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Management of DM and its complications. Complications are either… Acute---DKA ---hyperosmolor non ketotic coma ---hypoglycemia ---lactic acidosis

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  • Management of DM and its complications
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  • Complications are either Acute---DKA ---hyperosmolor non ketotic coma ---hypoglycemia ---lactic acidosis Chronic ---macrovascular ---microvascular
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  • Prevalance of complications at the time of diagnosis { UKPDS } newlydiagnosed diabetes ComplicationsPrevalance % Any complication50 % retinopathy21 % Abnormal ECG18 % Absent foot pulses 14 %
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  • Impaired reflexes +vibration sense 7% MI / angina / claudication 2.8 % stroke2.8 %
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  • Chronic complications Macrovascular microvascular
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  • Macrovascular complication 40-50 % of people with DM die from these complications Factors that contribute to the risk include 1- prevalance of hypertension in diabetics 2-- lipid profile 3abnoramlity in clotting system 4effect of hyperglycemia on progression of atherosclerotic lesions
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  • Macrovascular complications Stroke MI Peripheral vascular disease Foot problems
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  • Microvascular complications Retinopathy Nephropathy Neuropathy Foot problems
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  • Coronary artery disease Coronary artery disease accounts for the majority of diabetic deaths Certain features of CAD in diabetics include: Adjusted for age MI is 2-5 times more frequent in patients with diabetes Pts with DM who have MI have a lower survival rate compared to pts without DM incidence of silent MI 40% Silent MI may present as new onset of CCF Small vessel disease with relatively patent coronary arteries are more common
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  • Peripheral vascular disease {PVD} Special characteristics of PVD Locationtibial + popliteal arteries are common----aorta,ileal, femoral rare Extendmulti segmental occlusion Progressionaccelerated progression compared to non diabetics Gangrene---risk more than non diabetics over 40 yrs of age
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  • Retinopathy Backgroundthis is the most common type of retinopathy --not usually seen untill after 10 yrs of DM ---may be found in 30 % of pts with type 2 DM Proliferative maculopathy
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  • Nephropathy Consists of the following clinical stages: GFR > 150 mls /min Microalbuminurea 30-300 mg /24 hrs Clinical albuminuria also called macroalbuminuria > 300 mg/ 24 hrs Worsening of proteinuria, hypertension and GFR Kidney failure occurs when GFR to 10mls/min
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  • Factors influencing renal function in DM Glomerular basement membrane damage diabetic nephropathy Renal artery stenosis and ischaemia due to atherosclerosis Ascending infection Renal papillary necrosis
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  • Neuropathy Different clinical presentations Symmetrical sensory polyneuropathy Mononeuritis multilplex Autonomic neuropathy
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  • Sensory neuropathy Insidious onset of loss of sensation in feet and handsgloves and stockings Loss of vibration sense and reduced or absent ankle or knee jerk Loss of peripheral nerve function results in wasting of small muscles of feet and hands
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  • Mononeuritis multiplex Nerves commonly affected are 3rd and 6 th Amyotrophic motor neuropathy characterized by unilateral or bilateral pain and weakness of the quadricepsthey often recover spontanously Median nerve palsy leeds to carpal tunnel syndrome Peroneal nerve palsy leeds to foot drop
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  • Autonomic neuropathy CVSloss of vagal { parasympathetic tone} produces --resting tachycardia --loss of sinus rhythm change in heart rate with respiration---sinus arrythmia Loss of sympathetic activity in arterioles results in peripheral vasodilatation and postural hypotension Rxsupport stockings --fludrocortisone -alfa blockers
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  • GIT Gastroparesis--Delayed gastric emptying results in early statiety or recurrent vomiting --treated with dopamine agonist metochlorpramide domperidone erythromycin Nocturnal diarrhea loperamide Constipation due to colonic atony laxatives
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  • Autonomic bladder Loss of bladder smooth muscle tone results in incomplete emptying, stasis, and risk of infection In severe cases the bladder is persistantly distendedatonic which results in over flow incontinance sympathomimeticscarbachol antichilinesterase drugs
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  • Gustatory sweating Eating cause excessive facial sweating Anticholinergic drugs--probantheline Erectile dysfunction impotence
