Category Archives: Ailmemts & Remedies

Leprosy

Other name :  Hansen’s disease

Description:
Leprosy is a chronic infection caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis. Initially, infections are without symptoms and typically remain this way for 5 to as long as 20 years. Symptoms that develop include granulomas of the nerves, respiratory tract, skin, and eyes. This may result in a lack of ability to feel pain and thus loss of parts of extremities due to repeated injuries. Weakness and poor eyesight may also be present.

Leprosy is spread between people. This is believed to occur through a cough or contact with fluid from the nose of an infected person. Leprosy occurs more commonly among those living in poverty and is believed to be transmitted by respiratory droplets. It is not very contagious. The two main types of disease are based on the number of bacteria present: paucibacillary and multibacillary. The two types are differentiated by the number of poorly pigmented, numb skin patches present, with paucibacillary having five or fewer and multibacillary having more than five. The diagnosis is confirmed by finding acid-fast bacilli in a biopsy of the skin or via detecting the DNA by polymerase chain reaction.

Leprosy is curable with treatment.  Treatment for paucibacillary leprosy is with the medications dapsone and rifampicin for 6 months.Treatment for multibacillary leprosy consists of rifampicin, dapsone, and clofazimine for 12 months.  These treatments are provided for free by the World Health Organization.  A number of other antibiotics may also be used.  Globally in 2012, the number of chronic cases of leprosy was 189,000 and the number of new cases was 230,000.  The number of chronic cases has decreased from some 5.2 million in the 1980s.  Most new cases occur in 16 countries, with India accounting for more than half.  In the past 20 years, 16 million people worldwide have been cured of leprosy.  About 200 cases are reported per year in the United States.

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Leprosy has affected humanity for thousands of years.  The disease takes its name from the Latin word lepra, which means “scaly”, while the term “Hansen’s disease” is named after the physician Gerhard Armauer Hansen.  Separating people by placing them in leper colonies still occurs in places such as India,  China,   and Africa.   However, most colonies have closed since leprosy is not very contagious.   Leprosy has been associated with social stigma for much of history, which is a barrier to self-reporting and early treatment.  The word “leper” is considered insulting with the term leprosy being preferred.   World Leprosy Day was started in 1954 to draw awareness to those affected by leprosy.

Forms of Leprosy:
Leprosy may also be divided into the following forms:

*Early and indeterminate leprosy
*Tuberculoid leprosy
*Borderline tuberculoid leprosy
*Borderline leprosy
*Borderline lepromatous leprosy
*Lepromatous leprosy
*Histoid leprosy
*Diffuse leprosy of Lucio and Latapí
This disease may also occur with only neural involvement, without skin lesions

Symptoms:
Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions (light or dark patches) are the primary external sign. It first affects the skin and the nerves outside the brain and spinal cord, called the peripheral nerves. It may also strike the eyes and the thin tissue lining the inside of the nose.

The main symptom of leprosy is disfiguring skin sores, lumps, or bumps that do not go away after several weeks or months. The skin sores are pale-colored.

Nerve damage can lead to:
*Loss of feeling in the arms and legs
*Muscle weakness

It usually takes about 3 to 5 years for symptoms to appear after coming into contact with the leprosy-causing bacteria. Some people do not develop symptoms until 20 years later. The time between contact with the bacteria and the appearance of symptoms is called the incubation period. Leprosy’s long incubation period makes it very difficult for doctors to determine when and where a person with leprosy got infected.

If untreated, leprosy can progress and cause permanent damage to the skin, nerves, limbs, and eyes. Contrary to folklore, leprosy does not cause body parts to fall off, although they can become numb or diseased as a result of secondary infections; these occur as a result of the body’s defenses being compromised by the primary disease.  Secondary infections, in turn, can result in tissue loss.
How the infection produces the symptoms of the disease is not known.

Causes:
Leprosy is caused by a slow-growing type of bacteria called Mycobacterium leprae (M. leprae). Leprosy is also known as Hansen’s disease, after the scientist who discovered M. leprae in 1873.
M. leprae and M. lepromatosis are the causative agents of leprosy. M. lepromatosis is a relatively newly identified mycobacterium isolated from a fatal case of diffuse lepromatous leprosy in 2008.

An intracellular, acid-fast bacterium, M. leprae is aerobic and rod-shaped, and is surrounded by the waxy cell membrane coating characteristic of the Mycobacterium genus.

Due to extensive loss of genes necessary for independent growth, M. leprae and M. lepromatosis are obligate intracellular pathogens, and unculturable in the laboratory, a factor that leads to difficulty in definitively identifying the organism under a strict interpretation of Koch’s postulates. The use of nonculture-based techniques such as molecular genetics has allowed for alternative establishment of causation.

While the causative organisms have to date been impossible to culture in vitro, it has been possible to grow them in animals such as mice and armadillos.

Naturally occurring infection also has been reported in nonhuman primates, including the African chimpanzee, sooty mangabey, and cynomolgus macaque, as well as in armadillos and red squirrels.

Risk factors:
At highest risk are those living in areas with polluted water and poor diet or people suffering from diseases that compromise immune function. There appears to be little interaction between HIV and the risk of leprosy. Genetic predisposition appears to play a role in susceptibility.

Transmission:
Transmission of leprosy occurs during close contact with those who are infected.  Transmission is believed to be by nasal droplets.

Leprosy is not known to be either sexually transmitted or highly infectious. People are no longer infectious after as little as two weeks of treatment.

Leprosy may also be transmitted to humans by armadillos  and may be present in three species of non-human primates.

Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not  very clear. Lepromatous cases show large numbers of organisms deep in the dermis, but whether they reach the skin surface in sufficient numbers is doubtful.

The skin and the upper respiratory tract are most likely entry route. While older research dealt with the skin route, recent research has increasingly favored the respiratory route. Experimental transmission of leprosy through aerosols containing M. leprae in immune-suppressed mice was accomplished, suggesting a similar possibility in humans

Diagnosis:
Endemic areas:
Per the World Health Organization, diagnosis in an endemic area is based on one of these cardinal signs:

*Skin lesion consistent with leprosy and with definite sensory loss
*Positive skin smears
*Skin lesions can be single or multiple, usually hypopigmented, although occasionally reddish or copper-colored. The lesions may be macules (flat), papules (raised), or nodular. Sensory loss at the skin lesion is important because this feature can help differentiate from other causes of skin lesions such as tinea versicolor.

*Thickened nerves are associated with leprosy and can be accompanied by loss of sensation or muscle weakness. However, without the characteristic skin lesion and sensory loss, muscle weakness is not considered a reliable sign of leprosy.

*Positive skin smears: In some case, acid-fast leprosy bacilli are considered diagnostic; however, the diagnosis is clinical.

Treatment:
A number of leprostatic agents are available for treatment. For paucibacillary (PB or tuberculoid) cases, treatment with daily dapsone and monthly rifampicin for six months is recommended. While for multibacillary (MB or lepromatous) cases, treatment with daily dapsone and clofazimine along with monthly rifampicin for twelve months is recommended.

Multidrug therapy (MDT) remains highly effective, and people are no longer infectious after the first monthly dose.  It is safe and easy to use under field conditions due to its presentation in calendar blister packs.  Relapse rates remain low, and no resistance to the combined drugs is seen.

Prevention:
Early detection of the disease is important, since physical and neurological damage maybe irreversible even if cured. Medications can decrease the risk of those living with people with leprosy from acquiring the disease and likely those with whom people with leprosy come into contact outside the home. However, concerns are known of resistance, cost, and disclosure of a person’s infection status when doing follow-up of contacts. Therefore, the WHO recommends that people who live in the same household be examined for leprosy and only be treated if symptoms are present.

The Bacillus Calmette–Guérin (BCG) vaccine offers a variable amount of protection against leprosy in addition to tuberculosis. It appears to be 26 to 41% effective (based on controlled trials) and about 60% effective based on observational studies with two doses possibly working better than one.  Development of a more effective vaccine is ongoing as of 2011

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Leprosy
http://www.webmd.com/skin-problems-and-treatments/guide/leprosy-symptoms-treatments-history#1

Jet Lag

Definition:     Jet lag is nothing but circadian rhythm disorder of our body system.It is also known as time zone change syndrome or desynchronosis.It can occur when people travel rapidly from east to west, or west to east on a jet plane. Jet lag symptoms tend to be more severe when the person travels from westward compared to eastward. It is a physiological condition which upsets our body’s circadian rhythms –

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Circadian rhythm is the 24-hour cycle in the biochemical, physiological and behavioral process of our bodies. In layman’s terms, it means biological clock of our body. The word circadian comes from the Latin word circa meaning “about”, and the Latin word diem or dies meaning “day”. Our circadian rhythms are driven by an internal time-keeping system. This biological clock is entrained by external environmental occurrences, such as the light-dark cycle of night and day. Put simply, our circadian rhythm regulates our daily activities, such as sleep, waking, eating and body temperature regulation. Problems readjusting our internal biological clock causes jet lag, as do problems with shift work, and some sleeping disorders.

People with jet lag have their sleep-wake patterns disturbed. They may feel drowsy, tired, irritable, lethargic and slightly disoriented. The more time zones that are crossed rapidly, the more severe jet lag symptoms are likely to occur.

Researchers from the University of Washington revealed that the disruption occurs in two separate but linked groups of neurons in a structure called the suprachiasmatic nucleus, below the hypothalamus at the base of the brain. One group is synchronized with deep sleep that results from physical fatigue and the other controls the dream state of rapid eye movement, or REM, sleep

The condition of jet lag may last several days until one is fully adjusted to the new time zone, and a recovery rate of one day per time zone crossed is a suggested guideline. The issue of jet lag is especially pronounced for airline pilots, crew, and frequent travelers. Airlines have regulations aimed at combating pilot fatigue caused by jet lag.

The common term jet lag is used, because before the arrival of passenger jet aircraft, it was generally uncommon to travel far and fast enough to cause jet lag. Trips in propeller-driven aircraft and trains were slower and of more limited distance than jet flights, and thus did not contribute as widely to the problem.

Symptoms:
Symptoms of jet lag vary and depend on several factors, including how many time zones were travelled, the individual’s age, state of health, whether or not alcohol was consumed during the flight, how much was eaten during the flight, and how much sleep there was during the flight. Jet lag usually requires a change of three time zones or more to occur, though some individuals can be affected by as little as a single time zone or the single-hour shift of daylight saving time. Symptoms and consequences of jet lag can be a significant area of concern for athletes traveling east or west to competitions as performance is often dependent on a combination of physical and mental characteristics that are impacted by jet lag.

Light is the strongest stimulus for re-aligning a person’s sleep-wake schedule and careful control of exposure to and avoidance of bright lights can speed adjustment to a new time zone.
Traveling east causes more problems than traveling west, because the body clock has to be advanced, which is harder than delaying it, and the necessary exposure to light to realign the body clock does not tie in with the day/night cycle at the destination.Traveling east by six to nine time zones causes the biggest problems, as it is desirable to avoid light in the mornings.

General symptoms of jet lag are as follows:
*Headaches
*Head feels heavy
*Lethargy, fatigue
*Insomnia
*Irritability
*Mild depression
*Attention deficit – hard to concentrate on one thing for long
*Loss of appetite
*Slight confusion
*Dizzy unsettled feeling – this may be due to moving from the plane, which wobbles all the time, to firm land.
*Some gastrointestinal disturbances, such as diarrhea or constipation.

*Travel fatigue:
Travel fatigue is general fatigue, disorientation and headache caused by a disruption in routine, time spent in a cramped space with little chance to move around, a low-oxygen environment, and dehydration caused by limited food and dry air. It does not necessarily have the shift in circadian rhythms that cause jet lag. Travel fatigue can occur without crossing time zones, and it often disappears after a single day accompanied by a night of high-quality sleep
Causes:
Jet lag is a chronobiological problem, similar to issues often induced by shift work and the circadian rhythm sleep disorders. When travelling across a number of time zones, the body clock (circadian rhythm) will be out of synchronization with the destination time, as it experiences daylight and darkness contrary to the rhythms to which it has grown accustomed. The body’s natural pattern is upset, as the rhythms that dictate times for eating, sleeping, hormone regulation and body temperature variations no longer correspond to the environment nor to each other in some cases. To the degree that the body cannot immediately realign these rhythms, it is jet lagged.

The speed at which the body adjusts to the new schedule depends on the individual; some people may require several days to adjust to a new time zone, while others experience little disruption. Crossing one or two time zones does not typically cause jet lag.

The condition is not linked to the length of flight, but to the trans-meridian (west–east) distance traveled. A ten-hour flight from Europe to southern Africa does not cause jet lag, as travel is primarily north–south. A five-hour flight from the east to the west coast of the United States may well result in jet lag.

Crossing the International Date Line does not contribute to jet lag, as the guide for calculating jet lag is the number of time zones crossed, and the maximum possible disruption is plus or minus 12 hours. If the time difference between two locations is greater than 12 hours, subtract that number from 24. Note, for example, that the time zone GMT+14 will be at the same time of day as GMT-10, though the former is one day ahead of the latter.

Management & prevention:

Tip 1: Stay in shape

If you are in good physical condition, stay that way. In other words, long before you embark, continue to exercise, eat right, and get plenty of rest. Your physical stamina and conditioning will enable you to cope better after you land. If you are not physically fit, or have a poor diet, begin shaping up and eating right several weeks before your trip.

Tip 2: Get medical advice

If you have a medical condition that requires monitoring (such as diabetes or heart disease), consult your physician well in advance of your departure to plan a coping strategy that includes medication schedules and doctor’s appointments, if necessary, in the destination time zone.

Tip 3: Change your schedule

If your stay in the destination time zone will last more than a few days, begin adjusting your body to the new time zone before you leave. For example, if you are traveling from the U.S. to Europe for a one-month vacation, set your daily routine back an hour or more three to four weeks before departure. Then, set it back another hour the following week and the week after that. Easing into the new schedule gradually in familiar surroundings will save your body the shock of adjusting all at once.

If you are traveling east, try going to sleep earlier and getting up and out into the early morning sun. If traveling west, try to get at least an hour’s worth of sunlight as soon as possible after reaching your destination.

Tip 4: Avoid alcohol

Do not drink alcoholic beverages the day before your flight, during your flight, or the day after your flight. These beverages can cause dehydration, disrupt sleeping schedules, and trigger nausea and general discomfort.

