Endo(Ost529)-Dr.lookingland-Scribe 2

Front 1

STRUCTURE

Back 1

MECHANISM

Front 2

DRUG ADMIN.

Back 2

PLASMA CIRCULATION

Front 3

USE

Back 3

ONSET/DURATION

Front 4

HALF-LIFE

Back 4

ELIMINATION

Front 5

ADVERSE RXNS

Back 5

OTHER

Front 6

Crystalline, Semilente

Back 6

NPH (isophane), Lente

Front 7

Ultralente, Protamine Zinc

Back 7

Insulin Lispro, Insulin Aspart, Insulin Glulisine

Front 8

Insulin Detemir

Back 8

Insulin Glargine

Front 9

First Generation: Tolbutamine, Tolazamide Second Generation: Glyburide, Glipizide

Back 9

Repaglinide

Front 10

Exenatide

Back 10

Citagliptin & Vildagliptin ("gliptins")

Front 11

Metformin

Back 11

Rosiglitazone, Pioglitazone

Front 12

Acarbose

Back 12

Pramlintide (symlin)

Front 13

Synthetic analog of human amylin

Back 13

Blocks hepatic gluconeogenesis. Remember that in the absence of insulin, the liver will respond by making more glucose.

Front 14

Derived from the sulfonylurea containing compount, Butamide. These drugs have substitutions on the R1 and R2 chains.

Back 14

Glargine substitution at A-21 and B-30, which results in delayed absorption by causing precipitation of the molecule.

Front 15

Engineered to add a fatty acyl chain on to the lysine residue of the B-chain, so as to increase binding to albumin.

Back 15

Modified Insulin structure: Decreases hexameric association

Front 16

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).

Back 16

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.

Front 17

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.

Back 17

NPH (isophane): Contains protamine which binds the hexameric insulin, thus slowing the dissolution of the hexameric form to the dimeric forms.

Front 18

Decreased hexameric association allows for accelerated absorption.

Back 18

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.

Front 19

These drugs also act at the postassium channel, however they bind to a different site than the sulfonylureas.

Back 19

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

Front 20

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.

Back 20

These drugs potentiate the translocation of the glut 4 transporter to the cell membrane to promote glucose entrance.

Front 21

Reduces intestinal absorption of carbs which slows the rise in blood (glucose) and thereby decreases the insulin demand-->this reduces post prandial (glucose).

Back 21

Suppress post prandial glucose secretion, slows gastric emptying, and increases satiety just like endogenous amylin.

Front 22

Subcutaneous

Back 22

Oral administration

Front 23

Orally active.

Back 23

Must be injected

Front 24

Orally active.

Back 24

Injection

Front 25

ALL administered via sub-cutaneous injection.

Back 25

Once in the blood, it acts like endogenous insulin b/c it is the same thing! It circulates as a free hormone.

Front 26

Circulates bound to plasma proteins

Back 26

Unbound to plasma proteins

Front 27

Used for type I or II diabetics to facilitate insulin effects.

Back 27

Can be used by themselves, or in combination with Metformin and Rosiglitazone.

Front 28

Used mostly as adjunctive therapy for Type II diabetes with Metformin when adequate control is not achieved with Metformin alone.

Back 28

Marketed to be used before each meal in order to lower the incidence of hypoglycemic events in response to drugs.

Front 29

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.

Back 29

Long Acting Insulin Analog: Act to improve postprandial (after a meal) glycemic control. Matched to hepatic gluconeogenesis.

Front 30

Short-Acting Insulin Analogs are injected immediately prior to a meal for better glycemic control.

Back 30

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.

Front 31

Rapid action, short duration. Onset is typically about 15 minutes after the injection, and effects last 5-7 hours.

Back 31

Delayed onset, prolonged the duration of action.

Front 32

Duration of aciton is extended due to continued release of insulin that has been bound to circulating albumin.

Back 32

Delayed Absorption

Front 33

Half-lives and duration of action vary dependent upon chemical structure.

Back 33

Short-acting (2.5 hrs)

Front 34

Short-1/2 life (50 min)

Back 34

Short 1/2 life (1.5-4.5 hrs.)

Front 35

These drugs have short half-lifes.

Back 35

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.

Front 36

Half-life of natural endogenous insulin is 3-5 minutes.

Back 36

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.

Front 37

Metabolized in liver

Back 37

N/V and diarrhea and can cause hypoglycemia when used with insulin

Front 38

Malabsorption, flatulence, and abdominal bloating

Back 38

Diarrhea, abdominal discomfort, nausea, metallic taste, anorexia. Lactic acidosis is a possible adverse effect with chronic treatment but generally side effects are minimal.

Front 39

Cannot be given to pregnant women. Hypoglycemia related nausea, vomiting

Back 39

Same as insulin: mild hypoglycemia, and associated CNS abnormalities

Front 40

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

Back 40

Contraindications: Oral hypoglycemics cannot be used by TypeI diabetics b/c the B cells are not functional and therefore is not a target!

Front 41

TYPE I DIABETES MELLITUS

Back 41

TYPE II DIABETES MELLITUS

Front 42

RAPID

Back 42

INTERMEDIATE

Front 43

SLOW

Back 43

INSULIN PREPARATIONS

Front 44

INSULIN ANALOGS

Back 44

ORAL HYPOGLYCEMICS

Front 45

ORAL ANTI-HYPERGLYCEMIA

Back 45

SHORT-ACTING INSULIN ANALOGS

Front 46

INTERMEDIATE-ACTING INSULIN ANALOG

Back 46

LONG ACTING INSULIN ANALOG

Front 47

SULFONYLUREAS

Back 47

MEGLITINIDES

Front 48

INCRETIN MIMETICS

Back 48

DPP4-INHIBITORS

Front 49

BIGUANIDES

Back 49

THIAZOLIDINEDIONES

Front 50

ALPHA-GLUCOSIDASE INHIBITORS

Back 50

AMYLIN MIMETICS