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A FREE NAVIGATION THROUGH THE WAVES OF HYPER AND HYPOGLYCEMIA By Prof Morsi Arab University of Alexandria

A FREE NAVIGATION THROUGH THE WAVES OF HYPER AND HYPOGLYCEMIA By Prof Morsi Arab University of Alexandria. Glucose is the predominant fuel for the Brain. Because the brain cannot synthesize or store glucose ,it has to be provided from the circulation.

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A FREE NAVIGATION THROUGH THE WAVES OF HYPER AND HYPOGLYCEMIA By Prof Morsi Arab University of Alexandria

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  1. A FREE NAVIGATION THROUGH THE WAVES OF HYPER AND HYPOGLYCEMIA By Prof Morsi Arab University of Alexandria

  2. Glucose is the predominant fuel for the Brain. Because the braincannot synthesize orstore glucose ,it has to be provided from the circulation

  3. Factors involved in Gluco-regulation: I. Hormones : Insulin, Glucagon, adrenalin, Growth H. ,Cortisol . II. Neuro transmitters: Sympathetic – Parasypathetic., Autonomic neuropeptides III. Substrates : Glucose, FF Acids.

  4. The Glucoregulatory Hormones (main effects) : Insulin: decrease Hepatic Glucose production (HGP ) - and increase glucose utilization Glucagon:stimulates HGP Adrenalin :stimulate HGP and decrease Gluc utilization . Growth H. andCortisol: diminish Glucose utilization and increase glucose production .

  5. Sympathetic and parasympathetic Gluco regulation (cont ) Sympathetic and parasympathetic activation: Noradrenalin induces hyperglycemia Acetyl Cholinediminishes HGP . Substrates: GlucoseAuto regulation is independent of hormonal or neuroregulator mechanisms. Non-esterfied FA diminish glucose utilization and increase glucose production.

  6. Autonomic , neuroglycopenic and neuroendocrine responses to hypoglycemia

  7. THE PHYSIOLOGICAL RESPONSES TO HYPOGLYCEMIA I. CNS : - cognitive dysfunction - neurophysiological changes (EEG) II.Peripheral ( Extra CNS ) Effects: - in response to autonomic (sympathetic and parasympathetic activation) and release of catecholamines - Hemodynamic changes - Regional changes of blood flow - Tremors - Homeostatic effects

  8. Mean glycemic thresholds for different responses to hypoglycemia

  9. THE GLYCEMIC THRESHOLDS ( in nondiab) 1.The earliest response to lowered glucose is a diminished insulin secretion: at 82 mg) 2. Release of counter regulatory H: (at 66mg) 3. Growth H : (at 66 mg) 4. Cortisol : (at 57 mg) 5. Symptoms of Hypoglycemia start (at 54 mg) 6. Cognitive dysfunction develop ( at 48 mg ) -------------------------------------------------

  10. The CNS Cognitive Dysfunction in Hypoglycemia • It starts at a threshold of 3 m mol/L (54mg ) {but with marked individual variations}. • Affects selectivetasks requiring attention, memory, rapid decision taking, analysis of visual stimuli, hand eye coordination ……… - Recovery from it takes usually 40-90 min after normoglycemia is restored.

  11. Peripheral Hemodynamic Changes inhypoglycemia: - Increased Heart rate. - Increased pulse p (lowered diast. p). - Increased myocard. contraction. - Icreased card. output. - ECG: flat or inverted T , and long QT interv (with fall of Serum Potassium ).

  12. Regional changes in Blood flow in Hypoglycemia - Cerebral BF is 20 % increased (esp. in frontal and parietal areas ) • Renal BF & Glum filtration diminished (20%) • Increased Splanchnic BF - increased Hepatic BF - markedly diminished Splenic BF • Markedly increased Muscle BF • Cutaneous BF :Early increased (flushing and sense of warmth) {before sweating response },, then diminished (pallor)

  13. Other Changes in hypoglycemia : Tremors(a cardinal sympathetic feature) Homeostatic Changes: Increased : WBC activation, viscosity, fibrinolysis and platelet activation Increased Free Radical activity.

