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35 Cards in this Set
- Front
- Back
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-Nephropathy
-Neuropathy -Retinopathy are directly related to |
Level of glycemic control
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HBA 1C
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measures glycemic control; is proportional to average blood glucose over the last 3 to 4 months
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target HBA1c
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<7%
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things that DEcrease insulin resistance (in type 2)
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Exercise and weight loss
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insulin resistance + progressive beta cell decline over time
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Type 2
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a combination of oral agents and insulin may be needed for
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Type 2
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3 classes of oral agents
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insulin Secretagogues
insulin Sensitizers Alpha-Glucosidase Inhibitors |
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action of secretagogues
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help secrete more insulin
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action of sensitizers
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make existing insulin work better, thereby DEcrease insulin secretion
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action of glucosidase inhibitors
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inhibit the hydrolysis of oligosaccharides to glucose and other sugars;
therefore, blunt the postprandial increase in BG |
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classes of secretagogues
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Sulfonylureas:
-tolbutamide -Glimepiride -Glipizide -Glyburide Meglitinde Analogs: -nateglinide -repaglinide (~gogues are -gli, -gli, -gly, -glin, -glin) |
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The secretagogues famously cause
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HYPOglycemia and weight gain
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classes of insulin sensitizers
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Biguanide:
-meformin Glitazones: -pioglitazone -rosiglitazone (~ "met-a-glitzy" because they cause less/no hypoglycemia and no weight gain) |
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considered the DOC for newly diagnosed Type 2
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Metformin
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decreases hepatic gluconeogenesis (the major source of high BG), but may cause fatal lactic acidosis
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Metformin
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drugs which INcrease HDL and may be used in polycystic ovary disease to induce ovulation (obese women)
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metformin and the glitazones (insulin sensitizers)
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Side effect of a Glitazone
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hepatotoxicty - must my monitored w/ LFTs
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2 Glucosidase inhibitors
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acarbose (Precose)
miglitol (Glyset) |
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side effects of glucosidase inhibitors
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NO hypoglycemia, but
-GI distress: flatulence, diarrhea, abdm cramps, etc. |
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If glucosidase inhibitors are used w/ other agents like insulin, sulfonylureas, etc. ...
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may cause HYPOglycemia, which must be treated w/ glucose itself
(b/c the glucosidase inhibitor will prevent absorption of sucrose or fructose) |
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If the diabetic is so hypoglycemic that he/she can't take anything by mouth, the only option is
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call 911: glucagon IM or glucose IV
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2 types of physiologic insulin secretion
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Basal (background, constant) and Prandial (incr secretion w/ meals)
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Historically, basal insulin was supplied by
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intermediate acting insulins:
-NPH -Lente -Ultralente |
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Today, basal insulin is supplied by
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prolonged-acting insulins:
-Detimir -Glargine These last about 24 hours and are considered "peakless". |
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Historically, prandial insulin was supplied by
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short-acting regular insulin.
straight up, yo. just insulin. |
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Today, prandial insulin is supplied by
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ULTRAshort-acting insulins:
-Lispro -Aspart -Glulisine |
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Standard tx for Type 2 is insulin BID, whereas
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Intensive tx for Type 2 is insulin 3x to 5x per day
(increased incidence of hypoglycemia, seizures & coma) |
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severe hyperglycemia can lead to
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DKA
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Sx of DKA
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nausea, vomiting, severe dehydration, fruity breath, deep breathing (Kussmaul), stuporous, or comatose,
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more Sx of DKA
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hypothermia, hypotension, possible High serum potassium, but total BODY K+ depletion (from vomiting, etc.)
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Regular, run of the mill, straight up insulin
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bolus + hr infusion
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immediate fluid replacement
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Normal saline
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potassium replacement, starting 2-3 hrs into therapy
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due to K+ losses, and b/c of correction of the acidemia causes K+ to move back into the cells
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When BG falls to 250 mg/dl, give
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glucose IV (5%)
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if pH falls below 7.0 (acidosis)
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IV NaHCO3 to correct
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