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Diabetes Mellitus for ABIM

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Diabetes Mellitus for the American Board of Internal Medicine Exam
Diabetes Mellitus
  • Pathophysiology
    • Diabetes Mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both. It leads to chronic complications involving the eyes, kidneys, nerves, and cardiovascular system.
insulin actions
    • Types of Diabetes:
    • Type 1 Diabetes Mellitus (T1DM): An autoimmune disorder where the immune system attacks pancreatic beta cells, leading to absolute insulin deficiency. T1DM typically presents in childhood or adolescence, though it can develop at any age.
    • Type 2 Diabetes Mellitus (T2DM): Characterized by insulin resistance with an initial compensatory increase in insulin secretion, followed by beta-cell dysfunction over time. T2DM is closely linked to obesity and sedentary lifestyles.
    • Gestational Diabetes Mellitus (GDM): Hyperglycemia first identified during pregnancy. It increases the risk of T2DM for the mother later in life.
    • Other Specific Types: These include monogenic diabetes (e.g., MODY), secondary diabetes due to pancreatic disease, endocrinopathies (e.g., Cushing's syndrome), or medication-induced diabetes (e.g., glucocorticoid use).
  • Risk Factors
    • Type 1 DM: Family history of autoimmune diseases, certain genetic markers (e.g., HLA-DR3, HLA-DR4), and environmental factors (e.g., viral infections).
    • Type 2 DM: Obesity, physical inactivity, family history, age >45 years, history of gestational diabetes, hypertension, dyslipidemia, and ethnicity (higher risk in African American, Hispanic, Native American, and Pacific Islander populations).
  • Clinical Presentation
    • Classic Symptoms: Polyuria, polydipsia, polyphagia, and unexplained weight loss, which are more common in T1DM. These symptoms result from osmotic diuresis due to hyperglycemia and breakdown of fat and muscle for energy.
    • T2DM: Often asymptomatic or may present with subtle symptoms like fatigue, recurrent infections (e.g., candidiasis), and blurred vision. T2DM is frequently diagnosed during routine screenings or after the onset of complications (e.g., cardiovascular disease, neuropathy).
    • Diabetic Ketoacidosis (DKA): An acute complication primarily seen in T1DM, characterized by hyperglycemia, ketosis, and metabolic acidosis. It presents with nausea, vomiting, abdominal pain, dehydration, and altered mental status.
    • Hyperosmolar Hyperglycemic State (HHS): A complication of T2DM with severe hyperglycemia, dehydration, and hyperosmolarity without significant ketosis. Mental status changes and neurological deficits are common.
  • Diagnosis
    • Diagnostic Criteria (as per the ADA):
    • Fasting plasma glucose (FPG) ≥126 mg/dL.
    • 2-hour plasma glucose ≥200 mg/dL during a 75 g oral glucose tolerance test (OGTT).
    • HbA1c ≥6.5%.
    • Random plasma glucose ≥200 mg/dL with classic symptoms of hyperglycemia.
    • Screening:
    • Adults aged ≥45 should be screened every 3 years.
    • Screening is recommended earlier for those with risk factors such as obesity, family history of diabetes, or a history of gestational diabetes.
  • Management
    • Non-Pharmacological Management:
    • Lifestyle Modification:
    • Diet: Patients with T2DM benefit from a balanced diet rich in vegetables, whole grains, lean proteins, and healthy fats. Carbohydrate intake should be monitored.
    • Exercise: At least 150 minutes of moderate-intensity aerobic activity per week, along with resistance training, improves glycemic control and reduces cardiovascular risk.
    • Weight Loss: In overweight or obese individuals with T2DM, weight loss of 5-10% can significantly improve glycemic control and reduce cardiovascular risk.
    • Pharmacologic Therapy:
    • Type 1 Diabetes: Insulin therapy is essential. Various insulin regimens, such as basal-bolus therapy or continuous subcutaneous insulin infusion (CSII), are used to maintain glycemic control. Insulin pumps may be used for continuous delivery.
