Esophageal varices are abnormal, enlarged veins in the tube that connects the throat and stomach (esophagus). This condition occurs most often in people with serious liver diseases. Esophageal varices develop when normal blood flow to the liver is blocked by a clot or scar tissue in the liver. To go around the blockages, blood flows into smaller blood vessels that aren't designed to carry large volumes of blood. The vessels can leak blood or even rupture, causing life-threatening bleeding. A number of drugs and medical procedures can help prevent and stop bleeding from esophageal varices.

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.

Hepatitis is an inflammation of the liver. The condition can be self-limiting or can progress to fibrosis (scarring), cirrhosis or liver cancer. Hepatitis viruses are the most common cause of hepatitis in the world but other infections, toxic substances (e.g. alcohol, certain drugs), and autoimmune diseases can also cause hepatitis. There are 5 main hepatitis viruses, referred to as types A, B, C, D and E. These 5 types are of greatest concern because of the burden of illness and death they cause and the potential for outbreaks and epidemic spread. In particular, types B and C lead to chronic disease in hundreds of millions of people and, together, are the most common cause of liver cirrhosis and cancer. Hepatitis A and E are typically caused by ingestion of contaminated food or water. Hepatitis B, C and D usually occur as a result of parenteral contact with infected body fluids. Common modes of transmission for these viruses include receipt of contaminated blood or blood products, invasive medical procedures using contaminated equipment and for hepatitis B transmission from mother to baby at birth, from family member to child, and also by sexual contact. Acute infection may occur with limited or no symptoms, or may include symptoms such as jaundice (yellowing of the skin and eyes), dark urine, extreme fatigue, nausea, vomiting and abdominal pain.

Renal transplantation is the treatment of choice for a minority of patients with end-stage renal disease (ESRD). Most adult patients with ESRD are never referred for evaluation for transplantation, and have a 70% 5-year mortality on dialysis. Marked improvements in early graft survival and long-term graft function have made kidney transplantation a more cost-effective alternative to dialysis. In the United States, over 375,000 kidney transplants have been performed, and in 2012, 191,400 patients were alive and with a functioning transplanted kidney; currently, more than 101,000 patients are waiting for kidney transplants.[1, 2] Before the advent of immunosuppression, renal transplantation was limited to identical twins and was not applicable to the vast majority of patients with ESRD. The introduction of combined azathioprine-steroid therapy in 1963 produced encouraging results and became the mainstay of immunosuppression. Although this therapy improved the results of transplantation, acute rejection and complications associated with steroid therapy persisted. The introduction of cyclosporine in 1983 significantly improved the outcomes of all solid-organ transplants by reducing the risk of rejection. Further innovations, including anti–T cell antibodies (both monoclonal and polyclonal preparations), as well as other maintenance immunosuppressants (eg, tacrolimus, mycophenolate, sirolimus), have made a significant impact on both patient and graft survival. Currently, 1-year patient and graft survival rates exceed 90% in most transplant centers. For patient education information, see Kidney Transplant and the Mayo Clinic's kidney transplant information Web page.

intracranial hematoma occurs when a blood vessel ruptures within your brain or between your skull and your brain. The collection of blood (hematoma) compresses your brain tissue. An intracranial hematoma may occur because the fluid that surrounds your brain can't absorb the force of a sudden blow or a quick stop. Then your brain may slide forcefully against the inner wall of your skull and become bruised. Although some head injuries — such as one that causes only a brief lapse of consciousness (concussion) — can be minor, an intracranial hematoma is potentially life-threatening and often requires immediate treatment. An intracranial hematoma often, but not always, requires surgery to remove the blood.

An intracranial hematoma occurs when a blood vessel ruptures within your brain or between your skull and your brain. The collection of blood (hematoma) compresses your brain tissue. An intracranial hematoma may occur because the fluid that surrounds your brain can't absorb the force of a sudden blow or a quick stop. Then your brain may slide forcefully against the inner wall of your skull and become bruised. Although some head injuries — such as one that causes only a brief lapse of consciousness (concussion) — can be minor, an intracranial hematoma is potentially life-threatening and often requires immediate treatment. An intracranial hematoma often, but not always, requires surgery to remove the blood.

Retropharyngeal abscess (RPA) produces the symptoms of sore throat, fever, neck stiffness, and stridor. RPA occurs less commonly today than in the past because of the widespread use of antibiotics for suppurative upper respiratory infections. The incidence of RPA in the United States is rising, however. Once almost exclusively a disease of children, RPA is observed with increasing frequency in adults. It poses a diagnostic challenge for the emergency physician because of its infrequent occurrence and variable presentation.

Medial medullary syndrome, also known as Dejerine syndrome, represents less than 1% of brainstem stroke syndromes. Thrombotic or embolic occlusion of small perforating branches from vertebral or proximal basilar artery supplying the medial aspect of medulla oblongata cause this rare syndrome. It is characterized by contralateral hemiplegia/hemiparesis as well as hemisensory loss with ipsilateral hypoglossal palsy (ipsilateral tongue weakness and atrophy) from involvement of CN XII nucleus. Other manifestations e.g. vertigo, nausea, ipsilateral limb ataxia are also reported.

