Categories
Ailmemts & Remedies

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

Categories
Herbs & Plants

Chamomile

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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.

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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

Categories
Ailmemts & Remedies

Palmar hyperhidrosis

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

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

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

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

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

Causes:
Hyperhidrosis is either primary focal or secondary generalized.

1. Primary Palmar  Hyperhidrosis

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

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

2. Secondary Palmar Hyperhidrosis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

*Treatment should be directed at contributing factors.

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

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

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

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

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

Causes and Treatment of Palmar Hyperhidrosis – Sweaty Palms/Hands

Categories
immunisation

Immunisation

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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.

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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/

Categories
Pediatric Pregnancy & Child birth

Complications In Pregnancy

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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.

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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

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