Tip 5: Avoid caffeine

Likewise, do not drink caffeinated beverages before, during, or just after the flight. Caffeine can also cause dehydration and disrupt sleeping schedules. What’s more, caffeine can jangle your nerves and intensify any travel anxiety you may already be feeling.

Tip 6: Drink water

Drink plenty of water, especially during the flight, to counteract the effects of the dry atmosphere inside the plane. Take your own water aboard the airplane if allowed.

Tip 7: Move around on the plane

While seated during your flight, exercise your legs from time to time.Move them up and down and back and forth. Bend your knees. Stand upand sit down. Every hour or two, get up and walk around. Do not take sleeping pills, and do not nap for more than an hour at a time.

These measures have a twofold purpose. First, they reduce your risk of developing a blood clot in the legs. Research shows that long periods of sitting can slow blood movement in and to the legs, thereby increasing the risk of a clot. The seat is partly to blame. It presses against the veins in the leg, restricting blood flow. Inactivity also plays a role. It decelerates the movement of blood through veins. If a clot forms, it sometimes breaks loose and travels to the lungs (known as pulmonary embolism), lodges in an artery, and inhibits blood flow. The victim may experience pain and breathing problems and cough up blood. If the clot is large, the victim could die. Second, remaining active, even in a small way, revitalizes and refreshes your body, wards off stiffness, and promotes mental and physical acuity which can ease the symptoms of jet lag.
Tip 8: Break up your trip

On long flights traveling across eight, 10, or even 12 time zones, break up your trip, if feasible, with a stay in a city about halfway to your destination. For example, if you are traveling from New York to Bombay, India, schedule a stopover of a few days in Dublin or Paris. (At noon in New York, it is 5 p.m. in Dublin, 6 p.m. in Paris, and 10:30 p.m. in Bombay.)

Tip 9: Wear comfortable shoes and clothes

On a long trip, how you feel is more important than how you look. Wear comfortable clothes and shoes. Avoid items that pinch, restrict, or chafe. When selecting your trip outfit, keep in mind the climate in your destination time zone. Dress for your destination.

Tip 10: Check your accommodations

Upon arrival, if you are staying at a hotel, check to see that beds and bathroom facilities are satisfactory and that cooling and heating systems are in good working order. If the room is unsuitable, ask for another.

Tip 11: Adapt to the local schedule

The sooner you adapt to the local schedule, the quicker your body will adjust. Therefore, if you arrive at noon local time (but 6 a.m. your time), eat lunch, not breakfast. During the day, expose your body to sunlight by taking walks or sitting in outdoor cafés. The sunlight will cue your hypothalamus to reduce the production of sleep-inducing melatonin during the day, thereby initiating the process of resetting your internal clock.

When traveling with children, try to get them on the local schedule as well. When traveling east and you will lose time, try to keep the child awake until the local bedtime. If traveling west when you will gain time, wake your child up at the local time.

Tip 12: Use sleeping medications wisely — or not at all

Try to establish sleeping patterns without resorting to pills. However, if you have difficulty sleeping on the first two or three nights, it’s OK to take a mild sedative if your physician has prescribed one. But wean yourself off the sedative as soon as possible. Otherwise, it could become habit-forming.

There are also some homeopathic remedies that may be used. A product called No Jet Lag contains homeopathic remedies leopard’s bane (Arnica montana), daisy (Bellis perennis), wild chamomile (Matricaria chamomilla), ipecac (Cephalelis ipecacuanha), and club moss (Lycopodium).

Valerian root is an herb that can be used as treatment for insomnia. Do not take valerian with alcohol. It is important to consult your physician before taking these or any other homeopathic or herbal remedy.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Resources:
http://en.wikipedia.org/wiki/Jet_lag
http://www.medicinenet.com/jet_lag/page4.htm#how_long_does_jet_lag_last

Hot Flashes

Definition:
Hot flashes are sudden feelings of warmth, which are usually most intense over the face, neck and chest. Your skin may redden, as if you’re blushing. Hot flashes can also cause profuse sweating and may leave you chilled…..CLICK & SEE

Although other hormonal conditions can cause them, hot flashes most commonly are due to menopause — the time when a woman’s menstrual periods stop. In fact, hot flashes are the most common symptom of the menopausal transition.

Hot flashes are due to a reduction of FSH and reduced levels of estradiol. They are a form of flushing, a symptom which may have several other causes, but which is often caused by the changing hormone levels that are characteristic of menopause. They are typically experienced as a feeling of intense heat with sweating and rapid heartbeat, and may typically last from two to thirty minutes for each occurrence.

How often hot flashes occur varies from woman to woman, but usually the range is from one or two a day to one an hour. There are a variety of treatments for particularly bothersome hot flashes.
Symptoms:
Hot flashes, a common symptom of menopause and perimenopause, are typically experienced as a feeling of intense heat with sweating and rapid heartbeat, and may typically last from two to thirty minutes for each occurrence, ending just as rapidly as they began. The sensation of heat usually begins in the face or chest, although it may appear elsewhere such as the back of the neck, and it can spread throughout the whole body. Some women feel as if they are going to faint. In addition to being an internal sensation, the surface of the skin, especially on the face, becomes hot to the touch. This is the origin of the alternative term “hot flush”, since the sensation of heat is often accompanied by visible reddening of the face. Excessive flushing can lead to rosacea.

The symptoms of hot flashes are as follows:

*A sudden feeling of warmth spreading through the upper body and face
*A flushed appearance with red, blotchy skin
*Rapid heartbeat
*Perspiration, mostly on your upper body
*Feeling chilled as the hot flash subsides

Hot flashes vary in frequency — you may have few or many in a day — and each hot flash usually subsides in a few minutes. They’re particularly common at night. Most women who experience hot flashes have them for more than a year, but they usually stop on their own within four to five years.

The hot-flash event may be repeated a few times each week or every few minutes throughout the day. Hot flashes may begin to appear several years before menopause starts and last for years afterwards. Some women undergoing menopause never have hot flashes. Others have mild or infrequent flashes. The worst sufferers experience dozens of hot flashes each day. In addition, hot flashes are often more frequent and more intense during hot weather or in an overheated room, the surrounding heat apparently making the hot flashes themselves both more likely to occur, and more severe.

Severe hot flashes can make it difficult to get a full night’s sleep (often characterized as insomnia), which in turn can affect mood, impair concentration, and cause other physical problems. When hot flashes occur at night, they are called “night sweats”. As estrogen is typically lowest at night, some women get night sweats without having any hot flashes during the daytime.

Types:
Some menopausal women may experience both standard hot flashes and a second type sometimes referred to as “slow hot flashes” or “ember flashes”. The standard hot flash comes on rapidly, sometimes reaching maximum intensity in as little as a minute. It lasts at full intensity for only a few minutes before gradually fading.

Slow “ember” flashes appear almost as quickly but are less intense and last for around half an hour. Women who experience them may undergo them year round, rather than primarily in the summer, and ember flashes may linger for years after the more intense hot flashes have passed.
Young women:
If hot flashes occur at other times in a young woman’s menstrual cycle, then it might be a symptom of a problem with her pituitary gland; seeing a doctor is highly recommended. In younger women who are surgically menopausal, hot flashes are generally more intense than in older women, and they may last until natural age at menopause.

Men:
Hot flashes in men could have various causes. It can be a sign of low testosterone. Another is andropause, or “male menopause”. Men with prostate cancer or testicular cancer can also have hot flashes, especially those who are undergoing hormone therapy with antiandrogens, also known as androgen antagonists, which reduce testosterone to castrate levels. There are also other ailments and even dietary changes which can cause it. Men who are castrated can also get hot flashes

Causes:
The exact cause of hot flashes isn’t known, but it’s likely related to several factors. Research on hot flashes is mostly focused on treatment options. The exact cause and pathogenesis, or causes of vasomotor symptoms (VMS)—the clinical name for hot flashes—has not yet been fully studied. There is hints at reduced levels of estrogen as the primary cause of hot flashes. There are indications that hot flashes may be due to a change in the hypothalamus’s control of temperature regulation.

Diagnosis:
The doctor can usually diagnose hot flashes based on a description of symptoms. To confirm the cause of hot flashes, the doctor may suggest blood tests to check whether the patient is in menopausal transition or other causes.

Treatment:
Hormone replacement therapy:(HRT)……..CLICK & SEE
Hormone replacement therapy may relieve many of the symptoms of menopause. However, oral HRT may increase the risk of breast cancer, stroke, and dementia and has other potentially serious short-term and long-term risks. Since the incidence of cardiovascular disease in women has shown a rise that matches the increase in the number of post menopausal women, recent studies have examined the benefits and side effects of oral versus transdermal application of different estrogens and found that transdermal applications of estradiol may give the vascular benefits lowering the incidences of cardiovascular events with less adverse side effects than oral preparations.

Women who experience troublesome hot flashes are advised by some to try alternatives to hormonal therapies as the first line of treatment. If a woman chooses hormones, they suggest she take the lowest dose that alleviates her symptoms for as short a time as possible. The US Endocrine Society concluded that women taking hormone replacement therapy for 5 years or more experienced overall benefits in their symptoms including relief of hot flashes and symptoms of urogenital atrophy and prevention of fractures and diabetes.

When estrogen as estradiol is used transdermally as a patch, gel, or pessary with micronized progesterone this may avoid the serious side effects associated with oral estradiol HRT since this avoids first pass metabolism (Phase I drug metabolism). Women taking bioidentical estrogen, orally or transdermally, who have a uterus must still take a progestin or micronized progesterone to lower the risk of endometrial cancer. A French study of 80,391 postmenopausal women followed for several years concluded that estrogen in combination with micronized progesterone is not associated with an increased risk of breast cancer. The natural, plant-derived progesterone creams sold over the counter contain too little progesterone to be effective. Wild yam (Dioscorea villosa) extract creams are not effective since the natural progesterone present in the extract is not bioavailable.

Selective estrogen receptor modulators:
SERMs are a category of drugs that act selectively as agonists or antagonists on the estrogen receptors throughout the body. Tamoxifen, a drug used in the treatment of some types of breast cancer and which can cause hot flashes as a side effect, RAD1901, under development by Radius Health, Raloxifene and the soy-derived Femarelle (DT56a) are examples of SERMs. Menerba, a botanically derived selective estrogen receptor beta agonist currently under development by Bionovo, works like a SERM, but only activates on the estrogen receptor beta.

Selective serotonin reuptake inhibitors:
SSRIs are a class of pharmaceuticals that are most commonly used in the treatment of depression. They have been found as efficient in alleviating hot flashes. On 28 June 2013 FDA approved Brisdelle (low-dose paroxetine mesylate) for the treatment of moderate-to-severe vasomotor symptoms (e.g. hot flashes and night sweats) associated with menopause. Paroxetine became the first and only non-hormonal therapy for menopausal hot flashes approved by FDA.

Isoflavones:
Isoflavones are commonly found in legumes such as soy and red clover. The two soy isoflavones implicated[who?] in relieving menopausal symptoms are genistein and daidzein, and are also known as phytoestrogens. The half life of these molecules is about eight hours, which might explain why some studies have not consistently shown effectiveness of soy products for menopausal symptoms. Although red clover (Trifolium pratense) contains isoflavones similar to soy, the effectiveness of this herb for menopausal symptoms at relatively low concentrations points to a different mechanism of action.

Other phytoestrogens:
It is believed[who?] that dietary changes that include a higher consumption of phytoestrogens from sources such as soy, red clover, ginseng, and yam may relieve hot flashes.

Ginseng: Very few studies exist on the effect of ginseng for relief of menopausal symptoms. In a large double-blinded randomized controlled trial, reduction in hot flashes was not statistically significant but showed a strong trend towards improvement. Lack of statistical significance suggests future research, but does not meet the scientific bar for ginseng to be deemed effective.
Flaxseed: There have also been several clinical trials using flaxse Flaxseed is the richest source of lignans, which is one of three major classes of phytoestrogen. Lignans are thought to have estrogen agonist and antagonist effects as well as antioxidant properties. Flaxseed and its lignans may have potent anti-estrogenic effects on estrogen receptor positive breast cancer and may have benefits in breast cancer prevention efforts. One recent study done in France, looked at four types of lignans, including that found in flaxseed (Secoisolariciresinol) in a prospective cohort study to see if intake predicted breast cancer incidence. The authors report lowered risk of breast cancer among over 58,000 postmenopausal women who had the third highest quartile of lignan intake. There have been a few small pilot studies that have tested the effect of flaxseed on hot flashes. Currently there is a large study sponsored by the National Cancer Institute that is ongoing, but not accepting any new participants. The rationale for the study is that estrogen can relieve the symptoms of menopause, but can also cause the growth of breast cancer cells. Flaxseed may reduce the number of hot flashes and improve mood and quality of life in postmenopausal women not receiving estrogen therapy.

lLife style changes:
According to the North American Menopause Society (NAMS) there are foods and some unhealthy lifestyle habits that can aggravate or trigger hot flashes such as: hot/spicy foods, alcohol, or caffeine. Further, for women who are overweight or obese, a gradual weight loss can have potential benefits for menopausal symptom reduction.

Acupuncture:
Acupuncture has been suggested to reduce incidence of hot flashes in women with breast cancer and men with prostate cancer, but the quality of evidence is low.

Yoga:
Doing Yoga with Pranayama, meditation, slow, deep breathing or other stress-reducing techniques is the best way to get read of the symptoms.
Prevention:
If the hot flashes are mild, one may be able to manage them with lifestyle changes by following these tips:

*Keeping cool. Slight increases in the body’s core temperature can trigger hot flashes. It is adviced to dress in layers so that one can remove clothing at the time feeling warm.One can open windows or use a fan or air conditioner. Lower the room temperature, if possible. If one feels a hot flash coming on, sip a cold drink or water.

*Avoid : Hot and spicy foods, caffeinated beverages,smoking and alcohol can trigger hot flashes. So they are to be avoided as much as possible.

