Category Archives: Ailmemts & Remedies

SARS (Severe acute respiratory syndrome)

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Description:
SARS, or Severe acute respiratory syndrome, is the disease caused by SARS coronavirus. It causes an often severe illness marked initially by systemic symptoms of muscle pain, headache, and fever, followed in 2–10 days by the onset of respiratory symptoms,[3] mainly cough, dyspnea, and pneumonia. Another common finding in SARS patients is a decrease in the number of lymphocytes circulating in the blood.

You may click to see the picture:     (1)…….(2)

Virus classification:-

Group: Group IV ((+)ssRNA)

Order: Nidovirales

Family: Coronaviridae

Genus: Coronavirus

Species: SARS coronavirus

SARS coronavirus is a positive and single stranded RNA virus belonging to a family of enveloped coronaviruses. Its genome is about 29.7kb, which is one of the largest among RNA viruses. The SARS virus has 13 known genes and 14 known proteins. There are 265bp in the 5′UTR and 342bp in the 3′UTR. SARS is similar to other coronaviruses in that its genome expression starts with translation of two large ORFs 1a and 1b, which are two polyproteins.

The functions of several of these proteins are known:  ORFs 1a and 1b encode the replicase and there are four major structural proteins: nucleocapsid, spike, membrane and envelope. It also encodes for eight unique proteins, known as the accessory proteins, with no known homologues. The function of these accessory proteins remains unknown.
In the SARS outbreak of 2003, about 9% of patients with confirmed SARS infection died. The mortality rate was much higher for those over 50 years old, with mortality rates approaching 50% for this subset of patients.

Coronaviruses usually express pp1a (the ORF1a polyprotein) and the PP1ab polyprotein with joins ORF1a and ORF1b. The polyproteins are then processed by enzymes that are encoded by ORF1a. Product proteins from the processing includes various replicative enzymes such as RNA dependent polymerase, RNA helicase, and proteinase. The replication complex in coronavirus is also responsible for the synthesis of various mRNAs downstream of ORF 1b, which are structural and accessory proteins. Two different proteins, 3CLpro and PL2pro, cleave the large polyproteins into 16 smaller subunits.

SARS-Coronavirus follows the replication strategy typical of the Coronavirus genus.

In the SARS outbreak of 2003, about 9% of patients with confirmed SARS infection died. The mortality rate was much higher for those over 50 years old, with mortality rates approaching 50% for this subset of patients.

Causes:
SARS is caused by a strain of coronavirus, the same family of viruses that causes the common cold. Until now, these viruses have never been particularly dangerous in humans, although they can cause severe disease in animals. For that reason, scientists originally thought that the SARS virus might have crossed from animals to humans. It now seems likely that it evolved from one or more animal viruses into a completely new strain.
 
How do SARS spread:
Most respiratory illnesses, including SARS, spread through droplets that enter the air when someone with the disease coughs, sneezes or talks. Most experts think SARS spreads mainly through face-to-face contact, but the virus also may be spread on contaminated objects — such as doorknobs, telephones and elevator buttons.

Symptoms:
Once a person has contracted SARS, the first symptom that they present with is a fever of at least 38°C (100.4°F) or higher. The early symptoms last about 2–7 days and include non-specific flu-like symptoms, including chills/rigor, muscle aches, headaches, diarrhea, sore throat, runny nose, malaise, and myalgia (muscle pain). Next, they develop a dry cough, shortness of breath, and an upper respiratory tract infection.

SARS typically begins with flu-like signs and symptoms — signs and symptoms include:

*Fever of 100.4 F (38 C) or higher
* Dry cough
*Shortness of breath

Complications:
The main complication of SERS  is that most people develop pneumonia. Breathing problems can become so severe that a mechanical respirator is required. SARS is fatal in some cases, often due to respiratory failure. Other possible complications include heart and liver failure.

People older than the age of 60 — especially those with underlying conditions such as diabetes or hepatitis — are at highest risk of serious complications.

Risk Factors:
In general, people at greatest risk of SARS have had direct, close contact with someone who’s infected, such as family members and health care workers.

Diagnosis:
At that time, a chest x-ray is ordered to confirm pneumonia. If the chest appears clear and SARS is still suspected, a HRCT scan will be ordered, because it is visible earlier on this scan. In severe cases, it develops into respiratory failure and acute respiratory distress syndrome (ARDS), and in 70-90% of the cases, they develop lymphopenia (low count of lymphocyte white blood cells).

The incubation period for SARS-CoV is from 2–10 days, sometimes lasting up to 13 days, with a mean of 5 days.  So symptoms usually develop between 2–10 days following infection by the virus. As part of the immune response, IgM antibody to the SARS-CoV is produced. This peaks during the acute or early convalescent phase (week 3) and declines by week 12. IgG antibody is produced later and peaks at week 12.

Tests:
When SARS first surfaced, no specific tests were available to help doctors diagnose the disease. Now several laboratory tests can help detect the virus. But no known transmission of SARS has occurred anywhere in the world since 2004.

Treatment:
Although global efforts are still on, scientists have not yet found out any effective treatment for SARS. Antibiotic drugs don’t work against viruses and antiviral drugs haven’t shown much benefit.

Prevention:
Researchers are working on several types of vaccines for SARS, but none has been tested in humans.Engineering of SARS virus has been done. In a paper published in 2006, a new transcription circuit was engineered to make recombinant SARS viruses. The recombination allowed for efficient expression of viral transcripts and proteins. The engineering of this transcription circuit reduces the RNA recombinant progeny viruses. The TRS (transcription regulatory sequences) circuit regulates efficient expression of SARS-CoV subgenomic mRNAs. The wild type TRS is ACGAAC.

A double mutation results in TRS-1 (ACGGAT) and a triple mutation results in TRS-2 (CCGGAT). When the remodeled TRS circuit containing viruses are genetically recombined with wild type TRS circuits, the result is a circuit reduced in production of subgenomic mRNA. The goal of modifying the SARS virus with this approach is to produce chimeric progeny that have reduced viability due to the incompatibility of the WT and engineered TRS circuits.

Novel subunit vaccine constructs for an S protein SARS vaccine based on the receptor binding domain (RBD) are being developed by the New York Blood Center. The re-emergence of SARS is possible, and the need remains for commercial vaccine and therapeutic development. However, the cost and length of time for product development, and the uncertain future demand, result in unfavorable economic conditions to accomplish this task. In the development of therapeutics and next-generation vaccines, more work is required to determine the structure/ function relationships of critical enzymes and structural proteins.

If SARS infections resume, follow these safety guidelines if you’re caring for an infected person:-

 *Wash your hands. Clean your hands frequently with soap and hot water or use an alcohol-based hand rub containing at least 60 percent alcohol.

* Wear disposable gloves. If you have contact with the person’s body fluids or feces, wear disposable gloves. Throw the gloves away immediately after use and wash your hands thoroughly.

* Wear a surgical mask. When you’re in the same room as a person with SARS, cover your mouth and nose with a surgical mask. Wearing eye glasses also may offer some protection.

* Wash personal items. Use soap and hot water to wash the utensils, towels, bedding and clothing of someone with SARS.

* Disinfect surfaces. Use a household disinfectant to clean any surfaces that may have been contaminated with sweat, saliva, mucus, vomit, stool or urine. Wear disposable gloves while you clean and throw the gloves away when you’re done.

Follow all precautions for at least 10 days after the person’s signs and symptoms have disappeared. Keep children home from school if they develop a fever or respiratory symptoms within 10 days of being exposed to someone with SARS. Children can return to school if signs and symptoms go away after three days.

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

Resources:

http://en.wikipedia.org/wiki/SARS_coronavirus

http://www.mayoclinic.com/health/sars/DS00501/DSECTION=prevention

 

 

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Foot order or Smelly foot

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Description:
Our foot sometimes gives out an unpleasant smell which is very much embarrassing.It is a type of body odor that affects the feet of humans.The quality of foot odor is often reported as a thick smell. Some describe the smell like that of malt vinegar. However, it can also be ammonia-like. Brevibacteria are considered a major cause of foot odor because they ingest dead skin on the feet and, in the process, convert amino acid methionine into methanethiol, which has a sulfuric aroma. The dead skin that fuels this process is especially common on the soles and between the toes. The brevibacteria is also what gives cheeses such as Limburger, Bel Paese, Port du Salut, Pálpusztai and Munster their characteristic pungency.

Propionic acid (propanoic acid) is also present in many foot sweat samples. This acid is a breakdown product of amino acids by Propionibacteria, which thrive in the ducts of adolescent and adult sebaceous glands. The similarity in chemical structures between propionic acid and acetic acid, which share many physical characteristics such as odor, may account for foot odors identified as being vinegar-like. Isovaleric acid (3-methyl butanoic acid) is the other source of foot odor and is a result of actions of the bacteria Staphylococcus epidermidis which is also present in several strong cheese types.

Other implicated micro-organisms include Micrococcaceae, Corynebacterium and Pityrosporum.

Bart Knols, of Wageningen Agricultural University, the Netherlands, received an “IG Nobel” prize in 2006 for showing that the female malaria mosquito Anopheles gambiae “is attracted equally to the smell of limburger cheese and to the smell of human feet”. Fredros Okumu, of Ifakara Health Institute in Tanzania, received grants in 2009 and 2011 to develop mosquito attractants and traps to combat malaria. He uses a blend of eight chemicals, which is four times more effective than an actual human.

Causes;
The feet and hands contain more sweat glands than any other part of the body, with roughly 3,000 glands per square inch. Smelly feet are not only embarrassing, but can be physically uncomfortable as well.

Feet smell for two reasons: 1) shoe wear, and 2) sweating of the feet. The interaction between the perspiration and the bacteria that thrive in shoes and socks generates the odor.

Smelly feet or excessive sweating can also be caused by an inherited condition, called hyperhidrosis, which primarily affects men. Stress, some medications, fluid intake, and hormonal changes also can increase the amount of perspiration our bodies produce.

The main cause is foot sweat. Sweat itself is odorless, but it creates a beneficial environment for certain bacteria to grow and produce bad-smelling substances. These bacteria are naturally present on our skin as part of the human flora. Therefore, more smell is created with factors causing more sweating, such as wearing shoes and/or socks with inadequate air ventilation for many hours. Hair on the feet, especially on the toes, may contribute to the odor’s intensity by adding increased surface area in which the bacteria can thrive.

Given that socks directly contact the feet, their composition can have an impact on foot odor. Polyester and nylon are common materials used to make socks, but provide less ventilation than cotton or wool do when used for the same purpose. Wearing polyester or nylon socks may increase perspiration and therefore may intensify foot odor.[1] Because socks absorb varying amounts of perspiration from feet, wearing shoes without socks may increase the amount of perspiration contacting feet and thereby increase bacterial activities that cause odor

Treatments:
The best home remedy for foot odor is to soak feet in strong black tea for 30 minutes a day for a week. The acid in the tea kills the bacteria and closes the pores, keeping your feet dry longer. Use two tea bags per pint of water. Boil for 15 minutes, then add two quarts of cool water. Soak your feet in the cool solution. Alternately, you can soak your feet in a solution of one part vinegar and two parts water.

Persistent foot odor can indicate a low-grade infection or a severe case of hereditary sweating. In these cases, a prescription ointment may be required to treat the problem.

Treating Excessive Sweating:
A form of electrolysis, called iontophoresis, has been shown to reduce excessive sweating of the feet. However, it is more difficult to administer. In the worst cases of hyperhidrosis, a surgeon can cut the nerve that controls sweating. Recent advances in technology have made this surgery much safer, but may increase sweating in other areas of the body.

Prevention:
Methods of extinguishment may be used even before onset of the odor as prevention. However, a very effective and cheap way to prevent foot odor is with sodium bicarbonate (a mildly basic white salt also known as baking soda, bread soda, cooking soda, bicarbonate of soda, sodium bicarb, bicarb soda, or simply bicarb). Sodium bicarbonate will create a hostile environment unsuitable for the bacteria responsible for the bad smell. Four pinches of it on each foot everyday are usually enough (two inside the sock and two on the insole of the shoe). Sometimes it might take one or two days before the shoes completely lose their old smell. Washing your feet and applying the sodium bicarbonate daily are also potentially useful solutions.

