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Summary Chamberlain College of Nursing - NR 566 week 6 complete study guide NR566 Week 6 Study Guide Latest Spring 2021. $12.99   Add to cart

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Summary Chamberlain College of Nursing - NR 566 week 6 complete study guide NR566 Week 6 Study Guide Latest Spring 2021.

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Summary Chamberlain College of Nursing - NR 566 week 6 complete study guide NR566 Week 6 Study Guide Latest Spring 2021.Summary Chamberlain College of Nursing - NR 566 week 6 complete study guide NR566 Week 6 Study Guide Latest Spring 2021.

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  • February 15, 2021
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NR 566 Week 6 Study Guide
Chapter 22: Drugs Affecting the Reproductive System
 Know the pharmacodynamics, pharmacotherapeutics, clinical use, drug interactions, and ADRs for:
Erectile dysfunction (ED) drugs, Estrogens and Progesterone, and Antiandrogen drugs

 Androgen drugs
o Testosterone is the primary male androgen
o Responsible for:
 Growth, maturation, and maintenance of male sex organs and secondary sexual
characteristics
 Skeletal growth spurt in adolescence and termination of linear growth by fusion of the
epiphyseal growth plate
 Activation of sebaceous glands (acne during puberty)
 Enhances production of erythropoietic stimulating factor, increased RBCs production
 Libido
o Androgen Drugs: testosterone propionate (in oil, DepoTesterone), testosterone enanthate (in oil,
Delatestryl), testosterone cypionate (in oil, Depo-Testosterone), methyltestosterone (Android,
Methitest, Testred, Virilon), testosterone gel (AndroGel 1%, AndroGel 1.62%, Axiron, Testium),
fluoxymesterone, TD testosterone (Testoderm, Androderm), and buccal testosterone (Striant)
 Used to treat Indicated for the symptomatic Tx of
 1) deficiency states in males associated with hypogonadism and
 2) in both sexes for d/os such as CA and HIB, Tx libido, endometriosis, and
postmenopausal symptoms in women, have been used illicitly to enhance athletic
performance and increase muscle mass
o Contraindicated: male breast CA, prostate CA, and Pregnancy (Category X), and lactation

 Antiandrogens: several different categories
o Androgen hormone inhibitors (5-alpha-reductase inhibitors)
 Drugs: Finasteride (Propecia, Proscar) and dutasteride (Avodart)
 MOA: Block conversation of testosterone to dihydrotesterone
 Used to Tx BPH
 PSA levels and digital prostate examination are required monitoring for men on these agents
 Finasteride (Propecia, Proscar):
 Extensive hepatic metabolism
 BPH: 5mg/day, 6 to 12 months of therapy until therapeutic response
o Regression of prostate size increased urinary flow, and improve BPH
symptoms
 Approved for Male pattern baldness: 1 mg/day, three months until results
 Stopping the drugs reverses the effect within 12 months
 ADRs: decreased libido, impotence (can occur at both doses)
 Dutasteride (Avodart)
 Inhibits both type 1 and 2 (5-alpha-reductase)
 Peak clinical effect 6 to 12 months of therapy
 Extensively metabolized in the liver (CYP3A4 and CYP3A5)

