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Pharmacology > DM treatment > Flashcards

DM treatment Flashcards

0
Q

fasting plasma glucose OR

A

after 8hours of fasting

> or equal to 7.0 mmol/l 126 mg/dL

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1
Q

Diabetes mellitus is defined as

A

elevated blood glucose
absent or inadequate pancreatic insulin secretion
without concurrent impairment of insulin action

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2
Q

2 hour plasma glucose

A

75 g oral glucose load

> or equal to 11.1 mmol/l (200 mg/dl)

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3
Q

uncommon criteria in WHO DM

A

elevated RBS

glycosylated hemoglobin

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4
Q

signs and symptoms of DM

A 
polyphagia
polyuria
polydipsia
blurred vision
fatigue
nausea
dry skin
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5
Q

type 1 insulin dependent diabetes hallmark

A

selective Beta cell destruction

absolute insulin deficiency

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6
Q

type 2 noninsulin dependent diabetes hallmark

A

insulin resistance

relative insulin deficiency

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7
Q

fist diagnosis of gestational DM

A

during pregnancy

progresses to frank diabetes

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8
Q

interruption of insulin replacement therapy in type 1 DM can result to

A

diabetic ketoacidosis

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9
Q

type 2 DM dehydration can lead to

A

hyperketotic hyperosmolar coma

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10
Q

increases in response to different stimuli especially glucose

A

INSULIN

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11
Q

variability of insulin absorption is more prominent with

A

regular human insulin and NPH insulin

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12
Q

half life of insulin

A

3-5 minutes

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13
Q

endogenous insulin is secreted more by

A

liver 60%

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14
Q

exogenous insulin is excreted more by the

A

kidney. 60%

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15
Q

insulin binds with

A

alpha sub TKR

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16
Q

basal insulin value

A

5-15 uu/mL (30-90 pmol/l)

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17
Q

peak insulin value

A

60-90 uu/ml (369-540 pmol/l)

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18
Q

human sources of insulin made from

A

recombinant DNA

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19
Q

pork or beef insulin can cause

A

hyoersensitivity

not produced anymore

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20
Q

different concentrations of insulin prep

A

u-100
u-500
u-40

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21
Q

only concentration of insulin available in the Philippines

A

u-100

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22
Q

concentration used in other countries for insulin resistance

A

u-500

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23
Q

used in other countries for pedia DM

A

u-49

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24
Q

basis of classification of insulin preparations

A

time of onset

duration of action

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25
Q

for basal requirements use

A

intermediate or long acting insulin

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26
Q

postprandial hyperglycemia use

A

short acting or rapid acting insulin before meals

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27
Q

only cloudy suspension among preparations

A

NPH

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28
Q

only insulin preparation that can be mixed with other preparations

A

NPH

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29
Q

mixing how to

A

clear soln must be injected to the cloudy suspension

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30
Q

route of general prep

A

SC

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31
Q

preferable regular insulin route

A

IV

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32
Q

pH of almost all insulin prep

A

neutral

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33
Q

only prep that is acidic of pH. 4 and cant be mixed with other insulin

A

GLARGINE

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34
Q

types used in continuous SC insulin infusion

A

rapid acting- LISPRO, ASPART, GLULISINE

short acting- regular INSULIN

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35
Q

cant be mixed with other solutions

A

GLARGINE (Lantus)

DETEMIR (Levemir)

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36
Q

traditional and chepest way to administer INSULIN

A

vial

tuberculin syringe injection

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37
Q

mode of delivery for whose blood glucose fluctuate and is difficult to monitor and control

A

INSULIN pump

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38
Q

good range of blood glucose reading

A

80-120 fasting blood glucose early in the morning

140-180 after a meal

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39
Q

proline is moved from b28 to b29

lysine is moved from b29 to b28 making it faster acting

A

LISPRO (humalog)

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40
Q

b28 prolone substituted with a negatively charged aspartic acid

A

ASPART (novolog)

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41
Q

glycine substitutes aspargine at the end of alpha chain

2 arginines are added to the end of the b chain

A

GLARGINE (lantus)

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42
Q

myristic acid is added to the alpha chain

threonin is removed from the end of beta chain

A

DETERMIR (levemir)

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43
Q

lysine at b3 instead of aspargine

glutamic acid at b29 instead of lysine

A

GLULISINE (apidra)

