Monday, June 25, 2012

What Is Vocal Cord Paresis (Paralysis)? What Causes Vocal Cord Paresis?

Vocal cord paresis, also known as vocal cord paralysis is the inability of one or both vocal cords (vocal folds) to move. It can greatly impact on the daily life of the sufferer, including employment, choice of job, social interactions and leisure time activities. The damage is caused by damage to nerves going to the vocal cord - the nerve impulses in the larynx (voice box) are interrupted, resulting in paralysis of the vocal cord muscles. It can also be caused by brain damage.

Patients with vocal paresis typically experience hoarseness, vocal fatigue, mild to severe reduction in speech volume, a pain in the throat when speaking, and swallowing things down the wrong way and choking. The vocal cords, as well as allowing us to produce utterances (speak, etc.) also protect the airway, preventing food, drink and saliva from entering the trachea (windpipe). In extreme cases the resultant choking can lead to death.

Individuals with vocal cord paresis may find the effectiveness of coughing, swallowing or sneezing in removing laryngeal area waste is undermined reduced vocal cord mobility. This may result in accumulations in the area, allowing for bacterial and viral colonization, and subsequent infections and throat discomfort.

What are the signs and symptoms of vocal cord paresis (paralysis)?

A symptom is something the patient senses and describes, while a sign is something other people, such as the doctor notice. For example, drowsiness may be a symptom while dilated pupils may be a sign.

The vocal cords consist of two bands of muscle, located at the trachea (entrance to the windpipe). When we make an utterance (produce sound from the mouth) the two bands of muscle tissue touch each other and vibrate. When we are not uttering sounds the vocal cords are in an open, relaxed position, allowing air to flow freely into our windpipe - allowing us to breathe.

Most cases of vocal cord paresis involve just one cord being paralyzed. However, sometimes both are affected, and the patient is likely to experience swallowing as well as breathing difficulties.

The following signs and symptoms are possible:
  • The voice may change, and become more "breathy", like a loud whisper
  • Hoarseness, huskiness
  • The patients breathing may be noisier
  • Vocal pitch may be affected
  • When swallowing solids or liquids the patient might choke (including saliva sometimes)
  • While speaking the sufferer may have to catch his/her breathe more often than usual
  • Voice volume may be affected. The patient may not be able to raise their voice.
  • Pharyngeal reflex (gag reflex) may be lost - the pharyngeal reflex is a reflex contraction of the back of the throat, evoked by touching the soft palate. It prevents something from entering the throat except as part of normal swallowing and helps prevent choking.
  • Coughs that do not clear the throat properly

What are the risk factors and causes for vocal cord paresis (paralysis)?

A risk factor is something which increases the likelihood of developing a condition or disease. For example, obesity significantly raises the risk of developing diabetes type 2. Therefore, obesity is a risk factor for diabetes type 2. The following factors may raise the chances of developing vocal cord paresis:
  • Gender - females have a slightly higher risk than males.
  • Some types of surgery - especially chest or throat surgery. Breathing tubes used in surgery may damage vocal cord nerved. Cardiac surgery represents a risk to normal voice function as the nerves serving the larynx are routed near the heart - damage to this nerve during open heart surgery is not uncommon. The recurrent laryngeal nerve also runs close to the thyroid gland making, hoarseness of voice due to partial paralysis an important side effect of thyroid surgery.
  • Certain neurological conditions - people with multiple sclerosis (MS), Parkinson's disease, or myasthenia gravis have a higher risk of developing vocal cord paresis, compared to other individuals. The risk of vocal cord weakness is greater than paralysis.
  • Injury to the chest or neck - a trauma may damage the nerves that serve the vocal cords or the larynx.
  • Stroke - the part of the brain that sends messages to the larynx (voice box) may be damaged from a stroke.
  • Tumors - these may develop around or in the cartilages, nerves or muscles of the voice box. The tumors may be benign or malignant (cancerous).
  • Inflammation or scarring of the vocal cord joints, as well as the space between the two vocal cord cartilages may prevent the larynx from working properly. Although the cord nerves are usually working correctly, the inflammation can give vocal cord paresis-like signs and symptoms. Some infections may also cause inflammation.
Vocal cord paresis may also be idiopathic - there may be no identifiable cause.

Diagnosing vocal cord paresis (paralysis)

Initially, the patient will probable see a GP (general practitioner, primary care physician) who will ask about symptoms and check out for some signs, such as listening to their voice and asking how long there have been problems.

The following diagnostic tests may also be ordered:
  • Endoscopy - a long, thin, flexible tube (endoscope) is used to look at the vocal cords. A special device with a small camera at the end (videostrobolaryngoscopy) may be used. The doctor can get a good look at the vocal cords on a monitor.
  • Laryngeal electromyography (LEMG) - electric currents in the larynx muscles are measured. Small needles are inserted into the vocal cord muscles through the skin of the neck. The test measures the strength of the neuromuscular signal from the brain to the muscles controlling the vocal folds (cords). During an LEMG the doctor will ask the patient to perform a number of tasks that would normally activate the muscles.
  • Other tests - the doctor may order blood tests and imaging scans, such as x-rays, CT scans, MRI scans to help determine the cause of the paralysis.

What are the treatment options for vocal cord paresis (paralysis)?

Vocal cord paresis treatment depends on several factors, including what caused it, how severe symptoms are, and how long they have been present. The patient may be advised to have voice therapy, surgery, or both.

Voice therapy - the equivalent of physical therapy for large muscle paralysis. The therapist asks the patient to do special exercise and some other activities to strengthen their vocal cords, improve their breath and control while speaking, prevent unusual tensions in other muscles near the affected vocal cord(s), and protect the airway from liquids and solids.

Surgery - if the patient does not recover completely with voice therapy, the doctor may recommend surgical intervention:
  • Bulk injection - the vocal cord muscle will most likely be weak due to paralysis of the nerve. The otolaryngologist (ear, nose and throat specialist doctor) may inject fat, collagen or some filler into the vocal cord. The extra bulk brings the vocal cord nearer to the middle of the larynx (voice box), making it easier for the opposite cord muscle to move effectively when the patient coughs, swallows or speaks.
  • Phonosurgery (vocal cord repositioning) - this operation repositions and/or reshapes the vocal fold (cord) to improve voice functions.
  • Tracheotomy - if both vocal folds (cords) are affected and very close to each other, breathing will be more difficult because of decreased air flow. The doctor makes an incision (cut) in front of the neck and an opening is created into the trachea (windpipe). A breathing tube is inserted so that the patient can breathe with air bypassing the paralyzed vocal cords. Put simply, the patient breathes through a hole in the neck because the opening in the larynx is too small for proper breathing.


Breathing - if symptoms are severe enough the patient can have serious, life-threatening breathing problems.

Aspiration - because there is paralysis in the area where food or liquid may go down the wrong way (aspiration), there is a risk of choking. Aspiration can lead to severe pneumonia.
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What Is Diabetes Insipidus? What Causes Diabetes Insipidus?

Diabetes insipidus is a condition in which the body cannot retain enough water. The patient is excessively thirsty and excretes large amounts of extremely diluted urine - a reduction in fluid intake does not reduce amounts and consistency of urine excretion. It is a rare condition, affecting approximately 1 in every 25,000 people.

Diabetes insipidus is not related to diabetes mellitus (sugar diabetes). The term diabetes on its own nearly always refers to diabetes mellitus. This article is about diabetes insipidus - the condition characterized by intense thirst and polyuria (excretion of large amounts of urine).

In most cases diabetes insipidus occurs because the body does not properly produce, store or release a key hormone - arginine vasopressin (AVP), also known as antidiuretic hormone (ADH). It may also occur when the kidneys do not respond properly to ADH (antidiuretic hormone).

There are three types of diabetes insipidus:
  • Neurogenic diabetes insipidus - a deficiency with ADH (antidiuretic hormone).
  • Nephrogenic diabetes insipidus - insensitivity of the kidneys to ADH.
  • Gestational diabetes insipidus - in very rare cases diabetes insipidus may also occur during pregnancy.
According to Medilexicon's medical dictionary:
    Diabetes insipidus is "Chronic excretion of very large amounts of pale urine of low specific gravity, causing dehydration and extreme thirst; ordinarily results from inadequate output of pituitary antidiuretic hormone; the urine abnormalities may be mimicked as a result of excessive fluid intake, as in psychogenic polydipsia. Two types exist: central and nephrogenic. Autosomal dominant [MIM*125700, *125800, *192340], X-linked [MIM*304800 and *304900], and even autosomal recessive forms [MIM*222000] have been described."

What are the signs and symptoms of diabetes insipidus?

A symptom is something the patient senses and describes, while a sign is something other people, such as the doctor notice. For example, drowsiness may be a symptom while dilated pupils may be a sign.

The main signs and symptoms of diabetes insipidus include:
  • Extreme thirst - patients find themselves having to drink water all the time. The constant thirst and a dry feeling are persistent; even after consuming large quantities of water.
  • Polyuria - excretion of very large quantities of urine (diluted). Urine output can range from 2.5 liters (2.6 quarts) per day to 15 liters (16 quarts) per day, compared to about 1.5 to 2.5 liters per day in other adults without the condition.

