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Pharm Unit 4 > Wk 12 > Flashcards

Wk 12 Flashcards

1
Q

DM is a group of metabolic disorders characterized by:

A

hyperglycemia
impaired metabolism
impaired insulin secretion/insulin resistance

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2
Q

Percentage of Type I cases

A

5-10%

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3
Q

age of onset of type I

A

<30

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4
Q

genetic link for type I

A

weak

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5
Q

pathogenesis of type I

A

absolute deficiency of insulin production

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6
Q

percentage of cases of type II

A

90+

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7
Q

age of onset of type II

A

> 30

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8
Q

genetic link of type II

A

strong

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9
Q

pathogenesis of type II

A

insulin resistance, defective insulin release

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10
Q

diagnosis of DM is confirmed by ___

A

repeat

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11
Q

type I is typically due to an ____ mediated destruction of pancreatin B cells

A

autoimmune

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12
Q

4 main features of type I

A

long pre-clinical period
hyperglycemia when 80-90% of B cells are destroyed
transient remission (honeymoon period)
established disease

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13
Q

Type I tx is ____ to each patient

A

individualized

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14
Q

goal of type I tx

A

to mimic normal physiologic levels

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15
Q

single injection of long-acting insulin

A

basal

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16
Q

> 1 injection of short-acting insulin at meal time

A

bolus

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17
Q

basal bolus approach composed of a ___ for basal coverage and a ___ for bolus doses at mealtime

A

long acting insulin; short acting insulin

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18
Q

Human insulin

A

regular, short acting

100 units/mL, 500 u/mL

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19
Q

human insulin is ___ prone

A

error

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20
Q

insulin analogs

A

rapid acting

long acting

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21
Q

NPH insulin

A

intermediate acting

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22
Q

types of insulin

A

human insulin
insulin analogs
NPH
mixtures

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23
Q

oral administration of insulin destroys ___

A

protein

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24
Q

insulin must be given ___, usually by ___

A

parenterally; subQ injection

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25
Q

using a SC injection of insulin slows ___

A

absorption

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26
Q

regular insulin may be given ___

A

IV

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27
Q

rapid absorption of insulin may be due to ____

A

reduced self-association

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28
Q

advantage of rapid acting insulin

A

may inject closer to meal time

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29
Q

long acting insulin have reduced ___, slowing ___

A

solubility; absorption

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30
Q

advantaged of long acting insulin

A

continuous coverage w/o injections

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31
Q

long acting insulin analogs

A

glargine
detemir
degludec

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32
Q

duration of glargine

A

22-36h

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33
Q

Lantus dosage

A

100 units/mL

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34
Q

tujeo dosage

A

300+ units/mL

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35
Q

advantage of tujeo (glargine)

A

causes less nocturnal hypoglycemia

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36
Q

duration of detemir

A

12-20h

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37
Q

detemir is dosed ___ x /d

A

1-2

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38
Q

degludec is ___ prone

A

error

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39
Q

duration fo degludec

A

> 42h

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40
Q

dosage of tresiba (degludec)

A

100, 200 units/mL

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41
Q

NPH insulin =

A

neutral protamine hagedorn

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42
Q

NPH: suspension of:

A

crystalline zinc insulin

positively charged polypeptide, protamine

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43
Q

NPH is absorbed slower after ____

A

subQ injection

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44
Q

duration of action for NPH is:

A

longer than regular (or analog) insulin

shorter than glargine, detemir or degludec insulins

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45
Q

Humulin is manufactured by

A

Eli Lilly

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46
Q

Novolin is manufatured by

A

Novo Nordisk

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47
Q

Total daily dose of insulin required

A

~ 0.4-1 units/kg/d of actual body weight

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48
Q

decrease total daily dose of insulin during honeymoon period to ____

A

~0.2-0.5 units/kg/day

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49
Q

basal insulin in type I is approximately ____ total daily insulin dose

A

1/2

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50
Q

in type I, you Amy use _____ insulin

A

intermediate/long acting

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51
Q

in type I, ___ is perferred as it can be mixed

A

NPH

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52
Q

Detemir may require ___ dosing

A

q12h/BID

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53
Q

Meal time insulin in type I is ___% of total daily dose

A

50

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54
Q

meal time insulin for type I is divided between meals based on ___

A

type of meal

patient characteristics

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55
Q

for meal time insulin w/ type I, u se ___ or ___ insulin

A

rapid acting/regular

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56
Q

non intensive insulin therapy has ____ dosing

A

split-mixed (2 daily injections)

