Dwarfism

Dwarfism occurs when an individual person or animal is short in stature resulting from a medical condition caused by abnormal (slow or delayed) growth. In humans, dwarfism is sometimes defined as an adult height of less than 147 cm (4 feet 10 inches). Dwarfism can be caused by about 200 distinct medical conditions, such that the symptoms and characteristics of individuals with dwarfism vary greatly. Disproportionate dwarfism is characterized by one or more body parts being relatively large or small in comparison to those of an average-sized adult, with growth variations in specific areas being apparent. In cases of proportionate dwarfism, the body appears normally proportioned, but is unusually small. There is no single treatment for dwarfism. Individual differences, such as bonegrowth disorders, sometimes can be treated through surgery, some hormone disorders can be treated through medication, and by hormone replacement therapy; this treatment must be done before the childs' growth plates fuse. Individual accommodations, such as specialized furniture, are often used by people with dwarfism. Many support groups provide services to aid individuals with dwarfism in facing the challenges of an ableist society. For people, in addition to the medical aspect of the condition, there are social and sociological aspects as well. In the United States, Canada and New Zealand, any people with dwarfism prefer to be called little people. Historically, the term midget was used to describe "proportionate dwarfs"; however, this term is now sometimes regarded as offensive and pejorative (see terminology) in people. Another definition for midget is any thing (especially an animal), that is small in proportion to a typical specimen. Hypotonia, or low muscle tone, is common in dwarfs, but intelligence and lifespan are usually normal.

Defining dwarfism by height alone is problematic because short stature in itself is not a disorder. For example, in pygmy populations, a body height of less than 150 cm (59 inches) is normal.

Dwarfism is a highly visible condition and often carries negative connotations in society. Because of their unusual height, people with dwarfism often work as spectacles in entertainment and are often portrayed with stereotypes. For a person with dwarfism, heightism can lead to ridicule in childhood and discrimination in adulthood.[8][9] Classification
Dwarfism is a medical disorder. In humans, the sole requirement is being an adult height under 147 cm (4 ft 10 in) and it is almost always classified as to the underlying condition that is the cause for the short stature. Dwarfism is usually caused by a genetic disorder; achondroplasia is caused by a mistake on chromosome four. If dwarfism is caused by a medical disorder, the person is referred to by the underlying diagnosed disorder. Disorders causing dwarfism are often classified by proportionality. Disproportionate dwarfism describes disorders that cause unusual proportions of the body parts, while proportionate dwarfism results in a generally uniform stunting of the body. Disorders that cause dwarfism may be classified according to one of hundreds of names, which are usually permutations of the following roots:

location
o o o o

rhizomelic = root, e.g., bones of the upper arm or thigh mesomelic = middle, e.g., bones of the forearm or lower leg acromelic = end, e.g., bones of hands and feet. micromelic = entire limbs are shortened chondro = of cartilage osteo = of bone spondylo = of the vertebrae plasia = form trophy = growth

source
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Characteristics
A typical defining characteristic of dwarfism is an adult height of less than 147 cm (4 ft 10 in) Since those with dwarfism have such a wide range of physical characteristics, variations in individuals are identified by diagnosing and monitoring the underlying disorders.