    Patients may find that they need to pass pale, watery urine as often as every 15 to 20 minutes. This may make it very hard to be out of the house if there is no toilet nearby. In the UK patients may receive a toilet facility card which allows them to use toilets in non-public places.
The following signs and symptoms are also possible:
  • Nocturia - having to get up from sleep to urinate. Disrupted sleeping patterns can lead to fatigue (tiredness, irritability, and concentration problems.
  • Enuresis - bed-wetting
  • Feeling unwell - patients commonly feel run down for much of the time.
The following signs and symptoms may be present among young children with diabetes insipidus:
  • Cool hands and feet
  • Delayed growth (failure to thrive)
  • Diapers (UK: nappies) which are excessively wet
  • Diarrhea
  • Dry skin
  • Fever
  • Inconsolable crying
  • Unexplained fussiness
  • Vomiting
  • Weight loss (failure to thrive)
Anybody who has excessive thirst and urination should see their doctor as soon as possible.

What are the causes of diabetes insipidus?

Our kidneys remove excess body fluids from our bloodstream. This excess fluid waste is stored as urine in the bladder. If our body fluid levels drop due to, for example perspiration (sweating), our kidneys produce less urine in order to maintain a proper body fluid level balance.

Our fluid volume and composition remains balanced through a combination of fluid consumption and excretion in the kidneys. The amount we consume is mainly dictated by our thirst, even though individual habits may result in consuming more than we need. Our fluid excretion rate (through our kidneys) is influenced significantly by the production of ADH (anti-diuretic hormone), also known as vasopressin.

ADH is produced in the hypothalamus (a gland in the brain that also controls processes in the body, such as mood and appetite) and is stored in the pituitary gland (found just below the brain, behind the bridge of the nose). ADH is released into the bloodstream whenever it is needed. ADH also makes the kidney tubules reabsorb water back into the bloodstream - concentrating the urine.

Diabetes insipidus occurs when something goes wrong with this system and the body is unable to properly regulate body fluid levels. There are different types of diabetes insipidus:
  • Central diabetes insipidus (cranial diabetes insipidus) - usually caused by damage to the hypothalamus or the pituitary gland, often as a result of surgery, a tumor, meningitis, inflammation or a head injury, which disrupts ADH production, storage and release. Central diabetes insipidus that is caused by a head injury, or surgery to your pituitary gland, is sometimes only a temporary condition that lasts for just a couple of weeks. On some occasions the exact cause is never determined.
  • Nephrogenic diabetes insipidus - there is something wrong with the kidney tubules. The tubules cause fluids to be excreted or reabsorbed. Patients' kidneys do not respond properly to ADH. This may be caused by a congenital problem (inherited disorder) or some chronic (long-term) kidney disorder. Lithium, tetracycline and some other medications may also cause nephrogenic diabetes insipidus.
  • Gestational diabetes insipidus - occurs during pregnancy. An enzyme produced by the placenta may destroy AHD in the mother.

Diagnosing diabetes insipidus

A GP (general practitioner, primary care physician) will ask the patient about symptoms and recommend some tests. An endocrinologist - a doctor who specializes in hormone conditions - will carry out the tests.

Some of the signs and symptoms of diabetes insipidus are present in other conditions, including diabetes mellitus. If diabetes insipidus is diagnosed, the doctor will also have to determine which type it is, as treatment options will be different for each form of the disease. The following tests may be ordered:
  • Water deprivation test - the patient stops drinking liquids for two to three hours before starting the test so that the doctor may measure alterations in body weight, and urine output and composition. Sometimes blood levels of ADH may also be measured. If the patient has diabetes insipidus they will continue passing large amounts of diluted urine, compared to other people who would pass only a small amount of concentrated urine.

    This test also helps the doctor determine which form of diabetes insipidus the patient has. Pregnant women and children have to be monitored very closely during this test to make sure they do not lose more than 5% of body weight.
  • Urine test - a urinalysis examines the physical chemical content of urine. If urine water content is high and salt and waste concentrations are low, it may mean the patient has diabetes insipidus. If a large amount of sugar is found in the patient's urine, they may have diabetes mellitus rather than diabetes insipidus.
  • MRI (magnetic resonance imaging) scan - the doctor may wish to observe the pituitary gland or hypothalamus areas for any abnormalities. If any abnormality is found, such as a tumor, this will need to be treated first.
  • ADH (antidiuretic hormone) test - after the water deprivation test the doctor may give a small dose of ADH, usually in the form of an injection. This test shows how the patient reacts to the hormone, and can help determine which form of diabetes insipidus the patient has. If the ADH dosage stops the patient from producing urine, most likely their condition is caused by a shortage of ADH, and they will be diagnosed with central diabetes insipidus. If, on the other hand, the patient continues to produce excess urine despite the ADH dose, it probably means that the patient has nephrogenic diabetes insipidus (the kidneys are not responding to ADH).
The doctor may ask the patient whether any relatives have (had) excessive urination (polyuria). Genetic screening may be recommended if an inherited form of the disease is suspected.

What are the treatment options for diabetes insipidus?

Treatment depends on the type of diabetes insipidus the patient has.

Treatment for central (cranial) diabetes insipidus - if the patient's symptoms are mild; producing three to four liters of urine per 24-hour period, no medical treatment may be needed. In such mild cases the patient will be asked to increase their fluid intake in order prevent dehydration.

In more severe cases - when just consuming more water is not enough - the patient may be given desmopressin.
    Desmopressin - this is a man-made, more powerful version of ADH. Desmopressin, like ADH, stops the kidneys from producing urine when the body's water level is low. Desmopressin may be taken as a nasal spray or in tablet form. The nasal spray (Desmospray or DDAVP) is usually administered twice a day, while the tablets are taken more frequently. If the patient develops a cold or some condition which makes it more difficult to effectively use the nasal spray, they may have to switch to tablets.

    Desmopressin is safe to use and has very few side effects. If the patient takes too much desmopressin, or consumes too much water there is a risk the body may retain too much water, resulting in headaches, dizziness, a bloated feeling, and hyponatremia (excessively low levels of sodium in the blood). Hyponatremia can lead to drowsiness, confusion, and even coma. So, it is important to stay within the recommended desmopressin dosage, and to only drink fluids when thirsty.

    The patient will need to have follow-up checks to make sure blood sodium levels are OK.
Treatment for nephrogenic diabetes insipidus - if caused by taking lithium, tetracycline or some other medication, the doctor will recommend an alternative medication. It is important not to stop taking medications unless the doctor says so.

Desmopressin is not used for the treatment of nephrogenic diabetes insipidus. Patients will be encouraged to consume plenty of fluids.

If the condition is mild the doctor may recommend a diet which is very low in protein and salt, so that the kidneys produce less urine. Only embark on a new diet if the doctor tells you to.

In more severe cases that patient may be given a diuretic called hydrochlorothiazide. Although hydrochlorothiazide makes most people produce more urine, it has the opposite effect if the patient has nephrogenic diabetes insipidus.

Treatment for gestational diabetes insipidus - the patient is given desmopressin. In some very rare cases the gestational diabetes insipidus is caused by an abnormality in the thirst mechanism. In such cases the patient is not given desmopressin.

What are the possible complications of diabetes insipidus?

Complications may occur if the condition is either undiagnosed or not well controlled.

Dehydration - patients may find it more difficult to retain enough water in the body, resulting in dehydration. Dehydration may occur even if the patient drinks a lot of fluids. The following signs and symptoms may mean the patient with diabetes insipidus is dehydrated:
  • Dry mouth
  • Dry lips
  • Headaches
  • Confusion
  • Irritability
  • Dizziness
If the individual is very dehydrated it is better to consume re-hydration fluids, instead of just water. Rehydration fluids replace lost minerals, salts, sugars - as well as lost fluids. In very severe cases the patient may need to be hospitalized and given fluids through a drip into a vein (intravenously).

Electrolyte imbalance - diabetes insipidus can also cause an electrolyte imbalance. In our bodies, electrolytes include sodium (Na+), potassium (K+), calcium (Ca2+), bicarbonate (HCO3-, magnesium (Mg2+), chloride (C1-), hydrogen phosphate (HPO42-), and hydrogen carbonate (HCO3-). Electrolytes regulate our nerve and muscle function, our body's hydration, blood pH, blood pressure, the rebuilding of damaged tissue. Various mechanisms exist in our body that keep the concentrations of different electrolytes under strict control.

Our muscles and neurons are thought of as electric tissues of the body. They are activated by electrolyte activity between extracellular fluid or interstitial fluid, and intracellular fluid (fluid inside and outside or between cells).

A muscle contraction needs calcium (Ca2+), sodium (Na+) and potassium (K+) to be present. If levels of vital electrolytes are wrong, the muscles either become too weak, or their contractions are too severe. Our heart, muscle and nerve cells use electrolytes to maintain voltages across their cell membranes to carry electrical impulses across themselves and to other cells.

The level of an electrolyte in the blood can become too high or too low. Body electrolyte levels tend to change when water levels in the body change - when our level of hydration is altered.

An electrolyte imbalance can lead to several symptoms. The symptoms will depend on which electrolyte is out of balance, and whether that level is too high or low. An altered level of magnesium, sodium, potassium, or calcium may produce one or more of the following symptoms:
  • Weakness
  • Twitching
  • Seizures
  • Numbness
  • Nervous system disorders
  • Muscle spasm
  • Fatigue, lethargy
  • Irregular heartbeat
  • Convulsions
  • Confusion
  • Bone disorders
  • Blood pressure changes
An electrolyte imbalance is treated in the same was as dehydration, with fluids that contain electrolytes.
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What Is Infection? What Causes Infections?

A human with an infection has another organism inside them which gets its sustenance (nourishment) from that person, it colonizes that person and reproduces inside them. The human with that organism (germ) inside is called the host, while the germ or pathogen is referred to as a parasitic organism. Another name for an organism that causes infection is an infectious agent.

It is only an infection if the colonization harms the host. It uses the host to feed on and multiply at the expense of the host to such an extent that his/her health is affected. The normal growth of the bacterial flora in the intestine is not an infection, because the bacteria are not harming the host.