*Lose weight. If  one  is overweight or obese, losing weight might help to ease one’s hot flashes.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources
http://en.wikipedia.org/wiki/Hot_flash
http://www.mayoclinic.org/diseases-conditions/hot-flashes/basics/definition/con-20034883

Palmar hyperhidrosis

Description:
Palmer hyperhidrosis is profuse perspiration (excessive sweating) of the palms.It is one form of focal hyperhidrosis, meaning profuse perspiration affecting one area of the body. Sweaty palms may be accompanied by profuse perspiration of the feet, forehead, ckeeks, armpits (axillae) or be part of general hyperhidrosis (profuse perspiration throughout the body). Hyperhidrosis refers to profuse perspiration beyond the body’s thermoregulatory (temperature control) needs.

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Palmer  hyperhidrosis is a common condition in which the eccrine (sweat) glands of the palms and soles secrete inappropriately large quantities of sweat. The condition may become socially and professionally debilitating. The condition usually is idiopathic  and  it begins in childhood and frequently runs in families.

Symptoms:
The intensity of symptoms may vary among sufferers and trigger factors should be carefully noted. Common symptoms  are :

*Perspiration of the hands can vary from mild clamminess to severe perspiration resulting in dripping sweat.
*Temperature differences of palmar surface compared to surface temperature of other parts of the body may be noted.
*Sloughing (peeling) of skin may be noted in profuse perspiration.
*Episodes of profuse perspiration may be followed by periods of extreme dryness on the palmar surface.
*Hyperhidrosis often starts in puberty, and family history is often reported.

The secondary effects of palmar hyperhidrosis can result in both psychosocial effects as well as difficulty in undertaking certain tasks or handling equipment. Sufferers of palmar hyperhidrosis are often reluctant to partake in socially expected actions like shaking hands or touching loved ones. The embarrassment of dealing with this condition can affect the level of interactivity in both social and work situations. Difficulties with holding objects, gripping equipment or soiling electronic devices like keyboards may affect functioning at work. Daily activities such as writing with a pen or counting cash notes is often difficult.

Causes:
Hyperhidrosis is either primary focal or secondary generalized.

1. Primary Palmar  Hyperhidrosis

Focal palmar hyperhidrosis is usually localized and is referred to as primary (essential, idiopathic), meaning no obvious cause, except strong family predisposition can be found (4,5), and affected persons are otherwise healthy . Sweating on other locations as feet, armpits and face may appear. Primary palmar hyperhidrosis is caused by overactivity of the sympathetic nervous system, primarily triggered by emotional causes including anxiety, nervousness, anger and fear .

There may be a significant reduction in perspiration during sleep or sedation.

2. Secondary Palmar Hyperhidrosis

In secondary palmar hyperhidrosis hands sweat due to an obvious underlying disorder like:

*Infections including local infections, tuberculosis and tinea ugunium.
*Neurological disorders like peripheral autonomic neuropathy
*Frostbite
*Arteriovenous Fistulas
*Acromegaly
*Acrodynia
*Complex Regional Pain Syndromes
*Pachyonychia Congenita
*Primary Hypertrophic osteoarthropathy
*Dyskeratosis Congenita
*Blue rubber-bleb nevus
*Glomus tumor

*Secondary palmar hyperhidrosis as part of generalized hyperhidrosis due to  several  hormonal causes (diabetes, hyperthyroidism, thyrotoxicosis, menstruation, menopause), metabolic disorders, malignant disease (lymphoma, pheochromocitoma), autoimmune disorders (rheumatoid arthritis, systemic lupus erythrematosus), drugs like hypertensive drugs and certain classes of antidepressants (list of medications causing hyperhidrosis), chronic use of alcohol, Parkinson’s disease, neurological disorders (toxic neuropathy), homocystinuria, plasma cell disorders. Detailed list of conditions causing generalyzed hyperhidrosis.

How Sweat Glands Work:
In eccrine glands, the major substance enabling impulse conduction is acetylcholine, and in apocrine glands, they are catecholamines.

Body temperature is controlled by the thermoregulatory center in the hypothalamus and this is influenced not only by  by core body temperature but also by hormones, pyrogens, exercise and emotions.

Diagnosis:
The first step in diagnosing  the  Palmar  hyperhidrosis is to differentiate between generalized and focal hyperhidrosis.

A thorough case taking and medical history is usually sufficient to diagnose palmar hyperhidrosis and any trigger factors (scheduled drugs, narcotics, chronic alcoholism).

Diagnostic criteria for primary focal (including palmar) hyperhidrosis  are:

*Bilateral and relatively symmetric sweating
*Frequency of at least 1 episode per week
*Impairment of daily activities
*Age at onset before 25 years
*Family history
*Cessation of sweating during sleep

Tests may include:
*Hematological studies may be necessary to identify thyroid disorders (thyroid function test for T3 and T4 as well as thyroid antibodies) and diabetes (fasting blood glucose or a glucose tolerance test).

*X-rays and MRI scans will assist for diagnosing tuberculosis, pneumonia and tumors.

*Superficial electroconductivity can be monitored as any hyperhidrosis reduces skin electrical resistance.

*Thermoregulatory sweat test uses moisture-sensitive indicator powder to monitor moisture. Changes in the color of the powder at room temperature will highlight areas of increased perspiration.

Treatment:
Conservative management should be coupled with prescribed treatment by the Doctor to reduce the symptoms.

*Counseling may be effective in managing primary palmar hyperhidrosis in cases of mental-emotional etiology.

*Trigger foods and aggravating factors should be noted if possible and relevant dietary changes should be implemented.

*Effective prevention of secondary palmar hyperhidrosis is difficult with conservative management and drug therapy or surgery may be required.

*Excessive physical activity and extremes of heat may be two trigger factors that should be avoided as far as possible.

*In cases of diabetes, a glucose controlled diet with low glycemic index may improve glucose tolerance which could assist with palmar hyperhidrosis.

*Abstinence from alcohol and narcotics is advisable if it is the causative factor for sweaty palms.

*Stimulants such as caffeine and nicotine may aggravate palmar hypehidrosis and should relevant dietary and lifestyle changes should be implemented.

*Anti-perspirant compounds like aluminum chloride can be applied on the palms to reduce moisture or palmar surfaces. Recent research on an aluminum sesquichlorohydrate foam has shown that it is effective in reducing sweat in palmar hyperhidrosis

Treatment remains a challenge: options include topical and systemic agents, iontophoresis, and botulinum toxin type A injections, with surgical sympathectomy as a last resort. None of the treatments is without limitations or associated complications. Topical aluminum chloride hexahydrate therapy and iontophoresis are simple, safe, and inexpensive therapies; however, continuous application is required because results are often short-lived, and they may be insufficient. Systemic agents such as anticholinergic drugs are tolerated poorly at the dosages required for efficacy and usually are not an option because of their associated toxicity. While botulinum toxin can be used in treatment-resistant cases, numerous painful injections are required, and effects are limited to a few months.

Standard therapeutic protocol may differ among cases of palmar hyperhidrosis depending on medical history and underlying pathology.

*Anticholinergic drugs have a direct effect on the sympathetic nervous system although there are numerous side effects.

*Treatment should be directed at contributing factors.

*Ionophoresis involves the use of electrotherapeutic measures to reduce the activity of sweat glands.

*Botulinum injections at the affected area may be useful for its anticholinergic effects.

*Surgery should be considered if drug therapy proves ineffective. Endoscopic transthoracic sympathectomy involves resection of the sympathetic nerve supply to the affected area. This prevents nerve stimulation of the sweat gland of the palms. However surgery has a host of complications including exacerbating the problem or increasing generalized hyperhidrosis.

Surgical sympathectomy should be reserved for the most severe cases and should be performed only after all other treatments have failed. Although the safety and reliability of treatments for palmoplantar hyperhidrosis have improved dramatically, side effects and compensatory sweating are still common, potentially severe problems.

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Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.aafp.org/afp/2004/0301/p1117.html
http://www.healthhype.com/causes-treatment-of-palmar-hyperhidrosis-sweaty-palmshands.html

Spina bifida

Definition:
Spina bifida is a type of birth defect called a neural tube defect. It occurs when the bones of the spine (vertebrae) don’t form properly around part of the baby’s spinal cord. Spina bifida can be mild or severe….CLICK & SEE

Spina bifida malformations fall into three categories: spina bifida occulta, spina bifida cystica with meningocele, and spina bifida cystica with myelomeningocele. The most common location of the malformations is the lumbar and sacral areas. Myelomeningocele is the most significant and common form, and this leads to disability in most affected individuals. The terms spina bifida and myelomeningocele are usually used interchangeably.

Spina bifida meningocele and myelomeningocele are among the most common birth defects, with a worldwide incidence of about 1 in every 1000 births. The occulta form is much more common, but only rarely causes neurological symptoms.

Clasification:....CLICK & SEE
Spina bifida occulta:
Occulta is Latin for “hidden”. This is the mildest form of spina bifida. In occulta, the outer part of some of the vertebrae is not completely closed. The splits in the vertebrae are so small that the spinal cord does not protrude. The skin at the site of the lesion may be normal, or it may have some hair growing from it; there may be a dimple in the skin, or a birthmark.

Many people with this type of spina bifida do not even know they have it, as the condition is asymptomatic in most cases. The incidence of spina bifida occulta is approximately 10-20% of the population, and most people are diagnosed incidentally from spinal X-rays. A systematic review of radiographic research studies found no relationship between spina bifida occulta and back pain. More recent studies not included in the review support the negative findings.

However, other studies suggest spina bifida occulta is not always harmless. One study found that among patients with back pain, severity is worse if spina bifida occulta is present.

Incomplete posterior fusion is not a true spina bifida, and is very rarely of neurological significance.

Meningocele:
A posterior meningocele  or meningeal cyst  is the least common form of spina bifida. In this form, the vertebrae develop normally, but the meninges are forced into the gaps between the vertebrae. As the nervous system remains undamaged, individuals with meningocele are unlikely to suffer long-term health problems, although cases of tethered cord have been reported. Causes of meningocele include teratoma and other tumors of the sacrococcyx and of the presacral space, and Currarino syndrome.

A meningocele may also form through dehiscences in the base of the skull. These may be classified by their localisation to occipital, frontoethmoidal, or nasal. Endonasal meningoceles lie at the roof of the nasal cavity and may be mistaken for a nasal polyp. They are treated surgically. Encephalomeningoceles are classified in the same way and also contain brain tissue.

Myelomeningocele:
This type of spina bifida often results in the most severe complications. In individuals with myelomeningocele, the unfused portion of the spinal column allows the spinal cord to protrude through an opening. The meningeal membranes that cover the spinal cord form a sac enclosing the spinal elements. The term Meningomyelocele is also used interchangeably.

Myeloschisis:
Spina bifida with myeloschisis is the most severe form of myelomeningocele. In this type, the involved area is represented by a flattened, plate-like mass of nervous tissue with no overlying membrane. The exposure of these nerves and tissues make the baby more prone to life-threatening infections such as meningitis.

The protruding portion of the spinal cord and the nerves that originate at that level of the cord are damaged or not properly developed. As a result, there is usually some degree of paralysis and loss of sensation below the level of the spinal cord defect. Thus, the more cranial the level of the defect, the more severe the associated nerve dysfunction and resultant paralysis may be. People may have ambulatory problems, loss of sensation, deformities of the hips, knees or feet, and loss of muscle tone.

Signs and symptoms:
Physical complications:

*Leg weakness and paralysis
*Orthopedic abnormalities (i.e., club foot, hip dislocation, scoliosis)
*Bladder and bowel control problems, including incontinence, urinary tract infections, and poor renal function
*Pressure sores and skin irritations
*Abnormal eye movement

68% of children with spina bifida have an allergy to latex, ranging from mild to life-threatening. The common use of latex in medical facilities makes this a particularly serious concern. The most common approach to avoid developing an allergy is to avoid contact with latex-containing products such as examination gloves and condoms and catheters that do not specify they are latex free, and many other products, such as some commonly used by dentists.

The spinal cord lesion or the scarring due to surgery may result in a tethered spinal cord. In some individuals, this causes significant traction and stress on the spinal cord and can lead to a worsening of associated paralysis, scoliosis, back pain, and worsening bowel and/or bladder function

Neurological complications:
Many individuals with spina bifida have an associated abnormality of the cerebellum, called the Arnold Chiari II malformation. In affected individuals, the back portion of the brain is displaced from the back of the skull down into the upper neck. In about 90% of the people with myelomeningocele, hydrocephalus also occurs because the displaced cerebellum interferes with the normal flow of cerebrospinal fluid, causing an excess of the fluid to accumulate.  In fact, the cerebellum also tends to be smaller in individuals with spina bifida, especially for those with higher lesion levels.

The corpus callosum is abnormally developed in 70-90% of individuals with spina bifida myelomeningocele; this impacts the communication processes between the left and right brain hemispheres. Further, white matter tracts connecting posterior brain regions with anterior regions appear less organized. White matter tracts between frontal regions have also been found to be impaired.

Cortex abnormalities may also be present. For example, frontal regions of the brain tend to be thicker than expected, while posterior and parietal regions are thinner. Thinner sections of the brain are also associated with increased cortical folding. Neurons within the cortex may also be displaced.

Executive function:
Several studies have demonstrated difficulties with executive functions in youth with spina bifida, with greater deficits observed in youth with shunted hydrocephalus. Unlike typically developing children, youths with spina bifida do not tend to improve in their executive functioning as they grow older. Specific areas of difficulty in some individuals include planning, organizing, initiating, and working memory. Problem-solving, abstraction, and visual planning may also be impaired.  Further, children with spina bifida may have poor cognitive flexibility. Although executive functions are often attributed to the frontal lobes of the brain, individuals with spina bifida have intact frontal lobes; therefore, other areas of the brain may be implicated.

Individuals with spina bifida, especially those with shunted hydrocephalus, often have attention problems. Children with spina bifida and shunted hydrocephalus have higher rates of ADHD than typically developing children (31% vs. 17%). Deficits have been observed for selective attention and focused attention, although poor motor speed may contribute to poor scores on tests of attention.  Attention deficits may be evident at a very early age, as infants with spina bifida lag behind their peers in orienting to faces.

Academic skills:
Individuals with spina bifida may struggle academically, especially in the subjects of mathematics and reading. In one study, 60% of children with spina bifida were diagnosed with a learning disability.  In addition to brain abnormalities directly related to various academic skills, achievement is likely affected by impaired attentional control and executive functioning. Children with spina bifida may perform well in elementary school, but begin to struggle as academic demands increase.

