Chapter 13: Diabetes Flashcards Preview

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Flashcards in Chapter 13: Diabetes Deck (119):
1

 

 

Type 1 DM

 

 

2-5% of all cases

induced by auto-immune destruction of pacnreatic cells

2

 

 

Type 2 DM

 

 

90-95% of cases

prevalence varies by ethnicity

strong genetic predisposistion

plasma insulin levels drop as the body develops resistance

3

 

 

oral hypoglycemics

 

sulfonylureas

biquanides

alpha-glucosidase inhibitors

thiazolidines

meglitinides

DPP-4 inhibitors

4

 

 

glucosuria

 

glucose in urine d/t kidney excreting too much

5

 

 

polyuria

 

 

increased urination

6

 

 

polyphasia

 

 

increased appetitie

7

 

 

polydipsia

 

 

increased thirst

8

 

 

poor glycemic control places at a high risk for

 

 

retinopathy

neuropathy

MI

9

 

 

what is treatment for T2DM based on

 

 

HGBA1C results

10

 

 

what medications are obese patients more likely to benefit from and why

 

 

metformin because it acts more on glucose utilization and hepatic glucose storage and production 

11

 

 

which medication do non-obese diabetic patients respond better to

 

 

sulfonylureas

12

 

 

patients who are at risk for hypoglycemia benefit more from which drug and why

 

 

 

metformin because it is less likely to produce it

13

 

 

what do patients with a high postprsndial glucose level beneit most from

 

 

addition of a glucosidase inhibitor or a meglinitidine

14

 

 

steps for treatment of T2DM

 

 

  1. lifestyle intervention and metformin (titrated to maximum effective dose over 1-2 months) 
  2. additional medications
  3. glycemic control (start insulin)

15

 

 

sulfonylureas

mechanism of action

 

  • lowers blood glucose by increasing insulin secretion from pancreatic Bcell
  • decreases glycogenolysis
  • decreases glyconeogenesis
  • increase cell sensitivity to insulin

16

 

 

sulfonylureas clinical uses

 

 

monotherapy an in combination with other drug classes as well as insulin

17

 

 

sulfonylureas should not be used in combination with what

 

 

meglitinides

18

 

 

why is there controversy ove whether sulfonylureas should be as first line therapy for T2DM

 

 

only lowers A1C levels by 1-2%

1st class of drugs used to treat T2DM

19

 

 

conscientious prescribing of sulfonylureas

 

 

start low, go slow, watch for toxicity

mild-mod T2DM responds best

combination therapy is popular

20

 

 

the only sulfonylureas that doe not cause weight gain

 

 

metformin

21

 

 

patient education for sulfonylureas

 

 

take 30-40 minutes before eating and never on an empty stomach

watch for weight gain, GI upset, gas

avoid alcohol and ASA

accu-checks

22

 

 

what medications increase the effects of sulfonylureas

 

 

CYP450 inhibitors

(azoles, NSAIDs, sulfonamides, antidepressants, MAOIs, and digitalis)

23

 

 

what medications may decrease the effects of sulfonylureas

 

 

CYP450 inducers

(phenobarbital, beta blockers, and hydantoins)

24

 

 

sulfonylureas contraindications

 

 

cross-sensitivy to sulfonamides (including thiazide diuretics)

severe renal, hepatic, thyroid, or other endocrine disorders

uncontrolled infection, burns, and trauma

25

 

 

biguanides: Metformin (Glucophage)

 

 

first line therapy

lowers A1C 1-2%

26

 

 

metformin mechanism of action

 

 

reduces hepatic production of glucose and inhibits intestinal absorption of glucose

27

 

 

metformin clinical uses

 

 

monotherapy and in combination with other agents

28

 

 

conscientious considerations for metformin

 

  • decreases LDL, trigs, plasminogen, B12
  • combinations are more effective than monotherapy
  • monitor renal function for ketoacidosis
  • dc if hypoxic or surgery
  • assess for HF, septicemia metabolic acidosis, pregnancy
  • many drug interactions

29

 

 

patient education for metformin

 

take missed dose within an hour of scheduled dose or waite until next scheduled dose

healthy diet, avoid alcohol

regular follow-up is necessary

test for blood glucose and urine ketones

30

 

 

what medications may increase metformin levels

 

