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70 Cards in this Set
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increase insulin needs
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infection,e xacerbation of other medical problems, weight gain puberty,, inactivity, hyperthyroidism and cushing dz
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reduce insulin needs
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renal failure, adrenal insufficiency, nutrient malabasorption, hypopituitarism,weight loss and increased exercise
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abdomen
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fastest absorption of regular insulin
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physical exercise, hot shower, baths and massage
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increases blood flow to the exercising area, thus accelerating absorption of insulin injected at that site
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injection site rotated
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avoid lipohypertrophy and fibrosis
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insulin drip admin of regular insulin
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used for treatment of acute hyperglycemia, ketoacidosis, HHNK syndrome or during surgical procedures or delivery
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short acting or rapid acting insulin
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infused continuosly during the day in a patient-specific pattern to deliver low doses of insulin (basal insulin) to offset the glycemic effect of daily patterns of counterregulatory hormones
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before each meal, pt sets pump to deliver "bolus" dose of short acting or rapid acting insulin
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to control the glycemic effects of the meal
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bolus dose is determined
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by algorithms that consider the premeal glucose level, anticipated dietary intake and activity
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chemical classes
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sulfonyureas, meglitinides
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sulfonyureas
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tolbutamide, acetohexamide, chlorpropamide, glyburide, glipizide, glimepride
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meglitinides
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repaglinide and nateglinide
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type 2 dm
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1. monotherapy or in combo with other oral antidiabetes drugs or insulin 2. use in type 2 dm predicated on *adequate control not attained by medical nutrition therapy and physical activity alone * pharmacological intervention required based on the presenting blood glucose levels and diabetes symptomatology * sufficient number of functioning beta cells
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type 1 dm
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not indicated, pharmacological action depends on functioning beta cells
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mechanism of action
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1. predominant effect - stimulate pancreative secretion of insulin 2. improve 1st phase release of insulin/ increase sensitivity of beta cells to glucose stimulus 3. lessor eff-increase hepativ sensitivity to insulin, increase # and/or sensitivity of insulin rec in muscle and adipose tissue, reduce postreceptor defect in muscle and adipose tissue
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postreceptor defect
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transport defect
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most clinical significance of sulfonylureas
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duration of action, impacts frequency of dosing and potential compliance issues
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glimepride
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exhibits an insulin-sparing eff compared to other membersof this class, reportedly by its relatively greated extrapancreativ effect
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beta cell stimulation of insulin secretion
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more glucose dependent with repaglinide and nateglinide than with sulfonylurea agents, this action along with its very short action may present a reduced risk of late postprandial hypoglycemia for selected individuals
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chlorpropamide
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longest duration of action and poses a risk to patient with renal or hepatic impairment, It also causes more severe and frequent side eff- hypoglycemia and hyponatremia
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glyburide
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assoc with severe or prolonged hypoglycemia in the elderly
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insulin secretagogues (oral hypoglycemic agents)
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not recom for children, pregnant and lactating women or as monotherapy i pats without functioning pancreativ beta cells; not be used for metabolic control during stressful conditions such as severe infxn,injury or surgery
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sulfonulurea agents are contraindicated
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sulfa allergy
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acetohexamide
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metabolized in liver to active metabolite 2x as potent as parent compd, has diuretic activity , uricosuric activity
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chlorpropramide
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70% metabolized in liver to less-active metabolites, 30% excreted intact by kidneys, can potentiate ADH, 1/3 of patients have an antabuse-like reaction with alcohol
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tolazamide
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metabolized in liver to less active and inactive products, has diuretic activity
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tolbutamide
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metabolized in liver to inactive product
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glipizide
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metabolid in liver to inactive prodt that are excreted in the urine and to a lesser extenet in the bile
mild diuretic activity |
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glyburide
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metabolized in liver to weakly active and inactive prodts , excreted in urine and bile, mild diuretic activuty
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glimepride
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metabolid in liver, renal eliminated, less stimulation of insulin secretion
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repaglinide
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metabolized in liver to inactive metabolites. action is dose dependent and glucose dependent
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nateglinide
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metabolized in liver to less active metabolites by CYP2C9(70%) and CYP3A4(30%) . may elevate uric acid level
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hypoglycemia and alcohol intolerance
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sulfonylurea therapy - chlorpropramide and tolbutamide
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adverse eff with oral hypoglycemics
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gi disturbances (n/v, gastric discomfort,constipation)tachycardia, ha, skin rach and hematological prob(agranulocytosis, pancytopenia, hemolytic anemia
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cholestatic jaundice
