How does substance abuse affect parenting?

Introduction

In 2013 the American Psychiatric Association (APA) published a new version of their handbook of classification of mental disorders. The Diagnostic and Statistic Manual of Mental Disorders, fifth edition (DSM-5) sets forth the criteria used by mental health professionals in the United States to classify and diagnose any psychiatric disorder recognized within the US health care system. Substance use disorder is assessed and diagnosed on a continuum from mild to moderate to severe, with each substance classified as a separate disorder (alcohol use disorder, opiate use disorder, stimulant use disorder, and so on). A diagnosis of substance use disorder is used when the recurrent and repeated use of drugs and/or alcohol causes impairment such as failure to meet responsibilities at work, school, or home; physical or mental disability; and/or health problems. Furthermore, evidence of impairment of control or social impairment and/or risky or potentially life threatening behavior are additional indications that a diagnosis of substance use disorder would be appropriate.

Alcohol and substance abuse during pregnancy has been definitively proven to be detrimental to the fetus. In addition to the well-documented damages caused by fetal alcohol syndrome, both alcohol and drug abuse place the fetus at risk for intrauterine growth retardation, higher susceptibility for infectious disease before birth, and of being physically dependent on a substance at birth, requiring medical detoxification before the baby is able to leave the hospital setting.

Children who are reared by a parent or parents with substance use disorder have been shown to have impaired cognitive and social development skills, slowed learning skills, and a wide range of mental health problems, including depression and anxiety.

Alcohol Abuse

Data from the Substance Abuse and Mental Health Services Administration indicate that more than eight million children under the age of eighteen in the United States were living with a substance abusing parent and that approximately 10 percent of all children born in the United States were exposed to drugs or alcohol prenatally.

Young children of alcoholics are habitually given less attention than the alcohol itself by their parents. This leads to low self-esteem and decreased self-worth in the children, fostering fears of helplessness and abandonment.

The mood swings and erratic behavior of alcoholic parents also can lead to stress-induced nightmares, paranoia, and bedwetting in young children. Young children of alcoholics also are placed at a much higher risk of injuries, which result from inadequate supervision in the home or vehicular accidents caused by alcohol-impaired drivers.

Instances of incest and domestic violence also occur with considerably higher frequency in families in which alcoholism is prevalent. Because young children are poorly equipped to handle the emotional trauma that results from these incidents, they are at higher risk of lifelong psychological and mental disorders, including anxiety and depression.

The general alienation by and mistrust of adults also can lead young children into deviant behavior at school and in their community. This mistrust acts as a barrier for the children of alcoholic parents to seek solace or support from other adults, both outside the home and within their immediate families. The inability to relate and the lack of understanding in interactions with children from households unaffected by alcoholism also can lead to anger, hostility, and erratic behavior in peer interactions. This leads to further isolation and social abandonment.

Drug Abuse

Parental drug abuse is equally hazardous to the health and proper development of children as is parental alcohol abuse. As with abusive alcohol use, the number of potential prenatal dangers is lengthy and widely documented by medical research.

Pregnant women who use drugs, particularly those who ingest drugs intravenously, risk exposing the fetus to infectious disease. Severe brain damage, stroke, low birth weight, and organ failure are also common problems associated with prenatal use of illicit drugs. Additionally, newborn children of addicted individuals are at high risk for being born addicted to the drugs their mother ingested. The newborn must then be detoxed safely from the substance before being released to a family member or the department of social services.

Maltreatment such as sexual abuse and battery and habitual periods of neglect are of higher prevalence in families with one or more drug-using parent. The lack of structure and routine in the lives of children of substance abusers can also lead children to lash out at school and at day care.

While alcohol can be acquired legally and is readily available, controlled substances must be obtained through illicit trans-actions, often in environments that are unsuitable or unsafe for children. These environments include violent and crime-ridden neighborhoods.

Children of drug abusers are frequently exposed to these dangerous environments or experience lengthy periods of neglect in their own home while their parents seek the drugs. Lengthy neglect is particularly challenging for the older siblings of young children, who often have the responsibility of parenting their younger siblings when they are themselves lacking in the proper emotional, physical, and psychological abilities to navigate everyday life.

Similarly, children preoccupied with concern for their drug-abusing parents place education at a lower priority, resulting in less-than-adequate academic development and achievement. Shame, mistrust, and fear also hinder the children of drug-abusing parents. The children have trouble building trusting relationships both with their own peers and with adults, which further perpetuates feelings of isolation and helplessness.

Troubled Adulthoods

Children raised in drug-free homes or by parents with normative behaviors toward drugs and alcohol may experiment with such substances themselves. Children of substance-abusing parents, however, are raised in an environment that models alcohol and drug use as ways to cope with stress, anger, pain, or a host of other negative emotions. Many children of addicts resort to the use of drugs and alcohol to ease the psychological and emotional pains of childhood, or they simply view such behavior as normal, leaving them vulnerable to abuse themselves.

a history of abuse of other types of drugs and the presence of a mood or anxiety disorders.

Although there is little evidence to prove a genetic predisposition to illicit drug use, a large body of evidence exists to show a genetic connection between alcoholism in the children of alcoholic parents. According to the National Association of Children of Alcoholics (NACA), biological children of alcohol-dependent parents are four times as likely to become alcoholics themselves.

Children of substance abusers face difficult circumstances even if they manage to avoid the patterns of alcoholism and drug use demonstrated by their parents. Academic underachievement is common among children of substance abusers. These children repeatedly underperform on all standardized tests measuring academic skills, such as reading comprehension and mathematics. In one study reported by the NACA, 41 percent of children with drug- or alcohol-abusing parents repeat an academic grade because of poor performance or lagging academic comprehension. This lack of academic preparedness leaves children of substance abusers with fewer skills, interests, and motivations to apply toward careers and hobbies as adults.

