pharm drug list Flashcards

1
Q

short acting beta agonist

A
SABAs
albuterol (aka salbutamol)
levalbuterol
isoproterenol
terbutaline
epinephrine/ephedrine
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2
Q

SABA purpose

A

rescue meds

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3
Q

Long acting beta agonists

A
salmeterol
formoterol
indacaterol
arformoterol
olodaterol
vilanterol
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4
Q

LABAs purpose

A

some have a relatively fast onset and can reduce symptoms quickly but NOT a rescue medications

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5
Q

oral albuterol

A

oral syrups and tablets are available, but rarely used

  • slower onset <30 min peak effect 2-3 hours, duration 6-8 hours NOT a rescue med
  • more pronounced systemic side effects than inhalation due to large dose and systemic distribution
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6
Q

albuterol inhalation

A

onset 5 min
both inhaler and nebulizer are rescue

peak action:
ventolin 25 min
nebulizer: 1-2 hrs

duration 4-6 hours

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7
Q

SABAs can be used alone

A

with mild intermittent asthma or in patients with exercise induced bronchoconstriction
-good for occasional symptoms

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8
Q

indications that asthma is not well controlled

A

needing rescue medication more than twice a week - means enhance the controller medications

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9
Q

frequent use of SABA or routine use of LABAs

A

can result in tolerance

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10
Q

frequent use and poor response to SABAs

A

can indicate poor adherence to controller or incorrect technique

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11
Q

rescue medications

A

rapid acting bronchodilators are appropriate for rescue and should be made available to all patients with asthma

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12
Q

LABA box warning

A

can be useful in asthma as add on therapy to inhaled corticosteroids but should not be used as only controller therapy
-monotherapy increases risk of asthma related death and hospitalization

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13
Q

SAMA lists

A

ipratropium bromide

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14
Q

ipratropium dosing

A

quick action but not a rescue medication: onset 15 min
half life 1.6 hours/duration 4 hours
continuous treatment requires minimum of q6h dosing

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15
Q

indications for inhaled muscarinic antagonists

A

primary use: important bronchodilators in COPD

-some are approved as bronchodilators in asthma but are less effective than beta 2 agoinists

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16
Q

side effects of muscarinic antagonists

A

due to quarternary ammonium structure if swallowed may cause constipation

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17
Q

Long acting muscarinic antagonists lists

A

tiotropium bromide
aclidinium bromide
umeclidinium bromide
glycopyrronium

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18
Q

tiotropium

A
LAMA
onset 60 min 
duration 24-48 hrs
peak 5-7 min 
half life 5-6 days
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19
Q

aclindinium

A

LAMA
longer acting than tiotropium
plasma half live of 5-8 hours

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20
Q

Phosphodiesterase inhibitor (non-specific) list

A

theophylline

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21
Q

theophylline side effects

A
non-specific PDE inhibitor
is a methylxanthine
side effects:
CNS stimulation
bronchodilation
diuresis

compared with caffeine it causes less CNS stimulation and more bronchodilation

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22
Q

tobacco and theophyllines

A

theophylline is metabolized by CYP1A2

tobacco induces CYP1A2

the typical half-life of theophylline is 8 hours in smokers it is 4.5 hrs -problems of toxicity occur when patient quits smoking

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23
Q

theophylline toxicity reason

A

narrow therapeutic range (5-15 mg/L)

therapeutic index ED50/TD50 only 1 to 1.5 - toxic symptoms may occur at normal doses

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24
Q

theophylline toxic symptoms

A

Initial toxic symptoms: nausea/vomiting/abdominal pain, coarse muscle tremor.

Severe toxic symptoms: seizures, hypotension, and dysrhythmias.

If death occurs, usually due to intractable ventricular dysrhythmias.

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25
Q

MOA theophylline

A

inhibits phosphodiesterase isozymes and blocks the degradation of cAMP to 5’-AMP.

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26
Q

MOA ipratropium and tiotropium

A

block the stimulation of muscarinic receptors by acetylcholine (ACh) released from the vagus nerves and thereby attenuates reflex bronchoconstriction. The effect of ACh is mediated by IP3-induced calcium release and leads to smooth muscle contraction.

27
Q

PDE-4 inhibitors

A

roflumilast

28
Q

roflumilast MOA

A

phosphodiesterase (PDE) enzymes degrades cAMP
PDE-4 is a major isoform of PDE found in the lung tissue
this is a PDE-4 inhibitor

29
Q

roflumilast clinical role

A

prevent COPD exacerbation
used after LAMA and LABA and ICS
Very expensive

30
Q

roflumilast adverse effects

A

like the leukotrene antagonists may be associated with neuropsychiatric effects

-may decrease appetite/weight may cause nasuea and vomiting

31
Q

oral/systemic corticosteroids ie glucocorticoids list

A

prednisone
prednislone
methylprednisolone
dexamethasone

32
Q

risk of long term system glucocorticodids

A
  • infection risk
  • risk for developing diabetes, osteoporosis, weight gain, abnormal fat distribution
  • adrenal suppression (crisis)
  • hypertension
  • glaucoma, cataracts
  • restlessness/anxiety, insomnia/euphoria/psychosis
  • GI upset
  • hyperglycemia
33
Q

use of systemic oral glucocorticoids

A

acceptable and often required for SHORT term use in asthma or COPD exacerbation
-limit long term use

