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26 Cards in this Set

  • Front
  • Back
Rapid acting insulin
Lispro
Aspart
Short-acting insulin
Regular Insulin
Intermediate and long-acting insulin
Intermediate insulin = NPH
Long acting insulin = Glargine
Long acting insulin = Detemir
Insulin toxicity
Hypoglycemia
Hypersensitivity reaction (very rare)
Insulin Clinical use
Type 1 Dm
Type 2 Dm
Gestational Diabetes
Life-threatening Hyperkalemia
Stress-induced hyperglycemia
Insulin action on muscle
Protein synthesis and icnresed glycogen. Also Increase K+ uptake
Sulfonylureas - First Generation - list them
Tolbutamide
Chlorpropamide
Sulfonyureas - 2nd Generation - list them
The "Gly/Glis"
Glyburide
Glymepiride
Glipizide
Glitazones/Thiazolidinediones - List them
Proglitazone
Rosiglizatones
Alpha Glucosidase inhibitors
Acarbose
Miglitol
Pramlintide belongs to what drug class?
Mimetics
GLP-1 Analogs - name them
Exenatide

Analog - "example"=Examplatide(sounds similar)
Pramlintide : Action, use and toxicity
Action : Decrease glucagon
Clinical Use : Type 2 DM
Toxicities : Hypoglycemia, Nause, Diarrhea
Exentaide : Action, use and toxicity
Action : Increase in insulin, Decresae in glucagon release
Use : Type 2 DM
Toxicity : Nausea, vomiting, pancreatitis(site of action)
Alpha glucosidase inhibitors - Clinical use / toxicity
Clinical Use - Monotherapy in Type 2 DM or with combo therapy
Toxicity = GI disturbances (works there)
Metformin Action :
Exact mechanism unknown.
Decreased gluconeogenesis
Increased Glycolysis
Increased peripheral glucose uptake (increased insulin sensitivity)
Glitazones mechanism
"Glitters"(binds) peripheral tissues and increases their sensitivity to insulin. Binds to PPAR-gamma nuclear transcription regulator.
Glitazones Clinical use? Toxicity?
Monotherapy or combotherapy for Type 2 DM.

Toxicity :
Weight gain
Edema (can lead to weight gain)
Hepatotoxicity
Heart Failure
Alpha Glucosidase inhibitors - Action
Inhibits intestinal alpha glucosidase inhibitors on brush border cells.

Delayed sugar hydrolysis and glucose absorption leads to decreaseed postprandial hyperglycemia
Alpha glucosidase inhibitors - Clinical use / toxicity
Clinical Use - Monotherapy in Type 2 DM or with combo therapy
Toxicity = GI disturbances (works there)
Metformin Action :
Exact mechanism unknown.
Decreased gluconeogenesis
Increased Glycolysis
Increased peripheral glucose uptake (increased insulin sensitivity)
Metformin Clinical Use and Toxicity
Use : ORAL . First line treatment for type 2 DM.

Can be used in patients without Islet funciton

Toxicity : Worst effect is lactic acidosis (contraindicated in Renal Failure Patients)
Metformin contraindicated in?
Renal failure patients (b/c of lactic acidosis side effect)
Sulfonylurea Action:
Close K+ channel in beta cell pancreas membrane leading to depolarization which triggers Ca2+ influx leading to insulin release.
Sulfonylurea Use?
Use : Stimulate release of ENDOGENOUS insulin in type 2 DM. Useless in Type 1 DM (no endocrine pancreas fxn)
Sulfonylurea Toxicity:
First generation : Disulfiram-like effects
Second generation : Hypoglycemia