Children with spina bifida are more likely than their typically developing peers to have dyscalculia. Individuals with spina bifida have demonstrated stable difficulties with arithmetic accuracy and speed, mathematical problem-solving, and general use and understanding of numbers in everyday life. Mathematics difficulties may be directly related to the thinning of the parietal lobes (regions implicated in mathematical functioning) and indirectly associated with deformities of the cerebellum and midbrain that affect other functions involved in mathematical skills. Further, higher numbers of shunt revisions are associated with poorer mathematics abilities. Working memory and inhibitory control deficiencies have been implicated for math difficulties, although visual-spatial difficulties are not likely involved. Early intervention to address mathematics difficulties and associated executive functions is crucial.

Individuals with spina bifida tend to have better reading skills than mathematics skills. Children and adults with spina bifida have stronger abilities in reading accuracy than in reading comprehension. Comprehension may be especially impaired for text that requires an abstract synthesis of information rather than a more literal understanding. Individuals with spina bifida may have difficulty with writing due to deficits in fine motor control and working memory.

Causes:
The exact cause of this birth defect isn’t known. Experts think that genes and the environment are part of the cause. For example, women who have had one child with spina bifida are more likely to have another child with the disease. Women who are obese or who have diabetes are also more likely to have a child with spina bifida.

Spina bifida is sometimes caused by the failure of the neural tube to close during the first month of embryonic development (often before the mother knows she is pregnant). Some forms are known to occur with primary conditions that cause raised central nervous system pressure, which raises the possibility of a dual pathogenesis.

In normal circumstances, the closure of the neural tube occurs around the 23rd (rostral closure) and 27th (caudal closure) day after fertilization. However, if something interferes and the tube fails to close properly, a neural tube defect will occur. Medications such as some anticonvulsants, diabetes, having a relative with spina bifida, obesity, and an increased body temperature from fever or external sources such as hot tubs and electric blankets may increase the chances of delivery of a baby with a spina bifida.

Extensive evidence from mouse strains with spina bifida indicates that there is sometimes a genetic basis for the condition. Human spina bifida, like other human diseases, such as cancer, hypertension and atherosclerosis (coronary artery disease), likely results from the interaction of multiple genes and environmental factors.

Research has shown the lack of folic acid (folate) is a contributing factor in the pathogenesis of neural tube defects, including spina bifida. Supplementation of the mother’s diet with folate can reduce the incidence of neural tube defects by about 70%, and can also decrease the severity of these defects when they occur. It is unknown how or why folic acid has this effect.

Spina bifida does not follow direct patterns of heredity like muscular dystrophy or haemophilia. Studies show a woman having had one child with a neural tube defect such as spina bifida has about a 3% risk of having another affected child. This risk can be reduced with folic acid supplementation before pregnancy. For the general population, low-dose folic acid supplements are advised (0.4 mg/day)

Treatment:
There is no known cure for nerve damage caused by spina bifida. To prevent further damage of the nervous tissue and to prevent infection, pediatric neurosurgeons operate to close the opening on the back. The spinal cord and its nerve roots are put back inside the spine and covered with meninges. In addition, a shunt may be surgically installed to provide a continuous drain for the excess cerebrospinal fluid produced in the brain, as happens with hydrocephalus. Shunts most commonly drain into the abdomen or chest wall. However, if spina bifida is detected during pregnancy, then open or minimally-invasive fetal surgery can be performed.

In childhood:
Most individuals with myelomeningocele will need periodic evaluations by a variety of specialists:

*Physiatrists coordinate the rehabilitation efforts of different therapists and prescribe specific therapies, adaptive equipment, or medications to encourage as high of a functional performance within the community as possible.

*Orthopedists monitor growth and development of bones, muscles, and joints.

*Neurosurgeons perform surgeries at birth and manage complications associated with tethered cord and hydrocephalus.

*Neurologists treat and evaluate nervous system issues, such as seizure disorders.

*Urologists to address kidney, bladder, and bowel dysfunction – many will need to manage their urinary systems with a program of catheterization. Bowel management programs aimed at improving elimination are also designed.

*Ophthalmologists evaluate and treat complications of the eyes.

*Orthotists design and customize various types of assistive technology, including braces, crutches, walkers, and wheelchairs to aid in mobility. As a general rule, the higher the level of the spina bifida defect, the more severe the paralysis, but paralysis does not always occur. Thus, those with low levels may need only short leg braces, whereas those with higher levels do best with a wheelchair, and some may be able to walk unaided.

*Physical therapists, occupational therapists, psychologists, and speech/language pathologists aid in rehabilitative therapies and increase independent living skills.

Transition to adulthood:
Although many children’s hospitals feature integrated multidisciplinary teams to coordinate healthcare of youth with spina bifida, the transition to adult healthcare can be difficult because the above healthcare professionals operate independently of each other, requiring separate appointments and communicate among each other much less frequently. Healthcare professionals working with adults may also be less knowledgeable about spina bifida because it is considered a childhood chronic health condition.  Due to the potential difficulties of the transition, adolescents with spina bifida and their families are encouraged to begin to prepare for the transition around ages 14–16, although this may vary depending on the adolescent’s cognitive and physical abilities and available family support. The transition itself should be gradual and flexible. The adolescent’s multidisciplinary treatment team may aid in the process by preparing comprehensive, up-to-date documents detailing the adolescent’s medical care, including information about medications, surgery, therapies, and recommendations. A transition plan and aid in identifying adult healthcare professionals are also helpful to include in the transition process.

Further complicating the transition process is the tendency for youths with spina bifida to be delayed in the development of autonomy, with boys particularly at risk for slower development of independence. An increased dependence on others (in particular family members) may interfere with the adolescent’s self-management of health-related tasks, such as catheterization, bowel management, and taking medications.  As part of the transition process, it is beneficial to begin discussions at an early age about educational and vocational goals, independent living, and community involvement.

Prevention:
There is neither a single cause of spina bifida nor any known way to prevent it entirely. However, dietary supplementation with folic acid has been shown to be helpful in reducing the incidence of spina bifida. Sources of folic acid include whole grains, fortified breakfast cereals, dried beans, leaf vegetables and fruits.

Folate fortification of enriched grain products has been mandatory in the United States since 1998. The U.S. Food and Drug Administration, Public Health Agency of Canada  and UK recommended amount of folic acid for women of childbearing age and women planning to become pregnant is at least 0.4 mg/day of folic acid from at least three months before conception, and continued for the first 12 weeks of pregnancy.  Women who have already had a baby with spina bifida or other type of neural tube defect, or are taking anticonvulsant medication should take a higher dose of 4–5 mg/day.

Certain mutations in the gene VANGL1 are implicated as a risk factor for spina bifida: These mutations have been linked with spina bifida in some families with a history of spina bifida.

Pregnancy screening:
Open spina bifida can usually be detected during pregnancy by fetal ultrasound. Increased levels of maternal serum alpha-fetoprotein (MSAFP) should be followed up by two tests – an ultrasound of the fetal spine and amniocentesis of the mother’s amniotic fluid (to test for alpha-fetoprotein and acetylcholinesterase). AFP tests are now mandated by some state laws (including California). and failure to provide them can have legal ramifications. In one case a man born with spina bifida was awarded a $2 million settlement after court found his mother’s OBGYN negligent for not performing these tests. Spina bifida may be associated with other malformations as in dysmorphic syndromes, often resulting in spontaneous miscarriage. In the majority of cases, though, spina bifida is an isolated malformation.

Genetic counseling and further genetic testing, such as amniocentesis, may be offered during the pregnancy, as some neural tube defects are associated with genetic disorders such as trisomy 18. Ultrasound screening for spina bifida is partly responsible for the decline in new cases, because many pregnancies are terminated out of fear that a newborn might have a poor future quality of life. With modern medical care, the quality of life of patients has greatly improved.

Resources:
http://en.wikipedia.org/wiki/Spina_bifida
http://www.webmd.com/parenting/baby/tc/spina-bifida-topic-overview

Aphasia

Description:
Aphasia is the name given to a collection of language disorders caused by damage to the brain.  The word aphasia comes from the wordn aphasia, in Ancient Greek, which means A requirement for a diagnosis of aphasia is that, prior to the illness or injury, the person’s language skills were normal . The difficulties of people with aphasia can range from occasional trouble finding words to losing the ability to speak, read, or write, but does not affect intelligence. This also affects visual language such as sign language. The term “aphasia” implies a problem with one or more functions that are essential and specific to language function. It is not usually used when the language problem is a result of a more peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles or a general hearing impairment.
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Stroke is the most common cause of aphasia in the United States. Approximately 500,000 individuals suffer strokes each year, and 20% of these individuals develop some type of aphasia. Other causes of brain damage include head injuries, brain tumors, and infection. About half of the people who show signs of aphasia have what is called temporary or transient aphasia and recover completely within a few days. An estimated one million Americans suffer from some form of permanent aphasia. As yet, no connection between aphasia and age, gender, or race has been found.
Aphasia is sometimes confused with other conditions that affect speech, such as dysarthria and apraxia. These condition affect the muscles used in speaking rather than language function itself. Dysarthria is a speech disturbance caused by lack of control over the muscles used in speaking, perhaps due to nerve damage. Speech apraxia is a speech disturbance in which language comprehension and muscle control are retained, but the memory of how to use the muscles to form words is not.

Symptoms:
Aphasia is condition characterized by either partial or total loss of the ability to communicate verbally or using written words. A person with aphasia may have difficulty speaking, reading, writing, recognizing the names of objects, or understanding what other people have said. Aphasia is caused by a brain injury, as may occur during a traumatic accident or when the brain is deprived of oxygen during a stroke. It may also be caused by a brain tumor, a disease such as Alzheimer’s, or an infection, like encephalitis. Aphasia may be temporary or permanent. Aphasia does not include speech impediments caused by loss of muscle control.
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To understand and use language effectively, an individual draws upon word memory-stored information on what certain words mean, how to put them together, and how and when to use them properly. For a majority of people, these and other language functions are located in the left side (hemisphere) of the brain. Damage to this side of the brain is most commonly linked to the development of aphasia. Interestingly, however, left-handed people appear to have language areas in both the left and right hemispheres of the brain and, as a result, may develop aphasia from damage to either side of the brain.

People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems such as dysarthria or apraxia and not primarily due to aphasia. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication. Often those with aphasia will try to hide their inability to name objects by using words like thing. So when asked to name a pencil they may say it is a thing used to write.

*inability to comprehend language
*inability to pronounce, not due to muscle paralysis or weakness
*inability to speak spontaneously
*inability to form words
*inability to name objects (anomia)
*poor enunciation
*excessive creation and use of personal neologisms
*inability to repeat a phrase
*persistent repetition of one syllable, word, or phrase (stereotypies)
*paraphasia (substituting letters, syllables or words)
*agrammatism (inability to speak in a grammatically correct fashion)
*dysprosody (alterations in inflexion, stress, and rhythm)
*incomplete sentences
*inability to read
*inability to write
*limited verbal output
*difficulty in naming
*speech disorder
*Speaking gibberish
*inability to follow or understand simple requests

Causes:
Aphasia is most commonly caused by stroke. It can also be caused by other brain diseases, including cancer (brain tumor), epilepsy, and Alzheimer’s disease, or by a head injury. In rare cases, aphasia may also result from herpesviral encephalitis. The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia. In acute disorders, such as head injury or stroke, aphasia usually develops quickly. Aphasia usually develops more slowly from a brain tumor, infection, or dementia.

Although all of the disease listed above are potential causes, aphasia will generally only result when there is substantial damage to the left hemisphere of the brain, either the cortex (outer layer) and/or the underlying white matter. Substantial damage to tissue anywhere within the region shown in blue on the figure below can potentially result in aphasia.  Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, the internal and external capsules, and the caudate nucleus of the basal ganglia.  The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms.  A very small number of people can experience aphasia after damage to the right hemisphere only. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps greater overall reliance on the right hemisphere for language skills than in the general population.

Finally, certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom.  Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain.

Classification:
Aphasia is best thought of as a collection of different disorders, rather than a single problem. Each individual with aphasia will present with their own particular combination of language strengths and weaknesses. Consequently, it is a major challenge just to document the various difficulties that can occur in different people, let alone decide how they might best be treated. Most classifications of the aphasias tend to divide the various symptoms into broad classes. A common approach is to distinguish between the fluent aphasias (where speech remains fluent, but content may be lacking, and the person may have difficulties understanding others), and the nonfluent aphasias ( where speech is very halting and effortful, and may consist of just one or two words at a time).

However, no such broad-based grouping has proven fully adequate. There is a huge variation among patients within the same broad grouping, and aphasias can be highly selective. For instance, patients with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.

Classical-Localizationist approaches:
Localizationist approaches aim to classify the aphasias according to their major presenting characteristics and the regions of the brain that most probably gave rise to them. Inspired by the early work of nineteenth century neurologists Paul Broca and Carl Wernicke, these approaches identify two major subtypes of aphasia and several more minor subtypes:

*Broca’s aphasia (also known as Motor aphasia or Expressive aphasia), which is characterized by halted, fragmented, effortful speech, but relatively well-preserved comprehension. It has been associated with damage to the posterior left prefrontal cortex, most notably Broca’s area. Individuals with Broca’s aphasia often have right-sided weakness or paralysis of the arm and leg, because the left frontal lobe is also important for body movement, particularly on the right side.

*Wernicke’s aphasia (also known as Sensory aphasia or Receptive aphasia), which is characterized by fluent speech, but marked difficulties understanding words and sentences. Although fluent, the speech may lack in key substantive words (nouns, verbs adjectives), and may contain incorrect words or even nonsense words. This subtype has been associated with damage to the posterior left temporal cortex, most notably Wernicke’s area. These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement.

*Other, more minor subtypes include Conduction aphasia, a disorder where speech remains fluent, and comprehension is preserved, but the person may have disproportionate difficulty where repeating words or sentences. Other include Transcortical motor aphasia and Transcortical sensory aphasia which are similar to Broca’s and Wernicke’s aphasia respectively, but the ability to repeat words and sentences is disroportionately preserved.

Recent classification schemes adopting this approach, such as the “Boston-Neoclassical Model”  also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Broca’s aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernicke’s aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: Anomic aphasia, which is characterized by a selective difficulty finding the names for things; and Global aphasia where both expression and comprehension of speech are severely compromised.

