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Advanced Pharm > Respiratory Agents > Flashcards

Respiratory Agents Flashcards

1
Q

How do the SNS and PNS affect the pulmonary system?

A
  • SNS:
    • B2 adrenoceptors cause relaxation/dilation of smooth muscles in blood vessels, bronchi, the uterus, bladder, and other organs
    • done by increasing cAMP
  • PNS
    • stimulation of the vagus nerve leads to bronchoconstriction and increase in mucus secretion
    • M3 receptors are most important pharmacologically
      • found on bronchial smooth muscle
      • mediate bronchoconstriction by activating IP3 which increases intracellular Ca
      • mediates mucus secretion
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2
Q

How do non adrenergic, non cholinergic nerves affect the pulmonary system?

A
  • relax airway smooth muscle by releasing NO and vasoactive intestinal peptide (VIP)
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3
Q

What different parts of the asthma disease process do the drugs effect? (flow chart)

B2 agonists

glucocorticoids

A
  • B2- reverse the bronchospasm caused by the histamines and prostaglandins released
  • glucocorticoids- inhibit the chronic airway inflammation and hyperactivity
  • **It is important to address both the inflammation and bronchoconstrictive aspects of the disease
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4
Q

What are the advantages of inhalation drug therapy?

What are the different delivery methods (3)?

A
  • Advantages:
    • high local concentration of the drug in the bronchial tree, where it is needed
      • enhanced pulmonary effects
      • minimized systemic effects
      • drug onset is rapid, useful for acute attacks
  • delivery methods:
    • MDI- only 10% makes it into lungs
    • dry powder inhalers (DPIs)
    • Nebulizers
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5
Q

What are the anti-inflammatory drugs used to treat asthma?

how often are they taken?

which one is most effective?

A
  • Taken daily for long-term control
    • inhaled corticosteroids (glucocorticoids)
      • most effective preventative treatment for asthma
    • Cromolyns
    • leukotriene inhibitors
    • Anti- IgE antibodies
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6
Q

Glucocorticoids

MOA?

target?

what effect does it have?

A
  • MOA- suppress inflammation by altering genetic transcription
  • target: glucocorticoid receptor alpha in cytoplasm of airway epithelial cells
    • increases transcriptions of genes for B2 receptors and responsiveness
    • increases trans of genes for anti-inflammatory proteins
    • decreases trans of genes for pro-inflammatory proteins
    • induces apoptosis in inflammatory cells (eosinophils, TH2, lymphocytes)
    • indirect inhibition of mast cells over time
    • reverses bronchial hyperreactivity
    • used as suppressive therapy, does not change the progression of the disease NOT A CURE
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7
Q

What are the different corticosteroids that may be used to help with asthma?

inhaled

IV

PO

A
  • Inhaled:
    • Budesonide (MDI, neb, or DPI)
    • Beclomethasone
    • Triamcinolone
    • Fluticasone
  • IV (status asthmaticus)
    • Hydrocortisone
    • Methylprednisolone
  • PO (acute exacerbation, but limit time course)
    • Prednisone
    • Prednisolone
  • *These patients may need stress dose steroids, but NOT if the steroids they use are inhaled
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8
Q

How much of any MDI reaches the airway?

A

10-20%

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9
Q

What are some side effects of inhaled corticosteroids?

A
  • Adrenal suppression (mild compared with IV/PO routes)
  • oropharyngeal candidiasis
  • Hoarseness
  • Delayed growth in children
  • Osteopenia/osteoporosis
    • encourage vit D, Ca, and weight bearing exercise
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10
Q

What are side effects of IV/PO systemic corticosteroids?

A
  • Minor when taken acutely (<10 days), can be severe if used long-term
    • myopathy/weakness
    • adrenal suppression (taper, do not stop suddenly)
    • increased infection risk
    • suppression of growth and development
    • PUD- increased risk with NSAIDS
    • weight gain, edema, hypokalemia
    • hyperglycemia- may need to increase insulin dose in DM
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11
Q

Cromolyn

MOA?

Principle use?

administration?

