What is Rh factor? |

Structure and Functions

Blood replacement in emergency or surgery can be critical: blood loss exceeding 40 percent can lead to a condition called shock in which the heart cannot pump efficiently, resulting in death. In the search for human blood replacements, scientists have found that animal blood is not compatible. More important, they have discovered that even blood from different humans does not always mix. Sometimes the red blood cells will agglutinate, or settle out of the plasma in clumps. Consequently, these red blood cells are destroyed by the body, and jaundice and death may follow. To prevent this reaction, human blood must be classified into types and cross-matched. The two most important general groupings are the ABO and Rh types.

Human blood is classified into types according to the antigens that might be present on the red blood cells as a result of heredity. Antigens are usually large, complex molecules made of protein alone, protein with attached carbohydrates, or lipids with attached fatty acids and alcohol. They may be free molecules, as in the case of toxins released by invading bacteria, or they may be located on a cell’s surface and serve to label or mark the cell. The markers attached to cell surfaces identify the cell as “self” or “foreign.” Such antigens are the basis of blood types.

Karl Landsteiner
showed that there are four major blood types, based on two antigens that might be present or missing. He called the markers A and B. People with both markers on their cells are called type AB, people with one of the two are type A or type B, and those without either marker were originally called C but later changed to O. Landsteiner’s system of classifying blood according to the presence of the A and B antigens is now termed the ABO system. Landsteiner demonstrated the chemistry of the antigens and the antibodies by mixing blood from himself and coworkers in his laboratory and observing that some combinations agglutinated.

The next major breakthrough came with Philip Levine
and Rufus Stetson’s study of the blood of a woman whose fetus had died six weeks before birth. The mother’s immune system had produced antibodies against the Rh factors on the blood cells of her developing child. She was Rh negative while her child was positive, having inherited an Rh-positive gene from the father. The positive blood of the child caused the mother’s immune system to react. The importance of the discovery was twofold. It not only explained why some babies suffered from an immune reaction in their mothers but also showed that blood transfusions could be typed as ABO compatible and still fail if the Rh factor was not considered.

The term Rh factor came about because of a misunderstanding. Working independently and believing that they had found the same factor first in their laboratory animals, Landsteiner and Alexander Wiener claimed discovery and named the Rh antigen after the rhesus monkey. They injected the monkey blood into rabbits, and the rabbits developed antibodies against the foreign factor. Hypothesizing that closely related primates might share the factor, the rabbit antibodies in a serum were then mixed with samples of human blood. Further work verified that there was indeed a new important human factor, but it differed from the one in monkeys. By this time, however, it was too late to change the misleading name. To clear up the confusion, the factor in humans kept the name of Rh factor, while the monkey antigen was labeled the LW factor.

Even if it is inappropriately named, the Rh factor is an important discovery. People with the marker on their blood cells are Rh positive, while people without it are Rh negative. Rh-negative people can give blood to people who are positive if all other antigens such as those found in the ABO types are compatible. If the reverse is attempted, however, the Rh-negative person will develop antibodies against the Rh marker. Clumping of the red blood cells will occur, and illness and death are likely.

Discovery of the presence of these markers was the key to understanding both the blood types and what happens in immune responses. When a foreign protein or antigen enters the body, antibodies are produced by the immune system and released into the blood and lymph. These antibodies are specific in the sense that a particular antibody will only combine with a particular antigen. (If a particular antigen is present on a person’s own blood cells, the individual would not normally produce and carry antibodies for this molecule; otherwise, the antibodies would attack the person’s own blood cells.) The antibodies fasten the cells together in what is called agglutination. Agglutinated cells are destroyed by white blood cells.

Combining the ABO and Rh systems, a person could be A+, A-, AB+, AB-, B+, B-, O+, or O-. Because an AB+ individual has A, B, and Rh antigens and no antibodies against them, this person can receive blood from all others. An O- individual has no antigens and is a universal donor, assuming that the O- person has no other important antigen differences from other, more rare types. The importance of the ABO and Rh systems is shown by the standard practice of hospitals in typing and sorting by these systems.

Unlike the ABO types, Rh-negative blood does not normally contain antibodies for positive blood unless the person has been previously exposed (sensitized) to positive blood. The A and B antibodies are developed early in people because A and B antigens are common in the environment. They are found not only on red blood cells but also in milk, colostrum, saliva, and other body fluids. Should a transfusion of Rh-positive blood be given to an Rh-negative person, the negative blood produces the antibody, which will have a violent reaction with the next similar transfusion.

The Rh factor is inherited, as are all blood types. A person inherits one gene involving the factor from each parent. If the person inherits two genes (DD) for the factor, it will be present on the red blood cells. If a person inherits one gene for the factor and one that does not produce it (Dd), the individual will still be Rh positive. If a person inherits two recessive genes (dd), that person will be Rh negative. Consequently, the gene for production of the Rh factor is called dominant; the other gene is recessive.

The original Rh factor can also be called the D factor. Additional investigation has shown that the entire Rh factor is not a single factor caused by one pair of genes; rather, at least three pairs of genes may be involved. Antisera have been found not only for the most reactive D antigen but also for four other factors. The situation can be explained by imagining Rh to be determined by a combination of three genes, which are probably closely linked on the same chromosome. Ronald Fisher labeled the genes C, c, D, d, E, and e. An Rh gene complex could then be any of these combinations: CDE, CDe, CdE, Cde, cdE, cDe, cde, or cDE. An individual would have two of these complexes, one from each parent. The number of different Rh types then reaches sixty-four.

To illustrate, a person with CDe/cdE would test Rh positive using standard anti-D sera because of the D gene; so would people with any combination of C, c, E, and e with at least one D. Nevertheless, the other nearby genes can cause agglutination problems. Each of them, except d, produces an antigen on the red blood cells. The antigens cause antisera to form in human blood that recognizes them as foreign. One can also choose to think of the situation as having eight different alleles for Rh. Then a single symbol can stand for each combination: r = cde, r′ = Cde, r″ = CdE, ry = cdE, R0 = cDe, R1= CDe, R2 = cDE, and Rz = CDE. Any r is an Rh-negative combination in the classic sense, and any R is Rh positive. Additional discoveries of new Rh antisera have caused some investigators to hypothesize about the possibility of more than thirty antigens, some that are variant forms of the above and some that require more genes.

A 1948 paper by R. R. Race, A. E. Mourant, Sylvia D. Lawler, and Ruth Sanger reported that R1r (or CDe/cde) is the most common Rh blood gene combination in England, at about 33 percent of those tested. The R1R1 (or CDe/CDe) combination follows at 16.6 percent, rr (or cde/cde) at 15.8 percent, R1R2 (or CDe/cDE) at 12.9 percent, R2r (or cDE/cde) at 12.8 percent, and R2R2 (or cDE/cDE) at 2.7 percent. All the other combinations total about 6 percent.

Rh has turned out to be quite complex. Nevertheless, the system can be understood and applied at a very basic and useful level of Rh positive or Rh negative, which involves consideration of the very reactive D antigen on the blood cells. In that case, the Rh symbol is often labeled Rh0.

Disorders and Diseases

The discovery of the ABO system allowed transfusions to proceed with some confidence of success during World War I. Still, some transfusions produced problems, and some minor independent blood-type systems (MNS, P) were discovered. Clearly, people were members of more than one blood-type system. The additional discovery of the highly reactive Rh factor or D antigen was critical for safe transfusions.

Another immediate application of the discovery was in the area of childbirth. Rh incompatibility explained why some babies either died at birth or were born in serious trouble. The attack of the mother’s antibodies on the fetal blood cells can lead to various forms of hemolytic disease of newborns, or erythroblastosis fetalis. Incompatibility between mother and child is also one of the causes of spontaneous miscarriage early in pregnancy. Knowing the existence of the Rh factor has saved countless infants.

Recall that the Rh factor is inherited. If an Rh-negative woman (dd) marries an Rh-positive man (DD or Dd), the child may be Rh positive. During pregnancy, there is no direct blood flow from mother to child because red blood cells cannot cross the placenta. At some time during the pregnancy or at birth, however, blood will probably mix, and the mother will then be sensitized. She then will form antibodies against the Rh factor. Many of these antibodies are of the IgG type and are smaller than A or B antibodies (IgM). The small IgG antibodies can cross the placenta into the blood of the fetus. The first Rh-positive child usually escapes harm by being born, but a second positive child will be in great danger, as the mother’s preformed antibodies will cross the placenta and attack the red blood cells of the fetus. Blood cells are likely to be broken open, releasing hemoglobin. The fetus will become anemic and jaundiced and may suffer brain damage or be stillborn.

The occurrence of erythroblastosis fetalis can be prevented if an Rh-negative mother is given an injection of rhesus gamma globulin (RhoGAM) within seventy-two hours of the delivery of her first Rh-positive child. This approach was developed by C. A. Clark, P. M. Sheppard, and others working at Liverpool University. The gamma globulin destroys the fetal blood cells in the mother and prevents the production of antibodies that would affect the next positive child. Miscarriages or abortions of Rh-positive pregnancies count as an exposure to the antigen and can cause the mother’s immune system to react. Therefore, these events also require the injection to protect future children. Also, any Rh-negative woman accidentally given a transfusion of positive blood would be in danger herself, as would the fetuses in any of her future pregnancies.

Amniocentesis, a sampling of fluid from the sac around the developing fetus, can reveal such difficulties as Rh incompatibility. An Rh-negative woman can also be given a series of blood tests (Rh titers) during her pregnancy. If the tests show that the antibodies are increasing in number, intrauterine transfusion of negative blood may be attempted. Moreover, if the child is nearing full term, delivery may be induced to prevent the blood of the fetus from being completely destroyed. If the child is born with signs of circulatory problems, a blood transfusion can help.

Anthony Smith notes that the ABO type has an effect on trouble with Rh during pregnancy. If the mother is Rh negative, the child is positive, and their ABO types are also incompatible, then the Rh reaction is diminished. The reason may be that the mother already has antibodies against incompatible ABO types. When the red blood cells leak into the mother’s circulatory system, they are immediately destroyed by already-existing maternal ABO antibodies before any antibodies against Rh factor can be formed.

Some interesting associations with Rh have been discovered but are not yet understood. Typhoid, mumps, mononucleosis, and viral meningitis are more common in Rh-negative people. Viral diseases tend to be more common in the nonantigenic types of both the ABO and Rh systems (O and Rh negative).

