Endocrinology PANTS Series: Diabetes Lecture

Introduction

• Focus: Diabetes (Type 1 and Type 2)
• Importance: High relevance for exams, particularly for Type 2 diabetes

Type 1 Diabetes

• Cause: Pancreatic beta cell destruction
  • Complete absence of endogenous insulin
  • Initial "honeymoon period" where some insulin is produced
• Demographics: Mostly diagnosed under 30 years old
• Types:
  • Type 1A (Autoimmune, most common)
    • Presence of GAD antibodies, Islet cell antibodies
  • Type 1B (Non-autoimmune, idiopathic)
    • Strong hereditary component
• Presentation (Three P's):
  • Polyuria (frequent urination)
  • Polydipsia (excessive thirst)
  • Polyphagia (excessive hunger)
• Diagnosis: (Any one of the following)
  • Fasting Plasma Glucose ≥126 mg/dL on two occasions
  • 2-hour Glucose Tolerance ≥200 mg/dL
  • A1c ≥6.5%
  • Random Glucose ≥200 mg/dL (with symptoms)
• Treatment:
  • Focus on types of insulin:
    • Fast-acting: Lispro (Humalog), Aspart (Novolog) - 5-15 min onset
    • Intermediate: NPH - 2-hour onset, lasts up to 8 hours
    • Long-acting: Detemir, Glargine, Degludec - 12-24 hours

Phenomena in Type 1 Diabetes

• Somogyi Effect: Overnight low BS → Rebound Hyperglycemia
  • Treatment: Prevent nocturnal hypoglycemia (lower insulin, bedtime snack)
  • Memory Aid: "So much insulin"
• Dawn Phenomenon: Normal Overnight BS → Morning Hyperglycemia
  • Treatment: Increase basal insulin at night
  • Memory Aid: "Down Insulin"

Type 2 Diabetes

• Pathophysiology: Insulin resistance + impaired insulin secretion
  • Patients still produce insulin
• Risk Factors:
  • Obesity (90% of Type 2 patients)
  • Stronger genetic component
• Presentation:
  • Similar to Type 1 (Polyuria, Polydipsia, Polyphagia)
  • Poor wound healing, yeast infections, UTIs
  • More insidious onset
• Initial Management:
  • Lifestyle changes (diet, exercise)
  • Medication: Metformin (first-line after lifestyle)
  • Followed by other classes: SGLT2 inhibitors, GLP1 agonists, Sulfonylureas
• Note: Latent Autoimmune Diabetes in Adults (LADA) - Type 1 onset in adulthood

Diabetic Ketoacidosis (DKA)

• More common in Type 1 Diabetes
• Etiologies (Five I's):
  • Infection (most common), Iatrogenic (steroids), Infarction (MI, CVA), Ignorance (non-compliance), Infant on board (pregnancy)
• Presentation:
  • Nausea, vomiting, abdominal pain
  • Polyuria, polydipsia
  • Fruity/acetone breath
  • Kussmaul respirations
  • Dehydration (tachycardia, tachypnea)
• Diagnosis:
  • Elevated blood sugar (>250 mg/dL)
  • Metabolic acidosis, high anion gap
  • Positive ketones in urine
• Treatment (SIPS):
  • S: Saline (initial isotonic, then D5 when BS <250)
  • I: Insulin (regular insulin)
  • P: Potassium (unless serum K+ >5.3 or <3.3)
  • S: Search for underlying cause

Hyperosmolar Hyperglycemic State (HHS)

• More common in Type 2 Diabetes
• Etiology: Same as DKA (Five I's)
• Pathophysiology: Severe dehydration → Hyperglycemia (>600 mg/dL) → Hyperosmolarity (>320 mOsm/L)
• Presentation:
  • Altered mental status (more common than in DKA)
  • Similar symptoms as DKA (polyuria, polydipsia)
• Diagnosis:
  • Elevated blood sugar (>600 mg/dL)
  • Normal pH (≥7.30)
• Treatment: Same as DKA (SIPS)

Key Differences: DKA vs. HHS

• Blood Sugar:
  • DKA: >250 mg/dL
  • HHS: >600 mg/dL
• pH Levels:
  • DKA: <7.30 (Acidosis)
  • HHS: ≥7.30 (Normal)
• Onset:
  • DKA: Acute (hours to 1 day)
  • HHS: Insidious (days to weeks)
• Type:
  • DKA: More common in Type 1
  • HHS: More common in Type 2
• Ketones:
  • DKA: Always present
  • HHS: May have small amounts or not at all

Conclusion

• Next video: Detailed breakdown of Type 2 diabetes medications
• Importance of remembering key points for exams and real-life practice