Monday, December 28, 2015

Athetosis

Credit: tremorjournal.org

Athetosis is a symptom characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases, arms, legs, neck and tongue. Movements typical of athetosis are sometimes called athetoid movements. Lesions to the brain are most often the direct cause of the symptoms, particularly to the corpus striatum. This symptom does not occur alone and is often accompanied by the symptoms of cerebral palsy, as it is often a result of this disease. Treatments for athetosis are not very effective, and in most cases are simply aimed at the uncontrollable movement, rather than the cause itself.

Signs and Symptoms
Athetosis can vary from mild to severe motor dysfunction; it is generally characterized by unbalanced, involuntary movements of muscle tone and a difficulty maintaining a symmetrical posture. The associated motor dysfunction can be restricted to a part of body or present throughout the body, depending on the individual and the severity of the symptom. One of the pronounced signs can be observed in the extremities in particular, as the writhing, convoluted movement of the digits. Athetosis can appear as early as 18 months from birth with first signs including difficulty feeding, hypotonia, spasm, and involuntary writhing movements of the hands, feet, and face, which progressively worsen through adolescence and at times of emotional distress. Athetosis is caused by lesions in several brain areas such as the hippocampus and the motor thalamus, as well as the corpus striatum; therefore children during the developmental age could possibly suffer from cognitive deficits such as speech impairment, hearing loss, and failed or delayed acquirement of sitting balance.

Causes
Athetosis is a symptom primarily caused by the marbling, or degeneration of the basal ganglia. This degeneration is most commonly caused by complications at birth or by Huntington's disease, in addition to rare cases in which the damage may also arise later in life due to stroke or trauma. The two complications of particular interest are intranatal asphyxia and neonatal jaundice.

Sunday, December 27, 2015

Astigmatism and Your Eyes

Credit: www.eyesonyouseattle.com

Astigmatism and Your Eyes

What Is Astigmatism?
Astigmatism is a common eye condition that's usually corrected by eyeglassescontact lenses, or surgery.

Astigmatism is caused by an eye that is not completely round and occurs in nearly everybody to some degree. For vision problems due to astigmatism, glasses, contact lenses, and even vision correction procedures are all possible treatment options.
A person's eye is naturally shaped like a sphere. Under normal circumstances, when light enters the eye, it refracts, or bends evenly, creating a clear view of the object. However, the eye of a person with astigmatism is shaped more like a football or the back of a spoon. For this person, when light enters the eye it is refracted more in one direction than the other, allowing only part of the object to be in focus at one time. Objects at any distance can appear blurry and wavy.

What Causes Astigmatism?
Astigmatism is a natural and commonly occurring cause of blurred or distorted vision that is usually associated with an imperfectly shaped cornea. The exact cause in not known.

What Are the Symptoms of Astigmatism?
People with undetected astigmatism often have blurred vision which can be associated with fatigue and eyestrain. While these symptoms may not necessarily be the result of astigmatism, you should schedule an eye exam if you are experiencing one or more symptoms.

How Is Astigmatism Diagnosed?
Your eye doctor can diagnose astigmatism with a thorough eye exam. Astigmatism may occur with other vision problems such as nearsightedness and farsightedness. Because astigmatism may increase slowly, you should visit your eye doctor whenever you notice changes in your vision.

How Is Astigmatism Treated?
Almost all degrees of “normal” astigmatism can be corrected with properly prescribed eyeglasses or contact lenses. For a person with only a slight degree of astigmatism, corrective lenses may not be needed at all, as long as other conditions, such as nearsightedness or farsightedness, are not present. If the astigmatism is moderate to high, however, corrective glasses or contact lenses are probably needed.
Irregular astigmatism is far less common and is associated with abnormal conditions affecting the cornea (for example, keratoconus). This condition is more effectively treated with rigid gas permeable contact lenses or corneal procedures.
  • Corrective lenses (eyeglasses or contact lenses). Astigmatism correction can usually be easily incorporated into eye glasses. Alternatively, special soft contact lenses called toric lenses can be prescribed. Soft toric lenses have greater light-bending power in one direction than the other. Another option, particularly for higher amounts of astigmatism, is a gas-permeable rigid contact lens. After performing various tests, your eye doctor will determine the ideal prescription for your astigmatism.
  • Refractive surgery. Another method for correcting astigmatism is changing the shape of the cornea through refractive or laser eye surgery. While there is more than one type of refractive surgery, specific treatments are recommended on an individual basis. Refractive surgeries require healthy eyes that are free from retinal problems, corneal scars, and any eye disease.    Read more >>
Source: http://www.webmd.com/eye-health/astigmatism-eyes

Wednesday, September 16, 2015

Atherosclerosis

What Is Atherosclerosis?
Credit: www.azvascular.com

Atherosclerosis -- hardening and narrowing of the arteries -- gets a lot of bad press but with good reason. This progressive process silently and slowly blocks arteries, putting blood flow at risk.

