Diabetic medications- Do you know all the new diabetic medications?

Diabetic Medications

There are a myriad of diabetic drugs out there, all with strange and difficult to pronounce names. So how do we keep this straight? It’s not important that you know the specific names. Rather recognize the class. You can look the names up and quickly learn which class it belongs to. Once you know the class you should know what to do and what to worry about. 

There are 6 main classes of diabetic medications:

  • Metformin
  • Insulin
  • Sulfonylureas
  • GLP-1 agonists
  • DPP-4 inhibitors
  • SGLT2 inhibitors


Separate these into your hypoglycemics and non-hypoglycemics. 

Hypoglycemic agents 

  • Insulin

    • Replaces the body’s endogenous insulin
    • Insulin comes in a variety of forms classified by there duration and onset of action
      • Short acting- such as novolog (Aspart) and humalog (Lispro)
      • Moderate acting- such as regular insulin or NPH
      • Long acting- such as glargine (Lantus) and detemir (Levimir)
    • Again, it’s not important to recognize and memorize these. Instead recognize that insulin comes in 3 different formulations, all with a different time to peak onset and duration of action. If you recognize that, you can look up which category the insulin your patient took fits into and in turn what time you can expect to see it’s peak effect and how long you can expect it to last. 


  • Sulfonylureas– such as glimiperide, glipizide, glyburide
    • These directly stimulate insulin release from pancreatic beta-cells
    • These can be scary overdoses and are long acting too 
      • They can experience rebound hypoglycemia and often require a D10 drip and admission to the hospital for monitoring
      • Recognize one pill can cause serious harm and risk in a young pediatric patient
      • Treated with D10. Might also get octreotide in the hospital


  • GLP-1 agonists? – such as liraglutide (Victoza), dulaglutide (Trulicity), semaglutide (Ozempic)
    • Stimulates insulin release from the pancreas on a glucose dependant basis
    • Generally thought not to cause hypoglycemia but rare reports of these leading to hypoglycemia do exist in the literature
    • These are subcutaneous injections
      • Pen SQ injection which may resemble an insulin pen
      • Some are once weekly injections (Dulaglutid [Trulicity], semaglutide [Ozempic])


Non-hypoglycemic agents

  • Metformin

    • Guideline recommended first line agent for diabetes mellitus type 2
    • #5 most prescribed drug in the U.S. 
    • Lots of off-label uses (indications other than diabetes)
      • Weight loss
      • Slows cardiovascular progression
      • Slows colon and prostate tumor progression
      • Pre-diabetes
      • Improve fertility
    • Rare complication of severe and life threatening lactic acidosis
      • Occurs in an overdose 
      • Or in renal failure as metformin is cleared by the kidneys
      • Classic presentation is an OD or elderly patient who developed a renal insult
      • Will look like any other acidotic patient
        • Sick appearing, possibly altered
        • Deep rapid respirations in an attempt to compensate for the acidosis
      • Carries a 30-50% mortality rate 
  • DPP-4 inhibitors– such as inagliptin (Tradjenta), sitagliptin (Januvia)
    • These prevent the inactivation of the glucagon like peptide -1 (GLP-1) which is responsible for insulin release from the pancreas on a glucose dependant basis
    • Do not commonly cause complications that we need to be concerned about in the pre-hospital setting
  • SGLT2 inhibitors
    • These inhibit the ability for the sodium-glucose transport protein-2 from re-uptaking glucose in the kidney, thereby letting glucose “spill” into the urine
    • Can also act as an osmotic diuretic and as such have gained FDA approval for the treatment of heart failure even in the non-diabetic patient
    • Rare complication of euglycemic ketoacidosis
      • Occurs in the previously uncontrolled diabetic
      • They continue to have a suppression of insulin so despite spilingl glucose into the urine and effectively lowering blood glucose the patient still cannot get glucose into the cells where it is needed, thus, lipolysis must be performed in order to compensate
        • This breakdown of fatty acids leads to the production of ketone bodies
        • This is the same process that leads to classic DKA 
        • Difference here is the patient is spilling there extra blood glucose into the urine so when we obtain a finger stick glucose it is in the high normal range (150-200)
      • These patients present and look just like a DKA patient (and they are in DKA!) but will have a glucose in the 150-200 range


Take Home

Know the classes. Know which ones cause hypoglycemia. Know which ones have rare complications. Look up the rest. 


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