Alzheimer's Disease Animation, Causes, Sign symptoms And Treatment

Introduction:

Alzheimer's disease (AD) is a degenerative disease of the brain from which there is no recovery. The disease slowly attacks nerve cells in all parts of the cortex of the brain and some surrounding structures, thereby impairing a person's abilities to govern emotions, recognize errors and patterns, coordinate movement, and remember.

Causes:

Researchers are finding specific biologic factors involved with Alzheimer's disease. Various environmental and genetic players appear to contribute to or trigger the process by which these factors destroy nerve cells leading to this disease.

Biologic Factors in the Brain:

Imaging techniques in patients with Alzheimer's disease have found significant loss of cells and volume in the regions of the brain devoted to memory and higher mental functioning. Important abnormalities have specifically been observed during biopsies:

• Twisted nerve cell fibers, known as neurofibrillary tangles
• A sticky protein called beta amyloid

The Effects of Neurofibrillary Tangles and Beta Amyloid in Alzheimer's Disease. These biologic factors appear to be involved in the development Alzheimer's disease in the following ways:

• Neurofibrillary tangles are the damaged remains of microtubules, the support structure that allows the flow of nutrients through the neurons (nerve cells). A key component in these tangled fibers is an abnormal form of the tau protein, which in its healthy version helps in the assembly of the microtubule structure. The defective tau, however, appears to block the actions of the normal version.
• Beta Amyloid (also called A beta) is the second significant finding. This insoluble protein accumulates and forms sticky patches called neuritic plaque, which are found surrounded by the debris of dying nerve cells in the brains of Alzheimer's victims.
• Amyloid precursor protein (APP) is a large nerve-protecting protein that is the source of beta amyloid. In Alzheimer's certain enzymes, particularly those called gamma-secretases, snip APP into beta amyloid pieces. This process is controlled by factors called presenilin proteins. (Genetic abnormalities that affect either APP or presenilin proteins occur in some inherited cases of early-onset Alzheimer's.)
• High levels of beta amyloid are associated with reduced levels of the neurotransmitter acetylcholine. (Neurotransmitters are chemical messengers in the brain.) Acetylcholine is part of the cholinergic system, which is essential for memory and learning and is progressively destroyed in Alzheimer's disease.
• Beta amyloid may also disrupt channels that carry sodium, potassium, and calcium. These elements serve the brain as ions, producing electric charges that must fire regularly in order for signals to pass from one nerve cell to another. If the channels that carry ions are damaged, an imbalance can interfere with nerve function and signal transmission.

Other Proteins. Researchers have now identified other important proteins in the areas of the brain affected by Alzheimer's disease.

• ERAB (endoplasmic-reticulum associated binding protein) appears to combine with beta amyloid, which in turn attracts new beta amyloid from outside the cells. High amounts of ERAB may also enhance the nerve-destructive power of beta amyloid.
• AMY plaques resemble beta amyloid so closely that researchers were able to detect them only with the use of highly sophisticated techniques.
• Elevated levels of a protein called prostate apoptosis response-4 (Par-4) may cause nerve cells to self-destruct.

Oxidation and the Inflammatory Response:

Researchers are also attempting to discover why beta amyloid is so toxic to nerve cells. Some researchers are focusing on two processes in the body that may be involved with Alzheimer's disease: oxidation and the inflammatory process. There is some evidence that such events can begin decades before Alzheimer's disease actually develops. One scenario for their role in Alzheimer's is as follows:
The Role of Oxidation.

• As beta amyloid breaks down it releases unstable chemicals called oxygen-free radicals. Once released, oxygen-free radicals bind to other molecules through a process called oxidation.
• Oxidation is the result of many common chemical processes in the body, but when oxidants are overproduced, they can cause severe damage in cells and tissue, including even affecting genetic material in cells (its DNA). Oxidation is known to play a role in many serious diseases, including coronary artery disease and cancers, and experts believe it may also contribute to Alzheimer's.

The Inflammatory Response.

• One result of oxidation is the marshaling of immune factors to repair the cellular injuries it produces. Overproduction of some of these factors, however, produces the so-called inflammatory response, in which the immune process itself can actually damage the body's own cells themselves.
• Principle immune cells in the brain are called macrophage/microglia (M phi). In the healthy brain, they play an important protective role against invading organisms. However, when they are activated by beta amyloid oxidation, they release toxic molecules called cytokines, which are known to cause harm. For example, significantly high levels of interleukin-6, a specific cytokine, have been detected in people with Alzheimer's.
• Other inflammatory factors of specific interest in Alzheimer's research are the enzyme cyclooxygenase (COX) and its products called prostaglandins. Excess amounts of these factors may increase levels of glutamate. Glutamate is an amino acid that excites nerves and, when overproduced, is a powerful nerve-cell killer.
• The inflammatory process has also been associated with the release of soluble toxins called amyloid beta derived diffusible ligands, which some investigators believe may prove to key players in the destructive process.

Genetic Factors:

Major research targets in Alzheimer's disease are the factors responsible for beta amyloid build-up and concentration in certain people and not in others. Genetic factors are believed to play a role in many cases. In 2003, the National Institute on Aging (NIA) launched the ambitious AD Genetics Initiative, a 3-year national project to bank genetic material from families who have at least two members with late-onset Alzheimer's.
The ApoE Gene and Late-Onset Alzheimer's. The major target in genetic research on late-onset Alzheimer's disease (called LOAD) has been apolipoprotein E (ApoE), which plays a role in the movement and distribution of cholesterol for repairing nerve cells during development and after injury.