Atherosclerosis is the usual cause of heart attacks, strokes, and peripheral vascular disease -- what together are called "cardiovascular disease." Cardiovascular disease is the No. 1 killer in America, with more than 800,000 deaths in 2005.


How does atherosclerosis develop? Who gets it, and why? This deadly process is preventable and treatable. Read on, and get to know your enemy.

What Causes Atherosclerosis?
First, an Anatomy 101 review: Arteries are blood vessels that carry blood from the heart throughout the body. They're lined by a thin layer of cells called the endothelium. The endothelium works to keep the inside of arteries toned and smooth, which keeps blood flowing.
According to experts, atherosclerosis begins with damage to the endothelium caused by high blood pressuresmoking, or highcholesterol. That damage leads to the formation of plaque.
When bad cholesterol, or LDL, crosses the damaged endothelium, thecholesterol enters the wall of the artery. That causes your white blood cells to stream in to digest the LDL. Over years, the accumulating mess of cholesterol and cells becomes a plaque in the wall of the artery.

Plaque is a jumble of cholesterol, cells, and debris that creates a bump on the artery wall. As atherosclerosis progresses, that bump gets bigger. And when it gets big enough, it can create a blockage. That process goes on throughout your entire body. As a result, not only is your heart at risk but you are also at risk for stroke and other kinds of health problems.

Sunday, September 13, 2015

Asthma


Asthma (from the Greek ἅσθμα, ásthma, "panting") is a common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction and bronchospasm.Common symptoms include wheezing, coughing, chest tightness, and shortness of breath.
Asthma is thought to be caused by a combination of genetic and environmental factors. Its diagnosis is usually based on the pattern of symptoms, response to therapy over time and spirometry. It is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic) where atopy refers to a predisposition toward developing type 1 hypersensitivity reactions.
Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol) and oral corticosteroids. In very severe cases, intravenous corticosteroids, magnesium sulfate, and hospitalization may be required. Symptoms can be prevented by avoiding triggers, such as allergens and irritants, and by the use of inhaled corticosteroids. Long-acting beta agonists (LABA) or antileukotriene agents may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled. The occurrence of asthma has increased significantly since the 1970s. In 2011, 235–300 million people globally were diagnosed with asthma, and it caused 250,000 deaths.

Signs and symptoms
Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Sputum may be produced from the lung by coughing but is often hard to bring up. During recovery from an attack, it may appear pus-like due to high levels of white blood cells called eosinophils. Symptoms are usually worse at night and in the early morning or in response to exercise or cold air. Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked and persistent symptoms.

Associated conditions
A number of other health conditions occur more frequently in those with asthma, including gastro-esophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea. Psychological disorders are also more common, with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%. However, it is not known if asthma causes psychological problems or if psychological problems lead to asthma. Those with asthma, especially if it is poorly controlled, are at high risk for radiocontrast reactions.

Causes
Asthma is caused by a combination of complex and incompletely understood environmental and genetic interactions. These factors influence both its severity and its responsiveness to treatment. It is believed that the recent increased rates of asthma are due to changing epigenetics (heritable factors other than those related to the DNA sequence) and a changing living environment.

Environmental
Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. Low air quality from factors such as traffic pollution or high ozone levels, has been associated with both asthma development and increased asthma severity. Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. Also, phthalates in certain types of PVC are associated with asthma in children and adults.

There is an association between acetaminophen (paracetamol) use and asthma. The majority of the evidence does not, however, support a causal role. A 2014 review found that the association disappeared when respiratory infections were taken into account. Use by a mother during pregnancy is also associated with an increased risk.

Asthma is associated with exposure to indoor allergens. Common indoor allergens include dust mites, cockroaches, animal dander, and mold. Efforts to decrease dust mites have been found to be ineffective. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.

Hygiene hypothesis
The hygiene hypothesis attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses. It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies. Exposure to bacterial endotoxin in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.

