Meningitis: a rare but dangerous disease for students

Meningococcal meningitis is an uncommon disease, yet it affects college students at seven times the national average, and dorm residents are encouraged to be immunized.

Photo by Trung Le. Jean Haulman, associate medical director of public health and immunization at Hall Health, holds a meningococcal vaccine called “menactra”.

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The infection, which causes inflammation of the brain, can be deadly. Of those who contract it, there is a 10 to 15 percent mortality rate. Otherwise, serious debilitation is a possibility.
“Out of all the people in the United States who get meningitis and live, about 25 percent lose an arm or leg, become mentally retarded, or experience seizures,” said Jean Haulman, associate medical director of public health and immunization at Hall Health.
About one in every 100,000 people contracts the disease.
“There haven’t been any cases at UW in the four years I’ve been at Hall Health immunization — but if you get it, it has a high mortality rate and is dangerous,” she said.
The vaccine available in the United States is effective against four of the five types of meningitis. Among them, the B-strain is the most rare. Cuba has a vaccine for it, available since the 1980s, according to the BBC, yet no such vaccine is available in the United States because of the Cuban embargo, a ban on trade with the country.
Hall Health has Menactra, a vaccine available since 2005, which protects against the disease for up to 10 years, Haulman said.
Another vaccine, Menomune, is effective for five years. Both vaccines protect about 90 percent of those immunized and are made available to most young people through a federal program called Vaccines for Children (VFC). The program provides certain vaccines, including the one for meningitis, for free for all children up to age 19. Established in 1993, VFC is funded by both the Centers for Disease Control and Prevention and the state.
“The longevity of the new vaccine, along with the Vaccines for Children Program are … [leading to] more students coming to college already immunized,” Haulman said.
There is also heightened awareness about meningitis, said Jill Appel, nurse manager at Hall Health.
“The media hype around meningitis has also contributed to [getting] vaccines done [at an] earlier age. It’s also becoming standard among pediatric immunizations,” she said.
Thirty-five vaccinations have been given at Hall Health to people 19 and older in the past six months, Appel said. Most immunizations are provided during fall quarter, though students can take advantage of the program before the fall, Haulman said.
If a student is infected, Haulman must inform the campus community.
“We usually send out campus-wide e-mails,” she said. “With something like this, however, we would probably focus on students who were in close proximity to, or intimately involved with, the person infected.”
Symptoms may seem innocuous at first: a stiff neck, rash and high fever. However, Haulman said, “People can feel ok, but can get really sick quickly.”
If someone has these symptoms and starts feeling confused, they should immediately seek medical attention, she said.

Leucoderma

Leucoderma is a chronic disorder of the skin where the skin stops producing pigments that color the skin. As a result white patches appear randomly at different locations on the skin. These patches are white in color and as time passes may increase in number and size. Leucoderma is not a medical term. It is only a substitute name for vitiligo. Vitiligo is a more common name for this disease in the west where as in Asia leucoderma is used more.

The Skin is colored in different shades of brown due to a pigment called melanin.Special cells called melanocytes are responsible for the production of melanin. Sometimes, for reasons dubious, the melanocytes stop producing melanin which results in white skin patches.

There are many explanations as to why this happens but none of these explanations has been proven to be the right one. This also explains why there is no confirmed cure for leucoderma. Even after extensive scientific research, the treatments of leucoderma are still very scarce and have not been proven to work for a majority of people. The best patients can do is hide these marks with colored creams but it is to be noted, this only hides these marks and doesn't stop more patches of white skin from appearing. There is no explanation as to the location of these patches of skin. Also, a question that may rise is why only patches appear and not the whole body is affected. For this too there is no proven explanation.

About 0.5% to 2% of the worlds population currently suffer from leucoderma. Leucoderma is not a contagiuos disease so there is no way a person can have leucoderma just by being around another person having it. Even though this is a proven fact, patients suffering from leucoderma often aren't accepted well in the social world. This often results in the patients suffering from depressive disorders.

Causes
As mentioned above, the reason for leucoderma is still not very clear. However some theories are present and are as follows The first and most supported theory is autoimmune. In this case, the bodies self defense mechanism mistakes the melanocytes as foreign particles and destroys them thus putting melanin production to a halt. There is evidence that points towards this theory and tests are being carried out to determine if this is accurate and how to stop this.

The second theory suggests that the oxidant-antioxidant system of the body is, for an unknown reason, disturbed resulting in loss of melanocytes. A third theory is more based on statistical data than research. Statistics suggest that if a parent has leucoderma, his/her child will have a higher risk of having leucoderma than the rest of the population. So this theory suggests that a genetic factor is present in the causes of this disease. A fourth theory suggests that leucoderma is a direct cause of nerve damage. This can also be true as in a type of leucoderma called as segmental vitiligo, the areas of skin affected are often the areas in contact with the dorsal root of the spinal chord.

Treatments
Its very hard to find a proper cure for a disease, the reason to which is still unknown. There are many treatmets suggested for leucoderma but none of them are proven 100% successful.
Using colored creams and tanning creams to hide the patches of skin is a more common method. This hides the patches but requires a lot of time to apply the creams and the drawback is it doesnt prevent more spots from appearing.

Steroid creams are also very commonly used. Steroid affects the immune system of the body by weakening it. So when a steroid cream is applied to the skin, the antibodies in the skin are weakened and they stop attacking the melanocytes and melanin production is resumed. It is to be noted that this treatment does not guarantee that the patches will not appear again. Also, steroid creams can not be used continuously for as long as one wishes to use them. Steroids have serious side-affects which include permanent thinning of the skin and appearance of stretch marks on area of application, which are also permanent. Steroid creams also make the skin less resistant to infections.

A more advanced but complicated method is giving specific medicinal drugs and expose patient to ultra violet light in special UV radiation chambers. This causes serious sunburns and skin freckling. Also it is very time consuming and once again, doesn't guarantee results.

Whatever the reason maybe, patients who are dismayed and have lost hope as to the cure of leucoderma need not worry. Herbal medicine has been helping mankind to get rid of the worst diseases for a very very long time. In this case, we present a special oil that cures leucoderma and you can easily regain your skin color in no time. This oil has been proven to work and if you don't believe us, we offer you 100% money-back guarantee. If your scars do not disappear we will return you your money back.

What is leprosy?

Leprosy is a disease caused by the bacteria Mycobacterium leprae, which causes damage to the skin and the peripheral nervous system. The disease develops slowly (from six months to 40 years!) and results in skin lesions and deformities, most often affecting the cooler places on the body (for example, eyes, nose, earlobes, hands, feet, and testicles). The skin lesions and deformities can be very disfiguring and are the reason that infected individuals historically were considered outcasts in many cultures. Although human-to-human transmission is the primary source of infection, three other species can carry and (rarely) transfer M. leprae to humans: chimpanzees, mangabey monkeys, and nine-banded armadillos. The disease is termed a chronic granulomatous disease, similar to tuberculosis, because it produces inflammatory nodules (granulomas) in the skin and nerves over time.

What is the history of leprosy (Hansen's disease)?

Unfortunately, the history of leprosy and its interaction with man is one of suffering and misunderstanding. The newest research suggests that at least as early as 4000 B.C. individuals had been infected with M. leprae, while the first known written reference to the disease was found on Egyptian papyrus in about 1550 B.C. The disease was well recognized in ancient China, Egypt, and India, and there are several references to the disease in the Bible. Because the disease was poorly understood, very disfiguring, slow to show symptoms, and had no known treatment, many cultures thought the disease was a curse or punishment from the gods. Consequently, leprosy was left to be "treated" by priests or holy men, not physicians.