Perspective and Prospects

Few successful blood transfusions took place before 1900. In that year, Karl Landsteiner discovered that there are different types of blood. Some would mix, while others would clump. He and his coworkers identified four major human blood groups: A, B, AB, and O. Even so, eight years passed before the first transfusion using Landsteiner’s ABO types was attempted. Transfusions became more likely to succeed. People could be typed by the antigens on their blood cells, and donors could be matched with the patient. Yet sometimes the transfusions still did not work as predicted. In 1930, Landsteiner won the Nobel Prize in Physiology or Medicine for his discovery of ABO blood types.

Landsteiner and Philip Levine discovered the MNS types in 1927; these are not important in transfusions but are of great help in cases of doubtful paternity. When beginning his own work, Levine agreed with Landsteiner not to study new blood groups, as Landsteiner had reserved that project for himself. Nevertheless, in 1939, Levine and Rufus E. Stetson published a report showing that the blood of a mother with a stillborn child was able to react hemolytically with 80 out of 104 ABO-compatible donors. They correctly concluded that the mother’s blood lacked an antigen that many others had: an unknown marker that was independent of the known ABO, MNS, and P blood groups. Levine and Stetson had correctly analyzed the problem but did not name their new antigen. Clearly, they had discovered what would be called the Rh factor.

Less than a year later, Landsteiner and Alexander Wiener immunized rabbits and guinea pigs with the blood of the monkey Macacus rhesus. They found that the resulting rabbit serum agglutinated not only the rhesus monkey blood but also about 85 percent of blood samples from people in New York City. They called these people Rh positive and the remaining 15 percent Rh negative. Wiener and H. R. Peters attempted to show that the Rh antibody in the rabbits was the same as that found in the serum of people who had suffered incompatible transfusion reactions not explained by ABO blood typing.

A bitter exchange ensued between Levine and Wiener about who had discovered the Rh factor. This was resolved when it was shown that the antigen on the rhesus monkey cells was not the same as the human Rh factor. Unfortunately, the name Rh was too well established to be changed by this time. To avoid further confusion, Levine suggested that the factor in the monkeys be called the LW factor after Landsteiner and Wiener. Despite this controversy, R. R. Race and Ruth Sanger called the discovery of the Rh factor the most important event in blood-group science since the discovery of the ABO system forty years before.

Soon, different investigators were able to derive sera with different antibodies for the Rh factor. Clearly, the Rh factor was not simply a single antigen. In 1943, Ronald Fisher studied the different antisera that had been developed and proposed that eight different Rh gene complexes were involved.

The existence of the Rh factor is useful in other ways. In addition to transfusions, another application of blood typing (including the presence or absence of the Rh factor) is in criminology. Blood left at the scene of a crime can be powerful evidence against a suspect. Blood types can also eliminate individuals as possible fathers in paternity suits. For example, if both parents are Rh negative, the child cannot be Rh positive. A more complete typing of the blood would allow further strong evidence. Such typing does not prove paternity, however; it only shows whether paternity is possible.

Blood typing also allows anthropologists to develop theories about the relationships among various human groups and how people may have migrated. The breakdown between being Rh positive or negative varies among the races. The Basques, a group of people near the Bay of Biscay between Spain and France, are only 64 percent positive, while about 85 percent of the Caucasian population in general is Rh positive. Races other than Caucasian are generally nearly 100 percent Rh positive. According to Sir Peter Medawar, however, the advantages of being one type or another are obscure. Why there are so many different blood types remains an interesting question.

The discoveries of the ABO types and the Rh factor stand as fundamental achievements in medical science. Even though many other types continue to be uncovered, ABO and Rh determinations remain the most basic steps in matching blood for many purposes, especially for safe transfusions.

Bibliography

Alan, Rick, Andrea Chisholm, and Brian Randall. "Rh Incompatibility and Isoimmunization." Health Library, March 18, 2013.

Bibel, Debra Jan, ed. Milestones in Immunology: A Historical Exploration. New York: Springer, 1988.

Jandl, James H. Blood: Textbook of Hematology. 2d ed. Boston: Little, Brown, 1996.

Martin, Richard J., Avroy A. Fanaroff, and Michele C. Walsh, eds. Fanaroff and Martin’s Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant. 2 vols. 9th ed. St. Louis: Mosby/Elsevier, 2011.

Moore, Keith L., T. V. N. Persaud, and Mark G. Torchia. The Developing Human: Clinically Oriented Embryology. 9th ed. Philadelphia: Saunders/Elsevier, 2013.

Page, Jake. Blood: The River of Life. Washington, D.C.: US News Books, 1981.

Race, R. R., A. E. Mourant, Sylvia D. Lawler, and Ruth Sanger. "The Rh Chromosome Frequencies in England." Blood 3, no. 6 (June 1948): 689–695.

"Rh Factor Blood Test." Mayo Clinic, June 16, 2012.

Rodak, Bernadette F., George A. Fritsma, and Elaine M. Keohane, eds. Hematology: Clinical Principles and Applications. 4th ed. St. Louis, Mo.: Saunders/Elsevier, 2012.

Starr, Douglas P. Blood: An Epic History of Medicine and Commerce. New York: Alfred A. Knopf, 1998.

What is fatigue? |

Causes and Symptoms

Almost all people suffer from fatigue at some point in their lives. It is a nonspecific complaint including tiredness, lack of energy, listlessness, or malaise. Patients often confuse fatigue with weakness, breathlessness, or dizziness, which indicate the existence of other physical disorders. Rest or a change in the daily routine ordinarily alleviates fatigue in healthy individuals. Though normally short in duration, fatigue occasionally lasts for weeks, months, or even years in some individuals. In such cases, it limits the amount of physical and mental activity in which the person can participate.

Long-term fatigue can have serious consequences. Often, patients begin to withdraw from their normal activities. They may withdraw from society in general and may gradually become more apathetic and depressed. As a result of this progression, a patient’s physical and mental capabilities may begin to deteriorate. Fatigue may be aggravated further by a reduced appetite and inadequate nutritional intake. Ultimately, these symptoms lead to
malnutrition and multiple vitamin deficiencies, which intensify the fatigue state and trigger a vicious circle.

This fatigue cycle ends with a person who lacks interest and energy. Such patients may lose interest in daily events and social contacts. In later stages of fatigue, they may neglect themselves and lose track of their goals in life. The will to live and fight decreases, making them prime targets for accidents and repeated infections. They may also become potential candidates for suicide.

Physical and/or mental overactivity commonly cause recent-onset fatigue. Management of such fatigue is simple: Adequate physical and mental relaxation typically relieve it. Fortunately, many persistent fatigue states can be easily diagnosed and successfully treated. In some cases, however, fatigue does not respond to simple measures.

Fatigue can stem from depression. Depressed individuals often reflect boredom and a lack of interest, and frequently express uncertainty and anxiety about the future. These people usually appear “down.” They may walk slowly with their head down, slump their shoulders, and sigh frequently. They often take unusually long to respond to questions or requests. They also show little motivation. Depressed individuals typically relate feelings of dejection, sadness, worthlessness, or helplessness. Often, they complain of feeling tired when they wake up in the morning, and no amount of sleep or rest improves their condition. In fact, they feel weary all day and frequently complain of feeling weak. They often have poor appetites and sometimes lose weight. Once these patients are questioned by a physician, however, it may become apparent that their state of fatigue actually fluctuates. At times they feel exhausted, while at other times (sometimes only minutes later) they feel refreshed and full of energy.

Other manifestations of depression include sleep disorders (particularly early morning waking), reduced appetite, altered bowel habits, and difficulty concentrating. Depressed individuals sometimes fail to recognize their condition. They may channel their depression into physical complaints such as abdominal pain, headaches, joint pain, or vaguely defined aches and pains. In older people, depression sometimes manifests itself as impaired memory.

Anxiety, another major cause of fatigue, interferes with the patient’s ability to achieve adequate mental and physical rest. Anxious individuals often appear scared, worried, or fearful. They frequently report multiple physical complaints, including neck muscle tension, headaches, palpitations, difficulty in breathing, chest tightness, intestinal cramping, and trouble falling asleep. In some cases, both depression and anxiety may be present simultaneously.

Medications also constitute a major cause of fatigue. Most drugs—prescription, over-the-counter, or recreational—can cause fatigue. Medications for sleep, antidepressants, antianxiety medications, muscle relaxants, allergy medications, cold medications, and certain blood pressure medications can lead to problems with fatigue.

An excessive intake of stimulants, paradoxically, sometimes leads to easy fatigability. Stimulants can interfere with proper sleeping habits and relaxation. Common culprits include caffeine and medications (such as some diet pills and nasal decongestants) that can be purchased without a prescription. Recreational drugs can also contribute to chronic fatigue. Depending on their tendencies, they function to cause fatigue in much the same way as the prescription and over-the-counter drugs already discussed. Cocaine and amphetamines, for example, act as stimulants. Narcotics such as heroin and barbiturates (downers) possess strong sedative qualities. Alcohol consumption in an attempt to escape loneliness, depression, or boredom may further exacerbate a sense of fatigue. Alcohol produces fatigue in two ways. It has sedative qualities, and it also intensifies the sedative effects of other medications, if taken with them.

Other drugs that may induce fatigue include diuretics and those that lower blood pressure. These medications increase the excretions of many substances through the kidneys. If inappropriately given or regulated, these drugs may alter the blood concentration of other medications taken concurrently.

Painkillers can lead to fatigue in a different way. In some individuals, they irritate the lining of the stomach and cause it to bleed. Such bleeding usually occurs in small amounts and goes unnoticed by the patient. This slight blood loss can gradually lead to anemia and fatigue.

Medications are particularly likely to cause fatigue in elderly individuals. With many drugs, their elimination from the body through metabolism or excretion may decrease with age. This often leads to higher drug concentrations in the blood than intended, resulting in a state of constant sedation and lethargy. Also, elderly individuals’ brains may be more sensitive to sedation than those of younger individuals. Finally, the elderly tend to take more medication for more illnesses than younger adults. The additive side effects of multiple medicines can contribute to fatigue problems.

Sleep deprivation or frequent sleep interruptions lead to fatigue. A change in environment can induce sleep disorders, especially if accompanied by unfamiliar noises, excessive lighting, uncomfortable temperatures, or an excessive degree of humidity or dryness. Total sleep time may be adequate under such conditions, but quality of sleep is usually poor. Nightmares can also interrupt sleep, and if numerous and recurring, they also cause fatigue.

