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Pharmacology II - CP > Respiratory Agents > Flashcards

Respiratory Agents Flashcards

1
Q

Is asthma an obstructive disease or a restrictive disease?

A

Obstructive disease - problem with outflow

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2
Q

which obstructive disease is reversible?

A

Asthma

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3
Q

What is the airway smooth muscle influenced by?

A

PSNS and SNS

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4
Q

What does the SNS cause in the airway smooth muscle?

A

Bronchodilation

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5
Q

What does the PSNS cause in the airway smooth muscle?

A

Bronchoconstriction

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6
Q

Which receptors cause bronchodilation?

A

beta 2 receptors

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7
Q

PSNS innervation is via the ____

A

vagus nerve

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8
Q

Which receptors cause bronchoconstriction?

A

muscarinic (M3) receptors

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9
Q

Beta 2 receptors causes

A

smooth muscle relaxation in blood vessels, bronchi, uterus, and bladder, bronchodilation, increased intracellular cAMP

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10
Q

NonAdrenergic NonCholinergic Nerves (NANC)

A

influences on inflammation and smooth muscle tone

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11
Q

Stimulation of the vagus nerve leads to?

A

bronchoconstriction

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12
Q

How does M3 receptors mediate bronchoconstriction?

A

via the activation of IP3 which increases the intracellular Ca++ concentrations

also mediates mucus secretion

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13
Q

Asthma description

A

chronic inflammatory disorder of the airways characterized by increase responsiveness of the tracheobronchial tree to a variety of stimuli

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14
Q

Asthma recurrent symptoms

A

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

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15
Q

Main goal of therapy for treating asthma

A

decrease stimulus (flatten the response to mediators)

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16
Q

asthma creates airways that are

A

inflamed, edematous airways, bronchial hypersensitivity, reactivity to irritant stimuli, difficulty with outflow

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17
Q

asthma hyperresponsiveness and inflammation from allergen leads to

A

activation of T2 lymphocytes and cytokine release

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18
Q

bronchospasm

A

lower in the bronchus/in the lungs

treat with gas (sevo or iso)

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19
Q

laryngospasm

A

glottic closure

break with 3-5mg rocuronium

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20
Q

Mediators involved in asthma

A

eosinophils and mast cells mostly

other probable mediators - cytokines, interleukins, leukotrienes, histamine

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21
Q

What kinds of things can cause/lead to COPD?

A

genes, smoking, age/gender, lung growth/development, exposure to particles, socioeconomic status, asthma, chronic bronchitis, infections

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22
Q

COPD description

A

cell death and destruction of the alveoli due to impaired lung parenchyma, degraded matrix, and toxic actions of inflammatory cells that leads to enlargement of air spaces, fibrosis, and increased mucus production

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23
Q

Steroids have limited effect on inflammation in ___

A

COPD

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24
Q

Which type of treatments are used in airway outflow disorders?

A

short acting bronchodilators, regular inhaled corticosteroid, long acting bronchodilators, phosphodiesterase inhibitors, methylxanthines, leuokotriene inhibitors, oral corticosteroids, cromolyns

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25
Q

Example of bronchodilators

A

beta adrenergic agonists, anticholinergics, methylxanthines

26
Q

Short acting beta agonists

A

terbutaline, albuterol, levalbuterol, salbutamol

27
Q

Which short acting beta agonist is B2 selective?

A

levalbuterol

28
Q

what is an example of a long acting beta agonist

A

salmeterol

29
Q

MOA of beta agonists

A

GPCRs, activate adenlyl cyclase which increases the production of cAMP and decreases intracellular Ca++ release which leads to bronchodilation directly on beta 2 receptors

30
Q

Onset of action, DOA, route of administration of beta agonists

A

Onset - rapid, within minutes
DOA - short, 4-6 hours
Route - inhalation, aerosol, powder or nebulized, orally, SQ

31
Q

Side effects of beta agonists

A

minimized by inhalation delivery, tremor, increased HR, vasodilation, hyperglycemia, hypokalemia, hypomagnesemia

32
Q

Albuterol dosing

A

inhaler 100 mcg/puff; 2 puffs q 4-6hours

nebulizer 2.5-5 mg in 5mL of saline

33
Q

Albuterol effect with volatile anesthetics

A

additive effect on bronchomotor tone

34
Q

Albuterol side effects

A

tachycardia, hypokalemia, blunt airway responses to tracheal intubation

35
Q

Which volatile agent should be avoided in asthmatics?

