omen were preventing pregnancy long before there were any books about it—in fact, even before there was paper for printing the books. The first prescription for a contraceptive was written on papyrus around 1550 B.C. It seems to have called for crocodile dung to be inserted into the vagina, as the ancient Egyptians preferred. For ancient Arabians, elephant dung mixed with honey was the method of choice. And women in Northern Canada drank a potion of dried beaver testicles mixed with alcohol to avoid pregnancy.
Fortunately, technology has advanced to a point where we no longer have to rely on such methods of contraception. Modern science allows us to convert natural substances, such as the Mexican yam, into remarkably simple delivery systems, like tablets, subdermal implants, and shots.
Hormonal birth control methods— including oral contraceptives (the Pill), the Norplant implant, and DepoProvera Contraceptive Injection—have several things in common. They are all highly effective and safe for most women; they all reduce cramping and pain related to the menstrual cycle; and they all require a doctor's prescription. Unfortunately, these forms of birth control offer little protection from sexually transmitted diseases; and all may be accompanied by health risks and side effects.
How Hormonal Methods Work
Pills, implants, and injections all have one goal: to prevent your reproductive system from producing a mature egg. They do this by tricking the system into skipping a key step in the interlocking cycle of hormone production that triggers the egg's release from the ovary. The deception works like this:
Under ordinary circumstances, the brain's hypothalamus produces GnRH (gonadotropinreleasing hormone). This prompts the pituitary gland to release FSH (follicle stimulating hormone) which travels to the ovaries through the bloodstream and causes a follicle to grow. The development of the follicle produces estrogen, which after about 10 days reaches high enough levels to trip off a surge of LH (luteinizing hormone) from the pituitary gland. The ovarian follicle releases a mature egg into the fallopian tube about 24 hours after this surge of LH, and the empty follicle becomes known as the corpus luteum. The cells of the corpus luteum produce progesterone and estrogen, which together stimulate the uterine lining to thicken with blood in preparation for nurturing a fertilized egg. Once the corpus luteum wanes and the lining is left with no hormonal support, it sloughs off during your monthly period. The low levels of estrogen and progesterone also signal the hypothalamus to start the process over again.
Since oral contraceptives (OCs) provide a steady level of both progestin (a substitute for progesterone) and estrogen every day, and Norplant implants and DepoProvera provide steady daily levels of progestin, there is no signal to the hypothalamus to release GnRH and therefore no signal to the pituitary gland to produce FSH and LH. Because FSH stimulates the ovaries to grow egg follicles, and LH triggers ovulation, their absence causes the ovary to be relatively dormant, and no egg is produced to a point where it could be released. Hormonal contraception locks the system into the same late phase of the cycle on a continuous basis, perpetually skipping the allimportant release of GnRH.
Hormonal contraceptives work by damping down the two key hormones that trigger ovulation. Follicle stimulating hormone (FSH), the substance that coaxes an egg towards maturity, is the first to be suppressed. Luteinizing hormone (LH), which ordinarily triggers release of the egg at mid-cycle, is also held down. Production of both these substances usually starts when the body senses a shortage of two other hormones: progesterone and estrogen, both produced in the ovaries. Hormonal contraceptives supply just enough of these substances to prevent start-up of the FSH/LH production cycle. Constant levels of estrogen and progesterone thus produce constant levels of FSH and LH, and the eggs remain dormant.
Suppression of ovulation is the main mode by which OCs and DepoProvera prevent pregnancy; the implant system causes ovulation suppression about 50 percent of the time. However, throughout each pill cycle, and continuously with Norplant implants and DepoProvera, the mucous covering the cervix—the site where sperm enters the uterus—stays thick and sticky, making it very difficult for sperm to get through. This gooey impediment also acts on the sperm cell itself. It prevents fertilization by interfering with chemical changes inside the sperm that allow it to penetrate an egg's outer coating.
Even if ovulation and fertilization do take place, hormonal methods provide another measure of protection: changes to the uterine lining. Normally, estrogen initiates the thickening of the lining of the uterus in the first part of the cycle, while progesterone kicks in later to help the lining mature. Since both hormones are present throughout the pill cycle, and progestin is supplied continuously by implants and the shot, the usual hormonal variations are masked and the lining rarely has a chance to develop enough to nurture a fertilized egg.
All the hormonal methods currently available to us offer many benefits, including protection from cancer. However, they aren't 100 percent effective, and they aren't right for all women. To correct this, scientists are busy developing new forms of hormonal contraception which may be easier to use and may suit more women. These methods include biodegradable implants, pellets the size of a grain of rice, and a new product called the vaginal ring. Like a diaphragm, this device is removable. But unlike barrier contraceptives, it releases steady levels of progestins to prevent pregnancy.
Even without these new approaches, the array of choices at your disposal is varied and wide. Before you decide on a method take time to weigh the benefits and risks of all the forms of hormonal contraception available today. The following overview provides the basic information you'll need, but be sure to discuss any questions with your physician. Together you can find the approach that's optimal for you personally.