Some sleep interruptions are not so readily apparent. In sleep apnea, a specific and increasingly diagnosed sleep disorder, the patient temporarily stops breathing while sleeping. This results in reduced oxygen levels and increased carbon dioxide levels in the blood. When a critical level is reached, the patient awakens briefly, takes a few deep breaths, and then falls asleep again. Many episodes of sleep apnea may occur during the night, making the sleep interrupted and less refreshing than it should be. The next day, the patient often feels tired and fatigued but may not recognize the source of the problem. Obstructive sleep apnea normally develops in grossly overweight patients or in those with large tonsils or adenoids. Patients with obstructive sleep apnea usually snore while sleeping, and typically they are unaware of their snoring and sleep disturbance.

A number of diseases can lead to easy fatigability. In most illnesses, rest relieves fatigue and individuals awake refreshed after a nap or a good night’s sleep. Unfortunately, they also tire quickly. Unlike psychogenic fatigue or fatigue induced by drugs, disease-related fatigue is not usually the patient’s main symptom. Other symptoms and signs frequently reveal the underlying diagnosis. Individuals who suffer from severe malnutrition, anemia, endocrine system malfunction, chronic infections, tuberculosis, Lyme disease, bacterial endocarditis (a bacterial infection of the valves of the heart), chronic sinusitis, mononucleosis, hepatitis, parasitic infections, and fungal infections may all experience chronic fatigue.

In early stages of acquired immunodeficiency syndrome (AIDS), fatigue may be the only symptom. Persons at high risk for contracting the human immunodeficiency virus (HIV)—those with multiple sexual partners, those who have unprotected sex, those with a history of blood transfusion, or intravenous drug users—who complain of persistent fatigue should be tested for HIV infection.

Abnormalities of mineral or electrolyte concentrations—potassium, sodium, chloride, and calcium are the most important of these—may also cause fatigue. Such abnormalities may result from medications (diuretics are frequently responsible), diarrhea, vomiting, dietary fads, and endocrine or bone disorders.

Some less common medical causes of chronic fatigue include dysfunction of specific organs such as kidney failure or liver failure. Allergies can also produce chronic fatigue. Cancer can cause fatigue, but other symptoms usually surface and lead to a diagnosis before the patient begins to notice chronic weariness.

Treatment and Therapy

When an individual’s fatigue persists in spite of adequate rest, medical help becomes necessary in order to determine the cause. Common diseases known to be associated with fatigue should be considered. Initially, the physician makes detailed inquiries about the severity of the fatigue and how long ago it started. Other important questions include whether it is progressive, whether there are any factors that make it worse or relieve it, or whether it is worse during specific times of the day. An examination of the patient’s psychological state may also be necessary.

The physician should ask about the presence of any symptoms that occur along with the general sense of fatigue. For example, breathlessness may indicate a cardiovascular or respiratory disease. Abdominal pain might arouse the suspicion of a gastrointestinal disease. Weakness may point to a neuromuscular collagen disease. Excessive thirst and increased urine output may suggest diabetes mellitus, and weight loss may accompany metabolic or endocrinal abnormalities, chronic infections, or cancer.

Whether they have been prescribed by a physician or purchased over the counter, the medications taken regularly by a patient should be reviewed. The doctor should also inquire about alcohol and tobacco use and dietary fads. A thorough physical examination may be required. During an examination, the doctor sometimes uncovers physical signs of fatigue-inducing diseases. Blood tests and other laboratory investigations may also be needed, especially because a physical examination does not always reveal the cause.

Often, however, despite an extensive workup, no specific cause for the persistent fatigue appears. At this stage, the diagnosis of chronic fatigue syndrome should be considered. To fit this diagnosis, patients must have several of the symptoms associated with this syndrome. They must have complained of fatigue for at least six months, and the fatigue should be of such an extent that it interferes with normal daily activities. Since many of the symptoms associated with chronic fatigue syndrome overlap with other disorders, these other fatigue-inducing conditions must be considered and ruled out.

To fit the diagnosis of chronic fatigue syndrome, patients must have at least six of the classic symptoms. These include a mild fever and sore throat, painful lymph nodes in the neck or axilla, unexplained generalized weakness, and muscle pain or discomfort. Patients may describe marked fatigue lasting for more than twenty-four hours that is induced by levels of exercise that would have been easily tolerated before the onset of fatigue. They may suffer from generalized headaches of a type, severity, or pattern that is different from headaches experienced before the onset of chronic fatigue. Patients may also have joint pain without swelling or redness and neuropsychologic complaints such as a bad memory and excessive irritability. Confusion, difficulty in thinking, inability to concentrate, depression, and sleep disturbances are also on the list of associated symptoms.

No one knows the exact cause of chronic fatigue syndrome. Researchers continue to study the disease and come up with hypotheses, though none have proven entirely satisfactory. One theory argues that since patients with chronic fatigue syndrome appear to have a reduced aerobic work capacity, defects in the muscles may cause the condition. This, however, constitutes only one of many theories concerning the syndrome and its origin.

Many patients with chronic fatigue syndrome relate that they suffered from an infectious illness immediately preceding the onset of fatigue. This pattern causes some scientists to suspect a viral origin. Typically, the illness that precedes the patient’s problems with fatigue is not severe, and resembles other upper respiratory tract infections experienced previously. The implicated viruses include the Epstein-Barr virus, Coxsackie B virus, herpes simplex virus, cytomegalovirus, human herpesvirus 6, and the measles virus. It should be mentioned, however, that some patients with long-term fatigue do not have a history of a triggering infectious disease before the onset of fatigue.

Patients with chronic fatigue syndrome sometimes have a number of immune system abnormalities. Laboratory evidence exists of immune dysfunction in many patients with this syndrome, and there have been reports of improvement when immunoglobulin (antibody) therapy was given. The significance of immunological abnormalities in chronic fatigue syndrome, however, remains uncertain. Most of these abnormalities do not occur in all patients with this syndrome. Furthermore, the degree of immunologic abnormality does not always correspond with the severity of the symptoms.

Some researchers believe that the acute infectious disease that often precedes the onset of chronic fatigue syndrome forces the patient to become physically inactive. This inactivity leads to physical deconditioning, and the progression ends in chronic fatigue syndrome. Experiments in which patients with chronic fatigue syndrome were given exercise testing, however, do not support this theory completely. In the case of physical deconditioning, the heart rates of patients with chronic fatigue syndrome should have risen more rapidly with exercise than those without the syndrome. The exact opposite was found. The data were not determined consistent with the suggestion that physical deconditioning causes chronic fatigue syndrome.

A high prevalence of unrecognized psychiatric disorders exists in patients with chronic fatigue, especially depression. According to a 2012 article in American Family Physician, depression affects approximately 39 to 47 percent of chronic fatigue syndrome patients. Yet a critical question remains unanswered concerning chronic fatigue syndrome: Are patients with this syndrome fatigued because they have a primary mood disorder, or has the mood disorder developed as a secondary component of the chronic fatigue syndrome?

No completely satisfactory treatment exists for chronic fatigue syndrome. A group of researchers using intravenous immunoglobulin therapy met with varying degrees of success, but other investigators could not reproduce these results. Other therapeutic trials used high doses of medications such as acyclovir, liver extract, folic acid, and cyanocobalamine. A mixture of evening primrose oil and fish oil was also administered with some degree of success. Claims have also been made that patients administered magnesium sulfate improved to a larger extent than those receiving a placebo. Other therapeutic options include cognitive behavioral therapy, programs of gradually increasing physical activity, analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and antidepressants. Finally, a number of self-help groups exist for chronic fatigue sufferers.

The prognosis and natural history of chronic fatigue syndrome are still poorly defined. Chronic fatigue syndrome does not kill patients, but it does significantly decrease the quality of life for sufferers. For the physician, management of this syndrome remains challenging. In addition to correcting any physical abnormalities present, the physician should attempt to find an activity that interests the patient and encourage him or her to become involved in it.

Perspective and Prospects

Fatigue is generally considered a normal bodily response, protecting the individual from excessive physical and mental activity. After all, the normal levels of performance for individuals who do not rest usually decline. In the case of overactivity, fatigue should be viewed as a positive warning sign. Using relaxation and rest (both mental and physical), the individual can often alleviate weariness and optimize performance.

In some cases, however, fatigue does not derive from physical or mental overactivity, nor does it respond adequately to relaxation and rest. In these instances, it interferes with an individual’s ability to cope with everyday life and enjoy usual activities. The patient begins referring to fatigue as the reason for not participating in normal physical, mental, and social activities.

Unfortunately, physicians, health care professionals, society, and even the patients themselves dismiss fatigue as a trivial complaint. As a result, sufferers seek medical help only after the condition becomes advanced. This dangerous, negative attitude can delay the correct diagnosis of the underlying pathology and threaten the patient’s chances for a quick recovery.

The diagnosis and management of chronic fatigue syndrome prove challenging for both physician and patient. It is important to note that chronic fatigue syndrome often stems from nonmedical causes. While the possibility of a serious medical illness should be addressed, illness-related fatigue usually occurs along with other, more prominent symptoms. The causes of chronic fatigue syndrome are numerous and can take time to define. Patients need to answer all questions related to their complaints as thoroughly and accurately as possible, so that their physicians can reach accurate diagnoses using the minimum number of tests. Extensive testing for rare medical causes of fatigue can become extraordinarily expensive and uncomfortable, so doctors select the tests that they are ordering cautiously. They must balance the benefit, the cost, and the risk of each test to the patient. Such decisions should be based on their own experience and on the available data.

Open communication between the patient and doctor is of paramount importance. It ensures a correct diagnosis, followed by the most effective treatment. Follow-up visits and reassurance may be the best therapy in many cases. Professional counselors can offer assistance with fatigue-inducing psychological disorders. Examination of sleep and relaxation habits can reveal potential problems, and steps can be taken to ensure adequate rest.

Persistent fatigue should not be regarded lightly, and serious attempts should be made to determine its underlying causes. In this respect, it may be appropriate to recall one of Hippocrates’ aphorisms, “Unprovoked fatigue means disease.”

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Wilson, James L. Adrenal Fatigue: The Twenty-first Century Stress Syndrome. Petaluma, Calif.: Smart, 2004. Print.

Yancey, Joseph R., and Sarah M. Thomas. "Chronic Fatigue Syndrome: Diagnosis and Treatment." American Family Physician 86, no. 8 (October 15, 2012): 741–746.

Zgourides, George D., and Christie Zgourides. Stop Feeling Tired! Ten Mind-Body Steps to Fight Fatigue and Feel Your Best. Oakland: Harbinger, 2003. Print.