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44
Q

rapid acting insulin

A

LISPRO (humalog)
ASPART (novolog)
GLULISINE (apidra)

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45
Q

used for postprandial hyperglycemia

A

rapid acting

  • LISPRO
  • ASPART
  • GLULISINE
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46
Q

most physiologic insulin prep

A

rapid acting

  • LISPRO
  • ASPART
  • GLULISINE
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47
Q 
onset of action of 
rapid acting
-LISPRO
-ASPART
-GLULISINE
A

15 mins, not dose related

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48
Q 
duration of action of 
rapid acting
-LISPRO
-ASPART
-GLULISINE
A

3-5 hours

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49
Q

1st monomeric insulin analog to be marketed

produced by recombinant technology

A

LISPRO (humalog)

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50
Q

short acting insulin

A

HUMULIN R

ACTRAPID HM

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51
Q

onset of action of short acting
HUMULIN R
ACTRAPID HM

A

30min- 1hr

so give 30-45 min ac

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52
Q

peak of action of short acting
HUMULIN R
ACTRAPID HM

A

2-3 hours

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53
Q

duration of action of short acting
HUMULIN R
ACTRAPID HM

A

5-8 hours

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54
Q

delayed onset of action and peak action is caused by

short acting
HUMULIN R
ACTRAPID HM

A

hexameric structure

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55
Q 
NPH neutral protamine hagedorn
isophane insulin(HUMULIN N)
A

intermediate acting

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56
Q

use of protamine

A

added to prolong the action of insulin

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57
Q 
onset of action of NPH neutral protamine hagedorn
isophane insulin(HUMULIN N)
A

2-5 hours

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58
Q 
NPH neutral protamine hagedorn
isophane insulin(HUMULIN N)
duration of action
A

10-20h bid-qid

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59
Q

onset of action and duration of action of NPH are affected by the

A

dose

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60
Q

the only insulin used to provide for basal insulin requirements

A 
NPH neutral protamine hagedorn
isophane insulin(HUMULIN N)
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61
Q

long acting insulin analogs

A

GLARGINE (lantus)

DETEMIR

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62
Q

DETEMIR is given

A

2x a day

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63
Q

GLARGINE is peakless and is given

A

once a day

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64
Q

insulin combination’s onset will depend on

A 
short acting insulin 
LISPRO 
ASPART
GLULIGINE
regular
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65
Q

insulin combination duration will depend on

A

long acting -NPH

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66
Q

insulin regimens

A

basal bolus

split mixed

67
Q

most physiologic between two regimens

A

basal-bolus

68
Q

basal bolus dose

A

GLARGINE - hours after supper

+rapid acting or short acting - before meals:BLS

69
Q

split mised dose

A

before breakfast: NPH + rapid or short acting

70
Q

insulin absorption

A

directly into the bloodstream

71
Q

variability of insulin absorption more prominent with

A

regular human - short

NPH - intermediate

72
Q

absorption site of insulin

A

abdomen>arms>thighs>buttocks

73
Q

for px with kidney problem use

A

endo - liver 60%

74
Q

complications of insulin therapy

A 
hypoglycemia
insulin allergy, resistance
weight gain
lipodystrophy
increased cancer risk
75
Q

immune insulin resistance prone in

A

use of beef insulin
obese with type 2
interrupted tx

76
Q

rises insulin requirements in immune resistance

A

IgG anti insulin antibodies

77
Q

increased cancer risk is attributed to

A

insulin resistance

hyperinsulinemia- prediabetic and type 2

78
Q

insulin indications

A 
type 1 DM
pregnant diabetics
ketoacidosis, nonketotic coma
very ill patients
peri op control, patients in labor
hypersensitivity or inadequate response to oral hypoglycemic
kidney or liver disease
79
Q

why is insulin the DOC for pregnant diabetics

A

doesnt cross the placenta

wont cause fetal hypoglycemia

80
Q

biggest group of antihyperglycemic drugs other than insulin

A

sulfonylures

81
Q

2nd generation sulfonylureas

A

GLIPIZIDE (minidiab)
GLIBENCLAMIDE / GLYBURIDE (daonil)
GLICAZIDE (diamicron)
GLIPERAMIDE (norizec)

