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Justin Lyle Cards > Smooth Muscle Part 1 > Flashcards

Smooth Muscle Part 1 Flashcards

1
Q

what are the 3 big things that happen with asthma?

A
  1. narrowing of airways
  2. increased mucus production
  3. inflammation
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2
Q

what are the clinical characteristics of asthma?

A
  1. recurrent bouts of SOB
  2. chest tightness
  3. coughing
  4. wheezing
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3
Q

pathophysiology of asthma

A
  1. widespread, reversible narrowing of bronchial airways
  2. significant bronchial responsiveness to inhaled stimuli
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4
Q

pathology of asthma

A
  1. lymphocytic and eosinophilic inflammation of the bronchial mucosa 2. “remodelling” of the bronchial mucosa –> hyperplasia of the cells of the airway walls
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5
Q

what are the pharmacologic goals in the management of asthma

A
  1. treatment (w/ short-term relievers and long-term controllers) 2. prevention of inflammation, bronchoconstriction, and mucus
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6
Q

T/F: the more uncontrolled asthma is the more mucus production there is

A

TRUE

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7
Q

mild asthma

A
  1. occasional
  2. triggered via: exposure to allergens, pollutants, viral URI, and/or during exercise
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8
Q

severe asthma

A
  1. frequent
  2. associated with wheezing and dyspnea
  3. exacerbations occur often at night 4. chronic airway narrowing with chronic respiratory impairment
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9
Q

detail the pathogenesis (conceptual theory model) of asthma

A
  1. exposure to allergen –> synthesis of IgE –> binds to mast cells in airway mucosa
  2. on re-exposure to allergen –> Ag/Ab complex on mast cell surgace triggers release of mediators and anaphylaxis (histamine, tryptase, prostaglandin D2, leukotriene C4, and plt activating factor)
  3. these agents provoke contraction of airway smooth muscle –> immediate fall in FEV1
  4. re-exposure to allergen also causes the synthesis and release of a variety of cytokines
  5. these cytokins attract and activate eosinophils and neutrophils (which release mediators)
  6. mediator release –> edema, mucus hypersecretion, smM contraction, and increased bronchial reactivity associated with late asthmatic response indicated by second fall in FEV1 3-6 hours after exposure
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10
Q

bronchodilation is promoted by what secondary messenger?

A

cAMP

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11
Q

how do beta agonists promote bronchodilation with asthma?

A

increases cAMP by increasing the rate of cAMP synthesis via adenylyl cyclase

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12
Q

how do phosphodiesterase inhibitors, like theophylline promote bronchodilation in asthmatics

A

increases cAMP, by slowing the degradation of cAMP

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13
Q

what two med categories cause bronchodilation with asthma therapy by increasing cAMP?

A
  1. beta agonists
  2. PDE inhibitors (theophylline)
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14
Q

what class of medications tend to promote bronchodilation by inhibiting bronchoconstriction in asthma therapy

A
  1. muscarinic antagonists (M3)
  2. adenosine antagonists (theophylline)
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15
Q

which drug works in asthma therapy by both promoting bronchodilation through increasing intracellular cAMP and by inhibiting bronchoconstriction through adenosine antagonism?

A

theophylline

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16
Q

T/F: no med guarantees the break of a bronchospasm

A

TRUE

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17
Q

if a patient has a bronchospasm what should you do?

A
  1. take them off the vent and bag - seeing if you can move air 2. if you cannot move air –> no INH med, give double diluted epi IV 3. if can move air –> albuterol
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18
Q

what are the different symapthomimetics given for asthma ?

A
  1. epi (IV, INH, SQ)
  2. ephedrine
  3. isoproteronol
  4. albuterol (po, INH)
  5. terbutaline (PO, SQ, INH)
  6. metaproterenol (INH)
  7. Pirbuterol (INH)
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19
Q

epinephrine is a very effective bronchodilator that stimulates the ________& __________ receptor

A

alpha; B1

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20
Q

what meds were displaced (replaced) by beta 2 selective agents in asthma therapy

A
  1. epi 2. ephedrine
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21
Q

problematic s/e with using epinephrine with asthma?

A

tachycardia, arrhythmias, angina

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22
Q

compared to epi, what is different about ephedrine for use in asthma tx

A
  1. longer DOA
  2. oral availablity
  3. increased CNS effects
  4. decreased potency
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23
Q

why is isoproternol not used in asthma tx that often anymore

A

increased mortality 2/2 cardiac arrhythmias from high dose inhaled isopro

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24
Q

what are your long acting B2 agonists used in the tx of asthma?