What are viral hemorrhagic fevers?

Causes and Symptoms

Viral hemorrhagic fevers are caused by a variety of viruses, including
members of the Arenaviridae, Bunyaviridae, Flaviviridae, and Filoviridae families, with the last mentioned being the one associated with diseases such as Ebola hemorrhagic fever and Marburg hemorrhagic fever. Many of the hemorrhagic diseases are zoonoses
that exist in reservoir species, such as bats, and are transmitted to humans through various modes; others are vector-borne. Crimean-Congo hemorrhagic fever, for example, is carried by ticks; humans become infected when they are bitten. In contrast, Ebola hemorrhagic fever, caused by a filovirus, is suspected of making the leap from animals to humans through the handling and eating of infected wild game, while Lujo fever, which is caused by an arenavirus, apparently infects humans when they inhale dust from rodent droppings. However, some viral hemorrhagic fevers may have the ability to aerosolize and thus may be transmitted person-to-person from an infected patient to caregivers or family members when an infected person sneezes or coughs. Contact with body fluids, such as blood or vomit, from an infected person can also cause the disease to spread.

The initial clinical signs and symptoms for viral hemorrhagic fevers are similar to those of many common illnesses, such as influenza or dysentery, with the patient complaining of a fever, headache, generalized aches and pains, or nausea. In the case of Ebola hemorrhagic fever, clinical signs may include a skin
rash or red eyes. It is usually not until several days after the onset of the illness that the hemorrhagic signs, such as bloody diarrhea indicating internal bleeding, appear. Because the symptoms for many hemorrhagic fevers are similar to those of common tropical diseases, initial diagnosis and quarantine efforts may be delayed.

The virulence of the hemorrhagic fevers varies, depending both on the specific viral strain involved and how quickly medical treatment is obtained. Despite the name hemorrhagic fever, it is rarely the blood loss associated with the diseases that causes death but instead the failure of organs such as the kidneys. Some Ebola hemorrhagic fevers have resulted in death rates of close to 90 percent of infected patients, while others have been as low as 20 percent. Similarly, incubation periods vary for the different diseases, from only a few days for some diseases to as long as three weeks for others. The best-known hemorrhagic fever, Ebola, has an incubation period of two to twenty-one days.

Treatment and Therapy

Treatment for viral hemorrhagic fever varies from disease to disease. In many cases, the only care that can be given is that of relieving the suffering of the patient by treating the symptoms—giving liquids intravenously to replace fluids lost through vomiting or diarrhea, trying to keep electrolytes balanced, and giving drugs that may reduce the patient’s fever or body aches. In some cases, patients have been successfully treated with blood transfusions from persons who have survived a similar illness.

Because the exact transmission routes for many hemorrhagic fevers remain unclear, once patients are diagnosed, a strict quarantine must be instituted, with health care workers and family members alike wearing protective clothing to prevent becoming contaminated with any infectious material. When a patient dies, the body must also be handled carefully. In the case of Ebola, the World Health Organization (WHO) recommends burial or cremation as quickly as possible following death.

Perspective and Prospects

As the population has expanded globally and humans have encroached upon formerly isolated wildlife habitats, more viral hemorrhagic fevers have been discovered, sometimes through the case of just one or two persons becoming infected by a previously unknown pathogen and sometimes through devastating outbreaks resulting in many deaths. Despite many years of research, many of these diseases still remain scientific mysteries.

The best-known example, Ebola hemorrhagic fever virus, exists in multiple locations in Africa. Some strains are comparatively mild; some are extremely virulent, spreading quickly and causing high numbers of deaths within a population. Researchers now know that, as is true with many viruses, patients who have been infected by Ebola and survive retain antibodies to that strain of virus for decades. They do not yet know if that means those people are effectively immune to Ebola.

Theoretically, it should be possible to develop vaccines against the viral hemorrhagic diseases, but several factors mitigate such work. First is the reality that although many can be quite devastating in terms of death rates, outbreaks that have occurred to date have been in remote areas or have affected very low numbers of persons. It is easy to argue for funding vaccine research work when a disease is widespread, as in the historical example of polio; it becomes much more difficult for researchers when the disease in question is localized in a nonindustrialized country such as the Sudan or Uganda. In recent years, the threat of viruses such as Ebola being utilized for bioterrorism, however, has led to more effort being put into finding effective vaccines and treatments, but for most of the viral hemorrhagic diseases any vaccines or treatments developed to date remain classified as experimental.

Bibliography

"Ebola Haemorrhagic Fever." World Health Organization, Aug. 2012.

"Hemorrhagic Fevers." MedlinePlus, May 20, 2013.

"Haemorrhagic Fevers, Viral." World Health Organization, Jan. 2013.

Hewlitt, Barry S., and Bonnie L. Hewitt. Ebola, Culture, and Politics: The Anthropology of an Emerging Disease. Belmont, Calif.: Thomson Higher Education, 2008.

Shors, Teri. Understanding Viruses. 2d ed. Sudbury, Mass.: Jones and Bartlett, 2013.

Strauss, James H., and Ellen G. Strauss. Viruses and Human Disease. 2d ed. San Diego, Calif.: Academic Press, 2008.

"Viral Hemorrhagic Fevers." Centers for Disease Control and Prevention, Nov. 22, 2011.

What are diverticulitis and diverticulosis?

Causes and Symptoms

Diverticulosis is an acquired condition of the colon that involves a few to hundreds of blueberry-sized outpouchings of its wall, called diverticuli. Diverticular disease is usually manifested by the presence of multiple diverticuli that are at risk of causing abdominal pain, inflammation, or bleeding.

Although the wall of the colon is thin, microscopically it has four layers. The innermost layer is called the mucosa. Its main function is to absorb fluids from the substance entering the colon, turning it into a semisolid material called feces. Outside the mucosa is the submucosa, a layer that contains blood vessels as well as nerve cells that control the functions of mucosal cells. Outside the submucosa is the muscularis, which contains muscle cells that are able to contract, pushing feces along the colon and eventually out through the rectum. Outside the muscularis is the serosa, which forms a wrap around the colon and helps prevent infections in this organ from spreading beyond its walls.

The diverticuli that form in the colon are not true diverticuli, in that the entire wall is not present in the outpouching. Only the mucosal and submucosal layers pouch out through weakened areas in the muscularis layer. When examined by the naked eye, however, it appears as if the entire wall of the colon is involved in the tiny outpouching. The mucosa bulges out in the part of the colonic wall that is weakened; this is where arteries penetrate through clefts in the muscularis.

The large intestine begins with the cecum, which is connected to the small intestine. The cecum is a pouch leading to the colon, whose components are the ascending, transverse, descending, and sigmoid colon. The sigmoid colon leads to the rectum, which is connected to the outside of the body by the anal canal. Although diverticuli can appear at a variety of locations in the
gastrointestinal (GI) tract, they are usually located in the colon, most commonly in the sigmoid colon.

The most common form of diverticulosis is called spastic colon diverticulosis, which is a condition involving diverticuli that develop when the lumen (cavity) of the sigmoid colon is abnormally narrowed. Since the circumference of the colon alternately narrows and widens along its length, muscle contractions may result in local occlusions of the lumen at the narrowed sections. Occlusion may cause the lumen of the colon to become multiple, separate chambers. When this happens, the pressure within the chambers can increase to the point where the mucosa herniates out through small clefts in the muscularis, creating diverticuli.

Most people with diverticulosis never notice it. When abdominal pain related to painful diverticular disease develops, it is felt in the lower abdomen and may last for hours or days. Eating usually makes it worse, whereas passing gas or having a bowel movement may relieve it.

Besides causing abdominal pain, diverticuli may cause rectal bleeding, which may vary from mild to life threatening. Usually, there is a sudden urge to defecate followed by passage of red blood, clots, or maroon-colored stool. If the stool is black, the bleeding is probably from the upper GI tract.

Since the colon may be studded with multiple diverticuli, and the bleeding may stop by the time of evaluation, it is often difficult to tell which one bled. Diverticulosis is most common in elderly people, who may have other conditions of the colon that are associated with bleeding. Therefore, it is often impossible to confirm that the cause of bleeding was diverticular disease—even if the colon is lined with hundreds of diverticuli.

What is most important is to establish what part of the GI tract is bleeding. To find out if the bleeding could have come from the upper GI tract, a tube is passed through the nose into the stomach, and the contents are aspirated. If blood is not present, this suggests lower GI bleeding. In addition, the esophagus, stomach, and upper small intestine can be visualized with a flexible, snakelike instrument called an endoscope to exclude a source such as a bleeding ulcer.

It is more difficult to examine the lower GI tract. The simplest procedure is anoscopy, by which the physician can examine the inside of the anal canal for hemorrhoids. Proctosigmoidoscopy, a procedure similar to endoscopy, offers a view of the rectum and part of the sigmoid colon. It may reveal diverticuli or other lesions such as a bleeding growth called a polyp. Colonoscopy is most easily performed after bleeding has stopped. It requires cleaning out the contents of the colon and then inserting a long, flexible instrument called a colonoscope all the way to the cecum. The entire lining of the colon can be visualized while withdrawing the colonoscope.

Angiography
is a test done in the radiology department; it involves injecting dye into the vessels that lead to the colon. If there is active bleeding, it can help localize the source. Even if the bleeding has stopped, this procedure can sometimes identify abnormal blood vessel formations suggestive of cancer or a blood vessel abnormality called angiodysplasia.

Between 10 and 25 percent of people with diverticulosis suffer from one or more episodes of diverticulitis, which is an inflammatory condition that may progress to an infection. Initially, feces may become trapped and inspissated (thickened) in a diverticulum, irritating it and leading to inflammation. Inflammation is a tissue response to injury that involves local reactions that attempt to destroy the injurious material and begin the healing process. It is usually the first step in the body’s attempt to prevent infection and involves the migration of white blood cells out of blood vessels and into tissues, where they begin to fight off bacteria. The white blood cells release enzymes that cause tissue destruction. Because it is thin, the wall of the diverticulum may develop a tiny perforation.

Feces are made up of waste material and bacteria that normally do not cause problems when confined within the lumen of the colon. When a diverticulum perforates, however, they travel outside the colon and into other regions such as the peritoneal cavity, causing an infection. This infection along the outside of the colon is often limited, because many adjacent structures are able to wall off the bacteria, limiting their ability to extend through the peritoneal cavity. Although they become sealed off, they often form a pus-filled lesion called an abscess.