While there are a number of other remedies, sodium bicarbonate, if bought in a supermarket, costs approximately 20 times less than common odor-eaters or odor-killer powders.

Swabbing feet twice daily with isopropyl alcohol, found at your local drug store, for two weeks is a cheap and highly effective cure. One can also periodically remove their footwear, to reduce foot moisture and thereby reduce bacterial spawn.

Some types of powders and activated charcoal insoles, such as odor eaters, have been developed to prevent foot odor by keeping the feet dry. Special cedarsoles can be recommended for this purpose because of their antibacterial characteristics. Hygiene is considered important in avoiding odor, as is avoidance of synthetic shoes/socks, and rotation of the pairs of shoes worn

In general, smelly feet can be controlled with a few preventive measures:

•Always wear socks with closed shoes.
•Avoid wearing nylon socks or plastic shoes. Instead, wear shoes made of leather, canvas, mesh, or other materials that let your feet breathe.
•Bathe feet daily in lukewarm water, using a mild soap. Dry thoroughly.
•Change socks and shoes at least once a day.
•Check for fungal infections between toes and on the bottoms of your feet. If any redness or dry, patchy skin is observed, get treatment right away.
•Don’t wear the same pair of shoes two days in a row. If you frequently wear athletic shoes, alternate pairs so that the shoes can dry out. Give your shoes at least 24 hours to air out between wearings; if the odor doesn’t go away, discard the shoes.
•Dust your feet frequently with a nonmedicated baby powder or foot powder. Applying antibacterial ointment also may help.
•Practice good foot hygiene to keep bacteria levels at a minimum.
•Wear thick, soft socks to help draw moisture away from the feet. Cotton and other absorbent materials are best.

Extinguishment:

Once foot odor has begun, it can be extinguished, or at least alleviated, by either aromatic deodorants that neutralise the odor by their own smell, or by absorbers of the odor itself.

Among the earliest foot deodorants were aromatic herbs such as allspice, which nineteenth-century Russian soldiers would put in their boots.

Odor absorbers include activated charcoal foot insert wafers, such as Innofresh footwear odor absorbers.

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

Resources:

http://en.wikipedia.org/wiki/Foot_odor

http://www.wolfpodiatry.com/library/1932/SmellyFeetandFootOdor.html

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Neuropathy

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Definition:
Neuropathy is a general term that refers to diseases or malfunctions of the nerves. Any nerves at any location in the body can be damaged from injury or disease. Neuropathy is often classified according to the types or location of nerves that are affected. It is a disease caused by changes in the nerve cells. These changes may be age related. The degeneration is accelerated and aggravated if the patient suffers from diabetes, hypertension or has an abnormal lipid profile. Neuropathy can affect all three nervous systems — central, peripheral and autonomous.

If the central nervous system is affected, memory and cognitive skills decline. Forgetfulness becomes an accepted way of life. Peripheral neuropathy produces the most obvious, incapacitating, and distressing symptoms.

In some, the affected nerves may produce symptoms that are symmetrical (occurring in both limbs) and appear first in the furthest extremity. There may be paraesthesia (tingling, burning or numb sensation), hyperalgesia (abnormally acute pain sensation to innocuous stimuli) or deep aching. The symptoms tend to get worse at night and interfere with sleep.

Neuropathy can also be classified according to the disease causing it. (For example, neuropathy from the effects of diabetes is called diabetic neuropathy.)

You may click to see:
1.Slide show: How your brain works   :
2.Dementia Slideshow Pictures  :
3.Alzheimer’s Disease Slideshow Pictures  :
4.Brain Foods Slideshow Pictures 

Types of Neuropathy::

Peripheral neuropathy: Peripheral neuropathy is when the nerve problem affects the nerves outside of the brain and spinal cord. These nerves are part of the peripheral nervous system. Accordingly, peripheral neuropathy is neuropathy that affects the nerves of the extremities- the toes, feet, legs, fingers, hands, and arms. The term proximal neuropathy has been used to refer to nerve damage that specifically causes pain in the thighs, hips, or buttocks.

Cranial neuropathy: Cranial neuropathy occurs when any of the twelve cranial nerves (nerves that exit from the brain directly) are damaged. Two specific types of cranial neuropathy are optic neuropathy and auditory neuropathy. Optic neuropathy refers to damage or disease of the optic nerve that transmits visual signals from the retina of the eye to the brain. Auditory neuropathy involves the nerve that carries signals from the inner ear to the brain and is responsible for hearing.

Autonomic neuropathy: Autonomic neuropathy is damage to the nerves of the involuntary nervous system, the nerves that control the heart and circulation (including blood pressure), digestion, bowel and bladder function, the sexual response, and perspiration. Nerves in other organs may also be affected.

Focal neuropathy: Focal neuropathy is neuropathy that is restricted to one nerve or group of nerves, or one area of the body. Symptoms of focal neuropathy usually appear suddenly.

Symptoms:
Neuropathy is associated with varied characteristic symptoms. Although some people with neuropathy may not have symptoms, certain symptoms are common. The degree to which an individual is affected by a particular neuropathy varies.

Damage to the sensory nerves is common in peripheral neuropathy. Symptoms often begin in the feet with a gradual onset of loss of feeling, numbness, tingling, or pain and progress toward the center of the body with time. The arms or legs may be involved. The inability to determine joint position may also occur, which can result in clumsiness or falls. Extreme sensitivity to touch can be another symptom of peripheral neuropathy. The sensation of numbness and tingling of the skin is medically known as paresthesia.

The loss of sensory input from the foot means that blisters and sores on the feet may develop rapidly and not be noticed. Because there is a reduced sensation of pain, these sores may become infected and the infection may spread to deeper tissues, including bone. In severe cases, amputation may be necessary.

When damage to the motor nerves (those that control movement) occurs, symptoms include weakness, loss of reflexes, loss of muscle mass, cramping, and/or loss of dexterity.

Autonomic neuropathy, or damage to the nerves that control the function of organs and glands, may manifest with a wide variety of symptoms, including:

•Nausea, vomiting, or abdominal bloating after meals

•Urinary symptoms, such as incontinence, difficulty beginning to urinate, or feeling that the bladder was not completely emptied

•Impotence (erectile dysfunction) in men

•Dizziness or fainting

•Constipation or diarrhea

•Blurred vision

•Heat intolerance or decreased ability to sweat

•Hypoglycemia unawareness: Low blood sugar levels (hypoglycemia) are associated with trembling, sweating, and palpitations. In people with autonomic neuropathy, these characteristic symptoms may not occur, making dangerously low blood sugar levels difficult to recognize.

Causes:
Neuropathy or nerve damage may be caused by a number of different diseases, injuries, infections, and even vitamin deficiency states.
Some of them are :-

•Diabetes: Diabetes is the condition most commonly associated with neuropathy. The characteristic symptoms of peripheral neuropathy often seen in people with diabetes are sometimes referred to as diabetic neuropathy. The risk of having diabetic neuropathy rises with age and duration of diabetes. Neuropathy is most common in people who have had diabetes for decades and is generally more severe in those who have had difficulty controlling their diabetes, or those who are overweight or have elevated blood lipids and high blood pressure.

•Vitamin deficiencies: Deficiencies of the vitamins B12 and folate as well as other B vitamins can cause damage to the nerves.

•Autoimmune neuropathy: Autoimmune diseases such as rheumatoid arthritis, systemic lupus, and Guillain-Barre syndrome can cause neuropathies.

•Infection: Some infections, including HIV/AIDS, Lyme disease, leprosy, and syphilis, can damage nerves.

•Post-herpetic neuralgia: Post-herpetic neuralgia, a complication of shingles (varicella-zoster virus infection) is a form of neuropathy.

•Alcoholic neuropathy: Alcoholism is often associated with peripheral neuropathy. Although the exact reasons for the nerve damage are unclear, it probably arises from a combination of damage to the nerves by alcohol itself along with the poor nutrition and associated vitamin deficiencies that are common in alcoholics.

•Genetic or inherited disorders: Genetic or inherited disorders can affect the nerves and are responsible for some cases of neuropathy. Examples include Friedreich’s ataxia and Charcot-Marie-Tooth disease.

•Amyloidosis: Amyloidosis is a condition in which abnormal protein fibers are deposited in tissues and organs. These protein deposits can lead to varying degrees of organ damage and may be a cause of neuropathy.

•Uremia: Uremia (a high concentration of waste products in the blood due to kidney failure) can lead to neuropathy.

•Toxins and poisons can damage nerves. Examples include, gold compounds, lead, arsenic, mercury, some industrial solvents, nitrous oxide, and organophosphate pesticides.

•Drugs or medication: Certain drugs and medications can cause nerve damage. Examples include cancer therapy drugs such as vincristine (Oncovin, Vincasar), and antibiotics such as metronidazole (Flagyl), and isoniazid (Nydrazid, Laniazid).

•Trauma/Injury: Trauma or injury to nerves, including prolonged pressure on a nerve or group of nerves, is a common cause of neuropathy. Decreased blood flow (ischemia) to the nerves can also lead to long-term damage.

•Tumors: Benign or malignant tumors of the nerves or nearby structures may damage the nerves directly, by invading the nerves, or cause neuropathy due to pressure on the nerves.

•Idiopathic: Idiopathic neuropathy is neuropathy for which no cause has been established. The term idiopathic is used in medicine to denote the fact that no cause is known.

Diagnosis:
The diagnosis of neuropathy and its cause involve a thorough medical history and physical examination to help your health care professional determine the cause and severity of neuropathy. A neurological examination, testing the reflexes and function of sensory and motor nerves, is an important component of the initial examination.

Although there are no blood tests that are specific for determining whether of not neuropathy is present, when neuropathy is suspected, blood tests are often used to check for the presence of diseases and conditions (for example, diabetes or vitamin deficiencies) that may be responsible for nerve damage.

Imaging studies such as X-rays, CT scans, and MRI scans may be performed to look for sources of pressure on or damage to nerves.

Exams and Tests:

Specific tests of nerve function include:

•Electromyography (EMG) is a test that measures the function of the nerves. For this test a very thin needle is inserted through the skin into the muscle. The needle contains an electrode that measures the electrical activity of the muscle.

•A nerve conduction velocity test (NCV) measures the speed at which signals travel through the nerves. This test is often done with the EMG. In the NCV test, patches containing surface electrodes are placed on the skin over nerves at various locations. Each patch gives off a very mild electrical impulse, which stimulates the nerve. The electrical activity of the nerves is measured and the speed of the electrical impulses between electrodes (reflecting the speed of the nerve signals) is calculated.

•In some cases, a nerve biopsy may be recommended. A biopsy is the surgical removal of a small piece of tissue for examination under a microscope. A pathologist, a physician specially trained in tissue diagnosis, examines the specimen and can help establish the cause of the neuropathy. The procedure is performed using a local anesthetic. The sural nerve (in the ankle), or the superficial radial nerve (wrist) are the sites most often used for biopsy.

Treatment:
The treatment of neuropathy involves measures to control the symptoms as well as treatment measures that address the underlying cause of neuropathy, if appropriate. Medical treatments for diabetes, autoimmune diseases, infections, kidney disease, and vitamin deficiencies are varied and are directed at the specific underlying condition. In many cases, treatment of the underlying disease can reduce or eliminate the symptoms of neuropathy. Some cases, especially those involving compression or entrapment of nerves by tumors or other conditions, can be relieved by surgery.