It should be noted that short stature can be inherited without any coexisting disease. Short stature in the absence of a medical condition is not generally considered dwarfism. For example, a short man and a short woman with average health will tend to produce children who are also short and with average health. While short parents tend to produce short children, persons with dwarfism may produce children of average height, if the cause of their dwarfism is not genetically transmissible or if the individual does not pass on the genetic variation. Disproportionate dwarfism is characterized by one or more body parts being unusually large or small compared to the rest of the body. In achondroplasia one's trunk is usually of average size, one's limbs being proportionately shorter, one's head usually larger, and a prominent forehead.In at least one case achondroplasia resulted in a significantly smaller trunk and head.Facial features are often affected and individual body parts may have problems associated with them. Orthopedic problems can result from multiple conditions such as diastrophic dysplasia and pseudoachondroplasia. Proportionate dwarfism is marked by body parts being proportional but smaller. Height is significantly below average and there may be long periods without any significant growth. Sexual development is often delayed or impaired into adulthood. Unlike disproportionate dwarfism, in some cases intellectual disability may be a part of proportionate dwarfism. The overall stunted growth can lead to impaired intelligence when compared to physical age. Physical maleffects of malformed bones vary according to the specific disease. Many involve joint pain caused by abnormal bone alignment, or from nerve compression. Early degenerative joint disease, exaggerated lordosis or scoliosis, and constriction of spinal cord or nerve roots can cause pain and disability. Reduced thoracic size can restrict lung growth and reduce pulmonary function. Some forms of dwarfism are associated with disordered function of other organs, such as the brain or liver, sometimes severely enough to be more of an impairment than the unusual bone growth.Mental effects also vary according to the specific underlying syndrome. In most cases of skeletal dysplasia, such as achondroplasia, mental function is not impaired in any way. However, there are syndromes which can affect the cranial structure and growth of the brain, severely impairing mental capacity. Unless the brain is directly affected by the underlying disorder, there is little to no chance of mental impairment that can be attributed to dwarfism.

Causes
Dwarfism can result from myriad medical conditions, each with its own separate symptoms and causes. Extreme shortness in humans with proportional body parts usually has a hormonal cause, such as growth-hormone deficiency, once called pituitary dwarfism.[6][11] Two disorders, achondroplasia and growth hormone deficiency (also known as pituitary dwarfism), are responsible for the majority of human dwarfism cases.[3]

Achondroplasia The most recognizable and most common form of dwarfism in humans is achondroplasia, which accounts for 70% of dwarfism cases and produces rhizomelic short limbs, increased spinal curvature, and distortion of skull growth. With achondroplasia, the body's limbs are proportionately shorter than the trunk (abdominal area), with a larger head than average and characteristic facial features. Achondroplasia is an autosomal dominant disorder caused by the presence of a faulty allele in the genome. If a pair of achondroplasia alleles are present, the result is fatal. Growth hormone deficiency Growth hormone deficiency (GHD) is a medicalcondition in which the body produces insufficient growth hormone. Growth hormone, also called somatotropin, is a polypeptide hormone which stimulates growth and cell reproduction. If this hormone is lacking, stunted or even halted growth may become apparent. Children with this disorder may grow slowly and puberty may be delayed by several years or indefinitely. Growth hormone deficiency has no single definite cause. It can be caused by mutations of specific genes, damage to the pituitary gland, Turner's syndrome, poor nutrition,or even stress (leading to psychogenic dwarfism). Other Other causes of dwarfism include spondyloepiphyseal dysplasia congenita, diastrophic dysplasia, pseudoachondroplasia, hypochondroplasia, Noonan syndrome, primordial dwarfism, Turner syndrome, osteogenesis imperfecta (OI) and hypothyroidism. Severe shortness with skeletal distortion also occurs in several of the Mucopolysaccharidoses and other storage disorders.[24] Serious chronic illnesses may produce dwarfism as a side effect. Harsh environmental conditions, such as malnutrition, may also produce dwarfism. These types of dwarfism are indirect consequences of the generally unhealthy or malnourished condition of the individual, and not of any specific disease. The dwarfism often takes the form of simple short stature, without any deformities. In societies where poor nutrition is widespread, the average height of the population may be reduced below its genetic potential by the lack of proper nutrition.

Diagnosis
Dwarfism is often diagnosed in childhood on the basis of visible symptoms. A physical examination can usually suffice to diagnose certain types of dwarfism, but genetic testing and diagnostic imaging may be used to determine the exact condition.[ Short stature or stunted growth during youth is usually what brings the condition to medical In a person's youth, growth charts that track height can be used to

diagnose subtle forms of dwarfism that have no other striking physical characteristics. attention. Skeletal dysplasia is usually suspected because of obvious physical features (e.g., unusual configuration of face or shape of skull), because of an obviously affected parent, or because body measurements (arm span, upper to lower segment ratio) indicate disproportion. Bone X-rays are often key to diagnosing a specific skeletal dysplasia, but are not the sole diagnostic tool. Most children with suspected skeletal dysplasias are referred to a genetics clinic for diagnostic confirmation and genetic counseling. Since about the year 2000, genetic tests for some of the specific disorders have become available.