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  • Foot disease Neuropathic foot ulcer Ischaemic foot ulcer Charcots arthropathy
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  • Can we prevent type 2 DM Before pts develop DM,they almost always have pre diabetes Clinical trails have documented that dietary changes and regular exercise prevent or delay the development of overt DM in individuals at high risk
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  • Risk factors for type 2 DM Age > 45 1 st degree relative with type 2 DM History of gestational diabetes or delivery of infant >9 lbs PCO Abdominal obesity CVD, hypertension,dyslipidemia,other metabolic syndrome features
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  • Prediabetes Defined as- IFGFBS =100 -125 mg/dl5.6 - 6.9 mmol / l Impaired glucose tolerance---plasma glucose level 140 199 mg/dl 7,8 11.0 mmol / l, 2 hrs after 75 gms of glucose
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  • Evaluation and treatment FBG HbA1c Serum electrolytes Urine for protein and microalbuminuria ECG Fasting lipid profile
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  • Treatment Diet Exercise Stop smoking Treat hyperlipidemia ---statin group Treat hypertensionmainly ACEI Prevent proteinuria by prescribing ACEI Start ASA as prophylaxis for IHD OHG Insulin
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  • ADA Rx goals for glycemic control glycemianormalgoalFurther action required Average preprandial glucose mg / dl < 11080 - 120> 140 Average pp glucose < 140< 160> 180 HbA1c< 6< 7> 8
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  • OHG Biguanides Suppress hepatic glucose production Decrease intestinal glucose absorption Improve insulin sensitivity metformin Sulphonylurea Increase pancreatic insulin secretion glimepiride ---glipizide ---glyburide ---chlorpropamide
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  • Thiazolidinediones post prandial hyperglycemia ---Rosiglitazone ---poglitazone
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  • Cont.. Alfa glucosidase inhibitors post prandial hyperglycemia by decreasing GIT carbohydrate absorption arcabose Meglitinides--- Increase pancreatic insulin secretion through different glucose binding sites than used by sulphonylureas repaglinide
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  • Type 2 diabetes is a progressive disease Over time most pts will need insulin to control glucose
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  • Insulin therapy in type 2 diabetes Don,t wait forever Don,t be afraid of hypoglycemia Consider combination therapy Don,t under insulinize Consider insulin pump therapy
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  • DIABETIC KETOACIDOSIS Leading cause of death in pts with type 1 diabetes under the age of 20 yrs
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  • Risk factors for DKA Results from absolute or relative insulin deffeciency Missing the dose of insulin Infection Increase food intake Stress like MI or surgery
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  • Diagnosis Triad of. Hyperglycemiaglucose more than 15mmol /l Metabolic acidosisPH < 7.2 ---HCO3
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  • Principles of management Rehydration Insulin Correction of K+ Correction of acidosis + / - antibiotics
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  • Rehydration 1 litre NS over 30 min 1 litre over 1 hr 1 litre over 2 hrs 1 litre over 4 hrs I litre over 6 hrs Change saline once BS reaches 13 mmol / l
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  • Insulin therapy 10 -20 units of RI is given IM stat 4 - 6 units / hr by IV infusion untill BS to 10 15 mmol/l then to 1 - 4 units / hr Aim to BS 3 6 mmol / hr Change to SC once BS 13 mmol / l
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  • Potassium replacement 1 st 30 min if K+ > 5.5 mmol/l no K+ If 3.5 5.5 --give 20 meq in the 1 st litre If < 3.5 --give 40 meq in the 1 st litre Continue K+ infusion 20 meq in each litre to maintain K+ at the level of 3.5 4. 5
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  • Bicarbonte replacement Bicarbonate is replaced when the PH is between 7.0 7.1 Antibiotics These are used when there is strong suspicion of infection
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  • HYPOGLYCEMIA Causes Missed delayed or inadequate meal Unaccustomed exercise Alcohol Increase dose of drugs..insulin or OHG Gastroparesis Malabsorption factitious
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  • NON KETOTIC HYPEROSMOLAR DIABETIC COMA Characterized by Severe hyperglycemia--> 50 mmol / l No ketones in the urine Severe dehydration Occurs in the elderly Risk of thrombosis is high Mortality is high
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  • Management Differs from DKA in the following Very sensitive to insulin so very small dose should be started Calculate osmolality and start either or saline Plasma osmolality =2Na + 2K + glu + urea=280 - 295
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  • Cont.. Prophylactic SC heparin Fluid replacement should be adjusted according to CVP
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