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type I diabetes mellitus
autoimmune destruction of pancreatic beta cells, results in absolute insulin deficiency and hyperglycemia, insulin replacement therapy required
type II diabetes mellitus
primarily insulin resistance leads to hyperglycemia but also reduced insulin secretion; insulin may be required to achieve target blood sugar levels
oral medications and other innjectables used to treat
insulin secretagogoues
sulfonylureas
meglitinides
both stimulate release of insulin from the pancreas
meglitinides are significantly faster and shorter acting
sulfonylureas MOA
stimulates the release of insulin from the pancreas for type II diabetes, duration 12-24 hours
sulfonylureas and meglitinides adverse effects
hypoglycemia, weight gain
sulfonylureas nursing considerations
contraindiacted in pregnancy, caution with renal and hepatic disease, alcohol and beta blocker use
meglitinides MOA
stimulate release of insulin from the pancreas for type II diabetes, peak at one hour, duration four hours
meglitinides nursing considerations
dosing must be followed by a meal and caution with liver dysfunction
incretin mimetics
glucagon-like peptide-1 (GLP-1) receptor agonists
incretin promotors
dipeptidyl peptidase - IV (DPP-4) inhibitors
incretin hormones
two important incretin hormones secreted by the gut in response to eating are
glucogon-like peptide-1 (GLP-1) - stimulates the glucose-dependent release of insulin, inhibits the postprandial release of glucagon, slows gastric emptying, and suppresses appetite
rapidly inactivated by the enzyme dipeptidyl peptidase-IV (DPP-IV)
glucose-dependent insulinotropic polypeptide (GIP) - stimulates the glucose-dependent relese of insulin, promotes beta cell proliferation and is inactivated by DPP-IV
ORAL glucagon-like peptide 1 (GLP-1) receptor agonist MOA
stimulates glucose-dependent release of insulin, inhibits postprandial glucagon release, slows gastric emptying and promotes satiety
ORAL glucagon-like peptide 1 (GLP-1) receptor agonist - therapeutic use
oral adjuvant therapy for type 2 diabetes in patients taking metformin
ORAL glucagon-like peptide 1 (GLP-1) receptor agonist - AE
GI (N/V, abdominal pain), risk of pancreatitis thyroid cancers
dipeptidyl peptidase - IV (DPP-4) inhibitors MOA
enhances the action of incretin hormones by inhibiting dipeptidyl pepsidase and enzyme that inactivated incretin
dipeptidyl peptidase - IV (DPP-4) inhibitors AE
nasal inflammation, upper respiratory infection, risk of pancreatitis, headache
other oral agents that do not cause hypglycemia on their own
Biguanides
sodium-glucose co-transporter 2 inhibitors
thiazolidinediones (glitazones or TSDs)
alpha-glucosidase inhibitors
biguanide - metformin MOA
suppression of hepatic glucose production, enhances glucose uptake and utilization by muscle, decreases glucose absporption in the gut
biguanide - metformin Therapeutic use
type 2 diabetes and PCOS
biguanide - metformin ADVERSE EFFECT
GI disturbances, LACTIC ACIDOSIS
biguanide - metformin nursing considerations
do not use IV dye studies, contraindicated in renal insufficiency, caution in heart failure, avoid alcohol, can cause B-12 and folate deficiencies
sodium glucose Co-transporter 2 (SGLT2) inhibitors MOA
blocks the action of SGLT2. SGLT2 works in the kidney to reabsorb glucose. Blocking SGLT2 results in more glucose being excreted in the urine
sodium glucose Co-transporter 2 (SGLT2) inhibitors - therapeutic use
type 2 diabetes, cardiovascular and renal protective, reduce heart failure risk
sodium glucose Co-transporter 2 (SGLT2) inhibitors - AE
UTI and yeast infections because of more glucose in urine
sodium glucose Co-transporter 2 (SGLT2) inhibitors - nursing considerations
can cause postural hypotension in elderly due to increased urination reducing plasma volume. reduces blood sugar independent of insulin
thiazolidinediones - TZDs MOA
reduces insulin resistance of fat & muscle, may decrease glucose production
thiazolidinediones - TZDs AE
edema, URI, sinusitis, myalgia, HF d/t fluid retention is greatest concern
thiazolidinediones - TZDs nursing consideration
report signs of HF, weight gain, possible hepatotoxicity, monitor ALT levels, increased risk of bone fractures; contrindicated in bladder cancer
alpha-glucosidase inhibitors MOA
inhibit alpha-glucosidase which breaks dwon complex carbohydrates. delayes intestinal absorption of carbohydrates, reducing postprandial hyperglycemia
alpha-glucosidase inhibitors AE
GI disturbances, abdominal pain, diarrhea, liver dysfunction
alpha-glucosidase inhibitors nursing considerations
contradindicated with some GI disease but does not cause hypoglycemia