Many localizationist approaches also recognize the existence of additional, more “pure” forms of language disorder that may affect only a single language skill.  For example, in Pure alexia, a person may be able to write but not read, and in Pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them.

Cognitive neuropsychological approaches:
Although localizationist approaches provide a useful way of classifying the different patterns of language difficulty into broad groups, one problem is that a sizeable number of individuals do not fit neatly into one category or another. Another problem is that the categories, particularly the major ones such as Broca’s and Wernicke’s aphasia, still remain quite broad. Consequently, even amongst individuals who meet the criteria for classification into a subtype, there can be enormous variability in the types of difficulties they experience.

Instead of categorizing every individual into a specific subtype, cognitive neuropsychological approaches aim to identify the key language skills or “modules” that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with a number of modules. This type of approach requires a framework or theory as to what skills/modules are needed to perform different kinds of language tasks. For example, the model of Max Coltheart identifies a module that recognizes phonemes as they are spoken, which is essential for any task involving recognition of words. Similarly, there is a module that stores phonemes that the person is planning to produce in speech, and this module is critical for any task involving the production of long words or long strings of speech. One a theoretical framework has been established, the functioning of each module can then be assessed using a specific test or set of tests. In the clinical setting, use of this model usually involves conducting a battery of assessments, each of which tests one or a number of these modules. Once a diagnosis is reached as to the skills/modules where the most significant impairment lies, therapy can proceed to treat these skills.

In practice, the cognitive neuropsychological approach can be unwieldy due to the wide variety of skills that can potentially be tested. Also, it is perhaps best suited to milder cases of aphasia: If the person has little expressive or receptive language ability, sometimes test performance can be difficult to interpret. In practice, clinicians will often use a blend of assessment approaches, which include broad subtyping based on a localizationist framework, and some finer exploration of specific language skills based on the cognitive neuropsychological framework.
Other forms of aphasia:

Progressive aphasias:
Primary progressive aphasia (PPA) is associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimer’s disease, which is the gradual process of progressively losing the ability to think. It is characterized by the gradual loss of the ability to name objects. People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence. There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA)

Progressive Jargon Aphasia is a fluent or receptive aphasia in which the patient’s speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the patient has problems with the selection of nouns. Either they will replace the desired word with another that sounds or looks like the original one or has some other connection or they will replace it with sounds. As such, patients with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they cannot find with sounds. Substitutions commonly involve picking another (actual) word starting with the same sound (e.g., clocktower – colander), picking another semantically related to the first (e.g., letter – scroll), or picking one phonetically similar to the intended one (e.g., lane – late).

Deaf aphasia:
There have been many instances showing that there is a form of aphasia among deaf individuals. Sign language is, after all, a form of communication that has been shown to use the same areas of the brain as verbal forms of communication. Mirror neurons become activated when an animal is acting in a particular way or watching another individual act in the same manner. These mirror neurons are important in giving an individual the ability to mimic movements of hands. Broca’s area of speech production has been shown to contain several of these mirror neurons resulting in significant similarities of brain activity between sign language and vocal speech communication. Facial communication is a significant portion of how animals interact with each other. Humans use facial movements to create, what other humans perceive, to be faces of emotions. While combining these facials movements with speech, a more full form of language is created which enables the species to interact with a much more complex and detailed form of communication. Sign language also uses these facial movements and emotions along with the primary hand movement way of communicating. These facial movement forms of communication come from the same areas of the brain. When dealing with damages to certain areas of the brain, vocal forms of communication are in jeopardy of severe forms of aphasia. Since these same areas of the brain are being used for sign language, these same, at least very similar, forms of aphasia can show in the Deaf community. Individuals can show a form of Wernicke’s aphasia with sign language and they show deficits in their abilities in being able to produce any form of expressions. Broca’s aphasia shows up in some patients, as well. These individuals find tremendous difficulty in being able to actually sign the linguistic concepts they are trying to express

Diagnosis:
Following brain injury, an initial bedside assessment is made to determine whether language function has been affected. If the individual experiences difficulty communicating, attempts are made to determine whether this difficulty arises from impaired language comprehension or an impaired ability to speak. A typical examination involves listening to spontaneous speech and evaluating the individual’s ability to recognize and name objects, comprehend what is heard, and repeat sample words and phrases. The individual may also be asked to read text aloud and explain what the passage means. In addition, writing ability is evaluated by having the individual copy text, transcribe dictated text, and write something without prompting.
A speech pathologist or neuropsychologist may be asked to conduct more extensive examinations using in-depth, standardized tests. Commonly used tests include the Boston Diagnostic Aphasia Examination, the Western Aphasia Battery, and possibly, the Porch Index of Speech Ability.

The results of these tests indicate the severity of the aphasia and may also provide information regarding the exact location of the brain damage. This more extensive testing is also designed to provide the information necessary to design an individualized speech therapy program. Further information about the location of the damage is gained through the use of imaging technology, such as magnetic resonance imaging (MRI) and computed tomography scans.
Treatment:
Initially, the underlying cause of aphasia must be treated or stabilized. To regain language function, therapy must begin as soon as possible following the injury. Although there are no medical or surgical procedures currently available to treat this condition, aphasia resulting from stroke or head injury may improve through the use of speech therapy. For most individuals, however, the primary emphasis is placed on making the most of retained language abilities and learning to use other means of communication to compensate for lost language abilities.
Speech therapy is tailored to meet individual needs, but activities and tools that are frequently used include the following:

Exercise and practice. Weakened muscles are exercised by repetitively speaking certain words or making facial expressions, such as smiling.
Picture cards. Pictures of everyday objects are used to improve word recall and increase vocabulary. The names of the objects may also be repetitively spoken aloud as part of an exercise and practice routine.

Picture boards. Pictures of everyday objects and activities are placed together, and the individual points to certain pictures to convey ideas and communicate with others.
Workbooks. Reading and writing exercises are used to sharpen word recall and regain reading and writing abilities. Hearing comprehension is also redeveloped using these exercises.
Computers. Computer software can be used to improve speech, reading, recall, and hearing comprehension by, for example, displaying pictures and having the individual find the right word.

Prognosis:
The degree to which an individual can recover language abilities is highly dependent on how much brain damage occurred and the location and cause of the original brain injury. Other factors include the individual’s age, general health, motivation and willingness to participate in speech therapy, and whether the individual is left or right handed. Language areas may be located in both the left and right hemispheres in left-handed individuals. Left-handed individuals are, therefore, more likely to develop aphasia following brain injury, but because they have two language centers, may recover more fully because language abilities can be recovered from either side of the brain. The intensity of therapy and the time between diagnosis and the start of therapy may also affect the eventual outcome.

Prevention:
Because there is no way of knowing when a stroke, traumatic head injury, or disease will occur, very little can be done to prevent aphasia. However  it can be adviced to be careful in movement of aged person specially for those having high bloodpressure, diabetis and other form of diseases.

Following are some precautions that should be taken to avoid aphasia, by decreasing the risk of stroke, the main cause of aphasia:

*Exercising regularly
*Eating a healthy diet
*Keeping alcohol consumption low and avoiding tobacco use
*Controlling blood pressure

History:
The first recorded case of aphasia is from an Egyptian papyrus, the Edwin Smith Papyrus, which details speech problems in a person with a traumatic brain injury to the temporal lobe.During the second half of the 19th century, Aphasia was a major focus for scientists and philosophers who were working in the beginning stages in the field of psychology.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Aphasia
http://medical-dictionary.thefreedictionary.com/aphasia

Prostate cancer

Other Name : Carcinoma of the man’s prostate,adenocarcinoma, or glandular cancer
Definition:
Prostate cancer is cancer that occurs in a man’s prostate— a small walnut-shaped gland that produces the seminal fluid that nourishes and transports sperm for  male reproductive system.

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Prostate cancer is one of the most common types of cancer in men. Most prostate cancers are slow growing; however, some grow relatively fast.Initially remains confined to the prostate gland,  where it may not cause serious harm. While some types of prostate cancer grow slowly and may need minimal or no treatment, other types are aggressive and can spread quickly.

Prostate cancer that is detected early — when it’s still confined to the prostate gland — has a better chance of successful treatment.

Factors that increase the risk of prostate cancer include: older age, a family history of the disease, and race. About 99% of cases occur in those over the age of 50. Having a first degree relative with  the disease increases the risk 2 to 3 fold. In the United States it is more common in the African American population than the Caucasian population. Other factors that may be involved include a diet  high in processed, red meat, or milk products or low in certain vegetables. Prostate cancer is diagnosed by biopsy. Medical imaging may then be done to determine if the cancer has spread to other  parts of the body.

Symptoms:
Early prostate cancer usually causes no symptoms. Sometimes, however, prostate cancer does cause symptoms, often similar to those of diseases such as benign prostatic hyperplasia. These include frequent urination, nocturia (increased urination at night), difficulty starting and maintaining a steady stream of urine, hematuria (blood in the urine), and dysuria (painful urination). A study  based on the 1998 Patient Care Evaluation in the US found that about a third of patients diagnosed with prostate cancer had one or more such symptoms, while two thirds had no symptoms.

Prostate cancer is associated with urinary dysfunction as the prostate gland surrounds the prostatic urethra. Changes within the gland, therefore, directly affect urinary function. Because the vas  deferens deposits seminal fluid into the prostatic urethra, and secretions from the prostate gland itself are included in semen content, prostate cancer may also cause problems with sexual function  and performance, such as difficulty achieving erection or painful ejaculation.

Advanced prostate cancer can spread to other parts of the body, possibly causing additional symptoms. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis,  or ribs. Spread of cancer into other bones such as the femur is usually to the proximal part of the bone. Prostate cancer in the spine can also compress the spinal cord, causing leg weakness and  urinary and fecal incontinence.

Causes:
The  causes of prostate cancer  is still not very clear.
Doctors know that prostate cancer begins when some cells in your prostate become abnormal. Mutations in the abnormal cells’ DNA cause the cells to grow and divide more rapidly than normal cells  do. The abnormal cells continue living, when other cells would die. The accumulating abnormal cells form a tumor that can grow to invade nearby tissue. Some abnormal cells can break off and  spread (metastasize) to other parts of the body.

Risk Factors:
The primary risk factors are obesity, age and family history. Prostate cancer is very uncommon in men younger than 45, but becomes more common with advancing age. The average age at the time  of diagnosis is 70. However, many men never know they have prostate cancer. Autopsy studies of Chinese, German, Israeli, Jamaican, Swedish, and Ugandan men who died of other causes have  found prostate cancer in 30% of men in their 50s, and in 80% of men in their 70s. Men who have first-degree family members with prostate cancer appear to have double the risk of getting the  disease compared to men without prostate cancer in the family. This risk appears to be greater for men with an affected brother than for men with an affected father.   Men with high blood pressure are more likely to develop prostate cancer.  There is a small increased risk of prostate cancer associated with lack of exercise. A 2010 study found that prostate basal cells were the most common  site of origin for prostate cancers.

Genetic factors :
Genetic background may contribute to prostate cancer risk, as suggested by associations with race, family, and specific gene variants. Men who have a first-degree relative (father or brother) with prostate cancer have twice the risk of developing prostate cancer, and those with two first-degree relatives affected have a fivefold greater risk compared with men with no family history. In the

United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men. In contrast, the incidence and mortality rates for Hispanic men  are one third lower than for non-Hispanic whites. Studies of twins in Scandinavia suggest that 40% of prostate cancer risk can be explained by inherited factors.

No single gene is responsible for prostate cancer; many different genes have been implicated. Mutations in BRCA1 and BRCA2, important risk factors for ovarian cancer and breast cancer in women, have also been implicated in prostate cancer. Other linked genes include the Hereditary Prostate cancer gene 1 (HPC1), the androgen receptor, and the vitamin D receptor.  TMPRSS2-ETS gene  family fusion, specifically TMPRSS2-ERG or TMPRSS2-ETV1/4 promotes cancer cell growth.

Two large genome-wide association studies linking single nucleotide polymorphisms (SNPs) to prostate cancer were published in 2008. These studies identified several SNPs which substantially  affect the risk of prostate cancer. For example, individuals with TT allele pair at SNP rs10993994 were reported to be at 1.6 times higher risk of prostate cancer than those with the CC allele pair. This

SNP explains part of the increased prostate cancer risk of African American men as compared to American men of European descent, since the C allele is much more prevalent in the latter; this SNP is located in the promoter region of the MSMB gene, thus affects the amount of MSMB protein synthesized and secreted by epithelial cells of the prostate.

Dietary factors:
While some dietary factors have been associated with prostate cancer the evidence is still tentative.  Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence. Red  meat and processed meat also appear to have little effect in human studies.  Higher meat consumption has been associated with a higher risk in some studies.

Lower blood levels of vitamin D may increase the risk of developing prostate cancer.

Folic acid supplements have no effect on the risk of developing prostate cancer.

Viral factors:
In 2006, a previously unknown retrovirus, Xenotropic MuLV-related virus or XMRV, was associated with human prostate tumors,  but subsequent reports on the virus were contradictory,  and the original 2006 finding was instead due to a previously undetected contamination.

Sexual factors:
Several case-control studies have shown that having many lifetime sexual partners or starting sexual activity early in life substantially increases the risk of prostate cancer. This correlation suggests  a sexually transmissible infection (STI) may cause some prostate cancer cases; however, many studies have unsuccessfully attempted to find such a link, especially when testing for STIs shortly  before or after prostate cancer diagnosis.  Studies testing for STIs a decade or more prior to prostate cancer diagnosis find a significant link between prostate cancer and various STIs (HPV-16, HPV-18 and HSV-2). This evidence could be explained by a yet-to-be-identified sexually transmissible infection and a long latency period between onset of infection and prostate cancer.

On the other hand, while the available evidence is weak,  tentative results suggest that frequent ejaculation may decrease the risk of prostate cancer.  A study, over eight years, showed that those  that ejaculated most frequently (over 21 times per month on average) were less likely to get prostate cancer.  The results were broadly similar to the findings of a smaller Australian study

Medication exposure:
There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Use of the cholesterol-lowering drugs known as the statins may also decrease  prostate cancer risk.

Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer while another study shows infection may help prevent prostate cancer by increasing blood to the  area. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk. Finally, obesity  and elevated blood levels of testosterone   may increase the risk for prostate cancer. There is an association between vasectomy and prostate cancer however more research is needed to determine if this is a causative relationship.

