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.

CLICK & SEE THE PICTURES

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 –

CLICK & SEE THE PICTURES

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

Chronotherapy

 Definition:   Chronotherapy refers to the use of circadian or other rhythmic cycles in the application of therapy. Examples of this are treatments of psychiatric and somatic diseases that are administered according to a schedule that corresponds to a person’s rhythms in order to maximize effectiveness and minimize side effects of the therapy.

CLICK  & SEE 

Chronotherapy is used in different fields, examples of this are the treatment of asthma, cancer, hypertension, and multiple types of depression, among others seasonal affective disorder and bipolar disorder. Apart from the clinical applications, chronotherapy is becoming increasingly popular in non-clinical settings, for example on the work floor, where it is used to increase productivity and performance.

*Methods of pharmaceutical chronotherapy:
*Imitative/Mimetic: Imitating the natural changes in a certain substance in the body.
*Preventive/Precautionary: Taking medicines at the moment that they are most necessary, for example taking hypertension medicine at the time of day that the blood pressure is rising.
*Wake therapy

Chronotherapy is a successful treatment of diseases may depend on the time of day or month that a medicine is taken or surgery performed. Asthma and arthritis pain are examples of conditions now being treated by the clock or calendar.

How our bodies marshal defenses against disease depends on many factors, such as age, gender and genetics. Recently, the role of our bodies’ biological rhythms in fighting disease has come under study by some in the medical community.

Our bodies’ rhythms, also known as our biological clocks, take their cue from the environment and the rhythms of the solar system that change night to day and lead one season into another. Our internal clocks are also dictated by our genetic makeup. These clocks influence how our bodies change throughout the day, affecting blood pressure, blood coagulation, blood flow, and other functions.

Some of the rhythms that affect our bodies include:

*Ultradian, which are cycles shorter than a day (for example, the milliseconds it takes for a neuron to fire, or a 90-minute sleep cycle)
*Circadian, which last about 24 hours (such as sleeping and waking patterns)
*Infradian, referring to cycles longer than 24 hours (for example monthly menstruation)
*Seasonal, such as seasonal affective disorder (SAD), which causes depression in susceptible people during the short days of winter.

Chronotherapy (sleep phase)
In chronotherapy, an attempt is made to move bedtime and rising time later and later each day, around the clock, until the person is sleeping on a normal schedule. This treatment can be used by people with delayed sleep phase disorder who generally cannot reset their circadian rhythm by moving their bedtime and rising time earlier.

Here’s an example of how chronotherapy could work over a week’s course of treatment, with the patient going to sleep 3 hours later every day until the desired sleep and waketime is reached. (Shifting the sleep phase by 3 hours per day may not always be possible; shorter increments of 1–2 hours are needed in such cases.)[citation needed]

Day 1: sleep 04:00 to 12:00
Day 2: sleep 07:00 to 15:00
Day 3: sleep 10:00 to 18:00
Day 4: sleep 13:00 to 21:00
Day 5: sleep 16:00 to 00:00
Day 6: sleep 19:00 to 03:00
Day 7 to 13: sleep 22:00 to 06:00
Day 14 and thereafter: sleep 23:00 to 07:00
While this technique can provide temporary respite from sleep deprivation, patients may find the desired sleep and waketimes slip. The desired pattern can only be maintained by following a strictly disciplined timetable for sleeping and rising.
Other forms of sleep phase chronotherapy:
A modified chronotherapy is called controlled sleep deprivation with phase advance, SDPA. One stays awake one whole night and day, then goes to bed 90 minutes earlier than usual and maintains the new bedtime for a week. This process is repeated weekly until the desired bedtime is reached.

Sometimes, although extremely infrequently, “reverse” chronotherapy – i.e., gradual movements of bedtime and rising time earlier each day – has been used in treatment of patients with abnormally short circadian rhythms, in an attempt to move their bedtimes to later times of the day. Because circadian rhythms substantially shorter than 24 hours are extremely rare, this type of chronotherapy has remained largely experimental.

Chronotherapy is not well recognized in the medical community, but awareness is increasing. The implications are broad in every area of medicine.”

CLICK & SEE :Biologic Rhythms   & LEARN  HOW IT HELPS   Angina, Heart Attack,  Allergies,Asthma,High Blood Pressure, Symptoms of Illness and  Diagnostic Testing

Side effects:
The safety of chronotherapy is not fully known. While chronotherapy has been successful for some, it is necessary to rigidly maintain the desired sleep/wake cycle thenceforth. Any deviation in schedule tends to allow the body clock to shift later again.

Chronotherapy has been known to cause non-24-hour sleep–wake disorder in at least three recorded cases, as reported in the New England Journal of Medicine in 1992. Animal studies have suggested that such lengthening could “slow the intrinsic rhythm of the body clock to such an extent that the normal 24-hour day no longer lies within its range of entrainment.