The gene for ApoE comes in three major types:

• ApoE4. Studies have reported the greatest deposits of beta amyloid in people with ApoE4, which is now believed to be a major risk factor for late-onset Alzheimer's. Some evidence suggests that the ApoE protein removes beta amyloid but the ApoE4 variant does so less efficiently than other ApoE types. (ApoE4 has also been studied for years as a risk factor for heart disease.)
• ApoE3 and ApoE2. Fewer beta amyloid deposits have been observed in people with the ApoE3, and the fewest deposits have been observed in people with ApoE2, which may actually be protective.

People inherit a copy of one type from each parent, but Alzheimer's disease is not inevitable even in people with two copies of the ApoE4 gene. Reports vary widely in estimating the extent of risk:

• People without ApoE4 have an estimated risk of between 9 - 20% for developing Alzheimer's by age 85.
• In people with one copy of the gene, the risk is between 25 - 60%.
• In people with two copies, the risk ranges from 50 - 90%. (Only 2% of the population carries two copies of the ApoE4 gene.)

Some researchers suspect that some specific variation of the ApoE4 gene or combinations with other genes are critical for the disease, since many people who carry the ApoE4 exhibit no signs of Alzheimer's. For example, evidence suggests that genetic factors play a role in a common subtype of late-onset Alzheimer's disease that also includes psychosis. An important 2002 genetic study has identified certain genetic linkages associated with ApoE4 that appear to play a strong role in this subtype.

Genetic Factors for Early-Onset Alzheimer's. Scientists are coming closer to identifying defective genes responsible for early-onset Alzheimer's, an uncommon, but extremely aggressive form of the disease.

• Mutations in genes known as presenilin-1 (PS1) and presenilin-2 (PS2) account for most cases of early-onset inherited Alzheimer's disease. The defective genes appear to accelerate beta amyloid plaque formation and apoptosis, a natural process by which cells self-destruct.
• Genetic mutations in the genes that control amyloid precursor protein (APP) are also being targeted as causes of early-onset Alzheimer's. The genetic disease Down syndrome, for example, overproduces beta-amyloid precursor protein (APP), the source of beta amyloid, and almost always leads to early Alzheimer's. Other APP mutations are being identified.

Environmental Factors:

Researchers are also investigating environmental factors (infections, metals, industrial and other toxins) that may trigger oxidation, inflammation, and the disease process, particularly in people with a genetic susceptibility to Alzheimer's.
Infectious Organisms. Slow, infectious viruses cause a number of other degenerative neurologic diseases, such as kuru and Creutzfeldt-Jakob disease.

Risk Factors:

Alzheimer's disease is the seventh leading cause of death in Americans adults. It affects an estimated 4.5 million Americans and 8 million more people worldwide. Age is the greatest risk factor for Alzheimer's disease. The number of cases of Alzheimer's disease doubles every 5 years in people over 65. By age 85, almost half of all people are afflicted. People with the disease survive, on average, half as long as similarly aged adults without the disease.
With the increasing numbers of aging adults, unless effective methods for prevention and treatment are developed, Alzheimer's disease will reach epidemic proportions, afflicting an estimated 14 million Americans within 50 years. Evidence points to older age, high blood pressure, cholesterol levels, and a family history of the disease as the most important risk factors for Alzheimer's disease.

Gender and Estrogen Loss:

Several studies have reported that women have a much higher risk for Alzheimer's disease than men. If there is a gender difference, it is likely to be due estrogen, the primary female hormone, which appears to have properties that protect against the memory loss and lower mental functioning associated with normal aging. Such actions include blocking production of beta amyloid, offering antioxidant protection, and regulating blood sugar (glucose) levels in the brain. The drop in estrogen levels after menopause may explain a higher risk for Alzheimer's disease in older women than in men. (Testosterone, the male hormone, converts to estrogen, which may help protect men.) Studies have been mixed, however, on the association between the decline in natural estrogen levels and mental functioning in older women.

Family History and Populations Differences;

People with a family history of the disease are at higher than average risk for Alzheimer's disease. Researchers are identifying important genetic factors, notably the ApoE4 gene, that may be responsible for late- and early-onset cases.
Dietary and other cultural factors that increase the risk for hypertension and unhealthy cholesterol levels may also play a role. For example, a study of Japanese men showed that their risk increased if they emigrated to America. And the disease is much less common in West Africa than in African Americans, who share the same or higher risk with Caucasians Americans.

