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Resp > Bronchodilators, Corticosteroids, and the Pharmacotherapy of Asthma and COPD > Flashcards

Bronchodilators, Corticosteroids, and the Pharmacotherapy of Asthma and COPD Flashcards

1
Q

Short-acting bagonists (SABA)

list

A

*Albuterol, others

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2
Q

Long-acting bagonists (LABA)

list

A

Salmeterol, formoterol

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3
Q

Emergency, non-selective bagonist

list

A

Epinephrine*

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4
Q

Muscarinic Antagonists

list

A

Ipratropium, tiotropium

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5
Q

Methylxanthine

list

A

Theophylline*

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6
Q

Inhaled Corticosteroids (ICS)

list

A 
Beclomethasone
Budesonide
Ciclesonide
Flunisolide
Fluticasone
Mometasone
Triamcinolone
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7
Q

Oral Corticosteroids

list

A

Methylprednisolone

Prednisone

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8
Q

Leukotriene Receptor Antagonist (LTRA)

list

A

Montelukast

Zafirlukast

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9
Q

Cromolyn compounds

list

A

Cromolyn sodium

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10
Q

Anti-IgE Antibody

list

A

Omalizumab

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11
Q

Bronchospasm

A

In allergic asthmatics patients, immediate hypersensitivity-type reactions can be continuously present at a sub-threshold level, resulting in mild-to-moderate inflammation without overt bronchoconstriction.

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12
Q

Overt bronchospasm*

A

then occurs upon exposure to a specific allergen or to a variety of nonspecific stimuli, e.g., cold air, dust, air pollution, exercise, etc.

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13
Q

Inflammatory Mediators in Asthma

A

Enormous variety of mediators are released. Thus, blocker of a single mediator, e.g., antihistamine, is unlikely to be effective in alleviating the symptoms or the progression of asthma.

Corticosteroids, which are capable of blocking many key steps in the inflammatory process, come closest to this ideal therapy

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14
Q

Mast Cell Mediators of Inflammatory Processes

preformed (immediate)

A

mediator - histamine tnfa proteases heparin

effects - bronchoconstriction itch cough vasodilation edema

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15
Q

Mast Cell Mediators of Inflammatory Processes

lipids (minutes)

A

mediator - leukotrienes prostaglandins

effects - bronchoconstriction chemotaxis mucus secretion

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16
Q

Mast Cell Mediators of Inflammatory Processes

cytokines (hours)

A

mediator - interleukins GM-CSF

effects - bronchoconstriction, chemotaxis inflammatory cell proliferation

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17
Q

Aerosol Delivery of Drugs

A

Particle size of aerosol is important.
Rate of breathing and breath holding.
Even under ideal conditions, 90% of inhaled drug is swallowed.
Therefore, ideally the best drugs also have poor absoption from the GI tract and/or rapid first-pass metabolism in the liver.

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18
Q

Classification of asthma

intermittent

A

Symptoms - 80%, fev1/fvc normal

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19
Q

Classification of asthma

mild

A

Symptoms - > days /week but not daily

nighttime awakenings - 3-4Xmonth

short acting beta2 agonist use for symptom control - >2daysa week but no >1 a day

interference with normal activity - minor limitation

lung function - fev1>80% predicted, fev1/fvc normal

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20
Q

Classification of asthma

moderate

A

Symptoms - daily

nighttime awakenings - >1 time a week but not nightly

short acting beta2 agonist use for symptom control - daily

interference with normal activity - some limitation

lung function - fev1>60% predicted but less than80%, fev1/fvx reduced 5%

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21
Q

Classification of asthma

severe

A

Symptoms - throughout the day

nighttime awakenings - often nightly

short acting beta2 agonist use for symptom control - several times per day

interference with normal activity - extremely inhibited

lung function - fev15%

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22
Q

Stepwise approach for managing asthma adults

step 1

A

preferred

sabaprn

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23
Q

Stepwise approach for managing asthma adults

step 2

A

preferred

low dose ICS

alternative

cromolyn ltra nedocromil or theophyllin

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24
Q

Stepwise approach for managing asthma adults

step 3

A

preferred

low does ICS and laba or medium dose ICS

alternative

low dose ICS and either ltra theophylline or zileudon

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25
Q

Stepwise approach for managing asthma adults

step 4

A

preferred

medium dose ics and laba

alternative

medium dose ics and either ltra theophylline or zileuton

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26
Q

Stepwise approach for managing asthma adults

step 5

A

preferred high dose Ics and laba and consider omalizumab for patients who have allergies

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27
Q

Stepwise approach for managing asthma adults

step 6

A

preferred

high dose ics and laba and oral corticosteroid and consider omalizumab for pts who have allergies