Many adjuvant medications have been tried, such as mega doses of vitamins, iron, zinc, calcium, alpha lipoic acid, acetyl-L carnitine. Increasing doses of painkillers like tramadol are also used. Sometimes they are combined with anti histamines like diphendydramnine (Benadryl) and pain modifying drugs. Combinations with anti epileptics such as gabapentin and anti depressants like amitriptyline reduce the intensity of symptoms. None of these treatments has been 100 per cent successful. The pain is still present in 80 per cent of the patients 5-10 years later.

Control of blood glucose (sugar) levels is important in the treatment of diabetic neuropathy to help prevent further damage to nerves.

Clinical trials are underway to help find new and more effective treatments for neuropathy. For example, treatments that involve electrical nerve stimulation or magnetic nerve stimulation are being studied.

Self care at home:
Special and careful care of the feet is important in people with neuropathy to reduce the chance of developing sores and infections. The nerves to the feet are the nerves most commonly affected by neuropathy. Proper foot care includes:

•wash the feet with warm water each day and thoroughly dry feet after washing (especially between the toes);

•never go barefoot or wear improperly-fitting, damaged, or too-tight footwear;

•inspect the feet daily, looking for cuts, blisters, or other problems;

•cut and file toenails when needed;

•thick, seamless socks can help prevent irritation of the feet;

•call your health care practitioner if you have any problems with your feet;

•massaging the feet can improve circulation; and

•smoking cessation can further improve blood circulation, since smoking damages circulation to the extremities and may worsen foot problems.

.The intensity of the pain can be reduced by soaking the legs up to the knees in warm salted water for 10 minutes, half-an-hour before bed. Application of pain relieving ointments that contain capsaicin also provides relief. The ointment should be applied every 3-4 hours. Do not rub the ointment in too vigorously as it will damage the skin.

Prevention:

Neuropathy is preventable only to the extent that the underlying condition or cause is preventable. For those with diabetes, studies have conclusively shown that long-term control of blood glucose levels is critically important in preventing the development of neuropathy and other complications of diabetes. Neuropathy that arises due to poor nutrition or alcohol abuse may be preventable if these causes can be eliminated. Genetic or inherited causes of neuropathy are not preventable.

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

Resources:

http://www.emedicinehealth.com/neuropathy/article_em.htm

http://www.telegraphindia.com/1130211/jsp/knowhow/story_16546702.jsp

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Trigger finger

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Alternative Name : Stenosing tenosynovitis, trigger thumb, or trigger digit,

Definition:
Trigger finger is a common disorder of later adulthood characterized by catching, snapping or locking of the involved finger flexor tendon, associated with dysfunction and pain. A disparity in size between the flexor tendon and the surrounding retinacular pulley system, most commonly at the level of the first annular (A1) pulley, results in difficulty flexing or extending the finger and the “triggering” phenomenon. The label of trigger finger is used because when the finger unlocks, it pops back suddenly, as if releasing a trigger on a gun.
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One of your fingers or your thumb gets stuck in a bent position and then straightens with a snap — like a trigger being pulled and released. If trigger finger is severe, the finger may become locked in a bent position.

Often painful, trigger finger is caused by a narrowing of the sheath that surrounds the tendon in the affected finger. People whose work or hobbies require repetitive gripping actions are more susceptible. Trigger finger is also more common in women and in anyone with diabetes.

Symptoms:
Signs and symptoms of trigger finger may get progressed from mild to severe and include:

*Finger stiffness, particularly in the morning

*A popping or clicking sensation as you move your finger

*Tenderness or a bump (nodule) at the base of the affected finger

*Finger catching or locking in a bent position, which suddenly pops straight

*Finger locked in a bent position, which you are unable to straighten

Trigger finger more commonly occurs in your dominant hand, and most often affects your thumb or your middle or ring finger. More than one finger may be affected at a time, and both hands might be involved. Triggering is usually more pronounced in the morning, while firmly grasping an object or when straightening your finger.

Trigger finger is not the same as Dupuytren’s contracture — a condition that causes thickening and shortening of the connective tissue in the palm of the hand — though it may occur in conjunction with this disorder.

Causes:
The cause of trigger finger is a narrowing of the sheath that surrounds the tendon in the affected finger. Tendons are fibrous cords that attach muscle to bone. Each tendon is surrounded by a protective sheath — which, in turn, is lined with a substance called tenosynovium. The tenosynovium releases lubricating fluid that allows the tendon to glide smoothly within its protective sheath as you bend and straighten your finger — like a cord through a lubricated pipe.

But if the tenosynovium becomes inflamed frequently or for long periods, the space within the tendon sheath can become narrow and constricting. The tendon can’t glide through the sheath easily, at times catching the finger in a bent position before popping straight. With each catch, the tendon itself becomes more irritated and inflamed, worsening the problem. With prolonged inflammation, scarring and thickening (fibrosis) can occur and bumps (nodules) can form.

More than one potential causes have been described but the etiology remains idiopathic. It has also been called stenosing tenosynovitis (specifically digital tenovaginitis stenosans), but this may be a misnomer, as inflammation is not a predominant feature.

It has been speculated that repetitive forceful use of a digit leads to narrowing of the fibrous digital sheath in which it runs, but there is little scientific data to support this theory. The relationship of trigger finger to work activities is debatable and scientific evidence for and against hand use as a cause exist.

Risk Factors:
Risk Factors  developing trigger finger include:

Repeated gripping. If one routinely grips an item — such as a power tool or musical instrument — for extended periods of time, one may be more prone to developing a trigger finger.

Certain health problems. One is also at greater risk if he or she has certain medical conditions, including rheumatoid arthritis, diabetes, hypothyroidism, amyloidosis and certain infections, such as tuberculosis.Your sex. Trigger finger is more common in women.

Diagnosis:
Diagnosis is made almost exclusively by history and physical examination alone. More than one finger may be affected at a time, though it usually affects the thumb, middle, or ring finger. The triggering is usually more pronounced in the morning, or while gripping an object firmly.

Treatment:
Injection of the tendon sheath with a corticosteroid is effective over weeks to months in more than half of patients.

When corticosteroid injection fails, the problem is predictably resolved by a relatively simple surgical procedure (usually outpatient, under local anesthesia). The surgeon will cut the sheath that is restricting the tendon.

One recent study in the Journal of Hand Surgery suggests that the most cost-effective treatment is two trials of corticosteroid injection, followed by open release of the first annular pulley.  Choosing surgery immediately is the most expensive option and is often not necessary for resolution of symptoms.  More recently, a randomized controlled trial comparing corticosteroid injection with needle release and open release of the A1 pulley reported that only 57% of patients responded to corticosteroid injection (defined as being free of triggering symptoms for greater than 6 months). This is compared to a percutaneous needle release (100% success rate) and open release (100% success rate).  This is somewhat consistent with the most recent Cochrane Systematic Review of corticosteroid injection for trigger finger which found only 2 pseudo-randomized controlled trials for a total pooled success rate of only 37%. [5] However, this systematic review has not been updated since 2009.

There is a theoretical greater risk of nerve damage associated with the percutaneous needle release as the technique is performed without seeing the A1 pulley.

Investigative treatment options with limited scientific support include: non-steroidal anti-inflammatory drugs; occupational or physical therapy; steroid iontophoresis treatment; splinting; therapeutic ultrasound, phonophoresis (ultrasound with an anti-inflammatory dexamethasone cream); and Acupuncture.

Prognosis:
The natural history of disease for trigger finger remains uncertain.

There is some evidence that idiopathic trigger finger behaves differently in people with diabetes.

Recurrent triggering is unusual after successful injection and rare after successful surgery.

While difficulty extending the proximal interphalangeal joint may persist for months, it benefits from exercises to stretch the finger straighter.

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

Resources:

http://en.wikipedia.org/wiki/Trigger_finger

http://www.mayoclinic.com/health/trigger-finger/DS00155

http://assets.sbnation.com/imported_assets/71765/trigger_finger_2.jpg

http://www.trigger-finger.com/

http://www.drmomeni.com/hand/trigger.html

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Repetitive strain injury(RSI)

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Alternative Names:Repetitive stress injury, Repetitive motion injuries, Repetitive motion disorder (RMD), Cumulative trauma disorder (CT), Occupational overuse syndrome, Overuse syndrome, Regional musculoskeletal disorder

Definition:

Repetitive strain injury (RSI)  is an injury of the musculoskeletal and nervous systems that may be caused by repetitive tasks, forceful exertions, vibrations, mechanical compression (pressing against hard surfaces), or sustained or awkward positions.

The term “repetitive strain injury” is most commonly used to refer to patients in whom there is no discrete, objective, pathophysiology that corresponds with the pain complaints. It may also be used as an umbrella term incorporating other discrete diagnoses that have (intuitively but often without proof) been associated with activity-related arm pain such as carpal tunnel syndrome, cubital tunnel syndrome, thoracic outlet syndrome, DeQuervain’s syndrome, stenosing tenosynovitis/trigger finger/thumb, intersection syndrome, golfer’s elbow (medial epicondylosis), tennis elbow (lateral epicondylosis), and focal dystonia.

….click to see pictures..….(1).…...(2)….….(3)

Finally RSI is also used as an alternative or an umbrella term for other non-specific illnesses or general terms defined in part by unverifiable pathology such as reflex sympathetic dystrophy syndrome (RSDS), Blackberry thumb, disputed thoracic outlet syndrome, radial tunnel syndrome, “gamer’s thumb” (a slight swelling of the thumb caused by excessive use of a gamepad), “Rubik’s wrist” or “cuber’s thumb” (tendinitis, carpal tunnel syndrome, or other ailments associated with repetitive use of a Rubik’s Cube for speedcubing), “stylus finger” (swelling of the hand caused by repetitive use of mobile devices and mobile device testing.), “raver’s wrist”, caused by repeated rotation of the hands for many hours (for example while holding glow sticks during a rave).

Although tendinitis and tenosynovitis are discrete pathophysiological processes, one must be careful because they are also terms that doctors often use to refer to non-specific or medically unexplained pain, which they theorize may be caused by the aforementioned processes.

Doctors have also begun making a distinction between tendinitis and tendinosis in RSI injuries. There are significant differences in treatment between the two, for instance in the use of anti-inflammatory medicines, but they often present similar symptoms at first glance and so can easily be confused.

Types of RSIs that affect computer users may include non-specific arm pain or work related upper limb disorder (WRULD). Conditions such as RSI tend to be associated with both physical and psychosocial stressors.

Symptoms:

The following complaints are typical in patients who might receive a diagnosis of RSI:

*Short bursts of excruciating pain in the arm, back, shoulders, wrists, hands, or thumbs (typically diffuse – i.e. spread over many areas).

*The pain is worse with activity.

*Weakness, lack of endurance.

In contrast to carpal tunnel syndrome, the symptoms tend to be diffuse and non-anatomical, crossing the distribution of nerves, tendons, etc. They tend not to be characteristic of any discrete pathological condition.

1.The users experience constant pain in the hands, elbows, shoulders, neck, and the back. Other symptoms of Repetitive Stain Injury are cramps, tingling, and numbness in the hands. The hand movements of the user may become clumsy and the person may find it difficult even to fasten buttons.

2.Another variant of Repetitive Strain Injury is that, it may produce painful symptoms in the upper limbs, but the site may be difficult to locate.

3.The common diagnoses seen in Repetitive Strain Injury are Carpal Tunnel Syndrome, Tenosynovitis, Bursitis, White Limb, and Shoulder pain. A major cause is due to long unbroken periods of work. Ergonomics or the lack of it plays a very important role. Lack of information about the condition leads to neglect by the concerned individuals.

Frequency :A 2008 study showed that 68% of UK workers suffered from some sort of RSI, with the most common problem areas being the back, shoulders, wrists, and hands.

Physical examination and diagnostic testing; The physical examination discloses only tenderness and diminished performance on effort-based tests such as grip and pinch strength—no other objective abnormalities are present. Diagnostic tests (radiological, electrophysiological, etc.) are normal. In short, RSI is best understood as an apparently healthy arm that hurts. Whether there is currently undetectable damage remains to be established.

