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![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() | ![]() يوم الصحة العالمي – 7 نيسان/ أبريل 2013 ![]() يُحتفل بيوم الصحة العالمي في السابع من نيسان/ أبريل من كل عام بمناسبة الذكرى السنوية لتأسيس منظمة الصحة العالمية في عام 1948. ويُختار في كل عام موضوع ليوم الصحة العالمي يسلط الضوء على أحد المجالات ذات الأولوية والمثيرة للقلق على ساحة الصحة العمومية في العالم. والموضوع الرئيسي ليوم الصحة العالمي هذا العام هو ارتفاع ضغط الدم. عن ارتفاع ضغط الدم يؤدي ارتفاع ضغط الدم إلى زيادة مخاطر الإصابة بالنوبات القلبية والسكتات الدماغية والفشل الكلوي، وإذا تُرك دون سيطرة يمكن أن يسبب العمى وعدم انتظام ضربات القلب وقصور القلب. ويزداد احتمال حدوث هذه المضاعفات في حالة وجود أي من عوامل الخطر الأخرى المسببة لأمراض القلب والأوعية الدموية، مثل داء السكري. ويعاني واحد من كل ثلاثة بالغين على مستوى العالم من ارتفاع ضغط الدم. وتتزايد هذه النسبة مع التقدم في العمر، حيث تبدأ بواحد من كل عشرة أشخاص في العشرينات والثلاثينات من أعمارهم وترتفع إلى خمسة من كل عشرة أشخاص في الخمسينات من أعمارهم. وسُجلت أعلى معدلات انتشار مرض ارتفاع ضغط الدم في بعض البلدان المنخفضة الدخل في أفريقيا، حيث يُعتقد أن أكثر من 40٪ من البالغين في بلدان أفريقية عديدة يعانون من هذه الحالة. بيد أنه يمكن الوقاية والعلاج من ارتفاع ضغط الدم. فقد أثمر النجاح في الوقاية والعلاج من هذا الاعتلال، إلى جانب عوامل خطر أخرى مسببة لأمراض القلب والأوعية الدموية، عن خفض عدد الوفيات الناجمة عن أمراض القلب في بعض البلدان المتقدمة. ويمكن الحد من مخاطر الإصابة بارتفاع ضغط الدم عن طريق ما يلي:
الهدف النهائي ليوم الصحة العالمي 2013 هو خفض معدلات الإصابة بالنوبات القلبية والسكتات الدماغية. والأهداف المحددة للحملة هي:
بسمه تعالى المصدر: منتديات بني بحير بلقرن hgd,l hguhgld ggwpm - fpe w,v t]d, (hvjthu qy' hg]l ) 1434iJ -2013 2013 gg.dj hvjthu jpj |
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![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() | ![]() What is high blood pressure? High blood pressure (HBP) or hypertension means high pressure (tension) in the arteries. . High blood pressure does not mean excessive emotional tension, although emotional tension and stress can temporarily increase blood pressure. Normal blood pressure is below 120/80; blood pressure between 120/80 and 139/89 is called "pre-hypertension", and a blood pressure of 140/90 or above is considered high. The top number, the systolic blood pressure, corresponds to the pressure in the arteries as the heart contracts and pumps blood forward into the arteries. The bottom number, the diastolic pressure, represents the pressure in the arteries as the heart relaxes after the contraction. The diastolic pressure reflects the lowest pressure to which the arteries are exposed. An elevation of the systolic and/or diastolic blood pressure increases the risk of developing heart (cardiac) disease, kidney (renal) diseasصورة او فيديو e, hardening of the arteries(صورة او فيديو )atherosclerosis or arteriosclerosis), eye damageصورة او فيديو , and stroke (brain damage) صورة او فيديو . These complications of hypertension are often referred to as end-organ damage because damage to these organs is the end result of chronic (long duration) high blood pressure)(شرح). For that reason, the diagnosis of high blood pressure is important so efforts can be made to normalize blood pressure and prevent complications الترجمة ماهو ارتفاع ضغط الدم؟؟ ضغط الدم المرتفع:HBP او حالة ارتفاع ضغط الدمHypertension هو الضغط في الشرايين... ضغط الدم المرتفع لايعني الأضطراب العاطفي او الشد العصبي لانها حالات مؤقتة لأرتفاع ضغط الدم.ضغط الدم الطبيعي يجب ان يتراوح بين120/80 اما الضغط الذي يكون بين 120/80و139/89 يسمى ارتفاع ضغط الدم الابتدائي.. اما الذي يكون 140/90 او اكثر يكون حالة ارتفاع لضغط الدم.. الرقم العلوي(من قياس ضغط الدم)يسمى ضغط الدم العالي (الانقباضي)يعزى الى الضغط الموجود في الشرايين عند انقباض عضلة القلب وضخه للدم بأتجاه الشرايين... اما الرقم السفلي (من قياس ضغط الدم)يسمى بالضغط الواطيء(الانبساطي) يمثل الضغط في الشرايين في حالة استراحة القلب(بعد الانقباض) وهو يمثل اوطيء ضغط تتعرض له الشرايين.. ان ارتفاع معدلات كل من الضغط الانبساطي والانقباضي يزيد من خطر التعرض لامراض القلب..(cardiac) امراض الكلى(renal) تصلب الشرايين(atherosclerosis) ضرر العين..الجلطة الدماغية(ضرر الدماغ) ان المضاعفات الناتجة عن ارتفاع ضغط الدم ..تسمى(نهاية العضو) لان الضرر لهذه الاعضاء هو النتيجة النهائية للارتفاع المزمن لضغط الدم(التعرض لفترة طويلة) لذلك فمن المهم ان تتم اعادة الضغط الى قياسه الطبيعي بأقصى الجهود..