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Ailmemts & Remedies

Nightmare

Alternative Names: Dreams – bad; Bad dreams

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Definition:
A nightmare is a dream occurring during rapid eye movement (REM) sleep that arouses feelings of intense, inescapable fear, terror, distress, or extreme anxiety that usually awakens the sleeper.It is a bad dream which causes a strong unpleasant emotional response from the sleeper,it is typically fear or horror (scary stuff), being in situations of extreme danger, or the sensations of pain, falling, drowning or death or sometimes getting caused by giant animals. Such dreams can be related to physical causes such as a high fever, turned faced down on a pillow during sleep (most often in the case of drowning nightmares), or psychological ones such as psychological trauma or stress in the sleeper’s life, or can have no apparent cause. If a person has experienced a psychologically traumatic situation in life—for example, a person who may have been captured and tortured—the experience may come back to haunt them in their nightmares. Sleepers may waken in a state of distress and be unable to get back to sleep for some time. increased stress in daiy routines may also trigger nightmares and Eating before bed, which triggers an increase in the body’s metabolism and brain activity, is another potential stimulus for nightmares.

Occasional nightmares are commonplace, but recurrent nightmares can interfere with sleep and may cause people to seek medical help. A recently proposed treatment consists of imagery rehearsal. This approach appears to reduce the effects of nightmares and other symptoms in acute stress disorder and post-traumatic stress disorder.

Practitioners of lucid dreaming claim that it can help conquer nightmares of this type, rather than of the traditional type.

Nightmares, unlike night terrors, can be recalled afterward and are accompanied by much less anxiety and movement. These frightening dream experiences, which tend to occur at times of insecurity, emotional turmoil, depression, or guilt, can occur in all age groups.

Nightmares occur exclusively during REM sleep. REM sleep phases grow longer in the latter part of the sleep cycle, and the majority of nightmares occur from the middle of the night onward.

Night terrors, by contrast, take place in non-REM (nondream) sleep. During night terrors people wake up sweating heavily, their hearts pounding, and screaming in fear. They are unaware of their surroundings and unresponsive to attempts to comfort them. They may not calm down for 10 or 15 minutes, although they return to sleep quickly once the episode ends. Generally they do not remember what scared them, but rarely a person will retain a vague image of something terrifying. A few children and adults who experience night terrors will sleepwalk during the episode.

Considerations:-
Nightmares tend to be more common among children and become less frequent toward adulthood. About 50% of adults have occasional nightmares, women more often than men.

Eating just before going to bed, which raises the body’s metabolism and brain activity, may cause nightmares to occur more often. Adults who have repeated nightmares that become a significant problem should seek help.

Historic use of term
Nightmare was the original term for the state later known as (cf. Mary Shelley and Frankenstein‘s Genesis), and more currently as sleep paralysis, associated with rapid eye movement (REM) sleep. The original definition was codified by Dr Johnson in his A Dictionary of the English Language and was thus understood, among others by Erasmus Darwin and Henry Fuseli, to include a “morbid oppression during sleep, resembling the pressure of weight upon the breast.”

Such nightmares were widely considered to be the work of demons and more specifically incubi, which were thought to sit on the chests of sleepers. In Old English the name for these beings was mare or mære (from a proto-Germanic *mar?n, related to Old High German, -in modern german it would become “Nachtmar”-, and Old Norse mara), hence comes the mare part in nightmare. Etymologically cognate with Anglo-Saxon /mara/ (‘incubus’) may be Hellenic /Mar?n/ (in the Odusseid) and Samsk?ta /M?ra/ (supernatural antagonist of the Buddha).

Folk belief in Newfoundland, South Carolina and Georgia describe the negative figure of the Hag who leaves her physical body at night, and sits on the chest of her victim. The victim usually wakes with a feeling of terror, has difficulty breathing because of a perceived heavy invisible weight on his or her chest, and is unable to move i.e., experiences sleep paralysis. This nightmare experience is described as being “hag-ridden” in the Gullah lore. The “Old Hag” was a nightmare spirit in British and also Anglophone North American folklore.

Various forms of magic and spiritual possession were also advanced as causes. In nineteenth century Europe, the vagaries of diet were thought to be responsible. For example, in Charles Dickens‘s A Christmas Carol, Ebenezer Scrooge attributes the ghost he sees to “… an undigested bit of beef, a blot of mustard, a crumb of cheese, a fragment of an underdone potato…” In a similar vein, the Household Cyclopedia (1881) offers the following advice about nightmares:

“Great attention is to be paid to regularity and choice of diet. Intemperance of every kind is hurtful, but nothing is more productive of this disease than drinking bad wine. Of eatables those which are most prejudicial are all fat and greasy meats and pastry… Moderate exercise contributes in a superior degree to promote the digestion of food and prevent flatulence; those, however, who are necessarily confined to a sedentary occupation, should particularly avoid applying themselves to study or bodily labor immediately after eating… Going to bed before the usual hour is a frequent cause of night-mare, as it either occasions the patient to sleep too long or to lie long awake in the night. Passing a whole night or part of a night without rest likewise gives birth to the disease, as it occasions the patient, on the succeeding night, to sleep too soundly. Indulging in sleep too late in the morning, is an almost certain method to bring on the paroxysm, and the more frequently it returns, the greater strength it acquires; the propensity to sleep at this time is almost irresistible.

Causes  and Risk Factors :-
Anxiety and stress are the most common causes of nightmares. A major life event occurs before the nightmare in most cases.

Other causes of nightmares include:
*Illness with a fever
*Death of a loved one (bereavement)
*Reaction to or side effect of a drug
*Recent withdrawal from a drug, such as sleeping pills
*Excessive alcohol consumption
*Abrupt alcohol withdrawal
*Breathing disorder in sleep (sleep apnea)
*Sleep disorder (narcolepsy, sleep terror disorder)

Particularly among adults, prescription drugs such as levedopa, reserpine, beta blockers, and antidepressants, as well as withdrawal from addictive drugs, all can provoke nightmares. Heavy drinking also is strongly associated with nightmares.

Other drugs suspected of causing nightmares include heart drugs, antibiotics such as ciprofloxacin, antihistamines, appetite suppressers such as fenfluramine, antidepressants, Parkinson’s drugs such as levodopa, and ulcer drugs (cimetidine). However, many drugs cannot be stopped abruptly without side effects, so it is necessary to consult your physician before altering the use of medications.

In both adults and children, nightmares and night terrors can be caused by unresolved psychological conflicts or traumatic events. They are a frequent feature of post-traumatic stress disorder. Emotional traumas that disturb the sleep of children can be overlooked easily by adults – such as the loss of a favorite toy or overhearing a loud argument between parents.

Although nightmares and night terrors are considered normal developmental events in children, disappearing by adolescence, frequent episodes at any age warrant professional evaluation. Crisis intervention techniques can be very effective in dealing with the trauma.

