Diabetes Mellitus PDF

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Mr. Abdullah M. Khalil

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diabetes mellitus medical notes endocrinology human health

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This document provides a detailed overview of Diabetes Mellitus, covering definitions, types, complications, and treatment. It includes information on various aspects of the disease, suitable for undergraduate medical students.

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Diabetes Mellitus Mr. Abdullah M. Khalil ‫مقدمة‬ ‫لجً ِب ٔؾشذ ‪٠‬ؼٕ‪ ٟ‬ا‪" ٗ٠‬داء اٌغىش‪ٕ٘ ،"ٞ‬ؾشذ زبخخ ثغ‪١‬طخ خذا‪..‬األوً ٌّب ث‪١‬ذخً اٌدغُ ث‪١‬ز‪ٙ‬نُ ‪٠ٚ‬زسًٍ‬ ‫ٌٍؼٕبفش اٌغزائ‪١‬خ اٌشئ‪١‬غ‪١‬خ (وشث‪١٘ٛ‬ذساد أ‪ ٚ‬عىش...

Diabetes Mellitus Mr. Abdullah M. Khalil ‫مقدمة‬ ‫لجً ِب ٔؾشذ ‪٠‬ؼٕ‪ ٟ‬ا‪" ٗ٠‬داء اٌغىش‪ٕ٘ ،"ٞ‬ؾشذ زبخخ ثغ‪١‬طخ خذا‪..‬األوً ٌّب ث‪١‬ذخً اٌدغُ ث‪١‬ز‪ٙ‬نُ ‪٠ٚ‬زسًٍ‬ ‫ٌٍؼٕبفش اٌغزائ‪١‬خ اٌشئ‪١‬غ‪١‬خ (وشث‪١٘ٛ‬ذساد أ‪ ٚ‬عىش‪٠‬بد – د٘‪ – ْٛ‬ثش‪ٚ‬ر‪ – ٓ١‬ئٌخ‪)...‬‬ ‫اٌجش‪ٚ‬ر‪ ٛ٘ :ٓ١‬اٌٍ‪ ٟ‬ث‪١‬ى‪ ْٛ‬األٌ‪١‬بف اٌؼنٍ‪١‬خ‪ ،‬اٌذ٘‪ٚ ْٛ‬اٌغىش‪٠‬بد‪ ُ٘ :‬اٌٍ‪ ٟ‬ث‪ّ١‬ذ‪ٚ‬ا اٌخٍ‪١‬خ ثبٌطبلخ‪.‬‬ ‫األِالذ ‪ٚ‬اٌف‪١‬زبِ‪ٕ١‬بد‪ :‬ث‪١‬سغٕ‪ٛ‬ا ػًّ اٌخال‪٠‬ب‪.‬‬ ‫اٌغىش ثمب ف‪ ِٕٗ ٗ١‬أ‪ٛ‬اع وز‪١‬شح (خٍ‪ٛ‬و‪ٛ‬ص – فشوز‪ٛ‬ص – عىش‪ٚ‬ص – الوز‪ٛ‬ص – ئٌخ‪)....‬‬ ‫‪٠ ٛ٘ٚ‬ؼزجش أُ٘ ػٍّخ هبلخ خ‪ٛ‬ا اٌخٍ‪١‬خ‪ ،‬أ‪ ٞ‬خٍ‪١‬خ ثزبخذ "خٍ‪ٛ‬و‪ٛ‬ص" رطٍغ ‪ٚ ATP‬ؽ‪٠ٛ‬خ ِى‪ٔٛ‬بد ربٔ‪١‬خ‪.‬‬ ‫اإلخبثخ‪ :‬او‪١‬ذ ال‪ ،‬ف‪ ٟ‬زبخخ ثززسىُ ف‪ ٟ‬دخ‪ٛ‬ي ‪ٚ‬خش‪ٚ‬ج اٌغىش ٌٍخٍ‪١‬خ‪.‬‬ ‫‪ ً٘ ‬اٌغىش ٘‪١‬خؼ اٌخٍ‪١‬خ ٌ‪ٛ‬زذٖ ‪٠ٚ‬خشج ٌ‪ٛ‬زذٖ؟‬ ‫االخبثخ‪ :‬اٌجٕىش‪٠‬بط‪.‬‬ ‫‪ ٓ١ِ ‬ثمب اٌؼن‪ ٛ‬اٌّزسىُ ف‪ ٟ‬اٌؼٍّ‪١‬خ د‪ٞ‬؟‬ ‫اٌجٕىش‪٠‬بط ث‪١‬فشص ٘شِ‪ :ُ٘ٚ ،ٓ١ِّٙ ٓ١ٔٛ‬االٔغ‪ٚ ٓ١ٌٛ‬اٌدٍ‪ٛ‬وبخ‪ٚ.ْٛ‬االرٕ‪ ٓ١‬ػىظ ثؼل‪.‬‬ ‫االنسونٍن "‪ :"Insulin‬ث‪١‬مًٍ ِغز‪٠ٛ‬بد عىش اٌذَ ‪٠‬ؼٕ‪ ٟ‬ث‪١‬ؼٍ‪ِ ٟ‬غز‪٠ٛ‬بد اٌغىش ف‪ ٟ‬اٌخال‪٠‬ب‪ ،‬ػٓ هش‪٠‬ك أٗ ث‪١‬ذخً‬ ‫اٌغىش ٌٍخال‪٠‬ب (اػزجش٘ب اٌ‪ٛ‬اعطخ)‪.‬‬ ‫انجهوكاجون "‪ :"Glucagon‬ث‪١‬ؼٍ‪ِ ٟ‬غز‪٠ٛ‬بد عىش اٌذَ‪ٌّ ،‬ب ثزى‪ ْٛ‬فب‪ٚ ُ٠‬ثمبٌه وز‪١‬ش ِىٍزؼ‪ ،‬خغّه ث‪١‬سزبج‬ ‫هبلخ‪ٚ ،‬ػؾبْ ‪٠‬د‪١‬ت اٌطبلخ ث‪١‬سزبج أٗ ‪٠‬ىغش اٌدٍ‪١‬ى‪ٛ‬خ‪( "glycogen" ٓ١‬اٌغىش اٌّؼمذ اٌ ُّخضْ ثبٌىجذ‬ ‫‪ٚ‬اٌؼنالد)‪ ،‬اٌدٍ‪ٛ‬وبخ‪ ْٛ‬ث‪١‬ىغش اٌدٍ‪١‬ى‪ٛ‬خ‪ٌ ٓ١‬غىش ثغ‪١‬و ‪٠‬مذس اٌدغُ ‪٠‬غزخذِٗ ف‪ ٟ‬أزبج اٌطبلخ‪.‬‬ ‫‪ٚ‬ثبٌزبٌ‪ ٌٛ ٟ‬االٔغ‪ ٓ١ٌٛ‬ؽغبي رّبَ ‪ِٚ‬ف‪ٛٙ١‬ػ ِؾبوً‪ ،‬ف ٘‪ّٕ١‬غ رىغ‪١‬ش اٌدٍ‪١‬ى‪ٛ‬خ‪.ٓ١‬‬ ‫داء انسكري "‪ :"Diabetes Mellitus‬خًٍ ف‪ ٟ‬االٔغ‪ ،ٓ١ٌٛ‬اٌخًٍ ِّىٓ ‪٠‬ى‪ ْٛ‬ثغجت ٔمـ افشاصٖ ِٓ‬ ‫اٌجٕىش‪٠‬بط أ‪ِّ ٚ‬ىٓ ‪٠‬ى‪ ْٛ‬ثغجت مؼف وفبءرٗ‪.‬‬ ‫‪Diabetes Mellitus‬‬ ‫‪1. Definition of DM‬‬ ‫‪Diabetes mellitus is group of metabolic diseases characterized by high blood glucose‬‬ ‫‪level that results from defect in insulin secretion or action or both.‬‬ ‫‪ ‬داء اٌغىش‪ِ ٟ٘ :ٞ‬دّ‪ٛ‬ػخ ِٓ اٌّؾبوً رزّ‪١‬ض ثض‪٠‬بدح ِغز‪ ٜٛ‬عىش اٌذَ‪ ،‬ئِب ثغجت ٔمـ ئفشاص االٔغ‪ ،ٓ١ٌٛ‬ا‪ٚ‬‬ ‫ثغجت مؼف وفبءرٗ‪.‬‬ ‫‪ ‬روشٔب ف‪ ٟ‬اٌّمذِخ زبخخ ثخق‪ٛ‬ؿ رسًٍ اٌدٍ‪١‬ى‪ٛ‬خ‪ٌ ٓ١‬دٍ‪ٛ‬و‪ٛ‬ص‪ ،‬ثظ ِزوشٔبػ اعُ اٌؼٍّ‪١‬خ (ؽ‪ٛ‬ف اٌغطش‬ ‫اٌدب‪)ٞ‬‬ ‫‪ Glycogenolysis: The liver produces glucose through the breakdown of glycogen.‬‬ ٞ‫خ ص‬١‫ذسار‬١٘ٛ‫ش اٌىشث‬١‫اد غ‬ٌّٛ‫ش ا‬١‫ك رىغ‬٠‫ص ػٓ هش‬ٛ‫و‬ٍٛ‫ْ خ‬ّٛ ‫ى‬١‫ اٌىجذ ث‬،َ‫ْ هؼب‬ٚ‫ٍخ ثذ‬٠ٛ‫ اٌدغُ لؼذ فزشح ه‬ٌٛ .‫خ‬١ٕ١ِ‫االزّبك اال‬ Gluconeogenesis: After 8 to 12 hours without food, the liver forms glucose from the breakdown of non- carbohydrate substances, including amino acids. ‫ش ػٕذ‬ٙ‫ظ‬١‫ع ث‬ٛٔ ٟ‫ ثظ ف‬،ٓ١‫ػ‬ٛٔ ُ٘ ‫اع‬ٛٔ‫ اال‬،‫ّخ‬ِٙ ‫مر ٌه زبخخ‬ٚ‫ ازت ا‬:ٞ‫اع داء اٌغىش‬ٛٔ‫ أ‬ٟ٘ ْ‫ا‬ٕٛ‫ ػ‬ٟٔ‫رب‬.