Alimentos Para Controlar La Presion Arterial, Arterial Hypertension, Prevencion De Hipertension

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Para obtener los mismos beneficios que los medicamentos prescritos más comúnmente
sin los efectos secundarios negativos existen alternativas naturales. La dieta es la principal manera de aumentar las reacciones deseables, pero el ejercicio contribuye en gran medida también.

Por ejemplo, la misma reacción causada por los vasodilatadores puede ocurrir cuando usted obtiene suficiente L-Arginina. Este aminoácido permite que las paredes de los vasos sanguíneos se relajen. Usted puede tomar un suplemento o conseguirla a través de proteínas de origen animal, el maní y la soja.

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https://www.youtube.com/watch?v=SFUGz4IqbA0
Alimentos Para Controlar La Presion Arterial, Arterial Hypertension, Prevencion De Hipertension, Arterial Pdf, Hipertension Esencial, Hipertension Pulmonar Tratamiento,Tension Alta Sintomas, Dieta Hipertension, Guia Clinica Hipertension, Sal Marina Hipertension,
Sintomas De Tension Alta, Hipertension Portal Pdf, Hipertension Arterial Clasificacion, Hipertension Intracraneal, Tension Alta En, El Embarazo, Hipertension Primaria

The hepatitis E virus, responsible for major epidemics of viral hepatitis in subtropical and tropical countries, was cloned only 7 years ago.1 Hepatitis E was found to belong to the family of Caliciviridae, which includes the Norwalk virus—a common cause of gastroenteritis in humans—and consists of a single, plus-strand RNA genome of approximately 7.2 kb without an envelope (Fig. 1). The virus contains at least three open reading frames encoding viral proteins against which antibodies are made on exposure. These antibodies, especially those against the capsid protein derived from the second open reading frame2 and a protein of unknown function derived from the third open reading frame, are detected by currently available serologic assays. Retrospective studies on stored sera of past epidemics of viral hepatitis in Mexico, Africa, Afghanistan, Pakistan, India, Bangladesh, Burma, Nepal, and Borneo have revealed that all were caused by strains of hepatitis E. In addition, hepatitis E was found to be responsible for the hepatitis epidemic in the southern part of Xinjiang, China, in which 120,000 persons became infected between September 1986 and April 1988.3 Hepatitis E predominantly affects young adults (15 to 40 years old). The symptoms of hepatitis E are similar to those of hepatitis A. Frequently, a prodrome consisting of anorexia, nausea, low-grade fever, and right upper abdominal pain is present 3 to 7 days before jaundice develops. Aminotransferase levels peak (usually between 1,000 and 2,000 U/L) near the onset of symptoms; bilirubin levels (10 to 20 mg/dL) peak later. Jaundice usually resolves after 1 to 2 weeks. In about 10% of cases, the disease is fulminant—especially in pregnant women, among whom mortality rates as high as 20% due to hemorrhagic and thrombotic complications have been reported. No evidence has suggested that hepatitis E can cause chronic infection. Transmission is by the fecal-oral route, predominantly through fecally contaminated drinking water supplies. In addition, however, preliminary reports have suggested transmission of the hepatitis E virus through blood transfusions. Volunteer studies confirmed the presence of the virus in serum and feces before and during clinical disease.4 The virus is shed into feces approximately 1 week before symptoms develop. The incubation period varies from 2 to 9 weeks (mean duration, approximately 45 days). Until now, a few reports had described symptomatic hepatitis E acquired in Europe;5, 6 all patients with symptomatic hepatitis E in the United States were travelers returning from Mexico, Africa, or the Far East, in whom hepatitis E developed after their return home.7 In this issue of the Mayo Clinic Proceedings (pages 1133 to 1136), Kwo and associates describe a case of hepatitis E in a man who had not left the United States during the previous 10 years. Specific serologic tests for hepatitis E virus IgG (enzyme immunoassays and a fluorescent antibody blocking assay) and IgM8 (US strain-specific enzyme-linked immunosorbent assay with use of synthetic polypeptides deduced from the viral genome, as shown in Figure 1), developed at Abbott Laboratories (IgG and IgM) as well as at the Centers for Disease Control and Prevention (IgG), were used to prove that the patient indeed had acute hepatitis E. Researchers at Abbott Laboratories have prepared a report that describes most of the viral genome in this patient (Fig. I).8 Their results are interesting because this strain from the United States differs considerably from hepatitis E strains isolated in Mexico, Burma, Pakistan, or China. Furthermore, the sequence of the US strain is highly homologous (98% and 94% homology at the amino acid level to the second and third open reading frames, respectively) to a recently isolated hepatitis E strain from American swine.9 This finding suggests that, in the United States, hepatitis E is a zoonosis with the swine population as one of its hosts. This relationship would confirm earlier studies in Asia, where swine were also found to carry variants of the hepatitis E virus.10 Why are these two recent discoveries important for medicine in the United States? First, other sporadic, locally acquired cases of acute hepatitis may be caused by hepatitis E. Second, these back-to-back discoveries strongly suggest that a common natural host for hepatitis E is present in countries with more moderate climates. Because swine do not seem to experience any symptoms associated with infection and because symptoms in humans can be minor or absent, we now may also have an explanation for the 1 to 2% of positive hepatitis E serologic results in blood donors in the United States,11 Netherlands,12 and Italy,6 countries with large swine staples. Clearly, more research needs to be done to confirm this hypothesis. Third, in countries with more moderate climates, hepatitis E may often result in a subclinical infection. Is this variation in manifestation due to less virulent strains, and do sequence variations determine virulence? Fourth, swine may be used as an animal model for study of the disease as well as vaccine development.