Resources:
http://en.wikipedia.org/wiki/Chronotherapy_(treatment_scheduling)
http://www.medicinenet.com/script/main/art.asp?articlekey=551
http://www.medicinenet.com/script/main/art.asp?articlekey=551&page=5
http://en.wikipedia.org/wiki/Chronotherapy_(sleep_phase)

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

Chamomile

Botanical Name: Matricaria chamomilla
Family: Asteraceae
Tribe: Anthemideae
Genus: Matricaria
Species: M. chamomilla
Kingdom: Plantae
Order: Asterales

Synonym: Matricaria recutita

Common Names:Chamomile, German chamomile, Hungarian chamomile (kamilla), wild chamomile or scented mayweed,

Habitat:Chamomile is native to southern and eastern Europe. It is also grown in Germany, Hungary, France, Russia, Yugoslavia, and Brazil. It was introduced to India during the Mughal period, now it is grown in Punjab, Uttar Pradesh, Maharashtra, and Jammu and Kashmir. The plants can be found in North Africa, Asia, North and South America, Australia, and New Zealand. Hungary is the main producer of the plant biomass. In Hungary, it also grows abundantly in poor soils and it is a source of income to poor inhabitants of these areas. Flowers are exported to Germany in bulk for distillation of the oil. It often grows near roads, around landfills, and in cultivated fields as a weed, because the seeds require open soil to survive.

Description:
Chamomile is an annual plant with thin spindle-shaped roots only penetrating flatly into the soil. The branched stem is erect, heavily ramified, and grows to a height of 10–80 cm. The long and narrow leaves are bi- to tripinnate. The flower heads are placed separately, they have a diameter of 10–30 mm, and they are pedunculate and heterogamous. The golden yellow tubular florets with 5 teeth are 1.5–2.5 mm long, ending always in a glandulous tube. The flowers bloom in early to midsummer, and have a strong, aromatic smell. The flowers are 6–11 mm long, 3.5 mm wide, and arranged concentrically. The receptacle is 6–8 mm wide, flat in the beginning and conical, cone-shaped later, hollow—the latter being a very important distinctive characteristic of Matricaria—and without paleae. The fruit is a yellowish brown achene.

CLICK & SEE THE PICTURES

Cultivation:
German chamomile can be grown on any type of soil, but growing the crop on rich, heavy, and damp soils should be avoided. It can also withstand cold weather with temperature ranging from 2°C to 20°C. The crop has been grown very successfully on the poor soils (loamy sand) at the farm of the Regional Research Laboratory, Jammu. At Banthra farm of the National Botanical Research Institute, Lucknow, the crop has been grown successfully on soil with a pH of 9. Soils with pH 9–9.2 are reported to support its growth. In Hungary, it grows extensively on clayey lime soils, which are barren lands and considered to be too poor for any other crop. Temperature and light conditions (sunshine hours) have greater effect on essential oils and azulene content, than soil type. Chamomile possesses a high degree of tolerance to soil alkalinity. The plants accumulate fairly large quantity of sodium (66 mg/100 gm of dry material), which helps in reducing the salt concentration in the top soil.[43] No substantial differences were found in the characteristics of the plants grown 1500 km apart (Hungary–Finland). Under cooler conditions in Finland, the quantity of the oxide type in the essential oil was lower than in Hungary.

Propagation:
The plant is propagated by seeds. The seeds of the crop are very minute in size; a thousand seeds weigh 0.088–0.153 gm. About 0.3–0.5 kg of clean seed with a high germination percentage sown in an area of 200–250 m2 gives enough seedlings for stocking a hectare of land. The crop can be grown by two methods i.e. direct sowing of the seed and transplanting. Moisture conditions in the field for direct sowing of seeds must be very good otherwise a patchy and poor germination is obtained. As direct sowing of seeds usually results in poor germination, the transplanting method is generally followed. The mortality of the seedlings is almost negligible in transplanting.

Medicinal Uses:
Chamomile is used in herbal medicine for a sore stomach, irritable bowel syndrome, and as a gentle sleep aid. It is also used as a mild laxative and is anti-inflammatory and bactericidal. It can be taken as an herbal tea, two teaspoons of dried flower per cup of tea, which should be steeped for 10 to 15 minutes while covered to avoid evaporation of the volatile oils. The marc should be pressed because of the formation of a new active principle inside the cells, which can then be released by rupturing the cell walls, though this substance only forms very close to boiling point. For a sore stomach, some recommend taking a cup every morning without food for two to three months. It has been studied as a mouthwash against oral mucositis ]and may have acaricidal properties against certain mites, such as Psoroptes cuniculi.

One of the active ingredients of its essential oil is the terpene bisabolol. Other active ingredients include farnesene, chamazulene, flavonoids (including apigenin, quercetin, patuletin and luteolin) and coumarin.

Dried chamomile has a reputation (among herbalists) for being incorrectly prepared because it is dried at a temperature above the boiling point of the volatile components of the plant.