Picture of a person with leprosy (Hansen's disease)

Since the disease often appeared in family members, some people thought it was hereditary; other people noted that if there was little or no contact with infected individuals, the disease did not infect others. Consequently, some cultures considered infected people (and occasionally their close relatives) as "unclean" or as "lepers" and ruled they could not associate with uninfected people. Often infected people had to wear special clothing and ring bells so uninfected people could avoid them.
The Romans and the Crusaders brought the disease to Europe, and the Europeans brought it to the Americas. In 1873, Dr. Hansen discovered bacteria in leprosy lesions, suggesting leprosy was an infectious disease, not a hereditary disease or a punishment from the gods. However, patients with the disease were still ostracized by many societies and cared for only at missions by religious personnel. Patients with leprosy were encouraged or forced to live in seclusion up to the 1940s, even in the U.S. (for example, the leper colony on Molokai, Hawaii, and at Carville, La.), often because no effective treatments were available.
Because of Hansen's discovery of M. leprae, efforts were made to find treatments that would stop or eliminate M. leprae; in the early 1900s to about 1940, oil from Chaulmoogra nuts was used with questionable efficacy by injecting it into patients' skin. At Carville in 1941, promin, a sulfone drug, showed efficacy but required many painful injections. Dapsone pills were found to be effective in the 1950s, but soon (1960s-1970s), M. leprae developed resistance to dapsone. Fortunately, drug trials on the island of Malta in the 1970s showed that a three-drug combination (dapsone, rifampicin [Rifadin], and clofazimine [Lamprene]) was very effective in killing M. leprae. This multi-drug treatment (MDT) was recommended by the WHO in 1981 and remains, with minor changes, the therapy of choice. MDT, however, does not alter the damage done to an individual by M. leprae before MDT is started.
Currently, there are several areas (India, East Timor) of the world where the WHO and other agencies (for example, the Leprosy Mission) are working to decrease the number of clinical cases of leprosy and other diseases such as rabies and schistosomiasis that occur in remote regions. Although researchers hope to eliminate leprosy like smallpox, endemic (meaning prevalent or embedded in a region) leprosy makes complete eradication unlikely. In the U.S., leprosy has occurred infrequently but is considered endemic in Texas, Louisiana, Hawaii, and the U.S. Virgin Islands by some investigators.
Leprosy is often termed "Hansen's disease" by many clinicians in an attempt to have patients forgo the stigmas attached to being diagnosed with leprosy.

Insomnia Treatment

What Are Some  of the Treatments for Insomnia?

Generally, treatment of insomnia entails both non-pharmacologic (non-medical) and pharmacologic (medical) aspects. It is best to tailor treatment for individual person based on the potential cause. Studies have shown that combining medical and non-medical treatments typically is more successful in treating insomnia than either one alone.
Non-medical treatment and behavioral therapy include:

• sleep hygiene,
• relaxation therapy,
• stimulus control, and/or
• sleep restriction.

Examples of prescription and OTC sleep aids are:

• benzodiazepine sedatives,
• nonbenzodiazepine sedatives,
• antidepressants,
• and others.

Read more information about the OTC and prescription treatments for insomnia »

Insomnia Overview

Most adults have experienced insomnia or sleeplessness at one time or another in their lives. An estimated 30%-50% of the general population are affected by insomnia, and 10% have chronic insomnia.
Insomnia is a symptom, not a stand-alone diagnosis or a disease. By definition, insomnia is "difficulty initiating or maintaining sleep, or both" or the perception of poor quality sleep. Insomnia may therefore be due to inadequate quality or quantity of sleep. Insomnia is not defined by a specific number of hours of sleep that one gets, since individuals vary widely in their sleep needs and practices. Although most of us know what insomnia is and how we feel and perform after one or more sleepless nights, few seek medical advice. Many people remain unaware of the behavioral and medical options available to treat insomnia.
Insomnia is generally classified based on the duration of the problem. Not everyone agrees on one definition, but generally:

• symptoms lasting less than one week are classified as transient insomnia,
  
• symptoms between one to three weeks are classified as short-term insomnia, and
  
• those longer than three weeks are classified as chronic insomnia.

Statistics on Insomnia
Insomnia affects all age groups. Among adults, insomnia affects women more often than men. The incidence tends to increase with age. It is typically more common in people in lower socioeconomic (income) groups, chronic alcoholics, and mental health patients. Stress most commonly triggers short-term or acute insomnia. If you do not address your insomnia, however, it may develop into chronic insomnia.
Some surveys have shown that 30% to 35% of Americans reported difficulty falling asleep during the previous year and about 10% reported problems with long standing insomnia. There also seems to be an association between depression, anxiety, and insomnia. Although the nature of this association is unknown, people with depression or anxiety were significantly more likely to develop insomnia.

Rickets

Rickets is a disease of growing bone that is unique to children and adolescents. It is caused by a failure of osteoid to calcify in a growing person. Failure of osteoid to calcify in adults is called osteomalacia. Vitamin D deficiency rickets occurs when the metabolites of vitamin D are deficient. Less commonly, a dietary deficiency of calcium or phosphorus may also produce rickets. Vitamin D-3 (cholecalciferol) is formed in the skin from a derivative of cholesterol under the stimulus of ultraviolet-B light. Ultraviolet light or cod liver oil was the only significant source of vitamin D until early in the 20th century when ergosterol (vitamin D-2) was synthesized from irradiated plant steroids.
During the Industrial Revolution, rickets appeared in epidemic form in temperate zones where the pollution from factories blocked the sun’s ultraviolet rays. Thus, rickets was probably the first childhood disease caused by environmental pollution.
Natural nutritional sources of vitamin D are limited primarily to fatty, ocean-going fish. In the United States, dairy milk is fortified with vitamin D (400 IU/L) Human milk contains little vitamin D, generally less than 20-40 IU/L. Therefore, infants who are breastfed are at risk for rickets, especially those who receive no oral supplementation and those who have darkly pigmented skin, which blocks penetration of ultraviolet light.
Findings in rickets are illustrated in the image below.
Findings in patients with rickets.

Next Section: Pathophysiology

Pathophysiology

Cholecalciferol (ie, vitamin D-3) is formed in the skin from 5-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps. The first hydroxylation occurs at position 25 in the liver, producing calcidiol (25-hydroxycholecalciferol), which circulates in the plasma as the most abundant of the vitamin D metabolites and is thought to be a good indicator of overall vitamin D status. The second hydroxylation step occurs in the kidney at the 1 position, where it undergoes hydroxylation to the active metabolite calcitriol (1,25-dihydroxycholecalciferol). This cholecalciferol is not technically a vitamin but a hormone.
Calcitriol acts at 3 known sites to tightly regulate calcium metabolism. Calcitriol promotes absorption of calcium and phosphorus from the intestine, increases reabsorption of phosphate in the kidney, and acts on bone to release calcium and phosphate. Calcitriol may also directly facilitate calcification. These actions increase the concentrations of calcium and phosphorus in extracellular fluid. The increase of calcium and phosphorus in extracellular fluid, in turn, leads to the calcification of osteoid, primarily at the metaphyseal growing ends of bones but also throughout all osteoid in the skeleton. Parathyroid hormone facilitates the 1-hydroxylation step in vitamin D metabolism.

In the vitamin D deficiency state, hypocalcemia develops, which stimulates excess parathyroid hormone, which stimulates renal phosphorus loss, further reducing deposition of calcium in the bone. Excess parathyroid hormone also produces changes in the bone similar to those occurring in hyperparathyroidism. Early in the course of rickets, the calcium concentration in the serum decreases. After the parathyroid response, the calcium concentration usually returns to the reference range, though phosphorus levels remain low. Alkaline phosphatase, which is produced by overactive osteoblast cells, leaks to the extracellular fluids so that its concentration rises to anywhere from moderate elevation to very high levels.

