With normal glucose levels, the total amount of glucose in the blood at any given moment is only enough to provide energy to the body for 20–30 minutes, and so glucose levels must be precisely maintained by the bodys internal control mechanisms. When the mechanisms fail in a way that allows glucose to rise to abnormal levels, hyperglycemia is the result.Ketoacidosis may be the first symptom of immune-mediated diabetes, particularly in children and adolescents. Also, patients with immune-mediated diabetes, can change from modest fasting hyperglycemia to severe hyperglycemia and even ketoacidosis as a result of stress or an infection. Insulin resistance
Obesity has been contributing to increased insulin resistance in the global population. Insulin resistance increases hyperglycemia because the body becomes over saturated by glucose. Insulin resistance desensitizes insulin receptors, preventing insulin from lowering blood sugar levels.The leading cause of hyperglycemia in type 2 diabetes is the failure of insulin to suppress glucose production by glycolysis and gluconeogenesis due to insulin resistance. Insulin normally inhibits glycogenolysis, but fails to do so in a condition of insulin resistance, resulting in increased glucose production. In the liver, Fox06 normally promotes gluconeogenesis in the fasted state, but insulin blocks Fox06 upon feeding. In a condition of insulin resistance insulin fails to block Fox06, resulting in continued gluconeogenesis even upon feeding. Medications
Certain medications increase the risk of hyperglycemia, including: corticosteroids, octreotide, beta blockers, epinephrine, thiazide diuretics, statins, niacin, pentamidine, protease inhibitors, L-asparaginase, and antipsychotics. The acute administration of stimulants such as amphetamines typically produces hyperglycemia; chronic use, however, produces hypoglycemia.
History
The word chikungunya is believed to have been derived from a description in the Makonde language, meaning "that which bends up", of the contorted posture of people affected with the severe joint pain and arthritic symptoms associated with this disease. The disease was first described by Marion Robinson and W.H.R. Lumsden in 1955, following an outbreak in 1952 on the Makonde Plateau, along the border between Mozambique and Tanganyika (the mainland part of modern-day Tanzania).According to the initial 1955 report about the epidemiology of the disease, the term chikungunya is derived from the Makonde root verb kungunyala, meaning to dry up or become contorted. In concurrent research, Robinson glossed the Makonde term more specifically as "that which bends up". Subsequent authors apparently overlooked the references to the Makonde language and assumed the term to have been derived from Swahili, the lingua franca of the region. The erroneous attribution to Swahili has been repeated in numerous print sources. Many erroneous spellings of the name of the disease are also in common use. Since its discovery in Tanganyika, Africa, in 1952, Chikungunya virus outbreaks have occurred occasionally in Africa, South Asia, and Southeast Asia, but recent outbreaks have spread the disease over a wider range.The first recorded outbreak of this disease may have been in 1779. This is in agreement with the molecular genetics evidence that suggests it evolved around the year 1700. Research
Chikungunya is one of more than a dozen agents researched as a potential biological weapon.This disease is part of the group of neglected tropical diseases.