Chamomile is used topically in skin and mucous membrane inflammations and skin diseases. It can be inhaled for respiratory tract inflammations or irritations; used in baths as irrigation for anogenital inflammation; and used internally for GI spasms and inflammatory diseases. However, clinical trials supporting any use of chamomile are limited.

Possible Side Effects:
Chamomile, a relative of ragweed, can cause allergy symptoms and can cross-react with ragweed pollen in individuals with ragweed allergies. It also contains coumarin, so care should be taken to avoid potential drug interactions, e.g. with blood thinners.

While extremely rare, very large doses of chamomile may cause nausea and vomiting. Even more rarely, rashes may occur. A type-IV allergic reaction with severe anaphylaxis has been reported in a 38-year old man who drank chamomile tea.

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any
supplement, it is always advisable to consult with your own health care provider.

Resources:
http://en.wikipedia.org/wiki/Matricaria_chamomilla
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210003/
http://www.drugs.com/npp/chamomile.html

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.

CLICK & SEE THE PICTURES

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.

Ayurvedic Treatment ..click & see…>…….…(1) :....(2)

Home Remedies. click & see….>…....(1) :…(2) :.…...(3) :..

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

Immunisation

Definition:
Immunization, or immunisation, is the process by which an individual’s immune system becomes fortified against an agent (known as the immunogen).It  is the process whereby a person is made immune or resistant to an infectious disease.

CLICK & SEE

Immunization is done through various techniques, most commonly vaccination. Vaccines against microorganisms that cause diseases can prepare the body’s immune system, thus helping to fight or prevent an infection. The fact that mutations can cause cancer cells to produce proteins or other molecules that are known to the body forms the theoretical basis for therapeutic cancer vaccines. Other molecules can be used for immunization as well, for example in experimental vaccines against nicotine (NicVAX) or the hormone ghrelin in experiments to create an obesity vaccine.

Before the introduction of vaccines, the only way people became immune to an infectious disease was by actually getting the disease and surviving it. Smallpox (variola) was prevented in this way by inoculation, which produced a milder effect than the natural disease. It was introduced into England from Turkey by Lady Mary Wortley Montagu in 1721 and used by Zabdiel Boylston in Boston the same year. In 1798 Edward Jenner introduced inoculation with cowpox (smallpox vaccine), a much safer procedure. This procedure, referred to as vaccination, gradually replaced smallpox inoculation, now called variolation to distinguish it from vaccination. Until the 1880s vaccine/vaccination referred only to smallpox, but Louis Pasteur developed immunisation methods for chicken cholera and anthrax in animals and for human rabies, and suggested that the terms vaccine/vaccination should be extended to cover the new procedures. This can cause confusion if care is not taken to specify which vaccine is used e.g. measles vaccine or influenza vaccine.

When this system is exposed to molecules that are foreign to the body, called non-self, it will orchestrate an immune response, and it will also develop the ability to quickly respond to a subsequent encounter because of immunological memory. This is a function of the adaptive immune system. Therefore, by exposing an animal to an immunogen in a controlled way, its body can learn to protect itself: this is called active immunization.

The most important elements of the immune system that are improved by immunization are the T cells, B cells, and the antibodies B cells produce. Memory B cells and memory T cells are responsible for a swift response to a second encounter with a foreign molecule. Passive immunization is direct introduction of these elements into the body, instead of production of these elements by the body itself.

The most important elements of the immune system that are improved by immunization are the T cells, B cells, and the antibodies B cells produce. Memory B cells and memory T cells are responsible for a swift response to a second encounter with a foreign molecule. Passive immunization is direct introduction of these elements into the body, instead of production of these elements by the body itself.

Immunization is a proven tool for controlling and eliminating life-threatening infectious diseases and is estimated to avert between 2 and 3 million deaths each year. It is one of the most cost-effective health investments, with proven strategies that make it accessible to even the most hard-to-reach and vulnerable populations. It has clearly defined target groups; it can be delivered effectively through outreach activities; and vaccination does not require any major lifestyle change.

Immunizations are definitely less risky and an easier way to become immune to a particular disease than risking a milder form of the disease itself. They are important for both adults and children in that they can protect us from the many diseases out there. Through the use of immunizations, some infections and diseases have almost completely been eradicated throughout the United States and the World. One example is polio. Thanks to dedicated health care professionals and the parents of children who vaccinated on schedule, polio has been eliminated in the U.S. since 1979. Polio is still found in other parts of the world so certain people could still be at risk of getting it. This includes those people who have never had the vaccine, those who didn’t receive all doses of the vaccine, or those traveling to areas of the world where polio is still prevalent.

The Immunization can be achieved in an active or passive manner:
Vaccination is an active form of immunization.

Active immunization/vaccination has been named one of the “Ten Great Public Health Achievements in the 20th Century”.

Active immunization:.click & see
Active immunization can occur naturally when a person comes in contact with, for example, a microbe. The immune system will eventually create antibodies and other defenses against the microbe. The next time, the immune response against this microbe can be very efficient; this is the case in many of the childhood infections that a person only contracts once, but then is immune.

