‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬

‫‪(Pathology‬‬ ‫علم األمراض)‬

‫الپاثولوجٌا‪-:‬‬ ‫علم األمراض أو‬ ‫‪-‬‬
‫هو العلم الذي ٌقوم بدراسة مسببات المرض‪ ،‬أعراضه ونتابجه‪.‬‬
‫‪ -‬ما هو علم االمراض‬
‫فرع من فروع الطب‪ٌ ،‬عنى بدراسة طبابع األمراض والتؽٌٌرات التركٌبٌة والوظٌفٌة التً تقترن بمختلؾ األمراض‪،‬‬
‫وما تحدثه األمراض فً األنسجة من التؽٌٌرات‪ ،‬أو ما تستثٌر فٌاا من رد فع وتؽٌٌرات ٌضمن ظواهر تتى‬
‫كالتحو والضمور والتضخم وااللتااب‪.‬‬
‫‪ -‬علم األمراض (علم الباثولوجٌا)‪-:‬‬
‫هو عبارة عن فرع من فروع الطب ٌاتم بدارسة صفات األمراض والتؽٌرات التركٌبٌة وطبٌعة االمراض ووظٌفتاا‪،‬‬
‫التحو ‪ ،‬الضمور‪،‬‬
‫ّ‬ ‫وما تحدثه األمراض فً األنسجة من تؽٌٌرات‪ ،‬أو ما تستثٌر فٌاا من ردود فع تتى‪ ،‬مث ‪:‬‬
‫التورم‪ ،‬االلتااب‪ ،‬كذلك ٌاتم بتتخٌص األمراض عن طرٌق فحص العٌنات المأخوذة من الجسم تحت المجار‪ ،‬وٌعتنً‬
‫ّ‬
‫خاصة بتتخٌص األورام‪.‬‬
‫‪ٌ ‬عتمد علم الباثولوجٌا على دراسة التؽٌرات المرضٌة التً تحدث للخلٌة وأجازة الجسم عن طرٌق التحلٌ‬
‫المعملً‪ ،‬الفحص المٌكروسكوبً‪ ،‬التترٌح وتحلٌ األنسجة‪.‬‬
‫‪ ‬علم األمراض تباه العلماء بجذع التجرة الذي ٌربط بٌن معلومات الطب األساسٌة واإلكلٌنٌكٌة‪.‬‬
‫إن المرض هو‪-:‬‬
‫ظاهرة بٌولوجٌة تصٌب الجسم البتري وتؤثر على وظابفه أو أعضابه بطرق وأتكا مختلفة مث التضخم‪،‬‬
‫الضمور‪ ،‬االلتااب أو حتى النزٌؾ مما ٌستلزم أن ٌحظى اإلنسان المصاب بالظاهرة البٌولوجٌة بعناٌة طبٌة‬
‫وتمرٌضٌة حتى ٌمكن السٌطرة على تلك الظاهرة المرضٌة وإعادة الجسم إلى حالته الطبٌعٌة التً تمكنه من القٌام‬
‫بوظابفه الطبٌعٌة بدون تقصٌر أو اختال ‪ ،‬لذلك فالطبٌب المتخصص فً علم األمراض ٌعم على دراسة طبابع‬
‫األمراض وخصابصاا البٌولوجٌة الممٌزة لك مرض عن األخر‪.‬‬

‫اختصاصٌو علم األمراض‬ ‫‪‬‬

‫هم أطباء ٌقومون بتتخٌص المرض وتوصٌفه فً المرضى األحٌاء عن طرٌق فحص خزعات أو سواب الجسم‪.‬‬
‫أٌضا عملٌة تترٌح الجثث لبحث أسباب الوفاة‪.‬‬
‫وقد ٌُجري اختصاصٌو علم األمراض ً‬
‫أٌضا معلمون‪.‬‬
‫ً‬ ‫ربٌسا فً كلٌة الطب والعدٌد من اختصاصًٌ علم األمراض هم‬
‫ً‬ ‫فرعا دراس ًٌا‬
‫ً‬ ‫و ٌُعد علم األمراض‬
‫دورا ما ًما فً تطور نظم المعلومات‬
‫ً‬ ‫ومثلام مث مدٌري المختبرات الطبٌة‪ٌ ،‬لعب اختصاصٌو علم األمراض‬
‫ْ‬
‫المخت َبرٌة‪ .‬وعلى الرؼم من انبثاق الممارسة الطبٌة لعلم األمراض من تقالٌد علم األمراض االستقصابً‪ ،‬ال ٌقوم‬
‫معظم اختصاصًٌ علم األمراض المعاصرٌن بعم أبحاث ُمستحدَثة‪.‬‬
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 ‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬
‫ٌمث األخصابٌون فً علم األمراض مكونا ً أساسٌا ً فً نظام العناٌة الصحٌة‪ ،‬حٌث ٌتعلق اختصاصام بتتخٌص وتدبٌر‬
‫الحاالت المرضٌة من خال الطرق المخبرٌة‪ ،‬حٌث ٌقوم هؤالء األخصابٌون بدور كمتخصٌن مرضٌٌن‪ ،‬أطباء‬
‫استتارٌٌن‪ ،‬مدرسٌن وباحثٌن فً الدراسات السرٌرٌة والبحثٌة‪.‬‬
‫ٌقوم علماء األمراض بدمج المعلومات السرٌرٌة‪ ،‬المعرفة العلمٌة وفام النماذج المرضٌة مع طٌؾ واسع من‬
‫الطرابق التتخٌصٌة‪.‬‬
‫لكى تكون طبٌب متخصص بصورة كاملة فً علم األمراض فٌتطلب أن تكون أكملت الدراسة على مستوى الدراسات‬
‫العلٌا وفى الؽالب أن تكون حصلت على درجة الدكتورا ‪.‬‬

‫عم طبٌب علم األمراض وما هو دور فً خدمة وعالج المرضى‬

‫طبٌب علم االمراض )‪ (pathologist‬هو الطبٌب الذي ٌفحص هذ العٌنات تحت المجار وٌتخصاا وٌفام طبٌعة‬
‫المرض وسبب حدوثه وإمكانٌة استجابته للعالج والتنبؤ بمستقب المرض ثم ٌعطً رأٌه للطبٌب المعالج وعلى أساس‬
‫التتخٌص ٌكون العالج‪.‬‬
‫ؼالبا ما ٌطلق على طبٌب علم األمراض (طبٌب الطبٌب) وذلك آلن المرٌض عندما ٌمرض ٌذهب للطبٌب المعالج‬
‫وعندما ٌحتار الطبٌب المعالج فً التتخٌص ٌستتٌر وٌطلب مساعدة طبٌب علم األمراض فٌتخص طبٌب علم‬
‫االمراض الحالة وٌخبر باا الطبٌب المعالج‪ .‬فكما نالحظ ال ٌوجد تواص مباتر بٌن طبٌب علم األمراض والمرٌض‪.‬‬
‫إن مجاالت عم طبٌب علم األمراض هً مجاالت طبٌة كثٌرة حٌث ٌتواجد طبٌب علم األمراض فً كافة القطاعات‬
‫الطبٌة األخرى مث القطاعات الطبٌة البحثٌة‪ ،‬وفى المستتفٌات‪ ،‬والجامعات الطبٌة فً المناصب األكادٌمٌة‪.‬‬

‫فروع علم األمراض‪:‬‬

‫لعلم األمراض عدة فروع وهً‪:‬‬
‫‪ ‬علم األمراض السرٌري ‪ :‬وهو ٌعنى بطرق تتخٌص األمراض بوساب سرٌرٌة‪.‬‬
‫‪ ‬علم األمراض التجرٌبً ‪ :‬وٌعنى بدراسة التؽٌٌرات المرضٌة المحدثة بوساب مصطنعة‪.‬‬
‫‪ ‬علم األمراض الموازن ‪ :‬وٌعنى بمقابلة أمراض اإلنسان بأمراض الحٌوان‪.‬‬
‫ما لفرق بٌن علم األمراض االكلٌنٌكً )‪(Clinical pathology‬‬
‫وعلم األمراض التترٌحً)‪ (Anatomic pathology‬؟‬
‫ببساطة‪.‬‬
‫علم األمراض االكلٌنٌكً ٌاتم بالعٌنات المأخوذة من سواب الجسم‪.‬‬
‫أما علم األمراض التترٌحً ٌاتم بالعٌنات المأخوذة من أنسجة الجسم‪.‬‬

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 ‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬

‫مبادئ علم األمراض‬

‫عبارة عن ظاهرة تسود بٌن المجتمعات‪ ،‬وهذا المرض له صفاته وخصابصه االجتماعٌة‬ ‫األمراض‬ ‫‪‬‬
‫والبٌولوجٌة‪ ،‬وهناك الكثٌر من التعرٌفات التً تصؾ المرض‪ ،‬ولكن التعرٌؾ الواضح البسٌط‪:‬‬
‫‪ -‬هو عبارة عن اختالؾ ٌصٌب الجسم‪ ،‬وهذا االختالؾ ؼٌر مقبو به فً الجسم من حٌث وظٌفته‪ ،‬تركٌبه‪،‬‬
‫التعرض للحوادث‪ ،‬والحم ‪،‬‬
‫ّ‬ ‫حٌث ٌوجد حاالت خاصة ؼٌر األمراض والتً تتطلب االهتمام الطبً‪ ،‬وذلك مث ‪:‬‬
‫وقد ٌت ّم تصنٌؾ األمراض فً أتكا مختلفة‪ ،‬فاناك األمراض المصنفة حسب السبب‪ ،‬وأمراض تصنؾ بتأ ّثر‬
‫أجازة الجسم المختلفة‪ ،‬وأمراض تصنؾ حسب عالمات المرض‪ ،‬وؼٌر ذلك‪ ،‬وهناك األعراض المتتاباة‬
‫والتً تظار فً أكثر من مرض‪ ،‬لذلك ٌجب على الطبٌب إجراء الفحوصات المخبرٌة المتنوعة‪ ،‬ألخذ‬
‫والصحة‪ ،‬فاما تكالن ٌختلفان عن‬
‫ّ‬ ‫المالحظات الاامة الدقٌقة عن طبٌعة المرض‪ ،‬وٌفرق الطب بٌن المرض‬
‫بعضاما البعض فً المحتوى‪ ،‬لكناما ٌندمجان فً بعضاما‪ ،‬فك واحد مناما ٌعتبر ظاهرة من مظاهر الحٌاة‪.‬‬

