Diabetes Mellitus Part 2 (DKA)
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Diabetes mellitus..an introcution of Diabetic ketoacidosis
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Diabetes Mellitus Part 2 (DKA)
- 1. Pratap sagar Tiwari, MD, Internal Medcine, Lecturer, NMCTH UNDERSTANDING DIABETES..PART 2 DIABETES KETOACIDOSIS
- 2. •RECAP
- 3. CASE SUMMARY • A 30 yrs old M was brought in ERD in the state of unconsciousness. (Note: Coma is a symptom, not a diagnosis.) Pic taken from http://censorbugbear-reports.blogspot.com/2010/03/shocking-neglect-of-comatose-patient-at.html
- 4. RECAP • Causes of patient in state of coma • Definition of terms related to consciousness • Causes of Coma in a Diabetic Patient • Insulin Synthesis/ Secretion • Regulation of Glucose hemostasis • Response of hypoglycemia in normal & DM • Hypoglycemia & symptoms
- 5. DKA • DKA is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 DM, but it is not uncommon in some patients with type 2 DM. • This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Hyperglycemia Ketoacidosis
- 6. DKA Insulin def/ resistance Inhibition of “insulin inhibition of Glucagon” ↑ Glucagon ↑ fat/muscle breakdown ↑ Hepatic gluconeogenesis ↑ delivery of gluconeogenetic precursors to Liver ↑ Glycerol/ Alanine
- 7. Glycosuria ↓ Glucose excretion ↓ GFR Osmotic Diuresis Volume Depletion ↑ Blood GLucose
- 8. Action of Insulin: ↑ utilisation of peripheral glucose in skeletal muscle ↑ Blood Sugar X Insulin↓/ Resistance (Note: Insulin resistance is a condition in which cells fail to respond to the normal actions of the hormone insulin. The body produces insulin, but the cells in the body become resistant to insulin and are unable to use it as effectively, leading to hyperglycemia.)
- 9. Insulin def/ resistance Glucose utilization is impaired Alternate source of Energy : KETONES ↑ Lipolysis TG FFA Normally Plus increased catecholamines
- 10. DEVELOPMENT OF KETOACIDOSIS • The development of ketoacidosis requires a specific alteration in hepatic metabolism so that free fatty acyl CoA can enter the mitochondria, where conversion to ketones occurs. • Mitochondrial entry is regulated by the cytosolic enzyme carnitine palmitoyltransferase I (CPT I), the activity of which varies inversely with malonyl CoA [1]. • Glucagon decreases the production of malonyl CoA, thereby increasing CPT I activity and ketogenesis [2]. • Insulin does not appear to directly affect hepatic ketogenesis [3]. 1. McGarry JD, Woeltje KF, Kuwajima M, Foster DW. Regulation of ketogenesis and the renaissance of carnitine palmitoyltransferase. Diabetes Metab Rev 1989; 5:271. 2. Cook GA, Nielsen RC, Hawkins RA, et al. Effect of glucagon on hepatic malonyl coenzyme A concentration and on lipid synthesis. J Biol Chem 1977; 252:4421. 3. Miles JM, Haymond MW.. Effects of free fatty acid availability, glucagon excess, and insulin deficiency on ketone body production in postabsorptive man. J Clin Invest 1983; 71:1554.
- 11. NOTE • Moderate insulin deficiency, as seen in HHS, might be associated with sufficient insulin to block lipolysis (and therefore ketoacid formation) but not enough to promote glucose utilization and prevent the development of hyperglycemia [1]. 1. Hillman K. Fluid resuscitation in diabetic emergencies--a reappraisal. Intensive Care Med 1987; 13:4.
- 12. BREATHING PATTERNS: CHEYNE-STOKE • characterized by periods of respirations during which the tidal volume starts shallow and gets progressively deeper, and then gets progressively shallower. • This shallow-deep-shallow pattern is followed by periods of significant apnea that can last up to 30 seconds or longer, then the cycle starts over.
