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57 Cards in this Set

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Rapid acting insulins that do not self-aggregate

Insulin lispro, insulin aspart, and insulin glulisine

Note: Used to control postprandial glucose and used to treat emergency treatment of diabetic ketoacidosis.
Peakless basal acting insulin
Insulin glargine
Alpha cells in the pancreas
Produce glucagon
Beta cells in the pancreas
Produce insulin
Beta cells are found
Islets of Langerhans
Delta cells in the pancreas
Produce Somatostatin
Product of proinsulin cleavage used to assess insulin abuse
C-peptide
Exogenous insulin
Little C-peptide
Endogenous insulin
Normal C-peptide
Very rapid acting insulin, having fastest onset and shortest duration of action
Lispro (Humalog)
Rapid acting, crystalline zinc insulin used to reverse acute hyperglycemia
Regular (Humulin R)

Note: Before the development of rapid-acting insulins, it was the primary form of insulin used for controlling postprandial glucose concentrations, and requires 1 h or more before a meal.
Long acting insulin
Ultralente (humulin U)
Ultra long acting insulin, has over a day duration of action
Insulin glargine

Note: provides a peakless basal insulin level lasting more than 20 h.
Major SE of insulin?

How do you treat?
Hypoglycemia

Sugar or candy. Glucagon as well.
Important in synthesis of glucose to glycogen in the liver
GLUT 2
Important in muscle and adipose tissue for glucose transport across muscles and TG storage by lipoprotein lipase activation
GLUT 4
Examples of alpha-glucosidase inhibitors (AGI)
Acarbose, miglitol
MOA of AGI's
Act on intestine, delay absorption of glucose
SE of AGI's
Flatulence (do not use beano to tx), diarrhea, abdominal cramps
Alpha-glucosidase inhibitor associated with elevation of LFT's
Acarbose
Amino acid derivative
Nateglinide
MOA of nateglinide
Insulin secretagogue
What is the major drug in the class biguanide?
Metformin
MOA of metformin
Decreases hepatic glucose production, slows down intestinal glucose absorption, increase insulin sensitivity, and increases peripheral utilization of glucose.
Most important potential SE of metformin
Lactic acidosis.

Note: in liver disease, alcoholism, lactic acidosis can be further complicated.
What are some drugs that belong to the class meglitinides?
Repaglinide and nateglinide. Suffix: -glinide
MOA of repaglinide
Insulin release from pancreas; faster and shorter acting than sulfonylurea.

They bind to K channel, but a different binding site than sulfonylureas; therefore, they are secretagogues as well.
First generation sulfonylurea
Chlorpropamide, tolbutamide, tolazamide, etc.
Second generation sulfonylurea
Glyburide, glipizide, glimepiride, etc.
MOA of both generations
Insulin release from pancreas by modifying K+ channels
Common SE of sulfonylureas, repaglinide, and nateglinide
Hypoglycemia
Sulfonylurea NOT recommended for elderly because of very long half life
Chlorpropamide
What are some thiazolidinediones?
Pioglitazone, Rosiglitazone. Suffix: -glitazone


Note: Troglitazone (withdrawn/d from market)
Reason troglitazone was withdrawn from market
Hepatic toxicity
MOA of thiazolindinediones
Stimulate PPAR-gamma receptor to regulate CHO and lipid metabolism
SE of Thiazolindinediones
Fluid retention, edema, mild anemia
Hyperglycemic agent that increases cAMP and results in glycogenolysis, gluconeogenesis, reverses hypoglycemia, also used to reverse severe beta-blocker overdose and smooth muscle relaxation
Glucagon
Question: A 13 year old boy with T1DM is brought to the hospital complaining of dizziness. Laboratory findings include severe hyperglycemia, ketoacidosis, and blood pH of 7.15.

1) To achieve rapid control of the severe ketoacidosis, the appropriate antidiabetic agent to use is?

