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70 Cards in this Set

  • Front
  • Back
increase insulin needs
infection,e xacerbation of other medical problems, weight gain puberty,, inactivity, hyperthyroidism and cushing dz
reduce insulin needs
renal failure, adrenal insufficiency, nutrient malabasorption, hypopituitarism,weight loss and increased exercise
fastest absorption of regular insulin
physical exercise, hot shower, baths and massage
increases blood flow to the exercising area, thus accelerating absorption of insulin injected at that site
injection site rotated
avoid lipohypertrophy and fibrosis
insulin drip admin of regular insulin
used for treatment of acute hyperglycemia, ketoacidosis, HHNK syndrome or during surgical procedures or delivery
short acting or rapid acting insulin
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
before each meal, pt sets pump to deliver "bolus" dose of short acting or rapid acting insulin
to control the glycemic effects of the meal
bolus dose is determined
by algorithms that consider the premeal glucose level, anticipated dietary intake and activity
chemical classes
sulfonyureas, meglitinides
tolbutamide, acetohexamide, chlorpropamide, glyburide, glipizide, glimepride
repaglinide and nateglinide
type 2 dm
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
type 1 dm
not indicated, pharmacological action depends on functioning beta cells
mechanism of action
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
postreceptor defect
transport defect
most clinical significance of sulfonylureas
duration of action, impacts frequency of dosing and potential compliance issues
exhibits an insulin-sparing eff compared to other membersof this class, reportedly by its relatively greated extrapancreativ effect
beta cell stimulation of insulin secretion
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
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
assoc with severe or prolonged hypoglycemia in the elderly
insulin secretagogues (oral hypoglycemic agents)
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
sulfonulurea agents are contraindicated
sulfa allergy
metabolized in liver to active metabolite 2x as potent as parent compd, has diuretic activity , uricosuric activity
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
metabolized in liver to less active and inactive products, has diuretic activity
metabolized in liver to inactive product
metabolid in liver to inactive prodt that are excreted in the urine and to a lesser extenet in the bile
mild diuretic activity
metabolized in liver to weakly active and inactive prodts , excreted in urine and bile, mild diuretic activuty
metabolid in liver, renal eliminated, less stimulation of insulin secretion
metabolized in liver to inactive metabolites. action is dose dependent and glucose dependent
metabolized in liver to less active metabolites by CYP2C9(70%) and CYP3A4(30%) . may elevate uric acid level
hypoglycemia and alcohol intolerance
sulfonylurea therapy - chlorpropramide and tolbutamide
adverse eff with oral hypoglycemics
gi disturbances (n/v, gastric discomfort,constipation)tachycardia, ha, skin rach and hematological prob(agranulocytosis, pancytopenia, hemolytic anemia
cholestatic jaundice
primary failure
fails to control hyperglycemia within the 1st 4 weeks after initiation . represents indufficient numbers of functioning beta cells
2ndary failure
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
insulin sensitizers
biguanides - metformin

thiazolidinediones -
pioglitazone, rosiglitazone

combo prdts-met/gly;met/gli; met/rosiglitazone
indicated in those individuals with a significant component of insulin resisance
insulin sensitizers
antihyperglycemic agents
insulin sensitizers
major action for metformin
increase hepativ sensitivity to insulin thereby suppressing hepativ glucose production
major action for pioglitazone and rosiglitazone
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
metformin contraindications
lactic acidosis, chronic or binge ingestion of ethanol, liver dz
liver dz
hepatic function important for clearance of blood lactate
thiazolidinediones c/i
hepatic dz,severe heart failure, pregnancy,
alpha glucosidase inhibitors
indication of alpha glucosidase inhibitors
postprandial hyperglycemia- minimaleff on preprandial or fasting blood glucose levels
taken with meals to lessen gi eff, excreted unchanged i urine, warnings against use in situations with potential for lactic acidosis
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
metabolized CYP2C8-major and 2C9 -minor metabolites excreted via urine and feces
take with first bite of meal, negligible absorption of unchanged drug, metabolized in GI tract, 35% metabolites are absorbed and excreted in urine
take with 1st bite of meal, not metabolized, degree of absorption os dose dependent, excreted by kidneys(absorbed) and feces(unabasorbed)
moa of alpha glucosidase inhibitors
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
adverse eff of alpha glucosidase
pregnancy, breast feeding,inflammatory bowel disease, colonic ulceration, obstructive bowel disorders, chronic intestinal disorders of digestio oor absorption, cirrhosis of the liver,
secondary to autonomic neuropathic condition resulting in little or no perspiration
leading cause of vision impairment, blindness for individuals between ages 20-74 yrs old
urine glucose testing
reserved only for those individuals unable or unwilling to perform self monitoring of blood glucose
urine ketone monitoring
essential component of diabetes mgmt
long term monitoring of glycemic control
- hemoglobin A1C testing (glycohemoglobin; glycosylated hemoglobin test)
- glycosylated fructosamine test
7% or lower hemoglobin a1c level
indicates good overall glycemic control
>7% hg a1c level
need for additional intervention
glycosylated fructosamine test
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)
increase BG following prolonged or severe hypoglycemia
somogyi effect or rebound hyperglycemia
dawn phenomenon
increase BG occurring as a pattern in early morning
ketoacidosis physical findings
kussmaul's respirations, acetone breath odor, dehydrationm dry skin, poor sking turgor, reduced level of ocnsciousness and abdominal pain
treatment for ketoacidosis
fluid, iv insulin by continuos infusion and electrolyte replacement
adrenergic symptoms
tachycardia, palpitations, shakiness
cholinergic symptoms
cns glucopenia
inability to concentrate, dizzy, hunger blurred vision
delayed emptying of the stomach following a meal, an autonomic neuropathy complication of diabetes