A
  • MOA: Stabilizes pulmonary mast cells
    • inhibits antigen-induced release of histamine and the release of inflammatory mediators from eosinophils, neutrophils, monocytes, etc…
    • inhibits immediate allergic response to an antigen but not the allergic response once it has been activated
  • Principle use: Prophylactic therapy of bronchial asthma
    • can help prevent exercise induced bronchospasm
    • does not releive an allergic response after initiation- not a rescue inhaler
  • Administration via inhalation- 8-10% enters systemic circulation, poor oral absorption
    • taken 4 times daily
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12
Q

What are the SE of Cromolyn?

Route?

A
  • Side effects are rare and it is the safest of all anti-asthma medications
    • cough and/or bronchospasm
    • Laryngeal edema
    • angioedema
    • urticaria
    • anaphylaxis
  • route: Inhaled
    • MDI or neb
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13
Q

What are Leukotrienes?

A
  • Leukotrienes are made from Arachidonic Acid (AA) when inflammatory cells are activated
  • C4, D4, and E4 promote bronchoconstriction, eosinophil infiltration, mucus production, and airway edema
  • Inhibitors reduce these effects
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14
Q

What are the Leukotriene inhibitors?

How effective are they?

A
  • Zileuton (Zyflo)
  • Zafirlukast (Accolate)
  • Montelukast (Singulair)
  • efficacy:
    • Less effective than inhaled glucocorticoids
    • not effective in treatement of acute attacks
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15
Q

Zileuton

MOA?

pharmacokinetics?

What do you have to monitor?

SE?

A
  • MOA- lipoxygenase inhibitor which blocks the biosynthesis of leukotrienes from AA
    • produces bronchodilation, improves asthma symptoms, shows long-term improvement in PFT
  • Pharmacokinetics:
    • low bioavailability, low potency
    • Hepatotoxic- monitor LFTs once/month early in tx
  • SE:
    • neuropsychiatric issues- depression, anxiety, agitation, hallucinations, suicidal thinking and behavior
    • CYP450 interactions
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16
Q

Montelukast (Singulair)

MOA?

Uses?

effects?

PB?

Metab?

A
  • MOA- Leukotriene receptor antagonist that blocks the mechanism of bronchoconstriction and smooth muscle effects
    • prevents leukotrienes from binding to leukotriene-1 receptor
  • Uses
    • used to treat asthma in pts <1 year
    • prevents exercise induced bronchospasm >15 years old
    • treats allergic rhinitis
  • Effects:
    • improve bronchial tone, pulmonary function, and asthma symptoms
    • SE similar to placebo
  • 99% PB
  • Undergoes extensive metabolism by CYP450
    • minimal drug interactions
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17
Q

Omalizumab

Class?

target/MOA?

When is it used?

A
  • Anti-IgE antibody- Humanized mouse monoclonal antibody
  • Target: Prominence of IgE mediated allergenic responses in asthma
    • binds to IgE in the blood inactivating it (IgE levels decrease for a year)
    • decreased amt of circulating IgE prevents binding of IgE to mast cells
    • Down regulation of receptors d/t less circulating IgE
  • Only administered to pts who fail all other treatments because there are SO many SEs
18
Q

Omalizumab

Cost?

SE?

A
  • $10,000 per year
  • SQ, pt must be monitored at hospital, can’t be given at home
  • 1/2 life of 26 days
  • SE:
    • injection site reactions
    • viral infection
    • URI and sinusitis
    • pharyngitis
    • H/A
    • CV complications- get an EKG
    • possible increased risk of cancer
  • May trigger anaphylaxis
    • monitor for 2 hours after 1st 3 doses
    • monitor for 30 minutes after all later doses
19
Q

How do bronchodilators treat asthma?

What are the bronchodilators used?

A
  • Provide symptomatic relief but do not alter the underlying disease process (inflammation)
    • usually a pt requiring a bronchodilator will also be on glucocorticoid treatment for inflammation
  • Bronchodilators:
    • beta- adrenergic agonists (most effective in asthma)
    • anticholinergics
    • methylxanthines
20
Q

Beta Adrenergic receptors:

MOA?