Diagnosis:
Diagnosis will be based upon history and the absence of any underlying organic problems.

Tests that may be done include:
*Blood tests (such as CBC or blood differential)
*Liver function tests
*Thyroid function tests
*EEG

If therapies for stress and anxiety, medication side effects, and substance use do not treat the problem, your health care provider may want to send you to a sleep medicine specialist for a sleep study (polysomnography). In very rare cases, patients need to take special medications that suppress or reduce REM sleep to prevent nightmares.

Treatment :-
Some people have significant psychological problems that are causing bad dreams. It is important to consider psychotherapy to pinpoint major life stressors, past traumatic events and depression that might be causing bad dreams.

If one is taking medications, it is advisable to ask the prescribing physician if the pills might be the culprit.

Chronic nightmares have also been treated by a desensitization method that uses instruction about rehearsal of the nightmare and the imagining of a different ending.

In one study, patients were instructed to select a recent nightmare and write it down, change the nightmare in any way they wished, write down the changed version and rehearse the changed nightmare in an imagery relaxed state. Patients were instructed to rehearse the changed version once a day for three consecutive days after each nightmare or until the nightmare went away.

It was concluded that the use of desensitization or rehearsal techniques can reduce the frequency of nightmares and decrease distress.

Home Care
If you are under severe stress, you should ask for support from friends and relatives. Talking about what is on your mind can really help. Also, follow a regular fitness routine, with aerobic exercise if possible. You will find that you will be able to fall asleep faster, sleep more deeply, and wake up feeling more refreshed. Learn techniques to reduce muscle tension (relaxation therapy), which also will help reduce your anxiety.

Practice good sleep hygiene. Go to bed at the same time each night, and wake up at the same time each morning. Avoid long-term use of tranquilizers, as well as caffeine and other stimulants.

If you noticed that your nightmares started shortly after you began taking a new medication, contact your health care provider. He or she will let you know how to stop taking that medication if necessary, and recommend an alternative.

For nightmares caused by the effects of “street drugs” or regular alcohol use, ask for advice on the best ways to quit. An Alcoholics Anonymous group, for example, might suggest a safe way for you to stop drinking without putting your health at risk. You can also attend their regularly scheduled meetings. See also: Alcoholism – support group.

Also, look at your lifestyle — friends, work, family — to find and change factors that encourage substance abuse.

Questions To Ask Your Doctor About Nightmares:-
*Are these nightmares or night terror?
*Is there a psychological cause such as depression, emotional trauma, or stress?
*Is it related to any medications that are currently being taken?
*Should any changes be made in the medications currently being taken?
*Would psychotherapy help?
*What can be expected from psychotherapy?

Medical investigation:
Studies of dreams have found that about three quarters of dream content or emotions are negative.

One definition of “nightmare” is a dream which causes one to wake up in the middle of the sleep cycle and experience a negative emotion, such as fear. This type of event occurs on average once per month. They are not common in children under 5, more common in young children (25% experiencing a nightmare at least once per week), most common in adolescents, and less common in adults (dropping in frequency about one-third from age 25 to 55).

Fearfulness in waking life is correlated with the incidence of nightmares.

Scientists speculate that negative dreams are evolutionarily adapting, purging the brain of memories or associations which trigger fear.

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/Nightmare
http://www.healthscout.com/ency/68/612/main.html#cont
http://www.nlm.nih.gov/medlineplus/ency/article/003209.htm

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Categories
Ailmemts & Remedies

Breathing Disorders During Sleep

You Can Snore Your Life Away.
This sounds more like a joke than a warning. But, in fact, habitual loud snoring is the most common symptom of breathing disorders that occur during sleep. The person who snores not only sleeps restlessly, but also is at risk for serious disorders of the heart and lungs. Snoring can therefore be lifethreatening because it can lead to high blood pressure, irregular heart beats, heart attacks, and sudden death.

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Normal breathing must continue at all times whether awake or asleep. The act of breathing is an automatic, highly regulated mechanical function of the body. In healthy sleeping individuals, most muscular and neural activities will slow or even shut down but respiration goes on under a neuromuscular “auto pilot.” However, if something goes wrong with the auto pilot during sleep, breathing may become erratic and inefficient.

Understanding Sleep
Sleep is a complex neurological state. Its primary function is rest and restoring the body’s energy levels. Repeated interruption of sleep by breathing abnormalities such as cessation of breathing (apnea) or heavy snoring, leads to fragmented sleep and abnormal oxygen and carbon dioxide levels in the blood. Excessive daytime sleepiness and various disorders of the heart, lungs, and the nervous system result.

In the 1950’s scientists realized that sleep is not just a quiet state of rest. In fact, two stages of sleep occur with distinct physiological patterns-rapid-eye-movement sleep (REM), and non rapid-eye-movement sleep (NREM) or deep sleep. In normal sleep, REM occurs about 90 minutes after a person falls asleep. The two sleep stages recur in cycles of about 90 minutes each, with three non-REM stages (light to deep slumber) at the beginning and REM towards the end. The amount of sleep needed by each person is usually constant although there is a wide variation among individuals.

How sleep occurs and how it restores the body are not well understood. Scientists originally believed that sleep occurs because the brain lapses into a passive resting state from lack of stimulation. Another theory proposed that sleep occurs when the body generates and accumulates sufficient amounts of a “sleep-inducing substance.” However, research now suggests that sleep results when specific changes in brain function occur. By studying brain waves, scientists can define and measure various degrees, levels, and stages of sleep.

Sleep consists of a rhythmic combination of changes in physiological, biochemical, neurophysiological and psychological processes. When the rhythm is disturbed or the individual processes are abnormal during sleep, a variety of sleep-related disorders may result.

Sleep-Related Disorders
Sleep-related complaints appeared regularly in medical literature in the beginning of the 19th century. However, from 1900 to the mid-1960s little was published in scientific journals about the “sleepy patient” except for an occasional report on the normal or abnormal aspects of sleep physiology. Recent developments of research techniques in neurobiology, molecular biology, molecular genetics, physiology, neuropsychiatry, internal medicine, pulmonary medicine, and cardiology have allowed scientists to study the details of sleep. As a result, there has been an explosion in interest in understanding sleep and “sleep disorders.”

Some sleep-related disturbances are simply temporary inconveniences while others are potentially more serious. Sleep apnea is the major respiratory disorder of sleep. Other serious sleep-related disorders are narcolepsy and clinical insomnia. “Jet lag syndrome,” caused by rapid shifts in the biological sleep-wake cycle, is also an example of a temporary sleep-related disorder. So are the sleep problems experienced by shift workers. Sleep apnea is the condition of interrupted breathing while asleep. “Apnea” is a Greek word meaning “want of breath.” Clinically, sleep apnea, first described in 1965, means cessation of breathing during sleep.

