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Foundations of Medicine 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define pharmacology

A

The study of substances that interact with living systems through chemical processes, especially by binding to regulatory molecules and activating or inhibiting normal body processes.

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2
Q

define medical pharmacology

A

the science of substances used to prevent, diagnose, and treat disease.

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3
Q

Define toxicology

A

branch of pharmacology that deals with undesirable effects of chemical on living systems, from cells to humans to ecosystems.

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4
Q

What is diphenhydramine?

A

Benadryl, Sominex: a first gen anti-histamine used for tx of allergic rhinitis, sneezing, itching, urticaria, motion sickness, insomnia

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5
Q

What is the mechanism of action of diphenhydramine?

A

H1 receptor inverse agonist that stabilizes inactive conformation of H1 receptors, blocking effects of histamine on H1 in the GI tract, large bv’s, bronchial smooth muscle, uterus, and suppresses the formation of edema, flare, and pruritus.

Produces sedation in CNS

Antimuscarinic effects: relieves nausea, vomiting, and vertigo associated with motion sickness. Also has anti-Parkingsonian effects

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6
Q

Adverse reactions of diphenhydramine

A

CNS: confusion, dizziness, sedation

Antimuscarinic effects: myriasis, xerostomia, reduced bronchial secretions, tachycardia, constipation, urinary retention.

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7
Q

Precautions of diphenhydramine

A

Asthma, heart disease, hepatic disease, glaucoma, bladder obstruction, urinary retention, or in infants (SIDS)

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8
Q

Pharmacokinetics of diphenhydramine

A

Hepatic metabolism by CYP2D6, can be taken PO, topically, IV, or IM. PO onset 15-30 minutes, duration of 4-6 hours.

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9
Q

What is Cetirizine?

A

Zyrtec: a 2nd gen antihistamine, the active metabolite of first gen hydroxyzine for tx of allergic conditions. Also has sedation effects, but much less sedating than older anti-histamines. Zyrtec-D when formulated with pseudo ephedrine.

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10
Q

Mechanism of action of Cetirizine

A

H1 receptor inverse agonist, stabilizing inactive form of receptor and blocking histamine effects. Minimal antimuscarinic effects.

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11
Q

Pharmacokinetics of Cetirizine

A

PO tabs, usually 5-10 mg QD, last 24 hours. Low CNS accumulation, effluxed via P-glycoproteins pumps. 50% metabolized in liver by CYP3A4

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12
Q

Adverse effects and counter indications of Cetirizine

A

Few adverse reactions, CNS high doses can lead to sedation or fatigue, xerostomia. Avoid if renal CrCL is

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13
Q

What is Fexofenadine?

A

2nd generation antihistamine; active metabolite terfenadine. TX for allergic conditions (rhinitis, sneezing, itching, urticaria)

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14
Q

Mechanism of action of fexofenadine

A

H1 receptor inverse agonist, stabilizes the inactive conformation of H1 receptors; blocks the effects of histamine on H1 receptors in the GI tract, uterus, large blood vessels, and bronchial muscle and suppresses the formation of edema, flare, and pruritus. Virtually no antimuscarinic activity at therapeutic doses.

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15
Q

Pharmacokinetics of fexofenadine

A

Administered PO as tabs, disintegrating tabs, or suspension, usually 30-60 mg BID or 180 mg QD; duration

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16
Q

Adverse effects and counter indications of fexofenadine

A

Few adverse reactions. GI: nausea, dyspepsia (1.5%). CNS: drowsiness, sedation (1.3%)

Decrease dose in patients with decreased renal function
Avoid taking with fruit juices, get decreased absorption

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17
Q

What is loratadine?

A

2nd generation antihistamine. TX for allergic conditions (rhinitis, sneezing, itching, urticaria). Formulated with pseudoephedrine as Claritin-D®. Desloratidine (Clarinex®) is active metabolite of loratidine.

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18
Q

Mechanism of action of loratadine

A

H1 receptor inverse agonist, stabilizes the inactive conformation of H1 receptors; blocks the effects of histamine on H1 receptors in the GI tract, uterus, large blood vessels, and bronchial muscle and suppresses the formation of edema, flare, and pruritus. Little or no antimuscarinic activity at therapeutic doses.