لمنع حدوث المضاعفات Classification Classification Blood pressure is usually classified based on the systolic and diastolic blood pressures. Systolic blood pressure is the blood pressure in vessels during a heart beat. Diastolic blood pressure is the pressure between heartbeats. A systolic or the diastolic blood pressure measurement higher than the accepted normal values for the age of the individual is classified as prehypertension or hypertension. Hypertension[7] has several sub-classifications, including hypertension stage I, hypertension stage II, and isolated systolic hypertension. Isolated systolic hypertension refers to elevated systolic pressure with normal diastolic pressure and is common in the elderly. These classifications are made after averaging a patient's resting blood pressure readings taken on two or more office visits. Individuals older than 50 years are classified as having hypertension if their blood pressure is consistently at least 140 mmHg systolic or 90 mmHg diastolic. Patients with blood pressures higher than 130/80 mmHg with concomitant presence of diabetes mellitus or kidney disease require further treatment.[6] Hypertension is also classified as resistant if medications do not reduce blood pressure to normal levels.[6] Exercise hypertension is an excessively high elevation in blood pressure during exercise.[8][9][10] The range considered normal for systolic values during exercise is between 200 and 230 mm Hg.[11] Exercise hypertension may indicate that an individual is at risk for developing hypertension at rest التصنيف(تصنيف المرض) ضغط الدم يصنف عادة اعتمادا على كل من الضغطين الانقباضي والانبساطي.. الضغط الأنقباضي هو ضغط الدم في الأوعية الدموية اثناء نبض القلب(الضربة) اما ضغط الدم الأنبساطي فهو الضغط خلال الفترات المحصورة بين الضربات.. عندما يكون قياس كل من الضغط الأنقباضي اوالأنبساطي اعلى من القيم الطبيعية المتفق عليها بالنسبة لعمر الفرد فأن هذا الأرتفاع يصنف على انه حالة ارتفاع ابتدائية لضغط الدم.. ان لحالة ارتفاع ضغط الدم عدة اقسام: تشمل حالة ارتفاع ضغط الدم للمرحلة الاولى.. حالة ارتفاع ضغط الدم للمرحلة الثانية.. وكذلك حالة ارتفاع ضغط الدم الأنقباضية المعزولة.. وحالة ارتفاع ضغط الدم الأنقباضية المعزولة تشير الى ارتفاع ضغط الدم الأنقباضي يصاحبه ضغط انبساطي اعتيادي(طبيعي) وهي حالة شائعة في مرحلة الشيخوخة.. هذه الأقسام تم التعرف عليها بعد حساب معدل قراءات ضغط دم المريض المستقروالتي اعتمدت بعد زيارتين او اكثر... الاشخاص الذين هم فوق سن ال 50 سنة يصنفون على انهم يتعرضون لحالة ارتفاع ضغط الدم. اذا كان قياس ضغط دمهم هو 140ملم/زئبق انقباضي او 90 ملم/زئبق انبساطي بصورة ثابتة تقريبا..(اي لاتوجد حالة ارتفاع انفعالية مؤقته) المرضى الذين يكون ضغط دمهم فوق 130/80 ملم/زئبق مع تزامن وجود مرض البول السكري لديهم او احد امراض الكلية ,فهم يحتاجون لعناية اضافية.. كذلك تتصف حالة ارتفاع ضغط الدم على انها مقاومة (مستعصية)اذا كان العلاج او الدواء الموصوف لايعمل على خفض ضغط الدم واعادته للمستويات الطبيعية.. حالة ارتفاع ضغط الدم التي يسببها التمرين الرياضي :وهي حالة ارتفاع كبير في ضغط الدم خلال التمرين.. ان المدى الذي يعتبر طبيعيا للضغط الانقباضي خلال التمرين يتراوح بين 200و230 ملم/زئبق.. حالة ارتفاع ضغط الدم بسبب التمرين ربما تشير الى ان الشخص معرض لخطر الاصابه بأرتفاع ضغط الدم خلال الحالة الأعتيادية (خلال الاستراحة).. Signs and symptoms Mild to moderate essential hypertension is usually asymptomatic. Accelerated hypertension Accelerated hypertension is associated with headache, drowsiness, confusion, vision disorders, nausea, and vomiting. These symptoms are collectively called hypertensive encephalopathy. Hypertensive encephalopathy is caused by severe small blood vessel congestion and brain swelling, which is reversible if blood pressure is lowered Secondary hypertension Secondary hypertension Some additional signs and symptoms suggest that the hypertension is caused by disorders in hormone regulation. Hypertension combined with obesity distributed on the trunk of the body, accumulated fat on the back of the neck ('buffalo hump'), wide purple marks on the abdomen (abdominal striae), or the recent onset of diabetes suggests that an individual has a hormone disorder known as Cushing's syndrome. Hypertension caused by other hormone disorders such as hyperthyroidism, hypothyroidism, or growth hormone excess will be accompanied by additional symptoms specific to these disorders. For example, hyperthyrodism can cause weight loss, tremors, heart rate abnormalities, reddening of the palms, and increased sweating Signs and symptoms associated with growth hormone excess include coarsening of facial features, protrusion of the lower jaw, enlargement of the tongue excessive hair growth, darkening of the skin color, and excessive sweating Other hormone disorders like hyperaldosteronism may cause less specific symptoms such as numbness, excessive urination, excessive sweating, electrolyte imbalances and dehydration, and elevated blood alkalinity.[18] and also cause mental pressure. العلامات والاعراض من الحالة الغير مزمنة الى الحالة المتوسطة..فأن حالة ارتفاع ضغط الدم تكون عديمة الاعراض عادة.. حالة ارتفاع ضغط الدم المفرطة(المتطورة) تكون عادة مصحوبة بصداع..خمول..اضطراب..اختلاج بالرؤيا,غثيان وتقيء.. هذه الأعراض مجتمعة تسمى بحالة ارتفاع ضغط الدم الرأسية(hypertensive encephalopathy).. يكون سببها احتقان في الأوعية الدموية الصغيرة وتورم الدماغ..