The cyclical nature of damaging, abusive, and neglectful childhoods is perhaps the most severe consequence of substance abuse on parenting. Substance abuse can affect families for several generations. Early education on the dangers of alcohol abuse and illicit drug use has become a key tool in addressing the problem in the United States. Also critical is the establishment of effective outreach and social programs in which at-risk children can communicate about abusive behaviors and harmful home environments and can find support from their school or community.

Bibliography

Black, Claudia. It Will Never Happen to Me: Growing Up with Addiction as Youngsters, Adolescents, Adults. Center City: Hazelden, 2013. Print.

Brouwer, Thomas P. Parents with Substance Use Disorders and Child Protection Issues. Hauppauge: Nova Science, 2011. Print.

Calhoun, Stacy, et al. "Improving the Outcomes of Children Affected by Parental Substance Abuse: A Review of Randomized Controlled Trials." Substance Abuse and Rehabilitation 6 (2015): 15–24. Print.

“Children of Addicted Parents: Important Facts.” NACOA. National Association for Children of Alcoholics, n.d. Web. 5 Nov. 2015. PDF file.

“Children Living with Substance-Dependent or Substance-Abusing Parents: 2002 to 2007.” National Survey on Drug Use and Health. 16 Apr. 2009. Web. 20 Apr. 2012.

"Effects of Parental Substance Abuse on Children and Families." AAETS. American Academy of Experts in Traumatic Stress, 2014. Web. 2 Nov. 2015.

Sims, Armethia L. “A Substance Abuse Prevention Guide for Parents / Safe and Drug-Free Schools Program, Ann Arbor Public Schools.” DocPlayer. DocPlayer, 2006. Web. 20 Apr. 2012.

How does Aunt Alexandra become less objectionable?

Aunt Alexandra continually disagrees with her brother, Atticus, throughout in the novel in regards to several issues. She objects to the way he raises his children without teaching them about their family history, as well as his choice to defend Tom Robinson in front of the Maycomb community. There are several scenes throughout the novel where Alexandra argues with Atticus over these issues and more. In Chapter 13, Alexandra encourages her brother to speak with Jem and Scout about their family's background, but Atticus fails after his first attempt to talk with his children. In Chapter 14, Alexandra urges Atticus to fire Calpurnia, but Atticus defends Cal's reputation and refuses to fire her. Clearly, Aunt Alexandra learns quickly that Atticus will stand up to her and she will not get "her way," which is one reason she becomes less objectionable and more likable as the novel progresses.

Following the trial, Aunt Alexandra meets Atticus at the door and says, "I'm sorry brother" (Lee 284). Scout mentions that she is shocked because she has never heard Alexandra refer to Atticus as "brother." Alexandra shows compassion and sympathy towards Atticus because she realizes the stress and courage it took to defend Tom Robinson. In Chapter 24, Atticus interrupts the missionary circle to tell Calpurnia and Alexandra that Tom Robinson was shot dead in the prison earlier that day. Alexandra is numb and comments,

"I can't say I approve of everything he does, Maudie, but he's my brother, and I just want to know when this will ever end...It tears him to pieces. I've seen him when--what else do they want from him, Maudie, what else?" (Lee 316).

Alexandra displays her true feelings for her brother and shares Atticus' pain. She has witnessed firsthand how the Tom Robinson trial has negatively affected her brother. Alexandra's awareness of Atticus' burden is another reason why she becomes less objectionable to the reader and more likable. She understands that arguing about minor issues is trivial compared to the stress Atticus is under. She realizes that Atticus needs support, rather than criticism. 

Why does Charles Dickens contrast Lucie Manette and Madame Defarge so strongly in A Tale of Two Cities?

Charles Dickens makes use of the character of Lucie Manette as a foil to Madame Defarge in order to illuminate the frightening evil of the novel's antagonist, and to further the theme of Good vs. Evil.

The use of foils is a literary technique that can further the development both of theme and of character. In A Tale of Two Cities,Dickens designs his narrative with duality and foils; even the opening sentence starts with a classic parallelism that is a foil to his theme: "It was the best of times, it was the worst of times." Certainly, the duality of Lucie Manette and Madame Defarge also illustrates the theme of Good vs. Evil.

Lucie Manette - The quintessential Victorian heroine, Lucie swoons in men's arms, is often overcome with emotion, and is a delicate creature who needs protection. She is compassionate and loving, embracing her father, recently released from the Bastille, whom she does not know since he has been imprisoned most of her life. She bestows her kindness gratuitously upon even the dissolute as she befriends Sydney Carton. In fact, it is her friendship which raises Carton to a higher level as he finds purpose in his life and spiritual resurrection by sacrificing himself for Charles Darnay in his love for Lucie. Furthermore, Lucie is a devoted wife and mother. When she learns of her husband's imprisonment, she comes with her children and maid to France. Each day she patiently stands for long hours gazing at Charles's prison window in the hope that he will see her and be encouraged.

Thérèse Defarge - Certainly in sharp contrast to Lucie is her foil, Thérèse Defarge. The antithesis of Lucie's motherly love, tenderness, and kindness is Mme. Defarge's dark, sinister, even sadistic nature. Rather than supporting life, she destroys it, joining the Vengeance in cheering the decapitations at the guillotine. Indeed, she is the consummate villain. For instance, Mme. Defarge is intent upon revenge for the deaths of her brother and sister at the hands of the Evremonde brothers, and she registers into her knitting anyone she hates or suspects. She is absolutely resolved in her antipathy for the upper class, or anyone else who does not support the bloodbath of the revolution. 

It would be easier for the weakest poltroon that lives, to erase himself from existence, than to erase one letter of his name or crimes from the knitted register of Madame Defarge.