Intestinal malabsorption of fat and diseases of the liver or kidney may produce the clinical and secondary biochemical picture of nutritional rickets. Anticonvulsant drugs (eg, phenobarbital, phenytoin) accelerate metabolism of calcidiol, which may lead to insufficiency and rickets, particularly in children who are kept indoors in institutions.

Calcium and vitamin D intakes are low in infants who are fed vegan diets, particularly lactovegans, and monitoring of their vitamin D status is essential.^[1]

Studies have noted that disorders of increased fibroblast growth factor 23 (FGF-23) function are associated with rickets.^[2]

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Next Section: Pathophysiology

Epidemiology

Frequency

United States

In the United States, vitamin D deficiency rickets does not occur in formula-fed infants because formula and milk sold in the United States contains 400 IU of vitamin D per liter. Except in pediatric patients with chronic malabsorption syndromes or end-stage renal disease, nearly all cases of rickets occur in breastfed infants who have dark skin and receive no vitamin D supplementation.

International

Incidence in Europe is similar to that in the United States. In sunny areas, such as in the Middle East, rickets may occur when infants are bundled in clothing and are not exposed to sunlight. In some parts of Africa, deficiency of calcium, phosphorus, or both in the diet may also lead to rickets, especially in societies were corn is predominant in the diet.

Mortality/Morbidity

Skeletal deformity and short stature may occur. Severe rickets has been associated with respiratory failure in children, and resulting pelvic distortion in females may lead to problems with vaginal delivery later in life.

Race

Individuals with dark skin are at increased risk for vitamin D deficiency rickets.

Sex

No sexual predilection is noted.

Age

By definition, rickets is observed only in growing children, although the effects may be observed later in life.

Glaucoma

Glaucoma is a disease caused by increased intraocular pressure (IOP) resulting either from a malformation or malfunction of the eye's drainage structures. Left untreated, an elevated IOP causes irreversible damage the optic nerve and retinal fibers resulting in a progressive, permanent loss of vision. However, early detection and treatment can slow, or even halt the progression of the disease.
What causes glaucoma?
The eye constantly produces aqueous, the clear fluid that fills the anterior chamber (the space between the cornea and iris). The aqueous filters out of the anterior chamber through a complex drainage system. The delicate balance between the production and drainage of aqueous determines the eye's intraocular pressure (IOP). Most people's IOPs fall between 8 and 21.  However, some eyes can tolerate higher pressures than others. That's why it may be normal for one person to have a higher pressure than another.
Common types of glaucoma
Open Angle
Open angle (also called chronic open angle or primary open angle) is the most common type of glaucoma. With this type, even though the anterior structures of the eye appear normal, aqueous fluid builds within the anterior chamber, causing the IOP to become elevated. Left untreated, this may result in permanent damage of the optic nerve and retina. Eye drops are generally prescribed to lower the eye pressure. In some cases, surgery is performed if the IOP cannot be adequately controlled with medical therapy. 
Acute Angle Closure
Only about 10% of the population with glaucoma has this type. Acute angle closure occurs because of an abnormality of the structures in the front of the eye. In most of these cases, the space between the iris and cornea is more narrow than normal, leaving a smaller channel for the aqueous to pass through. If the flow of aqueous becomes completely blocked, the IOP rises sharply, causing a sudden angle closure attack.
While patients with open angle glaucoma don’t typically have symptoms, those with angle closure glaucoma may experience severe eye pain accompanied by nausea, blurred vision, rainbows around lights, and a red eye. This problem is an emergency and should be treated by an ophthalmologist immediately. If left untreated, severe and permanent loss of vision will occur in a matter of days.
Secondary Glaucoma
This type occurs as a result of another disease or problem within the eye such as: inflammation, trauma, previous surgery, diabetes, tumor, and certain medications. For this type, both the glaucoma and the underlying problem must be treated.
Congenital
This is a rare type of glaucoma that is generally seen in infants. In most cases, surgery is required.

Signs and Symptoms
Glaucoma is an insidious disease because it rarely causes symptoms.  Detection and prevention are only possible with routine eye examinations.  However, certain types, such as angle closure and congenital, do cause symptoms.
Angle Closure (emergency)

• Sudden decrease of vision
• Extreme eye pain
• Headache
• Nausea and vomiting
• Glare and light sensitivity

Congenital

• Tearing
• Light sensitivity
• Enlargement of the cornea

DETECTION AND DIAGNOSIS

Because glaucoma does not cause symptoms in most cases, those who are 40 or older should have an annual examination including a measurement of the intraocular pressure. Those who are glaucoma suspects may need additional testing. 
The glaucoma evaluation has several components. In addition to measuring the intraocular pressure, the doctor will also evaluate the health of the optic nerve (ophthalmoscopy), test the peripheral vision (visual field test), and examine the structures in the front of the eye with a special lens (gonioscopy) before making a diagnosis.

The above photos show progressive optic nerve damage (indicated by the cup to disc ratio) caused by glaucoma. Notice the pale appearance of the nerve with the 0.9 cup as compared to the nerve with the 0.3 cup.
The doctor evaluates the optic nerve and grades its health by noting the cup to disc ratio. This is simply a comparison of the cup (the depressed area in the center of the nerve) to the entire diameter of the optic nerve. As glaucoma progresses, the area of cupping, or depression, increases.  Therefore, a patient with a higher ratio has more damage.
The progression of glaucoma is monitored with a visual field test. This test maps the peripheral vision, allowing the doctor to determine the extent of vision loss from glaucoma and a measure of the effectiveness of the treatment. The visual field test is periodically repeated to verify that the intraocular pressure is being adequately controlled.
The structures in the front of the eye are normally difficult to see without the help of a special gonioscopy lens. This special mirrored contact lens allows the doctor to examine the anterior chamber and the eye's drainage system. 
At St. Luke's, another test called the Arden Screening Test is used to confirm the diagnosis of glaucoma. This color test may show vision changes that occur before problems appear on the visual field test.

TREATMENT

Most patients with glaucoma require only medication to control the eye pressure. Sometimes, several medications that complement each other are necessary to reduce the pressure adequately. Surgery is indicated when medical treatment fails to lower the pressure satisfactorily. There are several types of procedures, some involve laser and can be done in the office, others must be performed in the operating room. The objective of any glaucoma operation is to allow fluid to drain from the eye more efficiently.
Should you be treated for glaucoma?  Click here to learn more.
St. Luke's Cataract & Laser Institute provides this on-line information for educational and communication purposes only and it should not be construed as personal medical advice.  Information published on this St. Luke's website is not intended to replace, supplant, or augment a consultation with an eye care professional regarding the viewer/user's own medical care.  St. Luke's disclaims any and all liability for injury or other damages that could result from use of the information obtained from this site.

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Typhoid fever and paratyphoid fever

Typhoid fever is an infectious feverish disease, with severe symptoms in the digestive system in the second phase of the illness. The French used to call the disease a 'boil of the intestine'.
Classic typhoid fever is a serious disease. It can be life-threatening, but antibiotics are an effective treatment.
The disease lasts several weeks and convalescence takes some time.
The disease is transmitted from human to human via food or drinking water, and it's therefore mainly hygiene and sanitary conditions that determine its spread.
It's rarely seen in Europe, and 94 per cent of imported cases are from the Indian subcontinent.
In the UK, the Health Protection Agency (HPA) data indicates sources of infection as: India, Spain, Egypt, Turkey, Tunisia, Portugal and Morocco.

What causes typhoid fever and paratyphoid fever?