Narcolepsy is a neurological disorder whose main symptoms in uncontrollable, excessive sleep, regardless of the time of day or whether the person has had enough sleep during the previous night. The other features of this disorder can include brief episodes of muscle weakness or paralysis caused by laughter and anger (cataplexy), paralysis for brief periods upon awakening from sleep (sleep paralysis), and dreamlike images at sleep onset (hypnagogic hallucination). Narcolepsy, which may affect several members of the same family, is a life-long condition. Medications help to reduce the symptoms but do not cure the disease.

Insomnia is the commonly experienced difficulty in falling asleep, remaining asleep throughout the night, and the inability to return to sleep once awakened. Its causes may be physical or psychological and it may occur regularly or only occasionally.

Even a partial list of all the disorders caused by or associated with disturbed sleep adds up to some 70 items. The costs to society due to loss of productivity, industrial accidents and medical bills are estimated to be over $60 billion. These staggering statistics led to the creation by the U.S. Congress in 1988 of a National Commission of Sleep Disorders Research. This group is charged with task of developing a blueprint for a national effort to reduce the medical and economic consequences of sleep disorders.

Likely Candidates for Sleep-Related Disorders

Some of the people most likely to have or to develop a sleep-related disorder include:

* adults who fall asleep at inappropriate times and places (e.g., during conversation, lecturing, driving) and who exhibit nighttime snoring
* elderly men and women
* postmenopausal women
* people who are overweight, or have some physical abnormality in the nose, throat, or other parts of the upper airway
* night-shift workers
* people who habitually drink too much alcohol
* blind individuals who tend to develop impaired perception of light and darkness and have disturbed circadian rhythms, the cycles of biologic activities that occur at the same time during each 24 hours
* people with depression and other psychotic disorders.

Click to see:->Sleep related breathing disorders in adults with Down syndrome
Sleep and Breathing Disorders
In 1944, the important observation was made that ventilation (exchange of air between the lung and environment) normally decreases during sleep. Even in “normal” people, breathing patterns during sleep may show a few irregularities. For example, a person might experience an average of seven breathing pauses of up to 10 seconds per night without any associated symptoms or problems. However if the breathing irregularities are accompanied by reduced oxygen supply to tissue (hypoxia) and repeated loss of sleep, these people are at risk of developing more serious problems.

Sleep Apnea...
Sleep apnea is the most common sleep disorder in terms of mortality and morbidity, especially in middle-age men. Perhaps the best known sleep apnea “patient” is Charles Dickens’ Fat Joe in The Posthumous Papers of the Pickwick Club, the overweight, red-faced boy in a permanent state of sleepiness, who snored and breathed heavily. The term “Pickwickian” syndrome is now used to describe patients with the most severe form of sleep apnea that is associated with reduced levels of breathing even during the day. Click to see:->Sleep apnea patients have altered cardiovascular responses during exercise recovery

Sleep apnea occurs in all age groups and both sexes, but seems to predominate in males (it may be underdiagnosed in females) and in African Americans. The Association of Professional Sleep Societies estimates that as many as 20 million Americans have this condition. The conditions associated with sleep apnea are a cascade: apnea, arousal, sleep deprivation, and excessive daytime sleepiness. Each is related to the frequency of the prior condition.

Like obesity with which it is often associated, the clustering of sleep apnea in some families suggests a genetic abnormality. Ingestion of alcohol and sleeping pills increases the frequency and duration of breathing pauses during sleep in people with or without sleep apnea.

Because of serious disturbances in their normal sleep patterns, patients with sleep apnea feel sleepy during the day and their concentration and daytime performance suffer. The common consequences of sleep apnea range from annoying to life-threatening. They include personality changes, sexual dysfunction and falling asleep at work, on the phone, or driving.

Symptoms of Sleep Apnea
Patients with sleep apnea have many repeated involuntary breathing pauses during sleep. The length of the breathing pause can vary within a patient, and among patients, and can last for 10 seconds to 60 seconds. Fewer than 30 such breathing pauses during a 7-hour sleep, or shorter breathing pauses, are not considered indicative of sleep apnea. Most sleep apnea patients experience 20 to 30 “apneic events” per hour, more than 200 per night. These pauses may occur in clusters.

The breathing pauses are often accompanied by choking sensations which may wake up the patient, intermittent snoring, nighttime insomnia, early morning headaches, and excessive daytime sleepiness, although not all patients, for some reason, complain of daytime sleepiness. During the apneic events, a person may turn blue from low blood oxygen levels.

Other features of sleep apnea include slowing down of heart beat below 60 beats per minute (bradycardia), irregular heart beat (cardiac arrhythmias), high blood pressure (both systemic and pulmonary arterial), increase in red cells in the blood (polycythemia), and obesity. The absence of restful sleep may cause deterioration of performance, depression, irritability, sexual dysfunction, and defects in attention and concentration.

Types of Sleep Apnea
Scientists have distinguished three types of sleep apnea: obstructive, central, and mixed. However, since all three types can have the same symptoms and signs, a sleep evaluation is needed to tell the difference among them.

Obstructive Sleep Apnea (OSA) is the most common type. During OSA efforts to breath continue but air cannot flow out of the patient’s nose or mouth. The patient snores heavily and has frequent arousals (abrupt changes from deep sleep to light sleep) without being aware of them.

OSA occurs when the throat muscles and tongue relax during breathing and partially block the opening of the airway. When the muscles of the soft palate at the base of the tongue and the uvula (the small conical fleshy tissue hanging from the center of the soft palate) relax and say, the airway becomes obstructed marking breathing labored and noisy. Airway narrowing may also occur due to overweigh, possibly because of the associated increases in the amount of tissue in the airway.

The reduction in oxygen and increase in carbon dioxide which occur during apnea cause arousals. With each arousal, a signal is sent to the upper airway muscles to open the airway; breathing is resumed with a loud snort or gasp. Although arousals serve as a rescue mechanism and are necessary for a patient with apnea, they interrupt sleep, and the patient ends up with less restorative and sleep than normal individuals.

Central Apnea occurs less frequently than obstructive apnea. There is no airflow in or out of the airways because efforts to breathe have stopped for short periods of time. In central apnea, the brain temporarily fails to send the signals to the diaphragm and the chest muscles that maintain the breathing cycle. It is present more often in the elderly than in younger people but often goes unrecognized.

In central apnea, there is periodic loss of rhythmic breathing movements. The airways remain open but air dose not pass through the nose or mouth because activity of the diaphragm and the chest muscles stops. Patients with central apnea may not snore and they tend to be more aware of their frequent awakenings than those with obstructive apnea.

