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107 Cards in this Set
- Front
- Back
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What is Lispro?
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Ultra short acting insulin used in treatment of Type 1 diabetes
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What is aspart?
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Ultra short acting insulin used in treatment of Type 1 diabetes
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What is regular insulin?
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short acting insulin used in the treatment of Type 1 diabetes
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What is NPH insulin?
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intermediate acting insulin used in the treatment of Type 1 diabetes
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What is ultralente?
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long acting insulin used in the treatment of type 1 diabetes
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What is glargine?
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long acting insulin used in the treatment of type 1 diabetes
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What is novolin?
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mixture of 70% NPH insulin and 30% regular insulin
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What is tolbutamide?
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1st generation sulfonylurea secretagogue used in the treatment of type 2 diabetes
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What is chlorpropamide?
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1st generation sulfonylurea secretagogue used in the treatment of type 2 diabetes
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What is tolazamide?
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1st generation sulfonylurea secretagogue used in the treatment of type 2 diabetes
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What is glyburide?
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2nd generation sulfonylurea secretagogue used in the treatment of type 2 diabetes
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What is glipizide?
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2nd generation sulfonylurea secretagogue used in the treatment of type 2 diabetes
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What is glimepiride?
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2nd generation sulfonylurea secretagogue used in the treatment of type 2 diabetes
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What is repaglinide?
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non-sulfonylurea segretagogue used in the treatment of type 2 diabetes
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What is netaglinide?
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non-sulfonylurea segretagogue used in the treatment of type 2 diabetes
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What is metformin?
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biguanide insulin sensitizer used in the treatment of type 2 diabetes
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What is pioglitazone?
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thiazolidinedione insulin sensitizer used in the treatment of type 2 diabetes
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What is rosiglitazone?
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thiazolidinedione insulin sensitizer used in the treatment of type 2 diabetes
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What is sitagliptin?
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dipeptidyl-peptidase-4 inhibitor used in the treatment of type 2 diabetes
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What is exenatide?
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a type 2 diabetes drug that is similar to GLP-1 that decreases fasting and postpradial glucose levels and HbA1c levels
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What is avandamet?
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rosiglitazone + metformin
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What is ACTOplus met?
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pioglitazone + metformin
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What is precose (Acarbose)?
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an alpha-glucosidase inhibitor
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What is glyset (miglitol)?
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an alpha-glucosidase inhibitor
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What is the most common initial combination therapy for type 2 diabetes?
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sulfonylurea segretagogue and metformin
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What is the overall funciton of insulin?
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promotes growth and storage of energy, stops depletion of energy stores; stimulated by glucose
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What is the function of insulin in liver tissue?
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reversal of catabolic activity, inhibits glycogenolysis, conversion of FAs to amino acids and keto acids, inhibits the conversion of amino acids to glucose
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What is the function of insulin in muscle tissue?
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increases protein syntehsis by increasing aa transport and rRNA protein synthesis, increases glycogen stores by increasing glucose transport and glycogen synthesis and inhibiting phosphorylase
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What is the function of insulin in adipose tissue?
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incrases triglyceride storage by inducing lipoprotein lipase to hydrolyze triglycerides and increases glucose transport for glycerol phosphate (esterification of FAs)
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What is the structure of the insulin receptor?
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2 alpha subunits that bind insulin and 2 beta subunits that are transmembrane tyrosine kinases
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Which glucose transporter is inserted into the membrane of muscle and adipose in response to insulin?
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GLUT4
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What do the a cells of the islet of Langerhans produce?
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glucagon and proglucagon
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What do the b cells of the islet of Langerhans produce?
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insulin, C-peptide, islet amyloid polypeptide (makes up most of the islet)
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What do the d cells of the islet of Langerhans produce?
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somatostatin
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What do the f cells of the islet of Langerhans produce?
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pancreatic polypeptide
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What is secreted with insulin in equal amounts?
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C-Peptide
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What is Type 1 Diabetes?
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insulin dependent diabetes due to pancreatic beta cell destruction
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What is Type 2 Diabetes?
