Diabetes Flashcards
(47 cards)
What receptors are responsible for the release of insulin from beta cells in pancreas?
Beta 2 receptors
MOA of beta cells release of insulin in response to high serum glucose?
Glucose enters the beta cells, causing a rise in ATP, this leads to K channels to close shut, preventing their efflux, the cells depolarize as a result, Ca flows in and insulin vesicles are released
What is released in addition to insulin and why?What is the clinical significance of this?
C peptide, insulin is placed in the vesicles as pro insulin where it cleaved to insulin and C peptide, we can measure c peptide levels to measure the amount of insulin in the blood
Explain MOA of insulin on peripheral cells.
Binds to its receptor on cell surface membrane, leading to activation of tyrosine kinase, this causes the cell to express GLUT4 receptor to allow glucose to enter cells
What other effects does insulin have on metabolism.
- Increases glycogenesis in liver2. Increase fat synthesis and storage in adipose tissues3. Induces protein synthesis
What is the effect of insulin on serum [K] and what is the clinical significance of this?
Drives up K ions into the cells so it can lead to hypokalemia, can be used to treat hyperkalemia when administered together with glucose to prevent hypoglycemia
Name short acting insulins.
Glusin, Aspart and Lispro
What are the properties of short acting insulin?
Rapid onset of action, useful for post prandial glycemic control
Name intermediate acting insulins
Regular insulin and NPH - neutral protamine hagedorn
What are the properties of intermediate acting insulins?
Delayed onset and intermediate duration of action (NPH is more delayed) due to the formation of dimers and hexamers, takes time to breakdown
What do we use for diabetic ketoacidosis? what is an adverse effect of this?
IV insulin, have to watch out for K levels
Name long acting insulin and what are their properties.
Detemir and Glargine, have long durations of action and provide a steady background level of insulin (glargine has no peak)
MOA of sulfonyl ureas
Bind to ATP-dependent K+ channels on beta cells leading to depolarization of beta cells, lead to calcium influx and release of endogenous insulin
Name first generation sulfonyl ureas
tolbutamide, chloropropramide
Name second generation sulfonyl ureas
Glyburide, glipzide and glimeperide
What is the shortest acting sulfonyl ureas and what is a consequence of this?
Glipizide, less risk of development of hypoglycemia
Name meglitinides
repaglinide, nateglinide
MOA of meglitinides
MOA similar to sulfonureas bind the ATP-dependent K+ channels on beta cells leading to depolarization, calcium influx and release of endogenous insulin
Which ones mentioned are sulfa drugs
Meglitinides are not sulfa drugs, sulfonyl ureas are!
What are the adverse effect of meglitinides and sulfanyl ureas
Can cause hypoglycemia and weight gain.Sulfanyl ureas lile chloropropramide can cause disulfram like effect with ingestion of alcohol
Name GLP 1 agonists.
exenatide, liraglutide - tide suffix
Explain MOA of GLP1 agonists
GLP-1 agonists (exenatide, liraglutide) activate the Glucagon Like Peptide Receptor (GLP-1), this leads to increased insulin release and satiety, decreasing glucagon release and gastric emptying
Name DPP4 inhibitors.
“-gliptin” suffix of the DPP-4 inhibitors (stigaliptin, saxagliptin, linagliptin
MOA of DPP4 inhibitors.
Dipeptidyl peptidases inhibit the breakdown of GLP1, DPP-4 inhibitors (gliptins) increase levels of endogenously secreted GLP-1 (increased insulin release and satiety, decreased glucagon release and gastric emptying). All of this helps in decreasing glucose serum levels.