والتي تنعكس في حالة هبوط ضغط الدم.. حالة ارتفاع ضغط الدم الثانوية:تشمل بعض العلامات والاعراض الأضافية ويكون سببها حدوث اختلال في التنظيم الهرموني.. ارتفاع ضغط الدم يكون مصحوب بالبدانة ..عدم تناسق المنطقة الجذعية(السفلية)من الجسم..تجمع الدهون في المنطقة الخلفية من الرقبة (buffalo hump) (تضخم القفى) وعلامات او ندب ارجوانية عريضة على منطقة البطن(abdomenal striae) او ان بداية مرض السكري الذي يعاني فيه الفرد من اضطراب هرموني يعرف ب متلازمة cushing .. ارتفاع ضغط الدم يسببه اختلالات هرمونية اخرى مثل اختلال الغدة الدرقية(فرط افراز الثايروكسين) او انخفاض افراز الثايروكسين من قبل الغدة الدرقية( thyroid gland) او خلل في هرمونات النمو.. والذي يكون مصحوبا بأعراض اضافية مميزة لهذه الاختلالات.. مثال:انخفاض فعالية الغدة الدرقية قد يسبب انخفاض الوزن..رعشة(ارتجاف),عدم استقرار معدل نبض القلب(زيادة نبضة اونقصان او تسرع) احمرار راحة اليد,تعرق كثيف,واعراض متعلقة بهرمونات النمو تشمل:تخشن في ملامح الوجه.. ظهور نتوءات عظمية في الفك السفلي..تضخم اللسان ..نمو كثيف للشعر..اسمرار لون البشرة وتعرق كثيف.. اختلالات هرمونية اخرى:مثل مايسمى بال(hyperaldosteronism)وتسبب الاعراض التالية:فقدان الاحساس(خدر) زيادة الادرار,تعرق كثيف,انعدام التوازن الالكتروليتي(فقدان الاملاح),جفاف(فقدان السوائل),ارتفاع معدل قاعدية الدم (ارتفاع PH الدم عن 7.4)وكذلك يمكن ان تسبب ضغط عصبي.. In pregnancy Hypertension in pregnant women is one symptom of pre-eclampsia. Pre-eclampsia can progress to a life-threatening condition called eclampsia, which is the development of protein in the urine, generalized swelling, and severe seizures. Other symptoms indicating that brain function is becoming impaired may precede these seizures such as nausea, vomiting, headaches, and vision loss.[19] In addition, the systemic vascular resistance and blood pressure decrease during pregnancy. The body must compensate by increasing cardiac output and blood volume to provide sufficient circulation in the utero-placental arterial bed. في حالة الحمل ارتفاع ضغط الدم لدى المرأة الحامل هو من الاعراض او المؤشرات على وجود مايعرف بالتشنج الحملي_الأبتدائي..pre_eclampsia وتتلخص هذه الحالة في تطور او زيادة نوع من البروتينات في الأدرار..تورم عام ونوبات مرضية حادة.. كذلك اعراض اخرى مثل:غثيان,تقيأ,صداع,وفقدان الرؤيا.. يضاف الى ذلك فأن المقاومة الجهازية _الوعائية وضغط الدم ينخفضان اثناء الحمل.. لذلك فأن الجسم يجب ان يعوض ذلك بمضاعفة الانتاج القلبي وكميات الدم لكي يجهز كميات اكبر من الدوران الدموي في الشرايين المجهزة للمنطقة المشيمية_الرحمية(منطقة اتصال المشيمة بالرحم).. In children Some signs and symptoms are especially important in newborns and infants such as failure to thrive, seizures, irritability, lack of energy, and difficulty breathing In children, hypertension can cause headache, fatigue, blurred vision, nosebleeds, and facial paralysis Even with the above clinical symptoms, the true incidence of pediatric hypertension is not known. In *****s, hypertension has been defined due to the adverse effects caused by hypertension. However, in children, similar studies have not been performed thoroughly to link any adverse effects with the increase in blood pressure. Therefore, the prevalence of pediatric hypertension remains unknown due to the lack of scientific knowledge ارتفاع ضغط الدم في الأطفال.. بعض العلامات والاعراض تكون واضحة في المواليد الجدد والرضع.. مثل:فشل في النمو,نوبات مرضية,تهيج,انعدام الطاقة,صعوبة التنفس لدى الأطفال.. كذلك فأن حالة ارتفاع ضغط الدم ممكن ان تسبب :صداع,اعياء(انحطاط القوى),تشوش الرؤيا,نزيف الانف,عجز اوشلل في الوجه(عضلات الوجه).. وحتى مع هذه الأعراض السريرية المذكوره اعلاه,فأن الاسباب الحقيقية لأرتفاع ضغط الدم في طب الأطفال لاتزال غير معروفة.. تصنف حالة ارتفاع ضغط الدم استنادا الى المؤثرات المعاكسة(المؤاتية)التي يتسسب بها هذا الارتفاع.. بصورة عامة في الاطفال ,فأن الدراسات المماثلة لم يتم العمل بها للربط بين اي اعراض مؤاتية او جانبية مصاحبة لضغط الدم المرتفع... لذلك فأن تفشي حالة ارتفاع ضغط الدم تبقى غير معروفة الأسباب في طب الاطفال نتيجة لنقص او عدم وجود المعرفة العلمية الكافية.. Essential hypertension Essential hypertension Essential hypertension is the most prevalent hypertension type, affecting 90–95% of hypertensive patients.[2] Although no direct cause has been identified, there are many factors such as sedentary lifestyle,[23] smoking, stress, visceral obesity, potassium deficiency[24] (hypokalemia),[23] obesity[25] (more than 85% of cases occur in those with a body mass index greater than 25),[26] salt (sodium) sensitivity,[27] alcohol intake,[28] and vitamin D deficiency that increase the risk of developing hypertension.[29][30] Risk also increases with aging,[31] some inherited genetic mutations,[32] and having a family history of hypertension.[33] An elevated level of renin, a hormone secreted by the kidney, is another risk factor,[34] as is sympathetic nervous system overactivity.[35] Insulin resistance, which is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension.[34][36] Recent studies have implicated low birth weight as a risk factor for ***** essential hypertension بسمه تعالى حالة ارتفاع ضغط الدم الأساسية.. Essential hypertension حالة ارتفاع ضغط الدم الاساسية هي اكثر الانواع تفشيا... تصيب مايقارب 90_95 % من المرضى الذين يعانون من ارتفاع ضغط الدم .. ولم يتم تشخيص اي سبب مباشر..وهنالك العديد من العوامل: اسلوب الحياة الخاطيء,التدخين,الشد العصبي, البدانة في المنطقة البطنية(تجمع الشحوم حول الاحشاء),عوز البوتاسيوم,(hypokalmia),البدانة(حيث ان اكثر من85 % من الحالات تحدث للأشخاص الذين يزيد معدل كتلتهم عن 25)... الحساسية تجاه ملح الصوديوم,تناول المشروبات الكحولية ,نقص(عوز)فيتامين D ,(يزيد من مخاطر الاصابة بالمرض).. كذلك تزداد مخاطر الأصابة بالمرض مع تقدم العمر,وكذلك بعض الطفرات الجينية المتوارثة... وجود تاريخ عائلي للمرض,,ارتفاع مستوى الرينين(وهو هرمون تفرزه الكلية) عوامل خطورة اخرى:الفعالية الا_اعتيادية للجهاز العصبي الودي(السمبثاوي),مقاومة الانسولين (وهي من اعراض متلازمة X او المتلازمة الايضية)... كلها تساهم بحالة ارتفاع ضغط الدم,لقد بينت الدراسات الحديثة بأن نقصان اوزان المواليد هو عامل خطورة للاصابة بحالة ارتفاع ضغط الم الرئيسية... Risk factor Hypertension is one of the most common complex disorders. The etiology of hypertension differs widely amongst individuals within a large population.[8] And by definition, essential hypertension has no identifiable cause. However, several risk factors have been identified. Hypertension may be secondary to other diseases but over 95% of patients have essential hypertension which is of unknown origin. It is observed though that: • Having a personal family history of hypertension increases the likelihood that an individual develops HPT.[9] • Essential hypertension is four times more common in black than white people, accelerates more rapidly and is often more severe with higher mortality in black patients.[9][10][11][12] More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing. One of these genes is the angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number of AGT increases the blood pressure and hence this may cause hypertension.[8] Twins have been included in studies measuring ambulatory blood pressure; from these studies it has been suggested that essential hypertension contains a large genetic influence.[8] Supporting data has emerged from animal studies as well as clinical studies in human populations. The majority of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each has an elevated blood pressure as one of its phenotypic expressions. However, the genetic influence upon hypertension is not fully understood at the moment. It is believed that linking hypertension-related phenotypes with specific variations of the genome may yield definitive evidence of heritability.[13] Another view is that hypertension can be caused by mutations in single genes, inherited on a Mendelian basis.[14] Hypertension can also be age related, and if this is the case, it is likely to be multifactorial. One possible mechanism involves a reduction in vascular compliance due to the stiffening of the arteries. This can build up due to isolated systolic hypertension with a widened pulse pressure. A decrease in glomerular filtration rate is related to aging and this results in decreasing efficiency of sodium excretion. The developing of certain diseases such as renal microvascular disease and capillary rarefaction may relate to this decrease in efficiency of sodium excretion. There is experimental evidence that suggests that renal microvascular disease is an important mechanism for inducing salt-sensitive hypertension.[15] Obesity can increase the risk of hypertension to fivefold as compared with normal weight, and up to two-thirds of hypertension cases can be attributed to excess weight.[16] More than 85% of cases occur in those with a Body mass index greater than 25.[16] A definitive link between obesity and hypertension has been found using animal and clinical studies; from these it has been realized that many mechanisms are potential causes of obesity-induced hypertension. These mechanisms include the activation of the sympathetic nervous system as well as the activation of the renin–angiotensin-aldosterone system.[17] Another risk factor is salt (sodium) sensitivity which is an environmental factor that has received the greatest attention. Approximately one third of the essential hypertensive population is responsive to sodium intake.[18] When sodium intake exceeds the capacity of the body to excrete it through the kidneys, vascular volume expands secondary to movement of fluids into the intra-vascular compartment. This causes the arterial pressure to rise as the cardiac output increases. Local autoregulatory mechanisms counteract this by increasing vascular resistance to maintain normotension in local vascular beds. As arterial pressure increases in response to high sodium chloride intake, urinary sodium excretion increases and the excretion of salt is maintained at expense of increased vascular pressures.