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Biguanide
- Oral therapy
- Prototype: Metformin
- Mechanism of action: Exact mechanism unknown, but it works by decreasing hepatic production of glucose and intestinal glucose absorption, and by increasing insulin sensitivity
- SE: primarily GI (diarrhea, abdominal bloating, nausea), vitamin B12 deficiency with long term use, and lactic acidosis (the most severe but rare)
- Effect on plasma insulin: decreased
- Risk of hypoglycemia: not as monotherapy (because does not increase insulin secretion)
- Contraindicated in: renal impairement and acute/chronic metabolic acidosis
- Benefits: No weight gain (patient may actually have weight loss)
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Secretagogue
- Oral therapy
- Includes insulin secretagogues (sulfonylureas) and the glinides (repaglinide and nateglinide)
- MoA: Sulfonylureas block the potassium channel in beta cells (stimulating extra insulin release); glinides bind distinct sites on the potassium channel and also stimulate insulin release (these have rapid onset and short duration of action)
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Sulfonylurea
- Oral therapy
- First generation prototypes: tolbutamide and chlorpropamide
- Second generation prototypes: glyburide, glipizide/glipizide XL, glimepiride
- MoA: close potassium channel in beta cell membrane, causing the cell to depolarize and release insulin
- SE: Hypoglycemia (esp in elderly patients, those with hepatic/renal impairment, and when used as combo therapy), weight gain, decreased efficacy over time
- First generation SE: disulfiram-like effects (headache, drowsiness, tiredness, nausea, vomiting, etc)
- Useless in type 1 because they require some islet cell function
- Glyburide may be a safe alternative for pregnant diabetic patients
- Second generation SE: hypoglycemia
- Efficacy: has more rapid effect and decreases A1C 1.5%
- Effect on plasma insulin: increased for both generations
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Glinides
- Oral therapy
- Prototypes: repaglinide, nateglinide
- Short acting secretagogues that stimulate insulin release from pancreatic beta cells that have a shorter half life than sulfonylureas (insulin release is rapid and lasts only 1-2 hours)
- Targets postprandial glucose levels
- SE: Hypoglycemia (smaller risk than sulfonylureas), weight gain
- Effect on plasma insulin: increases it
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Thiazolidineodiones (TZDs)
- Oral therapy
- Prototype: Rosiglitazone and pioglitazone
- MoA: Insulin sensitizers that are PPAR-gamma receptor activators in muscle, fat, and liver to decrease insulin resistance (increases insulin, primarily in peripheral tissue)
- SE: Peripheral edema, weight gain (due to fluid retention), heart failure (greater risk if used in conjunction with insulin), increased fracture risk, potential bladder cancer risk, hepatotoxicity
- Contraindications: ATL > 2.5x ULN, pt with heart failure NYHA class III or IV (class I and II are okay so long as you monitor pt), alcohol abuse
- Effect on plasma insulin: decreased
- Risk of hypoglycemia: no
- Notes: effective in highly insulin-resistant pt; must monitor liver functions
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Alpha-glucosidase inhibitors
- Oral therapy
- Prototypes: acarbose, miglitol
- MoA: Inhibits alpha-glucosidase, a small intestinal brush border enzyme that cleaves oligosaccharides, thus preventing glucose absorption and decreasing post-prandial glucose levels
- SE: diarrhea, abdominal pain, flatulence (all not well tolerated)
- Contraindicated: chronic intestinal disease, cirrhosis
- Note: if tx someone on this who is hypoglycemic, it is important to use glucose and not sucrose, as these also inhibit sucrase
- Risk of hypoglycemia: no (not as monotherapy)
- Effect on plasma insulin: little or no change
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DDP-IV inhibitors
- Oral therapy
- Prototype: sitagliptin, saxagliptin, lingliptin
- MoA: inhibits DDP-IV, the enzyme that inactivates GLP-1; prolonged incretin activity increases insulin release in response to meals and reduces inappropriate glucagon secretion
- SE: well tolerated with few post-marketing reports of hypersensitivity rxns
- Contraindications: None yet known
- Effect on plasma insulin: increases
- Risk of hypoglycemia: No
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Glucagon-like peptide 1 (GLP-1) agonists
- Non-Oral therapy: given subcutaneously
- Prototypes: exenatide, exenatide LAR, liraglutide, bydureon (extended release exenatide)
- MoA: GLP-1 analog that mimics incretin to increase glucose-dependent insulin release, suppress high glucagon levels and delay gastric emptying
- SE: nausea, vomiting, weight loss, acute pancreatitis, hypoglycemia (if used in conjunction with sulfonylureas)
- Effect on plasma insulin: increases
- Risk of hypoglycemia: no
- Note: Because of the gastric emptying delay, this can affect absorption of other medications
- Contraindications: Type I DM, gastroparesis, hx of medullary thyroid cancer and MEN type II
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Major differences between DDP-4 inhibitors and GLP-1 receptor agonists
- Slows gastric emptying: DPP-4 inhibitors don't, GLP-1 agonists do
- Body weight effects: DDP-4 are neutral; GLP-1 cause weight loss
- SE: DDP-4 are well tolerated; GLP-1 has nausea/vomiting
- Administration: DDP-4 is oral once daily; GLP-1 is subcutaneous one or twice daily or once a week
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Pramlintide
- Synthetic analog of human amylin
- MoA: suppresses postprandial glucagon secretion, regulates rate of gastric emptying, and reduces food intake
- Amylin is co-secreted with insulin in response to a meal and is deficient in both type 1 and type 2 diabetes
- Note: should be given immediately prior to a meal; if used in conjunction with insulin, should lower the dose of insulin
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Types of Insulin
- Rapid acting (for pre-meal): Humalog (lispro), Novolog (aspart), and apidra (glulisine)
- Short acting (for pre-meal): Novolin R, Humulin R
- Intermediate acting: Novolin N, Humulin N
- Long acting (for basal insulin): Levemir (detemir), and lantus (glargine)
- Action: Bind insulin receptor
- In liver: causes increased glucose stored as glycogen
- In muscle: causes increased glycogen and protein synthesis and potassium uptake
- In fats: aids triglyceride storage
- Use: Type I DM, type 2 DM, gestational diabetes, life-threatening hyperkalemia, and stressed-induced hyperglycemia
- Tox: hypoglycemia and hypersensitivity rxn (very rare)
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Detemir (levemir)
- MoA: An attached fatty acid side chain that binds interstitial albumin at the subcutaneous injection site (prolongs absorption)
- Must dissociate from albumin to bind insulin receptors
- Onset: 2 hrs
- Peak: 6-9 hrs
- Duration: 24 hrs
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Glargine (lantus)
- MoA: Forms microprecipitates when injected into the body that slowly dissolves into monomers that are absorbed
- Is soluble at pH 4
- Onset: 4-5 hr
- Peak: none or blunted
- Duration: 24 hrs
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Neutral Protamine Hagedorn (NPH)
- Intermediate acting insulin
- Onset: 1 to 2 hr
- Peak: 6 to 10 hr
- Duration: 12-18 hr
- It an alternative basal insulin
- Novolin N and Humulin N work similarly
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Novolin R and Humulin R
- Short acting insulin
- Onset: 30 min
- Peak: 2 to 5 hr
- Duration: 4-6 hr
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Lispro (Humalog), Aspart (Novolog), Glulisine (Apidra)
- Rapid acting insulin
- Onset: 5-15 min
- Peak: 1-3 hr
- Duration: 3-5 hr
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