Artificial active immunization is where the microbe, or parts of it, are injected into the person before they are able to take it in naturally. If whole microbes are used, they are pre-treated.

The importance of immunization is so great that the American Centers for Disease Control and Prevention has named it one of the “Ten Great Public Health Achievements in the 20th Century”.  Live attenuated vaccines have decreased pathogenicity. Their effectiveness depends on the immune systems ability to replicate and elicits a response similar to natural infection. It is usually effective with a single dose. Examples of live, attenuated vaccines include measles, mumps, rubella, MMR, yellow fever, varicella, rotavirus, and influenza (LAIV).

Passive immunization:……...click & see
Passive immunization is where pre-synthesized elements of the immune system are transferred to a person so that the body does not need to produce these elements itself. Currently, antibodies can be used for passive immunization. This method of immunization begins to work very quickly, but it is short lasting, because the antibodies are naturally broken down, and if there are no B cells to produce more antibodies, they will disappear.

Passive immunization occurs physiologically, when antibodies are transferred from mother to fetus during pregnancy, to protect the fetus before and shortly after birth.

Artificial passive immunization is normally administered by injection and is used if there has been a recent outbreak of a particular disease or as an emergency treatment for toxicity, as in for tetanus. The antibodies can be produced in animals, called “serum therapy,” although there is a high chance of anaphylactic shock because of immunity against animal serum itself. Thus, humanized antibodies produced in vitro by cell culture are used instead if available.

Resources:
http://en.wikipedia.org/wiki/Immunization
http://www.who.int/topics/immunization/en/

Complications In Pregnancy

Pre-eclampsia, eclampsia or toxemia of pregnancy
Definition:
Pre-eclampsia or preeclampsia (PE) is a disorder of pregnancy characterized by high blood pressure and a large amount of protein in the urine. The disorder usually occurs in the third trimester of pregnancy and gets worse over time. In severe disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. PE increases the risk of poor outcomes for both the mother and the baby. If left untreated, it may result in seizures at which point it is known as eclampsia.

CLICK & SEE

Toxemia of pregnancy is a severe condition that sometimes occurs in the latter weeks of pregnancy. It is characterized by high blood pressure; swelling of the hands, feet, and face; and an excessive amount of protein in the urine. If the condition is allowed to worsen, the mother may experience convulsions and coma, and the baby may be stillborn.
The term toxemia is actually a misnomer from the days when it was thought that the condition was caused by toxic (poisonous) substances in the blood. The illness is more accurately called preeclampsia before the convulsive stage and eclampsia afterward.

Preeclampsia affects between 2–8% of pregnancies worldwide. Hypertensive disorders of pregnancy are one of the most common causes of death due to pregnancy. They resulted in 29,000 deaths in 2013 – down from 37,000 deaths in 1990. Preeclampsia usually occurs after 32 weeks; however, if it occurs earlier it is associated with worse outcomes. Women who have had PE are at increased risk of heart disease later in life. The word eclampsia is from the Greek term for lightning. The first known description of the condition was by Hippocrates in the 5th century BCE

Symptoms:
Swelling (especially in the hands and face) was originally considered an important sign for a diagnosis of preeclampsia. However, because swelling is a common occurrence in pregnancy, its utility as a distinguishing factor in preeclampsia is not great. Pitting edema (unusual swelling, particularly of the hands, feet, or face, notable by leaving an indentation when pressed on) can be significant, and should be reported to a health care provider.

In general, none of the signs of preeclampsia are specific, and even convulsions in pregnancy are more likely to have causes other than eclampsia in modern practice. Further, a symptom such as epigastric pain may be misinterpreted as heartburn. Diagnosis, therefore, depends on finding a coincidence of several preeclamptic features, the final proof being their regression after delivery.

The symptoms of toxemia of pregnancy (which may lead to death if not treated) are divided into three stages, each progressively more serious:
Mild preeclampsia symptoms include edema (puffiness under the skin due to fluid accumulation in the body tissues, often noted around the ankles), mild elevation of blood pressure, and the presence of small amounts of protein in the urine.

Severe preeclampsia symptoms include extreme edema, extreme elevation of blood pressure, the presence of large amounts of protein in the urine, headache, dizziness, double vision, nausea, vomiting, and severe pain in the right upper portion of the abdomen.
Eclampsia symptoms include convulsions and coma.