In Mixed Apnea, a period of central apnea is followed by a period of obstructive apnea before regular breathing resumes. People with mixed apnea frequently snore.

Snoring and Sleep Apnea
Snoring is a sign of abnormal breathing. It occurs when physical obstruction causes fluttering of the soft palate and the adjacent soft tissues between the mouth, external orifices of the nose (nares), the upper part of the windpipe (trachea), and the passage extending from the pharynx to the stomach (esophagus).

Snoring always occurs with obstructive sleep apnea. When diagnosing sleep disorders, obstructive sleep apnea is excluded if snoring is not a symptom. All snorers do not necessarily have sleep apnea; however, because they almost certainly have some physical obstruction in their airways, they may develop sleep apnea.

The prevalence of snoring is greater in the older population and apparently peaks in 60-year-old men and women, declining in older individuals. Men seem to snore more than women. Men also are more likely to develop sleep-disordered breathing. It is estimated that nearly half of all males over 40 snore habitually. Snoring is also more common in overweight people.

A visit to the doctor is not necessary when a person snores unless some of the other symptoms of sleep disordered breathing also occur. However, since snoring is an annoying or irritating symptom with some negative social aspects, many people have sought a “cure” for it. More than 300 devices have been patented in the U.S. which claim to control snoring. Many of these devices were developed even before medical scientists found out that heavy snoring is a potential marker of sleep apnea.

Sleep Apnea and the Heart
Sleep apnea and snoring seems to increase the likelihood of having a variety of cardiovascular diseases. These include high blood pressure, ischemic heart disease (a condition caused by reduced blood supply to the heart muscle), cardiac arrhythmias (abnormal heartbeat rhythm), and cerebral infarction (blood clot in the brain). It is not unusual for patients with sleep apnea to be mistakenly treated for primary heart disease because cardiac arrhythmias may be more prominent than the breathing disturbances.

Nearly 50 percent of sleep apnea patients have high blood pressure. Patients with the most severe sleep apnea seem to have the highest blood pressure levels and are also more likely to have trouble controlling their blood pressure than patients who do not have sleep apnea. No one knows whether a cause and effect relationship exists between high blood pressure and sleep apnea. If it does exist, the ways these conditions interact is unknown.

Snoring alone does not appear to be a risk factor for heart disease. Only when snoring occurs with sleep apnea or obesity does it seem to be associated with these conditions.

Sleep Apnea in Infants
Before a baby is born, the mother’s breathing takes care of its respiratory needs. Although the unborn baby’s lings are filled with fluid and are not ready to take in air, its respiratory muscles make breathing motions, as if “training” to take on the responsibilities of breathing after birth.

As soon as birth occurs, the normal newborn baby begins a continuous pattern of periodic breathing characterized by a succession of apneas followed by regular breathing. Apneas occasionally lasting longer than 10 to 15 seconds are common during the newborn period. Apneas are more frequent and longer in premature newborns than in full-term infants. The frequency of apnea decreases with age during the first 6 months of life.

Babies turn blue during sleep and appear limp may be undergoing episodes of insufficient breathing. They should be checked for a sleep-related disorder.

Sleep Apnea and Sudden Infant Death Syndrome
Sleep apnea is sometimes implicated in sudden infant death syndrome (SIDS), also called crib death. About 10,000 infants die every year in this country for SIDS. Scientists do not know the reasons for these deaths but sleep apnea may play a role because these babies die when they are asleep and show no evidence of trauma. On autopsy, pinpoint hemorrhages are sometimes noted in the thoracic cavity which may be caused by lack of oxygen prior to cardiac arrest and vigorous respiratory movements.

Diagnosis of Sleep Apnea
The general physician may sometimes recognize sleep apnea, but specialists in neurology, psychiatry, pulmonary medicine and cardiology may be needed for accurate diagnosis and management. Diagnosis of sleep apnea is difficult because disturbed sleep can cause various other diseases or make them worse. Several major medical centers now have pulmonologists, neurologists, and psychiatrists with specialty training in sleep disorders on their staff. Although an evaluation for sleep apnea can sometimes be done at home, it is more reliable if it is done in a sleep laboratory.

A variety of tests can be used to diagnose sleep apnea. These include pulmonary function tests, polysomnography, and the multiple sleep latency test. Physicians continue to try to develop other simple and economic procedures for the early diagnosis of sleep apnea.

Pulmonary function tests taken by sleep apnea patients may show normal results unless the patient has a coexisting lung disease. To make a definitive diagnosis of sleep apnea, the physician may order an all-night evaluation of the patient’s sleep stages, and of the status of breathing and gas exchange during sleep.

Polysomnography is a group of tests that monitors a variety of functions during sleep. These include sleep state, electrical activity of the brain (EEG), eye movement (EOG), muscle activity (EMG), heart rate, respiratory effort, airflow, blood oxygen and carbon dioxide levels. Other tests may be ordered depending on a particular patient’s needs. Polysomnography sometimes helps to distinguish between different sleep disorders. These test are used both to diagnose sleep apnea and to determine it severity.

The Multiple Sleep Latency Test is done during normal working hours. It consists of observations, repeated every 2 hours, of the time taken to reach various stages of sleep. In this test, people without sleep apnea take more than 10 minutes to fall asleep. On the other hand, patients with sleep apnea or narcolepsy fall asleep fairly rapidly. When it takes the patient an average of less than 5 minutes to fall asleep, it is considered pathological sleepiness. There is thus some uncertainty in the diagnosis if the sleep latency period (speed of falling asleep) is between 5 and 10 minutes. This test is important because it measures the degree of excessive daytime sleepiness and also helps to rule out narcolepsy, which is associated with onset of REM sleep (dream sleep) in many of the naps.

Treatment of Sleep Apnea…...
More than 50,000 patients are treated each year for breathing disorders of sleep. Physicians tailor therapy to the individual patient based on medical history, physical examination, and the results of laboratory tests and polysomnography.

Patients with sleep apnea can help themselves by trying avoid doing anything that can worsen the disease. Sleeping in improper positions can increase the frequency of apnea. Use of alcohol suppresses the activity of the upper airway muscles so that the airway is more likely to collapse. Sleeping pills and sedativehypnotic drugs suppress arousal mechanisms and prolong apneas. Moving to high altitudes may aggravate the condition because of low oxygen levels. Overweight sleep apnea patients should lose weight.

Because the exact mechanism responsible for obstructive sleep apnea is not known, there is still no treatment that directly addresses the underlying problem. In most cases, medications have not proved successful. Surgical procedures are effective only 50 percent of the time because the exact location of the airway obstruction is usually unclear.

Since patients with sleep apnea usually have significant family and work problems, the treatment should include strategies that will help them cope with these problems. Education of the patient, family, and employers is sometimes needed to help the patient return to an active normal life.

