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RALOXIFENE
Introduction
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.
ADvantages
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.
DISADVANTAGES
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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