Friday, June 17, 2016
Tuesday, June 14, 2016
Diabetes
What is Diabetes?
Either diabetes insipidus or diabetes mellitus, diseases having in common the symptom polyuria; when used without qualification, refers to diabetes mellitus.
Types of Diabetes
There are different many types of diabetes, Diabetes can cause by many things.
SEE HERE DIFFERENT TYPE OF DIABETES
- adult-onset diabetes
- alimentary diabetes
- alloxan diabetes
- brittle diabetes
- bronze diabetes
- bronzed diabetes
- calcinuric diabetes
- chemical diabetes
- diabetes innocens
- diabetes insipidus
- diabetes intermittens
- diabetes mellitus
- galactose diabetes
- gestational diabetes
- growth-onset diabetes
- insulin-dependent diabetes mellitus
- insulinopenic diabetes
- juvenile diabetes
- juvenile-onset diabetes
- ketosis-prone diabetes
- ketosis-resistant diabetes
- latent diabetes
- lipoatrophic diabetes
- lipogenous diabetes
- maturity onset diabetes of youth
- maturity-onset diabetes
- metahypophysial diabetes
- Mosler diabetes
- nephrogenic diabetes insipidus
- non-insulin-dependent diabetes mellitus
- pancreatic diabetes
- phlorizin diabetes
- phosphate diabetes
- piqûre diabetes
- pregnancy diabetes
- puncture diabetes
- renal diabetes
- starvation diabetes
- steroid diabetes
- steroidogenic diabetes
- subclinical diabetes
- thiazide diabetes
- type I diabetes
- type I diabetes mellitus
- type II diabetes
- vasopressin-resistant diabetes
What is diabetes mellitus
diabetes mellitus (DM)
a chronic metabolic disorder in which utilization of carbohydrate is impaired and that of lipid and protein enhanced; it is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma; long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessels, and increased susceptibility to infection.
Diabetes mellitus affects at least 16 million Americans, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. About 95% of persons with DM have type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have type 1, in which exogenous insulin is required for long-term survival. In type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in diabetes mellitus is an impairment of glucose tolerance of such a degree as to threaten or impair health. Revised diagnostic criteria for DM were published by the American Diabetes Association in June 1997. All criteria depend on the glucose concentration of venous plasma. The diagnosis is confirmed when any 2 tests performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7.0 mmol/L); 2 hours postprandially (after a 75-g glucose load), or at random, 200 mg/dL (11.1 mmol/L). Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism, obesity, hypertension, and impairment of renal function. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications (retinopathy, neuropathy, and nephropathy). Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in type 1 DM), drugs that stimulate endogenous insulin production (in type 2 DM), or both. Some studies suggest that the risk of cardiovascular disease may be increased in some patients by intensive treatment of DM because of elevation of body weight, blood pressure, triglycerides, and total and low-density cholesterol. Pharmaceutical agents developed during the 1990s have improved control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. See Also insulin resistance.
Tuesday, August 12, 2008
HEART DEVELOPMENT
Early development
The animal heart is derived from embryonic mesoderm germ-layer cells that differentiate after gastrulation into mesothelium, endothelium, and myocardium. Mesothelial pericardium forms the outer lining of the heart. The inner lining of the heart, lymphatic and blood vessels develop from endothelium. Myocardium develops into heart muscle.]
From splachnopleuric mesoderm tissue, the cardiogenic plate develops cranially and laterally to the neural plate. In the cardiogenic plate, two separate angiogenic cell clusters form on either side of the embryo. Each cell cluster coalesces to form an endocardial tube continuous with a dorsal aorta and a vitteloumbilical vein. As embryonic tissue continues to fold, the two endocardial tubes are pushed into the thoracic cavity and begin to fuse together and are completely fused at approximately 21 days.
The human embryonic heart begins beating around 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy. It is unknown how blood in the human embryo circulates for the first 21 days in the absence of a functioning heart. The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (BPM). The embryonic heart rate (EHR) then accelerates linearly for the first month of beating, peaking at 165-185 BPM during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 BPM per day, or about 10 BPM every three days, an increase of 100 BPM in the first month.
After peaking at about 9.2 weeks after the LMP, it decelerates to about 152 BPM (+/-25 BPM) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 BPM) BPM at term. The regression formula which describes this acceleration before the embryo reaches 25 mm in crown-rump length or 9.2 LMP weeks is Age in days = EHR(0.3)+6
There is no difference in male and female heart rates before birth.