ٟٔ‫ع اٌثب‬ٌٕٛ‫ فئخ ِؾزمخ ِٓ ا‬ٟ٘ٚ ،‫اًِ ثظ‬ٛ‫اٌس‬ 2. Types of DM Type 1 Type 2 Insulin-dependent DM Non-Insulin-dependent DM 5% - 10% 90% - 95% Onset Less 30 years Over 30 years Weight Thin Obese Etiology Genetic, immunologic, or Obesity, heredity, or environmental environmental factors (e.g., virus). factors. ‫بط‬٠‫ اٌجٕىش‬ٟ‫زب ف‬١‫ب ث‬٠‫بخُ خال‬ٙ١‫ اٌغىش اٌدغُ ث‬ٌٟ‫ثبٌزب‬ٚ ،ٓ١ٌٛ‫ِخ ٌإلٔغ‬ٚ‫ب رقجر ِمب‬٠‫اٌخال‬ ٓ١ٌٛ‫فشص االٔغ‬١‫ اٌدغُ ِؼ ث‬ٌٟ‫ثبٌزب‬ٚ ،‫ذِش٘ب‬١‫ث‬ٚ ٌٟ‫ثبٌزب‬ٚ ،‫ذ‬٠‫ض‬١‫ فغىش اٌذَ ث‬،‫ب‬٠‫ذخً اٌخال‬١‫ِؼ ث‬.‫أفال‬.‫ب اٌدغُ ٘زنشس ثغجت ٔمـ اٌطبلخ‬٠‫خال‬ Insulin Often have antibodies to insulin even No islet cell antibodies before insulin treatment. So, they have little or no endogenous insulin. Treatment Need insulin to preserve life. Most patients can control blood glucose through weight loss if obese. Oral anti- diabetic agents may improve blood glucose levels if dietary modification and exercise are unsuccessful. May need insulin on a short- or long-term basis to prevent hyperglycemia. Ketosis Ketosis-prone when insulin absent. Ketosis rare Complication DKA HHS )‫ ِؼ اوزش‬ٞ‫ خب‬ٌٍٟ ‫ أعبط‬ِٟ‫ً ػٓ اٌّنبػفبد (س‬١‫ب رفبف‬ٙ‫اٌقفسخ اٌمبدِخ ث‬ Gestational DM (‫)داء انسكر انهً بٍصٍب انحوامم‬  Onset: during pregnancy, usually in the second or third trimester..ًّ‫ اٌثبٌث ِٓ اٌس‬ٚ‫ أ‬ٟٔ‫اٌثٍث اٌثب‬  Due to: hormones secreted by the placenta, which inhibit the action of insulin.  Above-normal risk for perinatal complications, especially macrosomia (abnormally large babies). ‫٘م‪ٛ‬ي ٌه ٔجزح ػٓ وً زبخخ دٌ‪ٛ‬لذ ‪ٔٚ‬غ‪١‬ت اٌزفبف‪ٌّ ً١‬ب ٔ‪١‬د‪ٌٙ ٟ‬ب‬ ‫اٌّنبػفبد اٌخط‪١‬شح أ‪ٌّ ٞٚ‬شم‪ ٝ‬اٌغىش‪:ٟ٘ ،ٞ‬‬ ‫أ‪ٚ‬ي زبخخ ٘‪ ٟ‬اٌـ )‪:Diabetic Keto-acidosis (DKA‬‬ ‫اإلٔغ‪ِ ٓ١ٌٛ‬ؼ ِ‪ٛ‬خ‪ٛ‬د‪ ،‬فجبٌزبٌ‪ ٟ‬اٌغىش ِؼ ث‪١‬ذخً اٌخال‪٠‬ب ألْ ‪ٚ‬اعطزٗ اٌٍ‪ ٟ‬ثزذخٍٗ ِؼ ِ‪ٛ‬خ‪ٛ‬دح (عىش اٌذَ ث‪١‬ى‪ْٛ‬‬ ‫ػبٌ‪ 600 ،ٟ‬أ‪ ٚ‬أػٍ‪ )ٝ‬فبٌدغُ ‪ٍ٠‬دأ ٌألزّبك اٌذٕ٘‪١‬خ ػؾبْ ‪ٕ٠‬زح هبلخ‪ ،‬ث‪١‬ىغش اٌذ٘‪ٕ٠ٚ ْٛ‬زح ػٓ رىغ‪١‬ش٘ب‬ ‫ِخٍفبد اعّ‪ٙ‬ب األخغبَ اٌى‪١‬ز‪١ٔٛ‬خ (‪ )Ketone Bodies‬األخغبَ د‪ ٞ‬ثزىزش ف‪ ٟ‬اٌذَ‪ٚ ،‬هجؼب ثّب أ‪ٙ‬ب ِؾزمبد‬ ‫زّن‪١‬خ ف ثزغجت ص‪٠‬بدح ٌسّ‪ٛ‬مخ اٌذَ (‪ِ )Acidosis‬ؼٕ‪ ٝ‬وذح اْ اٌـ ‪ PH‬ثزبع اٌذَ ث‪١‬مً ػٓ ‪ٚ ،7.5‬هجؼب د‪ٌٛ ٞ‬‬ ‫وزشد ا‪ِّ ٞٚ‬ىٓ رذخً اٌّش‪٠‬ل ف‪ ٟ‬غ‪١‬ج‪ٛ‬ثخ )‪ )Coma‬ـــ ٔف‪ ِٓ ُٙ‬وذح اْ دٖ ؽبئغ اوزش ػٕذ ِشم‪Type 1 ٝ‬‬ ‫ألْ اإلٔغ‪ ٓ١ٌٛ‬ث‪١‬ى‪ِ ْٛ‬ؼ ِ‪ٛ‬خ‪ٛ‬د ػٕذُ٘‪.‬‬ ‫ربٔ‪ ٟ‬زبخخ ؽجٗ اٌـ ‪ DKA‬ؽ‪٠ٛ‬خ‪ Hyperglycemic Hyperosmolar State (HHS) ٟ٘ٚ ،‬ــــ اإلٔغ‪ٓ١ٌٛ‬‬ ‫ِ‪ٛ‬خ‪ٛ‬د ٌىٓ اٌخال‪٠‬ب ِمب‪ِٚ‬خ ٌٗ‪ ،‬فجبٌزبٌ‪ ٟ‬اٌغىش ِؼ ث‪١‬ذخً اٌخال‪٠‬ب (عىش اٌذَ ػبٌ‪ 444 ،ٟ‬أ‪ ٚ‬أػٍ‪ )ٝ‬اإلٔغ‪ٓ١ٌٛ‬‬ ‫ِ‪ٛ‬خ‪ٛ‬د ف‪ ٟ‬اٌدغُ‪ ،‬فجبٌزبٌ‪ِ ٟ‬بٔغ رىغ‪١‬ش األزّبك اٌذٕ٘‪١‬خ‪ ،‬ث‪١‬سقً خفبف ٌٍخال‪٠‬ب‪١ٌ ،‬ـــٗ‪..‬؟‬ ‫ف‪ ٟ‬زبخخ اعّ‪ٙ‬ب اٌخبف‪١‬خ االعّ‪ٛ‬ص‪٠‬خ‪ ،‬وً اٌٍ‪ ٟ‬ػب‪٠‬ضن رؼشفٗ ػٕ‪ٙ‬ب ٘‪ ٟ‬اٌدٍّخ اٌدب‪٠‬خ‪:‬‬ ‫اٌّ‪١‬بٖ األلً ثززسشن ٔبز‪١‬خ اٌّ‪١‬بٖ األوزش‪.‬‬ ‫‪ٚ‬ثّب اْ اٌّ‪١‬بٖ ف‪ ٟ‬اٌذَ الً (ػؾبْ رشو‪١‬ض٘ب ثبٌغىش ػبٌ‪ )ٟ‬فبٌّ‪١‬بٖ ثززسشن ِٓ اٌذَ ٌٍخال‪٠‬ب (اٌّش‪٠‬ل ث‪١‬ذخً ف‪ٟ‬‬ ‫زبٌخ خفبف ؽذ‪٠‬ذح)‪.‬‬ ‫ربٌذ زبخخ‪ Hypoglycemic Coma :‬غ‪١‬ج‪ٛ‬ثخ ٔمـ اٌغىش‬ 3. Clinical manifestation of DM A- Clinical manifestations of all types of diabetes: Polydipsia  Polyuria (increased urination).  Polyphagia (increased appetite). Polyphagia  Polydipsia. B- Other symptoms: Polyuria  Fatigue and weakness.  Sudden vision changes.  Tingling or numbness in hands or feet.  Dry skin.  Skin lesions or wounds that slow to heal.  Recurrent infections. 4. Diagnosis 1. Signs and symptoms 2. Fasting blood glucose level greater or equal to 126 mg\dl or 7 mmol\L ‫صيام‬ 3. 