Thursday, April 3, 2008
Wednesday, April 2, 2008
DIAGNOSIS OF INSULINOMA
- Hypoglycemia- extended fasting upto 72 hrs
- Insulin/glucose ratio >0.3
- Proinsulin levels
- Imaging techniques
- - CT scan
- - Ultrasound
- - Coeliac angiography
- - CT scan
FASTING HYPOGLYCEMIA- INSULINOMA
- ANY AGE BUT USUALLY 4-6TH DECADE
- EQUAL SEX DISTRIBUTION
- MAY TAKE YEARS BEFORE DIAGNOSIS IS MADE
- 75% ARE BENIGN SINGLE ADENOMAS, SMALL IN SIZE < 3 CM IN DIAMETER
- 10% MULTIPLE BENIGN ADENOSIS SCATTERED IN PANCREAS
- 10% MALIGNANT BETA CELL CARCINOMAS
FASTING HYPOGLYCEMIA
- INSULINOMA
- ISLET CELL HYPERPLASIA
- EXTRAPANCREATIC NEOPLASMS
- ADRENOCORTICAL DEFICIENCY
- GROWTH HORMONE DEFICIENCY
- HEPATIC FAILURE
- RENAL FAILURE
- AUTOIMMUNE HYPOGLYCEMIA
REACTIVE HYPOGLYCEMIA- EARLY DIABETES
- USUALLY SIGN OF EARLY DIABETES
- INSULIN SECRETION SHOWS AN INITIAL LAG FOLLOWED BY EXCESSIVE SECRETION
- USUALLY IN OBESE INDIVIDUALS
- SYMPTOMS DISAPPEAR IF OVERT DIABETES DEVELOPS
- TREATMENT: WEIGHT REDUCTION, SMALL FREQUENT MEALS
REACTIVE HYPOGLYCEMIA- FUNCTIONAL
- PSYCHIATRIC DISORDER
- INSULIN LEVELS NORMAL
- HYPOGLYCEMIA MAY NOT ACTUALLY BE PRESENT
REACTIVE HYPOGLYCEMIA
- ALIMENTARY
- IDIOPATHIC,FUNCTIONAL
- EARLY DIABETES MELLITUS
- IDIOPATHIC,FUNCTIONAL
- REACTIVE HYPOGLYCEMIA- ALIMENTARY
- Usually after gastrectomy, or gastrojejunostomy
- Rarely even without gastric surgery
- Hypo symptoms-occur 90-180 min. after food ingestion
- Insulin levels usually normal
- Intestinal factors; e.g. GIP, enteroglucagon & cholecystokinin
- Treatment: Small frequent meals, dietary fibre
- Usually after gastrectomy, or gastrojejunostomy
CLASSIFICATION OF HYPOGLYCEMIA IN ADULTS
- REACTIVE HYPOGLYCEMIA
- Alimentary
- Idiopathic,functional
- Early Diabetes mellitus
- Alimentary
- FASTING HYPOGLYCEMIA
- Insulinoma
- Islet cell hyperplasia
- Extrapancreatic neoplasms
- Adrenocortical deficiency
- Growth hormone deficiency
- Hepatic failure
- Renal failure
- Autoimmune hypoglycemia
- Insulinoma
- PHARMACOLOGIC HYPOGLYCEMIA
- Insulin reactions
- Factitious insulin injections
- Sulphonylureas
- Ethanol
- Beta blocking agents
- Insulinoma other medications (Rare)
- Insulin reactions
- ARTEFACTUAL HYPOGLYCEMIA
- Leukocytosis
- Hyperlipidemia
- Leukocytosis
METABOLIC RESPONSES TO HYPOGLYCEMIA
MECHANISMS TO PREVENT HYPO’S IN THE NON-DIABETIC STATE
- Function of various glucosensors which are able to ‘measure’ the blood glucose levels
- Stimulation of appetite and food-seeking behaviour to encourage food intake
- Ability to release glucose from stores,especially hepatic
glycogen, which can be used even in absence of food intake - Regulation of insulin secretion so that during fasting,secretion is quickly reduced with a falling blood glucose level
- Ability of the body to use alternate energy stores, especially
fat, thereby conserve glucose levels - Use of alternate energy substrates(ketone bodies, free fatty
acids,and to a lesser extent, lactate, glycerol and amino
acids) - Conversion of some amino acids into new glucose by process
of gluconeogenesis - Shift of metabolic processes from glucose as energy source
to free fatty acids and ketone acids for energy
Tuesday, April 1, 2008
HYPOGLYCEMIA
STANDARDS OF NORMALITY FOR PLASMA GLUCOSE CONCENTRATION AT 24-HOUR INTERVALS DURING THREE DAYS OF FASTING
SUBJECTS - - - PLASMA GLUCOSE*Mg/100 ML
24 hr:
Women(44) - - - 57.7 ± 11.6
Men(12) - - - 79.1 ± 12.9
48hr:
Women(35) - - - 49.6 ± 6.4
Men(12) - - - 74.6 ± 12.3
72hrs:
Women(45) - - - 41.3 ± 13.4
Men(12) - - - 67.5 ± 8.6
SUBJECTS - - - PLASMA GLUCOSE*Mg/100 ML
24 hr:
Women(44) - - - 57.7 ± 11.6
Men(12) - - - 79.1 ± 12.9
48hr:
Women(35) - - - 49.6 ± 6.4
Men(12) - - - 74.6 ± 12.3
72hrs:
Women(45) - - - 41.3 ± 13.4
Men(12) - - - 67.5 ± 8.6
Monday, March 31, 2008
Symptoms of Diabetes
- Excessive thirst and hunger
- Excess urination
- Tiredness
- Sudden weight loss
- Delayed wound healing
- Recurrent styes & boils
- Itching & infection in private parts
- Persistent ache in the limbs
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