Diabetes Management
Categories:
- 1) Insulin Sensitizers: Lower Glucose by their actions on the liver, muscle and adipose tissue
- A) Biguanides
- MOA: Increases hepatic AMPK, inhibits mitochondrial hepatic gluconeogenesis and lipogenesis, increases peripheral uptake
- Reduces hepatic gluconeogenesis and glycogenolysis
- Metformin (Glucophage)
- 500mg once to twice daily or 850mg once daily
- Double dose after 5-7 days if no GI SE
- Max: 850mg BID or 1000mg BID, lower dose if GI SE
- 1st line therapy for T2DM, works on the liver
- Inhibits mGPD and Complex 1
- Improves fasting and postprandial hyperglycemia and hypertriglyceridemia in obese w/DM w/o Weight gain
- Decreases A1c by 0.7-1.5%
- Potential ASCVD benefit
- SE: Lactic Acidosis in renal/liver failure (alcohol misuse), diarrhea
- 20% GI upset, nausea, vomiting, no hypoglycemia
- 2/2 decreasing glucose absorption in the GI tract
- B12 deficiency
- Good for obese patients
- 20% GI upset, nausea, vomiting, no hypoglycemia
- CI: Acute Renal Failure, Liver Failure, Sepsis, GFR <30
- Stop 48hrs before being given contrast
- 500mg once to twice daily or 850mg once daily
- MOA: Increases hepatic AMPK, inhibits mitochondrial hepatic gluconeogenesis and lipogenesis, increases peripheral uptake
- B) Glitazones/Thiazolidinediones (TZD)
- MOA: Bind PPPAR-gamma nuclear transcription regulator, agonists, sensitizing peripheral tissue to insulin and increasing adiponectin
- Increased GLUT1 and GLUT4, decreased FFA, decreased hepatic glucose output, increase adiponectin, and decreased adipocyte resistance, no hypoglycemia
- Works on muscle and adipose tissue
- Used in combo with metformin = no hypoglycemia
- Can reduce insulin dose up to 50%, but edema increases 10-15%
- Receptors also found in the collecting tubule of the nephron and stimulate increased sodium resorption (similar to aldosterone)
- May use spironolactone to treat
- Rosiglitazone (Avandia)
- SE: increase LDL (15%), total cholesterol, and HDL (10%), decrease FFA (8-15%), Angina or MI increase risk, edema
- Pioglitazone (Actos)
- Lowers TG (9%), and increases HDL (15%), edema
- SE: Weight gain, fluid retention and CHF, Hepatotoxic
- CI: NYHA Class III/IV, Liver dysfunction
- Black box for HF increased risk
- Generally, not used in CKD
- A) Biguanides
- 2) Secretagogues: Stimulate insulin secretion by binding the sulfonylurea receptor
- A) Sulfonylureas
- MOA: Closes K+ channels in pancreatic B cell membrane, causing the cell to depolarize, releasing insulin via increased Ca2+ influx
- 1st Gen:
- SE: Disulfram-like effects (Hyponatremia, flushing)
- Chlorpropamide
- Tolbutamide
- Tolazamide
- 2nd Gen:
- 100x more potent, use in caution with CVD
- Skip dose if pt too sick to eat (must be taken with meals, heavy sugar beverages, soda, juice, sweet tea)
- Glimepiride (Amaryl)
- Glipizide (Glucotrol)
- CI: Liver failure
- Glyburide (Diabeta)
- CI: Liver disease, CKD
- 100x more potent, use in caution with CVD
- SE: Hypoglycemia (especially on an empty stomach), weight gain
- Sulfonylurea poisoning
- Treatment
- Excessive amounts of Dextrose
- Severe: Octreotide
- Treatment
- B) Meglitinide analogs
- MOA: Similar to Sulfonylureas, different binding site on Beta cell membrane
- Take prior to meals
- No sulfur moiety, no disulfram reaction
- Repaglinide (Prandin)
- SE: Hypoglycemia (worse with renal failure), WT gain
- Nateglinide (Starlix)
- D-Phenylalanine Derivative
- Reduced postprandial risk in BP like Repaglinide
- SE: Hypoglycemia (worse with renal failure), Wt gain
- MOA: Similar to Sulfonylureas, different binding site on Beta cell membrane
- A) Sulfonylureas
- 3) Secretagogues: Mimic incretin effect or prolong incretin action
- A) Glucagon-like peptide 1 (GLP1) receptor agonists
- MOA: Increase glucose dependent insulin secretion, decreases glucagon release, delays gastric emptying, increases satiety
- Mimic incretins
- More potent than DPP-4 Inhibitors
- Decrease food intake, increase insulin, decrease glucagon, decrease gastric emptying
- Associated with weight loss
- Now preferred over insulin for most patients when injectable therapy is indicated
- Dulaglutide (Trulicity)
- 3rd most weight loss
- Exenatide (Byetta, Bydureon)
- CI: GFR <30
- Liraglutide (Victoza)
- 6mg subq once daily for a week, then 1.2mg daily
- 340B @ CAMC
- 2nd most weight loss
- LEADER Trial
- Has FDA indication for ASCVD benefit
- Decreased CV death by 22%, ACM by 15%
- Has shown CKD benefit
- 6mg subq once daily for a week, then 1.2mg daily
- Lixenatide
- Least weight loss
- Reduces CV mortality, may reduce CKD
- Semaglutide (Rybelsus, Ozempic)
- Ozempic: 0.25mg weekly for 4 weeks, then 0.5mg weekly up to 2mg weekly
- Rybelsus: 3mg oral tablet, once daily
- Only oral GLP-1 available
- Most weight loss of group
