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DIABETES CASE PRESENTATIONS

DIABETES CASE PRESENTATIONS. 3 rd – Chronic complications. 1. Diabetic retinopathy. Early subclinical abnormalities of the retinal vessels: thickening of the basement membrane loss of pericytes (the contractile cells that control vessel calibre and flow) increased blood flow

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DIABETES CASE PRESENTATIONS

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  1. DIABETES CASE PRESENTATIONS 3rd – Chronic complications

  2. 1. Diabetic retinopathy • Early subclinical abnormalities of the retinal vessels: • thickening of the basement membrane • loss of pericytes (the contractile cells that control vessel calibre and flow) • increased blood flow • increased capillary permeability (leakage)

  3. Simplified grading of diabetic retinopathy • Background (Level 1) • Microaneurysms • Retinal haemorrhages  any exudates (hard exudates) • Preproliferative (Level 2) • Venous beading • Venous loop or reduplication • Intraretinal microvascular abnormalities (IRMA) • Multiple deep, round haemorrhages • Cotton-wool spots • Proliferative (Level 3) • New vessels on disc (NVD) • New vessels elsewhere (NVE) • Preretinal or vitreous hemorrhage • Preretinal fibrosis  tractional retinal detatchment • Maculopathy • Exudate within a disc area (DA) of fovea • Retinal thickening within DA of fovea • Microaneurysm or hemorrhage within DA of fovea

  4. Screening for diabetic retinopathy • Regular examination of the eye in the diabetic patient is essential • visual acuity measurement • examination of the fundus through dilated pupils • digital fundus photography • yearly examinations for those with no retinopathy • from puberty / 5 yrs after diagnosis for T1DM • from diagnosis for T2DM • 6-monthly for those with background retinopathy

  5. Treatment for DR • Strict glycaemic control • Strict blood pressure control • ACE inhibitors • Early detection • Prompt treatment • Panretinal photocoagulation • Education

  6. 2. Diabetic nephropathy • Pathological changes: glomerulus + tubular interstitium • Glomerulus: • at diagnosis of DM - enlarged because of the increased capillary surface area • subsequently, glomerular enlargement is caused by basement membrane thickening and (usually) expansion of the mesangium • Tubular interstitium: • total kidney volume is also increased, mainly through expansion of tubular tissue • basement membrane thickening • atrophy • interstitial fibrosis • arteriosclerosis

  7. Glomerular filtration rate (GFR): • early in diabetes – increased because of the increased filtration area • later declines in parallel with mesangial expansion and the resultant glomerular occlusion • The natural history of diabetic nephropathy is marked by increasing loss of protein (mostly albumin) in the urine

  8. Urinary albumin excretion AER = albumin excretion rate

  9. 50 % Normoalbuminuria Sustained normoalbuminuria Diabetes duration Baseline AER Glycaemic control Genetic susceptibility Ethnic minorities 50 % 30 % 50 % Sustained microalbuminuria Microalbuminuria BP Glycaemic control 20 % Intermitent proteinuria BP Proteinuria End-stage renal disease The stages and determinants of DN

  10. Mogensen classification (1) Stage I (renal hyperfunction / hypertrophy) • from diagnosis of DM • good glycemic control → reversible • GFRby 20-50 % (>150 ml/min/1,73 m2) • possible microalbuminuria (transitory!) • size of kidneys (ultrasonography) and of glomerules (biopsy) • Electronic microscope: normal basal membrane • normal BP

  11. Mogensen classification (2) Stage II – asymptomatic, normoalbuminuria • first 5 yrs from diagnosis of DM • 5-7 yrs from onset of disease: 30-50 % → stage III • biopsy: thickening of glomerular basal membrane, mesangium expansion • GFRstill ↑ (by 20-50 %) • normal urine albumin excretion • possible microalbuminuria (transitory!) • normal BP

  12. Mogensen classification (3) Stage III (early diabetic nephropathy) • 6-15 yrs from diagnosis of DM • blood glucose and BP comtrol → stops/decreases progression • persistent microalbuminuria (30-300 mg/24 hrs) • GFRstill, but decreases by 3-5 ml/min/yr • BP normal or mildly (by 3 mmHg/yr)

  13. Mogensen classification (4) Stage IV (clinical diabetic nephropathy) • 15-25 yrsafter onset of DM • proteinuria (albuminuria> 300 mg/24 hrs) • GFR progressively (by 8-12 ml/min/yr) • 3 sub-classes: • early (GFR > 130 ml/min) • intermediate (GFR < 100 ml/min) • advanced (GFR < 70 ml/min) • BP (by 5 mmHg/yr)

  14. Mogensen classification (5) Stage V (end-stage renal failure) • 25-30 yrs after onset of DM • variable proteinuria • urine albumin excretion< 10 g/24 hrs • GFR < 10 ml/min • BP constantly  • Microscope: important glomerular modifications

  15. Screening for diabeticnephropathy Annual determining ofmicroalbuminuria: • Type 1 DM: • from puberty • 5 yrs after diagnosis • Type 2 DM : • from diagnosis • How? • minimum 3 samples in 3-6 months • avoid conditionsthat can produce transient urinary albumin excretions • persistent microalbuminuria= 2 out of 3 results of 30-300 mg/24 hrs, 20-200 µg/min or urine albumin/creatinine = 30-300 mg/g

  16. Tratament of diabeticnephropathy Objectives: • Good glycemic control • Treat high BP • Diet • Treat dyslipidemia • Prevent / treat related comorbidities • Treat renal anemia • Prevent / treat renal bone disease

  17. Treating hypertension in patients with diabetic nephropathy • Non-pharmacologically: • exercise • weight loss • low-sodium diet • low-protein diet • smoking cessation • avoid alcohol • coffee • Drugs: • ACE inhibitors • ARBs • diuretics • Calcium blockers • beta-blockers • -adrenergic blockers

  18. 3. Diabetic neuropathy • Acute reversible • hyperglycemic neuropathy • Persistent • Symmetrical • Distal symmetrical neuropathy (chronic sensory and autonomic polyneuropathy) • Acute painful neuropathy • Focal and multifocal • Mononeuropathies (diabetic amyotrophy)

  19. Symptoms in distal symmetrical neuropathy • Asymptomatic in some • Numbness • Altered sensation • paraesthesiae • allodynia • Pain

  20. Signs in distal symmetrical neuropathy • None • Loss of • vibration sense • pin prick • touch • temperature • joint position sense • Wasting and weakness rare • Autonomic involvement: • warm feet (dilated arteriovenous shunts) • dry feet (absent sweating) • Complications • ulcer • oedema • Charcot arthropathy

  21. Neuropathy Autonomic Motor Sensory -Charcot joint - Orthopaedic deformity Abnormal foot posture (raised arch, clawed toes) Absent sweating A-V Shunting Reduced pain sensation Micro-vascular disease Reduced tissue nutrition Trauma Increased pressure loading Callus formation Ischaemia Arterial disease Ulceration Infection Aetiology of foot ulceration in diabetic patients

  22. Charcot arthropathy • severe neuropathy • long-standing diabetes • initiating event = injury, causing bone fracture • gross deformity • cubic foot • acute Charcot foot

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