Use of antibiotics in early life has been linked to the development of asthma. Also, delivery via caesarean section is associated with an increased risk (estimated at 20–80%) of asthma—this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would have acquired from passage through the birth canal. There is a link between asthma and the degree of affluence.

Genetic
Family history is a risk factor for asthma, with many different genes being implicated. If one identical twin is affected, the probability of the other having the disease is approximately 25%. By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1, IL10, CTLA-4, SPINK5, LTC4S, IL4R and ADAM33, among others. Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested. In 2006 over 100 genes were associated with asthma in one genetic association study alone; more continue to be found.
Some genetic variants may only cause asthma when they are combined with specific environmental exposures. An example is a specific single nucleotide polymorphism in the CD14 region and exposure to endotoxin (a bacterial product). Endotoxin exposure can come from several environmental sources including tobacco smoke, dogs, and farms. Risk for asthma, then, is determined by both a person's genetics and the level of endotoxin exposure.

Medical conditions
A triad of atopic eczema, allergic rhinitis and asthma is called atopy. The strongest risk factor for developing asthma is a history of atopic disease; with asthma occurring at a much greater rate in those who have either eczema or hay fever. Asthma has been associated with Churg–Strauss syndrome, an autoimmune disease and vasculitis. Individuals with certain types of urticaria may also experience symptoms of asthma.

There is a correlation between obesity and the risk of asthma with both having increased in recent years. Several factors may be at play including decreased respiratory function due to a buildup of fat and the fact that adipose tissue leads to a pro-inflammatory state.

Beta blocker medications such as propranolol can trigger asthma in those who are susceptible. Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease. Other medications that can cause problems in asthmatics are angiotensin-converting enzyme inhibitors, aspirin, and NSAIDs.

Exacerbation
Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different individuals react to various factors in different ways. Most individuals can develop severe exacerbation from a number of triggering agents.


Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold. Perfumes are a common cause of acute attacks in women and children. Both viral and bacterial infections of the upper respiratory tract can worsen the disease. Psychological stress may worsen symptoms—it is thought that stress alters the immune system and thus increases the airway inflammatory response to allergens and irritants.

Source: https://en.wikipedia.org/wiki/Asthma

Friday, September 11, 2015

Asthenia

Credit: acner.org

Weakness or asthenia is a symptom of a number of different conditions. The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis.


Differential diagnosis
True vs. perceived weakness
True weakness (or neuromuscular) describes a condition where the force exerted by the muscles is less than would be expected, for example muscular dystrophy.

Perceived weakness (or non-neuromuscular) describes a condition where a person feels more effort than normal is required to exert a given amount of force but actual muscle strength is normal, for example chronic fatigue syndrome.

In some conditions, such as myasthenia gravis, muscle strength is normal when resting, but true weakness occurs after the muscle has been subjected to exercise. This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions.

Asthenia vs. myasthenia
Asthenia (Greek: ἀσθένεια, lit. lack of strength but also disease) is a medical term referring to a condition in which the body lacks or has lost strength either as a whole or in any of its parts. It denotes symptoms of physical weakness and loss of strength. General asthenia occurs in many chronic wasting diseases (such as tuberculosis and cancer), sleep disorders or chronic disorders of the heart, lungs or kidneys, and is probably most marked in diseases of the adrenal gland. Asthenia may be limited to certain organs or systems of organs, as in asthenopia, characterized by ready fatiguability. Asthenia is also a side effect of some medications and treatments, such as Ritonavir (a protease inhibitor used in HIV treatment), vaccines such as the HPV vaccine Gardasil and fentanyl patches (an opioid used to treat pain).

Differentiating psychogenic (perceived) asthenia and true asthenia from myasthenia is often difficult, and in time apparent psychogenic asthenia accompanying many chronic disorders is seen to progress into a primary weakness.

Myasthenia (my- from Greek μυο meaning "muscle" + -asthenia ἀσθένεια meaning "weakness"), or simply muscle weakness, is a lack of muscle strength. The causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular diseases, such as myasthenia gravis.

Types
Muscle fatigue can be central, neuromuscular, or peripheral muscular. Central muscle fatigue manifests as an overall sense of energy deprivation, and peripheral muscle weakness manifests as a local, muscle-specific inability to do work. Neuromuscular fatigue can be either central or peripheral.