Typhoid fever is caused by an infection with a bacterium.
This bacterium has different names in different places (UK experts prefer the name Salmonella enteritica serovar Typhi, but the US may still call it Salmonella typhi). It's only found in humans and may lead to serious illness.
When the bacterium passes down to the bowel, it penetrates through the intestinal mucosa (lining) to the underlying tissue.
If the immune system is unable to stop the infection here, the bacterium will multiply and then spread to the bloodstream, after which the first signs of disease are observed in the form of fever.
The bacterium penetrates further to the bone marrow, liver and bile ducts, from which bacteria are excreted into the bowel contents.
In the second phase of the disease the bacterium penetrates the immune tissue of the small intestine, and the often violent small-bowel symptoms begin.
Paratyphoid fever is caused by Salmonella paratyphi, a similar and generally milder disease.
Salmonella enteriditis and Salmonella typhimurium are other salmonella bacteria, which are unfortunately quite familiar within the UK and cause food poisoning and diarrhoea.
The term 'murine typhus' is used for salmonella in animals.

How is typhoid fever spread?

Salmonella typhi can only attack humans. So, the infection always comes from another human, either an ill person or a healthy carrier of the bacterium.
The bacterium is passed on with water and foods and can withstand both drying and refrigeration.
As it's necessary for someone to be exposed to a certain quantity of bacteria before symptoms occur, the storage of foods is also of great significance.
They must be kept refrigerated and prepared correctly, as required by general hygiene, so that any bacteria present are not able to multiply significantly.

Where does typhoid fever occur?

Typhoid fever is not a tropical disease and is related to hygiene and sanitary conditions rather than the climate itself.
Typhoid fever is found in large parts of Asia, Africa, Central and South America, where it occasionally causes epidemics.
The WHO estimates that there are approximately 16 million cases a year, which result in 600,000 deaths. Many of those infected get the disease in Asian countries.

What are the symptoms of the disease?

The incubation period is 10 to 20 days and depends on, among other things, how large a dose of bacteria has been taken in.
In the mild disease, the bacterium is eliminated very early in the course of the disease and there are perhaps only mild symptoms. It's possible to become a healthy carrier of infection.
There are two phases of classic typhoid fever:

• 1st phase: the patient's temperature rises gradually to 40ºC, and the general condition becomes very poor with bouts of sweating, no appetite, coughing and headache. Constipation and skin symptoms may be the clearest symptoms. Children often vomit and have diarrhoea. The first phase lasts a week and towards the end the patient shows increasing listlessness and clouding of consciousness.
• 2nd phase: in the second to third weeks of the disease, symptoms of intestinal infection are manifested and the fever remains very high and the pulse becomes weak and rapid. In the third week, the constipation is replaced by severe pea-soup-like diarrhoea. The faeces may also contain blood. It's not until the fourth or fifth week that the fever drops and the general condition slowly improves.

Complications

Intestinal perforation or profuse bleeding from the intestinal mucosa may occur if typhoid fever is left untreated.

Outlook

There are good prospects of cure with antibiotics, and the patient can be discharged from hospital when the general condition is stable.
But good general hygiene (as always) should be maintained in the home because bacteria may continue to be excreted for several more weeks.
If the patient is a food handler, they'll need to stay off work until at least two stool samples show absence of the infection.

What can you do yourself?

• There are several forms of vaccine that protect against Salmonella typhi. Most UK travel clinics use the injectable form (Typherix or Typhim Vi), rather than the oral form preferred in the USA (Vivotif). The injectable vaccine is easier to administer, since it only requires one dose and has less side-effects. It should be administered at least two weeks prior to potential typhoid exposure and is effective for three years.
• The routes of infection depend on hygiene conditions, and general kitchen hygiene should be maintained to prevent infection. For travel, the same precautions can be taken as described under cholera.

How is the disease diagnosed?

The clinical picture together with information on travel may be a good pointer for the doctor in moderate to severe cases. For the final diagnosis to be established, the bacteria have to be detected in samples from the stool, blood or other tissue. A serology test (Widal) not much used in the UK can be very useful overseas in areas where the infection is more common.
Malaria also needs to be considered as another possible explanation for the symptoms of the disease when the patient has been travelling in a malarial area.

How is typhoid fever treated?

Treatment may require admission to hospital, and loss of fluid and salt is treated with fluid therapy as appropriate.
The bacterium is controlled with antibiotics, and in rare cases steroid medicines are also included in the treatment.

MALARIA: A DEADLY DISEASE

• 
• Malaria is a potentially deadly tropical disease characterized by cyclical bouts of fever with muscle stiffness, shaking and sweating. It is caused by a tiny parasite (genus Plasmodium) that is transmitted by the female mosquito (genus Anopheles) when it feeds on blood for its developing eggs.
• Severe malaria is not readily distinguishable from other severe diseases, such as pneumonia typhoid and meningitis that require very different therapy.
• Almost all vertebrates, birds, snakes and monkeys, for example, can be infected by Plasmodium (malaria) parasites. Different animal species can only be infected by their own specific species of Plasmodium.
• Humans are generally host to four species of malaria parasites: Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae. Plasmodium falciparum causes the most dangerous complications, such as cerebral malaria. It is the species that is most virulent and potentially lethal to humans.
• Because of its dependence on human/vector (mosquito) contact, malaria is considered to be a disease of poverty. Poor people can be physically marginalized and live closer to degraded land and conditions where mosquitoes thrive. They are also less likely to have physical barriers such as screens or nets to protect them and they often lack the education and resources to access proper care and treatment.
• Intense and costly control programmes targeting malaria, that incorporate a variety of approaches such as environmental modification and indoor spraying with DDT, have succeeded in eliminating or significantly reducing the disease in many countries. Malaria has been eliminated in former Soviet Republics, the USA, Italy, Korea and many Caribbean Islands.
• The Anopheles gambiae mosquito selects small, sunlit collections of water to lay its eggs. The intact forest provides few such breeding sites so there are few malarious mosquitoes in dark jungles and tropical forests. Replacing tropical forests with agricultural land provides the mosquitoes with the conditions and proximity to human hosts that they require to thrive.
• Malaria is transmitted by an infected, female mosquito; Anopheles gambiae. It can also be acquired from an infected blood transfusion or even from the shared needles of drug addicts.
• Human malaria parasites only develop in Anopheles mosquitoes. The parasites move to the salivary glands of the mosquito and are injected into a human host by the feeding insect.

• The anopheline mosquito only feeds in the evening. The parasite is injected into the host when the mosquito feeds and then progresses through a number of stages and transformations. The threadlike malaria parasites enter the bloodstream and are carried to the liver where they invade liver tissue cells, transform into spores and replicate repeatedly.
• The spores, formed within cyst-like structures in the liver, are released into the bloodstream where they attack and destroy red blood cells. In the process, they undergo another transformation that allows a form of the parasite to attack and invade new red blood cells.
• The synchronized development of different stages of the parasite is responsible for the characteristic cycles of fever in infected humans. A form of the parasite periodically bursts from demolished cells and is released into the blood stream to invade new blood cells. Different species produce different fever cycles.
• Plasmodium falciparum has a forty-eight hour period between fever peaks. The process is repeated over and over until natural or acquired immunity, or antimalarial chemotherapy, or death brings the repetitive process to an end.
• When an anopheline mosquito takes blood from a malarious human, the parasite enters the mosquito and goes through a number of complex changes over a 14 to 21 day period. It becomes an infectious form and moves to the mosquito's salivary glands where it is ready to reinfect and complete the cycle.
• Many people in Africa and other areas with intense malaria transmission, carry parasites without being ill. Having been infected repeatedly, they have built up immunity to the disease.
• The malaria situation around the world is worsening. Social and environmental factors are bringing more humans into closer contact with the mosquito carrier. The widespread use of chloroquine has allowed the emergence of resistant strains of Plasmodium falciparum that no longer respond to the drug. Plasmodium falciparum has become resistant to the most common antimalarial drugs in most of its area of distribution. Mosquitoes are also becoming more resistant to chemical insecticides.
• Changes in the immune system make women particularly vulnerable to life threatening infections from malaria during pregnancy. In addition to the acute effects, malaria causes anaemia in children and pregnant women and increases their vulnerability to other diseases. Repeated bouts of malarial fever in young children reduces their immunity and interferes with feeding, thus increasing their vulnerability to other diseases and death

Enuresis ,Description

Enuresis, more commonly called bed-wetting, is a disorder of elimination that involves the voluntary or involuntary release of urine into bedding, clothing, or other inappropriate places. In adults, loss of bladder control is often referred to as urinary incontinence rather than enuresis; it is frequently found in patients with late-stage Alzheimer's disease or other forms of dementia .