2-hours post-prandial greater or equal to 200 mg\dl or 11,1 mmol\L ‫بعد األكل بساعتين‬ 4. Random blood glucose level equal or greater than to 200 mg\dl ‫عشوائي‬ 5. Assessment the Patient with Diabetes History Symptoms related to the diagnosis of diabetes:  Symptoms of hyperglycemia or hypoglycemia.  Results of blood glucose monitoring.  Status, symptoms, and management of chronic complications of diabetes such as eye, kidney, nerve, genitourinary and sexual, bladder, and gastrointestinal Cardiac, peripheral vascular, foot complications associated with diabetes  Dietary management plan.  Prescribed exercise regimen.  Pharmacologic treatment (insulin or oral anti-diabetic agents). Physical Examination  Blood pressure (sitting and standing to detect orthostatic changes).  Body mass index (height and weight).  Foot examination (lesions, signs of infection, pulses).  Skin examination (lesions and insulin-injection sites).  Neurologic examination.  Sensory examination.  Deep tendon reflexes.  Oral examination. Laboratory Examination  HgbA1C (A1C).  Fasting blood glucose level.  Glucose tolerance test.  Fasting lipid profile.  Test for micro-albuminuria.  Serum creatinine level  Urinalysis. ‫‪1. HgbA1C‬‬ ‫‪ ‬اخزجبس اٌ‪ّٛ١ٙ‬غٍ‪ٛ‬ث‪ ٓ١‬اٌغىش‪ ٛ٘ A1C ٞ‬أزذ أٔ‪ٛ‬اع رسبٌ‪ً١‬‬ ‫اٌذَ اٌؾبئؼخ اٌّغزخذِخ ٌزؾخ‪١‬ـ إٌ‪ٛ‬ع األ‪ٚ‬ي ‪ٚ‬اٌثبٔ‪ ِٓ ٟ‬داء‬ ‫اٌغىش‪٘.ٞ‬زا االخزجبس ‪ُ٠‬غزخذَ ٌّزبثؼخ ِغز‪ ٜٛ‬اٌمذسح ػٍ‪ ٝ‬اٌزسىُ‬ ‫ف‪ِ ٟ‬غز‪٠ٛ‬بد اٌغىش ف‪ ٟ‬اٌذَ‪.‬‬ ‫‪ٚ ‬رُظ‪ٙ‬ش ٔزبئح اخزجبس اٌ‪ّٛ١ٙ‬غٍ‪ٛ‬ث‪ ٓ١‬اٌغىش‪ِ A1C ٞ‬ز‪ٛ‬عو‬ ‫ِغز‪ ٜٛ‬اٌغىش ف‪ ٟ‬دِه ػٍ‪ِ ٝ‬ذاس اٌؾ‪ٙ‬ش‪ ٓ٠‬أ‪ ٚ‬اٌثالثخ أؽ‪ٙ‬ش‬ ‫اٌّبم‪١‬خ‪ٚ.‬ثؾىً خبؿ‪٠ ،‬م‪١‬ظ اخزجبس اٌ‪ّٛ١ٙ‬غٍ‪ٛ‬ث‪ ٓ١‬اٌغىش‪ٞ‬‬ ‫‪ A1C‬إٌغجخ اٌّئ‪٠ٛ‬خ ٌجش‪ٚ‬ر‪ٕ١‬بد اٌ‪ّٛ١ٙ‬غٍ‪ٛ‬ث‪ ٓ١‬ف‪ ٟ‬دِه اٌز‪ٟ‬‬ ‫ٍ‪ٛ‬صح)‪.‬‬ ‫‪٠‬غٍف‪ٙ‬ب اٌغىش (اٌّغ َ‬ ‫‪ ‬ثش‪ٚ‬ر‪ٕ١‬بد اٌ‪ّٛ١ٙ‬غٍ‪ٛ‬ث‪ ٓ١‬رٕمً األوغد‪( ٓ١‬اٌ‪ّٛ١ٙ‬غٍ‪ٛ‬ث‪ِٛ ٓ١‬خ‪ٛ‬د ف‪ ٟ‬وشاد اٌذَ اٌسّشاء)‪ٚ.‬وٍّب وبْ ِغز‪ٜٛ‬‬ ‫اٌ‪ّٛ١ٙ‬غٍ‪ٛ‬ث‪ ٓ١‬اٌغىش‪ A1C ٞ‬أػٍ‪ ،ٝ‬وبْ ٘زا ِإؽشًا ػٍ‪ ٝ‬أْ ع‪١‬طشره ػٍ‪ ٝ‬اٌغىش ف‪ ٟ‬دِه أمؼف‪ٚ ،‬أْ ِخبهش‬ ‫اٌزؼشك ٌّنبػفبد داء اٌغىش‪ ٞ‬أوثش‪.‬‬ ‫‪2. Fasting blood glucose level‬‬ ‫‪ ‬رإخز ػ‪ٕ١‬خ دَ ثؼذ اٌق‪١‬بَ ػٓ األوً ٌّذح ثّبٔ‪ ٟ‬عبػبد ػٍ‪ ٝ‬األلً أ‪ ٚ‬ه‪ٛ‬اي اٌٍ‪.ً١‬رمبط ل‪ ُ١‬عىش اٌذَ‬ ‫ثبٌٍٍّ‪١‬غشاَ ِٓ اٌغىش ٌىً د‪٠‬غ‪ٍ١‬زش (ٍِغُ‪/‬دي) أ‪ّٛ١ٍٍِ ٚ‬ي ِٓ اٌغىش ٌىً ٌزش (ٍٍِ‪ّٛ١‬ي‪ٌ/‬زش) ِٓ اٌذَ‪.‬ثقفخ ػبِخ‪:‬‬ ‫‪ّ٠ ‬ثً اٌّؼذي اٌطج‪١‬ؼ‪ ٟ‬ألً ِٓ ‪ 011‬مهغم‪/‬دل (‪ّٛ١ٍٍِ 5.6‬ي‪ٌ/‬زش)‪.‬‬ ‫‪٠ ‬ؾ َّخـ اٌّؼذي ‪ 011‬إنى ‪ 021‬مهغم‪/‬دل (‪ 5.6‬ئٌ‪ّٛ١ٍٍِ 6.6 ٝ‬ي‪ٌ/‬زش) ثّمذِبد اٌغىش‪ٌ( ٞ‬غخ ِزقبثؼ‬ ‫ثبٌغىش‪ٌ ،ٞ‬ىٓ ػٍ‪ٚ ٝ‬ؽه اإلفبثخ)‪.‬‬ ‫‪٠ ‬ؾ َّخـ اٌّؼذي ‪ 021‬مهغم‪/‬دل (‪ّٛ١ٍٍِ 0.4‬ي‪ٌ/‬زش) أ‪ ٚ‬أػٍ‪ ٝ‬ف‪ ٟ‬رسٍ‪ِٕ ٓ١ٍ١‬فقٍ‪ ٓ١‬ثّشك اٌغىش‪.ٞ‬‬ ‫)‪3. Glucose Tolerance Test (GTT / OGTT‬‬ ‫‪٠ ‬م‪١‬ظ اخزجبس رسًّ اٌدٍ‪ٛ‬و‪ٛ‬ص‪ ،‬اٌّؼش‪ٚ‬ف أ‪٠‬نًب ثبعُ اخزجبس رسًّ اٌدٍ‪ٛ‬و‪ٛ‬ص اٌفّ‪ ،ٞٛ‬ردب‪ٚ‬ة خغّه ٌٍغىش‬ ‫(اٌدٍ‪ٛ‬و‪ٛ‬ص)‪ّ٠.‬ىٓ أْ ‪ُ٠‬غزخذَ اخزجبس رسًّ اٌدٍ‪ٛ‬و‪ٛ‬ص ٌٍىؾف ػٓ اإلفبثخ ثبٌٕ‪ٛ‬ع ‪ ِٓ 2‬داء اٌغىش‪ٚ.ٞ‬اٌؾ‪ٟ‬ء‬ ‫األوثش ؽ‪ٛ١‬ػًب ٘‪ ٛ‬اعزخذاَ ٔغخخ ُِؼذٌخ ِٓ اخزجبس رسًّ اٌدٍ‪ٛ‬و‪ٛ‬ص ٌزؾخ‪١‬ـ اٌغىش‪ ٞ‬اٌسٍّ‪ٛٔ — ٟ‬ع ِٓ داء‬ ‫اٌغىش‪ ٞ‬رقبة ثٗ إٌغبء خالي اٌسًّ‪.‬‬ ‫‪ ‬لجً ‪ ٨‬عبػبد ِٓ ئخشاء االخزجبس‪ُ٠ ٌٓ ،‬غّر ٌٍّش‪٠‬ل ثبألوً أ‪ ٚ‬اٌؾشة‪ُ٠.‬فنً اٌق‪ َٛ‬أثٕبء اٌٍ‪ٚ ً١‬ئخشاء‬ ‫االخزجبس ف‪ٚ ٟ‬لذ ِجىش ِٓ فجبذ اٌ‪ َٛ١‬اٌزبٌ‪.ٟ‬‬ ‫‪ُ٠ ‬دش‪ ٜ‬اخزجبس رسًّ اٌغٍ‪ٛ‬و‪ٛ‬ص ػٍ‪ ٝ‬ػذح خط‪ٛ‬اد‪.‬ػٕذِب ‪٠‬قً اٌّش‪٠‬ل ئٌ‪ ٝ‬ػ‪١‬بدح اٌطج‪١‬ت أ‪ ٚ‬اٌّخزجش‪،‬‬ ‫ع‪١‬غست أزذ أفشاد اٌشػب‪٠‬خ اٌقس‪١‬خ ػ‪ٕ١‬خ ِٓ اٌذَ ِٓ أزذ األ‪ٚ‬سدح ف‪ ٟ‬اٌزساع‪ٚ.‬عزُغزخذَ ػ‪ٕ١‬خ اٌذَ ٘زٖ ف‪ ٟ‬ل‪١‬بط‬ ‫ِغز‪ ٜٛ‬عىش اٌذَ ف‪ ٟ‬اٌق‪١‬بَ‪.