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sulfonylurea
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primary failure
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fails to control hyperglycemia within the 1st 4 weeks after initiation . represents indufficient numbers of functioning beta cells
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2ndary failure
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drug controls hyperglycemia initially but fails to maintain control.represents progression of the dm with a diminishing # of functioning beta cells rather than a drug failure
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insulin sensitizers
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biguanides - metformin
thiazolidinediones - pioglitazone, rosiglitazone combo prdts-met/gly;met/gli; met/rosiglitazone |
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indicated in those individuals with a significant component of insulin resisance
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insulin sensitizers
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antihyperglycemic agents
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insulin sensitizers
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major action for metformin
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increase hepativ sensitivity to insulin thereby suppressing hepativ glucose production
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major action for pioglitazone and rosiglitazone
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reduce postreceptor defect in muscle and adipose tissue- this defect appears to be the major component of naturally occuring insulin resistance, and increase number and or sensitivity of insulin receptors in muscle and adipose tissue thereby addressing the cell-surface " binding defect" this defect correlates most sifnificantly with hyperinsulinemia
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metformin contraindications
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lactic acidosis, chronic or binge ingestion of ethanol, liver dz
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liver dz
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hepatic function important for clearance of blood lactate
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thiazolidinediones c/i
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hepatic dz,severe heart failure, pregnancy,
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alpha glucosidase inhibitors
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acarbose
miglitol |
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indication of alpha glucosidase inhibitors
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postprandial hyperglycemia- minimaleff on preprandial or fasting blood glucose levels
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metformin
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taken with meals to lessen gi eff, excreted unchanged i urine, warnings against use in situations with potential for lactic acidosis
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pioglitazone
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taken w/out regard to meals, food slightly delays the time to peack conc but does not reduce the extent of absorption, protein binding >99% mostly to albumin, metabolized in liver -CYP2C8 and 3A4) excreted primarily through feces
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rosiglitazone
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metabolized CYP2C8-major and 2C9 -minor metabolites excreted via urine and feces
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acarbose
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take with first bite of meal, negligible absorption of unchanged drug, metabolized in GI tract, 35% metabolites are absorbed and excreted in urine
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miglitol
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take with 1st bite of meal, not metabolized, degree of absorption os dose dependent, excreted by kidneys(absorbed) and feces(unabasorbed)
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moa of alpha glucosidase inhibitors
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1. inhibits the intestinal enzume alpha glucosidase. intestinal absorption of complex carbohydrates such as starch, dextrins and disaccharides (sucrose, maltose) requires the action of intestinal alpha glucosidase 2. inhibition retards the degradation and thus the absorption of carbohydrates resulting ina slower and smaller rise in blood glucose ff the meal
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adverse eff of alpha glucosidase
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pregnancy, breast feeding,inflammatory bowel disease, colonic ulceration, obstructive bowel disorders, chronic intestinal disorders of digestio oor absorption, cirrhosis of the liver,
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anhidrosis
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secondary to autonomic neuropathic condition resulting in little or no perspiration
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diabetes
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leading cause of vision impairment, blindness for individuals between ages 20-74 yrs old
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urine glucose testing
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reserved only for those individuals unable or unwilling to perform self monitoring of blood glucose
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urine ketone monitoring
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essential component of diabetes mgmt
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long term monitoring of glycemic control
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- hemoglobin A1C testing (glycohemoglobin; glycosylated hemoglobin test)
- glycosylated fructosamine test |
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7% or lower hemoglobin a1c level
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indicates good overall glycemic control
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>7% hg a1c level
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need for additional intervention
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glycosylated fructosamine test
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measures glycemic control over the preceding 2-3 weeks and useful for short term follow up of recently implemented interventions when timely assessment of the intervention is important (ex: changes in diabetes therapy druing pregnancy)
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increase BG following prolonged or severe hypoglycemia
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somogyi effect or rebound hyperglycemia
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dawn phenomenon
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increase BG occurring as a pattern in early morning
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ketoacidosis physical findings
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kussmaul's respirations, acetone breath odor, dehydrationm dry skin, poor sking turgor, reduced level of ocnsciousness and abdominal pain
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treatment for ketoacidosis
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fluid, iv insulin by continuos infusion and electrolyte replacement
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adrenergic symptoms
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tachycardia, palpitations, shakiness
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cholinergic symptoms
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sweating
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cns glucopenia
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inability to concentrate, dizzy, hunger blurred vision
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gastroparesis
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delayed emptying of the stomach following a meal, an autonomic neuropathy complication of diabetes
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