Symptoms;

The early symptoms of Alzheimer's disease (AD) may be overlooked because they resemble signs of natural aging. Older adults who begin to notice a persistent mild memory loss of recent events may have a condition called mild cognitive impairment (MCI). MCI is now believed to be a significant sign of early-stage Alzheimer's in older people. Studies now suggest that older individuals who experience such mild memory abnormalities can later develop Alzheimer's disease.
Early symptoms of Alzheimer's disease may include:

• Forgetfulness (particularly of recent events or information)
• Loss of concentration (having trouble planning or completing familiar tasks, difficulty with abstract thinking such as simple arithmetic problems)
• Language problems (forgetting the names of objects, mixing up words, difficulty completing sentences)
• Confusion about time and place (difficulty recognizing familiar neighborhoods or remembering how arrived at a location, confusion about months or seasons )
• Impaired judgement (dressing inappropriately or making poor financial decisions)
• Impaired movement and coordination (slowing of movements, halting gait, reduced sense of balance)
• Mood and behavior changes (rapid mood swings, emotional outbursts, personality changes, increased fear or suspicion)
• Apathy and depression (loss of interest in activities, increased sleeping, sitting in front of the television for long periods of time)

Diagnosis:

A definitive test to diagnose Alzheimer's disease, even in patients showing signs of dementia, has not yet been developed. A number of expert groups have developed criteria to help diagnose Alzheimer's disease and rule out other disorders. A diagnosis often involves answering questions about the patient:

• Do psychologic tests indicate dementia?
• Does the patient have deficits in two or more areas of mental functioning (such as language, motor skills, and perceptions)?
• Has memory and mental functions gotten progressively worse?
• Is consciousness disturbed? (It is not in Alzheimer's disease.)
• Is the patient over age 40?
• Are other medical or physical conditions present that could account for the same symptoms?
• Are daily activity impaired or has the behavior changed?
• Is there a family history of Alzheimer's disease?
• Are there other symptoms, such as depression, insomnia, incontinence, delusions, hallucinations, dramatic verbal, emotional or physical outbursts, sexual disorders, and weight loss?

Other steps involved in making a decision include laboratory tests (EEG and possibly tests to rule out other diseases) and psychological testing to determine the presence of dementia.

Ruling out Conditions of Normal Aging that Can Cause Alzheimer's-like Symptoms;

Although some memory impairment occurs in many people as they age, only some of these people develop Alzheimer's disease. Many similar symptoms can occur in healthy older individuals from other conditions associated with aging:

• Fatigue
• Grief or depression
• Illness
• Vision or hearing loss
• The use of alcohol or certain medications
• Simply the burden of too many details to remember at once

Ruling Out Other Causes Memory Loss or Dementia;

The first step in diagnosing Alzheimer's disease is to rule out other conditions that might cause memory loss or dementia. There are a number of causes for dementia in the elderly besides Alzheimer's disease:

• Vascular dementia (abnormalities in the vessels that carry blood to the brain)
• Lewy bodies variant (LBV), also called dementia with Lewy bodies
• Parkinson's disease
• Frontotemporal dementia

Experts believe that 60% of cases of dementia are due to Alzheimer's, 15% to vascular injuries, and the rest are a mixture of the two or caused by other factors.
Vascular Dementia. Vascular dementia is primarily caused by either multi-infarct dementia (multiple small strokes) or Binswanger's disease (which affects tiny arteries in the midbrain). One major analysis suggested that patients with vascular dementia have better long term verbal memory than patients with Alzheimer's disease, but poorer executive function (less ability to integrate and organize).

Lewy Bodies Variant. Lewy bodies are abnormalities found in the brains of patients with both Parkinson's disease and Alzheimer's. They can also be present in the absence of either disease; in such cases, the condition is called Lewy bodies variant (LBV). In all cases, the presence of Lewy bodies is highly associated with dementia. LBV was defined in 1997 and some experts believe it may be responsible for about 20% of people who have been diagnosed with Alzheimer's. They can be difficult to distinguish. Compared to Alzheimer's disease patients, those with LBV may be more likely to have hallucinations and delusions early on, to walk with a stoop (similar to Parkinson's disease), to have more fluctuating attention problems, and to perform better than Alzheimer's disease patients on verbal recall but less well with organizing objects.
Parkinson's Disease. Dementia is about six times more common in the elderly Parkinson patient than in the average older adult. It is most likely to occur in older patients who have had major depression. Unlike in Alzheimer's, language is not usually affected in Parkinson's related dementia. Visual hallucinations occur in about a third of people on long-term medications.

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ADHD Animation, Causes, Sign Symptoms And Treatment

DEFINITION:
ADHD is a problem with inattentiveness, over-activity, impulsivity, or a combination. For these problems to be diagnosed as ADHD, they must be out of the normal range for the child's age and development.

Alternative Names;
ADD; ADHD; Childhood hyperkinesis

Causes, incidence, and risk factors;
ADHD affects school performance and interpersonal relationships. Parents of children with ADHD are often exhausted and frustrated.
Neuroimaging studies suggest that the brains of children with ADHD are different from those of other children. These children handle neurotransmitters (including dopamine, serotonin, and adrenalin) differently from their peers.
ADHD is often genetic. Whatever the specific cause may be, it seems to be set in motion early in life as the brain is developing.
Depression, sleep deprivation, learning disabilities, tic disorders, and behavior problems may be confused with, or appear along with, ADHD. Every child suspected of having ADHD deserves a careful evaluation to sort out exactly what is contributing to the behaviors causing concern.
Attention Deficit Disorder (ADD) is the most commonly diagnosed behavioral disorder of childhood, affecting an estimated 3 - 5% of school aged children. It is diagnosed much more often in boys than in girls.
Most children with ADHD also have at least one other developmental or behavioral problem.

