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Raloxifene is in a class of drugs called selective estrogen receptor modulators, or SERMs. These drugs have been called 'designer estrogens' because they mimic the action of estrogen where it's wanted (i.e., in the cardiovascular and skeletal systems) but avoid estrogen-like action where it's not wanted (i.e., in breast and uterine tissue). It's not fully known how this works. But scientists theorize that individual SERMs cause changes in the shape of estrogen receptors in different organs, causing the SERM to stimulate some types of tissue but not others.


1. Raloxifene (Evista), is a drug that mimics estrogen's beneficial effects on bone density in postmenopausal women. It also mimics some of estrogen's beneficial effects on blood lipids (fats). Unlike estrogen, however, it has been shown to lower the risk for breast cancer and may lower the risk of uterine cancer.

2. Bone density Raloxifene increases bone mineral density significantly when compared to placebos. Increasing bone density is important to help protect against fractures of bones made vulnerable by osteoporosis. No study has yet evaluated raloxifene in a head-to-head comparison with estrogen. However, the placebo-controlled studies indicate that raloxifene increases bone density by about half what might be expected with estrogen or with alendronate (Fosamax).

3. Breast tissue Women taking raloxifene have no more breast tenderness or abnormalities on their mammograms than those taking placebos. There is evidence that raloxifene decreases the risk of breast cancer, but more study is needed

4. Uterine tissue Raloxifene does not cause precancerous changes of uterine tissue, and there's no spotting or bleeding as is commonly associated with oral estrogen.

5. (Overall/general advantages all summed up )

The advantage of raloxifene over HRT is having bone protection without the cancer risk. A great benefit will lie in adherence to the prescribed treatment plan. Women will be more likely to take this medication because their fears about a potential increased risk of breast or uterine cancer will be removed. They will also not be bothered by unwanted vaginal bleeding or breast pain. Women who take their medication will, in turn, see the benefits in terms of improved long-term health.


1.Hot flashes Unfortunately, raloxifene does not relieve hot flashes, and there is concern that in some doses it might even make hot flashes worse.

2. Blood fats It's not yet clear whether raloxifene and other SERMs will have long-term beneficial effects on the risk of heart disease.

Raloxifene does lower the blood level of total cholesterol and low-density lipoprotein cholesterol (the bad cholesterol). Unfortunately, unlike estrogen, raloxifene does not appear to increase high-density lipoprotein (the good cholesterol).

3.Leg cramps are also reported more frequently in women taking raloxifene. Women taking raloxifene are at an increased risk of developing a deep-vein thrombosis or clots.

4. While raloxifene prevents bone loss, it has not been proven to reverse osteoporosis that has already occurred. Therefore, a woman with osteoporosis or skeletal fractures would best be treated with a potent anti-resorptive medication, such as Fosamax.

5.Raloxifene does not alleviate menopausal symptoms of hot flashes, insomnia, mood swings, or night sweats. In fact, some women have noticed an increase in hot flashes during the first few months of treatment with raloxifene.

6.Raloxifene is contraindicated in women who are, or may become, pregnant. Women need to be aware of the potential hazard this drug poses to any pregnancy that occurs while taking the medication. Raloxifene is excreted in breast milk and is therefore also contraindicated in nursing women. A history of venous thrombosis is, similarly, an absolute contraindication to raloxifene use.

**A 42-year-old alcoholic male presents with a 6-day history of binge drinking. Serum chemistry tests reveal the following

Electrolytes (mmol/L): Na+ 145; K+ 5.0; Cl- 105; HCO3- 15
BUN: 7.1 mmol/L (20 mg/dL)
Creatinine: 133 g/L (1.5 mg/dL)
Glucose: 9.6 mmol/L (172 mg/dL)

The nitroprusside (Acetest) agent gives a minimally positive result. Optimal therapy to ameliorate the patient's acid-base disorder would include 5% dextrose in

A: water

B: normal saline

C: normal saline, insulin, and sodium bicarbonate

D: half normal saline and insulin

E: half normal saline, insulin, and sodium bicarbonate

The answer is B
A reasonable way to approach the diagnosis of metabolic acidosis is to separate patients into those with an increased anion gap and those with a normal anion gap (hyperchloremic acidosis). A calculation of these unmeasured anions consists of the sum of plasma bicarbonate and chloride minus the plasma sodium concentration (the normal value is 8 to 16 mmol/L). Reasons for increased acid production include diabetic ketoacidosis, alcoholic ketoacidosis (as in this patient), starvation, lactic acidosis caused by circulatory failure, certain drugs and toxins, and poisoning resulting from salicylates, ethylene glycol, or methanol. Finally, renal failure increases the anion gap because sulfate, phosphate, and organic acid ions are not excreted normally. Normal anion gap acidosis is due to renal tubular dysfunction or colonic losses. Since the ratio of beta-hydroxybutyrate to acetoacetate is high in alcoholic ketoacidosis, ketonemia can be missed by the routinely employed nitroprusside (Acetest) reagent, which detects acetoacetate but not beta-hydroxybutyrate. Patients suffering from alcoholic ketoacidosis do well on infusions of glucose and saline. Neither insulin nor alkali is required in these situations unless the acidosis is extreme (bicarbonate less than 6 to 8 mmol/L).

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