Diabetes mellitus Study Guide

High‑Yield Diabetes Study Guide (All information is drawn directly from the provided outline.) --- 📖 Core Concepts Diabetes mellitus = chronic hyperglycemia due to insulin deficiency, insulin resistance, or both. Insulin’s actions – drives glucose uptake into liver, adipose tissue, skeletal muscle; suppresses hepatic glucose output. Sources of blood glucose – intestinal absorption, glycogenolysis, gluconeogenesis. Classification (WHO) – six types: Type 1, Type 2, hybrid forms, diabetes first detected in pregnancy (gestational), other specific types, unclassified. Epidemiology – > 800 million people worldwide (2024); > 95 % are Type 2; mortality ≈ 2 million deaths/yr. --- 📌 Must Remember Diagnostic thresholds Fasting plasma glucose (FPG) ≥ 126 mg/dL (7.0 mmol/L) → diabetes. 2‑hr OGTT glucose ≥ 200 mg/dL (11.1 mmol/L) after 75 g load → diabetes. Random plasma glucose ≥ 200 mg/dL with classic symptoms → diabetes. HbA1c ≥ 6.5 % (48 mmol/mol) → diabetes. Prediabetes Impaired fasting glucose: 100–125 mg/dL (5.6–6.9 mmol/L). Impaired glucose tolerance: 140–199 mg/dL (7.8–11.0 mmol/L) 2‑hr OGTT. Target HbA1c < 7 % (avoid hypoglycemia). Classic triad – poly‑thirst, poly‑uria, poly‑phagia. Macrovascular risk – diabetes doubles CVD risk; accounts for 75 % of diabetes‑related deaths. First‑line therapy – Metformin (Type 2); basal‑bolus insulin (Type 1). Lifestyle “dose” – ≥150 min moderate‑intensity aerobic exercise/week (≈28 % risk reduction). --- 🔄 Key Processes Diagnosing Diabetes Assess symptoms → if present, obtain random glucose. If glucose ≥200 mg/dL → diagnosis. If asymptomatic, perform any of: FPG, 2‑hr OGTT, or HbA1c. Repeat abnormal test on a different day unless hyperglycemia is unequivocal. Basal‑Bolus Insulin Regimen (Type 1) Basal: long‑acting insulin (once/twice daily). Bolus: rapid‑acting insulin before meals, dosed per carbohydrate count or correction factor. Metformin Action ↓ hepatic gluconeogenesis. ↑ peripheral insulin sensitivity (muscle, adipose). Progression from Prediabetes → Diabetes Persistent hyperglycemia → β‑cell stress → gradual loss of insulin secretory capacity → overt diabetes. --- 🔍 Key Comparisons Type 1 vs. Type 2 Pathophysiology: Autoimmune β‑cell destruction → absolute insulin deficiency vs. insulin resistance + relative deficiency. Onset: Usually < 30 y (Type 1) vs. > 40 y (Type 2), but overlap (LADA, pediatric Type 2). Treatment: Insulin only (Type 1) vs. Metformin first, add other agents, possible insulin later (Type 2). DKA vs. HHS DKA: ↑ketones, metabolic acidosis, younger, type 1‑dominant, glucose ≈ 250‑600 mg/dL. HHS: No significant ketosis, profound hyperosmolarity, glucose > 600 mg/dL, older, type 2‑dominant. ACE Inhibitor vs. ARB (Renal Protection) Both ↓ progression of diabetic nephropathy; ACE‑I slightly superior for CV outcomes, but no added benefit when combined. --- ⚠️ Common Misunderstandings “All diabetes is type 2.” → Type 1 accounts for 5‑10 % and is the most common before age 20. “A normal fasting glucose rules out diabetes.” → May miss post‑prandial spikes; OGTT or HbA1c needed. “Aspirin is universally recommended.” → Only for intermediate/high CVD risk (5‑10 % 10‑yr risk); routine use in uncomplicated diabetes lacks benefit. “Weight loss surgery cures diabetes.” → It can normalize glucose in many, but not all, and requires lifelong follow‑up. --- 🧠 Mental Models / Intuition “Insulin = key, glucose = lock.” – When the key (insulin) is missing or the lock (tissues) is jammed, glucose stays in the bloodstream. “Glucose traffic jam” – Hyperglycemia overwhelms renal reabsorption → glucose spills into urine → osmotic diuresis → thirst. “Two‑hit model for Type 2” – First hit: insulin resistance; second hit: β‑cell failure → overt diabetes. --- 🚩 Exceptions & Edge Cases LADA (type 1.5) – Adult onset, slower β‑cell loss; may initially respond to oral agents but ultimately needs insulin. Pregnancy – Diagnosis at 24–28 wks via 75 g OGTT; treatment may be diet alone or insulin; metformin sometimes used but not first‑line. Elderly – HbA1c target relaxed to ≈ 8 % to avoid hypoglycemia. --- 📍 When to Use Which | Clinical Situation | Preferred Test / Therapy | |--------------------|--------------------------| | Screening (≥45 y or risk factors) | Annual FPG or HbA1c | | Confirmatory diagnosis | Repeat abnormal test on separate day | | First‑line pharmacology (Type 2) | Metformin (unless contraindicated) | | Add‑on when HbA1c > 7 % on Metformin | Sulfonylurea, DPP‑4i, SGLT‑2i, or GLP‑1 RA (based on CVD/CKD profile) | | Insulin requirement | Basal‑bolus for Type 1; basal insulin if oral agents fail in Type 2 | | Renal protection | ACE‑I or ARB in presence of albuminuria | | Primary CVD prevention | Low‑dose aspirin only if 10‑yr CVD risk 5‑10 % | | Weight‑centric patients | GLP‑1 RA or SGLT‑2i (favor weight loss) | | Pregnant with diabetes | Diet → insulin (avoid oral agents unless metformin shown safe) | --- 👀 Patterns to Recognize Polyuria + Polydipsia + Polyphagia → suspect hyperglycemia; check random glucose. Fruity breath, Kussmaul respirations → DKA (look for low pH, high ketones). Severe dehydration + hypernatremia + altered mental status → HHS. Acanthosis nigricans on neck/axilla → insulin resistance → consider Type 2. Retinopathy in a young adult → likely longstanding uncontrolled diabetes; trigger urgent ophthalmology referral. --- 🗂️ Exam Traps “HbA1c ≥ 6.0 %” → not diagnostic; threshold is 6.5 %. “FPG ≥ 110 mg/dL” → diagnostic cutoff is 126 mg/dL; 110 mg/dL defines impaired fasting glucose. “All patients with diabetes need aspirin” → only high‑risk or intermediate‑risk adults; routine use is not supported. “Metformin is contraindicated in pregnancy” – actually, it may be used in some cases, but insulin is preferred; the trap is assuming absolute contraindication. “SGLT‑2 inhibitors cause hypoglycemia” – they lower glucose via urinary excretion and have low hypoglycemia risk unless combined with insulin or sulfonylureas. --- Use this guide for rapid recall before your exam – focus on thresholds, classic presentations, and decision‑making algorithms.