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Hypoglicemia PowerPoint Presentation

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Description : hypoglicemia

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HYPOGLICEMIA Presentan : dr. Dazril Wiradinata Pembimbing : Dr. Hikmat Permana, dr., SpPD-KEMD Ervita, dr., SpPD. Mkes
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INTRODUCTION PHYSIOLOGY INSULIN PATOPHYSIOLOGY DIAGNOSIS HIPOGLIKEMIA WITH AND WITHOUT DIABETES INSULINOMA CONCLUSION
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INTRODUCTION Hypoglycemia can cause serious morbidity if severe and prolonged, it can be fatal. It should be considered in any patient with episodes of confusion, an altered level of consciousness, or a seizure.
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PHYSIOLOGY OF INSULIN Insulin is a peptide hormone synthesized from preproinsulin. The active form of insulin is produced by modification of proinsulin by cleavage of the C-peptide Both insulin and the cleaved C-peptide are packaged in secretory granules and are coreleased in response to glucose stimulation Molina, P. E. Endocrine physiology. M. H. Education. New York: Lange Medical Books/McGraw-Hill. Fourth Edition. 2013
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Insulin Release Insulin release occurs in a biphasic mode. First phase of insulin  rapid release of ready insulin in the first 10 minutes Second phase  slowly released insulin in 24 hours Molina, P. E. Endocrine physiology. M. H. Education. New York: Lange Medical Books/McGraw-Hill. Fourth Edition. 2013
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Regulation of Insulin Release Molina, P. E. Endocrine physiology. M. H. Education. New York: Lange Medical Books/McGraw-Hill. Fourth Edition. 2013
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Insulin effects on carbohydrate, fat, and protein metabolism Jameson, J. Harrison's Endocrinology, 3E. McGraw-Hill Education, 2013
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PATOPHYSIOLOGY Jameson, J. Harrison's Endocrinology, 3E. McGraw-Hill Education, 2013
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DEFINITION Whipple’s triad LEVEL 2 : threshold at which neuroglycopenic symptoms begin to occur. LEVEL 1 : threshold for neuroendocrine responses to falling glucose in people without diabetes LEVEL 3 : severe event characterized by altered mental and/or physical functioning American Diabetes Association. Standards of Medical Care in Diabetes—2019. Diabetes Care, 2019. Vol. 42(Supplement 1).2019
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CAUSE OF HYPOGLYCEMIA IN ADULTS Jameson, J. Harrison's Endocrinology, 3E. McGraw-Hill Education, 2013
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Clinical Manifestations Neuroglycopenic symptoms  behavioral changes, confusion, fatigue, seizure, loss of consciousness, Neurogenic (or autonomic) symptoms palpitations, tremor, and anxiety cholinergic symptoms  sweating, hunger, and paresthesias low plasma glucose concentration and their resolution after the glucose level is raised (Whipple’s triad) Heart rate and systolic blood pressure are typically increased but may not be raised in an individual who has experienced repeated, recent episodes of hypoglycemia Jameson, J. Harrison's Endocrinology, 3E. McGraw-Hill Education, 2013
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Hypoglycemia in Diabetes insulin (or insulin secretagogue) doses are excessive, ill-timed, or of the wrong type insulin-independent glucose utilization is increased endogenous glucose production is reduced Renal impairment You can simply impress your audience and add a unique zing and appeal to your Presentations. Your Text Here influx of exogenous glucose is reduced RISK FACTOR Jameson, J. Harrison's Endocrinology, 3E. McGraw-Hill Education, 2013
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HYPOGLICEMIA IN DM Intensive glycemic control Antecedent hypoglycemia AGE, BMI Cognitive dysfunction Yun, J. S., & Ko, S. H. Risk factors and adverse outcomes of severe hypoglycemia in type 2 diabetes mellitus. Diabetes & Metabolism Journal. 2016. 40(6), 423-432.
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69 Adverse Outcome severe hypoglicemia Yun, J. S., & Ko, S. H. Risk factors and adverse outcomes of severe hypoglycemia in type 2 diabetes mellitus. Diabetes & Metabolism Journal. 2016. 40(6), 423-432.
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Hypoglycemia-associated autonomic failure Jameson, J. Harrison's Endocrinology, 3E. McGraw-Hill Education, 2013
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Hypoglycemia Without Diabetes ACE-INHIBITOR, ARB, BETA BLOCKER, QUINOLONE, INDOMETACHINE, QUININE, SULFONAMID, INGESTION ALKOHOL Sepsis, renal failure, hepatic failure, inaniation Addison disease, hypopituitarism DRUGS CRITICAL ILLNESS Hormone deficiencies large mesenchymal or epithelial tumors (hepatomas, adrenocortical carcinomas) Non–beta-cell tumors Endogenous hyperinsulinism Beta cell tumor, antibody insulin, insulin receptor antibodies POST PRANDIAL REACTIVE HYPOGLICEMIA Desimone, M. E., & Weinstock, R. S. Non-diabetic hypoglycemia. In Endotext [Internet]. MDText. com, Inc. .2017.
