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SBM Pharm term 1 > respiratory I + II > Flashcards

respiratory I + II Flashcards

1
Q

how do B2-agonists work?

A
  • binds to 4th transmembrane beta agonist receptor
  • GTP for GDP
  • G-alpha/GTP stimulates adenylate cyclase
  • stimulates cAMP
  • stimulates protein kinases
  • phosphorylation decreases Ca++ influx, increases Ca++ uptake, decreases actin myosin interactions and relaxes smooth muscle
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2
Q

what are some positive secondary effects of B2-agonists?

A
  • enhance mucociliary clearance
  • decrease microvascular permeability
  • suppress mediator release from inflammatory cells
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3
Q

what is unique about inhaled doses?

A

micrograms because of effective absorption

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4
Q

what metabolizes B2 agonists?

A

COMT/MAO

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5
Q

inhaled bioavailability of B2 agonists?

A

8-15%

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6
Q

timing of inhaled vs oral B2 agonists

A

inhaled - onset within minutes, peak in 15 minutes, duration 4-6 hrs
oral - onset in 30-60 mins, peak 1-3 hrs, duration 6-8 hours

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7
Q

B2 agonists adverse CVS effects

A
  • tachycardia, palpitations, flushing
  • exacerbation of angina. arrhythmias
  • vasodilates pulmonary artery - V/Q mismatch
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8
Q

B2 agonists adverse CNS effects

A
  • tremor, anxiety
  • headache
  • insomnia
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9
Q

B2 agonists adverse metabolic effects

A
  • hypokalemia, hyperglycemia
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10
Q

which is longer acting, albuterol or salmeterol and why?

A

salmeterol, it has a projecting arm and binds longer and stronger to the agonists binding site, so it can be given twice per day rather than 6 times for albuterol

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11
Q

unique potential danger of salmeterol

A

slight increase in sudden death vs albuterol

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12
Q

what are the two important anticholinergic respiratory drugs?

A
  • ipratroprium

- tiotropium (once daily so easier for patient and therefor becoming more popular)

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13
Q

big differences between anticholinergic and B2 agonist respiratory drugs?

A
  • anticholinergics have a somewhat slower onset and don’t dilate bronchioles quite to the same degree
  • anticholinergics and taste very bitter and some patients can’t stand it
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14
Q

ipratropium bioavailability

A
  • 8-15% gets into lungs

- less than 1% reaches systemic circulation

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15
Q

ipratropium duration

A

6-8 hours

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16
Q

contraindication for use of respiratory anticholinergics

A

renal impairment

17
Q

tiotropium vs ipratropium duration?

A

tiotropium much longer (24 hours) vs 6-8 hours

18
Q

what is the inhaled respiratory corticosteroid?

A

fluticasone

19
Q

what are the systemic respiratory corticosteroids and order of potency?

A
  • hydrocortisone 1.0
  • prednisone 4.0
  • methylprednisolone 5.0
  • dexamethasone 25-30
20
Q

summarize the antiflammatory mechanisms of corticosteroids

A

1 - inhibits enzymes producing PGs, LTs, TX, for example PLA2 and COX2
2 - inhibits gene transcription of inflammatory cytokines, IL-1, 3, 4, 5, 6, TNFa, GM-CSF
3 - induces enzymes that degrade bradykinin and tachykinin
4 - increase B2 agonist receptor transcription
5 - reduces histamine producing cell trafficking into airways

21
Q

inhaled corticosteroids bioavailability

A

about 10%, the other 90% is swallowed.

22
Q

inhaled corticosteroids metabolism

A

liver CYP3A

23
Q

local adverse effects of inhaled corticosteroids

A
  • thrush - C. albicans (gargle with water)

- hoarse voice

24
Q

systemic adverse effects of inhaled corticosteroids (at very high doses)

A
  • suppression of adrenal axis
  • bruising
  • cataracts
  • inhibit bone growth in children
  • behavioral disturbances
25
Q

acute effects of systemic corticosteroids

A
  • CNS insomnia/psychosis
  • metabolic - hyperglycemia, Na/H2O retention
  • suppress signs of infection
  • proximal myopathy
26
Q

chronic effects of systemic corticosteroids

A
  • adrenal suppression, cushings-like
  • hypertension
  • opportunistic infections
  • peptic ulcer
  • osteoporosis
  • cataracts
  • growth suppression
  • pancreatitis
  • femoral head necrosis
27
Q

what is the most potent bronchoconstrictor the body manufactures?

A

leukotrienes

28
Q

what are the leuktriene antagonist drugs and what are the mostly used for?

A
  • montelukast and other “lukasts”
  • used for maintenance therapy with other asthma drugs
  • safe for children
  • useful for aspirin induced asthma
  • effective against cold air and allergen induced asthma
29
Q

montelukast pharmacodynamics

A
  • bronchodilation in 1-2 hours

- blockade as long as 10-14 hours

30
Q

what is the mechanism of montelukast action?

A
  • competitive inhibitor at cys LT1 receptor
31
Q

montelukast adverse effects

A
  • nausea and vomiting
  • CNS, mild headaches
  • hepatitis, transaminitis
  • churg-strauss vasculitis
32
Q

what are a few second line anti-asthma drugs and what is their class?

A

fexofenidine - antihistamine
methotrexate, azathioprine - steroid sparing
monoclonal antibody - omalizumab

33
Q

how does omalizumab work?

A
  • blocks IgE and reduces number of asthma exacerbations
34
Q

how is omalizumab given?

A

subcutaneous

35
Q

omalizumab adverse effects

A
  • hypersensitivity reaction
  • urticaria
  • thrombotic events??
  • local injection site reaction
36
Q

drugs absolutely contraindicated in asthma

A
  • b-blockers, never in acute asthma!!
  • cholinergic agonists like carbachol
  • adenosine
  • NSAIDs
37
Q

drugs relatively contraindicated in asthma

A

ACE inhibitors

38
Q

therapy for allergic rhinitis

A
  • reduce exposure to antigens
  • oral anti-histamine
  • topical disodium chromoglycate
  • topical glucocorticosteroids
  • topical ipratropium
39
Q

what is disodium chromoglycate used for and how does it work?

A
  • nasal rhinitis

- inhibits chloride channels and calcium flux, prevents release of cytokines from T-cells and eosinophils

SBM Pharm term 1 (9 decks)

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