 

lasix, nifedipine, cimetidine, cationic drugs (digoxin, amiloride, procainamide, quinidine, ranitidine, trimethoprim, vancomycin, triamterene, morphine)

31

 

 

what medications increase hyperglycemia risk when taken with metformin

 

thiazides and other diuretics, corticosteroids, phenothiazines, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, CCBs, and isoniazid

32

 

 

what can cause hypoglycemia when taken with metformin

 

 

alcohol

excess alcohol can increase risk for lactic acidosis

33

 

 

metformin contraindications

 

 

those at increased risk for lactic acidosis d/t renal impairment

hepatic dysfunction, HF, metabolic acidosis, dehydration, alcoholism

34

 

 

Meglitinides: secretagogues

mechanism of action

 

 

close ATP-dependent potassium channels in the beta cell membrane by binding at specific receptor sites causing insulin release

lowers A1C by 0.6-1%

35

 

 

examples of meglitinides

 

 

repaglinide (Prandin)

nateglinide (Starlix)

36

 

 

why must meglitinides be adminstered more often than sulfonylureas

 

 

they have a shorter half-life

37

 

 

meglitinides clinical usage

 

 

postprandial hyperglycemia

38

 

 

which meglitinide is almost as effective as metformin

 

 

repaglinide

39

 

 

meglitinide dosages are based on

 

 

A1C levels

40

 

 

meglitinide therapy

 

 

monotherapy has better long term effects

may need adjunct insulin in times of stress

41

 

 

what medications may lead to increased serum concentrations of meglitinides resulting in hypoglycemia

 

gemfibrozil, macrolide antibiotics, many herbals (St. John's wort, ethanol, garlic), any drug affected by the CYP450 system

42

 

 

meglitinides contraindications

 

 

hepatic impairment

43

 

 

meglitinide patient education

 

 

take with meals 2-4 times a day

watch for weight gain and hypoglycemia

44

 

 

thiazolidinediones (TZDs) mechanism of action

 

 

increase sensitivity of muscle, fat, and liver to endogenous and exogenous insulin

improves cellular response to insulin without increasing output of insulin from the pancreas

45

 

 

benefits of TZDs

 

 

do not produce hypoglycemia in diabetic or nondiabetic patients

46

 

 

most common adverse effects of TZDs

 

 

weight gain, fluid retention

47

 

 

clinical use of TZD

 

 

indicated as monotherapy and in combination with metformin, sulfonylureas, and insulin

 

 

48

 

 

TZD patient education

 

 

 

 

increased risk for HF

49

 

 

what should be monitored when on TZDs

 

LFTs (closely for 1st year d/t risk of hepatotoxicity)

edema, cytopenia HDL, trigs

50

 

 

TZDs with oral contraceptives

 

 

ovulation may resume

51

 

 

TZD medication interactions

 

 

phenobarbital, amiodarone, rifampim, fluconazole, medications metabolized by CYP450 system (carbamazepine, cyclosporine, felodipine, and some oral contraceptives)

52

 

 

TZD contraindications

 

 

CHF

hepatic impairment

53

 

 

alpha-glucosidase inhibitors

mechanism of action

 

 

reduce rate of digestion of polysaccharides in the proximal small intestine by lowering postpradnial glucose levels without causing hypoglycemia

(reduces A1C by approx 1%)

54

 

 

common side effects of alpha-glucosidase inhibitors

 

 

increased gas and GI symptoms

55

 

 

examples of alpha-glucosidase inhibitors

 

 

acarbose

miglitol

56

 

 

alpha-glucosidase inhibitors as monotherapy

 

 

seldom gives satisfactory results

57

 

 

conscientious prescribing for alpha-glucosidase inhibitors

 

 

start low, go slow

increase dose slowly over several weeks in increments of 2.5mg to minimize GI upset

58

 

 

Patients who show signs of hypoglycemia while being treated with alph-glucosidase inhibitors

 

 

treat with glucose not sucrose

59

 

 

why is periodic LFTs indicated with acarbose

 

 

has been associated with raised liver enzymes

60

 

 

what should be monitored for with alpha-glucosidase inhibitor therapy

GI/GU

 

 

diabetic ketoacidosis, IBD, colonic ulceration, partial intestinal obstruction, chronic intestinal disease, renal function, pregnancy statius

