Diabetes Flashcards
type 1 diabetes
autoimmune destruction of insulin producing pancreatic beta cells. insulin therapy required
incretin hormones
synthesized by L cells, primarily in ileum and colon. produced in response to incoming nutrients. stimulate insulin secretion.
glucagon-like hormone 1 (GLP-1) actions
enhances glucose dependent insulin secretion. slows gastric emptying. suppresses glucagon secretion. promotes satiety. receptors in the islet cells, CNS, elsewhere. metabolized rapidly by DPP-4 (2-3 minute half life)
metformin
activates AMP-kinase and inhibits mitochondrial isoform of glycerophosphate dehydrogenase. Reduces hepatic glucose production. biguanides.
glibenclamide, glipizide, gliclazide, glimepiride
closes Katp channels on B cell plasma membranes. increases insulin secretion. sulfonylureas.
repaglinide, nateglinide
closes Katp channels on B cell plasma membranes. increases insulin secretion. meglitinides.
pioglitazone, rosiglitazone
activates the nuclear transcription factor PPAR. increases peripheral insulin sensitivity. thiazolidinediones
acarbose, miglitol
inhibits intestinal alpha glucosidase. intestinal carbohydrate and consequently glucose absorption slowed. alpha glucosidase inhibitors
exenatide, liraglutide, albiglutide, dulaglutide
activates GLP-1 receptors. increases insulin secretion and satiety. decreases glucagon secretion. slows gastric emptying. GLP-1 receptor agonists
sitagliptin, alogliptin, saxagliptin, linagliptin
inhibits DPP-4 activity. increases active GLP-1 and GIP concentration, increases insulin secretion, decreases glucagon secretion. DPP-4 inhibitors
Canagliflozin, dapagliflozin, empagliflozin
reduces glucose resorption in the kidney; alpha cell agonist. urinary glucose excretion increases, glucagon secretion increases. SGLT2 inhibition.
colesevelam
binds bile acids/cholesterol. decreases hepatic glucose production. bile acid sequestrant.
hypoglycemia
most common with treatment with sulfonylurea drugs and insulin. more common in type 1 diabetes.
glucagon emergency kit
given only if unconscious or unable to swallow. patient never gives to self. turn on side. type 1 should always have prescription for this. type 2 with previous severe low blood sugar should have this.
amylin
released with insulin in response to eating. from beta cells. deficient in type 1, variable in type 2. slows gastric emptying, suppresses postprandial glucagon secretion, may reduce appetite
pramlintide
amylin analog. inject before each meal. reduces post-prandial glucose levels. significant risk of hypoglycemia.
indications for insulin therapy in type 2 diabetes
significant hyperglycemia at presentation. hyperglycemia on max doses of oral agents. surgery. pregnancy. decompensation. serious renal or hepatic disease.
rapid acting insulin analogs
lispro insulin, aspart insulin, glulisine insuin
intermediate acting insulin analogs
detemir insulin. neutral protamine lispro and neutral protamine aspart
insulin detemir
dose dependent duration of action. delayed release from subQ injection site due to self-association and binding to albumin. should not be diulted or mixed with any other insulin preparations
long acting insulin analogs
glargine insulin
ultra long acting basal insulin analog
degludec insulin
advantages/disadvantages of premixed insulins
A: Convenient, potentially longer shelf life, fewer dosing errors, simple.
D: loss of flexibility in matching to carb intake or physical activity. harder to treat short term glucose levels. lack of clinical outcome data. hypoglycemia risk.
rarely used in type 1 diabetes
inhaled insulin
oral inhalation, rapid acting. doses 4-8 unit increments. requires pulmonary function tests. contraindicated with chronic lung disease (asthma or COPD). may cause decreased FEV. long term risks unknown, possible increase of lung cancer