‬ئرا وبْ االخزجبس ٌّؼشفخ ً٘ اٌّش‪٠‬ل ِقبة ثبٌٕ‪ٛ‬ع اٌثبٔ‪ ٟ‬أَ ال‪:‬‬ ‫‪ ‬فغ‪١‬ؾشة اٌّش‪٠‬ل ِب ‪٠‬مشة ِٓ (‪ٍ١ٍِ 230‬زشًا) ِٓ ِسٍ‪ٛ‬ي اٌغٍ‪ٛ‬و‪ٛ‬ص اٌز‪٠ ٞ‬سز‪ ٞٛ‬ػٍ‪ 05( ٝ‬غشا ًِب ِٓ‬ ‫اٌغىش) ‪ٚ‬ع‪١‬زُ ل‪١‬بط ِغز‪ ٜٛ‬اٌغٍ‪ٛ‬و‪ٛ‬ص ف‪ ٟ‬اٌذَ ِشح أخش‪ ٜ‬ثؼذ عبػز‪.ٓ١‬‬ ‫‪ِ ‬غز‪ ٜٛ‬غٍ‪ٛ‬و‪ٛ‬ص اٌذَ اٌطج‪١‬ؼ‪ٌ ٟ‬قم عن ‪ 041‬مهغم‪/‬دل (‪ّٛ١ٍٍِ 0.٨‬ي‪ٌ/‬زش)‪.‬‬ ‫‪ُ٠ ‬ؼذ ِغز‪ ٜٛ‬اٌغٍ‪ٛ‬و‪ٛ‬ص ف‪ ٟ‬اٌذَ اٌز‪٠ ٞ‬مغ بٍن ‪ 041‬مهغم‪/‬دل و‪ 011‬مهغم‪/‬دل (‪ّٛ١ٍٍِ 11ٚ 0.٨‬ي‪ٌ/‬زش) ً‬ ‫خٍال‬ ‫ف‪ ٟ‬رسًّ اٌغٍ‪ٛ‬و‪ٛ‬ص‪ ،‬أ‪٠ ٚ‬ؼزجش ِمذِبد اٌغىش‪.ٞ‬ئرا وٕذ ِقبثًب ثّمذِبد اٌغىش‪ ،ٞ‬فأٔذ ػشمخ ٌخطش‬ ‫اإلفبثخ ثذاء اٌغىش‪ ِٓ ٞ‬إٌ‪ٛ‬ع ‪ 2‬ثّش‪ٚ‬س اٌ‪ٛ‬لذ‪.‬أٔذ أ‪٠‬نًب ػشمخ ٌخطش اإلفبثخ ثّشك اٌمٍت‪ ،‬زز‪ٝ‬‬ ‫ئرا ٌُ رقت ثذاء اٌغىش‪.ٞ‬‬ ‫‪٠ ‬ؾ‪١‬ش ِغز‪ ٜٛ‬اٌغٍ‪ٛ‬و‪ٛ‬ص ف‪ ٟ‬اٌذَ اٌز‪٠ ٞ‬جٍغ ‪ 211‬مهغم‪/‬دل (‪ّٛ١ٍٍِ 11.1‬ي‪ٌ/‬زش) أ‪ ٚ‬أػٍ‪ ٝ‬ئٌ‪ ٝ‬اإلفبثخ ثذاء‬ ‫اٌغىش‪.ٞ‬‬ ‫‪4. Fasting lipid profile‬‬ ‫‪ ‬فسـ اٌى‪١ٌٛ‬غزش‪ٚ‬ي اٌىبًِ‪ ٛ٘ ،‬رسٍ‪ ً١‬دَ ‪ّ٠‬ىٕٗ ل‪١‬بط وّ‪١‬خ اٌى‪١ٌٛ‬غزش‪ٚ‬ي ‪ٚ‬اٌذ٘‪ ْٛ‬اٌثالث‪١‬خ ف‪ ٟ‬اٌذَ‪.‬ع‪ُ١‬طٍت‬ ‫ِٓ اٌّش‪٠‬ل اٌق‪١‬بَ ‪ٚ‬ػذَ رٕب‪ٚ‬ي أ‪ ٞ‬هؼبَ أ‪ ٚ‬ع‪ٛ‬ائً ثخالف اٌّبء ٌّذح رزشا‪ٚ‬ذ ث‪ 12 - 6 ٓ١‬عبػخ لجً االخزجبس‪.‬‬ ‫‪ٚ‬ال رزطٍت ثؼل فس‪ٛ‬فبد اٌى‪١ٌٛ‬غز‪ٛ‬ي اٌق‪١‬بَ‪ٌ ،‬زا ‪٠‬دت ارجبع رؼٍ‪ّ١‬بد اٌطج‪١‬ت‪.‬‬ ‫‪ ‬فسـ اٌى‪١ٌٛ‬غزش‪ٚ‬ي ٘‪ ٛ‬رسٍ‪ ً١‬دَ‪ٚ ،‬ػبدحً ِب ‪ُ٠‬دش‪ ٜ‬ف‪ ٟ‬اٌقجبذ ئرا وبْ اٌّش‪٠‬ل فبئ ًّب ه‪ٛ‬اي اٌٍ‪.ً١‬عزُغست‬ ‫ػ‪ٕ١‬خ دَ ِٓ اٌ‪ٛ‬س‪٠‬ذ‪ٚ ،‬ػبدحً ِٓ اٌزساع‪ٚ.‬لجً ئدخبي اإلثشح‪ُٕ٠ ،‬ظَّف ِ‪ٛ‬لغ اٌجضي ثّط‪ٙ‬ش ‪ٍُ٠ٚ‬ف ؽش‪٠‬و ِطبه‪ ٟ‬ز‪ٛ‬ي‬ ‫اٌدضء اٌؼٍ‪ ِٓ ٞٛ‬اٌزساع‪٘ٚ.‬زا ‪٠‬إد‪ ٞ‬ئٌ‪ ٝ‬اِزالء أ‪ٚ‬سدح رساػه ثبٌذَ‪.‬‬ ‫‪ ‬ثؼذ ئدخبي اإلثشح‪ ،‬رُدّغ وّ‪١‬خ فغ‪١‬شح ِٓ اٌذَ ف‪ ٟ‬لٕ‪ٕ١‬خ أ‪ِ ٚ‬سمٕخ‪.‬ثُ ‪ُ٠‬ضاي اٌشثبه العزؼبدح اٌذ‪ٚ‬سح اٌذِ‪٠ٛ‬خ‪،‬‬ ‫خشج اإلثشح ‪ُ٠ٚ‬غط‪ِٛ ٝ‬لغ اٌجضي ثنّبدح‪.‬‬ ‫‪٠ٚ‬غزّش اٌذَ ف‪ ٟ‬اٌزذفك ئٌ‪ ٝ‬اٌمٕ‪ٕ١‬خ‪ٚ.‬ثّدشد خّغ وّ‪١‬خ وبف‪١‬خ ِٓ اٌذَ‪ ،‬رُ َ‬ ‫‪ٚ‬غبٌجًب ِب ‪٠‬غزغشق اإلخشاء دل‪١‬مز‪ ٛ٘ٚ.ٓ١‬غ‪١‬ش ِإٌُ ٔغج‪ً١‬ب‪.‬‬ ‫‪ ‬ال ر‪ٛ‬خذ ازز‪١‬بهبد رسزبج ئٌ‪ ٝ‬ارخبر٘ب ثؼذ ئخشاء فسـ اٌى‪١ٌٛ‬غزش‪ٚ‬ي‪ٕ٠ٚ.‬جغ‪ ٟ‬أْ ‪٠‬ى‪ ْٛ‬اٌّش‪٠‬ل لبدسًا ػٍ‪ٝ‬‬ ‫اٌسشوخ ‪ٚ‬اٌؼ‪ٛ‬دح ئٌ‪ ٝ‬إٌّضي ‪ٚ‬اٌم‪١‬بَ ثىً أٔؾطزٗ اٌؼبد‪٠‬خ‪ٚ.‬ئرا وبْ فبئ ًّب‪ ،‬فمذ ‪٠‬شغت ف‪ ٟ‬ئزنبس ‪ٚ‬خجخ خف‪١‬فخ‬ ‫ٌزٕب‪ٌٙٚ‬ب ثؼذ ئخشاء فسـ اٌى‪١ٌٛ‬غزش‪ٚ‬ي‪.‬‬ ‫‪5. Test for micro-albumin-uria‬‬ ‫‪ ٛ٘ ‬اخزجبس ‪٠‬م‪١‬ظ وّ‪١‬خ األٌج‪ ٓ١ِٛ‬اٌّ‪ٛ‬خ‪ٛ‬د ف‪ ٟ‬اٌج‪ٛ‬ي ثىّ‪١‬بد فغ‪١‬شح‪٠ٚ ،‬غزخذَ ٘زا اٌزسٍ‪ٌٍّ ً١‬غبػذح ف‪ٟ‬‬ ‫رؾخ‪١‬ـ أِشاك اٌىٍ‪ ٝ‬أ‪ ٚ‬رٍف اٌىٍ‪ ٝ‬إٌبخُ ػٓ اٌؼذ‪٠‬ذ ِٓ األِشاك ‪ِٕٙٚ‬ب اٌغىش‪.ٞ‬‬ ‫‪ ‬رم‪ َٛ‬اٌىٍ‪ ٝ‬ف‪ ٟ‬خغُ اٌفشد ثبٌزخٍـ ِٓ اٌفنالد اٌّ‪ٛ‬خ‪ٛ‬دح ف‪ ٟ‬اٌذَ‪ٚ ،‬اٌسفبظ ػٍ‪ِ ٝ‬غز‪ ٜٛ‬اٌغ‪ٛ‬ائً ف‪ ٟ‬اٌدغُ‪،‬‬ ‫‪ٚ‬اٌسفبظ ػٍ‪ ٝ‬اٌجش‪ٚ‬ر‪ٕ١‬بد ‪ٚ‬اٌؼٕبفش اٌنش‪ٚ‬س‪٠‬خ ف‪ ٟ‬اٌدغُ ثّب ف‪ ٟ‬رٌه األٌج‪٠ٚ ،ٓ١ِٛ‬ؼذ األٌج‪ ٓ١ِٛ‬أزذ ثش‪ٚ‬ر‪ٕ١‬بد‬ ‫اٌدغُ اٌز‪٠ ٞ‬غزخذَ ٌّٕ‪ ٛ‬اٌخال‪٠‬ب ‪ٚ‬ئفالذ االٔغدخ‪٠ٚ ،‬ى‪ِٛ ْٛ‬خ‪ٛ‬د ف‪ ٟ‬اٌذَ‪.‬‬ ‫‪ ‬ال ‪٠‬زز‪ٛ‬اخذ ثش‪ٚ‬ر‪ ٓ١‬األٌج‪ ٓ١ِٛ‬ثؾىً هج‪١‬ؼ‪ ٟ‬ف‪ ٟ‬اٌج‪ٛ‬ي‪ٌٚ ،‬ىٓ ‪ّ٠‬ىٓ أْ ‪٠‬زغشة ٘زا اٌجش‪ٚ‬ر‪ ٓ١‬ئٌ‪ ٝ‬اٌج‪ٛ‬ي ػٕذ ‪ٚ‬خ‪ٛ‬د‬ ‫ِؾىٍخ ف‪ ٟ‬اٌىٍ‪ٌ ،ٝ‬زا ‪٠‬غبػذ اٌىؾف ػٕٗ ف‪ ٟ‬اٌج‪ٛ‬ي ‪ٚ‬رسذ‪٠‬ذ وّ‪١‬برٗ ػٍ‪ ٝ‬االعزذالي ث‪ٛ‬خ‪ٛ‬د رٍف ف‪ ٟ‬اٌىٍ‪٘ٚ ،ٝ‬زا ِب‬ ‫‪٠‬زُ ئخشاؤٖ ف‪ ٟ‬رسٍ‪ ً١‬اٌّ‪١‬ىش‪ ٚ‬أٌج‪.ٓ١ِٛ‬‬ ‫‪6. Serum creatinine level‬‬ ‫‪ ‬اخزجبس اٌىش‪٠‬بر‪ ٛ٘ ٓ١ٕ١‬ل‪١‬بط ٌّذ‪ ٜ‬وفبءح وٍ‪١‬ز‪١‬ه ف‪ ٟ‬أداء ‪ٚ‬ظ‪١‬فز‪ّٙ‬ب ف‪ ٟ‬رشؽ‪١‬ر اٌفنالد ِٓ دِه‪ٚ.‬اٌىش‪٠‬بر‪ٓ١ٕ١‬‬ ‫٘‪ِ ٛ‬شوت و‪١ّ١‬بئ‪ِ ٟ‬زجك ِٓ ػٍّ‪١‬بد ئٔزبج اٌطبلخ ف‪ ٟ‬ػنالره‪.‬ز‪١‬ث رش ِّؽر اٌىٍ‪ ٝ‬اٌغٍ‪ّ١‬خ اٌىش‪٠‬بر‪ ٓ١ٕ١‬خبسج اٌذَ‪.‬‬ ‫‪٠ٚ‬خشج اٌىش‪٠‬بر‪ ِٓ ٓ١ٕ١‬خغّه مّٓ اٌفنالد اٌخبسخخ ِغ اٌج‪ٛ‬ي‪ُ٠ٚ.‬ؾبس ئٌ‪ ٝ‬أْ ل‪١‬بط ِغز‪ ٜٛ‬اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ٟ‬‬ ‫اٌذَ أ‪ ٚ‬اٌج‪ٛ‬ي ‪٠‬مذَ دالئً رغبػذ هج‪١‬جه ف‪ ٟ‬رسذ‪٠‬ذ وفبءح ػًّ وٍ‪١‬ز‪١‬ه‪.