‫‪ -‬المرض‪ :‬ظاهرة بٌولوجٌة واجتماعٌة‪ ،‬تقع فً وحدة جدلٌة مترابطة ‪ ،‬وٌمكن تعرٌؾ المرض بعدة اتكا ‪،‬‬
‫لكن التعرٌؾ البسٌط والتام هو ان المرض اختالؾ عن الحدود الطبٌعٌة المقبولة فً تركٌب الجسم‬
‫ووظٌفته ‪ ،‬او من جزء منه ‪ .‬وهناك حاالت خاصة ؼٌر االمراض تتطلب عناٌة طبٌة وتمرٌضٌة مث‬
‫الحوادث والحم ‪ ،‬وقد تصنؾ االمراض فً اتكا مختلفة ‪ ،‬فأحٌانا تصنؾ حسب السبب ‪ ،‬او حسب تأثر احد‬
‫اجازة الجسم او بحسب االعراض الممٌزة لاذا المرض ‪ ،‬وقد تظار االعراض فً اكثر من مرض فٌحتاج‬
‫الطبٌب عندها الى فحوص مخبرٌة متنوعة ومالحظات دقٌقة قب ان ٌتخص المرض ‪.‬‬
‫‪ -‬فالمرض هو اضطراب الصحة حٌث ٌراجع التخص المرٌض تاكٌا من مجموعة من االعراض والعالمات ‪.‬‬
‫‪ -‬فالمرض والصحة تكالن مختلفان فً حقٌقتاما ولكناما ٌرتبطان ببعضاما بان ك واحد مناما ٌتك ظاهرة‬
‫من مظاهر الحٌاة ‪.‬‬
‫‪ ‬األسباب‪:‬‬
‫وهً كثٌرة فالمرض إما مكتسب أو وراثً‪ .‬فلو كان وراثٌا ً فإنه ٌنتق عبر الجٌنات الوراثٌة‪.‬‬
‫أما إذا كان مكتسبا ً فاذا ٌعنً وجود سبب ربٌسً لإلصابة مث البكترٌا أو الفٌروسات أو الفطرٌات أو الطفٌلٌات أو‬
‫عوام خارجٌة كالبٌبة وما ٌحٌط باا من عوام مساعدة النتتار األمراض‪ .‬وتختلؾ األسباب من مرض آلخر‬
‫‪ -‬العرض ‪ :‬تكوى المرٌض من صداع ‪ ،‬الم ‪ ،‬تعب ‪ ،‬ضٌق تنفس ‪.‬‬
‫‪ -‬العالمة ‪ :‬وهً ما ٌالحظ بالفحص مث ‪ :‬الٌرقان ‪ ،‬الزرقة ‪ ،‬انتفاخ البطن ‪ ،‬وذمة الوجه االطراؾ ‪.‬‬
‫‪ ‬تصنٌؾ األمراض‬
‫‪ -‬األمراض الوراثٌة‬
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 ‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬
‫‪ -‬األمراض المزمنة‬
‫‪ -‬األمراض السارٌة‬
‫‪ -‬األمراض األٌضٌة‬
‫‪ -‬أمراض القصور‬
‫أمراض الحساسٌة‬ ‫‪-‬‬
‫‪ -‬أمراض االنحال أو التفسخ‬
‫‪ -‬األمراض الوظٌفٌة‬
‫‪ ‬أعراض األمراض بصفة عامة‬
‫تعور المرٌض باأللم والذي قد ٌكون موضعٌا ً أو عاما ً‪.‬‬ ‫‪‬‬

‫التورم‪.‬‬ ‫‪‬‬

‫حدوث السعا ‪.‬‬ ‫‪‬‬

‫التعور بضٌق فً التنفس‪.‬‬ ‫‪‬‬

‫وهناك األتخاص الذٌن ٌعانون من عسر فً التنفس‪.‬‬ ‫‪‬‬

‫النزٌؾ‪ ،‬سواء كان من الجلد أو مخارج الجسم األخرى‪.‬‬ ‫‪‬‬

‫التعرق‪ ،‬والتعرق التدٌد ٌسمى بالتعرق المرضً‪.‬‬ ‫‪‬‬

‫إفراط أو عسر فً التبو ‪.‬‬ ‫‪‬‬

‫الدوار والتق ٌّؤ‪ ،‬وهناك دوار مصحوب بالتقٌؤ وآخر ؼٌر مصحوب بالتقٌؤ‪ ،‬وٌعتبر الدوار والتقٌؤ واحد من‬ ‫‪‬‬

‫أهم العالمات المرضٌة‪ ،‬وقد ٌحدث التقٌؤ والدوار نتٌجة عوام عاطفٌة تصٌب التخص‪.‬‬
‫اإلمساك واإلساا ‪ :‬عندما ٌتم مالحظة أي تًء ؼٌر عادي فً براز التخص فً حالة اإلمساك أو اإلساا ‪،‬‬ ‫‪‬‬

‫فإ ّنه ؼالبا ً ٌد على إصابة التخص بمرض ما‪.‬‬

‫‪ ‬اعراض المرض ‪- :‬‬
‫‪ -‬االلم ‪ :‬قد ٌكون موضعٌا او عاما او قد ٌكون الما داال ‪ٌ ،‬تعر المرٌض بااللم فً مكان ما من جسمه‬
‫‪ ،‬بٌنما مكان تسببه فً ؼٌر ذلك المكان وٌحدث االلم لمجموعة مختلفة من االسباب ‪ ،‬عادة بسبب‬
‫تمزق فً االنسجة ناتج عن حادث او التااب او نمو‪.‬‬
‫التورم ‪ :‬قد ٌكون المرض ظاهرا وسببه تجمع الساب فً االنسجة ‪.‬‬ ‫‪-‬‬
‫السعا ‪ :‬عالمة مامة على المرض وقد ٌكون جافا او رطبا وٌقا ان السعا مخرج للمادة‬ ‫‪-‬‬
‫المخاطٌة اذا اخرج البصاق ‪ .‬وعلى الممرضة ان تراقب البصاق من حٌث اللون والكمٌة والتركٌب‬
‫واي اثار من الدم او القٌح قد تكون ذات دالله وال بد مع تعلٌم المرٌض ان ٌؽطً فمه عندما ٌسع ‪.‬‬

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 ‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬
‫ضٌق التنفس ‪ :‬قد ٌصاب المرٌض بصعوبة فً التنفس وال بد له ان ٌعتد فً جلوسه لكس ٌستطٌع‬ ‫‪-‬‬
‫التنفس هذا ما ٌسمى ضٌق التنفس ‪.‬‬
‫‪ -‬عسر التنفس ‪ٌ :‬نتج من نقص كمٌة االوكسجٌن فً الدم ‪ .‬ولعسر التنفس عدة اسباب ‪ :‬اكثرها حدوثا‬
‫حاالت معٌنة تصٌب اوعٌة القلب او جااز التنفس وفً بعض االحٌان قد ٌتسبب عسر التنفس عن‬
‫عوام عاطفٌة ‪ ،‬وعلى الممرضة ان تراقب المرٌض المصاب بعسر التنفس وتالحظ لونه ونبضه ‪،‬‬
‫والصوت فً المجاري التنفسٌة ‪ ،‬وقد ٌبدو المرٌض خابفا فعلى الممرضة ان تراقب زوا عسر‬
‫التنفس اذا ما ؼٌر المرٌض مكانه ‪ ،‬او وضعٌته ‪.‬‬
‫النزٌؾ ‪ :‬احد اعراض االخرى المامة هو ‪ :‬النزٌؾ من الجلد او فتحات الجسم وٌسمى النزٌؾ‬ ‫‪-‬‬
‫المتزاٌد بالنزؾ المرضً فقد ٌكون خارجٌا اي من الفم او المستقٌم او الماب ‪ ،‬او داخلٌا ضمن‬
‫المعدة او فً اي جااز اخر ففً حالة النزؾ الداخلً لن تكون هناك اي اتارة الى النزؾ ؼٌر نبض‬
‫المرٌض المتسرع وتنفس سطحً وجلد بارد ورطب ‪.‬‬
‫التعرق ‪ٌ :‬سمى التعرق التدٌد العرق المرضً فقد ٌتعرق المرٌض كثٌرا اثر اصابته ببعض‬ ‫‪-‬‬
‫االمراض وٌتعرق فً اللٌ اكثر من الناار اذا اصٌب بأمراض اخرى ‪.‬‬
‫البو ‪ٌ :‬جب فً الظروؾ العادٌة ان ٌفرز المرٌض كمٌة تتراوح بٌن ٓٓ٘ٔ‪ ٕٓٓٓ-‬ملمٖ فً ك‬ ‫‪-‬‬
‫ٕٗ ساعة وعلى اي حا فاناك بعض الحاالت التاذة التً ٌصاب فٌاا المرٌض بحصر البو اي انه‬
‫ؼٌر قادر على تفرٌػ البو ‪ .‬اما وقؾ البو او انحباسه فاً حالة خطٌرة جدا ناتجة عن فت‬
‫الكلٌتٌن فً افراز البو ‪،‬ولذلك لن ٌتفرغ المرٌض اي بو ‪ .‬اما ؼزارة البو فاً حالة اخرى ٌفرز‬
‫اثناباا جسم المرٌض كمٌة كبٌرة جدا من البو ‪ .‬عندما ٌكون التبو مؤلما فاذا ٌعنً عسر البو ‪.‬‬
‫وحالة اخرى كثٌرة الحدوث للمرض وهً سلس البو او العجز عن ضبط البو فً المثانة ‪ٌ ،‬تٌر‬
‫البو الى اتٌاء كثٌرة عن حالة المرٌض وعلى الممرضة ان تراقب البو لتتأكدا وجود دم او قٌح‬
‫فٌه فاذا ما لوحظ اي مناما فٌجب االحتفاظ بالعٌنة لكً ٌتاهدها الطبٌب ‪.‬‬
‫‪ -‬الدوار والتقٌؤ ‪ :‬الدوار المصحوب وؼٌر المصحوب بالتقٌؤ ‪ ،‬هو واحد من اهم االعراض المرضٌة ‪،‬‬
‫وقد ٌد على مرض فً الجااز الاضمً وقد ٌحدث لألطفا اثناء بداٌة االصابة بأمراض معدٌة ‪.‬‬
‫والدوار والتقٌؤ حالتان وظٌفٌتان عند بعض االتخاص تتأثران بالعوام العاطفٌة ‪ ،‬واي كمٌة قٌا‬
‫ٌخرجاا مرٌض ٌجب ان تقاس وتفحص للتحري عن الدم ‪ ،‬او الطعام الذي لم ٌاضم ‪ .‬كما ٌجد‬
‫مالحظة وقت حدوثه وتكرار ‪.‬‬
‫‪ -‬االمساك واالساا ‪ :‬تجب مالحظة اي تًء ؼٌر عادي فً البراز ومالحظة االمساك واالساا ‪ ،‬او‬
‫وجود مخاط او قٌح او دم وٌجب اخطار الطبٌب المسؤو ‪.‬‬