A
  1. salmeterol
  2. formeterol
  3. indacaterol (COPD only!)
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25
Q

characteristics of long acting beta 2 agonist

A
  1. highly lipid soluble 2. have to be combined with steroids
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26
Q

why do long acting beta 2 agonists like salmeterol and formeterol have to be combined with corticosteroids in the tx of asthma?

A

they have no anti-inflammatory effects; thus cannot be used as monotherapy

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27
Q

black box warning for long acting beta 2 agonists (salmeterol, formeterol, and indacaterol)

A

small but significant increase in the risk of death/near death from asthma attack, esp in african americans

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28
Q

T/F: you can use a NMB to break a bronchospasm

A

false; bronchospasm is smM, NMBA only work on skM (thus can use to break laryngospasm)

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29
Q

MOA of albuterol

A
  1. Beta-2 selective agonist
  2. relaxes airway smooth muscle by inhibiting bronchoconstricting mediators from mast cells
  3. inihbits microvascular leakage
  4. increases mucociliary transport via increased ciliary activity
  5. stimulates adenylyl cyclase to increase cAMP –> bronchodilation
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30
Q

albuterol systemic effects

A
  1. bronchodilation
  2. increase shunt (great perfusion, no oxygenation)
  3. tachycardia (B1)
  4. vasodilation (B2)
  5. potential for arrhythmias
  6. tremors
  7. increases activity of Na/K pump –> decrease potassium levels
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31
Q

how do you prevent the increasing of a pulmonary shunt with albuterol?

A

administer with O2

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32
Q

which can administer higher dose of medication? MDI or Neb?

A

nebulizer

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33
Q

which route of medication administration for asthma will provide the best local effect on airway smM with the least systemic toxicity

A

inhalation therapy

34
Q

with inhalation therapy, _______________ % of total dose is deposited in the mouth or pharynx, therefore it is important when administering to ____________________

A

80-90; hold breath

35
Q

how can you increase the absorption of inhalation agents in the bronchi?

A

slow full breath followed by 5 seconds of breath holding

36
Q

what medications are considered methylxanthines

A
  1. theophylline
  2. aminophylline
  3. theobromine
  4. caffeine
37
Q

why are methylxanthines not routinely used for asthma anymore?

A

safer INH B2 agonists and INH anti-inflammatory agents

38
Q

MOA of methylxanthines

A
  1. phosphodiesteras inhibitor –> increased cAMP & decreased release of cytokines and chemokines (decreasing immune cell activation)
  2. inihbition of cell surface adenosine receptors (relaxes airway smooth muscle & inhibits histamine release)
  3. enhancement of histone deacetylation (blocks inflammatory genes)
39
Q

aminophylline (compared to theophylline) has a ____________ half-life and is ___________ potent

A

shorter; less

40
Q

respiratory effects of methylxanthines

A
  1. bronchodilation
  2. inhibit antigen induced release of histamine
41
Q

CNS effects of methylxanthines

A
  1. mild cortical arousal
  2. increased alertness
  3. deferral of fatigue
  4. nervousness
  5. anxiety
  6. tremor
  7. HA
42
Q

toxic effects from high dose or OD of methylxanthines

A
  1. medullary stimulation 2. convulsions 3. death
43
Q

CV effects of methylxanthines

A
    • chronotropy
    • inotropy
  3. adenosine R antagonism –> increased SNS release
  4. increased cAMP –> increased Ca –> increased contractility
  5. decreased blood viscosity
  6. potential for arrhythmias
44
Q

GI/GU/endocrine effects of methylxanthines

A
  1. stimulate secretion of gastric acid
  2. stimulate digestive enzymes
  3. weak diuretics (not therapeutic)
  4. anorexia
  5. N/V
  6. abdominal pain
45
Q

skM effects of methylxanthines

A
  1. improve contractility 2. reverse fatigue of the diaphragm in patients
46
Q

of the methylxanthines, ______________ is most effective on smooth muscle, and ____________________ is most effective on neural tissue

A

theophylline; caffeine

47
Q

T/F: methylxanthines have a high risk for tolerance development

A

FALSE

48
Q

___________________ will increase the long term control of asthma when taken as sole maintenance, or when added to inhaled corticosteroids

A

methylxanthines

49
Q

methylxanthines are metabolized in the ___________________

A

liver

50
Q

__________________ if used in the tx of asthma, have a very narrow therapeutic window, thus require blood draws to monitor therapeutic levels