‬‬ ‫‪ُ٠ ‬غزخذَ اخزجبس اٌذَ اٌم‪١‬بع‪ٌ ٟ‬م‪١‬بط ِغز‪٠ٛ‬بد اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ ٟ‬اٌذَ (اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ِ ٟ‬قً اٌذَ)‪ّ٠ٚ.‬ىٓ أْ ‪٠‬طٍت‬ ‫اٌطج‪١‬ت ِٓ اٌّش‪٠‬ل ػذَ رٕب‪ٚ‬ي هؼبَ (اٌق‪١‬بَ) ػٍ‪ِ ٝ‬ذاس اٌٍ‪ٍ١‬خ اٌغبثمخ إلخشاء االخزجبس‪ٚ.‬إلخشاء اخزجبس‬ ‫اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ ٟ‬اٌج‪ٛ‬ي‪ ،‬لذ ‪٠‬زؼ‪ ٓ١‬ػٍ‪ ٝ‬اٌّش‪٠‬ل خّغ اٌج‪ٛ‬ي ػٍ‪ِ ٝ‬ذاس ‪ 24‬عبػخ ف‪ ٟ‬زب‪٠ٚ‬بد رمذِ‪ٙ‬ب ٌٗ اٌؼ‪١‬بدح‪.‬‬ ‫‪ٚ ‬لذ ‪ٍ٠‬ضَ اٌّش‪٠‬ل ػٕذ ئخشاء أ‪ ِٓ ٞ‬االخزجبس‪ ٓ٠‬ردٕت رٕب‪ٚ‬ي اٌٍس‪ٌ َٛ‬فزشح صِٕ‪١‬خ ِؼ‪ٕ١‬خ لجً االخزجبس‪ٚ.‬ئرا وبْ‬ ‫‪٠‬زٕب‪ٚ‬ي ِىّالً غزائ‪ً١‬ب ِسز‪ً٠ٛ‬ب ػٍ‪ ٝ‬اٌىش‪٠‬بر‪ ،ٓ١ٕ١‬فّٓ األسخر ع‪١‬زؼ‪ ٓ١‬ػٍ‪١‬ه ‪ٚ‬لفٗ‪.‬‬ ‫‪ ‬إلخشاء اخزجبس اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ِ ٟ‬قً اٌذَ‪ ،‬ع‪١‬غست أزذ أفشاد فش‪٠‬ك اٌشػب‪٠‬خ اٌقس‪١‬خ ػ‪ٕ١‬خ دَ ػٓ هش‪٠‬ك‬ ‫ئدخبي ئثشح ف‪ ٟ‬أزذ األ‪ٚ‬سدح ف‪ ٟ‬اٌزساع‪ٚ.‬ف‪ ٟ‬اخزجبس اٌج‪ٛ‬ي‪ٕ٠ ،‬جغ‪ ٟ‬ػٍ‪ ٝ‬اٌّش‪٠‬ل رمذ‪ ُ٠‬ػ‪ٕ١‬خ ‪ٚ‬ازذح ف‪ ٟ‬اٌؼ‪١‬بدح‪ ،‬أ‪ٚ‬‬ ‫خّغ ػ‪ٕ١‬بد ِٓ اٌج‪ٛ‬ي ف‪ ٟ‬إٌّضي ػٍ‪ِ ٝ‬ذاس ‪ 24‬عبػخ ‪ٚ‬ئػبدر‪ٙ‬ب ئٌ‪ ٝ‬اٌؼ‪١‬بدح‪.‬‬ ‫‪ ‬و‪١‬ف رُمبط ٔزبئح اخزجبس اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ ٟ‬اٌذَ‪:‬‬ ‫‪٠‬ذخً اٌىش‪٠‬بر‪ ٓ١ٕ١‬ػبدح ئٌ‪ِ ٝ‬دش‪ ٜ‬اٌذَ ‪٠ٚ‬دش‪ ٞ‬رشؽ‪١‬سٗ ثّؼذي ثبثذ ػّ‪ًِ ٛ‬ب‪ٕ٠ٚ.‬جغ‪ ٟ‬أْ رى‪ ْٛ‬وّ‪١‬خ‬ ‫اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ ٟ‬اٌذَ ثبثزخ ٔغج‪ً١‬ب‪ٚ.‬لذ ‪٠‬ى‪ ْٛ‬اسرفبع ِغز‪ ٜٛ‬اٌىش‪٠‬بر‪ِ ٓ١ٕ١‬إؽشًا ػٍ‪ ٝ‬مؼف ‪ٚ‬ظبئف اٌىٍ‪.ٝ‬‬ ‫رمبط وّ‪١‬خ اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ِ ٟ‬قً اٌذَ ثبٌٍٍّ‪١‬غشاَ ِٓ اٌىش‪٠‬بر‪ ٓ١ٕ١‬ئٌ‪ ٝ‬وً د‪٠‬غ‪ٍ١‬زش ِٓ اٌذَ (ٍِغُ‪/‬دي) أ‪ٚ‬‬ ‫اٌّ‪١‬ىش‪ِٛٚ‬ي ِٓ اٌىش‪٠‬بر‪ ٓ١ٕ١‬ئٌ‪ ٝ‬وً ٌزش ِٓ اٌذَ (ِ‪١‬ىش‪ِٛٚ‬ي‪ٌ/‬زش)‪٠ٚ.‬ى‪ ْٛ‬اٌّذ‪ ٜ‬اٌم‪١‬بع‪ٌ ٟ‬مشاءح ِغز‪ٜٛ‬‬ ‫اٌىش‪٠‬بر‪ ٓ١ٕ١‬ف‪ِ ٟ‬قً اٌذَ ػٍ‪ ٝ‬إٌس‪ ٛ‬اٌزبٌ‪:ٟ‬‬ ‫‪ 0.74 ِٓ ‬ئٌ‪ٍِ 1.35 ٝ‬غُ‪/‬دي نهرجال اٌجبٌغ‪ 65.4 ِٓ( ٓ١‬ئٌ‪١ِ 116.3 ٝ‬ىش‪ِٛٚ‬ي‪ٌ/‬زش)‬ ‫‪ 0.59 ِٓ ‬ئٌ‪ٍِ 1.04 ٝ‬غُ‪/‬دي نهنساء اٌجبٌغبد (ِٓ ‪ 52.2‬ئٌ‪١ِ 61.6 ٝ‬ىش‪ِٛٚ‬ي‪ٌ/‬زش)‬ ‫)تحهٍم بول( ‪7. Urinalysis‬‬ ‫رسٍ‪ِ ً١‬ى‪ٔٛ‬بد اٌج‪ٛ‬ي ‪ٔٚ‬غج‪ٙ‬ب‪.‬‬ 6. Five component of diabetes mellitus management 1) Exercise. 2) Diet. 3) Medication. 4) Monitoring glucose levels and ketones. 5) Patient education. Exercise 1. Patient with keton urine not exercise until the keton body become negative in test. 2. The patient should test blood glucose & take a dose of insulin if needed before engage of exercise and eat any snack such as fruits. 3. Use appropriate foot wear. 4. Avoid exercises in…  Extreme cold or hot  Poor metabolic control. 5. Gradually increase of length of exercise. Diet 1. Meal planning: To control of calories intake from carbohydrate rice cereal, bread, sugar. 2. Carbohydrate: It has a greater effect on blood glucose level so decrease amount of calories from bread & cereal and distribute it to fat and protein such as meat, fish. 3. Fats: Reduced to less than 30%, to prevent the development of coronary artery disease 4. Minerals: Iron improves hemoglobin and blood so improve metabolism and glycogeness in liver. 5. Vitamins: Diabetic patient must increase vitamins intake. Medication Types of hypoglycemic drugs: 1- Injection (insulin). 2- Oral hypoglycemic agent. 1) Insulin Indications of insulin:  In Type 1 DM: it is the only therapy.  In Type 2 DM: insulin is indicated for refractory hyperglycemia.  Complicated cases as DKA.  During pregnancy.  