Prevention
Many types of dwarfism are impossible to prevent because they are genetically caused. Genetic conditions that cause dwarfism may be identified with genetic testing, by screening for the specific variation that result in the condition. However, due to the number of causes of dwarfism, it may be impossible to determine definitively if a child will be born with dwarfism. Dwarfism resulting from malnutrition or a hormonal abnormality may be treated with an appropriate diet or hormonal therapy. Growth hormone deficiency may be remedied via injections of Human Growth Hormone (HGH) during early life.

Management
Genetic defects of most forms of dwarfism caused by bone dysplasia cannot be corrected, so therapeutic interventions are typically aimed at preventing or reducing pain or physical disability, increasing adult height, or mitigating psychosocial stresses and enhancing social adaptation. Forms of dwarfism associated with the endocrine system may be treated using hormonal therapy. If the cause is prepubescent hyposecretion of growth hormone, supplemental growth hormone may correct the abnormality. If the receptor for growth hormone is itself affected, the condition may prove harder to treat. Hypothyroidism is another possible cause of dwarfism that can be treated through hormonal therapy. Injections of thyroid hormone can mitigate the effects of the condition, but physical complications may be permanent. Pain and disability may be ameliorated by physical therapy, braces or other orthotic devices, or by surgical procedures. The only simple interventions that increase perceived adult height are dress enhancements, such as shoe lifts or hairstyle. Growth hormone is rarely used for shortness caused by bone dysplasias, since the height benefit is typically small (less than 5 cm [2 in]) and the cost high The most effective means of increasing adult height by several inches is distraction osteogenesis, though availability is limited and the cost is high in terms of money, discomfort, and disruption of life. Most people with dwarfism do not choose this option, and it remains controversial For other types of dwarfism, surgical treatment is not possible.

Myocardial infarction
From Wikipedia, the free encyclopedia Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, results from the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (cholesterol and fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and ensuing oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium). Typical symptoms of acute myocardial infarction include sudden retrosternal chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a sense of impending doom). Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigure A sizeable proportion of myocardial infarctions (2264%) are "silent", that is without chest pain or other symptoms.

Among the diagnostic tests available to detect heart muscle damage are an electrocardiogram (ECG), echocardiography, cardiac MRI and various blood tests. The most often used blood markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual nitroglycerin. Most cases of myocardial infarction with ST elevation on ECG (STEMI) are treated with reperfusion therapy, such as percutaneous coronary intervention (PCI) or thrombolysis. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although PCI may be required if the patient's risk warrants it. People who have multiple blockages of their coronary arteries, particularly if they also have diabetes mellitus, may benefit from bypass surgery (CAB The European Society of Cardiology guidelines in 2011 proposed treating the blockage causing the myocardial infarction by PCI and performing CABG later when the patient is more stable. Rarely CABG may be preferred in the acute phase of myocardial infarction, for example when PCI has failed or is contraindicated. Ischemic heart disease (which includes myocardial infarction, angina pectoris and heart failure when preceded by myocardial infarction) was the leading cause of death for both men and women worldwide in 2004. Important risk factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity and obesity, chronic kidney disease, excessive alcohol consumption, the abuse of illicit drugs (such as cocaine and amphetamines), and chronic high stress levels.[10][11][12]

Classification
There are two basic types of acute myocardial infarction based on pathology:

Transmural: associated with atherosclerosis involving a major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply. In addition, on ECG, ST elevation and Q waves are seen. Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia . In addition, ST depression is seen on ECG.

In the clinical context, a myocardial infarction can be further subclassified into a ST elevation MI (STEMI) versus a non-ST elevation MI (non-STEMI) based on ECG changes. The phrase heart attack is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction. A heart attack is different from, but can be the cause of cardiac arrest, which is the stopping

of the heartbeat, and cardiac arrhythmia, an abnormal heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired; however severe myocardial infarction may lead to heart failure. A 2007 consensus document classifies myocardial infarction into five main types:

Type 1 Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection Type 2 Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension Type 3 Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood Type 4 Associated with coronary angioplasty or stents:
o o

Type 4a Myocardial infarction associated with PCI Type 4b Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy

Type 5 Myocardial infarction associated with CABG

Signs and symptoms

Rough diagram of pain zones in myocardial infarction; dark red: most typical area, light red: other possible areas; view of the chest

Back view The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium,where it may mimic heartburn. Levine's sign, in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value. Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating),weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.