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57
Q

2 daily injections fo non-intensive insulin:

A

2/3 TDD in morning

1/3 TDD in evening

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58
Q

basal insulin should be ___ as morning dose, ___ as evening dose

A

2/3; 1/3 (even if using NPH)

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59
Q

non intensive insulin therapy also has 3 daily injections. Dose:

A

same as “split mixed” but moves NPH to bedtime

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60
Q

non intensive insulin therapy with 3 injections reduces ___ and increases ___

A

nocturnal hypoglycemia; effect at dawn

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61
Q

intensive insulin therapy requires multiple ___ each day

A

self monitoring blood glucose checks

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62
Q

sliding scale insulin has two categories:

A

tight control

regular control

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63
Q

blood glucose levels evaluates impact of ____

A

insulin on meals

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64
Q

SMBG measures:

A

fasting blood glucose

post prandial glucose

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65
Q

glycosylated hemoglobin (HbA1c) assess ____ over 2-3 months

A

glycemic control

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66
Q

in non diabetics, HbA1c should be ___

A

4-6%

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67
Q

AACE guidelines recommend ___ A1c

A

<6.5%

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68
Q

ADA guidelines recommend ___ A1c

A

<7%

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69
Q

process of hba1c is

A

irreversible

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70
Q

A1c lasts life of the ___ (__ days)

A

RBC; 120 days

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71
Q

a1c reflects average ____

A

glucose over 3 months

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72
Q

type II DM is a disease of:

A

insulin secretion
insulin resistance
excess glucose production
OR all of the above

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73
Q

treatment for type II DM is based on:

A

age/comorbidities

individualized

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74
Q

begin at diagnosis of type II DM with ___

A

pharmacotherapy

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75
Q

target weight loss for type II

A

> 7kg

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76
Q

Therapeutic lifestyle changes for type II DM

A

weight reduction
tobacco cessation
minimize alcohol intake
nutritional counseling

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77
Q

weight reduction in type II DM may decrease A1c by ___%

A

1-2

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78
Q

insulin
route:
weight:
HG:

A

SC/IV
gain
mod-severe

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79
Q

SUs
Weight:
HG:

A

gain

mod-severe

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80
Q

glinides
weight:
HG:

A

gain

mild-moderate

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81
Q

TZDs

weight:

A

gain

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82
Q

pramlintide

route:

A

SC

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83
Q

GLP-1 RAs

route:

A

SC

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84
Q

at dx of type II, start

A

TLCs and monotherapy w/ metformin

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85
Q

start dual therapy for type II if:

A

if not at target a1c after 3 mo of monotherapy OR

if baseline a1c >9%

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86
Q

start triple therapy for type II if

A

if not at target a1c after 3 months of dual therapy

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87
Q

start COMBO injection therapy for type II if:

A

not at target a1c after 3 mo of triple therapy
blood glucose is >300-350 mg/dL and/or
a1c >10-12%

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88
Q

highly effective hypoglycemic agents

A

insulin
biguanides (metformin)
sulfonyureas
rapid-acting secretagogues (glinides)

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89
Q

in type II, insulin is now used earlier in ___

A

pharmacotherapy

minimizes micro and macrovascular complications

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90
Q

in type II, ___ are being used earlier

A

multiple drugs

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91
Q

when to start insulin in type II DM

A

not at A1c goal arter >2 non insulin hypoglycemics
severe FBG levels
A1c levels >10%
DO NOT USE AS THREAT FOR NOT REACHING A1C GOALS

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92
Q

start with ___ insulin in type II DM

A

basal (long acting)

