Category Archives: Ailmemts & Remedies

Spina bifida

Definition:
Spina bifida is a type of birth defect called a neural tube defect. It occurs when the bones of the spine (vertebrae) don’t form properly around part of the baby’s spinal cord. Spina bifida can be mild or severe….CLICK & SEE

Spina bifida malformations fall into three categories: spina bifida occulta, spina bifida cystica with meningocele, and spina bifida cystica with myelomeningocele. The most common location of the malformations is the lumbar and sacral areas. Myelomeningocele is the most significant and common form, and this leads to disability in most affected individuals. The terms spina bifida and myelomeningocele are usually used interchangeably.

Spina bifida meningocele and myelomeningocele are among the most common birth defects, with a worldwide incidence of about 1 in every 1000 births. The occulta form is much more common, but only rarely causes neurological symptoms.

Clasification:....CLICK & SEE
Spina bifida occulta:
Occulta is Latin for “hidden”. This is the mildest form of spina bifida. In occulta, the outer part of some of the vertebrae is not completely closed. The splits in the vertebrae are so small that the spinal cord does not protrude. The skin at the site of the lesion may be normal, or it may have some hair growing from it; there may be a dimple in the skin, or a birthmark.

Many people with this type of spina bifida do not even know they have it, as the condition is asymptomatic in most cases. The incidence of spina bifida occulta is approximately 10-20% of the population, and most people are diagnosed incidentally from spinal X-rays. A systematic review of radiographic research studies found no relationship between spina bifida occulta and back pain. More recent studies not included in the review support the negative findings.

However, other studies suggest spina bifida occulta is not always harmless. One study found that among patients with back pain, severity is worse if spina bifida occulta is present.

Incomplete posterior fusion is not a true spina bifida, and is very rarely of neurological significance.

Meningocele:
A posterior meningocele  or meningeal cyst  is the least common form of spina bifida. In this form, the vertebrae develop normally, but the meninges are forced into the gaps between the vertebrae. As the nervous system remains undamaged, individuals with meningocele are unlikely to suffer long-term health problems, although cases of tethered cord have been reported. Causes of meningocele include teratoma and other tumors of the sacrococcyx and of the presacral space, and Currarino syndrome.

A meningocele may also form through dehiscences in the base of the skull. These may be classified by their localisation to occipital, frontoethmoidal, or nasal. Endonasal meningoceles lie at the roof of the nasal cavity and may be mistaken for a nasal polyp. They are treated surgically. Encephalomeningoceles are classified in the same way and also contain brain tissue.

Myelomeningocele:
This type of spina bifida often results in the most severe complications. In individuals with myelomeningocele, the unfused portion of the spinal column allows the spinal cord to protrude through an opening. The meningeal membranes that cover the spinal cord form a sac enclosing the spinal elements. The term Meningomyelocele is also used interchangeably.

Myeloschisis:
Spina bifida with myeloschisis is the most severe form of myelomeningocele. In this type, the involved area is represented by a flattened, plate-like mass of nervous tissue with no overlying membrane. The exposure of these nerves and tissues make the baby more prone to life-threatening infections such as meningitis.

The protruding portion of the spinal cord and the nerves that originate at that level of the cord are damaged or not properly developed. As a result, there is usually some degree of paralysis and loss of sensation below the level of the spinal cord defect. Thus, the more cranial the level of the defect, the more severe the associated nerve dysfunction and resultant paralysis may be. People may have ambulatory problems, loss of sensation, deformities of the hips, knees or feet, and loss of muscle tone.

Signs and symptoms:
Physical complications:

*Leg weakness and paralysis
*Orthopedic abnormalities (i.e., club foot, hip dislocation, scoliosis)
*Bladder and bowel control problems, including incontinence, urinary tract infections, and poor renal function
*Pressure sores and skin irritations
*Abnormal eye movement

68% of children with spina bifida have an allergy to latex, ranging from mild to life-threatening. The common use of latex in medical facilities makes this a particularly serious concern. The most common approach to avoid developing an allergy is to avoid contact with latex-containing products such as examination gloves and condoms and catheters that do not specify they are latex free, and many other products, such as some commonly used by dentists.

The spinal cord lesion or the scarring due to surgery may result in a tethered spinal cord. In some individuals, this causes significant traction and stress on the spinal cord and can lead to a worsening of associated paralysis, scoliosis, back pain, and worsening bowel and/or bladder function

Neurological complications:
Many individuals with spina bifida have an associated abnormality of the cerebellum, called the Arnold Chiari II malformation. In affected individuals, the back portion of the brain is displaced from the back of the skull down into the upper neck. In about 90% of the people with myelomeningocele, hydrocephalus also occurs because the displaced cerebellum interferes with the normal flow of cerebrospinal fluid, causing an excess of the fluid to accumulate.  In fact, the cerebellum also tends to be smaller in individuals with spina bifida, especially for those with higher lesion levels.

The corpus callosum is abnormally developed in 70-90% of individuals with spina bifida myelomeningocele; this impacts the communication processes between the left and right brain hemispheres. Further, white matter tracts connecting posterior brain regions with anterior regions appear less organized. White matter tracts between frontal regions have also been found to be impaired.

Cortex abnormalities may also be present. For example, frontal regions of the brain tend to be thicker than expected, while posterior and parietal regions are thinner. Thinner sections of the brain are also associated with increased cortical folding. Neurons within the cortex may also be displaced.

Executive function:
Several studies have demonstrated difficulties with executive functions in youth with spina bifida, with greater deficits observed in youth with shunted hydrocephalus. Unlike typically developing children, youths with spina bifida do not tend to improve in their executive functioning as they grow older. Specific areas of difficulty in some individuals include planning, organizing, initiating, and working memory. Problem-solving, abstraction, and visual planning may also be impaired.  Further, children with spina bifida may have poor cognitive flexibility. Although executive functions are often attributed to the frontal lobes of the brain, individuals with spina bifida have intact frontal lobes; therefore, other areas of the brain may be implicated.

Individuals with spina bifida, especially those with shunted hydrocephalus, often have attention problems. Children with spina bifida and shunted hydrocephalus have higher rates of ADHD than typically developing children (31% vs. 17%). Deficits have been observed for selective attention and focused attention, although poor motor speed may contribute to poor scores on tests of attention.  Attention deficits may be evident at a very early age, as infants with spina bifida lag behind their peers in orienting to faces.

Academic skills:
Individuals with spina bifida may struggle academically, especially in the subjects of mathematics and reading. In one study, 60% of children with spina bifida were diagnosed with a learning disability.  In addition to brain abnormalities directly related to various academic skills, achievement is likely affected by impaired attentional control and executive functioning. Children with spina bifida may perform well in elementary school, but begin to struggle as academic demands increase.

Children with spina bifida are more likely than their typically developing peers to have dyscalculia. Individuals with spina bifida have demonstrated stable difficulties with arithmetic accuracy and speed, mathematical problem-solving, and general use and understanding of numbers in everyday life. Mathematics difficulties may be directly related to the thinning of the parietal lobes (regions implicated in mathematical functioning) and indirectly associated with deformities of the cerebellum and midbrain that affect other functions involved in mathematical skills. Further, higher numbers of shunt revisions are associated with poorer mathematics abilities. Working memory and inhibitory control deficiencies have been implicated for math difficulties, although visual-spatial difficulties are not likely involved. Early intervention to address mathematics difficulties and associated executive functions is crucial.

Individuals with spina bifida tend to have better reading skills than mathematics skills. Children and adults with spina bifida have stronger abilities in reading accuracy than in reading comprehension. Comprehension may be especially impaired for text that requires an abstract synthesis of information rather than a more literal understanding. Individuals with spina bifida may have difficulty with writing due to deficits in fine motor control and working memory.

Causes:
The exact cause of this birth defect isn’t known. Experts think that genes and the environment are part of the cause. For example, women who have had one child with spina bifida are more likely to have another child with the disease. Women who are obese or who have diabetes are also more likely to have a child with spina bifida.

Spina bifida is sometimes caused by the failure of the neural tube to close during the first month of embryonic development (often before the mother knows she is pregnant). Some forms are known to occur with primary conditions that cause raised central nervous system pressure, which raises the possibility of a dual pathogenesis.

In normal circumstances, the closure of the neural tube occurs around the 23rd (rostral closure) and 27th (caudal closure) day after fertilization. However, if something interferes and the tube fails to close properly, a neural tube defect will occur. Medications such as some anticonvulsants, diabetes, having a relative with spina bifida, obesity, and an increased body temperature from fever or external sources such as hot tubs and electric blankets may increase the chances of delivery of a baby with a spina bifida.

Extensive evidence from mouse strains with spina bifida indicates that there is sometimes a genetic basis for the condition. Human spina bifida, like other human diseases, such as cancer, hypertension and atherosclerosis (coronary artery disease), likely results from the interaction of multiple genes and environmental factors.

Research has shown the lack of folic acid (folate) is a contributing factor in the pathogenesis of neural tube defects, including spina bifida. Supplementation of the mother’s diet with folate can reduce the incidence of neural tube defects by about 70%, and can also decrease the severity of these defects when they occur. It is unknown how or why folic acid has this effect.

Spina bifida does not follow direct patterns of heredity like muscular dystrophy or haemophilia. Studies show a woman having had one child with a neural tube defect such as spina bifida has about a 3% risk of having another affected child. This risk can be reduced with folic acid supplementation before pregnancy. For the general population, low-dose folic acid supplements are advised (0.4 mg/day)

Treatment:
There is no known cure for nerve damage caused by spina bifida. To prevent further damage of the nervous tissue and to prevent infection, pediatric neurosurgeons operate to close the opening on the back. The spinal cord and its nerve roots are put back inside the spine and covered with meninges. In addition, a shunt may be surgically installed to provide a continuous drain for the excess cerebrospinal fluid produced in the brain, as happens with hydrocephalus. Shunts most commonly drain into the abdomen or chest wall. However, if spina bifida is detected during pregnancy, then open or minimally-invasive fetal surgery can be performed.

In childhood:
Most individuals with myelomeningocele will need periodic evaluations by a variety of specialists:

*Physiatrists coordinate the rehabilitation efforts of different therapists and prescribe specific therapies, adaptive equipment, or medications to encourage as high of a functional performance within the community as possible.

*Orthopedists monitor growth and development of bones, muscles, and joints.

*Neurosurgeons perform surgeries at birth and manage complications associated with tethered cord and hydrocephalus.

*Neurologists treat and evaluate nervous system issues, such as seizure disorders.

*Urologists to address kidney, bladder, and bowel dysfunction – many will need to manage their urinary systems with a program of catheterization. Bowel management programs aimed at improving elimination are also designed.

*Ophthalmologists evaluate and treat complications of the eyes.

*Orthotists design and customize various types of assistive technology, including braces, crutches, walkers, and wheelchairs to aid in mobility. As a general rule, the higher the level of the spina bifida defect, the more severe the paralysis, but paralysis does not always occur. Thus, those with low levels may need only short leg braces, whereas those with higher levels do best with a wheelchair, and some may be able to walk unaided.

*Physical therapists, occupational therapists, psychologists, and speech/language pathologists aid in rehabilitative therapies and increase independent living skills.

Transition to adulthood:
Although many children’s hospitals feature integrated multidisciplinary teams to coordinate healthcare of youth with spina bifida, the transition to adult healthcare can be difficult because the above healthcare professionals operate independently of each other, requiring separate appointments and communicate among each other much less frequently. Healthcare professionals working with adults may also be less knowledgeable about spina bifida because it is considered a childhood chronic health condition.  Due to the potential difficulties of the transition, adolescents with spina bifida and their families are encouraged to begin to prepare for the transition around ages 14–16, although this may vary depending on the adolescent’s cognitive and physical abilities and available family support. The transition itself should be gradual and flexible. The adolescent’s multidisciplinary treatment team may aid in the process by preparing comprehensive, up-to-date documents detailing the adolescent’s medical care, including information about medications, surgery, therapies, and recommendations. A transition plan and aid in identifying adult healthcare professionals are also helpful to include in the transition process.

Further complicating the transition process is the tendency for youths with spina bifida to be delayed in the development of autonomy, with boys particularly at risk for slower development of independence. An increased dependence on others (in particular family members) may interfere with the adolescent’s self-management of health-related tasks, such as catheterization, bowel management, and taking medications.  As part of the transition process, it is beneficial to begin discussions at an early age about educational and vocational goals, independent living, and community involvement.

Prevention:
There is neither a single cause of spina bifida nor any known way to prevent it entirely. However, dietary supplementation with folic acid has been shown to be helpful in reducing the incidence of spina bifida. Sources of folic acid include whole grains, fortified breakfast cereals, dried beans, leaf vegetables and fruits.

Folate fortification of enriched grain products has been mandatory in the United States since 1998. The U.S. Food and Drug Administration, Public Health Agency of Canada  and UK recommended amount of folic acid for women of childbearing age and women planning to become pregnant is at least 0.4 mg/day of folic acid from at least three months before conception, and continued for the first 12 weeks of pregnancy.  Women who have already had a baby with spina bifida or other type of neural tube defect, or are taking anticonvulsant medication should take a higher dose of 4–5 mg/day.

Certain mutations in the gene VANGL1 are implicated as a risk factor for spina bifida: These mutations have been linked with spina bifida in some families with a history of spina bifida.

Pregnancy screening:
Open spina bifida can usually be detected during pregnancy by fetal ultrasound. Increased levels of maternal serum alpha-fetoprotein (MSAFP) should be followed up by two tests – an ultrasound of the fetal spine and amniocentesis of the mother’s amniotic fluid (to test for alpha-fetoprotein and acetylcholinesterase). AFP tests are now mandated by some state laws (including California). and failure to provide them can have legal ramifications. In one case a man born with spina bifida was awarded a $2 million settlement after court found his mother’s OBGYN negligent for not performing these tests. Spina bifida may be associated with other malformations as in dysmorphic syndromes, often resulting in spontaneous miscarriage. In the majority of cases, though, spina bifida is an isolated malformation.

Genetic counseling and further genetic testing, such as amniocentesis, may be offered during the pregnancy, as some neural tube defects are associated with genetic disorders such as trisomy 18. Ultrasound screening for spina bifida is partly responsible for the decline in new cases, because many pregnancies are terminated out of fear that a newborn might have a poor future quality of life. With modern medical care, the quality of life of patients has greatly improved.