‫‪5‬‬
 ‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬
‫‪ -‬االمراض الوراثٌة ‪ :‬هذ االمراض موجودة منذ الوالدة وٌمكن تورٌثاا ‪ ،‬مث فقر الدم فً الخالٌا المنجلٌة ‪،‬‬
‫او قد تكون نتٌجة نمو ؼٌر عادي اثناء الحٌاة الجنٌنٌة مث الحنك المتقوق وبعض حاالت تتو االقدام ‪ .‬وقد‬
‫تورث االم جنٌناا الزهري الوراثً ) ‪ (Congenital syphilis‬واالدمان على بعض االدوٌة ‪ .‬وال تعرؾ‬
‫حتى االن ك االمراض الوراثٌة ‪.‬‬
‫‪ -‬االمراض المزمنة ‪ٌ :‬ستمر المرض المزمن فترة طوٌلة وقد تؤثر فً وظٌفته اي جااز من اجازة الجسم او‬
‫فً تركٌب اي جزء فٌه او فً الوظٌفة والتركٌب معا ‪ .‬وٌعد كثٌر من االمراض امراضا مزمنة مث االورام‬
‫الخبٌثة وامراض القلب ‪ ،‬والربو ‪ ،‬والتااب المفاص ‪ٌ .‬فقد كثٌر من المصابٌن باألمراض قوتام كلٌا ‪ ،‬بٌنما‬
‫ٌستطٌع اخرون العناٌة بأنفسام ‪.‬‬
‫‪ -‬االمراض السارٌة ‪ :‬وهً االمراض الناجمة عن دخو عوام ممرضة الى العضوٌة ‪،‬‬
‫وهذ العوام تقسم الى ‪ :‬جراثٌم وفطور ‪ .‬فٌروسات ‪ .‬طفٌلٌات ‪:‬‬
‫ٔ‪ .‬وحٌدة الخلٌة ‪.‬‬
‫ٕ‪ .‬عدٌدة الخالٌا ‪ .‬وهً امراض تنتق من تخص ألخر فتؤدي لحدوث االصابة نفساا عند وطرق االنتقا هً ‪:‬‬
‫طرٌق هضمً ‪ :‬الؽذاء والماء الملوث ‪.‬‬
‫طرٌق تنفسً ‪ :‬الاواء (السعا والعطاس) ‪.‬‬
‫عن طرٌق الجلد ‪.‬‬
‫عن طرٌق الدم ‪.‬‬
‫الجنس ‪.‬‬
‫المتٌمة ‪.‬‬
‫وتمتاز هذ االمراض بان العدوى ال تظار مباترة وانما تحتاج لفترة زمنٌة حتى تظار اعراض المرض تدعى هذ‬
‫الفترة الحضانة ' وتختلؾ من مرض ألخر' فاً فً النزلة الوافدة عدة ساعات ‪ ،‬وفً الحصبة عدة اٌام ‪ .‬وعدة اتار‬
‫فً امراض اخرى مث االٌدز‬
‫االمراض االٌضٌة ‪ :‬تنتا عن فت الجسم فً تمث بعض العناصر الؽذابٌة المعٌنة فمثال ٌنتا مرض‬ ‫‪-‬‬
‫االختالطات السكرٌة من ضعؾ فعالٌة االنسولٌن الذي تولد البنكرٌاس ولذلك فالتخص المصاب به ال‬
‫ٌستطٌع تمث الكاربوهٌدرات والفٌنلكتونورٌا ‪ P.K.U‬هو مرض ٌصٌب الجسم فال ٌستطٌع عندها ان بتمث‬
‫الفٌنالٌن 'حمض الفٌنً' مادة مامة لتجزبة بعض االطعمة البروتٌنٌة ‪.‬‬
‫‪ -‬امراض القصور ‪ :‬تنتا عن فقدان مادة ضرورٌة للنمو العادي والتطور وقد ق انتتار هذا المرض فً‬
‫الوالٌات المتحدة االمرٌكٌة عن طرٌق العناٌة المتطورة بالطف و الرضٌع وبتقدٌم التؽذٌة الجٌدة لألسرة‬
‫بكاملاا وعلى سبٌ المثا نذكر ‪ :‬مرض الكساح الذي ٌسببه نقص الفٌتامٌن د‬

‫‪6‬‬
 ‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬
‫امراض الحساسٌة ‪ :‬تنتا من التحسس الزابد من بعض المواد التً قد ال تأثر باا معظم االتخاص وقد ٌكون‬ ‫‪-‬‬
‫سبب الحساسٌة ادوٌة واطعمة معٌنة ‪ ،‬او لدغ بعض الحترات ‪ ،‬او مالمسة بعض النباتات مث اللبالب السام‬
‫وقد تدخ المادة المثٌرة للحساسٌة عن طرٌق جااز التنفس او جااز الاضم او الجلد ‪.‬‬
‫‪ -‬امراض االنحال او التفسخ ‪ :‬هً امراض ٌسبباا التعب المستمر او التقدم فً السن وهذا النوع من االمراض‬
‫متطور وٌسبب تخرٌبا قد ٌستمر لمدة سنوات ومن هذ االمراض مرض تصلب التراٌٌن والتااب المفاص‬
‫المزمن وانواع اخرى من امراض القلب والكلٌتٌن ‪.‬‬
‫‪ -‬االمراض الوظٌفٌة ‪ :‬االمراض الوظٌفٌة اصطالح واسع عام ٌطلق على تلك الحاالت التً ال ٌحدث فٌاا اي‬
‫تؽٌر عضوي ‪ ،‬او بعبارة اخرى ال ٌستطٌع الطبٌب ان ٌجد اي حالة مرضٌة لٌفسر باا حالة المرٌض ‪.‬‬
‫وتصنؾ بعض االمراض الوظٌفٌة على اناا جسدٌة نفسٌة ‪ ،‬وهذا ال ٌعنً ان المرض ؼٌر موجود ب هو فعال‬
‫موجود ولكناا تعنً ان هذ االمراض تختلؾ عن االمراض العضوٌة التً سبق ذكرها ‪.‬‬
‫‪ ‬تتخٌص المرض ‪:‬‬
‫ٌقسم الى ‪- :‬‬
‫‪ ‬القصة السرٌرٌة ‪.‬‬
‫فحص الجسم ‪.‬‬ ‫‪‬‬
‫الفحوص المتممة ‪.‬‬ ‫‪‬‬
‫الفحوص المخبرٌة ‪ :‬تجرى على ‪:‬‬
‫ٔ‪ .‬الدم‬
‫ٕ‪ .‬البو‬
‫ٖ‪ .‬البواز‬
‫ٗ‪ .‬المفرزات االخرى‬
‫٘‪ .‬الفحوص التعاعٌة ‪ :‬بسٌطة ‪ :‬وتجرى دون تحضٌر مسبق مث صورة للجمجمة او الصدر او االطراؾ ‪.‬‬
‫الصورة التعاعٌة الظلٌلة ‪ :‬تحتاج للتحضٌر المرٌض تحضٌرا خاصا ‪ ،‬حسب الجااز المطلوب تصوٌر (معدة‬
‫–قولون‪ -‬كلٌة) وهنا ٌجب ان نعطً مواد ظلٌلة على االتعة مث (الٌورو ؼرافٌن ) و البارٌوم (فموٌا) ‪.‬‬
‫التصوٌر باألمواج فوق الصوتٌة ‪ :‬القلب – الكلٌة – الكبد و المرارة – الؽدة الدرقٌة ‪.‬‬
‫الدوبلر ‪ :‬للقلب واالوعٌة الدموٌة ‪.‬‬
‫الزرع ‪ :‬تجري على جمٌع مفرزات الجسم (الدم – المخاط – البو ) ‪ .‬والؽاٌة هً معرفة نوع الجراثٌم وعدد‬
‫المستعمرات والدواء االكثر فعالٌة للعالج ‪.‬‬
‫‪ ‬التترٌح المرضً ‪ :‬وهو اخذ قطعة من نسٌج مرضً لتحدٌد نوع االفة ه هً خبٌثة ام سلٌمة ام‬
‫التاابٌة ‪ ،‬وانتتارها ‪ .‬وٌجرى على العقد البلؽمٌة ‪ ،‬الكبد ‪ ،‬الطحا ‪ ،‬القلب ‪ ،‬الكلٌة ‪.‬‬
‫‪7‬‬
 ‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬
‫‪ ‬االختالطات ‪ :‬وهً المضاعفات التً تحدث خال سٌر المرض ‪ ،‬وهً تختلؾ حسب مكان االفة وطبٌعتاا‬
‫فمثال القرحة الاضمٌة تختلط باالنثقاب والنزؾ ‪ ،‬والتااب القصبات ٌختلط بالخراجة الربوٌة ‪.‬‬
‫‪ ‬المعالجة ‪ :‬وهً التدابٌر التً تقدم للمرٌض ‪ ،‬وتنفذ خطة الطبٌب فً العالج ‪ .‬وهناك انواع مختلفة‬
‫ومتعددة للعالج الؽاٌة مناا فابدة المرٌض التامة فقد ٌكون العالج تافٌا مث وصؾ دواء معٌن لتفاء‬
‫المرٌض من مرض تفاء تاما ‪ ،‬وهذ هً المعالجة النوعٌة وقد ٌكون العالج مسكنا اي تقدٌم مواد‬
‫تخفؾ من االعراض دون ان تتفً المرٌض من المرض وهذ هً المعالجة العرضٌة ‪ .‬وقد ٌكون‬
‫العالج جراحٌا عندما ٌصعب العالج الدوابً وهناك المعالجة الواسعة ‪ :‬التعاعٌة والكٌماوٌة‬
‫والفٌزٌابٌة‪ .‬وقد ٌكون العالج داعما اي ٌقدم الحاجات الؽذابٌة وٌأخذ مقدار مناسب من السواب اما‬
‫عن طرٌق الفم او عن طرٌق ؼٌر معوي – قد ٌحوي هذا العالج ادوٌة او كمٌة معٌنة من الدم تعطى‬
‫للمرٌض وتكون عملٌات السقاٌة او تنظٌم االكسجٌن جزءا من العالج الداعم للمرٌض وهناك انواع‬
‫اخرى من العالج لألمراض معٌنة ٌتم بعضاا استعما االدوٌة والارمونات والعالج بأتعة السٌنٌة‪.‬‬
‫‪ ‬االنذار ‪ :‬هً النتٌجة الناابٌة للمرض مع معالجة او دوناا وٌمكن ان ٌكون ‪ :‬تفاء عفوٌا ‪ ،‬تفاء‬
‫عالجٌا مع بقاء اختالطات ‪ ،‬تحسنا (تحسن االعراض دون زوالاا) تدهور الحالة العامة عندما ال‬
‫نستطٌع السٌطرة على المرض ‪ ،‬الوفاة ‪.‬‬

‫‪ALTERATIONS IN CELL FUNCTION AND‬‬

‫‪GROWTH‬‬
‫‪1.1 Cell injury and Cellular Adaptive Changes‬‬
‫‪The life cycle of a cell exists on continuum that includes normal activities and adaptation,‬‬
‫‪injury or lethal changes.‬‬

‫‪8‬‬
 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
Adaptation is a normal life cycle adjustment like in growth during puberty; changes
during pregnancy or aging and stressful life style produce physiologic changes that
may lead to adaptation or disease.
The cell constantly makes adjustments to a changing, hostile environment to keep the
organism functioning in normal steady state which is necessary to ensure the survival
of the organism. Prevention of disease by the body depends on the capacity of the
affected cells to undergo self-repair and regeneration i.e. adaptive-changes.
- When cells are confronted to one of the following stimulus, they may undergo
adaptive changes.
The common stimuli are:-
a) Physical agents
- Trauma, Burn, pressure, irradiation, etc
b) Chemical agents
- Poisons, drugs, simple compounds, etc.
c) Micro organisms
- Bacteria
- Virus
- Fungus
- Parasites
d) Hypoxia
- Is the most common stimuli (cause)
- Is because of inadequate oxygen in the blood or decreased tissue Perfusion.
e) Genetic defects
- Can affect cellular metabolism through inborn errors of metabolism or gross
malformation
f) Nutritional imbalances
- Under nutrition or over nutrition causes cellular injury or changes.
g) Immunologic reaction
E.g. - Hypersensitivity reaction.

