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Hypoglycemia PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Hypoglycemia" by Mahtab Niroomand MD.

This medical PowerPoint presentation talks about hypoglycemia, a condition characterized by low blood sugar levels, typically defined as a glucose level below 70 milligrams per deciliter (mg/dL). Glucose is the primary source of energy for the bodys cells, including the brain, so low blood sugar can cause a variety of symptoms and complications.

Hypoglycemia can be caused by a variety of factors, including Diabetes, Some medications, such as beta blockers and some antidepressants, Excessive alcohol consumption and Some medical conditions, such as liver disease and kidney failure.

Tags : hypoglycemia, low blood sugar levels, endocrinology, endocrinology PowerPoint presentation

Published on : Apr 18, 2023 | Views : 2315 | Downloads : 12

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Slide 1-

Hypoglycemia Mahtab Niroomand M.D. Shaheed Beheshti university of medical scienes
Slide 2-

Agenda Definition Pathophysiology Prevalence Prevention Treatment
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خانمي 67 ساله بعلت اختلال هوشياري به اورژانس بيمارستان آورده شده ،همراه بیمارسابقه حملات مشابه را دراز یکسال قبل ذکر می کند که در بعد از ظهر ها بوده وبا مصرف غذا بهتر مي شده. سابقه بيماري ديابت از 35 سال قبل که تحت درمان با انسولين NPH 60 واحد صبح و 30 واحد عصر, سابقه ی فشار خون و مصرف ايندرال mg 60 روزانه داشته از 5 روز قبل به دلیل قندهای بالا متفورمين به رژیم دارویی بیمار اضافه شده است. از 2 روز قبل بيمار تب و لرز و استفراغ و اسهال داشته است. بدنبال تزريق گلوكز هيپرتونيك هوشياري بهبود ميیابد.قند هنگام مراجعه 30 گذارش شده است . چه اقدام تشخيصي را پيشنهاد مي كنيد؟
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Definition All episodes of an abnormally low plasma glucose concentration that expose the individual to potential harm A single threshold value for plasma glucose concentration that defines hypoglycemia in diabetes cannot be assigned because there are varying threshold for symptoms
Slide 5-

Introduction Hypoglycemia is the most common endocrine medical emergency. Hypoglycemia is a clinical syndrome due to underproduction and or over utilization of glucose .
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Pathophysiology Metabolic state 50 – 140 mg/ dl G.H Insulin Cortisol Cathecholamines Glucagon Liver Fat cells
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Glucose is unique fuel for brain neurons Irreversible brain damage Hypoglycemia
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Glucose sources GI absorption Gluconeogenesis Glycogenolysis
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Liver glucose production Peripheral uptake Peripheral catabolism Liver uptake of nutrients Insulin Meal Fed state
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Fasting state Liver gluconeogenesis Liver gluconeogenesis Peripheral uptake Lipolysis - proteolysis Glucose production Insulin
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Defense against hypoglycemia B.S < 80 Insulin < 65 Glucagon Epinephrine G.H - Cortisol < 48 Glu.auto regulation < 40 Lethargy < 30 Coma, Convulsion < 20 Permanent damage < 10 Death Neuroglycopenic Neuradrenergic
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RESPONSE TO HYPOGLYCEMIA IN NORMAL SUBJECT Normal subject : Ability to suppress insulin release Increase counter-regulatory hormones
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Response to hypoglycemia in Diabetic patient Protective response to hypoglycemia impaired in many diabetic patient: Insulin release cannot turn off Effectiveness of counter-regulatory reduce
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IMPAIRMANT OF COUNTERREGULATORY RESPONSES IN DIABETIC PATIENT Glucagon response to hypoglycemia markedly impaired first few years Normal at onset of Diabetes Patient with glucagon secretion defect dependent to epinephrine protection which may impaired due to autonomous neuropathy.
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HYPOGLYCEMIA-ASSOCIATED AUTONOMIC FAILURE (1) Reduced counter regulatory hormone responses, which result in impaired glucose generation (2) Hypoglycemia unawareness, which precludes appropriate behavioral responses, such as eating.
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Hypoglycemia unawareness is reversible and require more than 2 weeks avoidance of hypoglycemia.
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Hypoglycemia-Associated Autonomic Failure(HAAF) Reduced counterregulatory hormone responses, which result in impaired glucose generation Hypoglycemia unawareness, which precludes appropriate behavioral responses, such as eating
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TIDMAbsolute insulin deficiency Insulin - Glucagon - Insulin therapy Hypoglycemia Hypoglycemia defective glucose unawareness counter regulation Autonomic Response Symptoms Epinephrine
Slide 21-

