Diabetes - E.

g:
lispro
Aspart
Type I (IDDM) Type II (NIDMM)
Glulisine (commonly used)
Insulin Absolute lack Relative lack

Age of onset Early onset. Late-onset. B. Rapid/Short-acting

Usually during Frequently over 35.
childhood or - E.g.
puberty (below
30-year-old)
Regular insulin
Semi-lente insulin
Nutritional Frequently Obesity usually - Prompt Insulin Zinc Suspension
status at time undernourishe present - Amorphous IZs
of onset d
- IV, SQ
Prevalence 5-10% of 90-95% of diagnosed
diagnosed diabetics - BOLUS insulin
diabetics
C. Intermediate-acting
Genetic Moderate Very strong
predisposition - E.g.
NPH (Neutral Promatine of Hagedorn)
Defect or B cells are Inability of B cells to Lente Insulin
Deficiency destroyed produce appropriate
eliminating the quantities of insulin; - BASAL insulin
production of Insulin Resistance;
insulin other defects
D. Long-acting

Ketoacidosis Prone Not prone - E.g.

Treatment Insulin Oral antidiabetic Ultralente

drug - Extended IZS

Glargine
- peakless insulin

• Treatment goal: Detemir

• Insulin Levemir

A. Ultra-rapid/Ultra-short E. Mixed Insulin

- DOA: 15-30 min - Rapid (bolus) + Intermediate (basal)

- BOLUS insulin - Regimen: Basal insulin

> Goal: ↑ glucose

 > Monitoring: CBG (Capillary Blood  Glicazide
Glucose), HbA1c(<7%)
- S/E: hypoglycemia, blood dyscrasia,
weight gain, disulfiram-like reaction

• Insulin Secretagogues

• MOA: (-) ATP sensitive K+ channels B. Meglitinides

A. Sulfonylureas - E.g. Nateglinide, Repaglinide

- MOA: Stimulate the pancreatic release of - Use: for post-prandial glucose control
insulin, Inhibit the pancreatic release of
glucagon, increase insulin receptor binding, - S/E: hypoglycemia, weight gain
Decrease hepatic extraction of insulin

- E.g. • Insulin Sensitizer

1st Generation (less potent but equally A. Biguanides
efficacious; associated with a number of
drug interactions) - E.g. Metformin

 Acetazolamide - MOA: decrease gluconeogenesis

 Tolazamide - 1st line

 Chlorpropamide - Only treatment for

(a very long t1/2,
not used for - Also used for PCOS
elderly with
kidney/liver - S/E: lactic acidosis, megaloblastic
problems) anemia, wieght loss

 Tolbutamide B. Thiazolidinediones
(fastest onset of
action 30 - E.g. Rosi-, Pio-, Tri-, -glitazone
minutes,
- MOA: (insulin sensitizer) activates
cardiotoxic)
PPAR-gamma (Peroxisome Proliferator
2nd Generation (more potent agents, Activator Receptor) resulting to
less common S/E) ↑↑glucose uptake in the muscle,
adipose tissue
 Glimepiride
- S/E: cardiotoxicity, hepatotoxicity
 Glibenclamide
- “Black box warning”
 Glipizide
• Alpha-Glucosidase Inhibitors
 • MOA: competitive inhibition of
intestinal alpha-glucosidase
hydrolase and alpha-amylase
preventing digestion of dextrins and
disaccharides into the absorbable
monosaccharides (used for T1 & T2
DM)

• E.g. Acarbose, Miglitol

• S/E: Flatulence, Hepatotoxicity

(Acarbose)

• Incretin-Acting Drugs/Incretin-
mimetics

• Goal: decrease glucose

A. GLP1 analogue

- e.g. exenatide, liraglutide

B. DPP-IV (DD4) inhibitors

- e.g. sitagliptin, linagliptin, saxagliptin

- vs type 1 & 2 DM
- causes weight loss
- hypoglycemia