9
 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬

1.1.1 Types of cellular Adaptive-changes

• When cells are exposed to one of the above noxious stimulus they will undergo one or
more of the following types of adaptive changes:-
i. Increased concentrations of normal cellular constituents.
ii. Accumulate abnormal substances
iii. Change the cellular size or number or
iv. Undergo a lethal change.
1.1.2 Abnormal and normal accumulation of intracellular substances
Intracellular accumulations often result from environmental changes or an inability of
the cell to process materials (substances) that cannot be metabolized by the cells. These
substances may accumulate in the cytoplasm.
As a result common changes include:-
- Cellular swelling Lipid accumulation (Fatty change process in the cytoplasm of
cells).
- Glycogen depositions (Excess deposition of glycogen in organs).
- Calcification (precipitation of calcium in dead or Chronic inflammation area)
- Hyaline infiltration( characteristic alteration within cells or in the Extra-cellular
spaces that appear as inclusion on stained histology).
1.1.3. Changes to cellular size or numbers
- Changes in size and numbers of the cells are usually as a result of response to adapt to
harmful agents.
- The changes include:-
I) Atrophy
 Atrophy refers to a decrease in cell size.
 Causes:
- Decreased work load (Disuse atrophy)
- Loss of nerve supply
- Decreased blood supply

11
 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
- Inadequate nutrition
- Loss of hormonal stimulation
Eg. - Uterine atrophy after menopause.
- Physiologic Atrophy
Eg. - Loss of muscle bulk with ageing.
II) Dysplasia:-
- Dysplasia refers to the appearance of cells that have undergone some atypical
changes in response to chronic irritation.
- It is not a true adaptive process in that it serves no specific functions.
- It is controlled reproduction of cells, but closely related to malignancy in that it may
transform into uncontrolled, rapid reproduction.
- It is complete loss of normal architectural orientation of one cell with the next both in
shape and size.
- Epithelial cells are common sites for dysplastic changes.
Eg: -Bronchial epithelium,
- Cervical epithelium, etc.
III) Hyperplasia:-
- It is defined as increase of tissue mass due to an increase in the number of cells.
- It occurs in cells that are under increased physiologic workload or stimulations.
I.e. the cells are capable of dividing thus increasing their numbers.
Types of Hyperplasia
a) Physiologic Hyperplasia: occurs when there hormonal stimulation
- Occurs in puberty and pregnancy
b) Compensatory-Hyperplasia
- Occurs in organs that are capable of regenerating lost tissues.
Eg. When part of liver is destroyed.
c) Pathologic Hyperplasia
- Is seen in abnormal stimulation of organs with cells that are capable of
regeneration.
11
 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
E.g. Enlargement of Thyroid gland due to TSH from pituitary gland.
IV) Hypertrophy
- Is an increase in the size of individual cells, resulting in increased tissue mass
with out an increase in the number of cells.
- It is usually response of a specific organ to an increased demand for work.
Example: - Enlargement of muscles in Athletes
V) Metaplasia
• Metaplasia is a reversible change in which one type of adult cell is replaced by
another type.
• It is an adaptive substitution of one cell type more suitable to the hostile environment
for another.
Eg. - Replacement of the normal columnar, ciliated goblet cells of the bronchial
mucosa by Stratified squamous epithelial cells in chronic smokers.

12
 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
Figure 1.1

Figure 1.1 Types of cellular adaptive changes

1.1.4. CELLULAR INJURY AND LETHAL CHANGES
(Cell Death)
Cell injury can be sub lethal or lethal. Sub lethal injury alters functions with out causing cell
death. The changes caused by this type of injury are potentially reversible if the injuring
stimuli are removed.
Causes of cell injury:-
Causes of cell injury are the same causes of cellular adaptive changes as mentioned above.
Classification of cell injury:-
Cellular injury can be reversible or it may progress to irreversible change (Lethal change).
1. Reversible cell injury:-

13
 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
Is cell injury which can be reversed when the stimulus or the cause of injury is
removed. Example
-Ischemia:
 Ischemia refers to a critical lack of blood supply to a localized area.
 It is reversible in that tissues are restored to normal function when oxygen is again
supplied to them, but if late progress to ischemic infraction
 It usually occurs in the presence of atherosclerosis in the major arteries.
 The classic conditions resulting from ischemia is Angina pectoris.
2. Irreversible Cell injury
It is cellular injury that can not be corrected (reversed) after the stimulus or cause has
been removed. Example:-
a. Infarction:-
 Is localized area of tissue death due to lack of blood supply.
 It is also called Ischemic Necrosis.
 It is due to occlusion of blood vessels by thrombus or embolus. Septic Infarction
is added when there is evidence of infection in the area.
 It is irreversible cellular death due to lack of blood supply, when ischemia is
persistent or late.
• Example:- Acute myocardial infarction (AMI)
b. Necrosis:-
 The term necrosis refers to cell or tissue death characterized by structural
evidence of this death.
 The structural changes are mitochondrial swelling, rupture of cell
membrane, shrinking of nucleus or fragmenting, and release of lysozomal
enzymes, etc.
 Based on the structural changes, Necrosis is classified in to two main classes:-
1. Coagulative-Necrosis
• Usually results from lack of blood supply to an area.

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
• The cell structure and its architectural outline is preserved, but the nucleus is lost
(structureless necrosis)
• Caseouse Necrosis: - is a good example of structureless necrosis. It is common in
tuberculosis and i s characterized by central area of necrosis which is soft, friable
and surrounded by an area with a cheesy, crumbly appearance.
2. Colliquative- Necrosis (liquefactive- Necrosis)
- It frequently occurs in brain tissues and results from break down of neurons by
released lysosomal enzymes resulting in formation of pockets of liquid, debris and
cyst like structures in the brain tissue.
Example:- Wet gangrene.
1.2. Neoplasm
1.2.1. Definition of terms:-
 Neoplasm: - New abnormal growth because of abnormal cellular- reproduction.
It is synonymously used with tumor.
 Aberrant cellular growth:- An alteration in normal cell growth
 Tumor: - A growth of Neoplastic cells clustered together to form a mass. It can
be benign or malignant.
 Benign tumor: - Is characterized by abnormal cell division but no metastasis or
invasion of the surrounding tissues.
 Malignant tumor: - Abnormal cell division characterized by ability to invade
locally, metastasize and reoccur. It is cancer cells.
 Carcinogenesis: - production or origination of cancer cells.
 Sarcoma: - Malignant growth from mesodermal tissues I.e. connective tissues,
blood-vessels, organs, etc.
 Metastasis: - Ability to establish secondary tumor growth at a new location
away from the primary tumor.
 Carcinoma: - Malignant growth originating in epithelial tissues
1.2.2. Benign and Malignant Neoplasia

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
- The capacity of undergoing mitosis is inherent in all cells. Mitosis is repressed or
controlled until specific stimulation for growth occurs. Every time a normal cell
passes through a cycle of division, the opportunity exists for it to become
Neoplastic.
 N.B. Cancer cells lack repression or lode control of Mitosis I.e. cancer cells are crazy
cells.
1.2.3. Epidemiology
- Neoplastic-disease affects 1 in 4 persons in the world.
- Cancer can strike at any age but the chance increase with age.
- It is the leading cause of children death aged 3-14 years old.
- The three leading death producing cancer in men are cancer of the lung, colo-rectal
and prostatic gland. For women the most common cancers are those of the breast,
lung, and colorectal respectively.
1.2.4. Classifications of Neoplasms
- Neoplasms are classified according to their cells of origin and their behavior of
growth as benign or malignant.
Table 1.1 A comparison of benign and malignant Neoplasms
Benign Malignant
- Similar to cell of origin - Dissimilar from cell of origin
- Edges move out word smoothly - Edges move out ward irregularly.
- Compress locally - Invade locally
- Slow growth rate - Rapid to very rapid growth rate.
- Seldom Recur after removal by surgery - Frequently recur after removal
- Necrosis and ulceration is uncommon - Necrosis and ulceration common.
- Systemic effect i s uncommon - Systemic effect common.
1.2.5. Nomenclature of Neoplasms
- Naming of Neoplasia based on two main important features of the tumor.
These are:-

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
A) Based on its Behavior of growth:-
i) Benign:
- Add “oma” at the end for connective tissue origin tumors.
- Add “papiloma” for epithelial origin.
- Add “adenoma” for glandular origin.
ii) Malignant:
– Add: - “sarcoma” at the end for malignant tumors of Connective tissues
origin.
- Add “carcinoma” at the end for malignant tumors of epithelial origin.
- Add “adenocarcinoma” at the end for malignant tumors of glandular origin.
B) Based on cells of origin:-
- Neoplasms are named at their prefix by their cells of origin and their suffixes are
added at the end to show whether they are benign or malignant.
Example: - Behavior of growth

Cells of origin Benign Malignant

- Fatty cells - Lipoma - Liposarcoma
- Bone cells - Osteoma - Osteosarcoma
- Blood vessels - Hemangioma - Hemangiosarcom
- Fibrous tissues - Fibroma - Fibrosarcoma
C) Exceptional Naming (Malignant Misnomers)
- There are some neoplasms that are named exceptionally to the above rules.
Examples:-
- Hepatoma: - malignant tumors of the liver cells. It is also called Hepato-cellular
carcinoma
- Hodgkin’s disease: - Malignant tumors of the lymphoid tissues.
- Multiple myeloma: - malignant tumors from the plasma cells.
- Others:- Leukemia, Ewing’s sarcoma, etc.
1.2.6. Mechanisms of carcinogenesis
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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
- There are large numbers of research done in the world to know the etiology of cancer
but none of the theories that attempt to explain the peculiarities of the cancer cells
have been completely successful. The following are some of the theories on
carcinogenesis:
a. Genetic Instability:-
- The theory of somatic cell mutation supports the concept that mutational carcinogenic
agents and heredity susceptibility can induce genetic abnormalities.
b. Carcinogens
- Carcinogens are those substances that are capable of inducing neoplastic growth.
They are also called oncogenes. Some substances induce neoplastic growth at higher
doses and exposure rates while others can be carcinogenic at lower doses and exposure
rate.
The three commonly encountered carcinogens are:
1. Chemical carcinogens
- Many chemical agents are capable of causing Neoplasms in either humans or
animals. Chemical carcinogens are grouped as:-
a. Polycyclic aromatic hydrocarbons:-
 They are common carcinogens; present in tobacco smoke or automobile
exhaust, .Usually cause cancer of lips, oral-cavity, lungs, neck, pancreases,
b. Aromatic amines
 Commonly found in insecticides, certain foods and Naphthalene.Usually
related with cancer of the bladder.
c. Alkylating agents
 They can cause cancer when given in large dose. Are usually used as
therapeutic agents. example:- Nitrogen mustard
- Mustard gas
d. Others
 Like aflatoxines, nitrosamides, drugs, etc.
2. Physical carcinogenic agents
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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
Ionizing radiation is a recognized cause of cellular mutations.
Damage to DNA may be direct or indirect.
A long latent period often exists between exposure and development of clinical
disease.
- Example:-
leukemia and skin cancers became very common long years later in Hiroshima
and Nagasaki,Japan;after atomic bomb detonation.
3. Viral carcinogens (oncogenic viruses)
Viruses are thought to cause some human and animals malignant neoplasms. Current
evidence shows that viruses alter the genome of the infected cells, which then alter
the offspring of the host cells. Some of the oncognic viruses are:-
1. EBV (Epstein-Barr virus) associated with Burkett’s lymphoma.
2. HPV (Human-papilloma-virus) associated with cervical cancer and skin
papilloma.
4. Other Factors in carcinogenesis
Epidemiologic studies have revealed other factors in the occurrence of neoplasms
besides chemical, physical and viral-carcinogens. Some of these factors are dietary
habits, sexuality, and other personal habits like smoking, alcohol consumption etc.