In fact, despite her husband's having been a servant for Dr. Manette, Mme. Defarge knits Lucie's name into her cloth for the simple reason that Lucie is going to marry Charles Darnay. She has mercy for no one. For instance, when her husband makes a plea to his wife to spare the Manettes from death, he alludes to the eighteen years of suffering of Dr. Manette, for whom he was once a servant, and mentions how his daughter Lucie has also suffered. Madame DeFarge reacts only with coldness to his suggestion to desist from her terrible vengeance:

“Then tell Wind and Fire where to stop,” returned madame; “but don’t tell me.”

Well, well,” reasoned Defarge, “but one must stop somewhere. After all, the question is still where?”

“At extermination,” said madame. (Bk. 3, Ch. 12)

Later in the narrative, when Mme. Defarge watches for the man she believes to be Charles Evrémonde (Darnay) to die,

[I]t was nothing to her that an innocent man was to die for the sins of his forefathers; she saw, not him, but them.

After the execution, she then takes her way along the streets to find Lucie Darnay and kill her. When Miss Pross discovers her standing in a room at the Darnay home, she demands what the woman wants. Mme. Defarge looks coldly at her and says, "The wife of Evrémonde; where is she?" Because she has come with a pistol to kill Lucie, Miss Pross wrestles with her until the gun goes off, leaving Thérèse Defarge dead and Miss Pross deaf.

Who do you think is the true hero (or protagonist) of Shakespeare's The Merchant of Venice, Portia or Antonio?

Your question is actually more complicated than it seems since it demands two interpretations of the term, 'hero.' In literature, the word normally refers to the lead character. Because the play is titled, 'The Merchant of Venice,' Antonio becomes the most obvious reference since he is the only merchant we read about from beginning to end. In this sense, he is, therefore, the protagonist.

Further support for him being deemed the true protagonist lies in the fact that all the major events revolve around his actions. The main theme of the play explores the antagonism between him and his opposition, Shylock, and delves into the origin and nature of their dispute, its development, and final resolution. The actions of most of the other characters are determined by events which he influences and by situations which have an impact on him. In essence, he is the core around whom almost everything revolves.

It is Antonio's decision to assist Bassanio by agreeing to act as surety that affects the major events in the play: Shylock's demand for restitution in the form of a pound of his flesh; Portia's decision to disguise herself as a lawyer; the trial scene. The major themes all have their origins in these particular situations. Although Portia's role is important, her actions later in the play are all affected by Antonio's dilemma.

In addition, your reference to 'true' suggests 'real' in the sense of, 'Who is the real hero in the play?' I suggest that this requires an alternative interpretation of the word. In this definition, a hero is someone who undertakes an arduous task and is admired for acting bravely in the face of adversity. A more common interpretation is a reference to someone who saves another from jeopardy. In this interpretation, Portia is a hero, for she saves Antonio from Shylock's vengeance. She becomes his savior and her deed is much admired and appreciated by her contemporaries.

Antonio, for all his magnanimity, does not accurately fit this definition. The fact that he extended assistance to Bassanio, against his advice, does not entirely qualify him. His attitude in accepting the harsh and punitive conditions of Shylock's bond was born from his naive overconfidence. He had no doubt that his merchant ships would dock safely and not come to harm. 

On the whole, you'll to weigh up the two definitions and determine which best suits the purpose of your task.        

Why is it important to study and understand the origins of humans?

Studying the origins of humans helps us to understand who we are, what we do, and where we fit in as humans. Looking at how Homo sapiens came to be, as well as considering our hominid and primate ancestors, tells an important part of the story of evolution.

Studying anthropology and the origins of humans can enrich understanding in almost any field of study. Even a mathematician should be interested in how humans developed a system of numbers and mathematics. What kind of changes in the brain enabled us to learn math? What might these changes in the brain have been in response to?

Even people with no interest in evolution or the hard sciences can benefit from studying human origins. As a species, we have a strong desire to make sense of where we fit in in the world. Why do you think religion (including folk or informal worldviews) have developed in every human culture? We want to make sense of the world and our place in it. 

I hope you will check out the Smithsonian Institute's webpages on Human Origins, if not to help answer your question, at least because they have one of the most comprehensive websites on human origins that is accessible to the public.

What are nails?

Structure and Functions

Nails function to protect fingers and toes against bumps and trauma. Fine touch is amplified and skillful manipulation of small objects with the fingers is enabled by the presence of nails. Nails also provide the ability to scratch, both as a temporary relief of an itch and in personal defense. Nails are important social communicators of beauty and sexuality and hence are the focus of a major cosmetic industry.

Biologically, nails are characterized as plates of tightly packed, hard epidermis cells filled with a protein called keratin. Nails are normally seen on the dorsal side (the side opposite the palm or sole) of all fingers and toes. The anatomy of the normal nail consists of a nail plate, proximal nail fold, nail bed, matrix, and hyponychium. These components are epithelial-derived structures, like skin and hair, which emerge from the live germinative zone of the epidermis. In nails, these cells differentiate and form the horny layer, which is considered to be dead.

The nail plate is a relatively hard and flat, transparent, horny structure that is rectangular in shape. It rests on the underlying nail bed but typically extends beyond the bed as an unattached, free-growing edge reaching toward or beyond the tip of the finger or toe. On the fingers, the thickness of the plate in adults increases from about 0.7 millimeters at the proximal edge to about 1.6 millimeters at the distal edge. The terminal tip thickness varies considerably between persons.

Normally, a pinkish nail bed is seen through the transparent nail plate. Frequently in the thumbnail and sometimes in the other fingernails, a whitish, semi-moon-shaped structure called the lunula is seen that extends under the proximal nail fold. The borders of the nail plate are covered by skin structures: two lateral folds and a single proximal fold.

