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N929 Pharmacology II > Respiratory agents > Flashcards

Respiratory agents Flashcards

1
Q

Airway smooth muscle is under the influence of

A

PSNS (bronchoconstriction) and SNS (Bronchodilation)

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2
Q

SNS fibers cause _____ through

A

bronchodilation via beta 2 receptors

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3
Q

PSNS innervation causes ____ through____

A

bronchoconstriction via muscarinic M3 receptors (also M1)
causes increased secretions
innervation is via the vagus nerve

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4
Q

Beta 2 adrenoreceptors cause

A

widening of the airways (Bronchodilation) via increased intracellular cyclic AMP which decreases Calcium binding

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5
Q

Stimulation of____ leads to bronchoconstriction

A

Vagus nerve (PSNS)

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6
Q

M3 receptors are found on the

A

bronchial smooth muscle & they cause bronchoconstriction by increasing intracellular Ca2+ concentrations
also cause mucus secretion

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7
Q

Pulmonary obstructive diseases

A

asthma & COPD

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8
Q

Describe asthma

A

reversible airflow obstruction disease

chronic inflammatory disorder of the airways characterized by increased responsiveness of the tracheobronchial tree

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9
Q

Asthma s/s

A

wheezing, breathlessness, chest tightness, cough, tachypnea, prolonged expiration phase of respiration, fatigue

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10
Q

asthma is characterized by

A

inflammation, hyper-reactivity & reversible airway obstruction

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11
Q

Asthma mediators include

A

eosinophils, mast cells, cytokines, interleukins, leukotrienes, & histamine

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12
Q

Medications for asthma are aimed at

A

flattening the response to mediators

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13
Q

COPD is characterized by

A

cell death & destruction of the alveoli
results in enlargement of air spaces, fibrosis, and increased mucus production
non-reversible

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14
Q

COPD therapy differs from asthma because

A

steroids have limited effect on inflammation process in COPD

inhaled corticosteroids help in reducing frequency of exacerbations

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15
Q

Steps of treatment for airway outflow disorders:

A 
step 1: short-acting bronchodilators
step 2: regular inhaled corticosteroid
step 3: long-acting bronchodilators
step 4: phosphodiesterase inhibitors, methylxanthines, or leukotriene inhibitors
Step 5: oral corticosteroid
other- cromolyns
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16
Q

Bronchodilators include

A

Beta-adrenergic agonists, anticholinergics, methylxanthines

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17
Q

Examples of beta adrenergic nonspecific drugs include

A

Epinephrine (beta 1, beta 2, and alpha)
Isoproterenol- (beta 1 & beta 2)
Metaproterenol (beta 1 & beta 2)

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18
Q

Examples of short-acting beta2 selective adrenergic drugs include

A

terbutaline, albuterol, levalbuterol (used mostly in OR since it is more B2 specific), and salbutamol

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19
Q

Examples of long-acting beta 2 selective adrenergic drugs include

A

salmeterol

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20
Q

Beta 2 adrenergic selective receptors are

A

200-400 times more strongly bound to beta 2 than beta 1

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21
Q

Mechanism of action of beta adrenergic agonists

A

attach to G proteins–> activates adenlyl cyclase which INCREASES production of cAMP–>bronchodilation
reduced intracellular calcium release & alters membrane conductance
primary effect is to DILATE the BRONCHI via direct action on beta 2 adrenoreceptors

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22
Q

By direct action on the beta 2 adrenoreceptors, beta 2 adrenergic agonists

A

result in smooth muscle relaxation & bronchodilation, inhibit mediator release from mast cells, and increase mucus clearance by action on the cilia

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23
Q

What is the onset of action and duration of action for bronchodilators?

A

onset: within minutes
duration of action: 4 to 6 hours
used as rescue inhalers for this reason

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24
Q

Beta adrenergic agonists are typically used as

A

rescue inhalers

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25
Q

Beta adrenergic agonists are given via

A

inhalation or aerosol, powder or nebulized, orally or injected (SC)

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26
Q

What are the side effects of beta 2 adrenergic agonists?

