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50 Cards in this Set

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STRUCTURE
MECHANISM
DRUG ADMIN.
PLASMA CIRCULATION
USE
ONSET/DURATION
HALF-LIFE
ELIMINATION
ADVERSE RXNS
OTHER
Crystalline, Semilente
NPH (isophane), Lente
Ultralente, Protamine Zinc
Insulin Lispro, Insulin Aspart, Insulin Glulisine
Insulin Detemir
Insulin Glargine
First Generation: Tolbutamine, Tolazamide Second Generation: Glyburide, Glipizide
Repaglinide
Exenatide
Citagliptin & Vildagliptin ("gliptins")
Metformin
Rosiglitazone, Pioglitazone
Acarbose
Pramlintide (symlin)
Synthetic analog of human amylin
Blocks hepatic gluconeogenesis. Remember that in the absence of insulin, the liver will respond by making more glucose.
Derived from the sulfonylurea containing compount, Butamide. These drugs have substitutions on the R1 and R2 chains.
Glargine substitution at A-21 and B-30, which results in delayed absorption by causing precipitation of the molecule.
Engineered to add a fatty acyl chain on to the lysine residue of the B-chain, so as to increase binding to albumin.
Modified Insulin structure: Decreases hexameric association
Modifications made to rapid acting insulin preparation-->adding more zinc or a bugger which will produce an amorphous precipitate with a longer duration of action (12-16 hr).
In the form of a hexamer, and are associated with zinc. Zinc is responsible for the binding of 6 molecules of insulin to form this hexamer configuration that we see.
Hexameric/Zinc complex is injected subcutaneously, where it breaks up into dimers, loses the zinc, and then can readily pass through membranes. As a result, it gets absorbed in the bloodstream.
NPH (isophane): Contains protamine which binds the hexameric insulin, thus slowing the dissolution of the hexameric form to the dimeric forms.
Decreased hexameric association allows for accelerated absorption.
Sulfonylurea drugs inhibit the ATP sensitive potassium channel causing a slow depolarization to threshold, which then causes the influx of calcium and subsequent release of endogenous insulin.
These drugs also act at the postassium channel, however they bind to a different site than the sulfonylureas.
These drugs are GLP-1 agonists (glucagon like peptide-1), which will stimulate the release of insulin from pancreatic B cells and suppress postprandial glucose secretions. Other effects include the slowing of gastric emptying and increased satiety
Block the metabolism of endogenous GLP-1 and GIP-1 (glucose dependent insulinatropic polypeptide). This results in an increase of insulin synthesis and release and decreased glucagon release. The decrease in glucagon causes a decrease in hepatic glucogneogenesis.
These drugs potentiate the translocation of the glut 4 transporter to the cell membrane to promote glucose entrance.
Reduces intestinal absorption of carbs which slows the rise in blood (glucose) and thereby decreases the insulin demand-->this reduces post prandial (glucose).
Suppress post prandial glucose secretion, slows gastric emptying, and increases satiety just like endogenous amylin.
Subcutaneous
Oral administration
Orally active.
Must be injected
Orally active.
Injection
ALL administered via sub-cutaneous injection.
Once in the blood, it acts like endogenous insulin b/c it is the same thing! It circulates as a free hormone.
Circulates bound to plasma proteins
Unbound to plasma proteins
Used for type I or II diabetics to facilitate insulin effects.
Can be used by themselves, or in combination with Metformin and Rosiglitazone.
Used mostly as adjunctive therapy for Type II diabetes with Metformin when adequate control is not achieved with Metformin alone.
Marketed to be used before each meal in order to lower the incidence of hypoglycemic events in response to drugs.
Target B cells to make more insulin, increase the # of insulin receptors on target tissues, these are very resitant to degradation in the liver, due to the moeieties that they have attached.
Long Acting Insulin Analog: Act to improve postprandial (after a meal) glycemic control. Matched to hepatic gluconeogenesis.
Short-Acting Insulin Analogs are injected immediately prior to a meal for better glycemic control.
Split mix: This is the way that most of the currently used insulin preparations are made. The name split mix refers to the fact that the preparation contains a mix of both short acting and intermediate or long acting insulin. This form requires two injections per day. With this type of administration, the rapid acting portion of the first injection covers you for your breakfast meal while the intermediate/long acting portion of that injection lasts until dinner, when you take your second injection.
Rapid action, short duration. Onset is typically about 15 minutes after the injection, and effects last 5-7 hours.
Delayed onset, prolonged the duration of action.
Duration of aciton is extended due to continued release of insulin that has been bound to circulating albumin.
Delayed Absorption
Half-lives and duration of action vary dependent upon chemical structure.
Short-acting (2.5 hrs)
Short-1/2 life (50 min)
Short 1/2 life (1.5-4.5 hrs.)
These drugs have short half-lifes.
The binding to albumin prolongs the life of the drug as it is protected from filtration in the kidney and circulates in the blood, slowly dissociating into the active form.
Half-life of natural endogenous insulin is 3-5 minutes.
Metabolized by the liver and kidney, as well as taken up by the target cells. All of these mechanisms remove injected insulin from the blood.
Metabolized in liver
N/V and diarrhea and can cause hypoglycemia when used with insulin
Malabsorption, flatulence, and abdominal bloating
Diarrhea, abdominal discomfort, nausea, metallic taste, anorexia. Lactic acidosis is a possible adverse effect with chronic treatment but generally side effects are minimal.
Cannot be given to pregnant women. Hypoglycemia related nausea, vomiting
Same as insulin: mild hypoglycemia, and associated CNS abnormalities
1.CNS: Mental confusion, bizarre behavior, coma 2. Autonomic Nervous System Effects: a.SNS: tachycardia, palpitations, sweating b.PNS: nausea and hunger 3.Anaphylaxis 4.Insulin Resistance
Contraindications: Oral hypoglycemics cannot be used by TypeI diabetics b/c the B cells are not functional and therefore is not a target!
TYPE I DIABETES MELLITUS
TYPE II DIABETES MELLITUS
RAPID
INTERMEDIATE
SLOW
INSULIN PREPARATIONS
INSULIN ANALOGS
ORAL HYPOGLYCEMICS
ORAL ANTI-HYPERGLYCEMIA
SHORT-ACTING INSULIN ANALOGS
INTERMEDIATE-ACTING INSULIN ANALOG
LONG ACTING INSULIN ANALOG
SULFONYLUREAS
MEGLITINIDES
INCRETIN MIMETICS
DPP4-INHIBITORS
BIGUANIDES
THIAZOLIDINEDIONES
ALPHA-GLUCOSIDASE INHIBITORS
AMYLIN MIMETICS