Resources:

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

http://www.webmd.com/parenting/baby/tc/spina-bifida-topic-overview

Aphasia

Description:
Aphasia is the name given to a collection of language disorders caused by damage to the brain.  The word aphasia comes from the wordn aphasia, in Ancient Greek, which means A requirement for a diagnosis of aphasia is that, prior to the illness or injury, the person’s language skills were normal . The difficulties of people with aphasia can range from occasional trouble finding words to losing the ability to speak, read, or write, but does not affect intelligence. This also affects visual language such as sign language. The term “aphasia” implies a problem with one or more functions that are essential and specific to language function. It is not usually used when the language problem is a result of a more peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles or a general hearing impairment.
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Stroke is the most common cause of aphasia in the United States. Approximately 500,000 individuals suffer strokes each year, and 20% of these individuals develop some type of aphasia. Other causes of brain damage include head injuries, brain tumors, and infection. About half of the people who show signs of aphasia have what is called temporary or transient aphasia and recover completely within a few days. An estimated one million Americans suffer from some form of permanent aphasia. As yet, no connection between aphasia and age, gender, or race has been found.
Aphasia is sometimes confused with other conditions that affect speech, such as dysarthria and apraxia. These condition affect the muscles used in speaking rather than language function itself. Dysarthria is a speech disturbance caused by lack of control over the muscles used in speaking, perhaps due to nerve damage. Speech apraxia is a speech disturbance in which language comprehension and muscle control are retained, but the memory of how to use the muscles to form words is not.

Symptoms:
Aphasia is condition characterized by either partial or total loss of the ability to communicate verbally or using written words. A person with aphasia may have difficulty speaking, reading, writing, recognizing the names of objects, or understanding what other people have said. Aphasia is caused by a brain injury, as may occur during a traumatic accident or when the brain is deprived of oxygen during a stroke. It may also be caused by a brain tumor, a disease such as Alzheimer’s, or an infection, like encephalitis. Aphasia may be temporary or permanent. Aphasia does not include speech impediments caused by loss of muscle control.
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To understand and use language effectively, an individual draws upon word memory-stored information on what certain words mean, how to put them together, and how and when to use them properly. For a majority of people, these and other language functions are located in the left side (hemisphere) of the brain. Damage to this side of the brain is most commonly linked to the development of aphasia. Interestingly, however, left-handed people appear to have language areas in both the left and right hemispheres of the brain and, as a result, may develop aphasia from damage to either side of the brain.

People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems such as dysarthria or apraxia and not primarily due to aphasia. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication. Often those with aphasia will try to hide their inability to name objects by using words like thing. So when asked to name a pencil they may say it is a thing used to write.

*inability to comprehend language
*inability to pronounce, not due to muscle paralysis or weakness
*inability to speak spontaneously
*inability to form words
*inability to name objects (anomia)
*poor enunciation
*excessive creation and use of personal neologisms
*inability to repeat a phrase
*persistent repetition of one syllable, word, or phrase (stereotypies)
*paraphasia (substituting letters, syllables or words)
*agrammatism (inability to speak in a grammatically correct fashion)
*dysprosody (alterations in inflexion, stress, and rhythm)
*incomplete sentences
*inability to read
*inability to write
*limited verbal output
*difficulty in naming
*speech disorder
*Speaking gibberish
*inability to follow or understand simple requests

Causes:
Aphasia is most commonly caused by stroke. It can also be caused by other brain diseases, including cancer (brain tumor), epilepsy, and Alzheimer’s disease, or by a head injury. In rare cases, aphasia may also result from herpesviral encephalitis. The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia. In acute disorders, such as head injury or stroke, aphasia usually develops quickly. Aphasia usually develops more slowly from a brain tumor, infection, or dementia.

Although all of the disease listed above are potential causes, aphasia will generally only result when there is substantial damage to the left hemisphere of the brain, either the cortex (outer layer) and/or the underlying white matter. Substantial damage to tissue anywhere within the region shown in blue on the figure below can potentially result in aphasia.  Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, the internal and external capsules, and the caudate nucleus of the basal ganglia.  The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms.  A very small number of people can experience aphasia after damage to the right hemisphere only. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps greater overall reliance on the right hemisphere for language skills than in the general population.

Finally, certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom.  Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain.

Classification:
Aphasia is best thought of as a collection of different disorders, rather than a single problem. Each individual with aphasia will present with their own particular combination of language strengths and weaknesses. Consequently, it is a major challenge just to document the various difficulties that can occur in different people, let alone decide how they might best be treated. Most classifications of the aphasias tend to divide the various symptoms into broad classes. A common approach is to distinguish between the fluent aphasias (where speech remains fluent, but content may be lacking, and the person may have difficulties understanding others), and the nonfluent aphasias ( where speech is very halting and effortful, and may consist of just one or two words at a time).

However, no such broad-based grouping has proven fully adequate. There is a huge variation among patients within the same broad grouping, and aphasias can be highly selective. For instance, patients with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.

Classical-Localizationist approaches:
Localizationist approaches aim to classify the aphasias according to their major presenting characteristics and the regions of the brain that most probably gave rise to them. Inspired by the early work of nineteenth century neurologists Paul Broca and Carl Wernicke, these approaches identify two major subtypes of aphasia and several more minor subtypes:

*Broca’s aphasia (also known as Motor aphasia or Expressive aphasia), which is characterized by halted, fragmented, effortful speech, but relatively well-preserved comprehension. It has been associated with damage to the posterior left prefrontal cortex, most notably Broca’s area. Individuals with Broca’s aphasia often have right-sided weakness or paralysis of the arm and leg, because the left frontal lobe is also important for body movement, particularly on the right side.

*Wernicke’s aphasia (also known as Sensory aphasia or Receptive aphasia), which is characterized by fluent speech, but marked difficulties understanding words and sentences. Although fluent, the speech may lack in key substantive words (nouns, verbs adjectives), and may contain incorrect words or even nonsense words. This subtype has been associated with damage to the posterior left temporal cortex, most notably Wernicke’s area. These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement.

*Other, more minor subtypes include Conduction aphasia, a disorder where speech remains fluent, and comprehension is preserved, but the person may have disproportionate difficulty where repeating words or sentences. Other include Transcortical motor aphasia and Transcortical sensory aphasia which are similar to Broca’s and Wernicke’s aphasia respectively, but the ability to repeat words and sentences is disroportionately preserved.

Recent classification schemes adopting this approach, such as the “Boston-Neoclassical Model”  also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Broca’s aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernicke’s aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: Anomic aphasia, which is characterized by a selective difficulty finding the names for things; and Global aphasia where both expression and comprehension of speech are severely compromised.

Many localizationist approaches also recognize the existence of additional, more “pure” forms of language disorder that may affect only a single language skill.  For example, in Pure alexia, a person may be able to write but not read, and in Pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them.

Cognitive neuropsychological approaches:
Although localizationist approaches provide a useful way of classifying the different patterns of language difficulty into broad groups, one problem is that a sizeable number of individuals do not fit neatly into one category or another. Another problem is that the categories, particularly the major ones such as Broca’s and Wernicke’s aphasia, still remain quite broad. Consequently, even amongst individuals who meet the criteria for classification into a subtype, there can be enormous variability in the types of difficulties they experience.

Instead of categorizing every individual into a specific subtype, cognitive neuropsychological approaches aim to identify the key language skills or “modules” that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with a number of modules. This type of approach requires a framework or theory as to what skills/modules are needed to perform different kinds of language tasks. For example, the model of Max Coltheart identifies a module that recognizes phonemes as they are spoken, which is essential for any task involving recognition of words. Similarly, there is a module that stores phonemes that the person is planning to produce in speech, and this module is critical for any task involving the production of long words or long strings of speech. One a theoretical framework has been established, the functioning of each module can then be assessed using a specific test or set of tests. In the clinical setting, use of this model usually involves conducting a battery of assessments, each of which tests one or a number of these modules. Once a diagnosis is reached as to the skills/modules where the most significant impairment lies, therapy can proceed to treat these skills.

In practice, the cognitive neuropsychological approach can be unwieldy due to the wide variety of skills that can potentially be tested. Also, it is perhaps best suited to milder cases of aphasia: If the person has little expressive or receptive language ability, sometimes test performance can be difficult to interpret. In practice, clinicians will often use a blend of assessment approaches, which include broad subtyping based on a localizationist framework, and some finer exploration of specific language skills based on the cognitive neuropsychological framework.
Other forms of aphasia:

Progressive aphasias:
Primary progressive aphasia (PPA) is associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimer’s disease, which is the gradual process of progressively losing the ability to think. It is characterized by the gradual loss of the ability to name objects. People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence. There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA)

Progressive Jargon Aphasia is a fluent or receptive aphasia in which the patient’s speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the patient has problems with the selection of nouns. Either they will replace the desired word with another that sounds or looks like the original one or has some other connection or they will replace it with sounds. As such, patients with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they cannot find with sounds. Substitutions commonly involve picking another (actual) word starting with the same sound (e.g., clocktower – colander), picking another semantically related to the first (e.g., letter – scroll), or picking one phonetically similar to the intended one (e.g., lane – late).

Deaf aphasia:
There have been many instances showing that there is a form of aphasia among deaf individuals. Sign language is, after all, a form of communication that has been shown to use the same areas of the brain as verbal forms of communication. Mirror neurons become activated when an animal is acting in a particular way or watching another individual act in the same manner. These mirror neurons are important in giving an individual the ability to mimic movements of hands. Broca’s area of speech production has been shown to contain several of these mirror neurons resulting in significant similarities of brain activity between sign language and vocal speech communication. Facial communication is a significant portion of how animals interact with each other. Humans use facial movements to create, what other humans perceive, to be faces of emotions. While combining these facials movements with speech, a more full form of language is created which enables the species to interact with a much more complex and detailed form of communication. Sign language also uses these facial movements and emotions along with the primary hand movement way of communicating. These facial movement forms of communication come from the same areas of the brain. When dealing with damages to certain areas of the brain, vocal forms of communication are in jeopardy of severe forms of aphasia. Since these same areas of the brain are being used for sign language, these same, at least very similar, forms of aphasia can show in the Deaf community. Individuals can show a form of Wernicke’s aphasia with sign language and they show deficits in their abilities in being able to produce any form of expressions. Broca’s aphasia shows up in some patients, as well. These individuals find tremendous difficulty in being able to actually sign the linguistic concepts they are trying to express

Diagnosis:
Following brain injury, an initial bedside assessment is made to determine whether language function has been affected. If the individual experiences difficulty communicating, attempts are made to determine whether this difficulty arises from impaired language comprehension or an impaired ability to speak. A typical examination involves listening to spontaneous speech and evaluating the individual’s ability to recognize and name objects, comprehend what is heard, and repeat sample words and phrases. The individual may also be asked to read text aloud and explain what the passage means. In addition, writing ability is evaluated by having the individual copy text, transcribe dictated text, and write something without prompting.
A speech pathologist or neuropsychologist may be asked to conduct more extensive examinations using in-depth, standardized tests. Commonly used tests include the Boston Diagnostic Aphasia Examination, the Western Aphasia Battery, and possibly, the Porch Index of Speech Ability.

The results of these tests indicate the severity of the aphasia and may also provide information regarding the exact location of the brain damage. This more extensive testing is also designed to provide the information necessary to design an individualized speech therapy program. Further information about the location of the damage is gained through the use of imaging technology, such as magnetic resonance imaging (MRI) and computed tomography scans.
Treatment:
Initially, the underlying cause of aphasia must be treated or stabilized. To regain language function, therapy must begin as soon as possible following the injury. Although there are no medical or surgical procedures currently available to treat this condition, aphasia resulting from stroke or head injury may improve through the use of speech therapy. For most individuals, however, the primary emphasis is placed on making the most of retained language abilities and learning to use other means of communication to compensate for lost language abilities.
Speech therapy is tailored to meet individual needs, but activities and tools that are frequently used include the following:

Exercise and practice. Weakened muscles are exercised by repetitively speaking certain words or making facial expressions, such as smiling.
Picture cards. Pictures of everyday objects are used to improve word recall and increase vocabulary. The names of the objects may also be repetitively spoken aloud as part of an exercise and practice routine.

Picture boards. Pictures of everyday objects and activities are placed together, and the individual points to certain pictures to convey ideas and communicate with others.
Workbooks. Reading and writing exercises are used to sharpen word recall and regain reading and writing abilities. Hearing comprehension is also redeveloped using these exercises.
Computers. Computer software can be used to improve speech, reading, recall, and hearing comprehension by, for example, displaying pictures and having the individual find the right word.

Prognosis:
The degree to which an individual can recover language abilities is highly dependent on how much brain damage occurred and the location and cause of the original brain injury. Other factors include the individual’s age, general health, motivation and willingness to participate in speech therapy, and whether the individual is left or right handed. Language areas may be located in both the left and right hemispheres in left-handed individuals. Left-handed individuals are, therefore, more likely to develop aphasia following brain injury, but because they have two language centers, may recover more fully because language abilities can be recovered from either side of the brain. The intensity of therapy and the time between diagnosis and the start of therapy may also affect the eventual outcome.

Prevention:
Because there is no way of knowing when a stroke, traumatic head injury, or disease will occur, very little can be done to prevent aphasia. However  it can be adviced to be careful in movement of aged person specially for those having high bloodpressure, diabetis and other form of diseases.

Following are some precautions that should be taken to avoid aphasia, by decreasing the risk of stroke, the main cause of aphasia:

*Exercising regularly
*Eating a healthy diet
*Keeping alcohol consumption low and avoiding tobacco use
*Controlling blood pressure

History:
The first recorded case of aphasia is from an Egyptian papyrus, the Edwin Smith Papyrus, which details speech problems in a person with a traumatic brain injury to the temporal lobe.During the second half of the 19th century, Aphasia was a major focus for scientists and philosophers who were working in the beginning stages in the field of psychology.

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/Aphasia

http://medical-dictionary.thefreedictionary.com/aphasia

Prostate cancer

Other Name : Carcinoma of the man’s prostate,adenocarcinoma, or glandular cancer
Definition:
Prostate cancer is cancer that occurs in a man’s prostate— a small walnut-shaped gland that produces the seminal fluid that nourishes and transports sperm for  male reproductive system.

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Prostate cancer is one of the most common types of cancer in men. Most prostate cancers are slow growing; however, some grow relatively fast.Initially remains confined to the prostate gland,  where it may not cause serious harm. While some types of prostate cancer grow slowly and may need minimal or no treatment, other types are aggressive and can spread quickly.