Pathophysiology:
The prostate is a part of the male reproductive system that helps make and store seminal fluid. In adult men, a typical prostate is about 3 centimeters long and weighs about 20 grams. It is located in the pelvis, under the urinary bladder and in front of the rectum. The prostate surrounds part of the urethra, the tube that carries urine from the bladder during urination and semen during ejaculation.  Because of its location, prostate diseases often affect urination, ejaculation, and rarely defecation. The prostate contains many small glands which make about 20 percent of the fluid  constituting semen.  In prostate cancer, the cells of these prostate glands mutate into cancer cells. The prostate glands require male hormones, known as androgens, to work properly. Androgens  include testosterone, which is made in the testes; dehydroepiandrosterone, made in the adrenal glands; and dihydrotestosterone, which is converted from testosterone within the prostate itself.

Androgens are also responsible for secondary sex characteristics such as facial hair and increased muscle mass.

Prostate cancer is classified as an adenocarcinoma, or glandular cancer, that begins when normal semen-secreting prostate gland cells mutate into cancer cells. The region of prostate gland where  the adenocarcinoma is most common is the peripheral zone. Initially, small clumps of cancer cells remain confined to otherwise normal prostate glands, a condition known as carcinoma in situ or  prostatic intraepithelial neoplasia (PIN). Although there is no proof that PIN is a cancer precursor, it is closely associated with cancer. Over time, these cancer cells begin to multiply and spread to the  surrounding prostate tissue (the stroma) forming a tumor. Eventually, the tumor may grow large enough to invade nearby organs such as the seminal vesicles or the rectum, or the tumor cells may develop the ability to travel in the bloodstream and lymphatic system. Prostate cancer is considered a malignant tumor because it is a mass of cells that can invade other parts of the body. This invasion of other organs is called metastasis. Prostate cancer most commonly metastasizes to the bones, lymph nodes, and may invade rectum, bladder and lower ureters after local progression.

The route of metastasis to bone is thought to be venous as the prostatic venous plexus draining the prostate connects with the vertebral veins.

The prostate is a zinc-accumulating, citrate-producing organ. The protein ZIP1 is responsible for the active transport of zinc into prostate cells. One of zinc’s important roles is to change the metabolism of the cell in order to produce citrate, an important component of semen. The process of zinc accumulation, alteration of metabolism, and citrate production is energy inefficient, and  prostate cells sacrifice enormous amounts of energy (ATP) in order to accomplish this task. Prostate cancer cells are generally devoid of zinc. This allows prostate cancer cells to save energy not  making citrate, and utilize the new abundance of energy to grow and spread. The absence of zinc is thought to occur via a silencing of the gene that produces the transporter protein ZIP1. ZIP1 is now called a tumor suppressor gene product for the gene SLC39A1. The cause of the epigenetic silencing is unknown. Strategies which transport zinc into transformed prostate cells effectively  eliminate these cells in animals. Zinc inhibits NF-?B pathways, is anti-proliferative, and induces apoptosis in abnormal cells. Unfortunately, oral ingestion of zinc is ineffective since high  concentrations of zinc into prostate cells is not possible without the active transporter, ZIP1.

Loss of cancer suppressor genes, early in the prostatic carcinogenesis, have been localized to chromosomes 8p, 10q, 13q, and 16q. P53 mutations in the primary prostate cancer are relatively low  and are more frequently seen in metastatic settings, hence, p53 mutations are late event in pathology of prostate cancer. Other tumor suppressor genes that are thought to play a role in prostate  cancer include PTEN (gene) and KAI1. “Up to 70 percent of men with prostate cancer have lost one copy of the PTEN gene at the time of diagnosis”   Relative frequency of loss of E-cadherin and  CD44 has also been observed.

RUNX2 is a transcription factor that prevents cancer cells from undergoing apoptosis thereby contributing to the development of prostate cancer.

The PI3k/Akt signaling cascade works with the transforming growth factor beta/SMAD signaling cascade to ensure prostate cancer cell survival and protection against apoptosis. X-linked
inhibitor of apoptosis (XIAP) is hypothesized to promote prostate cancer cell survival and growth and is a target of research because if this inhibitor can be shut down then the apoptosis cascade  can carry on its function in preventing cancer cell proliferation.  Macrophage inhibitory cytokine-1 (MIC-1) stimulates the focal adhesion kinase (FAK) signaling pathway which leads to prostate  cancer cell growth and survival.

The androgen receptor helps prostate cancer cells to survive and is a target for many anti cancer research studies; so far, inhibiting the androgen receptor has only proven to be effective in mouse  studies.   Prostate specific membrane antigen (PSMA) stimulates the development of prostate cancer by increasing folate levels for the cancer cells to use to survive and grow; PSMA increases  available folates for use by hydrolyzing glutamated folates.

Diagnosis :
The American Cancer Society’s position regarding early detection is “Research has not yet proven that the potential benefits of testing outweigh the harms of testing and treatment. The American  Cancer Society believes that men should not be tested without learning about what we know and don’t know about the risks and possible benefits of testing and treatment. Starting at age 50, (45 if African American or brother or father suffered from condition before age 65) the man should  talk to the doctor about the pros and cons of testing so  the person can decide if testing is the right choice for  him.”

The only test that can fully confirm the diagnosis of prostate cancer is a biopsy, the removal of small pieces of the prostate for microscopic examination. However, prior to a biopsy, less invasive  testing can be conducted.

There are also several other tests that can be used to gather more information about the prostate and the urinary tract. Digital rectal examination (DRE) may allow a doctor to detect prostate  abnormalities. Cystoscopy shows the urinary tract from inside the bladder, using a thin, flexible camera tube inserted down the urethra. Transrectal ultrasonography creates a picture of the prostate  using sound waves from a probe in the rectum.

Prostate screening tests :

*Digital rectal exam (DRE). During a DRE, your doctor inserts a gloved, lubricated finger into your rectum to examine your prostate, which is adjacent to the rectum. If your doctor finds any
abnormalities in the texture, shape or size of your gland, you may need more tests.

*Prostate-specific antigen (PSA) test. A blood sample is drawn from a vein in your arm and analyzed for PSA, a substance that’s naturally produced by your prostate gland. It’s normal for a small  amount of PSA to be in your bloodstream. However, if a higher than normal level is found, it may be an indication of prostate infection, inflammation, enlargement or cancer.
PSA testing combined with DRE helps identify prostate cancers at their earliest stages, but studies have disagreed whether these tests reduce the risk of dying of prostate cancer. For that reason,  there is debate surrounding prostate cancer screening.

If an abnormality is detected on a DRE or PSA test, your doctor may recommend tests to determine whether you have prostate cancer, such as:

*Ultrasound. If other tests raise concerns,  the doctor may use transrectal ultrasound to further evaluate your prostate. A small probe, about the size and shape of a cigar, is inserted into  the rectum. The probe uses sound waves to make a picture of the  prostate gland.

*Collecting a sample of prostate tissue. If initial test results suggest prostate cancer, your doctor may recommend a procedure to collect a sample of cells from your prostate (prostate biopsy).

Prostate biopsy is often done using a thin needle that’s inserted into the prostate to collect tissue. The tissue sample is analyzed in a lab to determine whether cancer cells are present.

Now to Determining whether prostate cancer is aggressive:

When a biopsy confirms the presence of cancer, the next step is to determine the level of aggressiveness (grade) of the cancer cells. In a laboratory, a pathologist examines a sample of the cancer cell to determine how much cancer cells differ from the healthy cells. A higher grade indicates a more aggressive cancer that is more likely to spread quickly.

The most common scale used to evaluate the grade of prostate cancer cells is called a Gleason score. Scoring combines two numbers and can range from 2 (nonaggressive cancer) to 10 (very aggressive cancer).

For  determining how far the cancer has spread:

Once a prostate cancer diagnosis has been made, your doctor works to determine the extent (stage) of the cancer. If your doctor suspects your cancer may have spread beyond your prostate, imaging tests such as these may be recommended:

*Bone scan
*Ultrasound
*Computerized tomography (CT) scan
*Magnetic resonance imaging (MRI)
*Positron emission tomography (PET) scan

It is not every person should have every test. The doctor will determine which tests are best for  every  individual case.

Once testing is complete,  the doctor assigns the stage and this helps determination of  treatment options. The prostate cancer stages are:

Stage I. This stage signifies very early cancer that’s confined to a small area of the prostate. When viewed under a microscope, the cancer cells aren’t considered aggressive.

Stage II. Cancer at this stage may still be small but may be considered aggressive when cancer cells are viewed under the microscope. Or cancer that is stage II may be larger and may have grown to  involve both sides of the prostate gland.

Stage III. The cancer has spread beyond the prostate to the seminal vesicles or other nearby tissues.

Stage IV. The cancer has grown to invade nearby organs, such as the bladder, or spread to lymph nodes, bones, lungs or other organs.

Treatment:
Prostate cancer treatment options depend on several factors, such as how fast your cancer is growing, how much it has spread and the overall health  and age of the patient , as well as the benefits  and the potential side effects of the treatment.Immediate treatment may not be necessary for men diagnosed with very early-stage of  prostate cancer. Some men may never need treatment. Instead, doctors sometimes recommend active  surveillance.

In active surveillance, regular follow-up blood tests, rectal exams and possibly biopsies may be performed to monitor progression of your cancer. If tests show your cancer is progressing, you may opt for a prostate cancer treatment such as surgery or radiation.

Active surveillance may be an option for cancer that isn’t causing symptoms, is expected to grow very slowly and is confined to a small area of the prostate. Active surveillance may also be

considered for a man who has another serious health condition or an advanced age that makes cancer treatment more difficult.

Active surveillance carries a risk that the cancer may grow and spread between checkups, making it less likely to be cured.

For other cases the the following treatment is recomended:

*Radiation therapy : Radiation therapy uses high-powered energy to kill cancer cells. Prostate cancer radiation therapy can be delivered in two ways:

Radiation that comes from outside of  the body (external beam radiation). During external beam radiation therapy, the patient   lie on a table while a machine moves around the body, directing high-

powered energy beams, such as X-rays or protons, to   prostate cancer.The patient  typically undergo external beam radiation treatments five days a week for several weeks.

Radiation placed inside  the body (brachytherapy). Brachytherapy involves placing many rice-sized radioactive seeds in your prostate tissue. The radioactive seeds deliver a low dose of radiation

over a long period of time. The doctor implants the radioactive seeds in patient’s prostate using a needle guided by ultrasound images. The implanted seeds eventually stop giving off radiation and  don’t need to be removed.

Side effects of radiation therapy can include painful urination, frequent urination and urgent urination, as well as rectal symptoms, such as loose stools or pain when passing stools. Erectile dysfunction can also occur.

Hormone therapy:
Hormone therapy is treatment to stop  the patient’s body from producing the male hormone testosterone. Prostate cancer cells rely on testosterone to help them grow. Cutting off the supply of hormones may cause cancer cells to die or to grow more slowly.

Options of hormone therapy:
*Medications that stop the body from producing testosterone. Medications known as luteinizing hormone-releasing hormone (LH-RH) agonists prevent the testicles from receiving messages to make testosterone. Drugs typically used in this type of hormone therapy include leuprolide (Lupron, Eligard), goserelin (Zoladex), triptorelin (Trelstar) and histrelin (Vantas). Other drugs sometimes used include ketoconazole and abiraterone (Zytiga).

*Medications that block testosterone from reaching cancer cells. Medications known as anti-androgens prevent testosterone from reaching your cancer cells. Examples include bicalutamide (Casodex), flutamide, and nilutamide (Nilandron). The drug enzalutamide (Xtandi) may be an option when other hormone therapies are no longer effective.

Surgery to remove the testicles (orchiectomy).
Removing  the testicles reduces testosterone levels in the body.
Hormone therapy is used in men with advanced prostate cancer to shrink the cancer and slow the growth of tumors. In men with early-stage prostate cancer, hormone therapy may be used to shrink tumors before radiation therapy. This can make it more likely that radiation therapy will be successful.

Side effects of hormone therapy may include erectile dysfunction, hot flashes, loss of bone mass, reduced sex drive and weight gain.

Surgery to remove the prostate:
Surgery for prostate cancer involves removing the prostate gland (radical prostatectomy), some surrounding tissue and a few lymph nodes. Ways the radical prostatectomy procedure can be performed include:

*Using a robot to assist with surgery. During robot-assisted surgery, the instruments are attached to a mechanical device (robot) and inserted into  the abdomen through several small incisions. The surgeon sits at a console and uses hand controls to guide the robot to move the instruments. Robotic prostatectomy may allow the surgeon to make more-precise movements with surgical tools than is possible with traditional minimally invasive surgery.

*Making an incision in  the abdomen. During retropubic surgery, the prostate gland is taken out through an incision in  the lower abdomen. Compared with other types of prostate surgery, retropubic prostate surgery may carry a lower risk of nerve damage, which can lead to problems with bladder control and erections.

*Making an incision between  the anus and scrotum. Perineal surgery involves making an incision between  the anus and scrotum in order to access  the prostate. The perineal approach to surgery may allow for quicker recovery times, but this technique makes removing the nearby lymph nodes and avoiding nerve damage more difficult.

*Laparoscopic prostatectomy. During a laparoscopic radical prostatectomy, the doctor performs surgery through small incisions in the abdomen with the assistance of a tiny camera (laparoscope). This procedure requires great skill on the part of the surgeon, and it carries an increased risk that nearby structures may be accidentally cut. For this reason, this type of surgery is not commonly performed for prostate cancer in the U.S. anymore.

The Doctor should decide which type of surgery is best for  the specific situation.

Radical prostatectomy carries a risk of urinary incontinence and erectile dysfunction. The riskfactors that the patient   may face based on the situation, the type of procedure the patient may select, according to his age, body type and  overall health.

Freezing of prostate tissue:
Cryosurgery or cryoablation involves freezing tissue to kill cancer cells.

During cryosurgery for prostate cancer, small needles are inserted in the prostate using ultrasound images as guidance. A very cold gas is placed in the needles, which causes the surrounding tissue to freeze. A second gas is then placed in the needles to reheat the tissue. The cycles of freezing and thawing kill the cancer cells and some surrounding healthy tissue.

