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MED602 — Metabolic and Endocrine Medicine: Lecture Note

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This is the complete lecture note for MED602 Metabolic and Endocrine Medicine. You can read it online below, open it in the full viewer, or download the PDF for offline study. It pairs with the course's video lectures, so you can read and watch together.

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la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS

la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS Course code: MED 602 Course title: Metabolic and Endocrine Medicine Course credit load: 2 Units Series 1: Diabetes Mellitus: Risk Factors, Pathogenesis, and Clinical Features • Part 1.1: Classification and Risk Factors of Diabetes Mellitus o Sub Part 1.1.1: Classification of diabetes mellitus o Sub Part 1.1.2: Risk factors for type 2 diabetes mellitus o Sub Part 1.1.3: Risk factors and triggers for type 1 diabetes mellitus • Part 1.2: Pathogenesis of Diabetes Mellitus o Sub Part 1.2.1: Pathogenesis of type 1 diabetes mellitus o Sub Part 1.2.2: Pathogenesis of type 2 diabetes mellitus and insulin resistance o Sub Part 1.2.3: Other specific types of diabetes mellitus • Part 1.3: Clinical Features of Diabetes Mellitus o Sub Part 1.3.1: Classic symptoms of hyperglycaemia o Sub Part 1.3.2: Clinical presentation of type 1 versus type 2 diabetes o Sub Part 1.3.3: Gestational diabetes mellitus • Part 1.4: Diagnostic Criteria and Screening o Sub Part 1.4.1: Diagnostic criteria for diabetes mellitus o Sub Part 1.4.2: Screening for diabetes and prediabetes o Sub Part 1.4.3: Differentiating diabetes types at presentation Introduction Few conditions in medicine touch as many patients, across as many organ systems, as diabetes mellitus, and few demand as thorough a theoretical grounding before meaningful clinical care can begin. This opening Series of Metabolic and Endocrine Medicine builds that grounding, working through the classification, risk factors, pathogenesis, and clinical features of diabetes

la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS mellitus, before turning to the diagnostic criteria and screening approaches that translate this theory into a confirmed diagnosis in an individual patient. The aim of this Series is to equip you with the ability to classify diabetes mellitus, list its risk factors, describe its pathogenesis in both major types, describe its classic clinical features including gestational diabetes, and apply the diagnostic criteria and screening approaches used to identify it. This theoretical and clinical foundation underpins everything that follows in Series 2, where the focus shifts to complications, investigation, and management. This Series opens with the classification and risk factors of diabetes mellitus, moves through its pathogenesis and clinical features, and closes with diagnostic criteria and screening. Series Learning Outcomes At the end of this Series, you should be able to: • SLO 1.1: classify diabetes mellitus • SLO 1.2: list the risk factors for type 1 and type 2 diabetes mellitus • SLO 1.3: describe the pathogenesis of type 1 diabetes mellitus • SLO 1.4: describe the pathogenesis of type 2 diabetes mellitus and insulin resistance • SLO 1.5: describe the classic symptoms and clinical presentation of diabetes mellitus • SLO 1.6: describe gestational diabetes mellitus • SLO 1.7: list the diagnostic criteria for diabetes mellitus • SLO 1.8: discuss screening for diabetes and differentiating diabetes types at presentation 1.1 Classification and Risk Factors of Diabetes Mellitus 1.1.1 classification of diabetes mellitus Four broad categories, each with a distinct underlying story Diabetes mellitus is classified into four broad categories: type 1 diabetes, resulting from autoimmune destruction of insulin-producing pancreatic beta cells leading to absolute insulin deficiency, type 2 diabetes, resulting from a combination of insulin resistance and relative insulin deficiency, gestational diabetes, diabetes first recognised during pregnancy, and other specific types, including monogenic diabetes and diabetes secondary to another medical condition or medication.