- 13. BIOT’S BREATHING (CLUSTER RESPIRATION) • A respiratory pattern characterized by periods or “clusters” of rapid respirations of near equal depth or followed by regular periods of apnea. • damage to the medulla oblongata by stroke (CVA) or trauma.
- 14. ATAXIA RESPIRATIONS • Completely irregular breathing pattern with irregular pauses and increasing episodes of apnea. • caused by damage to the medulla oblongata secondary to trauma or stroke.
- 15. KUSSMAUL’S RESPIRATIONS • A type of labored or hyperventilation characterized by a consistently deep and rapid respiratory pattern. • Most of the time a respiratory pattern secondary to a metabolic acidosis is rapid and shallow and a true kussmaul breathing pattern is rarely reached before the acidosis is corrected
- 16. APNEUSTIC RESPIRATIONS • have a prolonged inspiratory phase followed by a prolonged expiratory phase commonly believed to be apneic phases. • damage to the upper part of the pons
- 17. FEATURES OF HYPEROSMOLARITY • Excessive thirst despite frequently taking water / other liquids • Continued high level of blood sugar • Dry and/ or parched mouth • Frequency of urination increases • Pulse rate becomes rapid • Shortness of breath with exertion • Skin becomes dry and warm and there is no sweating • Sleepiness and/ or a condition of confusion http://www.mayoclinic.org/diseases-conditions/diabetic-hyperosmolar-syndrome/basics/definition/con-20026142
- 18. END OF SLIDES References: 1. Harrison's Principles of Internal Medicine, 18th Edition 2. Davidson Practice of Medicine 3. Uptodate 20.3 4. Standards of Medical Care in Diabetesd 2014. American Diabetes Association. Diabetes Care Volume 37, Supplement 1, January 2014 5. Medscape.com 6. Mercksmanual
Notes de l'éditeur
- Extra note: Insulin resistance (IR) is a condition in which cells fail to respond to the normal actions of the hormone insulin. The body produces insulin, but the cells in the body become resistant to insulin and are unable to use it as effectively, leading to hyperglycemia.
- The development of ketoacidosis requires a specific alteration in hepatic metabolism so that free fatty acyl CoA can enter the mitochondria, where conversion to ketones occurs
- The deficiency in insulin (absolute deficiency, or relative to excess counterregulatory hormones) is more severe in DKA compared with HHS. The residual insulin secretion in HHS is sufficient to minimize ketosis but does not control hyperglycemia. The serum glucose concentration in HHS frequently exceeds 1000 mg/dL (56 mmol/L), but in DKA is generally below 800 mg/dL (44 mmol/L). At least two factors contribute to the lesser degree of hyperglycemia in DKA: Patients with DKA often present early with symptoms of ketoacidosis (such as shortness of breath and abdominal pain), rather than late with symptoms due to hyperosmolality. Patients with DKA tend to be young and to have a glomerular filtration rate that, at least in the first five years of diabetes, may be as much as 50 percent above normal. As a result, they have a much greater capacity to excrete glucose than the usually older patients with HHS, thereby limiting the degree of hyperglycemia.
- Brainstem lesions: cerebrovascular event Encephalitis Raised intracranial pressure Heart failure Chronic pulmonary oedema Altitude sickness
- damage to the medulla oblongata by stroke (CVA) or trauma, pressure on the medulla due to uncal or tentorial herniation, prolonged opioid abuse.
- Ataxic respirations are most often caused by damage to the medulla oblongata secondary to trauma or stroke. This respiratory pattern usually indicates a very poor prognosis.
- Extra notes: This type of labored hyperventilation is usually seen in the late stages of a severe metabolic acidosis such as diabetic ketoacidosis. The patient becomes very “air-hungry” and the desperate gasping characteristic of Kussmaul’s breathing almost appears involuntary. Most of the time a respiratory pattern secondary to a metabolic acidosis is rapid and shallow and a true kussmaul breathing pattern is rarely reached before the acidosis is corrected.
- Extra notes: Apneustic breathing is caused by damage to the upper part of the pons, which is the upper portion of the brain stem. The pons contains, among other things, the “respiratory center” of the brain.