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19
Q

Pharmacokinetics of loratadine?

A

Administered PO as tabs, disintegrating tabs, or syrup, usually 10 mg QD; duration > 24 hr. Low CNS accumulation; effluxed from the CNS via the P-glycoprotein pump system. Extensive CYP3A4 metabolism in liver → drug interactions.

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20
Q

Adverse effects and counterindications of loratadine

A

Few adverse reactions. CNS: headache, sedation. Xerostomia (3%).

Hepatic disease.
If CrCL

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21
Q

What is cimetidine?

A

First commercially available drug for peptic ulcer disease. Indicated for GERD, peptic ulcer disease, intermittent dyspepsia.

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22
Q

Mechanism of action of Cimetidine

A

Inverse agonist, reduces constitutive activation of H2 receptors on parietal cells. Decreases acid secretion by 60-70%.

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23
Q

Pharmacokinetics of Cimetidine

A

Available for PO or IV dosing, usually 100-400 mg BID-QID or 800 mg HS. Nonselective inhibitor of CYP enzymes → many drug interactions possible.
Newer H2 blockers (ranitidine, nizatidine, famotidine) have little or no CYP inhibition.
~ 48% is excreted unchanged in the urine

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24
Q

Adverse effects and counter indications of Cimetidine

A

Moderate-to-severe headaches (3%). Rare blood dyscrasias: neutropenia, agranulocytosis, leukopenia, thrombocytopenia, pancytopenia.

Hepatic disease
Renal insufficiency

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25
Q

What is Ergotamine?

A

Ergot alkaloid used to relieve migraines; ~ 70% effective in controlling acute attacks

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26
Q

Mechanism of action of ergotamine.

A

MOA is complex; some of the pharmacologic actions are unrelated to each other and some actions are even mutually antagonistic. Partial agonist or antagonist activity at 5-HT, DA, and a-adrenergic receptors; causes vasoconstriction of arteries and veins and ↓ blood flow to the extremities. Oxytocic agent: ↑ force and frequency of uterine contractions, ↓ postpartum bleeding by constricting the placental vascular bed

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27
Q

Pharmacokinetics of ergotamine.

A

Formulated alone or with caffeine, atropine, and/or pentobarbital; administered PO or SL; absorption is incomplete and erratic. Migraine relief is obtained in 30-120 min; vasoconstricting effects last ~ 48 hr. Ergotamine is mostly metabolized by CYP3A4.

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28
Q

Adverse effects and counter indications of ergotamine.

A

GI: NVD (10%), xerostomia
Ergotism: angina, asthenia, coronary vasospasm, cramps, myalgia, paresthesias, changes in HR; vasoconstriction may result in hypothermia or tissue necrosis.

CV: angina, arteriosclerosis, coronary artery disease, hypertension, peripheral vascular disease, Raynaud’s disease, thrombophlebitis, MI, stroke
Hepatic disease, biliary tract disease, cholestasis
Renal failure or impairment
FDA Pregnancy Risk Category X

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29
Q

What is Sumatriptan?

A

Approved for the TX of acute migraine with or without aura; give ASAP after onset.
Not for long-term migraine prophylaxis

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30
Q

Mechanism of action of Sumatriptan.

A

Agonist at presynaptic 5-HT1D autoreceptors and at vascular 5-HT1B receptors → vasoconstriction

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31
Q

Pharmacokinetics of Sumatriptan.

A

Available PO, SC, or as nasal spray; PO dose of 25-100 mg give ~ 70% pt response rate after 60 min
SC gives most consistent peak blood levels; onset of pain relief after SC injection within ~ 10 min, and as many as 80% of patients experience relief within 60 min
Approximately 80% of a dose undergoes hepatic metabolism, mostly by MAO-A. Excretion of metabolites is via feces and urine.

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32
Q

Adverse effects and counter indications of Sumatriptan.

A

Potentially fatal CV events: coronary artery vasospasm, arrhythmias, MI, cardiac arrest.
GI: NVD, vasospastic effects leading to bowel ischemia, abdominal pain, bloody diarrhea, and cramping.
Injection site reaction (50%): pain, burning.