When exposure to stress from surgery or infection. Types of insulin According to its source: A. Conventional derived from beefs and less pure. B. Human insulin produced by genetic engineering, less allergic and pure. According to its bio availability: A. Short-acting Insulin: :ٗ١ٍ‫ أِثٍخ ػ‬،‫ خب٘ض‬ٟ‫ِزؼج‬ٚ ‫ ئمبفبد‬ٞ‫ْ أ‬ٚ‫ٓ هبٌغ ثذ‬١ٌٛ‫) دٖ ئٔغ‬Regular Insulin( ٟٔ‫ٌٗ اعُ رب‬  Insulinagypt R  Actrapid R  Humulin R.‫ٗ ئمبفبد‬١‫ؼ ف‬١‫ ِف‬ٚ‫ش ألٔٗ ِٕزظُ أ‬١‫ ثزؾ‬ٌٍٟ‫ا‬ٚ R ‫افزىش٘ب ثبٌـ‬ َٛ١ٌ‫ ا‬ٟ‫ زمٓ ف‬4 ‫ل‬٠‫ اٌّش‬ٞ‫ ِسزبج رذ‬:ٗ‫ث‬ٛ١‫ ػ‬،‫ عبػبد‬6 ‫ؾزغً ٌسذ‬١‫ث‬ٚ ،‫مخ‬١‫ دل‬30 ٗ‫ ثزبػ‬Onset ‫اٌـ‬ B. Intermittent-acting Insulin:.)Hagedorn( ْ‫س‬ٚ‫٘بخذ‬ ِ ٌُ‫ اعُ اٌؼب‬،‫ي‬ٚ‫ع األ‬ٌٕٛ‫ت ثزبع ا‬١‫ا اٌؼ‬ٛ‫زدٕج‬٠ ْ‫ع دٖ ػؾب‬ٌٕٛ‫ ػبٌُِ فٕغ ا‬ٟ‫ف‬ ،‫ اٌغّه‬ٟ‫د ف‬ٛ‫خ‬ِٛ ٓ١‫ر‬ٚ‫دٖ ثش‬ٚ )Neutral Protamine Hagedorn NPH( ّٗ‫ٕبد اع‬١‫ر‬ٚ‫ع ِٓ اٌجش‬ٛٔ ‫ا‬ٛ‫مبف‬ ‫ْ ِؼىش‬ٛ‫ى‬١‫ٓ ث‬١ٌٛ‫ْ اإلٔغ‬ٌٛ( ُٕٙ١‫ اٌشاثطخ ث‬ٞٛ‫م‬١‫) ث‬Ionic Bond( ‫خ‬١ٔٛ٠‫ْ ساثطخ أ‬ٛ‫ى‬٠ٚ ٓ١ٌٛ‫زسذ ِغ اإلٔغ‬١‫ث‬.)‫خ‬١ٔٛ٠‫ْ اٌشاثطخ األ‬ٛ‫ثغجت رى‬.‫ عبػخ‬18 ‫ؾزغً ٌسذ‬١‫ث‬ٚ )‫مخ (عبػخ‬١‫ دل‬60 ٗ‫ ثزبػ‬Onset ‫اٌـ‬.ًّ‫ ثزبع اٌؼ‬Duration ‫د اٌـ‬ٚ‫ض‬٠ ْ‫" ػؾب‬Protamine" ٌٗ ‫" مفٕب‬Regular Insulin" ٛ٘ :‫اٌخالفخ‬ ‫‪C. Rapid-acting Insulin:‬‬ ‫ٔفشك اْ ف‪ ٟ‬زبٌخ هبسئخ‪ٚ ،‬الصَ اٌّش‪٠‬ل ‪٠‬بخذ اإلٔغ‪ ٓ١ٌٛ‬ف‪ٛ‬سًا‪ ،‬ثبٌؾىً دٖ إٌ‪ٛ‬ػ‪ ٓ١‬اٌٍ‪ ٟ‬فبر‪ٛ‬ا ِؼ ٘‪ٕ١‬فؼ‪ٛ‬ا‪ ،‬ألْ‬ ‫ألً ِذح ٘زٕزظش٘ب ٘‪ٔ ٟ‬ـ عبػخ‪.‬فىبْ الصَ ‪٠‬الل‪ٛ‬ا زً‪...‬‬ ‫‪ ‬أ‪ٚ‬ي ٔ‪ٛ‬ع اعّٗ (‪ٕ٘ٚ )Insulin LISPRO‬ؼشف ٌ‪...ٗ١‬‬ ‫عٍغٍخ اإلٔغ‪ِ ٓ١ٌٛ‬ى‪ٔٛ‬خ ِٓ ‪ ُِٕٙ 53 Amino Acid‬اٌـ ‪ٚ Proline‬اٌـ ‪ٚ Lysine‬ث‪١‬ى‪ٛٔٛ‬ا الصل‪ ٓ١‬خٕت ثؼل‪،‬‬ ‫اٌدغُ ث‪١‬فىه عٍغٍخ اإلٔغ‪ ٓ١ٌٛ‬ػؾبْ ‪٠‬ؾغٍٗ‪ ،‬فـ ٘‪١‬بخذ ‪ٚ‬لذ ٌــ فقً اٌسّن‪( ٓ١‬ثش‪ٚ ٓ١ٌٚ‬ال‪٠‬غ‪ )ٓ١‬ػٓ ثؼل‪..‬‬ ‫ػٍّ‪ٛ‬ا زبخخ ثغ‪١‬طخ ا‪ ،ٞٚ‬أال ‪ :ٟ٘ٚ‬ث ّذٌ‪ٛ‬ا أِبوٓ اٌسّن‪٠ ،ٓ١‬ؼٕ‪ ٟ‬خٍ‪ٛ‬ا اٌال‪٠‬غ‪ ٓ١‬األ‪ٚ‬ي ثؼذ وذح اٌجش‪.ٓ١ٌٚ‬‬ ‫ػؾبْ وذح اعّٗ ‪ٚ LISPRO‬االعُ اٌزدبس‪Humalog ٌٗ ٞ‬‬ ‫ثبٌّٕبعجخ‪ :‬رمذس رجسث ػٕ‪ٙ‬ب ‪ٚ‬رؾ‪ٛ‬ف‪ٙ‬ب (اوزت عٍغٍخ االٔغ‪٘ ،ٓ١ٌٛ‬زالل‪ ٟ‬اْ اٌجش‪ ٛ٘ ٓ١ٌٚ‬اٌسّل االِ‪ ٟٕ١‬سلُ ‪28‬‬ ‫‪ٚ‬اٌال‪٠‬غ‪ ٛ٘ ٓ١‬اٌسّل األِ‪ ٟٕ١‬سلُ ‪)29‬‬ ‫‪ ‬ف‪ٛٔ ٟ‬ع ربٔ‪ ٟ‬اعّٗ (‪ )Insulin ASPART‬رسذ االعُ اٌزدبس‪NOVO RAPID ٞ‬‬ ‫‪ٚ‬دٖ ثذٌ‪ٛ‬ا ف‪ ٗ١‬زّل اٌجش‪ ٓ١ٌٚ‬ثسّل األعجبسر‪١‬ه (‪)Aspartic Acid‬‬ ‫‪ ‬ف‪ٛٔ ٟ‬ع ربٌذ اعّٗ (‪ )Insulin Glulisine‬رسذ االعُ اٌزدبس‪Apidra ٞ‬‬ ‫‪ٚ‬دٖ ثذٌ‪ٛ‬ا ف‪ ٗ١‬زّل اٌال‪٠‬غ‪ ٓ١‬ثسّّل اٌدٍ‪ٛ‬ربِ‪١‬ه (‪)Glutamic Acid‬‬ ‫اٌـ ‪ Onset‬ثزبػ‪٠ ُٙ‬زشا‪ٚ‬ذ ِٓ ‪ 5‬ئٌ‪ 15 ٝ‬دل‪١‬مخ‪ٚ ،‬ث‪١‬ؾزغً ٌسذ ‪ 5‬عبػبد‪.‬‬ ‫‪Long-acting Insulin:‬‬ ‫‪ ‬أ‪ٚ‬ي ِثبي‪ ،)Insulin Glargine( :‬ث‪١‬ن‪١‬ف‪ٛ‬ا ػٍ‪ ٝ‬اإلٔغ‪ ٓ١ٌٛ‬خضئ‪ ٓ١‬اسخٕ‪( ٓ١‬زّل أِ‪ٚ ،)ٟٕ١‬االعُ اٌزدبس‪ٞ‬‬ ‫ٌٗ ‪Lantus‬‬ ‫‪ ‬ربٔ‪ِ ٟ‬ثبي‪ ،)Insulin Detemir( :‬ث‪١‬ن‪١‬ف‪ٛ‬ا ػٍ‪ ٗ١‬عٍغٍخ أزّبك دٕ٘‪١‬خ (‪،)Fatty Acid Side Chain‬‬ ‫‪ٚ‬االعُ اٌزدبس‪Levemir ٌٗ ٞ‬‬ ‫االرٕ‪ :ٓ١‬اٌـ ‪ Onset‬ثزبػ‪( ُٙ‬عبػخ ٌـ ‪ 4‬عبػبد) ‪ٚ‬ث‪١‬مؼذ‪ٚ‬ا ف‪ ٟ‬اٌدغُ ٌّذح رقً ‪ 24‬عبػخ‬ ‫‪Mixed insulin:‬‬ ‫اٌؼٍّبء ػب‪٠‬ض‪ٛٔ ٓ٠‬ع ِخزٍو (‪٠‬ؾزغً ثغشػخ ‪٠ +‬مؼذ ف‪ ٟ‬اٌذَ أله‪ٛ‬ي فزشح)‬ ‫ػؾبْ وذح ػٍّ‪ٛ‬ا ٔ‪ٛ‬ع ِىظ (‪ٚ )Rapid/Short Acting + Intermediate‬عّ‪ ٖٛ‬رسذ االعُ اٌزدبس‪ٞ‬‬ ‫‪ ،MIXTARD‬إٌ‪ٛ‬ع دٖ ث‪١‬ى‪ ِٕٗ 70% + Regular Insulin ِٕٗ 30% ْٛ‬ث‪١‬ى‪NPH ْٛ‬‬ ‫أٔ‪ٛ‬اػٗ‪:‬‬ ‫‪ Insulin Mixtard 30/70‬‬ ‫رالر‪ٚ ٓ١‬عجؼ‪ٓ١‬‬ ‫‪ Humalog mix 25/75‬‬ ‫٘‪ ٟ‬إٌغت اٌّئ‪٠ٛ‬خ ٌالٔغ‪ٚ ٓ١ٌٛ‬اٌجش‪ٚ‬ر‪ ٓ١‬ػٍ‪ ٝ‬اٌز‪ٛ‬اٌ‪ٟ‬‬ ‫‪ Novomix 30/70‬‬ ‫‪٘ٚ‬ىزا ف‪ ٟ‬ثبل‪ ٟ‬االِثٍخ‬ Complication of insulin therapy  Insulin edema.  Hypoglycemia.  Pain.  Insulin allergy.  Insulin antibodies.  Liodystrophy.  Body weight gain. 2) Oral hypoglycemic agent Indicated for type 2 DM with stable and less complicated conditions Complication and side effects of Oral hypoglycemic agent:  Hypoglycemia  Diarrhea and abdominal pain  Weight gain  Hepatocelluar injury and fulminate failure Patient Education  Some home glucose monitoring devices  Older patients tend to skip meals. Assist them to identify easy but nutritious meals, such as frozen dinners.  