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What are metabolic events secondary to insulin deficiency?
- hyperglycemia = lack of insulin
- negative nitrogen balance =
- - breakdown of protein and amino acids + water loss --> weight loss
- - protein breakdown + glycosuria increase solutes in kidney = water loss
- weight loss
- acidosis = due to loss of HCO3-, which buffers excess H+
- deterioration of brain function & coma = if acidosis not corrected quickly
Identify ketone bodies that increase in ketoacidosis. (p.15)
- excess fatty acids coming into the liver lead to formation of ketones (bi-products of FA oxidation)
- = acetone
- = acetoacetate
- = beta-hydroxybutyrate
What cells use ketones as supplemental source of energy if glucose in short supply?
- conserves glucose for CNS
- in prolonged starvation, brain can use ketones for energy, which spares glucose
What are common s/s of ketoacidosis?
- anorexia, abdominal pain, N/V
- juicy-fruit breath - acetone/acetoacetic acid
- CNS depression --> stupor, coma, collapse of CV system
What is the compensatory response to ketoacidosis?
Kussmaul's respirations = deep and rapid
What are long-term complications of Type 1 and Type 2 diabetes?
- microangiopathy (capillaries)
- retinopathy (eyes)
- neuropathy (nerves)
- nephropathy (kidneys)
What effect will glycosylated hemoglobin (HgbA1c) and decreased levels of 2,3 DPG have on affinity of Hgb for O2?
- when hemoglobin is glycosylated, it forms HgbA1c
- glycosylated Hgb has high affinity for O2
- less O2 released to tissues
- decreased O2 to tissues --> microcirculation hypoxia --> microangiopathy
- also known as the sorbitol-aldose reductase pathway
- in cells that do not require insulin for glucose uptake, intracellular glucose similar to extracellular glucose
- = lens, kidney, nerves, blood vessels
- hyperglycemia --> high intracellular glucose --> the excess glucose is converted to sorbital via enzyme aldose reductase --> sorbitol converted to fructose
- neither sorbitol or fructose can readily leave the cell --> accumulation
- normally, little sorbitol is formed due to low affinity of aldose reductase for glucose
What are potential consequences of polyol pathway?
- 1) diabetic cataracts - osmotic cell injury
- = increased sorbitol --> increased intracellular osmolality --> influx of water --> osmotic cell injury
- 2) peripheral neuropathies
- = increased sorbitol --> decreased Ca2+ released from membrane and decreased ATP -->
- decreased energy for Na+/K+ pump --> decreased conduction
- 3) in RBCs
- = increased sorbitol --> displacement of 2,3 DPG --> decreased release of O2 to tissues
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