Pathophysiology of glucose counter-regulation
Slide 22-

Etiology
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Etiology in adults 1. Fasting ( more than 5 hours P.P ) 2. Postprandial (Less than 5 hours P.P)
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Fasting hypoglycemia a. Underproduction: Alcoholism Organ failure Diffuse hepatic failure Uremia Endocrine deficiency G.H Glucocorticoid Catecholamines Glucagon Hypothyroidism Drugs Inanition b. Over utilization: Prolong exercise Sever sepsis Mesenchymal tumors Hepatoma - Sarcoma Lymphoma - Carcinoma… Hyperinsulinism Drugs Autoimmune insulin syn. Insulinoma Insulin receptor Ab.
Slide 25-

2. Postprandial (Less than 5 hours P.P) G.I surgery (alimentary) Inborn error of metabolism Galactosemia Fructose intolerance Glycogen storage dis. Fructose 1,6 diphosphatase def. Autoimmun insulin syn. Functional (idiopathic) Insulinoma (rarely) Prediabetes 2. Postprandial (Less than 5 hours P.P) G.I surgery (alimentary) Inborn error of metabolism Galactosemia Fructose intolerance Glycogen storage dis. Fructose 1,6 diphosphatase def. Autoimmun insulin syn. Functional (idiopathic) Insulinoma (rarely) Prediabetes
Slide 26-

Drugs are the most common cause of hypoglycemia Insulin S.U Alcohol Sulfonamides Salicylates Quinine Pentamidine Beta blockers
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HYPOGLYCEMIA IN DIABETES
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HYPOGLYCEMIA IN DIABETES Never occurs in patients on diet and exercise . Rare occurs : α glucosidase inhibitors, biguanides and thiazolidinediones. exceptions: elderly chronically ill patients prolonged fasting. More frequent occurs on s.urea and especially insulin
Slide 29-

HYPOGLYCEMIA IN DIABETES Insulin (or oral agent) doses are excessive, ill timed, or of the wrong type 2) Influx of exogenous glucose is reduced (e.g., during an overnight fast or following missed meals or snacks) 3) Insulin-independent glucose utilization is increased (e.g., during exercise) 4) Insulin sensitivity is increased (e.g., with effective intensive therapy, in the middle of the night, late after exercise, or with increased fitness or weight loss) 5) Endogenous glucose production is reduced (e.g., following alcohol ingestion) 6) Insulin clearance is reduced (e.g., in renal failure).
Slide 30-

Clinical Manifestation
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Clinical manifestation 1. Neuroadrenergic: ( B.S < 55 - 60 ) Sweating Hunger Tremor Tingling Palpitation Anxiety Hypertension
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2. Neuroglycopenia: ( B.S < 45 - 50 ) Nonspecific: Headach - restlessness - aggressiveness - bizarre behavior - weakness Focal sign: Monoplegia - babinski - paresthesia - diplopia - trismus - vision loss Global sign: Stupor - convulsion - flaccidity - hypothermia - decerebrate rigidity - coma
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Symptoms thresholds The level of glucose that produces symptoms of hypoglycemia varies from person to person.
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Diagnosis
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Classification
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Harm of Clinically significant hypoglycemia Falling Motor vehicle accidents and other injueries Increased risk of dementia (older adults)
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Diagnosis 1. Pseudohypoglycemia: a. Lab.error b.Over utilization: Leukemoid reaction - Leukemia Hemolytic crisis - Polycytemia Vera c. Incorrect method for analysis: Lipemic serum
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Definition Hypoglycemia is threshold dependent B.S less than 45 - 50 mg/dl with symptoms recovery with treatment. ( Whipple triad )
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Differential Diagnosis T.I.A Epilepsy Orthostatic hypotension Arrhythmia
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Treatment
Slide 41-

