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Pharmacology > COPD/Asthma > Flashcards

COPD/Asthma Flashcards

1
Q

ANS mediation of the airway

A

SNS - bronchodilates (B2 agonism)

PNS - bronchoconstrictions, increases mucous secretion (M3 agonism)

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2
Q

what are the SABAs?

A

short acting beta agonists

  • - buterol: ​albuterol, levabuterol, pirbuterol
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3
Q

what are the LABAs?

A
  • - terol:
    • ​salmeterol
    • formoterol
    • vilanterol (always given in combination with fluticasone or umeclidinium)
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4
Q

SABAS & LABAS MOA

A
  • the B2 receptor is a Gs GCRP
    • the drug binds B2 receptor
    • which activates membrane adenylate cyclase (AC)
    • active AC cleaves ATP into cAMP
    • cAMP –> + PKA
    • PKA opens K+ channel
    • K+ effluxes along [] gradient –> hyperpolarization of smooth muscle ells –> smooth muscle relaxation (bronchodilation)
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5
Q

PDE inhibitors - MOA

A
  • PDE breaks down cAMP
    • PDE inhibitors inhibit PDE, maintaining high cAMP in cell
      • cAMP –> PKA
      • PKA –> open K+ channels
      • K+ efflux –> SMC hyperpolarization –> bronchodilation
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6
Q

contrast the SABAs and LABAs in terms of

  • drug names
  • speed of onset
  • duration of action
  • available formulations
  • metabolism
A
  • SABA: - buterol
  • LABA: - terol
    • note that formoterol, though classified as a LABA, has a rapid onset of action (3 min)
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7
Q

formoterol is

what kind of drug?

has what onset & duration of action?

A

is a LABA, but acts like a SABA-LABA hybrid

  • long duration of action: 12-24 hours - like a LABA
  • rapid onset of action: < 5 min (3 min) - like a SABA

can be used as an for acute asthma relief (given with ICS) for children 12 yrs +

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8
Q

SABAs & LABAs- clinical uses

A

LABAS always given with ICS*

SABS & LABAS:

  • acute asthma relief
    • LABAS: fomoterol + ICS only (used 12+ children)
  • prevention of exercise induced bronchospasm
  • COPD

SABAS only: asthma exacerbation

LABAS only: asthma prevention & long term control

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9
Q

SABAs & LABAs AEs

A

both:

  • muscle tremor
  • nervousness, excitement
  • tachycardia / arrythmias / prolonged QT
  • HTN
  • hyperglycemia
  • hypokalemia
  • paradoxical bronchospasm

In LABAS: the paradoxical bronchospasm can cause death. co-administration with ICS prevents risk of these asthma-related deaths

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10
Q

SABA & LABA drug drug interactions

A
  • non-selective B-blockers (propanolol, carvedilol): counteraction of bronchodilatory effects
  • SABA & LABA with eachother: worsen AEs
  • successive doses: can cause tachyphylaxis - a diminshing to response to B2 agonists as a result of desensitization
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11
Q

SABAs & LABAs should be used in caution with what patients?

A
  • CV issues:
    • arrythmias
    • HF
    • HTN
  • diabetes (risk of exacerbating hyperglycemia)
  • hyperthyroidism (B2 agonism cause thyroid hyperactivity)
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12
Q

SAMA & LAMAs - name of drugs

A

short acting/long acting M3 muscarinic receptor antagonists

- tropium

  • SAMA: ipratropium
  • LAMA: tiotropium
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13
Q

SAMA/LAMA MOA

A
  • M3 receptors are Gq GCPRs
    • normally, ACh binds M3 receptor
    • membrane phospholipase C (PLC) becomes activated
    • PLC cleaves PIP2 into –> IP3
    • IP3 releases Ca++ –> bronchial smooth muscle contraction
      • –> bronchoconstriction
  • LAMA/SAMA blocks M3, blocking contraction
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14
Q