Prostate cancer that is detected early — when it’s still confined to the prostate gland — has a better chance of successful treatment.

Factors that increase the risk of prostate cancer include: older age, a family history of the disease, and race. About 99% of cases occur in those over the age of 50. Having a first degree relative with  the disease increases the risk 2 to 3 fold. In the United States it is more common in the African American population than the Caucasian population. Other factors that may be involved include a diet  high in processed, red meat, or milk products or low in certain vegetables. Prostate cancer is diagnosed by biopsy. Medical imaging may then be done to determine if the cancer has spread to other  parts of the body.

Symptoms:
Early prostate cancer usually causes no symptoms. Sometimes, however, prostate cancer does cause symptoms, often similar to those of diseases such as benign prostatic hyperplasia. These include frequent urination, nocturia (increased urination at night), difficulty starting and maintaining a steady stream of urine, hematuria (blood in the urine), and dysuria (painful urination). A study  based on the 1998 Patient Care Evaluation in the US found that about a third of patients diagnosed with prostate cancer had one or more such symptoms, while two thirds had no symptoms.

Prostate cancer is associated with urinary dysfunction as the prostate gland surrounds the prostatic urethra. Changes within the gland, therefore, directly affect urinary function. Because the vas  deferens deposits seminal fluid into the prostatic urethra, and secretions from the prostate gland itself are included in semen content, prostate cancer may also cause problems with sexual function  and performance, such as difficulty achieving erection or painful ejaculation.

Advanced prostate cancer can spread to other parts of the body, possibly causing additional symptoms. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis,  or ribs. Spread of cancer into other bones such as the femur is usually to the proximal part of the bone. Prostate cancer in the spine can also compress the spinal cord, causing leg weakness and  urinary and fecal incontinence.

Causes:
The  causes of prostate cancer  is still not very clear.
Doctors know that prostate cancer begins when some cells in your prostate become abnormal. Mutations in the abnormal cells’ DNA cause the cells to grow and divide more rapidly than normal cells  do. The abnormal cells continue living, when other cells would die. The accumulating abnormal cells form a tumor that can grow to invade nearby tissue. Some abnormal cells can break off and  spread (metastasize) to other parts of the body.

Risk Factors:
The primary risk factors are obesity, age and family history. Prostate cancer is very uncommon in men younger than 45, but becomes more common with advancing age. The average age at the time  of diagnosis is 70. However, many men never know they have prostate cancer. Autopsy studies of Chinese, German, Israeli, Jamaican, Swedish, and Ugandan men who died of other causes have  found prostate cancer in 30% of men in their 50s, and in 80% of men in their 70s. Men who have first-degree family members with prostate cancer appear to have double the risk of getting the  disease compared to men without prostate cancer in the family. This risk appears to be greater for men with an affected brother than for men with an affected father.   Men with high blood pressure are more likely to develop prostate cancer.  There is a small increased risk of prostate cancer associated with lack of exercise. A 2010 study found that prostate basal cells were the most common  site of origin for prostate cancers.

Genetic factors :
Genetic background may contribute to prostate cancer risk, as suggested by associations with race, family, and specific gene variants. Men who have a first-degree relative (father or brother) with prostate cancer have twice the risk of developing prostate cancer, and those with two first-degree relatives affected have a fivefold greater risk compared with men with no family history. In the

United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men. In contrast, the incidence and mortality rates for Hispanic men  are one third lower than for non-Hispanic whites. Studies of twins in Scandinavia suggest that 40% of prostate cancer risk can be explained by inherited factors.

No single gene is responsible for prostate cancer; many different genes have been implicated. Mutations in BRCA1 and BRCA2, important risk factors for ovarian cancer and breast cancer in women, have also been implicated in prostate cancer. Other linked genes include the Hereditary Prostate cancer gene 1 (HPC1), the androgen receptor, and the vitamin D receptor.  TMPRSS2-ETS gene  family fusion, specifically TMPRSS2-ERG or TMPRSS2-ETV1/4 promotes cancer cell growth.

Two large genome-wide association studies linking single nucleotide polymorphisms (SNPs) to prostate cancer were published in 2008. These studies identified several SNPs which substantially  affect the risk of prostate cancer. For example, individuals with TT allele pair at SNP rs10993994 were reported to be at 1.6 times higher risk of prostate cancer than those with the CC allele pair. This

SNP explains part of the increased prostate cancer risk of African American men as compared to American men of European descent, since the C allele is much more prevalent in the latter; this SNP is located in the promoter region of the MSMB gene, thus affects the amount of MSMB protein synthesized and secreted by epithelial cells of the prostate.

Dietary factors:
While some dietary factors have been associated with prostate cancer the evidence is still tentative.  Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence. Red  meat and processed meat also appear to have little effect in human studies.  Higher meat consumption has been associated with a higher risk in some studies.

Lower blood levels of vitamin D may increase the risk of developing prostate cancer.

Folic acid supplements have no effect on the risk of developing prostate cancer.

Viral factors:
In 2006, a previously unknown retrovirus, Xenotropic MuLV-related virus or XMRV, was associated with human prostate tumors,  but subsequent reports on the virus were contradictory,  and the original 2006 finding was instead due to a previously undetected contamination.

Sexual factors:
Several case-control studies have shown that having many lifetime sexual partners or starting sexual activity early in life substantially increases the risk of prostate cancer. This correlation suggests  a sexually transmissible infection (STI) may cause some prostate cancer cases; however, many studies have unsuccessfully attempted to find such a link, especially when testing for STIs shortly  before or after prostate cancer diagnosis.  Studies testing for STIs a decade or more prior to prostate cancer diagnosis find a significant link between prostate cancer and various STIs (HPV-16, HPV-18 and HSV-2). This evidence could be explained by a yet-to-be-identified sexually transmissible infection and a long latency period between onset of infection and prostate cancer.

On the other hand, while the available evidence is weak,  tentative results suggest that frequent ejaculation may decrease the risk of prostate cancer.  A study, over eight years, showed that those  that ejaculated most frequently (over 21 times per month on average) were less likely to get prostate cancer.  The results were broadly similar to the findings of a smaller Australian study

Medication exposure:
There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Use of the cholesterol-lowering drugs known as the statins may also decrease  prostate cancer risk.

Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer while another study shows infection may help prevent prostate cancer by increasing blood to the  area. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk. Finally, obesity  and elevated blood levels of testosterone   may increase the risk for prostate cancer. There is an association between vasectomy and prostate cancer however more research is needed to determine if this is a causative relationship.

Pathophysiology:
The prostate is a part of the male reproductive system that helps make and store seminal fluid. In adult men, a typical prostate is about 3 centimeters long and weighs about 20 grams. It is located in the pelvis, under the urinary bladder and in front of the rectum. The prostate surrounds part of the urethra, the tube that carries urine from the bladder during urination and semen during ejaculation.  Because of its location, prostate diseases often affect urination, ejaculation, and rarely defecation. The prostate contains many small glands which make about 20 percent of the fluid  constituting semen.  In prostate cancer, the cells of these prostate glands mutate into cancer cells. The prostate glands require male hormones, known as androgens, to work properly. Androgens  include testosterone, which is made in the testes; dehydroepiandrosterone, made in the adrenal glands; and dihydrotestosterone, which is converted from testosterone within the prostate itself.

Androgens are also responsible for secondary sex characteristics such as facial hair and increased muscle mass.

Prostate cancer is classified as an adenocarcinoma, or glandular cancer, that begins when normal semen-secreting prostate gland cells mutate into cancer cells. The region of prostate gland where  the adenocarcinoma is most common is the peripheral zone. Initially, small clumps of cancer cells remain confined to otherwise normal prostate glands, a condition known as carcinoma in situ or  prostatic intraepithelial neoplasia (PIN). Although there is no proof that PIN is a cancer precursor, it is closely associated with cancer. Over time, these cancer cells begin to multiply and spread to the  surrounding prostate tissue (the stroma) forming a tumor. Eventually, the tumor may grow large enough to invade nearby organs such as the seminal vesicles or the rectum, or the tumor cells may develop the ability to travel in the bloodstream and lymphatic system. Prostate cancer is considered a malignant tumor because it is a mass of cells that can invade other parts of the body. This invasion of other organs is called metastasis. Prostate cancer most commonly metastasizes to the bones, lymph nodes, and may invade rectum, bladder and lower ureters after local progression.

The route of metastasis to bone is thought to be venous as the prostatic venous plexus draining the prostate connects with the vertebral veins.

The prostate is a zinc-accumulating, citrate-producing organ. The protein ZIP1 is responsible for the active transport of zinc into prostate cells. One of zinc’s important roles is to change the metabolism of the cell in order to produce citrate, an important component of semen. The process of zinc accumulation, alteration of metabolism, and citrate production is energy inefficient, and  prostate cells sacrifice enormous amounts of energy (ATP) in order to accomplish this task. Prostate cancer cells are generally devoid of zinc. This allows prostate cancer cells to save energy not  making citrate, and utilize the new abundance of energy to grow and spread. The absence of zinc is thought to occur via a silencing of the gene that produces the transporter protein ZIP1. ZIP1 is now called a tumor suppressor gene product for the gene SLC39A1. The cause of the epigenetic silencing is unknown. Strategies which transport zinc into transformed prostate cells effectively  eliminate these cells in animals. Zinc inhibits NF-?B pathways, is anti-proliferative, and induces apoptosis in abnormal cells. Unfortunately, oral ingestion of zinc is ineffective since high  concentrations of zinc into prostate cells is not possible without the active transporter, ZIP1.

Loss of cancer suppressor genes, early in the prostatic carcinogenesis, have been localized to chromosomes 8p, 10q, 13q, and 16q. P53 mutations in the primary prostate cancer are relatively low  and are more frequently seen in metastatic settings, hence, p53 mutations are late event in pathology of prostate cancer. Other tumor suppressor genes that are thought to play a role in prostate  cancer include PTEN (gene) and KAI1. “Up to 70 percent of men with prostate cancer have lost one copy of the PTEN gene at the time of diagnosis”   Relative frequency of loss of E-cadherin and  CD44 has also been observed.

RUNX2 is a transcription factor that prevents cancer cells from undergoing apoptosis thereby contributing to the development of prostate cancer.

The PI3k/Akt signaling cascade works with the transforming growth factor beta/SMAD signaling cascade to ensure prostate cancer cell survival and protection against apoptosis. X-linked
inhibitor of apoptosis (XIAP) is hypothesized to promote prostate cancer cell survival and growth and is a target of research because if this inhibitor can be shut down then the apoptosis cascade  can carry on its function in preventing cancer cell proliferation.  Macrophage inhibitory cytokine-1 (MIC-1) stimulates the focal adhesion kinase (FAK) signaling pathway which leads to prostate  cancer cell growth and survival.

The androgen receptor helps prostate cancer cells to survive and is a target for many anti cancer research studies; so far, inhibiting the androgen receptor has only proven to be effective in mouse  studies.   Prostate specific membrane antigen (PSMA) stimulates the development of prostate cancer by increasing folate levels for the cancer cells to use to survive and grow; PSMA increases  available folates for use by hydrolyzing glutamated folates.

Diagnosis :
The American Cancer Society’s position regarding early detection is “Research has not yet proven that the potential benefits of testing outweigh the harms of testing and treatment. The American  Cancer Society believes that men should not be tested without learning about what we know and don’t know about the risks and possible benefits of testing and treatment. Starting at age 50, (45 if African American or brother or father suffered from condition before age 65) the man should  talk to the doctor about the pros and cons of testing so  the person can decide if testing is the right choice for  him.”

The only test that can fully confirm the diagnosis of prostate cancer is a biopsy, the removal of small pieces of the prostate for microscopic examination. However, prior to a biopsy, less invasive  testing can be conducted.

There are also several other tests that can be used to gather more information about the prostate and the urinary tract. Digital rectal examination (DRE) may allow a doctor to detect prostate  abnormalities. Cystoscopy shows the urinary tract from inside the bladder, using a thin, flexible camera tube inserted down the urethra. Transrectal ultrasonography creates a picture of the prostate  using sound waves from a probe in the rectum.

Prostate screening tests :

*Digital rectal exam (DRE). During a DRE, your doctor inserts a gloved, lubricated finger into your rectum to examine your prostate, which is adjacent to the rectum. If your doctor finds any
abnormalities in the texture, shape or size of your gland, you may need more tests.

*Prostate-specific antigen (PSA) test. A blood sample is drawn from a vein in your arm and analyzed for PSA, a substance that’s naturally produced by your prostate gland. It’s normal for a small  amount of PSA to be in your bloodstream. However, if a higher than normal level is found, it may be an indication of prostate infection, inflammation, enlargement or cancer.
PSA testing combined with DRE helps identify prostate cancers at their earliest stages, but studies have disagreed whether these tests reduce the risk of dying of prostate cancer. For that reason,  there is debate surrounding prostate cancer screening.

If an abnormality is detected on a DRE or PSA test, your doctor may recommend tests to determine whether you have prostate cancer, such as:

*Ultrasound. If other tests raise concerns,  the doctor may use transrectal ultrasound to further evaluate your prostate. A small probe, about the size and shape of a cigar, is inserted into  the rectum. The probe uses sound waves to make a picture of the  prostate gland.

*Collecting a sample of prostate tissue. If initial test results suggest prostate cancer, your doctor may recommend a procedure to collect a sample of cells from your prostate (prostate biopsy).

Prostate biopsy is often done using a thin needle that’s inserted into the prostate to collect tissue. The tissue sample is analyzed in a lab to determine whether cancer cells are present.

Now to Determining whether prostate cancer is aggressive:

When a biopsy confirms the presence of cancer, the next step is to determine the level of aggressiveness (grade) of the cancer cells. In a laboratory, a pathologist examines a sample of the cancer cell to determine how much cancer cells differ from the healthy cells. A higher grade indicates a more aggressive cancer that is more likely to spread quickly.

The most common scale used to evaluate the grade of prostate cancer cells is called a Gleason score. Scoring combines two numbers and can range from 2 (nonaggressive cancer) to 10 (very aggressive cancer).

For  determining how far the cancer has spread:

Once a prostate cancer diagnosis has been made, your doctor works to determine the extent (stage) of the cancer. If your doctor suspects your cancer may have spread beyond your prostate, imaging tests such as these may be recommended:

*Bone scan
*Ultrasound
*Computerized tomography (CT) scan
*Magnetic resonance imaging (MRI)
*Positron emission tomography (PET) scan

It is not every person should have every test. The doctor will determine which tests are best for  every  individual case.