[9] The increased sodium ion concentration stimulates ADH and thirst mechanisms, leading to increased reabsorption of water in the kidneys, concentrated urine, and thirst with higher intake of water. Also, the water movement between cells and the interstitium plays a minor role compared to this. The relationship between sodium intake and blood pressure is controversial. Reducing sodium intake does reduce blood pressure, but the magnitude of the effect is insufficient to recommend a general reduction in salt intake.[19] Renin elevation is another risk factor. Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked with aldosterone in a negative feedback loop. In consequence, some hypertensive patients have been defined as having low-renin and others as having essential hypertension. Low-renin hypertension is more common in African Americans than white Americans, and may explain why African Americans tend to respond better to diuretic therapy than drugs that interfere with the Renin-angiotensin system. High renin levels predispose to hypertension by causing sodium retention through the following mechanism: Increased renin → Increased angiotensin II → Increased vasoconstriction, thirst/ADH and aldosterone → Increased sodium reabsorption in the kidneys (DCT and CD) → Increased blood pressure. Hypertension can also be caused by Insulin resistance and/or hyperinsulinemia, which are components of syndrome X, or the metabolic syndrome. Insulin is a polypeptide hormone secreted by cells in the islets of Langerhans, which are contained throughout the pancreas. Its main purpose is to regulate the levels of glucose in the body antagonistically with glucagon through negative feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin. It has been suggested that vitamin D deficiency is associated with cardiovascular risk factors.[20] It has been observed that individuals with a vitamin D deficiency have higher systolic and diastolic blood pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a "negative endocrine regulator of the renin-angiotensin system". Hence a deficiency in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed link between hypertension and vitamin D levels in the blood plasma.[21] Also, some authorities claim that potassium might both prevent and treat hypertension.[22] Recent studies claims that obesity is a risk factor for hypertension because of activation of the renin-angiotensin system (RAS) in adipose tissue,[23][24] and also linked renin-angiotensin system with insulin resistance, and claims that any one can cause the other.[25] Cigarette smoking, a known risk factor for other cardiovascular disease, may also be a risk factor for the development of hypertension.[26] عوامل الخطورة..Riskfactors حالة ارتفاع ضغط الدم وهي من اكثر الأضطرابات شيوعا.. المظاهر المرضية لحالة ارتفاع ضغط الدم,تختلف بشكل كبير وواسع بين الافراد ضمن المجتمع الكبير.. ومن خلال التعريف تبين ان حالة ارتفاع ضغط الدم الأساسية ليس لها مسبب متعرف عليه(ليس لها اي مسبب قابل للتشخيص) لذلك فأن هنالك بضعة عوامل خطورة تم تشخيصها.. ان حالة ارتفاع ضغط الدم ربما تكون ثانوية مقارنة مع الامراض الاخرى ولكن اكثر من 95% من المرضى يعانون من حالة ارتفاع ضغط الدم الرئيسية.. والتي هي غير معروفة المسبب .. وكذلك تم ملاحظة مايأتي: ان الشخص الذي لديه تاريخ عائلي لحالة ارتفاع ضغط الدم تزداد احتمالية اصابته بال HPT.. ان حالة ارتفاع ضغط الدم الأساسية تكون اكثر بأربع مرات في الاشخاص السود منها في الاشخاص البيض.. فهي اسرع تطورا واكثر حده واكثر احتمالية للتسبب بموت المرضى السود.. لقد تم فحص مايقارب ال 50 جين في دراسات متعلقة بحالة ارتفاع ضغط الدم والرقم لازال يرتفع بثبات واحد هذه الجينات هو AGT او Angiotensinogen وقد تمت دراسته بتوسع من قبل العالم KIM وجماعته .. لقد بينوا ان بأرتفاع اعداد هذا الجين ATG سيؤدي الى ارتفاع ضغط الدم وهو يقود الى الاصابة بحالة ارتفاع ضغط الدم(Hypertension عوامل الخطورة Risk factors التوائم تم شملهم بالدراسة بقياس ضغط دمهم غير الثابت(القابل للتغير).. ان هذه الدراسات اثبتت ان حالة ارتفاع ضغط الدم الاساسية تشمل تداخل وراثي كبير لقد تم الحصول على معلومات تدعيمية عن هذا الموضوع من الدراسات على الحيوانات وكذلك الدراسات السريرية على المجتمعات الانسانية.. اهمية هذه الدراسات تكمن في دعمها لفكرة ان انتقال الصفات الوراثية(inheritance) هي غالبا تكون متعددة العوامل او لها مصادر وراثية مختلفة مثلا:ارتفاع ضغط الدم يعتبر تعبيرا مظهريا عن طراز وراثي معين.. ان التأثير الوراثي لحالة ارتفاع ضغط الدم لم يفهم بصورة كاملة لحد الان.. ويعتقد ان هناك ارتباط حالة ارتفاع ضغط الدم والتعبير الوراثي المظهري مع تغيرات محددة بالمادة الوراثية الاساسية(genome)والتي والتي ربما تكون كدلائل تعريفية لأنتقال الصفات الوراثية.. من ناحية اخرى فأن حالة ارتفاع ضغط الدم ربما يكون سببها طفرات وراثية في جين مفرد..