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28
Q

intermittent asthma treatment

A

saba as needed

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29
Q

mild persistent asthma treaments

A

preferred - low dose ics

alternatives - montelukast or theophylline

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30
Q

moderate persistent asthma treatments

A

preffered - low dose ics and a laba or medium dose ics

alternatives - low dose ics and a leukotriene modifier or theophyllin

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31
Q

severe persistent asthma treatments

A

preferred - medium or high dose ics and a laba

alternatives - medium dose ics and a leukotrient modifier or theophylline

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32
Q

asthma treatment ages 5-11

step 1

A

preferred - saba prn

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33
Q

asthma treatment ages 5-11

step 2

A

preferred - low dose ics

alternative - cromolyn, ltra, nedocromil, or theophyllin

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34
Q

asthma treatment ages 5-11

step 3

A

preferred - lowe dose ics and either laba ltra or theophylline

or

medium dose ics

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35
Q

asthma treatment ages 5-11

step 4

A

preferred - medium dose ics and laba

alternative - medium dose ics and etiher ltra or theophylline

36
Q

asthma treatment ages 5-11

step 5

A

preferred - high dose ics and laba

alternative - high dose ics and either ltra or theophyllin

37
Q

asthma treatment ages 5-11

step 6

A

preferred - high dose ics and laba and oral systemic corticosteroid

alternative - high dose ics and either ltra or theophylline and oral systemic corticosteroid

38
Q

b-Adrenergic Agonists

Therapeutic Use in Asthma and COPD

A

Drug of choice for rapid relief of bronchospasm

Highly effective and safe for intermittent, prophylactic treatment of asthma.

39
Q

b-Adrenergic Agonists

Current Emphasis

A

Intermittent use on an as-needed basis for relief of acute, severe bronchospasm. Not general prophylaxis.

40
Q

b-Adrenergic Agonists

Overuse:

A

Side effects intensify will overuse, but a greater danger is the tendency to continue to self-medicate during periods when symptoms are escalating.
To avoid a medical emergency, patients should be encouraged to seek medical attention as soon as possible after they detect a decline in the efficacy of their usual therapeutic regimen.

41
Q

b-Adrenergic Agonists

Mechanism of Action:

A

Stimulate b2-adrenergic receptor on surface of bronchiolar smooth muscle cells.
b2-adrenergic receptor couples to Gs protein and activates adenylyl cyclase enzyme leading to increased cellular levels of cyclicAMP.
Cyclic AMP stimulates phosphorylation cascade that leads to decreased intracellular calcium and smooth muscle relaxation.
Also inhibit mediator release from mast cells.

42
Q

b-Adrenergic Agonists

Rapid Acting-Short Duration

A

Albuterolonset

43
Q

Long Actingb2-Selective Agonists (LABA

A

salmeterol:
slower onset
duration > 12 hours of useful bronchodilation
useful to control nighttime asthma attacks, also now used BID for prevention
not suitable for treatment of acute bronchospastic attacks because onset of action is too slow.

Formoterol
Similar to salmeterol
Not for acute attacks

44
Q

Less Selective or Nonselective b-Adrenergic Agonists

A

Epinephrine

Isoproterenol

Metaproterenol

Isoetharine
Because of their very short duration of action and their lack of b2-selectivity, these agents are not frequently used.
Low-strength epinephrine inhalers sometimes prescribed for mild asthma

Racemic Epinephrine
aerosol used for pediatric patients

45
Q

Long-term Use of LABA

A

Continued use of a LABA may cause down-regulation of b2 receptors with loss of the protective effect from rescue therapy with a short-acting agent.
LABA should not be used for monotherapy in patients with persistent asthma, especially in children.
LABA should be used in asthma only in combination with an inhaled corticosteroid.
“Stop use of a LABA, if possible, once asthma control is achieved and maintain the use of an asthma-controller medication such as an inhaled corticosteroid”.

46
Q

Oral Therapy withb-Adrenergic Agonists

Oral administration increases incidence of adverse side effects:

A

muscle tremor, cramps, cardiac tachyarrhythmias, metabolic disturbances, hypokalemia

47
Q

Oral Therapy withb-Adrenergic Agonists

Appropriate situations for oral therapy

A

brief therapy in children with upper respiratory tract infections who cannot manipulate inhaler
in severe asthma exacerbations where inhaler cannot be used or when aerosol is irritating
oral albuterol and terbutaline are available

48
Q

Adverse Side Effects ofb-Adrenergic Agonists

A

Patients with cardiovasculardisease or diabetesare at higher risk of adverse effects.
Skeletal muscle tremor (most frequent side effect)
CNS: restlessness, apprehension, anxiety, tremors
CVS: tachycardia, dysrhythmias, hyper-or hypotension
hypokalemia
worsen hyperglycemia in diabetics
drug interactions with thyroid, digitalis, methylxanthines