Once testing is complete,  the doctor assigns the stage and this helps determination of  treatment options. The prostate cancer stages are:

Stage I. This stage signifies very early cancer that’s confined to a small area of the prostate. When viewed under a microscope, the cancer cells aren’t considered aggressive.

Stage II. Cancer at this stage may still be small but may be considered aggressive when cancer cells are viewed under the microscope. Or cancer that is stage II may be larger and may have grown to  involve both sides of the prostate gland.

Stage III. The cancer has spread beyond the prostate to the seminal vesicles or other nearby tissues.

Stage IV. The cancer has grown to invade nearby organs, such as the bladder, or spread to lymph nodes, bones, lungs or other organs.

Treatment:
Prostate cancer treatment options depend on several factors, such as how fast your cancer is growing, how much it has spread and the overall health  and age of the patient , as well as the benefits  and the potential side effects of the treatment.Immediate treatment may not be necessary for men diagnosed with very early-stage of  prostate cancer. Some men may never need treatment. Instead, doctors sometimes recommend active  surveillance.

In active surveillance, regular follow-up blood tests, rectal exams and possibly biopsies may be performed to monitor progression of your cancer. If tests show your cancer is progressing, you may opt for a prostate cancer treatment such as surgery or radiation.

Active surveillance may be an option for cancer that isn’t causing symptoms, is expected to grow very slowly and is confined to a small area of the prostate. Active surveillance may also be

considered for a man who has another serious health condition or an advanced age that makes cancer treatment more difficult.

Active surveillance carries a risk that the cancer may grow and spread between checkups, making it less likely to be cured.

For other cases the the following treatment is recomended:

*Radiation therapy : Radiation therapy uses high-powered energy to kill cancer cells. Prostate cancer radiation therapy can be delivered in two ways:

Radiation that comes from outside of  the body (external beam radiation). During external beam radiation therapy, the patient   lie on a table while a machine moves around the body, directing high-

powered energy beams, such as X-rays or protons, to   prostate cancer.The patient  typically undergo external beam radiation treatments five days a week for several weeks.

Radiation placed inside  the body (brachytherapy). Brachytherapy involves placing many rice-sized radioactive seeds in your prostate tissue. The radioactive seeds deliver a low dose of radiation

over a long period of time. The doctor implants the radioactive seeds in patient’s prostate using a needle guided by ultrasound images. The implanted seeds eventually stop giving off radiation and  don’t need to be removed.

Side effects of radiation therapy can include painful urination, frequent urination and urgent urination, as well as rectal symptoms, such as loose stools or pain when passing stools. Erectile dysfunction can also occur.

Hormone therapy:
Hormone therapy is treatment to stop  the patient’s body from producing the male hormone testosterone. Prostate cancer cells rely on testosterone to help them grow. Cutting off the supply of hormones may cause cancer cells to die or to grow more slowly.

Options of hormone therapy:
*Medications that stop the body from producing testosterone. Medications known as luteinizing hormone-releasing hormone (LH-RH) agonists prevent the testicles from receiving messages to make testosterone. Drugs typically used in this type of hormone therapy include leuprolide (Lupron, Eligard), goserelin (Zoladex), triptorelin (Trelstar) and histrelin (Vantas). Other drugs sometimes used include ketoconazole and abiraterone (Zytiga).

*Medications that block testosterone from reaching cancer cells. Medications known as anti-androgens prevent testosterone from reaching your cancer cells. Examples include bicalutamide (Casodex), flutamide, and nilutamide (Nilandron). The drug enzalutamide (Xtandi) may be an option when other hormone therapies are no longer effective.

Surgery to remove the testicles (orchiectomy).
Removing  the testicles reduces testosterone levels in the body.
Hormone therapy is used in men with advanced prostate cancer to shrink the cancer and slow the growth of tumors. In men with early-stage prostate cancer, hormone therapy may be used to shrink tumors before radiation therapy. This can make it more likely that radiation therapy will be successful.

Side effects of hormone therapy may include erectile dysfunction, hot flashes, loss of bone mass, reduced sex drive and weight gain.

Surgery to remove the prostate:
Surgery for prostate cancer involves removing the prostate gland (radical prostatectomy), some surrounding tissue and a few lymph nodes. Ways the radical prostatectomy procedure can be performed include:

*Using a robot to assist with surgery. During robot-assisted surgery, the instruments are attached to a mechanical device (robot) and inserted into  the abdomen through several small incisions. The surgeon sits at a console and uses hand controls to guide the robot to move the instruments. Robotic prostatectomy may allow the surgeon to make more-precise movements with surgical tools than is possible with traditional minimally invasive surgery.

*Making an incision in  the abdomen. During retropubic surgery, the prostate gland is taken out through an incision in  the lower abdomen. Compared with other types of prostate surgery, retropubic prostate surgery may carry a lower risk of nerve damage, which can lead to problems with bladder control and erections.

*Making an incision between  the anus and scrotum. Perineal surgery involves making an incision between  the anus and scrotum in order to access  the prostate. The perineal approach to surgery may allow for quicker recovery times, but this technique makes removing the nearby lymph nodes and avoiding nerve damage more difficult.

*Laparoscopic prostatectomy. During a laparoscopic radical prostatectomy, the doctor performs surgery through small incisions in the abdomen with the assistance of a tiny camera (laparoscope). This procedure requires great skill on the part of the surgeon, and it carries an increased risk that nearby structures may be accidentally cut. For this reason, this type of surgery is not commonly performed for prostate cancer in the U.S. anymore.

The Doctor should decide which type of surgery is best for  the specific situation.

Radical prostatectomy carries a risk of urinary incontinence and erectile dysfunction. The riskfactors that the patient   may face based on the situation, the type of procedure the patient may select, according to his age, body type and  overall health.

Freezing of prostate tissue:
Cryosurgery or cryoablation involves freezing tissue to kill cancer cells.

During cryosurgery for prostate cancer, small needles are inserted in the prostate using ultrasound images as guidance. A very cold gas is placed in the needles, which causes the surrounding tissue to freeze. A second gas is then placed in the needles to reheat the tissue. The cycles of freezing and thawing kill the cancer cells and some surrounding healthy tissue.

Initial attempts to use cryosurgery for prostate cancer resulted in high complication rates and unacceptable side effects. However, newer technologies have lowered complication rates, improved cancer control and made the procedure easier to tolerate. Cryosurgery may be an option for men who haven’t been helped by radiation therapy.

Chemotherapy:
Chemotherapy uses drugs to kill rapidly growing cells, including cancer cells. Chemotherapy can be administered through a vein in your arm, in pill form or both.

Chemotherapy may be a treatment option for men with prostate cancer that has spread to distant areas of their bodies. Chemotherapy may also be an option for cancers that don’t respond to hormone therapy.

Biological therapy:
Biological therapy (immunotherapy) uses your body’s immune system to fight cancer cells. One type of biological therapy called sipuleucel-T (Provenge) has been developed to treat advanced, recurrent prostate cancer.

This treatment takes some of the patient’s own immune cells, genetically engineers them in a laboratory to fight prostate cancer, then injects the cells back into your body through a vein. Some men do respond to this therapy with some improvement in their cancer, but the treatment is very expensive and requires multiple treatments.

Alternative therapy:
It is believed that regular Yoga exercise with Pranayama  and Meditation under the guideline of some expart  may help a lot to cope with the distress of the patient.

Prevention:
Diet and lifestyle

The data on the relationship between diet and prostate cancer is poor.   In light of this the rate of prostate cancer is linked to the consumption of the Western diet.  There is little if any evidence to support an association between trans fat, saturated fat and carbohydrate intake and risk of prostate cancer.  Evidence regarding the role of omega-3 fatty acids in preventing prostate cancer does not suggest that they reduce the risk of prostate cancer, although additional research is needed. Vitamin supplements appear to have no effect and some may increase the risk.  High calcium intake has been linked to advanced prostate cancer. Consuming fish may lower prostate cancer deaths but does not appear to affect its occurrence.  Some evidence supports lower rates of prostate cancer with a vegetarian diet.  There is some tentative evidence for foods containing lycopene and selenium.  Diets rich in cruciferous vegetables, soy, beans and other legumes may be associated with a lower risk of prostate cancer, especially more advanced cancers.

Men who get regular exercise may have a slightly lower risk, especially vigorous activity and the risk of advanced prostate cancer.

Resources:

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

http://www.mayoclinic.org/diseases-conditions/prostate-cancer/basics/definition/con-20029597

Psoriatic arthritis

Other Names: Arthritis psoriatica,Arthropathic psoriasis or Psoriatic arthropathy

Definition:
Psoriatic arthritis is a form of arthritis that affects some people who have psoriasis — a condition that features red patches of skin topped with silvery scales. Most people develop psoriasis first and are later diagnosed with psoriatic arthritis, but the joint problems can sometimes begin before skin lesions appear.

Joint pain, stiffness and swelling are the main symptoms of psoriatic arthritis. They can affect any part of your body, including your fingertips and spine, and can range from relatively mild to severe. In both psoriasis and psoriatic arthritis, disease flares may alternate with periods of remission.

It is a type of inflammatory arthritis that will develop in up to 30 percent of people who have the chronic skin condition psoriasis. Psoriatic arthritis is classified as a seronegative spondyloarthropathy and therefore occurs more commonly in patients with tissue type HLA-B27.

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No cure for psoriatic arthritis exists, so the focus is on controlling symptoms and preventing damage to the joints. Without treatment, psoriatic arthritis may be disabling.

Classification:
There are five main types of psoriatic arthritis:

*Asymmetric: This type affects around 70% of patients and is generally mild. This type does not occur in the same joints on both sides of the body and usually only involves fewer than 3 joints.

*Symmetric: This type accounts for around 25% of cases, and affects joints on both sides of the body simultaneously. This type is most similar to rheumatoid arthritis and is disabling in around 50% of all cases.

*Arthritis mutilans (M07.1): Affects less than 5% of patients and is a severe, deforming and destructive arthritis. This condition can progress over months or years causing severe joint damage. Arthritis mutilans has also been called chronic absorptive arthritis, and may be seen in rheumatoid arthritis as well.

*Spondylitis (M07.2): This type is characterised by stiffness of the spine or neck, but can also affect the hands and feet, in a similar fashion to symmetric arthritis.

*Distal interphalangeal predominant (M07.0): This type of psoriatic arthritis is found in about 5% of patients, and is characterised by inflammation and stiffness in the joints nearest to the ends of the fingers and toes. Nail changes are often marked.

Symptoms:
*Pain, swelling, or stiffness in one or more joints is commonly present.

*Asymmetrical oligoarthritis (70%) (Involvement of the distal interphalangeal joints (DIP) is a characteristic feature).

*Sacroiliitis/spondylitis (40%)

*Symmetrical seronegative arthritis (15%)

*Distal interphalangeal joint arthritis (15%)

*Hand joints involved in psoriasis are proximal interphalangeal (PIP) + distal interphalangeal (DIP) + metacarpophalangeal (MCP) + wrist
Joints that are red or warm to the touch.

*Sausage-like swelling in the fingers or toes, known as dactylitis.

*Pain in and around the feet and ankles, especially tendinitis in the Achilles tendon or plantar fasciitis in the sole of the foot.

*Changes to the nails, such as pitting or separation from the nail bed.

*Pain in the area of the sacrum (the lower back, above the tailbone).

*Along with the above noted pain and inflammation, there is extreme exhaustion that does not go away with adequate rest. The exhaustion may last for days or weeks without abatement. Psoriatic arthritis may remain mild, or may progress to more destructive joint disease. Periods of active disease, or flares, will typically alternate with periods of remission. In severe forms, psoriatic arthritis may progress to arthritis mutilans which on X-ray gives pencil in cup appearance.

*Because prolonged inflammation can lead to joint damage, early diagnosis and treatment to slow or prevent joint damage is recommended.

*Scaly skin lesions are seen over extensor surfaces (scalp, natal cleft and umbilicus).

*The nail changes are pitting, onycholysis, sub–ungual hyperkeratosis and horizontal ridging.

Causes:
Psoriatic arthritis occurs when the body’s immune system begins to attack healthy cells and tissue. The abnormal immune response causes inflammation in your joints as well as overproduction of skin cells.

It’s not entirely clear why the immune system turns on healthy tissue, but it seems likely that both genetic and environmental factors play a role. Many people with psoriatic arthritis have a family history of either psoriasis or psoriatic arthritis. Researchers have discovered certain genetic markers that appear to be associated with psoriatic arthritis.

Physical trauma or something in the environment — such as a viral or bacterial infection — may trigger psoriatic arthritis in people with an inherited tendency.

Diagnosis:
There is no definitive test to diagnose psoriatic arthritis. Symptoms of psoriatic arthritis may closely resemble other diseases, including rheumatoid arthritis. A rheumatologist (a doctor specializing in diseases affecting the joints) may use physical examinations, health history, blood tests and x-rays to accurately diagnose psoriatic arthritis.

Factors that contribute to a diagnosis of psoriatic arthritis include:

*Psoriasis in the patient, or a family history of psoriasis or psoriatic arthritis.

*A negative test result for Rheumatoid factor, a blood factor associated with rheumatoid arthritis.

*Arthritis symptoms in the distal Interphalangeal articulations of hand (the joints closest to the tips of the fingers). This is not typical of rheumatoid arthritis.

*Ridging or pitting of fingernails or toenails (onycholysis), which is associated with psoriasis and psoriatic arthritis.

*Radiologic images indicating joint change.

*Other symptoms that are more typical of psoriatic arthritis than other forms of arthritis include inflammation in the Achilles tendon (at the back of the heel) or the Plantar fascia (bottom of the feet), and dactylitis (sausage-like swelling of the fingers or toes)

During the exam,the doctor may ask for the following tests:

Imaging tests:

*X-rays. Plain X-rays can help pinpoint changes in the joints that occur in psoriatic arthritis but not in other arthritic conditions.
Magnetic resonance imaging (MRI). MRI utilizes radio waves and a strong magnetic field to produce very detailed images of both hard and soft tissues in your body. This type of imaging test may be used to check for problems with the tendons and ligaments in your feet and lower back.
Laboratory tests:

*Rheumatoid factor (RF). RF is an antibody that’s often present in the blood of people with rheumatoid arthritis, but it’s not usually in the blood of people with psoriatic arthritis. For that reason, this test can help your doctor distinguish between the two conditions.