Causes:

RSI is believed by many to be caused due to lifestyle without ergonomic care,  E.g. While working in front of computers, driving, traveling etc. Simple reasons like ‘Using a blunt knife for everyday chopping of vegetables’, may cause RSI.

Repetitive Strain Injury occurs when the movable parts of the limbs are injured. Repetitive Strain Injury usually caused due to repetitive tasks, incorrect posture, stress and bad ergonomics. Repetitive Strain Injury generally causes numbness, tingling, weakness, stiffing, and swelling and even nerve damage. The chief complaint is the constant pain in the upper limbs, neck, shoulder and back.

The main cause of this main are the repetitive activities, forceful activities of arms and hand and awkward postures. The other causes of Repetitive Strain Injuries are sitting in a fixed posture and poor workplace ergonomics.

Other typical habits that some sources believe lead to RSI

*Reading or doing tasks for extended periods of time while looking down.

*Sleeping on an inadequate bed/mattress or sitting in a bad armchair and/or in an uncomfortable position.

*Carrying heavy items.

*Holding one’s phone between neck and shoulder.

*Watching TV in incorrect position e.g. Too much to the left/right.

*Sleeping with head forward, while traveling.

*Prolonged use of the hands, wrists, back, neck, etc.

*Sitting in the same position for a long period of time.

Diagnosis:

Repetitive task and stress affects the body parts causes RSI. An instance of this is using a screwdriver, if you keep using the screwdriver without a break, you feel your wrist become restricted and you feel pain and you may also experience the loss of movement. This is the initial stage of RSI.

RSI, or should we say the group of syndromes that make up repetitive strain injury only affects the back, neck and arms. A lot of people without even realizing may suffer with RSI.

You may have had pains in your wrists or arms that you explained as being tired if you are working on an assembly line or you’re an avid musician who can’t put their guitar down. These pains are more than likely the initial RSI symptoms.

Judging the Symptom:

The problem in diagnosing repetitive strain injury is the fact that is can be hard to judge the symptoms, after all RSI is just a name given to a group of different conditions that are all related in some way to the affects we attribute to RSI.

Not only do we have this issue, we also have the problem that some of the symptoms related with repetitive strain injury are found in other, more dangerous conditions such as angina.

Even though RSI only affects the upper torso and limbs, the symptoms can in fact appear in the lower half of the body; this is due to the vertebral nerves that can be affected in some cases so the pains appear in the legs.

Carpal Tunnel Syndrome:

Carpal tunnel syndrome is the most common out of all the syndromes that make up the condition called RSI.

Carpal tunnel syndrome is a condition that affects the median nerve situated in the carpal canal in the wrist, when the same movement is carried out frequently it can cause the tendons also situated in the carpal canal to become inflamed and compress the nerve causing pain and tightness causing loss of movement.

The most famous out of all the syndromes that make up repetitive stress injury is carpal tunnel syndrome because it affects a lot of people who spend long periods on the computer without supporting their wrists appropriately.

Other Conditions:

There are some conditions that the every day layman may be aware of golfers elbow, which is called medial epicondylitis, or like tennis elbow, which is officially called lateral epicondylitis.

You should visit your doctor if you suffer with pains, aches, stiffness, numbness or tingling sensations in your back, arms, wrists or hands. While RSI is not life threatening it can affect you more than you think.

Eventually without visiting a medical professional the symptoms can become ever worse, or you may even find the RSI could be something more risky. Learn more about ergonomics at safecomputingtips.com.

Treatment :Most common and simple measure of treatment, which is more common sense than anything is painkillers and anti inflammatory pills, these are available over the counter at any good pharmacy.When taking painkillers and anti inflammatory pills it is important that you rest the affected area, just because the pain is not there it doesn’t mean the condition has instantly been resolved.Another simple measure is speaking to your employer, you may find they have guidelines to work towards that may mean you can get some support in alleviating your condition. This means your work place may be assessed and improvements implemented.You can get a simple support bandage from your local pharmacy to help add strength to the affected area, if it is your wrist or arm. You may need to purchase a special keyboard and/or mouse or get speech recognition software in order to prevent further irritation to your injury.Speech recognition software is a great alternative for those who suffer due to computer work, speech recognition software works by the software writing what you say for you.Your medical professional might possibly prescribe that you wear an orthopedic hand brace. You don’t want to wear one of these if your doctor doesn’t prescribe it because it could lead to further injury.

Therapy:

Your doctor may prescribe physical therapy, a physical therapists role is to develop and maximize the movement of the body, and this can also include the provision of aids to alleviate symptoms.

Another prescribed therapy your doctor may request is occupational therapy, it may sound like occupational therapy and physical therapy are very similar but there are differences.

Occupational therapy helps develop and maintain the skills required to carry out all the general functions needed to live a comfortable life.

Occupational therapy includes assessing what a persons requirements are and supporting them with offering recommendations on adapting to their living or working space and offering simple exercises to regain movement.

Alternative Treatment:

Deep body massages have been reported to work wonders for those suffering with repetitive strain injury as it works deep into the body’s soft tissues like the muscles and tendons where the pain comes from.

Soft tissue therapy is a type of therapy that works by decompressing the area surrounding the RSI. This will increase your circulation and aid in healing. They may also try biofeedback. This is generally used to reduce tension in the muscles in your shoulders and neck.

Some people have reported that slow martial arts like Tai Chi can have a dramatic affect on their condition because they work on specific movements and improve strength and flexibility.

Surjury:

As a last resort, the medical professional might recommend to have surgery. one should keep in mind that it doesn’t always work and he or she  will be left without the use of one’s hand and arm for a long time. The above treatment methods have been proven to help heal even the worst types of RSI disorders when they are done correctly.

You may click to see the using of modern ergonomics in home office

Exercise:

Exercise decreases the risk of developing RSI.

*Doctors sometimes recommend that RSI sufferers engage in specific strengthening exercises, for example to improve posture.

*In light of the fact that a lifestyle that involves sitting at a computer for extended periods of time increases the probability that an individual will develop excessive kyphosis, theoretically the same exercises that are prescribed for thoracic outlet syndrome or kyphotic postural correction would benefit an RSI sufferer.

*Some sources[who?] recommend motoric exercises and ergo-aerobics to decrease chances of strain injury. Ergo-aerobics target touch typists and people who often use computer keyboard.

Resuming normal activities despite the pain:

Psychologists Tobias Lundgren and Joanne Dahl have asserted that, for the most difficult chronic RSI cases, the pain itself becomes less of a problem than the disruption to the patient’s life caused by

*avoidance of pain-causing activities

*the amount of time spent on treatment

They claim greater success from teaching patients psychological strategies for accepting the pain as an ongoing fact of life, enabling them to cautiously resume many day-to-day activities and focus on aspects of life other than RSI

Psychosocial factors:

Studies have related RSI and other upper extremity complaints with psychological and social factors. A large amount of psychological distress showed doubled risk of the reported pain, while job demands, poor support from colleagues, and work dissatisfaction also showed an increase in pain, even after short term exposure.

For example, the association of Carpal tunnel syndrome with arm use is commonly assumed but not well-established. Typing has long been thought to be the cause of carpal tunnel syndrome, but recent evidence suggests that, if anything, typing may be protective. Another study claimed that the primary risk factors for Carpal tunnel syndrome were “being a woman of menopausal age, obesity or lack of fitness, diabetes or having a family history of diabetes, osteoarthritis of the carpometacarpal joint of the thumb, smoking, and lifetime alcohol intake.


Prevention:
Risk of RSI can be reduced a lot by warming up and cooling down the muscles used, taking regular breaks throughout the day, having an appropriate workstation and seating position, and practising relaxation. If the job puts one  at risk of RSI he or she should seek out expert advice on prevention from your employer or professional body.

Repetitive Stress Injury symptoms when found, people should seek medical attention as early as possible. Measures that can be adopted to avoid Repetitive Stress Injury at an individual level include:
Position: The recommended position to sit in front of a computer is semi-reclined with the forearms resting in a cradle or on an extension of the keyboard support to prevent Repetitive Stress Injury.

There should be ample support for the back. The hands should be free and point in the direction of the forearms. The feet should rest on the ground or feet support. The distance of the monitor should be 18 inches or more and at a slightly lower level than the eye level. Using these measures Repetitive Stress Injury caused out of position can be avoided.

Hydration: The Repetitive Stress Injury can be prevented by drinking adequate fluids to keep the tendons and soft- tissues soft.

Shortcuts: Using keyboard shortcuts and less of mouse is the most effective preventive method to avoid Repetitive Stress Injury. Touch the ergonomic keyboard softly and do not pound at it. The wrist should rest on the table or wrist rest.

Telephone use: Don’t cradle the telephone between the face and shoulder while working, as this can lead to neck strain.

Messages: Don’t use the computer while conveying messages in person or through the intercom.

No games:One of the main Causes of Repetitive Stress Injury is Games. Games or surfing at work may increase stress on your hands. So games should be avoided.

Preventive Measures at the Organizational Level for Repetitive Stress injury : -
Organizations that use computers in a big way can also adopt certain preventive measures for avoiding Repetitive Strain Injury to their employees. These include:

…..

1.You need to educate your employees on the importance of adopting a proper posture which is one of the main cause of Repetitive Stress Injury.
2.Ensure that all your employees are using quality ergonomic furniture that will save loss of working hours by guaranteeing full comfort of the employees.
3.Give periodic reminders through lectures and audio-visual presentations by medical professionals on the importance of taking good care of health while using computers and Repetitive Stress Injury.
4.Try to avoid computer as much as possible: use voicemail instead of sending e-mail. Go for a walk or watch a movie instead of playing video games. Its better go for a book instead of searching the Web. You are in the danger zone for Repetitve Stress Injury if you are using a computer for as little as two hours a day.
5.Adjust your workstation properly. Make sure your monitor is directly in front of you, with the top of the screen at eye level. Be sure your keyboard (Ergonomic Keyboard) and mouse (Ergonomic Mouse) are low enough to allow you to relax your shoulders.
6.Sit up straight. Make sure your chair supports your spine in an erect position as it is the one of the main causes of Repetitive Stress Injury.
7.Practice proper technique: never rest your wrists on the desk, wrist pad or armrests while you are typing or using a mouse or trackball.
8.Pace yourself. Take a 5-to-10 minute break every 20 minutes and limit your overall time at the computer.
9.Get regular cardiovascular exercise.
10.Do appropriate upper-body strengthening and stretching exercises.
11.Stretch frequently while at the computer.
12.Do not work at the computer or other hand-intensive activities if you are experiencing pain, fatigue or soreness.
13.Avoid using the mouse and trackball whenever possible. Use keystrokes instead for preventing Repetitive Stress Injury.
14.When symptoms of Repetitive Stress Injury are set in, consult an orthopedic surgeon. If you find of the symptoms of Repetitive Stress Injury mentioned above, do not make the diagnosis yourself. The diagnosis will be made from the history and clinical findings as there will be no changes in X-rays, since the soft tissues are involved.

Nerve conduction studies can confirm the diagnosis. In cases detected earlier, attention to ergonomics will restore normalcy.
In cases of Repetitive Stress Injury when diagnosed late, orthopedic treatment like injections and even minor surgery may be necessary.

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

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Resources:

English: Untreated Carpal Tunnel Syndrome

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http://www.bbc.co.uk/health/physical_health/conditions/repetitivestrain1.shtml

http://www.rsiwarrior.com/ergonomics.html

http://www.hoverstop.com/eng/rsi.php

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Fainting

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Alternative Name : Syncope

Definition:
.Fainting is a temporary loss of consciousness due to a drop in blood flow to the brain. The episode is brief (lasting less than a couple of minutes) and is followed by rapid and complete recovery. You may feel light-headed or dizzy before fainting.

