Peds Pharm: Dm And Dka

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Diabetes mellitus (DM) =

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term used to describe a group of metabolic diseases characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both

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fasting plasma glucose

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no caloric intake for 8 hours

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oral glucose toloerance test

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administer 75g anhydrous glucose or 1.75g/kg body wieght glucose for max of 75 g

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impaired glucose tolerance

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2 h post load of 140-199

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impaired fasting glucose

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BG 100-125

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autoimmune DM 1

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beta cell destruction, absolute insulin deficiency and DKA

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insulin resistant DM2

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range from predominantly inuslin resistnace with relative insulin deficiency to predominantly secretory defect with or w/o insulin resistance

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clinical presentation of DM

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polyuria, polyphagia, polydipsia. also blurred vision, weight loss, fatigue, dry skin, slow healing wounds

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diagnostic critieria for DM

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must be confirmed next day if no unequivcal hyperglycemia. 1) symptoms + random BG>=200, 2) FPG>=126, 3) 2 hr post load>= 200

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normal fpg and ogtt

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fpg<100, OGTT<140

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impaired fpg and ogtt

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fpg100-125, OGTT 140-199

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DM fpg and ogtt

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fpg>=126, ogtt >=200

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3 presentations of DM 2

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asymptomatic, mild symptoms, BG>250 and ketosis

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asymptomatic, 1st line

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diet and exercise

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mild sympt, 1st line

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metformin

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bg>250, ketosis, symptoms 1st line

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insulin

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what is the action of inuslin

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Increases glucose uptake in tissues, inc liver glycogen, decreases glycogenolysis, increases fatty acid synthesis, decreases metabolism of fatty acids to ketones

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rapid acting insulin

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aspart, lispro, glulisine

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short acting insulin

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regluar

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intermediate acting insulin

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NPH

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long acting glucose

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glargine, detemir

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1 unit of insulin lowers BG by ___

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25-50 units

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honeymoon period

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for patients with DM 1- period that often follows diagnosis and initiation of insulin treatment. It is often suggestive of remission, but it is important to note that the two are unrelated - it is not a cure for type 1 diabetes. During this period some of the insulin-producing beta cells of the pancreas have not been completely destroyed yet and produce unpredictable amounts of endogenous insulin.

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sick day management

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keep taking insulin, stop metformin if npo. Reduce long acting insulin to basal levels and use sliding scale coverage

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somogyi effect

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post-hypoglycemic hyperglycemia, decrease bedtime NPH or give evening NPH later

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dawn phenomenon

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rise in BG in early AM, increase evening NPH dose

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metoformin acts to..

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decreases gluconeogenesis, decreases glucose absorption, increases insulin sensitivity, does not stimulate insulin secretion

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side effects of metforming

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n/v/d, metal taste, low b12, lactic acidosis

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combo of metformin with..

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glyburide

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1st gen sufonlyurea

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chlorpropamide, tolazamide, tolbutamide

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2nd gen sulfonylurea

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glimepiride, glipizide, glyburide

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ae 1st gen sulfonlyureas

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lo bg, weight gain, n/v/d/, rash, heme rxns

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ae 2nd gen sulfonylureas

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less than 1st gen

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moa of sulfonylureas

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binds to beta cells, stimulates insulin relsease

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late compliactions of DM and how to fix

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dislipidemia - statins, hypertension - acis, arbs, diuretics

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how much weight to lower insulin resistance

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10-20 lb

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bg in dka

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<600

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dm type of dka

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dm 1

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serum bicarb dka

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low to normal

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ketonemia in dka

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positive

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arterial ph in dka

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<7.3 (low)

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waht is the 4-2-1 rule

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is 10 kg 4, 11-20 kg 2, 20-50 kg 1 ml/hr

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max rate of K in mEq/kg/hr

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0.5

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do you use bicarb to replae acidosis in dka?

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NO

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dose of insulin per hour given in dka

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0.1 u/kg/hr for 1-2 hr after fluid replacement

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risk factors for cerebral edema

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low ca, inc bun, severe acidosis, treatment with bicarb, na inc during therapy, large volume in firts 4 h, insulin in 1st hour