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Graves disease is an autoimmune disorder that leads to an overactive thyroid gland (hyperthyroidism). An autoimmune disorder is a condition that occurs when the immune system mistakenly attacks healthy tissue. Causes The thyroid gland is an important organ of the endocrine system. The gland is located at the front of the neck above where the collarbones meet. This gland releases the hormones thyroxine (T4) and triiodothyronine (T3), which control body metabolism. Controlling metabolism is important for regulating mood, weight, and mental and physical energy levels. When the body makes too much thyroid hormone, the condition is called hyperthyroidism. (An underactive thyroid leads to hypothyroidism.) Graves disease is the most common cause of hyperthyroidism. It is due to an abnormal immune system response that causes the thyroid gland to produce too much thyroid hormone. Graves disease is most common in women over age 20. But the disorder can occur at any age and can affect men as well. Symptoms Younger people may have these symptoms: Anxiety or nervousness, as well as problems sleeping Breast enlargement in men (possible) Problems concentrating Fatigue Frequent bowel movements Hair loss Heat intolerance and increased sweating Increased appetite, despite having weight loss Irregular menstrual periods in women Muscle weakness of the hips and shoulders Moodiness, including irritability and anger Rapid or irregular heartbeat Shortness of breath with activity Tremor Many people with Graves disease have problems with their eyes: The eyeballs may seem to be bulging out and may be painful. Eyes can feel irritated and be tearing. Double vision may be present. Older people may have these symptoms: Rapid or irregular heartbeat Chest pain Memory loss Weakness and fatigue

New CPR Guidelines For Adults

New Minimally Invasive Procedure with No Pain or Downtime… From Dr. Michael Goodman, Caring For Women Wellness Center Laser Vaginal Tightening for Improved Sexual Pleasure and Relief from Minimal Urinary Incontinence Laser Vaginal Therapy for reversing Vaginal Atrophy (Good also for Breast Cancer Survivors with Vaginal Atrophy)

Factitious disorder is the term used to describe a pattern of behavior centered on the exaggeration or outright falsifications of one’s own health problems or the health problems of others. Some people with this disorder fake or exaggerate physical problems; others fake or exaggerate psychological problems or a combination of physical and psychological problems. Factitious disorder differs from a pattern of falsified or exaggerated behavior called malingering. While malingerers make their claims out of a motivation for personal gain, people with factitious disorder have no such motivation.

Keep tabs on your blood pressure. If it's too high, your risk of a heart attack and heart disease goes up. Stress management, a healthy diet, and regular exercise can help you manage your blood pressure. Your doctor may also prescribe medications to lower your levels.

