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  1. Pramlintide (Symlin)
  2. Incretin memetic exenatide injection
  3. Insulin - Aspart (Novolog)
  4. What are s/s of hyperglycemia?
  5. Gliptins
  6. Insulin Regular - Humulin R - Novolin R
  7. Biguanides;
    Metformin (Glucophage, Glucophage XR, Fotamet, Riomet)
  8. Insulin - Lispro (Humalog)
  9. Insulin - Glargine (Lantus)
    Insulin - Detemir (Levemir)
  10. Insulin Novolog Mix 70/30 (Neutral Protamine aspart and aspart)
  11. What are s/s of hypoglycemia?
  12. Thiazolidinediones aka glitazones;
    Rosiglitazone (Avandia)
    Pioglitazone (Actos)
  13. Glucagon
  14. Sulfonylureas- Oral hypoglycemic agents;
    1st Generation:
    Tolbutamide (Orinase)
    Tolazamide (Tolinase)
    Chlorpropamide (Diabinese)
    2nd Generation:
    Glipizide (Glucotrol)
    Glyburide (Diabeta, Micronase, Glynase)
    Gimepiride (Amaryl)
  15. Meglitinides;
    Repaglinide (Prandin)
    Nateglinide (Starlix)
  16. What are s/s of DKA?
  17. Hemoglobin A1C
  18. What is the best treatment for Type 2 diabetes?
  19. Alpha-Glucosidase Inhibitors;
    Acarbose (Precose)
    Miglitol (Glyset)
  20. What is HHNS?
  21. What is the best treatment for Type 1 diabetes?
  22. Insulin - Glulisine (Apidra)
  23. What are four major effects of insulin deficit?
  24. Insulin NPH (Novolin-N - Humulin-N - ReliOn N)
  25. What are lab values associated with DKA?
  1. a 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)
  2. b 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. c 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
  4. d Mixed insulin
    Onset: 15-30 minutes
    Peak: 2-10 hours
    Duration: 12-16 hours
    *70% NPH, 30% Regular
  5. e 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
  6. f 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.
  7. g Ex.: Sitagliptin (Januvia)
    -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
  8. h 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.
  9. i -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
    --injectable hypoglycemic agents (ie. Byetta)
  10. j 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
  11. k 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)
  12. l -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
  13. m 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
  14. n 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
  15. o -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
  16. p Rapid acting insulin
    Onset: 15-30 minutes
    Peak: 1-2 hours
    Duration: 3-4 hours
  17. q Rapid acting insulin
    Onset: 15-30 minutes
    Peak: 1-3 hours
    Duration: 3-5 hours
    *Can be used in insulin pump.
  18. r 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)
  19. s Long acting basal insulin
    Onset: 1-2 hours
    Duration: 24 hours
    *used overnight and between meals, 9am & 9pm
    *Do not mix with other insulin.
  20. t Rapid acting insulin
    Onset: 15-30 minutes
    Peak: 1-3 hours
    Duration: 3-5 hours
  21. u same MOA as sulfonylureas
    *Requires functioning pancreatic beta cells.
  22. v weak, tired, polyuria, polydipsia, polyphagia, blurry vision, itchy dry skin, fruity-smelling breath
  23. w MOA- Metabolized by intestinal bacteria and digestive enzymes; delay carbohydrate absorption from the small intestine.
    *Primary site of action: Gut
  24. x 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
  25. y Type 1 DM
    -Rapid onset- 1 to 24 hours
    -Polyuria, polydipsia, polyphagia
    --warm, dry skin
    --tachycardia, weak, thready pulse
    --acute weight loss
    --Nausea and vomiting, anorexia
    --Ketone breath -- sweet, fruity odor
    --Mental status changes
    ---lethargy, fatigue, stupor, coma
    COMPENSATION: Respiratory, Kussmaul's respirations (rapid, deep respirations)