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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
Tiotropium: enters the CNS?
No, because positively charged
26
Ipratropium: enters the CNS?
No, because positively charged
27
Cromolyn: class
Cromokalim derivative
28
Cromolyn: indications
prophylaxis in antigen and exercise induced asthma (especially in kids); allergic rhinitis and conjunctivitis (anti-inflammatory)
29
Cromolyn: PD
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
30
Cromolyn: tox
VERY RARE; cough/wheeze, headache, nausea
31
Cromolyn: special
cheap/old, but not used very often today because inhaled steroids are just much more effective
32
Fluticasone: class
inhaled Glucocorticosteroid
33
Fluticasone: indications
prophylaxis in mild/moderate asthma; can be combined with systemic steroids in chronic severe asthma to reduce systemic steroid requirement
34
Fluticasone: PD
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
35
Fluticasone: PK
more potent than beclomethasone, but shorter half life; ~10% reaches bronchi
36
Fluticasone: tox
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)
37
Fluticasone: excretion
metabolized by hepatic CYP3A
38
Fluticasone: special
not quite as effective as systemic steroids because NOT ABSORBED AS WELL ACROSS MUCUS MEMBRANES
39
Hydrocortisone: class
systemic Glucocorticosteroid
40
Hydrocortisone: indication
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)
41
Hydrocortisone: PD
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
Hydrocortisone: PK
Well absorbed (more so than inhaled steroids); one of the least potent steroids
43
Hydrocortisone: tox
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
Hydrocortisone: excr
metabolized by hepatic CYP3A
45
Hydrocortisone: special
VERY BAD SIDE EFFECTS!
46
Prednisone: class
Systemic glucocorticosteroid
47
Prednisone: indication
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
Prednisone: PD
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
Prednisone: PK
Well absorbed (more so than inhaled steroids); intermediate potency
50
Prednisone: tox
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
Prednisone: excr
metabolized by hepatic CYP3A
52
Prednisone: special
VERY BAD SIDE EFFECTS!
53
Methylprednisolone: class
Systemic glucocorticosteroid
54
Methylprednisolone: indication
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
Methylprednisolone: PD
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
Methylprednisolone: PK
Well absorbed (more so than inhaled steroids); intermediate potency
57
Methylprednisolone: tox
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
Methylprednisolone: excr
metabolized by hepatic CYP3A
59
Methylprednisolone: special
VERY BAD SIDE EFFECTS!
60
Montelukast: class
Leukotriene receptor inhibitor
61
Montelukast: indication
Asthma
62
Montelukast: PD
selective reversible inhibitor of cysteinyl leukotriene-1 receptor. blocks effects of cysteinyl leukotrienes (inflammatory cells which would bronchoconstrict)
63
Montelukast: special
Not as effective as β2 agonists | Used in patients with aspirin-induced asthma and kids
64
Montelukast: excr
Hepatic metabolism via CYP3A /2C9, excreted in bile and feces
65
Montelukast: PK
Bronchodilator effects within 1-2 hrs, lasting for 10-14 hrs | Oral absorption is good, but food ↓ bioavailability by 40%
66
Montelukast: tox
elevations in serum hepatic enzymes
67
Montelukast: monitor
serum hepatic enzymes
68
Montelukast: interactions
Does not inhibit CYP 450s in vitro or in vivo; CYP3A4 inducers (St. John’s Wort, phenobarbital) reduce its AUC by 40%
69
Fexofenadine: class
Histamine receptor (H1) blocker (2nd generation)
70
Fexofenadine: indication
allergic reactions, allergic rhinitis, mastocytosis, “cold” remedy, asthma; NO ANTI-EMETIC ACTIVITY!
71
Fexofenadine: PD
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
Fexofenadine: PK
well absorbed orally, T1/2 = 25h, enters CSF/CNS well
73
Fexofenadine: tox
unlike 1st generation, no Ach effects, less drowsiness, headaches, & GI disturbances
74
Fexofenadine: excr
hepatic metabolism by CYP3A
75
Fexofenadine: interactions
don’t give with drugs that have CNS depressant action (EtOH, other sedatives)
76
Fexofenadine: special
only of benefit to some asthmatics; NOT a primary treatment for asthma; more specific than 2nd generation drugs
77
Diphenhydramine: class
H1 blocker (central & periferal), Na channel blocker
78
Diphenhydramine: indication
Antihistamine (allergic reactions)
79
Diphenhydramine: PD
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
Diphenhydramine: PK
Well absorbed orally, T1/2 = 6-8h, enters CSF/CNS well
81
Diphenhydramine: tox
CNS (drowsiness/sedation, confusion), ACh side effects
82
Diphenhydramine: excr
Hepatic metabolism by CYP3A
83
Diphenhydramine: interactions
can prolong QTc; don’t give with drugs that have CNS depressant action (EtOH, other sedatives)
84
Diphenhydramine: special
less specific than 2nd generation drugs; Don’t use first generation agents in elderly --> confusion, sedation & ACh effects
85
Omalizumab: class
Anti-IgE monoclonal antibody
86
Omalizumab: indication
asthma
87
Omalizumab: PD
Binds to IgE and decreases effect of allergens that usually bind to these antibodies
88
Omalizumab: PK
??
89
Omalizumab: tox
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
Omalizumab: special
given every few weeks
91
Dextromethorphan: class
sigma opiate receptor agonist, NMDA antagonist
92
Dextromethorphan: indication
cough
93
Dextromethorphan: PK
good oral abs
94
Dextromethorphan: tox
NO opiate respiratory & gastrointestinal effects; confusion, drowsiness (both rare)
95
Dextromethorphan: excr
hepatic metabolism
96
Dextromethorphan: interactions
``` Adverse interaction with MAO inhibitor --> serotonin syndrome (due to increased serotonin levels (reuptake is blocked)) ```
97
Codeine: class
opiate mu receptor agonist
98
Codeine: indication
Analgesic, antitussive, & antidiarrheal
99
Codeine: PK
good oral absorption, hepatic metabolism by CYP2D6, metabolized to morphine, half-life 3-4 h
100
Codeine: tox
Opiate toxicity (CNS = euphoria or dysphoria, Respiratory = respiratory depression)
101
Codeine: special
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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