Patho 3

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Author:
cgordon05
ID:
17824
Filename:
Patho 3
Updated:
2010-05-06 14:27:32
Tags:
endocrine insulin ketones
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Description:
endocrine insulin ketones
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  1. 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
    • ketosis
    • acidosis = due to loss of HCO3-, which buffers excess H+
    • hyperlipidemia
    • deterioration of brain function & coma = if acidosis not corrected quickly
  2. 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
  3. What cells use ketones as supplemental source of energy if glucose in short supply?
    • cardiac
    • skeletal
    • conserves glucose for CNS
    • in prolonged starvation, brain can use ketones for energy, which spares glucose
  4. What are common s/s of ketoacidosis?
    (p.16)
    • anorexia, abdominal pain, N/V
    • juicy-fruit breath - acetone/acetoacetic acid
    • CNS depression --> stupor, coma, collapse of CV system
  5. What is the compensatory response to ketoacidosis?
    Kussmaul's respirations = deep and rapid
  6. What are long-term complications of Type 1 and Type 2 diabetes?
    (p.17)
    • microangiopathy (capillaries)
    • retinopathy (eyes)
    • neuropathy (nerves)
    • nephropathy (kidneys)
  7. What effect will glycosylated hemoglobin (HgbA1c) and decreased levels of 2,3 DPG have on affinity of Hgb for O2?
    (p.18)
    • 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
  8. polyol pathway
    • 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
  9. What are potential consequences of polyol pathway?
    (p.18)
    • 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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