*Joint fluid test. Using a long needle, your doctor can remove a small sample of fluid from one of your affected joints — often the knee. Uric acid crystals in your joint fluid may indicate that you have gout rather than psoriatic arthritis.

Treatments:
The underlying process in psoriatic arthritis is inflammation; therefore, treatments are directed at reducing and controlling inflammation. Milder cases of psoriatic arthitis may be treated with NSAIDS alone; however, there is a trend toward earlier use of disease-modifying antirheumatic drugs or biological response modifiers to prevent irreversible joint destruction.

Nonsteroidal anti-inflammatory drugs:
Typically the medications first prescribed for psoriatic arthritis are NSAIDs such as ibuprofen and naproxen followed by more potent NSAIDs like diclofenac, indomethacin, and etodolac. NSAIDs can irritate the stomach and intestine, and long-term use can lead to gastrointestinal bleeding. Other potential adverse effects include damage to the kidneys and cardiovascular system.

Disease-modifying antirheumatic drugs:
These are used in persistent symptomatic cases without exacerbation. Rather than just reducing pain and inflammation, this class of drugs helps limit the amount of joint damage that occurs in psoriatic arthritis. Most DMARDs act slowly and may take weeks or even months to take full effect. Drugs such as methotrexate or leflunomide are commonly prescribed; other DMARDS used to treat psoriatic arthritis include cyclosporin, azathioprine, and sulfasalazine. These immunosuppressant drugs can also reduce psoriasis skin symptoms but can lead to liver and kidney problems and an increased risk of serious infection.

Biological response modifiers:
Recently, a new class of therapeutics called biological response modifiers or biologics has been developed using recombinant DNA technology. Biologic medications are derived from living cells cultured in a laboratory. Unlike traditional DMARDS that affect the entire immune system, biologics target specific parts of the immune system. They are given by injection or intravenous (IV) infusion.

Biologics prescribed for psoriatic arthritis are TNF-(alfa) inhibitors, including infliximab, etanercept, golimumab, certolizumab pegol and adalimumab, as well as the IL-12/IL-23 inhibitor ustekinumab.

Biologics may increase the risk of minor and serious infections. More rarely, they may be associated with nervous system disorders, blood disorders or certain types of cancer.

Other treatments:
Retinoid etretinate 30mg/day is effective for both arthritis and skin lesions. Photochemotherapy with methoxy psoralen and long wave ultraviolet light (PUVA) are used for severe skin lesions. Doctors may use joint injections with corticosteroids in cases where one joint is severely affected. In psoriatic arthritis patients with severe joint damage orthopedic surgery may be implemented to correct joint destruction, usually with use of a joint replacement. Surgery is effective for pain alleviation, correcting joint disfigurement, and reinforcing joint usefulness and strength.

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Lifestyle and home remedies

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Prognosis:
Seventy percent of people who develop psoriatic arthritis first show signs of psoriasis on the skin, 15 percent develop skin psoriasis and arthritis at the same time, and 15 percent develop skin psoriasis following the onset of psoriatic arthritis.

Psoriatic arthritis can develop in people who have any level severity of psoriatic skin disease from mild to very severe.

Psoriatic arthritis tends to appear about 10 years after the first signs of psoriasis. For the majority of people this is between the ages of 30 and 55, but the disease can also affect children. The onset of psoriatic arthritis symptoms before symptoms of skin psoriasis is more common in children than adults.

More than 80% of patients with psoriatic arthritis will have psoriatic nail lesions characterized by nail pitting, separation of the nail from the underlying nail bed, ridging and cracking, or more extremely, loss of the nail itself (onycholysis).

Men and women are equally affected by this condition. Like psoriasis, psoriatic arthritis is more common among Caucasians than Africans or Asians

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/Psoriatic_arthritis

http://www.mayoclinic.org/diseases-conditions/psoriatic-arthritis/basics/tests-diagnosis/con-20015006

http://www.mayoclinic.org/diseases-conditions/psoriatic-arthritis/basics/causes/con-20015006

http://www.mayoclinic.org/diseases-conditions/psoriatic-arthritis/basics/definition/CON-20015006

Hemolytic Uremic Syndrome (HUS)

Alternative names:  Haemolytic-uraemic syndrome, HUS

Definition:
Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys‘ filtering system. Red blood cells contain hemoglobin—an iron-rich protein that gives blood its red color and carries oxygen from the lungs to all parts of the body.

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When the kidneys and glomeruli—the tiny units within the kidneys where blood is filtered—become clogged with the damaged red blood cells, they are unable to do their jobs. If the kidneys stop functioning, a child can develop acute kidney injury—the sudden and temporary loss of kidney function. Hemolytic uremic syndrome is the most common cause of acute kidney injury in children.

It is a disease characterized by hemolytic anemia (anemia caused by destruction of red blood cells), acute kidney failure (uremia), and a low platelet count (thrombocytopenia). It predominantly, but not exclusively, affects children. Most cases are preceded by an episode of infectious, sometimes bloody, diarrhea acquired as a foodborne illness or from a contaminated water supply and caused by E. coli O157:H7, although Shigella, Campylobacter and a variety of viruses have also been implicated. It is now the most common cause of acquired acute renal failure in childhood. It is a medical emergency and carries a 5–10% mortality; of the remainder, the majority recover without major consequences but a small proportion develop chronic kidney disease and become reliant on renal replacement therapy.

The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. Children produce less urine than adults and the amount produced depends on their age. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder.

Symptoms:
STEC-HUS occurs after ingestion of a strain of bacteria, usually types of E. coli, that expresses verotoxin (also called Shiga-like toxin). Bloody diarrhea typically follows. HUS develops about 5–10 days after onset of diarrhea, with decreased urine output (oliguria), blood in the urine (hematuria), kidney failure, thrombocytopenia (low levels of platelets) and destruction of red blood cells (microangiopathic hemolytic anemia). Hypertension is common. In some cases, there are prominent neurologic changes.

A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis—an inflammation of the lining of the stomach, small intestine, and large intestine—such as

*vomiting
*bloody diarrhea
*abdominal pain
*fever and chills
*headache

As the infection progresses, the toxins released in the intestine begin to destroy red blood cells. When the red blood cells are destroyed, the child may experience the signs and symptoms of anemia—a condition in which red blood cells are fewer or smaller than normal, which prevents the body’s cells from getting enough oxygen.

Signs and symptoms of anemia may include:-

*fatigue, or feeling tired
*weakness
*fainting
*paleness

As the damaged red blood cells clog the glomeruli, the kidneys may become damaged and make less urine. When damaged, the kidneys work harder to remove wastes and extra fluid from the blood, sometimes leading to acute kidney injury.

Other signs and symptoms of hemolytic uremic syndrome may include bruising and seizures.

When hemolytic uremic syndrome causes acute kidney injury, a child may have the following signs and symptoms:

*edema—swelling, most often in the legs, feet, or ankles and less often in the hands or face
*albuminuria—when a child’s urine has high levels of albumin, the main protein in the blood
*decreased urine output
*hypoalbuminemia—when a child’s blood has low levels of albumin
*blood in the urine

Causes:
A number of things can cause hemolytic uremic syndrome, but the most common cause — particularly in children — is an infection with a specific strain of E. coli, usually the strain known as O157:H7. However, other strains of E. coli have been linked to hemolytic uremic syndrome, too.

Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream. The toxins travel through the bloodstream and can destroy the red blood cells. E. coli O157:H7 can be found in:

*Contaminated meat or produce
*Swimming pools or lakes contaminated with feces
*undercooked meat, most often ground beef
*unpasteurized, or raw, milk
*unwashed, contaminated raw fruits and vegetables
*contaminated juice

Less common causes, sometimes called atypical hemolytic uremic syndrome, can include:-

*taking certain medications, such as chemotherapy
*having other viral or bacterial infections
*inheriting a certain type of hemolytic uremicsyndrome that runs in families

Children who are more likely to develop hemolytic uremic syndrome include those who
are younger than age 5 and have been diagnosedwith an E. coli O157:H7 infection

*have a weakened immune system
*have a family history of inherited hemolyticuremic syndrome
*Hemolytic uremic syndrome occurs in about two out of every 100,000 children.

Most people who are infected with E. coli, even the more dangerous strains, won’t develop hemolytic uremic syndrome. It’s also possible for hemolytic uremic syndrome to follow infection with other types of bacteria.

In adults, hemolytic uremic syndrome is more commonly caused by other factors, including:

*The use of certain medications, such as quinine (an over-the-counter muscle cramp remedy), some chemotherapy drugs, the immunosuppressant medication cyclosporine (Neoral, Sandimmune) and anti-platelet medications

*Pregnancy

*Certain infections, such as HIV/AIDS or an infection with the pneumococcal bacteria

*Genes, which can be a factor because a certain type of HUS — atypical hemolytic uremic syndrome — may be passed down from your parents

The cause of hemolytic uremic syndrome in adults is often unknown

Diagnosis:
The Doctor diagnoses hemolytic uremic syndrome with

*a medical and family history
*a physical exam
*urine tests
*a blood test
*a stool test
*kidney biopsy

The similarities between HUS, aHUS, and TTP make differential diagnosis essential. All three of these systemic TMA-causing diseases are characterized by thrombocytopenia and microangiopathic hemolysis, plus one or more of the following: neurological symptoms (e.g., confusion, cerebral convulsions, seizures); renal impairment (e.g., elevated creatinine, decreased estimated glomerular filtration rate [eGFR], abnormal urinalysis ); and gastrointestinal (GI) symptoms (e.g., diarrhea, nausea/vomiting, abdominal pain, gastroenteritis).The presence of diarrhea does not exclude aHUS as the etiology of TMA, as 28% of patients with aHUS present with diarrhea and/or gastroenteritis. First diagnosis of aHUS is often made in the context of an initial, complement-triggering infection, and Shiga-toxin has also been implicated as a trigger that identifies patients with aHUS. Additionally, in one study, mutations of genes encoding several complement regulatory proteins were detected in 8 of 36 (22%) patients diagnosed with STEC-HUS. However, the absence of an identified complement regulatory gene mutation does not preclude aHUS as the etiology of the TMA, as approximately 50% of patients with aHUS lack an identifiable mutation in complement regulatory genes.

Diagnostic work-up supports the differential diagnosis of TMA-causing diseases. A positive Shiga-toxin/EHEC test confirms an etiological cause for STEC-HUS, and severe ADAMTS13 deficiency (i.e., ?5% of normal ADAMTS13 levels) confirms a diagnosis of TTP

Complications:
Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.1
However, children with hemolytic uremic syndrome may have serious and sometimes life-threatening complications, including

*acute kidney injury
*high blood pressure
*blood-clotting problems that can lead to bleeding
*seizures
*heart problems
*chronic, or long lasting, kidney disease
*stroke
*coma

Treatment:
The Doctor will treat a child’s urgent symptoms and try to prevent complications by

*observing the child closely in the hospital
*replacing minerals, such as potassium and salt, and fluids through an intravenous (IV) tube
*giving the child red blood cells and platelets—cells in the blood that help with clotting—through an IV
*giving the child IV nutrition
*treating high blood pressure with medications

Treating Acute Kidney Injury:
If necessary,the Doctor will treat acute kidney injury with dialysis—the process of filtering wastes and extra fluid from the body with an artificial kidney. The two forms of dialysis are hemodialysis and peritoneal dialysis. Most children with acute kidney injury need dialysis for a short time only.

Treating Chronic Kidney Disease:
Some children may sustain significant kidney damage that slowly develops into CKD. Children who develop CKD must receive treatment to replace the work the kidneys do. The two types of treatment are dialysis and transplantation.

In most cases, The Doctor treat CKD with a kidney transplant. A kidney transplant is surgery to place a healthy kidney from someone who has just died or a living donor, most often a family member, into a person’s body to take over the job of the failing kidney. Though some children receive a kidney transplant before their kidneys fail completely, many children begin with dialysis to stay healthy until they can have a transplant. click to know more

Prevention:

Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys’ filtering system.
The most common cause of hemolytic uremic syndrome in children is an Escherichia coli (E. coli) infection of the digestive system.
Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream.
A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis, an inflammation of the lining of the stomach, small intestine, and large intestine.

Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.
Some children may sustain significant kidney damage that slowly develops into chronic kidney disease (CKD).

Parents and caregivers can help prevent childhood hemolytic uremic syndrome due to E. coli O157:H7 by

*avoiding unclean swimming areas
*avoiding unpasteurized milk, juice, and cider
*cleaning utensils and food surfaces often
*cooking meat to an internal temperature of at least 160° F
*defrosting meat in the microwave or refrigerator
*keeping children out of pools if they have had diarrhea
*keeping raw foods separate
*washing hands before eating
*washing hands well after using the restroom and after changing diapers

When a child is taking medications that may cause hemolytic uremic syndrome, it is important that the parent or caretaker watch for symptoms and report any changes in the child’s condition to the Doctor as soon as possible.

Prognosis:
Acute renal failure occurs in 55-70% of patients with STEC-HUS, although up to 70-85% recover renal function. Patients with aHUS generally have poor outcomes, with up to 50% progressing to ESRD or irreversible brain damage; as many as 25% die during the acute phase. However, with aggressive treatment, more than 90% of patients survive the acute phase of HUS, and only about 9% may develop ESRD. Roughly one-third of persons with HUS have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with HUS have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their colon removed. The overall mortality rate from HUS is 5-15%. Children and the elderly have a worse prognosis.

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://kidney.niddk.nih.gov/KUDiseases/pubs/childkidneydiseases/hemolytic_uremic_syndrome/

http://en.wikipedia.org/wiki/Hemolytic-uremic_syndrome

http://www.mayoclinic.org/diseases-conditions/hemolytic-uremic-syndrome/basics/causes/con-20029487

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Cholangitis

Definition:
Cholangitis is an infection of the common bile duct, the tube that carries bile from the liver to the gallbladder and intestines. Bile is a liquid made by the liver that helps digest food.

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Cholangitis can be life-threatening, and is regarded as a medical emergency. Characteristic symptoms include yellow discoloration of the skin or whites of the eyes, fever, abdominal pain, and in severe cases, low blood pressure and confusion. Initial treatment is with intravenous fluids and antibiotics, but there is often an underlying problem (such as gallstones or narrowing in the bile duct) for which further tests and treatments may be necessary, usually in the form of endoscopy to relieve obstruction of the bile duct.
Symptoms:
The following symptoms may occur:

*Pain on the upper right side or upper middle part of the abdomen. It may also be felt in the back or below the right shoulder blade. The pain may come and go and feel sharp, cramp-like, or dull.