What is the primary effect?

A
  • Beta adrenergic receptors are coupled to G-proteins
  • they activate adenlyl cyclase which increases the production of cAMP, causing bronchodilation
  • Decreases intracellular Calcium and increases membrane K conductance
  • Primary effect: dilate the bronchi by a direct action on the B2 adrenoreceptors
    • results in smooth muscle relaxation and bronchodilation
    • inhibits mediator release from mast cells
    • increases mucous action of cilia
21
Q

What are the Beta adrenergic agonists selective to?

What are the short acting agents?

What are the long acting agents?

A
  • Selective to B2
    • 200-400x more strongly than to B1
  • Short acting
    • albuterol
    • levalbuterol- even less B1 binding, but more expensive
  • Long acting
    • Salmeterol
    • terbutaline- IV/PO
22
Q

Beta adrenergic agonists

onset

use

administration route

A
  • Onset 15-30 minutes
  • Good for use as a rescue inhaler
  • administered via:
    • inhalation or aerosol
    • powder or nebulized
    • orally or injected (SC)
  • Short or long acting
23
Q

What are the side effects of Beta adrenergic agonists?

A
  • *SE are minimized by inhalation delivery
  • tremor
  • increased HR
  • vasodilation
  • metabolic changes
    • hyperglycemia
    • hypokalemia (increased K conductance into cell)
    • hypomagnesemia
  • With high doses of oral drugs:
    • angina, tachydysrhythmias
24
Q

What is the preferred Beta adrenergic agonist?

How is it administered?

doses?

DOA?

A
  • Albuterol
  • administered via MDI
    • 2 puffs, q 4-6 hrs
    • 100 mcg/puff
  • Nebulizer 2.5-5.0 mg in 5 ml of saline
  • DOA_ 4-8 hours
25
Q

What are the other Beta adrenergic (Beta2 selective) agonists used to treat asthma?

A
  • Metaproterenol-Alupent
    • beta2 agonist
    • MDI
    • not to exceed 16 puffs/day
    • longer lasting than albuterol
  • Bitolterol
    • longer asting
    • CV side effects are rare
    • Daily metered dose is 16-20 puffs/day
    • each dose is 270 mcg
26
Q

Terbutaline

class

use

administration/dose

A
  • Beta 2 selective adrenergic agonist
  • Used to treat asthma
  • administration:
    • SC peds: 0.01 mg/kg; adult: 0.25 mg q 15 min
    • MDI 16-20 puffs/day- 200 mcg/puff
27
Q

Salmeterol or Formoterol

Class?

what makes it last longer?

DOA?

What is it used for?

Warning?

A
  • Long acting B-agonist
  • Has a lipophillic side chain that resists degradation and binds to receptor tightly
  • DOA is 12-24 hours
  • Good for prevention NOT acute flare
  • BLACK BOX WARNING: may increase risk of fatal asthma attack
    • should always be given with a steroid as well
28
Q

What are the long acting beta agonist/steroid combo drugs?

Indications?

Warnings?

A
  • Available combination drugs:
    • Fluticasone/Salmeterol (advair)
    • Budesonide/Formoterol (symbicort)
  • Indicated for long-term maintenance in adults and children
    • convenient, but limited flexibility with dose
    • reduces symptoms, reduces the risk of exacerbation, and helps reduce steroid dose
  • Not recommended for initial treatments- many pts only need a glucocorticoid
  • BLACK BOX WARNING: increased risk of asthma related death
29
Q

Methylxanthines

class?

MOA?

Effect?

Clinical applications?

Examples?

A
  • Class: phosphodiesterase inhibitors
  • MOA: unclear; possible inhibition of phosphodiesterase isoenzymes (Type III and IV) which prevents cAMP degradation in airway smooth muscle as well as in inflammatory cells
    • possible adenosine receptor blockade at A1 and A2 receptors
    • may also have anti-inflammatory effect
  • Drug effect: airway relaxation and bronchodilation
  • Clinical applications:
    • COPD
    • asthma
  • Theophylline (prototype), Aminophylline
30
Q

What are the problems with Methylxanthines?

metabolization?