An organism which colonizes and harms a host's health is often called a pathogen. Examples include:
  • Parasites
  • Fungi
  • Bacteria
  • Prions
  • Viroids (plant pathogens, they affect the health of plants)
We all develop a wide range of infections, but fight them off rapidly. Some people, however, develop persistent, long-term (chronic) infections. The majority of chronic infections are caused by viruses, such as hepatitis or herpes. Chronic bacterial infections are more likely to affected patients with diabetes, as well as those with weakened immune systems.

Sometimes, if two organisms are present in the host together, they fight each other instead of the human body, and the levels of each colony remain balanced - their presence, together does not pose a problem for the host. An example could be some skin bacteria and yeast. Antibiotics may, in fact, upset the balance by destroying the good bacteria, allowing the other potential pathogen to multiply faster and cause health problems.

Viral infections

Infections caused by a virus. An individual may become infect by:
  • Inhaling the virus (breathing it in)
  • Being bitten by infected insects or parasites
  • Through sexual contact
Respiratory infections of the upper airways, nose and throat are the most common forms of viral infections.

Some antiviral medications may help, they either undermine the virus' ability to reproduce, or boost the patient's immune system.

Viruses are tiny organisms, much smaller than bacteria or fungi. The virus invades its host and attaches to a cell, entering it and releasing genetic material (DNA or RNA). This genetic material helps the virus multiply; it takes over control of the cell, making it replicate the virus. A cell that has this genetic material inserted into it cannot function properly and soon dies. When it does it releases new viruses, which infect new cells, etc.

Not all viruses destroy their host cell. Some of them just alter what the cell does. Experts say that some cells become cancerous as a result of a virus interfering with its functions.

Sometimes the genetic material lies dormant in a cell; some time in the future something triggers the cell and the virus starts multiplying again, making the host ill.

Viruses target specific cells in the body, such as those in the genitals or upper respiratory tract. Some target certain age groups, such as babies or young children, such as those that cause croup. The rabies virus targets the cells in the host's nervous system. Viruses may target skin cells and cause warts.

However, some viral infections can be systemic - they affect many different parts of the body, causing for example runny nose, sinus congestion, cough, and body aches. A viral infection that causes, for example viral conjunctivitis is local. Viral infections that cause pain, often trigger itching or burning.

Bacterial infections

Bacteria are tiny single-cell microorganisms, usually a few micrometers in length that normally exist together in millions - they are neither plants nor animals - they belong to a group all by themselves. A gram of soil typically contains about 40 million bacterial cells. A milliliter of fresh water usually holds about one million bacterial cells.

Planet Earth is estimated to hold at least 5 nonillion bacteria. Scientists say that much of Earth's biomass is made up of bacteria.
5 nonillion = 5,000,000,000,000,000,000,000,000,000,000 (or 5x1030).

Bacteria come in three main shapes:
  • Spherical (like a ball)
    These are usually the simplest ones. Bacteria shaped like this are called cocci (singular coccus).<.li>
  • Rod shaped
    These are known as bacilli (singular bacillus).
    Some of the rod-shaped bacteria are curved; these are known as vibrio. <.li>
  • Spiral
    These known are as spirilla (singular spirillus). If their coil is very tight they are known as spirochetes. <.li>
A bacterial cell differs somewhat from the cell of a plant or animal. Bacterial cells have no nucleus and other organelles (sub-units within a cell with a specific function) bound by a membrane, except for ribosomes. Bacteria have pili, flagella, and a cell capsule (most of them), unlike animal or plant cells. An organism without a nucleus is called a prokaryote.

Bacteria can live in virtually any kind of environment, from extremely hot to super cold, some even in radioactive waste. A number of bacteria live in our bodies, on our skin, airway, mouth, digestive and urinary tracts - most of the time without causing any harm to the host.

A relatively small number of bacteria causes diseases in humans. Some of the most deadly diseases and devastating epidemics in human history have been caused by bacteria, including:
  • Cholera
  • Diphtheria
  • Dysentery
  • Plague
  • Pneumonia
  • Tuberculosis
  • Typhoid
  • Typhus
Here is a list of infections and the names of the bacterium that commonly cause them (Source: Wikimedia Commons):
  • Brain (bacterial meningitis) - Streptococcus pneumoniae, Neisseria, meningitides, Haemuphilus influenzae, Streptococcus agalictaiae, Listeria monocytogenes.
  • Ear (otitis media ) - Streptococcus pneumoniae
  • Pneumonia
    Commonly acquired - Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus.
    Atypical - Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumophila
    Tuberculosis - Mycobacterium tuberculosis
  • Upper respiratory tract infection - Streptococcus pyogenes, Haemophilus influenzae
  • Gastritis (inflammation of the stomach) - Helicobacter pylori
  • Food poisoning - Campylobacter jejuni, Salmonella, Shigella, Clostridium, Staphylococcus aureus, Escherichia coli
  • Eye infections - Staphylococcus aureus, Neisseria gonorrheae, Chlamydia trachomatis
  • Sinusitis - Streptococcus pneumoniae, Haemophilus influenzae
  • Urinary tract infections - Escherichia coli, other Enterobacteriaceae, Staphylococcus saprophyticus, Pseudomonas aeruginosa
  • Skin infections - Staphylococcus aureus, Streptococcus pyogenes, Pseudomonas aeruginosa
  • STDs (sexually transmitted diseases) - Chlamydia trahomatis, Neisseria gonorrhoeae, treponema pallidum, Ureaplasma urealyticum, Haemophilus ducreyi
Bacterial infections typically present with localized redness and heat, inflammation (swelling) and pain. Bacterial infections tend to present localized pain more frequently than viral infections (not always). Even with a throat infection, a bacterial one will usually have more severe pain on one side of the throat. If there is pain in just one ear, it is more likely to be a bacterial infection.

Mycosis (fungal infection/disease)

Mycosis is a fungal infection in or on a part of the body, or a disease caused by a fungus. Some fungi reproduce through very small airborne spores which people either inhale or pick up on their skin - i.e. must fungal infections start in the lungs or the skin.

Patients on long-term strong antibiotics are at higher-than-normal risk of developing a fungal infection. Strong antibiotics can eventually reduce the population of good bacteria which help maintain the balance of microorganisms in the intestines, mouth, vagina and other parts of the body. If enough of these good bacteria are destroyed, the fungi have an opportunity to grow and cause health problems for the host.

Patients with weakened immune systems, such as those with HIV/AIDS and individuals receiving chemotherapy have a higher risk of developing a fungal infection. Diabetes patients, especially those who do not have good disease control are also more susceptible.

There are three types of fungal infections of the skin:
  • Superficial mycoses - limited to the surface of the skin and hair, such as Tinea versicolor, which commonly affects young people. The chest, back, upper arms or legs may be affected (very rarely the face). Light or reddish-brown spots appear on the skin. Sometimes the spots are not visible.
  • Cutaneous mycoses - occurs deeper in the skin, in the epidermis. The hair and nails may also be affected. Cutaneous mycoses are limited to the keratinized layers of skin, nails and hair. This type of mycosis is caused by dermatophytes (a group of three types of fungus that commonly causes skin disease in animals and humans), which may cause ringworm. Examples of dermatophytes are Microsporum, Trichophyton, and Epidermophyton fungi. Athlete's foot is another example of cutaneous micosis.
  • Subcutaneous mycoses - these types of infections go deeper into the skin, including the dermis, subcutaneous tissue, as well as muscle and fascia. The fascia is a band of tissue below the skin that covers underlying tissues - it separates different tissue layers and surrounds muscles. Subcutaneous mycoses tend to be long term (chronic) and are usually caused by skin penetration.
Systemic mycoses due to primary or opportunistic pathogens - a primary pathogen causes disease because of its very presence in a healthy human, while an opportunistic pathogen causes disease in a host (human) with a weakened immune system. Systemic means the entire body is affected.

Systemic mycoses due to primary pathogens tend to originate in the lungs, and then spread to other parts of the body; they are usually virulent (potent).

Candidiasis (thrush) is an example of systemic mycoses due to opportunistic pathogens; in other words, a patient is more likely to get thrush when their defenses (immune system) are down.

Prion disease

A prion is an infectious agent consisting mainly of protein - it contains no genetic material. It is neither bacterial nor fungal. It occurs normally in a harmless form, but when it folds into an abnormal shape it turns into a rogue agent and affects the structure of the brain or other parts of the nervous system. All forms of prion infections are currently untreatable and fatal.

Prions cause degenerative brain diseases, such as mad cow disease, CJD (Creutzfeldt-Jacob disease), kuru, fatal familial insomnia, and scrapie. Experts also link some cases of Alzheimer's disease to prion infection.

Prion diseases, also called transmissible spongiform encephalopathies, are brain wasting diseases that affect humans and animals. Made primarily of protein, prions are small active agents that act a bit like viruses: they don't replicate themselves but hijack material in the host and cause it to behave abnormally, for instance they force host proteins to fold into shapes that clump together into plaques that clog up the brain, causing it gradually to waste away.

A team of scientists from the US and the UK have found a new type of prion disease in mice that damages brain arteries and may help us better understand and treat types of Alzheimer's disease that cause similar damage.