Description

Enuresis is a condition that has been described since 1500 B.C. People with enuresis wet their bed or release urine at other inappropriate times. Release of urine at night (nocturnal enuresis) is much more common than daytime, or diurnal, wetting. Enuresis commonly affects young children and is involuntary. Many cases of enuresis clear up by themselves as the child matures, although some children need behavioral or physiological treatment in order to remain dry.
There are two main types of enuresis in children. Primary enuresis occurs when a child has never established bladder control. Secondary enuresis occurs when a person has established bladder control for a period of six months, then relapses and begins wetting. To be diagnosed with enuresis, a person must be at least five years old or have reached a developmental age of five years. Below this age, problems with bladder control are considered normal.

Causes and symptoms

Symptoms

The symptoms of enuresis are straightforward—a person urinates in inappropriate places or at inappropriate times. The causes of enuresis are not so clear. A small number of children have abnormalities in the anatomical structure of their kidney or bladder that interfere with bladder control, but normally the cause is not the physical structure of the urinary system. A few children appear to have to have a lower-than-normal ability to concentrate urine, due to low levels of antidiuretic hormone (ADH). This hormone helps to regulate fluid balance in the body. Large amounts of dilute urine cause the bladder to overflow at night. For the majority of bedwetters, there is no single clear physical or psychological explanation for enuresis.

Causes in children

The fourth edition of the Diagnostic and Statistical Manual of Mental Disorders , fourth edition, text revision, or ( DSM-IV-TR ), does not distinguish between children who wet the bed involuntarily and those who voluntarily release urine. Increasingly, however, research findings suggest that voluntary and involuntary enuresis have different causes.
Involuntary enuresis is much more common than voluntary enuresis. Involuntary enuresis may be categorized as either primary or secondary. Primary enuresis occurs when young children lack bladder control from infancy. Most of these children have urine control problems only during sleep; they do not consciously, intentionally, or maliciously wet the bed. Research suggests that children who are nighttime-only bed wetters may have a nervous system that is slow to process the feeling of a full bladder. Consequently, these children do not wake up in time to relieve themselves. In other cases, the child's enuresis may be related to a sleep disorder.
Children with diurnal enuresis wet only during the day. There appear to be two types of daytime wetters. One group seems to have difficulty controlling the urge to urinate. The other group consciously delays urinating until they lose control. Some children have both diurnal and nocturnal enuresis.
Secondary enuresis occurs when a child has stayed dry day and night for at least six months, then returns to wetting. Secondary enuresis usually occurs at night. Many studies have been done to determine if there is a psychological component to enuresis. Researchers have found that secondary enuresis is more likely to occur after a child has experienced a stressful life event such as the birth of a sibling, divorce or death of a parent, or moving to a new house.
Several studies have investigated the association of primary enuresis and psychiatric or behavior problems. The results suggest that primary nocturnal enuresis is not caused by psychological disorders. Bed-wetting runs in families, however, and there is strong evidence of a genetic component to involuntary enuresis.
Unlike involuntary enuresis, voluntary enuresis is not common. It is associated with such psychiatric disorders as oppositional defiant disorder , and is substantially different from ordinary nighttime bed-wetting. Voluntary enuresis is always secondary.

Causes in adults

Enuresis or urinary incontinence in elderly adults may be caused by loss of independent control of body functions resulting from dementia, bladder infections, uncontrolled diabetes, side effects of medications, and weakened bladder muscles. Urinary incontinence in adults is managed by treatment of the underlying medical condition, if one is present; or by the use of adult briefs with disposable liners.

Demographics

Enuresis is a problem of the young and is more common in boys than girls. At age five, about 7% of boys and 3% of girls have enuresis. This number declines steadily in older children; by age 18, only about 1% of adolescents experience enuresis. Studies done in several countries suggest that there is no apparent cultural influence on the incidence of enuresis in children. On the other hand, the disorder does appear to run in families; children with one parent who wet the bed as a child are five to seven times more likely to have enuresis than children whose parents did not have the disorder in childhood.

Diagnosis

Enuresis is most often diagnosed in children because the parents express concern to the child's doctor. The pediatrician or family physician will give the child a physical examination to rule out medical conditions that may be causing the problem, including structural abnormalities in the child's urinary tract. The doctor may also rule out a sleep disorder as a possible cause. In many cases the pediatrician can reassure the child's parents and give them helpful advice.
According to the American Psychiatric Association, to make a diagnosis of enuresis, a child must have reached the chronological or developmental age of five. Inappropriate urination must occur at least twice a week for three months; or the frequency of inappropriate urination must cause significant distress and interfere with the child's school and/or social life. Finally, the behavior cannot be caused exclusively by a medical condition or as a side effect of medication.

Treatments

Treatment for enuresis is not always necessary. About 15% of children who have enuresis outgrow it each year after age six. When treatment is desired, a physician will rule out obvious physical causes of enuresis through a physical examination and medical history. Several different treatment options are then available.

Behavior modification

Behavior modification is often the treatment of choice for enuresis. It is inexpensive and has a success rate of about 75%. The child's bedding includes a special pad with a sensor that rings a bell when the pad becomes wet. The bell wakes the child, who then gets up and goes to the bathroom to finish emptying his bladder. Over time, the child becomes conditioned to waking up when the bladder feels full.
Once this response is learned, some children continue to wake themselves help from without the alarm, while others are able to sleep all night and remain dry. A less expensive behavioral technique involves setting an alarm clock to wake the child every night after a few hours of sleep, until the child learns to wake up spontaneously. In trials, this method was as effective as the pad-and-alarm system. A newer technique involves an ultrasound monitor worn on the child's pajamas. The monitor can sense bladder size, and sets off an alarm once the bladder reaches a predetermined level of fullness. This technique avoids having to change wet bed pads.
Other behavior modifications that can be used alone or with the pad-and-alarm system include:

• restricting liquids starting several hours before bedtime
• waking the child up in the night to use the bathroom
• teaching urinary retention techniques
• giving the child positive reinforcement for dry nights and being sympathetic and understanding about wet nights

Treatment with medications

There are two main drugs for treating enuresis. Imipramine , a tricyclic antidepressant, has been used since the early 1960s. It is not clear why this antidepressant is effective in treating enuresis when other antidepressants are not. Desmopressin acetate (DDAVP) has been widely used to treat enuresis since the 1990s. It is available as a nasal spray or tablet. Both imipramine and DDAVP are very effective in preventing bed-wetting, but have high relapse rates if medication is stopped.

Alternative therapies

Some success in treating bed-wetting has been reported using hypnosis. When hypnosis works, the results are seen within four to six sessions. Acupuncture and massage have also been used to treat enuresis, with inconclusive results.

