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Pharm2 S.Horvath > oral hypoglycemic agents > Flashcards

oral hypoglycemic agents Flashcards

1
Q

what is the MOA for a sulfonylurea?

A

act at pancreatic beta cells to simulate release of insulin

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2
Q

T/F sulfs can cause hypoglycemia

A

TRUE

they have the HIGHEST incidence

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3
Q

Which drug class has high failure rates?

A

sulfonylureas

20% primary failures
10-15% secondary failures

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4
Q

which drug class should you avoid in patients with sulfa allergy?

A

sulfonylureas.

some that are allergic to sulfa ABX are OK though.

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5
Q

which drug has a high risk of hypoglycemia in renal failure patients

A

sulfonylureas.

because there are active and inactive metabolites

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6
Q

which is the safest sulf to use in renal dysfunction?

which is the worst?

A

gylpizide is safest

glyburide & chlorpropamide is worst - one your CC is less than 50, your risk of fluid retention and hypoglycemia increases dramatically

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7
Q

T/F Sulfonylureas may cause fetal hypoglycemia

A

TRUE

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8
Q

T/F Although hypoglycemia with sulfs is less frequent than with insulin, it is often more prolonged and more dangerous

A

TRUE

It can require prolonged infusions of glucose-containing solutions

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9
Q

sulfonylureas should be avoided in patients with liver disease, except ______

A

acetohexamide

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10
Q

____ are contraindicated in patients with hypoglycemia unawareness

A

Sulfonylureas

remember bc they have the greatest risk of hypoglycemia!

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11
Q

what is the shortest acting and least potent sulf?

A

tolbutamide (orinase)

also has the fewest side effects

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12
Q

most of the hypoglycemic action of acetohexamide is due to

A

its principle metabolite

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13
Q

what is the longest acting sulf

A

chlopropamide (diabeinese)

may approach 72h.

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14
Q

what sulf is associated with disulfiram-like reactions

A

chlopropamide (diabeinese)

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15
Q

what sulf is associated with severe hyponatremia? why?

A

chlopropamide (diabeinese)

when you have large glucose molecules floating around in the blood, it changes the osmolarity and in response to that, your body will start pulling water out of cells and into the blood stream - an osmotic type movement of water - body tries to combat the increase in osmolarity , causing a dilatational hyponatremia.

If you can treat the hyperglycemia, the sodium will correct itself.

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16
Q

what drugs are alpha-glucosidase inhibitors?

A

acarbose (precose)
miglitol (glyset)

alphas = acar + mig

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17
Q

whats the MOA of alpha-glucosidase inhibitors? (acar/mig)

A

think: alphas—absorption (inhibit)

decrease intestinal hydrolysis of complex carbs

inhibits the enzyme that breaks down complex carbs. you can’t absorb them, just eliminate them. so less glucose in the blood stream,.

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18
Q

whats the MOA of meglitinides

A

increase insulin secretion from islet cells (like sulfonylureas)

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19
Q

T/F Meglitinides have a faster onset and shorter duration than sulfs

A

TRUE

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20
Q

which drugs are meglitinides

A

RepaGLINIDE (Prandin)
NateGLINIDE (starlix)

meglitINIDES = repGLINIDE and NateGLINIDE

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21
Q

T/F Meglitinides are active whether glucose is present or not

A

FALSE - only active in the presence of glucose.

this decreases the risk of prolonged hypoglycemic episodes

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22
Q

meglitinies cause you to ___ weight

A

gain

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23
Q

the #1 med for new onset type!! diabetes that requires medication =

A

metformin

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24
Q

what class is metformin

A

bigauanides

bc metformin is the big dog

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25
Q

T/F Metformin has a high risk of hypoglycemia

A

FALSE - it decreases BG concentrations with only a very low risk of hypoglycemia - almost neutral when it comes to hypoglycemic events

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26
Q

what is the MOA of metformin? 3 points

A
  • decreases hepatic glucose production (reduces gluconeogenesis)
  • reduces glucose absorption from the intestine
  • increases insulin sensitivity
27
Q

why can someone who’s on metformin get off of their sulfonylurea?

A

because metformin reduces glucose absorption from the SI so you don’t need the sulf to increase beta islet insulin release

28
Q

which drug produces satisfactory results in 50% of the sulf failures

A

metformin

29
Q

whats the BB warning with metformin?

A

lactic acidosis

n/v, inc RR, HR, abd pain, shock

30
Q

how long before surgery should metformin be d/c’d?

A

48h

31
Q

whats the best way to prevent lactic acidosis

A

hydration

32
Q

hold metformin ___h prior to and after IV contrast because of

A

48, nephrotoxicity

33
Q

whats the package insert for metformin say

A

that withholding food/fluids during surgery may increase the risk for volume depletion, hOt, renal impairment.. so temporarily d/c metformin while patients have restricted food and fluid intake.