Fever and abdominal pain are the most common symptoms of diverticulitis. The fever may be high and associated with shaking chills. The pain is often sudden in onset, is often continuous, and may radiate from the left lower abdomen to the back. Laboratory findings usually include an elevated white blood cell count, a nonspecific finding that occurs with a variety of infections.

Radiographic studies are helpful for diagnosing and assessing the severity of diverticulitis. For example, a computed tomography (CT) scan can detect diverticuli or a thickening of the bowel wall associated with diverticulitis and can help assess whether abscesses are present.

Treatment and Therapy

There are two treatment goals in treating uncomplicated, painful diverticular disease: prevention of further development of diverticuli and pain relief. It is important to understand that the pressure that is able to develop inside the lumen of the colon is inversely related to the radius of the lumen. Therefore, if the lumen’s radius can be increased, the pressures within the lumen will lessen, theoretically decreasing the chance of diverticuli formation. One key to increasing the radius of the lumen of the colon is to increase the bulk of the stool by the addition of dietary
fiber.

A Western diet tends to be high in fiber-free animal products, and many foods that would ordinarily contain fiber, such as bread, lose much of their fiber during processing. This low-fiber diet may contribute to diverticulosis, which is prevalent in countries that have low-fiber diets. The typical American diet contains an average of ten to fifteen grams of fiber per day, whereas diets from regions such as Africa and Asia contain significantly more fiber. A high-fiber diet can increase stool bulk by 40 to 100 percent. Fiber adds bulk to the stool because it acts like a sponge, retaining water that would normally be reabsorbed by the colonic mucosa. Fiber also increases stool bulk because 50 to 70 percent of the fiber is degraded by the bacteria in the colon, and the products of degradation attract water by a process called osmosis.

The main fibers that increase stool bulk are the water-insoluble fibers, such as cellulose, hemicellulose, and lignin; they are derived from plants such as vegetables and whole-grain cereals. Diets high in these fibers have been shown to decrease the intraluminal pressure in the sigmoid colon as well as to relieve the pain associated with uncomplicated diverticular disease. Some research has suggested that adding ten to twenty-five grams per day of coarse, unprocessed wheat bran to various liquid and semisolid foods may provide the best results. The sudden addition of large amounts of bran to one’s diet, however, may cause bloating. Commercial preparations such as methylcellulose may be better tolerated during the first few weeks of therapy; their use may then be tapered off as bran is added to the diet. There are also various antispasmodic drugs available for inhibiting the muscle spasms of the colon, but many are not very effective for decreasing symptoms.

For diverticular bleeding, the most effective therapy is patience. Most episodes stop on their own, and conservative treatments such as maintaining the patient’s blood volume with intravenous fluids and possibly performing blood transfusions are all that is necessary. In those patients with continued active bleeding and in whom the source of the bleeding can be identified with angiography, a drug called
vasopressin may be administered into the artery over several hours. This causes constriction of the vessel and stops bleeding most of the time. Once the vasopressin is stopped, however, patients may resume bleeding.

If vasopressin fails, surgery may be necessary. Surgery is most often successful if the bleeding site has been well localized before the operation. In that case, only the involved segment of the colon needs to be removed. If the bleeding site cannot be identified, it may be necessary to remove a majority of the colon; this procedure is associated with a higher rate of postoperative complications.

Diverticulitis that warrants hospitalization is initially treated with intravenous antibiotics for seven to ten days. Antibiotics help prevent many patients from needing surgery. Most of those who respond to antibiotics will not have future attacks severe enough to warrant hospitalization.

Other measures may be necessary for the care of someone with diverticulitis, because the inflammation around the colon may be associated with problems such as narrowing of the bowel lumen to the point where it causes a partial or complete colonic obstruction. In this case, nothing should be given by mouth, and a tube should be passed through the nose into the stomach in order to suck out air and the stomach contents. This suction helps to reduce the amount of material that can pass through the colon and worsen the dilation of the colon that occurs proximal to the obstruction.

If the fever persists for more than a few days, the diverticulitis may be associated with complications. One complication is the formation of a large
abscess outside the colon, which may be detected by a CT scan. An abscess has a rim around it that makes it difficult for antibiotics to penetrate the liquid center. If it does not go away despite antibiotic therapy, surgery may be necessary. If the abscess is small, it is possible to remove the involved segment of bowel and reattach the two free ends. If the abscess is very large, it may be necessary first to drain the abscess and then to cut across the colon proximal to the diseased segment, attaching the free end of the proximal segment to the abdominal wall, a procedure called a diverting colostomy. Later, the diseased segment of colon can be removed, and the remaining two free ends of colon can be joined. Another option is to drain the abscess with the aid of visual guidance by the CT scan and then operate on the colon. Draining the abscess in this manner helps get the infection under control before surgery is performed. Other indications for surgery in diverticulitis include complications such as a persistent bowel obstruction. In this case, it is often necessary to use a two-stage approach rather than cure the problem in one operation.

Another complication of diverticulitis is a generalized infection of the peritoneal cavity, called
peritonitis. Surgery for peritonitis involves removing the leaking segment of bowel and attaching the remaining two free ends of the colon to the abdominal wall. In addition, the peritoneal cavity is rinsed with a sterile solution in an attempt to clean out the contaminating materials.

Diverticulitis may also be complicated by the presence of a perforation of a diverticulum leading to a fistula, an abnormally existing channel connecting two hollow organs. When there is a fistula between the colon and the bladder, stool can travel into the bladder. The bacteria in the stool can cause severe, recurrent urinary tract infections. Another symptom is that bowel gas gets into the bladder; when the patient urinates, there is an intermittent stream because of colonic gas being passed along with the urine. When a fistula exists, it is necessary to remove the diseased segment of colon, the fistula tract, and a small portion of the bladder where the tract entered it.

Even if a patient with diverticulitis seems to improve and is able to return home from the hospital without needing surgery, there is still a chance that surgery will be necessary in the future. Surgery may be needed if the patient continues to have repeated, severe attacks of diverticulitis or if a fistula between the colon and bladder causes recurring urinary tract infections. Another reason for surgery is persistent partial colonic obstruction and no possibility of inspecting the narrowed region of colon to exclude a constricting cancerous lesion as the cause of the obstruction.

Perspective and Prospects

Diverticuli are quite common in the United States and other countries in which much of the population tends to eat processed, low-fiber foods. Although residents of countries where a high-fiber diet is common tend to have a low prevalence of diverticulosis, their risk of developing this disease increases within ten years of moving to a country with a low-fiber diet. The prevalence of diverticulosis and diverticulitis appears to be increasing. For example, before 1900, colonic diverticuli were considered a curiosity in the United States, whereas by the early twenty-first century, they were found in more than half of Americans over the age of sixty. There are a few possible explanations for why this increasing prevalence is seen.

First, the change in the American diet probably plays a large part in the pathogenesis of diverticular disease. Fiber consumption may have fallen off by as much as 30 percent during the twentieth century. Many people in the United States eat foods such as quick-cooking rice, highly processed cereals, and processed flour, all of which contain less fiber than their unprocessed counterparts. In addition, the population tends to eat more fats and proteins and fewer carbohydrates. Many fibers are from food sources rich in carbohydrates and are carbohydrates themselves.

The increasing prevalence of diverticular disease may also be attributable to the changing survival pattern. The average life expectancy in the United States rose significantly over the course of the twentieth century, and the proportion of people over sixty-five has likewise risen. Thus, the American population is not only growing but also getting older. Since diverticulosis is seen in increasing frequencies with aging, it is understandable that more of it was seen in the late twentieth century and early twenty-first century than during the early twentieth century.

Another reason for the increase in the prevalence of diverticular disease could be improvements in detection. Now it is detected not only at autopsy but also by barium enema, during sigmoidoscopy, and during surgery. Thus, there are more opportunities for discovering diverticulosis.

Bibliography

Achkar, Edgar, Richard G. Farmer, and Bertram Fleshler, eds. Clinical Gastroenterology. 2d ed. Philadelphia: Lea & Febiger, 1992.

A.D.A.M. Medical Encyclopedia. "Diverticulitis." MedlinePlus, April 16, 2012.

A.D.A.M. Medical Encyclopedia. "Fiber." MedlinePlus, August 14, 2012.

Feldman, Mark, Lawrence S. Friedman, and Lawrence J. Brandt, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. New ed. 2 vols. Philadelphia: Saunders/Elsevier, 2010.

Ganong, William F. Review of Medical Physiology. 23d ed. New York: Lange Medical Books/McGraw-Hill Medical, 2009.

International Foundation for Functional Gastrointestinal Disorders. "Diverticula, Diverticulosis, Diverticulitis: What's the Difference?" International Foundation for Functional Gastrointestinal Disorders, January 17, 2013.

Kapadia, Cyrus R., James M. Crawford, and Caroline Taylor. An Atlas of Gastroenterology: A Guide to Diagnosis and Differential Diagnosis. Boca Raton, Fla.: Pantheon, 2003.

Kumar, Vinay, et al., eds. Robbins Basic Pathology. 8th ed. Philadelphia: Saunders/Elsevier, 2007.

National Digestive Diseases Information Clearinghouse. "Diverticulosis and Diverticulitis." National Institutes of Health, February 21, 2012.

Peikin, Steven R. Gastrointestinal Health. Rev. ed. New York: Quill, 2001.

Tortora, Gerard J., and Bryan Derrickson. Principles of Anatomy and Physiology. 12th ed. Hoboken, N.J.: John Wiley & Sons, 2009.

Wood, Debra. "Diverticulitis." HealthLibrary, March 5, 2013.

What is rat-bite fever? |

Definition

Rat-bite fever (RBF) is an infectious disease caused by two strains of
bacteria, Streptobacillus moniliformis
and Spirillum minus
. The bacteria are spread through the bite of rodents or through the
secretion of rodent fluids.

Causes

RBF primarily develops when rats bite or scratch humans, but infection can also occur simply by touching live or dead rats and by being exposed to secretions from their eyes, nose, or mouth. Additionally, cleaning rat cages and coming in contact with rat urine or feces can cause RBF. Living in rat-infested environments, such as impoverished areas, often leads to RBF, inadvertently ingesting food or water contaminated with rat feces or urine. Breathing in desiccated particles of rat feces may also result in RBF. Gerbils, squirrels, and weasels also carry RBF; furthermore, animals that hunt and ingest rodents, such as cats and dogs, may also infect humans with RBF through a bite, scratch, or secretions.