The animation shows how plaque buildup or a coronary artery spasm can lead to a heart attack and how blocked blood flow in a coronary artery can lead to a heart attack. Risk factors Myocardial infarction results from atherosclerosis. Smoking appears to be the cause of about 36% of coronary artery disease and obesity 20%. Lack of exercise has been linked to 7-12% of cases.stress appear to play a minor role accounting for about 3% of causes Risk factors for myocardial infarction include:

Age Gender: At any given age men are more at risk than women, particularly before menopause, but because in general women live longer than men ischemic heart disease causes slightly more total deaths in women. Diabetes mellitus (type 1 or 2 High blood pressure[37] Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides Tobacco smoking, including secondhand smoke[37] Short term exposure to air pollution including: carbon monoxide, nitrogen dioxide, and sulfur dioxide but not ozone.[38] Family history of ischaemic heart disease or myocardial infarction particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women).[10]

Obesity[39] (defined by a body mass index of more than 30 kg/m, or alternatively by waist circumference or waist-hip ratio). Lack of physical activity.[10]

Pathophysiology

Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated myocardial infarction and ST-elevated myocardial infarction, which are most frequently (but not always) a manifestation of coronary artery disease.The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades.Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the occluded coronary artery die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.As a result, the patient's heart will be permanently damaged. This myocardial scarring also puts the patient at risk for potentially life threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences.Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another lifethreatening arrhythmia is ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in

rapid heart rates that prevent the heart from pumping blood effectively. may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.

Diagnosis
The diagnosis of myocardial infarction can be made after assessing patient's complaints and physical status. ECG changes, coronary angiogram and levels of cardiac markers help to confirm the diagnosis. ECG gives valuable clues to identify the site of myocardial damage while coronary angiogram allows visualization of narrowing or obstructions in the heart vessels.At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist. In stable patients whose symptoms have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmacologic stress. Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.

Prevention
The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:

Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased. Beta blocker therapy such as metoprolol or carvedilol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia.Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI. ACE inhibitor therapy should be commenced 2448 hours post-MI in hemodynamically stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by

ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI.

Statin therapy has been shown to reduce mortality and morbidity post-MI.The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood li

Hypertension ( H T N ) o r h i g h b l o o d p r e s s u r e , s o m

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n t s , s y s t o l i c a n d d i a s t o l i c , w h i c h d e p e n d o n

w h e t h e r t h e h e a r t m u s c l e i s c o n t r a c t i n g ( s y

s t o l e ) o r r e l a x e d b e t w e e n b e a t s ( d i a s t o l e ) .

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i s p e r s i s t e n t l y a t o r a b o v e 1 4 0 / 9 0 m m H g . H y p

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i c a l c a u s e . T h e r e m a i n i n g 5 1 0 % o f c a s e s ( s e c

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c t i o n ( h e a r t a t t a c k s ) , h e a r t f a i l u r e , a n e u r y

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c i e n t .