B2 agonists vs M3 blockers - efficacy in tx of asthma & COPD

A

asthma: B2 >>> M3

COPD: B2 < /= M3; M3 has less AEs

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15
Q

contrast SAMAs and LAMAs in terms of

  • onset
  • duration of action
  • formulations available
  • metabolism
  • clinical uses
A

both: COPD

SAMA: ipratropium

  • for severe acute asthma exacerbation (not for maintenance)
    • like SABAs
    • MUST be given w/ SABAS

LAMA: tiotropium

  • asthma maintanence tx in patients over >/= 6 years (not for exacebation)
    • like LABAs
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16
Q

SAMAS/LAMAS AEs

A
  • most common: (seen way more in LAMA > SAMA)
    • ​upper RTI
    • dry mouth (xerostemia)
    • pharyngitis
  • systemic (rare)
    • dizziness / blurred vision
    • tachy / HTN
    • abdominal pain
    • urinary retention
17
Q

what is tiotroprium?

A

a LAMA

18
Q

what is iptratropium?

A

a SAMA

19
Q

what is theophylline?

  • where is found?
  • how does it treat airway disease (MOA)?
  • PK?
  • clinical uses?
  • what should it NOT be used for?
  • AEs?
A
  • a methylxanthine
  • found in tea
  • MOA:
    • blocks PDE-3 (& PDE-4) inhibiting cAMP breakdown
    • blocks adenosine A-1 recptor inhibiting bronchoconstriction
  • PK:
    • IV/ oral
    • half life - highly variable (2-40 hrs)
      • ​depends on age, hepatic function, lung function
    • therapeutic index - narrow
  • clinical use:
    • as an add on for long term asthma control in pts > 12 yrs
    • COPD
  • NOT used for
    • acute asthma
    • children under 12
  • AEs:
    • cardiac arrythmyias / seizures
    • like other bronchodilatory drugs (B2, M3) - muscle tremor / tachy
    • abdominal discomfort / peptic ulcer
20
Q

what are the i_nhaled_ corticosteroids (ICS)?

A

- asone:

  • fluticasone
  • beclomethasone
  • mometasone
  • budesonide: formoterol + ICS*
21
Q

what are the oral corticosteroids?

A

prednisone

22
Q

what is budesonide?

A

formoterol (LABA) + ICS

23
Q

corticosteroids MOA

A
  • drugs cross the cell membrane then bind to nuclear receptor
    • they modulate transcription to decrease expression of proteins - phospholipase A2 (PLA2), COX-2, other pro-inflammatory cytokines- that are involved in the prostaglandin synthesis pathway, reducing production of:
      • prostaglandins
      • leukotrienes
        • this takes time - thus, steroids have slow onset of action
24
Q

ICS

  • clinical uses
  • onset of action
  • PK
  • AEs
A
  • clinical uses:
    • persistent asthma, either
        1. alone
        1. with LABAS
    • acute bronchospasm relief: in combo with formoterol (budesonide)
  • onset of action: 24 hrs (slow, due to MOA).
    • max effects really seen 1-2 weeks post starting
  • PK: poor bioavailability - low systemic effects
  • AEs:
    • RTIs: rhinitis / nasal congestion , sinus infection
    • oral candidiasis*
25
Q

what are ICS not first choice for?

A

COPD

26
Q

what are the leukotriene modifers and their MOAs/

A

two classes

  • Zileuton
    • lipoxygenase inhibitor
      • inhibits an enzyme that generates luekotrienes (in arachadonic acid pathway)
  • -lukast: montelukast, zariflukast
    • block leukotrienes from binding receptors
27
Q

leukotriene modifers - clinical uses

A
  • alternative therapy for mild persistent asthma
    • severe persistent: add with ICS
  • prevention of exercise induced asthma (as an alternative to SABAs)
  • AERD/NERD (aspirin induced/NSAID induced respiratory disease)
    • as an add on
    • as prevention
28
Q

