All material is copyrighted and the property of mehlmanmedical.
Copyright © mehlmanmedical.
Privacy Policy and Terms and Conditions
HY points about each drug followed by a quiz at the end
—
Insulin preparations
- Insulin is the only treatment for type I diabetes (insulin deficiency).
- Insulin is used last resort for type II diabetes (insulin resistance).
| Insulin preparations | ||
| Type | When after administration does peak effect occur? | Name |
| Rapid-acting | 1 hour | LAG: Lispro, Aspart, Glulisine |
| Short-acting | 2-3 hours | Regular insulin |
| Intermediate-acting | 4-10 hours | NPH |
| Long-acting | Detemir (6-12 hours); Glargine (no real peak) | Detemir, Glargine |
Quiz yourself:
Type II diabetes meds (oral hypoglycemics)
Metformin
MOA of metformin?
- Inhibits mGPD (a mitochondrial enzyme called glycerophosphate dehydrogenase).
- “Increases glycolysis and decreases gluconeogenesis” is the MOA answer on the USMLE.
Side-effects of metformin?
- Lactic acidosis (HY)
- Increased risk in patients with renal insufficiency.
- 45M + T2DM + bicarb of 20 + creatinine of 1.6; next best step? –> answer = stop metformin.
Thiazolidinediones (pioglitazone, rosiglitazone)
MOA of thiazolidinediones?
- Activate PPAR-α, leading to increased insulin sensitivity.
Side-effects of thiazolidinediones?
- Heart failure
- Weight gain
- Edema
Sulfonylureas
- First generation: Tolbutamide, Chlorpropamide
- Second generation: Glyburide, Glipizide, Glibenclamide
- Third generation: Glimepiride
MOA of sulfonylureas?
- Insulin secretagogues (i.e., promote insulin release); require functioning beta-islet cells. If patient is on a sulfonylurea and his/her HbA1c is very high (e.g., 9+), it’s because he/she has most likely already has lost the beta-islet cells.
- Close K+ channel on β-islet cells –> more K+ trapped in the cell –> cell depolarizes –> Ca2+ then enters cell –> insulin-containing vesicles are released from the cell.
Side-effects of sulfonylureas?
- First generation: disulfiram-like reaction with EtOH.
- Second + third generation: hypoglycemia (especially 2nd-gen glibenclamide).
Meglitinides (Repaglinide, Nateglinide)
MOA of meglitinides?
- Same as sulfonylureas but structurally different.
- Just know the MOA.
GLP-1 analogues (Liraglutide, Exenatide)
MOA of GLP-1 analogues?
- ↓ glucagon release; ↑ glucose-dependent insulin release.
- GLP-1 (glucagon-like peptide-1) is an endogenous GI hormone that suppresses glucagon release and increases insulin release in response to oral glucose.
Side-effects of GLP-1 analogues?
- Pancreatitis
DPP-4 inhibitors (Linagliptin, Saxagliptin, Sitagliptin)
MOA of DPP-4 inhibitors?
- DPP-4 is an enzyme that breaks down GLP-1.
- Therefore the -gliptins help maintain levels of GLP-1.
- Since GLP-1 ↓ glucagon release and ↑ glucose-dependent insulin release, DPP-4 inhibitors produce the same effect as the GLP-1 analogues liraglutide and exenatide.
SGLT-2 inhibitors (Dapagliflozin, Canagliflozin)
MOA of SGLT-2 inhibitors?
- Inhibit sodium-glucose transporter 2 (SGLT-2), which normally reabsorbs glucose in the PCT of the kidney.
- These agents decrease serum glucose by promoting glycosuria.
Side-effects of SGLT-2 inhibitors?
- Increased risk of vulvovaginal candidiasis and UTIs (disruption of normal flora and pH balance).
α-glucosidase inhibitors (Acarbose, Miglitol)
MOA of α-glucosidase inhibitors?
- Decrease small bowel absorption of glucose at the brush border, resulting in ↓ postprandial hyperglycemia.
Side-effects of α-glucosidase inhibitors?
- Diarrhea
Amylin analogues (Pramlintide)
MOA of pramlintide?
- Amylin is a peptide normally co-secreted with insulin. It inhibits glucagon secretion, delays gastric emptying, and promotes satiety.
- It is deficient in type I diabetics (and late type II after the pancreas burns out).
—