Situs inversus is a condition in which the arrangement of the internal organs is a mirror image of normal anatomy. It can occur alone (isolated, with no other abnormalities or conditions) or it can occur as part of a syndrome with various other defects. Congenital heart defects are present in about 5-10% of affected people. The underlying cause and genetics of situs inversus are complex. Familial cases have been reported.[1][2]

Transjugular intrahepatic portosystemic shunt or transjugular intrahepatic portosystemic stent shunting (commonly abbreviated as TIPS or TIPSS) is an artificial channel within the liver that establishes communication between the inflow portal vein and the outflow hepatic vein.

The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Although many pathogenic processes have been implicated in the development of abdominal ascites, about 75% likely occur as a result of portal hypertension in the setting of liver cirrhosis, with the remainder due to infective, inflammatory, and infiltrative conditions. Three theories of ascites formation have been proposed: underfilling, overflow, and peripheral arterial vasodilation. The underfilling theory suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention. The overflow theory suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia. The most recent theory, the peripheral arterial vasodilation hypothesis, includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation theory proposes that underfilling is operative early and overflow is operative late in the natural history of cirrhosis. Although the sequence of events that occurs between the development of portal hypertension and renal sodium retention is not entirely clear, portal hypertension apparently leads to an increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those without ascites. Regardless of the initiating event, a number of factors contribute to the accumulation of fluid in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.

How are seizures and epilepsy treated? What should I do if someone has a seizure? When seizure medications don't work, what else can be tried? These are just a few of the questions that you'll find answered here. Some treatment goals are common to everyone. Everyone should know what to do when a person is having a seizure. All people with seizures and their families should know that the real goal of treating epilepsy is to stop seizures or control them as best as possible. But you are more than just a seizure and how epilepsy affects you and your family may be different from someone else. Don't forget the most important goal of the Epilepsy Foundation - helping people with seizures and their families lead full and unrestricted lives according to their own wishes. Patient and doctor discussing treatment options"No seizures, no side effects" is the motto for epilepsy treatment. Not every person will reach that goal right now, but research and getting the "right care at the right time" can help more people achieve it each year. You may learn things here that can help you right away or later on. While seizure medicines are the mainstay of epilepsy treatment, there are other approaches to think about too. We hope these sections will help you learn about different treatments and get the help you need. Learn about the basics of Treatment 101 to help you get started. Look at Receiving Quality Care to see what to expect when you have just been diagnosed or after you have already started treatment. Then learn about specific treatments, what to do if seizures don't stop, and how to develop your health care team. You'll also find tools to help you manage your epilepsy or learn about research studies in other sections, so don't stop here!

A stress ulcer is a single or multiple mucosal defect which can become complicated by upper gastrointestinal bleeding during the physiologic stress of serious illness.

Candida Albicans is more than just yeast- for most people, it's already mutated into a more aggressive fungal form that eats holes through the intestinal tract causing many of todays health problems like food allergies, autoimmune disorders, Crohn's disease, IBS, low energy and many more aggressive diseases. People need to know what it is and what to do about it.

How to examine a patient's wrist if you suspect a scaphoid fracture: by Cape Town Emergency Medicine

Chiari malformation (kee-AH-ree mal-for-MAY-shun) is a condition in which brain tissue extends into your spinal canal. It occurs when part of your skull is abnormally small or misshapen, pressing on your brain and forcing it downward.

Very small currents can be imperceptible. Larger current passing through the body may make it impossible for a shock victim to let go of an energized object. Still larger currents can cause fibrillation of the heart and damage to tissues. Death caused by an electric shock is called electrocution.

Each year, thousands of babies in the U.S. are born addicted to opiates. And the problem is getting worse.

What is a brain aneurysm? A brain (cerebral) aneurysm is a bulging, weak area in the wall of an artery that supplies blood to the brain. In most cases, a brain aneurysm causes no symptoms and goes unnoticed. In rare cases, the brain aneurysm ruptures, releasing blood into the skull and causing a stroke. When a brain aneurysm ruptures, the result is called a subarachnoid hemorrhage. Depending on the severity of the hemorrhage, brain damage or death may result.

Forehead wound repaired with "Liquiband" glue