61

 

 

is insulin needed with alpha-glucosidase inhibitor therapy

 

 

occasionally adjunct in time of stress

62

 

 

alpha-glucosidase inhibitor patient education

 

 

diet/exercise

side effects

follow-up

dosage may need adjustment during stress

63

 

 

miglitol interactions

 

 

may decrease absorption of digoxin, propranolol, and ranitidine

64

 

 

acarbose interactions

 

 

may decrease effects of digoxin, thiazide diuretics, thyroids, estrogens, oral contraceptives, and CCBs

65

 

 

alpha-glucosidase inhibitor contraindications

 

IBD

GI obstruction

colonic ulceration

cirrhosis

malabsorption syndrome

66

 

 

what is the only drug in the amylin analogue class and what is its make-up

 

 

pramlintide (Symlin)

synthetic analogue of human amylin

67

 

 

amylin analogue mechanism of action

 

 

neuroendocrine action that regulates glucose influx, including glucagon suppression, slowing of gastric emptying, and a potential effect on feeding behavior and weight control

68

 

 

clinical uses for amylin analogue

 

 

adjunct treatment in patient with either type DM who have not achieved desired insulin control despite optimal insulin therapy

with or without sulfonylureas and/or metformin in T2DM

69

 

 

amylin analogue conscientious prescribing

 

 

adjust dose after owering insulin dose

 

70

 

 

what tests are used to assess health in patients taking amylin analogues

 

 

FPG, HGBA1C, renal function, LFT, CBC

71

 

 

what should be adusted prior to begining therapy with amylin analogues

 

 

 

 

reduce insulin dose by 50% and monitor BG frequently

72

 

 

amylin analogue patient education

 

carry fast-acting sugar at all times

DO NOT mix with insulin (sepatate injections)

administer immediately prior to major meals

should be able to reduce insulin dose by 1/2

will need to frequently monitor BG

73

 

 

black box warning for amylin analogue

 

use with insulin

insulin induced severe hypoglycemia can occur within 3 hours of injection

74

 

 

amylin analogue interactions

 

 

do not administer with medications that alter GI motility or slow intestinal absorption

(anticholinergic agents like atropine or alpha-glucosidase inhibitors)

75

 

 

amylin analogue and analgesics

 

 

administer analgesics and other oral agents that require rapid onset 1 hour before or 2 hours after injection

76

 

 

amylin analogue contraindications

 

 

hypoglycemia unawareness

gastroparesis

77

 

 

glucagon-like peptide-1 (GLP-1) agonists

drug namess

 

 

exenatide (Byetta)

78

 

 

GLP-1 agonists

mechanism of action

 

 

analogue of the hormone incretin, which increases insulin secretion

high frequency of GI side effects

79

 

 

clinical uses of GLP-1 agonists

 

 

combination therapy only

for patients with T2DM that have not achieved glycemic control using metformin, a sulfonylurea, or both

80

 

 

byetta conscientious prescribing

 

 

not a substitute for insulin

monitor for pancreatitis

assess for T1DM, renal function, GI-paresis, HGBA1C

81

 

 

GLP-1 agonists patient education

 

take within 60 of morning and evening meal

if dose missed resume treatment at next dose

report side effects

keep drug away from light

discard pen after 30 days of first use

82

 

 

GLP-1 agonists and warfarin

 

 

may increase INR and cause bleeding

83

 

 

GLP-1 agonists interactions

 

 

drugs dependant on threshold concentrations for efficacy (contraceptives, antibiotics) should be taken 1 hour before

caution with drugs that require rapid GI absorption

84

 

 

GLP-1 agonists contraindications

 

 

T1DM

treatment of diabetic ketoacidosis

severe renal impairment

severe GI disease

85

 

 

dipeptidyl-peptidase-4 inhibitors (DDP-IV)

mechanism of action

 

 

slows the inactivation of incretin hormones (GLP-1 and gluosce-dependent insulinotropic polypeptide)

intestinal concentrations of these are decreased in T2DM

86

 

 

DDP-IV clinical uses

 

 

approved as monotherapy or in combination with metformin or thiazolidinedione

87

 

 

DDP-IV (Januvia) conscientious prescribing

 

may experience weight loss

watch for skin conditions (Steven's Johnson syndrome)

test for renal function, FPG, HGBA1C, hypoglycemia

88

 

