Type 1 and Type 2 diabetes. jan 2023.pptx

Dr Ali Chakera [email protected] Curriculum Objectives  Describe the global epidemiology of type 1 and type 2 diabetes  Explain why is it important to diagnose diabetes  Describe how a diagnosis of diabetes is made  Explain the basic principles of why and how diabetes is treated Learning out...

Dr Ali Chakera [email protected] Curriculum Objectives  Describe the global epidemiology of type 1 and type 2 diabetes  Explain why is it important to diagnose diabetes  Describe how a diagnosis of diabetes is made  Explain the basic principles of why and how diabetes is treated Learning outcome(s): To understand the global epidemiology of both T1 and T2 DM, to understand the importance of diabetes diagnosis and treatment, to understand how DM is diagnosed and treated. Epidemiology 537 million adults (20-79 years) are living with diabetes - 1 in 10. This number is predicted to rise to 643 million by 2030 and 783 million by 2045. Over 3 in 4 adults with diabetes live in low- and middle-income countries. Diabetes is responsible for 6.7 million deaths in 2021 - 1 every 5 seconds. Diabetes caused at least USD 966 billion dollars in health expenditure – a 316% increase over the last 15 years. 541 million adults have Impaired Glucose Tolerance (IGT), which places them at high risk of type 2 diabetes. https://diabetesatlas.org / https://diabetesatlas.org Prevalence of Diabetes (Adults) – England & Wales 2009 5.1%2,634,263 2016/7 6.7%3,192,745 2019/20 7.2%3,675,585 10% of NHS spend ~20% of inpatients have Diabetes Type 1 Type 2 MODY Why do we treat diabetes? www.nobelprize.org/prizes/medicine/1923/banting/l ecture/ https:// www.t1international.com/ Why do we treat diabetes? Acute symptoms High glucose - hyperglycaemia https://youtu.be/4LttAS3HpA0 s Hyperglycaemia Hypos https://youtu.be/4LttAS3HpA0 Chronic complications Stroke Heart disease Eye disease (retinopathy) Kidney disease (nephropathy) Nerve damage (neuropathy) The range of CCG/LHB 8 care process completion. England and Wales, 2019-20 and 2020-21 13 How do we define diabetes? Frequency Distribution of 2-Hour Post Challenge Glucose in Pima Indians Age > 25 Years Rushforth, Diabetes 1971 20 756-65 Rushforth, Diabetologia 1979 16 373-79 Rushforth, Diabetologia 1979 16 373-79 How do we diagnose diabetes? Symptoms + one of: • HbA1c ≥ 48 mmol/mol • Fasting glucose ≥ 7.0 mmol/L • Random glucose ≥ 11.1mmol/L 2-Hr  11.1 Or without symptoms: • Two raised results (of the same type) HbA1c 48 FPG  7.0 FPG  7.0 But what type of diabetes? Type 2 Type 1 Genetic Pancreatic Endocrine Drug induced Syndromic Gestational Is it Type 1 or Type 2 diabetes? Type 1 or Type 2 Age of onset Phenotype Rapidity of onset Past medical history T1T2 Classification // Diabetes G Family History enes Weight loss Ketosis GAD/ IA2/ Zn Transporter 8 antibodies C-Peptide Acute complications of diabetes Diabetic Ketoacidosis: Pathophysiology Unchecked gluconeogenesis  Hyperglycaemia Osmotic diuresis  Dehydration Unchecked ketogenesis  Ketosis Dissociation of ketone bodies into hydrogen ion and anions  Anion-gap metabolic acidosis • Often a precipitating event is identified (infection, lack of insulin administration) 21 Insulin Deficiency Hyperglycaemia (HyperOsmolality) Glycosuria Dehydration Renal Failure Shock Electrolyte Losses CV Collapse Insulin Deficiency Lipolysis  FFAs Ketones Acidosis CV Collapse Insulin Deficiency Hyperglycaemia (HyperOsmolality) Glycosuria Lipolysis  FFAs Ketones Dehydration Renal Failure Shock Electrolyte Losses Acidosis CV Collapse Hyperosmolar Hyperglycaemic State – clinical features HHS Age Usually >40years Precipitating causes previously undiagnosed, steroids, diuretics, sugar Serum sodium Usually high Blood glucose Often >40mmol/l Serum bicarbonate/pH Normal / pH 7.4 Serum ketones 0 Mortality 30% (thromboses) Subsequent