The proximal nail fold is the cutaneous or skin structure that is in continuity with the visible proximal border of the nail but overlies part of the nail root. The ventral side (underside) of the proximal nail fold provides physical protection to the germinative zone of the nail and aids in the physical attachment of the nail plate. About a fourth of the total surface area of the nail plate is located under the proximal fold. The cuticle is a layer of epidermis extending from the proximal nail fold and attached to the dorsal side of the nail. The cuticle functions to provide a physical seal against microbes and chemical irritants, which may otherwise enter the matrix and affect nail production.

The nail bed is the portion of the digit upon which the nail rests. The nail bed is highly vascular, with numerous capillaries. It consists of epithelial tissue and extends from the lunula to the point where the bed separates from the nail. A series of fine longitudinal folds in the nail bed corresponds to the undersurface structure of the nail. This arrangement enhances the adherence of the nail plate to the nail bed.

The nail matrix is generally considered the most proximal part of the nail bed and is bordered by the proximal nail fold. On the distal end it is bordered by the distal margin of the lunula. The nail matrix epithelium cells consist predominantly of keratinocytes in both a basal and a spinous layer. Melanocytes and Langerhans cells are intermingled with keratinocytes. It is within the matrix that the germinating center of nail growth is found. Basal epithelial cells increase in number through mitosis, or division, and then differentiate into keratinocytes, which are epithelial cells filled with keratin protein. These keratinocytes condense their cytoplasm, lose their nucleus, and form flat, horny-looking dead cells. As further cell division occurs in the nail matrix, more distal keratinocytes are pushed out to form the nail plate.

The hyponychium consists of epidermis tissue that underlies the edge of the nail plate and extends from the nail bed to the distal groove. It functions to provide a defense against entry of bacteria under the free edge of the nail plate. Excessively vigorous cleaning may damage the hyponychium and allow for bacteria to enter more readily under the nail plate.

The turnover rate of matrix cells determines the growth rate of the nail. This rate varies with age, environmental conditions, nutritional status, and the specific digit. The growth rate proportionately increases with the length of the digit; thus the middle finger nail grows the fastest while the growth rate in the little finger is the slowest. Fingernails grow three times as rapidly as toenails. The growth rate is more rapid in the winter than in the summer. Furthermore, nails grow faster in young children than in older adults. It takes about six months for a fingernail to completely grow in. Male nails grow faster than female nails. Nails on the dominant hand grow faster than those on the other hand.

If nails are protected and untrimmed, they can grow to considerable lengths. Such long nails were prized by the wealthy classes in imperial Chinese culture as an indication of status. The practice of painting toenails red may have originated in the Ottoman seraglio, where it was a signal of menstrual status.

Nails continue to grow throughout life without a resting phase. Contrary to folk belief, nails cease growing when an individual dies. The matrix cells stop producing deoxyribonucleic acid (DNA) and dividing soon after death, and thus the nail bed cannot grow longer. The appearance of nail growth after death is due to a retraction or shrinkage of nail matrix tissue, resulting in the apparent lengthening of the nail plate.

Professional grooming of the nails for both men and women is termed a manicure. Manicure procedures include cutting the nails according to fashion standards to improve their cosmetic appearance. A pedicure is the term applied to grooming the toenails. Typically, the nails are first soaked in a soapy solution to soften the nail plate and to remove dirt and debris. It is often fashionable to trim the nails to a delicate arc at the middle of the fingertip. The corners of the nail are typically filed. While this shape is attractive in creating the illusion of longer, slender fingers, it heightens the probability of nail plate fractures, hangnails, or ingrown nails. The cuticle, considered to be unattractive by manicurists, is typically minimized, partially removed, or traumatized. This may increase the incidence of fungal invasion and disease. Most of the problems associated with a manicure arise from excessive manipulation of the cuticle.

Nail polish typically consists of pigments suspended in a volatile solvent that also contains a film-forming agent. When the polish is applied to the finger, a covering film develops over the nail. The film is permeable to oxygen, which allows gas exchange to occur between the atmosphere and the nail plate. Resins and plasticizers are added to the polish to increase the flexibility of the film and to minimize chipping. The variety in nail polish color is due to the addition of coloring agents. Deep red nail polishes can cause a temporary yellowish staining of the nail plate.

Nail adornments are sometimes used. Frequently, small nail jewels or ribbons are applied to the fingernails immediately before the nail polish dries, allowing the decoration to adhere to the nail plate. Since some people frequently develop contact dermatitis in reaction to nickel, gold or nickel-free jewels should be selected. Artificial nail tips made of plastic also are glued to the nail tip to create the illusion of an elongated natural nail tip. The gluing may cause nail problems, since a portion of the natural nail is occluded by the glue. This occlusion inhibits oxygen transfer and stresses the nail plate. Frequently, the nail may thin and be unable to support its own weight after the plastic tip is removed. Removal of the plastic tip may result in nail pitting.

Disorders and Diseases

Nails are useful indicators of skin disease and internal disorders. An abnormally pigmented band in the nail may indicate a malignant melanoma. A yellow nail may indicate psoriasis or a fungal infection. Pulmonary disease or smoking may also cause yellow or brownish nails. Antimalarial drugs may cause the nail to darken in appearance. Frequently, psoriasis causes pitting of nails and an acceleration in their growth rate. Chronic chest disease or a cyanotic congenital heart disorder is frequently associated with club-shaped deformity of the nail plate. Beau’s lines, which are transverse depressions in the nail plates, are associated with illnesses such as coronary thrombosis, pneumonia, and severe injuries. Drug treatment may cause nail breakdown or destruction or complete shedding of the nail plate.