Risk Factors:
Known risk factors for preeclampsia include:

*Nulliparity (never given birth)
*Older age, and diabetes mellitus
*Kidney disease
*Chronic hypertension
*Prior history of preeclampsia
*Family history of preeclampsia
*Advanced maternal age (>35 years)
*Obesity
*Antiphospholipid antibody syndrome
*Multiple gestation
*Having donated a kidney.
*Having sub-clinical hypothyroidism or thyroid antibodies

It is also more frequent in a women’s first pregnancy and if she is carrying twins. The underlying mechanism involves abnormal formation of blood vessels in the placenta amongst other factors. Most cases are diagnosed before delivery. Rarely, preeclampsia may begin in the period after delivery. While historically both high blood pressure and protein in the urine were required to make the diagnosis, some definitions also include those with hypertension and any associated organ dysfunction. Blood pressure is defined as high when it is greater than 140 mmHg systolic or 90 mmHg diastolic at two separate times, more than four hours apart in a women after twenty weeks of pregnancy. PE is routinely screened for during prenatal care.
Causes:
There is no definitive known cause of preeclampsia, though it is likely related to a number of factors. Some of these factors include:

*Abnormal placentation (formation and development of the placenta)
*Immunologic factors
*Prior or existing maternal pathology – preeclampsia is seen more at a higher incidence in individuals with preexisting hypertension, obesity, antiphospholipid antibody syndrome, and those with history of preeclampsia
*Dietary factors, e.g. calcium supplementation in areas where dietary calcium intake is low has been shown to reduce the risk of preeclampsia.
*Environmental factors, e.g. air pollution
*Those with long term high blood pressure have a risk 7 to 8 times higher than those without.

Physiologically, research has linked preeclampsia to the following physiologic changes: alterations in the interaction between the maternal immune response and the placenta, placental injury, endothelial cell injury, altered vascular reactivity, oxidative stress, imbalance among vasoactive substances, decreased intravascular volume, and disseminated intravascular coagulation.

While the exact cause of preeclampsia remains unclear, there is strong evidence that a major cause predisposing a susceptible woman to preeclampsia is an abnormally implanted placenta. This abnormally implanted placenta is thought to result in poor uterine and placental perfusion, yielding a state of hypoxia and increased oxidative stress and the release of anti-angiogenic proteins into the maternal plasma along with inflammatory mediators. A major consequence of this sequence of events is generalized endothelial dysfunction. The abnormal implantation is thought to stem from the maternal immune system’s response to the placenta and refers to evidence suggesting a lack of established immunological tolerance in pregnancy. Endothelial dysfunction results in hypertension and many of the other symptoms and complications associated with preclampsia.

One theory proposes that certain dietary deficiencies may be the cause of some cases. Also, there is the possibility that some forms of preeclampsia and eclampsia are the result of deficiency of blood flow in the uterus.

Diagnosis:
Pre-eclampsia is diagnosed when a pregnant woman develops:

*Blood pressure >_ 140 mm Hg systolic or  >_  90 mm Hg diastolic on two separate readings taken at least four to six hours apart after 20 weeks gestation in an individual with previously normal blood pressure.
*In a woman with essential hypertension beginning before 20 weeks gestational age, the diagnostic criteria are: an increase in systolic blood pressure (SBP) of   >_ 30mmHg or an increase in diastolic blood pressure (DBP) of   >_15mmHg.
*Proteinuria  >_ 0.3 grams (300 mg) or more of protein in a 24-hour urine sample or a SPOT urinary protein to creatinine ratio  >_ 0.3 or a urine dipstick reading of 1+ or greater (dipstick reading should only be used if other quantitative methods are not available)

Suspicion for preeclampsia should be maintained in any pregnancy complicated by elevated blood pressure, even in the absence of proteinuria. Ten percent of individuals with other signs and symptoms of preeclampsia and 20% of individuals diagnosed with eclampsia show no evidence of proteinuria. In the absence of proteinuria, the presence of new-onset hypertension (elevated blood pressure) and the new onset of one or more of the following is suggestive of the diagnosis of preeclampsia:

*Evidence of kidney dysfunction (oliguria, elevated creatinine levels)
*Impaired liver function (impaired liver function tests)
*Thrombocytopenia (platelet count <100,000/microliter)
*Pulmonary edema
*Ankle edema pitting type
*Cerebral or visual disturbances
*Preeclampsia is a progressive disorder and these signs of organ dysfunction are indicative of severe preeclampsia. A systolic blood pressure ?160 or diastolic blood pressure ?110 and/or proteinuria >5g in a 24-hour period is also indicative of severe preeclampsia. Clinically, individuals with severe preeclampsia may also present epigastric/right upper quadrant abdominal pain, headaches, and vomiting. Severe preeclampsia is a significant risk factor for intrauterine fetal death.

Of note, a rise in baseline blood pressure (BP) of 30 mmHg systolic or 15 mmHg diastolic, while not meeting the absolute criteria of 140/90, is still considered important to note, but is not considered diagnostic.

