Drugs for Men’s Health and Reproductive DisordersAnabolic activity Any trenbolone acetate douleur injection activity that promotes the building up of body tissues, anabolic steroids nursing considerations as the activity produced by testosterone that causes the development of bone and muscle tissue; also called anabolism. Androgenic anabolic steroids nursing considerations The activity produced by testosterone that causes the development and maintenance of the male reproductive system and male secondary sex characteristics. Androgens Male sex hormones responsible for mediating the development and maintenance of male sex characteristics. Chief among these are testosterone and its various biochemical precursors. Benign prostatic hyperplasia BPH also called consideratiosn Nonmalignant noncancerous enlargement of the prostate gland.
Men’s Health Drugs | Nurse Key
Substances Related to Male Reproductive Disorders. Critical Thinking Case Study. The authors gratefully acknowledge the work of Karen Carmody, who updated this chapter for the eighth edition.
Reproductive health requires the production of adequate quantities of various hypothalamic, pituitary, and gonadal hormones as well as the appropriate hormone receptors. It requires normal development and patency of the reproductive tract. In addition, reproductive health implies that men and women at developmentally appropriate life stages are fertile i. Finally, reproductive health entails the ability to engage in sexual intercourse with ejaculation by the male.
Alterations in male reproductive health reflect a wide range of developmental, endocrine, infectious, inflammatory, hypertrophic, malignant, and psycho-emotional processes. Review the introduction to this unit to gain a better understanding of ways in which reproductive health is affected, including anatomy and physiology, sperm production, regulation of male sexual functioning, and sexual intercourse.
The drug family most clearly associated with male reproductive processes is the androgens. Because synthetic anabolic steroids and antiandrogens affect male reproduction, they are also discussed. Androgens , or male sex hormones, control the development and maintenance of sexual processes, accessory sexual organs, cellular metabolism, and bone and muscle growth.
Testosterone is the principal male sex hormone and is an anabolic steroid. It is the prototype of the androgen hormones, synthesized primarily in the testes and, to a lesser extent, in the adrenal cortex. In women, the ovaries synthesize small amounts of testosterone. Prototype Drug Chart lists the natural and synthetic androgens and their dosages, uses, and considerations. Prototype Drug Chart Testosterone secretion is greater in men than in women in most stages of life.
It is this unbound portion that is biologically active. Estrogen elevates the production of sex hormone—binding globulin, resulting in more protein-bound testosterone in women than in men. The half-life of endogenous naturally occurring free testosterone in the blood is 10 to 20 minutes. Synthetic androgens have longer half-lives, so only synthetic androgens are available in oral formulations in the United States. Testosterone can be combined with esters to form esterified testosterone, in an oil base for intramuscular IM injection.
Testosterone is excreted mainly in the urine as the metabolites androsterone and etiocholanolone. Synthetic androgens may be excreted as unaltered hormone or as metabolites. In some tissues the action of testosterone depends on its reduction to 5-alpha-dihydrotestosterone DHT , whereas in other tissues testosterone itself is the active hormone. In the central nervous system, the metabolite estradiol affects hormonal action. Testosterone is responsible for the development of male sex characteristics.
The biologic effects of testosterone may be mediated directly by testosterone or by its metabolites. Testosterone and dihydrotestosterone act as androgens by way of a single androgen receptor officially designated NR3A. The hormones bind to sites on certain responsive genes, causing a change to take place in the target cell.
The effects of the testosterone depend on which receptor it activates and the tissues in which these effects occur. The manufacture of protein within the target cells results in the buildup of cellular tissue anabolism , especially in muscles. This leads to development of secondary sex characteristics such as pubic hair growth, beard and body hair growth, baldness, deepening of the male voice, thickening of the skin, sebaceous gland activity, increased musculature, bone development, and red blood cell formation.
Fetal testes begin to produce testosterone during the first 3 months in utero. After birth until just before puberty, production is negligible. During puberty, production increases rapidly and continues until later adulthood. As men age, the number of Leydig cells decreases, sperm production declines, and luteinizing hormone LH and follicle-stimulating hormone FSH levels rise. Levels of unbound testosterone are reduced in older men to one-third to one-fifth the peak value.
Table lists the natural and synthetic androgens with their dosages, uses, and considerations. The most common clinical use is for androgen deficiency in males, specifically hypogonadism, replacement therapy for testicular failure in adult males, and delayed puberty in adolescents.
The clearest indication for exogenous androgen therapy is hypogonadism. Male hypogonadism is a defect of the reproductive system that results in failure of the testes to produce testosterone, sperm, or both.
