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NR507 Week 7 Quiz Study Guide - 09-02-19 ENDOCRINE

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NR507 Week 7 Quiz Study Guide - 09-02-19 WEEK 7 QUIZ STUDY GUIDE ENDOCRINE • Diabetes Insipidus (DI) o Disorder of posterior pituitary o Insufficiency of ADH leading to polyuria and polydipsia o Nephrogenic DI- caused by inadequate response of renal tubules to ADH (vasopressin) and inability to reabsorb filtered H20 back into the body o Usually acquired but can be genetic o Acquired is r/t disorders and drugs that damage renal tubules- pyelonephritis, amyloidosis, destructive uropathies, polycystic disease, intrinsic renal dx, all lead to irreversible DI o Drugs that induce reversible form= lithium, colchicines, loop diuretics, general anesthetics o Total inability to concentrate urine o Insufficient ADH activity causes excretion of large volumes of dilute urine increased plasma osmolality thirst mechanism is stimulated induces polydipsia o Dehydration develops rapidly without fluid replacement o Criteria for diagnosis includes- polyuria, polydipsia, low urine specific gravity and osmolality, hypernatremia, high serum osmolality, continued diuresis Type 1 DM (T1DM) • Most common pediatric chronic disease • Can be autoimmune or nonimmune (idiopathic) • Autoimmune Pathophys-Environmental-genetic factors (infections, cow’s milk proteins, lack of Vit D, vaccinations, stress) are thought to trigger cell-mediated destruction of pancreatic beta cells  absolute insulin deficiency o Loss of tolerance to self-antigens with formation of autoantigens expressed on surface of pancreatic beta cells and circulate in blood and lymph o Cellular immunity (T-cytotoxic cells and macrophages) and humoral immunity (autoantibodies) are stimulated resulting in beta-cell destruction and apoptosis • Nonimmune Pathophys- far less common does not have an autoimmune basis for beta- cell destruction, occurs secondary to other diseases (pancreatitis), mostly Asian and African descent. Varying degrees of insulin deficiency • S/S- glucose in urine d/t renal threshold of glucose is exceeded o Osmotic diuresis manifested as polyuria and polydipsia o Wide fluctuations in BGL o Protein and fat breakdown occurs because of lack of insulin  weight loss o Increased hepatic metabolism of fat leads to high levels of circulating ketones causing DKA • Diagnosis includes A1C 6.5% o FPG 126 o 2 hr plasma glucose 200 o In patient with symptoms of hyperglycemia and a random glucose 200

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NR507 Week 7 Quiz Study Guide - 09-02-19

WEEK 7 QUIZ STUDY
GUIDE ENDOCRINE
• Diabetes Insipidus (DI)
o Disorder of posterior pituitary
o Insufficiency of ADH leading to polyuria and polydipsia
o Nephrogenic DI- caused by inadequate response of renal tubules to
ADH (vasopressin) and inability to reabsorb filtered H20 back into the
body
o Usually acquired but can be genetic
o Acquired is r/t disorders and drugs that damage renal tubules- pyelonephritis,
amyloidosis, destructive uropathies, polycystic disease, intrinsic renal dx, all
lead to irreversible DI
o Drugs that induce reversible form= lithium, colchicines, loop diuretics, general
anesthetics
o Total inability to concentrate urine
o Insufficient ADH activity causes excretion of large volumes of dilute urine
increased plasma osmolality thirst mechanism is stimulated induces
polydipsia
o Dehydration develops rapidly without fluid replacement
o Criteria for diagnosis includes- polyuria, polydipsia, low urine specific gravity
and osmolality, hypernatremia, high serum osmolality, continued diuresis
Type 1 DM (T1DM)
• Most common pediatric chronic disease
• Can be autoimmune or nonimmune (idiopathic)
• Autoimmune Pathophys-Environmental-genetic factors (infections, cow’s milk
proteins, lack of Vit D, vaccinations, stress) are thought to trigger cell-mediated
destruction of pancreatic beta cells  absolute insulin deficiency
o Loss of tolerance to self-antigens with formation of autoantigens expressed on
surface of pancreatic beta cells and circulate in blood and lymph
o Cellular immunity (T-cytotoxic cells and macrophages) and humoral
immunity (autoantibodies) are stimulated resulting in beta-cell destruction and
apoptosis
• Nonimmune Pathophys- far less common does not have an autoimmune basis for
beta- cell destruction, occurs secondary to other diseases (pancreatitis), mostly Asian
and
African descent. Varying degrees of insulin deficiency
• S/S- glucose in urine d/t renal threshold of glucose is exceeded
o Osmotic diuresis manifested as polyuria and polydipsia
o Wide fluctuations in BGL
o Protein and fat breakdown occurs because of lack of insulin  weight loss
o Increased hepatic metabolism of fat leads to high levels of circulating ketones
causing DKA
• Diagnosis includes A1C > 6.5%
o FPG >126
o 2 hr plasma glucose > 200
This study source was downloaded by 100000834306259 from CourseHero.com on 02-14-2022 04:08:43 GMT -06:00


https://www.coursehero.com/file/72370214/NR507-Week-7-Quiz-Study-Guide-09-02-19docx/

, o In patient with symptoms of hyperglycemia and a random glucose > 200




This study source was downloaded by 100000834306259 from CourseHero.com on 02-14-2022 04:08:43 GMT -06:00


https://www.coursehero.com/file/72370214/NR507-Week-7-Quiz-Study-Guide-09-02-19docx/

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