course Diet/tablet controlled Insulin Deficiency Hyperglycaemia (HyperOsmolality) Glycosuria Dehydration Renal Failure Shock Electrolyte Losses CV Collapse 26 Long term complications of diabetes Neovascularisation – abnormal growth of blood vessels Hard Exudates Abnormal Cotton Wool Spots Normal Retinal Haemorrhages Pathological Findings of Diabetic Retinopathy Loss of pericytes Basement membrane thickening Capillary closure Ischaemia VEGF production Increased capillary permeability Clinical Stages of Retinopathy Non-proliferative Background (R1) Pre-proliferative (R2) Proliferative (R3) Macular Oedema Sight threatening Non sight threatening Peripheral Neuropathy Peripheral Neuropathy Callus Neuropathic Ulcer Charcot Foot Mononeuropathy Autonomic Neuropathy Gastroparesis Postural hypotension Erectile dysfunction Gustatory sweating (after eating) Diarrhoea Nephropathy Nephropathy Commonest cause of ESRD in Western World Accounts for deaths of 21% of type 1 and 11% of type 2 patients The Renal Microcirculation Fenestrated glomerular capillaries Basement membrane Highly specialised podocytes Basement membrane thickening Loss of negative charge Podocyte loss Loss of integrity of filtration barrier Glomerular sclerosis Mesangial expansion Clinical Stages of Diabetic Nephropathy Normoalbuminuria Microalbuminuria 20-200mg.min-1 30-300 mg.24hr -1 Dipstick negative Albuminuria >200mg.min-1 >300 mg.24hr -1 Dipstick positive Declining GFR % of patients with an event UKPDS: Microvascular renal failure or death, vitreous haemorrhage or photocoagulation Endpoints 346 of 3867 patients (9%) 30% Conventional Intensive p=0.0099 20% 10% Risk reduction 25% (95% CI: 7% to 40%) 0% 0 3 6 9 12 Years from randomisation 15 Type 1 diabetes – treatments Teplizumab •anti-CD3 monoclonal antibody The median time to the diagnosis of type 1 diabetes was 48.4 months in the teplizumab group and 24.4 months in the placebo group https://dafne.nhs.uk/ Structured education only completed by 7.2% of those with Type 1 diabetes Technology People with type 1 diabetes, by latest insulin treatment regimen and social deprivation, England and Wales, 2019-20 Basal-bolus insulin regimens are used equally by people from all areas of social deprivation. Insulin pumps are more likely to be used by people in the least deprived communities. Whereas, fixed mix insulin regimens are more likely to be used by people from the most deprived communities. 20 Insulin regimens for type 1 diabetes: Ethnicity 15 10 5 0 Basal-bolus Insulin pump** White Asian Black Mixed Fixed mix Other Monitoring Continuous Glucose Monitoring System - CGMS Type 2 diabetes treatments https://preventing-diabetes.co.uk/ Individualise care ©2018 by American Diabetes Association Melanie J. Davies et al. Dia Care 2018;41:2669-2701 Metformin Sulfonylur ea Pioglitazo ne e.g. gliclazide DDP4 inhibitor ‘gliptin Insulin SGLT2 inhibitor ‘gliflozin GLP1 receptor agonist ‘tide It’s complicated ©2018 by American Diabetes Association Melanie J. Davies et al. Dia Care 2018;41:2669-2701 Case - 36 year old woman Presents to GP with symptoms of feeling tired, and thirsty. What tests are you going to do? 1. Urine dip for glucose 2. Capillary blood test for glucose 3. HbA1c 4. Random laboratory glucose 5. Diabetes antibodies Case - 36 year old woman You diagnose diabetes. Her BMI is 36kg/m2 How are you going to determine what type of diabetes? 1. She’s < 50 years old – so it is Type 1 diabetes 2. You need to check diabetes antibodies to find out 3. She’s not unwell - so it is Type 2 diabetes 4. Her BMI is high - so it is Type 2 diabetes 5. Not sure Case - 36 year old woman Her glucose is 23mmol/L How are you going to treat her? 1. This is really high – she needs to go to hospital 2. Ask her to modify her diet and see her in a week 3. Start metformin 4. Start insulin 5. Call a specialist for advice.