ALTERATIONS IN BODY DEFENSE

2.1. Body Defense Mechanisms against Injury
To protect against injury and infection, the body has various defense mechanism.
These defense mechanisms are:-
2.1.1) The skin and mucous membranes
2.1.2) The mononuclear phagocyte system
2.1.3) The inflammatory response and
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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
2.1.4) The immune system
2.1.1. The skin and mucous membranes
The skin and mucous membranes are the first line of defense mechanisms. They serve
as a mechanical barrier for protection of the body against different injurious agents.
Break in these barriers give pave for way of injurious agents.
2.1.2. Mononuclear Phagocyte System
The mononuclear phagocyte system (MPS) consists of monocytes and macrophages
and their precursor cells. In the past, the MPS system was called the reticulo
endothealial system (RES). However, it is not a body system with distinctly defined
tissues and organs. Rather, it consists of phagocytic cells located in various tissues and
organs.
The phagocytic cells are either fixed or free (mobile). The macrophages of the liver,
spleen, bone marrow, lungs, lymph nodes, and nervous system (microglial cells) are
fixed phagocytes. The monocytes (in blood) and the macrophages found in connective
tissue, termed histolytic, are mobile, or wandering, phagocytes.
Monocytes and macrophages originate in the bone marrow.
Monocyts spend a few days in the blood and then enter tissues and change into
macrophages. Tissue macrophages are larger and more phagocytic than monocytes.
The functions of the macrophage system include recognition and phagocytes of foreign
material such as microorganisms, removal of old or damaged cells from circulation,
and participation in the immune system.
2.1.3. INFLAMMATORY RESPONSE
The inflammatory response is a sequential reaction to cell injury. It neutralizes and
dilutes the inflammatory agent, removes necrotic materials, and establishes an
environment suitable for healing and repair. The term inflammation is often but
incorrectly used as a synonym for the term infection. Inflammation is always present
with infection, but infection is not always present with inflammation. However, a
person who is neutropenic may not be able to mount an inflammatory response. An

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
infection involves invasion of tissues or cells by microorganisms such as bacteria,
fungi, and viruses. In contrast, inflammation can also be caused by nonliving agents
such as heat, radiation, trauma, and allergens.
The mechanism of inflammation is basically the same regardless of the injuring agent.
The intensity of the response depends on the extent and severity of injury and on the
reactive capacity of the injured person.
The inflammatory response can be divided in to:-
1) Vascular response,
2) Cellular response,
3) Formation of exudates
4) Healing.
1) VASCULAR RESPONSE
After cell injury, arterioles in the area briefly undergo transient vasoconstriction.
After release of histamine and other chemicals by the injured cells, the vessels
dilate. This vasodilatation results in hyperemia (increased blood flow in
the area), which raise filtration pressure. Vasodilatation and chemical mediators
cause endothelial cell retraction, which increases capillary permeability.
Movement of fluid from capillaries into tissue spaces is thus facilitated. Initially
composed of serous fluid, this inflammatory exudates later contains plasma
proteins, Primarily albumin. The proteins exert oncotic pressure that further draws
fluid from blood vessels. The tissue becomes edematous.
2)THE CELLULAR RESPONSE
This is characterized by extravasations of leucocytes from the lumen into
interstitial tissue followed by phagocytosis.
 Extravasations involve the following sequence of events: -
a) Margination
b) Transmigration across the endothelium to interstitical tissue (also called
diapedesis).

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Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
c) Migration in the interstitial tissues towards a chemotactic stimulus called
Chemotaxis.
a) Margination of leukocytes
 It is the adherence of leukocytes to the endothelial cells lining. Mainly to the
post Capillary venules.
b) Transmigration of leukocytes
 This is the movement of leukocytes by extending pseudopodia through the
vascular wall by a process called diapedesis.
 Leukocytes escape from venules and small veins but only occasionally from
capillaries.
c) Chemotaxis
 It is a unidirectional leukocyte attraction within tissue space guided by the
presence of bacteria and cellular debris.
 All granulocytes, monocytes and to a lesser extent lymphocytes respond to
chemotactic stimuli.
d) Phagocytosis
 Once the cell has reached to the site of injurious agent (in interstitial tissue)
phagocytosis ensues.
 Phagocytic cells include polymorphonuclear leukocytes (particularly
neutrophils), monocytes and tissue macrophages.
 Phagocytosis involves three distinct but interrelated steps:-
1. Recognition and attachment of the particle to be ingested by the leukocytes:
 Phagocytosis is enhanced if the material to be phagocyted is coated with
certain plasma proteins called opsonins.
2. Engulfment
 As a result of fusion between the phagosome and lysosom e , a
phagolysosome is formed and the engulfed particle is exposed to the
degradative lysosomal enzymes
3. Killing or degradation
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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
 The ultimate step in phagocytosis of bacteria (any foreign body) is killing
and degradation.
There are two forms of bacterial killing methods:
a. Oxygen independent mechanism:
 It is mediated by lysosomal enzymes (the primary and secondary granules)
of polymorphonuclear leukocytes.
b. Oxygen dependent killing of microbes:
 This is microbial killing by the generation of oxygen metabolites such as
super oxide, H2O2, HO-, etc.
Chemical mediators of inflammation
 Chemical mediators originate either from the plasma or from cells
(neutrophils, macrophages, lymphocytes, basophiles, mast cells and
platelets).
 Some of the chemical mediators of inflammation include histamine,
serotonin, lysosomal enzymes, prostaglandins, leukotriens, activated
oxygen species, nitric oxide, cytokines,
3) EXUDATES FORMATION
Exudates consist of fluid and leukocytes that move from the circulation to the site
of injury. The nature and quantity of exudates depend on the type and severity of
the injury and the tissues involved (see Table 2.3).
Table-2.3 TYPES OF INFLMMATIORY EXUDATE
TYPE DESCRIPTIN EXAMPLES
TYPE DESCRIPTIN EXAMPLES
Serous Serous exudates results from Skin blisters, pleural
outpouring of fluid that has low cell effusion
and protein content; it is seen in
early stages of inflammation or
when injury is mild

Catarrhal
Catarrhal exudates are found in Runny nose associated
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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
tissues where cells produce with URTI
mucus. Mucus production is
accelerated by inflammatory
response.

Fibrinous Furuncle(boil),abscess
Fibrinous exudates occur with cellulites ( diffuse
increasing vascular permeability inflammation in
and fibrinogen leakage into tissue connective tissue)
spaces.
Excessive amount of fibrin coating
tissue surfaces may cause them to
adhere. Hematoma
Hemorrhagic
Hemorrhagic exudates results from
rupture or necrosis of blood
vessels
walls; it consists of RBCs that
escape into tissue.
Clinical Manifestations of inflammations
The clinical manifestations of inflammation can be classified as
i. Local response to inflammation includes the manifestations of redeness, heat,
pain, swelling, and loss of function (see table 2.4).
ii. Systemic response to inflammations.
Table2.4 LOCAL MANIFESTATIONS OF INFLAMMATION
MANIFESTATIONS
1) Redness (rubor)
2) Heat (color)
3) Pain (dolor)
4) Swelling (tumor)
5) Loss of function
(function laesa)

Systemic manifestations of inflammation:-

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Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
Include leukocytosis with a shift to the left, malaise, nausea and anorexia,
Increased pulse and respiratory rate, and fever.
 Leukoctosis results from the increased release of leukoytes form the bone marrow.
An increase in the circulating number of one or more types of leukocytes may be
found. Inflammatory responses are accompanied by the vaguely defined
constitutional symptoms of malaise, nausea, anorexia, and fatigue.
The causes of these systemic changes are poorly understood but are probably due
to complement activation and the release of cytokines (soluble factors secreted by
WBCs that act as intercellular messengers) from stimulated WBCs.
Three of these cytokines, interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor
necrosis factor (TNF), are important in causing the constitutional manifestations
of inflammation, as well as inducing the production of fever.
An increase in pulse and respiration follows the rise in metabolism as a result of
an increase in body temperature.
 Fever
- The onset of fever is triggered by the release of cytokines. The most
potent of these cytokines are IL-1, IL- 6, and TNF (released from
mononuclear phagocytic cells).
- These cytokines cause fever by their ability to initiate metabolic changes
in the temperatureregulating center. The synthesis of prostaglandin E2
(PGE2) is the most critical metabolic change.
PGE2 acts directly to increase the thermostatic set point. The
hypothalamus then activates the sympathetic branch of the autonomic
nervous system to stimulate increased muscle tone and shivering and
decreased perspiration and blood flow to the periphery. Epinephrine
released from the adrenal medulla increases the metabolic rate.
The net result is fever.
- With the physiologic thermostat fixed at a higherthan –normal
temperature, the rate of heat production is increased until the body
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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
temperature reaches the new set point. As the set point is raised, the
hypothalamus signals and increases in heat production and conservation
to raise the body temperature to the new level. At this point the
individual feels chilled and shivers. The shivering response is the body’s
method of raising the body’s temperature until the new set point is
attained. This seeming paradox is dramatic: the body is hot yet an
individual piles on blankets and may go to bed to go warm. When the
circulating body temperature reaches the set point of the core body
temperature, the chills and warmth- seeking behavior cease.
The classifications of febrile response
 The febrile response is classified into four stages:
Prodromal, chill, flush and defervescence. (See Table2.5)

Table-2.5 STAGES OF THE FEBRILE RESPONSES

STAGE CHARACTERSTICS
Prodromal • Nonspecific complaints such as mild headache, fatigue, general
malaise, and muscle aches
Chill • Cutaneous vasoconstriction, “ goose pimples,” pale skin; feeling of
being cold; generalized shaking chill; shivering causing body to
reach new temperature set by control center in hypothalamus
Flush Sensation of warmth throughout body; cutaneous vasodilatation;
warming and flushing of the skin
Defervescence Sweating ; decrease in body temperature
The released cytokines and the fever they trigger activate the body’s defense
mechanisms. Beneficial aspects of fever include increased killing of
microorganisms, increased phagocytes by neutrohils, and increased proliferation of
T cells. Higher body temperature may also enhance the activity of interferon,
body’s natural virus- fighting substance.
Types of Inflammation

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
The basic types of inflammation are acute, sub- acute, and chronic.
 In acute inflammation the healing occurs in 3 to 3 weeks and usually leaves
no residual damage. Neutorphils are the predominate cell type at the site of
inflammation.
 A sub acute inflammation has the features of the acute process but lasts
longer. For example, infective endocarditic is a smoldering infection with
acute inflammation, but it persists throughout weeks or months.
 Chronic Inflammation lasts for weeks, months, or even years. The injurious
agent persists or repeatedly injures tissue. The predominate cell types at the
site of inflammation are lymphocytes and macrophages. Chronic
inflammatory process are debilitating and can be devastating. The
prolongation and chronicity of any inflammation may be the result of an
alteration in the immune response.
4) HEALING PROCESS
The final phase of the inflammatory response is healing.
Healing includes the two major components of regeneration and repair.
 Regeneration
is the replacement of lost cells and tissues with cells of the same type.
 Repair
is healing as a result of lost cells being replaced by connective tissue of
different origin. Repair is the more common type of healing and usually results
in scar formation.
Example of healing processes:-
A) Wound Healing
B) Fracture Healing

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬

Mechanism of respiration

PULMONARY CONGESTION
PATHOPHYSIOLOGY OF PULMONARY CONGESTION
Pulmonary congestion is defined as accumulation of fluid in the lungs, resulting in
impaired gas exchange and arterial hypoxemia.
It occurs sequentially, first developing in the hilar region of the lungs, followed by
filling of the interstitial space and finally, in its most severe form, by alveolar
flooding. High left ventricular (LV) filling pressure leading to pulmonary venous
hypertension (increased PCWP) is the main underlying mechanism of pulmonary
congestion. Elevation of LV diastolic pressure (LVDP) results from fluid overload
caused either by fluid retention or by fluid redistribution. On the other hand, a rapid
increase in blood pressure (afterload), particularly in patients with diastolic
dysfunction, may precipitate severe pulmonary congestion. Often, elevation of
LVDP (hemodynamic congestion) precedes clinical congestion by days or even
weeks.

