Most intact aortic aneurysms do not produce symptoms. As they enlarge, symptoms such as abdominal pain and back pain may develop. Compression of nerve roots may cause leg pain or numbness. Untreated, aneurysms tend to become progressively larger, although the rate of enlargement is unpredictable for any individual. Rarely, clotted blood which lines most aortic aneurysms can break off and result in an embolus. They may be found on physical examination. Medical imaging is necessary to confirm the diagnosis. Symptoms may include: anxiety or feeling of stress; nausea and vomiting; clammy skin; rapid heart rate. In patients presenting with aneurysm of the arch of the aorta, a common symptom is a hoarse voice as the left recurrent laryngeal nerve (a branch of the vagus nerve) is stretched. This is due to the recurrent laryngeal nerve winding around the arch of the aorta. If an aneurysm occurs in this location, the arch of the aorta will swell, hence stretching the left recurrent laryngeal nerve. The patient therefore has a hoarse voice as the recurrent laryngeal nerve allows function and sensation in the voicebox. Abdominal aortic aneurysms, hereafter referred to as AAAs, are the most common type of aortic aneurysm. One reason for this is that elastin, the principal load-bearing protein present in the wall of the aorta, is reduced in the abdominal aorta as compared to the thoracic aorta (nearer the heart). Another is that the abdominal aorta does not possess vasa vasorum, hindering repair. Most are true aneurysms that involve all three layers (tunica intima, tunica media and tunica adventitia), and are generally asymptomatic before rupture. The most common sign for the aortic aneuysm is the Erythema nodosum also known as leg lesions typically found near the ankle area. The prevalence of AAAs increases with age, with an average age of 65–70 at the time of diagnosis. AAAs have been attributed to atherosclerosis, though other factors are involved in their formation. An AAA may remain asymptomatic indefinitely. There is a large risk of rupture once the size has reached 5 cm, though some AAAs may swell to over 15 cm in diameter before rupturing. Before rupture, an AAA may present as a large, pulsatile mass above the umbilicus. A bruit may be heard from the turbulent flow in a severe atherosclerotic aneurysm or if thrombosis occurs. Unfortunately, however, rupture is usually the first hint of AAA. Once an aneurysm has ruptured, it presents with a classic pain-hypotension-mass triad. The pain is classically reported in the abdomen, back or flank. It is usually acute, severe and constant, and may radiate through the abdomen to the back. The diagnosis of an abdominal aortic aneurysm can be confirmed at the bedside by the use of ultrasound. Rupture could be indicated by the presence of free fluid in potential abdominal spaces, such as Morison's pouch, the splenorenal space (between the spleen and left kidney), subdiaphragmatic spaces (underneath the diaphragm) and peri-vesical spaces. A contrast-enhanced abdominal CT scan is needed for confirmation. Only 10–25% of patients survive rupture due to large pre- and post-operative mortality. Annual mortality from ruptured abdominal aneurysms in the United States alone is about 15,000. Another important complication of AAA is formation of a thrombus in the aneurysm.

Bipolar Disorder Types Overview

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This Underbalanced Drilling Animation demonstrates new oil drilling technology.

At one time, women who had delivered by cesarean section in the past would usually have another cesarean section for any future pregnancies. The rationale was that if allowed to labor, many of these women with a scar in their uterus would rupture the uterus along the weakness of the old scar. Over time, a number of observations have become apparent: Most women with a previous cesarean section can labor and deliver vaginally without rupturing their uterus. Some women who try this will, in fact, rupture their uterus. When the uterus ruptures, the rupture may have consequences ranging from near trivial to disastrous. It can be very difficult to diagnose a uterine rupture prior to observing fetal effects (eg, bradycardia). Once fetal effects are demonstrated, even a very fast reaction and nearly immediate delivery may not lead to a good outcome. The more cesarean sections the patient has, the greater the risk of subsequent rupture during labor. The greatest risk occurs following a “classical” cesarean section (in which the uterine incision extends up into the fundus.) The least risk of rupture is among women who had a low cervical transverse incision. Low vertical incisions probably increase the risk of rupture some, but usually not as much as a classical incision. Many studies have found the use of oxytocin to be associated with an increased risk of rupture, either because of the oxytocin itself, or perhaps because of the clinical circumstances under which it would be contemplated. Pain medication, including epidural anesthetic, has not resulted greater adverse outcome because of the theoretical risk of decreasing the attendant’s ability to detect rupture early. The greatest risk of rupture occurs during labor, but some of the ruptures occur prior to the onset of labor. This is particularly true of the classical incisions. Overall successful vaginal delivery rates following previous cesarean section are in the neighborhood of 70 This means that about 30of women undergoing a vaginal trial of labor will end up requiring a cesarean section. Those who undergo cesarean section (failed VBAC) after a lengthy labor will frequently have a longer recovery and greater risk of infection than had they undergone a scheduled cesarean section without labor. Women whose first cesarean was for failure to progress in labor are only somewhat less likely to be succesful in their quest for a VBAC than those with presumably non-recurring reasons for cesarean section. For these reasons, women with a prior cesarean section are counseled about their options for delivery with a subsequent pregnancy: Repeat Cesarean Section, or Vaginal Trial of Labor. They are usually advised of the approximate 70successful VBAC rate (modified for individual risk factors). They are counseled about the risk of uterine rupture (approximately 1in most series), and that while the majority of those ruptures do not lead to bad outcome, some of them do, including fetal brain damage and death, and maternal loss of future childbearing. They are advised of the usual surgical risks of infection, bleeding, anesthesia complications and surgical injury to adjacent structures. After counseling, many obstetricians leave the decision for a repeat cesarean or VBAC to the patient. Both approaches have risks and benefits, but they are different risks and different benefits. Fortunately, most repeat cesarean sections and most vaginal trials of labor go well, without any serious complications. For those choosing a trial of labor, close monitoring of mother and baby, with early detection of labor abnormalities and preparation for