,  Used to Tx BPH
 Absorbed through the skin, women who are pregnant or may become pregnant should
not handle dutasteride capsules r/t risk of fetal anomaly to a male fetus
 ADR: decreased libido and impotence
o Gonadotropin-releasing hormone analogue: luteinizing hormone-releasing hormone
antagonist
 Leuprolide acetate (Lupron)
 Create a reversible chemical orchiectomy state in males and an oophorectomy state in
females
 Used to Tx: advanced prostatic CA and for management of endometriosis and uterine
leiomyomata (fibroids)
 1 mg SC daily or IM every 3 months (depot formulation)
 Increased suppression when used with flutamide (direct antiandrogen)
 Peds: Tx central precocious puberty
 Women: reducing uterine fibroids, endometriosis, and PCOS (pain relief, regain fertility)
o Direct antiandrogens
 Flutamide (Eulexin), bicalutamide (Casodex), and nilutamide (Nilandron)
 Inhibit androgen uptake or nuclear binding of androgen at target tissues
 Uses as part of combo therapy Tx of prostatic carcinoma
 Flutamide: competitive antagonist at the androgen receptor site
 Truly a nonsteroidal agent
 ADRs: gynecomastia and reversible liver toxicity
 Renal doses: less than 29 mL/min
 BLACK BOX WARNING: hepatic failure, hepatic encephalopathy, and death
o Usually within the first 3 months of therapy
o Baseline and monthly LFTs for the first 4 months of therapy and periodically
o D/c if any symptoms of hepatic injury or jaundice develop
o Spironolactone (Aldactone): aldosterone antagonist and inhibitor of 5-alpha-reductase
 used as a K sparing diuretic
 Off label use for Tx of female hirsutism and acne due to antiandrogenic properties
 50 to 200 mg/day
 Competitive inhibitor of the dihydrotestosterone, aldosterone, and interferes with the
androgen receptors in the prostate
 Also reduces 17-alpha-hydroxylase activity: lowers plasma levels of testosterone and
androstenedione
 Metabolized by the liver
 Short term use for primary hyperaldosteronism in patients preoperatively
 Long term: for those who are not good candidates for Sx with idiopathic hyperaldosteronism
 PMS/PMDD symptoms may be relieved by spironolactone (25 mg QID beginning on day 14
of the menstrual cycle)
 ADRs: dose-related and reversible when the drug is d/c GI upset, drowsiness, gynecomastia,
impotence, cutaneous eruptions, and urticaria
 BLACK Box Warning: r/t animal chronic toxicity studies demonstrated tumorigenicity
 Contraindications: pregnancy

 Drug Interactions

, o Finasteride: Nevirapine: Combo induces hepatic metabolism of finasteride: monitor for effectiveness
of finasteride
o Leuprolide: Pituitary, gonadotropic, and gonadal function lab test: misleading results: consider if lab
test reports show unexpected values
o Flutamide: Warfarin: Increased INR and risk of bleeding: monitor INR closely
o Spironolactone:
 renal impairment and agents that affect renal function: alternation in renal function and
electrolytes: monitor K in young patients with reduced renal function and patients greater
than 65 y/o
 Digitals: may increase or decrease digitalis half-life: Monitor closely for s/s of dig toxicity
and electrolyte and digitalis levels. Consider alternative Tx.
 Potassium: additive effect increases risk of hyperkalemia: recommend alternative
 Eplerenone (aldosterone receptor antagonist used for CHF): severe hyperkalemia:
Combination is contraindicated, do not use together, choose different therapy

Estrogens:
Drugs: estrogen (conjugated A/Synthetics)(Cenestin), esterified estrogen/methyltestosterone (Covaryx,
Covaryx HS, EEMT, EEMT HS), estrogen (conjugated B/Synthetic)(Enjuvia), estrogen (esterified)(Menest),
estrogen (conjugated/equine)(Premarin), estrogen (conjugated/equine) and Medroxyprogesterone (Premphase,
Prempro)
 Endogenous hormone with multiple actions
 Primary role: maturation and function of the female reproductive system
 Nonreproductive effects: bone, CV system, CNS, and GI tract
 Contraindication: estrogen-only products in women with an intact uterus
o Combo estrogen and progesterone products in these patients
Pharmacodynamics
 Estrogen occurs naturally in several forms
 Primary sources of estrogen in the normally cycling adult women is the ovarian follicle (70 to 500 mcg of
estradiol daily)
 This estradiol is converted to estrone: circulates in about equal amounts to the estradiol and too small
amounts of estriol
 After menopause: endogenous estrogen is generated from conversion by peripheral tissues of
androstenedione, secreted by the adrenal cortex, to estrone
 Effects of estrogen on the reproductive system
o Maturation of reproductive organs
o Development of secondary sex characteristics
o Regulation of the menstrual cycle
o Endometrial regeneration post menstruation
 Other physical effects:
o Closure of long bones after the pubertal growth spurt
o Maintenance of bone density by decreasing the rate of bone resorption through antagonizing the
effects of parathyroid hormone (PTH)
o Maintenance of the normal structure of skin and blood vessels through its actions on the endothelial
cells in the arterial wall, including the induction of NO to facilitate vasodilation and O2 uptake by
cells
o Reduction of the motility of the bowel through its modulation of SNS control over smooth muscle

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