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Endo II Exam 2 > Diabetes Pharmacotherapy > Flashcards

Diabetes Pharmacotherapy Flashcards

1
Q

rapid acting insulin

A

lispro
aspart
glulisine

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2
Q

short acting insulin

A

regular - human

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3
Q

intermediate acting insulin

A

NPH

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4
Q

log acting insulin

A

glargine

detemir

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5
Q

fixed mix insulin

A

NPH/regular

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6
Q

metformin

A

biguanine

-antihyperglycemic

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7
Q

glimepiride

A

sulfonylurea

-stimulate insulin secretion

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8
Q

glipizide

A

sulfonylurea

-stimulate insulin secretion

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9
Q

glyburide

A

sulfonylurea

-stimulate insulin secretion

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10
Q

repaglinide

A

non-sulfonylurea secretagogue

-stimulate insulin secretion

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11
Q

nateglinide

A

non-sulfonylurea secretagogue

-stimulate insulin secretion

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12
Q

pioglitazone

A

insulin sensitizer

-thiazolidinediones - TZD

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13
Q

acarbose

A

alpha-glucosidase inhibitor

prevent complex carb hydrolysis and delay carb absorption

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14
Q

miglitol

A

alpha-glucosidase inhibitor

prevent complex carb hydrolysis and delay carb absorption

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15
Q

exenatide

A

GLP-1 agonist

potentiate glucose-dependent insulin secretion

suppress glucagon secretion

slow gastric emptying

promote satiety

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16
Q

C peptide

A

removed from proinsulin when insulin released

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17
Q

insulin chemistry

A

solution as monomer, dimer, hexamer

Zn coordinated

crystallize differently - determine how fast dissolve after subQ injection

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18
Q

stimulus for insulin release

A

glucose

also, AAs, FAs, ketone bodies

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19
Q

alpha2

A

inhibit insulin release

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20
Q

beta2

A

stimulate insulin release

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21
Q

vagus

A

stimulate insulin release

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22
Q

GLUT2

A

glucose transport into beta cell

ATP generation - results in influx of extracellular Ca

leading to fusion of insulin granules with membrane
-insulin release

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23
Q

insulin release

A

two phases

DMII - missing first

DMI - missing both

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24
Q

insulin after meal

A

greater frequency and higher amplitude pulses

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25
Q

insulin in circulation

A

free monomer

-half life - 5-8 minutes

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26
Q

insulin receptor

A

tyrosine kinase

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27
Q

GLUT4

A

insulin sensitive receptors

go to membrane when have increased insulin stimulation

-muscle and adipose tissue

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28
Q

long term insulin resistance

A

GLUT1 and GLUT4

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29
Q

diminished insulin secretion in DM II

A

GLUT4

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30
Q

phosphoinositol 3-kinase

A

activated insulin receptor brings GLUT4 receptors to membrane via this

31
Q

DM I

A

lack beta cell activity - absent insulin

associated with HLA

insulin-dependent

32
Q

DM II

A

defective insulin secretion
tissue resistance
increased hepatic glucose

with obesity

strong fam hx

33
Q

therapeutic insulin subQ

A

1 doesn’t match normal up and down of insulin levels