2) The most likely complication of insulin therapy in this PT is?
1) Crystalline zinc insulin (rapid-acting insulin given intravenously)

2) Hypoglycemia
Question: A 24 year old women with T1DM wishes to try tight control of her diabetes to improve her long-term prognosis. What regimen is appropriate?
Morning injections of insulin glargine, supplemented by small amounts of insulin lispro at mealtimes. (glargine controls basal level; lispro is short-acting)
Question: What drug promotes the release of endogenous insulin?
Glipizide. Also, glyburide and glimepiride. All three are sulfonylureas.

Also meglitinides (repaglinide and nateglinide)
Question: An important effect of insulin is?
Increased glucose transport into cells
Question: A 54 year old obese PT with T2DM and a history of alcoholism probably should not receive metformin because it can increase the risk of?
Lactic acidosis.
Question: The PPAR-gamma receptor that is activated by thiazolidinediones increases tissue sensitivity to insulin by?
Regulating transcription of genes involved in glucose utilization--metabolism of carbohydrates and lipids.
Question: What drug is taken during the first meal for the purpose of delaying the absorption of dietary carbohydrates?
Acarbose or miglitol, which inhibits alpha-glucosidase.

Note: inhibition of alpha-glucosidase delays uptake of carbohydrates.
Question: What drug is MOST likely to cause hypoglycemia when used as monotherapy in the treatment of T2DM?
Insulin secretagogues (glyburide, glipizide, glimepiride, tolbutamide, chlorpropamide, repaglinide, and nateglinide).

Note: biguanides, thiazolidinediones, and alpha-glucosidase inhibitors are unlikely to cause hypoglycemia when used alone.
Question: What type of PT is MOST likely to be treated with IV of glucagon?
A 62 year old man with severe bradycardia and hypotension resulting from ingestion of an overdose of atenolol.

Note: Atenolol is a beta blocker--could be the most effective for stimulating the depressed heart because it increases cardiac cAMP without requiring access to beta receptors.
What is alpha glucosidase?

What drug can inhibit it for T2DM?

What is the reason for this?
An enzyme in the GI tract that converts complex starches and oligosaccharides to monosaccharides.

Acarbose and miglitol

By inhibiting this enzyme, absorption of glucose from the GI is slowed down.
What is an intermediate acting insulin?
NPH insulin.

Is often combined with regular and rapid-acting insulins.
What are the four noninsulin drugs used to treat T2DM?
Secretagogues (sulfonylureas), biguanide (metformin), thiazolidinediones (rosiglitazone), and alpha0glucosidase inhibitors (acarbose, miglitol)
What is the MOA of secretagogues?
Promotes closure of K channels in beta-cells which result in depolarization of the cell that triggers insulin release.
SE of secretagogues?
Hypoglycemia and weight gain.
Why is metformin the DOC for T2DM?
Unlike insulin, secretagogues, or thiazolidineiones, it does not increase weight gain. It also does NOT cause hypoglycemia.
What is the SE of alpha-glucosidase inhibitors?
Acarbose and miglitol cause flatulence and diarrhea.

Note: flatulence from fermentation of unabsorbed carbohydrates by flora.
What is pramlintide, and its SE?
Injectable synthetic analog of amylin, which is produced by beta-cells.

Pramlintide suppresses glucagon release, slows gastric emptying, and works in the CNS to reduce appetite.

Hypoglycemia and GI disturbances.
What is glucagon-like peptide-1 (GLP-1)?

What is an analog that can treat T2DM and its SE?
It is released from endocrine cells in the epi of the bowel in response to food. It augments glucose-stimulated insulin release. It produces a feeling of satiety.

Exenatide.

SE: hypoglycemia and pancreatitis.
What the MOA of sitagliptin and its SE?
An inhibitor of dipeptidyl peptidase-4 (DPP-4), an enzyme that degrades GLP-1 and other incretins.

Upper respiratory tract infection.
Metformin MOA?
mechanism is unknown
possibly decrease gluconeogenesis
increase glycolysis
decrease serum glucose levels
overall acts as an insulin senstitizer