Hyperglycemia o type i diabetes mellitus insulin

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

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