explain the role of leukotriene inhibirs in the treatment of AERD/NERD

A

zileuton, - lukast

AERD/NERD: aspirin/nsaid induced respiriatory disease ​

  • taking aspirin blocks COX-1/COX-2 from converting AAs into prostaglandins
  • AA accumulates and is redirected to leukotriene synthesis pathway
  • excess leukotrienes cause bronchospasm / mucus secretion /nasal congestion in URT
  • inhibitors work by:
    • inhibit 5-lipooxygenase enzyme converting AA –> LTs (zilueton)
    • blocking LTs from their receptor (-lukast)
29
Q

montelukast

  • what type of drug
  • clinical uses
  • PK
    • onset
    • duration of action
    • dosing
  • AEs
A
  • leukotriene inhibitor
    • uses: persistent asthma (monotherpy in mild, + severe) / AERD (add on) / exercise induced asthma (as prevention)
  • PK: metabolized by CYP-3A4, 2C8, 2C9
  • dosing: oral once daily
    • _duration > 24 hr_s
  • AEs: serious neuropsychiatric events (behavior/mood changes)
30
Q

zafirlukast

  • what kind of drug
  • clinical uses
  • PK
    • dosing
    • duration of action
  • AEs
A
  • leukotriene inhibitor
    • clinical uses: uses: persistent asthma (monotherpy in mild, + severe) / AERD (add on) / exercise induced asthma (as prevention)
  • PK
    • dosing: oral 2x daily
      • ​duration of action: 12 hrs
  • AES: n/a
31
Q

zilueton

  • what kind of drug
  • clinical uses
  • PK
    • duration of action
    • dosing
  • AEs
A
  • leukotriene inhibitor (lipooxygenase inhibitor)
    • clinical uses: persistent asthma (monotherpy in mild, + severe) / AERD (add on) / exercise induced asthma (as prevention)
  • PK
    • dosing: oral 4x daily
  • AEs
    • headache
    • hepatotoxicity (elevates ALT)
32
Q

cromolyn

  • what kind of drug
  • MOA
  • clinical uses
A
  • mast cell stabilizer
    • MOA: inhibits degranulation of mast cells & response of esionophils to inhaled antigens
  • clinical uses:
    • prevention of
      • exercise indueed asthma
      • allergen indued asthma
    • mild persistent asthma (as an alternative)
  • AEs
    • transient cough
    • mild wheez
    • bronchospasm after cough (rare)
33
Q

what are leukotriene inhibitors not to be used for?

A

acute asthma exacerbation

34
Q

what can be given to relieve bronchospasm secondary to use of cromolyn?

A

SABAs (- buterol)

35
Q

omalizumab

  • what kind of drug?
  • MOA?
  • clinical uses?
  • AEs?
A
  • a biologic
  • MOA: neutralizes IgE (is an anti IgE antibody)
  • cinical uses: as an on add on for maintence of severe allergic asthma with elevated IgE in patients that
    • =/ > 6 yrs old
    • are not responding to ICS + LABA
  • AEs
    • anaphylaxis
36
Q

reslizumab, mepoliaumab, benralizumab

  • what kind of drug?
  • MOA?
  • clinical uses
A
  • biologics
  • MOA: inhibit IL-5
    • reslinzumab, mepolizumab = anti- IL-5 antibodies
    • benralizumab = anti-IL-5 receptor antibodies
  • uses: add on maintenane treatment of severe asthma in adults with an esionophillic phenotype
  • AEs
    • reslizumab = anaphylaxis
    • benralizumab = antibody development
37
Q

duplimumab

  • what kind of drug?
  • MOA?
  • clinical uses
  • AE
A
  • biologic
  • inhibits IL-4Aa (IL4-4Ra antagonist)
  • clinical uses:
    • as add on maintenance treatment of moderate and severe asthma in patients with an eiosonophillic phenotype
    • in severe, corticosteroid dependent asthma
  • AE: antibody development
38
Q

what are the best medications to use for prevention of exercise induced bronchoconstriction?

A

given as prophylaxis:

  • SABAS (albuterol)
    • ​given 5-30 minutes before exercise
  • montelukast
    • give 2 hrs before exercise
    • last 24 hours
    • useful in young children**

Pharmacology (4 decks)

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