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬

pulmonary edema
Pulmonary edema is a condition in which the lungs fill with fluid. It’s also known as
lung congestion, lung water, and pulmonary congestion. When pulmonary edema
occurs, the body struggles to get enough oxygen and you start to have shortness of
breath.
Causes of pulmonary edema
Congestive heart failure
The most common cause of pulmonary edema is congestive heart failure (CHF).
Heart failure happens when the heart can no longer pump blood properly
throughout the body. This creates a backup of pressure in the small blood vessels
of the lungs, which causes the vessels to leak fluid.
In a healthy body, the lungs will take oxygen from the air you breathe and put it into
the bloodstream. But when fluid fills your lungs, they cannot put oxygen into the
bloodstream. This deprives the rest of the body of oxygen.
Other medical conditions
Other less common medical conditions that can cause pulmonary edema include:
 heart attack, or other heart diseases
 leaking, narrowed, or damaged heart valves
 sudden high blood pressure
 pneumonia
 kidney failure
 lung damage caused by severe infection
 severe sepsis of the blood, or blood poisoning caused by infection
External factors
Some external factors can also put extra pressure on the heart and lungs and
cause pulmonary edema. These outside factors are:
 high altitude exposure
 illicit drug use or drug overdose

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
 lung damage caused by inhalation of toxins
 severe trauma
 major injury
 near drowning
Symptoms of pulmonary edema
In cases of pulmonary edema, your body will struggle to gain oxygen. This is due to
the amount of increasing fluid in the lungs preventing oxygen moving into the
bloodstream. Symptoms may continue to worsen until you get treatment.
Symptoms depend on the type of pulmonary edema.
Long-term pulmonary edema
The symptoms for long-term pulmonary edema include:
 shortness of breath when being physically active
 difficulty breathing when lying down
 wheezing
 waking up at night with a breathless feeling that goes away when you sit up
 rapid weight gain, especially in the legs
 swelling in the lower part of the body
 fatigue
High-altitude pulmonary edema
Pulmonary edema due to altitude sickness, or not getting enough oxygen in the air,
will have symptoms that include:
 headaches
 irregular, rapid heartbeat
 shortness of breath after exertion and during rest
 coughing
 fever
 difficulty walking uphill and on flat surfaces
Diagnosis of pulmonary edema

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
They will perform a basic physical examination and listen to your lungs with a
stethoscope, looking for:
 an increased heart rate
 rapid breathing
 a crackling sound from your lungs
 any abnormal heart sounds
Examples of tests used in diagnosing pulmonary edema include:
 complete blood count
 echocardiogram, or an ultrasound, to check for abnormal heart activity
 chest X-ray to see fluid
 blood tests to check oxygen levels
 electrocardiogram (ECG) to look for heart rhythm problems or signs of a heart
attack
Risk factors of pulmonary edema
People with heart problems or heart failure are the most at risk for pulmonary
edema. Other factors that may put a person at risk include:
 history of pulmonary edema.
 history of lung disease, such as tuberculosis or chronic obstructive pulmonary
disorder (COPD).
 vascular (blood) disorders.

Orthopnea
It comes from the Greek words “ortho,” which means straight or vertical, and
“pnea,” which means “to breathe.”
Orthopnea is shortness of breath or difficulty breathing when you’re lying down.
It should improve once you sit up or stand.
In most cases, orthopnea is a sign of heart failure.
Orthopnea is different from dyspnea, which is difficulty breathing during non-
strenuous activities.

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
Other variations on this symptom include:
 Platypnea. This disorder causes shortness of breath when you stand.
 Trepopnea. This disorder causes shortness of breath when you lie on your
side.
Orthopnea is a symptom. You’ll feel short of breath when you lie down.
Sitting propped up on one or more pillows can improve your breathing.
For example, “three pillow orthopnea” means your orthopnea is very severe.
The medical term for shortness of breath is dyspnea. Orthopnea is a type of
dyspnea that only occurs when a person is lying down.
People often describe orthopnea as a sensation of tightness in the chest that
makes breathing difficult or uncomfortable. Some individuals may also experience
chest pain.
Causes
Orthopnea is caused by increased pressure in the blood vessels of your lungs.
When you lie down, blood flows from your legs back to the heart and then to your
lungs.
But if you have heart disease or heart failure, your heart may not be strong enough
to pump the extra blood back out of the heart. This can increase the pressure in the
veins and capillaries inside your lungs, causing fluid to leak out into the lungs. The
extra fluid is what makes it hard to breathe.
Other possible causes of orthopnea include:
 excess fluid in the lungs (pulmonary edema)
 severe pneumonia
 obesity
 fluid buildup around the lung (pleural effusion)
 fluid buildup in the abdomen (ascites)
 diaphragm paralysis
Diagnosis
Depending on the suspected cause recommend one or more of the following tests:

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
 X-ray or CT scan of the chest. These tests create an image of the inside of
the chest, which allows the doctor to see if there are any problems with the
lungs or heart.
 Electrocardiogram (ECG). This test involves placing sensors on a person’s
skin to measure electrical signals from the heart. Doctors use an ECG to
check the functioning of the heart.
 Echocardiogram. Also known as an “echo,” this is a type of ultrasound
scan that uses sound waves to create an image of the heart. Doctors use this
test to check for any problems with this organ.
 Pulmonary function tests. These tests include spirometry, which involves
breathing into a machine. A doctor can use the results to determine how well
the lungs are functioning.
 Arterial blood gas. This is a type of blood test that checks whether a person
is getting enough oxygen.
 Blood tests. These involve taking a small sample of a person’s blood, and
doctors use them to check for signs of a wide range of conditions.
Associated conditions
Orthopnea can be a sign of several different medical conditions, including:
- Heart failure
- Chronic obstructive pulmonary disease (COPD)
- Pulmonary edema

dyspnea
Dyspnea is the medical term for shortness of breath, sometimes described as “air
hunger.” It is an uncomfortable feeling.
Shortness of breath can range from mild and temporary to serious and long-lasting.
It is sometimes difficult to diagnose and treat dyspnea because there can be many
different causes.

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
A person can feel short of breath after intense exercise, when traveling to a high
altitude, or going through major temperature changes. However, dyspnea usually
relates to health problems. Sometimes, it is just a case of being out of shape, and
exercise can improve symptoms. But dyspnea can be a sign of a serious health
issue.
Symptoms
Dyspnea can happen as a result of overexertion, spending time at high altitude, or
as a symptom of a range of conditions.
Signs that a person is experiencing dyspnea include:
 shortness of breath after exertion or due to a medical condition
 feeling smothered or suffocated as a result of breathing difficulties
 labored breathing
 tightness in the chest
 rapid, shallow breathing
 heart palpitations
 wheezing
 coughing
If dyspnea occurs suddenly or if symptoms are severe, it may be a sign of a serious
medical condition.
Causes
An episode of dyspnea is not always directly related to an individual’s health.
If shortness of breath starts suddenly, it is called an acute case of dyspnea.
Acute dyspnea could be due to:
 asthma
 anxiety
 pneumonia
 choking on or inhaling something that blocks breathing passageways
 allergic reactions
 anemia

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 serious loss of blood, resulting in anemia
 exposure to dangerous levels of carbon monoxide
 heart failure
 hypotension, which is low blood pressure
 pulmonary embolism, which is a blood clot in an artery to the lung
 collapsed lung
 hiatal hernia
Dyspnea is also common among people with a terminal illness.
If a person experiences shortness of breath for over a month, the condition is called
chronic dyspnea.
Chronic dyspnea could be due to:
 asthma
 COPD
 heart problems
 obesity
 interstitial pulmonary fibrosis, a disease that causes scarring of the lung tissue
Some additional lung conditions may also cause shortness of breath.
Examples are:
 croup
 traumatic lung injury
 lung cancer
 tuberculosis
 pleurisy, an inflammation in the tissues surrounding the lungs
 pulmonary edema, when too much fluid collects in the lungs
 pulmonary hypertension, when the blood pressure in the arteries to the lungs
rises
 sarcoidosis, when clusters of inflammatory cells grow in the lungs
Shortness of breath has also been linked to the following heart problems:
 cardiomyopathy, a range of diseases affecting the heart muscle

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 heart rhythm problems
 heart failure
 pericarditis, when the tissue that surrounds the heart becomes inflamed
Complications
Dyspnea can be associated with hypoxia or hypoxemia, which is a low blood
oxygen levels. This can lead to a decreased level of consciousness and other
severe symptoms.
If dyspnea is severe and continues for some time, there is a risk of either temporary
or permanent cognitive impairment.
It can also be a sign of an onset or worsening of other medical problems.
Diagnosis
diagnose dyspnea based on a complete physical examination of the person, along
with a full description of their experiences, .
- chest X-rays
- computed tomography (CT) images
- electrocardiogram (ECG)
- Spirometry tests to measure airflow and the patient’s lung capacity.

CYANOSIS
Cyanosis is the abnormal blue discolouration of the skin and mucous membranes
caused by an increased concentration of deoxygenated haemoglobin in the
capillary bed.
Central Cyanosis
In central cyanosis there is systemic hypoxia and therefore cyanosis is visible
throughout the body including the tongue, lips and mucous membranes.
Central cyanosis usually develops when SpO2 is less than 85%.
Peripheral Cyanosis

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In peripheral cyanosis systemic arterial oxygen saturation is normal but there is
slow movement of blood through the capillary bed resulting in increased extraction
of oxygen from the blood. Vasoconstriction, venous obstruction and low cardiac
output are all causes. Cyanosis will be seen in the affected regions only and will not
be seen in the tongue, lips and mucous membranes.
PATHOPHYSIOLOGY
In order for circulating blood to appear blue, it requires an elevated amount of blue
pigment to accumulate. Central cyanosis is generally of greater concern, as it
requires reduced arterial oxygen saturation (PaO2) or abnormal hemoglobin
derivatives to be present (methemoglobin or sulf hemoglobin), and is generally a
relatively late finding in the course of illness. The increased amount of
deoxygenated hemoglobin is due to either an increased amount of venous
admixture (due to vasodilatory effects on the venous plexi) or by reduced arterial
oxygen tension in the capillaries. In central cyanosis, either SaO2 is reduced or
abnormal (nonfunctional) hemoglobin is present, which is why central structures
and mucosae are affected; this is in contrast to peripheral cyanosis, where there is
a normal SaO2 but increased extraction of oxygen in the setting of peripheral
vasoconstriction and thus, decreased peripheral blood flow.
Causes of Cyanosis
Central Cyanosis Peripheral Cyanosis
Severe respiratory illness Reduced cardiac output (shock/heart failure)
Congenital cyanotic heart disease Peripheral arterial disease
Eisenmenger’s syndrome Cold exposure
Airway obstruction Raynaud’s phenomenon
High altitude Venous obstruction
Methaemoglobinaemia Acrocyanosis

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Acrocyanosis
Acrocyanosis: a cause of peripheral cyanosis affecting the hands, feet and
circumoral region due to benign vasomotor changes. It does not affect the mucous
membranes and this differentiates it from central cyanosis.
Methaemoglobinaemia Methaemoglobin is an altered state of haemoglobin in which
Fe2+ in haem is oxidised to Fe3+. Fe3+ is unable to bind to oxygen and the oxygen
carrying-capacity of the blood is reduced. It is caused by congenital genetic
abnormalities or acquired through oxidative stress from drugs or toxins.

Symptoms become more severe with the degree of methaemoglobinaemia and

result from reduced oxygen delivery to the tissues. Headache, fatigue, SOB and
lethargy may progress to altered consciousness, end-organ damage and seizure.
Suspect methaemoglobinaemia when central cyanosis is present but normal PaO2
is seen on arterial blood gas (PaO2 represents dissolved O2 in the plasma rather
than O2 bound to haemoglobin). Methaemoglobin is also measured by the blood
gas machine and will be elevated. SpO2 may be low but rarely to the level required
to cause central cyanosis.

Treat symptomatic patients with high-flow oxygen and methylene blue 1-2mg/kg IV.
Methylene blue encourages reduction of iron in methaemoglobin by providing an
artificial electron receptor.