Watch that video to know if it is safe to have anal sex

Twin Childbirth Video

The gastric balloon procedure (endoscopic intragastric balloon) leaves an inflated silicon balloon in the stomach for 6 months, making less room for food. As a result, patients: Feel full sooner while eating and therefore eat less. Lose about 30% of their excess weight in 6 months.

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Urogenital neoplasms spreading to the inguinal lymph nodes are penile carcinoma (the most frequent), urethral and scrotum cancers, tumors of the testis with scrotal violation. Penile carcinoma is an uncommon malignant disease and accounts for as many 0.4-0.6% of male cancers. Most patients are elder...ly. It rarely occurs in men under age 60 and its incidence increases progressively until it reaches a peak in the eighth decade 1. The risk of a lymph node invasion is greater with high grade and high stage tumors 2. Some investigators have reported the inaccuracy of the sentinel node biopsy 3, 4, described by Cabanas 5. Patients with metastatic lymph node penis cancer have a very poor prognosis if penectomy only is performed. Ilioinguinal lymphadenectomy is basically carried out as a treatment modality and not only as a staging act. Patients with lymph node invasion have a 30-40% cure rate. Ilioinguinal lymphadenectomy should be also performed in patients with disseminated neoplasms for the local control of the disease. The 5 years survival rate of patients with clinically negative lymph nodes treated with a modified inguinal lymphadenectomy is 88% versus 38% in patients not initially treated with lymphadenectomy 6. This video-tape clearly shows a therapeutic algorithm, the anatomy of the inguinal lymph nodes, according to Rouviere 7 and Daseler 8, the radical ilioinguinal node dissection with transposition of the sartorius muscle and the modified inguinal lymphadenectomy proposed by Catalona 9. References: 1. Lynch D.F. and Schellhammer P: Tumors of the penis. In Campbell’s Urology Seventh Edition, edited by Walsh P.C., Retik A.B., Darracott Vaughan E. and Wein A.J. W.B. Saunders Company, Vol. 3, chapt. 79, p. 2458, 1998. 2. Pizzocaro G., Piva L., Bandieramonte G., Tana S. Up-to-date management of carcinoma of the penis. Eur. Urol. 32: 5-15, 1997 3. Perinetti E., Crane D.B. and Catalona W.J. Unreliability of sentinel lymph node biopsy for staging penile carcinoma. J. Urol. 124: 734, 1980 4. Fowler J.E. Jr. Sentinel lymph node biopsy for staging penile cancer. Urology 23: 352, 1984 5. Cabanas R.M. An approach for the treatment of penile carcinoma. Cancer 39: 456, 1977 6. Russo P. and Gaudin P. Management strategies for carcinoma of the penis. Contemporary Urology;5:48-66, 2000 7. Rouviere H. Anatomy of the human lymphatic system. Edwards Brothers, p. 218, 1938 8. Daseler E.H., Anson B.J., Reimann A.F. Radical excision of the inguinal and iliac lymph glands: a study based on 450 anatomical dissections and upon supportive clinical observations. Surg. Gynecol. Obstet. 87: 679, 1948 9. Catalona W.J. Modified inguinal lymphadenectomy for carcinoma of the penis with preservation of saphenous veins: technique and preliminary results. J. Urol. 140: 306-310, 1988

EKG/ECG Interpretation Explained Clearly

The fetal circulation is the circulatory system of a human fetus, often encompassing the entire fetoplacental circulation that also includes the umbilical cord and the blood vessels within the placenta that carry fetal blood.