Central fatigue
The central fatigue is generally described in terms of a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output. It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity. The exact mechanisms of central fatigue are unknown, though there has been a great deal of interest in the role of serotonergic pathways.

Neuromuscular fatigue
Nerves control the contraction of muscles by determining the number, sequence, and force of muscular contraction. When a nerve experiences synaptic fatigue it becomes unable to stimulate the muscle that it innervates. Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue.

For extremely powerful contractions that are close to the upper limit of a muscle's ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice strength trainers, the muscle's ability to generate force is most strongly limited by nerve’s ability to sustain a high-frequency signal. After an extended period of maximum contraction, the nerve’s signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply ‘stop listening’ and gradually cease to move, often lengthening. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle soreness following the workout. Part of the process of strength training is increasing the nerve's ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force. It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force.

Peripheral muscle fatigue
Peripheral muscle fatigue during physical work is considered[by whom?] an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. This is the most common case of physical fatigue—affecting a national[where?] average of 72% of adults in the work force in 2002. This causes contractile dysfunction that manifests in the eventual reduction or lack of ability of a single muscle or local group of muscles to do work. The insufficiency of energy, i.e. sub-optimal aerobic metabolism, generally results in the accumulation of lactic acid and other acidic anaerobic metabolic by-products in the muscle, causing the stereotypical burning sensation of local muscle fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy.

The fundamental difference between the peripheral and central theories of muscle fatigue is that the peripheral model of muscle fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. Peripheral regulation therefore depends on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore, the feedback that is read by this central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors will depend on the nature of the fatigue-inducing work that is being performed.

Though not universally used, "metabolic fatigue" is a common alternative term for peripheral muscle weakness, because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the myocytes. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca2+ to stimulate actin and myosin to contract.

Lactic acid hypothesis
It was once believed that lactic acid build-up was the cause of muscle fatigue. The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.

Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles. This can lower the sensitivity of contractile apparatus to calcium ions (Ca2+) but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell. This counters inhibiting effects of potassium ions (K+) on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving K+ as the only restricting influence on muscle contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.

Pathophysiology
Main article: muscle contraction
Muscle cells work by detecting a flow of electrical impulses from the brain, which signals them to contract through the release of calcium by the sarcoplasmic reticulum. Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle cell. This makes less calcium available for the muscle cell. In addition, the Columbia researchers propose that an enzyme activated by this released calcium eats away at muscle fibers.

Substrates within the muscle generally serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model. Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct. Contrary to common belief, lactic acid accumulation doesn't actually cause the burning sensation we feel when we exhaust our oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce pyruvate in the liver, which is known as the Cori cycle.
Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so.

Source: https://en.wikipedia.org/wiki/Weakness

Thursday, September 10, 2015

Arthritis

Credit: mamapacks.eu

Arthritis (from Greek arthro-, joint + -itis, inflammation; plural: arthritides) is a form of joint disorder that involves inflammation of one or more joints. There are over 100 different forms of arthritis. The most common form of arthritis is osteoarthritis (degenerative joint disease), a result of trauma to the joint, infection of the joint, or age. Other arthritis forms are rheumatoid arthritis, psoriatic arthritis, and related autoimmune diseases. Septic arthritis is caused by joint infection.


The major complaint by individuals who have arthritis is joint pain. Pain is often a constant and may be localized to the joint affected. The pain from arthritis is due to inflammation that occurs around the joint, damage to the joint from disease, daily wear and tear of joint, muscle strains caused by forceful movements against stiff painful joints and fatigue.

Classification
There are several diseases where joint pain is primary, and is considered the main feature. Generally when a person has "arthritis" it means that they have one of these diseases, which include:
  • Osteoarthritis
  • Rheumatoid arthritis
  • Gout and pseudo-gout
  • Septic arthritis
  • Ankylosing spondylitis
  • Juvenile idiopathic arthritis
  • Still's disease

Joint pain can also be a symptom of other diseases. In this case, the arthritis is considered to be secondary to the main disease; these include:

  • Psoriasis (Psoriatic arthritis)
  • Reactive arthritis
  • Ehlers-Danlos Syndrome
  • Haemochromatosis
  • Hepatitis
  • Lyme disease
  • Sjogren's disease
  • Hashimoto's Thyroiditis
  • Inflammatory bowel disease (including Crohn's disease and ulcerative colitis)
  • Henoch-Schönlein purpura
  • Hyperimmunoglobulinemia D with recurrent fever
  • Sarcoidosis
  • Whipple's disease
  • TNF receptor associated periodic syndrome
  • Granulomatosis with polyangiitis (and many other vasculitis syndromes)
  • Familial Mediterranean fever
  • Systemic lupus erythematosus


An undifferentiated arthritis is an arthritis that does not fit into well-known clinical disease categories, possibly being an early stage of a definite rheumatic disease. 