34
Q

metformin is contraindicated if GFR is

A

30

35
Q

do not initiate or re-evaulate patents with GFR

A

45

36
Q

metformin is contradicted in patents aged >__

A

80

37
Q

metformin has high rates of ____ upset

A

GI

38
Q

new recommendations for metformin are based on ___ NOT ___ and ____

A

GFR..

not gender and cr

39
Q

T/F metformin is contraindicated in CHF and hepatic impairment

A

TRUE

40
Q

which drugs are thiazolidinediones

A

rosiglitaZONE and pioglitaZONE

Thia is in the ZONE

41
Q

which drug class is esp effective in the obese

A

TZD’s

42
Q

whats the MOA of TZD’s

A

decrease hepatic glucose output and decrease insulin resistance

so TZD’s stop the liver and stop resistance

43
Q

which drug class cause hepatotoxicity

A

TZD’s

think: they work in the liver decreasing hepatic glucose output

44
Q

which drug class has a bizarre risk of bone fx

A

TZD’s

45
Q

TZDs cause weight ___

A

gain

46
Q

T/F: higher rates of CV deaths and MI’s in patients that take TZD’s

A

TRUE - avandia (ros)

aVan = cV death

47
Q

TZD’s have Three Terrible side effects like:

A

hepatotoxic, peripheral edema, CHF exacerbations

48
Q

DPP-4 inhibitor drugs =

A

gliptins

sitagliptin (Januvia)
Saxagliptin (onglyza)
linagliptin (tradjenta)
alogliptin

49
Q

DPP4 MOA

A
  • increases pancreatic insulin secretion
  • limits glucagon secretion
  • slows gastric emptying
  • promotes satiety

glucagon-like peptide.. when you eat, it is released.. tells you youre full and not to eat anymore and also kick starts a couple of processes to prep for glucose load.. pancreas/liver. so DPP4 is dipeptidyl peptidase and that reduces the breakdown of GLP1. so it lasts longer and continues to stimulate satiety

so it is working at different places where your glucagon like peptide normally works, to inc the amt of it.. to then limit glucagon sectretion, increase insulin secretion, slow gastric emptying , making you feel full

revise this card…..

50
Q

which drugs basically cause a forced gastroparesis

A

DDP4 inhibitors - the gliptins

51
Q

DPP4 inhibitors have 4 really bad side effects that were discovered post-marketing =

A

pancreatitis, angioedema, Stevens johnsons, anaphylaxis `

52
Q

which drugs have infection risk

A

DDP4 inhibitors - the gliptins

risk of URI + UTI’s

53
Q

which 2 drug classes fall under incretin mimetics

A

GLP-1 analogs & amylin analogs

54
Q

how do GLP1 analogs work

A

prolong gastric emptying, reduce post-prandial glucagon secretion

think: DPP4 inhibitors work like this too bc they reduce the breakdown of GLP1

55
Q

which drugs are GLP1 analogs?

A

the TIDES

exanatide (byetta, bydureon)
liraglutide (victoza)
albiglutide (tandem)
dulaglutida (trulicity)

56
Q

avoid which GLP1 analog in renal failure

A

exanatide (byetta)

BYEpass Byetta in RF

57
Q

avoid which GLP1 analog in thyroid carcinoma

A

liraglutide (victoza)

vicotza is NOT a victory in thyroid cancer

58
Q

how do amylin analogs work?

A

they increase insulin secretion, slow gastric emptying, increase beta cell growth, central appetite suppression

59
Q

which drug is an amylin analog

A

pramlinide (symlin)

slimy like the gila monster

60
Q

whats the BB warning with Amylin

A

hypoglycemia (esp type1)

61
Q

which drugs are SLGT2 inhibitors

A

the gliflozin’s

canagliflozin (invokana)
dapagliflozin (farxiga)
empagliflozin (jardiance)

gliFLOZIN’s get the glucose FLO goin

62
Q

how do SLGT2 inhibitors work

A

increase urinary glucose excretion.

make you pee it out.

within the kidneys there is a sodium and glucose transporter and by inhibiting this, we are now holding on to less glucose, we are peeing more out.

think STG = sodium glucose transporter

63
Q

SLGT2 inhibitors are contraindicated with

A

crcl <30
ESRD
HD

64
Q

since SLGT2’s increase urinary glucose excretion, what side effects are you thinking of

A

s/e r/t fluid shifts so hOtn

UTI (d/t extra glucose in urinary tract)

toe amputations (bc of the dehydration/fluid shifts/PVD)

Pharm2 S.Horvath (13 decks)

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