Predictive tests:
There have been many assessments of tests aimed at predicting preeclampsia, though no single biomarker is likely to be sufficiently predictive of the disorder. Predictive tests that have been assessed include those related to placental perfusion, vascular resistance, kidney dysfunction, endothelial dysfunction, and oxidative stress. Examples of notable tests include:

*Doppler ultrasonography of the uterine arteries to investigate for signs of inadequate placental perfusion. This test has a high negative predictive value among those individuals with a history of prior preeclampsia.
*Elevations in serum uric acid (hyperuricemia) is used by some to “define” preeclampsia,[14] though it has been found to be a poor predictor of the disorder. Elevated levels in the blood (hyperuricemia) are likely due to reduced uric acid clearance secondary to impaired kidney function.
*Angiogenic proteins such as vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) and anti-angiogenic proteins such as soluble fms-like tyrosine kinase-1 (sFlt-1) have shown promise for potential clinical use in diagnosing preeclampsia, though evidence is sufficient to recommend a clinical use for these markers.
*Recent studies have shown that looking for podocytes, specialized cells of the kidney, in the urine has the potential to aid in the prediction of preeclampsia. Studies have demonstrated that finding podocytes in the urine may serve as an early marker of and diagnostic test for preeclampsia. Research is ongoing.

Differential diagnosis:
Pre-eclampsia can mimic and be confused with many other diseases, including chronic hypertension, chronic renal disease, primary seizure disorders, gallbladder and pancreatic disease, immune or thrombotic thrombocytopenic purpura, antiphospholipid syndrome and hemolytic-uremic syndrome. It must be considered a possibility in any pregnant woman beyond 20 weeks of gestation. It is particularly difficult to diagnose when preexisting disease such as hypertension is present. Women with acute fatty liver of pregnancy may also present with elevated blood pressure and protein in the urine, but differs by the extent of liver damage. Other disorders that can cause high blood pressure include thyrotoxicosis, pheochromocytoma, and drug misuse
Treatment:
Preeclampsia and eclampsia cannot be completely cured until the pregnancy is over. Until that time, treatment includes the control of high blood pressure and the intravenous administration of drugs to prevent convulsions. Drugs may also be given to stimulate the production of urine. In some severe cases, early delivery of the baby is needed to ensure the survival of the mother.

Prevention:
Recommendations for prevention include: aspirin in those at high risk, calcium supplementation in areas with low intake, and treatment of prior hypertension with medications. In those with PE delivery of the fetus and placenta is an effective treatment. When delivery becomes recommended depends on how severe the PE and how far along in pregnancy a person is. Blood pressure medication, such as labetalol and methyldopa, may be used to improve the mother’s condition before delivery. Magnesium sulfate may be used to prevent eclampsia in those with severe disease. Bedrest and salt intake have not been found to be useful for either treatment or prevention.

Diet:
Protein or calorie supplementation have no effect on preeclampsia rates, and dietary protein restriction does not appear to increase preeclampsia rates. Further, there is no evidence that changing salt intake has an effect.

Supplementation with antioxidants such as vitamin C and E has no effect on preeclampsia incidence, nor does supplementation with vitamin D. Therefore, supplementation with vitamins C, E, and D is not recommended for reducing the risk of pre-eclampsia.

Calcium supplementation of at least 1 gram per day is recommended during pregnancy as it prevents preeclampsia where dietary calcium intake is low, especially for those at high risk. Low selenium status is associated with higher incidence of preeclampsia.

Aspirin:
Taking aspirin is associated with a 1% to 5% reduction in preeclampsia and a 1% to 5% reduction in premature births in women at high risk. The WHO recommends low-dose aspirin for the prevention of preeclampsia in women at high risk and recommend it be started before 20 weeks of pregnancy. The United States Preventive Services Task Force recommends a low-dose regimen for women at high risk beginning in the 12th week.

Physical activity:
There is insufficient evidence to recommend either exercise or strict bedrest as preventative measures of pre-eclampsia.

Smoking cessation:
In low-risk pregnancies the association between cigarette smoking and a reduced risk of preeclampsia has been consistent and reproducible across epidemiologic studies. High-risk pregnancies (those with pregestational diabetes, chronic hypertension, history of preeclampsia in a previous pregnancy, or multifetal gestation) showed no significant protective effect. The reason for this discrepancy is not definitively known; research supports speculation that the underlying pathology increases the risk of preeclampsia to such a degree that any measurable reduction of risk due to smoking is masked. However, the damaging effects of smoking on overall health and pregnancy outcomes outweighs the benefits in decreasing the incidence of preeclampsia. It is recommended that smoking be stopped prior to, during and after pregnancy

Restriction of salt in the diet may help reduce swelling, it does not prevent the onset of high blood pressure or the appearance of protein in the urine. During prenatal visits, the doctor routinely checks the woman’s weight, blood pressure, and urine. If toxemia is detected early, complications may be reduced.

Resources:
http://health.howstuffworks.com/pregnancy-and-parenting/pregnancy/complications/a-guide-to-pregnancy-complications-ga13.htm
http://en.wikipedia.org/wiki/Pre-eclampsia

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

Spirulina (Blue-green algae)

Other Names:
AFA, Algae, Algas Verdiazul, Algues Bleu-Vert, Algues Bleu-Vert du Lac Klamath, Anabaena, Aphanizomenon flos-aquae, Arthrospira maxima, Arthrospira platensis, BGA, Blue Green Algae, Blue-Green Micro-Algae, Cyanobacteria, Cyanobactérie, Cyanophycée, Dihe, Espirulina, Hawaiian Spirulina, Klamath, Klamath Lake Algae, Lyngbya wollei, Microcystis aeruginosa, Microcystis wesenbergii, Nostoc ellipsosporum, Spirulina Blue-Green Algae, Spirulina Fusiformis, Spirulina maxima, Spirulina platensis, Spirulina pacifica, Spiruline, Spiruline d’Hawaii, Tecuitlatl.