Worldwide deaths from infectious diseases

Source: World Health Organization (WHO)
  • Lower respiratory infections
    Deaths 2002 - 3.9 million
    Percentage of all deaths - 6.9% 4.1 million
    Deaths 2002 - 2.8 million
    Percentage of all deaths - 4.9%
  • Diarrheal diseases
    Deaths 2002 - 1.8 million
    Percentage of all deaths - 3.2%
  • Tuberculosis (TB)
    Deaths 2002 - 1.6 million
    Percentage of all deaths - 2.7%
  • Malaria
    Deaths 2002 - 1.3 million
    Percentage of all deaths - 2.2%
  • Measles
    Deaths 2002 - 0.6 million
    Percentage of all deaths - 1.1%
  • Pertussis (whooping cough)
    Deaths 2002 - 0.29 million
    Percentage of all deaths - 0.5%
  • Tetanus
    Deaths 2002 - 0.21 million
    Percentage of all deaths - 0.4%
  • Meningitis
    Deaths 2002 - 0.17 million
    Percentage of all deaths - 0.3%
  • Syphilis
    Deaths 2002 - 0.16 million
    Percentage of all deaths - 0.3%
  • Hepatitis B
    Deaths 2002 - 0.10 million
    Percentage of all deaths - 0.2%
  • Tropical diseases
    Deaths 2002 - 0.13 million
    Percentage of all deaths - 0.2%
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Cancer Is Probably Man Made Caused By Pollution And Diet

Why was cancer detected in only one in a few hundred Egyptian mummies? Why is there such scarce reference to cancer in ancient Greek or Egyptian texts? A study carried out by researchers from the University of Manchester, England and published in Nature suggests that cancer, especially cancer among children and young adults is not simply due to our living longer these days - it must be a man-made disease. The scientists say theirs is "the first histological diagnosis of cancer in an Egyptian mummy".

Investigators at Manchester University's KNH Centre for Biomedical Egyptology say their study proves that during the Egyptian mummies' time, cancer was extremely rare. After investigating hundreds of mummies, they came across just one case of cancer - worldwide only two cases have ever been detected. Incidence of cancer, especially childhood cancer exploded after the Industrial Revolution.

Professor Rosalie David, at Manchester University's Faculty of Life Sciences, said:

In industrialized societies, cancer is second only to cardiovascular disease as a cause of death. But in ancient times, it was extremely rare. There is nothing in the natural environment that can cause cancer. So it has to be a man-made disease, down to pollution and changes to our diet and lifestyle.

The important thing about our study is that it gives a historical perspective to this disease. We can make very clear statements on the cancer rates in societies because we have a full overview. We have looked at millennia, not one hundred years, and have masses of data.

Professor Michael Zimmerman, a visiting professor at the KNH Centre, made the first ever histological diagnosis of cancer in an Egyptian mummy. The mummy was said to be an ordinary person, from the Ptolemaic period.

Zimmerman said:

In an ancient society lacking surgical intervention, evidence of cancer should remain in all cases. The virtual absence of malignancies in mummies must be interpreted as indicating their rarity in antiquity, indicating that cancer causing factors are limited to societies affected by modern industrialization.

The investigators examined literary evidence from ancient Greece and Egypt, as well as mummified remains from ancient Egypt. They also carried out medical examinations of animal and human remains further back in history, as far back as the period of the dinosaurs.

They found that:
  • According to animal, non-human primates, and early human remains and fossil evidence, cancer was extremely uncommon. One Edmontosaurus fossil of unknown primary origin had evidence of metastatic cancer.
  • Virtually all evidence of tumors, which were extremely uncommon anyway, were benign.
  • The few malignancies were found were in non-human primates, but none of them are cancers found in modern adult humans.
Atherosclerosis, Paget's disease of bone, and osteoporosis did exist in ancient Greece and Egypt - diseases that affect humans when they are older; old enough to develop common modern cancers. If humans at that time lived long enough to develop those diseases, the extreme rarity of cancer cannot be put down to very short life spans. People in those days lived long enough to develop the cancer adults develop today. Also, there is no evidence of any childhood cancers in ancient Greece or Egypt. Cancer among children is definitely much more common today than it was in ancient Greece/Egypt.

Some people have suggested that tumors do not preserve well, so evidence of them disappears over time. However, Zimmerman says mummification preservers malignancy features; in fact, it preserves tumors much better than normal tissue.

Of all the hundreds of mummies examined all over the world, just two have microscopic evidence of cancer. Radiologists have examined all the mummies at museums in Cairo and Europe and found no evidence of cancer at all.

Evidence of cancer and medical procedures, such as operations for cancers does not appear until the 17th century, the researchers reveal. Scientific literature depicting distinctive tumors have only been about for the last 200 years, when data started to be documented about chimney sweeps with scrotal cancer in 1775, nasal cancer in snuff users in 1761, and Hodgkin's disease in 1832.

Professor David said:

Where there are cases of cancer in ancient Egyptian remains, we are not sure what caused them. They did heat their homes with fires, which gave off smoke, and temples burned incense, but sometimes illnesses are just thrown up.

The ancient Egyptian data offers both physical and literary evidence, giving a unique opportunity to look at the diseases they had and the treatments they tried. They were the fathers of pharmacology so some treatments did work.

They were very inventive and some treatments thought of as magical were genuine therapeutic remedies. For example, celery was used to treat rheumatism back then and is being investigated today. Their surgery and the binding of fractures were excellent because they knew their anatomy: there was no taboo on working with human bodies because of mummification. They were very hands on and it gave them a different mindset to working with bodies than the Greeks, who had to come to Alexandria to study medicine.

(Conclusion) Yet again extensive ancient Egyptian data, along with other data from across the millennia, has given modern society a clear message - cancer is man-made and something that we can and should address.
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What Is Ventricular Fibrillation? What Causes Ventricular Fibrillation?

Ventricular fibrillation is an abnormally irregular heart rhythm caused by rapid, uncoordinated fluttering contractions of the ventricles - the lower chambers of the heart. These fluttering replace normal contractions. Ventricular fibrillation puts the heartbeat and pulse beat out of synch.

The pumping chambers in the ventricles quiver uselessly, instead of pumping blood, resulting in a serious drop in blood pressure, and the cutting off of oxygen-rich blood to body organs.

Ventricular fibrillation is a life-threatening medical emergency. It is most commonly linked to heart attacks or scarring of the heart muscle from previous heart attack. A patient with ventricular fibrillation generally collapses within seconds - and it won't be long before his/her breathing or pulse stops.

What is the difference between ventricular fibrillation and atrial fibrillation?

The human heart has two upper chambers and two lower chambers. The upper chambers are called the left atrium and the right atrium - the plural of atrium is atria. The two lower chambers are the left ventricle and the right ventricle. When the two upper chambers - the atria - contract at an excessively high rate, and in an irregular way, the patient has atrial fibrillation. When the two lower chambers beat irregularly and flutter, the patient has ventricular fibrillation.

Put simply - atrial fibrillation refers to the two upper heart chambers while ventricular fibrillation refers to the two lower heart chambers; in either case there abnormally irregular rhythm.

Ventricular fibrillation is more serious than atrial fibrillation. Ventricular fibrillation frequently results in loss of consciousness and death, because ventricular arrhythmias are more likely to interrupt the pumping of blood, or undermine the heart's ability to supply the body with oxygen-rich blood.

Sudden cardiac death (SCD) accounts for about 300,000 deaths annually in the USA, of which 75% to 80% are due to ventricular fibrillation, according to the NIH (National Institutes of Health). The NIH adds that more deaths are attributable to ventricular fibrillation than to breast, cancer, AIDS or lung cancer.

Ventricular fibrillation is typically the first expression of coronary artery disease (CAD) and is responsible for approximately 50% of deaths from CAD.

According to Medilexicon's medical dictionary:

Ventricular fibrillation is "coarse or fine, rapid, fibrillary movements of the ventricular muscle that replace the normal contraction."

What are the signs and symptoms of ventricular fibrillation?

A symptom is something the patient senses and describes, while a sign is something other people, such as the doctor notice. For example, drowsiness may be a symptom while dilated pupils may be a sign.

The most common sign of ventricular fibrillation is:
    Sudden collapse, loss of consciousness or fainting; because the brain and muscles have stopped receiving blood from the heart.
Early ventricular fibrillation signs and symptoms - approximately an hour before the heart goes into ventricular fibrillation and the patient faints, the following may be experienced:
  • Dizziness
  • Nausea
  • Pain in the chest
  • Tachycardia - accelerated heartbeat, palpitations

What are the risk factors for ventricular fibrillation?

A risk factor is something which increases the likelihood of developing a condition or disease. For example, obesity significantly raises the risk of developing diabetes type 2. Therefore, obesity is a risk factor for diabetes type 2.

The following risk factors are linked to ventricular fibrillation:
  • Having had ventricular fibrillation before
  • A previous heart attack
  • Cardiomyopathy - disease of the heart muscle (myocardium)
  • Cocaine and/or methamphetamine use
  • Congenital heart disease - being born with a heart defect
  • Electrocution or other injuries that resulted in heart muscle damage

What are the causes of ventricular fibrillation?

When the human heart beats, electrical impulses that trigger a contraction need to follow a specific route (pathway) to the heart. If there is something wrong with the path of these impulses, i.e. if there is an interruption to these impulses, arrhythmia (irregular heartbeat) may occur.

The heart is divided into four hollow chambers - the upper chambers are called the atria (singular: atrium) and the lower chambers are called the ventricles. The walls of the atria and ventricles are made virtually of 100% pure muscle. A heartbeat is caused by the tightening of these muscles. When the muscles tighten the chambers squeeze closed and push out the blood which is inside them.

During a heartbeat the muscular atria (the smaller chambers) contract and fill the relaxed ventricles with blood. The contraction begins when the sinus node (small group of cells in the right atrium) emits an electrical impulse which makes the right and left atria contract.