  14. In the DCCT Study severe hypoglycemic episodes occurred in 50% during sleep , and in 1/3rd during day butwithout warning.

  15. Who are the special groups at high riskbecause of hypoglycemia ( esp. if withoutwarning or monitoring ): * The Elderly, esp. on Insulin or strong oral ( e,g. glibenclamide ) * Pts with angina or cerebro-vascdis. * Pts on B-Blockers

  16. Hypoglycemic Unawareness Definition : loss of the known warning autonomic symptoms which were present before. Occurs in 50% of very long standing Type 1 DM and in 25% of all DM .

  17. Hypoglycemic Unawareness Elevation of the Hypoglycemic threshold means that more profound hypoglycemia is needed to induce awareness

  18. Hypoglycemic Unawareness (cont. ) Patients with history of hypoglycemic unawareness have 6-folds risk of getting severe hypoglycemia

  19. After development of Hypoglycemic unawareness , the meticulous avoidance of hypoglycemic episodes leads to restoration of awareness .

  20. Self Monitoring of Blood Glucose (SMBG) • It is an essential tool in management, unless unaffordable or unavailable • 1961: first suggested ---1970s technical revolution – supported by studies relating glycemic control to prevention of complications .

  21. SMBG • Advantage over Glycated HB : it shows the excursions , not just an average. * In strict glycemic control management proper pt. selection is essential : ( motivated - accepting frequent performance of SMBG – sufficiently educated – skilled staff assistance )

  22. Frequency of monitoring in SMBG • Individualized More frequent with : insulin Trt - unstable DM (brittle) - pts at high risk . • In Tight Glycemic Control: 4 times or more (+ once /wk overnight) . + at any time if hypoglyc. is suspected . + before performing critical activities (e.g. driving)

  23. The More Frequent Monitoring 7- 9 times/day ! For a 24 H profile During initiation of intensive treatment , in pregnancy .etc A Modified Concise Profile by ” once/day over a week “ monitoring Sat : overnight morning fast Sun : 2H pp (brkfst) Mon : before lunch Tues : 2H pp after lunch Wed : before supper Thrs : 2H pp after supper Friday : before retiring to bed Any day : when hypoglyc episode is suspected (especially at early morning hours ) Any day to monitor the effect of exercise , change of treatment , or dietary irregularities

  24. SMBG IN TYPE 2 Diabetes Frequency ? Controversial. With Good control : Just daily Fasting test may be sufficient to detect onset of disruption of control. Otherwise, (at initiation of additional oral agent, increasing doses or initiating insulin therapy ): morefrequent monitoring is needed , to see a day profile. Reasonable targets Fasting 80-120 mg PP 100-180 mg Bed time 100-140 mg

  25. It is important to”keep records”with SMBS To monitor the impact of diet , exercise and changes in treatment But too much data may induce “ Data Overload ”, transfer to “Graphic Display “.

  26. The Future ? A Continuous Monitoring System “ Gluco-watch “

  27. STRESS HYPERGLYCEMIA IN STROKE Cerebral ischemia ( bld flow < 15ml /100g /min ) induces cerebral infarction:. with irreversible changes in the centre and reversible changes surrounding it. * The Hyperglycemia is usually mild (< 200 mg) but it enhances the isch. cerebral damage * There is no known threshold for the hyperglyc. level which enhances this risk.

  28. Associated Hyperglycemia with stroke leads to : 1. slower recovery of the reversible changes. 2. increased capil. permeability --.increases the risk of hemorrhagic transformation. 3. increases by 5 folds the risk inthrombolytic therapy ( by fatal or nonfatal hemorrhage .

  29. Clinical trials are not yet conclusive but probably control of hyperglycemia affects the safety and efficacy of stroke interventions

  30. Alexandrie – Palais du Montazah Thank You

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