An unexplained aspect of nail physiology is its relationship to lung physiology. Hippocrates first described a connection between lung parenchymal disorders and an edema in the connective tissue beneath the lunula that results in clubbing. The relationship has long been recognized, but the causal link is still unknown.

An ingrown nail
results when a deformed nail grows improperly into the skin or when the skin around the nails engulfs part of the nail. Wearing narrow, tight shoes can cause or worsen this pathology. Initially, symptoms may be slight or mild, but with time may come increasing pain. The affected area becomes reddish and, if not treated, may become infected. If infected, the area becomes swollen, inflamed, and painful. Blisters may develop. Treatment involves trimming away the nail from the infected area, allowing the inflammation to decline and the area to heal.

Clubbing is a disorder characterized by a bulblike enlargement of the nail with increased horizontal and longitudinal curvatures. Clubbing involves both fingers and toes and commonly begins at puberty. The disorder may be genetically inherited or acquired. Clubbed nails often have a spongy feel when pressure is placed on the proximal nail fold. This is due to the expanded soft tissue that underlies the nail. Acquired clubbing is often associated with another clinical pathology, most commonly pulmonary or cardiovascular disease. However, at times it is also associated with gastrointestinal inflammatory disease or cystic fibrosis.

A fungal infection is the cause of onychomycosis, which is the most common nail disorder. About half of all nail problems can be linked to this disease, which affects as many as 15 to 20 percent of people in North America. It is uncommon in children and more frequently seen in aged adults.

Several fungi may cause onychomycosis, although most belong to the group called dermatophytes. The fungi are present in soil, and indirect transmission to humans frequently occurs through public swimming pools and shower floors. Some yeasts and molds are also thought to cause this clinical condition. Alternatively, this infection is associated with athlete’s foot infection. Typically this condition is found in toenails more frequently than fingernails. The presence of the fungus is further evidenced by scaling on the plantar surface of the foot, where it is often harbored.

In onychomycosis, the fungal organism invades the nail bed, causing a progressive change in the color, texture, and structure of the nail. The nail may turn white, thicken, and even detach from the nail bed. Debris from the infected nail often collects under its free edge. If untreated, the pathology may involve the entire nail plate, and rarely will the nail unit spontaneously heal itself.

Since several organisms may induce the pathology, effective treatment depends on matching the curative with the causal agent. Topically applied antifungals are seldom effective because most cannot penetrate the nail-plate barrier to reach the causal organism. Systemically (orally) administered antifungal therapy frequently uses one of several drugs such as griseofulvin, thiabendazole, or ketoconazole. These drugs are generally effective in halting further invasion of the fungus. While treatment continues, the new nail growth is usually normal, so treatment typically continues until the old nail is replaced by new nail and is then discontinued.

More than seventy tumors have been associated with parts of the nail. They may originate from the epidermis, dermis, subcutaneous tissues, or bone and may be found in the nail bed, nail matrix, hyponychium, or nail fold. The tumors may take various forms, including warts, erosion or ulceration of the nail bed, malignant neoplasms from underlying melanocytes, benign fibromas of the connective tissue, or squamous cell carcinomas. Diagnosis usually is made by taking a biopsy of the affected area. Treatment typically involves surgical removal of the tumor.

Perspective and Prospects

The earliest cellular growth leading to nail formation can be seen histologically at eight weeks of human development, the end of the embryonic period. Microscopically, the cells forming the proximal edge of the nail field and the future matrix can be distinguished at this time. The earliest gross anatomical appearance of nails is seen on the finger digit surface at about nine weeks of development, the very early fetal stage. By eleven weeks of age, the nail field is seen clearly on the hand digits of the fetus. By twenty weeks of age, the fetus shows a nail plate and bed and a proximal cuticle. By thirty-two weeks, the third trimester of pregnancy, adult-type nail structures are visible in the fetus, including a nail plate, matrix, and bed and a forming hyponychium.

Aging results in changes and disorders in nails. When people get older, the color, contour, growth rate, surface texture, and thickness of the nail plate change. Some disorders are more prevalent with aging, such as brittle nails, splitting or fissuring of the nail plate, and increased infections. Aged nails appear dull and opaque, with their color varying from yellow to gray. Frequently in older persons, the lunula is decreased in size or is absent. The growth rate of nails decreases with aging. The most rapid period of growth is during the first thirty years, after which the rate steadily declines. Nail plate thickness frequently increases with advanced age, in combination with discoloration and loss of translucency of the nail plate.

For many years, blood and urine specimens have been used to detect and measure body concentrations of therapeutic drugs or drugs of abuse. During the past decade, alternative biological specimens such as nails and hair have been frequently used as the basis for drug detection. The basis for drug detection in nail clippings is that the dividing epidermal cells that form the nail plate also incorporate drugs from the systemic circulation. The subsequent cornification of these cells traps the drug within the forming nail plate. Drug-detection methods involve taking a sample of nail clippings and extracting and identifying drug molecules via immunochemical or chromatographic techniques. These techniques are extremely sensitive and capable of detecting minute quantities of drug in the samples; as little as ten milligrams of nail clippings is required to detect the presence of drugs. Twenty-first-century drug-screening methods have detected amphetamines and cocaine in nail clippings. Using nail clippings for drug analysis and screening provides a long-term measure of drug exposure that may potentially represent months of drug use. Furthermore, nail clippings are relatively easy to collect and involve a noninvasive procedure; samples are easily stored, and once incorporated in the nail tissue, most of the drugs are presumably stable.

Modern medicine in the early twenty-first century still lacks adequate descriptive science as well as understanding of the molecular mechanisms that control nail development and growth. To date, the specific genes or gene products that initiate nail growth have not been identified. The molecular basis for brittle nails, clubbing, and other nail pathologies is not known. Is onychomycosis affected by a systemic immune deficit? What causes yellow nail syndrome? Answers to these questions as well as additional information about the molecular control of nail physiology will greatly increase understanding and lead to better treatments for nail disorders.