The electrical impulse continues to the center of the heart, to the atrioventricular node. This node is located on the pathway between the atria and the ventricles. From the atrioventricular node the impulse travels through the ventricles, making them contract, resulting in blood being pumped out of the heart and into the body.

How does ventricular fibrillation start? In the majority of cases ventricular tachycardia occurs. Ventricular tachycardia is an abnormally rapid heart rhythm that originates from a ventricle. It is caused by abnormal electrical impulses that travel around a scar which developed from a previous heart attack. Ventricular tachycardia occurs in patients with some kind of heart defect.

Ventricular tachycardia can occur and then go away about 30 seconds later and cause no symptoms - this is known as non-sustained ventricular tachycardia. If it continues for more than about 30 seconds it will generally cause palpitations, dizziness and/or loss of consciousness. If left untreated, ventricular tachycardia can lead to ventricular fibrillation.

Ventricular fibrillation is when the ventricles quiver uselessly, pumping virtually no blood into the body - this is caused by disordered electrical impulses. The heart ends up without an effective heartbeat; blood stops flowing around the body and vital organs, including the brain lose their much needed blood supply.

A patient with ventricular fibrillation will typically lose consciousness very quickly and will require immediate, emergency medical assistance, including CPR (cardiopulmonary resuscitation). If CPR is delivered until the heart can be shocked back into a normal rhythm with a defibrillator, the patient's chance of survival are much better.

Diagnosing ventricular fibrillation

Diagnosis of ventricular fibrillation is usually done in emergency circumstances, because most likely the patient has lost consciousness. The following diagnostic checks can confirm ventricular fibrillation:
  • A heart monitor - this device reads the electrical impulses that cause the heart to beat and will detect either no heart beat or an erratic one.
  • Checking the pulse - the pulse will be difficult to detect, it may either be very weak or not there at all.
Diagnostic tests to find out what caused the ventricular fibrillation:
  • ECG (electrocardiogram) - a medical device that monitors the electrical activity of the heart muscles. Our hearts produce a small electric signal at every beat. A heart specialist (cardiologist) can use this device to see how well the heart is functioning, whether there is any damage to the heart muscle, or abnormalities with the heart rhythm. A doctor can tell, when checking the data coming from the ECG, whether the patient has had a heart attack recently, or even earlier. Heart attack is a common cause of ventricular fibrillation.
  • Cardiac enzyme test - when a person has a heart attack some enzymes make their way into the bloodstream. A blood test can detect these enzymes. Usually, enzyme blood levels are checked regularly over a few days.
  • Chest X-ray - this can be useful to see if the heart has any swelling, or if there is anything unusual with the heart's blood vessels.
  • Nuclear scan - can detect blood flow problems to the heart. Thallium, or some other radioactive material is injected into the bloodstream. The radioactive material is detected by special cameras as it flows through the lungs and heart. This test can detect where areas of reduced blood flow to the muscles are.
  • Echocardiogram - This is a type of ultrasound test that utilizes high-pitched sound waves that are sent through a transducer - a wand-like device that is held on the chest. The transducer picks up echoes of the sound waves as they bounce off different parts of the patient's heart. The data is presented on a video screen where the doctor can see the heart as it moves. This test can help a doctor identify underlying structural heart disease.
  • Angiogram (coronary catheterization) - a catheter (thin, flexible tube) is introduced into a blood vessel until it goes through the aorta into the patient's coronary arteries. The catheter usually enters the body at the groin or arm. A dye is injected through the catheter into the arteries. This dye stands out on images created by an X-ray and helps doctors detect coronary artery disease (arteries to the heart that have narrowed).
  • Cardiac MRI (magnetic resonance imaging) or CT (computed tomography) scan - they can measure ejection fraction as well as the heart arteries and valves. They can also determine whether the patient had a heart attack. These scans are also useful in seeking out unusual heart failure causes.

What are the treatment options for ventricular fibrillation?

In emergency treatment, focus is on restoring blood flow to organs throughout the body, including the brain - in other words, restoring blood flow as soon as possible. When this is done, the patient may receive treatment to prevent or minimize a recurrence.

Emergency treatments may, and will probably include:
  • CPR (cardiopulmonary resuscitation) - can restore blood flow through the body. CPR can be done by anybody with some basic life support training.

    Manual chest compressions and mouth-to-mouth

    • 30 chest compressions to the heart
    • and then
    • Two mouth-to-mouth resuscitation breaths (mouth-to-mouth)
    Mouth-to-mouth not necessary

    Most health care professionals these days say that breathing into the person's mouth is not necessary. The patient should receive about two compressions per second, or between 100 and 120 per minute - the chest should be allowed to rise back between compressions. This should be continued until either emergency personnel arrive or somebody comes with a portable defibrillator.
  • Defibrillator - This is a CPS medical device. It sends electric shocks across the patient's chest - the aim is to use electricity to shock the heart back into proper activity. Initially, the electric shock stops the heart momentarily - but it also stops the chaotic heart rhythm, which usually restores normal heart rhythm.

    A public-use defibrillator can be used by a lay person. These devices often have voice instructions on their use. A public-use defibrillator is programmed to detect ventricular fibrillation and emit a shock at the right moment. In most countries, especially industrialized nations, public-use (portable) defibrillators will be available in public places, such as airports, major train and bus stations, shopping malls, community centers, places where elderly people gather, casinos, etc.
Preventing ventricular fibrillation from occurring again

If a physician determines that the ventricular was cause by scarred tissue from a heart attack, or some structural defect in the heart, medications and medical procedures may be recommended to minimize the risk of recurrence. The following may be recommended:
  • Medications:

    • Beta blockers are commonly used to prevent sudden cardiac arrest or ventricular fibrillation. These drugs make the heart beat more slowly and with less force, thus easing the heart's workload. They also stabilize the heart's electrical activity. Examples include metoprolol, propranolol, timolol, and atenolol.
    • ACE (angiotensin-converting enzyme) inhibitors - these drugs help ease the workload on the heart by opening up blood vessels and lowering blood pressure. Experts say ACE inhibitors also protect the heart from further damage. Patient will have a blood test to make sure their kidneys are working properly before starting on this type of medication. Then, about ten days after starting treatment, the patient will undergo further tests to make sure his/her kidneys are still working fine. Over a period of about 3 weeks the patient's dose is gradually increased. Examples of ACE inhibitors include lisinopril, perindopril and ramipril.
    • Amiodarone (Cordarone) or calcium channel blockers may also be prescribed.
  • ICD (implantable cardioverter-defibrillator) - this device is placed inside the body. It is designed to recognize certain types of arrhythmias (abnormal heart rhythms) and correct them by emitting electric shocks to reset the heart to a normal rhythm.
  • Coronary angioplasty - this surgical procedure is sometimes necessary in severe cases of coronary artery disease. Angioplasty opens up the coronary artery. A small wire goes up the artery from the patient's groin or arm and is pushed until it reaches where the clot is in the coronary artery. There is a small balloon, shaped like a sausage, at the end of the wire. The balloon is placed at the narrowest part of the artery and is then inflated, squashing the clot away. A flexible metal mesh, called a stent, is then placed there to keep that part of the artery open.
  • CABG (Coronary artery bypass graft) - the damaged blood vessel is by-passed with grafts taken from blood vessels elsewhere in the body. The bypass effectively goes around the blocked area of the artery, allowing blood to pass through into the heart muscle. If blood supply to the heart is improved, the risk of ventricular fibrillation goes down.
  • Ventricular tachycardia ablation - catheters are inserted through a vein, usually in the groin and threaded to the heart, to correct structural heart problems that cause an arrhythmia. The aim is to clear the signal pathway (of electrical impulses) so that the heart may beat normally again. Put simply, tissue that blocks the electrical signal is either destroyed or scarred.
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West Nile Virus Positive Mosquitoes Identified In 20 Connecticut Towns

Twenty Connecticut towns are reported to have West Nile Virus positive mosquitoes, Department of Public Health Commissioner Dr. J. Robert Galvin informs. Connecticut's Mosquito Management Program announced that a resident of Clinton recently tested positive for WNV (West Nile Virus) and has been admitted to hospital.

The elderly resident showed symptoms of fever, severe headache, weakness and fatigue during the first month of September and is in hospital for meningitis. Laboratory tests confirmed the presence of WNV antibodies.

Six people have been reported with WNV infection in the state so far this year, the other five are from Bridgeport, Greenwich, New Haven, Stamford and Trumbull. Health authorities say two more individuals who travelled out of state also became infected.

Dr. Galvin said:

West Nile virus can cause serious illness, especially in people over 50. In Connecticut, this is the time of year when the risk of getting sick from West Nile virus is the greatest. West Nile virus is transmitted by mosquitoes, and simple things like wearing long-sleeved shirts, using insect repellant, and minimizing time outside at dusk and dawn when mosquitoes are most active can help you reduce your risk of getting this virus.

The 20 towns where WNV-positive mosquitoes have been identified include Bethel, Bridgeport, Darien, Fairfield, Greenwich, Manchester, Meriden, Milford, Newtown, Norwalk, New Britain, New Haven, Orange, Stamford, Stratford, Trumbull, Wallingford, West Haven, Westport and Wethersfield.

Dr. Theodore G. Andreadis, Ph.D., Chief Medical Entomologist, The Connecticut Agricultural Experiment Station, said:

Although cooler weather is expected which should slow virus build-up, we continue to repeatedly identify infected mosquitoes throughout central and southern regions of the state. We anticipate that virus activity will continue for several more weeks.

