLT receptor (inhibits further down the pathway
  • – Zafirlukast
  • – Montelukast
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25
Q

Leukotriene Modifiers

Considerations for Use

A

ALL ORAL

- all have different mechanisms

26
Q

Zileuton

  • dosage
  • inhibits
A

Leukotriene Modifiers

  • dosed 2 or 4x/day
  • inhibits multiple CYPs
27
Q

Zafirlukast

A

Leukotriene Modifiers

  • dosed 2x/day
  • inhibits multiple CYPs
28
Q

Montelukast

A

Leukotriene Modifiers

  • dosed 1x/day
  • no hepatic toxicity and does NOT inhibit CYPS
  • most widely used
29
Q 
Corticosteroids
Therapeutic use in Asthma
- target
- effects
- how administered
A

target: glucocorticoid receptors
- inhibit eosinophilic influx
- inhibit airway mucosal inflammation
- reduce frequency of exacerbations if administered chronically
- potentiate effects of B2 agonists (make effective for longer)
- oral steroids for urgent, short-term treatment (can be given high dose oral if emergent)

30
Q

Corticosteroid Considerations

A
  • ** Aerosol Rx most effective at minimizing systemic adverse effects ***
  • lots of side effects when used long term
  • use as little as possible to get desired results
31
Q

Inhaled Corticosteroids

  • bioavailability
  • name 2
A
  • extremely low bioavailability due to extensive first-pass hepatic metabolism
  • – budesonide
  • – fluticasone
32
Q

Dual Controller Therapy in Asthma

A

ICS + LABA vs. increased-dose ICS

  • much safer than LABA alone (DO NOT DO)
  • helps mitigate patient being refractory to LABA or SABA
  • escalating doses of ICS detrimental

ICS + LABA vs ICS + LTRA
*** patient dependent

Asthma control in patients using ICS + LABA

  • dependent on severity
  • used for exacerbation treatment
33
Q

As disease gets more severe

A

add on additional therapies

- monoclonal antibodies only for those with severe asthma who is not responding to anything else

34
Q

Biologics

Used For

A

used for:

  • eosinophilic asthma
  • allergic eosinophilic inflammation
  • nonallergic eosinophilic inflammation
35
Q

Omalizumab: Anti-IgE therapy

A
  • mast cells BIG for allergic asthma: inhibit IgE & cut asthma off at the source (stops mast cell production)
  • – lowers plasma IgE to undetectable levels
  • injection
  • lowers amount of corticosteroids needed

* indicated for use in patients with a positive skin test or in vitro reactivity to perennial aeroallergen*

36
Q

Omalizumab Indication

A

Anti-IgE therapy

* indicated for use in patients with a positive skin test or in vitro reactivity to perennial aeroallergen*

37
Q

Anti-IL5 or IL-5 Receptor therapy

A
  • eosinophilic asthma
  • affects maturation and differentiation of eosinophils; can also effect basophils
  • injection
  • ** Indicated for use in patients with eosinophilic asthma
38
Q

Mepolizumab

A

Anti-IL5 or IL-5 Receptor therapy

39
Q

Reslizumab

A

Anti-IL5 or IL-5 Receptor therapy

40
Q

Benralizumab

A

Anti-IL5 or IL-5 Receptor therapy

41
Q

Anti-IL5 or IL-5 Receptor therapy Indication

A

*** Indicated for use in patients with eosinophilic asthma

42
Q

Anti-IL5 or IL-5 Receptor therapy
Benralizumab
Reslizumab
Mepolizumab

A

Mepolizumab & Reslizumab target CIRCULATING IL5

Benralizumab targets receptor level IL5

43
Q

Clinical Pharmacology of Mild to Moderate Asthma

A
  • bronchodilators are rapidly effective, safe, and inexpensive
  • inhaled SABA on “as needed” basis

Additional treatment is necessary if:

  • “rescue” therapy is required >2x/week
  • nocturnal symptoms occur >2x/month
  • FEV is <80% predicted
44
Q

Clinical Pharmacology of Refractory and Severe Asthma

A
  • ICS + LABA
  • – marketed 2 in one inhalers
  • if asthma is inadequately controlled– candidates for biologics
45
Q

COPD

A

Irreversible

  • common preventable and treatable disease
  • progressive with enhanced chronic inflammatory response in the airways and lungs to noxious particles or gases
  • mainly effects older people
  • symptoms worsen over time, with limited relief because so much destruction of lung
46
Q

Drugs used in COPD

A

Bronchodilators

  • anti-cholinergics
  • B2 agonists
47
Q

Clinical Pharmacology of COPD

A

inhaled bronchodilator and brochodilator-steroid combinations

48
Q

Tiotropium Bromide (Spiriva)

A

COPD

- long-acting muscarinic receptor antagonists (LAMRAs)

49
Q

Aclidinium Bromide (Tudorza)

A

COPD

- long-acting muscarinic receptor antagonists (LAMRAs)

50
Q

Fluticasone-Vilanterol (Breo)

A

COPD

- corticosteroid-LABA combination

51
Q

Budesonide-Formoterol (Symbicort)

A

COPD
- corticosteroid-LABA combination
Also used for asthma treatment

52
Q

Revefenacin (Yupelri)

A

COPD

- LAMRA that specifically TARGETS M3 MUSCARINIC RECEPTORS OVER M2

53
Q

Clinical Pharmacology of Acute COPD Symptoms

A
  • inhalation of SABA, a SAMRA, or SABA-SAMRA combination
54
Q

Clinical Pharmacology of Chronic COPD Symptoms

A
  • LAMRA or a Corticosteroid-LABA combination is indicated
55
Q

B2 Agonists

- naming

A
  • Albuterol, Salmeterol, Formoterol

OL

56
Q

Anti-muscarinics

- naming

A
  • Tiotropium Bromide, Aclidinium Bromide

IUM Bromide

57
Q

Leukotriene Receptor Antagonists

A
  • Zafirlukast, Montelukast

KAST

58
Q

Corticosteroids

A
  • Fluticasone, Beclomethasone, Budesonide

SONE

59
Q

Biologics

A
  • Omalizumab, Mepolizumab, Benralizumab

MAB

60
Q

budesonide

A

Inhaled corticosteroids

61
Q

fluticasone

A

Inhaled corticosteroids

Pharmacology Test 2 (8 decks)

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