The patient can discard used syringes and needles in a hard plastic container such as a Clorox bottle with a screw top.  The patient can use a mirror to look at the bottom of the feet or have a family member examine the patient’s feet.  Hot water heaters should be set below (50 c° = 120° F). 7. Complications of diabetes mellitus:  Acute Complications of DM:  Hyperglycemic hyperosmolar state (HHS).  Ketoacidosis coma.  Hypoglycemic coma.  Long-Term Complications:  Macro-vascular complications: involve large blood vessels in the body  Micro-vascular complications: the tiny blood vessels, such as those in the eyes or kidneys.‫شح‬١‫خ اٌقغ‬٠ِٛ‫خ اٌذ‬١‫ػ‬ٚ‫ اال‬ٟ‫ِنبػفبد ثزسقً ف‬ٚ ،‫شح‬١‫خ اٌىج‬٠ِٛ‫خ اٌذ‬١‫ػ‬ٚ‫ اال‬ٟ‫ ِنبػفبد ثزسقً ف‬ٟ‫ف‬ 1. Macro vascular Complications Circulatory system: Individuals with diabetes develop atherosclerosis and arteriosclerosis faster than the general population. The risk of cardiovascular disease and strokes is two to four times more common in persons with diabetes than in the general population. 2. Micro vascular Complications 2.1. Eyes Small blood vessels may become diseased, eventually leading to retinopathy in most patients with diabetes. Retinopathy involves damage to the tiny blood vessels that supply the eye. Small hemorrhages occur, which can cause blindness if not corrected. - Diabetes is also associated with a high incidence of cataracts. 2.2. Kidneys: Nephropathy is caused by damage to the tiny blood vessels within the kidneys. A primary risk factor for diabetic nephropathy is poor control of blood glucose. If nephropathy occurs, the kidneys are unable to remove waste products and excess fluid from the blood. 2.3. Nerves Another complication of diabetes is neuropathy, which is damage to nerves as a result of chronic hyperglycemia. Neuropathy can cause numbness and pain in the extremities, erectile dysfunction (impotence) in males, gastroparesis (delayed stomach emptying), and other problems. Unfortunately, pain caused by neuropathy is difficult to treat with traditional analgesics. 2.4. Infection Persons with diabetes are prone to infection for several reasons. If injuries occur, healing may be slow because of impaired circulation. There may not be enough blood supply to heal the wound or fight an infection. For the same reason, it may be difficult for IV antibiotics to reach an infected site, and topical antibiotics may be preferable. In the presence of hyperglycemia, white blood cells become sluggish and ineffective, further reducing the body’s ability to fight infection. The incidence of periodontal (gum) disease, caused by bacteria in plaque, is also increased in individuals with diabetes. Patients must be taught to maintain good oral hygiene and make regular visits to the dentist. Hyperglycemic Hyperosmolar Hypoglycemic coma State (HHS) Because basal insulin levels are Hypoglycemia is a well- unaffected. recognized complication among patients with type 1 diabetes. Excessive ketone production does not 1. Definition occur. The acidosis that these patients develop is attributed to lactic acidosis from poor tissue perfusion. 