CV: angina, arteriosclerosis, arrhythmias, coronary artery disease, hypertension, peripheral vascular disease, Raynaud’s disease, thrombophlebitis, MI, stroke; evaluate CV function before prescribing
Ischemic bowel disease
Hepatic disease
Renal insufficiency

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33
Q

What is natural hydrocortisone and what does it do?

A

the main glucocorticoid in humans, released from adrenals by adrenocorticotropic hormone.

Stimulates gluconeogenesis → ↑ blood glucose, ↑ insulin secretion
Promotes lipolysis and lipogenesis → ↑ fat deposition
Stimulates protein, bone catabolism
CNS: ↑ mood, ↑ motor activity, ↓ sleep, ↓ memory
Immunosuppressive, antiinflammatory effects

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34
Q

What is medicinal hydrocortisone?

A

Natural steroid hormone secreted by the adrenal cortex
Main uses are antiinflammatory: anaphylaxis, asthma, COPD, inflammatory bowel disease, rheumatic disorders, dermatoses (pruritus, psoriasis, contact dermatitis, urticaria, insect stings). DOC for glucocorticoid replacement therapy in patients with adrenal insufficiency. Low potency topical corticosteroids are the safest for chronic use and may be used in infants and young children

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35
Q

Mechanism of action of hydrocortisone.

A

Acts via nuclear receptors to modulate gene expression
Anti-inflammatory: represses COX-2 expression; ↓ cytokine production, decreased formation and release of endogenous inflammatory mediators; causes apoptosis of eosinophils

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36
Q

Pharmacokinetics of hydrocortisone

A

Available in various forms for IV, IM, PO, or topical administration. Biological half-life of hydrocortisone is 8-12 hr.

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37
Q

Adverse effects and counterindications of hydrocortisone

A

Essentially none, even with large doses, if given for

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38
Q

What is prednisone?

A

Immunosuppressive oral corticosteroid; most-prescribed oral corticosteroid. TX for autoimmune disorders, allograft rejection, asthma, inflammatory bowel disease, rheumatoid arthritis, and other inflammatory states.

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39
Q

Mechanism of action of prednisone

A

Prodrug of prednisolone, must be metabolized in vivo to prednisolone. Acts via nuclear receptors to modulate gene expression.
Anti-inflammatory: represses COX-2 expression; ↓ cytokine production, decreased formation and release of endogenous inflammatory mediators; causes apoptosis of eosinophils.

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40
Q

Pharmacokinetics of prednisone

A

Given PO, doses range from 5-100 mg QD depending on disease. Metabolized in the liver to prednisolone
t1/2 ~ 18-36 hr.

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41
Q

Adverse effects and counterindications of prednisone.

A

CNS: headache, insomnia, vertigo, depression, anxiety, euphoria, personality changes, psychosis
GI: NVD, anorexia, gastritis
Cataracts
Opportunistic infections

Cushing’s syndrome
High doses and long-term therapy can suppress hypothalamic-pituitary-adrenal system; avoid abrupt DC of prolonged therapy
Preexisting bacterial, viral, fungal infections
Patients receiving corticosteroids chronically should be periodically assessed for cataracts

42
Q

What is aspirin?

A 
The first NSAID, synthesized in 1853 and marketed in the late 1890s
NSAID of the salicylate chemical class
Used for thrombosis prevention; prevents or reduces the risk of MI in patients with a history of MI, coronary bypass, angioplasty, angina, stroke, transient ischemic attacks (TIAs)
43
Q

Mechanism of action of aspirin

A

Irreversible inhibitor of COX enzymes, ~ 5-fold selective for COX-1 vs. COX-2

44
Q

Pharmacokinetics of aspirin

A

Dosing is usually 325-650 mg PO QID PRN for inflammation, pain, fever.
For thrombosis prevention, dosing is usually 80-325 mg QD.
Antiplatelet effect lasts 8-10 days; in other tissues, synthesis of new COX replaces inactivated COX so that ordinary doses have a duration of action of 6-12 hr
Metabolized in the liver to salicylic acid and related compounds which are excreted in the urine.