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Mechanism of digestion and absorption

Mechanism of Nausea and Vomiting

vomiting
Nausea and vomiting are basic human protective reflexes against the absorption of
toxins, as well as responses to certain stimuli.
Vomiting is the means by which the upper gastrointestinal tract rids itself of its
contents when almost any part of the upper tract becomes excessively irritated,
overdistended, or even overexcitable.
Nausea which is often a prodrome of vomiting, and is the conscious recognition of
subconscious excitation in an area of the medulla closely associated with or part of
the vomiting center.
Etiology
The main etiologies for nausea and vomiting include iatrogenic, that is almost any
medication that can cause nausea and vomiting, such as, chemotherapeutic
agents.
Toxic infectious causes, which is mainly caused by ingestion of a toxin.
The other causes contain gastrointestinal disorders, central nervous system or
psychiatric conditions, and some conditions caused by metabolism such as
Pregnancy, which is the most common endocrinologic cause of nausea and
vomiting.
Pathophysiology
There are many conditions out there that cause nausea and vomiting, but we know
that there are at least three kinds of nausea and vomiting, the first of which has
been attributed to anaesthetics such as ether, the second to reflex responses, the
last to opioids.
Nausea and vomiting occurs via different mechanisms and pathways.

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The afferent and efferent reflexes involved in nausea and vomiting are integrated
with two distinct centers at brainstem level, which are the vomiting center, where it
is proposed that, it is multiple distributed nuclei located in the medulla, that contain
histamine (H1), acetylcholine (ACh) and 5hydroxytryptamine2 (5HT2) receptors,
however, it is now thought that an anatomically discrete vomiting center is unlikely
to exist, as proposed nearly 60 years ago by Wang and Borison. Rather, a number
of loosely organized neuronal areas within the medulla probably interact to
coordinate the emetic reflex, and the neurons coordinating the complex series of
events that occur during emesis have been termed the “central pattern generator”.6
And the second center is chemoreceptor trigger zone (CTZ), which is located
bilaterally on the floor of the fourth ventricle in area postrema near the obex, where
this part has no blood-brain barrier and may be accessible to humoral stimuli in
either blood or cerebrospinal fluid, so various drugs, toxins and metabolites can
access it, and has dopamine (D2), 5HT3 and Neurokinin-1 receptors. The vomiting
center receives afferent stimulation via the CTZ, the cerebral cortex, and the
vestibular system, and peripheral stimulation via the vagal and sympathetic nerves
which, in turn, leads to emesis.
Once the vomiting center stimulated, the vomiting reflex occurs which is divided into
two phases:
(1) Pre-ejection phase, which is characterized by a sensation of nausea associated
with cold, sweating, pupil dilatation, salivation and tachycardia mediated by
sympathetic and parasympathetic nerves,
(2) Ejection phase, where it comprises of retching and vomiting with expulsion of
gastric contents.
Nausea Which is the prodrome of vomiting, is excitation of part of the medulla that
is closely associated with vomiting center, which can be caused by
(1) irritative impulses coming from the gastrointestinal tract,
(2) impulses that originate in the lower brain associated with motion sickness,

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(3) impulses from the cerebral cortex to initiate vomiting. But it doesn’t mean that
Nausea and Vomiting are coupled together, because vomiting can occasionally
occur without the prodromal sensation of nausea, indicating that only certain
portions of the vomiting center area associated with the sensation of nausea.
Vomiting usually starts with salivation and the sensation of nausea, and the
vomiting reflex occurs only when through stimulation of the vomiting center.
There are several ways that vomiting center is stimulated, the First way is when the
stomach and the upper portions of the small intestine faces irritation, excessive
distention or overexcitation, it causes antiperistalisis -the prelude of vomiting-, often
appears many minutes before vomiting, which is peristalsis up the digestive tract
rather than downward. This may begin as far down in the intestinal tract as the
ileum, and the antiperistaltic wave travels backward up the intestine at a rate of 2 to
3 cm/sec; this process can actually push a large share of the lower small intestine
contents all the way back to the duodenum and stomach within 3 to 5 minutes.
Then, as these upper portions of the gastrointestinal tract, especially the
duodenum, become overly distended, this distention becomes the exciting factor
and an impulse is formed by stimulation of H1 and ACh receptors, leading to an
afferent stimulus that terminates in the brain stem by both vagal and sympathetic
afferent nerve fibers, primarily in the nucleus tractus solitarius, and subsequently
activates the vomiting center, which is shown in figure (1).
The emetic stimuli in gut are detected by two types of vagal afferent fibres,
mechanoreceptors and chemoreceptors, and the abdominal vagal afferents appear
to have the greatest relevance for chemotherapy-induced nausea and vomiting, and
post-operative nausea and vomiting.
Second way is arising nervous signals in chemoreceptor trigger zone. Electrical
stimulation and administration of certain drugs, including apomorphine, morphine,
and some digitalis derivatives, can directly stimulate this chemoreceptor trigger
zone and in return stimulating Vomiting center, as shown in figure(1). Destruction of

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this area blocks this type of vomiting but does not block vomiting resulting from
irritative stimuli in the gastrointestinal tract itself.

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Third way, is through stimulation of Ach or H1 receptors in the vestibular labyrinth of
the inner ear, when direction or rhythm of motion of the body is changed, which
then transmitted to vestibular nuclei that mediates the nausea and vomiting of
motion sickness, from there, it is transmitted into the cerebellum, then to the
chemoreceptor trigger zone, and finally to the vomiting center to cause vomiting.
Fourth way is stimulation of the Vomiting Center from higher centers of the brain.
When a stimulation is formed from the diencephalon, limbic system and cerebral
cortex, then transmitted to the cortical center, after that to vomiting center to cause
vomiting. Because emetic responses to emotionally charged stimuli such as
nauseating smells, sickening sights and pain occur. In addition to the pathways
already described, when there is raised intracranial pressure cerebral histamine
receptors may be stimulated and meningeal mechanoreceptors stimulate the
vomiting center. Also vestibular cardiac afferent induce nausea and vomiting as in
MI, and pharyngeal stimulation may induce nausea and vomiting, too. Figure (2)
demonstrates the most of the pathways for the stimulation of the vomiting center,
which we talked about before.
Once the vomiting center has been sufficiently stimulated and the vomiting act
instituted, the vomiting act takes place, where motor impulses that cause the actual
vomiting are transmitted from the vomiting center by way of the 5th, 7th, 9th, 10th,
and 12th cranial nerves to the upper gastrointestinal tract, through vagal and
sympathetic nerves to the lower tract, and through spinal nerves to the diaphragm
and abdominal muscles, which cause the following effects that are

(1) a deep breath,

(2) raising of the hyoid bone and larynx to pull the upper esophageal sphincter
open,
(3) closing of the glottis to prevent vomitus flow into the lungs,
(4) lifting of the soft palate to close the posterior nares. Also Serotonin (5-HT)
released from enterochromaffin cells in the small intestine that initiate impulses via
5-HT 3 receptors trigger vomiting, where reverse peristalsis empties material from
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the upper part of the small intestine into the stomach, and it causes distention of the
stomach, which means further stimulation of the vomiting center. Next comes a
strong downward contraction of the diaphragm along with simultaneous contraction
of all the abdominal wall muscles, along with partial relaxation of the esophageal-
stomach sphincter, thus allowing vomitus to begin moving from the stomach into the
esophagus. This squeezes the stomach between the diaphragm and the abdominal
muscles, building the intragastric pressure to a high level. Finally, the lower
esophageal sphincter relaxes completely, allowing expulsion of the gastric contents
upward through the esophagus, then the vomitus is expelled to the exterior easily.
1, 4,6,8 The vomiting act is simply shown in Figure (3). 7

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Anorexia (Loss of Appetite)

Anorexia is a general loss of appetite or a loss of interest in food.
When some people hear the word “anorexia,” they think of the eating
disorder anorexia nervosa. But there are differences between the two.
Anorexia nervosa doesn’t cause loss of appetite. People with anorexia nervosa
purposely avoid food to prevent weight gain. People who suffer from anorexia (loss
of appetite) unintentionally lose interest in food. Loss of appetite is often caused by
an underlying medical condition.

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Causes of loss of appetite
Since anorexia is often a symptom of a medical problem, Common causes of loss
of appetite can include the following:
- Depression
During episodes of depression, a person may lose interest in food or forget to eat.
This can lead to weight loss and malnourishment. The actual cause of loss of
appetite is not known. Sometimes, people with depression can overeat.
- Cancer
Advanced cancer can cause loss of appetite, so it’s not uncommon for people with
end-stage cancer to decline food. As the disease progresses, the body of a person
with end-stage cancer begins to conserve energy. Since their body is unable to use
food and fluids properly, loss of appetite typically occurs as the end of life
approaches. If you’re a caregiver, don’t be overly concerned if a loved one chooses
not to eat, or only prefers liquids such as ice cream and milkshakes.
Side effects caused by some cancer treatments (radiation and chemotherapy) can
also affect appetite. People who receive these treatments may lose their appetite if
they experience nausea, difficulty swallowing, difficulty chewing, and mouth sores.
- Hepatitis C
Hepatitis C is a liver infection that spreads from person to person through contact
with infected blood. This infection is caused by the hepatitis C virus. If left
untreated, it can cause liver damage. Advanced liver damage can cause nausea
and vomiting, which affects appetite. If you experience loss of appetite, your doctor
can order blood work to check for the hepatitis C virus. Other types of hepatitis can
also cause loss of appetite in the same way.
- Kidney failure
People with kidney failure will often have a condition called uremia, which means
there is excess protein in the blood. This protein would normally be flushed out in
the urine, however, the damaged kidneys are unable to filter it properly. Uremia can
cause people with kidney failure to feel nauseated, and not want to eat. Sometimes

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food will taste different. Some will find that the foods they once enjoyed no longer
appeal to them.
- Heart failure
People with heart failure may also experience loss of appetite. This is because you
have less blood flow to the digestive system, causing problems with digestion. This
can make it uncomfortable and unappealing to eat.
- HIV/AIDS
Loss of appetite is also a common symptom of HIV/AIDS. There are different
reasons for loss of appetite with HIV and AIDS. Both can cause painful sores on the
mouth and tongue. Because of pain, some people reduce their food intake or
completely lose the desire to eat.
Nausea caused by AIDS and HIV can also affect appetite. Nausea can also be a
side effect of a medication used to treat HIV and AIDS. Talk to your doctor if you
develop nausea or loss of appetite after beginning treatment. Your doctor may
prescribe a separate medication to help you cope with nausea.
- Alzheimer’s disease
In addition to other symptoms, some people with Alzheimer’s disease (AD) also
experience loss of appetite. Loss of appetite in people with AD has several possible
explanations. Some people with AD battle depression which causes them to lose
interest in food. This disease can also make it difficult for people to communicate
pain. As a result, those who experience oral pain or difficulty swallowing may lose
interest in food.
Decreased appetite is also common with AD because the disease damages the
hypothalamus, which is the area of the brain that regulates hunger and appetite. A
change in appetite may start to develop years before a diagnosis, and become
more apparent after a diagnosis.
Loss of appetite can also occur if a person with AD isn’t active or doesn’t burn
enough calories throughout the day.

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Diarrhea
Pathophysiology of Diarrhea
Diarrhea is an increase in the volume of stool or frequency of defecation. It is one of
the most common clinical signs of gastrointestinal disease, but also can reflect
primary disorders outside of the digestive system. Certainly, disorders affecting
either the small or large bowel can lead to diarrhea.