Position Therapy
In mild cases of sleep apnea, breathing pauses occur only when the individual sleeps on the back. Thus using methods that will ensure that patients sleep on their side is often helpful.

Nasal Continuous Positive Airway Pressure (CPAP)
CPAP is the most common effective treatment for sleep apnea. In this procedure, the patient wears a mask or a pillow over the nose during sleep and pressure from an air compressor forces air through the nasal passages. The air pressure is adjusted so that it is just enough to hold the throat open when it relaxes the most. The pressure is constant and continuous. Nasal CPAP prevents obstruction while in use but apneas return when CPAP is stopped.

The major disadvantage of CPAP is that about 40 percent of patients have difficulty using it for long periods of time. Irritation and drying in the nose occur in some patients. Facial skin irritation, abdominal bloating, mask leaks, sore eyes, and headaches are some of the other problems. Because many patients stop using nasal CPAP due to the discomfort arising form exhaling against positive pressure, the search goes on for more comfortable devices. Modifications of CPAP in the treatment of sleep apnea are currently being defined.

One device, which some patients find more comfortable, is the bilevel positive airway pressure (BiPAP). Unlike CPAP where the pressure is equal during inhalation and exhalation, BiPAP is designed to follow the patient’s breathing pattern. It lowers the pressure during expiration and maintains a constant inspiratory pressure.

The ramp system, a modification of CPAP, allows the pressure to be applied only when the patient goes to sleep, increasing pressure slowly over a 30-minute period. The purpose of the ramp system is to make CPAP more comfortable.

Nocturnal Ventilation
Patients can be ventilated non-invasively during sleep with positive pressure ventilation through a CPAP mask. This technique is now used in patients whose breathing is impaired to the point that their blood carbon dioxide level is elevated, as happens in patients with obesity-hypoventilation syndrome and certain neuromuscular disease.

Pharmacologic Therapies
No medications are effective in the treatment of sleep apnea. However some physicians believe that mild cases of sleep apnea respond to drugs that either stimulate breathing or suppress deep sleep. Acetazolamide has been used to treat central apnea. Tricyclic antidepressants inhibit deep sleep (REM) and are useful only in patients who have apneas in the REM state.

Oxygen administration sometimes benefits patients without andy side effects. However, the role of oxygen in the treatment of sleep apnea is controversial and it is difficult to predict which patients will respond to oxygen therapy.

Dental Appliances
Dental appliances which reposition the lower jaw and the tongue have been helpful to some patients with obstructive sleep apnea. Possible side effects include damage to teeth, soft tissues, and the jaw joint.

Surgery
Some patients with sleep apnea may require surgical treatment. Useful procedures include removal of adenoids and tonsils, nasal polyps or other growths, or other tissue in the airway, or correction of structural deformities. Younger patients seem to benefit from surgery better than older patients.

Tracheostomy
Tracheostomy is used only in patients with severe, life-threatening obstructive sleep apnea. In this procedure a small hole is make in the windpipe (trachea) below the Adam’s apple. A T-shape tube is inserted into the opening. This tub stays closed during waking hours and the person breathes normally. It is opened for sleep so that air flows directly into the lungs, bypassing any upper airway obstruction. Its major drawbacks are that it is a disfiguring procedure and the tracheostomy tube requires proper care to keep it clean.

Uvulopalatopharyngoplasty (UPPP)
UPPP is a procedure used to remove excess tissue at the back of the throat (tonsils, adenoids, uvula, and part of the soft palate). This technique probably helps only half of the patients who choose it. Its negative effects include nasal speech and backflow (regurgitation) of liquids into the nose during swallowing. UPPP is not considered as universally effective as tracheostomy but does seem to be a cure for snoring. It does not appear to prevent mortality form cardiovascular complications of severe sleep apnea.

Some patients whose sleep apnea is due to deformities of the lower jaw (mandible) benefit from reconstruction of surgical advancement of the mandible. Gastric stapling procedures to treat obesity are sometimes recommended for sleep apnea patients who are morbidly obese.

Treatment of Patients with Coexisting Lung Diseases
Asthma, chronic bronchitis, emphysema, or other lung diseases can cause breathing problems during sleep. Patients with these diseases may be frequently awakened by cough, aspiration of secretions, choking sensations, and apnea-like sleep disturbances. The treatment in these cases depends on whether the sleep disturbances are due to lung disease or sleep apnea.

Pathophysiology of Sleep and Breathing:

Highlights of the National, Heart, Lung, and Blood Institute Programs

Sleep
The modern era of sleep research started in the mid-1950’s with the discovery that sleep is not a homogeneous phenomenon. Rather it fluctuates cyclically between two distinct sequential stages of sleep.

The first sleep stage is variously called synchronized sleep, slow sleep, slow-wave sleep, quite sleep, or nonrapid-eye-movement (NREM) sleep. In this state the EEG is dominated by large-amplitude slow waves; body functioning generally slows: there are slow, rolling eye movements; the pupils constrict; the respiratory and heart rates decline; blood pressure decreases; and total body oxygen consumption is reduced. It is believed that NREM sleep is a recuperative state.

The second state of sleep is called synchronized sleep, fast sleep, fast-wave sleep, dream sleep, or rapid-eye-movement (REM sleep. The EEG is synchronized, with low-voltage fast waves and there are intermittent eye movements. It is also called paradoxical sleep because of the paradox that the EEG in this sleep stage is similar to that in wakefulness or light sleep, although this is deep sleep in terms of arousability. During REM sleep, central-nervous-system (CNS) activity generally increases, and body system are variously activated and inactivated in a complex physiological pattern. The normal adult spends some 15 to 20 percent of the sleeping hours in REM sleep; this percentage decreases with aging. In contrast, the human fetus of 30 weeks spends 80 percent of its sleep in REM sleep. This declines to 50 percent at term. The amount of quiet sleep (NREM) increases for 50 to 60 percent by 3 months and to 70 percent between 6 and 23 months.

At the biochemical level, hormone-like prostaglandins and cytokines, which are intercellular messengers found in the brain, are implicated in the mechanisms that control sleep. Some speculate that a balance between prostaglandin D2 which increases sleep, and prostaglandin E2 which increases wakefulness, may be involved in the controlling mechanism. The prostaglandins produce their effects when injected into the preoptic area of the hypothalamus, an area responsible for temperature regulation. This may explain the link between sleep and fall in temperature, and also may unify the neurophysiological and biochemical mechanisms of sleep.

Interleukin-1 is localized in the brain in areas associated with control of sleep, and is believed to play a sleep regulatory role. The amount of interleukin-1 in cerebrospinal fluid fluctuates in parallel with the normal sleep/wake cycle.

There is no clear biological answer to the fundamental question of why we sleep. A wide variety of medical and psychiatric illnesses and factors related to age and gender can pathophysiological sequelae. A major goal of sleep research is the characterization of the etiology and pathophysiology of the causes and effects of disturbed sleep.

