Diabetes and Insulin Flashcards

1
Q

Insulin concentration

A

100U/ml

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2
Q

very rapid acting insulin

A

lisper, insulin aspart, glulisine

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3
Q

rapid acting insulin

A

regular

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4
Q

intermediate acting insulin

A

NPH

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5
Q

long acting insulin

A

detemir, glargine

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6
Q

ultra long acting

A

degludec

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7
Q

lispro

A

onset within 15 minutes, peak of action 45-75 minutes, duration 2-4h.

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8
Q

insulin aspart and glulisine

A

onset 10-15 minutes, peak 45-75 minutes, duration 2-4h

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9
Q

aspart (fiasp)

A

vitamin B3 added which may increase speed of absorption. onset 15-20 minutes, time to peak plasma concentration 1 hour, DOA 5-7h

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10
Q

regular insulin

A

onset 30 minutes, peak 2-4h after SQ injection because of insulin hexamers. duration 6-8h. periop single dose 1-5U or infusion .5-2U/h

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11
Q

Five Main SE:

A
  1. hypoglycemia
  2. allergic reactions
  3. lipodystrophy
  4. insulin resistance
  5. drug interactions
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12
Q

Oral Antidiabetic Drugs

A
  1. secretagogues
  2. biguanides
  3. thiazolidinediones or glitazones
  4. alpha glucosidase inhibitors
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13
Q

Metformin drug class and contraindications

A

oral biguanide, can be used in combination with insulin and sulfonylureas. contraindications: lactic acidosis, AKI, GI intolerance, acute hepatic disease

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14
Q

Metformin MOA

A

blood glucose lowering effect is not mediated through stimulation of endogenous insulin secretion

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15
Q

Metformin and Lactic Acidosis

A
  • possible SE of metformin therapy
  • discontinue 48h before elective surgery
  • monitor for lactic acidosis, ABG, lactate, RFP
  • anaerobic metabolism results in pyruvate–>reduced to lactate
  • do not administer in patients with hepatic metabolism, renal insufficiency (creatinine >1.5mg/dL), IV contrast dye, acute MI, CHF, arterial hypoxemia, sepsis
  • treatment: hemodialysis, bicarbonate administration
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16
Q

Sulfonylureas

A
  • can lower glucose levels to hypoglycemic levels
  • improved BG control, decreased hepatic production of very low density lipoproteins, improved hypertriglyceridemia
  • up to 20% of patients do not have adequate hypoglycemic response to maximal doses (primary failures), and another 10-15% of patients who initially respond will fail to respond to therapy each year (secondary failure).
  • successful treatment requires beta cell function
  • do not administer to patients with sulfa allergy
17
Q

Sulfonylureas MOA

A

act on sulfonylurea receptors on pancreatic and cardiac cells: inhibit adenosine triphosphate sensitive K channels on pancreatic beta cells resulting in calcium influx and stimulation of insulin release

18
Q

How does sulfonylurea affect cardiovascular mortality

A

close potassium-ATPase channels and inhibit ischemic preconditioning aka the cardioprotective mechanism

19
Q

Glyburide MOA

A

stimulates insulin secretion over 24 hour period. increases insulin sensitivity and inhibits liver production of glucose

20
Q

glipizide MOA

A

increases glucose uptake and suppresses liver glucose output- effects persist for prolonged periods without tolerance. rapid plasma clearance minimizes risk for hypoglycemia

21
Q

glimepiride MOA

A

decreases blood glucose by stimulating release of insulin from pancreas and may decrease hepatic glucose production. combined with insulin therapy when sulfonylureas are not effective

22
Q

metglinide

A

exert effects on beta cells (similar to sulfonylureas). repaglinide, nateglinide.

23
Q

repaglinide

A

stimulates release of insulin from beta islet cells of pancreas

24
Q

nateglinide

A

lowers blood glucose by stimulating release of insulin from pancreas. accumulation of active metabolites may cause hypoglycemia

25
Q

alpha glucosidase inhibitors

A

acarbose and miglitol

26
Q

thiazolidinesiones (TZD’s)

A

rosiglitazone and pioglitazone. act at skeletal muscle, liver and adipose tissue via peroxisome proliferator activator receptor-gamma to decrease insulin resistance and hepatic glucose production, and to increase use of glucose by liver.

27
Q

glucagon like peptide 1 receptor agonists

A

exenatide and lireglutide. injectable agents that bind to receptors in pancreas, GI tract and brain to increase insulin secretion from beta cells, (glucose dependent), decrease glucagon production from alpha cells and reduce gastric emptying