For many people, diarrhea represents an occasional inconvenience or annoyance,

yet at least 2 million people in the world, mostly children, die from the
consequences of diarrhea each year.

There are numerous causes of diarrhea, but in almost all cases, this disorder is a
manifestation of one of the four basic mechanisms described below. It is also
common for more than one of the four mechanisms to be involved in the
pathogenesis of a given case.

Osmotic Diarrhea

Absorption of water in the intestines is dependent on adequate absorption of

solutes. If excessive amounts of solutes are retained in the intestinal lumen, water
will not be absorbed and diarrhea will result. Osmotic diarrhea typically results from
one of two situations:

 Ingestion of a poorly absorbed substrate: The offending molecule is usually a

carbohydrate or divalent ion. Common examples include mannitol or sorbitol,
epson salt (MgSO4) and some antacids (MgOH2).

 Malabsorption: Inability to absorb certain carbohydrates is the most common

deficit in this category of diarrhea, but it can result virtually any type of
malabsorption. A common example of malabsorption, afflicting many adults
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humans and pets is lactose intolerance resulting from a deficiency in
the brush border enzyme lactase. In such cases, a moderate quantity of
lactose is consumed (usually as milk), but the intestinal epithelium is deficient
in lactase, and lactose cannot be effectively hydrolyzed into glucose and
galactose for absorption. The osmotically-active lactose is retained in the
intestinal lumen, where it "holds" water. To add insult to injury, the
unabsorbed lactose passes into the large intestine where it is fermented by
colonic bacteria, resulting in production of excessive gas.

A distinguishing feature of osmotic diarrhea is that it stops after the patient is fasted
or stops consuming the poorly absorbed solute.

Secretory Diarrhea

Large volumes of water are normally secreted into the small intestinal lumen, but a
large majority of this water is efficienty absorbed before reaching the large intestine.
Diarrhea occurs when secretion of water into the intestinal lumen exceeds
absorption.

Many millions of people have died of the secretory diarrhea associated with
cholera. The responsible organism, Vibrio cholerae, produces cholera toxin, which
strongly activates adenylyl cyclase, causing a prolonged increase in intracellular
concentration of cyclic AMP within crypt enterocytes. This change results in
prolonged opening of the chloride channels that are instrumental in secretion of
water from the crypts, allowing uncontrolled secretion of water. Additionally, cholera
toxin affects the enteric nervous system, resulting in an independent stimulus of
secretion.

Exposure to toxins from several other types of bacteria (e.g. E. coli heat-labile toxin)
induce the same series of steps and massive secretory diarrhea that is often lethal
unless the person or animal is aggressively treated to maintain hydration.

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In addition to bacterial toxins, a large number of other agents can induce secretory
diarrhea by turning on the intestinal secretory machinery, including:

 some laxatives

 hormones secreted by certain types of tumors (e.g. vasoactive intestinal

peptide)

 a broad range of drugs (e.g. some types of asthma medications,

antidepressants, cardiac drugs)

 certain metals, organic toxins, and plant products (e.g. arsenic, insecticides,
mushroom toxins, caffeine)

In most cases, secretory diarrheas will not resolve during a 2-3 day fast.

Inflammatory and Infectious Diarrhea

The epithelium of the digestive tube is protected from insult by a number of

mechanisms constituting the gastrointestinal barrier, but like many barriers, it can
be breached. Disruption of the epithelium of the intestine due to microbial or viral
pathogens is a very common cause of diarrhea in all species. Destruction of the
epithelium results not only in exudation of serum and blood into the lumen but often
is associated with widespread destruction of absorptive epithelium. In such cases,
absorption of water occurs very inefficiently and diarrhea results. Examples of
pathogens frequently associated with infectious diarrhea include:

 Bacteria: Salmonella, E. coli, Campylobacter

 Viruses: rotaviruses, coronaviruses, parvoviruses (canine and feline),

norovirus

 Protozoa: coccidia species, Cryptosporium, Giardia

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The immune response to inflammatory conditions in the bowel contributes
substantively to development of diarrhea. Activation of white blood cells leads them
to secrete inflammatory mediators and cytokines which can stimulate secretion, in
effect imposing a secretory component on top of an inflammatory diarrhea.
Reactive oxygen species from leukocytes can damage or kill intestinal epithelial
cells, which are replaced with immature cells that typically are deficient in the brush
border enyzmes and transporters necessary for absorption of nutrients and water.
In this way, components of an osmotic (malabsorption) diarrhea are added to the
problem.

Diarrhea Associated with Deranged Motility

In order for nutrients and water to be efficiently absorbed, the intestinal contents
must be adequately exposed to the mucosal epithelium and retained long enough
to allow absorption. Disorders in motility than accelerate transit time could decrease
absorption, resulting in diarrhea even if the absorptive process per se was
proceeding properly.

Alterations in intestinal motility (usually increased propulsion) are observed in many

types of diarrhea. What is not usally clear, and very difficult to demonstrate, is
whether primary alterations in motility are actually the cause of diarrhea or simply
an effect.

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Cardiac Arrest
Cardiac arrest is the cessation of cardiac mechanical activity resulting in the
absence of circulating blood flow.
Cardiac arrest stops blood from flowing to vital organs, depriving them of oxygen,
and, if left untreated, results in death. Sudden cardiac arrest is the unexpected
cessation of circulation within a short period of symptom onset (sometimes without
warning). Sudden cardiac arrest occurs outside the hospital in more than 350,000
people/year in the US, with a 90% mortality.
Respiratory arrest and cardiac arrest are distinct, but without treatment, one
inevitably leads to the other. (See also respiratory failure, dyspnea, and hypoxia.)
(See also the American Heart Association's 2018 update of heart disease and
stroke statistics for out-of-hospital and in-hospital cardiac arrest.)
Etiology
In adults, sudden cardiac arrest results primarily from cardiac disease (of all
types, but especially coronary artery disease). In a significant percentage of
patients, sudden cardiac arrest is the first manifestation of heart disease. Other
causes include circulatory shock due to noncardiac disorders
(especially pulmonary embolism, gastrointestinal hemorrhage, or trauma),
ventilatory failure, and metabolic disturbance (including drug overdose).
In infants and children, cardiac causes of sudden cardiac arrest are less
common than in adults. The predominant cause of sudden cardiac arrest in infants
and children is respiratory failure due to various respiratory disorders (eg, airway
obstruction, smoke inhalation, drowning, infection, sudden infant death syndrome
[SIDS]). Other causes of sudden cardiac arrest include trauma and poisoning.
Pathophysiology

Cardiac arrest causes global ischemia with consequences at the cellular level that
adversely affect organ function after resuscitation. The main consequences
involve direct cellular damage and edema formation. Edema is particularly harmful
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in the brain, which has minimal room to expand, and often results in increased
intracranial pressure and corresponding decreased cerebral perfusion
postresuscitation. A significant proportion of successfully resuscitated patients
have short-term or long-term cerebral dysfunction manifested by altered alertness
(from mild confusion to coma), seizures, or both.
Decreased adenosine triphosphate (ATP) production leads to loss of membrane
integrity with efflux of potassium and influx of sodium and calcium. Excess sodium
causes cellular edema. Excess calcium damages mitochondria (depressing ATP
production), increases nitric oxide production (leading to formation of damaging
free radicals), and, in certain circumstances, activates proteases that further
damage cells.
Abnormal ion flux also results in depolarization of neurons, releasing
neurotransmitters, some of which are damaging (eg, glutamate activates a specific
calcium channel, worsening intracellular calcium overload).
Inflammatory mediators (eg, interleukin-1B, tumor necrosis factor-alpha) are
elaborated; some of them may cause microvascular thrombosis and loss of
vascular integrity with further edema formation. Some mediators trigger apoptosis,
resulting in accelerated cell death.
Symptoms and Signs

In critically or terminally ill patients, cardiac arrest is often preceded by a period of

clinical deterioration with rapid, shallow breathing, arterial hypotension, and a
progressive decrease in mental alertness. In sudden cardiac arrest, collapse
occurs without warning, occasionally accompanied by a brief (< 5 seconds)
seizure.
Diagnosis

 Clinical evaluation
 Cardiac monitor and electrocardiography (ECG)

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 Sometimes testing for cause (eg, echocardiography, chest x-ray, or chest
ultrasonography)

arrhythmia
DEFINITION •
The term "arrhythmia" refers to any change from the normal sequence of electrical
impulses. The electrical impulses may happen too fast, too slowly, or erratically –
causing the heart to beat too fast, too slowly, or erratically. When the heart doesn't
beat properly, it can't pump blood effectively.
ABNORMAL RHYTHM
CAN BE OF TWO EXTREME FORMS
1. Bradycardia - Cardiac beats below 60 beats per minute .
2. Tachycardia – Cardiac beat above 100 beats per minute.
ETIOLOGY
- Coronary artery disease.
- Electrolyte imbalances in your blood (such as sodium or potassium).
- Changes in your heart muscle.
- Injury from a heart attack.
- Healing process after heart surgery.
- Irregular heart rhythms can also occur in "normal, healthy" hearts.
- Ischemic Heart Disease
- Drugs related
- Others
Arrhythmia Presentation
(SYMPTOMS)
Palpitation.
Dizziness.
Chest Pain.
Dyspnea.
Fainting.
Sudden cardiac death
Swelling
Shortness of Breath
Exercise Intolerance

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Mechanism of Arrhythmias
Bradycardia
1. SA node : Slowed / Absent
Causes
• Decreased Sympathetic Signals
• Increased Parasympathetic Signals
• SA node Damage

2. Blockage of Conduction from SA node

AV node Blockage
Causes
• Ischemia
• Fibrosis
• Viral Infection
RESULTS in HEART ATTACK

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬

LEFT BUNDLE BRUNCH BLOCK (LBBB)

• No Impulse conduction through Bundle Brunch
• Action Potential transferred through Right Ventricle to Left Ventricle
RESULTS in Wide QRS complex

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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬

Tachycardia
1. Increased Pacemaker Activity (SA Node)- Sinus Tachycardia
Causes
• Increased Sympathetic Signals
• Decreased Parasympathetic Signals
• SA node Dysfunction
Example : Sick Sinus Syndrome

2.Re-entry Tachycardias
Atrial Fibrillation

• loss of the normal organised propagation of electrical activity

• atria fibrillate, they no longer contract in a mechanically useful way
• a degree of stasis to blood flow and predisposing to clot (thrombus)
formation within the chambers
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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
Ventricular Fibrillation

• Uncoordinated contraction of the Cardiac Muscle

• Quiver rather than contract properly
• Commonly identified arrhythmia in Cardiac Arrest patients
• As a consequence, Sudden Cardiac Death.

Wolf Parkinson White Syndrome (WPW)

• WPW is caused by the presence of an abnormal accessory electrical

conduction pathway between the atria and the ventricles.
• Electrical Signals through abnormal pathway stimulate the ventricles to
contract prematurely
• A unique type of supraventricular tachycardia referred to as an
”atrioventricular reciprocating tachycardia”.
Atrioventricular nodal re-entrant tachycardia
• Most common regular supraventricular tachycardia
• Re-entry circuit forms within or just next to the atrioventricular node.
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 Pathology theory ) ‫علم األمراض نظري مستوى ثانً (تمرٌض‬
• Same as WPW except reentry is in or around AV node

3. Delayed Repolarization

Causes
• Ischemia
• Drugs related (Potassium Blockers)
• Electrolyte Imbalance

Effects
Long QT interval
R on T Phenomenon
Premature Ventricular Beat
Ventricular Fibrillation
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‫‪Pathology theory‬‬ ‫علم األمراض نظري مستوى ثانً (تمرٌض )‬

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