Breathing
The two major components of breathing are inspiration and expiration. Inspiration is an active process involving contraction of the diaphragm, external intercostal, and in certain circumstances, accessory muscles. It serves to increase intrathoracic volume, decrease intrapleural pressure and allow exchange of air and carbon dioxide within the alveoli of the lungs. Oxygen is transported from the alveoli to the pulmonary bloodstream by passive diffusion and is made available to tissues. Expiration, on the other hand, is a relatively passive process, requiring little or no contraction of the muscles during quiet breathing. A main function of the breathing process is to bring about the exchange of oxygen and carbon dioxide and other gaseous products from biological system.

At birth, the baby switches from dependence on placental gas exchange to air breathing. At the moment of birth there is also a switch from intermittent breathing efforts of the fetal stage to sustained breathing efforts. Since the infants’ respiratory muscles are not well-equipped to sustain high workloads, respiratory muscle fatigue is a problem for premature infants, and apneic episodes requiring intervention occur in at least 50 percent of surviving infants weighing less than 1,500 grams.

Breathing disorders during sleep occur either when there are deficiencies in neurally generated rhythmic respiratory efforts or when there is normal generation of rhythmic efforts but mechanically impeded airflow in upper airways. Metabolic and behavioral control systems in the brain are believed to be the control mechanisms for sleep and breathing. The metabolic system that responds to changes in carbon dioxide and oxygen seems to exert its major influence over NREM sleep. On the other hand, the behavioral control system is involved in voluntary respiratory activities and appears to influence REM sleep; many of the ventilatory changes that occur in REM sleep are similar to the behavioral ventilatory activities such as swallowing, voluntary breath holding, and hyperventilation.

Subjects without any clinical problems may exhibit obstructive or central apnea during periods of REM sleep. Although severe changes in respiratory behavior often occur during the REM sleep, sleep apnea can occur in both NREM and REM sleep. However, sleep staging in patients with severe sleep apnea syndrome is difficult because of severe sleep fragmentation. Thus it is difficult to define the relative importance of abnormal respiration detected during REM or NREM sleeps.

Research Highlights
A recent basic research advance of potential clinical implication relates to the application of modern three dimensional medical imaging techniques to the study of pathogenesis of sleep apnea. Magnetic resonance imaging (MRI) and ultrafast X-ray computed tomography (CT) of the upper airways, combined with computer graphics and reconstructions, have begun to provide exquisite details of the geometry of the upper airway. These approaches now permit identification of the precise anatomical sites of collapse or areas of abnormal compliance to determine if the problem is in a specific area or is a more generalized multifocal abnormality. This information will impact on the treatment options, particularly if there is more diffuse involvement since this wold predict failure of localized surgical procedures.

Only 50 percent of patients with sleep apnea undergoing uvulopalatopharyngoplasty benefit from this procedure. Investigators are exploring ways to identify those patients most likely to benefit from this procedure. A small scale clinical trial conducted to determine predictors of success for UPPP revealed that 86 percent of patients who had documented (by fiberoptic endoscopy) preoperative nasopharyngeal obstruction at the level of the soft palate, showed significant improvement in the number of apneas, arousals and in the cumulative time in apnea-hypopnea following surgery. In contrast, only 18 percent of the patients who had a collapsing segment in regions of the pharynx other than the soft palate showed any improvement following UPPP. This is the first prospective clinical study to demonstrate that closure of the passive pharynx at the level of the soft palate predicts a favorable surgical outcome.

An important opportunity for research on the pathophysiology and treatment of sleep apnea has open up with the finding that the English bulldog seems to be a suitable animal model of sleep apnea. This model is permitting the study of the regularly occurring periodicities in neural activity of the upper airways and the inspiratory muscles, and the role of neural mechanisms in the genesis of sleep apnea. Studies with this model revealed that the consequences of intermittent apnea (sleepiness or hypox emia) serve to increase the magnitude and frequency of neural inhibitory activity, thereby worsening the apnea.

Other studies exploring new treatments for obstructive sleep apnea in animals and humans have identified buspirone, a hypnotic agent as a potentially effective drug for sleep apnea. Buspirone seems to increase ventilation in both anesthetized and awake rats and cats without producing the traditional respiratory depressive effect. In a small scale, controlled clinical trial, this drug decreased sleep apnea and improved respiratory status in the patients receiving the drug.

Associations between snoring, hypertension, heart disease, and stroke raise the possibility of common factors and/or causal relationships between sleep apnea and cardiovascular disorders. Such links may be related to biochemical factors such as insulin, catecholamine, or cortisol that are increased in stress. Sleep apnea may itself be a stress that produces hormonal imbalances that lead to the hypertensive state. Alternately obesity, sleep apnea, and other cardiovascular risk factors may share common metabolic pathways and therefore may be genetically determined. These relationships are being explored by studying families with a history of sleep apnea and/or sudden infant death syndrome as well as by studying racial and genetic differences in the prevalence of sleep apnea-related illnesses.

THE MOST EFFECTIVE  TREATMENT IS REGULAR YOGA EXERCISE  WITH MEDITATION (BREATHING EXERCISE)

Research Opportunities
Since 1986, the Division of Lung Diseases, National Heart, Lung, and Blood Institute, has been engaged in a concerted national program in cardiopulmonary disorders in sleep designed to fill critical gaps in the understanding of the pathogenesis, diagnosis, treatment, and prevention of sleep-disordered breathing. Some research areas of current emphasis include the following.

1. Natural history of sleep apnea with the goal of determining the magnitude of the problem and designing the most effective therapy.
2. Scientific basic for the influence of age, gender, ethnicity, smoking obesity, and snoring on the development of sleep apnea.
3. Assessment of the severity of sleep apnea and defining the relationships of disease severity, response to treatment and prognosis.
4. Cellular and molecular basis of the role of hypoxia in excessive daytime sleepiness and sleep apnea.
5.Cardiovascular consequences of sleep apnea and the underlying neural cellular and respiratory mechanisms.
6.Improved therapeutic modalities for sleep apnea when associated with blood pressure, asthma, chronic heart failure, angina pectoris, chronic pulmonary disease and stroke.
For More Information
Additional information about breathing-related sleep disorders and other disorders of sleep can be obtained form your local sleep disorders center and the following sources:

Unites States
American Sleep Apnea Association
P.O. Box 3893
Charlottesville, VA 22903

The American Sleep Disorders Association 604 Second Street Southwest
Rochester, MN 55902

Association of Sleep Disorders Centers

P.O. Box 2604
Del Mar, CA 92014

AWAKE NETWORK
P.O. Box 534
Bethel Part, PA 15102

American Narcolepsy Association
P.O. Box 1187
San Carlos, CA 94070

Narcolepsy Network
155 Van Brackle Rd.
Aberdeen, NJ 07747

National Heart, Lung, and Blood Institute (NHLBI) Communications and Public Information Branch 9000 Rockville Pike
Bethesda, MD 20892

(Other institutes at NIH that have information about sleep disorders include the National Institute of Neurological Disorders and Stroke, National Institute od Child Health and Human Development, National Institute of Mental Health, National Institute on Aging. The address for each is 9000 Rockville Pike, Bethesda, MD 20892.)