The fetal circulation works differently from that of born humans, mainly because the lungs are not in use: the fetus obtains oxygen and nutrients from the mother through the placenta and the umbilical cord.

Tension pneumothorax develops when a lung or chest wall injury is such that it allows air into the pleural space but not out of it (a one-way valve). As a result, air accumulates and compresses the lung, eventually shifting the mediastinum, compressing the contralateral lung, and increasing intrathoracic pressure enough to decrease venous return to the heart, causing shock. These effects can develop rapidly, particularly in patients undergoing positive pressure ventilation.

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.

http://crohnsulcerativecolitis.plus101.com/
----Crohn's Disease Symptoms Pain. Are you suffering from diarrhea that sometimes leaves you feeling that you've completely emptied your intestine from eveything you've eaten that week?
Have you seen bright red blood traces in your stool or on the toilet paper at least once?
Do you sometimes have abdominal cramps after your meals?
Do you at times feel so nauseous that food doesn't have any appeal to you?
Have you had at least one onset of unexplained low grade fever?
Do you joints sometimes feel itchy, sore or painful?
Did you ever notice red spots or blisters on your arms or legs?
Did you ever experience episodes of itchy and even painfull pink eye (conjuctivitis)?
Have you lost weight?
Do you have episodes of overwhelming fatigue?
Do you experience increased frequency of bowel movement?
Did you ever get up during the night to defecate?


Crohn's, Disease, Symptoms, Pain, symptoms of crohns, chrons disease symptoms , ulcerative colitis symptoms, symptoms of colitis, United States, United Kingdom, Canada, ulcerative colitis diet, ulcerative colitis treatment, irritable bowel symptoms

Doctor makes magic - Doctor hace magia (Sorprendente) - Doctor Magic

Are most spiders poisonous? The majority of the 3,000 spiders in the United States aren’t poisonous. Even if most spiders did bite, their fangs are too small or weak to puncture human skin. Their bites may leave itchy, red wounds that heal within a week or so. The spiders that do manage to bite through our skin and insert toxic venom can cause serious health complications. Read on to learn what spider bites look like, what spider varieties leave certain bites, and how to treat spider bites. What do spider bites look like? Identifying a spider bite is easier if you saw the spider that bit you, but it’s possible that you won’t notice the wound until hours later. Look for things like: swelling a red welt skin damage any troubling symptoms that accompany the bite Other possible symptoms that may accompany a spider bite include: itching or rash pain around the area of the bite muscle pain or cramping blister that’s red or purple in color sweating difficulty breathing headache nausea and vomiting fever chills anxiety or restlessness rashes swollen lymph glands high blood pressure Spider bites often take longer to heal than other insect bites, and they may affect skin tissues. It’s important to keep the bite clean to reduce the risk of infection. How to treat a spider bite at home In some cases, you can treat spider bites at home. For nonvenomous spider bites, follow these steps: Apply an ice pack on and off the bite for 10 minutes at a time. Elevate the area to reduce swelling. Take an antihistamine, such as diphenhydramine (Benadryl), to help with itching. Clean the area with soap and water to prevent infection. Apply antibiotic ointment to the area if blisters develop. Seek medical attention if you’re showing symptoms of a spider bite or if the symptoms don’t go away over time. Always seek medical attention if you suspect you’ve been bitten by one of the following species: brown recluse black widow hobo spider tarantula Brazilian wandering spider

Asthma is a condition in which your airways narrow and swell and produce extra mucus. This can make breathing difficult and trigger coughing, wheezing and shortness of breath. For some people, asthma is a minor nuisance. For others, it can be a major problem that interferes with daily activities and may lead to a life-threatening asthma attack. Asthma can't be cured, but its symptoms can be controlled. Because asthma often changes over time, it's important that you work with your doctor to track your signs and symptoms and adjust treatment as needed.

Vascular dementia is a general term describing problems with reasoning, planning, judgment, memory and other thought processes caused by brain damage from impaired blood flow to your brain. You can develop vascular dementia after a stroke blocks an artery in your brain, but strokes don't always cause vascular dementia. Whether a stroke affects your thinking and reasoning depends on your stroke's severity and location. Vascular dementia also can result from other conditions that damage blood vessels and reduce circulation, depriving your brain of vital oxygen and nutrients