Create a PowerPoint presentation for Section 1: Essential Physiology (Slides 2-5) Slide 2: Normal Glucose Homeostasis • Blood glucose maintained ~4-6 mmol/L (70-110 mg/dL) fasting • Sources: Dietary carbohydrates, hepatic gluconeogenesis/glycogenolysis • Key hormones: Insulin (lowers), Glucagon (raises) • Other: Cortisol, catecholamines, growth hormone (counter-regulatory) Slide 3: Role of Insulin • Produced by pancreatic beta cells • Actions: o Promotes glucose uptake (GLUT4 in muscle/adipose) o Glycogen synthesis (liver/muscle) o Inhibits lipolysis and gluconeogenesis • Anabolic hormone Slide 4: Role of Glucagon • Produced by pancreatic alpha cells • Actions: o Stimulates glycogenolysis and gluconeogenesis in liver o Promotes ketogenesis in prolonged fasting • Released in response to low blood glucose Slide 5: Pancreatic Islets and Regulation • Diagram of islets of Langerhans (beta, alpha cells) • Feedback loop: High glucose → insulin release; Low glucose → glucagon release • Postprandial vs. fasting states Section 2: Definitions and Classification (Slides 6-8) Slide 6: Definition of Diabetes Mellitus • Group of metabolic disorders characterized by chronic hyperglycemia due to defects in insulin secretion, insulin action, or both • Leads to disturbances in carbohydrate, fat, and protein metabolism Slide 7: Main Types of Diabetes • Type 1 DM (5-10%): Autoimmune beta-cell destruction → absolute insulin deficiency • Type 2 DM (90-95%): Insulin resistance + relative insulin deficiency • Gestational DM • Other: MODY, secondary (steroids, pancreatitis, etc.), prediabetes Slide 8: Diagnostic Criteria • Fasting plasma glucose ≥7.0 mmol/L (126 mg/dL) • 2h OGTT ≥11.1 mmol/L (200 mg/dL) • HbA1c ≥6.5% (48 mmol/mol) • Random glucose ≥11.1 mmol/L + symptoms • (Note: Confirm with repeat test unless symptomatic) Section 3: Pathophysiology (Slides 9-13) Slide 9: Pathophysiology of Type 1 DM • Autoimmune destruction of beta cells (T-cell mediated) • Genetic predisposition (HLA) + environmental triggers (viruses?) • Absolute insulin deficiency → hyperglycemia, lipolysis, ketogenesis Slide 10: Pathophysiology of Type 2 DM • Insulin resistance (muscle, liver, adipose) • Compensatory hyperinsulinemia initially • Progressive beta-cell dysfunction/failure • Contributing factors: Obesity, visceral fat, inflammation, genetics Slide 11: Hyperglycemia Consequences • Osmotic diuresis (polyuria, polydipsia, dehydration) • Glycosuria • Long-term: Advanced glycation end-products (AGEs), oxidative stress, vascular damage Slide 12-13: Flowcharts • One for T1DM, one for T2DM progression Section 4: Clinical Features and Natural History (Slides 14-18) Slide 14: Classic Symptoms of Hyperglycemia • Polyuria, polydipsia, polyphagia • Weight loss (especially T1) • Fatigue, blurred vision, recurrent infections • Slow-healing wounds Slide 15: Natural History of Type 1 DM • Rapid onset (weeks) • Often presents with DKA in children/young adults • Lifelong insulin dependence Slide 16: Natural History of Type 2 DM • Insidious onset (years) • Often diagnosed incidentally • Prediabetes phase → overt diabetes → complications • Strongly associated with obesity/metabolic syndrome Slide 17-18: Chronic Complications • Microvascular: Retinopathy, nephropathy, neuropathy • Macrovascular: CAD, stroke, peripheral artery disease • Others: Diabetic foot, infections, skin changes • Timeline graphic showing progression with poor control Section 5: Investigations (Slides 19-21) Slide 19: Diagnostic & Monitoring Tests • Blood glucose (fasting/random) • HbA1c (glycated hemoglobin) – reflects 2-3 months • OGTT • C-peptide/insulin levels (to differentiate T1 vs T2) • Autoantibodies (GAD, islet cell) for T1 Slide 20: Screening for Complications • Eye exam (fundoscopy/retinopathy screening) • Urine ACR (albumin-creatinine ratio) • eGFR/renal function • Lipid profile, ECG/foot exam • Neuropathy assessment Slide 21: Other Labs • Electrolytes, ketones (in illness), arterial blood gas Section 6: Management (Slides 22-28) Slide 22: General Principles • Patient education, lifestyle modification (diet, exercise, weight loss) • Glycemic targets (individualized, e.g., HbA1c <7%) • Multidisciplinary care: Dietitian, educator, podiatrist, etc. • Cardiovascular risk reduction (BP, lipids, smoking) Slide 23: Type 1 DM Management • Insulin therapy (basal-bolus, pump) • Carbohydrate counting, self-monitoring/CGM • Sick day rules Slide 24: Type 2 DM Management • Lifestyle first • Metformin (first-line) • Other orals: SGLT2i, GLP-1RA, sulfonylureas, DPP4i • Insulin if needed • Note benefits of SGLT2i/GLP-1 for CV/renal protection Slide 25: Monitoring and Follow-up • Regular HbA1c, self-monitoring • Annual complication screening Section 7: Diabetic Emergencies (Slides 26-34) Slide 26: Overview of Emergencies • Hyperglycemic: DKA, HHS • Hypoglycemia • Others: Hyperosmolar hyperglycemic state, lactic acidosis Slide 27: Diabetic Ketoacidosis (DKA) • Triad: Hyperglycemia (>11-13.9 mmol/L), ketonemia/acidosis (pH<7.3, bicarb<15), anion gap • Mostly T1DM (can occur in T2) • Precipitants: Infection, insulin omission, illness Slide 28: DKA Clinical Features • Polyuria/polydipsia, nausea/vomiting, abdominal pain • Kussmaul breathing, fruity breath (acetone) • Dehydration, altered mental status/coma Slide 29: HHS (Hyperosmolar Hyperglycemic State) • Severe hyperglycemia (>33 mmol/L), hyperosmolality (>320 mOsm), profound dehydration • Minimal/no ketoacidosis • Mostly elderly T2DM, insidious onset (days-weeks) • Higher mortality than DKA Slide 30: Hypoglycemia • Blood glucose <4 mmol/L (or <3.9 with symptoms) • Causes: Excess insulin/meds, missed meals, exercise • Symptoms: Adrenergic (sweating, tremor) + neuroglycopenic (confusion, seizure) Slide 31-32: Management of DKA/HHS • ABC, fluids (normal saline initially), insulin (after K+ check), electrolytes (esp. potassium), treat precipitant • Monitoring: Hourly glucose, electrolytes, gap closure • Key differences table (DKA vs HHS) Slide 33: Hypoglycemia Management • Conscious: Oral carbs (15g) • Unconscious: IV dextrose or IM glucagon • Prevent recurrence Slide 34: Prevention of Emergencies • Education, sick day rules, access to supplies, regular follow-up Conclusion & References (Slides 35-36) • Summary key points • Importance of early diagnosis, tight control, and education • References (ADA, NICE, or key sources) • Q&A slide Additional Tips for Creation: • Use simple diagrams (glucose regulation loop, DKA pathway). • Include tables for comparisons (DKA vs HHS, T1 vs T2). • Add high-yield images: Fundus photo of retinopathy, foot ulcer (with sensitivity). • Total timing: 30-45 minutes presentation. • Sources: Base on guidelines (e.g., ADA, WHO) for accuracy.