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Pharm 7 > diabetes > Flashcards

diabetes Flashcards

1
Q

rapid acting insulins

A

insulin aspart

insulin lispro

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2
Q

short-acting insulins

A

regular insulin (humulin R, novolin R)

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3
Q

intermediate-acting insulins

A

NPH insulin (humulin N, novolin N)

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4
Q

long-acting insulins

A

insulin glargine

detemir

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5
Q

inhaled insulins

A

rapid-acting: afrezza

*very new, no data on efficacy, ADRs, and cost

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6
Q

why do insulins have different durations of action

A

amino acid sequence alterations of biological insulins

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7
Q

tx for type 1 vs type 2 DM

A

1: insulin
2: oral drugs (everything else)

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8
Q

sulfonylurea drugs

A

glyburide, glipizide, glimepiride, meglitinides (repa- and nate-glinide)

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9
Q

biguanide drugs

A

metformin

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10
Q

thiozolidinediones

A

pioglitazone

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11
Q

incretin mimetics

A

DPP4 inh: -gliptans

GLP-1 agonists: exenatide, liraglutide

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12
Q

DPP4 inhibitors

A

sitagliptins, linagliptin, saxagliptin

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13
Q

alfa-glucosidase inhibitors

A

acarbose, miglitol

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14
Q

Na/glucose cotransporter-2 (SGLT2) inhibitors

A

canagliflozin, dapagliflozin

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15
Q

basal vs bolus insulin

A

basal- continuous secretion, accounts for ~50% body’s daily insulin production
bolus- stimulates glucose disposal and storage, limits post-prandial hyperglycemia, accounts for the rest of body’s daily insulin production

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16
Q

uses, advantages, limitations of rapid-acting insulins

A

use: prior to eating (w/i 15 min) bc quick release, to cover mealtime sugars
adv: mealtime dose, 2x speed of regular insulin, rapid onset, short duration, convenient delivery
limits: must eat immediately after dosing, multiple injections/day, no basal insulin coverage, expensive

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17
Q

advantages and limitations of short-acting insulins

A

adv: no Rx needed, only 2/day, can provide postprandial control
limit: 30-60 min onset, duration 2-5 hr increases risk hypoglycemia after meals, must dose 30 min before eating

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18
Q

uses, advantages, limitations of intermediate-acting insulins

A

use: in insulin mixtures (w rapid and short-acting), to mimic basal insulin
adv: long duration (up to 20 h), mixed w regular insulin to reduce injection #, no Rx required
limits: contains protamine and Zn (rare immunologic rxn at injection site), longer acting = inc risk hypoglycemia, can’t be given IV

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19
Q

mechanism, advantages, limitations of long-acting insulins

A

MOA: injected, microprecipitate forms “depot” that releases insulin over 24 hours

adv: low risk nocturnal/any hypoglycemia, lower risk weight gain vs NPH, can be prescribed w oral agents
limits: expensive, no mixing w other insulin, no bolus = use w rapid/short-acting insulin, can’t give IV

20
Q

2/3 1/3 rule for starting insulin therapy

A

with regular and NPH insulin
2 injections per day: 2/3 total insulin dose given in AM
1/3 total dose given before dinner
2/3 dose = NPH (intermediate) and 1/3 = short-acting or regular insulin

21
Q

pre-mixed insulins

A

have rapid/short and intermediate combos
ex: 70% NPH + 30% regular or aspart, or 75% NPL + 25% lispro
eliminates difficulty of mixing and combines rapid and extended insulins

22
Q

drugs that sensitize body to insulin and/or control hepatic glucose production

A

biguanides

thiazolidinediones

23
Q

drugs that stimulate pancreas to make more insulin

A

sulfonylureas

meglitinides

24
Q

drugs that slow absorption of starches

A

alpha-glucosidase inhibitors

25
Q

incretin mimetics and MOA

A

dipeptidyl peptidase-IV (DPP4) inhibitors: enhance incretin levels by inhibiting enzyme responsible for incretin inactivation, prolonging action of GLP-1 and GIP
glucagon-like (GLP-1)-R agonists: stimulate insulin secretion in presence of glucose, block glucagon release

26
Q

synthetic amylin analogs MOA

A

slow gastric emptying and decrease post-meal glucagon levels

27
Q

SGLT-2 inhibitors MOA

A

decrease renal absorption of glucose (proximal tubule) to increase urinary glucose excretion and decrease blood glucose

28
Q

bromocriptine for diabetes

A

ergot-derived dopamine agonist that mildly lowers blood glucose by unknown mechanism

29
Q

metformin classification and MOA

A

biguanide

decreases hepatic glucose production, also an insulin-R sensitizer

30
Q

metformin advantages and disadvantages

A

adv: a/w weight loss, little/no hypoglycemia
dis: nausea, diarrhea, abd discomfort (50%), renal elim, CI w renal insufficiency, accumulation -> lactic acidosis

31
Q

MOA sulfonylureas

A

bind ATP-sensitive K channels in beta-cell membrane causing depolarization -> Ca influx = degranulation and release of insulin
independent of food intake

32
Q

adverse effects of sulfonylureas

A

hypoglycemia (dose-dependent), weight gain, sulfa allergy

33
Q

specific adverse effect of glyburide

A

sulfonylurea with active metabolites accumulate in renal failure

34
Q

meglitinides MOA and ADRs

A

similar to sulfonylureas but no sulfa compound = no sulfa allergy
*must take w meal d/t rapid onset and short duration of action

35
Q

thiazolidinediones (glitazones) MOA

A

selective agonist for peroxisome proliferator activated receptor (PPAR), which regulates txn of insulin-responsive genes
promotes sk mm glucose uptake and reduce insulin resistance

36
Q

thiazolidinediones (glitazones) ADR

A

rosiglitazone - withdrawn for CV side effects

requires 30% less insulin (d/t increased sensitivity)

37
Q

a-glucosidase inhibitors MOA and ADR

A

inhibits intestinal breakdown of carbohydrates and delay absorption of monosaccharides
*useful for high post-prandial glucose
ADR: bloating, diarrhea, flatulence

38
Q

GLP-1 sites of action and effects

A

brain: dec food intake, inc satiety
stomach: dec motility
pancreas: inc insulin secretion, dec glucagon secretion; -> liver/peripheral tissues: dec endogenous postprandial glucose production (liver), inc insulin action (tissue)

39
Q

GLP-1 and GIP

A

released by GI tract in response to food

stimulate insulin secretion, reduce glucagon, slow gastric emptying, and increase satiety

40
Q

CD26

A

DPP-4 peptide, many diverse immunological functions

41
Q

use of DPP4 inhibitors

A

sitagliptin (prototype) for type 2 DM as monotherapy or in combo w metformin, sulfonylurea, glitazone, or insulin
*metformin is DOC, but consider this if metformin CI d/t liver failure, inc risk lactic acidosis, etc

42
Q

DPP4 inhibitor ADRs

A

renal elimination = reduce dose if CrCl less than 50 ml/min

43
Q

exenatide

A

synthetic form of Gila monster saliva protein similar to GLP-1, for type 2 DM unable to control w metformin and/or sulfonylurea

44
Q

GLP-1-R agonist ADRs

A

nausea, vomiting, diarrhea, hypoglycemia if given w sulfonylurea
hemorrhagic or necrotizing pancreatitis, may result in death

45
Q

SGLT-2 inhibitors (flozins) ADRs

A

increased genital mycotic infections (women), UTIs, increased diuretic effect

Pharm 7 (7 decks)

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