34
Q

Inhaled corticosteroids list

A

beclomethasone, Triamcinolone, budesonide, fluticasone

35
Q

inhaled corticosteroids are

A

the most effective controllers

-because with proper technique 20-30% of dose is deposited at the site of action

36
Q

inhaled corticosteroids and the need for a rescue medication

A

inhaled corticosteroids exert a delayed onset of action. Acute exacerbations require “rescue” medication, and may require systemic glucocorticoids

37
Q

ICS adverse effects

A
-thrush; candidias of the mouth/esophagus
     rinse mouth with water after use
-dysphonia
-throat irritation
-URI
-osteoporosis
38
Q

rare but serious side effects of ICS

A

hypercortisolism, anaphylaxis, hypersensitvity reaction, raised intraocular pressure, penumonia

39
Q

fluticasone

A

one of the most potent and most commonly ICS used ‘flovent -when alone
‘advair when in combination with salmeterol LABA

40
Q

budesonide

A

the only FDA ICS for pregnancy

lowest oral bioavalibilty

41
Q

triamcinolone

A

ICS lower potency than others, may requires more puffs to achieve moderate to high dose (3-4 per day)

42
Q

properties of ICS

A

full response can take 8 weeks

-not started during exacerbation (systemic are helpful not inhaled during exacerbation)

43
Q

regular use of ICS

A

Asthma symptoms nearly —absent, and prevent progression.

  • Reduce bronchial hyper-reactivity.
  • Decrease airway mucus production.
  • Increase the number of bronchial beta2 receptors as well as their responsiveness to beta2 agonists.- this reverses the tolerance and maintain B2 effect
44
Q

Degranulation inhibitors drug list

A

cromolyn

mast cell stabilizer

45
Q

antibody therapy drug list

A

omalizumab

46
Q

leukotriene inhibitor drug list

A

zileutin (a 5-lipoxygenase inhibitor)
montelukast (leukotriene receptor antagonists)
zafirlukast

47
Q

cromolyn MOA

A

inhibits mast cell degranulation

  • prevents histamine release
  • reduce the release of inflammatory leukotrienes
48
Q

cromolyn onset and use

A

onset may take 1-2 weeks
full benefit 3-4 weeks
for asthma, now only used by nebulizer (usually not used at all)

49
Q

omalizumab MOA

A

IgE binders

binds IgE and prevents activation of mast cells and basophils

50
Q

omalizumab limitations

A

only for refractory “allergic” asthma -eosinophilia
EXPENSIVE
and only administered in healthcare setting 3 injections in office for two hours

51
Q

omalizumab only in health care settings reason

A

Should only be administered in a healthcare setting by providers who are prepared to identify and treat anaphylaxis
-delayed hypersensitivity can occur (should dispense an epinephrine auto injector)

52
Q

omalizumab dose and frequency

A

based on serum IgE levels

300 mg injected SC every 2-4 weeks

53
Q

omalizumab pharmacokinetics

A

degraded in liver - excreted in bile
half life in 25 days
peak time after single SC injection 8 days

54
Q

montelukast MOA

A

cysLT1 receptor antagonists

cysLT1 creates sustained bronchoconstriction, mucus secretion and edema.

55
Q

montelukast in asthma

A

Prophylaxis and chronic treatment of asthma in patients 12 months of age and older.
Once daily in the evening.

56
Q

montelukast for EIB

A

Acute prevention of exercise-induced bronchoconstriction (EIB) in patients 6 years of age and older.
Dose = once daily PRN, 2 hours before exercise.

57
Q

montelukast for AR

A

Relief of symptoms of allergic rhinitis (AR): seasonal allergic rhinitis (SAR) in patients 2 years of age and older, and perennial allergic rhinitis (PAR) in patients 6 months of age and older.
Once daily.

58
Q

clinical role of leukoriene

A

Less effective than inhaled corticosteroids for asthma.

An accepted asthma-controller medication alternative to ICS (or adjunct) in mild, persistent asthma. (people or parents that don’t want to or don’t want their kids to take a inhaled corticosteroid)
receptor

59
Q

montelukast clinical role

A

For allergic rhinitis usually combined with an antihistamine and/or intranasal glucocorticoid…

  • A “compelling indication” for patients with allergic asthma?
  • Leukotrienes are released from nasal mucosa in response to allergen exposure symptoms: sneezing, nasal itching, & congestion
60
Q

zileuton MOA

A

inhibits 5-lipxygenase

only approved for asthma

61
Q

drugs for TB

A

rifampin, isoniazid, ethambutol, pyrazinamide, and bedaquiline

62
Q

Parameters to monitor when taking fluticasone

A
  • Bone mineral density (at baseline and periodically thereafter)
  • Ocular changes (IOP, catatracts)
  • Signs/symptoms of oral/systemic infection
  • Hypercotrisolism for adrenal suppression
63
Q

Parameters to monitor when taking a beta agonist (umeclidinium)

A

BP, HR, serum K+, glucose