Symptoms:
The Diagnostic and Statistical Manual (DSM-IV) divides the symptoms of ADHD into those of inattentiveness and those of hyperactivity and impulsivity.
To be diagnosed with ADHD, children should have at least 6 attention symptoms or 6 activity and impulsivity symptoms -- to a degree beyond what would be expected for children their age.
The symptoms must be present for at least 6 months, observable in 2 or more settings, and not caused by another problem. The symptoms must be severe enough to cause significant difficulties. Some symptoms must be present before age 7.
Older children have ADHD in partial remission when they still have symptoms but no longer meet the full definition of the disorder.
Some children with ADHD primarily have the Inattentive Type, some the Hyperactive-Impulsive Type, and some the Combined Type. Those with the Inattentive type are less disruptive and are easier to miss being diagnosed with ADHD.

Inattention symptoms:

1. Fails to give close attention to details or makes careless mistakes in schoolwork
2. Difficulty sustaining attention in tasks or play
3. Does not seem to listen when spoken to directly
4. Does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace
5. Difficulty organizing tasks and activities
6. Avoids or dislikes tasks that require sustained mental effort (such as schoolwork)
7. Often loses toys, assignments, pencils, books, or tools needed for tasks or activities
8. Easily distracted
9. Often forgetful in daily activities

Hyperactivity symptoms:

1. Fidgets with hands or feet or squirms in seat
2. Leaves seat when remaining seated is expected
3. Runs about or climbs in inappropriate situations
4. Difficulty playing quietly
5. Often "on the go," acts as if "driven by a motor," talks excessively

Impulsivity symptoms:

1. Blurts out answers before questions have been completed
2. Difficulty awaiting turn
3. Interrupts or intrudes on others (butts into conversations or games)

Signs and tests:
Too often, difficult children are incorrectly labeled with ADHD. On the other hand, many children who do have ADHD remain undiagnosed. In either case, related learning disabilities or mood problems are often missed. The American Academy of Pediatrics (AAP) has issued guidelines to bring more clarity to this issue.
The diagnosis is based on very specific symptoms, which must be present in more than one setting. The child should have a clinical evaluation if ADHD is suspected.
Evaluation may include:

• Parent and teacher questionnaires (Connors, Burks)
• Psychological evaluation of the child AND family including IQ testing and psychological testing
• Complete developmental, mental, nutritional, physical, and psychosocial examination

Treatment:
The American Academy of Pediatrics has guidelines for treating ADHD:

• Set specific, appropriate target goals to guide therapy.
• Medication and behavior therapy should be started.
• When treatment has not met the target goals, evaluate the original diagnosis, the possible presence of other conditions, and how well the treatment plan has been implemented.
• Systematic follow-up is important to regularly reassess target goals, results, and any side effects of medications. Information should be gathered from parents, teachers, and the child.

ADHD is a frustrating problem. Alternative remedies have become quite popular, including herbs, supplements, and chiropractic manipulation. However, there is little or no solid evidence for many remedies marketed to parents.
Children who receive both behavioral treatment and medication often do the best. Medications should not be used just to make life easier for the parents or the school. There are now several different classes of ADHD medications that may be used alone or in combination. Some ADHD medicines have been linked to sudden death in children with heart problems. Talk to your doctor about which drug is best for your child.
The following may also help:

• Limit distractions in the child's environment.
• Provide one-on-one instruction with teacher.
• Make sure the child gets enough sleep.
• Make sure the child gets a healthy, varied diet, with plenty of fiber and basic nutrients.

Expectations (prognosis):
ADHD is a long-term, chronic condition. About half of the children with ADHD will continue to have troublesome symptoms of inattention or impulsivity as adults. However, adults are often more capable of controlling behavior and masking difficulties.
Statistics show that there is an increased incidence in juvenile delinquency and adult encounters with the law among individuals who had ADHD as a child.
Every effort should be made to manage symptoms and direct the child's energy to constructive and educational paths.

Complications:
Many adults with ADHD are in successful jobs. Possible complications, if ADHD is not adequately treated, could include failure in school or other similar problems.

Prevention:
While there is no proven way to prevent ADHD itself, early identification and treatment can prevent many of the problems associated with ADHD.

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Actinic Keratosis Animation, Causes, Sign Symptoms and Treatment

DEFINITION:
Actinic keratosis is a precancerous skin growth usually caused by sun exposure.

Alternative Names;
Solar keratosis; Sun-induced skin changes - keratosis; Keratosis - actinic (solar)

Causes, incidence, and risk factors:
Actinic keratosis occurs most commonly in fair skin, especially in the elderly and in young individuals with light complexions. The growths occur in sun-exposed skin areas. The growths begin as flat, scaly areas that later develop a hard wart-like surface.
They are classified as precancerous growths. If left untreated, approximately 1% of actinic keratoses develop into squamous cell carcinoma.

Symptoms:

• Rough and dry textured skin lesion
• A macule, patch, or growth on the skin
  • Limited to a discrete area (localized)
  • Located on the face, scalp, back of the hands, chest or other sun-exposed areas
  • Gray, pink, red (erythematous), or the same color as the skin
  • Initially flat and scaly on the surface, becoming slightly raised
  • Becoming hard and wart-like or gritty, rough, and "sandpapery" -- may develop a horn-like texture from overgrowth of skin keratin layer (hyperkeratosis)

Signs and tests:
The health care provider bases the diagnosis on the appearance of the skin growth. A skin biopsy could reveal signs of cancerous changes, if present.

