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The HEENT, or Head, Eye, Ear, Nose and Throat Exam is usually the initial part of a general physical exam, after the vital signs. Like other parts of the physical exam, it begins with inspection, and then proceeds to palpation. It requires the use of several special instruments in order to inspect the eyes and ears, and special techniques to assess their special sensory function. This module reviews some of the relevant surface anatomy and describes the basic HEENT exam. The module includes an introduction to use of the ophthalmoscope.
Your baby's sex is set at conception. At around 7 weeks, your baby's internal sex organs – such as ovaries and testes – begin to form in the abdomen. Male and female sex organs and genitalia look the same at this stage because they're derived from the same structures. At around 9 weeks, boys and girls begin to develop differently. In girls, a tiny bud emerges between the tissue of the legs. This bud will become the clitoris. The membrane that forms a groove below the bud separates to become the labia minora and the vaginal opening. By 22 weeks, the ovaries are completely formed and move from the abdomen to the pelvis. They already contain a lifetime supply of 6 million eggs. In boys, the bud develops into the penis and starts to elongate at around 12 weeks. The outer membrane grows into the scrotal sac that will later house the testicles. By 22 weeks, the testes have formed in the abdomen. They already contain immature sperm. Soon they'll begin their descent to the scrotum, but it's a long journey. They'll reach their destination late in pregnancy, or for some boys, after birth. If you're eager to find out whether you're having a girl or a boy, you'll have to wait until you're at least 17 weeks pregnant. That's when the genitals have developed enough to be seen on an ultrasound.
Vasculitis is an inflammation of your blood vessels. It causes changes in the walls of blood vessels, including thickening, weakening, narrowing and scarring. These changes restrict blood flow, resulting in organ and tissue damage. There are many types of vasculitis, and most of them are rare. Vasculitis might affect just one organ, such as your skin, or it may involve several. The condition can be short term (acute) or long lasting (chronic). Vasculitis can affect anyone, though some types are more common among certain groups. Depending on the type you have, you may improve without treatment. Or you will need medications to control the inflammation and prevent flare-ups. Vasculitis is also known as angiitis and arteritis.
Nosebleeds are common. Most often they are a nuisance and not a true medical problem. But they can be both. Nosebleed care Sit upright and lean forward. By remaining upright, you reduce blood pressure in the veins of your nose. This discourages further bleeding. Sitting forward will help you avoid swallowing blood, which can irritate your stomach. Pinch your nose. Use your thumb and index finger to pinch your nostrils shut. Breathe through your mouth. Continue to pinch for five to 10 minutes. Pinching sends pressure to the bleeding point on the nasal septum and often stops the flow of blood. To prevent re-bleeding, don't pick or blow your nose and don't bend down for several hours after the bleeding episode. During this time remember to keep your head higher than the level of your heart. If re-bleeding occurs, blow out forcefully to clear your nose of blood clots and spray both sides of your nose with a decongestant nasal spray containing oxymetazoline (Afrin, Mucinex Moisture Smart, others). Pinch your nose again as described above and call your doctor. When to seek emergency care The bleeding lasts for more than 20 minutes The nosebleed follows an accident, a fall or an injury to your head, including a punch in the face that may have broken your nose
Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear in their mid-60s. Estimates vary, but experts suggest that more than 5 million Americans may have Alzheimer’s. Alzheimer's disease is currently ranked as the sixth leading cause of death in the United States, but recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people. Alzheimer’s is the most common cause of dementia among older adults. Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living. The causes of dementia can vary, depending on the types of brain changes that may be taking place. Other dementias include Lewy body dementia, frontotemporal disorders, and vascular dementia. It is common for people to have mixed dementia—a combination of two or more disorders, at least one of which is dementia. For example, some people have both Alzheimer's disease and vascular dementia. Alzheimer’s disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems, and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary, or tau, tangles). These plaques and tangles in the brain are still considered some of the main features of Alzheimer’s disease. Another feature is the loss of connections between nerve cells (neurons) in the brain. Neurons transmit messages between different parts of the brain, and from the brain to muscles and organs in the body.
Plantar warts are hard, grainy growths that usually appear on the heels or balls of your feet, areas that feel the most pressure. This pressure also may cause plantar warts to grow inward beneath a hard, thick layer of skin (callus). Plantar warts are caused by the human papillomavirus (HPV). The virus enters your body through tiny cuts, breaks or other weak spots on the bottom of your feet. Most plantar warts aren't a serious health concern and may not require treatment. But plantar warts can cause discomfort or pain. If self-care treatments for plantar warts don't work, you may want to see your doctor to have them removed.
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.