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Pharmacology > Chapter 13: Diabetes > Flashcards

Chapter 13: Diabetes Flashcards

1
Q

Type 1 DM

A

2-5% of all cases

induced by auto-immune destruction of pacnreatic cells

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2
Q

Type 2 DM

A

90-95% of cases

prevalence varies by ethnicity

strong genetic predisposistion

plasma insulin levels drop as the body develops resistance

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3
Q

oral hypoglycemics

A

sulfonylureas

biquanides

alpha-glucosidase inhibitors

thiazolidines

meglitinides

DPP-4 inhibitors

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4
Q

glucosuria

A

glucose in urine d/t kidney excreting too much

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5
Q

polyuria

A

increased urination

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6
Q

polyphasia

A

increased appetitie

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7
Q

polydipsia

A

increased thirst

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8
Q

poor glycemic control places at a high risk for

A

retinopathy

neuropathy

MI

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9
Q

what is treatment for T2DM based on

A

HGBA1C results

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10
Q

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

A

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

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11
Q

which medication do non-obese diabetic patients respond better to

A

sulfonylureas

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12
Q

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

A

metformin because it is less likely to produce it

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13
Q

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

A

addition of a glucosidase inhibitor or a meglinitidine

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14
Q

steps for treatment of T2DM

A
  1. lifestyle intervention and metformin (titrated to maximum effective dose over 1-2 months)
  2. additional medications
  3. glycemic control (start insulin)
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15
Q

sulfonylureas

mechanism of action

A
  • lowers blood glucose by increasing insulin secretion from pancreatic Bcell
  • decreases glycogenolysis
  • decreases glyconeogenesis
  • increase cell sensitivity to insulin
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16
Q

sulfonylureas clinical uses

A

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

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17
Q

sulfonylureas should not be used in combination with what

A

meglitinides

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18
Q

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

A

only lowers A1C levels by 1-2%

1st class of drugs used to treat T2DM

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19
Q

conscientious prescribing of sulfonylureas

A

start low, go slow, watch for toxicity

mild-mod T2DM responds best

combination therapy is popular

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20
Q

the only sulfonylureas that doe not cause weight gain

A

metformin

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21
Q

patient education for sulfonylureas

A

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

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22
Q

what medications increase the effects of sulfonylureas

A

CYP450 inhibitors

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

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23
Q

what medications may decrease the effects of sulfonylureas

A

CYP450 inducers

(phenobarbital, beta blockers, and hydantoins)

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24
Q

sulfonylureas contraindications

A

cross-sensitivy to sulfonamides (including thiazide diuretics)

severe renal, hepatic, thyroid, or other endocrine disorders

uncontrolled infection, burns, and trauma

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25
Q

biguanides: Metformin (Glucophage)

A

first line therapy

lowers A1C 1-2%

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26
Q

metformin mechanism of action

A

reduces hepatic production of glucose and inhibits intestinal absorption of glucose

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27
Q

metformin clinical uses

A

monotherapy and in combination with other agents

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28
Q

conscientious considerations for metformin

A
  • 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
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29
Q

patient education for metformin

A

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

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30
Q

what medications may increase metformin levels

A

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

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31
Q

what medications increase hyperglycemia risk when taken with metformin

A

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

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32
Q

what can cause hypoglycemia when taken with metformin

A

alcohol

excess alcohol can increase risk for lactic acidosis

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33
Q

metformin contraindications

A

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

hepatic dysfunction, HF, metabolic acidosis, dehydration, alcoholism

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34
Q

Meglitinides: secretagogues

mechanism of action

A

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%

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35
Q

examples of meglitinides

A

repaglinide (Prandin)

nateglinide (Starlix)

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36
Q

why must meglitinides be adminstered more often than sulfonylureas

A

they have a shorter half-life

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37
Q

meglitinides clinical usage

A

postprandial hyperglycemia

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38
Q

which meglitinide is almost as effective as metformin

A

repaglinide

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39
Q

meglitinide dosages are based on

A

A1C levels

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40
Q

meglitinide therapy

A

monotherapy has better long term effects

may need adjunct insulin in times of stress

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41
Q

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

A

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

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42
Q

meglitinides contraindications

A

hepatic impairment

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43
Q

meglitinide patient education

A

take with meals 2-4 times a day

watch for weight gain and hypoglycemia

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44
Q

thiazolidinediones (TZDs) mechanism of action

A

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

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45
Q

benefits of TZDs

A

do not produce hypoglycemia in diabetic or nondiabetic patients

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46
Q

most common adverse effects of TZDs

A

weight gain, fluid retention

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47
Q

clinical use of TZD

A

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

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48
Q

TZD patient education

A

increased risk for HF

49
Q

what should be monitored when on TZDs

A

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

edema, cytopenia HDL, trigs

50
Q

TZDs with oral contraceptives

A

ovulation may resume

51
Q

TZD medication interactions

A

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

52
Q

TZD contraindications

A

CHF

hepatic impairment

53
Q

alpha-glucosidase inhibitors

mechanism of action

A

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
Q

common side effects of alpha-glucosidase inhibitors

A

increased gas and GI symptoms

55
Q

examples of alpha-glucosidase inhibitors

A

acarbose

miglitol

56
Q

alpha-glucosidase inhibitors as monotherapy

A

seldom gives satisfactory results

57
Q

conscientious prescribing for alpha-glucosidase inhibitors

A

start low, go slow

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

58
Q

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

A

treat with glucose not sucrose

59
Q

why is periodic LFTs indicated with acarbose

A

has been associated with raised liver enzymes

60
Q

what should be monitored for with alpha-glucosidase inhibitor therapy

GI/GU

A

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

61
Q

is insulin needed with alpha-glucosidase inhibitor therapy

A

occasionally adjunct in time of stress

62
Q

alpha-glucosidase inhibitor patient education

A

diet/exercise

side effects

follow-up

dosage may need adjustment during stress

63
Q

miglitol interactions

A

may decrease absorption of digoxin, propranolol, and ranitidine

64
Q

acarbose interactions

A

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

65
Q

alpha-glucosidase inhibitor contraindications

A

IBD

GI obstruction

colonic ulceration

cirrhosis

malabsorption syndrome

66
Q

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

A

pramlintide (Symlin)