45
Q

Adverse effects of counter indications of aspirin

A 
GI disturbances (2-30%; dose-dependent): NVD, mucosal damage, bleeding, pain. Tinnitus or hearing loss with high doses. Hypersensitivity and anaphylactic reactions
Incidence: patients with chronic urticaria (20%), asthma (4%), or chronic rhinitis (1.5%). Sensitivity manifests as bronchospasm in asthmatics and is commonly associated with nasal polyps; the correlation of aspirin hypersensitivity, asthma, and nasal polyps is known as the aspirin triad.

Children

46
Q

What is the aspirin triad?

A

aspirin hypersensitivity, asthma, and nasal polyps

47
Q

What is ketorolac?

A

Promoted mainly as a strong analgesic, not as an anti-inflammatory drug.
Used short term (≤ 5 days) for postsurgical pain that requires analgesia at the opioid level.

48
Q

Mechanism of action of ketorolac

A

Competitive inhibitor of COX enzymes, ~ 100-fold selective for COX-1 vs. COX-2

49
Q

Pharmacokinetics of ketorolac

A

Formulated as tables, parenteral solution, and ophthalmic solution. Usual regimen is a single IV (30 mg) or IM (60 mg) dose. Parenteral dosing followed by 10 mg PO QID. Well-absorbed, oral F = 1
> 90% excreted in the urine, 40% as hepatic metabolites and 60% unchanged

50
Q

Adverse effects and counter indications of ketorolac

A

CNS: headaches, dizziness, drowsiness
GI (1-10%): NVD, damage to mucosa, gastric bleeding, abdominal pain

Salicylate sensitivity
Aspirin triad
CrCL

51
Q

What is indomethacin?

A

NSAID of the indole and indene acetic acid class.

In premature infants, indomethacin is used to accelerate closure of patent ductus arteriosus (PDA).

52
Q

Mechanism of action of indomethacin.

A

Competitive inhibitor of COX enzymes, ~ 3-5-fold selective for COX-1 vs. COX-2

53
Q

Pharmacokinetics of indomethacin

A

Administered PO, rectally, or IV (for PDA closure; 3 doses 12 hr apart). Usual anti-inflammatory dose is 50–70 mg TID. Metabolized in the liver and undergoes enterohepatic recirculation. About 60% is recovered in the urine as drug and metabolites and 33% is recovered in the feces.

54
Q

Adverse effects and counter indications of indomethacin

A 
CNS: dizziness (3-9%), headache (> 10%), fatigue/malaise (1-3%), depression, tremor, ataxia
GI disturbances (1-9%): NVD, damage to mucosa, gastric bleeding, abdominal pain

Salicylate sensitivity
Aspirin triad
Heart disease
Hepatic disease
Prior history of GI bleeding or perforation
Bleeding disorders: hemophilia, thrombocytopenia, vitamin K deficiency
CNS: seizure disorder, Parkinson’s disease, major depression or other psychiatric disturbance
Pregnancy Risk Category D if in 3rd trimester, otherwise Category B

55
Q

What is naproxen?

A 
Naphthylpropionic acid class NSAID
Marketed as S-enantiomer
56
Q

Mechanism of action of naproxen

A

Competitive inhibitor of COX enzymes, ~ 3-5-fold selective for COX-1 vs. COX-2

57
Q

Pharmacokinetics of naproxen

A

Available as tablets, gel caps, enteric-coated tablets, oral suspension; usual dose for RA is 250-500 mg BID
F = 0.95, t1/2 = 12-17 hr, steady state reached in 3-5 days
Extensive hepatic metabolism and conjugation, ~ 95% excreted in urine,

58
Q

Adverse effects and counter indication of naproxen

A

GI: NVD, damage to mucosa, gastric bleeding, abdominal pain; risk of upper GI bleeding is double that of OTC ibuprofen
DERM: rashes, urticaria, alopecia

Salicylate sensitivity
Aspirin triad
Heart disease
Hepatic disease
Prior history of GI bleeding or perforation
Bleeding disorders: hemophilia, thrombocytopenia, vitamin K deficiency

59
Q

What is ibuprofen?