Fainting  is  a sudden, usually temporary, loss of consciousness generally caused by insufficient oxygen in the brain either through cerebral hypoxia or through hypotension, but possibly for other reasons. A pre- or near-syncope is diagnosed if the individual can remember events during the loss of consciousness (i.e., reports remembering dizziness, blurred vision, and muscle weakness, and the fall previous to hitting his or her head and losing consciousness). As loss of consciousness is a symptom for a variety of conditions and syncope is difficult to rule out outside of a hospital, a thorough examination is required in order to determine the cause, including interviews with witnesses as well as evaluation with an electrocardiogram. If the individual remembers feeling dizzy and loss of vision, but not the fall, then it is considered a syncoptic episode. Typical symptoms progress through dizziness, clamminess of the skin, a dimming of vision or greyout, possibly tinnitus, complete loss of vision, weakness of limbs to physical collapse. These symptoms falling short of complete collapse, or a fall down, may be referred to as a syncoptic episode. A breathing gas containing less than 16% oxygen can still contain enough to prevent hypoxia. On the other hand, mountaineers, pilots, and astronauts breathe oxygen-enriched gas because the partial pressure of oxygen in normal air mixture is not enough to prevent hypoxia, since the total pressure is reduced at high altitude. Syncope due to hypoxia can also occur because the lungs are not working properly, because a person is not breathing, because the blood is not circulating, or because the blood’s ability to transport oxygen is destroyed or blocked, e.g., by carbon monoxide, which, if present, binds itself to the blood’s hemoglobin.

The most common is a vasovagal attack, where overstimulation of a major nerve (called the vagus) slows the heart rate and lowers blood pressure. This overstimulation may be caused by intense stress, fear, pain or anything that suddenly increases pressure inside the body, such as blowing a trumpet.

Fainting may also result from low blood pressure (hypotension), often when someone stands up suddenly or is dehydrated and low in body fluids.

More rarely, fainting is due to abnormalities of the heartbeat.

A longer, deeper state of unconsciousness is often called a coma.
Anyone may be affected by fainting, but people who are unwell or dehydrated are at greater risk. Fainting – or feeling faint – is also common in pregnancy.

Symptoms:-
The person may start to feel light-headed, dizzy, nauseous and sweaty. They may have ringing in their ears and feel weak. Some people, however, have little or no warning symptoms.

They then collapse to the ground and are unconscious for a few moments before coming round. They may feel woozy or nauseous for a little while afterwards and may vomit.

Causes:-
Central nervous system ischaemiaThe central ischaemic response is triggered by an insufficient level of oxygenated blood in the brain.

The respiratory system may contribute to oxygen levels through hyperventilation, though a sudden ischaemic episode may also proceed faster than the respiratory system can respond. These processes cause the typical symptoms of fainting: pale skin, rapid breathing, nausea and weakness of the limbs, particularly of the legs. If the ischaemia is intense or prolonged, limb weakness progresses to collapse. An individual with very little skin pigmentation may appear to have all color drained from his or her face at the onset of an episode. This effect combined with the following collapse can make a strong and dramatic impression on bystanders.

The weakness of the legs causes most sufferers to sit or lie down if there is time to do so. This may avert a complete collapse, but whether the sufferer sits down or falls down the result of an ischaemic episode is a posture in which less blood pressure is required to achieve adequate blood flow. It is unclear whether this is a mechanism evolved in response to the circulatory difficulties of human bipedalism or merely a serendipitous result of a pre-existing circulatory response.

Vertebro-basilar arterial disease
Arterial disease in the upper spinal cord, or lower brain, causes syncope if there is a reduction in blood supply, which may occur with extending the neck or after drugs to lower blood pressure.

VasovagalMain article: Vasovagal syncope
Vasovagal (situational) syncope—one of the most common types—may occur in scary, embarrassing or uneasy situations, or during blood drawing, coughing, urination or defecation. Other types include postural syncope (caused by a changing in body posture), cardiac syncope (due to heart-related conditions), and neurological syncope (due to neurological conditions). There are many other causes of syncope, including low blood-sugar levels and lung disease such as emphysema and a pulmonary embolus. The cause of the fainting can be determined by a doctor using a complete history, physical, and various diagnostic tests.

The vasovagal type can be considered in two forms:

Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group, and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.
Recurrent syncope with complex associated symptoms. This is so-called Neurally Mediated Syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance (“spots before the eyes”), sweating, light-headedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive.
A pattern of background factors contributes to the attacks. There is typically an unsuspected relatively low blood volume, for instance, from taking a low-salt diet in the absence of any salt-retaining tendency. Heat causes vaso-dilatation and worsens the effect of the relatively insufficient blood volume. That sets the scene, but the next stage is the adrenergic response. If there is underlying fear or anxiety (e.g., social circumstances), or acute fear (e.g., acute threat, needle phobia), the vaso-motor centre demands an increased pumping action by the heart (flight or fight response). This is set in motion via the adrenergic (sympathetic) outflow from the brain, but the heart is unable to meet requirement because of the low blood volume, or decreased return. The high (ineffective) sympathetic activity is always modulated by vagal outflow, in these cases leading to excessive slowing of heart rate. The abnormality lies in this excessive vagal response. The tilt-table test typically evokes the attack.

Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defence mechanism when confronted by danger (“playing possum”). This reflex occurs in only some people and may be similar to that described in other animals.

The mechanism described here suggests that a practical way to prevent attacks would be, what might seem to be counterintuitive, to block the adrenergic signal with a beta-blocker. A simpler plan might be to explain the mechanism, discuss causes of fear, and optimise salt as well as water intake.[citation needed]

Deglutition syncope
Syncope may occur during deglutition. Manisty et al. note: “Deglutition syncope is characterised by loss of consciousness on swallowing; it has been associated not only with ingestion of solid food, but also with carbonated and ice-cold beverages, and even belching.”

CardiacCardiac arrhythmias
Most common cause of cardiac syncope. Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which requires DC cardioversion.

Obstructive cardiac lesion
Aortic stenosis and mitral stenosis are the most common examples. Aortic stenosis presents with repeated episodes of syncope. Pulmonary embolism can cause obstructed blood vessels. High blood pressure in the arteries supplying the lungs (pulmonary artery hypertension) can occur during pulmonary embolism. Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.

Structural cardiopulmonary disease
These are relatively infrequent causes of faints. The most common cause in this category is fainting associated with an acute myocardial infarction or ischemic event. The faint in this case is primarily caused by an abnormal nervous system reaction similar to the reflex faints. In general, faints caused by structural disease of the heart or blood vessels are particularly important to recognize, as they are warning of potentially life-threatening conditions. Among other conditions prone to trigger syncope (by either hemodynamic compromise or by a neural reflex mechanism, or both), some of the most important are hypertrophic cardiomyopathy, acute aortic dissection, pericardial tamponade, pulmonary embolism, aortic stenosis, and pulmonary hypertension.

Other cardiac causes
Sick sinus syndrome, a sinus node dysfunction, causing alternating bradycardia and tachycardia. Often there is a long pause asystole between heartbeat.

Adams-Stokes syndrome is a cardiac syncope which may occur with seizures caused by complete or incomplete heart block. Symptoms include deep and fast respiration, weak and slow pulse and respiratory pauses that may last for 60 seconds.

Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope.

Other causesFactors that influence fainting are fasting long hours, taking in too little food and fluids, low blood pressure, hypoglycemia, growth spurts, physical exercise in excess of the energy reserve of the body, emotional distress, and lack of sleep. Orthostatic hypotension caused by standing up too quickly or being in a very hot room can also cause fainting.

More serious causes of fainting include cardiac (heart-related) conditions such as an abnormal heart rhythm (an arrhythmia), wherein the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening. Other important cardio-vascular conditions that can be manifested by syncope include subclavian steal syndrome and aortic stenosis.

Orthostatic (postural) hypotensive faints are as common or perhaps even more common than vasovagal syncope. Orthostatic faints are most often associated with movement from lying or sitting to a standing position. Apparently healthy individuals may experience minor symptoms (“lightheadedness”, “greying-out”) as they stand up if blood pressure is slow to respond to the stress of upright posture. If the blood pressure is not adequately maintained during standing, faints may develop. However, the resulting “transient orthostatic hypotension” does not necessarily signal any serious underlying disease. The most susceptible individuals are elderly frail individuals, or persons who are dehydrated from hot environments or inadequate fluid intake. More serious orthostatic hypotension is often the result of certain commonly prescribed medications such as diuretics, ?-adrenergic blockers, other anti-hypertensives (including vasodilators), and nitroglycerin. In a small percentage of cases, the cause of orthostatic hypotensive faints is structural damage to the autonomic nervous system due to systemic diseases (e.g., amyloidosis or diabetes) or in neurological diseases (e.g., Parkinson’s disease).

Fainting may occur while you are urinating, having a bowel movement (especially if straining), coughing very hard, or when you have been standing in one place too long. Fainting can also be related to fear, severe pain, or emotional distress.

A sudden drop in blood pressure can cause you to faint. Your blood pressure may drop suddenly if you are bleeding or severely dehydrated. It can also happen if you stand up very suddenly from a lying position.

Certain medications may lead to fainting by causing a drop in your blood pressure or for another reason. Common drugs that contribute to fainting include those used for anxiety, high blood pressure, nasal congestion, and allergies.

Other reasons you may faint include hyperventilation, drug or alcohol use, and low blood sugar.

Less common but more serious reasons for fainting include heart disease (such as abnormal heart rhythm or heart attack) and stroke. These conditions are more likely in persons over age 65 and less likely in those younger than 40.

Other causes:
Factors that influence fainting are fasting long hours, taking in too little food and fluids, low blood pressure, hypoglycemia, growth spurts,[citation needed] physical exercise in excess of the energy reserve of the body, emotional distress, and lack of sleep. Orthostatic hypotension caused by standing up too quickly or being in a very hot room can also cause fainting.

More serious causes of fainting include cardiac (heart-related) conditions such as an abnormal heart rhythm (an arrhythmia), wherein the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening. Other important cardio-vascular conditions that can be manifested by syncope include subclavian steal syndrome and aortic stenosis.

Diagnosis:
Clinical testsIf one is suffering from syncope, there are many underlying causes that may be contributing to the episodes. It is important to understand that there is no master list of tests that are currently being used to diagnose the underlying cause(s). However, there are some common diagnostic tests for fainting.

A hemoglobin count may indicate anemia or blood loss. However, this has been shown to be useful in only about 5% of patients being evaluated for fainting.[4]

An electrocardiogram (ECG) records the electrical activity of the heart. It is estimated that from 20%-50% of patients will have an abnormal ECG. However, while an ECG may identify conditions such as atrial fibrillation, heart block, or a new or old heart attack, it typically does not provide a definite diagnosis for the underlying cause for fainting.

Sometimes, a Holter monitor may be used. This is a portable ECG device that can record the wearer’s heart rhythms during daily activities over an extended period of time. Since fainting usually does not occur upon command, a Holter monitor can provide a better understanding of the heart’s activity during fainting episodes.

The Tilt table test is performed to elicit orthostatic syncope secondary to autonomic dysfunction (neurogenic).

For patients with more than two episodes of syncope and no diagnosis on “routine testing”, an insertable cardiac monitor might be used. It lasts 14 to 18 months. Smaller than a pack of gum, it is inserted just beneath the skin in the upper chest area. The procedure typically takes 15 to 20 minutes. Once inserted, the device continuously monitors the rate and rhythm of the heart. Upon waking from a “fainting” spell, the patient places a hand held pager size device called an Activator over the implanted device and simply presses a button. This information is stored and retrieved by their physician.

