Insulin and Diabetes Regulation Quiz

Diabetes Mellitus

• Diabetes mellitus (DM) is a group of metabolic diseases characterized by high blood glucose levels. This results from defects in insulin secretion, insulin action, or both.
• DM is also a chronic systemic disease, characterized by either a deficiency of insulin or a decreased ability of the body to use insulin. It's often referred to as "high sugars."
• As of 1995, there were 135 million DM patients worldwide. In 2010, this rose to 285 million and 366 million in 2011. The global estimate is expected to reach 552 million by 2030, with 80% of these cases in low and middle-income countries.
• A significant portion (up to 50%) of DM patients are over 65 years old. Approximately 183 million (50%) of those with diabetes remain undiagnosed, and 4.6 million deaths globally were associated with DM in 2011.
• Data from 2011 indicates that Diabetes Mellitus deaths in Ghana reached 2,752, accounting for 1.47% of the total deaths.
• The global increase in DM cases is attributed to an aging population and a rise in unhealthy lifestyles, poor dietary practices, and decreased physical activity.

Classification

• There are four major classifications of DM:
  • Type 1 (Juvenile or Insulin Dependent Diabetes Mellitus): Affects 5-10% of people, typically diagnosed before age 30, and requiring daily insulin treatment. Causes include genetic, immunologic, and environmental factors.
  • Type 2 (Non-Insulin Dependent Diabetes Mellitus): Affects 90-95% of people, usually diagnosed after age 40, and often associated with certain ethnic and racial groups; also sometimes referred to as stable diabetes. Causes include heredity, obesity, and environmental factors.
  • Gestational Diabetes Mellitus (GDM): Develops in up to 14% of pregnant women, increasing their risk for hypertensive problems. Occurs primarily in the second half of pregnancy, potentially leading to larger babies. Women with a family history of DM and obesity are at a higher risk.
  • DM associated with other conditions: This type is linked to certain medications (like oral contraceptives and corticosteroids) and hormonal conditions (such as adrenal insufficiency or Cushing's Syndrome). This accounts for 1-2% of diagnosed cases.

Pathophysiology

• In healthy individuals, insulin, secreted by beta cells in the pancreas, increases after meals. It facilitates the transfer of glucose from the bloodstream into muscle, liver, and fat cells.

• Insulin's function in these cells is to: metabolize glucose for energy, stimulate glucose storage as glycogen in the liver and muscles, and signal the liver to stop glucose release, enhance dietary fat storage, and accelerate amino acid transport from dietary proteins into cells. Insulin also inhibits the breakdown of stored glucose, protein, and fat.

• Between meals (fasting periods) or overnight the pancreas continues releasing small amounts of insulin (basal insulin).

• During low blood glucose levels, glucagon, another pancreatic hormone (secreted by alpha cells), is secreted to stimulate the liver to release stored glucose.

• In Type 1 DM, there's destruction of pancreatic beta cells, leading to an absolute deficiency of insulin. This could be due to genetic, immunologic, or environmental (e.g., viral) factors, though the exact process of destruction isn't fully understood. People with particular Human Leukocyte Antigen (HLA) types are known to be genetically predisposed. Also, evidence shows that autoimmune responses, where antibodies target the body's normal tissues as if they were foreign, can play a role in destruction. Environmental factors like viruses or toxins have been considered as initiating factors of beta cell destruction. All these result in decreased insulin production, unchecked glucose production by the liver, and fasting hyperglycemia. Glucose from food then remains in the blood after a meal, contributing to post-prandial hyperglycemia.

• In Type 2 DM, the primary issues are insulin resistance and impaired insulin secretion. Insulin resistance is characterized by a decreased sensitivity to insulin. Normal insulin receptors initiate intracellular glucose metabolic processes. But in type 2 diabetes, these intracellular actions are diminished, causing insulin to be less effective in promoting glucose uptake by tissues and regulating glucose release. The exact mechanisms causing insulin resistance and impaired insulin secretion in type 2 are unknown, but genetic factors are implicated. The body tries to compensate, leading to higher insulin production in an attempt to maintain glucose levels; if beta cells cannot meet the heightened demand, blood glucose levels rise, resulting in type 2 DM. Despite this impaired secretion, there's usually enough insulin to prevent fat breakdown and ketone body production, making diabetic ketoacidosis (DKA) less common in type 2. However, severe cases of uncontrolled type 2 DM can lead to hyperglycemic hyperosmolar non-ketotic syndrome (HHNS). The slow progression of glucose intolerance in type 2 DM can often cause its onset to go undetected for years.

