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*OldPharm > Diabetes Type 2 > Flashcards

Diabetes Type 2 Flashcards

1
Q

released from distal ileum and colon in response to food containing carbs and fats

A

GLP-1 (glucagon-like peptide)

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2
Q

T2DM Patients have a loss of what?

A

first phase insulin response

loss of amylin

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3
Q

a fasting plasma glucose of greater than what is considered a diagnosis of DM?

A

FPG>126

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4
Q

what is an impaired fasting glucose (IFG) “pre diabetes”

A

100-125

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5
Q

what is an impaired glucose tolerance test (2 hour post-load glucose)

A

140-199

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6
Q

who should be screened for DM?

A

any patient BMI >25

age >45 (no risk factors) and repeat every 3 years

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7
Q

what children should be screened for T2DM?

A 
BMI>85th percentile Plus 2 of the following
Family hx
ethnicity associated w/ risk
signs of insulin resistance
maternal hx or gestational DM
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8
Q

what is involved w/ Polycystic ovarian syndrome

A 
Hyperandrogenism
Hirsutism
Menstrual irregularities
Obesity 
infertility
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9
Q

condition w/ excess growth hormone

A

acromegaly

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10
Q

condition w/ excessive corticosteroids

A

cushing’s syndrome

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11
Q

what are microvascular complications of DM?

A

Retinopathy
Nephropathy
Neuropathy

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12
Q

what are macrovascular complications of DM?

A

Atherosclerotic Cardiovascular diagnosis

Dyslipidemia

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13
Q

what is the A1C goal for people w/ T2DM?

A

<7.0%

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14
Q

what can patients who have IGT or IFG do you prevent progression of DM?

A

weight loss <7%) and increase physical activity

14 grams dietary fiber/ 1000 kcals

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15
Q

what are complications w/ gestational DM?

A

maternal morbidity
fetal macrosomia
higher rate of pre-eclampsia
mother at risk for developing T2DM later

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16
Q

risk factors for GDM?

A 
severely obese
previous GDM or large infant
presence of glycosuria
diagnosis of PCOS
strong family hx
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17
Q

when are women screened for GDM?

A

at 24-26 weeks gestation

do an OGTT

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18
Q

women with GDM should be screened for DMT2 when?

A

6-12 weeks postpartum

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19
Q

what is the cornerstone of management of T2DM?

A

diet (>7% weight loss) and exercise (150 min/wk minimum)

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20
Q

what other changes changes can help someone w/ T2DM lower CV risk

A

Smoking cessation
Lipid management
Blood Pressure control
Antiplatelet therapy

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21
Q

patient on oral meds for glucose control use SMBG to do what?

A

help them achieve their glycemia goals

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22
Q

when should A1C be taken for someone at goal?

A

twice a yaer

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23
Q

when should A1C be checking for someone not at goal?

A

every 3 months

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24
Q

what drugs class has the MOA of “Direct stimulation of insulin release from viable pancreatic beta-cells thus reducing blood glucose levels (↑ insulin secretion)”

A

sulfonylureas

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25
Q

at high doses what do sulfonylureas do?

A

decrease hepatic glucose production (decrease levels of glucagon)

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26
Q

how much do sulonylureas decrease A1C by?

A

1.5%

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27
Q

why are 1st generation sulfonylureas not used?

A

resulted in hypoglycemia

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28
Q

what are the names of the 2nd generation sulfonylureas

A

Glyburide
Glipizide
Glimepride

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29
Q

what type DM can’t you use sulfonylureas in?

A

GDM

T1DM

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30
Q

ADRs of sulfonylureas?

A

Hypoglycemia (elderly, hepatic or renal impairment)

weight gain

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31
Q

when should glyburide be administered?