San Francisco syncope rule:
The San Francisco syncope rule was developed to isolate patients who have higher risk for a serious cause of syncope. Anyone with high risk criteria needs to be further investigated. They are summed up by the CHESS mnemonic: congestive heart failure, hematocrit <30%, electrocardiogram abnormality, shortness of breath, or systolic blood pressure <90 mm Hg

Treatment :
Recommended treatment involves returning blood to the brain by positioning the person on the ground, with legs slightly elevated or leaning forward and the head between the knees for at least 10-15 minutes, preferably in a cool and quiet place. As the dizziness and the momentary blindness passes, the person may experience a brief period of visual disturbances in the form of phosphenes, sudden sore throat, nausea, and general shakiness. For individuals who have problems with chronic fainting spells, therapy should focus on recognizing the triggers and learning techniques to keep from fainting. At the appearance of warning signs such as lightheadedness, nausea, or cold and clammy skin, counter-pressure maneuvers that involve gripping fingers into a fist, tensing the arms, and crossing the legs or squeezing the thighs together can be used to ward off a fainting spell. After the symptoms have passed, sleep is recommended. If fainting spells occur often without a triggering event, syncope may be a sign of an underlying heart disease.

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

Resources:

http://en.wikipedia.org/wiki/Syncope_(medicine)

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Sjogren’s syndrome

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Alternative Names: Mikulicz disease” and “Sicca syndrome

Definition:
Sjögren’s syndrome (SHOW-grins)is a systemic autoimmune disease in which immune cells attack and destroy the exocrine glands  that produce tears and saliva.In some cases, other organs of the body are also affected, including the:

•Kidneys
•Liver
•Pancreas
•Lungs
•Blood vessels
•Brain

It is named after Swedish ophthalmologist Henrik Sjögren (1899–1986), who first described it.

Nine out of ten Sjögren’s patients are women  and the average age of onset is late 40s, although Sjögren’s occurs in all age groups in both women and men. It is estimated to strike as many as 4 million people in the United States alone, making it the second most common autoimmune rheumatic disease.

Sjogren’s syndrome may be classified as primary or secondary. Primary Sjogren’s syndrome occurs alone; secondary Sjogren’s syndrome is seen alongside another disease, such as rheumatoid arthritis and systemic lupus erythematosis (SLE).

The disorder should not be confused with the Sjögren–Larsson syndrome, which was also denoted T. Sjögren syndrome in early studies.

Symptoms:
There are many different symptoms of Sjogren’s. However, not everyone experiences the same ones or to the same degree.

The characteristic dryness of Sjogren’s means the eyes often feel very uncomfortable and may burn, itch or feel gritty. Mouth dryness makes talking, chewing and swallowing difficult.

Other symptoms include:

•A sore or cracked tongue
•Dry nose and skin
•Digestive problems
•Joint pains
•Fatigue
•Dental problems are more likely (because of the lack of saliva)
As is often the case with any long-term condition, a person’s quality of life may be adversely affected. This may result in depression and make social life, work and relationships more difficult to maintain and enjoy.

Sjogren’s is also associated with an increased risk of miscarriage, Raynauds phenomenom and adverse reactions to medication such as antibiotics.

 

Causes:
Sjogren’s syndrome is an autoimmune disorder. This means that your immune system mistakenly attacks your body’s own cells and tissues.

Scientists aren’t certain why some people develop Sjogren’s syndrome and others don’t. Certain genes put people at higher risk for the disorder, but it appears that a triggering mechanism — such as infection with a particular virus or strain of bacteria — is also necessary.

In Sjogren’s syndrome, your immune system first targets the moisture-secreting glands of your eyes and mouth. But it can also damage other parts of your body, such as your:

*Joints
*Thyroid
*Kidneys
*Liver
*Lungs
*Skin
*Nerves
Risk Factors:
Although anyone can develop Sjogren’s syndrome, it typically occurs in people with one or more known risk factors. These include:

*Age. Sjogren’s syndrome is usually diagnosed in people older than 40.
*Sex. Women are much more likely to have Sjogren’s syndrome.
*Rheumatic disease. It’s common for people who have Sjogren’s syndrome to also have a rheumatic disease — such as rheumatoid arthritis or lupus.

Complications:
The most common complications of Sjogren’s syndrome involve your eyes and mouth.

*Dental cavities. Because saliva helps protect the teeth from the bacteria that cause cavities, you’re more prone to developing cavities if your mouth is dry.

*Yeast infections. People with Sjogren’s syndrome are much more likely to develop oral thrush, a yeast infection in the mouth.

*Vision problems. Dry eyes can lead to light sensitivity, blurred vision and corneal ulcers.

Less common complications may affect your:

*Lungs, kidneys or liver. Inflammation may cause pneumonia, bronchitis or other problems in your lungs; may lead to problems with kidney function; and may cause hepatitis or cirrhosis in your liver.

*Unborn baby. If you’re a woman with Sjogren’s syndrome and you plan to become pregnant, talk with your doctor about being tested for certain autoantibodies that may be present in your blood. In rare cases, these antibodies have been associated with heart problems in newborns

*Lymph nodes. A small percentage of people with Sjogren’s syndrome develop cancer of the lymph nodes (lymphoma).

*Nerves. You may develop numbness, tingling and burning in your hands and feet (peripheral neuropathy).

 

Diagnosis:
Diagnosing Sjögren’s syndrome is complicated by the range of symptoms a patient may manifest, and the similarity between symptoms of Sjögren’s syndrome and those of other conditions. Nevertheless, the combination of several tests can lead to a diagnosis of Sjögren’s syndrome.

Blood tests can be done to determine if a patient has high levels of antibodies that are indicative of the condition, such as anti-nuclear antibody (ANA) and rheumatoid factor (because SS frequently occurs secondary to rheumatoid arthritis), which are associated with autoimmune diseases. Typical Sjögren’s syndrome ANA patterns are SSA/Ro and SSB/La, of which SSB/La is far more specific; SSA/Ro is associated with numerous other autoimmune conditions but are often present in Sjögren’s.

Schirmer’s test measures the production of tears: a strip of filter paper is held inside the lower eyelid for five minutes, and its wetness is then measured with a ruler. Producing less than five millimeters of liquid is usually indicative of Sjögren’s syndrome. However, lacrimal function declines with age or may be impaired from other medical conditions. An alternative test is nonstimulated whole saliva flow collection, in which the patient spits into a test tube every minute for 15 minutes. A resultant collection of less than 1.5 mL is considered a positive result. It takes longer to perform than Schirmer’s test, but does not require special equipment.

A slit-lamp examination can reveal dryness on the surface of the eye. Salivary gland function can be tested by collecting saliva and determining the amount produced in a five minute period. A lip biopsy can reveal lymphocytes clustered around salivary glands, and damage to these glands due to inflammation.

Ultrasound examination of the salivary glands is the simplest confirmatory test and has the added advantage of being non-invasive with no complications. The parenchyma of the gland demonstrates multiple, small-2-6 mm hypoechoic lesions which are representations of the lymphocytic infiltrates. Often sialectasis with calculi are demonstrated if the disease is advanced. The sonographic findings have excellent symptom correlation. The other advantage of ultrasound is that complications of the disease such as extra-nodal lymphomas can often be detected as larger 1–4 cm hypoechoic intra-parenchymal masses.

There is also a radiological procedure which is a reliable and accurate test for Sjögren’s syndrome. A contrast agent is injected into the parotid duct, which opens from the cheek into the vestibule of the mouth opposite the neck of the upper second molar tooth. Widespread puddling of the injected contrast scattered throughout the gland indicates Sjögren’s syndrome.

The Revised Classification Criteria for Sjögren’s Syndrome requires the presence of signs, symptoms, and lab findings.

Patient-reported symptoms must include both ocular symptoms, such as daily, persistent, troublesome dry eyes for more than three months, and oral symptoms, such as needing to drink water to swallow food.

Objective evidence of eye involvement relies on Schirmer’s test and the Rose bengal score (or similar). Histopathology studies should show focal lymphocytic sialadenitis. Objective evidence of salivary gland involvement is tested through ultrasound examinations, the level of unstimulated whole salivary flow, a parotid sialography, or salivary scintigraphy. Autoantibodies against Ro (SSA) and/or La (SSB) antigens are also expected.

SS can be excluded from people with past head and neck radiation therapy, hepatitis C infection, Acquired immunodeficiency syndrome (AIDS), pre-existing lymphoma, sarcoidosis, graft-versus-host disease, and use of anticholinergic drugs (since a time shorter than four times the life of the drug).

 

Treatment:
It’s not possible to prevent Sjogren’s syndrome and there’s no cure, but treatments can help to relieve many of the symptoms. Treatment varies depending on which parts of the body are affected and may include:

•Artificial tears to help with dry eyes
•Saliva stimulants and mouth lubricants for dry mouth
•Anti-inflammatory medication for joint or muscle pain
•Corticosteroids or immunosuppressive drugs for lung, kidney, blood vessel or nervous system problems

Lifestyle and home remedies:

Many symptoms of Sjogren’s syndrome respond well to self-care measures.

To relieve dry eyes:

*Use artificial tears, an eye lubricant or both. Artificial tears (in eyedrop form) and eye lubricants (in eyedrop, gel or ointment form) help relieve the discomfort of dry eyes. Both types of product are available over-the-counter. You don’t have to apply eye lubricants as often as artificial tears. Because of their thicker consistency, though, eye lubricants can blur your vision and collect on your eyelashes. Your doctor may recommend artificial tears without preservatives because the preservatives can be irritating for people with dry eye syndrome.

* Increase humidity. Increasing the indoor humidity and reducing your exposure to blowing air may help keep your eyes from getting uncomfortably dry. For example, avoid sitting in front of a fan or air-conditioning vent, and wear goggles or protective eyewear when you go outdoors.

To help with dry mouth:

*Increase  fluid intake. Drinking lots of fluids, particularly water, helps to reduce dry mouth.

*Stimulate saliva flow. Sugarless gum or hard candies can boost saliva flow. Because Sjogren’s syndrome increases your risk of dental cavities, limit sweets, especially between meals. Lemon juice in water can also help stimulate saliva flow.

*Try artificial saliva. Saliva replacement products often work better than plain water because they contain a lubricant that helps your mouth stay moist longer. These products may come as a spray or lozenge.

*Use nasal saline spray. A nasal saline spray can help moisturize and clear nasal passages so you can breathe freely through your nose. A dry, stuffy nose can increase mouth breathing.

Oral health:

Dry mouth increases your risk of dental cavities and tooth loss. The following precautions may help prevent those types of problems.

*Brush your teeth and floss after every meal.

*Schedule regular dental appointments, at least every six months.

*Use daily topical fluoride treatments and antimicrobial mouthwashes.

Other areas of dryness:

If dry skin is a problem, avoid hot water when you bathe and shower. Pat your skin — don’t rub — with a towel and apply moisturizer when your skin is still damp. Use rubber gloves when doing dishes or housecleaning. Vaginal moisturizers and lubricants help women who experience vaginal dryness.

 

Prognosis:-
Sjögren’s can damage vital organs of the body with symptoms that may plateau or worsen, but the disease does not go into remission as with other autoimmune diseases. Some people may experience only the mild symptoms of dry eyes and mouth, while others have symptoms of severe disease. Many patients are able to treat problems symptomatically. Others are forced to cope with blurred vision, constant eye discomfort, recurrent mouth infections, swollen parotid glands, hoarseness, and difficulty in swallowing and eating. Debilitating fatigue and joint pain can seriously impair quality of life. Some patients can develop renal involvement (autoimmune tubulointerstitial nephritis) leading to proteinuria, urinary concentrating defect and distal renal tubular acidosis.

Patients with Sjögren’s syndrome have a higher rate of non-Hodgkin lymphoma compared to both patients with other autoimmune diseases and healthy people.  About 5% of patients with Sjögren’s syndrome will develop some form of lymphoid malignancy. Patients with severe cases are much more likely to develop lymphomas than patients with mild or moderate cases. The most common lymphomas are salivary extranodal marginal zone B cell lymphomas (MALT lymphomas in the salivary glands)   and diffuse large B-cell lymphoma.