Treatment Urgent Treatment necessary. When possible sample for documentation of plasma glucose should be obtained prior to treatment glucose administration need not delay until the result for initial sample report.
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Treatment ( emergency ) 1. Conscious patient: Ingestion of 5-20 gr. Soft drink or sugar… 2. Unconscious patient: a) Bolus : I.V 0.5 - 1 g/kg of hypertonic glucose b) maintenance : 5 - 10 g/h of glucose infusion. c) Glucagon : 0.5 - 1 mg I.v - I.m - S.c ( repeat ) 3. Post hypoglycemic coma: Hydrocortison 100 mg /t.I.d 20% Mannitol 200 cc/20 min
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Treatment(emergency) For treatment of BG <70 mg/dl in a patient who is alert and able to eat and drink, administer 15–20 g of rapid-acting carbohydrate such as:a one–15–30 g tube glucose gel or (4 g) glucose tabs (preferred for patients with end stage renal disease). 4–6 ounces orange or apple juice. 6 ounces regular sugar sweetened soda.
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Treatment(emergency) For treatment of BG <70 mg/dl in an alert and awake patient who is NPO or unable to swallow, administer 20 ml dextrose 50% solution iv and start iv dextrose 5% in water at 100 ml/h.
Slide 45-

Treatment (emergency) For treatment of BG <70mg/dl in a patient with an altered level of consciousness, administer 25 ml dextrose 50% (1/2 amp) and start iv dextrose 5% in water at 100 ml/h. In a patient with an altered level of consciousness and no available iv access, give glucagon 1 mg im. Limit, two times. Recheck BG and repeat treatment every 15 min until glucose level is at least 80 mg/dl
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hypoglycemic patient cause by regular insulin excess-nutritional deficit or alcohol can be stabilized and discharged. hypoglycemia caused by intermediate or long acting insulin, First generation or second generation sulfonylurea at risk for prolong hypoglycemia Treatment (emergency)
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ADA Recommendation Individuals at risk for hypoglycemia should be asked about symptomatic and asymptomatic hypoglycemia at each encounter
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ADA Recommendation Glucose (15–20 g) is the preferred treatment for the conscious individual with hypoglycemia (glucose alert value of <70 mg/dL), although any form of carbohydrate that contains glucose may be used. Fifteen minutes after treatment, if SMBG shows continued hypoglycemia, the treatment should be repeated.
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ADA Recommendation Once SMBG returns to normal, the individual should consume a meal or snack to prevent recurrence of hypoglycemia
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ADA Recommendation Glucagon should be prescribed for all individuals at increased risk of clinically significant hypoglycemia, defined as blood glucose ,54 mg/dL,so it is available should it be needed. Caregivers, school personnel,or family members of these individuals should know where it is and when and how to administer it. Glucagon administration is not limited to health care professionals
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ADA Recommendation Hypoglycemia unawareness or one or more episodes of severe hypoglycemia should trigger reevaluation of the treatment regimen. E
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ADA Recommendation Insulin-treated patients with hypoglycemia unawareness or an episode of clinically significant hypoglycemia should be advised to raise their glycemic targets to strictly avoid hypoglycemia for at least several weeks in order to partially reverse hypoglycemia unawareness and reduce risk of future episodes. A
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ADA Recommendation Ongoing assessment of cognitive function is suggested with increased vigilance for hypoglycemia by the clinician, patient, and caregivers if low cognition or declining cognition is found. B
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Prevention
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Patient education Close observation and control SMBG Sick day monitoring
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Case study
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خانم چاق 40 ساله ای با دو نوبت آزمایش قند ناشتای 165 و 180 مراجعه کرده است . با تشخیص دیابت توصیه به پرهیز غذایی- ورزش و مصرف گلیبن کلامید یک عدد روزانه میشود. یکماه بعد با تعریق و خواب آلودگی به بیمارستان آورده میشود در حالیکه قند 28 برای وی گذارش میشود . آیا با تشخیص دیابت وی موافق هستید ؟ توصیه شما جیست؟ بیمار دیابتیک محسوب میشود. قطع گلیبن کلامید ادامه ورزش و پرهیز تغذیه ای
Slide 58-