Signs and symptoms
Pain, which can vary in severity, is a common symptom in virtually all types of arthritis. Other symptoms include swelling, joint stiffness and aching around the joint(s). Arthritic disorders like lupus and rheumatoid arthritis can affect other organs in the body, leading to a variety of symptoms. Symptoms may include:

  • Inability to use the hand or walk
  • Stiffness, which may be worse in the morning, or after use
  • Malaise and fatigue
  • Weight loss
  • Poor sleep
  • Muscle aches and pains
  • Tenderness
  • Difficulty moving the joint

It is common in advanced arthritis for significant secondary changes to occur. For example, arthritic symptoms might make it difficult for a person to move around and/or exercise, which can lead to secondary effects, such as:

These changes, in addition to the primary symptoms, can have a huge impact on quality of life.

Disability
Arthritis is the most common cause of disability in the USA. More than 20 million individuals with arthritis have severe limitations in function on a daily basis. Absenteeism and frequent visits to the physician are common in individuals who have arthritis. Arthritis can make it very difficult for individuals to be physically active and some become home bound.

It is estimated that the total cost of arthritis cases is close to $100 billion of which almost 50% is from lost earnings. Each year, arthritis results in nearly 1 million hospitalizations and close to 45 million outpatient visits to health care centers.

Decreased mobility, in combination with the above symptoms, can make it difficult for an individual to remain physically active, contributing to an increased risk of obesity, high cholesterol or vulnerability to heart disease. People with arthritis are also at increased risk of depression, which may be a response to numerous factors, including fear of worsening symptoms.


Diagnosis is made by clinical examination from an appropriate health professional, and may be supported by other tests such as radiology and blood tests, depending on the type of suspected arthritis. All arthritides potentially feature pain. Pain patterns may differ depending on the arthritides and the location. Rheumatoid arthritis is generally worse in the morning and associated with stiffness; in the early stages, patients often have no symptoms after a morning shower. Osteoarthritis, on the other hand, tends to be worse after exercise. In the aged and children, pain might not be the main presenting feature; the aged patient simply moves less, the infantile patient refuses to use the affected limb.
Elements of the history of the disorder guide diagnosis. Important features are speed and time of onset, pattern of joint involvement, symmetry of symptoms, early morning stiffness, tenderness, gelling or locking with inactivity, aggravating and relieving factors, and other systemic symptoms. Physical examination may confirm the diagnosis, or may indicate systemic disease. Radiographs are often used to follow progression or help assess severity.

Blood tests and X-rays of the affected joints often are performed to make the diagnosis. Screening blood tests are indicated if certain arthritides are suspected. These might include: rheumatoid factor, antinuclear factor (ANF), extractable nuclear antigen, and specific antibodies.

Osteoarthritis
Osteoarthritis is the most common form of arthritis. It can affect both the larger and the smaller joints of the body, including the hands, wrists, feet, back, hip, and knee. The disease is essentially one acquired from daily wear and tear of the joint; however, osteoarthritis can also occur as a result of injury. In recent years, some joint or limb deformities, such as knock-knee or acetabular overcoverage or dysplasia, have also been considered as a predisposing factor for knee or hip osteoarthritis. Osteoarthritis begins in the cartilage and eventually causes the two opposing bones to erode into each other. The condition starts with minor pain during physical activity, but soon the pain can be continuous and even occur while in a state of rest. The pain can be debilitating and prevent one from doing some activities. Osteoarthritis typically affects the weight-bearing joints, such as the back, spine, and pelvis. Unlike rheumatoid arthritis, osteoarthritis is most commonly a disease of the elderly. More than 30 percent of women have some degree of osteoarthritis by age 65. Risk factors for osteoarthritis include prior joint trauma, obesity, and a sedentary lifestyle.