- SE: Weight loss, Nausea/Vomiting, pancreatitis, weight loss
- Lower risk of hypoglycemia, decrease CVD/MI/Stroke, decrease progression of albuminuria
- Black box warning of increased risk of thyroid C-cell tumors
- RCI: History of Pancreatitis
- MOA: Increase glucose dependent insulin secretion, decreases glucagon release, delays gastric emptying, increases satiety
- B) DPP4 Inhibitors
- MOA: Inhibits DPP-4 enzyme that deactivates GLP-1
- Block the degradation of GLP-1 and GIP, thereby increasing insulin
- Can’t be used with GLP-1s
- Once daily, few SE
- Linagliptin (Tradjenta)
- No dose adjustment for renal failure
- Saxagliptin (Onglyza)
- Increased risk of HF (only one in class)
- Sitagliptin (Januvia)
- Alogliptin
- Increased risk of HF (not used)
- SE: weight neutral, mild urinary or respiratory infections, nasopharyngitis
- Potential increased risk of HF, joint pain, increased risk of pancreatitis
- MOA: Inhibits DPP-4 enzyme that deactivates GLP-1
- A) Glucagon-like peptide 1 (GLP1) receptor agonists
- 4) Slow intestinal absorption of glucose
- A) Alpha-glucosidase inhibitors
- MOA: Inhibits intestinal brush-border alpha-glucosidases, decreasing disaccharide absorption
- Delayed carbohydrate hydrolysis and glucose absorption in the SI, increasing absorption in the large intesine
- Decreases postprandial hyperglycemia
- Acarbose (Precose)
- Decreases postprandial hyperglycemia by 30-50%, decrease A1c by 0.5-1%, flatulence in 20-30%, abdominal pain
- 3 times daily
- Decreases intestinal CHO absorption
- Miglitol (Glyset)
- CI: Decreased renal function
- SE: Diarrhea, Flatulence
- MOA: Inhibits intestinal brush-border alpha-glucosidases, decreasing disaccharide absorption
- A) Alpha-glucosidase inhibitors
- 5) Inhibit reabsorption of filtered glucose in the kidney
- A) Sodium glucose co-transporter 2 inhibitors (SGLT2 Inhibitors)
- MOA: Blocks reabsorption of glucose in proximal convoluted tubule
- Causes glucosuria, weight loss is common
- Causes osmotic diuresis, decreasing BP
- Decreases progression of renal disease, Decreases CVD and MI risk if ASCVD
- May improve CKD, still do not use if GFR <30
- Canagliflozin (Invokana)
- Has shown CKD benefit, decreased CV death by 38%, ACM by 32%, HF hospitalization by 35%
- EMPA-REG Outcome Trail
- Dapagliflozin (Farxiga)
- Has shown CKD benefit
- Empagliflozin (Jardiance)
- Has shown CKD benefit
- Has FDA indication for ASCVD benefit, improving HF outcomes
- EMPEROR Trials
- HFpEF: Improved outcomes/Hospitalizations/QOL, Not mortality, reduced instance of hyperkalemia
- HFrEF: Improved outcomes/Hospitalizations, improved eGFR, reduced instance of hyperkalemia
- Ertugliflozin (Steglatro)
- Check Cr prior to initiation
- Indication: Type 2 DM or ASCVD (or give GLP-1) with metformin
- Careful in amputation, severe PVD, neuropathy, diabetic foot ulcers
- SE: Increases glucosuria, weight loss, UTIs, Genital infections, vaginal yeast infections, hyperkalemia, dehydration, orthostatic hypotension, Fournier’s gangrene, Triple risk of DKA (Euglycemic DKA), risk of lower limb infection/ulceration/amputations
- Hold for 24hrs prior to surgery or extreme sports
- Decreases risk of MI, stroke, CVD death
- MOA: Blocks reabsorption of glucose in proximal convoluted tubule
- A) Sodium glucose co-transporter 2 inhibitors (SGLT2 Inhibitors)
- 6) Glucagon suppression and slowing gastric emptying
- A) Amylin Analogs
- Pramlintide (Symlin)
- Delays gastric emptying and decreases glucagon
- SE: hypoglycemia (always given with insulin), nausea/V
- Pramlintide (Symlin)
- A) Amylin Analogs
- 7) Other
- Aldose Reductase Inhibitors
- Epalrestat
- Colesevelam (Welchol)
- Bromocriptine (Cycloset)
- Sitagliptin/Metformin (Janumet)
- Aldose Reductase Inhibitors
Insulin Preparations
- Fast Acting:
- Lispro (Humalog), Aspart (Novolog), Glulisine (Apidra)
- Peak: 0.5-1.5 hours
- Duration: 3-5 hours
- Peak coincides with food peak
- Short Acting:
- Regular Insulin (Humulin R, Novolin R)
- Peak: 2-4 hours
- Duration: 5-8 hours
- Peak may follow food peak
- Intermediate Acting:
- NPH Insulin (Humulin N, Novolin N)
- Peak: 4-12 hours
- Duration: 14+ hours
- Long Acting:
- Detemir (Levemir)
- Peak: 4-9 hours
- Duration: 12-24 hours
- May require BID administration
- Glargine (Lantus)
- Peak: None
- Duration: 14+ hours
- Peakless effect less likely to cause hypoglycemia
- Formulations with higher concentrations of glargine (300 vs 100u/mL) have longer duration (30+ hours)
- Detemir (Levemir)
- Ultra-Long Acting:
- Degludec (Tresiba)
- Peak: None
- Duration: 42+ hours
- Formation of a soluble hexamer at the injection site
- Degludec (Tresiba)
- Sliding Scale
- No basal insulin given, only reactively
- Good with Basal-Bolus patient with Sliding scale on top prn