Diabetes Mellitus PDF
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Mr. Abdullah M. Khalil
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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.