A

tremor, increased heart rate, vasodilation, metabolic changes (hyperglycemia, hypokalemia & hypomagnesemia)
minimized by inhalation delivery

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27
Q

Albuterol (drug class & duration of action)

A

is a preferred selective beta 2 agonists & duration of action is 4-8 hours

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28
Q

Albuterol is administered via

A

metered dose- 100 mcg/puff
2 puffs q4-6 hours
nebulizer 2.5-5.0 mg in 5 mL of saline

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29
Q

Albuterol has an additive effect

A

with volatile anesthetics on bronchomotor tone

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30
Q

There are 2 isomers of albuterol:

A

R-albuterol levalbuterol has more affinity for beta 2

S-albuterol has more affinity for beta 1 (more side effects)

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31
Q

Side effects of albuterol include

A

tachycardia, hypokalemia, anesthesia use: 4 puffs blunt AW responses to tracheal intubation in asthmatic patients

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32
Q

Do not use ____ in patients with reactive airways

A

desflurane

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33
Q

Metaproterernol-Alupent (drug class & administration)

A

beta 2 agonists for tx of asthma
administered via metered dose
not to exceed 16 puffs/day

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34
Q

Prbuterol-Maxair (drug class & administration)

A

Beta 2 agonists
2 puffs (400 mcg) via metered dose
not to exceed 12 inhalations/day

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35
Q

Terbutaline (drug class & administration)

A

beta 2 agonist
administered oral, SC, inhalation
SC administration resembles the response of epi

36
Q

Terbutaline dosages

A

SC dose for child: 0.01 mg/kg
Adult SC dose is 0.25 mg q15 min
Metered dose inhaler 16-20 puffs/day
Each dose is 200 mcgs

37
Q

Long acting beta agonists include

A

Salmeterol (combination drug-fluticasone & salmeterol)

formoterol

38
Q

Long-acting beta agonists (chemical structure & duration of action)

A

have a liphophilic side chain that resist degradation
duration in 12-24 hours
Good for prevention NOT for acute flare-up

39
Q

Long-acting beta agonists can be used for

A

prevention NOT acute flare-up

40
Q

The mechanism of action for muscarinic receptor antagonists is

A

competitive antagonists at muscarinic acetylcholine receptors
muscarinic 1 & 3 subtype are the targets
By antagonizing endogenous Ach–> broncho-relaxation & decreased mucus secretion

41
Q

Muscarinic receptor antagonists are used for

A

treatment of COPD

SECONDARY LINE for asthma in patients resistant to beta agonist or significant cardiac disease

42
Q

Examples of muscarinic receptors antagonists include

A

atropine, ipratropium bromide, and tiotropium

43
Q

Atropine administration

A

formally used for tx of asthma

administered 1-2 mg diluted in 3 to 5 ml of saline via nebulizer

44
Q

Atropine signs and symptoms

A

highly absorbed across respiratory epithelium which causes systemic anticholinergic effects including: tachycardia, nausea, dry mouth, and GI upset

45
Q

Tiotropium (structure & drug type)

A

quaternary ammonium salt

LONG acting anticholinergic

46
Q

Tiotropium is used for ____ & side effects include

A

approved for COPD & not significantly absorbed across respiratory epithelium which results in few side effects

47
Q

Ipratropium bromide structure & MOA

A

quaternary ammonium salt derivative of atropine
antagonizes the effect of endogenous acetylcholine at M3 receptor subtypes
not significantly absorbed compared to atropine

48
Q

What is the onset & duration of action of ipratropium bromide?

A

Onset: 30 minutes

Duration of action: 4 to 6 hours

49
Q

Administration of ipratropium bromide

A

metered dose inhaler 40-80 mcg in 2-4 puffs via neb

inadvertent oral administration leads to dry mouth and GI upset

50
Q

The mechanism of action of methylxanthines-phosphodiesterase inhibitors is

A

nonspecific inhibition of phosphodiesterase isoenzymes which prevents cAMP degradation and inflammatory cells–> airway relaxation & bronchodilation

51
Q

Examples of methylxanthines-phosphodiesterase inhibitors include

A

theophylline, aminophylline

52
Q

Methylxanthines-phosphodiesterase inhibitors uses

A

COPD & asthma (more historically used b/c of many side effects & need to monitor blood levels)

53
Q

Side effects of methylxanthines phosphodiesterase inhibitors include

A

headache, nausea/vomiting, irritability/restlessness, insomnia, cardiac arrhythmias, seizures, Stevens Johnson syndrome

54
Q

How is methylxanthine-phosphodiesterase inhibitors metabolized and excreted?

A

metabolized- liver
excreted-kidney
susceptible to drug-drug interactions d/t metabolism by CYP450 (cimetidine & antifungals which are CYP-450 inhibitors)

55
Q

Theophylline concerns

A

caution with halothane b/c sensitizes myocardium
& toxicity
therapeutic plasma level of 10-20mcg/ml
toxic >20 mcg/ml

56
Q

Anti-inflammatory agents include

A

Inhaled corticosteroids, cromolyns, leukotriene inhibitors, anti-IgE antibodies

57
Q

Anti-inflammatory agents work to

A

flatten response to mediators that cause inflammation

58
Q

Inhaled corticosteroids are used

A
  • ***as major preventive treatment for patients with asthma

* ***used as suppressive therapy, NOT A CURE

59
Q

The mechanism of action of inhaled corticosteroids is

A

alters genetic transcription
Increases transcription of genes for beta 2 receptor and anti-inflammatory proteins
decreases transcription of genes for pro-inflammatory proteins
induces apoptosis in inflammatory cells
indirect inhibition of mast cells over time

60
Q

What is considered the most important drug in management of asthma?