Bibliography

Baran, R., et al., eds. Baran and Dawber’s Diseases of the Nails and Their Management. 3d ed. Malden, Mass.: Blackwell Science, 2001.

Du Vivier, Anthony. Atlas of Clinical Dermatology. 4th ed. Edinburgh: Churchill Livingstone, 2012.

"Fingernails: Dos and Don'ts for Healthy Nails." Mayo Clinic, December 8, 2011.

Hordinsky, Maria K., Marty E. Sawaya, and Richard K. Scher, eds. Atlas of Hair and Nails. Philadelphia: Churchill Livingstone, 2000.

Mix, Godfrey F. The Salon Professional’s Guide to Foot Care. Albany: Milday SalonOvations, 1999. .

"Nail Diseases." MedlinePlus, July 9, 2013.

Porter, Robert S., et al., eds. The Merck Manual Home Health Handbook. Whitehouse Station, N.J.: Merck Research Laboratories, 2009.

Standring, Susan, et al., eds. Gray’s Anatomy. 40th ed. New York: Churchill Livingstone/Elsevier, 2008.

Zaias, Nardo. The Nail in Health and Disease. 2d ed. Norwalk, Conn.: Appleton & Lange, 1992.

What are lymphadenopathy and lymphoma?

Causes and Symptoms

The lymphatic system consists of a large complex of lymph vessels and groups of lymph nodes (“lymph glands”). The lymph vessels include a vast number of capillaries that collect fluid and dissolved proteins, carbohydrates, and fats from tissue fluids. The lacteals of the intestinal villi are lymph vessels that serve to absorb fats from the intestine and transport them to the bloodstream.

Lymph nodes are found throughout the body but are concentrated most heavily in regions of the head, neck, armpits, abdomen, and groin. Nodes function to filter out foreign materials, such as bacteria or viruses, which make their way into lymphatic vessels.

The sizes of lymph nodes vary: some are as small as a pinhead, some as large as a bean. In general, they are shaped much like kidney beans, with an outer covering. Internally, they consist of a compartmentalized mass of tissue that contains large numbers of B and T lymphocytes as well as antigen-presenting cells (APC). The lymphatic circulation into the lymph nodes consists of a series of entering, or afferent, vessels, which empty into internal spaces, or sinuses. A network of connective tissue, the reticulum, regulates the lymph flow and serves as a site of attachment for lymphocytes and macrophages. The lymphatic circulation leaves the node through efferent, or exiting, vessels in the lower portion of the organ, the hilum.

Among the functions of lymph nodes are those of the immune response. B and
T lymphocytes tend to congregate in specialized areas of the lymph nodes: B cells in the outer region, or cortex, and T cells in the underlying paracortex. When antigen is presented by an APC, T- and B-cell interaction triggers B-cell maturation and proliferation within the germinal centers of the cortex. The result may be a significant enlargement of the germinal centers and subsequently of the lymph node itself.

Lymphadenopathy, or enlarged lymph nodes, may signify a lymphoma, or cancer of the lymphatic system. More commonly, however, the enlarged node is secondary to other phenomena, usually local infections. For example, an ear infection may result in the entrance of bacteria into local lymphatic vessels. These vessels drain into regional nodes of the neck. The result is an enlargement of the nodes in this area, as an immune response is carried out.

Enlarged nodes caused by infections can, in general, be easily differentiated from those caused by malignancies. Infectious nodes are generally smaller than 2 centimeters in diameter, soft, and tender. They usually occur in areas where common infections occur, such as the ears or the throat. Malignant lymph nodes are often large and occur in groups. They are generally firm and hard, and they often appear in unusual areas of the body (for example, along the diaphragm). To confirm a malignancy, a biopsy of material may be necessary.

Infectious nodes can also be caused by diseases such as infectious mononucleosis, tuberculosis, and
Acquired immunodeficiency syndrome (AIDS). Lymphadenopathy syndrome (LAS), a generalized enlargement of the lymph nodes, is a common feature of the prodromal
AIDS-related complex (ARC).

Since lymphadenopathy can be caused by any immune proliferation in the germinal centers, allergy-related illnesses may also cause enlargement of the lymph nodes. Consequently, immune disorders such as rheumatoid arthritis, systemic
lupus erythematosus, and even hay fever
allergies may show enlarged nodes as part of their syndromes.

As is the case for any cell in the body, cells constituting the lymphatic system may undergo a malignant transformation. The broadest definition of these lymphoproliferative diseases, or lymphomas, can include both
Hodgkin disease and Hodgkin lymphomas, in addition to acute and chronic lymphocytic leukemias (ALL and CLL). With the understanding of, and ability to detect, specific cell markers, it is possible to classify many of these lymphomas on the basis of their cellular origin. Such is the case for ALL, CLL, Burkitt lymphoma, and many other forms of non-Hodgkin lymphomas. The cell type that ultimately forms the basis for Hodgkin disease remains uncertain.

Hodgkin disease is a malignant lymphoma that first manifests itself as a painless enlargement of lymphoid tissue. Often, this is initially observed in the form of swollen lymph nodes in the neck or cervical region. Occasionally, the victim may exhibit a mild fever, night sweats, and weight loss. Untreated, the disease spreads from one lymphatic region to another, resulting in diffuse adenopathy. An enlarged spleen (splenomegaly) is a common result. As the disease spreads, other organs such as the liver, lungs, and bone marrow may be involved.

