diabetes Flashcards by J N

rapid acting insulins

insulin aspart

insulin lispro

How well did you know this?

Not at all

Perfectly

short-acting insulins

regular insulin (humulin R, novolin R)

How well did you know this?

Not at all

Perfectly

intermediate-acting insulins

NPH insulin (humulin N, novolin N)

How well did you know this?

Not at all

Perfectly

long-acting insulins

insulin glargine

detemir

How well did you know this?

Not at all

Perfectly

inhaled insulins

rapid-acting: afrezza

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

How well did you know this?

Not at all

Perfectly

why do insulins have different durations of action

amino acid sequence alterations of biological insulins

How well did you know this?

Not at all

Perfectly

tx for type 1 vs type 2 DM

1: insulin
2: oral drugs (everything else)

How well did you know this?

Not at all

Perfectly

sulfonylurea drugs

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

How well did you know this?

Not at all

Perfectly

biguanide drugs

metformin

How well did you know this?

Not at all

Perfectly

thiozolidinediones

pioglitazone

How well did you know this?

Not at all

Perfectly

incretin mimetics

DPP4 inh: -gliptans

GLP-1 agonists: exenatide, liraglutide

How well did you know this?

Not at all

Perfectly

DPP4 inhibitors

sitagliptins, linagliptin, saxagliptin

How well did you know this?

Not at all

Perfectly

alfa-glucosidase inhibitors

acarbose, miglitol

How well did you know this?

Not at all

Perfectly

Na/glucose cotransporter-2 (SGLT2) inhibitors

canagliflozin, dapagliflozin

How well did you know this?

Not at all

Perfectly

basal vs bolus insulin

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

How well did you know this?

Not at all

Perfectly

uses, advantages, limitations of rapid-acting insulins

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

How well did you know this?

Not at all

Perfectly

advantages and limitations of short-acting insulins

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

How well did you know this?

Not at all

Perfectly

uses, advantages, limitations of intermediate-acting insulins

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

How well did you know this?

Not at all

Perfectly

mechanism, advantages, limitations of long-acting insulins

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

2/3 1/3 rule for starting insulin therapy

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

pre-mixed insulins

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

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

biguanides

thiazolidinediones

drugs that stimulate pancreas to make more insulin

sulfonylureas

meglitinides

drugs that slow absorption of starches

alpha-glucosidase inhibitors

incretin mimetics and MOA

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

synthetic amylin analogs MOA

slow gastric emptying and decrease post-meal glucagon levels

SGLT-2 inhibitors MOA

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

bromocriptine for diabetes

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

metformin classification and MOA

biguanide | decreases hepatic glucose production, also an insulin-R sensitizer

metformin advantages and disadvantages

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

MOA sulfonylureas

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

adverse effects of sulfonylureas

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

specific adverse effect of glyburide

sulfonylurea with active metabolites accumulate in renal failure

meglitinides MOA and ADRs

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

thiazolidinediones (glitazones) MOA

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

thiazolidinediones (glitazones) ADR

rosiglitazone - withdrawn for CV side effects | requires 30% less insulin (d/t increased sensitivity)

a-glucosidase inhibitors MOA and ADR

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

GLP-1 sites of action and effects

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)

GLP-1 and GIP

released by GI tract in response to food | stimulate insulin secretion, reduce glucagon, slow gastric emptying, and increase satiety

CD26

DPP-4 peptide, many diverse immunological functions

use of DPP4 inhibitors

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

DPP4 inhibitor ADRs

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

exenatide

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

GLP-1-R agonist ADRs

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

SGLT-2 inhibitors (flozins) ADRs

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