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35 Cards in this Set

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-Nephropathy
-Neuropathy
-Retinopathy
are directly related to
Level of glycemic control
HBA 1C
measures glycemic control; is proportional to average blood glucose over the last 3 to 4 months
target HBA1c
<7%
things that DEcrease insulin resistance (in type 2)
Exercise and weight loss
insulin resistance + progressive beta cell decline over time
Type 2
a combination of oral agents and insulin may be needed for
Type 2
3 classes of oral agents
insulin Secretagogues
insulin Sensitizers
Alpha-Glucosidase Inhibitors
action of secretagogues
help secrete more insulin
action of sensitizers
make existing insulin work better, thereby DEcrease insulin secretion
action of glucosidase inhibitors
inhibit the hydrolysis of oligosaccharides to glucose and other sugars;
therefore, blunt the postprandial increase in BG
classes of secretagogues
Sulfonylureas:
-tolbutamide
-Glimepiride
-Glipizide
-Glyburide

Meglitinde Analogs:
-nateglinide
-repaglinide

(~gogues are -gli, -gli, -gly, -glin, -glin)
The secretagogues famously cause
HYPOglycemia and weight gain
classes of insulin sensitizers
Biguanide:
-meformin

Glitazones:
-pioglitazone
-rosiglitazone

(~ "met-a-glitzy" because they cause less/no hypoglycemia and no weight gain)
considered the DOC for newly diagnosed Type 2
Metformin
decreases hepatic gluconeogenesis (the major source of high BG), but may cause fatal lactic acidosis
Metformin
drugs which INcrease HDL and may be used in polycystic ovary disease to induce ovulation (obese women)
metformin and the glitazones (insulin sensitizers)
Side effect of a Glitazone
hepatotoxicty - must my monitored w/ LFTs
2 Glucosidase inhibitors
acarbose (Precose)
miglitol (Glyset)
side effects of glucosidase inhibitors
NO hypoglycemia, but
-GI distress: flatulence, diarrhea, abdm cramps, etc.
If glucosidase inhibitors are used w/ other agents like insulin, sulfonylureas, etc. ...
may cause HYPOglycemia, which must be treated w/ glucose itself
(b/c the glucosidase inhibitor will prevent absorption of sucrose or fructose)
If the diabetic is so hypoglycemic that he/she can't take anything by mouth, the only option is
call 911: glucagon IM or glucose IV
2 types of physiologic insulin secretion
Basal (background, constant) and Prandial (incr secretion w/ meals)
Historically, basal insulin was supplied by
intermediate acting insulins:
-NPH
-Lente
-Ultralente
Today, basal insulin is supplied by
prolonged-acting insulins:
-Detimir
-Glargine
These last about 24 hours and are considered "peakless".
Historically, prandial insulin was supplied by
short-acting regular insulin.
straight up, yo. just insulin.
Today, prandial insulin is supplied by
ULTRAshort-acting insulins:
-Lispro
-Aspart
-Glulisine
Standard tx for Type 2 is insulin BID, whereas
Intensive tx for Type 2 is insulin 3x to 5x per day
(increased incidence of hypoglycemia, seizures & coma)
severe hyperglycemia can lead to
DKA
Sx of DKA
nausea, vomiting, severe dehydration, fruity breath, deep breathing (Kussmaul), stuporous, or comatose,
more Sx of DKA
hypothermia, hypotension, possible High serum potassium, but total BODY K+ depletion (from vomiting, etc.)
Regular, run of the mill, straight up insulin
bolus + hr infusion
immediate fluid replacement
Normal saline
potassium replacement, starting 2-3 hrs into therapy
due to K+ losses, and b/c of correction of the acidemia causes K+ to move back into the cells
When BG falls to 250 mg/dl, give
glucose IV (5%)
if pH falls below 7.0 (acidosis)
IV NaHCO3 to correct