Glucose homeostasis


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Dr Anand Tiwari
approach to blood sugar management

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Glucose homeostasis

  1. 1. Glucose homeostasisDr Anand.TiwariHead of dept.ICUWanowrie Ruby hall
  2. 2. Emergency prespective• When do you advise a blood sugar ?
  3. 3. • Brain is the biggest user of glucoseALTERED MENTAL STATUS
  4. 4. Pinprick for BSL• Altered glucose metabolism shouldbe considered in the• differential diagnosis of all patientswith mental status changes,• neurologic deficits, and severeillnessDo not neglect the initial assessment of ABC
  5. 5. Insulin and glucagoan
  6. 6. Toronto university…..1921
  7. 7. Insulin• Hormone required to transfer glucose fromthe blood to the tissues and the cell where itcan be used as fuel.• Anabolic hormone• Ant catabolic action• Liver acts as a buffer
  8. 8. The Diabetic patient• Diabetes is a medical condition whenpersons pancreas will no longer produce anadequate supply of insulin or when thebody loses ability to utilize insulin properly
  9. 9. Gluocose tolerance curve
  10. 10. Glycosylated Hemoglobin• 6.5%• 7%• 7.5%
  11. 11. Pathophysiology of Diabetic Emergencies• type 1 diabetes (previously known asjuvenile onset,• ketosis-prone, insulin-dependent, orbrittle diabetes) or• type 2 diabetes (previously, adult-onset, non-ketosis-prone,• non-insulin-dependent, or obesity-related diabetes• T3Gestational
  13. 13. Diabetes video
  14. 14. Diabetic emergencies• HYPERGLYCEMIA• HYPOGLYCEMIA
  15. 15. • You receive a patient in ER who isobtunded,what is your approach to thepatient /?????????????
  16. 16. Emergency care• SAMPLE• What did you last eat?• Do you take diabetic medication?• Have you taken your medication asprescribed?
  17. 17. life-threatening disorders of glucosemetabolism.• DKA• HHNC• hypoglycemiaAtherosclerosisInfectionRetinopathyCataractHypertensionCkdNeuropathyFoot
  19. 19. • TYPICAL SYMPTOMS OFHYPOGLYCEMIA OCCURSBELOW?/?• A-120mg%• B-80mg%• C-50mg%• D-400mg%
  20. 20. • Q- which of the following iscontraindication for administrating oralglucose to a known diabetic patient?• A-low blood glucose reading• B-unresponsive patient• C-patient able to swallow easily• D-patient taken insulin recently
  21. 21. Insulin deficiency• in lipolysis and unrestrained fatty acidoxidation, producing• acetone,• β-hydroxybutyrate,• acetoacetate—
  22. 22. IntracellularInterstitialIntravascular2/3 1/33/4 1/4ECF osmolality = ICF osmolalityK, ATPCreatinine PO4phospholipidsNa, ClHCO3
  23. 23. Osmotic diuresis• The glucose remains largely in theextracellular• space and shifts water osmotically fromthe intracellular compartment.• of the renal tubules for glucose has amaximum of approximately 200 mg/min,an osmotic diuresis occurs, with water lost in• excess of salts.
  24. 24. DKA• Hyperglycemic condition in which absenceof insulin causes the body to metabolizeother sources of energy such as fat .Theblood becomes acidic and condition mayresult in fruity breath odor and alteredmental status• (
  25. 25. Kussmaul respiration• )• Respiration that are both rapid anddeep seen in patient with extremehyperglycemia associated with thefruity odor of acetone.
  26. 26. Enumerate medical causes of•• ACUTE ABDOMEN???
  27. 27. Diabetic ketoacidosis• Dyspnea• Normotension• Hypo- and hyperthermia• Nausea• Tachycardia
  28. 28. S/symptoms• Lethargy to coma• Vomiting• Tachypnea• Fruity breath• Abdominal pain• Abdominal tenderness• Orthostatic• Cerebral edema
  29. 29. Lab paradox• nitroprusside reaction commonly usedto detect ketone bodies• detects acetoacetate much better thanacetone and does• not react with β-hydroxybutyrate at all.Particularly in severe• DKA, β-hydroxybutyrate is thepredominant ketone,
  30. 30. Laboratory findings• 1. Serum glucose level >300 mg/dL• 2. pH <7.35, pCO2 <40 mm Hg• 3. Bicarbonate level below normal with anelevated anion gap• 4. Presence of ketones in the serum
  31. 31. What next• CHECK ANION GAP• Causes of raised anion gap• MUDPIES
  32. 32. Differential diagnosis• A. Differential diagnosis of ketosis-causing conditions• 1. Alcoholic ketoacidosis occurs with heavy drinking• and vomiting. It does not cause an elevated• glucose.• 2. Starvation ketosis occurs after 24 hours without• food and is not usually confused with DKA because• glucose and serum pH are normal.
  33. 33. Treatment of diabetic ketoacidosis• Fluid resuscitation• Which fluid???• When to introduce 5% dex
  34. 34. Insulin• loading dose consists of 0.1 U/kg IV• . then infused at 0.1 U/kg per hour.• glucose decline does not• exceed 100 mg/dL per hour.• 2. The insulin infusion rate may be decreasedwhen the bicarbonate level is greater than 20mEq/L, the anion gap is less than 16 mEq/L, or theglucose is <250 mg/dL.
  35. 35. Potassium• deficit is between 300 and 500 mEq• potassium replacement is 20 mEq/h, but• hypokalemia. All patients should receive potassium replacement,• except for those with renal failure, no urine output,• or an initial serum potassium level greater than 6.0• mEq/L.