93
Q

long acting insulin in type II DM causes less ___

A

hypoglycemia

94
Q

both NPH and LA analogs are ____

A

equally effective

95
Q

NPH is available ___ and is much ___

A

OTC; cheaper

96
Q

starting insulin for type II DM:

A
  1. start basal insulin once daily
  2. adjust once or twice weekly
  3. if not at Goa (or dose >0.5 u/kg/d) begin prandial rapid acting before largest meal (0-15 mins) or premixed insulin
  4. if still not controlled, begin basal-bolus insulins (30 mins before meals)
97
Q

biguanides route

A

PO

98
Q

first line DOC for type II DM

A

metformin

99
Q

MOA of metformin

A

reduces hepatic glucose production
reduces intestinal glucose absorption
increases insulin sensitivity
improves peripheral glucose uptake and utilization

100
Q

metformin promotes modest ___ or ___

A

weight loss; weight neutral

101
Q

metformin lowers fasting BC ___%, and A1c __%

A

20%; 1-2%

102
Q

metformin has a synergistic effect with ___

A

SUs

103
Q

metformin has minimal ___ as monotherapy

A

HG

104
Q

metformin has a generally minimal ____

A

s/e profile

105
Q

adverse reactions of metformin

A 
primairly GI effects: N/V, diarrhea, flatulence
Lactic acidosis (death)
106
Q

C/I of metformin

A

Male: SCr >1.5 mg/dL
Female: Screaming >1.4 mg/dL
CrCl <30 (CKD sag 4/5)

107
Q

first biguanide was

A

phenformin

108
Q

monitor metformin users with CrCL of

A

30-59

109
Q

monitor metformin users for:

A

renal failure, dehydration
infections/sepsis
metformin overdose

110
Q

SUs are usually given ___

A

once daily

111
Q

downside of SUs

A

greater risk of HG w/ glimepiride

112
Q

second line therapy after metformin for type II

A

SUs

113
Q

all SUs are equally effective ____

A

within class

114
Q

Cus are ___ effective as a class

A

moderately

115
Q

efficacy of SUs ___ over time

A

decreases (beta cell burnout)

116
Q

___ SUs are rarely used

A

first generation

117
Q

___ SUs are preferred

A

second generation (less HG)

118
Q

dose of glimepiride

A

q24h

119
Q

s/e of glimepiride

A

causes more HG than glipizide

120
Q

glipizide dosage

A

q12-24h

121
Q

glyburie is not preferred due to ___

A

most HG of the 3 second generation SUs

122
Q

dose of glyburide

A

q12-24h

123
Q

MOA of SUs

A

stimulate release of insulin
requires presence of insulin (functioning pancreas)
not effective in type I

124
Q

greatest concern with SUs

A

HG

125
Q

rapid acting secretagogues AKA ___

A

glinides

126
Q

nateglinide is dosed

A

ac tid

127
Q

repaglinde is dosed

A

ac, 2-4xd

128
Q

rapid acting secretagogues are ____ agents

A

oral antidiabetic

129
Q

rapid acting secretagogues have ____ dosing than SUs

A

more frequent

130
Q

MOA of rapid acting secretagogues

A

stimulates insulin release from pancreas
similar to SUs but shorter half life
Faster than SUs (rapid acting)

131
Q

repaglinide is ____ effective than nateglinide

A

slightly more effective at A1c reduction

132
Q

adverse effects of rapid acting secretagogues

A

hypoglycemia (less than SUs)

weight gain

133
Q

adrenergic manifestations of HG

A

shakiness, nervous, anxiety

palpitations, achy, sweating (absent if on B blockers)

134
Q

glucagon manifestations of HG

A

hunger, n/v , HA

135
Q

neuroglycopenic manifestations of HG

A

impaired judgement, mentation
fatigue, lethargy, ataxia (mistaken for drunkenness)
stupor, coma, seizures