 

DDP-IV patient education

 

 

adjunct to diet and exercise

counsel about adverse effects (nasopharyngitis, headache, URIs)

advise dosing may need adjusted during stress

89

 

 

examples of DDP-IV

 

sitagliptin (Januvia)

saxagliptin (Onglyza)

saxagliptin/metformin (Kombiglyze)

sitagliptin/metformin (Janumet)

90

 

 

DDP-IV interactions

 

 

may increase digoxin levels

may require lower dose of sulfonylurea to reduce risk of hypoglycemia

91

 

 

DDP-IV contraindications

 

 

anaphylaxis

angioedema

92

 

 

glucagon mechanism of action

 

 

increases BG levels 

93

 

 

glucagon clinical uses

 

 

treat severe hypoglycemia

diagnstic aid for radiologic exam of the stomach, duodenum, small bowel, colon

94

 

 

when is glucagon not effective

 

 

states of starvation, adrenal insufficiency, chronic hypoglycemia, insufficient liver glycogen

95

 

 

glucagon contraindication

 

 

pheochromocytoma

96

 

 

what is the oldest available medication to treat T1DM

 

 

injectable insulins

97

 

 

what are injectable insulins ade from

 

 

 

 

derived from beef or prok or synthesized using recombinant DNA technology using strands of E. Coli

98

 

 

four categories of injectable insulins

 

 

regular

protamines

lentes

modifieds

99

 

 

insulin for special populations

 

used for gestational diabetes

less stringent glycemic control set for elderly

children should be referred to pediatric endocrinologist if multiple drugs are needed

100

 

 

why are glycemic controls less stringent for elderly

 

 

increased risk for hypotension and long-term microvascular complications

101

 

types of insulins

 

rapid acting

short acting

intermediate acting

long acting

102

 

 

examples of rapid acting insulins

 

 

aspart (Novolog)

lispro (Humalog)

103

 

 

examples of short acting insulins

 

 

regular insulin (Humalog-R, Humalin-R)

104

 

 

examples of intermediate acting insulins

 

 

NPH

insulin zinc (Humulin N) lente

isophane insulin suspension

105

 

 

examples of long acting insulins

 

 

insuline glargine (Lantus)

insulin detmir (Levimir)

extended zinc (UltraLente)

protomine zinc (PZ)

106

 

 

injectable insulins conscientious prescribing

 

have a plan for starting/maintainingg dosages

may need higher doses for T2DM

dosage adjustments should be step-wie

change regimen if goals not met in 2-3 days

can change from rapid to long acting at largest meal of the day

107

 

 

injectable insulin patient education

 

 

measure BG at least twice daily

 

108

 

 

effect of insulin on glucose cell membrane

 

 

 

acts on the membranes transporters that regulate insulin release and glucose homeostasis

109

 

 

why is it so hard to induce weight loss as part of a diabetes management regien

 

 

total number of insulin receptors acan be downregulated by obesity

110

 

 

insulin and liver

 

 

where glucose increases storage of glucose as glycogen and resets the liver;s catabolic activity after ingesting food

111

 

 

insulin and adipose tissue

 

 

where insulin reduces circulating free fatty acids and promotes storage of triglycerides in adipose tissue

112

 

 

insulin and muscle cell growth

 

 

where insulin promotes protein synthesis by increasing amino acid activity and glycogen synthesis to replace glycogen that has been depleted during work or exercise

113

 

 

general rule of insulin dosing

 

 

0.6-1 unit per kilogram of body weight

114

 

 

lente insulins

 

 

modified by a fish protein which prolongs insulin action

115

 

 

protamine insulin

 

 

modified by zinc moiety which prolongs insulin action

116

 

 

symptoms of diabetic ketoacidosis (DKA)

 

 

drowsiness, dim vision, and labored breathing preceded by a lengthy episode of polyuria, polydipsia, polyphagia, weight loss, vomiting, dehydration, and ketone odor to breath

117

 

 

what is DKA usually the result of

 

 

undue stress, illness, infection, missed insulin

118

 

 

treatment of DKA

 

 

requires hospitalization and correction of acid/base, fluid, and glucose imbalances

119

 

 

drugs that interact with insulin

 

 

page 239