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Sunday, June 3, 2007

Clearing Pus From the Ear

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male evacuates pus filled earlobe; warning - extremely graphic.



Monday, April 2, 2007

All About Genital warts

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Genital warts (or condyloma, condylomata acuminata, or venereal warts) is a highly contagious sexually transmitted infection. Caused by some sub-types of the human papillomavirus (HPV) genital warts are spread through direct skin-to-skin contact during oral, genital, or anal sex with an infected partner. Genital warts are the most easily recognized sign of genital HPV infection. Of the multiple strains of genital HPV, strains 6, 11, 30, 42, 43, 44, 45, 51, 52, and 54 can cause genital warts; types 6 and 11 are the most common.[1] Most people who acquire those strains never develop warts or any other symptoms. HPV is also responsible for over 90% of all cases of cervical cancer. (However, the HPV strains responsible for cervical cancer differ from the strains that cause genital warts.)

Genital warts often occur in clusters and can be very tiny or can spread into large masses in the genital or anal area. In women the warts occur on the outside and inside of the vagina, on the opening (cervix) to the womb (uterus), or around the anus. While genital warts are approximately as prevalent in men, the symptoms of the disease may be less obvious. When present, they usually are seen on the tip of the penis. They also may be found on the shaft of the penis, on the scrotum, or around the anus. Rarely, genital warts also can develop in the mouth or throat of a person who has had oral sex with an infected person.

Treatment

Genital warts often disappear even without treatment. In other cases, they eventually may develop a fleshy, small raised growth. There is no way to predict whether the warts will grow or disappear.

Depending on factors such as the size and location of the genital warts, a doctor will offer one of several ways to treat them.

* Imiquimod, (Aldara®) a topical immune response cream which can be applied to the affected area
* A 20% podophyllin anti-mitotic solution, which can be applied to the affected area and later washed off
* A 0.5% podofilox solution, applied to the affected area but should not be washed off
* A 5% 5-fluorouracil (5-FU) cream
* Trichloroacetic acid (TCA)
* Pulsed dye laser
* Liquid nitrogen cryosurgery
* Electric or Laser cauterization

With pregnancy, podophyllin or podofilox should not be used as they are absorbed by the skin and may cause birth defects in the fetus. In addition, 5-fluorouracil cream should not be used while trying to become pregnant or if there is a possibility of pregnancy.

In case of small warts, they can be removed by freezing (cryosurgery), burning (electrocautery), or laser treatment. Surgery is occasionally used to remove large warts that have not responded to other treatment.

Some doctors use the antiviral drug interferon-alpha, which they inject directly into the warts, to treat warts that have returned after removal by traditional means. The drug is expensive, however, and does not reduce the rate that the genital warts return.

Although treatments can get rid of the warts, they do not get rid of the HPV virus, so warts can recur after treatment. The body's immune system typically clears the virus anywhere from 8 to 13 months, but it occasionally remains in the body for a lifetime.[2] The state of the immune system determines the chances of ridding the virus entirely and can be affected by factors such as HIV infection, certain medications, stress, or illness.[3] There is even some suggestion that effective treatment of the wart may aid the body's immune response[citation needed].

Prevention

The virus that causes genital warts is spread by skin-skin contact. Condoms do not adequately protect against genital warts, because the infected spot may not be covered by a condom. The only reliable prevention is to have no skin contact with potentially infected tissue.

Gardasil, an HPV vaccine, protects women from the strains of HPV that cause 70% of all cervical cancers and 90% of all genital warts and has been approved by the Food and Drug Administration.[4] The license allows prescription to females between the ages of 9-26. This vaccine is most effective when administered before the girl has contacted any of the HPV strains which the virus protects. For this reason, the vaccine should be preferably administered before a girl becomes sexually active. This vaccine is currently being tested for males. Gardasil does not contains the preservative thimerosal.[5]

Hirsuties papillaris genitalis

It is a common misconception among men that hirsuties papillaris genitalis are in fact genital warts. Hirsuties papillaris genitalis is not contagious and no treatment for the condition is necessary. Some may deem it unsightly and there are various methods of ridding the penis of the condition such as carbon dioxide laser treatment.

Fordyce's spots

Genital warts should not be confused with Fordyce's spots, which are considered benign.

Pregnancy and childbirth

Genital warts may cause a number of problems during pregnancy. Sometimes the warts get larger during pregnancy, making it difficult to urinate. If the warts are in the vagina, they can make the vagina less elastic and cause obstruction during child birth.