136
Q

mild HG tx

A

glucose tablets
fruit juice
hard candy (no artificial sweeteners)
glucose gen

137
Q

severe HG tx

A

glucagon injection

50% dextrose

138
Q

moderately effective HG agents

A

TZDs
DPP4Is
SGLT2Is

139
Q

available TZDs

A

rosiglitazone

Pioglitazone

140
Q

doseing of rosiglitazone

A

1-2xd

141
Q

dosing of pioglitazone

A

once daily

142
Q

TZDs have a synergistic effect when combined with

A

SUs
metformin
insulin

143
Q

MOA of TZDs

A

increase insulin sensitivity by;
increasing glucose utilization
decreasing glucose production
(requires presence of insulin)

144
Q

adverse effects of TZDs

A

weight gain (~9lbs)
increased total cholesterol, LDL, HDL
edema
hepatic metabolism

145
Q

when should you avoid TZDs

A

if LFTs >2.5 ULN

146
Q

rosiglitazone has an increased risk of ____

A

MI

(FDA warning 5/21/2007(

147
Q

record finding in 2013 found no difference in ___ between rosiglitazone or metformin/SU

A

CV risk

148
Q

restrictions on TZDs removed in

A

2013

149
Q

pioglitazone:
cost:
dose:

A

~$10

once/d

150
Q

rosiglitazone
cost:
dose:

A

~$90

1-2xd

151
Q

intestinal incretin hormones

A

GLP1

GIP

152
Q

incretin hormones increase ____ in response to meals

A

insulin secretion

153
Q

prolonging incretin levels (in DPP4Is):

A

stimulates insulin synth & release

decreases glucagon secretion from pancreatic alpha cells

154
Q

DDP4Is are ___ enhancers

A

incretin

155
Q

net result of DPP4Is

A

prolonged basal insulin secretion

156
Q

DPP4Is are __ anti diabetic agents, used ___

A

oral; once/daily

157
Q

DPP4Is cause minimal __ and are weight ___

A

HG; neutral

158
Q

DPP4Is are are costly:

A

$380/mo

159
Q

renal adjustment for lingaliptin

A

NONE

160
Q

DPP4Is have increased risk of ___, but no increased risk of hospitliization ___

A

HF; HF

161
Q

SGLT2Is are a new class of ___ antidiabetics which are __ effective

A

oral; moderately

162
Q

MOA of SGLT2I

A

SGLT2 recovers filtered glucose from urine
inhibition increase urinary glucose loss
lowers BP and decreases weight

163
Q

adverse effects of SGLT2Is increase risk ooo ___

A

genital fungal infection, dehyration

164
Q

recent FDA safety communication for SGLT2Is:

A

ketosis (73 cases)

UTis, pyelonephritis (19 cases)

165
Q

minimally effect HG agents

A

a-glucosidase inhibitors
pramlintide
glucagon-like peptide receptor agonists

166
Q

AGIs are __ HG agents, dosed ___

A

oral; TID

167
Q

most of AGI

A

$30-60 / 30 days of therapy

168
Q

MOA fo AGI

A

inhibits pancreatic alpha-amylase and GI brush border alpha glucosidases
delays hydrolysis of ingested carbs
reduces postprandial insulin and glucose peaks

169
Q

AGIs are effective for ___

A

type I and type II

170
Q

AGIs do NOT cause ___

A

HG

171
Q

AGIs are ___ between agents

A

equally effective

172
Q

AGIs are typically combined with _____

A

metformin; SUs; insulin

173
Q

SE of AGIs

A

flatulence (73%)

diarrhea (31%)

174
Q

pramlintide is a synthetic analog of ___

A

human amylin

175
Q

pramlintide decreases ____

A

post prandial glucose levels

176
Q

pramlintide does not act on ___

A

B cells (effective for type I and type II)

177
Q

pramlintide
risk of HG:
affect on weight:

A

neutral

loss

178
Q

pramlintide has additional ___ separate from insulin injection prior to each ___

A

subcutaneous injection; meal

179
Q

glucagon requires ___

A

SC injection

180
Q

dose of liraglutide

A

once daily

181
Q

dose of exenatide IR

dose of eventide ER

A

BID

once weekly

182
Q

dose of albiglutide

A

once weekly (requires reconstitution before use)

183
Q

MOA of GLP 1

A 
incretin mimetic
enhances glucose dependent insulin secretion
inhibits release of glucagon
slows rate of gastric emptying 
increases satiety
184
Q