The Connecticut Agricultural Experiment Station says it has a network of 91 mosquito-trapping stations in 72 municipalities throughout the state, operating from June till the end of October. The traps are set every ten days at each site on a rotating basis. The mosquitoes are pooled according to collection site, date and species. Each pool is tested for West Nile Virus and eastern equine encephalitis viruses.

What is West Nile Virus?

West Nile Virus, or WNV, is a virus of the Flaviviridae family which is spread by the bite of an infected mosquito. The Flaviviridae virus family also includes dengue fever, Japanese encephalitis, and yellow fever.

WNV affects birds mainly, but horses, dogs, cats, bats, skunks, squirrels, chipmunks and domestic rabbits may also become infected, as well as humans.

In most cases, an infected human either has no signs or symptoms at all, or just a skin rash and headache. About 1% of infected individuals, unfortunately, develop complications such as encephalitis (inflammation of the brain), myelitis (inflammation of the spinal cord), or meningitis (inflammation of tissues surrounding the brain and spinal cord), which are potentially life-threatening.

People with weakened immune systems as well as elderly individuals have a higher risk of developing complications.

West Nile Virus (WNV) is found in both tropical and temperate regions. WNV outbreaks occur in Egypt, Israel, Pakistan, France, the northern Mediterranean and some parts of Eastern Europe. In 1996 there was a major outbreak in Budapest, Hungary. In 1999 it appeared in New York and has since been found in all 48 US contiguous states. More recently it has been found in Canada, Mexico, Central America and the West Indies.

According to the National Health Service (NHS), UK, the WNV spread in mainland Europe and North America has made many experts fear that it is only a question of time before it reaches the United Kingdom. So far, there has only been one reported case in the UK - a tourist who arrived home after becoming infected while on vacation in Portugal.

People in areas known to have infected mosquitoes can reduce their risk of infection by using mosquito repellent, wearing clothing that covers most of their skin, and taking some other preventive measures.

According to the CDC (Centers for Disease Control and Prevention), USA, over 15,000 people in the United States have tested positive for WNV since 1999 - over 500 of them have died. Authorities say the real number of infected people is much higher, because those with either no symptoms or very mild ones would not have sought medical help.

A bird-mosquito life cycle maintains West Nile virus in the environment. According to the U.S. Geological Survey's National Wildlife Health Center, American crows (Corvus brachyrhynchos) and other corvids (e.g., blue jays) seem more susceptible to fatal infection - nobody knows why. The death of these birds has allowed many local health departments to utilize dead birds as an indicator of the virus emergence or re-emergence in their areas.
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What Is Triple X Syndrome? What Causes Triple X Syndrome?

Triple X syndrome, also known as Trisomy X, 47,XXX aneuploidy, and Triplo-X, XXX Syndrome is a chromosomal abnormality that affects approximately 1 in every 1,000 females. A healthy female has two X chromosomes, one from her father and one from her mother. A female with triple-X syndrome has three X chromosomes.

According to the NIH (National Institutes of Health), USA, 5 to 10 girls with triple X syndrome are born in the USA each day.

A female with triple-X syndrome does not inherit it from her parents. The syndrome generally results from a mistake in the formation of the father's sperm cell or the mother's egg. In some cases triple-X syndrome may be the result of something that went wrong in the development of the embryo.

A girl with triple X syndrome may either have no symptoms, just mild ones, or more severe ones with developmental delays. Developmental delays may include learning disabilities, delayed development of speech and language skills, as well as motor skills. There may be behavioral and emotional difficulties. Approximately 10% of affected females have seizures or kidney abnormalities. Among those who do have symptoms, they will vary widely from person-to-person.

Triple X syndrome treatment varies and depends on which symptoms are present, and how severe they are.

Unlike the majority of other chromosomal conditions, there is usually no clear visual difference between a female with triple X syndrome and other females. Some females with triple X syndrome may be taller than average. Most individuals with the syndrome have normal sexual development and can conceive children. Infertility is possible in some cases, but it is rare.

Most medical professionals do not regard the condition a disability.

According to Medilexicon's medical dictionary:

Triple X Syndrome is "trisomy of the X chromosome; original observations (made in mental institutions) were seriously biased and the phenotypic changes spurious. Intelligence may be at the lower range of normal, stature is usually tall, there may be speech and behavioral problems. The outstanding feature of the syndrome is the occurrence of twin Barr bodies in a typical cell."

What are the signs and symptoms of triple X syndrome?

A symptom is something the patient senses and describes, while a sign is something other people, such as the doctor notice. For example, drowsiness may be a symptom while dilated pupils may be a sign.

In all female cells, only one X chromosome is active at any time. Consequently, triple X syndrome generally does not cause unusual physical features or medical problems. In other words, in the majority of cases there are no signs or symptoms. If symptoms do occur, they may include:
  • If physical features are present they will be very mild:

    • Tall stature
    • Microcephaly (small head)
    • Epicanthal folds - a vertical fold of skin that comes down across the inner angle of the eye.
    • Increased width between the eyes
  • Delayed language skill development
  • Delayed motor skill development, resulting in poor coordination, awkwardness, and/or clumsiness.
  • In very rare cases, infertility
  • Some may have menstrual irregularities
  • Some may experience an early onset of menstruation
If signs and symptoms are present, they will vary a lot between individuals.

What are the causes of triple X syndrome?

What are genes, chromosomes and DNA?

Anything that lives has genes. Genes are a set of instructions that decide what the organism is like, how it survives, and how it behaves in its environment. The genes lie in long strands of DNA (deoxyribonucleic acid) called chromosomes. Humans have 23 pairs of chromosomes - or a total of 46. A donkey has 31 pairs of chromosomes, a hedgehog has 44, and a fruit fly has just 4. An enormous number of genes lie in each chromosome strand. Scientists say that a chromosome is a single piece of DNA which has many genes, regulatory elements and other nucleotide sequences (sequences of the letters ACGT).

A chromosome consists of DNA and has proteins attached to it. These chromosomes are located in your body's cells, which then contain this important genetic information held in the long strands of DNA.

Your genes decide virtually everything about you. Your genes decide whether you are tall or not, the color of your hair, the color of your skin, whether you are more likely to develop certain diseases, whether you are good at sports, how you respond to environmental triggers, what you look like inside and out, and what sex you are.

Chromosomes that determine our sex

One of the 23 chromosome pairs that humans have determine our sex. We receive:
  • One sex chromosome from our mother, whose chromosome pair is XX. Females have an XX pair. A mother can only pass on an X chromosome.
  • One sex chromosome from our father, whose chromosome pair is XY. Males have an XY pair. A father can pass on either an X or a Y chromosome.
If an offspring receives an X chromosome from the father she will be female - because the mother will pass on an X chromosome, giving the offspring an XX chromosome pair; making her female. If the father passes on a Y chromosome, the offspring will have an XY chromosome pair, making him a male.

Individuals with triple X syndrome have an extra X chromosome, on top of the XX pair - in other words, they are females (XX) with an extra X chromosome (XXX).

Experts say this occurs because either:
  • The mother's egg was not formed properly (nondisjunction)
  • The father's sperm was not formed properly (nondisjunction)
  • Something went wrong during the development of the embryo (mosaic form of triple X syndrome)
Triple X syndrome is not an inherited condition.

The presence or severity of symptoms depends partly on how many body cells have the extra X chromosome. If the syndrome is caused by a badly formed egg or sperm every cell in the body has that extra chromosome. In the mosaic form of triple X syndrome only a number of body cells have the extra chromosome. Most cases of triple X syndrome are caused by a malformed egg or sperm.

Triple X syndrome is sometimes called 47, XXX syndrome because the extra chromosome gives that human 47 chromosomes (instead of the usual 46).

Diagnosing triple X syndrome

Triple X syndrome is diagnosed before the baby is born, through CVS (chorionic villus sampling) or amniocentesis, and a blood test after she is born.
  • CVS (chorionic villus sampling) - tissue is taken from the villi (vascular fingers) of part of the placenta (chorion) and examined. It is usually done between the 8th and 10th week of pregnancy, usually to diagnose severe abnormalities afflicting the fetus (unrelated to triple X syndrome).
  • Amniocentesis - also known as an amnio. Done during pregnancy in which some amniotic fluid is collected and diagnosed for a genetic or some other condition. The fetus/embryo floats in amniotic fluid.
  • Blood test - a chromosome analysis is done if the doctor notices unusual physical features of delays in development.
All three tests can look at the person's Karotype (collection of chromosomes).

There is no routine screening for triple X syndrome. If an embryo/fetus is found to have the syndrome, it is usually after screening for something else.

What are the treatment options for triple X syndrome?

It is not possible to remove the extra X chromosome. Treatment will depend on the needs of the girl. The patient may have been seen by physical, developmental, occupational or speech therapists if developmental or speech problems have occurred. If there are social problems she may have also been seen by a pediatric psychologist.

Treatment for developmental or psychological symptoms will be the same as for any child with such problems. If she has a learning disability she should receive the same counseling and support as anybody else with that type of learning disability.

A supportive environment is crucial, especially for girls with triple X syndrome who may be more susceptible to stress.

A girl with triple X syndrome who receives proper help and support can lead a full and normal life.

What are the possible complications of triple X syndrome?

If the girl has developmental delays, motor skill delays and difficulties, and does not get proper and prompt help and support, she may suffer from undue stress and anxiety which may eventually lead to psychological problems and social isolation.

The right help and support is extremely helpful for a girl with triple X syndrome who has symptoms.
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What Is Discoid Eczema (Nummular Dermatitis)? What Causes Discoid Eczema?

