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Flashcards in Diabetes Deck (74):
1

Diabetes is the leading cause of what?

blindness and ESRD

2

The effects of insulin

promotes glucose removal, glycogen storage, fatty acid storage and protein synthesis, inhibition of ketone body formation in the liver occurs at lower insulin concentrations than that required to stimulate muscle uptake of glucose

3

postprandial metabolism starts with the release of insulin and results in

conversion of glucose to glycogen, conversion of amino acids to protein, conversion of ffa to triglycerides

4

decreased glucose concentrations causes what

shuts off conversion of energy sources to storage, causes release of glucagon, epi, cortisol, growth hormone, glycogenolysis, gluconeogenesis

5

What are signs and symptoms of diabetes?

polyuria, polydipsia, polyphagia, wt loss, fatigue, recurrent UTI, ketoacidosis

6

Gestational diabetes

glucose intolerance during pregnancy, 1-14% of all pregnancies, most common in third trimester, screen conducted three months post partum to test for resolution

7

Drug induced diabetes

antiretrovirals, glucocorticoids, nicotinic acid atypical antipsychotics

8

Drugs that increase insulin resistance

thiazides, niacin

9

drugs that decrease insulin secretion

phenytoin

10

Drugs that mask S/Sx of hypoglycemia

beta blockers

11

diagnostic criteria for diabetes

FPG>126, 2hr GTT >200mg/dL, random plasma glucose >200, A1c>6.5%

12

How often do you check A1c?

every 3 months until at goal and then 6 months

13

Diagnostic criteria for prediabetes

FPG 100-125mg/dL, 2hr plasma glucose 140-199, A1c 5.7-6.4%

14

Metformin (Glucophage) MOA

increases insulin sensitivity, decrease in hepatic glucose production, decreases intestinal absorption of glucose

15

Metformin dosage

500 mg PO BID is starting can increase up to 2000

16

How much does metformin decrease A1c

up to 1-2%

17

Advantages of metformin

no wt gain, no risk for hypoglycemia, decreases risk for micro and macro vascular complications, stroke, MI

18

Disadvantages of metformin

GI side effects, lactic acidosis, contraindicated in renal failure, NYHAIII and IV (CHF), men SCr>1.5, women >1.4

19

When should metformin be held?

temporarily for a few days pre and post any radiographic studies where iodinated contrast is employed

20

What other disease is metformin used in?

polycystic ovarian disease

21

oral sulfonylureas

dlyburide (diabeta), glipizide (glucotrol), glimepiride (Amaryl), glicazide, chlorpromamide, tolazamide, tolbutamide

22

MOA of sulfonylureas

increases insulin secretion from pancreas, may increase insulin sensitivity and reduce glucose production but to a lesser ectent

23

Sulfonylureas place in therapy

first tier option after pt fails metformin and lifestyle modifications, can be used in combination w/ other agents except meglitinides, reduces A1c by 1.5-2%

24

Advantages of sulfonylureas

well tolerated, first tier, old, inexpensive

25

Disadvantages of sulfonylureas

wt. gain, drug interactions, hypoglycemia

26

Dose of Flimepiride (Amaryl)

2-8mg PO daily

27

Dose of glipizide (Glucotrol)

5-15 mgPO daily, XL

28

dose of glycuride (Diabeta)

5-20 mg PO daily

29

Sulfonylurea pearls

start low, go slow, no value if max exceeded, use with caution with insulin due to increased risk of hypo glycemia, 15% of pts may never respond, 50% fail after 5 years

30

Hypoglycemia symptoms

slurred speech, drowsiness, tachycardia, confusion, agitation, diaphoresis, tremors, coma

31

Treatment of hypoglycemia

goal of 15-30gm carbs, dectrose 50% IVP, glucose tabs, cola, orange juice, hard candy, sugar packets

32

What do you not give for treatment of hypoglycemia

chocolate

33

What is the minimum CNS glucose concentration

40-60 mg/dL

34

How often should you recheck blood glucose after hypoglycemia

15 mins

35

What should be given to a hypoglucose pt who is unconscious

IM glucagon

36

What are the meglitinides

repaglinide (Prandin), Nateglinide (Starlix)

37

MOA of meglitinides

increase in insulin secretion, similar to sulfonylurea but lacks sulfa allergy, faster onset, short duration

38

When should meglitinides be used

in combo with metformin or TZD, not with sulfonylureas because similar MOA, minimal use overall

39

Advantages of meglitinides

accentuated effects around meal ingestion, particularly useful for pts w/ elevated postprandial hyperglycemia