A
  • Multiple side effects and a narrow therapeutic index
    • TI plasma level of 10-20 mg/ml
    • Toxic >20 mg/ml
    • wide 1/2 life variation; smokers metabolize 50% faster
  • Susceptible to drug-drug interactions (CYP450)
    • Cimetidine, Cipro, and antifungals (CYP450 inhibitors) increase plasma levels
    • phenobarb and phytoin can decrease levels
    • Caffeine is also a methylxanthine and can increase levels and promote CNS and CV toxicity
  • Metabolized in liver and excreted in kidney
  • Sustained release only
31
Q

What are the SE of methylxanthines?

A
  • Almost always at toxic levels
    • Cardiac arrhythmias
    • N/V
    • irritability
    • insomnia
    • sz
    • brain damage
    • hyperglycemia
    • hypokalemia
    • hypotension
    • death from CV collapse
32
Q

Anticholinergic bronchodilators

MOA?

Uses?

A
  • MOA: competative antagonists at muscarinic acetylcholine receptors
    • promote smooth muscle relaxation and decreased mucus gland secretion by antagonizing endogenous Ach
    • M3 is most important
  • Uses
    • treatment of COPD
    • second line treatment of asthma
33
Q

Atropine

Class?

dose?

A
  • Naturally occurring alkaloid
    • formally considered 1st line treatment for asthma
  • 1-2 mg diluted in 3-5 ml of saline via nebulizer
    • Highly absorbed across respiratory epithelium, causing systemic anticholinergic effects
      • tachycardia, nausea, dry mouth, GI upset
34
Q

Ipratroprium bromide (atrovent)

structure?

MOA?

dose?

onset?

DOA?

A
  • Quanternary ammonium salt derivative of atropine
    • does not easily absorb across pulmonary epithelium compared to atropine
  • MOA: antagonizes the effect of endogenous acetylcholine at M3 receptor subtypes
  • MDI 40-80 mcg in 2-4 puffs
  • Onset: 30-90 minutes
  • DOA: 4-6 hours
35
Q

Tiotropium

structure?

class?

use?

A
  • Quaternary ammonium salt
  • Long acting anticholinergic
  • Not significantly absorbed across the resp. epithelium
  • FDA approved for COPD
36
Q

How is initial treatment of asthma determined?

Goals of asthma treatment?

How can this be achieved chronically?

A
  • Stepwise therapy
    • step chosen for initial therapy is based on pre-treatment classification of asthma severity
    • moving up or down a step is based on ongoing assessment of asthma control
  • Goals: to reduce impairment and risk
    • reduce exposure to allergens and triggers (dust mites, pets, mold, cockroaches)
    • other factors: tobacco smoke, wood smoke, household sprays
37
Q

What should you do for acute exacerbation in the OR?

A
  • This requires immediate attention
  • Goal is to relieve airway obstruction and hypoxemia and normalize lung function as quickly as possible
  • initial therapy:
    • oxygen
    • systemic glucocorticoid to reduce inflammation
    • nebulized high dose SABA
    • nebulized ipratroprium
  • Try ketamine before epi
38
Q

Are steroids very helpful in COPD?

A
  • Not really, sometimes a trial will be done, but they arent usually very useful
  • Bronchodilators might work better, but only show modest improvement
39
Q

What drugs are usually used to treat COPD?

A
  • Usually started on one agent and then will add another if one is not enough
    • Long acting inhaled beta 2 agonist (salmeterol)
    • long acting anticholinergic (tiotropium)
    • Inhaled glucocorticoid (budesonide) is last choice
    • If using two agents, usually LABA and steroid
40
Q

What is the new drug used to treat COPD?

MOA?

SE?

A
  • Roflumilast (Daliresp)- a selective phosphodiesterase type 4 inhibitor that appears to reduce exacerbations
  • MOA: increases cAMP levels resulting in reduced cough, inflammation, and mucus
  • SE: diarrhea, weight loss, loss of appetite, nausea, HA, back pain, depression

Advanced Pharm (27 decks)

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