hyperglycemia o Type I diabetes mellitus insulin dependent diabetes mellitus

Hyperglycemia o type i diabetes mellitus insulin

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hyperglycemia: o Type I diabetes mellitus ( insulin-dependent diabetes mellitus ) – disease caused by destruction of beta islet cells that produce and secrete insulin Target cells are unable to take in circulating glucose Glucose is overproduced in liver because of unopposed actions of glucagon; glucagon also elevates level of ketone bodies in blood Leads to glucose and ketones in urine; draws water from ECF by osmosis, causing polyuria (frequent urination) and polydipsia (excessive thirst) from dehydration o Type II diabetes mellitus ( non–insulin-dependent diabetes mellitus ) – disease in which insulin’s target tissues become insensitive to insulin and target cells do not initiate proper responses to increases in blood glucose concentration ( insulin resistance ) Results in hyperglycemia and accompanying characteristic signs and symptoms, such as glucosuria, polyuria, and polydipsia; unlike individuals with type 1 diabetes, those with type 2 diabetes generally produce enough insulin to prevent ketoacidosis Development of type 2 diabetes is strongly associated with heredity and obesity Chronic hyperglycemia has wide-ranging effects on body: o Damages blood vessels , particularly those in heart and lower limbs; results in decreased circulation to these tissues; increases risk of heart attack, nonhealing wounds, and amputation o Damages peripheral nerves , again particularly in lower limbs; leads to peripheral neuropathy (numbness, tingling, and burning pain in affected areas) o Other tissues affected include lens of the eye and capillaries of retina and kidneys; possibly results in blindness and kidney failure Insulin and glucagon are antagonists in a complicated feedback loop that maintains blood glucose homeostasis: Following feedback responses are initiated when blood glucose level increases : o Stimulus – Blood glucose level increases above its normal range, in response to feeding or hormones such as cortisol o Receptor – Beta cells of pancreas detect increased glucose concentration o Control center – beta cells increase insulin secretion; alpha cells reduce glucagon secretion o Effector/response – insulin decreases blood glucose level by increasing glucose uptake by cells and storage of glucose, amino acids, and fats o Homeostatic range and negative feedback – as blood glucose level returns to its normal range, negative feedback to beta cells decreases insulin secretion Following feedback responses are initiated when blood glucose level decreases : 17
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o Stimulus – Blood glucose level decreases below its normal range o Receptor – alpha cells of pancreas detect decreased blood glucose concentration, as well as presence of ingested protein o Control center – alpha cells increase glucagon secretion; beta cells decrease insulin secretion o Effector/response – glucagon triggers breakdown of glycogen ( glycogenolysis ) into glucose and formation of new glucose ( gluconeogenesis ) o Homeostatic range and negative feedback – as blood glucose level returns to its normal range, negative feedback to alpha cells decreases glucagon secretion Other Endocrine Glands and Hormone-Secreting Tissues The Gonads – Sex Hormones Testes and ovaries are primary male and female reproductive organs or gonads
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