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STEP2 CK, ENDOCR(1)

  1. Definition: Hyperglycemia resulting from the autoimmune distruction of the insulin-producing beta cells of the pancreas
    DM-1
  2. most common HLA genotypes in DM-1; (2)HLA DR3; HLA DR4
  3. Dx: woman has a recurrent vaginal candidiasis that is refractory to treatment; what test should be done?
    Diabetes mellitus; Get a blood glucose
  4. Antibody types for DM-1; (2)
    Anti-cytoplasmic Ab against: Beta cells; and Glutamic Acid Carboxylate (GAD)
  5. (2) environmental factors that may play a role in the etiology of DM-1
    Viral infection; Exposure to cow's milk during infancy
  6. (3) Viral infections that may play a role in the etiology of DM- 1
    Congenital Rubella; Mumps; Coxsackie B
  7. Dx: polyuria, polydipsia, weight loss, dehydration, blurred vision, fatigue
    DM-1
  8. Dx tests for Diabetes; (3)
    1. Fasting glucose > 126; 2. Random plasma glucose > 200; 3. HbA1c > 7%
  9. (4)* Bugs that occur in DM patients due to their decreased efficacy of granulocytes
    MA and PA:; Mucormycoses;; Actinomycoses;; Pseudomonas;; Aspergillosis (pneumonia)
  10. How do you determine the time the daily dose of insulin (NPH or 70/30 preparations) is given for a DM-1 patient?
    Give 2/3 daily dose before breakfast; Give 1/3 daily dose before dinner
  11. How should new DM-1 patients monitor their glucose?
    Finger-stick levels 5 times a day: morning fasting;; breakfast postprandial;; lunch postprandial;; dinner postprandial;; before bed
  12. Which insulin preparation is considered "Rapid-acting" and used right before meals?; (2); List: Onset of action; Peak action; Duration of action
    Humalog or Lispro; Onset of action = 15 min; Peak action = 60 min (ave 30-90 min); Duration of action = 3 hr (ave 2-4 hr)
  13. Regular insulin: Onset of action; Peak action; Duration of action
    Onset of action = 30-60 min; Peak action = 2-4 hr; Duration of action = 6-8 hr
  14. (2) Intermediate-acting Insulin preparations; List: Onset of action; Peak action; Duration of action
    NPH and Lente; Onset of action = 1-3 hr; Peak action = 6-12 hr; Duration of action = 18-26 hr
  15. (2) Long-Acting Insulin preparations; List: Onset of action; Peak action; Duration of action
    Ultralente and PZI; Onset of action = 4-8 hr; Peak action = 14-24 hr; Duration of action = 24+
  16. Longest acting Insulin preparation; (2 names); List: Onset of action; Peak action; Duration of action
    Glaragine (Lantus); Onset of action = 1 hr; Peak action = no peak; Duration of action = 24+
  17. Definition: exaggeration of the normal tendancy of plasma glucose to rise in the early morning hours before breakfast; what may it be caused by?; First step in Tx?
    Dawn phenomenon; By: inc in GH secretion; Tx: move nighttime insulin closer to bedtime
  18. what is "postprandial"?
    2 hours after meal
  19. Definition: nighttime hypoglycemia followed by dramatic inc in fasting glucose levels and inc plasma ketones; what confirms dx?; Tx?
    Somogyi Effect; confirms: Hypoglycemia at 3am; Tx: give Long-acting insulin at bedtime (instead of NPH)
  20. Dx: patient presents with persistent morning hyperglycemia, despite increasing his nighttime NPH insulin dose. He complains of frequent nightmares and his wife witnessed him having a seizure in the middle of the night