What is Wallenberg syndrome? Wallenberg syndrome is a rare condition in which an infarction, or stroke, occurs in the lateral medulla. The lateral medulla is a part of the brain stem. Oxygenated blood doesn’t get to this part of the brain when the arteries that lead to it are blocked. A stroke can occur due to this blockage. This condition is also sometimes called lateral medullary infarction. The cause of the syndrome isn’t always clear, however.

LDL (Bad) Cholesterol LDL cholesterol is considered the “bad” cholesterol because it contributes to plaque, a thick, hard deposit that can clog arteries and make them less flexible. This condition is known as atherosclerosis. If a clot forms and blocks a narrowed artery, heart attack or stroke can result. Another condition called peripheral artery disease can develop when plaque buildup narrows an artery supplying blood to the legs. View an animation of cholesterolHDL (Good) Cholesterol HDL cholesterol is considered “good” cholesterol because it helps remove LDL cholesterol from the arteries. Experts believe HDL acts as a scavenger, carrying LDL cholesterol away from the arteries and back to the liver, where it is broken down and passed from the body. One-fourth to one-third of blood cholesterol is carried by HDL. A healthy level of HDL cholesterol may also protect against heart attack and stroke, while low levels of HDL cholesterol have been shown to increase the risk of heart disease.

Although drug treatment of hypertension is associated with improved survival and decreased vascular complications, drug compliance is a major problem in the control of hypertension. All antihypertensive medications are associated with side effects; thus, it is a physician's responsibility to explain to each patient the side effects of the drugs he prescribes to treat hypertension, and to instill in the patient a sense of necessity for the treatment of hypertension. The choice of antihypertensive drug should be made based on each patient's lifestyle, overall health and ability to tolerate the drug. Ideally, the antihypertensive regimen should be simple, effective, convenient to take and have very few side effects.

Myocardial infarction (MI), commonly known as a heart attack, is defined pathologically as the irreversible death of myocardial cells caused by ischemia. Clinically, MI is a syndrome that can be recognized by a set of symptoms, chest pain being the hallmark of these symptoms in most cases, supported by biochemical laboratory changes, electrocardiographic (ECG) changes, or findings on imaging modalities able to detect myocardial injury and necrosis. According to the third universal definition of MI, implemented by a joint task force from the European Society of Cardiology (ESC), American College of Cardiology (ACC) Foundation, American Heart Association (AHA), and the World Heart Federation (WHF), MI is diagnosed when either of the following two criteria are met

Fifth disease is a mild rash illness caused by parvovirus B19. This disease, also called erythema infectiosum, got its name because it was fifth in a list of historical classifications of common skin rash illnesses in children. It is more common in children than adults. A person usually gets sick with fifth disease within 4 to 14 days after getting infected with parvovirus B19.

What causes rheumatic fever? Rheumatic fever is not an infection itself, but rather the result of an untreated strep infection. When your body senses the strep infection, it sends antibodies to fight it. Sometimes, these antibodies attack the tissues of your joints or heart instead. If the antibodies attack your heart, they can cause your heart valves to swell, which can lead to scarring of the valve "doors" (called leaflets or cusps). Who is at risk for rheumatic fever? Fewer than 0.3% of people who have strep throat also get rheumatic fever. Rheumatic fever is most common among children aged 5 to 15, but adults may have the condition as well. Doctors think that a weakened immune system may make some people more likely to get rheumatic fever. And, although antibiotic medicines have reduced the number of cases of rheumatic fever in developed countries, there are still thousands of reported cases. What are the symptoms of rheumatic fever and how is it diagnosed? Symptoms of rheumatic fever usually begin 1 to 6 weeks after you have had a strep infection. They are Fever Joint pain or swelling in your wrists, elbows, knees, or ankles Small bumps under the skin over your elbows or knees (called nodules) A raised, red rash on your chest, back, or stomach Stomach pain or feeling less hungry Weakness, shortness of breath, or feeling very tired Your doctor will begin by doing a throat culture to find out if you have a strep infection. Then, your doctor will use a stethoscope to listen to your heart. He or she will also look for nodules on your joints. Sometimes, blood tests, chest x-rays, or an electrocardiogram (ECG or EKG) may be needed for a more definite diagnosis. How is rheumatic fever treated? Rheumatic fever must be treated right away. If you have a sore throat that lasts longer than 3 days, or if you have a fever and headache along with your sore throat, you should see your doctor for a throat culture. Even if you do not have a sore throat but have a fever and a skin rash, this could also mean a strep infection, and you should get tested. Remember rheumatic fever can result from an untreated strep infection, so it is very important to treat the infection before it leads to a worse condition.

Kawasaki disease is a condition that causes inflammation in the walls of medium-sized arteries throughout the body, including the coronary arteries, which supply blood to the heart muscle. Kawasaki disease is also called mucocutaneous lymph node syndrome because it also affects lymph nodes, skin, and the mucous membranes inside the mouth, nose and throat. Signs of Kawasaki disease, such as a high fever and peeling skin, can be frightening. The good news is that Kawasaki disease is usually treatable, and most children recover from Kawasaki disease without serious problems.

