Anti Diabetic Flashcards
What are the Insulin Regulators?
Positive: Glucose, Amino Acids, Incretins, Epi/Beta stimulation, Vagus stimulation
Neg:
NE/alpha stimulation,
Amylin
Glucose enters beta cell and increase ATP, this closes the ATP sensitive K channel, causes depolarization, Ca entering and Insulin released.
It binds receptors and increases GLUT4 on membrane to uptake glucose
What are the organ targets of insulin and how insulin regulates glucose homeostasis in these organs.
In the Muscle and Adipose Tissue, Insuilin triggers the insertion of GLUT4 receptors into the membrane of the cells that facilitates the uptake of glucose from the extracellular environment
Insulin also works on the liver to increase glycogen formation, Protein in muscles, and triglycerides in adipose tissue
Describe Diabetes Mellitus
type 1: insulin dependent, juvenile onset, mostly autoimmune destruction of beta cells
Type 2: non insulin dependent, adult onset, insensitivity of insulin receptors, could be insulin secretion defect, obesity/nutrition, physical activity
Signs: freq urination, excessive thirst, unexplained wt loss, extreme hunger, sudden vision changes, tingling, fatigue, dry skin, slow to heal, more infections
Dx: Random blood glucose: 200+mg/dl,
Fasting blood glu: 126+mg/dl
2 hr blood glu: 200+ during oral glucose tolerance test
Hbg A1C: above 6.5%
What pharmacological features of insulin dictate teh peak periods of insulin action?
we can manipulate the complex formation of the insulins (stickiness) to affect absorption. This will in turn effect the peak. Less complex formation = rapid onset, Regular insulin forms complexes and therefore is slower onset.
Long Acting (Glargine, Detemir)`
MOA: AA substitution that forms precipitate in neutral pH of body
AE: Hypoglycemia, Hypersensitivity, Resistance, Lipohypertrophy at injection site, Lipoatrophy
Short Acting (Regular Insulin)
MOA
AE
MOA: Identicle to human insulin
AE: Hypoglycemia, Hypersensitivity, Resistance, Lipohypertrophy at injection site, Lipoatrophy
Glimepiride, Glipizide, Glyburide (Sulfonylureas)
MOA
AE
Type 2 DM
MOA: Increase Insulin Release from Beta cells
AE: Wt. gain, GI, Hypoglycemia
Repaglinide, Nateglinide (Meglitinides)
Type 2 DM
MOA: Increase Insuline release from beta cells
AE: Wt Gain, GI, Hypoglycemia
Metformin (Biguanide)
MOA
AE:
MOA: decrease hepatic Glucose output
AE: Diarrhea, N/V, Vit B12 deficiency
Always start Type 2 Diabetics on this plus exercise then increase meds based on response.
Pioglitazone, Rosigliazone (Thiazolidinediones)
Type 2 DM
MOA: Activation of PPARgamma
AE: Abdominal Pain, Hypoglycemia, Cardiovascular (MI)
Pramlinitide
Type 1 and 2 MOA: Synthetic Amylin - Inhibits glucagon release - Inhibits gastric emptying - anorectic effect AE: Nausea, Hypoglycemia
Acarbose, Miglitol (Glucosidase Inhibitors)
Type 2 DM
MOA: Impair carbohydrate digestion and subsequent absorption
AE: abdominal pain, Diarrhea, FLATULENCE
Contraindicated in pnts with GI diseases
Pioglitazone, Rosigliazone (Thiazolidinediones)
Type 2 DM
MOA: Activation of PPARgamma To increase GLUT4 in membrane
AE: Abdominal Pain, Hypoglycemia, CARDIOVASCULAR (MI)
Pramlinitide (Amylinomimetic)
Type 1 and 2 MOA: Synthetic Amylin - Inhibits glucagon release - Inhibits gastric emptying - anorectic effect AE: NAUSEA, HYPOglycemia
Exenatide (Incretins)
Type 2 DM MOA: Synthetic incretin - Potentiates insulin secret - Inhib glucagon release - Inhib gastric emptying - Anorectic effect AE: NAUSEA, HYPOGLYCEMIA