*Fever and chills

*Dark urine and clay-colored stools

*Nausea and vomiting

*Yellowing of the skin (jaundice), which may come and go
Physical examination findings typically include jaundice and right upper quadrant tenderness.Charcot’s triad is a set of three common findings in cholangitis: abdominal pain, jaundice, and fever. This was assumed in the past to be present in 50–70% of cases, although more recently the frequency has been reported as 15–20%.Reynolds’ pentad includes the findings of Charcot’s triad with the presence of septic shock and mental confusion. This combination of symptoms indicates worsening of the condition and the development of sepsis, and is seen less commonly still.

In the elderly, the presentation may be atypical; they may directly collapse due to septicemia without first showing typical features. Those with an indwelling stent in the bile duct (see below) may not develop jaundice.

Causes:
Cholangitis is most often caused by a bacterial infection. This can occur when the duct is blocked by something, such as a gallstone or tumor. The infection causing this condition may also spread to the liver.

Bile duct obstruction, which is usually present in acute cholangitis, is generally due to gallstones. 10–30% of cases, however, are due to other causes such as benign stricturing (narrowing of the bile duct without an underlying tumor), postoperative damage or an altered structure of the bile ducts such as narrowing at the site of an anastomosis (surgical connection), various tumors (cancer of the bile duct, gallbladder cancer, cancer of the ampulla of Vater, pancreatic cancer, cancer of the duodenum), anaerobic organisms such as Clostridium and Bacteroides (especially in the elderly and those who have undergone previous surgery of the biliary system). Parasites which may infect the liver and bile ducts may cause cholangitis; these include the roundworm Ascaris lumbricoides and the liver flukes Clonorchis sinensis, Opisthorchis viverrini and Opisthorchis felineus. In people with AIDS, a large number of opportunistic organisms has been known to cause AIDS cholangiopathy, but the risk has rapidly diminished since the introduction of effective AIDS treatment. Cholangitis may also complicate medical procedures involving the bile duct, especially ERCP. To prevent this, it is recommended that those undergoing ERCP for any indication receive prophylactic (preventative) antibiotics.

The presence of a permanent biliary stent (e.g. in pancreatic cancer) slightly increases the risk of cholangitis, but stents of this type are often needed to keep the bile duct patent under outside pressure

Diagnosis:
Routine blood tests show features of acute inflammation (raised white blood cell count and elevated C-reactive protein level), and usually abnormal liver function tests (LFTs). In most cases the LFTs will be consistent with obstruction: raised bilirubin, alkaline phosphatase and ?-glutamyl transpeptidase. In the early stages, however, pressure on the liver cells may be the main feature and the tests will resemble those in hepatitis, with elevations in alanine transaminase and aspartate transaminase.

Blood cultures are often performed in people with fever and evidence of acute infection. These yield the bacteria causing the infection in 36% of cases, usually after 24–48 hours of incubation. Bile, too, may be sent for culture during ERCP (see below). The most common bacteria linked to ascending cholangitis are gram-negative bacilli: Escherichia coli (25–50%), Klebsiella (15–20%) and Enterobacter (5–10%). Of the gram-positive cocci, Enterococcus causes 10–20%.

You may have the following tests to look for blockages:

*Abdominal ultrasound

*Endoscopic retrograde cholangiopancreatography (ERCP)

*Magnetic resonance cholangiopancreatography (MRCP)

*Percutaneous transhepatic cholangiogram (PTCA)

*You may also have the following blood tests:

#Bilirubin level
#Liver enzyme levels
#Liver function tests
#White blood count (WBC)
Treatment:
Quick diagnosis and treatment are very important.Antibiotics to cure infection is the first treatment done in most cases. ERCP or other surgical procedure is done when the patient is stable.Patients who are very ill or are quickly getting worse may need surgery right away.

Cholangitis requires admission to hospital. Intravenous fluids are administered, especially if the blood pressure is low, and antibiotics are commenced. Empirical treatment with broad-spectrum antibiotics is usually necessary until it is known for certain which pathogen is causing the infection, and to which antibiotics it is sensitive. Combinations of penicillins and aminoglycosides are widely used, although ciprofloxacin has been shown to be effective in most cases, and may be preferred to aminoglycosides because of fewer side effects. Metronidazole is often added to specifically treat the anaerobic pathogens, especially in those who are very ill or at risk of anaerobic infections. Antibiotics are continued for 7–10 days. Drugs that increase the blood pressure (vasopressors) may also be required to counter the low blood pressure.
Prognosis:
Acute cholangitis carries a significant risk of death, the leading cause being irreversible shock with multiple organ failure (a possible complication of severe infections). Improvements in diagnosis and treatment have led to a reduction in mortality: before 1980, the mortality rate was greater than 50%, but after 1980 it was 10–30%. Patients with signs of multiple organ failure are likely to die unless they undergo early biliary drainage and treatment with systemic antibiotics. Other causes of death following severe cholangitis include heart failure and pneumonia.

Risk Factors:
Risk factors include a previous history of gallstones, sclerosing cholangitis, HIV, narrowing of the common bile duct, and, rarely, travel to countries where you might catch a worm or parasite infection.

Risk factors indicating an increased risk of death include older age, female gender, a history of liver cirrhosis, biliary narrowing due to cancer, acute renal failure and the presence of liver abscesses. Complications following severe cholangitis include renal failure, respiratory failure (inability of the respiratory system to oxygenate blood and/or eliminate carbon dioxide), cardiac arrhythmia, wound infection, pneumonia, gastrointestinal bleeding and myocardial ischemia (lack of blood flow to the heart, leading to heart attacks).

Prevention:
Treatment of gallstones, tumors, and infestations of parasites may reduce the risk for some people. A metal or plastic stent that is placed in the bile system may be needed to prevent the infection from returning.
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.nlm.nih.gov/medlineplus/ency/article/000290.htm

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

Gastroparesis

Definition:
Gastroparesis (gastro-, “stomach” + -paresis, “partial paralysis”), also called delayed gastric emptying, is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for an abnormally long time. Normally, the stomach contracts to move food down into the small intestine for additional digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not properly function. Food then moves slowly or stops moving through the digestive tract….CLICK & SEE

YOU MAY CLICK & SEEOur Digestive System and How It Works 
Symptoms:
The most common symptoms of gastroparesis are the following:
*Chronic nausea (93%)
*Vomiting (especially of undigested food) (68-84%)
*Abdominal pain (46-90%)
*A feeling of fullness after eating just a few bites (60-86%)

Other symptoms include the following:
*Palpitations
*Heartburn
*Abdominal bloating
*Erratic blood glucose levels
*Lack of appetite
*Gastroesophageal reflux
*Spasms of the stomach wall
*Weight loss and malnutrition

Morning nausea may also indicate gastroparesis. Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.

Symptoms may be aggravated by eating greasy or rich foods, large quantities of foods with fiber—such as raw fruits and vegetables—or drinking beverages high in fat or carbonation. Symptoms may be mild or severe, and they can occur frequently in some people and less often in others. The symptoms of gastroparesis may also vary in intensity over time in the same individual. Sometimes gastroparesis is difficult to diagnose because people experience a range of symptoms similar to those of other diseases.

Causes:
Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.

It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may affect chemical changes in the nerves.The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Other possible causes include anorexia nervosa and bulimia nervosa, which may also damage the vagus nerve. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers-Danlos syndrome, and neurological conditions such as Parkinson’s disease. It may also occur as part of a mitochondrial disease.

Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery.  Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.

Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. “Stomach flu”, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.

Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.

Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCL) in order to properly empty itself of a meal.

Other identifiable causes of gastroparesis include intestinal surgery and nervous system diseases such as Parkinson’s disease or multiple sclerosis. For reasons that are not very clear, gastroparesis is more commonly found in women than in men.

Complications:
The complications of gastroparesis can include

*severe dehydration due to persistent vomiting

*gastroesophageal reflux disease (GERD), which is GER that occurs more than twice a week for a few weeks; GERD can lead to esophagitis— irritation of the esophagus

*bezoars, which can cause nausea, vomiting, obstruction, or interfere with absorption of some medications in pill form

*difficulty managing blood glucose levels in people with diabetes

*malnutrition due to poor absorption of nutrients or a low calorie intake

*decreased quality of life, including work absences due to severe symptoms

Diagnosis:
Gastroparesis is diagnosed through a physical exam, medical history, blood tests, tests to rule out blockage or structural problems in the GI tract, and gastric emptying tests. Tests may also identify a nutritional disorder or underlying disease. To rule out any blockage or other structural problems, the doctor may perform one or more of the following tests:

*Upper gastrointestinal (GI) endoscopy. This procedure involves using an endoscope—a small, flexible tube with a light—to see the upper GI tract, which includes the esophagus, stomach, and duodenum—the first part of the small intestine. The test is performed at a hospital or outpatient center by a gastroenterologist—a doctor who specializes in digestive diseases. The endoscope is carefully fed down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A person may receive a liquid anesthetic that is gargled or sprayed on the back of the throat. An intravenous (IV) needle is placed in a vein in the arm if general anesthesia is given. The test may show blockage or large bezoars—solid collections of food, mucus, vegetable fiber, hair, or other material that cannot be digested in the stomach—that are sometimes softened, dissolved, or broken up during an upper GI endoscopy.

*Upper GI series. An upper GI series may be done to look at the small intestine. The test is performed at a hospital or outpatient center by an x-ray technician, and the images are interpreted by a radiologist—a doctor who specializes in medical imaging. Anesthesia is not needed. No eating or drinking is allowed for 8 hours before the procedure, if possible. If the person has diabetes, a health care provider may give different instructions about fasting before the test. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Barium coats the small intestine, making signs of gastroparesis show up more clearly on x rays. Gastroparesis is likely if the x ray shows food in the stomach after fasting. A person may experience bloating and nausea for a short time after the test. For several days afterward, barium liquid in the GI tract causes stools to be white or light colored. A health care provider will give the person specific instructions about eating and drinking after the test.

*Ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The procedure is performed in a health care provider’s office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist; anesthesia is not needed. The images can show whether gallbladder disease and pancreatitis could be the cause of a person’s digestive symptoms, rather than gastroparesis.

*Gastric emptying scintigraphy. The test involves eating a bland meal—such as eggs or an egg substitute—that contains a small amount of radioactive material. The test is performed in a radiology center or hospital by a specially trained technician and interpreted by a radiologist; anesthesia is not needed. An external camera scans the abdomen to show where the radioactive material is located. The radiologist is then able to measure the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. If more than 10 percent of the meal is still in the stomach at 4 hours, the diagnosis of gastroparesis is confirmed.

*SmartPill. The SmartPill is a small electronic device in capsule form. The SmartPill test is available at specialized outpatient centers. The images are interpreted by a radiologist. The device is swallowed and moves through the entire digestive tract, sending information to a cell-phone-sized receiver worn around the person’s waist or neck. The recorded information provides a detailed record of how quickly food travels through each part of the digestive tract.

* Breath test. With this test, the person eats a meal containing a small amount of radioactive material; then breath samples are taken over a period of several hours to measure the amount of radioactive material in the exhaled breath. The results allow the health care provider to calculate how fast the stomach is emptying.
Treatment:
Treatment of gastroparesis depends on the severity of the person’s symptoms. In most cases, treatment does not cure gastroparesis, which is usually a chronic, or long-lasting, condition. Gastroparesis is also a relapsing condition—the symptoms can come and go for periods of time. Treatment helps people manage the condition so they can be as comfortable and active as possible.

Treatment includes dietary changes (low-fiber and low residue diets and, in some cases, restrictions on fat and/or solids); oral prokinetic medications such as metoclopramide (Reglan, Maxolon, Clopra), cisapride (Propulsid) (no longer available in the US or Australia), erythromycin (E-Mycin, Erythrocin, Ery-Tab, EES) and domperidone (Motilium) (not approved in the US; can be prescribed/obtained in Canada); adjustments in insulin dosage for those with diabetes; a jejunostomy tube; parenteral nutrition; implanted gastric neurostimulators (“stomach pacemakers”); or botulinum toxin (botox injected into the pylorus).

Sildenafil citrate, which increases blood flow to the genital area in men, is being used by some practitioners to stimulate the gastrointestinal tract in cases of diabetic gastroparesis.

The antidepressant mirtazapine has proven effective in the treatment of gastroparesis unresponsive to conventional treatment. This is due to its anti-emetic and appetite stimulant properties. Mirtazapine acts on the same serotonin receptor (5-HT3) as does the popular anti-emetic ondansetron.

When a person has severe symptoms, a liquid or puréed diet may be prescribed. As liquids tend to empty more quickly from the stomach, some people may find a puréed diet helps improve symptoms. Puréed fresh or cooked fruits and vegetables can be incorporated into shakes and soups. A health care provider may recommend a dietitian to help a person plan meals that minimize symptoms and ensure all nutritional needs are met.

When the most extreme cases of gastroparesis lead to severe nausea, vomiting, and dehydration, urgent care may be required at a medical facility where IV fluids can be given.

CLICK & SEE.……..Home remidies..1……Home remidies..2

In most of the cases if the patient starts Yoga exercise & meditation and does it regularly under the guidance of an expart with dietary changes he or she will get total recovery.

Hope through Research:
The National Institute of Diabetes and Digestive and Kidney Diseases’ (NIDDK’s) Division of Digestive Diseases and Nutrition supports basic and clinical research into GI motility disorders, including gastroparesis.

Researchers are studying whether new medications or surgery can improve gastric emptying and reduce gastroparesis symptoms. Researchers are evaluating the safety and effectiveness of nortriptyline for treatment of gastroparesis.

Participants in clinical trials can play a more active role in their own health care, gain access to new research treatments before they are widely available, and help others by contributing to medical research.
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/Gastroparesis

http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/gastroparesis/Pages/facts.aspx

Dumping Syndrome

Other Names: Gastric dumping syndrome, or rapid gastric emptying

Definition:
Gastric dumping syndrome, or rapid gastric emptying is a condition where ingested foods bypass the stomach too rapidly and enter the small intestine largely undigested. It happens when the small intestine expands too quickly due to the presence of hyperosmolar (having increased osmolarity) contents from the stomach. This causes symptoms due to the fluid shift into the gut lumen with plasma volume contraction and acute intestinal distention. “Early” dumping begins concurrently within 15 to 30 minutes from ingestion of a meal. Symptoms of early dumping include nausea, vomiting, bloating, cramping, diarrhea, dizziness, and fatigue. “Late” dumping happens one to three hours after eating. Symptoms of late dumping include weakness, sweating, and dizziness. Many people have both types. The syndrome is most often associated with gastric bypass (Roux-en-Y) surgery.