  36. 36. Sodium.• . For every 100 mg/dL that glucose iselevated, the sodium level should beassumed to be higher than the measuredvalue by 1.6 mEq/L.
  37. 37. Other electrolytes• Phosphate. Diabetic ketoacidosis depletes phosphate• stores. Serum phosphate level should be• checked after 4 hours of treatment. If it is below 1.5• mg/dL, potassium phosphate should be added to the• IV solution in place of KCl.• F. Bicarbonate therapy is not required unless the• arterial pH value is <7.0. For a pH of <7.0, add 50• mEq of sodium bicarbonate to the first liter of IV fluid.• G. Magnesium. The usual magnesium deficit is 2-3 gm.• If the patients magnesium level is less than 1.8• mEq/L or if tetany is present, magnesium sulfate is• given as 5g in 500 mL of 0.45% normal saline over 5• hours.
  38. 38. Say no to soda bicarbonate??• Therapy of DKA and HHNC requiresreplacement of deficits of• fluids, electrolytes, and insulin
  39. 39. Freezing point depression method• Osmolarity (mOsm/L) = 2 × [sodium]• + [glucose]/18 + [BUN]/2.8 +[ethanol]/4.6
  40. 40. disastrous consequences ofaggressivetherapy• —cerebral edema,• pulmonary edema,• hypoglycemia,• hypokalemia, and• hyperchloremic metabolic acidosis.
  41. 41. Why decompensation?Search for Infection
  42. 42. BS control in acute illness• Maintaining BS between 80-100 mg/dl• Surgical ICU (Van den Berghe et al, 2001)– In-hospital mortality 11 to 7%– Reduction in severe infections, polyneuropathy andorgan failure• Medical ICU (Van den Berghe et al, 2006)– Prevent acute renal failure, accelerated weaning fromventilator, reduced ICU and hospital stay– Mortality reduced in people who stayed in icu for morethan 3 days• Control population had BS control once BS > 215mg/dl
  43. 43. Review questions• All of the following pathways occur as diabetic• ketoacidosis develops EXCEPT• (A) hyperglycemia → glycosuria → dehydration• and loss of electrolytes• (B) hyperglycemia → cell dehydration → altered• level of consciousness• (C) insulin and glucagon deficiency → increased• hepatic gluconeogenesis• (D) lipolysis → ketosis → acidosis• (E) muscle breakdown → azotemia →• loss of sodium
  44. 44. Which of the following statements is TRUE regardingadministration of sodium bicarbonate solution duringthe management of diabetic ketoacidosis (DKA)?• (A) It prevents paradoxical spinal fluid acidosis• and cerebral edema• (B) It shifts potassium ions extracellularly and• corrects the hypokalemia• (C) It shifts the oxyhemoglobin dissociation curve• to the right, facilitating off-loading of oxygen• at the tissue level• (D) Complications include rebound alkalosis and• sodium overload• (E) It is recommended in all DKA patients with• severely altered levels of consciousness
  45. 45. All of the following are appropriate treatmentsforDKA EXCEPT• (A) administering 3 to 5 L normal saline in the• first 4 to 6 h• (B) replacing the 3 to 5 mEq KCl/kg deficit• gradually over the first 2 to 3 days• (C) infusing insulin at 0.1 U/kg/h after the initial• bolus is given• (D) stopping insulin administration when glucose• levels fall to 250 mg/dL• (E) administering phosphate if levels fall below• 1.0 mg/dL
  46. 46. Which of the following statements concerninghyperosmolarhyperglycemic nonketotic syndrome (HHNS) isTRUE?• (A) The mortality rate of HHNS is less than that• of DKA• (B) HHNS and DKA are easily distinguishable• (C) A majority of HHNS patients present• with coma• (D) Metabolic acidosis excludes the diagnosis• (E) Seizures occur in up to 15 percent of patients• with HHNS
  47. 47. • What is the MOST common cause ofhypoglycemia• in patients presenting to the ED?• (A) First time presentation of diabetes• (B) Alcohol related• (C) Oral hypoglycemics• (D) Insulinoma• (E) Liver failure
  48. 48. Which of the following statementsregarding hypoglycemiais FALSE?• (A) Counterregulatory hormones are released in a• hypoglycemic state• (B) Hypoglycemia causes both autonomic and neuroglycopenic• symptoms• (C) Hypoglycemic patients commonly present with• altered levels of consciousness, lethargy, confusion,• or agitation• (D) Hypoglycemia is diagnosed when the blood• glucose is less than 60 mg/dL• (E) Glucagon is ineffective in the treatment of• alcohol-induced hypoglycemia
  49. 49. • A patient presents to the ED and has the following• laboratory values: sodium 139 mEq/L, potassium 4.1• mEq/L, chloride 112 mEq/L, bicarbonate 15 mEq/L,• blood urea nitrogen (BUN) 22, creatinine 1.5, andglucose 180. All of the following could be the etiology of• these laboratory findings EXCEPT• (A) salicylates• (B) renal tubular acidosis, type II• (C) acute diarrhea• (D) ureterosigmoidostomy• (E) pancreatic fistula
  50. 50. • What is the calculated osmolarity for the patient in• question 300?• (A) 157 mOsm/L• (B) 274 mOsm/L• (C) 296 mOsm/L• (D) 310 mOsm/L• (E) 347 mOsm/L
  51. 51. • The etiologies of this patient’s normal AG• (hyperchloremic) metabolic acidosis can beremembered by a helpful mnemonic,• HARDUP: H for hypoaldosteronism (Addison’sdisease), A for acetazolamide, R for renal• tubular acidosis, D for diarrhea, U forureterosigmoidostomy, and P for pancreaticfistula.