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Pharm > Endocrine: DM > Flashcards

Endocrine: DM Flashcards

1
Q

T1 DM

A

cellular mediated beta cell destruction

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2
Q

T2 DM

A

insulin resistance in muscle and liver

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3
Q

maturity onset DM of the young

A

genetic disorder: impaired secretion of insulin

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4
Q

gestational DM

A

15% of pregnancies

common in 3rd tri

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5
Q

pre-diabetic

A

impaired glucose tolerance/fasting glucose

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6
Q

drug induced DM can be caused by which drugs?

A

glucocorticoids
protease inhibitors
atypical antipsychotics

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7
Q

screening for t1 DM is done why

A

if someone has relatives with T1

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8
Q

how is T1 DM screened for?

A

by measuring islet abs

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9
Q

T2 diabetes screening happens when

A

at age 45, q3 years

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10
Q

T2 Diabetes screening happens at what weight?

A

> 25kg/m2

>23kg/m2 for Asians

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11
Q

t2 dm may be seen with

A 
CVD
PCOS
HDL < 35 
TG > 250
HTN
physical inactivity
severe obesity
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12
Q

gestational DM screening

A

screen at 1st prenatal visit and again at 24-28 weeks with OGTT

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13
Q

if diagnosis of gestational DM is made,

A

screen for diabetes 4-12wks after delivery.

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14
Q

fasting plasma glucose in diabetes

A

> 126

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15
Q

random plasma glucose in diabetes

A

> 200

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16
Q

OGTT

A

administer 75g of glucose, obtain plasma glucose in 2 hours. if >200 and symptoms of hyperglycemia, diagnosis can be made.

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17
Q

A1C in diabetes

A

> 6.5%

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18
Q

one step OGTT

A

75g at 24-28 wks
fasting: >92
after 1 hr: >180
after 2 hr: >153

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19
Q

two step OGTT

A

50g at 24-28 weeks
after 1 hr if glucose < 140, no need for further workup
if >140, perform another OGTT using 100g.

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20
Q

microvascular complications of DM

A

retinopathy
neuropathy
nephropathy

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21
Q

glycemic goals of therapy:

A1C

A

<7%

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22
Q

glycemic goals of therapy:

preprandial:

A

70-130

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23
Q

glycemic goals of therapy:

postprandial

A

<180

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24
Q

BP mgmt for pt with DM

A

keep < 140/90

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25
Q

lipid mgmt for pt c DM

A

no specific LDL goal, use ACC/AHA guidelines.

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26
Q

T1 DM

insulin pump

A

hourly basal and bolus dosing
rapid acting insulins
requires patient education and carb counseling.

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27
Q

neurotransmitter dysfunction in DM

meds (3)

A

GLP1 receptor agonists
amylin
bronocriptine

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28
Q

increased lipolysis and reduced glucose uptake

meds

A

thiazolidinediones

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29
Q

dec glucose uptake meds

A

metformin
insulin
thiazolidinediones

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30
Q

decrease incretin effect

meds

A

metformin
alpha glucosidase inhibitors
colesevelam

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31
Q

increased hepatic glucose production:

meds

A

metformin
insulin
thiazolidinediones

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32
Q

increased glucagon secretion

meds

A

GLP1 receptor agonists
DPP 4 inhibitors
Amylin

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33
Q

impaired insulin secretion

meds

A

sulfonylurea
meglitinide
GLP1 receptor agonists
DPP 4 inhibitors

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34
Q

mono therapy DM

A

metformin
-high efficacy
-no risk hypoglycemia
weight neutral/loss

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35
Q

AE metformin

A

GI

lactic acidosis

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36
Q

dual therapy: DM

metformin PLUS

A

either

sulfonylurea, thiazolidinedione, DPP4 inhibitor, SGL2 inhibitor, GLP1 receptor agonist, or insulin

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37
Q

metformin plus sulfonylurea

A

high efficacy
moderate risk hypoglycemia
weight: gain
cost:low

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38
Q

dual therapies with highest efficacy and lowest costs

A

metformin+sulfo

metformin+thiazo

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39
Q

highest risk dual therapy for hypoglycemia

A

metformin and insulin

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40
Q

combination injectable therapy for DM

A

basal insulin + mealtime insulin + GLP-1RA

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41
Q

GLP1 receptor agonists

A

high cost

high efficacy

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42
Q

highest costing dual therapies

A

DPP4 inhibitor
SGLT2 inhibitor
GLP1 RA

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43
Q

highest efficacy dual therapy

A

sulfo
thiazo
GLP1 RA
insulin*

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44
Q

T2 DM pharmacotherapy

first line

A

metformin

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45
Q

DPP4 inhibitors

A

dipeptidyl peptidase 4 inhibitor

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46
Q

SGLT2

A

sodium glucose cotransporter 2 inhibitors

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47
Q

GLP1 agonists

A

glucose like peptide 1 agonists

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48
Q

diabetic pts should be started on insulin for the following parameters

A

A1C > 10%

glucose >300-350

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49
Q

MoA metformin:

A

reduces hepatic gluconeogenesis and can inc insulin sensitivity. can also inc uptake of glucose from blood into other tissues.