حسب قوانين مندل الاساسية في الوراثة.. عوامل الخطورة Risk factors حالة ارتفاع ضغط الدم يمكن كذلك ان تكون مرتبطة بالعمر وفي هذه الحالة تكون متعددة الأسباب والعوامل.. هناك ميكانيكية واحدة ممكنة في مايتعلق بأختزال التلين الوعائي, والذي يعزى الى تصلب الشرايين .. وهذا البناء يعزى الى حالة ارتفاع ضغط الدم الأنقباضية المنعزلة والتي يرافقها ضغط نبضي متوسع.. ان انخفاض معدل الترشيح بواسطة الكبيبة(وهي تجمع شرياني في الكلية) يكون مرتبطا بالعمر والذي ينتج عنه انخفاض في افراغ الصوديوم بكمية كافية... ان تطور امراض معينة مثل مرض تضيق الاوعية الدموية الكلوية..Microvascular disease وكذلك مرض زيادة مسامية او تخلخل الأوعية الدموية الشعرية..capillary rarefaction والذي يكون مرتبطا بنقص افراغ الصوديوم..... Pathophysiology of essential hypertension The pathophysiology of hypertension is an area of active research, attempting to explain causes of hypertension, which is a chronic disease characterized by elevation of blood pressure. Hypertension can be classified as either essential or secondary. Essential hypertension indicates that no specific medical cause can be found to explain a patient's condition. About 90-95% of hypertension is essential hypertension.[1][2][3][4] Secondary hypertension indicates that the high blood pressure is a result of another underlying condition, such as kidney disease or tumours (adrenal adenoma or pheochromocytoma). Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure.[5] Most mechanisms leading to secondary hypertension are well understood. The pathophysiology of essential hypertension remains an area of active research, with many theories and different links to many risk factors. Cardiac output and peripheral resistance are the two determinants of arterial pressure.[6] Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles. Contents • 1 Genetics • 2 Autonomic nervous system • 3 Renin-angiotensin-aldosterone system • 4 Endothelial dysfunction • 5 References Genetics Evidence for genetic influence on blood pressure comes from various sources.[7] There is greater similarity in blood pressure within families than between families, which indicates a form of inheritance.[8] And it was proved that this finding wasn't due to shared environmental factors.[9] Single gene mutations is proved to cause Mendelian forms of high and low blood pressure.[10] almost 10 genes have been identified to cause this forms of hypertension.[10][11] These mutations affect blood pressure by altering renal salt handling.[12] Recently and with the aid of newly developed genetic analysis techniques researchers found statistically significant linkage of blood pressure to several chromosomal regions, including regions linked to familial combined hyperlipidemia.[13][14][15][16][17] These findings suggest that there are many genetic loci, each with small effects on blood pressure in the general population. Overall, however, identifiable single-gene causes of hypertension are uncommon, consistent with a multifactorial cause of essential hypertension.[2][7][18][19] The best studied monogenic cause of hypertension is the Liddle syndrome, a rare but clinically important disorder in which constitutive activation of the epithelial sodium channel predisposes to severe, treatment-resistant hypertension.[20] Epithelial sodium channel activation resulting in inappropriate sodium retention at the renal collecting duct level. Patients with the Liddle syndrome typically present with volume-dependent, low renin, and low aldosterone, and hypertension. Screenings of general hypertensive populations indicate that the Liddle syndrome is rare and does not contribute substantially to the development of hypertension in the general population.[21] Autonomic nervous system Also the autonomic nervous system, plays a central role in maintaining the cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. Done by altering peripheral vasculature, and kidneys, causing increased cardiac output, increased vascular resistance, and fluid retention. Disorder of the system, as in case of sympathetic nervous system overactivity, increases blood pressure and contributes to the development and maintenance of hypertension.[22][23][24][25] In addition, autonomic imbalance (i.e. increased sympathetic tone accompanied by reduced parasympathetic tone) has been associated with many metabolic and hemodynamic abnormalities that result in increased cardiovascular morbidity and mortality.[24][26] The mechanisms of increased sympathetic nervous system activity in hypertension are complex and involve alterations in baroreflex and chemoreflex pathways at both peripheral and central levels. Arterial baroreceptors are reset to a higher pressure in hypertensive patients, and this peripheral resetting reverts to normal when arterial pressure is normalized.