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non-insulin dependent diabetes due to insulin resistance with relative insulin deficiency due to predominately secretory defect with insulin resistance
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What is Type 3 Diabetes?
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diabetes linked to pancreatic disease, hormonal changes, drug side effects or genetic defects
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What is Type 4 Diabetes?
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gestational diabetes
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What is the therapeutic goal of type 1 diabetes treatment?
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insulin replacement
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How long until lispro and aspart are efficacious after injection?
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10 minutes
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What are lispro and aspart used for?
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used immediately before meals to provide insulin for the meal
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Why are lispro and aspart ultra short acting?
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they are recombinant forms of insulin with low propensity to form hexamers due to point mutations on the C terminus of the B chain
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When is regular human insulin efficacious?
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30 minutes after injection
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What is a problem with regular human insulin?
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patient must eat within 30 minutes or there is a risk of severe hypoglycemia
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What structural changes to NPH insulin delay its onset?
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it is combined with protamine so that neither is present in an uncomplexed form
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What allows ultralente insulin to be long lastin?
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it is a zinc insulin and thus is poorly soluable
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How is ultralente insulin administered?
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by injection - it is slowly absorbed by the body
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What accounts for the long action of glargine?
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it is bioengineered to be soluable at pH of 4 and insoluable at pH of 7.4 = when injected it forms microprecipitates delaying its absorption and prolonging its duration
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What are the 3 insulin delivery systems?
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protable pen injectors, continuous pumps, inhaled insulin
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What are the benefits of insulin therapy in type 1 diabetes?
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decreased glycated hemoglobin, reduces diabetic retinopathy, nephropathy and neurpathy
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What are the complications of insulin therapy?
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hypoglycemia, lipodystrophy at the injection site, weight gain and immunpathology (to the insulin)
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What are the therapeutic goals of type 2 diabetes therapy?
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insulin release, increased sensitization to insulin, decreased blood glucose
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What is the mechanism of action of sulfonylurea secretagogues?
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they release insulin by promoting closure of potassium channels in beta cel membranes
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What are the adverse effects of secretagogues?
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hypoglycemia (especially elderly with impaired renal and hepatic function) and weight gain
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In addition to promoting closure of potassium channels what other action do sulfonylurea secretagogues do to release insulin?
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additional sulfonylurea binding proteins are localized to the intracelllular membrane which facilitate exocytosis of insulin granules
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What occurs with chronic use of sulfonylurea secretagogues?
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chronic use decreases serum glucagon levels - thought to contribute to hypoglycemia
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What is the duration of tobutamide?
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rapid onset, half life 4-5 hours
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Where is tolbutamide eliminated?
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in the liver - not for patients with hepatic impairment
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What is the duration of chlorpropamide?
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half life 31 hours
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Where is chlorpropamide eliminated?
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metabolized by the liver mostly; 20-30% excreted unchanged by the kidneys; not for patients with renal or hepatic impairment
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What is the duration of tolazamide?
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short duration; half life 7 hours; slowly absorbed!
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Which patients should not receive glyburide?
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contraindicated for paitents with liver and kidney problems
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What is the half life of glipizide?
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half life 2-4 hours = less propensity for hypoglycemia!
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How is glipizide administered?
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taken orally 30 minutes before breakfast
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Who should not receive glipizide?
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patients with liver, kidney, heart or thyroid problems or a severe infection
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What drugs interact with glipizide?
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antibiotics, anticoagulants, dexamethasone, diuretics, estrogens, isoniazid, MAO inhibitors, medications for HTN or heart disease, niacin, phenytoin, prednisone, probenecid and vitamins
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What is the half life of glimepiride?
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half life is 5 hours
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How often is glimpiride administered?
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once a day
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Where is glimpiride administered
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in the liver
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What is the action of repaglinide and nateglinide?
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increase insulin secretion by decreasing potassium influx (like sulfonylureas)
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What effect do repaglinide and nateglinide have on the exocytosis of insulin?
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None, unlike sulfonylureas
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Where are repaglinide and netaglinide eliminated?