Rarely, infants born to women with genital warts develop warts in their throats (laryngeal papillomatosis). Although uncommon, it is a potentially life-threatening condition for the child, requiring frequent laser surgery to prevent obstruction of the breathing passages. Research on the use of interferon therapy in combination with laser surgery indicates that this drug may show promise in slowing the course of the disease.

References

1. ^ eMedicine med/1037
2. ^ What is HPV? at plannedparenthood.org
3. ^ Learn about HPV > Myths and Misconceptions at American Social Health Association
4. ^ FDA Licenses New Vaccine for Prevention of Cervical Cancer and Other Diseases in Females Caused by Human Papillomavirus
5. ^ GARDASIL® Questions and Answers. CBER - Quadrivalent Human Papillomavirus (Types 6, 11, 16, 18) Recombinant Vaccine. Retrieved on 2007-03-19.

All About Blisters

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A blister or bulla is a defense mechanism of the human body. When the outer (epidermis) layer of the skin separates from the fibre layer (dermis), a pool of lymph and other bodily fluids collect between these layers while the skin re-grows from underneath. Blisters can be caused by chemical or physical injury. An example of chemical injury would be an allergic reaction. Physical injury can be caused by heat, frostbite, or friction.

Treatment

Unless infection occurs, blisters usually heal quickly without additional treatment. If a blister is punctured, it forms an open wound so it is a good idea to bandage it when one is working around unsanitary conditions. If the blister has 'popped,' the excess skin should not be removed, unless it is dirty or torn. Removing the excess skin often makes the wound more prone to further infection (Kaiser Permanente, 2001). As with all wounds, it is a good idea to keep blisters clean.

Variations

If a blister is associated with sub-dermal bleeding it will partially fill with blood, forming a blood blister. Certain autoimmune diseases feature extensive blistering as one of their symptoms. These include pemphigus and pemphigoid. Blistering also occurs as part of foodborne illness with Vibrio vulnificus (seafood). The class of chemical weapons known as vesicants acts by causing blisters (often within the respiratory tract). Mustard gas and lewisite are examples of such agents.

See also

* Buboe
* Dracunculiasis
* Herpangina
* Herpes zoster
* Ulcer

All About Erythroderma

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Erythroderma is defined as a generalized skin disorder characterized by reddening and scaling of 100% of the skin. It is also known as erythrodermatitis, generalized exfoliative dermatitis, and red man syndrome. There may also be normal areas of skin present.

Causes

Erythroderma is produced by several skin diseases, such as psoriasis, contact dermatitis, drug reactions, and mycosis fungoides (a cutaneous lymphoma). A dermatologist must first diagnose the cause, usually with a skin biopsy, a blood smear examined by a pathologist and patch testing (if the eruption can be temporarily cleared).

Treatment

The treatment is dependent on the cause.

See also

* List of skin diseases
* Eczema

All About Erysipelas

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Erysipelas (Greek ερυσίπελας - red skin) is an acute streptococcus bacterial skin infection, resulting in inflammation and characteristically extending into underlying fat tissue.

(Erysipelas is also the name given to an infection in animals caused by the bacterium Erysipelothrix rhusiopathiae. Infection by Erysipelothrix rhusiopathiae in humans is known as erysipeloid.)

Risk factors

This disease is most common among the elderly, infants, and children. People with immune deficiency, diabetes, alcoholism, skin ulceration, fungal infections and impaired lymphatic drainage (e.g., after mastectomy, pelvic surgery, bypass grafting) are also at increased risk.

Signs and symptoms

Patients typically develop symptoms including high fevers, shaking, chills, fatigue, headaches, vomiting, and general illness within 48 hours of the initial infection. The erythematous skin lesion enlarges rapidly and has a sharply demarcated raised edge. It appears as a red, swollen, warm, hardened and painful rash, similar in consistency to an orange peel. More severe infections can result in vesicles, bullae, and petechiae, with possible skin necrosis. Lymph nodes may be swollen, and lymphedema may occur. Occasionally, a red streak extending to the lymph node can be seen.

The infection may occur on any part of the skin including the face, arms, fingers, legs and toes, but it tends to favor the extremities. Fat tissue is most susceptible to infection, and facial areas are typically around the eyes, ears, and cheeks. Repeated infection of the extremities can lead to chronic swelling (lymphadenitis).

