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M2 Pharmacology Jen > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Albuterol: classes

A

beta-2 adrenergic agonist

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2
Q

Albuterol: indications

A

asthma, COPD

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3
Q

Albuterol: PK

A

intermediate acting (3-6 hours); quick onset

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4
Q

Albuterol: PD

A

Binds to beta-2 receptor, produces stimulation of adenylyl cyclase (via G protein), cAMP and protein kinase levels increase, intracellular [Ca] drops, and bronchodilation occurs; also enhances mucociliary clearance, decreases microvascular permeability, and suppresses mediator release from inflammatory cells

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5
Q

Albuterol: tox

A

tachycardia, exacerbation of angina, arrhythmias, pulmonary artery vasodilation (increased V/Q mismatch), tremor, headache, hypokalemia, hyperglycemia

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6
Q

Albuterol: excretion

A

metabolized by hepatic COMT/MAO

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7
Q

Albuterol: special

A

loses selectivity with increased dose (will start to bind to beta-1 receptors); Tolerance/Tachyphylaxis –> decreased response to drug after repeated doses over a short period of time (due to decreased receptor expression)

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8
Q

Salmeterol: class

A

long-acting beta-2 adrenergic agonist

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9
Q

Salmeterol: indications

A

asthma, COPD (for prevention of bronchospasm)

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10
Q

Salmeterol: PD

A

Binds to beta-2 receptor, produces stimulation of adenylyl cyclase (via G protein), cAMP and protein kinase levels increase, intracellular [Ca] drops, and bronchodilation occurs; also enhances mucociliary clearance, decreases microvascular permeability, and suppresses mediator release from inflammatory cells

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11
Q

Salmeterol: PK

A

long acting (>12 hours), slower onset (hours)

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12
Q

Salmeterol: tox

A

tachycardia, exacerbation of angina, arrhythmias, pulmonary artery vasodilation (increased V/Q mismatch), tremor, headache, hypokalemia, hyperglycemia

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13
Q

Salmeterol: excretion

A

metabolized by hepatic COMT/MAO

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14
Q

Salmeterol: special

A

only prescribed with inhaled steroid (studies show increased risk of sudden cardiac death when taken alone); loses selectivity with increased dose (will start to bind to beta-1 receptors); Tolerance/Tachyphylaxis –> decreased response to drug after repeated doses over a short period of time (due to decreased receptor expression)

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15
Q

Formeterol: class

A 
beta-2, long acting
same class as Salmeterol
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16
Q

Formeterol: indication

A

asthma, COPD

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17
Q

Ipratropium: class

A

muscarinic receptor blocker (anticholinergic)

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18
Q

Ipratropium: indications

A

asthma, COPD (a bronchodilator)

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19
Q

Ipratropium: PD

A

binds to muscarinic receptor (M3), which is on smooth muscle, and blocks parasympathetic signals, leading to bronchodilation

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20
Q

Ipratropium: PK

A

slower onset than beta-2 agonists (albuterol, etc); 1% reaches systemic circulation; duration 6-8 hrs;

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21
Q

Ipratropium: tox

A

rare and only at high doses; horrible taste; Paradoxical bronchoconstriction; other rarities including tachycardia, GI dysfunction, bladder dysfunction (due to decreased parasympathetic signals)

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22
Q

Ipratropium: excretion

A

Inactive metabolites excreted in urine

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23
Q

Tiotropium: class

A 
Muscurinic blocker, long acting
same class as Atropine and Ipatropium
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24
Q

Tiotropium: indication

A

asthma, COPD

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25
Q

Tiotropium: enters the CNS?

A

No, because positively charged

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26
Q

Ipratropium: enters the CNS?

A

No, because positively charged

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27
Q

Cromolyn: class

A

Cromokalim derivative

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28
Q

Cromolyn: indications

A

prophylaxis in antigen and exercise induced asthma (especially in kids); allergic rhinitis and conjunctivitis (anti-inflammatory)

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29
Q

Cromolyn: PD

A

NOT a direct bronchodilator; Inhibits release of inflammatory mediators from mast cells; Suppresses effects of kinins on inflammatory cells; may inhibit sensory C-fiber endings –> reduced cough

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30
Q

Cromolyn: tox

A

VERY RARE; cough/wheeze, headache, nausea

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31
Q

Cromolyn: special

A

cheap/old, but not used very often today because inhaled steroids are just much more effective

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32
Q

Fluticasone: class

A

inhaled Glucocorticosteroid

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33
Q

Fluticasone: indications

A

prophylaxis in mild/moderate asthma; can be combined with systemic steroids in chronic severe asthma to reduce systemic steroid requirement

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34
Q

Fluticasone: PD

A

binds to glucocorticoid receptor, which then travels to nucleus and acts as transription factor; inhibits transcription of pro-inflammatory genes (cytokines) and promotes transcription of anti-inflammatory genes; induces apoptosis in eosinophils; acts on many types of cells (lymphocytes, mast cells, etc); net effect = bronchodilation a few hours after taking drug