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REACTIVE HYPOGLICEMIA 01 02 03 04 Hipoglycemia 2-5 hours after food intake 3 type : Early Idhiopatic Late Terapi : Life style OAD (Metformin, AGI, DPP IV Inhibitor Prediabetic state Altuntaş, Y. Postprandial Reactive Hypoglycemia. Şişli Etfal Hastanesi tıp Bülteni, 2019. 53(3), 215.
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POST PRANDIAL REACTIVE HYPOGLICEMIA Overweight, DM History in family Altuntaş, Y. Postprandial Reactive Hypoglycemia. Şişli Etfal Hastanesi tıp Bülteni, 2019. 53(3), 215.
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INSULINOMA ETIOLOGY Epidemiology 4 Most common functional Neuroendocrin Tumor (NET)  Hiperinsulin. Solitary Benign Tumor 5% Malignant Introduction Zhuo, F., & Anastasopoulou, C. Insulinoma. In StatPearls [Internet]. StatPearls Publishing. 2019 Prognosis
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DIAGNOSTIC TEST Zhuo, F., & Anastasopoulou, C. Insulinoma. In StatPearls [Internet]. StatPearls Publishing. 2019 Diagnostic Test INITIAL EVALUATION TESTING APPROACH ANAMNESIS, PHYSICAL EXAM WHIPPLE’S TRIAD THE 72-HOURS FAST IMAGING
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THE 72 HOURS FASTING Gold Standard no food, non-essential medications should be discontinued. Simultaneous insulin, c-peptide and glucose samples are obtained at the beginning of the fast and every 4-6 hours. When the plasma glucose falls to <60 mg/dL, specimens should be taken every 1-2 hours under close supervision. The fast continues until plasma glucose less than 55 mg/dL is an alternative end point if Whipple’s triad has been previously documented] and symptoms of neuroglucopenia develop. At this time insulin, glucose, c-peptide, oral insulin secretagogues, proinsulin are obtained and the fast is terminated Desimone, M. E., & Weinstock, R. S. Non-diabetic hypoglycemia. In Endotext [Internet]. MDText. com, Inc. 2017
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Distinguishing Causes of Symptomatic Hypoglycemia [glucose < 55 mg/dl After a Prolonged Fast Approximately 75% of patients with insulinomas are diagnosed after a 24 hour fast and 90-94% at 48 hours. Desimone, M. E., & Weinstock, R. S. Non-diabetic hypoglycemia. In Endotext [Internet]. MDText. com, Inc. 2017
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IMAGING computed tomography (CT), magnetic resonance imaging (MRI), GLP-1 receptor imaging. Imaging studies are successful in identifying insulinomas approximately 75% (CT scan), 85% (MRI), 66-97% (GLP-1) Negative imaging  Endoscopic ultrasonography (EUS) or selective arterial calcium stimulation test (SACST) EUS has sensitivy 70 – 95% identifying insulinomas SACST has sensitivity 93 % identifying insulinomas Zhuo, F., Anastasopoulou, C. Insulinoma. In StatPearls [Internet]. StatPearls Publishing. 2019
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Spesific Treatment Diazoxide Inhibits insulin secretion and enhance glycogenolysis 3-8 mg/kg/day divided 8-12 hours up to 1200 mg/day Dietary Modification Somatostatin analogs (ocreotide and lanreotide) Injection subcutan 2x 100 mcg-1500 mcg Surgical Resection (Enucleation of the insulinoma and partial distal pancreatectomy) EUS-guided ablation Zhuo, F., Anastasopoulou, C. Insulinoma. In StatPearls [Internet]. StatPearls Publishing. 2019
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GENERAL TREATMENT Immediate treatment should be focused on reversing the hypoglicemia. Stopping antidiabetic drugs and other drugs that cause hypoglycemia. If the patient is able to ingest simple glucose 15-20 grams (2-3 tablespoons of sugar) dissolved in water  eat or consume snacks if blood glucose stable Unable to ingest carbohydrate  parenteral glucose Evaluate the triggers for hypoglycemia Pedoman Pengelolaan dan Pencegahan Diabetes Melitus Tipe 2 Dewasa di Indonesia. 2019
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CONCLUSION hypoglycemia is characterized by a decrease in blood glucose levels <70 mg / dl Whipple’s Triad Identification of cause to prevent recurrent hypoglicemia by anamnesis, physical examination and supportive investigation Drugs, particulary those used to treat diabetes or alcohol should be the first consideration. Other considerations include critical illness, hormone deficiencies and rarely non beta cell tumor In well individual, consider endogenous hyperinsulinism Urgent treatment  oral or parenteral therapy Identification of cause to prevent recurrent hypoglicemia
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THANK YOU