Initial attempts to use cryosurgery for prostate cancer resulted in high complication rates and unacceptable side effects. However, newer technologies have lowered complication rates, improved cancer control and made the procedure easier to tolerate. Cryosurgery may be an option for men who haven’t been helped by radiation therapy.

Chemotherapy:
Chemotherapy uses drugs to kill rapidly growing cells, including cancer cells. Chemotherapy can be administered through a vein in your arm, in pill form or both.

Chemotherapy may be a treatment option for men with prostate cancer that has spread to distant areas of their bodies. Chemotherapy may also be an option for cancers that don’t respond to hormone therapy.

Biological therapy:
Biological therapy (immunotherapy) uses your body’s immune system to fight cancer cells. One type of biological therapy called sipuleucel-T (Provenge) has been developed to treat advanced, recurrent prostate cancer.

This treatment takes some of the patient’s own immune cells, genetically engineers them in a laboratory to fight prostate cancer, then injects the cells back into your body through a vein. Some men do respond to this therapy with some improvement in their cancer, but the treatment is very expensive and requires multiple treatments.

Alternative therapy:
It is believed that regular Yoga exercise with Pranayama  and Meditation under the guideline of some expart  may help a lot to cope with the distress of the patient.

Prevention:
Diet and lifestyle

The data on the relationship between diet and prostate cancer is poor.   In light of this the rate of prostate cancer is linked to the consumption of the Western diet.  There is little if any evidence to support an association between trans fat, saturated fat and carbohydrate intake and risk of prostate cancer.  Evidence regarding the role of omega-3 fatty acids in preventing prostate cancer does not suggest that they reduce the risk of prostate cancer, although additional research is needed. Vitamin supplements appear to have no effect and some may increase the risk.  High calcium intake has been linked to advanced prostate cancer. Consuming fish may lower prostate cancer deaths but does not appear to affect its occurrence.  Some evidence supports lower rates of prostate cancer with a vegetarian diet.  There is some tentative evidence for foods containing lycopene and selenium.  Diets rich in cruciferous vegetables, soy, beans and other legumes may be associated with a lower risk of prostate cancer, especially more advanced cancers.

Men who get regular exercise may have a slightly lower risk, especially vigorous activity and the risk of advanced prostate cancer.

Resources:
http://en.wikipedia.org/wiki/Prostate_cancer
http://www.mayoclinic.org/diseases-conditions/prostate-cancer/basics/definition/con-20029597

Psoriatic arthritis

Other Names: Arthritis psoriatica,Arthropathic psoriasis or Psoriatic arthropathy

Definition:
Psoriatic arthritis is a form of arthritis that affects some people who have psoriasis — a condition that features red patches of skin topped with silvery scales. Most people develop psoriasis first and are later diagnosed with psoriatic arthritis, but the joint problems can sometimes begin before skin lesions appear.

Joint pain, stiffness and swelling are the main symptoms of psoriatic arthritis. They can affect any part of your body, including your fingertips and spine, and can range from relatively mild to severe. In both psoriasis and psoriatic arthritis, disease flares may alternate with periods of remission.

It is a type of inflammatory arthritis that will develop in up to 30 percent of people who have the chronic skin condition psoriasis. Psoriatic arthritis is classified as a seronegative spondyloarthropathy and therefore occurs more commonly in patients with tissue type HLA-B27.

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No cure for psoriatic arthritis exists, so the focus is on controlling symptoms and preventing damage to the joints. Without treatment, psoriatic arthritis may be disabling.

Classification:
There are five main types of psoriatic arthritis:

*Asymmetric: This type affects around 70% of patients and is generally mild. This type does not occur in the same joints on both sides of the body and usually only involves fewer than 3 joints.

*Symmetric: This type accounts for around 25% of cases, and affects joints on both sides of the body simultaneously. This type is most similar to rheumatoid arthritis and is disabling in around 50% of all cases.

*Arthritis mutilans (M07.1): Affects less than 5% of patients and is a severe, deforming and destructive arthritis. This condition can progress over months or years causing severe joint damage. Arthritis mutilans has also been called chronic absorptive arthritis, and may be seen in rheumatoid arthritis as well.

*Spondylitis (M07.2): This type is characterised by stiffness of the spine or neck, but can also affect the hands and feet, in a similar fashion to symmetric arthritis.

*Distal interphalangeal predominant (M07.0): This type of psoriatic arthritis is found in about 5% of patients, and is characterised by inflammation and stiffness in the joints nearest to the ends of the fingers and toes. Nail changes are often marked.

Symptoms:
*Pain, swelling, or stiffness in one or more joints is commonly present.

*Asymmetrical oligoarthritis (70%) (Involvement of the distal interphalangeal joints (DIP) is a characteristic feature).

*Sacroiliitis/spondylitis (40%)

*Symmetrical seronegative arthritis (15%)

*Distal interphalangeal joint arthritis (15%)

*Hand joints involved in psoriasis are proximal interphalangeal (PIP) + distal interphalangeal (DIP) + metacarpophalangeal (MCP) + wrist
Joints that are red or warm to the touch.

*Sausage-like swelling in the fingers or toes, known as dactylitis.

*Pain in and around the feet and ankles, especially tendinitis in the Achilles tendon or plantar fasciitis in the sole of the foot.

*Changes to the nails, such as pitting or separation from the nail bed.

*Pain in the area of the sacrum (the lower back, above the tailbone).

*Along with the above noted pain and inflammation, there is extreme exhaustion that does not go away with adequate rest. The exhaustion may last for days or weeks without abatement. Psoriatic arthritis may remain mild, or may progress to more destructive joint disease. Periods of active disease, or flares, will typically alternate with periods of remission. In severe forms, psoriatic arthritis may progress to arthritis mutilans which on X-ray gives pencil in cup appearance.

*Because prolonged inflammation can lead to joint damage, early diagnosis and treatment to slow or prevent joint damage is recommended.

*Scaly skin lesions are seen over extensor surfaces (scalp, natal cleft and umbilicus).

*The nail changes are pitting, onycholysis, sub–ungual hyperkeratosis and horizontal ridging.

Causes:
Psoriatic arthritis occurs when the body’s immune system begins to attack healthy cells and tissue. The abnormal immune response causes inflammation in your joints as well as overproduction of skin cells.

It’s not entirely clear why the immune system turns on healthy tissue, but it seems likely that both genetic and environmental factors play a role. Many people with psoriatic arthritis have a family history of either psoriasis or psoriatic arthritis. Researchers have discovered certain genetic markers that appear to be associated with psoriatic arthritis.

Physical trauma or something in the environment — such as a viral or bacterial infection — may trigger psoriatic arthritis in people with an inherited tendency.

Diagnosis:
There is no definitive test to diagnose psoriatic arthritis. Symptoms of psoriatic arthritis may closely resemble other diseases, including rheumatoid arthritis. A rheumatologist (a doctor specializing in diseases affecting the joints) may use physical examinations, health history, blood tests and x-rays to accurately diagnose psoriatic arthritis.

Factors that contribute to a diagnosis of psoriatic arthritis include:

*Psoriasis in the patient, or a family history of psoriasis or psoriatic arthritis.

*A negative test result for Rheumatoid factor, a blood factor associated with rheumatoid arthritis.

*Arthritis symptoms in the distal Interphalangeal articulations of hand (the joints closest to the tips of the fingers). This is not typical of rheumatoid arthritis.

*Ridging or pitting of fingernails or toenails (onycholysis), which is associated with psoriasis and psoriatic arthritis.

*Radiologic images indicating joint change.

*Other symptoms that are more typical of psoriatic arthritis than other forms of arthritis include inflammation in the Achilles tendon (at the back of the heel) or the Plantar fascia (bottom of the feet), and dactylitis (sausage-like swelling of the fingers or toes)

During the exam,the doctor may ask for the following tests:

Imaging tests:

*X-rays. Plain X-rays can help pinpoint changes in the joints that occur in psoriatic arthritis but not in other arthritic conditions.
Magnetic resonance imaging (MRI). MRI utilizes radio waves and a strong magnetic field to produce very detailed images of both hard and soft tissues in your body. This type of imaging test may be used to check for problems with the tendons and ligaments in your feet and lower back.
Laboratory tests:

*Rheumatoid factor (RF). RF is an antibody that’s often present in the blood of people with rheumatoid arthritis, but it’s not usually in the blood of people with psoriatic arthritis. For that reason, this test can help your doctor distinguish between the two conditions.

*Joint fluid test. Using a long needle, your doctor can remove a small sample of fluid from one of your affected joints — often the knee. Uric acid crystals in your joint fluid may indicate that you have gout rather than psoriatic arthritis.

Treatments:
The underlying process in psoriatic arthritis is inflammation; therefore, treatments are directed at reducing and controlling inflammation. Milder cases of psoriatic arthitis may be treated with NSAIDS alone; however, there is a trend toward earlier use of disease-modifying antirheumatic drugs or biological response modifiers to prevent irreversible joint destruction.

Nonsteroidal anti-inflammatory drugs:
Typically the medications first prescribed for psoriatic arthritis are NSAIDs such as ibuprofen and naproxen followed by more potent NSAIDs like diclofenac, indomethacin, and etodolac. NSAIDs can irritate the stomach and intestine, and long-term use can lead to gastrointestinal bleeding. Other potential adverse effects include damage to the kidneys and cardiovascular system.

Disease-modifying antirheumatic drugs:
These are used in persistent symptomatic cases without exacerbation. Rather than just reducing pain and inflammation, this class of drugs helps limit the amount of joint damage that occurs in psoriatic arthritis. Most DMARDs act slowly and may take weeks or even months to take full effect. Drugs such as methotrexate or leflunomide are commonly prescribed; other DMARDS used to treat psoriatic arthritis include cyclosporin, azathioprine, and sulfasalazine. These immunosuppressant drugs can also reduce psoriasis skin symptoms but can lead to liver and kidney problems and an increased risk of serious infection.

Biological response modifiers:
Recently, a new class of therapeutics called biological response modifiers or biologics has been developed using recombinant DNA technology. Biologic medications are derived from living cells cultured in a laboratory. Unlike traditional DMARDS that affect the entire immune system, biologics target specific parts of the immune system. They are given by injection or intravenous (IV) infusion.

Biologics prescribed for psoriatic arthritis are TNF-(alfa) inhibitors, including infliximab, etanercept, golimumab, certolizumab pegol and adalimumab, as well as the IL-12/IL-23 inhibitor ustekinumab.

Biologics may increase the risk of minor and serious infections. More rarely, they may be associated with nervous system disorders, blood disorders or certain types of cancer.

Other treatments:
Retinoid etretinate 30mg/day is effective for both arthritis and skin lesions. Photochemotherapy with methoxy psoralen and long wave ultraviolet light (PUVA) are used for severe skin lesions. Doctors may use joint injections with corticosteroids in cases where one joint is severely affected. In psoriatic arthritis patients with severe joint damage orthopedic surgery may be implemented to correct joint destruction, usually with use of a joint replacement. Surgery is effective for pain alleviation, correcting joint disfigurement, and reinforcing joint usefulness and strength.

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Lifestyle and home remedies

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Prognosis:
Seventy percent of people who develop psoriatic arthritis first show signs of psoriasis on the skin, 15 percent develop skin psoriasis and arthritis at the same time, and 15 percent develop skin psoriasis following the onset of psoriatic arthritis.

Psoriatic arthritis can develop in people who have any level severity of psoriatic skin disease from mild to very severe.

Psoriatic arthritis tends to appear about 10 years after the first signs of psoriasis. For the majority of people this is between the ages of 30 and 55, but the disease can also affect children. The onset of psoriatic arthritis symptoms before symptoms of skin psoriasis is more common in children than adults.

More than 80% of patients with psoriatic arthritis will have psoriatic nail lesions characterized by nail pitting, separation of the nail from the underlying nail bed, ridging and cracking, or more extremely, loss of the nail itself (onycholysis).

Men and women are equally affected by this condition. Like psoriasis, psoriatic arthritis is more common among Caucasians than Africans or Asians

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Psoriatic_arthritis
http://www.mayoclinic.org/diseases-conditions/psoriatic-arthritis/basics/tests-diagnosis/con-20015006
http://www.mayoclinic.org/diseases-conditions/psoriatic-arthritis/basics/causes/con-20015006
http://www.mayoclinic.org/diseases-conditions/psoriatic-arthritis/basics/definition/CON-20015006

Hemolytic Uremic Syndrome (HUS)

Alternative names:  Haemolytic-uraemic syndrome, HUS

Definition:
Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys‘ filtering system. Red blood cells contain hemoglobin—an iron-rich protein that gives blood its red color and carries oxygen from the lungs to all parts of the body.

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When the kidneys and glomeruli—the tiny units within the kidneys where blood is filtered—become clogged with the damaged red blood cells, they are unable to do their jobs. If the kidneys stop functioning, a child can develop acute kidney injury—the sudden and temporary loss of kidney function. Hemolytic uremic syndrome is the most common cause of acute kidney injury in children.

It is a disease characterized by hemolytic anemia (anemia caused by destruction of red blood cells), acute kidney failure (uremia), and a low platelet count (thrombocytopenia). It predominantly, but not exclusively, affects children. Most cases are preceded by an episode of infectious, sometimes bloody, diarrhea acquired as a foodborne illness or from a contaminated water supply and caused by E. coli O157:H7, although Shigella, Campylobacter and a variety of viruses have also been implicated. It is now the most common cause of acquired acute renal failure in childhood. It is a medical emergency and carries a 5–10% mortality; of the remainder, the majority recover without major consequences but a small proportion develop chronic kidney disease and become reliant on renal replacement therapy.

The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. Children produce less urine than adults and the amount produced depends on their age. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder.

Symptoms:
STEC-HUS occurs after ingestion of a strain of bacteria, usually types of E. coli, that expresses verotoxin (also called Shiga-like toxin). Bloody diarrhea typically follows. HUS develops about 5–10 days after onset of diarrhea, with decreased urine output (oliguria), blood in the urine (hematuria), kidney failure, thrombocytopenia (low levels of platelets) and destruction of red blood cells (microangiopathic hemolytic anemia). Hypertension is common. In some cases, there are prominent neurologic changes.

A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis—an inflammation of the lining of the stomach, small intestine, and large intestine—such as

*vomiting
*bloody diarrhea
*abdominal pain
*fever and chills
*headache

As the infection progresses, the toxins released in the intestine begin to destroy red blood cells. When the red blood cells are destroyed, the child may experience the signs and symptoms of anemia—a condition in which red blood cells are fewer or smaller than normal, which prevents the body’s cells from getting enough oxygen.