Signs and symptoms

Hypertension is rarely accompanied by any symptoms, and its identification is usually through screening, or when seeking healthcare for an unrelated problem. A proportion of people with high blood pressure report headaches (particularly at the back of the head and in the morning), as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes.[3] These symptoms however are more likely to be related to associated anxiety than the high blood pressure itself.[4] On physical examination, hypertension may be suspected on the basis of the presence of hypertensive retinopathy detected by examination of the optic fundus found in the back of the eye using ophthalmoscopy.[5] Classically, the severity of the hypertensive retinopathy changes is graded from grade IIV, although the milder types may be difficult to distinguish from each other.[5] Ophthalmoscopy findings may also give some indication as to how long a person has been hypertensive.[3] Secondary hypertension Some additional signs and symptoms may suggest secondary hypertension, i.e. hypertension due to an identifiable cause such as kidney diseases or endocrine diseases. For example, truncal obesity, glucose intolerance, moon facies, a "buffalo hump" and purple striae suggest Cushing's syndrome.[6] Thyroid disease and acromegaly can also cause hypertension and have characteristic symptoms and signs.[6] An abdominal bruit may be an indicator of renal artery stenosis (a narrowing of the arteries supplying the kidneys), while decreased blood pressure in the lower extremities and/or delayed or absent femoral arterial pulses may indicate aortic coarctation (a narrowing of the aorta shortly after it leaves the heart). Labile or paroxysmal hypertension accompanied by headache, palpitations, pallor, and perspiration should prompt suspicions of pheochromocytoma.[6] Hypertensive crisis Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 110 sometime termed malignant or accelerated hypertension) is referred to as a "hypertensive crisis", as blood pressures above these levels are known to confer a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches (22% of cases)[7] and dizziness than the general population.[3] Other symptoms accompanying a hypertensive crisis

may include visual deterioration or breathlessness due to heart failure or a general feeling of malaise due to renal failure.[6] Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.[8] In pregnancy Hypertension occurs in approximately 810% of pregnancies.[6] Most women with hypertension in pregnancy have pre-existing primary hypertension, but high blood pressure in pregnancy may be the first sign of pre-eclampsia, a serious condition of the second half of pregnancy and puerperium.[6] Pre-eclampsia is characterised by increased blood pressure and the presence of protein in the urine.[6] It occurs in about 5% of pregnancies and is responsible for approximately 16% of all maternal deaths globally.[6] Pre-eclampsia also doubles the risk of perinatal mortality.[6] Usually there are no symptoms in pre-eclampsia and it is detected by routine screening. When symptoms of pre-eclampsia occur the most common are headache, visual disturbance (often "flashing lights"), vomiting, epigastric pain, and edema. Pre-eclampsia can occasionally progress to a life-threatening condition called eclampsia, which is a hypertensive emergency and has several serious complications including vision loss, cerebral edema, seizures or convulsions, renal failure, pulmonary edema, and disseminated intravascular coagulation (a blood clotting disorder).[6][9] In infants and children Failure to thrive, seizures, irritability, lack of energy, and difficulty breathing[10] can be associated with hypertension in neonates and young infants. In older infants and children, hypertension can cause headache, unexplained irritability, fatigue, failure to thrive, blurred vision, nosebleeds, and facial paralysis.[11][10]

Cause
Primary hypertension Primary (essential) hypertension is the most common form of hypertension, accounting for 9095% of all cases of hypertension.[2] In almost all contemporary societies, blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable.[12] Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified[13] as well as some rare genetic variants with large effects on blood pressure[14] but the genetic basis of hypertension is still poorly understood. Several environmental factors influence blood pressure. Lifestyle factors that lower blood pressure include reduced dietary salt intake,[15] increased consumption of fruits and low fat products (Dietary Approaches to Stop Hypertension (DASH diet)), exercise,[16] weight loss[17] and reduced alcohol intake.[18] Stress appears to play a minor role[4] with specific relaxation techniques not supported by the evidence.[19] The possible role of other factors such as caffeine consumption,[20] and vitamin D deficiency[21] are less clear

cut. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension.[22] Recent studies have also implicated events in early life (for example low birth weight, maternal smoking and lack of breast feeding) as risk factors for adult essential hypertension,[23] although the mechanisms linking these exposures to adult hypertension remain obscure.[23] Secondary hypertension Secondary hypertension results from an identifiable cause. Renal disease is the most common secondary cause of hypertension.[6] Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, hyperparathyroidism and pheochromocytoma.[6][24] Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive liquorice consumption and certain prescription medicines, herbal remedies and illegal drugs.[6][25]

Pathophysiology

In most people with established essential (primary) hypertension, increased resistance to blood flow (total peripheral resistance) accounting for the high pressure while cardiac output remains normal.[26] There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension.[27] These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age.[27] Whether this pattern is typical of all people who ultimately develop hypertension is disputed.[28] The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles,[29] although a reduction in the number or density of capillaries may also contribute.[30] Hypertension is also associated with decreased peripheral venous compliance[31] which may increase venous return, increase cardiac preload and, ultimately, cause diastolic dysfunction. Whether increased

active vasoconstriction plays a role in established essential hypertension is unclear.