82
Q

preferred less AE and DI of sulfonylureas

A

2nd generation

83
Q

short acting sulfonylureas

A

TOLBUTAMIDE- 2-3x a day

84
Q

Intermediate acting sulfonylureas

A

1-2 per day

GLIPIZIDE (minidiab)
GLIBENCLAMIDE / GLYBURIDE (daonil)
GLICAZIDE (diamicron)
GLIPERAMIDE (norizec)

85
Q

long acting sulfonylureas

A

CHLORPROPAMIDE

1x day

86
Q

moa of sulfonylureas, glinides, d phenylalanine derivatives

A

stimulate insulin release from pancreas by interacting with ATP sensitive K channels on pancreatic beta cells

87
Q

additional MOA of sulfonylureas

A

⬇️ serum glucagon secretion

bind to extrapancreatic receptors and close K channels

88
Q

CI of sulfonyureas

A

type 1 DM, ketoacidosis
renal and hepatic impairment
pregnancy

89
Q

only sulfonylurea for pregnancy

A

GLYBURIDE (daonil)

90
Q

GLIBENCAMIDE dose

A

5-10 mg tab OD

91
Q

GLIBENCAMIDE is given

A

30 mins before breakfast

92
Q

AE of sulfonylureas

A 
hypoglycemia
GIT
weight gain
Disulfram like rxn with alcohol
agranulocytosis, thrombocytopenia
93
Q

meglitinide or glinides

A

REPAGLINIDE (novonorm)

94
Q

pk of REPAGLINIDE

A

short half life

onset: 1hr

95
Q

use of REPAGLINIDE

A

lower postprandial glucose-given at start of meals

monotherapy or combination with Biguanides

96
Q

SE of REPAGLINIDE

A

hypoglycemia

weight gain

97
Q

REPAGLINIDE CI

A

hepatic impairment

98
Q

d phenylalanin derivatives

A

NATEGLINIDE (starlix)

99
Q

NATEGLINIDE PK

A

short half life

onset : 20 mins

100
Q

use of NATEGLINIDE

A

lower postprandial glucose given at start of meals

101
Q

NATEGLINIDE se

A

hypoglycemia-lowest

weight gain

102
Q

insulin secretagogue that can be given to DM px with renal impairment

A

D phenylalanine derivatives- NATEGLINIDE (starlix)

103
Q

moa of biguanides

A

❤️ decrease hepatic glucose production by activating AMP activated protein kinase (AMPK)➡️ suppress ATP dependent processes like gluconeogenesis➡️ block glucose

increase glucose uptake in muscle and fat

lipid lowering effect

104
Q

half life of biguanides

A

1.5- 3 hrs

105
Q

duration of action of biguanides

106
Q

extended release biguanide duration

107
Q

biguanide dosing

A

once a day

108
Q

interesting pk of biguanide

A

not metabolized, excreted as an active compound

109
Q

AE of biguanides

A 
dose related GIT
anorexia
lactic acidosis
decreased b12 absorption during long term
metallic taste
110
Q

uses of biguanides

A

first line tx of t2 DM
prevention of t2 DM in impaired glucose tolerance test
PCOS

111
Q

the only biguanide in the market

A

METFORMIN (glucophage)

112
Q

dosage form of METFORMIN

A

500 mg
500 mg XR
850 mg
1 g tablets

113
Q

METFORMIN dose

A

500 mg to max 2.5 g per day on 3 divided doss with meals

114
Q

METFORMIN CI

A

withold in conditions predisposing to renal insufficiency and or hypoxia

  • CV collapse
  • severe infection
  • alcoholism
  • renal, liver dysfxn
  • ⬆️risk of lactic acidosis
115
Q

resume METFORMIN 48 hours after the following

A

use of IV iodinated contrast material

major surgical procedures

116
Q

thiazolidinediones

A

PIOGLITAZONE (actos)

117
Q

moa of PIOGLITAZONE

A

bind to peroxisome proliferator activated receptor PPAR y
➡️activates insuline responsive genes that reg cho and lipid metab
➡️ increase tissue sensitivity to insulin