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35
Q

Fluticasone: PK

A

more potent than beclomethasone, but shorter half life; ~10% reaches bronchi

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36
Q

Fluticasone: tox

A

local (thrush/C. albicans infection, hoarseness) and systemic (HPA axis suppression, bruising, cataracts, inhibition of long bone growth in kids, hypercholesterolemia, behavioral disturbances (out of control kids)

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37
Q

Fluticasone: excretion

A

metabolized by hepatic CYP3A

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38
Q

Fluticasone: special

A

not quite as effective as systemic steroids because NOT ABSORBED AS WELL ACROSS MUCUS MEMBRANES

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39
Q

Hydrocortisone: class

A

systemic Glucocorticosteroid

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40
Q

Hydrocortisone: indication

A

acute severe asthma (status asthmaticus) (still takes a couple of hours for effects to be seen), chronic maintenance therapy (to minimize the ongoing inflammatory process)

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41
Q

Hydrocortisone: PD

A

binds to glucocorticoid receptor, which then travels to nucleus and acts as transription factor; inhibits transcription of pro-inflammatory genes (cytokines) and promotes transcription of anti-inflammatory genes; induces apoptosis in eosinophils; acts on many types of cells (lymphocytes, mast cells, etc); net effect = bronchodilation a few hours after taking drug

42
Q

Hydrocortisone: PK

A

Well absorbed (more so than inhaled steroids); one of the least potent steroids

43
Q

Hydrocortisone: tox

A

Acute (Insomnia/psychosis/depression, hyperglycemia, Na and H20 retention, proximal myopathy, suppress signs of infection) and Chronic (HPA axis suppression, Cushingoid appearance, peptic ulcer, opportunistic infection, osteoporosis, posterior cataracts, growth suppression (kids), pancreatitis, aseptic necrosis of the femoral head)

44
Q

Hydrocortisone: excr

A

metabolized by hepatic CYP3A

45
Q

Hydrocortisone: special

A

VERY BAD SIDE EFFECTS!

46
Q

Prednisone: class

A

Systemic glucocorticosteroid

47
Q

Prednisone: indication

A

acute severe asthma (status asthmaticus) (still takes a couple of hours for effects to be seen), chronic maintenance therapy (to minimize the ongoing inflammatory process)

48
Q

Prednisone: PD

A

binds to glucocorticoid receptor, which then travels to nucleus and acts as transription factor; inhibits transcription of pro-inflammatory genes (cytokines) and promotes transcription of anti-inflammatory genes; induces apoptosis in eosinophils; acts on many types of cells (lymphocytes, mast cells, etc); net effect = bronchodilation a few hours after taking drug

49
Q

Prednisone: PK

A

Well absorbed (more so than inhaled steroids); intermediate potency

50
Q

Prednisone: tox

A

Acute (Insomnia/psychosis/depression, hyperglycemia, Na and H20 retention, proximal myopathy, suppress signs of infection) and Chronic (HPA axis suppression, Cushingoid appearance, peptic ulcer, opportunistic infection, osteoporosis, posterior cataracts, growth suppression (kids), pancreatitis, aseptic necrosis of the femoral head)

51
Q

Prednisone: excr

A

metabolized by hepatic CYP3A

52
Q

Prednisone: special

A

VERY BAD SIDE EFFECTS!

53
Q

Methylprednisolone: class

A

Systemic glucocorticosteroid

54
Q

Methylprednisolone: indication

A

acute severe asthma (status asthmaticus) (still takes a couple of hours for effects to be seen), chronic maintenance therapy (to minimize the ongoing inflammatory process)

55
Q

Methylprednisolone: PD

A

binds to glucocorticoid receptor, which then travels to nucleus and acts as transription factor; inhibits transcription of pro-inflammatory genes (cytokines) and promotes transcription of anti-inflammatory genes; induces apoptosis in eosinophils; acts on many types of cells (lymphocytes, mast cells, etc); net effect = bronchodilation a few hours after taking drug

56
Q

Methylprednisolone: PK

A

Well absorbed (more so than inhaled steroids); intermediate potency

57
Q

Methylprednisolone: tox

A

Acute (Insomnia/psychosis/depression, hyperglycemia, Na and H20 retention, proximal myopathy, suppress signs of infection) and Chronic (HPA axis suppression, Cushingoid appearance, peptic ulcer, opportunistic infection, osteoporosis, posterior cataracts, growth suppression (kids), pancreatitis, aseptic necrosis of the femoral head)

58
Q

Methylprednisolone: excr

A

metabolized by hepatic CYP3A

59
Q

Methylprednisolone: special

A

VERY BAD SIDE EFFECTS!

