Diabetes Management

Diabetes Management

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  Diabetes BENJAMIN WAMALWA
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  Investigations 1. Urine testing •Glucose– best if dipstick done on urine passed 1- 2hrs after a meal(maximize sensitivity) •One must confirm with blood testing because some individuals may have a low renal threshold for glucose, ‘renal glycosuria’ (eg. In pregnancy)
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  •Ketones – itis not pathognomonic for diabetes but if ass. with glycosuria, diabetes is likely. •They may be present in normal individuals who: •Have been fasting •Exercising strenuously for long periods •Have been vomiting repeatedly •Have been eating diet high in fat, low in carbs •Proteins – presence of microalbuminuria or proteinuria in the absence of UTI indicates development of diabetic nephropathy
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  2. Blood testing •Glucose •Glycatedhaemoglobin •This is not a diagnostic tool. It is used to assess glycaemic control over a period of weeks to months in patients with diabetes (usually up to 3 months). Normal IGT Diabetes FBS 3.5 - 6.0 6.1 – 6.9 >= 7.0 RBS 3.5 – 7.7 7.8 – 11.0 >= 11.1
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  • It measuresthe amount of glycated haemoglobin relative to the non-glycated haemoglobin. An increase in glycated haemoglobin indicates an increase in blood glucose (1% : 2mmol/L) • Therapeutic goal <7% (<8% in pts > 60yrs) • NB: levels may be increased (iron deficiency)/ decreased (Hb variants) in anemia. 3. Oral Glucose Tolerance Testing-Test done to test for diabetes, insulin resistance, impaired pancreatic beta cell function. Normal Pre-D Diabetic HbA1c 4 – 5.6% 5.7- 6.4% >6.5%
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  - Indicated ifRBS and FBS values are within the impaired glucose tolerance ranges - How is it performed?? •Preparation: - unrestricted carbohyrate diet for 3 days - fast overnight for at least 8 hrs - rest for 30 mins - remain seated during the test, no smoking •Sampling: plasma glucose measured before and 2hrs after a 75g oral glucose drink
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  •Interpretation: •Others 1. Blood pressure 2.FHG 3. UECs 4. Lipid profile Fasting 2hrs after glucose load Fasting hyperglycaemia 6.1 – 6.9 < 7.8 Impaired glucose tolerance <7.0 7.8 – 11.0 Diabetes >= 7.0 >= 11.1
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  Management •Multidisciplinary approach… 1. Nutritionist 2.Endocrinologist 3. Ophthalmologist 4. Nephrologist 5. Physiotherapist 6. Podiatrist •In new cases of diabetes, adequate glycaemic control can be achieved by diet and lifestyle alone(50%), oral antidiabetic drugs(20-30%)and insulin(20-30%)
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  Anti-diabetic drugs • Type2 diabetes as they depend on a supply of endogenous insulin 1. Biguanides (Metformin) • MOA: not well defined but it is thought to: - inhibit hepatic gluconeogenesis - increase peripheral glucose uptake - impairs glucose gut absorption • 1st line therapy, dose 500mg BD – max of 1g TDS • CI: impaired renal(GFR < 36ml/min) and hepatic function • SE: nausea, diarrhoea, abdominal pain, worsens lactic acidosis • If HbA1c is >7% 16 weeks after starting it, add a sulphonylurea
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  2. Sulphonylureas (tolbutamide,glibenclamide, gliclazide, glipizide) • MOA: ‘insulin secretagogues’ • Tolbutamide(mildest, good for elderly), glibenclamide(should be avoided in the elderly as it induces severe hypoglycaemia,) • Gliclazide, glipizide and glimepiride have few side effects. • All sulphonylureas effects are achieved at low doses. Little benefit when maximal doses are used. • SE: hypoglycaemia, weight gain • If HbA1c is >7.4% 6 months after starting it, consider insulin/ add a -glitazone 3. Meglitinides (repaglinide, nateglinide) • MOA: insulin secretagogue, prandial glucose regulator • Reduced risk of hypoglycaemia
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  4. Alpha- glucosidaseinhibitors (acarbose, miglitol) • MOA: delay carbohydrate absorption in the gut by selectively inhibiting disaccharidases, reduced postprandiol glucose • SE: flatulence, bloating, diarrhoea 5. Thiazodilinediones (pioglitazone, rosiglitazone) • MOA: increase insulin sensitivity in peripheral tissues • Administred as 2nd line with metformin or 3rd line with metformin + sulphonylureas • SE: hypoglycemia, fractures, fluid retention and increased LFTs
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  insulin • Insulin preparations Timein hours Insulin Onset Peak Duration Rapid-acting (insulin analogues:lispro, aspart, glulisine) < 0.5 0.5 – 2.5 3 – 4.5 Short-acting (soluble; regular) 0.5 -1 1 - 4 4 - 8 Intermediate-acting (isophane(NPH), lente) 1 - 3 3 - 8 7 - 14 Long-acting (bovine ultralente) 2 - 4 6 - 12 12 - 30 Long-acting (insulin analogues: glargine, detemir) 1 - 2 none 18 - 24 mixtard
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  • Side effects •Hypoglycemia • Weight gain • Peripheral edema • Insulin antibodies • Local allergy • Lipodystrophy • Dawn’s phenomenon: Hyperglycemia in the morning due to hormonal release (GH, Cortisol & epinephrine), without adequate insulin production in the body. • Somogyi phenomenon: Hyperglycemia in the morning due to hormone release following a period of hypoglycemia in the early hours of the morning (2 to 3 am). Maybe due to high doses of insulin given at night or lack of eating at night. • Honeymoon phenomenon: Occurs in newly diagnosed type 1 diabetes in which low blood glucose levels are recorded. This is because when insulin is administered, remaining beta cells are stimulated to produce insulin before they are eventually destroyed.