Symptoms

• DM symptoms arise from elevated blood glucose levels. Common signs include:
  • Polyuria (increased urination)
  • Polydipsia (increased thirst)
  • Polyphagia (increased appetite)
  • Weight loss due to the body switching to fats and proteins as energy sources if glucose isn't available
  • Fatigue and weakness (as cells lack energy from glucose)
  • Glycosuria (glucose in urine) leading increased risk to infection (like candidiasis)
  • Visual disturbances (secondary to ocular lens & retina exposure to hyperosmolar fluids).
  • Paraesthesia (tingling or numbness) in extremities, poor wound healing, sexual dysfunction, and acetone (fruity, sweet) breath (due to ketoacidosis).
  • Type 1 DM may show additional symptoms like lethargy, stupor, Kussmaul breathing (hyperventilation), nausea, vomiting, and abdominal pain.

Diagnostic Investigations

• Urine chemistry: testing for elevated glucose and ketones.
• Blood chemistry panel: assessing fasting blood glucose (levels > 7.0 mmol/L suggests DM). Random blood sugar (levels > 11.1mmol/L). Oral glucose tolerance test (OGTT) (levels > 11.1 mmol/L).
• HbA1c: Average blood glucose over 3 months (normal values typically 4-8%).
• Blood Urea and Electrolytes: annually
• Eye exams: annually

Diagnostic Criteria

• Symptoms of Diabetes plus Random blood glucose concentration ≥ 200mg/dL (11.1 mmol/L). Random level is for any time of day, regardless of time since last meal.
• Fasting Plasma Glucose ≥ 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 hours.
• 2-hour postload glucose level ≥ 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test. A glucose load containing 75 g anhydrous glucose dissolved in water is used.
• In the absence of unequivocal hyperglycemia, repeat testing on a different day should confirm these results. A third measure is not normally necessary.

Management

• Goal is euglycemia (normal blood glucose) without hypoglycemia or disrupting daily life.
• Management includes:
  • Nutritional management
  • Exercise
  • Self-monitoring of blood glucose (SMBG)
  • Pharmacologic therapy
  • Education
• Treatment varies due to lifestyle and emotional changes, requiring ongoing assessment and adjustments by practitioners and patients.

Medications

• Two or more types of medications are often used.
• Initially, older patients may be managed with dietary changes.
• Sulphonylureas: Stimulate the pancreas to secrete more insulin. Needed for functioning pancreas. Cannot be used for type 1. Examples include Acetohexamide, Chlorpropamide, Tolazamide, Tolbutamide.
• Biguanides: Improve insulin action on peripheral receptor sites. Need insulin. Example: Metformin. (Glucophage, Glucophage XL)
• Alpha Glucosidase Inhibitors: Slow absorption of glucose in the intestines, thus reducing post-meal blood glucose. Examples: Acarbose, Miglitol.
• Thiazolidinediones (TZDs): Enhance insulin action at receptor sites. Examples: Pioglitazone, Rosiglitazone.
• Non-sulfonylurea insulin secretagogues: Stimulate insulin release from beta cells. Examples: Repaglinide, Nateglinide.
• Dipeptidyl Peptidase-4 (DPP-4) inhibitors: Increase and prolong incretin action, which increases insulin and decreases glucagon. Examples include Sitaglipton and Vildaglipton.

Insulin Treatment

• Used for type 1 DM and in cases where other treatments are insufficient in type 2.
• Also used temporarily in type 2 DM during periods of stress (e.g., surgery), pregnancy, or when other medications are insufficient.
• Different types of insulin:
  • Rapid-acting (e.g., Lispro, Aspart, Glulisine).
  • Short-acting (e.g., Regular).
  • Intermediate-acting (e.g., NPH).
  • Long-acting (e.g., Glargine, Detemir).
  • Combination therapies (premixed).
• Storage: Refrigerate insulin not in use. Keep in use insulin at room temperature unless temps over 86F (30C) or freezing conditions.

Insulin Delivery Equipments

• Syringe and needle
• Insulin pen
• Insulin pump

Insulin Administration

• Insulin is inactivated by stomach acid; oral intake is not effective. Subcutaneous injection is the most common method except in immediate needed cases (IV).
• Inhaled insulin was once available but is no longer widely used.
• U100 insulin (1 mL = 100 units) requires U100 marked syringes.
• Proper handwashing, assembling equipment, inspecting insulin for lumps or crystals, confirmation of type and concentration are all critical steps prior to administration.
• Insulin types needing mixing, require that the entire vial is rolled before use.
• Specific injection sites are typically used for injection.
• Techniques for administration (e.g., pinching skin for injection). Single use syringes should be safely disposed of.

Test your knowledge on the roles of insulin and glucagon in glucose metabolism and regulation. This quiz also covers the factors leading to type 1 diabetes and the implications of insulin resistance in type 2 diabetes. Challenge yourself with questions on related medications and physiological responses.