[8][27][28] Furthermore, there is central resetting of the aortic baroreflex in hypertensive patients, resulting in suppression of sympathetic inhibition after activation of aortic baroreceptor nerves. This baroreflex resetting seems to be mediated, at least partly, by a central action of angiotensin II.[29][30][31] Additional small-molecule mediators that suppress baroreceptor activity and contribute to exaggerated sympathetic drive in hypertension include reactive oxygen species and endothelin.[32][33] Some studies shown that hypertensive patients manifest greater vasoconstrictor responses to infused norepinephrine than normotensive controls.[34] And that hypertensive patients doesn't show the normal response to increased circulating norepinephrine levels which generally induces downregulation of noradrenergic receptor, and its believed that this abnormal response is genetically inherited.[35] Exposure to stress increases sympathetic outflow, and repeated stress-induced vasoconstriction may result in vascular hypertrophy, leading to progressive increases in peripheral resistance and blood pressure.[2] This could partly explain the greater incidence of hypertension in lower socioeconomic groups, since they must endure greater levels of stress associated with daily living. Persons with a family history of hypertension manifest augmented vasoconstrictor and sympathetic responses to laboratory stressors, such as cold pressor testing and mental stress, that may predispose them to hypertension. This is particularly true of young African Americans. Exaggerated stress responses may contribute to the increased incidence of hypertension in this group.[36] Renin-angiotensin-aldosterone system Another system maintaining the extracellular fluid volume, peripheral resistance and that if disturbed may lead to hypertension, is the renin-angiotensin-aldosterone system. Renin is a circulating enzyme that participates in maintaining extracellular volume, and arterial vasoconstriction, Thus it contributing to regulation of the blood pressure, it performs this function through breaking down (hydrolyzes) angiotensinogen secreted from the liver into the peptide angiotensin I, Angiotensin I is further cleaved by an enzyme that is located primarily but not exclusively in the pulmonary circulation bound to endothelium, that enzyme is angiotensin converting enzyme (ACE) producing angiotensin II, the most vasoactive peptide.[37][38] Angiotensin II is a potent constrictor of all blood vessels. It acts on the musculature of arteries and thereby raises the peripheral resistance, and so elevates blood pressure. Angiotensin II also acts on the adrenal glands too and releases Aldosterone, which stimulates the epithelial cells of the kidneys to increase re-absorption of salt and water leading to raised blood volume and raised blood pressure. So elevation of renin level in the blood, which is normally in ***** human is 1.98-24.6 ng/L in the upright position.[39] will lead to hypertension.[2][40] Recent studies claims that obesity is a risk factor for hypertension because of activation of the renin-angiotensin system (RAS) in adipose tissue,[41][42] and also linked renin-angiotensin system with insulin resistance, and claims that anyone can cause the other.[43] Local production of angiotensin II in various tissues, including the blood vessels, heart, adrenals, and brain, is controlled by ACE and other enzymes, including the serine proteinase chymase. The activity of local renin–angiotensin systems and alternative pathways of angiotensin II formation may make an important contribution to remodeling of resistance vessels and the development of target organ damage (i.e. left ventricular hypertrophy, congestive heart failure, atherosclerosis, stroke, end-stage renal disease, myocardial infarction, and arterial aneurysm) in hypertensive persons.[40] Endothelial dysfunction The endothelium of blood vessels produces an extensive range of substances that influence blood flow and, in turn, is affected by changes in the blood and the pressure of blood flow. For example, local nitric oxide and endothelin, which are secreted by the endothelium, are the major regulators of vascular tone and blood pressure. In patients with essential hypertension, the balance between the vasodilators and the vasoconstrictors is upset, which leads to changes in the endothelium and sets up a “vicious cycle” that contributes to the maintenance of high blood pressure. In patients with hypertension, endothelial activation and damage also lead to changes in vascular tone, vascular reactivity, and coagulation and fibrinolytic pathways. Alterations in endothelial function are a reliable indicator of target organ damage and atherosclerotic disease, as well as prognosis.[44] Multiple evidences suggest that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone. Inactivation of nitric oxide (NO) by superoxide and other reactive oxygen species (ROS) seems to occur in conditions such as hypertension.