60
Q

Montelukast: class

A

Leukotriene receptor inhibitor

61
Q

Montelukast: indication

A

Asthma

62
Q

Montelukast: PD

A

selective reversible inhibitor of cysteinyl leukotriene-1 receptor. blocks effects of cysteinyl leukotrienes (inflammatory cells which would bronchoconstrict)

63
Q

Montelukast: special

A

Not as effective as β2 agonists

Used in patients with aspirin-induced asthma and kids

64
Q

Montelukast: excr

A

Hepatic metabolism via CYP3A /2C9, excreted in bile and feces

65
Q

Montelukast: PK

A

Bronchodilator effects within 1-2 hrs, lasting for 10-14 hrs

Oral absorption is good, but food ↓ bioavailability by 40%

66
Q

Montelukast: tox

A

elevations in serum hepatic enzymes

67
Q

Montelukast: monitor

A

serum hepatic enzymes

68
Q

Montelukast: interactions

A

Does not inhibit CYP 450s in vitro or in vivo; CYP3A4 inducers (St. John’s Wort, phenobarbital) reduce its AUC by 40%

69
Q

Fexofenadine: class

A

Histamine receptor (H1) blocker (2nd generation)

70
Q

Fexofenadine: indication

A

allergic reactions, allergic rhinitis, mastocytosis, “cold” remedy, asthma; NO ANTI-EMETIC ACTIVITY!

71
Q

Fexofenadine: PD

A

unclear mechanism for asthma, but effect may be due to reduced secretions into the airway; competitively inhibits H1 receptors found on SM and endothelium, causing decreased IP3, which leads to reduced Ca2+ and decreased endothelial contraction (gaps in vessel wall close up); decreases itching by reducing sensitivity of peripheral nociceptors.

72
Q

Fexofenadine: PK

A

well absorbed orally, T1/2 = 25h, enters CSF/CNS well

73
Q

Fexofenadine: tox

A

unlike 1st generation, no Ach effects, less drowsiness, headaches, & GI disturbances

74
Q

Fexofenadine: excr

A

hepatic metabolism by CYP3A

75
Q

Fexofenadine: interactions

A

don’t give with drugs that have CNS depressant action (EtOH, other sedatives)

76
Q

Fexofenadine: special

A

only of benefit to some asthmatics; NOT a primary treatment for asthma; more specific than 2nd generation drugs

77
Q

Diphenhydramine: class

A

H1 blocker (central & periferal), Na channel blocker

78
Q

Diphenhydramine: indication

A

Antihistamine (allergic reactions)

79
Q

Diphenhydramine: PD

A

competitively inhibits H1 receptors found on SM and endothelium, causing decreased IP3, which leads to reduced Ca2+ and decreased endothelial contraction (gaps in vessel wall close up); also has some anticholinergic effect (thus anti-emetic); decreases itching by reducing sensitivity of peripheral nociceptors.

80
Q

Diphenhydramine: PK

A

Well absorbed orally, T1/2 = 6-8h, enters CSF/CNS well

81
Q

Diphenhydramine: tox

A

CNS (drowsiness/sedation, confusion), ACh side effects

82
Q

Diphenhydramine: excr

A

Hepatic metabolism by CYP3A

83
Q

Diphenhydramine: interactions

A

can prolong QTc; don’t give with drugs that have CNS depressant action (EtOH, other sedatives)

84
Q

Diphenhydramine: special

A

less specific than 2nd generation drugs; Don’t use first generation agents in elderly –> confusion, sedation & ACh effects

85
Q

Omalizumab: class

A

Anti-IgE monoclonal antibody

86
Q

Omalizumab: indication

A

asthma

87
Q

Omalizumab: PD

A

Binds to IgE and decreases effect of allergens that usually bind to these antibodies

88
Q

Omalizumab: PK

A

??

89
Q

Omalizumab: tox

A

Gastrointestinal upsets, local injection site reactions, rashes/urticaria, secondary malignancies (very rare), delayed anaphylaxis (very rare) weeks after drug administration, ongoing study suggests increased cardiovascular and cerebrovascular events

90
Q

Omalizumab: special

A

given every few weeks

91
Q

Dextromethorphan: class

A

sigma opiate receptor agonist, NMDA antagonist

92
Q

Dextromethorphan: indication

A

cough

93
Q

Dextromethorphan: PK

A

good oral abs

94
Q

Dextromethorphan: tox

A

NO opiate respiratory & gastrointestinal effects; confusion, drowsiness (both rare)

95
Q

Dextromethorphan: excr

A

hepatic metabolism

96
Q

Dextromethorphan: interactions

A 
Adverse interaction with MAO inhibitor -->
serotonin syndrome (due to increased serotonin levels (reuptake is blocked))
97
Q

Codeine: class

A

opiate mu receptor agonist

98
Q

Codeine: indication

A

Analgesic, antitussive, & antidiarrheal

99
Q

Codeine: PK

A

good oral absorption, hepatic metabolism by CYP2D6, metabolized to morphine, half-life 3-4 h

100
Q

Codeine: tox

A

Opiate toxicity (CNS = euphoria or dysphoria, Respiratory = respiratory depression)

101
Q

Codeine: special

A

can be a drug of abuse; when nursing mothers are ultra-metabolizers (extra-active 2D6) and take codeine, high levels of morphine can be found in breast milk (can be lethal for baby)

M2 Pharmacology Jen (11 decks)

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