Rheumatoid arthritis
Rheumatoid arthritis is a disorder in which the body's own immune system starts to attack body tissues. The attack is not only directed at the joint but to many other parts of the body. In rheumatoid arthritis, most damage occurs to the joint lining and cartilage which eventually results in erosion of two opposing bones. Rheumatoid arthritis often affects joints in the fingers, wrists, knees and elbows. The disease is symmetrical (appears on both sides of the body) and can lead to severe deformity in a few years if not treated. Rheumatoid arthritis occurs mostly in people aged 20 and above. In children, the disorder can present with a skin rash, fever, pain, disability, and limitations in daily activities. Often, it is not clear why the rheumatoid arthritis occurred. With earlier diagnosis and aggressive treatment, many individuals can lead a decent quality of life. The drugs to treat rheumatoid arthritis range from corticosteroids to monoclonal antibodies given intravenously. The latest drugs like Remicade can significantly improve quality of life in the short term. In rare cases, surgery may be required to replace joints but there is no cure for the illness.
This adaptive immune response is initiated in part by CD4+ T helper (Th) cells, specifically Th17 cells. Th17 cells are present in higher quantities at the site of bone destruction in joints and produce inflammatory cytokines associated with inflammation, such as interleukin-17 (IL-17).

Bone erosion is a central feature of rheumatoid arthritis. Bone continuously undergoes remodeling by actions of bone resorbing osteoclasts and bone forming osteoblasts. One of the main triggers of bone erosion in the joints in rheumatoid arthritis is inflammation of the synovium, caused in part by the production of pro-inflammatory cytokines and receptor activator of nuclear factor kappa B ligand (RANKL), a cell surface protein present in Th17 cells and osteoblasts. Osteoclast activity can be directly induced by osteoblasts through the RANK/RANKL mechanism.

Lupus
Lupus is a common collagen vascular disorder that can be present with severe arthritis. Other features of lupus include a skin rash, extreme photosensitivity, hair loss, kidney problems, lung fibrosis and constant joint pain.

Gout
Gout is caused by deposition of uric acid crystals in the joint, causing inflammation. There is also an uncommon form of gouty arthritis caused by the formation of rhomboid crystals of calcium pyrophosphate known as pseudogout. In the early stages, the gouty arthritis usually occurs in one joint, but with time, it can occur in many joints and be quite crippling. The joints in gout can often become swollen and lose function. Gouty arthritis can become particularly painful and potentially debilitating when gout cannot successfully be treated. When uric acid levels and gout symptoms cannot be controlled with standard gout medicines that decrease the production of uric acid (e.g., allopurinol, febuxostat) or increase uric acid elimination from the body through the kidneys (e.g., probenecid), this can be referred to as refractory chronic gout or RCG.

Other
Infectious arthritis is another severe form of arthritis. It presents with sudden onset of chills, fever and joint pain. The condition is caused by bacteria elsewhere in the body. Infectious arthritis must be rapidly diagnosed and treated promptly to prevent irreversible joint damage.

Psoriasis can develop into psoriatic arthritis. With psoriatic arthritis, most individuals develop the skin problem first and then the arthritis. The typical features are of continuous joint pains, stiffness and swelling. The disease does recur with periods of remission but there is no cure for the disorder. A small percentage develop a severe painful and destructive form of arthritis which destroys the small joints in the hands and can lead to permanent disability and loss of hand function.

Treatment
There is no known cure for either rheumatoid or osteoarthritis. Treatment options vary depending on the type of arthritis and include physical therapy, lifestyle changes (including exercise and weight control), orthopedic bracing, and medications. Joint replacement surgery may be required in eroding forms of arthritis. Medications can help reduce inflammation in the joint which decreases pain. Moreover, by decreasing inflammation, the joint damage may be slowed.

Physical therapy
In general, studies have shown that physical exercise of the affected joint can have noticeable improvement in terms of long-term pain relief. Furthermore, exercise of the arthritic joint is encouraged to maintain the health of the particular joint and the overall body of the person.

Individuals with arthritis can benefit from both physical and occupational therapy. In arthritis the joints become stiff and the range of movement can be limited. Physical therapy has been shown to significantly improve function, decrease pain, and delay need for surgical intervention in advanced cases. Exercise prescribed by a physical therapist has been shown to be more effective than medications in treating osteoarthritis of the knee. Exercise often focuses on improving muscle strength, endurance and flexibility. In some cases, exercises may be designed to train balance. Occupational therapy can provide assistance with activities as well as equipment.

Medications
There are several types of medications that are used for the treatment of arthritis. Treatment typically begins with medications that have the fewest side effects with further medications being added if insufficiently effective.

