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Pharmacology N929 > Respiratory Agents > Flashcards

Respiratory Agents Flashcards

1
Q

SNS lung innervation

A

from thoracic ganglia, innervates smooth muscles of bronchi and pulmonary blood vessels

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2
Q

PSNS lung innervation

A

via vagus nerve, bronchoconstriction via mostly M3 and a little bit of M1

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3
Q

B2 adrenoreceptors cause (intracellular response)

A

increased intracellular cAMP which changes membrane potential of cells and decreases calcium release intracellularly, greater sensitivity to EPI v NE

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4
Q

Non adrenergic non cholinergic nerves (NANC)

A

excitatory: related to substance p and neurokinin
inhibitory: NO, peptide release

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5
Q

How do M3 mediate bronchoconstriction

A

via activation of IP3 (inositol triphosphate) which increases intracellular Ca2+ concentrations. also mediates mucous secretion.

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6
Q

asthma histologic mediators include

A

eosinophils, mast cells, neutrophils, macrophages, basophils, t lymphocytes, cytokines, interleukins, arachidonic acid metabolites, leukotrienes, prostaglandins, histamine, adenosine, platelet activating factor

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7
Q

emphysema/bronchitis pathological result

A

enlargement of air spaces, fibrosis, increased mucous production

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8
Q

treatment of airway outflow disorders (5 steps)

A
  1. short acting bronchodilators
  2. inhaled corticosteroids
  3. long acting bronchodilators
  4. PD3 inhibitors, methylxanthines, leukotriene inhibitor
  5. oral corticosteroid
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9
Q

bronchodilator med classes

A

beta agonists
anticholinergics
methylxanthines

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10
Q

short acting beta agonists (SALT)

A

terbutaline, albuterol, levalbuterol, salbutamol

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11
Q

long acting beta agonists

A

salmeterol, formoterol

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12
Q

B2 agonist bronchodilator MOA (general)

A

(3,5 cAMP production)
activate adenyl cyclase which increases production of cAMP (adenosine monophosphate) which causes bronchodilation. reduced intracellular calcium release and alters membrane conductance

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13
Q

B2 agonist bronchodilator effects (general desirable effects)

A

dilates bronchi, smooth muscle relaxation, inhibits mediator release from mast cells, increase mucus clearance by action in cells

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14
Q

B2 agonist SE’s (general)

A 
minimized by inhalation delivery
tremor
increased HR
vasodilation
metabolic changes including hyperglycemia, hypokalemia, hypomagnesemia
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15
Q

Albuterol class, dose, route of administration (2), duration of action, SE’s

A

beta 2 agonist
administered via metered dose at 100mcg/puff
2 puffs q4-6h
neb 2.5-5mg in 5ml of saline
can give 4 puffs to blunt AW response to tracheal intubation for asthmatics
duration 4 hours with relief evident up to 8h (additive effect with volatile anesthetics)
SE: tachycardia, hypokalemia,

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16
Q

isomers of albuterol

A

R albuterol levalbuterol- more affinity for B2

S albuterol more affinity for B1

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17
Q

Metaproterenol-Alupent class, route of administration, dose max

A

beta 2 agonist used for tx of asthma, administered via metered dose, dont exceed 16 puffs per day

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18
Q

Pirbuterol-Maxair class, dose, dose max

A

beta 2 agonist, administered via metered dose (400mcg), do not exceed 12 puffs/day

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19
Q

Terbutaline class, use, route of admin, dosage, drug comparison

A 
beta agonist
used to treat asthma
administered oral, SQ(SC), inhaled
SQ dose pedes .01mg/kg
SQ dose adults .25mg q15min
metered dose inhaler 16-20puffs/day
each dose 200mcg
SQ administration resembles response of epi
20
Q

Salmeterol and Formoterol class, duration, use, chemical consideration

A 
beta agonist
long acting, 12-24h duration
asthma prevention of flare
lipophilic side chains that resist degradation
salmeterol has fluticasone (steroid)
21
Q

Muscarinic Receptor Antagonist MOA

A

M1 and M3 most important in mediating smooth muscle relaxation and decreased mucous gland secretion, which produces bronchorelaxation and decreased secretions.

22
Q

Muscarinic Receptor Antagonist uses

A

tx of COPD

secondary line of tx for asthma (in patients resistant to B agonist or significant cardiac disease

23
Q

Atropine class, use, dose, route of administration, distribution, SE

A

muscarinic antagonist (naturally occurring alkaloid)
formally considered 1st line for asthma tx
1-2mg diluted in 3-5ml of saline via nebulizer
highly absorbed across respiratory epithelium
SE: systemic anticholinergic effects including tachycardia, nausea, dry mouth, GI upset

24
Q

Iatropium Bromide class, chemical structure, MOA, route of administration, dose, onset, duration of action, absorption consideration, SE

