DM pharm Flashcards

1
Q

rapidly acting insulins

A

lispro
aspart
glulisine

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2
Q

short acting insulins

A

regular insulin

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3
Q

intermediate acting insulins

A

NPH and NPL

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4
Q

ultra-long actin insulins

A

glargine

detemir

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5
Q

sulfonylureas

A

glipizide
glyburide
glimepiride

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6
Q

non-sulfonylurea insulin releasers

A

repaglinide

nateglinide

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7
Q

alpha glucosidase inhibitors

A

acarbose

miglitol

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8
Q

TZDs

A

rosiglitazone

pioglitazone

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9
Q

adjuncts

A

exenatide
sitagliptin
saxagliptin

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10
Q

regulation of insuline secretion

A

glut 2 transports glucose into beta cells -> high ATP -> opens ATP sensitive KCh -> depolarizes membrane -> opens CaChs -> insulin release

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11
Q

degradation of insuline

A

primarily liver
kidney
t1/2= 5-15min

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12
Q

recommended hA1C

A

6.5-7%

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13
Q

Dx of DM

A

classic signs and symptoms
FBG >126
random glucose >200
failure of oral glucose tolerance test

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14
Q

typical insulin regimen

A

30 U/day
2/3 before breakfast (2/3 NPH 1/3 regular)
1/3in evening (1/3 regular before dinner, 2/3 NPH at bed)

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15
Q

metformin

A

first line
antihyperglycemic
does not cause hypoglycemia

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16
Q

metformin affects

A
  • increases action of insulin
  • increases glycolysis
  • increases glucose uptake and utilization by mm
  • decreases gluconeogenesis and hepatic glucose output
  • decreases GI absorption of glucose
17
Q

advantages of metformin

A

no hypoglycemia
no weight gain
favorable lipid profile

18
Q

adverse effects of metformin

A

GI: anorexia, nausea, diarrhea, abdominal discomfort

lactic acidosis

19
Q

complications of metformin induced lactic acidosis

A

renal or hepatic insufficiency

CV disease

20
Q

second generation sulfonylureas

A

glipizide

glyburide

21
Q

third generation sulfonylureas

A

glimeperide

22
Q

MOA sulfonylureas

A

bind ATP sensitive KCh -> continuously open -> Ca influx -> insulin secretion

indirectly increase insulin sensitivity

23
Q

adverse effects of sulfonylureas

A

weight gain and hypoglycemia

24
Q

glimerperide advantages

A

less weight gain then 2nd gen

doses once daily PO

25
Q

glimerperide CI

A
sulfa allergy
pregnancy
type I DM
ketoacidosis
renal failure
hepatic failure
major surgery
26
Q

glipizide

A

dose 1-2x/day PO
inactive metabolites
no CIs

27
Q

glyburide

A

freater incidence of hypoglycemia

use with caution

28
Q

non-sulfonylurea secretagogues

A

same MOA as sulfonylureas, but have different binding site
short half-life
rapid action
can be taken right before meal

29
Q

alpha-glucosidase inhibitors

A

not very popular b/c block glucose absorption -> more gut bacteria digestion -> serious gas
can also cause hypoglycemia

30
Q

GLP-1 agonists

A

peptide hormone cleaved from pro-glucagon precursor
secreted by intestinal L cells
highly resistant to DPP-4 degredation

31
Q

actions of GLP-1 agonists

A

glucose dependent enhancement of insulin secretion
inhibition of glucagon secretion
appetite suppression and satiety induction
reduce gastric emptying
possible stimulation of islet cell growth
Decrease HbA1c
decrease postprandial glucose
weight loss
little hypoglycemia

32
Q

GLP-1 combos

A

with metformin, TZDs, and/or sulfonylurea
NOT with insulin
must be injected

33
Q

DDP-4 inhibitors

A

prevents break down of GLP-1 and GIP
oral
cannot be combined with insulin

34
Q

actions of DDP-4 inhibiots

A
increase insulin secretion
decrease glucagon
decrease hepatic glucose production
increase peripheral glucose uptake and utilization
little hypoglycemia
35
Q

pramlintide

A

synthetic analog of amylin
4th line drug
used with DMI or II when already on insulin
cannot be dosed with insulin and must be injected

36
Q

TZDs MOA

A
insulin sensitizers
act as steroid hormone -> PPAR-gamma RXR R complex
decrease insulin resistance
decrease hepatic glucose output
increase glucose uptake
37
Q

risks of TZDs

A

very controversial
risk of MI with rosiglitazone
risk of bladder CA with pioglitazone

38
Q

SGLT2 inhibitors

A

-flozin
PO 1/day for DMII
used in combo

39
Q

SGLT2 inhibitors MOA

A

SGLT2 is membrane protein expressed in kidney and inhibition of this protein blocks glucose reabsorption