Treatment:
Because actinic keratoses represent precancerous changes, you should have them examined promptly and follow the health care provider's advice for treatment.
Growths may be removed by cryotherapy (freezing), electrical cautery (burning), or surgery. Growths may also be treated with medications that cause skin peeling or removal. More recently, lasers and other light sources have been used to treat actinic keratoses.

Expectations (prognosis):
Actinic keratosis itself is benign, but it may develop into skin cancer. Removal of the growth is usually effective.

Complications:

• Squamous cell carcinoma
• Irritation and discomfort of the skin growth

Calling your health care provider:
Call for an appointment with your health care provider if areas of persistent roughness or scaliness develop in sun-exposed skin.

Prevention:
Reduce sun exposure and protect your skin from the sun. Wear protective clothing such as hats, long-sleeved shirts, long skirts, or pants. Ultraviolet light is most intense midday, so try to avoid sun exposure during these hours.
Use high-quality sunscreens, preferably with SPF (sun protection factor) ratings of at least 15. Pick a sunscreen that blocks both UBA and UVB light. Apply sunscreen at least 30 minutes before going out into the sun, and reapply frequently. Sunscreen should be used year-round, including in the winter.

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Acne Animation, Causes and Description, Diagnosis and Treatment

Boils and carbuncles are bacterial infections of hair follicles and surrounding skin that form pustules (small blister-like swellings containing pus) around the follicle. Boils are sometimes called furuncles. A carbuncle is formed when several furuncles merge to form a single deep abscess with several heads or drainage points.



DESCRIPTION:

Boils and carbuncles are firm reddish swellings about 0.2-0.4in (5-10 mm) across that are slightly raised above the skin surface. They are sore to the touch. A boil usually has a visible central core of pus; a carbuncle is larger and has several visible heads. Boils occur most commonly on the face, back of the neck, buttocks, upper legs and groin area, armpits, and upper torso. Carbuncles are less common than single boils; they are most likely to form at the back of the neck. Males are more likely to develop carbuncles.
Boils and carbuncles are common problems in the general population, particularly among adolescents and adults.

People who are more likely to develop these skin infections include those with:

• diabetes, especially when treated by injected insulin
• alcoholism or drug abuse
• poor personal hygiene
• crowded living arrangements
• jobs or hobbies that expose them to greasy or oily substances, especially petroleum products
• allergies or immune system disorders, including HIV infection.
• family members with recurrent skin infections

CAUSES AND SYMPTOMS:

Boils and carbuncles are caused by Staphylococcus aureus, a bacterium that causes an infection in an oil gland or hair follicle. Although the surface of human skin is usually resistant to bacterial infection, S. aureus can enter through a break in the skin surface--including breaks caused by needle punctures for insulin or drug injections. Hair follicles that are blocked by greasy creams, petroleum jelly, or similar products are more vulnerable to infection. Bacterial skin infections can be spread by shared cosmetics or washcloths, close human contact, or by contact with pus from a boil or carbuncle.
As the infection develops, an area of inflamed tissue gradually forms a pus-filled swelling or pimple that is painful to touch. As the boil matures, it forms a yellowish head or point. It may either continue to swell until the point bursts open and allows the pus to drain, or it may be gradually reabsorbed into the skin. It takes between one and two weeks for a boil to heal completely after it comes to a head and discharges pus. The bacteria that cause the boil can spread into other areas of the skin or even into the bloodstream if the skin around the boil is injured by squeezing. If the infection spreads, the patient will usually develop chills and fever, swollen lymph nodes (lymphadenitis), and red lines in the skin running outward from the boil.
Furunculosis is a word that is sometimes used to refer to recurrent boils. Many patients have repeated episodes of furunculosis that are difficult to treat because their nasal passages carry colonies of S. aureus. These bacterial colonies make it easy for the patient's skin to be reinfected. They are most likely to develop in patients with diabetes, HIV infection, or other immune system disorders.
Carbuncles are formed when the bacteria infect several hair follicles that are close together. Carbunculosis is a word that is sometimes used to refer to the development of carbuncles. The abscesses spread until they merge with each other to form a single large area of infected skin with several pus-filled heads. Patients with carbuncles may also have a low-grade fever or feel generally unwell.

DIAGNOSIS:

The diagnosis of boils and carbuncles is usually made by the patient's primary care doctor on the basis of visual examination of the skin. In some cases involving recurrent boils on the face, the doctor may need to consider acne as a possible diagnosis, but for the most part boils and carbuncles are not difficult to distinguish from other skin disorders.

TREATMENT:

Patient and Family education
Patient education is an important part of the treatment of boils and carbuncles. Patients need to be warned against picking at or squeezing boils because of the danger of spreading the infection into other parts of the skin or bloodstream. It is especially important to avoid squeezing boils around the mouth or nose because infections in these areas can be carried to the brain. Patients should also be advised about keeping the skin clean, washing their hands carefully before and after touching the boil or carbuncle, avoiding the use of greasy cosmetics or creams, and keeping their towels and washcloths separate from those of other family members. Some doctors may recommend an antiseptic soap or gel for washing the infected areas.

If the patient has had several episodes of furunculosis, the doctor may examine family members or close contacts to see if they are carriers of S. aureus. In many cases they also need treatment for boils or carbuncles. Skin infections and reinfections involving small groups or clusters of people are being reported more frequently in the United States.