The disease is characterized by the presence of a characteristic cell type—the Reed-Sternberg cell.Reed-Sternberg cells appear to be of macrophage origin, with multilobed nuclei or multiple nuclei. They may also be present in other lymphatic disorders, but their presence is considered to be indicative of all cases of Hodgkin disease. The precise relationship of the cell to the lymphoma is unclear, but some researchers in the field believe that the Reed-Sternberg cell is the actual malignant cell of the disease. The other infiltrative cells present in the node, including many B and T lymphocytes, may simply represent the reaction to the neoplasm. This interpretation, however, has been disputed.

Lymphoma
staging is a system of classifying lymphomas according to the stage of development of the disease. Staging is important in that the prognosis and basis for treatment are in part determined by the stage of disease. Characterizing the form of Hodgkin disease, therefore, involves two forms of classification. The first is a four-part classification based on the histology or cell type (Rye Conference classification). This scheme is based upon the proportion of Reed-Sternberg cells, ranging from their being “hard to find” to their being the predominant type. The prognosis becomes less favorable as the proportion of these cells increases.

Clinical staging, like that based on histology, is a four-part classification scheme (it is actually six parts, since stage III can be divided into subclasses). In this system, classification is based upon the extent of spread or extralymphatic involvement. For example, stage I features the involvement of a single lymph node region or a single extralymphatic site. Stage IV involves multiple disseminated foci. Early-stage disease is more easily treated and has a better prognosis than late-stage disease.

Non-Hodgkin lymphomas (NHLs) represent a multitude of malignant disorders. Unlike Hodgkin disease, they frequently arise in lymphatic tissue that is not easily observed; for example, in the gastrointestinal tract, tonsils, bone, and central nervous system. They have a tendency to spread rapidly, with malignant cells being released into the bloodstream early in the disease. Consequently, by the time diagnosis of NHL is made, the disease has often spread and the prognosis may be poor.

Though the etiology of most forms of NHL remains unknown, certain characteristics are evident in some forms of these diseases. For example, a portion of chromosome 14 is elongated in about 60 percent of NHL patients. Nearly one-third of patients with NHLs of B-cell origin demonstrate a chromosomal translocation, often involving a piece of chromosome 14 being translocated to chromosome 18. Though the relationship of these changes to disease is unclear, one can surmise that chromosomal defects play at least some role in the development of some forms of these disorders.

At least two forms of NHL are either caused by viruses or related to their presence:
Burkitt lymphoma and adult T-cell lymphoma/leukemia. Burkitt lymphoma, which was first described by Denis Burkitt in central Africa, is a B-cell tumor that occurs primarily in children. It is generally manifested as a large tumor of the jaw. This type of lymphoma is associated with early infection by the Epstein-Barr virus, or EBV (also the etiological agent of infectious mononucleosis). The relationship of the disorder to the virus remains unclear, and EBV may be either a specific cause or a necessary cofactor.

Specific chromosomal abnormalities are also associated with Burkitt lymphoma. In 75 percent of cases, a translocation from chromosome 8 to chromosome 14 is evident, while in most other cases, a portion of chromosome 8 is translocated to either chromosome 2 or chromosome 22. Each of these translocations involves the transfer of the same gene from chromosome 8, the c-myc gene. The site to which the c-myc is translocated is in each instance a region that encodes protein chains for antibody production, proteins that are produced in large quantities. The c-myc gene product normally plays a role in committing a cell to divide. By being translocated into these specific regions, the c-myc gene product is overproduced, and the B cell undergoes continual replication.

Approximately 80 percent of NHL tumors are of B-cell origin; the remainder are primarily of T-cell origin. Those lymphomas that arise within the thymus, the organ of T-cell maturation, are called lymphoblastic lymphomas. Those that originate as more differentiated and mature T cells outside the thymus include a heterogeneous group of diseases (for example, peripheral T-cell lymphomas and Sézary syndrome). Often, by the time of diagnosis, these disorders have spread beyond the early stage of classification and have become difficult to treat.

Treatment and Therapy

Treatment and other means of dealing with lymphadenopathy depend on the specific cause. In the case of lymph node enlargement that is secondary to infections, treatment of the primary cause is sufficient to restore the normal appearance of the node. For example, in a situation in which nodes in the neck region are enlarged as the result of a throat infection, antibiotic treatment of the primary cause—that is, the bacterial infection—is sufficient. The nodes will resume their normal size after a short time.

Dealing with lymph node enlargement caused by lymphoma requires a much more aggressive form of treatment. There are many kinds of lymphomas, which differ in type of cell involvement and stage of differentiation of the involved cells. The manifestations of most lymphomas, however, are similar. In general, these disorders first present themselves as painless, enlarged nodes. Often, this occurs in the neck region, but in many forms of NHL, the lymphadenopathy may manifest itself elsewhere in the lymphatic system. As the disease progresses, splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may manifest themselves. Frequently, the bone marrow becomes involved. If the enlarged node compresses a vital organ or vessel in the body, immediate surgery may be necessary. For example, if one of the veins of the heart is compressed, the patient may be in immediate, life-threatening danger. Treatment generally includes radiation therapy and/or chemotherapy.

As is true for lymphomas in general, Hodgkin disease is found more commonly in males than in females. In the United States, it occurs at a rate of 3.2 per 100,000 population per year for men and 2.4 per 100,000 for women, with more than nine thousand cases expected to be diagnosed in 2013. More than one thousand persons die of the disease each year. The cause of the disease is unknown, though attempts have been made to assign the Epstein-Barr virus to this role.

Hodgkin disease has an unusual age incidence. The age-specific incidence exhibits a bimodal curve. The disease shows an initial peak among young adults between fifteen and thirty years of age. The incidence drops after age thirty, only to show an additional increase in frequency after age fifty. This is in contrast to NHL, which shows a sharp increase in incidence only after age forty-five. The reasons are unknown.