A

NSAID of the phenylpropionic acid class

60
Q

Mechanism of action of ibuprofen

A

Competitive inhibitor of COX enzymes, ~ 2-fold selective for COX-1 vs. COX-2

61
Q

Pharmacokinetics of ibuprofen

A

Administered PO, 200-800 mg TID-QID PRN

Excreted in the urine, 50-60% as metabolites

62
Q

Adverse effects of counter indication of naproxen

A

CNS (

63
Q

What is meloxicam?

A

Potent enolcarboxamide NSAID

Indicated for rheumatoid arthritis or osteoarthritis

64
Q

Mechanism of action of meloxicam

A

Competitive inhibitor of COX enzymes, ~ 10-fold selective for COX-2 vs. COX-1

65
Q

Pharmacokinetics of meloxicam.

A

Available as tablets or oral suspension, usual dose is 7.5-15 mg QD
Highly bound to serum albumin, Vd ~ 10L
About 70% metabolized in the liver by CYP2C9 and CYP3A4, another 20% by peroxidases
Excretion of metabolites occurs equally through urine and feces

66
Q

adverse effects and counter indications of meloxicam.

A

GI: pain, dyspepsia, nausea

Salicylate sensitivity
Aspirin triad
Heart disease
Hepatic disease
Prior history of GI bleeding or perforation
Bleeding disorders: hemophilia, thrombocytopenia, vitamin K deficiency

67
Q

What is celecoxib?

A

First FDA-approved selective COX-2 inhibitor

68
Q

Mechanism of action of celecoxib.

A

Competitive inhibitor of COX enzymes, 10-20-fold selective for COX-2 vs. COX-1

69
Q

Pharmacokinetics of celecoxib.

A

Administered PO, usually 100-200 mg BID

> 97% is metabolized in the liver by CYP2C9

70
Q

Adverse effects and counter indications of celecoxib.

A

GI disturbances: dyspepsia (9%), NVD (3-6%), abdominal pain (4%)
Dizziness
Rash (2%)

Salicylate sensitivity
Aspirin triad
Heart disease
Hepatic disease
Prior history of GI bleeding or perforation
Bleeding disorders: hemophilia, thrombocytopenia, vitamin K deficiency

71
Q

What is diclofenac?

A

NSAID of the phenylacetic acid class

72
Q

Mechanism of action of diclofenac.

A

Competitive inhibitor of COX enzymes, ~ 10-20 fold selective for COX-2 vs. COX-1

73
Q

Pharmacokinetics of diclofenac.

A

Formulated as tablets, solution, and gel (topical); PO dosing is usually 50-75 mg BID; ER form available for 100 mg QD dosing
Metabolized in the liver mainly by CYP2C9 followed by glucuronidation or sulfation
Excretion is ~65% renal and ~35% biliary

74
Q

Adverse effect and counter indications of diclofenac.

A

GI disturbances: upset stomach, heartburn, bleeding, ulceration, perforation, elevated LFTs (2-4%)
Renal: ↓ blood flow, ↓ GFR

Salicylate sensitivity
Aspirin triad
Heart disease
Hepatic disease
Prior history of GI bleeding or perforation
Bleeding disorders: hemophilia, thrombocytopenia, vitamin K deficiency

75
Q

What is acetaminophen?

A

Has analgesic and antipyretic activity but no anti-inflammatory activity and no platelet effects.
Preferred analgesic/antipyretic for patients in whom aspirin is contraindicated.

76
Q

Mechanism of action of acetaminophen.

A

Competitive inhibitor of COX-1 and COX-2 enzymes within the CNS but not the periphery.
Binds to cannabinoid receptors in spinal cord.

77
Q

Pharmacokinetics of acetaminophen.

A

Administered PO, PR, IV, usually 325-500 mg QID, not to exceed 4 g QD.
In the liver, 85-90% is harmlessly metabolized but 10-15% is converted via CYP2E1, 1A2, or 3A4 to a chemically reactive, potentially hepatotoxic metabolite.
85% of a dose is renally excreted.