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

Resources:

http://halter4sen.org/wp-content/uploads/2011/09/sjogren_syndrome.jpg

http://en.wikipedia.org/wiki/Sj%C3%B6gren’s_syndrome

http://www.mayoclinic.com/health/sjogrens-syndrome/DS00147

http://www.bbc.co.uk/health/physical_health/conditions/sjogrensyndrome1.shtml

http://pubs.acs.org/subscribe/archive/mdd/v05/i04/html/04disease.html

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Silicosis

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Alternative Names :P otter’s rot,  Acute silicosis; Chronic silicosis; Accelerated silicosis; Progressive massive fibrosis; Conglomerate silicosis; Silicoproteinosis

Definition:
Silicosis is a respiratory disease caused by breathing in (inhaling) silica dust. It is an occupational lung disease that develops over time when dust that contains silica is inhaled into the lungs. Other examples of occupational lung disease include coalworker’s pneumoconiosis and asbestosis.

The name silicosis (from the Latin silex, or flint) was originally used in 1870 by Achille Visconti (1836-1911), prosector in the Ospedale Maggiore of Milan. The recognition of respiratory problems from breathing in dust dates to ancient Greeks and Romans. Agricola, in the mid-16th century, wrote about lung problems from dust inhalation in miners. In 1713, Bernardino Ramazzini noted asthmatic symptoms and sand-like substances in the lungs of stone cutters. With industrialization, as opposed to hand tools, came increased production of dust. The pneumatic hammer drill was introduced in 1897 and sandblasting was introduced in about 1904, both significantly contributing to the increased prevalence of silicosis.

Classification:
Classification of silicosis is made according to the disease’s severity (including radiographic pattern), onset, and rapidity of progression. These include:

Chronic simple silicosis
Usually resulting from long-term exposure (10 years or more) to relatively low concentrations of silica dust and usually appearing 10–30 years after first exposure. This is the most common type of silicosis. Patients with this type of silicosis, especially early on, may not have obvious signs or symptoms of disease, but abnormalities may be detected by x-ray. Chronic cough and exertional dyspnea are common findings. Radiographically, chronic simple silicosis reveals a profusion of small (<10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones.
…..Click to see the pictures………..(2)….(1)
Accelerated silicosis
Silicosis that develops 5–10 years after first exposure to higher concentrations of silica dust. Symptoms and x-ray findings are similar to chronic simple silicosis, but occur earlier and tend to progress more rapidly. Patients with accelerated silicosis are at greater risk for complicated disease, including progressive massive fibrosis (PMF).

Complicated silicosis
Silicosis can become “complicated” by the development of severe scarring (progressive massive fibrosis, or also known as conglomerate silicosis), where the small nodules gradually become confluent, reaching a size of 1 cm or greater. PMF is associated with more severe symptoms and respiratory impairment than simple disease. Silicosis can also be complicated by other lung disease, such as tuberculosis, non-tuberculous mycobacterial infection, and fungal infection, certain autoimmune diseases, and lung cancer. Complicated silicosis is more common with accelerated silicosis than with the chronic variety.
...Click to see the picture
Acute silicosis
Silicosis that develops a few weeks to 5 years after exposure to high concentrations of respirable silica dust. This is also known as silicoproteinosis. Symptoms of acute silicosis include more rapid onset of severe disabling shortness of breath, cough, weakness, and weight loss, often leading to death. The x-ray usually reveals a diffuse alveolar filling with air bronchograms, described as a ground-glass appearance, and similar to pneumonia, pulmonary edema, alveolar hemorrhage, and alveolar cell lung cancer.

Symptoms:
Because chronic silicosis is slow to develop, signs and symptoms may not appear until years after exposure. Signs and symptoms include:

*Dyspnea (shortness of breath) exacerbated by exertion

*Cough, often persistent and sometimes severe

*Fatigue

*Tachypnea (rapid breathing) which is often labored

*Loss of appetite and weight loss

*Chest pain

*Fever

*Gradual dark shallow rifts in nails eventually leading to cracks as protein fibers within nail beds are destroyed.

In advanced cases, the following may also occur:

*Cyanosis (blue skin)

*Cor pulmonale (right ventricle heart disease)

*Respiratory insufficiency

Patients with silicosis are particularly susceptible to tuberculosis (TB) infection—known as silicotuberculosis. The reason for the increased risk—3 fold increased incidence—is not well understood. It is thought that silica damages pulmonary macrophages, inhibiting their ability to kill mycobacteria. Even workers with prolonged silica exposure, but without silicosis, are at a similarly increased risk for TB.

Pulmonary complications of silicosis also include Chronic Bronchitis and airflow limitation (indistinguishable from that caused by smoking), non-tuberculous Mycobacterium infection, fungal lung infection, compensatory emphysema, and pneumothorax. There are some data revealing an association between silicosis and certain autoimmune diseases, including nephritis, Scleroderma, and Systemic Lupus Erythematosus, especially in acute or accelerated silicosis.

In 1996, the International Agency for Research on Cancer (IARC) reviewed the medical data and classified crystalline silica as “carcinogenic to humans.” The risk was best seen in cases with underlying silicosis, with relative risks for lung cancer of 2-4. Numerous subsequent studies have been published confirming this risk. In 2006, Pelucchi et al. concluded, “The silicosis-cancer association is now established, in agreement with other studies and meta-analysis

Causes:
Silica in crystalline form is toxic to the lining of the lungs. When the two come into contact, a strong inflammatory reaction occurs. Over time this inflammation causes the lung tissue to become irreversibly thickened and scarred – a condition known as fibrosis.

Common sources of crystalline silica dust include:

•Sandstone
•Granite
•Slate
•Coal
•Pure silica sand

People who work with these materials, as well as foundry workers, potters and sandblasters, are most at risk. Other forms of silica, such as glass, are less of a health risk as they aren’t as toxic to the lungs.

Men tend to be affected more often than women, as they are more likely to have been exposed to silica.

Risk Factors:
Silicosis is most commonly diagnosed in people over 40, as it usually takes years of exposure before the gradually progressive lung damage becomes apparent.

There are now fewer than 100 new cases of silicosis diagnosed each year in the UK. This is mostly the result of better working practices, such as wet drilling, appropriate ventilation, dust-control facilities, showers and the use of face masks. Many foundries are also replacing silica sand with synthetic materials.

With these measures and an increased awareness of the risks of silica exposure, the number of cases should fall even further in the future.

When silicosis is suspected, a chest x-ray will look for any damaged areas of the lungs to confirm the diagnosis. Lung function tests are often performed to assess the amount of damage the lungs have suffered and to guide treatment.

Possible Complications:
•Connective tissue disease, including rheumatoid arthritis, scleroderma (also called progressive systemic sclerosis), and systemic lupus erythematosus
•Lung cancer
•Progressive massive fibrosis
•Respiratory failure
•Tuberculosis

You may click to see the pictures:    ->(1) Simple  silicosis    :   (2)  Complicated silicosis    :(3) Silicosis.ILO Classification 2-2 R-R  :

Diagnosis:
There are three key elements to the diagnosis of silicosis. First, the patient history should reveal exposure to sufficient silica dust to cause this illness. Second, chest imaging (usually chest x-ray) that reveals findings consistent with silicosis. Third, there are no underlying illnesses that are more likely to be causing the abnormalities. Physical examination is usually unremarkable unless there is complicated disease. Also, the examination findings are not specific for silicosis. Pulmonary function testing may reveal airflow limitation, restrictive defects, reduced diffusion capacity, mixed defects, or may be normal (especially without complicated disease). Most cases of silicosis do not require tissue biopsy for diagnosis, but this may be necessary in some cases, primarily to exclude other conditions.

For uncomplicated silicosis, chest x-ray will confirm the presence of small (< 10 mm) nodules in the lungs, especially in the upper lung zones. Using the ILO classification system, these are of profusion 1/0 or greater and shape/size “p”, “q”, or “r”. Lung zone involvement and profusion increases with disease progression. In advanced cases of silicosis, large opacity (> 1 cm) occurs from coalescence of small opacities, particularly in the upper lung zones. With retraction of the lung tissue, there is compensatory emphysema. Enlargement of the hilum is common with chronic and accelerated silicosis. In about 5-10% of cases, the nodes will calcify circumferentially, producing so-called “eggshell” calcification. This finding is not pathognomonic (diagnostic) of silicosis. In some cases, the pulmonary nodules may also become calcified.

A computed tomography or CT scan can also provide a mode detailed analysis of the lungs, and can reveal cavitation due to concomitant mycobacterial infection.

Treatment:
Silicosis is an irreversible condition with no cure.  Treatment options currently focus on alleviating the symptoms and preventing complications. These include:

*Stopping further exposure to silica and other lung irritants, including tobacco smoking.

*Cough suppressants.

*Antibiotics for bacterial lung infection.

*TB prophylaxis for those with positive tuberculin skin test or IGRA blood test.

*Prolonged anti-tuberculosis (multi-drug regimen) for those with active TB.

*Chest physiotherapy to help the bronchial drainage of mucus.

*Oxygen administration to treat hypoxemia, if present.

*Bronchodilators to facilitate breathing.

*Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.

*For acute silicosis, Whole-lung lavage (see Bronchoalveolar lavage) may alleviate symptoms, but does not decrease overall mortality.

Experimental treatments include:

*Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.

*Corticosteroid therapy.

*The herbal extract tetrandine may slow progression of silicosis.

Support Groups:
Joining a support group where you can meet other people with silicosis or related diseases can help you understand your disease and adapt to its treatments.

Prognosis:
The outcome varies depending on the amount of damage to the lungs.

Prevention:
The best way to prevent silicosis is to identify work-place activities that produce respirable crystalline silica dust and then to eliminate or control the dust (“primary prevention”). Water spray is often used where dust emanates. Dust can also be controlled through dry air filtering.

Following observations on industry workers in Lucknow (India), experiments on rats found that jaggery (a traditional sugar) had a preventive action against silicosis.

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

Resources:

http://en.wikipedia.org/wiki/Silicosis

http://www.nlm.nih.gov/medlineplus/ency/article/000134.htm

http://www.smianalytical.com/dust-sampling/what-is-silicosis.html

http://www.bbc.co.uk/health/physical_health/conditions/silicosis1.shtml

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Sepsis

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Alternative Names: Systemic inflammatory response syndrome (SIRS),blood poisoning or septicaemia.

Definition:
Sepsis is a bacterial infection of the blood.It is a severe illness in which the bloodstream is overwhelmed by bacteria.While sepsis can happen to anyone, it’s most common and most dangerous in people who are elderly or who have weakened immune systems.

CLICK TO SEE THE PICTURE
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Sepsis occurs when chemicals released into the bloodstream to fight the infection trigger inflammation throughout the body. This inflammation creates microscopic blood clots that can block nutrients and oxygen from reaching organs, causing them to fail. If sepsis progresses to septic shock, blood pressure drops dramatically and the person may die.

Early treatment of sepsis, usually with antibiotics and large amounts of intravenous fluids, improves chances for survival.

Symptoms:
In addition to symptoms related to the provoking infection, sepsis is characterized by presence of acute inflammation present throughout the entire body, and is, therefore, frequently associated with fever and elevated white blood cell count (leukocytosis) or low white blood cell count and lower-than-average temperature, and vomiting. The modern concept of sepsis is that the host’s immune response to the infection causes most of the symptoms of sepsis, resulting in hemodynamic consequences and damage to organs. This host response has been termed systemic inflammatory response syndrome (SIRS) and is characterized by an elevated heart rate (above 90 beats per minute), high respiratory rate (above 20 breaths per minute or a partial pressure of carbon dioxide in the blood of less than 32), abnormal white blood cell count (above 12,000, lower than 4,000, or greater than 10% band forms) and elevated or lowered body temperature, i.e. under 36 °C (97 °F) or over 38 °C (100 °F). Sepsis is differentiated from SIRS by the presence of a known or suspected pathogen. For example SIRS and a positive blood culture for a pathogen indicates the presence of sepsis. However, in many cases of sepsis no specific pathogen is identified.

This immunological response causes widespread activation of acute-phase proteins, affecting the complement system and the coagulation pathways, which then cause damage to the vasculature as well as to the organs. Various neuroendocrine counter-regulatory systems are then activated as well, often compounding the problem. Even with immediate and aggressive treatment, this may progress to multiple organ dysfunction syndrome and eventually death.