49
Q

Epinephrine: Emergency Use

A

Epinephrine is the drug of choice for treatment of anaphylactic reactions.
Give SQ (or IM or IV with dextrose)
Bronchodilation (mediated by b2receptors)
Vasoconstriction (mediated by 1receptors)
maintains BP & decreases edema
Inhibition of mediator release (b2receptors)

50
Q

Anaphylaxis Treatments

A 
Albuterol via nebulizer
IV fluids
Oxygen
Secondary therapy
H1 antagonist -diphenhydramine
H2 antagonist -ranitidine
Corticosteroid -hydrocortisone, methylprednisolone
Aminophylline
NE, glucagon -for hypotension
51
Q

Bronchodilators:Ipratropium bromide OVERVIEW

A

A quaternary muscarinic receptor antagonist
If given parenterally, effects are like atropine
But, only given as inhaled aerosol
 few side effects, even when swallowed because is poorly absorbed from GI and does not cross into brain
 quaternary amine-poor diffusion across membranes

52
Q

Bronchodilators:Ipratropium bromide

parasympathetic

A

mediated bronchospasm is a significant component of airway resistance in some asthmatics and COPD patients, especially psychogenic exacerbations

53
Q

Ipratropium bromide

Therapeutic Use:

A

Bronchodilation develops more slowly and is usually less intense than that produced by b-agonists.
Useful bronchodilationlasts up to 6 hours.
Principal use of ipratropium is in COPD.
Combined with albuterol = COMBIVENT
Also used intranasally to reduce secretions in the upper and lower respiratory tract in allergic rhinitisand chronic postnasal drip syndrome

54
Q

Tiotropium

A

newer long-acting agent (QD dosing) used for maintenance therapy in chronic bronchitis and emphysema; dry powder inhaler device

55
Q

Methylxanthines

drugs

A

theophylline, caffeine, theobromine

found in coffee, tea, chocolate, cocoa, colas

56
Q

Methylxanthines

Diverse cellular actions

A

adenosine receptor antagonists
block cyclic AMP degradation –PDE inhibitor
lower intracellular calcium
hyperpolarize cell membranes

57
Q

Theophylline

A

Bronchodilationis a clinically relevant effect of theophylline
Other effects include CNS stimulation, modest peripheral vasodilation, improved skeletal muscle contractility, and a thiazide-like diuresis

58
Q

Theophylline

Therapeutic Use:

A

Formerlya first-line agent for treatment of asthma
Nowhas a far less prominent role because:
benefits are modest
 narrow therapeutic window
 considerable variation in absorption and elimination between different patients
 monitoring of plasma concentrations is often required

59
Q

Theophylline

Nocturnal asthma

A

can be improved with slow-release theophylline, but inhaled corticosteroids and salmeterol are probably more effective.
IV formulation = aminophylline

60
Q

Anti-Inflammatory AgentsCorticosteroids

overview

A

In asthma (and some COPD) an inflammatory responseis responsible for the underlying disease process.
So many inflammatory mediators are involved that a blocker of any given autocoid or cytokine, e.g., antihistamine, is ineffective in alleviating the symptoms of asthma.
Corticosteroids block many of the steps involved in the inflammatory cascade.

61
Q

Anti-Inflammatory AgentsCorticosteroids

Mechanism of Action

A

corticosteroids are steroid receptor agonists that bind to intracellular receptors that translocate to the cell nucleus and positively or negatively regulate gene transcription. This takes time.
corticosteroids inhibit the production and release of cytokines, vasoactive and chemoattractivefactors, lipolytic and proteolytic enzymes, decrease mobilization of leukocytes to areas of injury, and decrease fibrosis.
General anti-inflammatory response

62
Q

Inhaled Corticosteroids

A 
Beclomethasone dipropionate (Beclovent)
Budesonide dipropionate (Pulmicort)
Ciclesonide (Alvesco)
Flunisolide (AeroBid)
Fluticasone (Flovent)
Mometasone (Asmanex Twisthaler)
Triamcinolone acetonide (Azmacort)
63
Q

Systemic Corticosteroids

IV or oral

A

Prednisone
Methylprednisolone
Hydrocortisone

64
Q

Corticosteroids overview asthma

A

Corticosteroids have potentially important adverse side effects.
Aerosol delivery of the steroid has significantly improved the safety of treatment for moderate to severe asthma.
Asthmatics who require inhaled b-adrenergic agonist therapy 3 -4 or more times weekly are candidates for inhaled steroid therapy.

65
Q

Corticosteroids

Available preparations

A

have equivalent efficacy and potential side effects, but differ in the amount of drug aerosolized per inhaler activation, i.e., high-dose and low-dose.
Therefore, the dose of inhaled steroid must be empirically determined for each patient.