MEDICATION:

Boils are usually treated with application of antibiotic creams--usually clindamycin or polymyxin--following the application of hot compresses. The compresses help the infection to come to a head and drain.

Carbuncles and furunculosis are usually treated with oral antibiotics as well as antibiotic creams or ointments. The specific medications that are given are usually dicloxacillin (Dynapen) or cephalexin (Keflex). Erythromycin may be given to patients who are allergic to penicillin. The usual course of oral antibiotics is 5-10 days; however, patients with recurrent furunculosis may be given oral antibiotics for longer periods. Furunculosis is treated with a combination of dicloxacillin and rifampin (Rifadin).

Patients with bacterial colonies in their nasal passages are often given mupirocin (Bactroban) to apply directly to the lining of the nose.

SURGICAL TREATMENT:

Boils and carbuncles that are very large, or that are not draining, may be opened with a sterile needle or surgical knife to allow the pus to drain. The doctor will usually give the patient a local anesthetic if a knife is used; surgical treatment of boils is painful and usually leaves noticeable scars.

ALTERNATIVE TREATMENT:

Naturopathic therapy
Naturopathic practitioners usually recommend changes in the patient's diet as well as applying herbal poultices to the infected area. The addition of zinc supplements and vitamin A to the diet is reported to be effective in treating boils. The application of a paste or poultice containing goldenseal (Hydrastis canadensis) root is recommended by naturopaths on the grounds that goldenseal helps to kill bacteria and reduce inflammation.

Homeopathy
Homeopaths maintain that taking the proper homeopathic medication in the first stages of a boil or carbuncle will bring about early resolution of the infection and prevent pus formation. The most likely choices are Belladonna or Hepar sulphuris. If the boil has already formed, Mercurius vivus or Silica may be recommended to bring the pus to a head.

Western herbal therapies
A variety of herbal remedies can be applied topically to boils to fight infection. These include essential oils of bergamot (Citrus bergamia), chamomile (Matricaria recutita), lavender (Lavandula officinalis), and sage (Salvia officinalis), as well as tea tree oil (Melaleuca spp.). Herbalists also recommend washing the skin with a mixture of goldenseal and witch hazel. To fight the inflammation associated with boils, herbalists suggest marsh mallow (Althaea officinalis) ointment, tinctures (herbal solutions made with alcohol) of blue flag (Iris versicolor) or myrrh (Commiphora molmol), and slippery elm (Ulmus fulva) made into a poultice.

Prognosis
The prognosis for most boils is excellent. Some patients, however, suffer from recurrent carbuncles or furunculosis. In addition, although the spread of infection from boils is relatively unusual, there have been deaths reported from brain infections caused by squeezing boils on the upper lip or in the tissue folds at the base of the nose.

Prevention

• There are some precautions that people can take to minimize the risk of developing bacterial skin infections:
• cleanse skin properly with soap and water, and take showers rather than tub baths
• do not share washcloths, towels, or facial cosmetics with others
• cut down on greasy or fatty foods and snacks
• always wash hands before touching the face
• consider using antiseptic soaps and shower gels
• consult a doctor if furunculosis is a persistent problem--it may indicate an underlying disease such as diabetes

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Allergy Animation, Description, Causes, Sign symtoms and treatment

Definition

Allergic rhinitis is a collection of symptoms, predominantly in the nose and eyes, caused by airborne particles of dust, dander, or plant pollens in people who are allergic to these substances.
When these symptoms are caused by pollen, the allergic rhinitis is commonly called hay fever.

Alternative Names

Hay fever; Nasal allergies

Causes, incidence, and risk factors

Allergies are caused by an over-sensitive immune response. The immune system normally protects the body against harmful substances such as bacteria and viruses. Allergy symptoms occurs when the immune system reacts to substances (allergens) that are generally harmless and in most people do not cause an immune responseWhen a person with allergies breathes in an allergen such as pollen or dust, antibodies are produced. When the antibodies are stimulated by pollen and dust, histamine and other chemicals are released. This causes itching, swelling, and mucus production. Symptoms vary from person to person. Very sensitive individuals can experience hives or other rashes.
Hay fever involves an allergic reaction to pollen. A similar reaction occurs with allergy to mold, animal dander, dust, and similar inhaled allergens.
The pollens that cause hay fever vary from person to person and from region to region. Large, visible pollens are seldom responsible for hay fever. Tiny, hard to see pollens more often cause hay fever. Examples of plants commonly responsible for hay fever include:

• Trees (deciduous and evergreen)
• Grasses
• Ragweed

The amount of pollen in the air can play a role in whether hay fever symptoms develop. Hot, dry, windy days are more likely to have increased amounts of pollen in the air than cool, damp, rainy days when most pollen is washed to the ground.
Some disorders may be associated with allergies. These include eczema and asthma.
Allergies are common. Your genes and environmental may make you more prone to allergies.
Symptoms

• Coughing
• Headache
• Itching nose, mouth, eyes, throat, skin, or any area
• Runny nose
• Problems with smell
• Sneezing
• Stuffy nose (nasal congestion)
• Tearing eyes
• Sore throat
• Wheezing

Signs and tests

The health care provider will perform a physical exam and ask you questions about your symptoms. Your history of symptoms is important in diagnosing allergic rhinitis, including whether the symptoms vary according to time of day or the season, exposure to pets or other allergens, and diet changes.