40

Disadvantages of meglitinides

hypoglycemia, poor efficacy, wt gain, dosing frequency (TID), DI

41

When should meglitinides be taken

15-30 mins before a meal, if no meal, skip dose, if add meal, add ose, can adjust dose weekly

42

Thiazolidinedione (TZD)

pioglitazone (actos), rosiglitazone (Avandia)

43

Dose of pioglitazone (actos)

15-45 mg PO daily

44

MOA of TZD

imporves target cell responses to insulin w/out increasing pancreatic insulin secretion, multi-modal MOA

45

What is TZD place in therapy

second tier option after pt fails metformin and lifestyle modifications, combo w/ other agents, reduces A1c by .5-1.4%, take 2-3 months to see full effect

46

Advantages of TZD

no hypoglycemia, increase HDL by 3-9%, decrease triglycerides by 10-20%

47

Disadvantages of TZD

wt. gain, edema, does not decrease LDL, FDA box warning to CHF exacerbation (lifted recently), hepatotoxic

48

Pearls of TZD

not first line, combo w/ OSU, metformin or insulin

49

Incretin physiology

GLP-1: naturally occurring hormone stimulates glucose dependent insulin secretion, dec glucagon release, slows gastric emptying and dec food intake, degrades DPP-4; GIP: inc insulin release, degraded by DPP

50

GLP-1 agonist

exenatide (Byetta), albiglutide (Tanzeum), liraglutide (Victoza), dulaglutide (Trulicity)

51

MOA of GLP-1 receptor agonists

incretin mimetic, inc glucose dependent insulin secretion, dec glucagon secretion, slows gastric emptying, inhibits B cell death

52

Place in therapy of GLP-1 receptor agonists

second tier option for Type 2 DM after pt fails metformin and lifestyle modifications, can be used in combo w/ other agents

53

Advantages of GLP-1 receptor agonist

wt reduction, potential for improved B cell function

54

Disadvantages of GLP-1 receptor agonist

GI- N/V/D, cases of acute pancreatitis reported, long term safety unknown, injectable (sq BID)

55

Dose of exenatide (Byetta)

5-10 mcg sub cut BID, extended release 2 mg weekly

56

Dose of liraglutide (Victoza)

.6-3 mg subcut daily

57

Dipeptidyl peptidase inhibitors

Sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina)

58

Dose of sitagliptin (Januvia)

50-100 mg PO daily, adjust renal

59

Dose Saxagliptin (Onglyza)

2.5-5 mg PO once daily

60

Dose of Linagliptin (Tradjenta)

5 mg PO daily

61

DPP-4 inhibitors MOA

inhibits DPP-4 activity which prolongs the survival of endogenously release incretin hormones, results in greater GLP-1 concentrations

62

Place of DPP-4 inhibitors in therapy

may be used as monotherapy or in combo with OSU, metformin, TZD, or insulin, may be first line eventually

63

DPP-4 inhibitors advantages

no hypoglycemia, PO, wt neutrality, well tolerated

64

Disadvantages of DPP-4 inhibitors

cases of angioedema, acute pancreatitis observed, long term safety unknown, $$, $200/ month

65

Sodium glucose costransporter 2 inhibitors

Canagliflozin (Invokana), dapagliflozin (Farxiga), empagliflozin (jardiance)

66

MOA of SGLT2 inhibitors

work to reduce reabsorption of filtered glucose from the tubular lumen in proximal renal tubules. lower renal threshold for glucose

67

place in therapy of SGLT2 inhibitors

new products, no established recommendations, FDA approved for type II, monotherapy

68

Advantages of SGLT2 inhibitors

already available in combo w/ metformin, oral, once daily formulation, novel MOA, quick onset, dec A1c by .7-1%, efficacy best if taken in am

69

Disadvantages of SGLT2 inhiitors

avoid CrCl

70

a-Glucosidase inhibitors

acarbose (Precose), miglitol (glyset)

71

MOA of a Glucosidase inhibitors

inhibits intestinal a glucosidase resulting in slowed carbohydrate digestion and absorption

72

Place in therapy for a glucosidase inhibitors

as adjunct with other agents for post prandial hyperglycemia, .4-1% A1c reduction

73

advantages of a-glucosidase inhibitors

no systemic effects, no wt gain, specific for post-prandial hyperglycemia

74

Disadvantages of a-glucosidase inhibitors

GI, flatulence is sig, diarrhea, dosing frequency, bad if pt on low carb