66
Q

Corticosteroids

Asthmatic patients maintained on inhaled

A

corticosteroids show improvement of symptoms and lower requirements for “rescue” with a bronchodilator.

67
Q

Corticosteroids

Systemic Therapy

A

Systemic (i.v. or oral) steroid therapy is used in severe asthmatic attacks requiring hospitalization.
For severe asthma, prednisoneor methylprednisoloneis given i.v., followed by oral doses and gradual tapering of the dose.
For acute, sever exacerbations, oral prednisone is administered for 1 -2 weeks.
Longer treatments require tapering of the dose to account for hypothalamic-pituitary-adrenal suppression.

68
Q

Corticosteroids:Potential Side Effects

A

HPA suppression -low risks until high doses
Bone resorption -modest risks
Carbohydrate and lipid -minor risks
Cataracts and skin thinning -dose-related
Purpura -dose-related
Dysphonia -usually resolves
Candidiasis -use spacer device and rinse mouth
Growth retardation -of concern in children

69
Q

Combination Products

A

Fluticasone propionate +Salmeterol (Advair Diskus, Advair HFA)
Budesonide + Formoterol(Symbicort HFA)
Mometasone + Formoterol (Dulera)
Not useful for acutebronchospastic attack
Cost Range: ~$145-$175/month

70
Q

Chronic Obstructive Pulmonary Disease (COPD)

A

Emphysema and chronic bronchitis
Smoking cessation
Alveolar destruction is the main pathophysiological component (irreversible component)
Some patients have inflammation and bronchospasm (reversible components)
Drug therapy is applicable to the reversible component of COPD

71
Q

COPD Treatment

Group A

A

preferred - short acting anticholinergic prn or saba prn

aleternative - long acting anticholinergic or laba or saba and short ancting anticholinergic

72
Q

COPD Treatment

Group B

A

preferred - long acting anticholinergic or laba

alternative - long acting anticholinergic and laba

73
Q

COPD Treatment

Group C

A

preferred - ics and laba or long acting anticholinergic

alternative long acting anticholinrgic and laba or ics, or pde4 inhibitor and long acting anticholinergic or laba

74
Q

COPD Treatment

Group D

A

preferred - ics and laba and/or long acting anticholinergic

alternative - ics and laba and long acting anticholinergic or ics and laba and pde4 inhibitor or long acting anticholinergic and laba or long acting anticholinergic and pde4 inhibitor

75
Q

Chronic Obstructive Pulmonary Disease (COPD)

Inhaled ipratropium bromide or tiotropium

A

especially useful in patients with a vagally-mediated psychogenic component

76
Q

Chronic Obstructive Pulmonary Disease (COPD)

Inhaled b2-adrenergic agonists

A

As with asthma, continuous (overuse) of bronchodilators may be associated with worsening of symptoms

77
Q

Chronic Obstructive Pulmonary Disease (COPD)

A subgroup of COPD patients

A

may benefit from corticosteroid therapy, but generally mixed results of steroids in COPD.

78
Q

Cromolyn Compounds

A

Cromolyn sodium (Intal)
Cromolyn sodium is an anti-inflammatoryagent that indirectly inhibits antigen-induced bronchospasm and directly inhibits the release of histamine and other autocoids from sensitized mast cells.
May suppress the activating effects of chemoattractant peptides on eosinophils, neutrophils, and monocytes.

79
Q

Cromolyn Compounds:Therapeutic Use

A

Cromolyn compounds do not directly relax smooth muscle, therefore they are not useful for control of acute bronchospasm.
Cromolyn compounds are primarily prophylactic. When inhaled several times daily, they inhibit both the immediate and late asthmatic responses to antigenic challenge or exercise.

80
Q

Leukotriene inhibitors

A

Zafirlukast
LTD4 receptor antagonist
Montelukast
LTD4 receptor antagonist
Alternative or adjunctive therapy to low-dose corticosteroids for mild persistent asthma.
Useful as oral prophylaxis in exercise-induced asthma.

81
Q

muscarinic antagonists are used mainly for

A

copd

82
Q

ltras are less effective but

A

less side effects

83
Q

theophylline increases

A

dynamic contraction of diaphragm

84
Q

theophylline is not used bc

A

too many side effects and have to monitor too much

85
Q

corticosteroids pic

A

croticosteroids related to cortisol

affect glucose metabolism

hypdrophobic and cross into cell bind to recptr in cell forms a dimer attaches to dna and transcritipon to shutdown of it takes place

86
Q

CORTICOSTEROIDS ARE DANGEROUS WHEN

A

LONG term use

low dose are ok

87
Q

once you destroy the alveoli

A

there is no way to really fix that

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