آقای 58 ساله مبتلا به دیابت از 8 سال قبل و تحت درمان 4 عدد گلیبن کلامید و 6 عدد مت فرمین بدلیل عدم کنترل قند در طی یکسال اخیر و با قند 580 بستری شده و تحت درمان 4 تزریق روزانه انسولین قرار میگیرد . 24 ساعت بعد دچار سردرد و طپش قلب و گرسنگی میشود اما قند همزمان 98 گذارش میگردد . توجیه شما چیست؟ کاهش سریع قند در بیماریکه مدتها کنترل نبوده است.
Slide 59-

خانم 63 ساله دیابتی تحت درمان گلیبن کلامید 2 عدد و مت فرمین 3 عدد روزانه که از 3 روز قبل بدلیل سکته مغزی در بیمارستان بستری شده است و سپس دچار پنومونی بیمارستانی نیز گردیده در حال حاضر تغذیه از راه لوله معده دارد . امروز صبح دچار افت سطح هوشیاری شده و قند همزمان 30 و کراتنین 7/1 گذارش شده است . علت افت قند وی چیست و چه روش درمانی را توصیه میکنید؟ تغذیه ناکافی عفونت مت فرمین قطع داروهای خوراکی و شروع انسولین
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آقای 65 ساله دیابتی که تحت درمان 3 قرص روزانه گلیبن کلامید بوده بعلت مصرف اشتباه دارو و با اختلال سطح هوشیاری در اورژانس بستری میشود قند 35 و کراتنین 2/2 گذارش میشود . پس از دریافت سرم قندی هیپرتونیک هوشیاری وی کامل بهبود میابد و قند وی نیز به 120 میرسد . بیمار تمایل به ترخیص دارد . توصیه شما چیست؟ بستری در بیمارستان و دریافت انفوزیون سرم قندی بررسی علت نارسایی کلیه در صورت نیاز شروع انسوین
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خانمي 67 ساله بعلت اختلال هوشياري به اورژانس بيمارستان اورده شده و با تزريق گلوكوز هيپرتونيك بهبود يافته است سابقه حملات مشابه عصرگاهي كه با مصرف غذا بهتر مي شده رااز يكسال قبل مي دهد . سابقه بيماري ديابت از 35 سال قبل و مصرف انسولين NPH 60 واحد صبح و 30 واحد عصر, فشار خون و مصرف ايندرال mg 60 روزانه واستفاده از مت فرمين بدليل قند بالا از 5 روز قبل وجود دارد. از 2 روز قبل بيمار تب و لرز و استفراغ و اسهال داشته است. معاينه باليني نكته خاصي ندارد. بدنبال تزريق گلوكز هيپرتونيك هوشياري بهبود ميابد.قند هنگام مراجعه 30 گذارش شده است . چه اقدام تشخيصي را پيشنهاد مي كنيد؟
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Lab data: CBC = nl Na = 146 K= 6 BUN = 120 Cr = 3
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علل افت قند در اين بيمار چيست؟
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Poor intake Prerenal azotemia Metformine
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علت عدم وجود علايم نورآدرنرژيك چيست؟
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Long duration of DM. Hypoglycemia unawareness β blocker usage
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با توجه به بهبود هوشياري بيمار توصيه شما براي ادامه درمان وي چيست؟ Admission for at least 72 hours Serum : DW5% 100 cc / h saline for hydration
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Thank you
Slide 69-

