Endocrine- Clinical DM and Insulin Resistance

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Endocrine- Clinical DM and Insulin Resistance
2015-09-16 22:54:47
vetmed diabetes

vetmed diabetes
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  1. Persistent fasting hyperglycemia and glucosuria should be verified with _________.
  2. What will you see on UA of a diabetic patient?
    glycosuria, proteinuria, ketonuria, bacteruria
  3. What will you see on CBC of a diabetic patient?
    increased hematocrit if dehydrated, increased WBC with infection
  4. What will you see on the blood chem of a diabetic patient?
    liver enzyme abnormalities due to hepatic lipidosis and pancreatitis, increased cholesterol, pre-rena azotemia, electrolyte abnormalities
  5. What might you feel when palpating the abdomen of a diabetic patient?
    hepatomegaly due to fatty liver
  6. Diabetic dogs should be put on a ____________ diet.
    high fiber, complex carb
  7. Diet for diabetic dogs should avoid excess __(2)__.
    fat and protein
  8. The most important aspect of dietary management of diabetes is ___________.
  9. Diabetic cats should be put on a ___________ diet.
    high protein, low carb, low fiber
  10. In cats, _________ are strong stimulators of insulin release.
    amino acids
  11. __________ diets are better for diabetic cats because they have lower carbs.
    Canned food
  12. The goal of insulin therapy is the minimize ____________, which is critical for minimizing the risk of ___________.
    day-to-day variability; hypoglycemia
  13. In order to extend the duration of action of regular insulin, it is formulated with... (3)
    zinc (lente), protamine (NPH), or both (protamine-zinc formulation).
  14. Protamine and zinc increase the tendency of insulin to _________ to slow its absorption.
  15. Lente, NPH, and PZI are injected as _________; the cons to this are... (2)
    suspensions; decreased accuracy of dosing ad variability of time-action of de-precipitation.
  16. What is the major advantage to recombinant insulin?
    MUCH less variability throughout the day
  17. Insulin glargine (Lantus) is ____________; there is an altered _______, making it stable in ________ but crystallized in __________, slowing its absorption.
    recombinant human insulin analog; AA; pH4; physiologic pH
  18. Which insulin is long-acting and peakless?
    insulin glargine
  19. Lente, NPH, and PZI formulations are ________ insulin.
  20. Insulin detemir (Levemir) is ____________; there is an altered _________, which facilitates self-association and association with ________ to slow absorption.
    recombinant human insulin analog; AA to FA; albumin
  21. What insulin formulation has the lowest within-patient pharmacokinetic and pharmcodynamic variability?
    insulin detemir
  22. A duration of action increases, _________ decreases.
  23. Canine and _______ insulin have 100% homology.
  24. What insulin is the best for dogs?
    BID vetsulin
  25. The most common type of insulin used for dogs is ___________; it is given in a(n) ______ syringe; its dose interval is _________.
    porcine lente; U-40; 12-24h
  26. The 3 most common types of insulin used in cats.
    human PZI, glargine, detemir
  27. Detemir is given to cats in a(n) _______ syringe; its dosing interval is ________.
    U-100; 12-24hr
  28. Glargine is given to cat in a(n) ________ syringe; its dosing interval is _________.
    U-100; 12h
  29. Human PZI is given to cats in a(n) _______ syringe; its dosing interval is _________.
    U-40; 12-24hr
  30. ___________ is formed as a result of non-enzymatic glycation of blood proteins; it is not affected by ___(2)___; it is affected by __________.
    Fructosamine; stress and food intake; half-life of proteins
  31. Fructosamine reflects __________, which is proportional to ___________.
    glycemic control over the past 2-3 weeks; average BG
  32. When analyzing fructosamine levels, use _______ more than ________.
    trends; reported guidelines
  33. Normal fructosamine might be indicative of...
    excellent control, prolonged periods of hypoglycemia due to insulin overdose (usually), diabetic remission (in cats)
  34. A glucose curve is a plot of ______ vs. ______; samples taken every ________.
    BG; time; 2 hrs (at least 4 samples)
  35. Using a glucose curve, you can estimate... (2)
    duration of insulin effect, efficacy of dose.
  36. How can you use a glucose curve to determine the efficacy of the dose?
    based on degree of decline from pre-injection to nadir (never change dose based on one curve)
  37. If the duration of insulin is too short,...
    switch to longer-acting insulin
  38. If the blood glucose curve shows hypoglycemia,...
    decrease the insulin dose (hypoglycemia is bad in all contexts)
  39. What are possible causes of excessively high glucose on a glucose curve? (5)
    incidental, technical problems with insulin handling/administration, stress hyperglycemia, inadequate dosage, insulin resistance
  40. Insulin-induced hyperglycemia occurs when there is an ___________, causing _________ followed by ______________; ___________ is necessary.
    excessively high insulin dosage; hypoglycemia; excessive counter-regulatory hormone release; insulin dose reduction
  41. Always correlate blood glucose curves with... (2)
    clinical signs and fructosamine.