A

muscarinic antagonist
quaternary ammonium salt derivative of atropine
antagonizes effect of endogenous Ach at M3 receptor subtypes
administered via metered dose inhaler
40-80mcg in 2-4 puffs via nebulizer
slow onset of 30 min
duration 4-6h
not significantly absorbed compared to atropine
SE: dry mouth, Gi upset if oral absorption

25
Q

Tiotropium class, chemical structure, duration of action, absorption considerations, use

A 
muscarinic antagonist
quarternary ammonium salt
long acting 
not significantly absorbed across respiratory epithelium which results in few side effects
COPD
26
Q

Methylxanthine class, MOA, uses

A

(Inhibit breakdown of 3,5 cAMP)
PDE inhibitors
nonspecific inhibition of PDE isoenzymes (types III and V) which prevents cAMP degradation in airway smooth muscle as well as in inflammatory cells. causes airway relaxation and bronchodilation
used for COPD or asthma

27
Q

theophylline TI, caution, metabolism, excretion

A

TI 10-20mcg/ml
caution with halothane
drug-drug interactions r/t CYP450 metabolism (cimetidine, antifungals)
excreted in kidney

28
Q

methylxanthine (PDI) consideration r/t SE

A

because they have multiple MOA’s and are nonselective, have many SE’s and narrow TI

29
Q

methylxanthine PDI SE’s (general)

A 
headache
n/v
irritability, restlessness
insomnia
cardiac arrhythmias
seizures
SJS
30
Q

Inhaled corticosteroids MOA, use

A

alter genetic transcription by:

  • increasing transcription of genes for B2 receptor and anti inflammatory proteins
  • decreasing transcription of genes for pro inflammatory proteins
  • induce apoptosis in inflammatory cells (eosinophils, TH2, lymphocytes)
  • indirect inhibition of mast cells over time
  • reducing number of inflammatory cells in airways reduced damage to epithelium
  • vascular permeability is reduced which decreases airway edema
  • overall reduction in airway hyper-responsiveness
  • used as suppressive therapy, major preventive tx for patients with asthma (most important asthma mgmt)
31
Q

Inhaled Corticosteroid Examples (4)

A

beclomethasone
traimcinolone
fluticasone
budesonide

32
Q

Inhaled corticosteroid anesthesia considerations (periop use)

A

may consider use of corticosteroid 1-2h postop
prolong response of B agonists
may consider 5 day course of combined corticosteroid and albuterol to minimize risk of intubation invoked bronchospasm

33
Q

Corticosteroid inhaled and PO route considerations

A

80-90% of inhaled dose reaches oropharynx and is swallowed
higher airway concentration than same dose given PO
systemic effects decreased through inhalation

34
Q

Inhaled Corticosteroid SE’s

A 
oropharyngeal candidiasis
osteopenia/osteoporosis
delayed growth in children
hoarseness
hyperglycemia
35
Q

Cromolyn MOA

A

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

36
Q

Cromolyn use, administration, SE’s

A

prophylactic therapy of bronchial asthma (does not relieve allergic response after initiation, and is therefore not to be used as a rescue inhaler)
-administered via inhalation, take 4x daily
SE are rare but include laryngeal edema, angioedema, urticaria, anaphylaxis

37
Q

Leukotriene Inhibitors use

A

useful for bronchial asthma

38
Q

synthesis of leukotriene

A

from arachidonic acid when inflammatory cells are activated

39
Q

Zileuton class MOA, use, bioavailability, potency, SE

A

leukotriene inhibitor
lipoxygenase inhibitor which blocks biosynthesis of leukotrienes from arachidonic acid
produces bronchodilation, improves asthma symptoms, has shown long term improvement in PFT
low bioavailability and potency
hepatotoxicity is SE, not widely used because of many adverse effects

40
Q

Monteuklast-Singulair class, MOA, co administration considerations

A

leukotriene inhibitor
block mechanism of bronchoconstriciton and smooth muscle effects by blocking ability of leukotrienes to bind to cysteinyl leukotriene 1 receptor
improves bronchial tone, pulmonary function, and asthma symptoms
caution with co admin with warfarin which would prolong PT

41
Q

Anti IgE Antibodies and Asthma

A

since asthma is an IgE mediated allergic response, the idea is that the removal of the IgE antibodies from circulation would mitigate acute response of inhaled allergen

42
Q

Omalizumab class, use, route of administration, duration of administration, SE, drug considerations

A

monoclonal antibody derived from DNA, binds to IgE to decrease the quantity of IgE and prevent binding of IgE to mast cells. in response to lower levels of IgE, mask cells, basophils, and dendritic cells are down regulated

  • given in early and late phase of asthmatic response
  • given SQ for 2-4w/parenterally infused
  • SE: rare but triggering of immune response
  • high cost and inconvenience
43
Q

which drug class is most utilized for COPD

A

anticholinergics

44
Q

what are the two ways in which leukotriene inhibitors work

A

block synthesis of leukotriene via arachidonic acid or block receptors

45
Q

Methylxanthine examples

A

theophylline, aminophylline

Pharmacology N929 (11 decks)

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