This document summarizes different types of treatments for type 1 and type 2 diabetes mellitus. It describes the composition, absorption, and effects of various insulin preparations used to treat type 1 diabetes. It also outlines the mechanisms of action, pharmacokinetics, clinical uses, and adverse effects of oral medications commonly used to treat type 2 diabetes, including sulfonylureas, biguanides, glitazones, glucagon-like peptide-1 analogs, and alpha-glucosidase inhibitors. Key points are that oral anti-diabetic drugs depend on endogenous insulin production and can only cause hypoglycemia if they increase blood insulin levels.
This document summarizes different types of treatments for type 1 and type 2 diabetes mellitus. It describes the composition, absorption, and effects of various insulin preparations used to treat type 1 diabetes. It also outlines the mechanisms of action, pharmacokinetics, clinical uses, and adverse effects of oral medications commonly used to treat type 2 diabetes, including sulfonylureas, biguanides, glitazones, glucagon-like peptide-1 analogs, and alpha-glucosidase inhibitors. Key points are that oral anti-diabetic drugs depend on endogenous insulin production and can only cause hypoglycemia if they increase blood insulin levels.
This document summarizes different types of treatments for type 1 and type 2 diabetes mellitus. It describes the composition, absorption, and effects of various insulin preparations used to treat type 1 diabetes. It also outlines the mechanisms of action, pharmacokinetics, clinical uses, and adverse effects of oral medications commonly used to treat type 2 diabetes, including sulfonylureas, biguanides, glitazones, glucagon-like peptide-1 analogs, and alpha-glucosidase inhibitors. Key points are that oral anti-diabetic drugs depend on endogenous insulin production and can only cause hypoglycemia if they increase blood insulin levels.
Insulins Composition Absorbtion Secreted by B cells w/ C-pep Secreted by a cells cellular glucose uptake Used to treat insulin Soluble monomeric rapid gluconeogenesis and glycogenolysis overdose NPH protamine mix intermediate fatty acid and TG synthesis Lente Amorphous insulin-zinc suspension slow lipolysis, protein syn.
mutated B chain, causing decreased self Insulin Synthesis Initial translation product has N-terminal signal, Lispro/aspart association. very fast which is removed upon ER insertion. C peptide is cleaved out in golgi. mutations, causing precipitation at Secretion: blood glucose cell uptake/catabolism ATP Glargine injection site ultra long acting ATP-sensitive K+ channel closure depolarization opening inhaler. Contraindicated in smokers or of voltage sensitive Ca+ channel exocytotic release of insulin. EXUBERA lung disease rapid Metabolism: Extensive first pass met. So liver sees higher concentration than other tissues. Type 2 DM Treatments Drug Mechanism Pharmacokinetics Clinical use Adverse reactions ~Effective GI abs., end up mostly bound to albumin 1st gen Risk of inducing severe Tolbutamide: 4-7 hr t1/2 hypoglycemia Stimulation of insulin release Chlorpromamide: 24-48 hr t1/2 from the pancreas, via reduced 2nd gen Appetite stimulants obesity conductance through ATP Glyburide/glipizide: 2-4 hr t1/2 Primary agents, in combo with sensitive K+ channels. Requires ~ Yet, effects from one does last 24- dietary control. High failure rate (7%) prob due Sulfonylureas functional B cells. 48 hr. 100X more potent than 1st gen. Oral administration to pancreatic insuff. Glinides Induce insulin secretion through Taken orally at mealtimes to reduce Repaglinide + closure of the ATP sensitive K+ Very rapid acting, short duration. post-prandial peak. Flexible dosing Less potential for hypoglycemia Nateglinide channel. depending on meals. since short acting. Metformin reduces blood Lactic acidosis much less glucose via unknown common than with phenformin mechanism. 2 actions: reduced (off market) liver gluconeogenesis, reduced Often given synergistically with No hypoglycemia Biguanides insulin resistance. Oral administration sulfonylureas Anorexia Agonistic binding to PPAR, to Not recommended for first line Glitazones suppress resistin release from Low incidence of liver tox. (TZDs) white adipocytes. When used, monthly liver tests. Induces insulin release Nausea, which often goes away Glucagon-like-peptide homolog, Depresses glucagon release Twice daily injections with persistant use derived from gila monster Delays gastric emptying Approved as combo with metformin Increased risk of hypoglycemia if Exenatide salivary glands Net result: significant weight loss (good!) and sulfonylureas used with sulfonylureas -glucosidase Not effective as primary therapy inhibitors Slow intestinal degradation of used with other oral agents when (acarbose, complex carbs to reduce glucose failure to adequately control post- miglitol) absorbtion/ prandial glucose levels Flatulence, diarrhea ALL of the oral anti-diabetics depend on endogenous insulin production. If insulin production is insufficient, need Type 1 DM drugs Only have risk of hypoglycemia if you are increasing insulin levels in the blood.