78
Q

Adverse effect and counter indications of acetaminophen

A 
Rash, pruritus, urticaria
GI disturbances (high dose): NV, anorexia, and abdominal pain usually occur within 2-3 hr after ingestion of toxic doses
Hepatotoxicity; in acute overdose, 2-3 days pass before maximum liver damage becomes apparent; antidote is IV N-acetyl cysteine
Renal tubule necrosis with high or chronic doses

Alcoholism
Hepatic disease
Renal disease; if CrCL

79
Q

What is alprostadil?

A

Synthetic PGE1 used for the treatment of erectile dysfunction (ED) in males and to temporarily maintain the patency of the ductus arteriosus in newborns until corrective or palliative surgery can be performed

80
Q

Mechanism of action of alprostadil

A

Agonist at EP receptors → ↑ cAMP production → vasodilation
Alprostadil induces erection by relaxation of trabecular smooth muscle and by dilation of cavernosal arteries; blood is entrapped by compression of venules (corporal veno-occlusive mechanism)
In neonates, prevents or reverses the functional closure that occurs shortly after birth, resulting in increased pulmonary or systemic blood flow in infants

81
Q

Pharmacokinetics of alprostadil

A

For ED, supplied as sterile lyophilized powder for intracavernosal use in 5, 10, 20 and 40 mg sizes; reconstituted with water for injection
For pediatric use, supplied as solution in alcohol which is diluted and administered by constant IV infusion, usually 0.05-0.1 mg/kg/min; t1/2 5-10 min
81% albumin-bound
Metabolized by one pass through the lungs, duration of action in ED is 12-70 min

82
Q

Adverse effects of alprostadil

A

ED: most common adverse effect is mild-to-moderate penile pain (37%); prolonged erection (4%) is a potential medical emergency; penile fibrosis (3%)
PEDS: fever (14%), apnea (12%), flushing (10%)

ED: regular follow-up of patients, with careful examination of the penis, is strongly recommended to detect signs of penile fibrosis
PEDS: infuse for the shortest time and at the lowest dose that will produce the desired effects

83
Q

What is latanoprost?

A

Synthetic PGF2 analog prodrug that is used to reduce elevated IOP in patients with open-angle glaucoma or ocular hypertension

84
Q

Mechanism of action for latanoprost

A

Selective FP receptor agonist, believed to reduce the IOP by increasing the outflow of aqueous humor
Produces 6-9 mm Hg reduction in IOP

85
Q

Pharmacokinetics of latanoprost

A

Formulated as a 0.005% ophthalmic solution, usual dose 1 gtt QV
Reduction of IOP begins 3-4 hr after administration and maximum effect is reached in 8-12 hr
Hydrolyzed by esterases in the cornea to the biologically active acid

86
Q

Adverse effects of latanoprost

A

OPT (5-15%): blurred vision, burning, itching, increased iris pigmentation (↑ melanin), eyelash changes

Active intraocular inflammation
Remove contact lenses for 15 min

87
Q

What is misoprostol?

A

Very potent synthetic prostaglandin analog used for the prevention of gastric ulcers, but slightly less effective than H2 antagonists
PO following mifepristone for early (

88
Q

Mechanism of action of misoprostol

A

Agonist at EP receptors on parietal cells in stomach → ↓cAMP → decreases acid secretion, promotes mucous and bicarbonate ion secretion, enhances mucosal gel protection
Agonist at EP receptors in uterus, stimulates and increases amplitude and frequency of uterine contractions, dilates cervix

89
Q

Pharmacokinetics of misoprostol

A

Formulated as 100 mg and 200 mg tablets for PO administration. To decrease stomach acidity, 100-200 mg given QID with food. In medical abortions, 48 hr following mifepristone, given as 2 x 200 mg for labor induction
Rapidly absorbed, peak levels are reached in 9-15 min and t1/2 = 20-40 min. Activity is apparent 30 min after PO administration and persists for at least 3 hr.