Risk Factors

Those who live in rat-infested environments are at greatest risk for RBF. Persons living in Asian countries, such as Japan, where the farming of rice attracts large numbers of rats, are more likely to be infected. However, RBF is also present in impoverished North American cities, which often provide a haven for rodent populations. Sanitation and sewage workers are also at high risk of RBF because of daily rodent contact. Laboratory staff are equally vulnerable to RBF because they regularly handle rats and clean their cages; pet store staff are also susceptible to RBF because of increased exposure to pet rats.

Symptoms

Symptoms of RBF include a rash, headache, chills, fever, vomiting, swelling of
the lymph
nodes, skin irritation, wounds that do not heal, and muscle,
joint, and back pain. In particular, the area around the rat bite sometimes
becomes reddish purple and swollen and ulcerated.

Screening and Diagnosis

After a physical examination, blood and culture tests are performed to confirm
a diagnosis of RBF. The tests determine if S. moniliformis or
S. minus bacteria are in the person’s blood, skin, joint
fluid, or lymph nodes. Polymerase chain reaction tests and
blood antibody tests aid in the diagnosis of RBF.

Treatment and Therapy

RBF can be treated successfully in early stages of the disease with seven to
fourteen days of antibiotics, primarily penicillin,
doxycycline, and erythromycin. If left untreated, RBF is extremely dangerous and
can damage the heart, brain, and other vital organs; it can sometimes lead to death.

Prevention and Outcomes

Avoiding rat-populated environments is the best way to prevent RBF; however, if
contact with rats cannot be avoided, one should always wear gloves when handling
them or their droppings; one should also wash his or her hands often. Persons who
have been bitten by a rat should treat the wound with antiseptic immediately to
help prevent infection and should contact a physician for further
care.

Bibliography

Dvorak, Glenda, Anna Spickler, and James Roth. Handbook for Zoonotic Diseases of Companion Animals. Ames: College of Veterinary Medicine, Iowa State University, 2008.

Gratz, Norman. The Vector- and Rodent-Borne Diseases of Europe and North America: Their Distribution, Public Health Burden, and Control. New York: Cambridge University Press, 2006.

Hayashimoto, N., et al. “Isolation of Streptobacillus moniliformis from a Pet Rat.” Journal of Veterinary Medical Science 70 (2008): 493-495.

Peters, C. J. “Infections Caused by Arthropod- and Rodent-Borne Viruses.” In Harrison’s Principles of Internal Medicine, edited by Joan Butterton. 17th ed. New York: McGraw-Hill, 2008.

Suckow, Mark, Steven Weisbroth, and Craig Franklin. The Laboratory Rat. 2d ed. Burlington, Mass.: Academic Press/Elsevier, 2006.

What are some of the concerns shown by Steinbeck in the story "The Chrysanthemums"?

Elisa has a decent husband. He is steady and a good provider. So, Elisa has no real concerns about money or stability. However, as a result of her encounter with the stranger, she realizes that her life lacks any sense of romance or adventure. Her marriage and her role in that marriage are quite traditional. So, her desire for something more emerges as a feminist theme in that she dreams of something more than her...

Elisa has a decent husband. He is steady and a good provider. So, Elisa has no real concerns about money or stability. However, as a result of her encounter with the stranger, she realizes that her life lacks any sense of romance or adventure. Her marriage and her role in that marriage are quite traditional. So, her desire for something more emerges as a feminist theme in that she dreams of something more than her limited role will allow. When the stranger says he will take some of her chrysanthemums to a woman down the road, Elisa is very excited. Even if she can not get away from her routine life, she takes some solace in the knowledge that her flowers will. 

Elisa actually divulges her desire to escape and live more adventurously. Speaking to the stranger, she says: 

I've never lived as you do, but I know what you mean. When the night is dark—why, the stars are sharp-pointed, and there's quiet. Why, you rise up and up! Every pointed star gets driven into your body. It's like that. Hot and sharp and—lovely. 

Her description is about life on the road, but the language is laden with sexual connotations. The phrase "driven into your body" is clearly sexual. So, here she is conflating sex, romance, and an adventurous life. Her main concern following the encounter with the stranger is how to address this urge for something more. When Henry takes her out, she sees the chrysanthemums along the side of the road and this symbolically suggests that she can not escape from her traditional role. The story ends with Elisa trying to hide the fact that she's crying. 

What is epididymitis? |

Definition

Acute epididymitis is an
inflammation of the epididymis. This is a structure shaped like a tube that surrounds and attaches to each testicle. The epididymis helps transport and store sperm cells.

Chronic epididymitis causes pain and inflammation in the epididymis. There is often no swelling of the scrotum. Symptoms can last six weeks or more, but this type is less common.

Causes

Epididymitis is most often caused by bacterial infections such as those of
the urinary tract, by sexually transmitted diseases (STDs)
such as chlamydia and gonorrhea, by infection of the urethra
(urethritis), by infection of the prostate (prostatitis),
and by tuberculosis. Other causes include injury, viral infections
such as mumps, genital abnormalities, treatment with the heart rhythm drug
amiodarone (cordarone), and chemotherapy to treat bladder cancer.

Risk Factors

Risk factors for epididymitis include infection of the genitourinary tract (bladder, kidney, prostate, or testicle), narrowing of the urethra, use of a urethral catheter, infrequent emptying of the bladder, recent surgery or instrumentation of the genitourinary tract (especially prostate removal), birth disorders of the genitourinary tract, unprotected sex, and disease that affects the immune system. Most at risk are boys and men ages fifteen to thirty years and men older than age sixty years.

Symptoms

Symptoms usually develop within a day and include pain in the testes; sudden redness or swelling of the scrotum; hardness, a lump, or soreness (or all three) in the affected testicle; tenderness in the nonaffected testicle; groin pain; chills; fever; inflammation of the urethra; pain during intercourse or ejaculation; pain or burning, or both, during urination; increased pain while having a bowel movement; lower abdominal discomfort; discharge from the penis; and blood in the semen.

Screening and Diagnosis

A doctor will ask about symptoms and medical history and will perform a physical exam. Tests may include a urinalysis to check for a high white blood cell (WBC) count and the presence of bacteria; a urine culture to identify the type of bacteria present; a culture of discharge from the penis; a blood test to measure the white blood cell count (WBC); and an ultrasound (a test that uses sound waves to examine the scrotum).

Treatment and Therapy

Treatment is essential to prevent the infection from worsening. Treatment may
include bed rest. The patient should stay in bed to keep the testicles from moving
and to promote healing. Bed rest might be necessary until the swelling subsides.
Another treatment is antibiotics, prescribed for bacterial
infections. If the patient has an STD, his partners will also need treatment.
Another treatment is oral anti-inflammatory medication, which includes drugs such
as ibuprofen, to help reduce swelling.

The patient may need to wear an athletic supporter for several weeks. Taking baths can ease the pain and help relieve swelling. One should not have sex until treatment is completed. Finally, surgery may be needed in severe cases that return.

Prevention and Outcomes

To help decrease the risk of developing epididymitis, one should practice safer sex. One can protect against STDs by using condoms. Finally, one should empty one’s bladder when feeling the need to do so.

Bibliography

Centers for Disease Control and Prevention. “Sexually Transmitted Diseases Treatment Guidelines 2010.”Available at http://www.cdc.gov/std/treatment/ 2010.

Lunenfeld, Bruno, and Louis Gooren, eds. Textbook of Men’s Health. Boca Raton, Fla.: Parthenon, 2007.

National Institutes of Health. “Men’s Health.” Availableat http://health.nih.gov/category/menshealth.

Schrier, Robert W., ed. Diseases of the Kidney and Urinary Tract. 8th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2007.

Simon, Harvey B. The Harvard Medical School Guide to Men’s Health. New York: Free Press, 2004.

Who is responsible for red tape in management? Why is it only seen in bureaucratic organizations?

In essence there are two questions here:

1) Who in management is responsible for "red tape" in a bureaucratic organization, and

2) Why is "red tape" only prevalent in bureaucratic organizations, and not in other types of organizations such as scientific or administrative ones (even though formal procedures are often used in those types of organizations as well)?

First, note that "red tape" is in quotes, as it is a form of jargon.  Merriam-Webster defines...

In essence there are two questions here:

1) Who in management is responsible for "red tape" in a bureaucratic organization, and

2) Why is "red tape" only prevalent in bureaucratic organizations, and not in other types of organizations such as scientific or administrative ones (even though formal procedures are often used in those types of organizations as well)?

First, note that "red tape" is in quotes, as it is a form of jargon.  Merriam-Webster defines it as:

"official routine or procedure marked by excessive complexity which results in delay or inaction."

As such, it is generally thought of as a pejorative.  The key to the question is in the idea of complexity which is "excessive" relative to the desired outcome or purpose of the task.  Quite simply, what is excessive to one person may make perfect sense to another, so the existence of red tape is often the perception on the part of the person being delayed or frustrated.  For example, to a builder who wants to drain a tidal pool and build a new high rise apartment, the number of studies and permits required, often by multiple entities, may seem like red tape.  However, to the people whose interests are being protected by those studies and permits, they are important and add value.

That being said, people on both sides of an issue will generally agree that red tape exists when the process of addressing and balancing these competing interests could be more efficient and transparent.  In other words, you minimize red tape by engineering the process to require minimum time and minimum expense on all sides, by making the need for each step clear, and by making the required steps easy to understand and comply with.

The association between red tape and governmental organizations (bureaucracies) is common usage, but red tape can be perceived in any type of organization, consistent with the principles above.  However, it is generally believed that governmental bureaucracies evolve red tape, because they are not subjected to market disciplines which for other types of organizations motivate them to be efficient and transparent.  This leads to another principle, namely, that the more insulated a function is from market-type interactions, and therefore the more arbitrary power it wields over its "customers," the easier it is for it to survive despite being inefficient and/or non-transparent (opaque).  Further reading in this regard should be directed to areas of market economics and forms of economic organization.

With reference to the ways Steinback presents Slim in Of Mice and Men, show how far you agree that he is someone to be admired.

Slim is the one character in Of Mice and Men who seems to have it all. He is a good listener, an excellent thinker and a great problem solver. His energy is above the negative and miserable essence that all the other characters give out; this is perhaps because Slim's outlook in life is naturally positive, making him a much needed light in the middle of the dark, silent and sad life in the ranch. 

As far as his job goes, we learn that Slim is the jerkline skinner, which is the top mule rider on the ranch. However, Steinbeck has special words with which to describe Slim, to whom he dubs 

The prince of the ranch

Steinbeck uses this descriptor to specify how far above Slim is, mentally, spiritually, and even physically, from the other men. He is the "go-to" problem solver and he mentor of these lost souls. Steinbeck also describes Slim's personality as quite unique in comparison to the others

There was a gravity in his manner and a quiet so profound that all talk stopped when he spoke. His authority was so great that his word was taken on any subject….