Causes:
Sepsis is often a complication of another infection, such as of the lungs or kidneys, and occurs when the bacteria escape that part of the body and get into the bloodstream.

This bacteria can also come from burns, infected wounds, boils and tooth abscesses. Sometimes it isn’t obvious how it has got into your blood.

Anyone can develop sepsis. The people most at risk are those with weakened immune systems, because of an existing illness, for example, or medication.

Older people, children and intravenous drug users are also more susceptible.

In children, sepsis may accompany infection of the bone (osteomyelitis). In hospitalized patients, common sites of infection include intravenous lines, surgical wounds, surgical drains, and sites of skin breakdown known as bedsores (decubitus ulcers).

Risk Factors:
Sepsis is more common and more dangerous in people who:

*Are very young or very old
*Have compromised immune systems
*Are already very sick, often in a hospital’s intensive care unit
*Have invasive devices, such as intravenous catheters or breathing tubes

Complication:
As sepsis worsens, blood flow to vital organs, such as your brain, heart and kidneys, becomes impaired. Sepsis can also cause blood clots to form in your organs and in your arms, legs, fingers and toes — leading to varying degrees of organ failure and tissue death (gangrene).

Most people recover from mild sepsis, but the mortality rate for severe sepsis or septic shock is close to 50 percent.

Diagnosis:
The infection is often confirmed by a blood test. However, a blood test may not reveal infection in people who have been receiving antibiotics.

Other tests that may be done include:
•Blood gases
•Kidney function tests
•Platelet count
•White blood cell count
•Blood differential
•Fibrin degradation products
•Peripheral smear

Treatment;
Early, aggressive treatment boosts your chances of surviving sepsis. People with severe sepsis require close monitoring and treatment in a hospital intensive care unit. If one has severe sepsis or septic shock, lifesaving measures may be needed to stabilize breathing and heart function.

Medications
A number of different types of medications are used in treating sepsis. They include:

*Antibiotics. Treatment with antibiotics begins immediately — even before the infectious agent is identified. Initially you’ll receive broad-spectrum antibiotics, which are effective against a variety of bacteria. The antibiotics are administered intravenously (IV). After learning the results of blood tests, your doctor may switch to a different antibiotic that’s more appropriate against the particular bacteria causing the infection.

*Vasopressors. If your blood pressure remains too low even after receiving intravenous fluids, you may be given a vasopressor medication, which constricts blood vessels and helps to increase blood pressure.

*Others. Other medications you may receive include low doses of corticosteroids, insulin to help maintain stable blood sugar levels, drugs that modify the immune system responses, and painkillers or sedatives.Therapy

People with severe sepsis usually receive supportive care including oxygen and large amounts of intravenous fluids. Depending on your condition, you may need to have a machine help you breathe or dialysis for kidney failure.

Surgery
Surgery may be needed to remove sources of infection, such as collections of pus (abscesses).

Prognosis:
This section requires expansion.

Prognosis can be estimated with the Mortality in Emergency Department Sepsis (MEDS) score.  Approximately 20–35% of patients with severe sepsis and 40–60% of patients with septic shock die within 30 days. Others die within the ensuing 6 months. Late deaths often result from poorly controlled infection, immunosuppression, complications of intensive care, failure of multiple organs, or the patient’s underlying disease.

Prognostic stratification systems such as APACHE II indicate that factoring in the patient’s age, underlying condition, and various physiologic variables can yield estimates of the risk of dying of severe sepsis. Of the individual covariates, the severity of underlying disease most strongly influences the risk of death. Septic shock is also a strong predictor of short- and long-term mortality. Case-fatality rates are similar for culture-positive and culture-negative severe sepsis.

Some patients may experience severe long-term cognitive decline following an episode of severe sepsis, but the absence of baseline neuropsychological data in most sepsis patients makes the incidence of this difficult to quantify or to study. A preliminary study of nine patients with septic shock showed abnormalities in seven patients by MRI.

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


Resources:

http://www.mayoclinic.com/health/sepsis/DS01004

http://www.nlm.nih.gov/medlineplus/ency/article/000666.htm

http://en.wikipedia.org/wiki/Sepsis

http://www.bbc.co.uk/health/physical_health/conditions/sepsis.shtml

http://www.humenhealth.com/sepsis/sepsis.asp

http://images.emedicinehealth.com/images/4453/4453-4482-12996-21147.jpg

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Scarlet fever

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Alternative Names : Scarlatina

Definition:
Scarlet fever is a disease caused by infection with the group A Streptococcus bacteria (the same bacteria that causes strep throat).Once a major cause of death, it is now effectively treated with antibiotics. The term scarlatina may be used interchangeably with scarlet fever, though it is commonly used to indicate the less acute form of scarlet fever that is often seen since the beginning of the twentieth century.
click to  see the picture
It can affect people of any age. However, it’s most common between the ages of six and 12.

Symptoms:

The time between becoming infected and having symptoms is short, generally 1 – 2 days. The illness typically begins with a fever and sore throat.

 

click to see the pictures..….(1).……..(2)..……...(3).……………………………
The rash usually first appears on the neck and chest, then spreads over the body. It is described as “sandpapery” in feel. The texture of the rash is more important than the appearance in confirming the diagnosis. The rash can last for more than a week. As the rash fades, peeling (desquamation) may occur around the fingertips, toes, and groin area.

The common signs and symptoms that give scarlet fever are as follows:

*Red rash. The rash looks like a sunburn and feels like sandpaper. It typically begins on the face or neck and spreads to the trunk, arms and legs. If pressure is applied to the reddened skin, it will turn pale.

*Red lines. The folds of skin around the groin, armpits, elbows, knees and neck usually become a deeper red than the surrounding rash.

*Flushed face. The face may appear flushed with a pale ring around the mouth.

*Strawberry tongue. The tongue generally looks red and bumpy, and it’s often covered with a white coating early in the disease.

The rash and the redness in the face and tongue usually last about a week. After these signs and symptoms have subsided, the skin affected by the rash often peels. Other signs and symptoms associated with scarlet fever include:

*Fever of 101 F (38.3 C) or higher, often with chills

*Very sore and red throat, sometimes with white or yellowish patches

*Difficulty swallowing

*Enlarged glands in the neck (lymph nodes) that are tender to the touch

*Nausea or vomiting

*Headache

*Abdominal pain

*Bright red color in the creases of the underarm and groin (Pastia’s lines)

*Chills

*General discomfort (malaise)

*Muscle aches

*Sore throat

*Swollen, red tongue (strawberry tongue)

Causes:
Scarlet fever is caused by the same type of bacteria that cause strep throat. In scarlet fever, the bacteria release a toxin that produces the rash and red tongue.

The infection spreads from person to person via droplets expelled when an infected person coughs or sneezes. The incubation period — the time between exposure and illness — is usually two to four days.

Risk Factors:
Children 6 to 12 years of age are more likely than are other people to get scarlet fever. Scarlet fever germs spread more easily among people in close contact, such as family members or classmates.

Complications:
If scarlet fever goes untreated, the bacteria may spread to the:

*Tonsils
*Sinuses
*Skin
*Blood
*Middle ear

Rarely, scarlet fever can lead to rheumatic fever, a serious condition that can affect the:

*Heart
*Joints
*Nervous system
*Skin

Diagnosis:
Diagnosis of scarlet fever is clinical. The blood test shows marked leukocytosis with neutrophilia and conservated or increased eosinophils, high erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) (both indications of inflammation), and elevation of antistreptolysin O titer. Blood culture is rarely positive, but the streptococci can usually be demonstrated in throat culture. The complications of scarlet fever include septic complications due to spread of streptococcus in blood and immune-mediated complications due to an aberrant immune response. Septic complications—today rare—include ear and sinus infection, streptococcal pneumonia, empyema thoracis, meningitis and full-blown sepsis, upon which the condition may be called malignant scarlet fever.

Immune complications include acute glomerulonephritis, rheumatic fever and erythema nodosum. The secondary scarlatinous disease, or secondary malignant syndrome of scarlet fever, includes renewed fever, renewed angina, septic ear, nose, and throat complications and kidney infection or rheumatic fever and is seen around the eighteenth day of untreated scarlet fever.

The rash is the most striking sign of scarlet fever. It usually begins looking like a bad sunburn with tiny bumps, and it may itch. The rash usually appears first on the neck and face, often leaving a clear unaffected area around the mouth. It spreads to the chest and back, then to the rest of the body. In body creases, especially around the underarms and elbows, the rash forms classic red streaks (on very dark skin, the streaks may appear darker than the rest of the skin). Areas of rash usually turn white (or paler brown, with dark complected skin) when pressed on. By the sixth day of the infection, the rash usually fades, but the affected skin may begin to peel. Usually there are other symptoms that help to confirm a diagnosis of scarlet fever, including a reddened sore throat, a fever at or above 101 °F (38.3 °C), and swollen glands in the neck. Scarlet fever can also occur with a low fever. The tonsils and back of the throat may be covered with a whitish coating, or appear red, swollen, and dotted with whitish or yellowish specks of pus. Early in the infection, the tongue may have a whitish or yellowish coating. Also, an infected person may have chills, body aches, nausea, vomiting, and loss of appetite.

When scarlet fever occurs because of a throat infection, the fever typically stops within 3 to 5 days, and the sore throat passes soon afterward. The scarlet fever rash usually fades on the sixth day after sore throat symptoms started, and begins to peel (as above). The infection itself is usually cured with a 10-day course of antibiotics, but it may take a few weeks for tonsils and swollen glands to return to normal.

In rare cases, scarlet fever may develop from a streptococcal skin infection like impetigo. In these cases, the person may not get a sore throat.

Treatment:
Other than the occurrence of the diarrhea, the treatment and course of scarlet fever are no different from those of any strep throat. In case of penicillin allergy, clindamycin or erythromycin can be used with success. Patients should no longer be infectious after taking antibiotics for 24 hours. People who have been exposed to scarlet fever should be watched carefully for a full week for symptoms, especially if aged 3 to young adult. It is very important to be tested (throat culture) and if positive, seek treatment.

A drug-resistant strain of scarlet fever has emerged in Hong Kong, accounting for at least two deaths in that city – the first such in over a decade. The mutant strain of the bacterium is about 60% resistant to the antibiotics, says Professor Kwok-yung Yuen, head of Hong Kong University’s microbiology department. This is compared to a previous strain of the disease, which demonstrated a 10-30% resistance. This new strain may have spread to neighboring Macau and mainland China.

Prognosis:
With proper antibiotic treatment, the symptoms of scarlet fever should get better quickly. However, the rash can last for up to 2 – 3 weeks before it fully goes away.

Prevention :
Bacteria are spread by direct contact with infected people, or by droplets exhaled by an infected person. Avoid contact with infected people.

Children should be taught  to practice the following healthy habits:

*Wash  hands. Show your child how to wash his or her hands thoroughly with warm soapy water.

*Don’t share dining utensils or food. As a general rule, your child shouldn’t share drinking glasses or eating utensils with friends or classmates. And that rule applies to food, too.

*Cover your mouth and nose. Tell your child to cover his or her mouth and nose when coughing and sneezing to prevent the potential spread of germs.If your child has scarlet fever, wash his or her drinking glasses, utensils and, if possible, toys in hot soapy water or in a dishwasher.

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

Resources:

http://www.mayoclinic.com/health/scarlet-fever/DS00917

http://en.wikipedia.org/wiki/Scarlet_fever

http://www.bbc.co.uk/health/physical_health/conditions/scarletfever1.shtml

http://www.nlm.nih.gov/medlineplus/ency/article/000974.htm

http://www.umm.edu/imagepages/19082.htm

http://www.healthofchildren.com/S/Scarlet-Fever.html

http://sigma.ontologyportal.org:4010/sigma/Browse.jsp?kb=SUMO&term=ScarletFever

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