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50
Q

A1c reduction c metformin

A

1-2%

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51
Q

blackbox warning for metformin

A

lactic acidosis

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52
Q

dosing for metformin is based on

A

GFR

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53
Q

metformin is CI in

A

acute or chronic metabolic acidosis

GFR <30

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54
Q

onset and full effect of metformin

A

onset: days

full effect: 2 weeks

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55
Q

metabolism of metformin

A

not hepatic

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56
Q

elimination of metformin

A

urine, 90% unchanged.

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57
Q

dosing of metformin

A

500-100mg BID

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58
Q

max dose of metformin

A

2550 mg/day

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59
Q

metformin and IV contrast

A

avoid administration within 48 hr of contrast

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60
Q

pregnancy category of metformin

A

B

61
Q

sulfonylurea examples

A

glipizide
glimepride
glyburide

62
Q

A1c reduction of sulfonylureas

A

1-2%

63
Q

MoA sulfonylurea

A

binds to receptors on pancreatic beta cells which causes the K channel to close so that K cannot leave the cell - which causes depo of the membrane. there is then an influx of calcium which stimulates insulin secretion

64
Q

AE sulfos

A

hypoglycemia

weight gain

65
Q

CI to sulfos

A

hypersensitivity to sulfonamides

poor renal function

66
Q

pt edu for sulfos

A

take c food

67
Q

protein binding of sulfos

A

high

>95%

68
Q

onset of sulfo

A

Reduces blood glucose within hours

69
Q

elimination of sulfos

A

hepatic

70
Q

monitoring for sulfos

A

fasting BG
A1C
s/s hypoglycemia

71
Q

CI sulfos

A

hepatic insufficiency

renal failure

72
Q

meglitinides A1C reduction

A

.5 - 1.5%

73
Q

meglitinide meds

A

repaglinide

nateglinide

74
Q

MoA of meglitinides

A

similar to sulfos but faster

75
Q

AEs of meglitinides

A

hypoglycemia
weight gain
URI

76
Q

CI c meglitinides

A

hypersensitivity

use of gemfibrozil

77
Q

thiazos examples

A

pioglitazone

rosiglitazone

78
Q

MoA thiazos

A

decrease plasma glucose by increasing insulin sensitivity of adipose tissue, skeletal muscle, and the liver.

79
Q

primary site of action of thiazos

A

adipose tissue

80
Q

what receptor does thiazo bind to?

A

PPARy

81
Q

thiazo A1C reduction

A

0.5 - 1.4 %

82
Q

onset of thiazos

A

1-3 months

83
Q

AE of thiazos

A 
weight gain
edema
CHF exacerbation
inc risk fractures in women
myalgia
headache
macular edema
inc LFT
84
Q

protein binding of thiazo

A

high

>99%

85
Q

Thiazo excretion

A

urine and feces as metabolites

86
Q

CI c thiazos

A

NYHA class 3-4 of HF at initiation of therapy

87
Q

thiazo monitoring

A 
BG 
A1c
LFT
s/s HF
bone health
88
Q

DPP4 inhibitors examples

A

sitagliptin
saxagliptin
linagliptin
alogliptin

89
Q

DPP4 A1c reduction

A

0.5 - 0.8%

90
Q

MoA DPP4

A

inhibits breakdown of GLP1 during meals thus increasing insulin secretion, reducing glucagon secretion, and promoting satiety.

91
Q

DPP4 inhibitors on fasting blood glucose

A

low impact

92
Q

side effect profile for DPP4 inhibitors

A

minimal but monitor for s/s pancreatitis

93
Q

hypoglycemia and DPP4 as monotherapy

A

uncommon

94
Q

dose adjust DPP4 inhibitors based on

A

GFR

95
Q

elimination and metabolism of DPP4 inhibitors

A

renal elimination

minor metabolism thru CYPs

96
Q

SGLT2 inhibitor examples

A

-flozins

97
Q

MoA SGLT2 inhibitors

A

inc urinary glucose excretion by blocking normal reabsorption in the proximal convoluted tubule

98
Q

AE of SGLT2 inhibitors

A

inc urination
UTI
hypotension
inc risk fractures

99
Q

SGLT2 inhibitors are CI in

A

renal impairment

100
Q

alpha glucosidase inhibitor med

A

acarbose

101
Q

MoA alpha glucosidase inhibitor

A

reduce absorption of glucose from intestine to bloodstream by slowing breakdown of large carbs into smaller, easier to absorb sugars

102
Q

AEs of alpha glucosidase inhibitors

A

flatulence
diarrhea
abd pain
inc LFTs

103
Q

alpha glucosidase inhibitors are CI in

A

IBD
colonic ulcerations
intestinal obstruction

104
Q

once insulin binds,

A

autophosphorylations occur. CAP/Cbl protein complex and PI3 kinase facilitates glucose transporter translocation. transporter gets to membrane, pulls glucose from bloodstream (BG decreases) and glucose stored as energy.