A

Administer with breakfast or first main meal

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32
Q

what sulfonylureas has the greatest risk of hypoglycemia due to longer 1/2 life and no recommended with CrCl<50
not a first line agent

A

Glyburide

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33
Q

sulfonylurea that is administered 30 minutes before first main meal and not recommended with CrCl<10

A

glipizide

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34
Q

sulfonylureas that you Administer with first main meal

Not recommended if CrCl < 22 ml/min

A

glimepiride

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35
Q

when is there reduced GI absorption w/ sulonylureas

A

Reduced GI absorption if blood glucose > 250 mg/dL

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36
Q

when do you monitor FPG w/ sulfonylureas

A

in 2 weeks

A1C in 3 months

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37
Q

contraindications w/ sulfonylureas

A

sulfa allergy
avoid with ETOH
pregnant

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38
Q

drug interactions w/ sulfonylureas

A 
Sulfonamide antibacterials
Propranolol
Salicylates
Phenylbutazone
ETOH
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39
Q

oral diabetic med that Stimulate insulin release from pancreatic beta-cells
Shorter half life than sulfonylureas
Rapid release of insulin that only lasts 1-2 hours

A

meglitinides

40
Q

when do you take meglitinides?

A

with meals

targetes postprandial glucose levels

41
Q

what are the 2 meglitinides?

A

repaglinide

nateglinide

42
Q

meglitinide that is Approved for monotherapy or in combination w/metformin.
Taken before meals 3 X/day
Allergy to sulfas not an issue
ADR hypoglycemia

A

repaglinide

43
Q

meglitinide that is Phenylalanine derivative
Faster onset of action and shorter duration of action than repaglinide; less A1C reduction than repaglinide
Approved for monotherapy an combination w/metformin.
Taken 3X/d before meals

A

nateglinide

44
Q

adrs w/ meglitinides?

A

hypoglycemia

weight gain

45
Q

monitoring w/ meglitinides

A

FPG at 2 weeks
Postprandial glucose at initiation
A1C at 3 months

46
Q

DOC for treatment of T2DM

47
Q

MOA of metformin

A

Does not affect insulin secretion but requires the presence of insulin to be effective.
decreases production of hepatic glucose production.
decreases intestinal glucose absorption.
increases peripheral glucose uptake.
increases insulin sensitivity

48
Q

what type patient does metformin work best in?

A

patients w/ significant hyperglycemia

49
Q

ADRs w/ metformin

A 
GI symptoms (decrease if taken w/ food)
lactic acidosis (increase w/ renal failure, CHF, hypoxemia, ETOH)
50
Q

monitoring for metformin

A

SCr at baseline
FPG at 2 weeks
A1C at 3 months

51
Q

worst side effect w/ metformin

A

lactic acidosis

52
Q

contraindications w/ metformin

A

SCr >1.5 in men and 1.4 in women

acute or chronic metabolic acidosis

53
Q

precautions to use w/ metformin

A 
radiocontrast studies
Age >80 (unless normal GFR)
hypoxic states
liver dysfunction
alcoholism
heart failure requiring pharmacologic tx
54
Q

benefits of metformin

A

No weight gain
No hypoglycemia as monotherapy
Inexpensive
Approved for use as monotherapy and in combination with other therapy

55
Q

what are 2 thiazolidinediones (TZDs) (Insulin sensitizers)

A

rosiglitazone and pioglitazone

56
Q

how much do TZDs decrease A1C?

A

0.5%-1.4% (May take 4 weeks for effect)

57
Q

what is required for TZD action?

A

endogenous insulin

58
Q

beneficial CV effects w/ pioglitazone

A

increased HDL

decreased triglycerides

59
Q

with rosiglitazone what CV benefits are there?

A 
increase LDL (not beneficial)
but increase HDL
60
Q

ADRs w/ TZDs

A

fluid retention
weight gain
redistribution of adipose tissue
new onset heart failure (higher when combined w/ insulin)

61
Q

Contraindications w/ TZDs

A

alcohol abuse
elevated liver enzymes (D/C if LFTs elevated 2-3 times ULN)
Hf NYHA class III or IV

62
Q

BBW and TZDs

A

increased risk of CHF and MI risk

63
Q

what drugs Delays intestinal carbohydrate absorption
Inhibits alpha-glucosidase found in the small intestinal brush border
Prevent glucose absorption and  post-prandial glucose levels

A

alpha-glucosidase inhibitors

64
Q

what are 2 alpha-glucosidase inhibitors

A

acarbose

miglitol

65
Q

how much do alpha-glucosidase inhibitors decrease A1C by?