    Somogyi effect
  21. MC negative complication with: 1. DM-1; 2. DM-2
    1. DKA; 2. Non-Ketonic Hyperglycemic Hyperosmolar Coma (NKHC); [either can occur with either DM]
  22. What type of immunity is impaired with diabetes?; what type of infections can this lead to?
    Cell-mediated immunity; leads to: Fungal infections
  23. What should be done if the am finger-sticks show hypoglycemia?
    decrease the bedtime NPH even if the bedtime finger-sticks are high
  24. (3) causes of DM-2 hyperglycemia
    1. Impaired secretion of Insulin; 2. Decreased insulin effectiveness at glucose uptake; 3. Impaired inhibition of hepatic gluconeogenesis
  25. How can hyperglycemia cause further glucose intolerance?; (2)
    1. it Decreases insulin sensitivity; 2. it Increases hepatic glucose production
  26. Drug class of Metformin; MOA (3); AE
    Biguanides; MOA: sensitizes skeletal muscle and fat to insulin; Dec hepatic gluconeogenesis; Dec GIT absorption; AE: Lactic Acidosis
  27. (4)* drugs in Sulfonylurea class
    . Goes To Cancel Glucose:; Glyburide;; Tolbutamide;; Chlorpropamide;; Glipizide
  28. MOA of Sulfonylureas; AE
    MOA: increase postprandial insulin secretion from beta cells; AE: Hypoglycemia
  29. (3) drugs in the Thiazolidinediones class
    GLITAZONES: Troglitazone;; Rosiglitazone;; Pioglitazone
  30. (2) MOA of the Thiazolidinediones; AE
    MOA: Reduces insulin resistance; dec. hepatic glucose output; AE: Hepatotoxicity
  31. Example of an Alpha-glucosidase inhibitor; MOA; AE
    Example: Acarbose; MOA: inhibits monosaccharides and oligosaccharide hydrolysis in the small intestines; AE: Diarrhea and nausea (and farting)
  32. MC combination of DM oral drugs; (plus 2 drugs in it)
    Glucovance; (Metformin + Glyburide)
  33. Basic Etiology behind DKA
    Severe insulin deficiency causes body to switch from metabolizing carbs to metabolizing and oxidizing lipids
  34. What (2) ketones are produced with DKA?; what is normal raio of these two?; ratio in DKA?
    Beta-hydroxybutyric Acid (BOH); Acetoacetic Acid; Normal ratio: 3:1; DKA ratio: 8:1
  35. Pathophysiology of DKA and how it leads to "fruity breath"; (4)
    1. insulin deficiency causes hyperglycemia -> osmotic diuresis; 2. loss of fluids, Na and K; 3. inhibition of FFA oxidation in liver -> ketosis; 4. Met Acidosis results in respiratory compensation and blowing off of breakdown products (acetone)
  36. Dx: dehydration, polyuria, N/V, rapid deep (Kussmal) breathing, + anion gap, scent to breath
    DKA
  37. (3) main parts of Dx DKA
    D: high glucose (400-800 mg); K: + Ketones; A: pH < 7.3 (inititially casues K to rise)
  38. (3) Tx rules for DKA
    1. Hydrate (usu 3-4L loss): replace with NS; 2. Insulin (and glucose if pt becomes normoglycemic); 3. Replace K
  39. Causes of death with DKA; (3)
    circulatory failure;; HypoK;; Infection
  40. MC DM-2 patient profile to get Nonketotic Hyperosmolar Coma
    . DM-2 nursing home patient
  41. Etiology of Nonketotic Hyperosmolar Coma; (4--2 are drugs)
    Sepsis;; Dehydration;; Diuretics;; Glucocorticoids
  42. Sx: Altered mental status, signs of profound dehydration, neurologic deficits, DM-2
    Nonketotic Hyperosmolar Coma
  43. What is serum glucose levels for Nonketotic Hyperosmolar Coma?; serum Osmolarity?; what is the other indicator, with relation to the kidneys?
    glucose > 1000 mg/dL; serum osmloarity around 385 mOsm/kg; Pre-renal Azotemia: BUN/creatinine levels are increased
  44. Tx for Nonketotic Hyperosmolar Coma; (3)
    1. Expand IV volume: infuse 2-3L NS over 1-2hrs; 2. K replacement; 3. withhold insulin therapy for up to 1 hour (to help with IV osmolality)
  45. Whipple's triad of Hypoglycemia
    1. plasma glucose < 60mg/dL; 2. Sx of hypoglycemia; 3. improvement of Sx with Glucose
  46. MCC of altered mental status in Healthcare environments
    Hypoglycemia
  47. Etiology of Hypoglycemia; (6)*
    DIAL HI:; 1. Drug induced; 2. Islet cell tumor/adenoma; 3. Adrenal insufficiency; 4. Liver/renal Dz (severe); 5. Hypopituitarism from low GH and cortisol; 6. Insulin receptor Ab
  48. Dx: possible History of insulin or sulfonylurea Tx, adrenergic Sx (diaphoresis, anxiety, tremor, hunger, palpitations); confusion, inappropriate behavior, mistaken for alcohol intoxication
    A049. Hypoglycemia
  49. Dx Tests for Hypoglycemia; (2)
    . 1. Low serum glucose < 50mg/dL; 2. ask lab to test C-peptide to distinguish b/t Endogenous insulin (high C-peptide) or Exogenous insulin(low)
  50. If alcoholism or nutritional deficiency is a suspected reason for hypoglycemia, what should be placed with the IV of dextrose?; Why?