Deficiency of sex hormones can result in defective primary or secondary sexual development. Defective sperm development can result in infertility. Hypogonadism is either primary, reflecting testicular abnormality, or secondary, reflecting hypothalamic or pituitary failure. A combination of disorders can also occur. Inadequate pituitary function will severely affect young boys and results in lack of secondary sex characteristics and infertility.
Adult men may experience lack of libido, testicular atrophy, impotence, decreased bone density, loss of muscle tone, increased hair growth, or the onset of vasomotor flushing may occur. The timing and extent of treatment depend on the clinical manifestations. Because accelerated bone maturation can lead to premature closure of bone epiphyses and short stature, androgen therapy should be used cautiously in children and only by specialists aware of the adverse effects on bone maturation.
Skeletal maturation must be monitored every 6 months by x-ray of the hand and wrist. Artificial induction of puberty is undertaken only after boys reach age 15 to 17 years and hypothalamic and pituitary function has been assessed. A 4- to 6-month trial of androgen therapy is implemented, followed by a like period of rest for reevaluation. It should be given deep in the gluteal muscle. Inspect vials visually for particulate matter and discoloration before administration.
Warm and shake the vial to dissolve any crystals that may have formed during storage. It takes 3 or 4 years for sexual development to occur. Plasma testosterone levels should be monitored and dosages adjusted as needed to maintain normal levels. If the serum testosterone level is below the normal range, the provider will adjust the dose upward. Therapy may be lifelong. Some young, hypogonadal men are able to resolve erectile dysfunction with testosterone replacement therapy by way of oral, parenteral, or direct injection of drugs into the penis.
These therapies may be associated with hypotension, dizziness, pain, and priapism; some of these drugs can cause hepatotoxicity. Given the success and high efficacy of oral erectile dysfunction therapy, discussed later, the use of these medications for adult hypogonadism has decreased markedly.
Testosterone may be administered buccally, orally, transdermally, or parenterally. The selection of an androgen or anabolic steroid depends on the balance of growth and sexual maturation desired and on the preferred route of administration. A buccal muco-adhesive system Striant is available at a mg dose every 12 hours. Advise the patient to place the rounded side surface of the system against the gum above an incisor tooth and hold firmly in place with finger over lip and against product for 30 seconds.
To remove, slide gently downwards toward tooth to avoid scratching gums. Sites must be rotated with each application. If the product falls off within the hour dosing interval or falls out of position within 4 hours before next dose, remove and apply a new system.
The patient should not chew or swallow the tablet. Advise the patient to regularly inspect gums where the system has been applied. With the exception of the buccal system, androgens are considered controlled substances Schedule III.
Many brands of testosterone transdermal patches are available. Testoderm patches are applied to the scrotum; scrotal skin is about five times more permeable than normal skin, and Testoderm will not achieve desired serum concentrations if applied to other skin sites. Serum concentrations of testosterone maximize after 2 to 4 hours, returning to baseline 2 hours after patch removal.
Serum concentrations of testosterone approach those of normal males and reach a plateau after 3 to 4 weeks. Testoderm TTS patches achieve adequate serum concentrations when applied to the arm, back, or upper buttocks. Androderm patches can be applied to any healthy skin site other than the scrotum or bony areas. Daily application of two Androderm 2. The first day of dosing results in morning serum testosterone concentrations within the normal range.
There is no testosterone accumulation with continued use. After removal of Androderm, hypogonadal status returns within 24 hours. Keep testosterone gel out of reach of children. An underarm solution Axiron is applied to one or both axillary areas at the same time each day.
The patient should not apply Axiron to the genitals. These skin application products can be transferred to others through personal contact with skin or clothing. The treatment eliminates the need for injections and provides circadian fluctuations in dosage. Other uses of androgens include treatment of refractory anemia in men and women, hereditary angioedema, tissue wasting associated with severe or chronic illness, advanced carcinoma of the breast in women, and endometriosis.
The effectiveness of androgens for treatment of cryptorchidism undescended testis and impotence has not been established.
Androgens may be used in combination with estrogens for management of severe menopausal symptoms in women. Hypogonadal men on androgen therapy may experience frequent erections or priapism painful, continuous erection , gynecomastia mammary gland enlargement in men , or urinary urgency. Continued use of androgens by normal men can halt spermatogenesis formation of spermatozoa.
The sperm count may be low oligospermia for 3 or more months after therapy is stopped. Other side effects of androgen therapy include abdominal pain, nausea, insomnia, diarrhea or constipation, hives or redness at the injection site, increased salivation, mouth soreness, and increased or decreased sexual desire.
Advise the patient to notify the health care provider if side effects persist, worsen, or are bothersome. Androgen therapy may cause hypercalcemia by stimulating bone resorption in patients with breast cancer or immobilized patients. The drug should be discontinued and appropriate measures instituted if signs of hypercalcemia occur including: