Endocrine- DKA

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  1. What usually precipitates a DKA episode and why?
    concurrent illness- increased stress, stress hormones are counter-regulatory to insulin, making hyperglycemia worse
  2. _________ shifts the body to a catabolic state, causing _______ in adipose tissue, __(3)__ in the liver, and _________ in muscles.
    decreased insulin/increased glucagon; lipolysis; FA oxidation, gluconeogenesis, glycogen breakdown; AA mobilization
  3. Normally, acetylCoA enters the TCA cycle, but if all the oxaloacetate is being diverted to __________, acetylCoA is converted to __(2)__, causing severe _________.
    gluconeogenesis; acetoacetate and beta-hydroxybutyrate; metabolic acidosis
  4. Why are acetoacetate and beta-hydroxybutyrate such strong acids in the body?
    they have extremely low pKa, so they are completely ionized at physiologic pH
  5. Hyperglycemia leads to _______ and ________, ultimately _______; eventually dehydration results because of __(3)__; dehydration leads to decreased __(2)__, impairing _________; glucose spirals out of control.
    glucosuria; osmotic diuresis; PU/PD; PU, anorexia, vomiting; RBF, GFR; urinary excretion of glucose
  6. Although rare, non-ketotic hyperglycemia syndrome is characterized by __________, but _________ may prevent ketosis.
    severe hyperglycemia; small amounts of insulin
  7. Why is non-ketotic hyperglycemia syndrome so dangerous?
    no ketoacidosis--> no/mild clinical signs--> disorder not recognized right away--> impaired consciousness and coma
  8. How do you diagnose DKA?
    hyperglycemia and ketonuria
  9. What clinical signs are associated with DKA? (5 main ones, 2 +/-)
    PU/PD, anorexia, lethargy, vomiting, hepatomegaly, +/- weight loss and diarrhea
  10. What do you find on the CBC of a DKA patient? (4)
    dehydration, increased TP, increase WBC (inflammatory +/- stress leukogram)
  11. In a DKA patient __(2)__ can make CBC results difficult to interpret.
    dehydration and lipemia (mask anemia, artificially increased TP)
  12. What do you find on the blood chem of a DKA patient? (4)
    hyperglycemia, hyponatremia, hypochloremia, increased ALP
  13. What 3 factors contribute to decreased Cl- and NA+?
    volume depletion stimulates ADH (impairs water and solute excretion, dilutes blood), hyperlipemia can cause psuedoyponatremia, vomiting (hypochloremia> hyponatremia)
  14. It is difficult to assess the extend of hypokalemia because...
    it is mostly intracellular, always assume they need K+ supplements
  15. Total body K+ deficit in DKA is due to... (5)
    polyuria, loss of muscle mass, anorexia, vomiting, and weight loss
  16. Why does K+ always drop dramatically after treatment of DKA, making it necessary to supplement K+? (2)
    insulin drives K+ intracellularly, administered fluids dilute serum K+
  17. Why is phosphorous difficult to assess in DKA patients? (2)
    mostly intracellular, dehydration and decreased RBF/GFR mask hypophosphatemia
  18. Why does phosphorous always decrease after treatment of DKA? (3)
    serum Ph decreases after insulin and fluid administration due to dilution, increased urinary excretion, and entry into cells
  19. Severe hypophosphatemia can cause _________ because...
    hemolysis; RBC need ATP for for cell membrane pump
  20. Not all diabetics have increase blood osmolality (you'd think they would because of hyperglycemia) because...
    hyponatremia decreased blood osmolality.
  21. Anion gap is the difference b/w _________ and ________; normal anion gap should represent ___________.
    commonly measured cations; anions; net negative charge on plasma proteins
  22. In DKA, ________ cause a(n) ________ in the anion gap.
    ketoanions; increase
  23. Why is ALP increased in DKA patients?
    hepatic lipidosis, possibly biliary obstruction
  24. What do you find on UA of a DKA patient? (3)
    glucosuria, ketonuria, ALWAYS culture (UTI could be concurrent disease that incited DKA)
  25. What is the first thing you do to treat DKA?
    restore volume with LRS or plasmalyte
  26. Why should you use LRS or plasmalyte in DKA patients over saline?
    b/c saline has too much Cl-, driving bicarb down--> worsens acidosis; also, when you give an organic ion (lactate), results in a net gain of bicarb--> alkalinizing, allowing ketoanions to be metabolized to bicarb
  27. What is the most desirable but least practical method of insulin administration for DKA txt?
    constant rate of infusion
  28. What is the least desirable but most practical method of insulin administration for DA txt?
    IM injections of regular insulin every 4-6 hours
  29. Why is fluid replacement the first thing you should do when treating DKA?
    increases GFR, allowing excretion of glucose
  30. It is important to lower glucose _________.
  31. What are two substances that you must absolutely supplement when treating DKA?
    potassium and phosphate
  32. Do not exceed _________ K+ supplementation because it can cause ____________.
    0.5mEq/kg/hr; cardiac arrhythmia
  33. What is a good rule of thumb for supplementing K+ and Ph?
    estimate K+ needs based on chart and 50% is given as KCl and 50% is given as K phosphates
  34. What should you monitors every 4 hours when treating a DKA patient? (4)
    BG, serum elctrolytes, acid base status, BUN/Cre
  35. What are potential complications of DKA treatment? (2)
    hypoglycemia; osmolality drops too rapidly, idiogenic osmoles in brain don't follow right away, brain takes up water, edema, coma, death
  36. If you accidentally drop the BG too quickly and cause cerebral edema, give _________ to reverse it.
Card Set:
Endocrine- DKA
2015-09-18 01:52:51
endocrinology vetmed DKA

vetmed endocrinology DKA
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