Endocrine Disorders II (NURS 5315 Mod 8 Exam 4) | Questions & Answers (100 %Score)
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Diabetes Mellitus - -metabolic disorder marked by hyperglycemia and alteration in
protein and fat metabolism
-may result from endocrine pancreas dysfunction or from lack of cellular response to
insulin
-type 1 and type 2
Diabetes Mellitus Type 1 - -usually dx'd before 30
-many dx between 9 months and 12 years
-autoimmune destruction of beta cells of pancreas which produce insulin
-more common in whites
-must receive insulin since they do not produce it
-sensitive to insulin
-more likely to have problems with hypoglycemia than type 2
-hard to control
Diabets Mellitus Type 2 - -more common
-onset middle age, dx in children increasing
-more common in native americans, hispanics, african americans, family history
-defect is insulin resistance
-decreased number of insulin cel receptors and/or insufficient amounts of insulin
secretion to meet metabolic needs
-risk factors: obesity and high risk group
-treatment starts with lifestyle modification and oral meds
Secondary Diabetes Mellitus - -DM with clear etiology and not related to type 1 or type 2
-etiologies include: pancreatic disease (cancer, pancreatitis), steroid use, Cushing
syndrome, acromegaly, and excess glucagon secretion
Gestational diabetes - -hyperglycemia in pregnancy
-risk factors: obesity, family hx of DM, high maternal age
-usually resolves after birth
-increased risk of DM later in life
-baby may have hyperplasia of pancreatic islet cells and hypoglycemia
Diabetes diagnostics - -only need one for diagnosis
-fasting glucose >/=126mg/dl
-random glucose >/=200mg/dl with diabetic symptoms
-Glycosylated Hemoglobin(Hgb A1-C)>/=6.5%
(tx goal <7%)
, DM Type 1 Clinical manifestations - -hyperglycemia >200
-polydipsia
-polyuria
-dehydration if untreated (HHS)
-ketonuria
-acetone breath
-weight LOSS
-nutritional deficiency
-polyphagia (increased hunger)
-fatigue
-DKA
DM Type 1 hyperglycemia >200 - -glucose cannot be reabsorbed by the kidneys and
spills into urine causing glycosuria and increasing urine osmolality
-high urine osmolality pulls water into the urine
-increased water loss causes increased urination and dehydration if untreated
-unable to use glucose as energy so gluconeogenesis (non-carb sources) initiated with
ketone byproduct causing ketonuria
-untreated causes DKA
DM Type 2 Clinical manifestations - -mild polydipsia
-polyphagia
-polyuria
-usually does not have gluconeogenesis (non-carb) or DKA
-glucose can slowly go higher than type 1 (400-900)
DM acute complications - -hypoglycemia
-DKA
-hyperosmolar hyperglycemic state
hypoglycemia - -low blood glucose level
-caused by insulin therapy or not eating
-causes pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis, headache,
dizziness, irritability, fatigue, poor judgment, confusion, seizures and coma
-symptoms from release of epinephrine and cortisol
-beta blockers can block many symptoms
Diabetic Ketoacidosis (DKA) - -life-threatening event from insulin deficiency and the
release of counter regulatory hormones (catecholamines, glucagon, cortisol)
-more common in type 1
-lack of insulin causes increase in hepatic glucose production, decrease in peripheral
glucose utilization, initiates gluconeogenesis (non-carb), and forms ketones and
metabolic acidosis
-can cause coma
DKA diagnostic criteria - -glucose >250mg/dl
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