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Pharmacology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Diabetes is the leading cause of what?

A

blindness and ESRD

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2
Q

The effects of insulin

A

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

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3
Q

postprandial metabolism starts with the release of insulin and results in

A

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

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4
Q

decreased glucose concentrations causes what

A

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

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5
Q

What are signs and symptoms of diabetes?

A

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

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6
Q

Gestational diabetes

A

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

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7
Q

Drug induced diabetes

A

antiretrovirals, glucocorticoids, nicotinic acid atypical antipsychotics

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8
Q

Drugs that increase insulin resistance

A

thiazides, niacin

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9
Q

drugs that decrease insulin secretion

A

phenytoin

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10
Q

Drugs that mask S/Sx of hypoglycemia

A

beta blockers

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11
Q

diagnostic criteria for diabetes

A

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

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12
Q

How often do you check A1c?

A

every 3 months until at goal and then 6 months

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13
Q

Diagnostic criteria for prediabetes

A

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

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14
Q

Metformin (Glucophage) MOA

A

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

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15
Q

Metformin dosage

A

500 mg PO BID is starting can increase up to 2000

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16
Q

How much does metformin decrease A1c

A

up to 1-2%

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17
Q

Advantages of metformin

A

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

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18
Q

Disadvantages of metformin

A

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

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19
Q

When should metformin be held?

A

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

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20
Q

What other disease is metformin used in?

A

polycystic ovarian disease

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21
Q

oral sulfonylureas

A

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

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22
Q

MOA of sulfonylureas

A

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

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23
Q

Sulfonylureas place in therapy

A

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%

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24
Q

Advantages of sulfonylureas

A

well tolerated, first tier, old, inexpensive

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25
Q

Disadvantages of sulfonylureas

A

wt. gain, drug interactions, hypoglycemia

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26
Q

Dose of Flimepiride (Amaryl)

A

2-8mg PO daily

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27
Q

Dose of glipizide (Glucotrol)

A

5-15 mgPO daily, XL

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28
Q

dose of glycuride (Diabeta)

A

5-20 mg PO daily

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29
Q

Sulfonylurea pearls

A

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

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30
Q

Hypoglycemia symptoms

A

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

31
Q

Treatment of hypoglycemia

A

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

32
Q

What do you not give for treatment of hypoglycemia

A

chocolate

33
Q

What is the minimum CNS glucose concentration

A

40-60 mg/dL

34
Q

How often should you recheck blood glucose after hypoglycemia

A

15 mins

35
Q

What should be given to a hypoglucose pt who is unconscious

A

IM glucagon

36
Q

What are the meglitinides

A

repaglinide (Prandin), Nateglinide (Starlix)

37
Q

MOA of meglitinides

A

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

38
Q

When should meglitinides be used

A

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

39
Q

Advantages of meglitinides

A

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

40
Q

Disadvantages of meglitinides

A

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

41
Q

When should meglitinides be taken

A

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

42
Q

Thiazolidinedione (TZD)

A

pioglitazone (actos), rosiglitazone (Avandia)

43
Q

Dose of pioglitazone (actos)

A

15-45 mg PO daily

44
Q

MOA of TZD

A

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

45
Q

What is TZD place in therapy

A

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
Q

Advantages of TZD

A

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

47
Q

Disadvantages of TZD

A

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

48
Q

Pearls of TZD

A

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

49
Q

Incretin physiology

A

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
Q

GLP-1 agonist

A

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

51
Q

MOA of GLP-1 receptor agonists

A

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

52
Q

Place in therapy of GLP-1 receptor agonists

A

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

53
Q

Advantages of GLP-1 receptor agonist

A

wt reduction, potential for improved B cell function

54
Q

Disadvantages of GLP-1 receptor agonist

A

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

55
Q

Dose of exenatide (Byetta)

A

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

56
Q

Dose of liraglutide (Victoza)

A

.6-3 mg subcut daily

57
Q

Dipeptidyl peptidase inhibitors

A

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

58
Q

Dose of sitagliptin (Januvia)

A

50-100 mg PO daily, adjust renal

59
Q

Dose Saxagliptin (Onglyza)

A

2.5-5 mg PO once daily

60
Q

Dose of Linagliptin (Tradjenta)

A

5 mg PO daily

61
Q

DPP-4 inhibitors MOA

A

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

62
Q

Place of DPP-4 inhibitors in therapy

A

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

63
Q

DPP-4 inhibitors advantages

A

no hypoglycemia, PO, wt neutrality, well tolerated

64
Q

Disadvantages of DPP-4 inhibitors

A

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

65
Q

Sodium glucose costransporter 2 inhibitors

A

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

66
Q

MOA of SGLT2 inhibitors

A

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

67
Q

place in therapy of SGLT2 inhibitors

A

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

68
Q

Advantages of SGLT2 inhibitors

A

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
Q

Disadvantages of SGLT2 inhiitors

A

avoid CrCl

70
Q

a-Glucosidase inhibitors

A

acarbose (Precose), miglitol (glyset)

71
Q

MOA of a Glucosidase inhibitors

A

inhibits intestinal a glucosidase resulting in slowed carbohydrate digestion and absorption

72
Q

Place in therapy for a glucosidase inhibitors

A

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

73
Q

advantages of a-glucosidase inhibitors

A

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

74
Q

Disadvantages of a-glucosidase inhibitors

A

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

Pharmacology (61 decks)

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