Allergy testing may reveal the specific allergens the person is reacting to. Skin testing is the most common method of allergy testing. This may include scratch, patch, or other tests.

If your doctor determines you cannot undergo skin testing, the RAST blood test may help determine which allergens you are sensitive to.

Treatment

The goal of treatment is to reduce allergy symptoms caused by the inflammation of affected tissues. The best "treatment" is to avoid what causes your allergic symptoms in the first place. It may be impossible to completely avoid all allergens to which you are sensitive, but you can often take steps to reduce exposure. Medication options include the following:

• Short-acting antihistamines can relieve mild to moderate symptoms, but can cause drowsiness. Many may be bought without a prescription. A pediatrician should be consulted before using these medicines in children, as they may affect learning. Loratadine (Claritin) is now available over the counter. It does not tend to cause drowsiness or affect learning in children.
• Longer-acting antihistamines are available by prescription. They cause less drowsiness and can work just as well. They usually do not interfere with learning. These medications include fexofenadine (Allegra), and cetirizine (Zyrtec).
• Nasal corticosteroid sprays work very well for people with symptoms not relieved by antihistamines alone. These prescription medications include fluticasone (Flonase), mometasone (Nasonex), and triamcinolone (Nasacort).
• Azelastine (Astelin) is a new, nasal antihistamine that is used to treat allergic rhinitis.
• Decongestants may also be helpful in reducing symptoms such as nasal congestion, but they should not be used for long periods.
• Cromolyn sodium is a nasal spray (Nasalcrom) for treating hay fever. Eye drop versions of cromolyn sodium and antihistamines are available for itchy, bloodshot eyes.
• The leukotriene inhibitor Singulair is a prescription medicine approved to help control asthma and to help relieve the symptoms of seasonal allergies.

The most appropriate medication depends on the type and severity of symptoms. Specific illnesses that are caused by allergies (such as asthma and eczema) may require other treatments.
Allergy shots (immunotherapy) are occasionally recommended if the allergen cannot be avoided and if symptoms are hard to control. This includes regular injections of the allergen, given in increasing doses (each dose is slightly larger than the previous dose) that may help the body adjust to the antigen.

Expectations (prognosis)

Most symptoms of allergic rhinitis can be readily treated.
In some cases (particularly children), people may outgrow an allergy as the immune system becomes less sensitive to the allergen. However, as a general rule, once a substance causes allergies for an individual, it can continue to affect the person over the long term.
More severe cases of allergic rhinitis require immunotherapy (allergy shots) or removal of tissue in the nose or sinuses.

Complications

• Drowsiness and other side effects of antihistamines
• Side effects of other medications
• Sinusitis
• Nasal polyps
• Disruption of lifestyle (usually not severe)

Prevention

Symptoms can sometimes be prevented by avoiding known allergens. During the pollen season, people with hay fever should remain indoors in an air-conditioned atmosphere whenever possible:

• Most trees produce pollen in the spring.
• Grasses usually produce pollen during the late spring and summer.
• Ragweed and other late-blooming plants produce pollen during late summer and early autumn.

For people who are sensitive to certain indoor allergens, dust mite covers for mattresses and pillowcases are recommended, as well as avoiding culprit pets or other triggers.

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Breast Cancer Causes, Examination and Treatment

Aims of breast cancer surgery

• To achieve cure if excised before metastatic spread has occurred
• To prevent unpleasant sequelae of local recurrence

Surgical options for the breast

• Breast Conserving Surgery (BCS) + radiotherapy
  • BCS is regarded as either wide local excision, quadrantectomy or segmentectomy
• Simple mastectomy
• Radical mastectomy - obsolete
• Mastectomy + reconstruction (immediate or delayed)

Tumours suitable for breast conservation

• Small single tumours in a large breast
• Peripheral location
• No local advancement or extensive nodal involvement
• For tumours that are suitable for breast conservation there is no difference in local recurrence or overall survival when BCS + radiotherapy is compared to mastectomy

Aims of axillary surgery

• 30-40% of patients with early breast cancer have nodal involvement
• The aims of axillary surgery is to:
  • To eradicate local disease
  • To determine prognosis to guide adjuvant therapy
• Clinical evaluation of the axilla is unreliable (30% false positive, 30% false negative)
• No reliable imaging techniques available
• Surgical evaluation important and should be considered for all patients with invasive cancer
• Levels of axillary clearance are assessed relative to pectoralis minor
  • Level 1 - below pectoralis minor
  • Level 2 - up to upper border of pectoralis minor
  • Level 3 - to the outer border of the 1st rib
• Axillary samplings removes more than 4 nodes
• Pre-operative axillary ultrasound and biopsy may allow a tailored approach to the axilla

Arguments for axillary clearance

• Axillary clearance both stages and treats the axilla
• Sampling potentially misses nodes and understages the axilla
• Surgical clearance possibly gains better local control
• Avoids complications of axillary radiotherapy
• Avoids morbidity of axillary recurrence

Arguments for axillary sampling

• Only stages the axilla
• Must be followed by axillary radiotherapy
• The 60% of patients with node negative disease have unnecessary surgery
• Radical lymphadenectomy in other cancers (e.g. melanoma) produces disappointing results
• Avoids morbidity of axillary surgery
• The combination of axillary clearance and radiotherapy is to be avoided
• Produces unacceptable rate of lymphoedema