    • Type 2 Diabetes:
    • Metformin: First-line therapy unless contraindicated (e.g., renal dysfunction). It improves insulin sensitivity and reduces hepatic gluconeogenesis.
    • Second-Line Agents:
    • GLP-1 Receptor Agonists (e.g., liraglutide): Improve glycemic control, promote weight loss, and have cardiovascular benefits.
    • SGLT-2 Inhibitors (e.g., empagliflozin): Reduce blood glucose by promoting glucosuria. These drugs also have cardiovascular and renal protective effects.
    • DPP-4 Inhibitors (e.g., sitagliptin): Increase incretin levels, improving insulin secretion and decreasing glucagon secretion.
    • Insulin: May be required as the disease progresses, especially in patients with severe hyperglycemia or during times of stress (e.g., infections, surgery).
    • Gestational Diabetes: Managed with diet and exercise initially. Insulin is the preferred treatment if medications are needed, as most oral hypoglycemics cross the placenta.
  • Monitoring:
    • HbA1c: Measured every 3-6 months. The target HbA1c is <7% in most adults, though more stringent targets (<6.5%) may be appropriate for some without significant comorbidities, while less stringent targets (<8%) are considered for older adults or those with a limited life expectancy.
    • Self-Monitoring of Blood Glucose (SMBG): Important for patients on insulin therapy or those experiencing frequent hypoglycemia.
  • Complications
    • Microvascular Complications:
    • Diabetic Retinopathy: Caused by chronic hyperglycemia damaging retinal vessels. Annual eye exams are recommended.
    • Diabetic Nephropathy: Hyperglycemia leads to kidney damage, progressing to end-stage renal disease (ESRD). Monitoring includes annual urine albumin-to-creatinine ratios.
    • Diabetic Neuropathy: Sensory neuropathy leads to pain, tingling, and numbness, commonly affecting the feet and increasing the risk of ulcers and infections.
    • Macrovascular Complications:
    • Cardiovascular Disease (CVD): Diabetes significantly increases the risk of myocardial infarction, stroke, and peripheral artery disease (PAD). Blood pressure and lipid management are critical.
    • Hypoglycemia: A risk of intensive insulin therapy, especially in T1DM and advanced T2DM. Symptoms include tremors, palpitations, sweating, and confusion, and it may lead to seizures or coma if severe.
  • Prevention:
    • Prevention of T2DM: Lifestyle interventions, including weight loss, regular physical activity, and dietary changes, have been shown to delay or prevent the onset of T2DM in high-risk individuals (e.g., those with prediabetes).
    • Management of Cardiovascular Risk Factors: Tight control of blood pressure, lipid levels, and smoking cessation are critical in reducing the long-term complications of diabetes.
Key Points
  • Types of Diabetes: T1DM involves autoimmune destruction of beta cells, while T2DM is primarily due to insulin resistance with progressive beta-cell dysfunction. GDM occurs during pregnancy, increasing future T2DM risk.
  • Diagnosis: Diagnostic criteria include FPG ≥126 mg/dL, 2-hour OGTT ≥200 mg/dL, HbA1c ≥6.5%, or random plasma glucose ≥200 mg/dL with classic symptoms.
  • Management: T1DM requires insulin therapy, while T2DM management focuses on lifestyle modification, metformin as first-line therapy, and additional agents (e.g., GLP-1 agonists, SGLT-2 inhibitors) for glycemic control and cardiovascular protection.
  • Complications: Long-term complications include microvascular issues (retinopathy, nephropathy, neuropathy) and macrovascular disease (myocardial infarction, stroke). Monitoring and early intervention can help prevent or delay these complications.
  • Prevention: Preventing T2DM involves lifestyle interventions, and managing cardiovascular risk factors reduces complications in all forms of diabetes.

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