Depending on the type of arthritis, the medications that are given may be different. For example, the first-line treatment for osteoarthritis is acetaminophen (paracetamol) while for inflammatory arthritis it involves non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen. Opioids and NSAIDs are less well tolerated.
Rheumatoid arthritis (RA) is autoimmune so in addition to using pain medications and anti-inflammatory drugs, this type uses another category of drug called disease modifying anti-rheumatic drugs (DMARDS). An example of this type of drug is Methotrexate. These types of drugs act on the immune system and slow down the progression of RA.

Other treatments
Arthroscopic surgery for osteoarthritis of the knee provides no additional benefit to optimized physical and medical therapy.

A Cochrane review in 2000 concluded that transcutaneous electrical nerve stimulation (TENS) for knee osteoarthritis was more effective in pain control than placebo.

PEMF - Pulsed Electromagnetic Field Therapy has been shown to effectively treat pain associated with arthritic conditions. The FDA has not approved PEMF for the treatment of arthritis. In Canada, PEMF devices are legally licensed by Health Canada for the treatment of pain associated with arthritic conditions. These devices consist of cylindrical coils of wire that are energized by frequency generators to produce an electromagnetic field.

Epidemiology
Arthritis is predominantly a disease of the elderly, but children can also be affected by the disease. More than 70% of individuals in North America affected by arthritis are over the age of 65. Arthritis is more common in women than men at all ages and affects all races, ethnic groups and cultures. In the United States a CDC survey based on data from 2007–2009 showed 22.2% (49.9 million) of adults aged ≥18 years had self-reported doctor-diagnosed arthritis, and 9.4% (21.1 million or 42.4% of those with arthritis) had arthritis-attributable activity limitation (AAAL). With an aging population, this number is expected to increase.

History

While evidence of primary ankle (kaki) osteoarthritis has been discovered in dinosaurs, the first known traces of human arthritis date back as far as 4500 BC. In early reports, arthritis was frequently referred to as the most common ailment of prehistoric peoples. It was noted in skeletal remains of Native Americans found in Tennessee and parts of what is now Olathe, Kansas. Evidence of arthritis has been found throughout history, from Ötzi, a mummy (circa 3000 BC) found along the border of modern Italy and Austria, to the Egyptian mummies circa 2590 BC.
In 1715, William Musgrave published the second edition of his most important medical work, De arthritide symptomatica, which concerned arthritis and its effects.

Source: https://en.wikipedia.org/wiki/Arthritis

Wednesday, September 9, 2015

Argyria

Credit: en.wikipedia.org

Argyria or argyrosis (from Ancient Greek: ἄργυρος argyros silver) is a condition caused by inappropriate exposure to chemical compounds of the element silver, or to silver dust.  The most dramatic symptom of argyria is that the skin turns blue or bluish-grey. It may take the form of generalized argyria or local argyria. Generalized argyria affects large areas over much of the visible surface of the body. Local argyria shows in limited regions of the body, such as patches of skin, parts of the mucous membrane or the conjunctiva.

Tuesday, September 8, 2015

Apraxia

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What Is Apraxia?
Apraxia is a poorly understood neurological condition. People who have it find it difficult or impossible to make certain motor movements, even though their muscles are normal. Milder forms of apraxia are known as dyspraxia.

Monday, September 7, 2015

Appendicitis


Credit: imagekb.com

Appendicitis is an inflammation of the appendix, a 3 1/2-inch-long tube of tissue that extends from the large intestine. No one is absolutely certain what the function of the appendix is. One thing we do know: We can live without it, without apparent consequences.


Sunday, September 6, 2015

Anthrax

(Credit: Wikipedia) Skin reaction to anthrax

Anthrax is an acute disease caused by the bacterium Bacillus anthracis. Most forms of the disease are lethal, and it affects mostly animals. It is contagious and can be transmitted through contact or consumption of infected meat. Effective vaccines against anthrax are available, and some forms of the disease respond well to antibiotic treatment.

Thursday, September 3, 2015

Anotia

Credit: Wikipedia.org

Anotia ("no ear") describes a rare, congenital deformity, that involves the complete absence of the pinna, the outer projected portion of the ear, and narrowing or absence of the ear canal. This contrasts with microtia, in which a small part of the pinna is present. Anotia and microtia may occur unilaterally (only one ear affected) or bilaterally (both ears affected). This deformity results in conductive hearing lossdeafness.