Sentinel node biopsy

• Currently under investigation and should still be regarded as experimental
• Aims to accurately stage the axilla without the morbidity of axillary clearance
• Technique used to identify the first nodes that tumour drains to
• Can be located following the injection of either
  • Radioisotope
  • Blue dye
  • Combination of isotope and blue dye
• Can be injected in peritumoural, subdermal or subareolar site
• Allows more detailed examination of nodes removed
• Significance of micrometastatic deposits identified in sentinel nodes is unclear

Prognostic factors

• 50% women with operable breast cancer who receive locoregional treatment alone will die from metastatic disease.
• Prognostic factors have three main uses:
  • To select appropriate adjuvant therapy according to prognosis
  • To allow comparison of treatment between similar groups of patient at risk of recurrence or death
  • To improve the understanding of the disease
• Prognostic factors can be:
• Chronological
  • Indication of how long disease has been present
  • Relate to stage of the disease at presentation
• Biological
  • Relate to intrinsic behaviour of tumour

Chronological prognostic factors

• Age
  • Younger women have poorer prognosis of equivalent stage
• Tumour size
  • Diameter of tumour correlates directly with survival
• Lymph node status
  • Single best prognostic factor
  • Direct correlation between number and level of nodes involved and survival
• Metastases
  • Distant metastases worsen survival

Biological prognostic factors

• Histological type
  • Some histological types associated with improved prognosis:
    • Tubular
    • Cribriform
    • Mucinous
    • Papillary
    • Micro-invasive
• Histological grade
  • Three characteristics allow scoring of grade into grades one, two or three depending on:
    • Tubule formation
    • Nuclear pleomorphism
    • Mitotic frequency
• Lymphatic / vascular invasion
  • 25% operable breast cancers have lympho-vascular invasion
  • Double risk of local relapse
  • Higher risk of short term systemic relapse

Biochemical measurements

• Hormone and growth factor receptors
  • ER positivity predicts for response to endocrine manipulation
  • EGF receptors are negatively correlated with ER and poorer prognosis
• Oncogenes
  • Tumours that express C-erb-B2 oncogene likely to be
  • resistant to CMF chemotherapy
  • resistant to hormonal therapy
  • respond to anthracycline
  • respond to taxols
• Proteases
  • Urokinase and cathepsin D found in breast cancer
  • Presence confers a poorer prognosis

Chemotherapy in breast cancer

• Can be given as:
  • Primary systemic therapy prior to locoregional treatment
  • Adjuvant therapy following locoregional treatment
• Post-operative adjuvant chemotherapy
• Depends primarily on:
  • Age / menopausal status
  • Nodal status
  • Tumour grade
• Combination chemotherapy more effective than single drug
• Most commonly used regimen = CMF (Cyclophosphamide, Methotrexate, 5-Flurouracil)
• Given as six cycles at monthly intervals
• No evidence that more than 6 months treatment is of benefit
• Greatest benefit is seen in premenopausal women
• High -dose chemotherapy with stem cell rescue produces no overall survival benefit

Primary (neoadjuvant) chemotherapy

• Chemotherapy prior to surgery for large or locally advanced tumours
• Shrinks tumour often allowing breast conserving surgery rather than mastectomy
• 70% tumours show a clinical response
• In 20–30% this is response is complete
• Surgery required even in those with complete clinical response
• 80% of these patients still have histological evidence of tumour
• Primary systemic therapy has not to date been shown to improve survival

Endocrine therapy in breast cancer

• It is just over 100 years since Beatson described response to oophorectomy in women with advanced breast cancer

Tamoxifen

• Tamoxifen is an oral anti-oestrogen
• Effective in both the adjuvant setting and in advanced disease
• 20 mg per day is as effective as higher doses
• 5 years treatment is better than 2 years
• Value of treatment beyond 5 years is unknown
• Risk of contralateral breast cancer reduced by 40%
• Greater benefit seen in oestrogen receptor rich tumours
• Benefit still seen in oestrogen receptor negative tumours
• Benefit observed in both pre and post menopausal women

Aromatase inhibitors

• Several new endocrine therapies are available
• Reduced the peripheral conversion of androgens to oestrogens
• Only effective in post menopausal women
• May be superior to tamoxifen
• To date have not been shown to have survival benefit compared with tamoxifen

Locally advanced breast cancer

• Regarded as a tumour that is not surgically resectable
• Clinical features include
  • Skin ulceration
  • Dermal infiltration
  • Erythema over the tumour
  • Satellite nodules
  • Peau d'orange
  • Fixation to chest wall, serratus anterior or intercostal muscles
  • Fixed axillary nodes

• Often associated with the development of metastatic disease
• Restaging is therefore essential
• Commonest sites for ductal carcinoma are liver, bone and lung
• Lobular carcinoma less predictable often spreading to bowel, retroperitoneum etc
• Recurrence whilst on adjuvant tamoxifen consider:
  • Further surgery for
  • Isolated 'spot' recurrence after mastectomy
  • Local recurrence in the conserved breast
  • Radiotherapy if not previously given
  • Change of hormonal agent to anastozole or megestrol acetate

Male breast cancer

• 1% of all breast cancers occur in men
• Pathologically, the disease is similar to that which occurs in women
• The principles of treatment are the same
• The proportion of men undergoing mastectomy is higher
• Adjuvant therapy is the same as for women

Bibliography

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