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65 Cards in this Set

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approaches to tx of DMII
-lifestyle changes
-stimulate insulin secretion(secretagogue)
-stimulate insulin secretion(sensitizer)
-decrease glucose absorption(alpha-glucosidase inhibitors)
secretagogues (stimulate insulin secretion)
sulfonylureas, repaglinide
sensitizers (stimulate insulin action)
metformin, thiazolidinediones
relation of weight control with management of diabetes
-obesity is a major cause of insulin resistance; decreased amount of adipose tissue helps to restore insulin sensitivity
contraindications for the use of sulfonylureas
-DM type 1
-preganant or lactating
-severe, acute, concurrent illness, surgery, or other stress during which glycemic control fluctuates
MOA of sulfonylureas
-pancreatic effects:: secretagogue
-stimulate insulin release and increase beta cell sensitivity to glucose
-bind to specific beta cellreceptor(SUR) linked to the potassium ion channel; binding of the sulfonylurea closes the potassium channel preventing K+ efflux
-makes membrane potential more positive resulting in depolarization to open Ca2+ channels stimulating insulin release
-completely ineffective in pts with no pancreatic fx
second generation sulfonylureas
glyburide, glipizide, and glimepiride
comparison of first generation and second generation sulfonylureas
-2nd generation have greater potency, shorter halflife, and longer duration of action
characteristics of glyburide compared with other sulfonylureas
-12-24 hr duration of action(dosed once daily)
-most effective in pts with fasting hyperglycemia
-less effective in pts with postprandial hyperglycemia
-high incidence of severe prolonged hypoglycemia
characteristics of glimepiride with other sulfonylureas
-more potent than glyburide, but actsmore like glipizide
-more effective for postprandial hyperglycemia, with less incidence of hypoglycemia
ADR of sulfonylureas
-most common and severe is hypoglycemia(esp with glyburide)
-2nd most common ADR is weight gain
Repaglinide MOA
-secretagogue
-binds to beta cell membranes and closes ATP-dependent K+ channels; depolarizes cell to open Ca2+ channels; induces insulin secretion
-insulin secretion is glucose-dependent and diminishes at low glucose concentrations
indications of Repaglinide in DM type 2
- adjunct to diet and exercise in pts whose hyperglycemia cannot be controlled satisfactorily by diet and exercise alone
contraindications of Repaglinide
DM type 1 or DKA
ADR of Repaglinide
-hypoglycemia
-weight gain
dosing of Repaglinide
-15-30min before meals 2-4x daily based on blood glucose response
-taken before meals to stimulate insulin release and reduce postprandial hyperglycemia
-must eat within 30 min; hypoglycemia is a risk of meal is delayed or inadequate carbs are eaten
Metformin MOA
-insulin sensitizer:
-increased peripheral glucose utilization; direct stimulation of tissue glycolysis, with increased glucose uptake from blood into tissue
-decreases hepatic glucose production: inhibition of gluconeogenesis
-decreases GI glucose absorption; achieves high concentration of GI epithelium after po dosing, with increased glucose conversion to lactate in enterocytes
Actions of Metformin
-lowers both preprandial and postprandial blood glucose
-euglycemic drug(no reports of hypoglycemia or weight gain)
-insulin sparing::insulin secretion remains unchanged while fasting and plasma insulin response may actually decrease
-stabilization or decrease in body weight
Metformin is the DOC for ?
obese, dyslipidemic type 2 diabetics
indications for metformin
-should be used in all type 2 pts since it is the only oral antihyperglycemic drug that may reduce the risk of total mortality and CV death
contraindications of metformin
-renal dysfunction
-pts prone to metabolic acidosis or hypoxic states
-temporarily withhold in pts undergoing radiologic studies with iodinated contrast agents
Boxed warning for metformin
very rarely associated with lactic acidosis
-predisposing risk factors include decreased renal function and advanced age
Due to the DI between iodinated parenteral contrast agents and metformin you should?
-withhold metformin 48hrs prior and 48hrs subsequent to the procedure and restart only after renal function is normal
Thiazolidiones (TZD, "glitazones")
rosiglitazone and pioglitazone
pharmacological actions of TZD agents
"insulin sensitizers"-increase insulin sensitivity through activation of PPARgamma
-lowers blood glucose by improving cell response to insulin without increasing pancreatic insulin secretion
-decreases insulin resistance; stimulates glucose uptake into skeletal muscle and fat
-decreases hepatic gluconeogenesis
net effects of PPARgammma agonists (TZD agents)
- lowers blood glucose (fasting and postprandial), without causing hypoglycemia when used alone
-enhance insulin sensitivity in metabolic tissues
PPARgamma stands for?
peroxisome proliferation-activated receptor gamma; nuclear transcription factor
rosiglitazone in tx of DM2
-as adjunct to diet and exercise when used as monotherapy
-used in combo with sulfonylurea or metformin when diet, exercise, or rosiglitazone, or the single agent alone insuficient to control blood glucose
risk of hepatotoxicity with rosiglitazone
-do not initiate therapy in hepatocellular dz
-some cases of hepatic failure have been reported from Phase IV postmarketing surveillance
rosiglitazone warning
increased risk of heart attacks and possibly death
-may be associated with myocardial ischemic events such as angina or MI
pioglitazone indication for DM2
-use alone as monotherapy or
-use in combo with sulfonylureas, metformin, or insulin when diet plus single agent is inadequate for glycemic control
ADR of TZDs
-weight gain/contribution of fluid retention
-increased CV risk:fluid retentionand edema-->HF
-increased CV risk::MI
-increased risk of fractures
TZD CV risks-HF
-fluid retention and edema increase risk for HF
-both meds double the risk of HF or worsen existing HF
-TZD-induced cardiomyopathy probable
-TZDs are contraindicated in stage III and IV HF
TZD CV risks-MI
-increased risk limited to rosiglitazone
-rosiglitazone no longer recommended for use in DM2
TZD risks of fractures
-1 of 2 studies showed increased fx in men, but both showed increased fx in women
-mechanism: activation of nuclear hormone(PPARgamma)may affect differentiation of stem cells to adipocytes and osteoblasts in bone marrow
-increased adipocytes and decreased osteoblasts--decreasd bone formation/mass
Acarbose pharmacologic effects
-complex oligosaccharide that reduces the increase in peak postprandial blood glucose
-most useful in pts with exagerrated postprndial increase in blood glucose
-slight improvement of FBG with absence of weight gain
Acarbose MOA
-competitive reversible inhibitor of intestinal brush border alpha-glucosidases, pancreatic alpha-amylase, and sucrase which are responsible for digestion of complex carbohydrates
-results in smaller rise in blood glucose and insulin following meals
Why is acarbose the DOC for elderly DM2 pts with postprandial hyperglycemia?