A

Desflurane

36
Q

Dosing considerations for Metaproterenol-Alupent

A

not to exceed 16 puffs/day

administered via a metered dose

37
Q

Dosing considerations for Pirbuterol-Maxair

A 
2 puffs (400 mcg) via metered dose
not to exceed 12 inhalations/day
38
Q

Terbutaline dosing and route administration(s)

A 
oral, SQ, inhalation 
SQ = response of epi
Child SQ dose = 0.01 mg/kg
Adult SQ dose = 0.25 mg q 15 minutes
inhaler = 16-20 puffs/day (200 mcgs per dose)
39
Q

Long acting beta agonists

A

have a lipophilic side chain that resists degradation
duration 12-24 hours
good for prevention

40
Q

Anticholinergics MOA

A

competitive antagonist at muscarinic acetylcholine receptors

41
Q

by antagonizing endogenous ACh leads to

A

bronchorelaxation, decreased mucus secretion

42
Q

what are anticholingeric used for?

A

treatment of COPD, secondary treatment of asthma that are resistant to beta agonist or significant cardiac disease

43
Q

should asthma patients be on long acting beta agonists?

A

not unless they’re on a corticosteroid otherwise high risk of death

44
Q

atropine

A

1-2mg diluted in 3-5 mL of saline via neb

highly absorbed and can cause systemic effects including tachycardia, nausea, dry mouth, GI upsest

45
Q

ipratropium bromide

A

antagonizes the effect of endogenous acetylcholine at M3 receptors

46
Q

ipratropium bromide dosing

A

inhaler 40-80 mcg in 2-4 puffs
slow onset 30 minutes
DOA 4-6 hours

47
Q

Methylxanthines- Phosphodiesterase Inhibitors MOA

A

nonspecific inhibition of phosphodiesterase isoenzymes which prevents cAMP degradation in airway smooth muscle as well as in inflammatory cells that leads to airway relaxation and bronchodilation

48
Q

What is something you want to monitor with someone taking theophylline?

A

blood levels
has narrow therapeutic index
therapeutic level 10-20mcg/mL
toxic level >20 mcg/mL

49
Q

Which inhalational agent should you take caution using with theophylline?

A

halothane

50
Q

Which bronchodilator is contraindicated with drugs metabolized by the CYP450 system?

A

theophylline

51
Q

side effects of methylxanthines- PIs

A

HA, N/V, irritability, insomnia, cardiac arrhythmias, seizures, stevens johnson syndrome

52
Q

inhaled corticosteroids MOA

A

major preventive treatment for asthma
alter genetic transcription
reduce the number of inflammatory cells in the airways and the damage to airway epithelium

53
Q

which drug class is considered the most important in managing asthma?

A

inhaled corticosteroids

54
Q

Anesthesia considerations for inhaled corticosteroids

A

give 1-2 hours preop, prolongs the response of beta agonists, may have 5 day course of combined corticosteroid and albuterol to minimize the risk of intubation evoked bronchospasm

55
Q

side effects of corticosteroids

A

oropharyngela candidiasis, osteopenia/osteoporosis, delayed growth, hoarseness, hyperglycemia

56
Q

Cromolyn MOA

A

stabilize mast cells
inhibits antigen-induced release of histamine and immediate allergic response to an antigen
administered via inhalation 4x/day

57
Q

Cromolyn side effects

A

infrequent but serious!

laryngeal edema, angioedema, urticaria, anaphylaxis

58
Q

leukotriene inhibitors MOA

A

inhibit leuokotriene pathways which are synthesized by arachidonic acid when inflammatory cells are activated

59
Q

Examples of leukotriene inhibitors

A

zileuton and montelukast

60
Q

zileuton MOA and why it isn’t widely used

A

blocks biosynthesis of leukotrienes from arachidonic acid leading to bronchodilation and improves asthma symptoms

not widely used because it is hepatotoxic and can cause hepatitis

61
Q

montelukast-singulair MOA and which drug to use with caution

A

block the mechanism of bronchoconstriction and smooth muscle effects improving bronchial tone, pulmonary function, and asthma symptoms

use caution with warfarin because it can prolong the PT

62
Q

Omalizumab

A

anti-IgE monoclonal antibody derived from DNA that is given in the early and late phase of asthmatic response
decreases quantity of IgE and prevents binding to mast cells
very expensive and inconvenient
last ditch effort

Pharmacology II - CP (12 decks)

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