A

inhaled corticosteroids

61
Q

Inhaled corticosteroids work to

A

reduce the # of inflammatory cells in the airways & damage to airway epithelium
vascular permeability is reduced which decreases airway edema
overall reduction in airway hyper-responsiveness

62
Q

Inhaled corticosteroid drugs include

A

beclomethasone
triamcinolone
fluticasone
budesonide

63
Q

Inhaled corticosteroids administration considerations:

A

may consider the use of corticosteroid administration 1-2 hours pre-op
prolong the response of beta agonists
may consider 5 day course of combined corticosteroid and albuterol to minimize the risk of intubation evoked bronchospasm

64
Q

Side effects of inhaled corticosteroids include

A

oropharyngeal candidiasis, osteopenia/osteoporosis, delayed growth in children, hoarseness, hyperglycemia
systemic effects are decreased thru inhalation
(rinse mouth after inhaler)

65
Q

With inhaled corticosteroids,

A

25% of inhaled corticosteroids reach the airway

80-90% of the inhaled dose reaches oropharynx and is swallowed

66
Q

The mechanism of action of cromolyn drugs

A

stabilize mast cells
MOA: inhibits antigen-induced release of histamine
including the release of inflammatory mediators from eosinophils, neutrophils, monocytes, macrophages, lymphocytes, and leukotrienes from pulmonary mast cells
inhibits immediate allergic response to antigen but not the allergic response once it has been activated

67
Q

Cromolyn is administered via

A

inhalation w/ 8-10% entering the systemic circulation
taken 4 times daily
must be used for 7 days to see effect

68
Q

Cromolyn is NOT

A

used as a rescue inhaler

69
Q

Side effects of cromolyn include

A

infrequent: urticaria, anaphylaxis, angioedema, and laryngeal edema

70
Q

The principle use of cromolyn is

A

prophylactic therapy of bronchial asthma

does not relieve an allergic response after initiation

71
Q

Leukotriene inhibitors are used for

A

bronchial asthma

NOT effective in the tx of ACUTE asthma attacks Zi

72
Q

Drug prototypes of leukotriene inhibitors include

A

Zileuton & montelukast

73
Q

Zileuton works by

A

blocks the biosynthesis of leukotrienes from arachidonic acid
produces bronchodilation, improves asthma symptoms, and has shown long-term improvement in PFT

74
Q

Zileuton is not widely used because

A

it has low bioavailability, low potency, and significant adverse effects including hepatotoxic & hepatitis

75
Q

Montekulast-Singulair works by

A

block the mechanism of bronchoconstriction and smooth muscle effects
leukotriene receptor antagonists
blocks the ability of leukotrienes to bind to cysteinyl-leukotriene 1 receptor

76
Q

Montelukast-Singulair is caution with

A

co-administration with warfarin which can result in prolonged PT

77
Q

Montekulast is used to

A

improve bronchial tone, pulmonary function, and asthma symptoms

78
Q

Anti-IgE antibodies are used for patients with

A

asthma

79
Q

Anti-IgE antibodies work by

A

removal of IgE antibodies from circulation mitigate the acute response of the inhaled allergen

80
Q

____ is an example of an anti-IgE antibody

A

Omalizumab

81
Q

Omalizumab is a (admin)

A

monoclonal antibody derived from DNA
given in the early & late phase of asthmatic response
given SQ for 2-4 weeks/parenterally infused
High cost & inconvenience

82
Q

Omalizumab works by

A

binds to IgE- decreases quantity of circulating IgE & prevents binding of IgE to mast cells
also causes down-regulation of receptors

83
Q

An adverse effect of omalizumab is

A

rare: triggering of an immune response

84
Q

Drugs that are used for bronchodilation include:

A

B2 adrenergic agonists (cAMP production–> bronchodilation), anticholinergics (competitive inhibitor of cholinergic), methylxanthines/PDE inhibitors (inhibit breakdown of cAMP)

85
Q

Drugs that are used for inflammation and mucous include:

A

steroids- decrease mucosal edema

cromolyn- mast cell stabilization

N929 Pharmacology II (16 decks)

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