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  Complications Microvascular/neuropathic • Retinopathy, cataract •Impaired vision • Nephropathy • Renal failure • Peripheral neuropathy • Sensory loss, pain, motor weakness • Autonomic neuropathy • Postural hypotension, GI(gasroparesis, altered bowel habits) • Foot disease • Ulceration, arthropathy Macrovascular • Coronary circulation • Myocardial ischaemia/infarction • Cerebral circulation • TIA, stroke • Peripheral circulation • Claudication, ischaemia
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  References • ^ "WhatIs MicrovascularCranialNerve Palsy?". aao.org. 1 September 2017. Archivedfromthe original on 22 December 2017. • ^ Behl T, Kaur I, Kotwani A (Jun 2015). "Implication of oxidative stress in progression of diabetic retinopathy". Surv Ophthalmol. 61 (2): 187– 196. doi:10.1016/j.survophthal.2015.06.001. PMID 26074354. • ^ Forbes, JM; Coughlan MT; Cooper ME (June 2008). "Oxidative stress as a major culprit in kidney disease in diabetes". Diabetes. 57 (6): 1446–1454. doi:10.2337/db08- 0057. PMID 18511445. Archived from the original on 2009-04-15. • ^ Javed S, Petropoulos IN, Alam U, Malik RA (Jan 2015). "Treatment of painfuldiabetic neuropathy". Ther Adv Chronic Dis. 6 (1): 15– 28. doi:10.1177/2040622314552071. PMC 4269610. PMID 2555323 9. • ^ Jump up to:a b Kanji JN, Anglin RE, Hunt DL, Panju A (April 2010). "Does this patient with diabeteshave large-fiber peripheral neuropathy?". JAMA. 303 (15): 1526– 32. doi:10.1001/jama.2010.428. PMID 20407062. • ^ Aristidis Veves; John M. Giurini;Frank W. LoGerfo (2012-06-12) SurgicalManagement (3rd ed.). SpringerScience & Business Media. p. 34. ISBN 978-1-61779-791-0. • ^ Pop-Busui, Rodica;Boulton, Andrew J.M.; Feldman, Eva L.; Bril, Vera; Freeman, Roy; Malik, Rayaz A.; Sosenko, Jay M.; Ziegler, Dan (20 December 2016). "Diabetic Neuropathy:A Position Statement by the American Diabetes Association". Diabetes Care. 40 (1): 136– 154. doi:10.2337/dc16-2042. PMID 27999003. • ^ Jump up to:a b Griebeler, ML; Morey-Vargas, OL; Brito, JP; Tsapas, A; Wang, Z; Carranza Leon, BG; Phung, OJ; Montori, VM; Murad, MH (November 2014). "Pharmacologicinterventionsfor painful diabetic neuropathy:An umbrella systematic review and comparative effectiveness network meta-analysis". Annals of Internal Medicine(Systematic Review & Meta-Analysis). 161 (9): 639– 49. doi:10.7326/M14-0511. PMID 25364885. • ^ Derry, S; Rice, AS; Cole, P; Tan, T; Moore, RA (13 January 2017). "Topicalcapsaicin (high concentration)for chronic neuropathic pain in adults". The Cochrane Databaseof Systematic Reviews (Systematic Review). 1: CD007393. doi:10.1002/14651858.CD007393.pub4. PMID 28085183 .
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