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25 Multiple choice questions

  1. MOA- Metabolized by intestinal bacteria and digestive enzymes; delay carbohydrate absorption from the small intestine.
    *Primary site of action: Gut
  2. Given to increase blood glucose (opposite of insulin)
    -naturally produced by alpha cells of the pancreas
    -break down of glycogen to glucose
    decreases conversion of glucose to glycogen
    -stimulates biosynthesis of glucose
    -Administered parentally
    -Used only if IV glucose is not an option
  3. Ex.: Sitagliptin (Januvia)
    MOA:
    -increases insulin release by enhancing the activity of incretins
    -Reduces glucagon release
    -Decreases hepatic glucose production
    onset: rapid, peak: 1-4 hr, duration: 24 hr
  4. Ex. Exenatide (Byetta)
    -MOA: enhances glucose dependent insulin secretion
    -Indication: as adjunct to metformin or sulfonylurea or a combination therapy when have not achieved adequate glycemic control
    -Stimulates glucose-dependent release of insulin, inhibits postprandial release of glucagon, and suppresses appetite
    -Major SE are nausea and hypoglycemia
    -Given SC within 1H of AM & PM meal(BID)
    -Peak 2 hours, half life 2.4 hours
    -Excreted unchanged in urine (contraindicated in ESRD)
    -NOT GIVEN with Type 1 DM or DKA
  5. Lower blood glucose by:
    1. stimulating secretion of insulin from the pancreas
    2. increasing the body's sensitivity or response to insulin
    3. reducing the release of glucose from the liver
    -Classified by generations based on potency, duration and drug interactions/SE
    -Adverse effects: hypoglycemia (most likely with kidney or liver dysfxn), effects potentiated by ETOH, NSAIDs, Tagamet
    *Safe with Metformin.
    *Not used for gestational diabetes.
    *Primary site of action: Pancreas
  6. MOA: Increase insulin sensitivity at insulin receptor sites on the cell. Most appropriate for adults whose bodies produce insulin but cannot use it because of inadequate or ineffective receptor sites.
    -onset & peak unknown, duration 12-24 hr
    -Adverse Effects:
    --*Risk of MI and heart-related deaths in people taking Avandia
    --edema, wt gain, fluid retention, avoid if pt has liver dysfunction, elevated liver enzymes, raises plasma lipids (TG, LDL, HDL)
    *Primary site of action: Muscle
  7. -Prevent longterm complications by keeping blood glucose and lipids under tight control.
    -Diet & exercise (promotes glucose uptake by muscles)
    -Weight loss
    -drug therapy, if diet & exercise fail
    --oral hypoglycemic agents
    --insulin
    --injectable hypoglycemic agents (ie. Byetta)
  8. New injectable drug for DM
    MOA: amylin (peptide hormone in the pancreas, released with insulin) mimetic, delays gastric emptying & suppresses glucagon secretion, decrease postprandial levels of glucose; lowers calorie intake by increasing satiety
    Therapeutic use: supplement mealtime insulin (SC injection)
    Adverse effects: hypoglycemia, nausea, injection site reaction
  9. -Prevent longterm complications by keeping blood glucose and lipids under tight control.
    1. Diet:
    -CHO and Mono-fats together = 60-70% cal
    -Protein= 10%
    -Saturated fat < 10%
    -Cholesterol < 300 mcg/day
    -Total caloric intake spread evenly with meals spaced 4-5 hours apart
    2. Regular exercise that includes monitoring blood glucose pre- and post-
    3. Insulin replacement
  10. same MOA as sulfonylureas
    *Requires functioning pancreatic beta cells.