Discoid eczema, also known as discoid dermatitis, gravitational eczema, nummular dermatitis, and nummular eczema is a form of dermatitis. It is a chronic (long-term) or recurrent condition. A rash appears on the skin in the form of red coin shaped discs - plaques of eczema - which can affect different parts of the body, but primarily the lower legs, hands and forearms, and sometimes the trunk. It is extremely itchy and uncomfortable. Dermatitis means "inflammation of the skin".

The round or oval plaques, made of tiny raised red spots and scaling on a red base, have well defined edges. Affected areas of skin can range in size from just a few millimeters to a few centimeters.

Discoid eczema is not contagious - you cannot catch it by touching an affected person, or being near him/her. Experts say there is no link between food allergies and the condition. It is solely a dermatological (skin) condition; no other systems are affected. Although infection is common, it is secondary and not causative. People with discoid eczema are at risk of developing other forms of dermatitis.

It is also known as nummular eczema because of the Latin word nummus, meaning "coin".

Symptoms of discoid eczema are more frequently reported to doctors during the winter months, when indoor humidity levels are lower. Although discoid eczema symptoms can occur at any age, they are more commonly seen in males in their 60s and 70s. There is also a lesser peak during the teen years to mid 20s. Discoid eczema is extremely rare in children.

According to the National Health Service (NHS), UK, approximately 2 in every 1,000 people are affected.

According to Medilexicon's medical dictionary, Nummular eczema is "discrete, coin-shaped patches of eczema".

What are the signs and symptoms of discord eczema?

A symptom is something the patient senses and describes, while a sign is something other people, such as the doctor notice. For example, drowsiness may be a symptom while dilated pupils may be a sign.
  • The affected areas are red and have well-defined edges.
  • On top of the coin-shaped plaques there may be small blisters, scales or yellowish crusts - often a sign of a staphylococcal (bacterial) infection.
  • Typically, the affected areas are symmetrical, especially on the limbs.
  • The lesions (affected areas) are extremely itchy, often resulting in lichenification (see next line).
  • Lichenification - constant scratching and rubbing leads to thick, leathery skin. Prolonged scratching and rubbing causes the epidermis (outer layer of skin) to become overgrown (hypertrophied). The skin thickens and there are exaggerated skin markings; giving the skin an appearance like leathery bark.
  • Apart from itching, affected areas may also burn or sting.
  • Itching tends to be worse at night.
  • Symptoms most commonly appear on the legs, but may also do so on the arms, trunk, hands or feet. The face and scalp are not affected.
Put simply - discoid eczema generally starts off as round/oval plaques of very small red spots and blisters. They are red, oozy and crusty. The plaques eventually dry and become scalier, sometimes with a clear middle.

Signs and symptoms may be confused for ringworm infection (a type of fungal infection) or contact eczema.

What are the causes of discoid eczema?

We do not know what causes discoid eczema. We know that it can be triggered by:
  • An insect bite
  • A burn
  • Some other minor skin injury
  • Administration of interferon or ribavirin for hepatitis C treatment
We also know that:
  • Discoid eczema is not usually linked to an allergy
  • People with discoid eczema often also have atopic eczema
  • The condition does not appear to have a genetic link (does usually not run in families)
  • Most individuals with discoid eczema have dry, sensitive skin
  • Venous insufficiency and stasis (stoppage or slowdown in blood flow) may aggravate symptoms on the lower legs.

Diagnosing discoid eczema

A GP (general practitioner, primary care physician) may be able to make a diagnosis after seeing the hallmark signs and symptoms. In some cases the patient may be referred to a dermatologist (specialist skin doctor).
  • Samples - the doctor may take scrapings of lesions for analysis and to rule out tinea (ringworm). Ringworm is a fungal skin infection which has similar signs to discoid eczema. The fungi that cause ringworm are called dermatophytes.
  • Secondary infection - if there is evidence of any secondary infection the doctor will take a swab for analysis.
A biopsy is not generally needed.

What are the treatment options for discoid eczema?

Although there is no straightforward cure for discoid eczema, there are treatments which may help prevent recurrences, as well as symptoms. Treatment focuses on:
  • Rehydrating the skin
  • Identifying and treating infections
  • Alleviating inflammation
The following measures are known to help patients with discoid eczema:
  • Bathe/shower once or twice a day. The water should be cool. In order to seal the water in the skin medicated topical preparations or moisturizers should be used.
  • Apply medication to damp skin. This helps seal it, so that the medication can penetrate.
  • Topical steroids - in medicine topical means "applied on to the skin". Corticosteroids rapidly reduce inflammation. If the patient's skin is very red and inflamed the doctor may prescribe a topical corticosteroid. In patients with severe symptoms oral steroids may be required.

    Applying a corticosteroid - apply to the affected area sparingly. Follow the instructions on the leaflet carefully. You can also ask the doctor, and if you cannot remember, ask a qualified pharmacist.

    Applying a corticosteroid during a flare-up - the corticosteroid should not be applied more than twice daily. Most patients will only require one application per day. After the flare-up has cleared up you should continue for another 48 hours.

    If the patient is using corticosteroids on a long-term basis, he/she should check carefully with the doctor on how and when to apply it.

    Discoid eczema is harder to treat than atopic eczema and may require higher dosages and longer treatment courses with steroids (than atopic eczema).

    Remember that steroid creams can mask or further spread an infection.

    If you have tried corticosteroids and symptoms have not improved you should see your doctor.
  • Secondary infections - if there is a secondary infection the patient may be given an antibiotic; usually one against streptococci. Good hand hygiene can help prevent eczema from becoming infected - keep hands clean and nails clean and short. Try to avoid scratching.
  • Antihistamines - they may help sleep more than the itching. Hence, the older sedating ones tend to be better if the aim is to get a good night's sleep. They should be taken about one hour before going to bed. Sometimes drowsiness is still present the following day. If the patient feels drowsy the following morning he/she should not drive or operate heavy machinery.
  • Tar preparations - these may help reduce inflammation if there are older, thickened, scaly plaques.
  • Environments - the patient will find that cool and moist environments help reduce symptoms, while the opposite - hot and dry ones - make them worse. If possible, seek out cool and moist environments.
  • Phototherapy - involves the use of natural or artificial light. In its most simple form, all the patient has to do is expose himself/herself to controlled amounts of natural sunlight.

    Other forms of phototherapy include using artificial ultraviolet A (UVA) or ultraviolet B (UVD) light, either on its own or in combination with drugs.

    Light therapy is very effective. It is important that it is done with a qualified health care professional. Exposure to sunlight has many beneficial effects, but it does, however, also have risks if not controlled properly. Examples of risks include premature skin aging and a higher risk of developing skin cancer. There is also a risk that the heat worsens the itching.
  • Emollients - agents that soften and smooth the skin - it can be a cream, bath oil, soap substitute, lotion or ointment. They keep the skin supple and moist. Emollients are an important part of eczema treatment. The skin of people with eczema is usually dry; emollients help keep them moisturized, which helps prevent cracking and irritation.

    Finding the right emollient may be a question of trial-and-error at first. The patient may have to try several different ones before hitting on a suitable one. Patients usually end up needing different types of emollients for different parts of their body.

    Some emollients are specific for very dry skin, while others are aimed at less dry skin. Ointments are generally prescribed for drier skin, while creams and lotions are usually prescribed for other skin types.

    It is not uncommon for patients to find that an emollient is no longer as effective as it used to be. Others may start experiencing skin irritation after long-term use. If either case happens you should see your GP.

    Individuals who use an emollient in the bath should remember that they make things slippery - care should be taken when getting in and out.
  • OTC (over the counter) medications - these are medications which can be purchased without a doctor's prescription. For discoid eczema they may include shampoos, emollient products and some low-dose topical steroids. A good source of advice on different products and their usage is a pharmacist.

    Peanuts - if the patient has a peanut allergy it is important to let the pharmacist know, because some products contain peanuts. The doctor should also know about any peanut allergy.

    Patients should see their doctor if OTC preparations have not improved symptoms after a week.
  • Wet wraps - the use of dampened bandages to reduce inflamed eczema is an old remedy. Sometimes diluted steroids and/or emollients are added to the preparation that dampens the bandages.
  • Complementary treatments - very popular among patients with atopic eczema, and used by some with discoid eczema. They include aromatherapy, massage, homeopathy, and some herbal remedies, to mention but a few. It is important to remember that although patients do report benefits, a lot of information one reads in books and on the internet is anecdotal. For therapy to be convincing, it should undergo proper clinical tests, usually carried out and compared to a placebo (dummy treatment).

    Before undergoing any complementary/alternative therapy, check it out carefully and make sure you get it from a reputable source.

    Patients should inform their doctor about all complementary treatments they are taking. Asking a qualified pharmacist about complementary therapies is useful.

    A study, carried out by Scientists at the Chinese University of Hong Kong found that a traditional Chinese herbal concoction, consisting of Flos lonicerae (Japanese honeysuckle), Herba menthae (peppermint), Cortex moutan (root bark of peony tree), Atractylodes Rhizome (underground stem of the atractylodes herb) and Cortex phellodendri (Amur cork-tree bark) may help people with eczema and reduced their needs for medications.

What are the possible complications of discoid eczema?

  • Secondary infections
  • Infections may cause permanent scars
  • Excoriation (scratching and picking the skin) may cause scars
  • If lesions are slow to heal there may be permanent brown blemishes (macules) on the skin, especially on the legs.

Reducing recurrences

  • Keep the skin well hydrated with liberal use of moisturizers. Add oils to the bath.
  • Do not have hot baths or showers.
  • Do not use soaps.
  • Wear clothing that does not irritate the skin. This usually means choosing natural, rather than man-made fabrics.
  • Loose clothing is better than tight clothing.
  • If your home has air-conditioning or central heating you may find an air-humidifier helps ease symptoms and reduce the number of recurrences.
  • Try to avoid scratching.
  • After a bath/shower - when you dry yourself, gently pat the skin dry with a soft towel (do not rub).
  • Adherence - follow your doctor's instructions and recommendations carefully.
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What Is Raynaud's Disease? What Causes Raynaud's Phenomenon?