-does not cause hypoglycemia in the fasting or postprandial state
ADR of acarbose
abd pain, diarrhea, flatulence
--60%d/c rate in trials
Step 1 of ADA guidelines for tx of DM2
-lifestyle changes: diet, exercise
-metformin: Tier 1 drug (only drug that has shown mortality benefit)
Step 2 of the ADA guidelines for tx of DM2
-add a sulfonylurea or basal insulin:other Tier 1 drugs
What are now considered the core therapies for DM2?
-metformin, sulfonylureas, and insulin
-they lower A1C to a greater extent, cost less, and have longer safety hx
Step 3 of the ADA guidelines for tx of DM2
-intensify insulin therapy
Analternative therapy for tx of DM2
-Step 1 plus a Tier 2 drug (pioglitazone or exenatide)
insulin therapy in tx of DM2 is most commonly started with?
-basal insulin added to oral therapy
insulin glargine was originally approved for use at bedtime, but is now approved for?
use any time of day as long as same time everyday is used
if A1C goal is not met with insulin glargine in tx of DM2, then?
add a rapid-acting insulin analog just before meals PRN
If hyperglycemia continues (A1C>7) in DM2 with use of basal and rapid acting insulin, then
-d/c basal insulin and use a premixed insulin containing either a rapid or short-acting insulin
-twice daily admin gives better BG control and lower A1C than daily regimen
physiologic actions of endogenous incretins and exogenous GLP1
-normalizes fasting and postprandial glucose by enhancing glucose-mediated insulin secretion; very little effect in normoglycemicso not much tendency to cause hypoglycemia
-suppress glucagon secretion in glucose-dependent manner; no suppression during hypoglycemia
-slows gastric emptying and delays nutrient absorption
-reduces appetite and food intake
Incretin enhancers
exenatide (Byetta) and sitagliptin (Januvia)
exenatide (Byetta) interacts with human GLP1 receptors to cause WHAT ACTIONS?
-restores 1st phase fast insulin response
-increases 2nd phase slow insulin response
-lowers serum glucagon during hyperglycemia resulting in decreased hepatic glucose output
-slows gastric emptying and reduces rate of glucose absorption
-reduces food intake
indications for use of exenatide (Byetta)
-adjunct therapy to improve glycemic control in DM2 in pts who are taking metformin, a sulfonylurea, or a combo of the two, but have not yet achieved glycemic control
-tx of DM2 in adults as monotherapy along with diet and exercise
dosing of exenatide (Byetta)
-initiate at any time within 60 min period before the am and pm meals; do not admin after meals
-SC injections
precaution/ADR for exenatide (Byetta)
-not for use in DM1, pts using insulin, pts with DKA,orin pts with severe renal dysfunction or ESRD
sitagliptin (Januvia) indications
-DM2 as monotherapy or in combo with metformin or a TZD
labeling on sitaglipitin (Januvia) updated to warn of?
-anaphylaxis, angioedema, andexfoliative skin conditions; frequency unknown and causal relationship uncertain
sitagliptin/metformin (Janumet)
combo drug with the advantage of lack of weight gain, edema, or hypoglycemia
Amylinomimetics MOA
-mimic effects of endogenous hormone amylin which is secreted by beta cellswith insulin postprandially
effects of amylinomimetics
-reduces postprandial glucose levels
-slows/delays gastric emptying
-induces satiety and regulates food intake
-suppresses postprandial glucagon secretion to decrease hepatic glucose production
Pramlintide
amylinomimetic agent
-slows gastric emptying, decreasespostprandial elevation in BG, decreases glucagon secretion postprandial, and induces satiety leading to decreased appetite and caloric intake/weight loss
indications for use of Pramlintide
DM1 and DM2
-as adjunct tx in pts who use mealtime insulin therapy
dosing for Pramlintide
-when initiating therapy, initial insulin dose reduction required to reduce risk of insulin-induced hpoglycemia
-reduce all insulin by 50%
-a 0.3 mL U-100 insulin syrince is used
-increase dosage to next increment when no significant nausea has occured
-if nausea persists, decrease dose and if still presists d/c
-admin SC immediately prior to meals
reasons to d/c Pramlintide therapy?
-recurrent unexplained hypoglycemia requiring medical assistance
-persistent clinically significant nausea
-pt noncompliance
what types of pts should not be considered for Pramlintide therapy?
-recurrent or severehypoglycemia requiring medical assistance during past 6mo or hypoglycemic unawareness
-confirmed gastroparesis or tequire GI motility stimulating agents
-pediatric pts
Colesevelam (Welchol)
combo agent of antidiabetic and antihyperlipidemic meds
-FDA approved to decrease both A1C and LDL
used as adjunct to other therapy