CLICK & SEE

Rapid loading of the small intestine with hypertonic stomach contents can lead to rapid entry of water into the intestinal lumen. Osmotic diarrhea, distension of the small bowel (leading to crampy abdominal pain), and hypovolemia can result.

In addition, people with this syndrome often suffer from low blood sugar, or hypoglycemia, because the rapid “dumping” of food triggers the pancreas to release excessive amounts of insulin into the bloodstream. This type of hypoglycemia is referred to as “alimentary hypoglycemia.”
Dumping Syndrome occurs when food, especially sugar, moves too fast from the stomach to the duodenum—the first part of the small intestine—in the upper gastrointestinal (GI) tract. This condition is also called rapid gastric emptying. Dumping syndrome has two forms, based on when symptoms occur:

*early dumping syndrome—occurs 10 to 30 minutes after a meal

*late dumping syndrome—occurs 2 to 3 hours after a meal

Symptoms:
Symptoms of dumping syndrome are most common during a meal or within 15 to 30 minutes following a meal. They include:

Gastrointestinal:-

*Nausea
*Vomiting
*Abdominal cramps
*Diarrhea
*Feeling of fullness

Cardiovascular:

*Flushing
*Dizziness, lightheadedness
*Heart palpitations, rapid heart rate
Signs and symptoms also can develop later, usually one to three hours after eating. This is due to the dumping of large amount of sugars into the small intestine (hyperglycemia). In response, the body releases large amounts of insulin to absorb the sugars, leading to low levels of sugar in the body (hypoglycemia).

Symptoms of late dumping can include:-

*Sweating
*Hunger
*Fatigue
*Dizziness, lightheadedness
*Confusion
*Heart palpitations, rapid heart rate
*Fainting

A study of more than 1,100 people who had their stomachs surgically removed found that about two-thirds experienced early symptoms and about a third experienced late symptoms of dumping syndrome. Some people experience both early and late signs and symptoms.

No matter when problems develop, however, they may be worse following a high-sugar meal, especially one that’s rich in table sugar (sucrose) or fruit sugar (fructose).
Causes:
Dumping syndrome is caused by problems with the storage of food particles in the stomach and emptying of particles into the duodenum. Early dumping syndrome results from rapid movement of fluid into the intestine following a sudden addition of a large amount of food from the stomach. Late dumping syndrome results from rapid movement of sugar into the intestine, which raises the body’s blood glucose level and causes the pancreas to increase its release of the hormone insulin. The increased release of insulin causes a rapid drop in blood glucose levels, a condition known as hypoglycemia, or low blood sugar.

In dumping syndrome, food and gastric juices from your stomach move to your small intestine in an uncontrolled, abnormally fast manner. This is most often related to changes in your stomach associated with surgery, such as when the opening (pylorus) between your stomach and the small intestine (duodenum) has been removed during an operation.

The pylorus acts as a brake so that stomach emptying is gradual. When it’s removed, stomach material dumps rapidly into the small intestine. The ill effects of this are thought to be caused by the release of gastrointestinal hormones in the small intestine, as well as insulin secreted to process the sugar (glucose).

Dumping syndrome can occur after any operation on the stomach as well as after removal of the esophagus (esophagectomy). Gastric bypass surgery for weight loss is the most common cause today. It develops most commonly within weeks after surgery, or as soon as you return to your normal diet. The more stomach removed or bypassed, the more likely that the condition will be severe. It sometimes becomes a chronic disorder.
Diagnosis:
The doctor will diagnose dumping syndrome primarily on the basis of symptoms. A scoring system helps differentiate dumping syndrome from other GI problems. The scoring system assigns points to each symptom and the total points result in a score. A person with a score above 7 likely has dumping syndrome.

The following tests may confirm dumping syndrome and exclude other conditions with similar symptoms:-

*A modified oral glucose tolerance test checks how well insulin works with tissues to absorb glucose. A health care provider performs the test during an office visit or in a commercial facility and sends the blood samples to a lab for analysis. The person should fast—eat or drink nothing except water—for at least 8 hours before the test. The health care provider will measure blood glucose concentration, hematocrit—the amount of red blood cells in the blood—pulse rate, and blood pressure before the test begins. After the initial measurements, the person drinks a glucose solution. The health care provider repeats the initial measurements immediately and at 30-minute intervals for up to 180 minutes. A health care provider often confirms dumping syndrome in people with

#low blood sugar between 120 and 180 minutes after drinking the solution

#an increase in hematocrit of more than 3 percent at 30 minutes

#a rise in pulse rate of more than 10 beats per minute after 30 minutes
*A gastric emptying scintigraphy test involves eating a bland meal—such as eggs or an egg substitute—that contains a small amount of radioactive material. A specially trained technician performs this test in a radiology center or hospital, and a radiologist—a doctor who specializes in medical imaging—interprets the results. Anesthesia is not needed. An external camera scans the abdomen to locate the radioactive material. The radiologist measures the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. The test can help confirm a diagnosis of dumping syndrome.

The doctor may also examine the structure of the esophagus, stomach, and upper small intestine with the following tests:

#An upper GI endoscopy involves using an endoscope—a small, flexible tube with a light—to see the upper GI tract. A gastroenterologist—a doctor who specializes in digestive diseases—performs the test at a hospital or an outpatient center. The gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A person may receive general anesthesia or a liquid anesthetic that is gargled or sprayed on the back of the throat. If the person receives general anesthesia, a health care provider will place an intravenous (IV) needle in a vein in the arm. The test may show ulcers, swelling of the stomach lining, or cancer.

#An upper GI series examines the small intestine. An x-ray technician performs the test at a hospital or an outpatient center and a radiologist interprets the images. Anesthesia is not needed. No eating or drinking is allowed before the procedure, as directed by the health care staff. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Barium coats the small intestine, making signs of a blockage or other complications of gastric surgery show up more clearly on x rays.

A person may experience bloating and nausea for a short time after the test. For several days afterward, barium liquid in the GI tract causes white or light-colored stools. A health care provider will give the person specific instructions about eating and drinking after the test.
Treatment:
Dumping syndrome is largely avoidable by avoiding certain foods that are likely to cause it; therefore, having a bigger digestive tract balanced diet is important. Treatment includes changes in eating habits and medication. People who have gastric dumping syndrome need to eat several small meals a day that are low in carbohydrates, avoiding simple sugars, and should drink liquids between meals, not with them. Fiber delays gastric emptying and reduces insulin peaks. People with severe cases take medicine (such as octreotide and cholestyramine) or proton pump inhibitors (such as pantoprazole and omeprazole) to slow their digestion. Doctors may also recommend surgery. Surgical intervention may include conversion of a Billroth I to a Roux-en Y gastrojejunostomy.

Medication:
A doctor may prescribe octreotide acetate (Sandostatin) to treat dumping syndrome symptoms. The medication works by slowing gastric emptying and inhibiting the release of insulin and other GI hormones. Octreotide comes in short- and long-acting formulas. The short-acting formula is injected subcutaneously—under the skin—or intravenously—into a vein—two to four times a day. A health care provider may perform the injections or may train the patient or patient’s friend or relative to perform the injections. He or she may injects the long-acting formula into the buttocks muscles once every 4 weeks. Complications of octreotide treatment include increased or decreased blood glucose levels, pain at the injection site, gallstones, and fatty, foul-smelling stools.

Hope through Research:
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) conducts and supports basic and clinical research into many digestive disorders, including dumping syndrome.

Clinical trials are research studies involving people. Clinical trials look at safe and effective new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. To learn more about clinical trials, why they matter, and how to participate, visit the NIH Clinical Research Trials and You website at www.nih.gov/health/clinicaltrialsExternal NIH Link. For information about current studies, visit www.ClinicalTrials.govExternal Link

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/Gastric_dumping_syndrome

http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/dumping-syndrome/Pages/facts.aspx

http://www.mayoclinic.org/diseases-conditions/dumping-syndrome/basics/symptoms/con-20028034

Bowel control

Other Names: Bowel incontinence,Fecal incontinence

Description:
Bowel incontinence is the loss of bowel control, leading to an involuntary passage of stool. This can range from occasionally leaking a small amount of stool and passing gas, to completely losing control of bowel movements..CLICK & SEE

You have a bowel control problem if you accidentally pass solid or liquid stool or mucus from your rectum.* Bowel control problems include being unable to hold a bowel movement until you reach a toilet and passing stool into your underwear without being aware of it happening. Stool, also called feces, is solid waste that is passed as a bowel movement and includes undigested food, bacteria, mucus, and dead cells. Mucus is a clear liquid that coats and protects tissues in your digestive system.

Among people over age 65, most surveys find that women experience bowel incontinence more often than men. One to three out of every 1,000 women report a loss of bowel control at least once per month.

To hold stool and maintain continence, the rectum, anus, pelvic muscles, and nervous system must function normally. You must also have the physical and mental ability to recognize and respond to the urge to have a bowel movement.

Ringlike muscles called sphincters close tightly around your anus to hold stool in your rectum until you’re ready to release the stool. Pelvic floor muscles support your rectum and a woman’s vagina and also help with bowel control.

Causes:
Bowel control problems are often caused by a medical issue and can be treated.

*Chronic constipation, causing the muscles of the anus and intestines to stretch and weaken, and leading to diarrhea and stool leakage (see: encopresis)

*Chronic laxative use

*Colectomy or bowel surgery

*Decreased awareness of sensation of rectal fullness

*Emotional problems

*Gynecological, prostate, or rectal surgery

*Injury to the anal muscles due to childbirth (in women)

*Nerve or muscle damage (from trauma, tumor, or radiation)

*Severe diarrhea that overwhelms the ability to control passage of stool

*Severe hemorrhoids or rectal prolapse

*Stress of unfamiliar environment

*A disease or injury that damages your nervous system

*Poor overall health from multiple chronic, or long lasting, illnesses

*A difficult childbirth with injuries to your pelvic floor—the muscles, ligaments, and tissues that support your uterus, vagina, bladder, and rectum

Diagnosis:
To diagnose what is causing your bowel control problem, your doctor will take your medical history, including asking the questions listed in “What do I tell my doctor about my bowel control problem?” Your doctor may refer you to a specialist who will perform a physical exam and may suggest one or more of the following tests:

* anal manometry
* anal ultrasound
* magnetic resonance imaging (MRI)
* defecography
* flexible sigmoidoscopy or colonoscopy
* anal electromyography (EMG)

Anal manometry. Anal manometry uses pressure sensors and a balloon that can be inflated in your rectum to check how sensitive your rectum is and how well it works. Anal manometry also checks the tightness of the muscles around your anus. To prepare for this test, you should use an enema and not eat anything 2 hours before the test. An enema involves flushing water or a laxative into your anus using a special squirt bottle. A laxative is medicine that loosens stool and increases bowel movements. For this test, a thin tube with a balloon on its tip and pressure sensors below the balloon is put into your anus. Once the balloon reaches the rectum and the pressure sensors are in the anus, the tube is slowly pulled out to measure muscle tone and contractions. No sedative is needed for this test, which takes about 30 minutes.

Anal ultrasound. Ultrasound uses a tool, called a transducer, that bounces safe, painless sound waves off your organs to create an image of their structure. An anal ultrasound is specific to the anus and rectum. The procedure is performed in a doctor’s office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist—a doctor who specializes in medical imaging. A sedative is not needed. The images can show the structure of your anal sphincter muscles.

MRI. MRI machines use radio waves and magnets to produce detailed pictures of your internal organs and soft tissues without using x rays. The procedure is performed in an outpatient center or hospital by a specially trained technician, and the images are interpreted by a radiologist. A sedative is not needed, though you may be given medicine to help you relax if you have a fear of confined spaces. An MRI may include the injection of special dye, called contrast medium. With most MRI machines, you lie on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some newer machines are designed to allow you to lie in a more open space. MRIs can show problems with your anal sphincter muscles. MRIs can provide more information than anal ultrasound, especially about the external anal sphincter.

Defecography. This x ray of the area around your anus and rectum shows whether you have problems with

* pushing stool out of your body
* the functioning of your anus and rectum
* squeezing and relaxing your rectal muscles

The test can also show changes in the structure of your anus or rectum. To prepare for the test, you perform two enemas. You can’t eat anything for 2 hours before the test. During the test, the doctor fills your rectum with a soft paste that shows up on x rays and feels like stool. You sit on a toilet inside an x-ray machine. The doctor will ask you to first pull in and squeeze your sphincter muscles to prevent leakage and then to strain as if you’re having a bowel movement. The radiologist studies the x rays to look for problems with your rectum, anus, and pelvic floor muscles.

Flexible sigmoidoscopy or colonoscopy. These tests are similar, but a colonoscopy is used to view your rectum and entire colon, while a flexible sigmoidoscopy is used to view just your rectum and lower colon. These tests are performed at a hospital or outpatient center by a gastroenterologist—a doctor who specializes in digestive diseases. For both tests, a doctor will give you written bowel prep instructions to follow at home. You may be asked to follow a clear liquid diet for 1 to 3 days before either test. The night before the test, you may need to take a laxative. One or more enemas may be needed the night before and about 2 hours before the test.

In most cases, you will be given a light sedative, and possibly pain medicine, to help you relax during a flexible sigmoidoscopy. A sedative is used for colonoscopy. For either test, you will lie on a table while the doctor inserts a flexible tube into your anus. A small camera on the tube sends a video image of your bowel lining to a computer screen. The test can show problems in your lower GI tract that may be causing your bowel control problem. The doctor may also perform a biopsy, a procedure that involves taking a piece of tissue from the bowel lining for examination with a microscope. You won’t feel the biopsy. A pathologist—a doctor who specializes in diagnosing diseases—examines the tissue in a lab to confirm the diagnosis.

You may have cramping or bloating during the first hour after these tests. You’re not allowed to drive for 24 hours after a colonoscopy or flexible sigmoidoscopy to allow the sedative time to wear off. Before the test, you should make plans for a ride home. You should recover fully by the next day and be able to go back to your normal diet.

