1. What is the function of the endocrine system?
    It regulates secretion of hormones that alter metabolic functions
  2. What is metabolic syndrome?
    • Waist size greater than 40in in men and 30in in women
    • HDL less than 40 in men and 50 in women
    • Triglycerides greater than 150
    • BP greater than 125/85
    • Fasting Blood sugar greater than 110
  3. What is the definition of DI?
    A clinical condition characterized by impaired renal conservation of water, resulting in polyuria, low urine specific gravity, dehydration and low serum Na
  4. What causes DI?
    A deficiency of ADH(from the pituitary) or decreased renal responsiveness to ADH
  5. What is the clinical presentation of DI?
    • Polyuria- 5-15 Liters/day
    • Thirst/fatigue
    • Dehydration:weight loss, poor skin turgor, postural hypotension
    • <CVP, <RAP,<PAP,<PCWP. <CO/CI
    • Nerologic: restlessness, confusion, irritability, seizures, lethargy, coma
  6. What lab values can be expected with DI?
    • Urine specific gravity <1.005
    • Serum sodium >145
    • BUN>>
    • HCT>>
    • Serum osmolality >>
    • Serum ADH level <<
    • Water deprivation test and vasopressin test differentiate neuro-nephro genic DI
  7. What is the treatment for DI?
    • Correct fluid deficit- with hypotonic solutions
    • Administer exogenous ADH, aqueous vasopressin, DDAVP, Diapid (intranasal)
  8. What are the cardinal signs of DI?
    Dehydration and High Na
  9. What is the definition of SIADH?
    Clinical condition characterized by impaired renal excretion of water, resulting in olguria, high urine specific gravity, water intoxication and hyponatremia.
  10. What causes neurogenic SIADH?
    Pituitary tumor, CNS trauma, stroke, ICH, CNS infection, Guillain-Barre syndrome, CVA, nonmalignant pulmonary disease
  11. What causes Ectopic SIADH?
    • Production of a substance indistinguishable from ADH by tissue
    • - Oat-cell CA
  12. What causes Nephrogenic SIADH?
    General anesthetics, narcotics, tricyclics, tylenol, anticonvulsants
  13. What is Oliguria?
    Urine output of less than 0.5ml/kg/hr
  14. What are the clinical signs of SIADH?`
    • Oliguria
    • Urine specific gravity of >1.03
    • Clinical indications of overhydration: >CVP.>RAP, >PAOP
    • anorexia, N/V, diarrhea
    • Syspnea and pulmondary edema
    • HA, personality changes, altered LOC
    • Seizures
    • Muscle weakness or cramps
    • Serum NA < 120
    • <<<BUN  with normal Creatinine
    • <<HCT
    • << Serum osmolality
    • Serum ADH level >> in neurogenic
  15. How is SIADH treated?
    • Treat the cause:
    • Decrease water intake
    • Surgery to remove maligancy
    • Demeclocycline, phenytoin, lithium to inhibit the effect of ADH on renal tubules
    • DC causative drugs
  16. What is the cardinal sign of SIADH
    Swimming in water/Low Na
  17. What is DM?
    A group of metabolic diseases characterized by hyperglycemia that results from defects in insulin secretion, insulin action or both
  18. What is DKA?
    A hyperglycemic crisis associated with metabolic acidosis and elevated serum ketenes, the most serious metabolic disturbance of type I DM
  19. What is Hyperglycemic Hypersomolar Nonketotic Condition (HHNC)?
    A hyperglycemic crisis associated with the absense of Ketone formation. This is the most serious metabolic disturbance of type 2 DM
  20. What does DKA normally occur?
    • Ungiagnosed type 1 DM
    • Illness, infection, omission of insulin, trauma, surgery and noncompliance in a know type 1 diabetic
    • In an nondiabetic- Cushing's syndrome, hyperthyroidism, pancreatitis, drugs(steroids, thiazide diuretics, dilantin), pregnancy
  21. What is the lab presentation of DKA?
    • Glucose > 300-800
    • Na=, K > then <<
    • >>Ketones
    • >>BUN/Creatinine
    • Serum osmolality >>295-330
    • ABG's metabolic acidosis
    • >>WBC's
  22. What symptoms does a pt have in DKA?
    • N/V, abd pain, polyphagia, polydipsia, polyuria
    • weakness, fatifue, wt loss
    • Clinical indications of dehydration(tachycardia, orthostatic hypotension)
    • Kussmaul's breathing
    • Lethargy progressing to coma
  23. What is the treatment for DKA?
    • ABC's
    • Identify and treat cause
    • Correct fluid volume deficit
    • Normalize serum glucose- Regular insulin 0.1-0.15u/kg followed by infusion
    • Correct acid base imbalance (fluids)
  24. How fast should insulin drop when treating DKA with a insulin drip and why?
    Glucose level should be decreased by no more than 75-100 per hour to avoid hpoglycemia, hypokalemia and cerebral edema
  25. What are the potential complications of DKA?
    • Cardiovascular: Hypovolemic shock, dysrhythmias, embolism, MI, pulmonary edema
    • Neurologic: seizures, cerebral edema, coma
    • Renal:ARF, electrolyte imbalance
  26. What causes Metabolic Acidosis?
    • Diabetic or ETOH ketoacidosis
    • Renal failure
    • lactic acidosis
    • poisoning
  27. What causes HHNC?
    • Usually seen in patients over 50 years old with glucose intolerance
    • THis can follow: pancreatitis, burns, hepatitis, trauma, ETOH, hypertonic nutrition, durgs (Beta blocers, thiazide, dilantin, steroids)
  28. What is the clinical presentation of HHNC?
    • Tachycardia, orthostatic hypotension,< CVP, RAP, PAP<PCWP, CO/CI, tachypnea, motor deficits< DTR's, seizures, lethargy-coma
    • Glucose >600-2000
    • Na < (BS), K<<, BUN/Cr >>, Serum osmolality >>330-450
    • ABG's: Normal pH, acidosis if present is lactic acidosis
  29. Complications of HHNC?
    Hypocolemic shock, dysrhythmias, ARF, thromboembolism, MI, PE, Cerebral edema
  30. Hypoglycemia?
    • Females>Males
    • More common in the elderly
    • ETOH
    • Infection
  31. What is normal serum osmolarity?
  32. SIADH is clinically manifested by?
    • Hyperosmolar state
    • Low output state
    • Myxedema state
    • water intoxication state
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