118
Q

target tissues of PIOGLOTAZONE

A

fat
muscle
liver

119
Q

secondary effect of PIOGLITAZONE

A

decrease hepatic glucose production

120
Q

onset of PIOGLITAZONE

A

4-12 weeks

121
Q

ppar alpha effect of PIOGLITAZONE

A

⬇️ TAG

slight ⬆️ HDL, LDL

122
Q

Use of PIOGLITAZONE

A

add on to other insulin therapies

123
Q

AE of PIOGLITAZONE

A

❤️edema and weight gain
hepatotoxic : TROGLITAZONE
risk of bone fractures

124
Q

PIOGLITAZONE CI

A

pregnancy
significant liver disease
CHF

125
Q

alpha glucosidase inhibitors

A

ACARBOSE (glucobay, gluconase)
VOGLIBOSE (basen)
MIGLITOL

126
Q

moa of AG inhibitors

A

inhibit alpha gluconidase - no weight gain or hypoglycemia

127
Q

alpha gluconidase fxn

A

breaks down polysaccharides to monosaccharides in intestinal brush border, delaying CHO absorption

128
Q

dose of ACARBOSE (glucobay, gluconase)

A

50-100 mg od-tid after 1st spoonful of meal

129
Q

VOGLIBOSE dose

A

0.2-0.3 mg TID AC

130
Q

AE dose related AG inhibitors

A 
malabsorption
flatulence 
diarrhea
abdominal pain
bloating
reversible elevated liver fxn test
131
Q

why should AG inhibitors be started at low doses

A

flatulence AE

132
Q

CI AG inhibitors

A

IBD
intestinal conditions
renal, hepatic impairment

133
Q

advantage of using AG inhibitors

A

type 1 and 2 DM

because it is limited to the gut only

134
Q

disadvantage of using AG inhibitor

A

not very effective, only a secondary drug

135
Q

enteric hormones that segment glucose dependent insulin secretion when glucose is taken orally

136
Q

enzyme that degrades incretins

A

DPP4 dipeptidyl peptidase 4 inhibitor

137
Q

moa of GLP1 analogs

A

stimulate b cell to release insulin in response to oral glucose load

138
Q

GLP1 analog

A

EXENATIDE (byetta)

139
Q

SC injections of EXENATIDE are absorbed

A

equally

arm, ab, thigh

140
Q

EXENATIDE peak

141
Q

EXENATIDE duration

A

til 10 hours

142
Q

major SE of EXENATIDE

143
Q

SE of EXENATIDE

A

GI
weight loss
headache
hemorrhagic pancreatitis

144
Q

dosage of EXENATIDE

A

5 mcg BID SC to 10 mcg SC 60 mins A

before meals

145
Q

when should dose of EXENATIDE be adjusted?

A

if crea clearance is <30 ml/min

146
Q

DPP 4 inhibitors

A

SITAGLIPTIN (januvia)

147
Q

bioavailability of SITAGLIPIN

148
Q

half life of SITAGLIPIN

A

8-14 hours

149
Q

preparations of SITAGLIPIN

A

25 mg
50 mg
100 mg

150
Q

dosage of SITAGLIPIN

A

25-100 mg OD

151
Q

unchanged SITAGLIPIN in urine

152
Q

advantage of SITAGLIPIN to EXENATIDE

A

oral

relatively safe

153
Q

adv of GLP 1 agonists

A

increases GLP 1 levels promoting satiety and prolonging gastric emptying time resulting in weight loss

154
Q

DPP 4 inhibitors adv

A

maintains physiologic level of GLP 1 in the body

155
Q

amylin analogs

A

PRAMLINTIDE

156
Q

37 aa compound secreted with insulin from beta cells
deficient in type1,2
renal clearance

157
Q

physiologic effects of AMYLIN

A

inh glucagon secretion esp in postprandial state

reduction of gastric emptying time

158
Q

synthetic analog of AMYLIN

A

PRAMLINTIDE

159
Q

an effect of PRAMLIMTIDE on appetite

160
Q

PRAMLINTIDE admin

A

SC injection

161
Q

PRAMLINTIDE AE

A

hypoglycemia
nausea
vomiting

162
Q

how is PRAMLINTIDE used with INSULIN

A

separate admin
preprandially
for type 1,2

163
Q

initial therapy

A

1-2% lifestyle change to dec wt and inc activity

1.5% METFORMIN- biguanides

164
Q

additional therapy

A

INSULIN
SULFONYLUREAS- Gs
TZDs - PIOGLITAZONE

165
Q

weight neutral advantage

A

ACARBOSE- AG inh

Pharmacology (8 decks)

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