synthetic analogue of human amylin

67
Q

amylin analogue mechanism of action

A

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

68
Q

clinical uses for amylin analogue

A

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
Q

amylin analogue conscientious prescribing

A

adjust dose after owering insulin dose

70
Q

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

A

FPG, HGBA1C, renal function, LFT, CBC

71
Q

what should be adusted prior to begining therapy with amylin analogues

A

reduce insulin dose by 50% and monitor BG frequently

72
Q

amylin analogue patient education

A

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
Q

black box warning for amylin analogue

A

use with insulin

insulin induced severe hypoglycemia can occur within 3 hours of injection

74
Q

amylin analogue interactions

A

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

(anticholinergic agents like atropine or alpha-glucosidase inhibitors)

75
Q

amylin analogue and analgesics

A

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

76
Q

amylin analogue contraindications

A

hypoglycemia unawareness

gastroparesis

77
Q

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

drug namess

A

exenatide (Byetta)

78
Q

GLP-1 agonists

mechanism of action

A

analogue of the hormone incretin, which increases insulin secretion

high frequency of GI side effects

79
Q

clinical uses of GLP-1 agonists

A

combination therapy only

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

80
Q

byetta conscientious prescribing

A

not a substitute for insulin

monitor for pancreatitis

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

81
Q

GLP-1 agonists patient education

A

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
Q

GLP-1 agonists and warfarin

A

may increase INR and cause bleeding

83
Q

GLP-1 agonists interactions

A

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

caution with drugs that require rapid GI absorption

84
Q

GLP-1 agonists contraindications

A

T1DM

treatment of diabetic ketoacidosis

severe renal impairment

severe GI disease

85
Q

dipeptidyl-peptidase-4 inhibitors (DDP-IV)

mechanism of action

A

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

intestinal concentrations of these are decreased in T2DM

86
Q

DDP-IV clinical uses

A

approved as monotherapy or in combination with metformin or thiazolidinedione

87
Q

DDP-IV (Januvia) conscientious prescribing

A

may experience weight loss

watch for skin conditions (Steven’s Johnson syndrome)

test for renal function, FPG, HGBA1C, hypoglycemia

88
Q

DDP-IV patient education

A

adjunct to diet and exercise

counsel about adverse effects (nasopharyngitis, headache, URIs)

advise dosing may need adjusted during stress

89
Q

examples of DDP-IV

A

sitagliptin (Januvia)

saxagliptin (Onglyza)

saxagliptin/metformin (Kombiglyze)

sitagliptin/metformin (Janumet)

90
Q

DDP-IV interactions

A

may increase digoxin levels

may require lower dose of sulfonylurea to reduce risk of hypoglycemia

91
Q

DDP-IV contraindications

A

anaphylaxis

angioedema

92
Q

glucagon mechanism of action

A

increases BG levels

93
Q

glucagon clinical uses

A

treat severe hypoglycemia

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

94
Q

when is glucagon not effective

A

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

95
Q

glucagon contraindication

A

pheochromocytoma

96
Q

what is the oldest available medication to treat T1DM

A

injectable insulins

97
Q

what are injectable insulins ade from

A

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

98
Q

four categories of injectable insulins

A

regular

protamines

lentes

modifieds

99
Q

insulin for special populations

A

used for gestational diabetes

less stringent glycemic control set for elderly

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

100
Q

why are glycemic controls less stringent for elderly

A

increased risk for hypotension and long-term microvascular complications

101
Q

types of insulins

A

rapid acting

short acting

intermediate acting

long acting

102
Q

examples of rapid acting insulins

A

aspart (Novolog)

lispro (Humalog)

103
Q

examples of short acting insulins

A

regular insulin (Humalog-R, Humalin-R)

104
Q

examples of intermediate acting insulins

A

NPH

insulin zinc (Humulin N) lente

isophane insulin suspension

105
Q

examples of long acting insulins

A

insuline glargine (Lantus)

insulin detmir (Levimir)

extended zinc (UltraLente)

protomine zinc (PZ)

106
Q

injectable insulins conscientious prescribing

A

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
Q

injectable insulin patient education

A

measure BG at least twice daily

108
Q

effect of insulin on glucose cell membrane

A

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

109
Q

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

A

total number of insulin receptors acan be downregulated by obesity

110
Q

insulin and liver

A

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

111
Q

insulin and adipose tissue

A

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

112
Q

insulin and muscle cell growth

A

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
Q

general rule of insulin dosing

A

0.6-1 unit per kilogram of body weight

114
Q

lente insulins

A

modified by a fish protein which prolongs insulin action

115
Q

protamine insulin

A

modified by zinc moiety which prolongs insulin action

116
Q

symptoms of diabetic ketoacidosis (DKA)

A

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
Q

what is DKA usually the result of

A

undue stress, illness, infection, missed insulin

118
Q

treatment of DKA

A

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

119
Q

drugs that interact with insulin

A

page 239

Pharmacology (28 decks)

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