Anal EMG. Anal EMG checks the health of your pelvic floor muscles and the nerves that control your muscles. The doctor inserts a very thin needle wire through your skin into your muscle. The wire on the needle picks up the electrical activity given off by the muscles. The electrical activity is shown as images on a screen or sounds through a speaker. Another type of anal EMG uses stainless steel plates attached to the sides of a plastic plug instead of a needle. The plug is put in your anus to measure the electrical activity of your external anal sphincter and other pelvic floor muscles. The test can show if there is damage to the nerves that control the external sphincter or pelvic floor muscles by measuring the average electrical activity when you

* relax quietly
* squeeze to prevent a bowel movement
* strain to have a bowel movement

Treatment:
Home Care:
Incontinence is not a hopeless situation. Proper treatment can help most people, and can often eliminate the problem.

Treating bowel incontinence should begin by identifying the cause of the incontinence. There are several ways to strengthen the anal and pelvic muscles and promote normal bowel function.

Rutine pelvic floor exercise  may improve the condition.

FECAL IMPACTION:
Fecal impaction is usually caused by chronic constipation. It leads to a mass of stool that partially blocks the large intestine. If constipation or fecal impaction contributes to fecal incontinence, usually laxatives and enemas are of little help. A health care provider may need to insert one or two fingers into the rectum and break the mass into smaller pieces that can pass more easily.

Take measures to prevent further fecal impaction. Add fiber to your diet to help form normal stool. Use other medications your health care provider recommends. In addition, drink enough fluids and get enough exercise to enhance normal stool consistency.

DIET:
Bowel incontinence often occurs because the rectal sphincter is less able to handle large amounts of liquid stool. Often, simply changing the diet may reduce the occurrence of bowel incontinence.

Certain people develop diarrhea after eating dairy foods because they are unable to digest lactose, a sugar found in most dairy products. Some food additives such as nutmeg and sorbitol may cause diarrhea in certain people.

Adding bulk to the diet may thicken loose stool and decrease its amount. Increasing fiber (30 grams daily) from whole-wheat grains and bran adds bulk to the diet. Psyllium-containing products such as Metamucil can also add bulk to the stools.

Formula tube feedings often cause diarrhea and bowel incontinence. For diarrhea or bowel incontinence caused by tube feedings, talk to your health care provider or dietitian. The rate of the feedings may need to be changed, or bulk agents may need to be added to the formula.

Eating, Diet, and Nutrition:
Changes in your diet that may improve your bowel control problem include

*Eating the right amount of fiber. Fiber can help with diarrhea and constipation. Fiber is found in fruits, vegetables, whole grains, and beans. Fiber supplements sold in a pharmacy or health food store are another common source of fiber to treat bowel control problems. The Academy of Nutrition and Dietetics recommends getting 20 to 35 grams of fiber a day for adults and “age plus five” grams for children. A 7-year-old child, for example, should get “7 plus five,” or 12, grams of fiber a day. Fiber should be added to your diet slowly to avoid bloating.

*Getting plenty to drink. Drinking eight 8-ounce glasses of liquid a day may help prevent constipation. Water is a good choice. You should avoid drinks with caffeine, alcohol, milk, or carbonation if they give you diarrhea.

MEDICATIONS:
In people with bowel incontinence due to diarrhea, medications such as loperamide (Imodium) may be used to control the diarrhea and improve bowel incontinence.

Other antidiarrheal medications include anti-cholinergic medications (belladonna or atropine), which reduce intestinal secretions and movement of the bowel. Opium derivatives (paregoric or codeine) or diphenoxylate (lomotil), as well as loperamide (Imodium) increase intestinal tone and decrease movement of the bowel.

Other medications used to control bowel incontinence include drugs that reduce water content in the stools (activated charcoal or Kaopectate) or that absorb fluid and add bulk to the stools (Metamucil).

MEDICATION EVALUATION: With your health care provider, review all the medications you take. Certain medications can cause or increase bowel incontinence, especially in older people. These medications include:

*Antacids
*Laxatives

OTHER THERAPIES:
If you often have bowel incontinence, you can use special fecal collection devices to contain the stool and protect your skin from breakdown. These devices consist of a drainable pouch attached to an adhesive wafer. The wafer has a hole cut through the center, which fits over the opening to the anus.

Most people who have bowel incontinence due to a lack of sphincter control, or decreased awareness of the urge to defecate, may benefit from a bowel retraining program and exercise therapies to help restore normal muscle tone.

Special care must be taken to maintain bowel control in people who have a decreased ability to recognize the urge to defecate, or who have impaired mobility that prevents them from independently and safely using the toilet. Such people should be assisted to use the toilet after meals, and promptly helped to the toilet if they have the urge to defecate.

If toileting needs are often unanswered, a pattern of negative reinforcement may develop. In this case people no longer take the correct actions when they feel the urge to have a bowel movement

You may click & See : Toileting safety

SURGERY
People who have bowel incontinence that continues even with medical treatment may benefit from surgery to correct the problem. Several different options exist. The choice of surgery is based on the cause of the bowel incontinence and the person’s general health.

RECTAL SPHINCTER REPAIR
Sphincter repair is performed on people whose anal muscle ring (sphincter) isn’t working well due to injury or aging. The procedure consists of re-attaching the anal muscles to tighten the sphincter and helping the anus close more completely.

GRACILIS MUSCLE TRANSPLANT
In people who have a loss of nerve function in the anal sphincter, gracilis muscle transplants may be performed to restore bowel control. The gracilis muscle is taken from the inner thigh. It is put around the sphincter to provide sphincter muscle tone.

ARTIFICIAL BOWEL SPHINCTER
Some patients may be treated with an artificial bowel sphincter. The artificial sphincter consists of three parts: a cuff that fits around the anus, a pressure-regulating balloon, and a pump that inflates the cuff.

The artificial sphincter is surgically implanted around the rectal sphincter. The cuff remains inflated to maintain continence. You have a bowel movement by deflating the cuff. The cuff will automatically re-inflate in 10 minutes.

FECAL DIVERSION
Sometimes a fecal diversion is performed for people who are not helped by other therapies. The large intestine is attached to an opening in the abdominal wall called a colostomy. Stool passes through this opening to a special bag. You will need to use a colostomy bag to collect the stool most of the time.

Regular Yoga exercise & Meditation under the supervision of an expart  will defenitely help a lot to get rid of the problem.

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.niddk.nih.gov/health-information/health-topics/digestive-diseases/bowel-control/Pages/ez.aspx

http://www.nlm.nih.gov/medlineplus/ency/article/003135.htm

leukonychia

Description::
Leukonychia (or leuconychia), also known as white nails or milk spots, is a medical term for white discoloration appearing on nails. It is derived from the Greek words leuko (“white”) and onux (“nail”). The most common cause is injury to the base of the nail (the matrix) where the nail is formed…..CLICK & SEE

It is harmless and most commonly caused by minor injuries that occur while the nail is growing. Contrary to popular belief, leukonychia is not a sign of excess or deficiency of calcium and zinc or other vitamins in the diet but rather less commonly a medical sign of hypoalbuminemia or chronic liver disease. It is more commonly found on fingernails than toenails. There is no effective treatment for leukonychia. However, the white marks and spots gradually disappear as the nail grows outward from the matrix with the nail plate.

Leukonychia is a nail condition. It manifests as the nail changing color either partially or fully. This disease can be caused by systemic problems or most commonly, it is a genetic disorder. The nail appears to have the standard shape and appearance, except for the fact that the nail turns white. This is caused by the presence of “parakeatotic cells”. These cells have an undeveloped and bulky nucleus, which contain ‘keratohyalins’. This cell variation causes the nail to reflect light and makes the nail appear opaque white.

Types:
Leukonychia totalis :
This condition is a whitening of the entire nail. This may be a clinical sign of hypoalbuminaemia (low albumin), which can be seen in nephrotic syndrome (a form of kidney failure), liver failure, protein malabsorption and protein-losing enteropathies. A genetic condition, and a side effect of sulphonamides, a family of antibiotics can also cause this appearances.

Leukonychia partialis:
This condition is whitening of parts of the nail plate in form of small white dots. There are several types of this condition. There are three variations of partial leukonychia; punctate, transverse and longitudinal leukonychia. Some more serious variations of leukonychia partialis may lead to Leukonychia totalis.

Leukonychia striata:
Leukonychia striata, transverse leukonychia, or Mees’ lines are a whitening or discoloration of the nail in bands or “stria” that run parallel the lunula (nail base). This is commonly caused by physical injury or disruption of the nail matrix. Common examples include excessive tapping of the nails, slamming a car door or extensive use of manicure. It may also occur in great toenails as a result of trauma from footwear. Alternatively, the condition can be caused by heavy metal poisoning most commonly by lead or arsenic. It can also be caused by cirrhosis or chemotherapy. The tendency toward leukonychia striata is sometimes inherited in an autosomal dominant fashion. In other cases, it can be attributed to vigorous manicuring and trauma aforementioned, or to a wide variety of systemic illnesses. Serious infections known for high fevers, measles, malaria, herpes, and leprosy may also cause this condition. In many patients, there is no obvious cause, and the streaks resolve spontaneously. There is a similar condition called Muehrcke’s lines (apparent leukonychia) which differs from leukonychia in that the lines fade with digital compression and does not migrate with the growth of the nail.

Leukonychia punctata:
Also known as “true” leukonychia, this is the most common form of leukonychia, in which small white spots appear on the nails. Picking and biting of the nails are a prominent cause in young children and nail biters. Besides parakeratosis, air that is trapped between the cells may also cause this appearance. It is also caused by trauma. In most cases, when white spots appear on a single or a couple of fingers or toes, the most common cause is injury to the base (matrix) of the nail. When this is the case, white spots disappear after around eight weeks, which is the amount of time necessary for nails to regrow completely. The pattern and number of spots may change as the nail grows.

Longitudinal leukonychia:
Longitudinal leukonychia is far less common and features smaller 1mm white longitudinal lines visible under the nail plate. It may be associated with Darier’s disease.

Symptoms :
Some of the obvious signs of leukonychia are white spots on the fingernail. It is observed in the form of small white lines on the nails and change in color of the nails which become totally white. The white spots may also occur on toenails. The nails become colorless and brittle losing the original texture. The nail may change its color to fully white (leukonychia totalis) or half white (leukonychia partialis).
Apart from the above signs, the person affected with leukonychia may also have problems like deafness, gingivitis, and hyperkeratosis and hammer toes if they are suffering from systemic disorders.

Causes:
It can be due to nail injury or infection. Sometimes it can be due to nail disorder or bacterial infection on the nail-bed. The white spots and change of nail to full-white color is due to the presence of para-karyotic cells that contains a compound called keratohyalins. On reflection to the light the normal color of the nail looks fully white.

Leukonychia can also occur due to heavy poisoning, heart problem, kidney disease, malnutrition, vitamin deficiency and stress.
Lack of essential nutrients like zinc and protein can also cause discoloration of nails. Ulcer in advance form can affect the fingernails. Further it can be caused due to pneumonia and hepatic cirrhosis and various other skin problems.People with diseases like typhoid, cholera, rheumatic fever, and colitis may also show this symptom of white spots on fingernails.

Individuals with family history of leukonychia have more chance of developing this problem than others. Patients who are undergoing chemotherapy or radiation treatment for cancer may also get this disease. Prolonged use of nail enamels and nail hardeners can be the reason for white spots on the fingernail. Bacterial or fungal infection on the nails can cause this problem.

True Leukonychia:
This type of Leukonychia is broken into two variations, total leukonychia and partial leukonychia. The difference seems to lie in the nail being either fully white, or only two thirds discolored as it takes a while for the maturation of the keratin to occur and change.

Total Leukonychia is an autosomal dominant condition. Other circumstances that may cause total leukonychia to occur are;
*Leprosy
*Typhoid
*Cytotoxic drugs
*Nail Biting
*Partial Leukonychia is viewed as a phase of total leukonychia. The most common causes of partial leukonychia are:

*Metastatic carcinoma
*Tuberculosis
*Leprosy

There are three different variants of partial leukonychia.

1.Transverse leukonychia – This causes the nail plate to be multi colored in its opacity. It is seen mostly in women’s fingernails. Possible causes are:
*Acute respiratory infections
*High fever
*Malaria
*Leprosy

2.Punctuate leukonychia This is the most common form and can happen to anyone. The telltale symptom is that the nail appears to have tiny opaque spots which fade with time.

3.Longitudinal leukonychia – A small white line under the nail plate
Pseudo Leukonychia

*This occurs when a discoloration in the nail appears due to a change in the nail bed. Pseudo leukonychia has three different forms:

*Terry’s nails – This affects the majority of the nail and makes it multi-colored. The majority of the nail is white, the rest, pink or brown.
Muhrecke’s nails – The nail appears to have several white transverse bands

*Half and half nails – This is seen as a larger part of the nail being dull white and the rest being brownish in color.

Diagnoses :
It is easy to identify this disease by physically examining the nails of the person affected. If needed, your doctor will ask you to do blood culture and other test for measuring the nutrients like zinc and vitamins. The doctor will take a thorough medical history, and may take blood tests as well as examining liver and kidney function.

Treatment :
You can get some relief from the symptoms by including lot of nutrition in your daily diet. Proteins, vitamins and zinc are essential elements that are to be added in daily food. You can eat nuts and green leafy veggies that carry lot of zinc.

The white spots on the fingernail will gradually diminish if you start taking zinc in daily food.In case if the problem is due to anemia then you will be given folic acid and iron supplement pills. If the symptoms are due to renal failure, then your doctor will initiate treatment for the condition. Suitable medicines will be given for treating the underlying disease like liver problem or ulcer or anemia.

Do not change your nail polish frequently and always use trusted brands. Limit the usage of nail enamels and polish to certain occasions. Avoid biting your nails since it may worsen the condition.

In case if the white spots or white coloration on the fingernails does not improve for more than 2 months, you can consult your doctor who would help you to find the actual cause.

Almost in many cases, the symptoms of leukonychia are due to deficiency of nutrients and zinc and only in rare cases, it will be due to underlying systemic disorders.

Increasing the quantity of grains, vegetables and nuts and even taking a zinc supplement (as zinc deficiency is a cause of leukonychia) is a good preventative and treatment, as is keeping affected nails out of harms way when using chemicals of any kind as they can further damage the nail.

Resources:

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

http://www.nailsfungus.org/nail-fungus/leukonychia.html

http://diseasespictures.com/leukonychia/