Moreover, Slim is respected by Curley, who does not dare to even come close to confront Slim, even when he believes that his wife is interested in the farmer. Slim's presence is strong enough to scare off a bully like Curley, and as such, he defends the others in the same manner. 

All this being said, Slim is literally the knight of the farm. He defends others, communicates effectively with everyone, and uses his power to help and make the best out of the dire circumstances in Soledad. He is, in every way, someone to be admired. 

What is sickle cell disease?

Causes and Symptoms

Sickle cell disease is a genetic disorder of hemoglobin, which gives the red color to blood. The hemoglobin
molecule is made up of two pairs of globin polypeptide chains (two α chains and two β chains) and four heme molecules containing iron. Normal hemoglobin (hemoglobin A) is a remarkable protein that changes the biophysical configuration of its amino acid chains so that it can deliver oxygen safely to the tissues without oxidizing iron. Oxygen removal occurs during each cycle of blood flow from the lungs to the tissues. Sickle hemoglobin has a single amino acid substitution of valine for glutamic acid at the sixth position from the end of the β chain. Sickle hemoglobin has the unfortunate propensity to condense as rods in red blood cells when the oxygen is removed during the normal circulation of the blood. These rods distort the cells, making them stiff and rigid and unable to transverse the smaller blood vessels rapidly. The result is vasocclusion (obstruction) of the small and medium-sized blood vessels, damaging the endothelial inner lining of the blood vessel and thereby resulting in tissue necrosis (ischemia).

The most common genotypes of sickle cell disease are sickle cell anemia, or homozygous sickle cell disease (SS disease); sickle cell hemoglobin C disease (SC disease); sickle cell β0
thalassemia (Sβ0
thalassemia); and sickle cell β0 thalassemia (Sβ0 thalassemia). Less common genotypes include sickle cell hemoglobin E disease (SE disease), sickle cell hemoglobin D Los Angeles (SD Los Angeles), and sickle cell hemoglobin O Arab (SO Arab). In addition to these conditions, more than four hundred other abnormal human hemoglobins can combine with sickle hemoglobin. This genetic heterogeneity accounts for the wide spectrum of clinical severity in patients with sickle cell disease, with some forms essentially asymptomatic, such as Hb SE or S deer lodge.

Sickle cell anemia
(SS disease) is the most common and the most severe form of sickle cell disease. It results from the inheritance of the sickle cell gene from both parents. Its hallmark clinical manifestations are anemia and severe episodes of pain; similar but less frequent manifestations are seen with other forms of sickle cell disease. In sickle cell anemia, anemia is caused by the rapid destruction of the red blood cells as they circulate because of a shortened peripheral survival time of less than 30 days (normal is 120 days).

Acute painful episodes—particularly in the older child, adolescent, or adult—are characteristic of sickle cell anemia. Sickle cell crisis often begins with pain in the abdomen or extremities and joints. Painful sickle crisis in the young child is usually precipitated by an acute fever, with excruciatingly tender swelling of the hands and feet (dactylitis) caused by small infarctions of the small growing bones of the hands and feet. Approximately 25 percent of SS patients have endless and repeated painful episodes throughout life requiring frequent hospital care.

The clinical course of sickle cell anemia involves intermittent episodes of acute painful illnesses interspersed with periods of clinical quiescence and relative well-being. Commonly occurring acute complications necessitating intensive medical care are septicemia and meningitis during childhood, recurrent sickle cell pain crises, cerebral infarction with stroke, acute chest
syndrome (often termed pneumonia), severe upper respiratory tract infections, gallbladder disease with gallstones, aplastic crisis, hypersplenism with splenic sequestration crisis, bone infarctions, priapism (a painful erection of the penis not associated with sexual desire), and pyelonephritis (infection of the kidney).

An increased incidence of invasive infections caused by the bacteria
Streptococcus pneumoniae is found in children with SS disease who are between the ages of four months and five years; this is thirty to one hundred times that which would be expected in a healthy population of the same race and age. Blood infections in SS infants and young children are associated with a rapid elevation of temperature, often to 104 degrees Fahrenheit, and the patient becomes even more anemic. In the untreated patient, death occurs within eight to twelve hours.

Chronic major organ failure in SS disease is the direct consequence of irreversible and ongoing damage to the endothelial lining of the small blood vessels as a result of sickle cells (sickle vasculopathy). Vascular damage begins years before the overt clinical symptoms are apparent. The spleen is the first organ to be destroyed, usually by five years of age. During childhood (three to ten years of age), 10 percent of children with this disease will have strokes
, with resulting severe brain damage. Strokes cause paralysis and weakness of the extremities and difficulties in learning. This devastating complication in young children often makes functioning in school or living as self-sustaining adults difficult. Brain
infarction can be accurately identified using computed tomography (CT) brain scans, magnetic resonance imaging (MRI), positron emission tomography (PET), and other diagnostic procedures. Sickle
vasculopathy eventually culminates in young adulthood as end-stage kidney failure (glomerulosclerosis), sickle chronic restrictive lung disease, intracranial hemorrhages and brain damage, retinopathy with blindness, disabling leg ulcers, and painful generalized osteonecrosis of many of the bones of the body. Specialized medical care is required for the diagnosis and management of these permanent incurable complications.

Treatment and Therapy

Most acute complications of SS disease can be treated successfully so that the patient can attend school, be involved in social activities, and have a pleasant childhood and adolescence. Intensive care units with sophisticated monitoring equipment that are dedicated to infants and young children can manage and maintain the vital function of patients during severe illness episodes.

The institution of appropriate immunization programs for children with sickle cell anemia has substantially decreased their mortality and morbidity throughout the world. The importance of preventing the usual childhood infectious diseases such as hepatitis, whooping cough (pertussis), red measles (rubeola), rubella (German measles), diphtheria, tetanus, mumps, poliomyelitis, and Hemophilus influenzae
septicemia allows 90 percent of these children to reach adulthood. The use of prophylactic antibiotics such as penicillin during young childhood (four months to five years) decreases the incidence of invasive pneumococcal blood infections. However, a recent ominous increase has been seen in penicillin resistance to pneumococcal serotype-specific strains, making prophylactic antibiotic prevention less effective. Salmonella contamination of chicken is still a major source of septicemia and salmonella
osteomyelitis (bone infection).

Over time, children with sickle cell disease and their families begin to recognize the things that may precipitate a painful sickle cell crisis. Severe episodes require hospitalization and analgesic treatment, often with narcotic agents in addition to intravenous fluids.

Perspective and Prospects

Sickle cell anemia is the prototypical molecular disease. The causative gene modifying the chemical structure of the hemoglobin β chain (βA to βS)—replacing the amino acid glutamic acid with valine—originated in Africa. The disorder was transmitted to the United States, Arabia, Europe, and South and Central America as part of the slave trade. At that time, healthy persons carrying the sickle gene, who are said to have sickle cell trait, survived the rigors of a slave ship. As persons carrying the sickle cell trait migrated throughout the North and South American continents and Europe, genetic drift occurred, accounting for the 15 percent of patients with the various forms of sickle cell disease who are not phenotypically African in appearance.

Improvements in acute medical care during childhood and in the social and environmental situation for patients, as factors taken together, have made it possible for most children with sickle cell anemia and other forms of sickle cell disease to survive childhood. In the United States, Great Britain, and most European countries, umbilical cord blood diagnosis or peripheral blood sampling of newborns can diagnose the disorder at birth. This allows the children to be provided with responsive, knowledgeable medical care and complete immunizations early in life.

The current focus of clinical investigations is prevention of the tissue destruction induced by the repeated endothelial damage caused when sickle cells obstruct blood vessels. Such prevention requires lifelong medical treatment. Drugs that can modify the rate of hemoglobin polymerization (precipitation) in the red blood cells include hydroxyurea, cytosine arabinoside, 5-azosididine, and other agents that increase the amount of fetal hemoglobin in red blood cells. By increasing the fetal hemoglobin, the rate of polymerization of hemoglobin S is modified so that there is less propensity for insoluble rods to be formed. The membranes of red blood cells become more flexible, allowing the cells to traverse the microvasculature and thereby decreasing the damage to blood vessels. Adhesion molecules (such as VCAM-1) act to provide the glue that binds the damaged sickle cell to the inner lining of the blood vessel, inducing permanent endothelial damage. An intensive search is underway to identify blocking agents for these adhesion molecules that can prevent the blood vessel occlusion.

Bone marrow transplantation

with normal bone marrow (normal red blood cell precursors) from a donor with identical human leukocyte antigens (HLAs) is the only cure now available for sickle cell anemia. Bone marrow
transplantation is limited by the paucity of HLA-compatible sibling donors who do not have sickle cell anemia.

Gene therapy holds the promise of a cure but has not been successfully developed for use in patients with sickle cell anemia. The advantage of gene therapy is that no HLA-compatible donor is required.

Bibliography

Ballas, S. K. “Sickle Cell Anaemia: Progress in Pathogenesis and Treatment.” Drugs 62 (2002): 1143–1172.

Edelstein, Stuart J. The Sickled Cell: From Myths to Molecules. Cambridge, Mass.: Harvard University Press, 1986.

Embury, Stephen H., Robert P. Hebbel, Narla Mohandas, and Martin H. Steinberg, eds. Sickle Cell Disease: Basic Principles and Clinical Practice. New York: Raven Press, 1994.

Genetics Home Reference. "Sickle Cell Disease." Genetics Home Reference, May 20, 2013.

Health Library. "Sickle Cell Anemia (Sickle Cell Disease)." Health Library, September 30, 2013.

National Institutes of Health. "When Blood Cells Bend: Understanding Sickle Cell Disease." NIH News In Health, April, 2012.

O’Malley, Paul D., ed. New Developments in Sickle Cell Disease Research. New York: Nova Science, 2006.

Pauling, Linus, H. Itano, S. J. Singer, and I. C. Wells. “Sickle Cell Anemia: A Molecular Disease.” Science 110 (1949): 543–548.

Powars, Darleen R. “Management of Cerebral Vasculopathy in Children with Sickle Cell Anaemia.” British Journal of Haematology 108 (2000): 666–678.

Serjeant, Graham R., and Beryl E. Serjeant. Sickle Cell Disease. 3d ed. New York: Oxford University Press, 2001.