Raynaud's disease, also known as Raynaud's phenomenon and sometimes simply Raynaud's, is a condition that causes some areas of the body to feel numb and cool in response to cold temperatures or emotional stress, caused by a problem with the blood supply to the skin. Raynaud's disease is a vasospastic disorder - spasms in the blood vessels lead to vasoconstriction (narrowing).

The disease mostly affects the fingers, toes, tip of the nose and the ears. The problem is in the blood vessels that supply the skin. Smaller arteries narrow and limit blood circulation to affected areas. Areas of the body subsequently become cold and very pale. Patients typically feel pins and needles, numbness, and even burning. The sensation can be unpleasant and painful.

According to Medilexicon's medical dictionary:

Raynaud's phenomenon is an idiopathic paroxysmal bilateral cyanosis of the digits due to arterial and arteriolar contraction; caused by cold or emotion.

The disease is named for Maurice Raynaud (1834 - 1881), a French physician who first described it in 1862.

The condition is either:
  • Primary Raynaud's. This is the most common form, there is no apparent cause (idiopathic). It is possible for the primary form to move to the secondary form.
  • Secondary Rayndaud's. It is associated with an underlying disease, such as rheumatoid arthritis. In extreme cases this form can progress to necrosis or gangrene of the fingertips.
Doctors may measure hand-temperature to distinguish between primary and secondary forms of the condition.

The National Health Service (NHS), UK, says that there could be as many as 10 million British people affected by Raynaud's disease. The NHS adds that a significant number of individuals never see their doctor about it because they think it is just part of their makeup, not knowing it is a disease with a name and treatment.

Raynaud's disease will usually affect people during or after middle age, although it can develop in all age groups. The majority of sufferers are women. As cold temperatures is one of the possible triggers, the condition becomes more common the further you move from the equator.

Most people have mild symptoms and do not find their daily tasks or general quality of life is affected. Even if symptoms are more severe, treatment (with medications) is usually effective.

What are the signs and symptoms of Raynaud´s disease?

A symptom is something the patient feels and reports, while a sign is something other people, such as the doctor detect. For example, pain may be a symptom while a rash may be a sign.

Generally, primary Reynaud's disease symptoms are mild, while the secondary form's may be more severe. In the primary form both hands are affected simultaneously, usually all fingers at the same time. In the secondary form the development and appearance of symptoms is more patchy, with perhaps a couple of fingers on one side being affected.

The affected areas will become very pale (pallor), and then take on a bluish color (cyanosis) due to hypoxia (lack of oxygen to that area). They will feel very cold and numb. If all fingers are affected, trying to rummage in your pockets for specific coins becomes much more difficult. This can sometimes be distressing.

When the episode subsides and bloodflow returns to the affected area the skin may turn red (rubor). During the recovery period there may be tingling and swelling.

Meanings in medicine:
  • Pallor - whiteness.
  • Cyanosis - a bluish color of skin (or mucous membranes) due to lack of oxygen in the blood.
  • Rubor - redness
Not all sufferers go through the three color process - pallor, cyanosis, rubor - especially those with mild symptoms.

Symptoms may not only affect the fingers, but also the toes, lips, ears and nose.

An episode may range from a few minutes to a number of hours.

Breastfeeding - Raynaud's-type symptoms may occur during breastfeeding; the nipples will turn white and become extremely painful.

What are the risk factors?

A risk factor is something which increases the likelihood of developing a condition or disease. For example, obesity significantly raises the risk of developing diabetes type 2. Therefore, obesity is a risk factor for diabetes type 2.
  • Gender. The phenomenon is more common in women than men; the Framingham Study found that 5% of men and 8% of women suffer from it.
  • Age. Although any age group can be affected, middle-aged and elderly individuals have a higher risk, compared to young people.
  • Geography. A significantly higher percentage of adults in, for example, Alaska suffer from the phenomenon compared to individuals in Florida.
  • Genes. A significant number of individuals with Raynaud's disease have a parent or sibling who also has it.
  • Underlying diseases - people with some other underlying diseases have a much higher risk of developing the phenomenon, such as people:

    • with connective tissue disorders, including scleroderma, systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, dermatomyositis, polymyositis, mixed connective tissue disease, cold agglutinin disease, and Ehlers-Danlos Syndrome.
    • with eating disorders, such as anorexia nervosa.
    • with obstructive disorders, such as atherosclerosis, Buerger's disease, Takayasu's arteritis, subclavian aneurysms, and thoracic outlet syndrome.
    • on certain medications, such as beta-blockers, cytotoxic drugs - particularly chemotherapeutics and most especially bleomycin, ciclosporin, ergotamine, sulfasalazine, and anthrax vaccines whose primary ingredient is the Anthrax Protective Antigen.
    • some other conditions, such as hypothyroidism, cryoglobulinemia, malignancy, reflex sympathetic dystrophy, carpal tunnel syndrome, and Magnesium Deficiency Erythromelalgia

What causes Raynaud's disease?

When the body is exposed to the cold, heat is lost through the extremities (fingers and toes) as capillaries (small blood vessels) under the skin constrict - become narrower, resulting in less blood getting to tissue in that area. For people with Raynaud's disease, the narrowing is more severe, and the consequent blood supply is much less than other people. If the blood supply is very low, that part of the body experiences an abnormal drop in temperature - hence the sensation of cold fingers.

For some people it needs to get really cold for symptoms to appear, while for others even a slight drop in temperature can trigger symptoms.

Stress, specifically emotional stress, which includes anxiety or anger can also trigger symptoms.

In secondary Raynaud's, where there is an underlying condition/disease, we know that the cause is that condition. In primary Raynaud's, nobody really knows why the blood vessels narrow so much.

Some occupations - there may be a link between repetitive movements and Raynaud's type symptoms, as may happen with a typist whose fingertips receive little blows for prolonged periods. Certain occupations may make individuals more susceptible, especially those where vibrating equipment is used, such as hammer drills, chainsaws or hedge trimmers (vibration white finger). Some people who work in the plastics industry develop Raynaud's type symptoms.

Smoking - smoking causes the blood vessels to narrow, increasing the risk of developing Raynaud's disese.

What are the complications of Raynaud´s disease?

A combination of thickening blood vessel walls and narrowing can lead to permanent reduction of blood flow to susceptible areas. If blood flow is seriously impaired there is a risk of finger or toe deformity, and even gangrene.

Some people with Raynaud's syndrome go on to develop scleroderma, where scar tissue (fibrosis) forms in the skin and sometimes other organs of the body.

How is Raynaud´s disease diagnosed?

Most doctors, after a careful examination, will be able to determine whether the patient has the primary or secondary form of Raynaud's. Possible secondary causes need to be identified or excluded. The following diagnostic tests may be ordered:
  • Digital artery pressure - the pressure of the arteries of the fingers are measured before and after they are cooled. A drop of 15mmHg or more allows for a positive diagnosis.
  • Blood test - to determine blood count (may reveal anemia or renal failure). Urea and electrolyte levels may also be tested to rule out a kidney problem (renal impairment).
  • Thyroid function test - to rule out hypothyroidism (underactive thyroid gland)
  • An auto-antibody screen - to test for rheumatoid factor, Erythrocyte sedimentation rate, or C-reactive protein. These may reveal either an inflammatory process or some illnesses.
  • Nail fold vasculature capillaroscopy - a fold of hard skin overlapping the base and sides of a finger/toe nail is examined under a microscope and the tiny blood vessels are observed. This test can help determine whether the patient has the primary or secondary form of the disease.

What is the treatment for Raynaud´s disease?

Treatment options depend on the type (secondary or primary), and the severity of symptoms. Treatment for primary Raynaud's concentrates primarily on avoiding triggers.

If symptoms are mild, most patients find that simply avoiding the triggers, such as staying warm, learning to relax (to avoid stress, anxiety and anger), and avoiding vibrating machines is all they need to do. Smokers should seriously consider giving up.

Avoiding caffeine, stimulants and substances that cause the blood vessels to constrict (vasoconstrictors) may help alleviate symptoms.

If the fingers become extremely white, run tepid to slightly warm water over them and massage them gently. If no warm water is available, place your fingers under your arms, crotch, or even in your mouth. Keep the affected digits warm until their normal color is restored.

  • Nifedipine - this medication, a dihydropyridine calcium channel blocker, rapidly lowers blood pressure and opens up the capillaries (tiny blood vessels); this helps speed up the return of proper bloodflow to affected areas. Patients should not drink grapefruit juice while on this medication.
  • Angiotensin blocking vasodilators - angiotensin is a protein that makes our blood vessels narrow (constrict) and drives up blood pressure. A vasodilator is anything which opens up (widens) blood vessels. An angiotensin blocking vasodilator is a medication that blocks angiotensin and widens the blood vessels.
  • Iloprost - if symptoms are severe and other therapies were not effective, this medication may be administered by intravenous infusion (through a drip). Iloprost widens the blood vessels, helping proper blood flow reach the affected areas.
Counseling - if the patient has the primary form of Raynaud's and emotional stress is identified as one of the triggers, counseling may help control stress, anger, frustration and anxiety. In some cases the patient may be prescribed an antidepressant.

Surgery - in extreme cases that have not responded to other therapies, some nerves in the affected area may be cut. This procedure is known as sympathectomy.
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