GLP 1 RAs

weight:

A

loss

185
Q

GLP1 RAs were recently ___

A

discontinued

186
Q

type II recommendation: ___ initially

A

metformin

187
Q

mono, dual, or triple therapy for ______

A

mild, moderate of severe type II DM

188
Q

most type II diabetics will require ____

A

multiple medications eventually

189
Q

DKA is mainly seen in ___

A

type I diabetics

190
Q

DKA is most often precipitated by

A

omission of treatment (medication non-adherence)
infection (if percent, usually hyperthermic)
alcohol abuse

191
Q

DKA presentation:

A 
polyuria
polydipsia
polyphagia
weakness
N/V
dehydration
192
Q

tx mild DKA ___

A

outpatient

193
Q

tx mod-severe DKA ___

A

inpatient

194
Q

if severe DKA admit to __

A

ICU

195
Q

DKA tx

A 
fluids
insulin
potassium
bicarb
sodium
196
Q

biologically active thyroid hormones:

A

t4 (thyroxine)

t3 (tri-iodothyronine)

197
Q

___% of T3 produced in the thyroid gland

A

20%

198
Q

___% of T3 produced peripherally by breakdown of T4

A

80

199
Q

steady state of thyroid hormone

A

4-5 half lives

200
Q

thyroid gland purpose:

A

regulation of hormone production

hypothalamic-pituitary-thyroid axis

201
Q

production of thyroid hormone regulated by two mechanisms:

A

TSH secretion by ant pit

extra thyroidal conversion of t4 to t3.

202
Q

primary hypothyroid:

A

disorder of thyroid gland

hashimoto’s thyroiditis

203
Q

secondary hypothyroidism:

A

pituitary or hypothalalmic disorder

204
Q

sx of hypothyroid

A

weight gain

depression

205
Q

when working up a pt for depression, ___ is essential

A

eval of thyroid function

206
Q

hypothyroid lab tests

A

serum TSH

free or total T4

207
Q

subclinical hypothyroid:
TSH:
Free/total T4

A

high

normal

208
Q

hypothyroidism
TSH:
free/total t4

A

high

low

209
Q

DOC for hypothyroid

A

levothyroxine

synthetic t4 – long half life – once daily dosing

210
Q

dose IV dose at ___ of oral dose

A

50%

211
Q

note: doses are in ___

A

MICROGRAMS

212
Q

other hypothyroid tx

A

dessicated beef or pork thyroid gland (dosed in mg not mcg)

t3 and t4 mixtures (liotrix)

213
Q

S/E of desiccated beef or pork thyroid gland

A

potential for allergy

considered obselete

214
Q

cons of t3 and t4 mixtures

A

expensive, lacks therapeutic rationale

215
Q

dosing for levothyroxine

A

take once daily in AM on empty stomach

216
Q

typical dose of levo

A

100-112 mcg/day

217
Q

use lower initial dose of levo in ___

A

elderly

patients with CV disorder

218
Q

pregnancy usually requires an __ in levo dose

A

increase

219
Q

clinical presentaiton of hyperthyroid

A

nervousness/anxiety/palpitations
heat intolerance
finger tremor
cardinal sign: loss of weight

220
Q

classic triad of grave’s disease

A

hyperthyroidism
ophthalmopathy
dermopathy

221
Q

hyperthyroidism
TSH
free/total t4

A

low

high

222
Q

tx of hyperthyroidism

A

antithyroid medications

propylthiouracil PTU, methimazole

223
Q

MOA of PTU

A

inhibits peripheral conversion fo t4 to t3

224
Q

dosing of PTU

A

TID

225
Q

eval patient ___ for recurrence of hyperthyroidism with PTU

A

q3mo

226
Q

methimazole is ___ as potent as PTU

A

10x

227
Q

MOA of methimazole

A

blocks oxidation of iodine in thyroid

no effect on circulating t3 or t4

228
Q

dosing of methimazole

A

TID

229
Q

s/e of antithyroid medications

A

agranulocytosis
aplastic anemia
thrombocytopenia

Pharm Unit 4 (3 decks)

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