  11. 1. Hyperglycemia (>300 mg/dL)
    2. Low bicarb (<15 mEq/L)
    3. Low pH (<7.3)
    4. Ketonemia (positive ketones or acetones in blood)
    5. Ketonuria (ketones or acetones in urine)
  12. A serum blood test which reflects glucose level over the preceding 2-3 months that is a better indicator of glycemic control over time than the FBS
    6% reflects pretty good control
  13. Type 2 DM
    -Hyperglycemic Hyperosmolar Nonketotic Syndrome
    -Characterized by:
    --Serum osmolality of 310 mOsm/L
    --Serum glucose of >600 mg/dL
    --Absence of ketoacidosis/ketones
    --Associated with Type 2 diabetes mellitus (most common)
    Rate of onset: 24 hours to 2 weeks
    Dehydration: Dry mucous membranes and thirst
    Neurologic manifestations: decreased level of consciousness (sometimes coma); potential for seizures
  14. Short acting insulin
    Onset: 30-60 minutes
    Peak: 2-4 hours
    Duration: 6-8 hours
    *Regular insulin can be administered intravenously, thus it is used in emergencies.
    *Can be used in insulin pump.
  15. Rapid acting insulin
    Onset: 15-30 minutes
    Peak: 1-3 hours
    Duration: 3-5 hours
  16. 1. Impaired carbohydrate metabolism-glucose can't enter the cell, serum becomes hyperglycemic
    2. Impaired fat metabolism - fat broken down in cholesterol & phospholipids (ie. atherosclerosis) or ketone bodies (potential ketosis)
    3. Impaired protein metabolism - can't store or synthesize protein, but increased catabolism causes muscle wasting, elevated BUN, aminoacidemia and multiple organ dysfunction
    4. Fluid & electrolyte imbalance-increased serum glucose, inc. plasma osmotic P, fluid shift to intravascular compartment, intracellular dehydration (polydipsia)
  17. Type 1 DM
    -Rapid onset- 1 to 24 hours
    -Polyuria, polydipsia, polyphagia
    -Dehydration
    --warm, dry skin
    --tachycardia, weak, thready pulse
    --acute weight loss
    --hypotension
    -Ketoacidosis
    --Nausea and vomiting, anorexia
    --Ketone breath -- sweet, fruity odor
    --Mental status changes
    ---lethargy, fatigue, stupor, coma
    COMPENSATION: Respiratory, Kussmaul's respirations (rapid, deep respirations)
  18. MOA- lowers blood glucose by decreasing production of glucose in the liver:
    --Enhances glucose uptake and utilization by muscle
    --DOES NOT promote insulin release from the pancreas or cause hypoglycemia
    -Onset several days; peak 2-4 weeks
    -Adverse effects: abdominal bloating, nausea, vomiting, diarrhea, risk for lactic acidosis in pts with elevated creatinine
    -NIC - monitor serum glucose levels; give 30 minutes AC
    Other uses: prevent Type 2 DM, polycystic ovarian syndrome.
    *Primary site of action: Liver.
  19. Intermediate acting insulin
    Onset: 1-3 hours
    Peak: 6-12 hours
    Duration: 18-26 hours
    *NPH is the only intermediate insulin suitable for mixing with short acting insulin.
    Cloudy solution-gently roll between palms before administration. Short acting before long acting. (clear before cloudy)
  20. Mixed insulin
    Onset: 15-30 minutes
    Peak: 2-10 hours
    Duration: 12-16 hours
    *70% NPH, 30% Regular
  21. Rapid acting insulin
    Onset: 15-30 minutes
    Peak: 1-2 hours
    Duration: 3-4 hours
  22. Rapid acting insulin
    Onset: 15-30 minutes
    Peak: 1-3 hours
    Duration: 3-5 hours
    *Can be used in insulin pump.
  23. -Impaired cerebral function
    -H/A, altered emotional behavior
    -Difficulty problem solving, feelings of vagueness,
    -Slurred speech, impaired motor function,
    -Seizures, coma
    -Nervous, shaky, dizzy, confused, hunger, cold & clammy skin, tachycardia, irritability
  24. weak, tired, polyuria, polydipsia, polyphagia, blurry vision, itchy dry skin, fruity-smelling breath
  25. Long acting basal insulin
    Onset: 1-2 hours
    PeakLESS
    Duration: 24 hours
    *used overnight and between meals, 9am & 9pm
    *Do not mix with other insulin.