Description:
Spirulina is obtained from a plant in form of blue-green algae that springs from warm, fresh water bodies………..CLICK & SEE
Spirulina is a cyanobacterium that can be consumed by humans and other animals. There are two species, Arthrospira platensis and Arthrospira maxima.

Arthrospira is cultivated worldwide; used as a dietary supplement as well as a whole food; and is also available in tablet, flake and powder form. It is also used as a feed supplement in the aquaculture, aquarium and poultry industries.

Blue-green algae have a high protein, iron, and other mineral content which is absorbed when taken orally. Blue-green algae are being researched for their potential effects on the immune system, swelling (inflammation), and viral infections.

Chlorella is another form of algae that is sometimes confused with spirulina. The fundamental difference between spirulina and chlorella is that spirulina is many thousands of years older and does not possess the hard cell wall that makes chlorella closer to being a plant than algae.

Chlorella is an excellent way to detoxify  our body from mercury, which most of you are contaminated with if you’ve ever had dental fillings, received a vaccine, used certain types of cookware or eaten fish. Spirulina simply is unable to remove heavy metals like chlorella does, as it lacks a cell membrane.

Chlorella has also been proven to be of benefit to those who suffer from degenerative disease. This report, however, will focus on the specific benefits that can be attributed to spirulina in particular.

“Blue-green algae” describes a large and diverse group of simple, plant-like organisms found in salt water and some large fresh water lakes.

Blue-green algae products are used for many conditions, but so far, there isn’t enough scientific evidence to determine whether or not they are effective for any of them.

Blue-green algae are used as a source of dietary protein, B-vitamins, and iron. They are also used for weight loss, attention deficit-hyperactivity disorder (ADHD), hayfever, diabetes, stress, fatigue, anxiety, depression, and premenstrual syndrome (PMS) and other women’s health issues.

Some people use blue-green algae for treating precancerous growths inside the mouth, boosting the immune system, improving memory, increasing energy and metabolism, lowering cholesterol, preventing heart disease, healing wounds, and improving digestion and bowel health.

Blue-green algae are commonly found in tropical or subtropical waters that have a high-salt content, but some types grow in large fresh water lakes. The natural color of these algae can give bodies of water a dark-green appearance. The altitude, temperature, and sun exposure where the blue-green algae are grown dramatically influence the types and mix of blue-green algae in the water.

Some blue-green algae products are grown under controlled conditions. Others are grown in a natural setting, where they are more likely to be contaminated by bacteria, liver poisons (microcystins) produced by certain bacteria, and heavy metals. Choose only products that have been tested and found free of these contaminants.

You may have been told that blue-green algae are an excellent source of protein. But, in reality, blue-green algae is no better than meat or milk as a protein source and costs about 30 times as much per gram.

Protein:
Dried spirulina contains about 60% (51–71%) protein.  It is a complete protein containing all essential amino acids, though with reduced amounts of methionine, cysteine and lysine when compared to the proteins of meat, eggs and milk. It is, however, superior to typical plant protein, such as that from legumes.

The U.S. National Library of Medicine said that spirulina was no better than milk or meat as a protein source, and was approximately 30 times more expensive per gram

Other nutrients:
Spirulina’s lipid content is about 7% by weight,  and is rich in gamma-linolenic acid (GLA),  and also provides alpha-linolenic acid (ALA), linoleic acid (LA), stearidonic acid (SDA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA).  Spirulina contains vitamins B1 (thiamine), B2 (riboflavin), B3 (nicotinamide), B6 (pyridoxine), B9 (folic acid), vitamin C, vitamin A, and vitamin E.  It is also a source of potassium, calcium, chromium, copper, iron, magnesium, manganese, phosphorus, selenium, sodium, and zinc. Spirulina contains many pigments which may be beneficial and bioavailable, including beta-carotene,  zeaxanthin,  7-hydroxyretinoic acid,  isomers, chlorophyll-a, xanthophyll, echinenone, myxoxanthophyll, canthaxanthin, diatoxanthin, 3′-hydroxyechinenone, beta-cryptoxanthin, and oscillaxanthin, plus the phycobiliproteins  c-phycocyanin and allophycocyanin.

Vitamin B12 controversy:
Spirulina is not considered to be a reliable source of Vitamin B12. Spirulina supplements contain predominantly pseudovitamin B12, which is biologically inactive in humans. Companies which grow and market spirulina have claimed it to be a significant source of B12 on the basis of alternative, unpublished assays, although their claims are not accepted by independent scientific organizations. The American Dietetic Association and Dietitians of Canada in their position paper on vegetarian diets state that spirulina cannot be counted on as a reliable source of active vitamin B12. The medical literature similarly advises that spirulina is unsuitable as a source of B12.