World Health Organization. "Sickle-Cell Disease and Other Haemoglobin Disorders. (Fact Sheet No. 308)." World Health Organization: Media Centre, January, 2011.

What is family systems theory?

Introduction

Family systems theory developed from several prominent influences during the 1950s. These influences include general systems theory (GST), psychoanalysis, developmental psychology, and the disruption of family relationships during World War II (and their subsequent rebuilding). Austrian-born biologist Ludwig von Bertalanffy developed general systems theory, which later influenced the development of family systems theory. Von Bertalanffy examined scientific and social phenomena holistically (exploring the whole) as opposed to using a reductionist or mechanistic approach (emphasizing the parts). In other words, he explored how parts of an organization or system interact and connect with one another to form a holistic working system.

American psychiatrist Murray Bowen is one of the foundational theorists of family systems theory. Bowen was born in the small town of Waverly, Tennessee. He was the oldest of five children and frequently had difficult relationships with his family members. Bowen readily drew on his own problematic family experiences in developing his systemic view of families. Bowen believed that the primary source of human emotional experience is the extended family unit. He believed that family members are emotionally interdependent and functional in reciprocal relationships with one another. Bowen’s family therapy is often referred to as Bowen family systems theory or Bowenian therapy.

Argentine psychiatrist and family therapist Salvador Minuchin is another foundational family theorist. Minuchin examined the structure of the family and the way the family system interrelates. He believes that the way in which a family deals with stressors indicates whether a family system is functional or dysfunctional. He especially explored how family members developed appropriate social boundaries with one another. Minuchin pioneered such techniques as joining, whereby the family therapist enters into the family system and joins it so that it can be positively restructured or so that the family system can be a catalyst for positive change. Minuchin is credited with developing
structural family therapy. He continues his work in family therapy through the Minuchin Center for Family Therapy.

American psychotherapist Jay Haley was also an influential figure in founding family therapy. He was the founding editor of the family therapy journal Family Process, and he significantly contributed to and shaped the empirical study of psychotherapy and family systems theory. He is credited with coining the term “strategic therapy” to describe a new type of family therapy, which differs from Bowenian family therapy. He worked with Minuchin and was involved in the evolution of structural family therapy.

American Virginia Satir
is also credited with significantly shaping the family therapy movement. Satir studied how self-esteem develops in families and influences interpersonal relationships and relationship choices. For example, she asserted that in choosing romantic partners, individuals often choose a partner who matches their level of self-esteem, low or high. She called her system the human validation process model and incorporated humanism (a philosophy that affirms the dignity and worth of all people) and existentialism (a philosophy that focuses on the holistic experiences of an individual—thinking, feeling, and sensing) into her family systems work. She was often criticized for her humanistic focus by other family therapists. Although Satir made important contributions to the family therapy field, she eventually stopped doing family therapy because she was not embraced by her family therapy colleagues.

Theoretical Overview

In general, all family theorists subscribe to some basic beliefs. One significant belief is that the family is an interconnected unit or system wherein the actions of one family member affect all members in the family system. Family systems theory examines the organization, structure, and complexity of families and familial relationships. Family theorists explore patterns in families over generations, which in Bowen’s family therapy is known as the multigenerational transmission process. An example of a multigenerational pattern might be if a grandfather, a father, and his son are all alcoholics. The substance abuse experienced in this family over generations would be considered a multigenerational pattern. Most family theorists also explore family members’ emotional, social, and psychological boundaries with one another. Minuchin’s work with families frequently focused on familial boundaries. Boundaries are respectful limits or social rules that govern the development and maintenance of interpersonal relationships. In family systems theory, healthy interpersonal boundaries permit appropriate degrees of emotional intimacy between two people. Families with few boundaries may be considered enmeshed or so deeply involved with one another that individual family members have difficulty establishing individual identities separate from their families. Family therapists often examine healthy and unhealthy boundaries within a family system.

Although family systems theory does explore past family history within a family system, its focus is primarily on the present. Family systems therapy can be done with individuals, couples, or the entire family. Families can be broken down into subsystems, which are often organized hierarchically, by gender or by generation. Family therapists explore relationship patterns among familial subsystems as well as how these subsystems affect the entire family unit. The two most popular forms of family systems therapy are Bowen family systems therapy and structural family therapy.

The Bowen family systems theory explores how individual family members differentiate themselves from their families of origin. The differentiation process is how individuals can remain a member of a family system and still be a separate individual, emotionally and psychologically. Bowen also explored relationship alliances in families, called triangles. Triangles are the basic building blocks of an emotional system and begin with a relationship alliance between two people. Bowen believed that when there is tension or stress in the relationship between these two people, a third person or thing is brought in to relieve this tension. This is known as triangulation, where two individuals are on the inside and another is on the outside of the relationship. For example, if a married couple is having difficulty with each other, they may focus on their children instead of confronting the problems within their marriage. Another example of triangulation is if the couple introduces their children into their marital conflicts so that the couple does not have to face their problems with one another. Bowen frequently drew family diagrams to examine relational patterns, identify family members, and highlight important family history and events. These diagrams are known as genograms and are still considered an important technique in family therapy.

At the heart of Bowen’s work was his idea that within the nuclear family, relationships are shaped by how family members deal with anxiety within (and outside) the family. When families experience stress, members sometimes draw closer to one another or distance themselves. He describes the distancing as an emotional cutoff. Sometimes individuals who experience high levels of family conflict may cut themselves off from family members when they become adolescents or adults.

Minuchin’s structural family therapy (SFT) differs from Bowen’s family therapy in that Minuchin focused more on the social contexts in which families exist and the structure of families. Structural family therapy has its own unique terminology. Minuchin formally introduced the concept of exploring family subsystems. He stresses the exploration of boundaries within the family system in structural family therapy. Minuchin believes that family relationships are frequently organized by power hierarchies. For example, in a nuclear family, the parents may have the most power. This is usually considered an appropriate family structure. Healthy families show some flexibility in boundaries over time. For example, when young children become adolescents, they are usually allowed more freedom in making decisions than they were as children. However, dysfunctional families tend to be inflexible and unchanging over time. Minuchin believed that dysfunctional families develop inappropriate coalitions (alliances) among familial subsystems, which disrupt appropriate family hierarchies or subsystems. An example of this would be if a mother and daughter align themselves against the father. In such a case, Minuchin’s goal would be to restructure the family system so that the mother and father develop a healthy coalition, which would rebalance the family system. In doing so, the appropriate hierarchy between parents and children is maintained. Minuchin would use the technique of joining or becoming a part of the family system so that it can be restructured.

Structural family therapy restructures families by unbalancing the current family system. Minuchin would often intentionally cause the family conflict and upheaval, which requires the family to change. In family therapy sessions, Minuchin would frequently isolate family coalitions from one another (either physically in the room or by asking family members to leave the room), deliberately break family rules, or have some family members watch other members in session, from behind a two-way mirror. These interventions were specifically designed to restructure unhealthy family patterns into more healthy ones.

Some key concepts of structural family therapy include family rules, family homeostasis, quid pro quo, the redundancy principle, symmetrical and complementary relationships, and circular causality. A structural family therapist would examine the covert and overt rules that govern the family. Minuchin believed that it was critical to understand a family’s rules so that the therapist can then join the family system. Families tend to remain in the same pattern of functioning over time unless challenged to change. This is known as homeostasis. When structural family therapists unbalance a family system, they disrupt homeostasis. This is disruptive for families but allows them to be restructured. Family members often treat one another in the ways in which they are treated. This is known as quid pro quo. Families behave in repetitive ways over time (redundancy principle). Structural family therapy describes relationships between family members in terms of power. Symmetrical relationships occur between equals (mother-father), and complementary relationships occur between unequals (parent-child). Finally, the idea that events are interconnected and that behaviors are caused by multiple factors is known as circular causality. Structural family therapy is considered brief therapy (about ten sessions). It focuses on what needs to be changed and what solutions the family has already tried.

Treatment Success

Almost all family therapy is based on family systems theory. Family therapy has been successfully used with several different clinical populations, including families with members who have substance abuse issues, anorexia, schizophrenia, developmental delays, autism, and mood disorders. Family therapy is also successful with nonclinical populations and helps families adjust to changes, crises, and other problematic issues that develop within them. Family therapy is frequently considered the treatment of choice for these sorts of issues. Family therapy has expanded its focus from the nuclear family to explore nontraditional families, such as those with stepparents, stepsisters, and stepbrothers.

African American family therapist Nancy Boyd-Franklin has criticized traditional family therapy approaches that did not incorporate cultural sensitively within their treatment frameworks. Training of family therapists has come to incorporate multicultural family therapy approaches, which emphasize understanding how culture and ethnicity influence concepts such as differentiation, the multigenerational transmission process, and other traditional family therapy concepts. Boyd-Franklin highlighted the necessity of incorporating woman-led (single-mother) families and families in which extended family members are as important as the nuclear family into family therapy treatment frameworks. Some family therapists are also trained to work with families in which there are one or two gay parents.

Bibliography

Bregman, Ona Cohn, and Charles M. White. Bringing Systems Thinking to Life: Expanding the Horizons for Bowen Family Systems Theory. New York: Routledge, 2011. Print.

Bowen, M. Family Therapy in Clinical Practice. Northvale: Aronson, 1968. Print.

Boyd-Franklin, N., and B. Hafer Bry. Reaching Out in Family Therapy: Home-Based, School, and Community Interventions. New York: Guilford, 2001. Print.

Haley, J. Problem-Solving Therapy. 2d ed. San Francisco: Jossey, 1991. Print.

MacKay, Linda. "Trauma and Bowen Family Systems Theory: Working with Adults Who were Abused as Children." Australian & New Zealand Journal of Family Therapy 33.3 (2012): 232–41. Print.

Minuchin, Salvador. Families and Family Therapy. London: Routledge, 1993. Print.

Nichols, Michael P. The Essentials of Family Therapy. 6th ed. Boston: Pearson, 2014. Print.

Satir, V., J. Banmen, J. Gerber, and M. Gomori. Satir Model: Family Therapy and Beyond. Palo Alto: Science and Behavioral, 1991. Print.

Steinglass, P. “A Systems View of Family Interaction and Psychopathology.” Family Interaction and Psychopathology. Ed. T. Jacob. New York: Plenum, 1987. Print.

Whitchurch, G., and L. Constantine. “Systems Theory.” Sourcebook of Family Theories and Methods: A Contextual Approach. Ed. P. Boss, et al. New York: Plenum, 1993. Print.