CHAPTER 23 Women’s Health Issues
I. Osteoporosis
B. Pathophysiology
1. In normal bones, there is a regulated balance between the activity of cells that create bone and those that break it down, a process called bone remodeling. There are three main cell types that compose bone:
2. Healthy bone remains stable because osteoblasts and osteoclasts are working at a similar rate, allowing bone to continuously remodel and heal when damaged. If osteoclast activity outpaces osteoblast activity, bones become weakened. In other words, if resorption is greater than formation, bone loss occurs.
3. By the mid-30s, most men and women gradually begin to lose bone strength. When bones become less dense and structurally weaker, this condition is known as osteopenia. Osteopenia refers to mild bone loss that is not as severe as osteoporosis. Individuals with osteopenia are at increased risk of developing osteoporosis. As the condition progresses, bones lose calcium, phosphorus, boron, and other minerals and they become lighter, less dense, and more porous. If untreated, osteopenia can progress painlessly to osteoporosis, increasing likelihood of fracture. Although any bone is susceptible to fracture, the most common fractures due to osteoporosis occur at the spine, wrists, and hips. Spine and hip fractures in particular may lead to chronic pain, long-term disability, and even death.
4. Extracellular levels of calcium, vitamin D, and parathyroid hormone (PTH) are key regulators in maintaining bone remodeling. PTH enhances the release of calcium and stimulates bone resorption and formation. Estrogen is thought to have a direct effect on bone cells. It enhances bone formation by stimulating the estrogen receptors, which are located on the osteoblasts. There is a direct link between the estrogen loss after menopause and the development of osteoporosis. Low hormone levels that occur in early menopause can significantly increase the risk of osteoporosis. Using anti-inflammatory corticosteroids may also significantly affect bone health. Corticosteroids are commonly taken by women greater than 55 years of age for conditions such as arthritis but are known to directly lead to bone loss. It is estimated that 20% of all osteoporosis cases may be attributed to corticosteroid use.
F. Treatment
3. Adequate intake of vitamin D needed to help with absorption of calcium and maintain muscle strength
5. Medications
a. Therapies that increase BMD and prevent fractures
(1) Calcium
(a) Important for attaining peak bone mass and preventing osteoporosis, antiresorptive, beneficial effects enhanced with other therapies and exercise
b. “Bone-building” treatments
T-score | |
---|---|
Normal | > −1 |
Osteopenia | −1 to −2.5 |
Osteoporosis | < −2.5 |
(1) Bisphosphonates
(a) Mechanism of action: bisphosphonates adsorb to the bone, preventing osteoclasts from adhering to the same bone surfaces, thereby inhibiting osteoclast activity.
(c) Provide the greatest BMD increases, effect is dose-dependent, combination therapy with estrogen/hormone replacement therapy (HRT) results in greater increases in BMD
(e) Adverse effects: nausea, dyspepsia, abdominal pain, diarrhea; esophageal, gastric, or duodenal irritation, perforation, ulceration or bleeding, acid reflux; osteonecrosis of jaw
(f) Considerations, if patient is taking medication orally
(i) Take on an empty stomach, with plain water only, first thing in the morning before having anything to eat or drink.
(ii) Patient must not lie down, eat, drink, or take other medications for at least 30 minutes. If patient wants to lie down after 30 minutes, the patient must eat breakfast first. These directions are necessary to avoid irritation of esophagus
(2) Hormone replacement therapy
(a) Estrogen alone or estrogen plus progestin
(i) Mechanism of action: The bone-protective effects of estrogen may involve suppression of inflammatory chemicals called cytokines, as discussed previously. There are estrogen receptors on osteoblasts and osteoclasts. Estrogens decrease osteoclast recruitment and activity, inhibit PTH peripherally, increase calcitriol concentrations and intestinal calcium absorption, and decrease renal calcium excretion. Estrogens also decrease cytokine levels.
(ii) Consideration: The progestin component is added only in women with an intact uterus to prevent endometrial overgrowth and endometrial cancer.
(iii) Caution: Use is contraindicated in active/suspected estrogen-dependent cancer, abnormal vaginal bleeding, severe liver disease, and active vascular thrombosis. Relative contraindications include migraines, thromboembolic disease, hypertriglyceridemia, uterine fibroids, endometriosis, gallbladder disease, family history of breast cancer, and chronic hepatic dysfunction.
c. Medications that increase BMD only
G. Prevention
6. Adequate calcium and vitamin D are essential for the prevention of osteoporosis in general, including postmenopausal osteoporosis. Postmenopausal women are especially susceptible to fractures of the hip, wrist, and spine; therefore, it is recommended by healthcare professionals for postmenopausal women to have about 1200–1500 milligrams of calcium and 800 IU of vitamin D daily.
II. Vaginitis due to Yeast Infection
A. A yeast infection is a fungal infection called vulvovaginal candidiasis (VVC). It is rare before menarche. Incidence is likely after age 20, and 50% of women who have had a yeast infection before will have another yeast infection.
B. Yeast is part of the normal flora in the vagina. Usually, changes in the patient’s vaginal environment triggers the infection. Changes include hormonal changes, such as in pregnancy, or the use of antibiotics, which disrupt the normal flora in the vagina.
C. The major pathogen is Candida albicans. With increasing use of over-the-counter (OTC) products, short-course therapies, and the increased use of preventive or long-term maintenance therapy, there is an increased incidence of non-albicans candidiasis (e.g., Candida glabrata). A diagnosis for a yeast infection or VVC entails a positive vaginal culture for Candida.
D. Yeast infections can be sporadic or recurrent. They could also be defined as uncomplicated sporadic infections, which most likely, will be susceptible to all forms of antifungal therapy regardless of the duration of treatment. Complicated or recurrent VVC occurs in immunocompromised patients or those who have uncontrolled diabetes. Therapy in these populations requires longer duration (10–14 days), regardless of the route of administration.
F. Symptoms generally worsen during menstruation because the hormonal changes provide a better environment for fungal growth.
G. Treatment
2. Prescription antifungal suppositories/vaginal creams (Table 23-2)
a. Vaginal yeast infections are treated with antifungal medications that are inserted directly into the vagina as suppositories or as cream-filled applicators.
3. Common OTC vaginal medications
a. Selection of product is based on patient’s preference for the preparation used and the duration of treatment.
III. Menopause
Active Ingredient | Duration | |
---|---|---|
Terconazole (Terazol, Zazole) | 0.4% cream | 7 days |
0.8% cream or 80 mg suppository | 3 days | |
Nystatin | 100,000 unit vaginal tablet | 14 days |
Active Ingredient | Duration | |
---|---|---|
Butoconazole (Femstat) | 2% cream | 3 days |
Clotrimazole (Gyne-Lotrimin, Mycelex, Canesten) | 1% cream or 100-mg tablet | 7 days |
2% cream or 200-mg tablet | 3 days | |
10% cream or 500-mg tablet | 1 day | |
Miconazole (Monistat, Vagistat-3, Monistat-1 Ovule Pak) | 2% cream or 100-mg suppository | 7 days |
200-mg suppository | 3 days | |
1200-mg ovule | 1 day | |
Tioconazole (Vagistat-1) | 6.5% ointment or 300-mg ovule | 1 day |
A. Risk factors associated with early menopause
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