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by CYP3A4
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Is hypoglycemia more common or less commonly seen with repaglinide and netaglinide compared to sulfonylureas?
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less frequent
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What is the action of metformin?
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decreases blood glucose levels independent of funcitoning beta cells, increases pheripheral glucose utilization somewhat
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When is metformin used?
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in patients with refractory obesity whose hyperglycemia is due to ineffective insulin action or with sulfonylureas when they are not adequate alone
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Does metformin cause hypoglycemia?
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there is little incidence of hypoglycemia = 'euglycemic'
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What are the adverse effects of metformin?
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anorexia, nausea, vomiting, abdominal discomfort, diarrhea, metallic taste, rarely lactic acidosis
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What are the contraindications of metformin?
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contraindicated in patients with renal disease, alcoholism, hepatic disease, heart disease and conditions predisposing to tissue anoxia
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What are the interactions with metformin?
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furosemide, nifedipine, cimetidine, amiloride, morphine, procainamide, quinidine, trimethoprim, vancomycin
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What is the action of pioglitazone and rosiglitazone?
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enhances insulin target tissue senstivity by enhancing PPRPgamma which regulates genes involved in glucose and lipid metabolism
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Do pioglitazone and resiglitazone cause hypoglycemia?
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no, they incrase glucose uptake into muscles and adipose without causing hypoglycemia "euglycemic"
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What are the effects of pioglitazone and resiglitazone on fat?
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they cause redistribution of body fat, increased peripheral small adipocytes from visceral fat mass
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Where are pioglitazone and resiglitazone eliminated?
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by P450 in the liver
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What are the adverse effects of pioglitazone and rosiglitazone?
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weight gain and fluid retention - can lead to CHF
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When should pioglitazone and rosiglitazone not be used?
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during pregnancy - retards fetal development
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What is the action of alpha-glucosidase inhibitors?
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inhibits the enteric enzymes of the brush border preventing the breakdown of complex starches, oligosaccharides and disaccharides
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When are alpha-glucosidase inhibitors used?
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they are taken with meals to minimize absorptio and digestion of starch and disaccharides
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What are the adverse effects of alpha-glucosidease inhibitors?
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severe flatulence, diarrhea, abdominal pain - slowly increasing dosage helps with these
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What are the contraindicatios of are alpha-glucosidase inhibitors?
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patients with chronic intestinal disease, IBD, colonic ulceration, intestinal obstruction
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Hypoglycemia can occur with alpha-glucosidase inhibitors when given with what other drug?
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sulfonylurea therapy
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What is used to treat hypoglycemia in patients taking alpha-glucosidase inhibitors?
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dextrose, NOT sucrose
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What is the action of sitagliptin?
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increases glucagon-like peptide-1 (GLP1) and glucose dependent inuliotropic polypeptide (GIP) which release insulin
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What are the actions of GLP1 and GIP?
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GLP1 and GIP are released by the intestine, potentiate insulin synthesis and release and decrease glucagon produciton
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How is sitagliptin administered?
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orally as monotherapy or in combo with metformin, pioglitazone and resiglitazone
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What are the side effects of sitagliptin?
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few, less likely to cause hypoglycemia and decreased weight gain compared to glipizide
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How is sitagliptin eliminated?
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mostly be the kidney, some in the feces
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How is exenatide administered?
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subcutaneous injections
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How is exenatide eliminated?
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by proteolysis and renal excretion
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What is the action of glucagon?
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increases blood glucose, decreases hepatic glycogen
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When is glucagon used?
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to treat severe hypoglycemia, in the diagnosis of endocrine disorders, in treatment of beta blocker poisoning, and radiology of the bowel
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How is glucagon eliminated?
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it is degraded by the liver
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What composes the glucagon receptor?
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7 transmembrane Gprotien coupled receptor
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What are the metabolic effects of glucagon?
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increased cAMP production, facilitates storage of glycogen, increases gluconeogensis and ketogenesis
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What is the cardiac effect of glucagon?
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increases cAMP mediated by beta receptor like effects
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What is the effect of glucagon on smooth muscle?
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profound relaxation of the small intestine
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