 Spirulina Helped Save Millions from Arsenic Poisoning:
Bangladeshi researchers conducted a three-month-hospital-based study, where spirulina was given to 33 patients while 17 received placebo doses. 82 percent of those taking spirulina showed tremendous improvement.

An Immune-System Power-Boost — Spirulina’s Impact on Candida and AIDS:
According to a study done by the Department of Aquataculture in Taiwan,4 spirulina shows significant immune-boosting properties. Researchers exposed white shrimp to seawater containing a hot-water extract of spirulina before transferring them to seawater with a pH level of 6.8. The control group was not exposed to spirulina.

The shrimp exposed to the spirulina seawater showed a faster and more promising recovery rate to the high levels of pH than those not given the dose of spirulina first.

Now, let’s take a look at what this immune-system boosting power can mean for  us:

Candida:
If  we have an autoimmune disease such as Crohn’s disease, chronic fatigue syndrome, Lupus or fibromyalgia, chronic candida yeast can both cause and worsen your symptoms. Spirulina has been shown to encourage and support the growth of healthy bacterial flora in our gut,  which can help keep candida overgrowth under control.

HIV and AIDS:
Drugs such as AZT used to treat HIV and AIDS patients can actually cause the symptoms they are supposed to cure. However, spirulina has been shown to help inactivate the human immunodeficiency virus associated with HIV and AIDS.

Seasonal Allergy:
Millions of people are allergic to pollen, ragweed, dust, mold, pet dander, and a myriad other environmental contaminants, ensuring the makers of Kleenex will always stay in business.

Unfortunately, many people who have allergic rhinitis treat it with prescription and over-the-counter (OTC) drugs that often do more harm than good. Antihistamines are designed to suppress our immune system, which leads to decreased resistance to disease and dependence on the drug. Certain asthma drugs have been linked to serious side effects as well.

This is where natural methods such as the use of spirulina come in. According to one study,  patients treated with spirulina reported relief of symptoms commonly associated with allergic rhinitis, such as nasal discharge and congestion, sneezing and itching, when given spirulina.

Blood Pressure Balancing:
According to a study done by the Department of Biochemistry in Mexico,7 4.5 grams of spirulina given each day was shown to regulate blood pressure among both women and men ages 18-65 years with no other dietary changes made during the six weeks the experiment was run.

Lowers Stroke Risk:
In a study done at the Institute of Pharmaceutical Technology in India, it was found that a dosage of 180mg/kg of spirulina had a protective effect on the brain and nervous system of rats exposed to high amounts of free radicals, compared to rats not given the spirulina before the experiment. This lab test shows the promising effect of spirulina on stroke prevention.

Helps Reduce Cancer Risk:
According to a study done in China,10 selenium-infused spirulina inhibited the growth of MCF-7 breast cancer cells.

Potential Adverse Reactions:
Spirulina is a safe source of protein, nutrients, vitamins, and minerals that has been used for centuries. Though there are no known side effects associated with spirulina,  our body may react to it based on  our current state of health. Let’s take a look at some of those reactions,  what they mean, and what you can do to alleviate them.

The most prominent reactions  one may experience are:
*Slight Fever –– The high protein content in spirulina increases metabolism, which may elevate body temperature.

*Dark Green Waste Matter — Spirulina can remove accumulated waste product in our colon, which may cause darker stool. Also, spirulina is high in chlorophyll. This will also turn waste matter green.

*Excessive Passing of Gas — This may indicate that your digestive system is not functioning properly or you have an extreme build-up of gas.

*Feelings of Excitement — Our body is converting protein into heat energy, which may cause temporary feelings of restlessness.

*Breakouts and Itchy Skin — This is caused by colon cleansing process and is only temporary.

*Sleepiness — This is caused by the detoxification process and may indicate our body is exhausted and needs better rest.

Remember, our body may go through an adjustment period with spirulina, and our best bet to reduce reaction is to dose gradually to see how  our body will react.  Water intake should be increased and ,  stress levels should be  reduced, we should eat according to our nutritional type, and get plenty of rest.

Important Contraindications for Spirulina:
Even though spirulina is entirely natural and generally considered a healthful food, there are some contraindications  we need to be aware of.  No one should  take spirulina if he or she has a severe seafood or iodine allergy. And, if one is pregnant or nursing or have hyperthyroidism, it is adviced  to  consult with the healthcare provider before taking spirulina.

Resources:
http://en.wikipedia.org/wiki/Spirulina_(dietary_supplement)
http://www.webmd.com/vitamins-supplements/ingredientmono-923-spirulina%20(blue-green%20algae).aspx?activeingredientid=923&activeingredientname=spirulina%20(blue-green%20algae)
http://articles.mercola.com/sites/articles/archive/2011/07/01/spirulina-the-amazing-super-food-youve-never-heard-of.aspx