Diagnosis 1. Overnight F.B.S 2. 72 hours fasting test: Admit and discontinue all nonessential medication. Patient may consume calorie and caffeine free liquids and should ambulate. Baseline glucose - Insulin - G.H - (Glucagon - Cortisol). Check B.S every 6 hours (B.S >60) then every 1 hour. The fast is ended at 72 hrs. or earlier if the patient has a B.S <45 with neuroglicopenic symptoms and check B.S - Insulin - G.H - Proinsulin - C.Peptid - Glucagon - Cortisol - S.U.
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2. Reactive or alimentary: Omit simple sugar and alcohol. Frequent small high protein - low C.H.O. meal Fiber Drug: Anticholinergic drugs: Atropin Propantheline A- glucosidase inh. : Acarbose - Miglitol
Slide 71-

Etiologic management 1. Fasting: Tumors : Surgery Autoimmune: Glucocorticoid - Plasmapheresis Insulinoma: Surgery Drug : Diazoxide Dilantin Calcium blockers Octerotide Chemotherapy
Slide 72-

B.S < 45 mg/dl Insulin<6 uU/m : with symptoms Autoimmune Tumors Insulin >6uU/ml Endocrine def. Organ failure.. < 200 pmol/L > 200pmol/L Autoimmune Insulin inj. Iatrogenic Insulinoma Hyperinsulinism C.peptide S.U + _
Slide 73-

Clinical suspicion Medication Fasting P.P Systemic illness Sepsis - Malignancy mixed meal + -- B.S > 45 B.S < 45 motility Idiopathatic exclude with symptom study Exclude Insulin C.Peptide S.U 72 hr test
Slide 74-

2. Clinical data: Fasting or p.p With or without activity First attack or recurrent D.H F.H of diabetes Signs and symptoms Reversible or irreversible Neurologic deficit Weight loss or weight gain PH.Exam.
Slide 75-

خانمي 54 ساله بعلت اختلال هوشياري به اورژانس بيمارستان اورده شده و با تزريق گلوكوز هيپرتونيك بهبود يافته است سابقه حملات مشابه عصرگاهي كه با مصرف غذا بهتر مي شده رااز يكسال قبل مي دهد . سابقه بيماري مصرف دارو ويا ديابت در خانواده نمي دهد , معاينه باليني نيز نكته خاصي ندارد. قند هنگام مراجعه 30 گذارش شده است . چه اقدام تشخيصي را پيشنهاد مي كنيد؟
Slide 76-

تست 72ساعته: پس از 12ساعت از شروع تست بيمار علامتدار شد . ازمايشات همزمان : B.S = 32 mg / dl Insulin = 21 uU / ml C. Peptide = 860 pmol / L Proinsulin = 19 Pmol / L S.U = Negative با تشخيص انسولينوما اقدامات تصويربرداري درخواست گرديد.
Slide 77-

Fasting hypoglycemia a. Underproduction: Alcoholism Organ failure Diffuse hepatic failure Uremia Endocrine deficiency G.H Glucocorticoid Catecholamines Glucagon Drugs b. Over utilization: Prolong exercise Malnutrition Sever sepsis Mesenchymal tumors Hepatoma - Sarcoma Lymphoma - Carcinoma… Hyperinsulinism Drugs Autoimmune insulin syn. Insulinoma Insulin receptor Ab.
Slide 78-

2. Postprandial (Less than 5 hours P.P) G.I surgery (alimentary) Inborn error of metabolism Galactosemia Fructose intolerance Glycogen storage dis. Fructose 1,6 diphosphatase def. Autoimmun insulin syn. Functional (idiopathic) Insulinoma (rarely) Prediabetes
Slide 79-

Classification 1- Ill appearance: Mesenchymal tumors Organ failure Sepsis T.P.N Dialysis… 2 - Healthy appearance: Drugs Hyperinsulinism Functional Endocrinopathies...