A

A1C 0.5-0.8%

66
Q

ADRs of alpha-glucosidase inhibitors

A

loose stools

flatulence

67
Q

monitoring w/ alpha-glucosidase inhibitors

A

Post prandial glucose at initiation

A1C in 3 months

68
Q

contraindications w/ Alpha-Glucosidase Inhibitors

A

Chronic intestinal disease

Cirrhosis

69
Q

what drug class Prevent degradation of endogenous glucagon-like peptide-1 (GLP-1) and insulinotropic polypeptide (GIP)
Incretin hormones released in response to meal
Increase insulin synthesis and release from beta cells
Intracellular signaling
GLP-1 also lowers glucagon secretion from pancreatic alpha cells

A

Dipeptidyl peptidase-4 (DPP-4) inhibitor

70
Q

what drugs are Dipeptidyl peptidase-4 (DPP-4) inhibitors

A

Sitagliptin (Januvia®)

Saxagliptin (Onglyza)

71
Q

how much do Dipeptidyl peptidase-4 (DPP-4) inhibitors decrase A1C

A

A1C 0.5-0.7%

72
Q

benefits for DPP-4 inhibitors

A

weight neutral
approved for monotherapy or combo
weight neutral

73
Q

Bile acid sequestrant: received FDA indication in January 2008 for Type 2 diabetes as an adjunct to diet and exercise
previously approved for LDL reduction

A

Colesevelam (WelChol)

74
Q

efficacy of Colesevelam (WelChol)

A

0.4-0.8% A1C decrease

75
Q

has Colesevelam (WelChol) been studied as monotherapy

76
Q

ADRs of Colesevelam (WelChol)

A

constipation/ nausea/ indigestion

increase triglycerides

77
Q

Contraindications w/ Colesevelam (WelChol)

A

Bowel obstruction
History of hypertriglyceridemia-induced pancreatitis
Triglycerides >500 mg/dL

78
Q

what is a glucagon-like peptide peptide 1 (GLP-1) agonist?

A

exenatide (byetta)

79
Q

what is the efficacy of exenatide?

A

decrease A1c by 0.5-1%

80
Q

what is exenatide FDA approved for?

A

T2DM in patients on metformin, sulfonylurea, TZD or a combo who aren’t at goal

81
Q

is exenatide approved with use for basal insulin?

82
Q

ADRs w/ exenatide

A

N/V/D
modest weight loss
anti-exenatide antibodies

83
Q

what ADR can exenatide cause w/ espeically sulonylureas

A

hypoglycemia

84
Q

what monitoring needs to be done w/ exenatide?

A

renal function

A1C in 3 months

85
Q

contraindications w/ exenatide?

86
Q

precautions w/ exenatide

A

ClCr <30 (changes dose)
gastroparesis
hypoglycemia

87
Q

SubQ injection that is FDA approved for Type 1 or 2 diabetes in patients on optimal insulin therapy who are still not at goal
With or without metformin and/or sulfonylurea therapy

A

pramlintide

88
Q

what is pramlintide administered in conjuction w/?

A

mealtime insulin

89
Q

additional med for people with CHD and DM?

A

81 mg aspirin

90
Q

what are the first lines for HTN for people w/ DM?

A

ACEI or ARB in combo w/ thiazide diuretic

91
Q

what is the goal BP for a diabetic patient?

92
Q

if a DM patients is over the age of 40 w/ a risk factor or overt CVD what should be added?

93
Q

if a statin isn’t tolerated what should a DM be placed on as well?

A

BAR (bile acid resin)
niacin
fibrate

94
Q

is a life threatening condition similar to DKA
Extreme hyperglycemia and fluid deficits
Arises from inadequate insulin but occurs primarily in older type II patients

A

hyperosmolar hyperglycemic state (HHS)

95
Q

what is the different between hyperosmolar hyperglycemic states (HHS) and DKA?

A

HHS lacks lipolysis, ketonemia, and acidosis

96
Q

Diagnostic criteria for hyperosmolar hyperglycemic states (HHS)

A

Plasma glucose > 600mg/dL

Serum osmolality of > 320 mOsm/kg

97
Q

Tx for hyperosmolar hyperglycemic states (HHS)

A

Rehydration
Correction of electrolyte imbalances
Continuous insulin infusion
Reduce blood glucose levels gradually to avoid cerebral edema

*OldPharm (12 decks)

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