  42. Insulin therapeutic range overlaps with ___________; therefore, start with _________.
    hypoglycemia; low dose and increase as necessary
  43. What do you usually start the insulin dose at for dogs and cats?
    • cats: 1U/inj
    • dogs: 0.25U/kg/inj (determir 0.1 U/kg)
    • BID!!!
  44. What should you expect following the onset of insulin therapy? (5)
    decrease urine volume and water intake, decreased appetite, weight gain, overall improvement in health and attitude
  45. What are the goals on insulin therapy? (3)
    resolve clinical signs, prevent consequences, avoid hypoglycemia
  46. Hypoglycemia causes...(5)
    weakness, ataxia, disorientation, seizures, death
  47. Insulin resistance is suspected when there is ...
    a perceived inappropriate response to insulin therapy.
  48. If compliance issue have been ruled out, insulin resistance may be caused by... (6)
    bacterial infections, organ failure, pancreatitis, concurrent endocrinopathies, drugs, heat cycles, insulin induced hyperlgycemia
  49. Insulin-induced hyperglycemia can result in... (5)
    increased BG, massive fluctuations in BG, worsening signs of uncontrolled DM, worse PU/PD, increased fructosamine
  50. ________ is a good screening test for pancreatitis in non-diabetic patients, but it is unreliable in diabetic patients because...
    PLI; it is frequently elevated in diabetics that are not symptomatic for pancreatitis.
  51. Obesity can cause _________, but is not usually ________ in diabetic patients in vetmed.
    insulin resistance; significant
  52. Hypothyroidism occurs mainly in _______; it causes weight ______ in the face of _______ appetite; it can be masked by DM, which causes...
    dogs; weight gain; decreased appetite; weight loss in the face of polyphagia.
  53. What are the overlapping parameters b/w hypothyroidism and DM? (2)
    increased liver enzymes, high cholesterol
  54. Why is fructosamine unreliable in hypothyroid dogs?
    it can increase as a result of decreased protein catabolism
  55. Hyperthyroid occurs mainly in _______; the overlapping parameters with DM include... (5)
    cats; PU/PD, polyphagia, increased liver enzymes, hyperglycemia, glucosuria
  56. Why is there often hyperglycemia and glucosuria in hypothyroid cats?
  57. Why is fructosamine unreliable in hyperthyroid cats?
    it can decrease as a result on increased protein catabolism
  58. Hypercortisolism (Cushing's) causes the following overlapping parameters with DM... (6)
    PU/PD, polyphagia, increased liver enzymes, increased cholesterol, dilute urine, UTIs
  59. When is it difficult to discern Cushing's and DM?
    in a cushings animal, concurrent DM is easy to confirm by hyperglycemia, fructosamine, glucouria; in a diabetic, it is difficult to confirm cushings because DM causes chronic stress and will result in false positive ACTH stim tests
  60. Hypersomatotropism occurs in cats with __________ and in dogs with __(2)__.
    acidophil adenoma; mammary gland tumors or increased progesterone (diestrus)
  61. What are the effects of excessive GH? (5)
    decreased insulin sensitivity, increased protein synthesis, increased bone growth, increased lipolysis, increased IGF-1 production
  62. GH _________ IGF-1 production; insulin has __________ effects on IGF-1 production.
    stimulates; permissive (ie. without insulin, IGF-1 will not be produced)
  63. What 2 syndromes are associated with hypersomatotropism?
    insulin resistance (and DM), acromegaly
  64. How do hypersomatotropic cats usually present?
    PU?PD, polyphagia (acromegaly often not present, or develops in late stages)
  65. What is an important clue that a diabetic cat may also have hypersomatotropism?
    lack of weight loss in a diabetic cat that is otherwise uncontrolled
  66. What are common clinical signs of hypersomatotropism? (7)
    PU/PD, polyphagia, weight gain, renomegaly, hepatomegaly, systolic murmur, plantigrade stance
  67. What are clinical signs in late stages of hypersomatotropism? (4)
    proganthia inferior, broad face, stridor/stertor (enlarged soft palate), enlarged organs
  68. __________ is a good screening test in a cat that is difficult to regulate when other differentials have been ruled out.
    IGF-1 measurment
  69. When do you screen cats for hypersomatotropism?
    treat diabetes first and consider IGF-1 measurment after diagnosis of insulin resistance; confirm hypersomtatropism with brain imaging
  70. Why is measurement of GH not used to diagnose hypersomatotropism?
    because of its pulsatile secretion
  71. Left untreated, hypersomatotropism will lead to...
    death from heart failure, laryngeal obstruction, brain compression
  72. How can you treat hypersomatotropism?
    radiation therapy, hypophysectomy (best chance for DM remission- not in USA), Pasireotide (somatostatin analog- EXPENSIVE)