contraindications
A patient with T2DM and NYHA Class III heart failure is started on a new oral agent. He presents 3 weeks later with a 10-lb weight gain and 2+ pitting edema.
Question: This presentation is a classic contraindication for this drug class, which acts as a PPAR-gamma agonist and causes fluid retention.
What are thiazolidinediones (TZDs)
While adults with T2DM often experience a slow decline, adolescents with T2DM are noted to have a more precipitous failure of this specific cell type and a reduced incretin effect.
What are pancreatic beta cells
A T2DM patient on basal insulin complains of fasting hyperglycemia (~200 mg/dL). A 3 AM glucose check reveals a value of 55 mg/dL.
Question: This 3 AM finding confirms the morning hyperglycemia is a rebound phenomenon caused by a counter-regulatory hormone surge in response to nocturnal hypoglycemia
What is the Somogyi effect?
For a 58-year-old patient with Type 2 Diabetes, established coronary artery disease, hypertension, and microalbuminuria (UACR = 60 mg/g), evidence-based guidelines mandate initiating three specific drug classes for organ protection, independent of their A1c or baseline metformin use.
Name these three classes.
What are:
An SGLT-2 inhibitor or GLP-1 receptor agonist (for cardiovascular & renal benefit)
An ACE inhibitor or ARB (for renal protection/hypertension)
A Statin (for hyperlipidemia/ASCVD risk reduction)
A T2DM patient with an eGFR of 25 mL/min/1.73 m² is scheduled for a clinic visit.
Question: This first-line oral agent is absolutely contraindicated in this patient due to the high risk of lactic acidosis associated with severe renal impairment.
What is metformin?
While this entire lipid-lowering class carries a slight risk of new-onset T2DM, this specific agent is a prodrug with <5% oral bioavailability due to extensive first-pass metabolism by CYP3A4.
What is simvastatin?
A 32-year-old female, G1P1, had gestational diabetes (GDM) during her pregnancy 4 years ago. Her A1c is now 6.8%.
Question: Her prior GDM is a major non-modifiable risk factor that served as an early "stress test," unmasking her underlying beta cell dysfunction and predisposition to T2DM, which was exacerbated by this
What are the hormonal changes of pregnancy
A 19-year-old T1DM patient presents with Kussmaul respirations and confusion. Labs show glucose 480 mg/dL, pH 7.18, and positive serum ketones.
Question: The Kussmaul breathing is a respiratory compensation for the severe metabolic acidosis, which is a direct result of this alternative energy pathway being activated by absolute insulin deficiency.
What is ketogenesis (or uncontrolled lipolysis and ketone body production)?
This lab test, a marker of endogenous insulin secretion, is crucial for differentiating T1DM from T2DM in an insulin-treated patient; a level < 0.20 nmol/L strongly suggests T1DM.
What is C-peptide?
A 50-year-old T2DM patient with "walking pneumonia" is prescribed a 5-day course of azithromycin and a 5-day prednisone taper. His home glucose readings, normally 130-160, are now consistently >350 mg/dL.
Question: While the infection and antibiotic are factors, this profound hyperglycemia is a direct pharmacodynamic effect of this other prescribed medication, which rapidly induces insulin resistance and stimulates gluconeogenesis.
What are corticosteroids (prednisone)?
This class of insulin secretagogues, particularly long-acting agents like glyburide, is generally avoided in patients with CKD due to the high risk of severe, prolonged hypoglycemia as its active metabolites accumulate.
What are sulfonylureas?
A patient on basal insulin consistently wakes up with a fasting glucose of 210 mg/dL. A 3 AM glucose check is 185 mg/dL.
Question: This pattern, without nocturnal hypoglycemia, is attributed to the "dawn phenomenon," a physiological surge of growth hormone and this other counter-regulatory hormone.
What is cortisol?
A 62-year-old T2DM patient with CKD Stage 4 (eGFR 22) is on metformin (at an inappropriate dose) and develops a severe UTI. He is prescribed trimethoprim-sulfamethoxazole. He presents to the ED with an anion-gap metabolic acidosis, but his lactate is only mildly elevated. His serum creatinine has jumped from 2.8 to 4.5.
Question: The trimethoprim component is causing this specific renal adverse effect that can both worsen metformin accumulation and independently raise creatinine, complicating the diagnosis of lactic acidosis.
What is competitive inhibition of creatinine secretion at the proximal tubule?
DAILY DOUBLE
For a T2DM patient with established atherosclerotic cardiovascular disease, ADA guidelines recommend adding an agent from one of these two drug classes, independently of A1c, due to their proven cardiovascular benefits.
What are GLP-1 receptor agonists and SGLT-2 inhibitors?
Case: A 72-year-old T2DM patient with an eGFR of 25 mL/min/1.73 m² is reviewed. His provider notes that both metformin and glyburide are contraindicated.
Question: While both drugs must be avoided, they pose two distinct, life-threatening risks due to their clearance pathways. Metformin accumulation, due to its renal excretion, causes [THIS], while the accumulation of glyburide's active metabolites causes [THIS].
What are lactic acidosis and severe, prolonged hypoglycemia?
A 75-year-old T2DM patient on glyburide is admitted for community-acquired pneumonia and started on IV levofloxacin. The nurse reports erratic glucose levels: 410 mg/dL before the dose and 55 mg/dL two hours after the dose.
Question: This antibiotic class is known to cause severe dysglycemia (both hyper- and hypoglycemia) by interfering with this specific ion channel in pancreatic beta cells.
What are fluoroquinolones and their effect on the ATP-sensitive potassium (K-ATP) channel?