la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS Correctly classifying a patient's diabetes matters considerably, since the underlying pathophysiology directly shapes the most appropriate treatment approach, and a patient with type 1 diabetes who is mistakenly managed as though they have type 2 diabetes, or vice versa, risks genuinely serious harm, underlining why accurate classification at presentation, covered in more detail later in this Series, is a genuinely essential clinical skill rather than an academic formality. Fill in the blank: Type 1 diabetes results from autoimmune destruction of insulin-producing pancreatic beta ________. 1.1.2 risk factors for type 2 diabetes mellitus A condition shaped heavily by modifiable factors Risk factors for type 2 diabetes include obesity, particularly central or visceral adiposity, physical inactivity, a family history of type 2 diabetes, increasing age, and certain ethnic backgrounds known to carry higher population-level risk, alongside a history of gestational diabetes or polycystic ovary syndrome in women, each contributing to the underlying insulin resistance that characterises this type of diabetes. Many of these risk factors are genuinely modifiable, particularly obesity and physical inactivity, making type 2 diabetes a condition where individual and population-level prevention strategies can meaningfully reduce future disease burden, a theme that will recur throughout this course given its genuine public health importance alongside the purely clinical management of established disease. Fill in the blank: Central or visceral ________ is a particularly significant risk factor for type 2 diabetes. 1.1.3 risk factors and triggers for type 1 diabetes mellitus A different risk profile, rooted in autoimmunity Risk factors for type 1 diabetes differ fundamentally from those for type 2, centring on genetic susceptibility, particularly certain human leukocyte antigen gene variants, alongside a family history of type 1 diabetes or other autoimmune conditions, reflecting the autoimmune basis of this type rather than the metabolic and lifestyle factors more relevant to type 2 diabetes. Environmental triggers, including certain viral infections, are hypothesised to precipitate the autoimmune process in genetically susceptible individuals, though the precise mechanism remains incompletely understood, and, unlike type 2 diabetes, type 1 diabetes is not preventable through lifestyle modification, a genuinely important distinction to communicate clearly to

la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS patients and families who may otherwise, understandably but incorrectly, attribute the diagnosis to diet or lifestyle choices. Fill in the blank: Unlike type 2 diabetes, type 1 diabetes is not preventable through lifestyle ________. Figure 1.1: A clinician measuring waist circumference to assess central adiposity as a diabetes risk factor. Pilot questions 1.1 1. List the four broad categories of diabetes mellitus. (Linked to SLO 1.1) 2. Explain why accurate classification of diabetes matters clinically. (Linked to SLO 1.1) 3. List the risk factors for type 2 diabetes. (Linked to SLO 1.2) 4. List the risk factors for type 1 diabetes. (Linked to SLO 1.2) 5. Explain why type 1 diabetes is not preventable through lifestyle modification. (Linked to SLO 1.2)

la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS 1.2 Pathogenesis of Diabetes Mellitus 1.2.1 pathogenesis of type 1 diabetes mellitus The immune system turning against its own pancreas Type 1 diabetes develops through progressive autoimmune destruction of pancreatic beta cells, mediated by autoreactive T lymphocytes and marked by circulating autoantibodies against beta cell antigens, a process that typically proceeds silently for months to years before sufficient beta cell mass is lost to produce clinically apparent hyperglycaemia and the classic symptoms this eventually causes. Once beta cell mass falls below a critical threshold, usually around eighty to ninety percent destruction, absolute insulin deficiency results, and, without exogenous insulin replacement, the body shifts towards unrestrained lipolysis and ketogenesis, since insulin's normal restraining effect on these processes is entirely lost, a pathophysiological cascade that, left untreated, progresses towards the genuine medical emergency of diabetic ketoacidosis. Fill in the blank: Absolute insulin deficiency in type 1 diabetes typically results once beta cell mass falls below a critical ________. 1.2.2 pathogenesis of type 2 diabetes mellitus and insulin resistance A gradual failure of both supply and demand Type 2 diabetes develops through a combination of insulin resistance, reduced tissue sensitivity to insulin's normal effects, particularly in skeletal muscle, liver, and adipose tissue, and progressive beta cell dysfunction, an initially compensatory increase in insulin secretion that gradually fails to keep pace with the body's rising insulin resistance, eventually resulting in relative insulin deficiency and clinically apparent hyperglycaemia. Excess visceral adiposity contributes directly to insulin resistance through several interlinked mechanisms, including altered adipokine secretion and chronic low-grade inflammation, and this pathophysiological link between obesity and insulin resistance explains why weight loss remains one of the most effective interventions available for improving glycaemic control in appropriately selected patients with type 2 diabetes, a genuinely important therapeutic principle covered further in the following Series. Fill in the blank: Type 2 diabetes develops through a combination of insulin resistance and progressive beta cell ________.

la-NET | ONLINE LEARNING VIDEO PLATFORM FOR POST-SECONDARY & HIGHER INSTITUTION STUDENTS 1.2.3 other specific types of diabetes mellitus A smaller but genuinely important category Monogenic diabetes, resulting from a mutation in a single gene, includes maturity-onset diabetes of the young, typically presenting in adolescence or early adulthood with a strong family history across multiple generations, and neonatal diabetes, presenting within the first six months of life, both genuinely important to recognise since their specific genetic cause can, in certain subtypes, meaningfully alter the most appropriate treatment choice compared with standard type 1 or type 2 management. Secondary diabetes, resulting from another underlying condition or its treatment, includes diabetes

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