Type 2 Diabetes Mellitus Oral Medications – Medical Institution

Diabetes Mellitus:

Diabetes is metabolic disorder that causes blood glucose (sugar) levels to rise higher than normal. This is also called hyperglycemia. Diabetes is one of the major causes of early illness and death worldwide. Type 2 diabetes is the most common form of diabetes and it accounts for over 90 percent of patients with diabetes. Type 2 diabetes is primarily due to obesity and its onset is now common in Adolescence. It is characterized by insulin resistance leading to high level of insulin.

Managing diabetes:

– Lifestyle change (healthy nutrition, increase activity and weight loss)
– Medication
– Prevention of and screening for complications
– Surgery

Management Goals:

– Preprandial glucose < 100 mg/dl
– Bedtime glucose < 120 mg/dl
– A1C < 7%** (many now using 6.5%), Monitor every 3 months
– Blood pressure < 130/80
– LDL cholesterol < 100 mg/dl, (< 70 mg/dl with cardiovascular disease)


– Influenza yearly
– Pneumococcal vaccine once and repeat at age 65 (but 5 years after the 1st)
– Hepatitis B now recommended for all ≤ age 60 (after age 60 at high risk for hep-B)
– Tdap (replaces dT one time only): OK after age 65 and no minimum time after last Td

Screening for Comorbid Conditions

– Routine blood pressure check at every doctor visit
– Yearly Lipid panel
– Screen for hypothyroidism as it can contribute to dyslipidemia
– Screen for tobacco use
– Screen for depression (more prevalent in patients with chronic disease)


– Macrovascular (e.g. heart disease and stroke)
– Microvascular (e.g. retinopathy, neuropathy and nephropathy)
– Diabetic foot problems (e.g. ulcers, osteomyelitis, charcot foot)
– Ketoacidosis and Hyperosmolar hyperglycemia





– Metformin
– Exact mechanism is unknown
– Works primary in liver: Decreases gluconeogenesis and increase glycolysis leading to decrease serum glucose
– Increases peripheral glucose uptake (insulin sensitivity) 
– Lactic acidosis
– Renal failure
– Gastrointestinal disturbance (e.g. nausea, vomiting, diarrhea and Flatulence)
FIRST generation:
– Tolbutamide
– Chlorpropamide
SECOND generation:
– Glyburide
– Glimepiride
– Glipizide
– Blocks the potassium (K+) channels in Beta-cells membranes of pancreas. This causes cells depolarization and influx of calcium (Ca+) into the cells, triggering insulin release


FIRST generation:
– Disulfiram-like reactionSECOND generation:
– Hypoglycemia
– Repaglinide
– Nateglinide
– Stimulate the pancreatic Beta-cells to release insulin (similar to sulfonylureas)


– Headache
– Hypoglycemia
– Upper respiratory tract infection

– Pioglitazone
– Rosiglitazone
– Binds and activates PPARs (peroxisome proliferator-activated receptors) a group of nuclear receptors, with greatest specificity for PPARγ (gamma), leading to increase cell sensitivity to glucose.


– Weight gain
– Edema, fluid retention and subsequent heart failure
– Hepatotoxicity (liver failure)
– Decrease bone density and increase fracture risk, especially in women
Alpha-glucosidase inhibitors:
– Acarbose
– Miglitol
– Inhibits intestinal brush border alpha-glucosidase enzymes, which reduces the rate of digestion of carbohydrates.
– This delays glucose absorption from the gut and subsequently decreases postprandial hyperglycemia. 
– Gastrointestinal disturbance (e.g. flatulence, diarrhea and abdominal pain)
– Rash (rare)
– Pramlintide
– Decreases secretion of glucagon, which is a catabolic hormone that opposes the effects of insulin.
– NOTE: Glucagon increases blood glucose 
– Headache
– Severe hypoglycemia
– Gastrointestinal disturbance (e.g. nausea, anorexia and vomiting)
GLP-1 (glucagon-like peptide-1 agonist) analogs:
– Exenatide
– Increases insulin release and decreases glucagon release – Headache and dizziness
– Hypoglycemia
– Gastrointestinal disturbance (e.g. nausea, vomiting and diarrhea) 
DPP-4 (dipeptidyl peptidase 4) inhibitors:
– Sitagliptin
– Increases incretin levels (GLP-1 and GIP), which inhibit glucagon release, which in turn increases insulin secretion, decreases gastric emptying, and decreases blood glucose levels.


– Peripheral edema
– Hypoglycemia
– Gastrointestinal disturbance (e.g. nausea, diarrhea and constipation)
– Osteoarthritis
SGLT2 ( sodium-glucose transporter 2) Inhibitors:
– Gliflozin
– SGLT2 works in the kidney to reabsorb glucose, SGLT2 inhibitors, block this action, causing excess glucose to be eliminated in the urine.


– Hypoglycemia
– Ketoacidosis
– Increased risk of urinary tract infections and candidal vulvovaginitis
Bile Acid Sequestrants:
– Colesevelam
– The exact mechanism in reducing serum glucose is unknown


– Gastrointestinal disturbance (e.g. nausea, diarrhea, Flatulence and constipation)
– Weakness and muscle pain
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