Psychotherapy

Primary enuresis does not require psychotherapy . Secondary enuresis, however, is often successfully treated with therapy. The goal of the treatment is to resolve the underlying stressful event that has caused a relapse into bed-wetting. Unlike children with involuntary enuresis, children who intentionally urinate in inappropriate places often have other serious psychiatric disorders. Enuresis is usually a symptom of another disorder. Therapy to treat the underlying disorder is essential to resolving the enuresis.

Prognosis

Enuresis is a disorder that most children outgrow. For those who do receive treatment, the overall success rate of behavioral therapy is 75%. The short-term success rate with drug treatments is even higher than with behavioral therapy. Drugs do not, however, eliminate the enuresis. Many children who take drugs to control their bed-wetting relapse when the drugs are stopped.

Prevention

Although enuresis cannot be prevented, one side effect of the disorder is the shame and social embarrassment it causes. Children who wet may avoid sleepovers, camp, and other activities where their bed-wetting will become obvious. Loss of these opportunities can cause a loss of self-esteem, social isolation, and adjustment problems. A kind, low-key approach to enuresis helps to prevent these problems

Enuresis (Bed-Wetting)

What is enuresis?

Enuresis (say "en-yur-ee-sis") is the medical term for bed-wetting during sleep. Bed-wetting is fairly common among children and is often just a stage in their development. Bed-wetting is more common among boys than girls.

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What causes bed-wetting?

A number of things can cause bed-wetting. Some of the more common causes of bed-wetting include the following:

• Genetic factors (it tends to run in families)
• Difficulties waking up from sleep
• Stress
• Slower than normal development of the central nervous system (which reduces the child's ability to stop the bladder from emptying at night)
• Hormonal factors (not enough antidiuretic hormone is produced, which is the hormone that slows urine production at night)
• Urinary tract infections
• Abnormalities in the urethral valves in boys or in the ureter in girls or boys
• Abnormalities in the spinal cord
• A small bladder

Bed-wetting is not a mental or behavior problem. It doesn't happen because the child is too lazy to get out of bed to go to the bathroom.

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When do most children achieve bladder control?

Children achieve bladder control at different ages. By the age of 6 years, most children no longer urinate in their sleep. Bed-wetting up to 6 years of age is not unusual, even though it may be frustrating to parents. If a child is younger than 6 years of age, treatment for bed-wetting usually is not necessary.

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How can my family doctor help?

Although most children who wet the bed are healthy, your doctor can help you determine whether your child’s bed-wetting is caused by a medical problem. First, your doctor will ask questions about your child's daytime and nighttime bathroom habits. Then your doctor will do a physical exam and probably a urine test (called a urinalysis) to check for infection or diabetes.

Your doctor may also ask about how things are going at home and at school for your child. Although you may be worried about your child's bed-wetting, studies have shown that children who wet the bed are not more likely to be emotionally upset than other children. Your doctor will also ask about your family life, because treatment may depend on changes at home.

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What are the treatments for bed-wetting?

Most children outgrow bed-wetting without treatment. However, you and your doctor may decide your child needs treatment. There are 2 kinds of treatment: behavior therapy and medicine. Behavior therapy helps teach your child not to wet the bed. Some behavioral treatments include the following:

• Limit fluids before bedtime.
• Have your child go to the bathroom at the beginning of the bedtime routine and then again right before going to sleep.
• Use an alarm system that rings when the bed gets wet and teaches the child to respond to bladder sensations at night.
• Create a reward system for dry nights.
• Ask your child to change the bed sheets when he or she wets.
• Bladder training: have your child practice holding his or her urine for longer and longer times during the day, in effort to stretch the bladder so it can hold more urine.

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What kinds of medicines are used to treat bed-wetting?

Your doctor may give your child medicine if your child is 7 years of age or older and if behavior therapy has not worked. But medicines aren't a cure for bed-wetting. One kind of medicine helps the bladder hold more urine, and the other kind helps the kidneys make less urine. These medicines may have side effects, such as dry mouth and flushing of the cheeks.

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How can I help my child cope with wetting the bed?

Bed-wetting can lead to behavior problems because a child may feel guilt and embarrassment. It's true that your child should take responsibility for bed-wetting (this could mean having your child help with the laundry). But your child shouldn't be made to feel guilty. It's important for your child to know that bed-wetting isn't his or her "fault." Punishing your child for wetting the bed will not solve the problem.

It may help your child to know that no one knows the exact cause of bed-wetting. Explain that it tends to run in families (for example, if you wet the bed as a child, you should share that information with your child).

Remind your child that it's okay to use the bathroom during the night. Place nightlights leading to the bathroom so your child can easily find his or her way. You may also cover your child's mattress with a plastic cover to make cleanup easier. If accidents occur, praise your child for trying and for helping clean up.

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More Information

For Parents

• Toilet Training
• Toilet Teaching Your Child
• Stool Soiling
• Constipation
• Vomiting and Diarrhea
• Urinary Tract Infections
• Proteinuria

Moisturizing and Cleansing Key to Treating Atopic Dermatitis

When it comes to treating atopic dermatitis, dermatologists consider moisturizing and gentle cleansing to be indispensable. Yet, a recent survey revealed that 23% of adults living with atopic dermatitis say they do not do not apply moisturizer and 29% do not use a cleanser. The researchers also found that most of the people who participated in the survey wanted more information about moisturizers and cleansers.

Why is Moisturizing So Important?
Our skin is our barrier. It protects us from unseen invaders such as bacteria, viruses, and other potentially harmful organisms and toxins. Our skin also prevents us from losing large amounts of water. The outermost layer of skin, the stratum corneum, serves as our first line of defense. Some dermatologists call this our “bricks and mortar.”

When atopic dermatitis develops, the stratum corneum breaks down. With gaps in our bricks and mortar, the skin is more easily irritated. These gaps also make it easier for bacteria and viruses to enter the body. Easier access and the weakened immune system of atopic dermatitis make people more susceptible to infection. The skin also loses moisture more readily, causing dry skin.

Studies have shown that when patients with atopic dermatitis properly use a recommended moisturizer, it can help:

• Alleviate dry skin. Moisturizer forms a protective coating that reduces the amount of water lost through the skin. This, in turn, decreases dryness, itch, and cracking skin.
  
  Depending on the patient’s signs and symptoms, it may be necessary to apply moisturizer 4 or more times per day. Moisturizer should always be applied after a shower or bath while the skin is still damp. This locks in moisture.
   
• Boost the skin’s protective abilities. Moisturizer forms a protective membrane on the skin. One type of product called a barrier-repair emollient may provide the skin with essential components that can actually repair the damaged stratum corneum.
  
  Two small studies showed that a barrier-repair emollient produced dramatic improvement. In one of these studies, 24 children with stubborn to recalcitrant (not responding to treatment) atopic dermatitis were treated with a barrier-repair emollient containing ceramide (a molecule that helps regulate our skin cells and an effective emollient). Fifteen of the children were previously treated with other emollients.
  
  The emollient containing ceramide was applied twice a day for 12 weeks. All 24 children showed improvement within 3 weeks. By the end of 12 weeks, there was such significant improvement in all children that the researchers asked for the emollient be applied once a day. With regular once-a-day use, the skin continued to improve.
  
  Larger studies are needed to determine if a barrier-repair emollient actually repairs the skin. Research, to date, has not shown whether or not barrier-repair emollients offer any benefit not provided by other emollients.
   
• Increase the effectiveness of topical corticosteroids, and possibly reduce the need for long-term corticosteroid treatment. Researchers have found that using both a topical corticosteroid and a moisturizer decreases the signs and symptoms of atopic dermatitis better than use of a topical corticosteroid alone. Studies also have found that proper use of a moisturizer along with a topical corticosteroid can reduce the amount of corticosteroid needed. This suggests that using an appropriate moisturizer may reduce the need for long-term corticosteroids.
   