Centers for Disease Control and Prevention 1600 Clifton Road, NE
Atlanta, GA 30333

International
Sleep Apnea Research Association, Inc.
65 Kitchener Avenue
Earlwood NSW 2206
Australia

Sleep Apnea Society of Alberta
Faculty of Nursing
University of Calgary
2500 University Drive NW
Calgary, Alberta T2N 1N4

Nederlandse Vereniging Van Slaap Apnoe Patienten De Nye Oanliz 25
9084 AN GOUTOM
The Netherlands

British Sleep Society
Sleep Disorder Clinic
Leicestershire General Hospital
Leicester, LE5 4PW
United Kingdom

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.

Sources:http://www.medhelp.org/lib/breadiso.htm

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Ailmemts & Remedies

Renal Tubular Acidosis

Definition:-Your body’s cells use chemical reactions to carry out tasks such as turning food into energy and repairing tissue. These chemical reactions generate acids. But too much acid in the blood—acidosis—can disturb many bodily functions. Healthy kidneys help maintain acid-base balance by excreting acids into the urine and returning bicarbonate—an alkaline, or base, substance—to the blood. This “reclaimed” bicarbonate neutralizes much of the acid that is created when food is broken down in the body.

Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person’s blood to remain too acidic. Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, and progressive renal failure.

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One researcher, pediatric neurologist Donald Lewis, has theorized that Charles Dickens may have been describing a child with RTA when he created the character of Tiny Tim in his famous story, “A Christmas Carol.” Tiny Tim’s small stature, malformed limbs, and periods of weakness are all possible consequences of the chemical imbalance caused by RTA. Among the evidence cited to support this theory is the fact that Tiny Tim’s condition, while fatal in one scenario, is reversible when Scrooge pays for medical treatments, which in those times would likely have included sodium bicarbonate and sodium citrate, which are alkaline agents that would neutralize the acid in Tiny Tim’s blood. Whether the literary diagnosis of Tiny Tim is correct or not, the good news is that medical treatment can indeed reverse the effects of RTA.

Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine. When blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine. The metabolic acidosis that results from RTA may be caused either by failure to recover sufficient (alkaline) bicarbonate ions from the filtrate in the early portion of the nephron (proximal tubule) or by insufficient secretion of (acid) hydrogen ions into the latter portions of the nephron (distal tubule). Although a metabolic acidosis also occurs in those with renal insufficiency, the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. Several different types of RTA exist, which all have different syndromes and different causes.

The word acidosis refers to the tendency for RTA to lower the blood’s pH. When the blood pH is below normal (7.35), this is called acidemia. The metabolic acidosis caused by RTA is a normal anion gap acidosis.

Diagnosis :-
To diagnose RTA, your doctor will check the acid-base balance in samples of your blood and urine. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed first to rule out other causes. If RTA is suspected, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which of the three types of RTA you have. In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis .
Types of RTA:-
At one time, doctors divided RTA into four types.

*Type 1 is also called classic distal RTA. “Distal,” which means distant, refers to the point in the urine-forming tube where the defect occurs. It is relatively distant from the point where fluid from the blood enters the tiny tube, or tubule, that collects fluid and wastes to form urine.

*Type 2 is called proximal RTA. The word “proximal,” which means near, indicates that the defect is closer to the point where fluid and wastes from the blood enter the tubule.

*Type 3 is rarely used as a classification today because it is now thought to be a combination of type 1 and type 2.

*Type 4 RTA is caused by another defect in the distal tubule, but it is different from classic distal RTA and proximal RTA because it results in high levels of potassium in the blood instead of low levels. Either low potassium (hypokalemia) or high potassium (hyperkalemia) can be a problem because potassium is important in regulating heart rate.

Type I-Distal RTA:-
This disorder may be inherited as a primary disorder or may be one symptom of a disease that affects many parts of the body. Researchers have now discovered the abnormal gene responsible for the inherited form. More often, however, classic distal RTA is a complication of diseases that affect many organ systems (systemic diseases), like the autoimmune disorders Sjögren’s syndrome and lupus.

Other diseases and conditions associated with distal RTA include hyperparathyroidism, a hereditary form of deafness, analgesic nephropathy, rejection of a transplanted kidney, renal medullary cystic disease, obstructive uropathy, and chronic urinary tract infections

Distal RTA (dRTA) is the most common and also the classical form of RTA, being the first described. It has a number of causes which cause a common underlying problem, which is a failure of acid secretion by the alpha intercalated cells of the cortical collecting duct of the distal nephron. This leads to a failure to acidify the urine to a pH of less than 5.3 even if the blood is too acidic (ie there is systemic acidemia), and consequently there is a tendency towards acidemia. This leads to the clinical features of dRTA;

*Normal anion gap metabolic acidosis/acidemia

*Hypokalemia (which may be severe)

*Urinary stone formation

*Nephrocalcinosis (deposition of calcium in the substance of the kidney)

*Bone demineralisation (causing rickets in children and osteomalacia in adults)

The acidosis is variable, and one may have dRTA with alpha intercalated cell failure without necessarily being acidemic, this is termed incomplete dRTA. The diagnosis of dRTA can be made by the observation of a urinary pH of greater than 5.3 in the face of a systemic acidemia (usually taken to be a serum bicarbonate of 20 mmol/l or less). In the case of an incomplete dRTA, failure to acidify the urine following an oral acid loading challenge is often used as a test. The test usually performed is the short ammonium chloride test, in which ammonium chloride capsules are used as the acid load. More recently, an alternative test using furosemide and fludrocortisone has been described.

The symptoms and sequelae of dRTA are variable and ranging from being completely asymptomatic, through loin pain and hematuria from kidney stones to failure to thrive and severe rickets in childhood forms as well as possible renal failure and even death.

Interestingly, dRTA has been proposed as a possible diagnosis for the unknown malady plaguing Tiny Tim in Charles Dickens’ A Christmas Carol.

Causes:
*Autoimmune disease. Classically Sjögren’s syndrome, but it is also associated with systemic lupus erythematosus, rheumatoid arthritis and even hypergammaglobulinemia. Hypokalaemia is often severe in these cases.

