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Alfuzosin (uroxatral ®)

Oral: Adults:
: 10 mg once daily

Dosage adjustment in renal impairment: Bioavailability and maximum serum concentrations are increased by ~50% with mild, moderate, or severe renal impairment

Note: Safety has not been evaluated in patients with creatinine clearances <30 mL/minute.

Dosage adjustment in hepatic impairment:
Mild hepatic impairment: Use has not been studied.
Moderate or severe hepatic impairment (Child-Pugh class B and C): Clearance is decreased 1 /3 to 1 /4 and serum concentration is increased three- to fourfold; use is contraindicated

Tablet should be swallowed whole; do not crush or chew. Administer once daily (with a meal); should be taken at the same time each day.

[ Supplied: 10mg extended release tablet.]

Doxazosin (cardura ®)  

Mechanism of Action
The mechanism of action of CARDURA (doxazosin mesylate) is selective blockade of the alpha1 (postjunctional) subtype of adrenergic receptors. Studies in normal human subjects have shown that doxazosin competitively antagonized the pressor effects of phenylephrine (an alpha1 agonist) and the systolic pressor effect of norepinephrine. Doxazosin and prazosin have similar abilities to antagonize phenylephrine.

Oral:  Adults: 1 mg once daily in morning or evening; may be increased to 2 mg once daily. Thereafter titrate upwards, if needed, over several weeks, balancing therapeutic benefit with doxazosin-induced postural hypotension

Hypertension: Maximum dose: 16 mg/day

BPH: Goal: 4-8 mg/day; maximum dose: 8 mg/day

Elderly: Initial: 0.5 mg once daily

[Supplied 1 mg, 2 mg, 4 mg, 8 mg tablets]

Dutasteride (avodart ®) 

Mechanism of Action
Dutasteride inhibits the conversion of testosterone to dihydrotestosterone (DHT). DHT is the androgen primarily responsible for the initial development and subsequent enlargement of the prostate gland. Testosterone is converted to DHT by the enzyme 5α-reductase, which exists as 2 isoforms, type 1 and type 2. The type 2 isoenzyme is primarily active in the reproductive tissues, while the type 1 isoenzyme is also responsible for testosterone conversion in the skin and liver.

Dutasteride is a competitive and specific inhibitor of both type 1 and type 2 5α-reductase isoenzymes, with which it forms a stable enzyme complex. Dissociation from this complex has been evaluated under in vitro and in vivo conditions and is extremely slow. Dutasteride does not bind to the human androgen receptor.

AVODART is indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to:
improve symptoms,
reduce the risk of acute urinary retention (AUR), and
reduce the risk of the need for BPH-related surgery.

Combination With Alpha-Blocker:
AVODART in combination with the alpha-blocker tamsulosin is indicated for the treatment of symptomatic BPH in men with an enlarged prostate.

Adult (usual) - (BPH): 0.5 mg orally once daily.

[Supplied: 0.5 mg capsule]

Finasteride (proscar ®) 

The development and enlargement of the prostate gland is dependent on the potent androgen, 5α-dihydrotestosterone (DHT). Type II 5α-reductase metabolizes testosterone to DHT in the prostate gland, liver and skin. DHT induces androgenic effects by binding to androgen receptors in the cell nuclei of these organs.

Finasteride is a competitive and specific inhibitor of Type II 5α-reductase with which it slowly forms a stable enzyme complex. Turnover from this complex is extremely slow (t1/2~ 30 days). This has been demonstrated both in vivo and in vitro. Finasteride has no affinity for the androgen receptor. In man, the 5α-reduced steroid metabolites in blood and urine are decreased after administration of finasteride.

In man, a single 5 mg oral dose of finasteride produces a rapid reduction in serum DHT concentration, with the maximum effect observed 8 hours after the first dose. The suppression of DHT is maintained throughout the 24 hour dosing interval and with continued treatment. Daily dosing of finasteride at 5 mg/day for up to 4 years has been shown to reduce the serum DHT concentration by approximately 70%. The median circulating level of testosterone increased by approximately 10 to 20% but remained within the physiologic range.

Finasteride tablets are indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to:
Improve symptoms
Reduce the risk of the need for surgery including transurethral resection of the prostate (TURP) and prostatectomy.

Finasteride tablets are contraindicated in the following:

Hypersensitivity to any component of this medication.

Pregnancy. Finasteride use is contraindicated in women when they are or may potentially be pregnant. Because of the ability of Type II 5α-reductase inhibitors to inhibit the conversion of testosterone to DHT, finasteride may cause abnormalities of the external genitalia of a male fetus of a pregnant woman who receives finasteride. If this drug is used during pregnancy, or if pregnancy occurs while taking this drug, the pregnant woman should be apprised of the potential hazard to the male fetus.

Dosing -  Oral: Adults:
Male:  Benign prostatic hyperplasia (Proscar®): 5 mg/day as a single dose; clinical responses occur within 12 weeks to 6 months of initiation of therapy; long-term administration is recommended for maximal response
Male pattern baldness (Propecia®): 1 mg daily
Female hirsutism (unlabeled use): 5 mg/day

Tablet [film coated]:
Propecia®: 1 mg
Proscar®: 5 mg

Tamsulosin  (flomax ®)

Mechanism of Action
Tamsulosin, an alpha1 adrenoceptor blocking agent, exhibits selectivity for alpha1 receptors in the human prostate. At least three discrete alpha1-adrenoceptor subtypes have been identified: alpha1A, alpha1B and alpha1D; their distribution differs between human organs and tissue. Approximately 70% of the alpha1-receptors in human prostate are of the alpha1A subtype.

Flomax® (tamsulosin hydrochloride) capsules are not intended for use as an antihypertensive drug

Dosage - Oral: Adults:   BPH:   0.4 mg once daily ~30 minutes after the same meal each day; dose may be increased after 2-4 weeks to 0.8 mg once daily in patients who fail to respond. If therapy is interrupted for several days, restart with 0.4 mg once daily.

Dosage adjustment in renal impairment:
Clcr >/= 10 mL/minute: No adjustment needed
Clcr<10 mL/minute: Not studied

[Supplied: 0.4 mg capsule]

Terazosin (hytrin ®) 

Mechanism of Action
BPH: The reduction in symptoms and improvement in urine flow rates following administration of terazosin is related to relaxation of smooth muscle produced by blockade of alpha-1 adrenoceptors in the bladder neck and prostate. Because there are relatively few alpha-1 adrenoceptors in the bladder body, terazosin is able to reduce the bladder outlet obstruction without affecting bladder contractility.

HTN: The vasodilatory hypotensive action of terazosin appears to be produced mainly by blockade of alpha-1 adrenoceptors. Terazosin decreases blood pressure gradually within 15 minutes following oral administration.

Oral: Adults:
Hypertension: Initial: 1 mg at bedtime; slowly increase dose to achieve desired blood pressure, up to 20 mg/day; usual dose range (JNC 7): 1-20 mg once daily

Dosage reduction may be needed when adding a diuretic or other antihypertensive agent; if drug is discontinued for greater than several days, consider beginning with initial dose and retitrate as needed; dosage may be given on a twice daily regimen if response is diminished at 24 hours and hypotensive is observed at 2-4 hours following a dose

Benign prostatic hyperplasia: Initial: 1 mg at bedtime, increasing as needed; most patients require 10 mg day; if no response after 4-6 weeks of 10 mg/day, may increase to 20 mg/day

[Supplied 1, 2, 5, 10 mg capsule]


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