Signs and symptoms of anemia may include:-

*fatigue, or feeling tired
*weakness
*fainting
*paleness

As the damaged red blood cells clog the glomeruli, the kidneys may become damaged and make less urine. When damaged, the kidneys work harder to remove wastes and extra fluid from the blood, sometimes leading to acute kidney injury.

Other signs and symptoms of hemolytic uremic syndrome may include bruising and seizures.

When hemolytic uremic syndrome causes acute kidney injury, a child may have the following signs and symptoms:

*edema—swelling, most often in the legs, feet, or ankles and less often in the hands or face
*albuminuria—when a child’s urine has high levels of albumin, the main protein in the blood
*decreased urine output
*hypoalbuminemia—when a child’s blood has low levels of albumin
*blood in the urine

Causes:
A number of things can cause hemolytic uremic syndrome, but the most common cause — particularly in children — is an infection with a specific strain of E. coli, usually the strain known as O157:H7. However, other strains of E. coli have been linked to hemolytic uremic syndrome, too.

Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream. The toxins travel through the bloodstream and can destroy the red blood cells. E. coli O157:H7 can be found in:

*Contaminated meat or produce
*Swimming pools or lakes contaminated with feces
*undercooked meat, most often ground beef
*unpasteurized, or raw, milk
*unwashed, contaminated raw fruits and vegetables
*contaminated juice

Less common causes, sometimes called atypical hemolytic uremic syndrome, can include:-

*taking certain medications, such as chemotherapy
*having other viral or bacterial infections
*inheriting a certain type of hemolytic uremicsyndrome that runs in families

Children who are more likely to develop hemolytic uremic syndrome include those who
are younger than age 5 and have been diagnosedwith an E. coli O157:H7 infection

*have a weakened immune system
*have a family history of inherited hemolyticuremic syndrome
*Hemolytic uremic syndrome occurs in about two out of every 100,000 children.

Most people who are infected with E. coli, even the more dangerous strains, won’t develop hemolytic uremic syndrome. It’s also possible for hemolytic uremic syndrome to follow infection with other types of bacteria.

In adults, hemolytic uremic syndrome is more commonly caused by other factors, including:

*The use of certain medications, such as quinine (an over-the-counter muscle cramp remedy), some chemotherapy drugs, the immunosuppressant medication cyclosporine (Neoral, Sandimmune) and anti-platelet medications

*Pregnancy

*Certain infections, such as HIV/AIDS or an infection with the pneumococcal bacteria

*Genes, which can be a factor because a certain type of HUS — atypical hemolytic uremic syndrome — may be passed down from your parents

The cause of hemolytic uremic syndrome in adults is often unknown

Diagnosis:
The Doctor diagnoses hemolytic uremic syndrome with

*a medical and family history
*a physical exam
*urine tests
*a blood test
*a stool test
*kidney biopsy

The similarities between HUS, aHUS, and TTP make differential diagnosis essential. All three of these systemic TMA-causing diseases are characterized by thrombocytopenia and microangiopathic hemolysis, plus one or more of the following: neurological symptoms (e.g., confusion, cerebral convulsions, seizures); renal impairment (e.g., elevated creatinine, decreased estimated glomerular filtration rate [eGFR], abnormal urinalysis ); and gastrointestinal (GI) symptoms (e.g., diarrhea, nausea/vomiting, abdominal pain, gastroenteritis).The presence of diarrhea does not exclude aHUS as the etiology of TMA, as 28% of patients with aHUS present with diarrhea and/or gastroenteritis. First diagnosis of aHUS is often made in the context of an initial, complement-triggering infection, and Shiga-toxin has also been implicated as a trigger that identifies patients with aHUS. Additionally, in one study, mutations of genes encoding several complement regulatory proteins were detected in 8 of 36 (22%) patients diagnosed with STEC-HUS. However, the absence of an identified complement regulatory gene mutation does not preclude aHUS as the etiology of the TMA, as approximately 50% of patients with aHUS lack an identifiable mutation in complement regulatory genes.

Diagnostic work-up supports the differential diagnosis of TMA-causing diseases. A positive Shiga-toxin/EHEC test confirms an etiological cause for STEC-HUS, and severe ADAMTS13 deficiency (i.e., ?5% of normal ADAMTS13 levels) confirms a diagnosis of TTP

Complications:
Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.1
However, children with hemolytic uremic syndrome may have serious and sometimes life-threatening complications, including

*acute kidney injury
*high blood pressure
*blood-clotting problems that can lead to bleeding
*seizures
*heart problems
*chronic, or long lasting, kidney disease
*stroke
*coma

Treatment:
The Doctor will treat a child’s urgent symptoms and try to prevent complications by

*observing the child closely in the hospital
*replacing minerals, such as potassium and salt, and fluids through an intravenous (IV) tube
*giving the child red blood cells and platelets—cells in the blood that help with clotting—through an IV
*giving the child IV nutrition
*treating high blood pressure with medications

Treating Acute Kidney Injury:
If necessary,the Doctor will treat acute kidney injury with dialysis—the process of filtering wastes and extra fluid from the body with an artificial kidney. The two forms of dialysis are hemodialysis and peritoneal dialysis. Most children with acute kidney injury need dialysis for a short time only.

Treating Chronic Kidney Disease:
Some children may sustain significant kidney damage that slowly develops into CKD. Children who develop CKD must receive treatment to replace the work the kidneys do. The two types of treatment are dialysis and transplantation.

In most cases, The Doctor treat CKD with a kidney transplant. A kidney transplant is surgery to place a healthy kidney from someone who has just died or a living donor, most often a family member, into a person’s body to take over the job of the failing kidney. Though some children receive a kidney transplant before their kidneys fail completely, many children begin with dialysis to stay healthy until they can have a transplant. click to know more

Prevention:

Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys’ filtering system.
The most common cause of hemolytic uremic syndrome in children is an Escherichia coli (E. coli) infection of the digestive system.
Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream.
A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis, an inflammation of the lining of the stomach, small intestine, and large intestine.

Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.
Some children may sustain significant kidney damage that slowly develops into chronic kidney disease (CKD).

Parents and caregivers can help prevent childhood hemolytic uremic syndrome due to E. coli O157:H7 by

*avoiding unclean swimming areas
*avoiding unpasteurized milk, juice, and cider
*cleaning utensils and food surfaces often
*cooking meat to an internal temperature of at least 160° F
*defrosting meat in the microwave or refrigerator
*keeping children out of pools if they have had diarrhea
*keeping raw foods separate
*washing hands before eating
*washing hands well after using the restroom and after changing diapers

When a child is taking medications that may cause hemolytic uremic syndrome, it is important that the parent or caretaker watch for symptoms and report any changes in the child’s condition to the Doctor as soon as possible.

Prognosis:
Acute renal failure occurs in 55-70% of patients with STEC-HUS, although up to 70-85% recover renal function. Patients with aHUS generally have poor outcomes, with up to 50% progressing to ESRD or irreversible brain damage; as many as 25% die during the acute phase. However, with aggressive treatment, more than 90% of patients survive the acute phase of HUS, and only about 9% may develop ESRD. Roughly one-third of persons with HUS have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with HUS have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their colon removed. The overall mortality rate from HUS is 5-15%. Children and the elderly have a worse prognosis.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://kidney.niddk.nih.gov/KUDiseases/pubs/childkidneydiseases/hemolytic_uremic_syndrome/
http://en.wikipedia.org/wiki/Hemolytic-uremic_syndrome
http://www.mayoclinic.org/diseases-conditions/hemolytic-uremic-syndrome/basics/causes/con-20029487

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Cholangitis

Definition:
Cholangitis is an infection of the common bile duct, the tube that carries bile from the liver to the gallbladder and intestines. Bile is a liquid made by the liver that helps digest food.

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Cholangitis can be life-threatening, and is regarded as a medical emergency. Characteristic symptoms include yellow discoloration of the skin or whites of the eyes, fever, abdominal pain, and in severe cases, low blood pressure and confusion. Initial treatment is with intravenous fluids and antibiotics, but there is often an underlying problem (such as gallstones or narrowing in the bile duct) for which further tests and treatments may be necessary, usually in the form of endoscopy to relieve obstruction of the bile duct.
Symptoms:
The following symptoms may occur:

*Pain on the upper right side or upper middle part of the abdomen. It may also be felt in the back or below the right shoulder blade. The pain may come and go and feel sharp, cramp-like, or dull.

*Fever and chills

*Dark urine and clay-colored stools

*Nausea and vomiting

*Yellowing of the skin (jaundice), which may come and go
Physical examination findings typically include jaundice and right upper quadrant tenderness.Charcot’s triad is a set of three common findings in cholangitis: abdominal pain, jaundice, and fever. This was assumed in the past to be present in 50–70% of cases, although more recently the frequency has been reported as 15–20%.Reynolds’ pentad includes the findings of Charcot’s triad with the presence of septic shock and mental confusion. This combination of symptoms indicates worsening of the condition and the development of sepsis, and is seen less commonly still.

In the elderly, the presentation may be atypical; they may directly collapse due to septicemia without first showing typical features. Those with an indwelling stent in the bile duct (see below) may not develop jaundice.

Causes:
Cholangitis is most often caused by a bacterial infection. This can occur when the duct is blocked by something, such as a gallstone or tumor. The infection causing this condition may also spread to the liver.

Bile duct obstruction, which is usually present in acute cholangitis, is generally due to gallstones. 10–30% of cases, however, are due to other causes such as benign stricturing (narrowing of the bile duct without an underlying tumor), postoperative damage or an altered structure of the bile ducts such as narrowing at the site of an anastomosis (surgical connection), various tumors (cancer of the bile duct, gallbladder cancer, cancer of the ampulla of Vater, pancreatic cancer, cancer of the duodenum), anaerobic organisms such as Clostridium and Bacteroides (especially in the elderly and those who have undergone previous surgery of the biliary system). Parasites which may infect the liver and bile ducts may cause cholangitis; these include the roundworm Ascaris lumbricoides and the liver flukes Clonorchis sinensis, Opisthorchis viverrini and Opisthorchis felineus. In people with AIDS, a large number of opportunistic organisms has been known to cause AIDS cholangiopathy, but the risk has rapidly diminished since the introduction of effective AIDS treatment. Cholangitis may also complicate medical procedures involving the bile duct, especially ERCP. To prevent this, it is recommended that those undergoing ERCP for any indication receive prophylactic (preventative) antibiotics.

The presence of a permanent biliary stent (e.g. in pancreatic cancer) slightly increases the risk of cholangitis, but stents of this type are often needed to keep the bile duct patent under outside pressure

Diagnosis:
Routine blood tests show features of acute inflammation (raised white blood cell count and elevated C-reactive protein level), and usually abnormal liver function tests (LFTs). In most cases the LFTs will be consistent with obstruction: raised bilirubin, alkaline phosphatase and ?-glutamyl transpeptidase. In the early stages, however, pressure on the liver cells may be the main feature and the tests will resemble those in hepatitis, with elevations in alanine transaminase and aspartate transaminase.

Blood cultures are often performed in people with fever and evidence of acute infection. These yield the bacteria causing the infection in 36% of cases, usually after 24–48 hours of incubation. Bile, too, may be sent for culture during ERCP (see below). The most common bacteria linked to ascending cholangitis are gram-negative bacilli: Escherichia coli (25–50%), Klebsiella (15–20%) and Enterobacter (5–10%). Of the gram-positive cocci, Enterococcus causes 10–20%.

You may have the following tests to look for blockages:

*Abdominal ultrasound

*Endoscopic retrograde cholangiopancreatography (ERCP)

*Magnetic resonance cholangiopancreatography (MRCP)

*Percutaneous transhepatic cholangiogram (PTCA)

*You may also have the following blood tests:

#Bilirubin level
#Liver enzyme levels
#Liver function tests
#White blood count (WBC)
Treatment:
Quick diagnosis and treatment are very important.Antibiotics to cure infection is the first treatment done in most cases. ERCP or other surgical procedure is done when the patient is stable.Patients who are very ill or are quickly getting worse may need surgery right away.

Cholangitis requires admission to hospital. Intravenous fluids are administered, especially if the blood pressure is low, and antibiotics are commenced. Empirical treatment with broad-spectrum antibiotics is usually necessary until it is known for certain which pathogen is causing the infection, and to which antibiotics it is sensitive. Combinations of penicillins and aminoglycosides are widely used, although ciprofloxacin has been shown to be effective in most cases, and may be preferred to aminoglycosides because of fewer side effects. Metronidazole is often added to specifically treat the anaerobic pathogens, especially in those who are very ill or at risk of anaerobic infections. Antibiotics are continued for 7–10 days. Drugs that increase the blood pressure (vasopressors) may also be required to counter the low blood pressure.
Prognosis:
Acute cholangitis carries a significant risk of death, the leading cause being irreversible shock with multiple organ failure (a possible complication of severe infections). Improvements in diagnosis and treatment have led to a reduction in mortality: before 1980, the mortality rate was greater than 50%, but after 1980 it was 10–30%. Patients with signs of multiple organ failure are likely to die unless they undergo early biliary drainage and treatment with systemic antibiotics. Other causes of death following severe cholangitis include heart failure and pneumonia.

Risk Factors:
Risk factors include a previous history of gallstones, sclerosing cholangitis, HIV, narrowing of the common bile duct, and, rarely, travel to countries where you might catch a worm or parasite infection.

Risk factors indicating an increased risk of death include older age, female gender, a history of liver cirrhosis, biliary narrowing due to cancer, acute renal failure and the presence of liver abscesses. Complications following severe cholangitis include renal failure, respiratory failure (inability of the respiratory system to oxygenate blood and/or eliminate carbon dioxide), cardiac arrhythmia, wound infection, pneumonia, gastrointestinal bleeding and myocardial ischemia (lack of blood flow to the heart, leading to heart attacks).

Prevention:
Treatment of gallstones, tumors, and infestations of parasites may reduce the risk for some people. A metal or plastic stent that is placed in the bile system may be needed to prevent the infection from returning.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Resources:
http://www.nlm.nih.gov/medlineplus/ency/article/000290.htm
http://en.wikipedia.org/wiki/Ascending_cholangitis