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Definitions
Type I Diabetes
Autoimmune B-cell destruction insulin deficiency loss of insulin production
Type II Diabetes
Progressive loss of B-cell insulin secretion insulin resistance decreased insulin production over time
Identify and treat other CV risk factors
Gestational Diabetes
Develops during pregnancy
Risk of macrosomia (high birth weight), hypoglycemia
Clinical Presentation
Polyuria, polyphagia, polydipsia, blurred vision, fatigue
Screening
Overweight + 1 additional risk factor
Age 45 if no risk factors
FPG, 2h plasma glucose after 75g oral glucose tolerance test, and A1C
Risk Factors/Complications
First degree relatives
High risk races/ethnicities
Overweight (BMI ≥ 25 kg/m^2)
Autoimmune disease (thyroid)
Microvascular Complications: retinopathy, nephropathy, neuropathy
Macrovascular Complications: CHD, CVD, and PAD
Anxiety disorders, depression, eating disorders, mental illnesses
HTN, Dyslipidemia
Smoker
Non-Pharmacologic Measures
Nutrition therapy (carbohydrate counting, omega 3 fatty acids. fiber)
Limit saturated fat, cholesterol, trans fat, and sodium
3500 kcal weekly reduction = 1 lb weight loss/week
Waist circumference < 35 inches (females) and < 40 inches (males)
Physical activity (30 min/day, 4-5x/week)
Smoking cessation
Comprehensive Treatment
1. Primary Prevention ASA 81 mg
- Men or women ≥ 50 years old with 1 additional risk factor
2. Secondary Prevention ASA 81 mg
3. Blood Pressure Control Thiazide, CCB, ACEi, ARB
4. Cholesterol Control Mod/High Statin
5. Nephropathy
- Annual urine test screening for protein
- Urinary albumin excretion ≥ 30 mg/24 hours (kidney damage) ACEi, ARB
6. Retinopathy
7. Neuropathy
- Foot and visual examinations
Treatment Algorithm
Biguanides
MOA: Acts on liver to reduce hepatic glucose production, acts on intestine to enhance glucose uptake, acts on kidneys
to impair renal gluconeogenesis
Sulfonylureas
MOA: Stimulate insulin secretion from pancreatic beta cells
GLP-1 Analogs
MOA: Pharmacological increase in incretin glucose dependent increase in insulin, while inhibiting glucagon
Restores first phase insulin response
Albiglutide (Tanzeum)
30-50 mg SQ weekly
Dulaglutide (Trulicity)
0.75-1.5 mg SQ weekly
Thiazolidinediones (TZDs)
MOA: Act on PPAR gamma agonists (nuclear receptors) found in muscle, fat, and liver to induce gene expression
Increase peripheral muscle and adipose tissue insulin sensitivity decrease insulin resistance
Slow onset and offset because they are dependent on gene expression changes
Long lag time; max effect seen in 8-12 weeks
SGLT2 Inhibitors
MOA: Blocks early segment SGLT2 receptors in proximal tubule of kidneys, blocking reabsorption of glucose
Results in excretion of glucose and salt/water loss
Dapagliflozin works on kidney and pancreas therefore it can lead to increased levels of glucagon secretion
Alogliptin (Nesina)
Meglitinides
MOA: Stimulate insulin secretion from pancreatic beta cells
Miglitol (Glyset)
Taken with first bite of meal
Amylin Analogs
MOA: Amylin is produced by pancreatic beta cells to control glucose. This is synthetic amylin that slows gastric
emptying leading to inhibition of glucagon secretion in a glucose dependent manner (no effect on insulin)
Common:
N/V
Weight loss
Conversions
Can occur in a 1:1 (unit per unit) conversion of the total daily dose for most cases
Dose Reduction Exceptions
- Twice daily NPH once daily Glargine
- Use 80% of total daily NPH dose as initial insulin Glargine dose
- Once daily Toujeo once daily Lantus or Basaglar
- Use 80% of total daily Toujeo dose as initial Lantus or Basaglar dose
Rapid Acting: Bolus Insulin Carbs: Rule of 500 Can mix with NPH
4 units or 0.1 u/kg before meals Correction Dose/Factor: Rule of 1800
Inhaled (Afrezza)
- BBW: Do not use in
patients with asthma,
COPD, or smokers
Short Acting Carbs: Rule of 450 Can mix with NPH IV Use – DKA and
Regular (Humulin R, Novolin R) Correction Dose/Factor: Rule of 1500 Hyperkalemia
- Available w/o prescription
- Can be used IV Onset: 0.5-1 hr
Peak: 2-4 hrs
Duration: 4-8 hrs