2 goes to peripheral circulation, instead of portal circulation

34
Q

detemir

A

long acting insulin - binds albumin

35
Q

glargine

A

long acting insulin - acidic pH

36
Q

lispro, aspart, glulisine

A

rapid acting insulin - 2AA substitution - faster than regular insulin

37
Q

intermediate insulin

A

crystalline suspension

38
Q

NPH

A

added protamine, Zn, phosphate buffer

intermediate acting insulin - crystalline suspension

39
Q

rapid acting insulin

A

action - 15 minutes

taken immediately before meal

lower risk of hypoglycemia**

40
Q

IV insulin

A

only regular, aspart, glulisine, lispro

rapid acting and regular**

IV or subQ pump

41
Q

neutral protamine hagedorn

A

NPH insulin - intermediate acting

complex with protamine and zinc

42
Q

changes in subQ blood flow

A

important indicator in variability of response to insulin

43
Q

exubera

A

inhalation insulin

44
Q

CSII

A

continuous subQ insulin infusion

timed throughout day
-regular or rapid acting

45
Q

measure of long term hyperglycemic control

A

HbA1C < 6.5%

46
Q

IIT

A

intensive insulin therapy

basal - long acting QD

bolus - rapid acting before meal

47
Q

split mix insulin therapy

A

mix dose of NPH/regular insulin

48
Q

adverse effect insulin

A

hypoglycemia

more rigorous attempt to achieve euglycemia - greater risk hypoglycemia

49
Q

counter-regulatory hormones

A

epi, glucagon, cortisol, GH

dominant - glucagon

type I DM - long duration - glucagon secretion becomes deficient and epi becomes dominant

50
Q

tx of hypoglycemia

A

ingestion glucose

severe - glucagon injection or IV glucose

51
Q

lipoatrophy and lipohypertrophy

A

subQ fat at site of insulin injection

patient advised to rotate injection site

52
Q

DKA tx

A

IV insulin continuous infusion

also - replacement of fluid and electrolytes

53
Q

perioperative and childbirth

A

when diabetic patient gets IV insulin - more control

54
Q

drug-induced hypoglycemic state

A

ethanol
beta antagonist
salicylates

ethanol - inhibitor of gluconeogenesis

55
Q

inhibit insulin secretion

A

phenytoin
clonidine
CCBs

56
Q

inhibit insulin secretion

A

diuretics

57
Q

hyperglycemic effect

A

epi
glucocorticoid
contraceptives

58
Q

initial therapy for DMII patient who fails diet and exercise therapy

A

metformin

59
Q

DM I tx

A

insulin

-don’t respond to oral hypoglycemic agents

60
Q

metformin effect

A

antihyperglycemic effect

does not cause hypoglycemia**

  • inhibits gluconeogenesis
  • increased insulin action
  • increased glucose uptake
  • reduces intestinal glucose absorption
61
Q

obese insulin resistant pt with DM II tx

A

metformin**

also has lipid lowering effect

62
Q

lipid lowering effect

A

metformin

63
Q

sulfonylurea MOA

A

stimulate insulin release from beta cells of pancreas

-bind and block ATP sensitive K channel - causes Ca influx - insulin release**

64
Q

extrapancreatic effects

A

sulfonylureas

  • increased insulin receptors
  • increased glucose transporters
  • enhanced tissue response to insulin
65
Q

second generation sulfonylureas

A

100x more potent

66
Q

pt older than 30, not obese, residual beta cell fxn, fasting glucose <300

A

sulfonylurea tx

67
Q

adverse sulfonylurea

A

hypoglycemia - including coma

CI - sulfa allergy, DMI, pregnant/nursing mother, hepatic/renal insufficiency

68
Q

meglitinide MOA

A

bind ATP sensitive K channels - different site than sulfonylureas

opens Ca channels - rapid increase in insulin release

rapid acting - meal skipped - so is drug dose**

69
Q

alpha glucosidase inhibitors

A

competitive inhibition of sugar digestion

-limits postprandial rise in glucose

for new DM II pt with mild hyperglycemia

70
Q

adverse of alpha glucosidase inhibitors

A

flatulence, diarrhea, GI upset

71
Q

TZDs

A

insulin sensitizers
-removed from market

bind nuclear transcription factors involving insulin receptor signaling cascade

resensitize target tissue to insulin

increase GLUT 1 and 4 transport proteins

72
Q

rosiglitazone

A

risk of MI

TZD

73
Q

GLP-1 analogs

A

secreted by intestinal L cells

agonist at GLP-1 receptor

74
Q

exenatide

A

GLP-1

reduction of HbA1c levels

need for BID subQ injections

Endo II Exam 2 (16 decks)

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