Diabetes Flashcards
pathogenesis of hyperglycemia (2 points)
1 - Beta cell dysfunction
2 - insulin resistence in tissues
Insulin secreted when
elevation of blood glucose
vagal stimulation
B2-adrenergic agonists
Insulin MOA liver
promotes glucose storage
inhibits gluconeogenesis and ketogenesis
Insulin MOA muscle
Increased AA transport, protein synthesis and glycogen synthesis
Insulin MOA Fat cells
Inhibits intracellular lipolysis
increased TG storage and FA synthesis
Mechanism of hyperglycemia in diabetes
reduced glucose transport into muscle
reduced conversion of glucose storage as glycogen
increased conversion of protein to glucose
Mechanism of ketoacidosis in diabetes
increased mobilization of peripheral fat –> increased lipolysis –> increased FFA –> increased acetyl CoA –> increased ketone bodies
Prandial insulin are given before meals –> covers between meals and are rapid-acting and short-acting
:)
Humalog
Novolog
Apidra
are examples of
Rapid- acting insulins
onset 5-15 minutes and duration ~4hours
Intermediate acting basal insulin are given…
before breakfast –> covers between lunch and dinner.
before dinner or at bedtime –> covers overnight
Example: NPH
Long acting basal insulin is given…
once (Lantus) or twice (Levemir) daily –> provides “background” insulin levels
SSx of hypoglycemia with long acting insulin
CNS impairment: night sweats, HA, visual disturbance, confusion etc. come on more gradually
SSx of hypoglycemia with short acting insulin
Mimic autonomic hyperactivity: tachycardia, palpitations, tremor, nausea, hunger. Come on more rapidly
SSx of ketoacidosis (not enough insulin)
Gradual onset (hours or days)
Acetone breath, dry/flushed skin, thirst
TX: saline, insulin, possible replacement of K+ and PO4
Biguanides (Metformin, Glucophage) MOA
Increase the suppression of insulin on hepatic glucose production
Initial Pharm tx after lifestyle modifications