*Hereditary causes include mutations of Band 3 the basolateral bicarbonate transporter of the intercalated cell, which may transmit in an autosomal dominant fashion in western European cases, or in an autosomal recessive fashion in South East Asian cases. The South East Asian cases are associated with more severe hypokaemia. Other Hereditary causes include mutations of subunits of the apical proton pump vH+-ATPase, which transmit in an autosomal recessive fashion, and may be associated with sensorineural deafness.

*Liver cirrhosis.

*Nephrocalcinosis. While it is a consequence of dRTA, it can also be a cause; related to calcium-induced damage of the cortical collecting duct.

*Renal transplantation.

*Sickle cell anemia.

*Toxins, including ifosfamide, toluene, lithium carbonate and amphotericin B.

*Chronic urinary tract obstruction.

Cartoon of the alpha intercalated cell, showing the apical proton pump and the basolateral band 3 (kAE1)

Treatment:
This is relatively straightforward. It involves correction of the acidemia with oral sodium bicarbonate or sodium citrate. This will correct the acidemia and reverse bone demineralisation. Hypokalemia and urinary stone formation and nephrocalcinosis can be treated with potassium citrate tablets which not only replace potassium but also inhibit calcium excretion and thus exacerbate stone disease as sodium bicarbonate or citrate may do.

Type 2-Proximal RTA:-
This form of RTA occurs most frequently in children as part of a disorder called Fanconi’s syndrome. The symptoms of Fanconi’s syndrome include high levels of glucose, amino acids, citrate, and phosphate in the urine, as well as vitamin D deficiency and low blood-potassium.

Proximal RTA (pRTA) is caused by a failure of the proximal tubular cells to reabsorb filtered bicarbonate from the urine, leading to urinary bicarbonate wasting and subsequent acidemia. The distal intercalated cells function normally, so the acidemia is less severe than dRTA and the urine can acidify to a pH of less than 5.3. pRTA also has several causes, and may occasionally be present as a solitary defect, but is usually associated with a more generalised dysfunction of the proximal tubular cells called Fanconi’s syndrome where there is also phosphaturia, glycosuria, aminoaciduria, uricosuria and tubular proteinuria. The principal feature of Fanconi’s syndrome is bone demineralisation due to phosphate wasting.

Causes:


Familial disorders

* Cystinosis
*Galactosemia
*Glycogen storage disease (type I)
*Hereditary fructose intolerance
*Lowe’s syndrome
*Tyrosinemia
*Wilson’s disease

Acquired disorders

*Amyloidosis
*Multiple myeloma
*Paroxysmal nocturnal hemoglobinuria
*Toxins, such as HAART, ifosfamide, lead, and cadmium

Treatment
Again this depends on oral bicarbonate supplementation. However, this will increase urinary bicarbonate wasting and may well promote a bicarbonate diuresis. The amount of bicarbonate given may have to be very large, to stay ahead of the urinary losses. Correction with oral bicarbonate may exacerbate urinary potassium losses and precipitate hypokalemia.As with dRTA, reversal of the chronic acidosis should reverse bone demineralisation.

Type 3 RTA:-
This was previously used to designate a rare and transient mixed dRTA and pRTA of uncertain aetiology. Now it is used to describe a genetic defect in type 2 carbonic anhydrase (CA2), which is found in both the proximal and distal tubular cells, as well in bone. As a result it causes;

*proximal renal tubular acidosis
*distal renal tubular acidosis
*osteopetrosis
*cerebral calcification and subsequent mental impairment;

It is very rare and cases from all over the world have been reported, of which about 70% are from the Magreb region of North Africa, possibly due to the high prevalence of consanguinity there. The kidney problems are treated as described above. There is no treatment for the osteopetrosis or cerebral calcification.

Type 4 RTA (Hypoaldosteronism):-
This form of RTA is most often referred to as type 4. It occurs when blood levels of the hormone aldosterone are low or when the kidneys do not respond to it. Aldosterone directs the kidneys to regulate the levels of sodium, potassium, and chloride in the blood. Type 4 RTA is distinguished by a high blood-potassium level.

Hyperkalemic distal RTA may result from sickle cell disease, urinary tract obstruction, lupus, amyloidosis, or transplantation.

Type 4 RTA is not actually a tubular disorder at all, and nor does it have a clinical syndrome similar to the other types of RTA described above. It was included in the classification of renal tubular acidoses as it is associated with a mild (normal anion gap) metabolic acidosis due to a physiological reduction in distal tubular ammonium excretion, which is secondary to hypoaldosteronism. Its cardinal feature is hyperkalemia, and measured urinary acidification is normal.

Causes:
*Aldosterone deficiency-Primary (rare)

1.Primary adrenal insufficiency
2.Congenital adrenal hyperplasia
3.Aldosterone synthase deficiency

*Hyporeninemic hypoaldosteronism (due to decreased angiotensin 2 production as well as intra-adrenal dysfunction)

1.Renal dysfunction-most commonly diabetic nephropathy
2..HIV infection
3..ACE inhibitors
4..NSAIDs
5..Cyclosporine

*Aldosterone resistance

1.Drugs (Amiloride, Spironolactone,Trimethoprim, Pentamidine)
2.Pseudohypoaldosteronism

Treatment:
*Aldosterone deficiency should be treated with a mineralocorticoid (such as fludrocortisone), as well as possibly a glucocorticoid for cortisol deficiency, if present.

*Hyporeninemic hypoaldosteronism is ammenable to fludrocortisone treatment, but the accompanying hypertension and edema can prove a problem in these patients, so often a diuretic (such as the thiazide diuretic, bendrofluazide,or a loop diuretic, such as furosemide) is used to control the hyperkalemia.

Hope through Research:-
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) conducts and supports research into many kinds of kidney disease, including renal tubular acidosis. NIDDK-supported researchers are exploring the genetic and molecular mechanisms that control acid-base regulation in the kidney. These studies will point the way to more effective treatments for RTA.

Click to See also:-
Hyperchloremic acidosis
Hypokalemia
Kidney stone

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.

For More Information you may contact:

American Association of Kidney Patients
3505 East Frontage Road
Suite 315
Tampa, FL 33607
Phone: 1–800–749–2257 or 813–636–8100
Fax: 813–636–8122
Email: info@aakp.org
Internet: www.aakp.org

American Kidney Fund
6110 Executive Boulevard
Suite 1010
Rockville, MD 20852
Phone: 1–800–638–8299 or 301–881–3052
Email: helpline@akfinc.org
Internet: www.kidneyfund.org

National Kidney Foundation
30 East 33rd Street
New York, NY 10016
Phone: 1–800–622–9010 or 212–889–2210
Fax: 212–689–9261
Email: info@kidney.org
Internet: www.kidney.org
Resources:
http://kidney.niddk.nih.gov/kudiseases/pubs/tubularacidosis/index.htm
http://en.wikipedia.org/wiki/Renal_tubular_acidosis

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