Pancreatitis is inflammation in the pancreas. The pancreas is a long, flat gland that sits tucked behind the stomach in the upper abdomen. The pancreas produces enzymes that assist digestion and hormones that help regulate the way your body processes sugar (glucose). Pancreatitis can occur as acute pancreatitis — meaning it appears suddenly and lasts for days. Or pancreatitis can occur as chronic pancreatitis, which describes pancreatitis that occurs over many years. Mild cases of pancreatitis may go away without treatment, but severe cases can cause life-threatening complications.

Esophageal cancer is cancer that occurs in the esophagus — a long, hollow tube that runs from your throat to your stomach. Your esophagus carries food you swallow to your stomach to be digested. Esophageal cancer usually begins in the cells that line the inside of the esophagus. Esophageal cancer can occur anywhere along the esophagus, but in people in the United States, it occurs most often in the lower portion of the esophagus. More men than women get esophageal cancer. Esophageal cancer isn't common in the United States. In other areas of the world, such as Asia and parts of Africa, esophageal cancer is much more common.

http://barretts-esophagus-cure.info-pro.co Barrett's Esophagus, Barrett's Esophagus Metaplasia, Barrett's Esophagus Bulimia. Are you lost, scared, frustrated, or confused? Have you been recently diagnosed with Barrett’s? Maybe your loved one or a close family member is now a victim of this painful disease. If so, I’d like to share with you some possibly life changing information on how I personally cured my own Barrett’s Esophagus. But before I do I’d like you to take a deep breath, relax for a moment, and let your worry subside because. Even though the Society of Thoracic Surgeons has determined that people with Barrett’s Esophagus are 40x’s more likely to get esophageal cancer, this diagnosis isn’t always a death sentence. Having been a victim of Barrett’s myself, I can relate to the excruciating pain this disease can cause. Maybe you’re like I was, trying to hide the symptoms when the burning, the heartburn, and the PAIN would become so unbearable I’d try doing anything to block it out. I can clearly recall the feeling of those scorching corroding acids inside my throat that would burn like fire, tearing up my esophagus from the inside out. It’s a pain I will NEVER forget. For me, maybe like you, many of my days were spent in anguish and painful agony. Barrett’s Reversed Without Surgery, Pills, PPI Pumps, Antacids, or Drugs. Clicking Here http://barretts-esophagus-cure.info-pro.co

Middle cerebral artery syndrome is a condition whereby the blood supply from the middle cerebral artery (MCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the lateral aspects of frontal, temporal and parietal lobes, the corona radiata, globus pallidus, caudate and putamen. The MCA is the most common site for the occurrence of ischemic stroke.[1] Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with MCA syndrome. More distal blockages tend to produce milder deficits due to more extensive branching of the artery and less ischemic response. In contrast, the most proximal occlusions result in widespread effects that can lead to significant cerebral edema, increased intracranial pressure, loss of consciousness and could even be fatal.[1] In such occasions, mannitol (osmotic diuretic) or hypertonic saline are given to draw fluid out of the oedematus cerebrum to minimise secondary injury. Hypertonic saline is better than mannitol, as mannitol being a diuretic will decrease the mean arterial pressure and since cerebral perfusion is mean arterial pressure minus intracranial pressure, mannitol will also cause a decrease in cerebral perfusion. Contralateral hemiparesis and hemisensory loss of the face, upper and lower extremities is the most common presentation of MCA syndrome.[1] Lower extremity function is more spared than that of the faciobrachial region.[2] The majority of the primary motor and somatosensory cortices are supplied by the MCA and the cortical homunculus can, therefore, be used to localize the defects more precisely.it is important to note that middle cerebral artery lesions mostly affect the dominant hemisphere i.e. the left cerebral hemisphere.

LBD is not a rare disease. It affects an estimated 1.4 million individuals and their families in the United States. Because LBD symptoms can closely resemble other more commonly known diseases like Alzheimer’s and Parkinson’s, it is currently widely underdiagnosed. Many doctors or other medical professionals still are not familiar with LBD. LBD is an umbrella term for two related diagnoses. LBD refers to both Parkinson’s disease dementia and dementia with Lewy bodies. The earliest symptoms of these two diseases differ, but reflect the same underlying biological changes in the brain. Over time, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms. While it may take more than a year or two for enough symptoms to develop for a doctor to diagnose LBD, it is critical to pursue a formal diagnosis. Early diagnosis allows for important early treatment that may extend quality of life and independence. LBD is a multisystem disease and typically requires a comprehensive treatment approach. This approach involves a team of physicians from different specialties who collaborate to provide optimum treatment of each symptom without worsening other LBD symptoms. Many people with LBD enjoy significant improvement of their symptoms with a comprehensive approach to treatment, and some can have remarkably little change from year to year. Some people with LBD are extremely sensitive or may react negatively to certain medications used to treat Alzheimer’s or Parkinson’s in addition to certain over-the-counter medications.