• Reduce skin irritation. One study found that pre-treating skin affected by atopic dermatits with moisturizer before exposing it to dust mite or grass pollen significantly reduced patients’ reactions to these substances. More than half of the patients said they would continue using the moisturizer after the study ended. The researchers concluded that moisturizer may help prevent exacerbation in patients with atopic dermatitis; however, more research is needed.
   
• Improve the skin’s appearance. A large-scale study found that applying certain lipid-rich moisturizers significantly improved the condition of skin affected by atopic dermatis. During this study, patients either applied a lipid-rich moisturizer alone or the lipid-rich moisturizer and a topical corticosteroid. In many cases, the moisturizer alone was as effective as the moisturizer plus corticosteroid in relieving dryness and scaling in patients. However, when it came to reducing the redness and itch, the corticosteroid plus moisturizer was more effective. This finding suggests that once the atopic dermatitis is under control, a moisturizer alone may be all that is needed.

Gentle Cleansing Essential
Cleansing the skin helps keep it healthy. Washing removes oils, dirt, bacteria, dead skin cells, and a number of other substances. The key to cleansing skin affected by atopic dermatitis is to be gentle because the outer layer of skin, the stratum corneum, is damaged and fragile.

Rubbing, scrubbing, peeling, microdermabrasion, and exfoliating can cause more damage as can harsh soaps. Soap can dry the skin and worsen itching. Mesh sponges, abrasive scrubs, and woven face cloths should not be used as they also can further damage the skin. Anything that increases damage to the skin can cause a flare-up and block the effects of treatment.

When washing, be sure to use a mild cleanser and to gently apply it with your fingertips. Cleanser should be rinsed off with lukewarm water. Dermatologists recommend that cleanser never be applied to skin that has flared. Even the mildest cleanser can be quite irritating when skin has flared.

Ask a Dermatologist for Product Recommendations
With the number of moisturizers, emollients, and cleansers on the market, trying to choose suitable products can boggle the mind. Typing the word “moisturizer” in a popular Internet search engine yields more than 2 million results. If that is not challenge enough, certain ingredients in these products can cause folliculitis (a type of skin inflammation that may resemble acne) or prickly heat in people living with atopic dermatitis. And, did you know that products containing glycerin and rose water — ingredients used to effectively moisturize skin — can increase dryness in skin affected by atopic dermatitis?

To help sort through the options, you may want to schedule an appointment with a dermatologist. After considering a number of factors, such as the severity of your atopic dermatitis and overall health, the dermatologist can recommend suitable products. This can save you time and money. During this appointment, the dermatologist also can show you how to apply cleanser and moisturizer to get optimal results

Daily Skin Care Essential to Control Atopic Dermatitis

When looking for a safe and effective way to control atopic dermatitis, do not overlook dermatologist-recommended skin care. It can reduce flare-ups, decrease the need for medication, and improve response to treatment.

Despite these benefits, dermatologists find that patients and caregivers seldom follow the skin care guidelines given to them. Often the reason is misconceptions about skin care. The following should help clear up some of this confusion.

Myth: Keep Bathing to a Minimum
It is a common misconception that bathing dries the skin and should be kept to a bare minimum.

What dermatologists recommend: People with atopic dermatitis tend to have excessively dry skin. To hydrate the skin, take a short, daily bath(s) in warm — not hot — water. A mild, non-irritating soap should be used only when needed.

The facts: Daily bathing as recommended by a dermatologist helps to hydrate the skin, which can reduce flare-ups and relieve discomfort when moisturizers also are used as directed.

For severe atopic dermatitis, a dermatologist may recommend up to 3 short baths a day. Even patients who avoid water because getting wet can be painful tend to get relief after some initial discomfort.

Myth: Moisturizers Add Moisture to the Skin
The word “moisturizer” causes a great deal of confusion. People often think that a moisturizer adds moisture to the skin and can be applied any time.

What dermatologists recommend: Apply moisturizer within 3 minutes of bathing. This will trap moisture in the skin. Continue to apply moisturizer throughout the day to very dry areas.

The facts: A moisturizer cannot add moisture to the skin. Moisturizer seals in the water from the bath, preventing water from evaporating. This is why moisturizer is most effective when applied within 3 minutes of bathing.

To apply a moisturizer after bathing:

1. Gently pat the skin partially dry.
2. Apply medication directly on the lesions.
3. Apply moisturizer on top of the medication and to the rest of the skin. For best results, dermatologists recommend using a thick, oily moisturizer and applying it in the same way that you would apply icing to a cake.

Applying moisturizer within 3 minutes of bathing and frequently throughout the day will help the skin to retain moisture from bathing. This, in turn, helps prevent dryness and cracking, which is especially important when the air is dry. With regular use, moisturizer can help to reduce discomfort and flare-ups as well as decrease the need for medication.

The new barrier repair moisturizers (also called barrier repair creams) can be especially helpful. Barrier repair moisturizers are generally applied twice daily to flare-prone skin and can be used along with a traditional moisturizer. These products do more than traditional moisturizers, which sit on top of the skin and prevent water loss. Barrier repair moisturizers, also known as physiologic moisturizers, not only reduce water loss; they help rebuild the skin. Patients say barrier repair moisturizers also calm the burning and itching.

Myth: Identify and Avoid Allergens to Prevent Flare-ups
Dermatologists often hear their patients and caregivers say that if only a patient’s allergies could be identified, then the patient could avoid these and prevent atopic dermatitis flares.

What dermatologists recommend: No one thing — not even allergen (substance to which the patient is allergic) avoidance — can control atopic dermatitis. Successfully managing this complex condition requires a multi-faceted approach. Proper skin care, using medication as directed, and avoiding one’s personal triggers all play a role. A trigger is anything that irritates the skin. A trigger need not be an allergen.

The facts: Laundry detergents, soaps, smoke, skin care products that contain alcohol or fragrance, and rough-textured clothing such as wool are common triggers that cause atopic dermatitis to flare. Triggers vary from person to person though, so it is important to learn what irritates the skin and avoid contact with individual triggers.

Discover the Benefits of Skin Care
Dermatologists stress that control of atopic dermatitis is nearly always possible. A key part of gaining control is good skin care. If skin care has not been a regular part of caring for atopic dermatitis, be sure to see a dermatologist. Including dermatologist-recommended guidelines can help one discover the relief possible with skin care.

Types of Eczema

Eczema, also called “dermatitis,” is not one specific skin condition. Several types of eczema exist, and sometimes a person develops more than one type. The links below take you to more information about common types of eczema.

Atopic dermatitis

Contact dermatitis

Dyshidrotic dermatitis

Hand dermatitis

Neurodermatitis

Nummular dermatitis

Occupational dermatitis

Seborrheic dermatitis

Stasis dermatitis

Eczema Treatment

What happens if I have eczema?
If the diagnosis is eczema, the dermatologist will explain what type of eczema you have and prescribe an appropriate treatment plan.

Before prescribing a treatment plan, a dermatologist considers the type of eczema, extent and severity of the eczema, patient’s medical history, and a number of other factors. Medication and other therapies will be prescribed as needed to:

• Control itching
• Reduce skin inflammation
• Clear infection
• Loosen and remove scaly lesions
• Reduce new lesions

It is important to realize that in most cases no one treatment will be effective. Medical research continues to show that the most effective treatment plan for eczema — regardless of type — involves using a combination of therapies to treat the skin and making lifestyle changes to control flare-ups. Doing so tends to increase effectiveness and reduce side effects from medications.