2. Onset Gradual Rapid 3. Type of DM Type 2 Type 1 4. Age of patient Usually older than 60 years Usually younger than 40 years 5. Mortality risk 20% - 40% 6. Drug history Steroids, thiazides, oral agents Insulin or oral agents Extreme stress associated with  Insulin shock. severe medical illness such as  Inborn errors of metabolism. stroke, MI, pancreatitis, trauma,  Stress. sepsis, burns, or pneumonia.  Weight loss.  Post-gastrectomy. Excessive carbohydrate intake:  Alcohol-related. - Peritoneal dialysis.  Glucocorticoid deficiency. 7. Predisposing - Drugs. factors  Fasting hypoglycemia.  Profound malnutrition.  Prolonged exercise.  Severe liver disease.  Severe sepsis.  Drug effects  Salicylates.  Insulin. Hyperglycemic Hyperosmolar Hypoglycemic coma State (HHS) Symptoms result from either the sympathetic nervous system response to hypoglycemia or 8. Manifestation from the neuroglycopenic response.  Dehydration.  Tachycardia.  Hypothermia.  Palpitation.  Toxic appearance.  Pallor.  Flushed skin.  Sweating.  Lethargy.  Anxiety.  Coma.  Tremor stupor.  Seizure.  Coma. 9. Glucose level Mean, more than 400 mg/dL 50 mg/dL or less 10. Ketones Absent Blood glucose.  Serum blood glucose 11. Lab Chemistries. investigation Osmolality. PH. ABGs. Urine acetone & glucose. Sodium. Potassium. Creatinine. BUN. 12. Diagnostic The same as DKA Studies Hyperglycemic Hyperosmolar Hypoglycemic coma State (HHS) Treatment goals for the patient Treatment of insulin reactions is with DKA include the always glucose. following: Improve circulatory volume If the patient can swallow, the and tissue perfusion. glucose is most conveniently Correct electrolyte given as a glucose- or sucrose imbalances. containing drink. Decrease serum glucose. Determine precipitating If the patient is too groggy, events. stuporous, or uncooperative to 13. Treatment drink, a bolus of 50% dextrose 1. IV fluids, IV insulin. is given intravenously over several minutes. 2. Glucose should be added to the IV when the blood glucose If this route or dosage is drops to 250 mg/dL to avoid unavailable, 1 mg of glucagon hypoglycemia. given subcutaneously or intramuscularly reverses the 3. Potassium should also be symptoms by inducing a rapid monitored, because the serum breakdown and release of potassium level drops rapidly as glucose into the blood stream it reenters the cells. from hepatic glycogen stores. Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) It is a critical illness that manifests with severe hyperglycemia, metabolic acidosis, and fluid and electrolyte imbalances elevation of counter-regulatory hormones such as growth hormone, cortisol, and glucagons. Diabetic ketoacidosis (DKA) occurs when blood glucose levels become very high (mean, 600 mg/dL) and insulin is deficient Signs and symptoms of DKA 1. Kussmaul’s respirations 2. The expired air has a fruity odor caused by the ketones 3. Polyuria, the body becomes dehydrated very quickly 4. Tachycardia, hypotension, and shock can result. 5. High blood glucose also causes potassium to leave the cells and accumulate in the blood (hyperkalemia). 6. The patient loses consciousness and death occurs if DKA is not treated. Treatment of DKA 1. IV fluids, IV insulin, and blood glucose monitoring  Assist with monitoring blood glucose levels closely and notify the RN or physician when the desired level is reached. 2. Glucose should be added to the IV when the blood glucose drops to 250 mg/dL to avoid hypoglycemia. 3. Potassium should also be monitored, because the serum potassium level drops rapidly as it reenters the cells. 4. The cause of the DKA should be identified and treated.

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