[32]

Hypertension is diagnosed on the basis of a persistently high blood pressure. Traditionally,[45] this requires three separate sphygmomanometer measurements at one monthly intervals.[46] Initial assessment of the hypertensive people should include a complete history and physical examination. With the availability of 24hour ambulatory blood pressure monitors and home blood pressure machines, the importance of not wrongly diagnosing those who have white coat hypertension has led to a change in protocols. In the United Kingdom, current best practice is to follow up a single raised clinic reading with ambulatory measurement, or less ideally with home blood pressure monitoring over the course of 7 days.[45] Pseudohypertension in the elderly or noncompressibility artery syndrome may also require consideration. This condition is believed to be due to calcification of the arteries resulting an abnormally high blood pressure readings with a blood pressure cuff while intra arterial measurements of blood pressure are normal.[47]

Prevention
Much of the disease burden of high blood pressure is experienced by people who are not labelled as hypertensive.[50] Consequently, population strategies are required to reduce the consequences of high blood pressure and reduce the need for antihypertensive drug therapy. Lifestyle changes are recommended to lower blood pressure, before starting drug therapy. The 2004 British Hypertension Society guidelines[50] proposed the following lifestyle changes consistent with those outlined by the US National High BP Education Program in 2002[53] for the primary prevention of hypertension:

maintain normal body weight for adults (e.g. body mass index 2025 kg/m2) reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride or <2.4 g of sodium per day) engage in regular aerobic physical activity such as brisk walking (30 min per day, most days of the week) limit alcohol consumption to no more than 3 units/day in men and no more than 2 units/day in women consume a diet rich in fruit and vegetables (e.g. at least five portions per day);

Effective lifestyle modification may lower blood pressure as much an individual antihypertensive drug. Combinations of two or more lifestyle modifications can achieve even better results.[50]

Management
Lifestyle modifications The first line of treatment for hypertension is identical to the recommended preventative lifestyle changes[54] and includes: dietary changes[55] physical exercise, and weight loss. These have all been shown to significantly reduce blood pressure in people with hypertension.[56] If hypertension is high enough to justify immediate use of medications, lifestyle changes are still recommended in conjunction with medication. Different programs aimed to reduce psychological stress such as biofeedback, relaxation or meditation are advertised to reduce hypertension. However, in general claims of efficacy are not supported by scientific studies, which have been in general of low quality.[57][58][59] Dietary change such as a low sodium diet is beneficial. A long term (more than 4 weeks) low sodium diet in Caucasians is effective in reducing blood pressure, both in people with hypertension and in people with normal blood pressure.[60] Also, the DASH diet, a diet rich in nuts, whole grains, fish, poultry, fruits and vegetables promoted in the USA by the National Heart, Lung, and Blood Institute lowers blood pressure. A major feature of the plan is limiting intake of sodium, although the diet is also rich in potassium, magnesium, calcium, as well as protein.[61] Medications Several classes of medications, collectively referred to as antihypertensive drugs, are currently available for treating hypertension. Prescription should take into account the person's cardiovascular risk (including risk of myocardial infarction and stroke) as well as blood pressure readings, in order to gain a more accurate picture of the person's cardiovascular profile.[62] Evidence in those with mild hypertension (SBP less than 160 mmHg and /or DBP less than 100 mmHg) and no other health problems does not support a reduction in the risk of death or rate of health complications from medication treatment.[63] If drug treatment is initiated the Joint National Committee on High Blood Pressure (JNC-7)[1] recommends that the physician not only monitor for response to treatment but should also assess for any adverse reactions resulting from the medication. Reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34%, of ischaemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease.[64] The aim of treatment should be to reduce blood pressure to <140/90 mmHg for most individuals, and lower for those with diabetes or kidney disease (some medical professionals recommend keeping levels below 120/80 mmHg).[62][65] If the blood pressure goal is not met, a change in treatment should be made as therapeutic inertia is a clear impediment to blood pressure control.[66]