The type of medication prescribed will depend on many factors, including the type of eczema, past treatment, and the patient’s preference. Topical (applied to the skin) medication is frequently prescribed. If the eczema is more severe, phototherapy (a type of treatment that uses light therapy) or systemic (circulates throughout the body) medication may be prescribed.

Today, there are many effective therapies available to treat the different types of eczema. With proper treatment, most eczema can be controlled.

Keep in mind that eczema can be stubborn. If the signs and symptoms persist, be sure to tell your dermatologist. Sometimes it helps to change how you use the medications or to set aside more time for relaxing activities. Stress triggers flare-ups in many people. Others find relief with stronger medication. Keeping a diary to learn what triggers the eczema and avoiding these triggers helps others. A dermatologist can work with you to tailor a treatment plan that meets your needs.

What is Eczema?

5 most dangerous diseases to humans.

The survival of mankind has historically seen as a key part in the development of the species.There have been many dangers that threaten human beings, including the 5 most dangerous diseases to humans.

AIDS:-Scientifically known as Syndrome Immune Deficiency Syndrome, is one of the most STDs dangerous and common. In Addition AIDS can be infected by drug use, especially by sharing needles. This disease is wiping out your defenses.

Alzheimer’s:-It’s a terrible disease. I do not know if it will be the most dangerous, but I think it’s one that we most fear humans.Think that gradually we will lose the memory stick to almost like a vegetable … it is a fact that may distress to more than one. Moreover, we can consider it as a mysterious disease because they are not very well known source.

Hepatitis B:-Is a liver disease that causes the liver to gradually stop working. We understand it as a chronic disease, which is precisely to be chronic, is difficult to bear. That is, you will damage your liver slowly.

Cancer:-We can say that stress and diabetes are epidemics of the twenty-first century.  Well, cancer does not stay behind, and I daresay that even the disease of greatest concern to humans.

Osteoporosis:-In general, any bone disease is dangerous and that bones are the structure that holds us upright.

Dangerous Effects of Smoking on Human Body

Tobacco is considered as the greatest cause of preventable deaths in the United States and throughout the world. According to the American Heart Association and the National Health Interview Survey of 2008, 24.8 million men and 21.1 million women in the United States are smokers. Tobacco smoking causes many diseases affecting major organs of the body including heart, brain, and lungs.

Effects
Nicotine is the most active and important chemical component that causes dangerous effects in human body. It is a major risk factor for heart attacks; lung and mouth cancers and chronic obstructive pulmonary disease (COPD). Here, we will discuss about some of the dangerous effects of smoking on human body.

Oral cancer:
It was revealed by the National Institutes of Health that a variety of cancers including cancers of oral cavity, esophagus, larynx, and lungs are caused by cigar smoking. It was observed that around 90% of the patients with oral cancer are smokers. Laryngeal cancer is caused about 20 to 30 times more in smokers than non-smokers. Smoking causes inflammation around the teeth which is termed as periodontitis. Adherent white plaques and patches occur on the membranes of oral cavity and is called as leukoplakia.

Effect on heart rate and blood pressure:
Increase in rate of heartbeat and a sharp rise in blood pressure are the immediate effects of smoking on heart and blood circulation. The heart rate increases by about 30 times during the first 10 minutes of smoking. Nicotine causes the blood vessels to get narrowed resulting in rise of blood pressure. The oxygen carrying capacity of the blood is decreased by carbon monoxide which increases heart rate. Long term effects of smoking include increase in levels of fibrinogen and cholesterol in blood increasing risk of heart attacks. Coronary heart disease (CHD), Peripheral vascular disease (PVD), aneurysm, artherosclerosis, and others are caused by the heart and circulation attacks.

Effect on lungs:
More than 80% lung cancer cases are accounted by tobacco. Inability of cilia to remove the tar content of cigarette smoke leads to lung and laryngeal cancer. Chronic Obstructive Pulmonary Disease (COPD) is caused by smoking and is characterized by shortness of breath; persistent cough with sputum; and damage to lungs including emphysema and chronic bronchitis.

Effect on liver:
Numerous toxins are present in the cigarettes that lead to chronic inflammation and scarring of liver. This may increase the risk of diseases such as liver cancer, liver fibrosis, and Hepatitis B and C. Chemicals such as N-Nitrosodiethylamine, N-Nitrosopyrrolidine, and arsenic present in cigarettes are responsible for cause of liver tumors. The ability of liver to detoxify dangerous substances gets diminished by smoking.

Effect on brain dysfunction:
Nicotine reaches the brain within 10 seconds after inhalation. Carotid artery is the main artery that supplies blood to the brain. Fatty substances are built up in the carotid artery due to cigarette smoking. This decreases the supply of blood to the brain cells and results in stroke called as cerebral thrombosis. The risk of this stroke in smokers is about 1.5 times to that of non-smokers. Thickening and clotting of blood in brain may also be caused due to smoking.

Effect on digestive system:
Harmful effects of smoking can be seen on all parts of the digestive system. The decrease in strength of lower esophageal valve allows the acids of stomach to reflux into esophagus. This situation is termed as heartburn. The movement of bile salts from intestine to stomach is also promoted by smoking. Smoking increases the rate of formation of peptic ulcers.

Effect of skin and hair:
Collagen, a protein in skin, keeps the skin elastic. As nicotine affects collagen, elasticity of the skin is reduced. The tiny capillaries which nourish the skin are also constricted by nicotine, leading to formation of wrinkles. Healing process also gets affected by smoking and longer time is taken to heal a wound. The immune system is suppressed by the nicotine which leads to increase in susceptibility of viral infections of skin.

Premature thinning and graying of hair is seen in smokers. The chances of people becoming bald are twice in smokers than in non-smokers. Premature graying of hair is also 3 to 6 times common in smokers.

Effect on bone and muscle:
Healing of fractures is delayed by smoking. Blood flow to all tissues is restricted by nicotine. Mostly it is restricted in newly forming tissues, which are involved in bone repair. The chemicals of tobacco are responsible for inhibition of development of new muscle and bone tissue cells. The risk of osteoporosis is increased by smoking. Significantly lower bone densities are seen among women smokers and are more likely to suffer fractures. The risk of osteoporosis among women is 50% more in smokers than non-smokers.

Effect on respiratory system:
Entry of chemicals of tobacco into mouth and trachea causes irritation and chemical burns. It causes sore throat and pain. Cancer causing properties of certain chemicals may cause burns on trachea resulting in throat cancer. Many fatal diseases are caused by smoking including cancers of mouth, nasopharynx, larynx and lung. Increased risk of asthma, cough, bronchitis and pneumonia are seen in children who are exposed to passive smoking.

Psychological effects:
The feeling of euphoria and calmness are considered as the root cause for addiction to cigarettes. Nicotine triggers the release of dopamine in brain giving pleasure reaction. The psychological effects of smoking are dependent on the physical effect of nicotine on brain. When a person quits smoking, the psychological desire for cigarettes can last for many years, whereas the physical desire can be overcome within 2 weeks.

Smoking causes many dangerous effects on human body. American Cancer Society estimated that 168,000 Americans died of cancer due to tobacco smoking in 2007. Yearly smoking causes 1 in 5 deaths in America. Hence, it is necessary to take serious steps for eradication of smoking habits. Many educational programs have to be conducted to make people aware of the harmful effects of smoking on human body.

Tobacco is considered as the greatest cause of preventable deaths in the United States and throughout the world. Tobacco smoking causes many diseases affecting major organs of the body including heart, brain, and lungs. According to the American Heart Association and the National Health Interview Survey of 2008, 24.8 million men and 21.1 million women in the United States are smokers.

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