    Thiamine to prevent Wernicke's encephalopathy
  51. Hospital Tx for Hypoglycemia; (3 steps)
    1. IV amp of 50% dextrose; 2. if no improvement, give a second amp; 3. continue to infuse 10% dextrose until serum glucose is > 100mg/dL
  52. if hypoglycemia is refractory after Tx and there are associated signs of adrenal insufficiency, what is Tx?
    give Hyrdocortisone 100-200mg IV
  53. what is used to resuscitate hypoglycemic coma?; what type of patient will this Tx not work on?
    Glucagon IM; won't work on Alcoholic with liver failure
  54. What does a glucagonoma present with?; (3)
    1. new-onset DM; 2. weight loss; 3. characteristic rash (necrolytic migratory erythema)
  55. How is insulin related to Catecholamines?; (2)
    1. Inc insulin leads to hypoglycemia, leading to tachycardia, sweating and anxiety; 2. Pheochomocytoma patient have inc risk of hyperglycemia and DM
  56. How does Cortisol relate to glucose levels?; (2)
    . Too much cortisol (Cushings) leads to hyperglycemia and DM; 2. Too little cortisol (Addisons) leads to hypoglycemia
  57. How does GH relate to glucose levels?; (2)
    1. high GH in acromegaly, leads to hyperglycemia and DM; 2. neonatal hypoglycemia is a cardinal sign of GH deficiency
  58. List the 5 signs (any 3 of which can confirm Dx) to properly Dx Metabolic syndrome
    1. Fasting glucose > 110 mg/dL; 2. Abdominal obesity; 3. Serum TG > 150 mg/dL; 4. HDL-C < 40 in men and < 50 in women; 5. Blood Pressure > 130/85 (or on BP meds)
  59. (3) causes of Macroglossia
    Acromegaly;; Myxedema;; Amyloidosis
  60. Definition: Increased synthesis and secretion of free thyroid hormones resulting in hypermetabolism
    Hyperthyroidism
  61. Etiology of Hyperthyroidism; (4)
    Grave's Dz;; Toxic Nodular Goiter;; Plummer's Dz (toxic adenoma);; Subacute thyroiditis
  62. Dx: heat intolerance, sweating, palpitations, weight loss, tremor, nervousness, weakness, hyperdefication
    Hyperthyroidism
  63. When is the only time TSH is increased and TRH is decreased?
    Pituitary tumor (secretes TSH)
  64. When is the only time TSH and TRH are both increased (with T3 and T4 decreased)?
    Primary Hypothyroidism
  65. Definition: A medical emergency consisting of an exaggerated manifestation of hyperthyroidism
    Thyroid Storm
  66. Etiology of a Thyroid Storm; (4)
    1. Trauma, infection;; 2. DKA;; 3. MI, CVA, PE;; 4. Withdrawl from anti-hyperthyroid meds
  67. Dx: fever, tachycardia, high-output CHF and volume depletion, exhaustion, diarrhea, abdominal pain, agitation and confusion, possible jaundice
    Thyroid Storm
  68. What is the BP change with hyperthyroidism?
    Isolated systolic HTN
  69. (4) Primary stabilization Tx for a Thyroid Storm
    Airway protection;; Oxygenation;; Assess circulation and BP;; IV hydration
  70. Aside from primary stabilization, how is a Thyroid Storm treated?; (4 together)
    1. Beta-blocker - block adrenergic effects;; 2. Acetaminophen - fever;; 3. PTU - block new thyroid hormones; 4. Iodine - 1.5 hrs after PTU to decrease release of preformed thyroid hormones
  71. Definition: Autoimmune Dz causing hyperthyroidism due to Ab, which stimulates TSH receptor
    Graves Dz
Author
icbcc
ID
136292
Card Set
STEP2 CK, ENDOCR(1)
Description
FA, ENDOCR(1)
Updated

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