[45][46][47] Normally nitric oxide is an important regulator and mediator of numerous processes in the nervous, immune and cardiovascular systems, including smooth muscle relaxation thus resulting in vasodilation of the artery and increasing blood flow, suppressor of migration and proliferation of vascular smooth-muscle cells.[2] It has been suggested that angiotensin II enhances formation of the oxidant superoxide at concentrations that affect blood pressure minimally.[48] Endothelin is a potent vasoactive peptide produced by endothelial cells that has both vasoconstrictor and vasodilator properties. Circulating endothelin levels are increased in some hypertensive patients,[49][49][50] particularly African Americans and persons with hypertension Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which by definition is caused by an identifiable underlying secondary cause. It is much less common than the other type, called essential hypertension, affecting only 5% of hypertensive patients. It has many different causes including endocrine diseases, kidney diseases, and tumors. It also can be a side effect of many medications types of secondary hypertension Renovascular hypertension (I15.0) 1.2 Hypertension secondary to other renal disorders (I15.1) 1.3 Hypertension secondary to endocrine disorders (I15.2) 1.4 Other secondary hypertension (I15.8) 1.5 Adrenal 1.6 Kidney 1.7 Medication side effects 1.8 Pregnancy 1.9 Sleep disturbances 1.10 Arsenic exposure 1.11 Potassium deficiency Renovascular hypertension (or "renal hypertension") is a syndrome which consists of high blood pressure caused by narrowing of the arteries supplying the kidneys (renal artery stenosis). It is a form of secondary hypertension - a form of hypertension whose cause is identifiable. Cause: It induces renin secretion that causes the angiotensin conversion, causing aldosterone release and then water retention and potassium depletion. Hypertension secondary to other renal disorders (I15.1) Chronic renal failure Kidney disease / renal artery stenosis: the normal physiological response to low blood pressure in the renal arteries is to increase cardiac output (CO) to maintain the pressure needed for glomerular filtration. Here, however, increased CO cannot solve the structural problems causing renal artery hypotension, with the result that CO remains chronically elevated. Renal segmental hypoplasia Hypertension secondary to endocrine disorders (I15.2) Pheochromocytoma - caused by an excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction Hyperaldosteronism (Conn's syndrome) - idiopathic hyperaldosteronism, liddle's syndrome (also called pseudoaldosteronism), glucocorticoid remediable aldosteronism Cushing's syndrome - an excessive secretion of glucocorticoids causes the hypertension Hyperparathyroidism Acromegaly Hyperthyroidism Hypothyroidism Other secondary hypertension (I15.8) Hormonal contraceptives Neurologic disorders Obstructive sleep apnea Liquorice (when consumed in excessive amounts) Scleroderma Neurofibromatosis Pregnancy: unclear etiology. Cancers: tumours in the kidney can operate in the same way as kidney disease. More commonly, however, tumors cause inessential hypertension by ectopic secretion of hormones involved in normal physiological control of blood pressure. Drugs: In particular, alcohol, nasal decongestants with adrenergic effects, NSAIDs, MAOIs, adrenoceptor stimulants, and combined methods of hormonal contraception (those containing ethinyl-estradiol) can cause hypertension while in use. Heavy alcohol use Steroid use Nicotine use. [1] Malformed aorta, slow pulse, ischemia: these cause reduced blood flow to the renal arteries, with physiological responses as already outlined. Aortic valve disease: unclear etiology. Coarcation of the aorta Atherosclerosis Anemia: unclear etiology. Fever: unclear etiology. White coat hypertension, that is, elevated blood pressure in a clinical setting but not in other settings, probably due to the anxiety some people experience during a clinic visit. Perioperative hypertension is development of hypertension just before, during or after surgery. It may occur before surgery during the induction of anesthesia; intraoperatively e.g. by pain-induced sympathetic nervous system stimulation; in the early postanesthesia period, e.g. by pain-induced sympathetic stimulation, hypothermia, hypoxia, or hypervolemia from excessive intraoperative fluid therapy; and in the 24 to 48 hours after the postoperativ period as fluid is mobilized from the extravascular space. In addition, hypertension may develop perioperatively because of discontinuation of long-term antihypertensive medication.[2] |
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