Type 2 Diabetes Mellitus

• Type 2 Diabetes Mellitus arises when the body doesn't produce enough insulin or cannot use insulin effectively, despite the pancreas still producing some insulin.

Metabolic Abnormalities

• Insulin resistance or inadequate insulin secretion from pancreatic beta cells results in the insulin receptors not functioning properly and/or insufficient insulin production, preventing glucose from entering cells and causing hyperglycemia.
• Liver abnormality means the liver responds erratically to blood glucose levels, releasing too much or too little glucose.
• Adipose tissue releases cytokines, leading to chronic inflammation associated with Type 2 diabetes.

Risk Factors

• Non-modifiable risk factors include being at least 45 years old, having a family history of diabetes, or a history of gestational diabetes.
• Modifiable risk factors, often linked to adipose tissue, include being overweight or obese, physical inactivity, hyperlipidemia, hypertension (vasoconstriction reduces pancreatic perfusion leading to dysfunction), and cigarette smoking (causing inflammation and vasoconstriction).

Clinical Features

• Type 2 diabetes typically has a gradual onset and may present with asymptomatic hyperglycemia.
• The "3 Ps" of diabetes:
  • Polydipsia (increased thirst)
  • Polyuria (frequent urination)
  • Polyphagia (excessive hunger), are caused by high glucose levels and the osmotic gradient pulling water into the bloodstream.
• Blurry vision can occur as high blood sugar damages the lenses of the eyes.

Diagnostic Criteria

• Hemoglobin A1C level of 6.5% or higher indicates diabetes.
• Fasting glucose level of 126 mg/dL or higher is a diagnostic criterion.
• Random glucose level of 200 mg/dL or higher, along with hyperglycemia symptoms, points to diabetes.
• Oral glucose tolerance test is used for diagnosis during pregnancy.

Complications

• Macrovascular complications of atherosclerosis include coronary artery disease, stroke/transient ischemic attack, and peripheral artery disease.
• Microvascular complications affect small blood vessels, leading to peripheral neuropathy (due to poor circulation), retinopathy, nephropathy, delayed wound healing, and recurrent infections.

Hyperosmolar Hyperglycemic State (HHS)

• HHS is a life-threatening condition with gradual onset.
• The pancreas produces enough insulin to prevent ketoacidosis, with no ketones present in the urine.
• Severe hyperglycemia leads to dehydration as water is drawn out of cells due to concentrated blood.
• Clinical Features: Blood glucose levels are typically > 600 mg/dL, usually triggered by underlying infection, medication, or acute/chronic illness, and severe polyuria leads to dehydration
• Neurologic manifestations include blurry vision, lethargy, altered level of consciousness, and potentially coma.
• Treatment Goals: Lower glucose levels to within normal limits; administer IV fluids, insulin, and electrolytes to correct severe dehydration.

Lifestyle Modifications

• Engage in moderate activity to reduce insulin resistance, blood pressure, and cholesterol.
• Follow a low-fat, high-fiber diet with a low glycemic index.
• Reduce weight if the client is obese.
• Avoid alcohol consumption due to the risk of hypoglycemia.
• Use oral antidiabetic medications as prescribed
• Consider prescribed insulin if oral medications are insufficient.
• Treat hyperlipidemia with statins, if necessary.
• Monitor regularly for hyperglycemia and HHS.

Proper Foot Care

• Inspect feet every day for signs of infection.
• Wear protective shoes, avoiding open-toe sandals.
• Separate overlapping toes using silk fabric.
• Wash feet daily with lukewarm water.
• Avoid using heating pads.
• Follow sick day management, and continue insulin treatment as directed.
• Schedule routine dilated eye exams to monitor for retinopathy.
• Practice stress reduction techniques.
• Get vaccinated and up to date to help prevent infections.

DKA vs. HHS

• DKA is more common in Type 1 diabetes, while HHS is more common in Type 2 diabetes.
• Blood glucose levels in DKA range from 250-600 mg/dL, while in HHS they are typically 600-1200 mg/dL.
• Acidosis is present in DKA (pH < 7.3, bicarbonate < 15 mEq/L) but absent in HHS (pH > 7.3, bicarbonate > 15 mEq/L).
• Ketones are present in DKA (ketonuria and ketonemia) but absent in HHS.
• Onset in DKA is rapid (hours to a day), while in HHS it is slow (days to weeks).
• Dehydration is moderate to severe in DKA and severe in HHS.
• Neurological symptoms are less pronounced in DKA and more prominent in HHS.