As noted earlier, the staging of Hodgkin disease is important in determining methods of treatment; the earlier the stage, the better the prognosis. Patients in stage I (single node or site of involvement) or stage II (two or more nodes on the same side of the diaphragm involved, or limited extralymphatic involvement) have a much better prognosis than patients in stages III and IV (splenic or disseminated disease). Prior to the mid-1960s, a diagnosis of Hodgkin disease was almost a death sentence. The development of radiation therapy and chemotherapy has dramatically increased the chances for survival; long-term remission can be achieved in nearly 70 percent of patients, and the “cure” rate may be higher than 90 percent with early detection. In part, this has been the result of understanding the progression of the disease (reflected in the process of staging) and utilizing a therapeutic approach to eradicate the disease both at its current site and at likely sites of spreading.

Radiation therapy
is the treatment of choice for patients in stages I and II; spreading beyond local nodes is still unlikely in these stages. The body is divided into three regions to which radiation may be delivered: The mantle field covers the upper chest and armpits; the para-aortic field is the region of the diaphragm and spleen; and the third field is the pelvic area. For example, a patient manifesting lymphadenopathy in a single node in the neck region may undergo only “mantle” irradiation. As noted above, with early detection, such treatment is effective 90 percent of the time (based on five-year disease-free survival).

Beyond stage II, a combination of radiation therapy and chemotherapy treatment is warranted. A variety of chemotherapy programs have been developed, the most common of which is known by the acronym MOPP (nitrogen mustard/Oncovin/procarbazine/prednisone). With combined radiation therapy and chemotherapy, even stage III disease may go into remission 60 to 70 percent of the time, while 40 to 50 percent of stage IV patients may enter remission. In general, therapy takes six to twelve months.

Non-Hodgkin lymphomas represent a heterogeneous group of malignancies. Eighty percent are of B-lymphocyte origin. The wide variety of types has made classification difficult. The most useful method of classification for clinical purposes is based on the relative aggressiveness of the disease, low-grade being the slowest growing, followed by intermediate-grade and high-grade, which is the most aggressive.

NHLs often arise in lymphoid areas outside the mainstream. For example, the first sign of disease may be an abdominal mass or pain. Fever and night sweats are uncommon, at least in the early stages. Consequently, once the disease is manifested, it is often deep and widespread. Because the disorder is no longer localized by this stage, radiation therapy by itself is of limited use. For comparison, nearly half of Hodgkin disease patients are in stage I at presentation; not quite 15 percent of NHL patients are in stages I and II. Consequently, treatment almost always involves extensive chemotherapy.

A variety of aggressive forms of chemotherapy may be applied. These may include either single drugs such as alkaloids (vincristine sulfate) and alkylating agents (chlorambucil) or combination programs such as that of MOPP. Low-grade types of NHL are frequently slow growing and respond well to less aggressive forms of therapy. Low-grade NHL patients often enter remission for years. Unfortunately, the disorder often recurs with time and may become resistant to treatment; remission may occur in 50 percent of the patients, but only about 10 percent survive disease-free after ten years. High-grade lymphomas are rapidly growing, and the prognosis for most patients in the short term is not good. Those patients who do achieve remission with aggressive therapy, however, often show no recurrence of disease. As many as 50 percent of these persons may be “cured.” The difference in prognosis between low-grade and high-grade disease may relate to the characteristics of the malignant cell. A rapidly growing cancer cell may be more susceptible to aggressive therapy than a slow-growing cancer and more likely to die as a result. Thus, if a patient enters remission following therapy, there is greater likelihood that the cancer has been eradicated.

Perspective and Prospects

What was likely Hodgkin disease was first described in 1666 as an illness in which lymphoid tissues and the spleen had the appearance of a “cluster of grapes.” The disorder was invariably fatal. In 1832, Thomas Hodgkin published a thorough description of the disease, including its progression from the cervical region of the body to other lymphatic regions and organs. The unusual histological appearance of the cellular mixture characteristic of Hodgkin disease was noted during the nineteenth century. It was early in the twentieth century, however, that Dorothy Reed and Karl Sternberg described the cell that is characteristic of the disorder: the Reed-Sternberg cell. As noted earlier, the number and proportion of such cells are the bases for the classification of the disease.

Two forms of non-Hodgkin lymphoma are known to be associated with specific viruses: Burkitt lymphoma (BL) and adult T-cell leukemia (ATL). BL was described by Denis Burkitt, who studied the pattern of certain forms of lymphomas among Ugandan children during the late 1950s. He noted that nearly all cases were found in children between the ages of two and fourteen, and noted that most cases in Africa were found in the malarial belt. Burkitt suspected that a mosquito might be involved in the transmissions of BL. Though no link has been found with arthropod transmission, the idea that BL might be associated with a viral agent bore fruit. In 1964, Michael Epstein and Yvonne Barr reported the presence of a particle in BL tissue that resembled the herpes virus. The Epstein-Barr virus was eventually linked to BL, though the specific role played by the virus remains elusive.

Adult T-cell leukemia was first noted in Japan during the 1970s. Japanese scientists observed that the majority of NHLs there were of T-cell origin and exhibited a similar clinical spectrum. The disease was later observed in the Caribbean basin, the southeastern United States, South America, and central Africa. In 1980, Robert Gallo isolated the etiological agent, the human T-cell lymphotrophic type I virus (HTLV-I).

The treatment of Hodgkin disease represents one of the few success stories in dealing with cancers. In addition, some forms of NHL—notably, Burkitt lymphoma—respond well to treatment. The prognosis for most patients with NHL, however, is less than optimal. In addition, the specific causes of most NHL syndromes are not known. Those with which a virus is linked may, in theory, be prevented by means of vaccination. The etiological agents or factors associated with the development of other forms of lymphomas remain elusive.

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