90
Q

Adverse effects and counter indications of misoprostol

A

CNS: headache (2%)
GI: diarrhea (14-40%), pain (7-20%), NV (3%)

Pregnancy Risk Category X; DC immediately if pregnancy occurs
♀ of childbearing potential should 1) exhibit a negative serum pregnancy test within 2 weeks of initiating therapy, 2) use effective and reliable means of contraception, 3) receive both oral and written warnings on potential hazards, and 4) should initiate therapy only on the 2nd or 3rd day of the next normal menstrual period

91
Q

What is Zileuton?

A

Benzothiophene derivative of N-hydroxyurea.

Indicated for the prophylaxis and chronic treatment of asthma.

92
Q

Mechanism of action of zileuton

A

Specific 5-LOX inhibitor → ↓ leukotriene (LTB4, LTC4, LTD4, and LTE4) formation.
Clinical response is inhibition of neutrophil and eosinophil migration, neutrophil and monocyte aggregation, leukocyte adhesion, decreased capillary permeability, decreased leukotriene-induced smooth muscle contractions.

93
Q

Pharmacokinetics of zileuton

A

Formulated as 600 mg tablets for QID dosing
Rapidly absorbed, mean time to peak plasma concentration ~1.7 hr, t1/2 ~2.5 h
Apparent Vd = 1.2 L/kg, 93% bound to plasma proteins
Substrate for CYP1A2, CYP2C9 and CYP3A4.

94
Q

Adverse effects and counter indications of zileuton

A

GI: dyspepsia (8%), elevated LFTs (2-5%)

Active liver disease
LFTs before treatment begins, monthly for the first 3 months, every 2-3 months for the remainder of the first year, and periodically thereafter
Not a bronchodilator, not used for acute episodes of asthma.

95
Q

What is Zafirleukast?

A

Synthetic, selective peptide leukotriene receptor antagonist indicated for the prophylaxis and chronic treatment of asthma in adults and children 5 years of age and older; prophylaxis only
First example of the leukotriene receptor antagonists, FDA approved in 1996

96
Q

Mechanism of action of zafirleukast.

A

Antagonist at G protein-coupled cysteinyl leukotriene receptors (cysLT1) in airway smooth muscles, mast cells, and neutrophils
Inhibits bronchoconstriction, edema, mucous secretion

97
Q

Pharmacokinetics of zafirleukast.

A

Supplied as 10 and 20 mg tablets for PO administration, usual adult dose is 20 mg BID. Rapidly absorbed, peak plasma concentrations are achieved in ~ 3 hr
Food can reduce the bioavailability; dosing should be with an empty stomach.
Zafirlukast is more than 99% bound to plasma proteins, predominantly albumin.
Extensively metabolized by CYP3A4 and CYP2C9, mean plasma half-life is 8-16 hr.
Most excretion of metabolites is via the feces with 10% excreted in the urine.

98
Q

Adverse effects and counter indications of zafirleukast.

A

Well-tolerated, adverse effects are rare; most common effects include headache, nausea, diarrhea; rare elevated LFTs.

Hepatic status: cirrhosis, acute hepatitis, cholestasis, alcoholism, smoking, age
Not a bronchodilator, not used for acute episodes of asthma.

99
Q

What is monetleukast?

A

Used for asthma maintenance therapy, prophylaxis only

Also used for TX of allergic rhinitis

100
Q

Mechanism of action of monteleukast

A

Antagonist at G protein-coupled cysteinyl leukotriene receptors (cysLT1) in airway smooth muscles, mast cells, and neutrophils
Inhibits bronchoconstriction, edema, mucous secretion

101
Q

Pharmacokinetics of monteleukast.

A

Given PO, usual adult dose is 10 mg QD
Rapidly absorbed; peak plasma concentration is achieved in 3-4 hr
Greater than 99% bound to plasma proteins resulting in a Vd of 8-11 L
Extensive hepatic metabolism via CYP3A4 and CYP2C9
Excreted almost exclusively in the bile with less than 0.2% excreted renally

102
Q

Adverse effects and counter indications of monteleukast

A

Rare: fever, indigestion, gastritis, cough

Hepatic status: cirrhosis, acute hepatitis, cholestasis, alcoholism, smoking, age
Not a bronchodilator, not used for acute episodes of asthma

Foundations of Medicine 1 (4 decks)

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