A

methylxanthines

51
Q

what are your anti-muscarinic drugs used in the tx of asthma

A
  1. ipatropium bromide (atrovent)
  2. atropine
  3. tiotropium
52
Q

MOA of anti-muscarinics for asthma

A
  1. competitively inhibits Ach at the Muscarinic R of the ANS
  2. blocks airway smM contraction
  3. blocks the increase of mucus secretion that occurs with vagal stimulation
53
Q

inhaled anti-muscarinics (ipatropium - ex) does NOT enter ____________, and is _______________ absorbed into circulation

A

CNS; poorly

54
Q

anti-muscarinics for asthma tx are used in pts who are intolerant to __________

A

B2 agonists

55
Q

Antimuscarinics are used in asthma tx as an _________________ therapy; enhances the effects of _______________ in acute severe attacks

A

adjunct; albuterol

56
Q

what are the corticosteroids used in the tx of asthma?

A
  1. prednisone (PO/IV)
  2. beclomethasone (beconase) (INH)
  3. budesonide (pulmicort) (INH)
57
Q

MOA of corticosteroids for asthma

A
  1. blocks lymphocytes, eosinophils, and mast cells from infiltrating the airways (primary action)
  2. has broad anti-inflammatory effects
  3. inhibits production of inflammatory cytokines
  4. potentiates B-receptor agonists
58
Q

T/F: corticosteroids when used for asthma tx work by directly relaxing smooth muscle

A

false; - reduces bronchial activity

59
Q

____________________ meds used in the tx of asthma work by decreasing bronchial reactivity, and decreasing contraction of engorged vessels in the bronchial mucosa

A

inhaled corticosteroids

60
Q

with oral corticosteroids for asthma treatment, the dose must be tapered slowly to avoid _____________________

A

adrenal insufficiency

61
Q

what is a common s/e with inhaled corticosteroids and how can it be prevented?

A

oropharyngeal candidiasis; mouthwash after dose

62
Q

______________________ used for asthma treatment in adults long term will increase the risk of catarcts and osteoporosis

A

corticosteroids

63
Q

_________________ used for asthma tx will slow the rate of growth in children

A

corticosteroids

64
Q

what med will decrease the frequency of asthma exacerbations if taken regularly d/t decreasing airway reactivity

A

corticosteroids

65
Q

T/F: corticosteroids for asthma is reserved for urgent tx

A

TRUE

66
Q

montelukast (singluar) used in the tx of asthma is what type of med?

A

leukotriene (LDT4) receptor antagonist

67
Q

____________________ is an oral asthma therapy medication that is used in pts who’s sx persist for more than 2x a week or awaken from sleep by astham more than 2x per month

A

montelukast (LDT4 receptor antagonist)

68
Q

what med is widely used in the tx of asthma in children ages 6 and up

A

montelukast

69
Q

which med improves asthma control, decreasing exacerbations, and is a once/day oral medication?

A

montelukast

70
Q

this medication is appropriate as a single therapy for someone with mild asthma, but requires supplementation with corticosteroids in severe asthma

A

B2 agonists

71
Q

use of 2 or more canisters of inhaled Beta agonist per month for asthma is the marker for _________________

A

increased risk of asthma fatality

72
Q

with B2 agonists, indications that additional (supplemental) treatment is needed are:

A
  1. sx requiring “rescue” therapy more than 2x per week
  2. nocturnal sx occuring more than 2x per month
  3. FEV1 is less than 80% of predicted
73
Q

____________________ is an asthma med that is reserved for patients who are poorly controlled with inhaled anti-inflammatory agents (pulmicort) and PRN B2 agonist (albuterol)

A

Theophylline

74
Q

what drug is largely used as an alternative in asthma tx for pts who are intolerant to B2 agonists?

A

ipratropium bromide (anti-muscarinics)

75
Q

inhaled corticosteroids are started in the tx of asthma under what conditions?

A
  1. significant airflow obstruction persists despite bronchodilator tx
76
Q

in severe asthma, a standard inhaled corticosteroid may NOT be enough. in this situation, what are the tx options?

A
  1. double the dose
  2. combine with another drug like: theophylline, montelukast, long acting Beta2 receptor agonist
77
Q

combination inhalers for asthma consist of a _________________ + _____________

A

corticosteroid; long acting B2 agonist

78
Q

advantages of Combo inhalers

A
  1. convenient
  2. very effective
  3. decrease asthmatic exacerbations
79
Q

what are some comination inhalers on the market

A
  1. advair 2. symbicort
80
Q

black box warning for combination inhalers

A

mild to moderate asthma should be tx with low dose INH corticosteroid alone d/t increase risk of death

Justin Lyle Cards (27 decks)

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