105
Q

rapid acting insulin onset

A

15-30 min

106
Q

short acting insulin onset

A

30-60 min

107
Q

intermediate acting insulin onset

A

2-4

108
Q

rapid acting insulin examples

A

lispro
aspart
glulisine

109
Q

short acting insulin examples

A

regular (humulin)

110
Q

intermediate acting insulin example

A

neutral protamine hagedorn (humulin)

111
Q

long acting insulin examples

A

lantus

levemir

112
Q

rapid acting insulin peaks

A

.5 - 3

113
Q

duration of rapid onset insulins

A

3-5 hr

114
Q

short acting insulin, regular, peak

A

2-3 hr

115
Q

short acting insulin, regular, duration

A

3-6 hr

116
Q

intermediate acting insulin peak

A

4-6 hr

117
Q

duration of intermediate acting insulin

A

8-12

118
Q

short acting and intermediate acting insulin are typically dosed

A

BID

119
Q

long acting insulins are typically dosed

A

1x a day

basal

120
Q

long acting insulin onset

A

3-5 hr

121
Q

long acting insulin peak

A

no peak

122
Q

duration of long acting insulin

A

up to 24 hr.

123
Q

basal dosing of insulin

A

either 10u daily or

.1-.2 units/kg/daily

124
Q

titration of basal dose insulin

A

patient can do it, 2u q3 days to target A1C.

125
Q

for basal insulin pt, fasting plasma glucose level should be consistent with

A

A1c goal

126
Q

initiation of prandial dosing

A

appropriate if above A1c goal but basal dose is titrated and fasting is at goal

127
Q

prandial dosing

start with

A

1 dose at largest meal

either 4u/day or 10% of total basal dose

128
Q

increasing prandial dosing

A

1-2 units or 10-15% twice weekly.

129
Q

dose insulin at _ - _ units/kg/day

A

0.3 to 0.6 u/kg/day

130
Q

total insulin can be divided into

A

2/3 NPH + 1/3 regular divided in AM and PM meal
or
50% basal and 50% prandial divided in 3 meals

131
Q

AE insulin

A

hypoglycemia
weight gain
allergy
lipoatrophy or lipohypertrophy

132
Q

GLP1 analogs end in

A

-tide

133
Q

A1C reduction of GLP1 analogs

A

0.5-1.5%

134
Q

MoA GLP1 analogs

A

increases glucose dependent insulin secretion, reduction of glucagon secretion, and reduced gastric emptying

135
Q

AE GLP1

A

N/V/D
hypoglycemia
AKI

136
Q

CI GLP1

A

impaired renal function

137
Q

monitoring for GLP1

A 
bg 
a1c
s/s pancreatitis
hypogly
weight loss
138
Q

tx hypoglycemia

A

treat at < 70

admin 15-20 glucose, reassess in 15. if glucose still <70, admin another 15-20.

139
Q

tx hypoglycemia c bg <54

A

admin glucagon 1mg IM or IV dextrose if no response.

140
Q

DKA is more common in

A

T1

141
Q

tx DKA

A

fluid replacement c 1/2NS or NS
bolus and infusion of insulin
potassium
sodium bicarb

142
Q

bolus and infusion insulin rates for DKA

A

bolus: 0.1unit/kg
infusion: 0.1u/kg/hr

143
Q

when to reduce insulin infusion in DKA

A

reduce by .02-.05 u/kg/hr when serum glu reaches 200

144
Q

when do we give bicarb in dka?

A

if serum pH is <6.9

145
Q

when is DKA considered resolved?

A

venous pH > 7.3
bicarb >15
anion gap <12

146
Q

tx nephropathy in DM

A

screen yearly for urine album/creat ratio (normal is < 30) - if >30, use ace/arb.
obtain CrCl yearly
reduce dietary protein

147
Q

retinopathy in DM

A

screen annually

treat extreme cases c IV steroids

148
Q

neuropathy tx DM

A

TCAs - amitriptyline
SNRIs - duloxetine
or
anticonvulsants - gapapentin/pregabalin

Pharm (31 decks)

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