Etiology

Most cases of erysipelas are due to Streptococcus pyogenes (also known as group A streptococci), although non-group A streptococci can also be the causative agent. Historically, the face was most affected; today the legs are affected most often. [1]

Erysipelas infections can enter the skin through minor trauma, eczema, surgical incisions and ulcers, and often originate from strep bacteria in the subject's own nasal passages.

Diagnosis

This disease is mainly diagnosed by the appearance of the rash and its characteristics. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erypsipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast.

Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevaiton of the antistreptolysin O titre occurs after around 10 days of illness.

Treatment

Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.

Complications

* Spread of infection to other areas of body through the bloodstream (bacteremia), including septic arthritis and infective endocarditis (heart valves).
* Septic shock.
* Recurrence of infection – Erysipelas can recur in 18-30% of cases even after antibiotic treatment.
* Lymphatic damage
* Necrotizing fasciitis -- AKA "the flesh-eating bug." A potentially-deadly exacerbation of the infection if it spreads to deeper tissue.

All About Epidermolysis bullosa

In medicine (dermatology) Epidermolysis bullosa (EB) is a rare genetic disease characterized by the presence of extremely fragile skin and recurrent blister formation, resulting from minor mechanical friction or trauma. The condition was brought to public attention in the UK through the Channel 4 documentary The Boy Whose Skin Fell Off, chronicling the life and death of English sufferer Jonny Kennedy.

Forms

There are three main forms of inherited EB. These different subtypes are defined by the depth of blister location within the skin layers, and the location of the dissolution of the skin.

EB Simplex (EBS) -- ABOVE the basement membrane

See main article at Epidermolysis bullosa simplex.

Blister formation of EB simplex is within the basal keratinocyte of the epidermis. Sometimes EB simplex is called epidermolytic. There are four subtypes of EBS:

1. EBS - Weber-Cockayne (EBS-WC)
2. EBS - Koebner (EBS-K)
3. EBS - Dowling-Meara (EBS-DM) -- caused by missense mutation in KRT5 (E477K) or one of two missense mutations in KRT14 (R125C and R125H)
4. EBS - Mottled Pigmentation (EBS-MP) - caused by one missense mutation in KRT5 (I161S) or by missense mutations in the plectin gene (Koss-Harnes et al., 1997;Koss-Harnes et al., 2002).

Junctional EB (JEB) -- THROUGH the basement membrane

Condition characterized by spontaneous blistering of the skin and mucous membranes at the level of the lamina lucida within the basement membrane zone. Condition is caused by defects in the structures of laminin 5 or laminin 6, proteins that contribute to the cohesion of the dermis and epidermis A severe form of the disease, JEB gravis is often fatal early in life. Death occurs as a result of epithelial blistering of the respiratory, digestive and genitourinary systems.

Dystrophic EB (DEB) -- UNDER the basement membrane

Dystrophic EB (DEB) forms which can lead to scarring occur in a deeper tissue level; the sub-lamina densa region (the beneath the lamina densa) within the upper dermis. The disease DEB is caused by genetic defects (or mutations) within the molecule type VII collagen (collagen VII). Collagen VII is a very large molecule (780 nm) that dimerizes to forms a semicircular looping structure: the anchoring fibril. Anchoring fibrils are thought to form a structural link between the epidermal basement membrane and the fibrillar collagens in the upper dermis.

Collagen VII is also present in the epithelial tissue of the esophagus, which leads to chronic scarring, webbing, and obstruction. Affected individuals are often severely malnourished due to trauma to the oral and esophageal mucosa and require feeding tubes for nutrition. They also suffer from iron-deficiency anemia of uncertain origin, which leads to chronic fatigue.

Open wounds on the skin heal slowly or not at all, often scarring extensively, and are particularly susceptible to infection. Many individuals bathe in a bleach and water mixture to fight off these infections.

The chronic inflammation leads to errors in the DNA of the affected skin cells, which in turn causes squamous cell carcinoma (SCC). The majority of these patients die before the age of 30, either of SCC or complications related to DEB.

Laymen's Terms

The skin has two layers; the outer layer is called the epidermis and the inner layer the dermis. In normal individuals there are "anchors" between the two layers that prevent them from moving independently from one another. In people born with EB the two skin layers lack the anchors that hold them together, and any action that creates friction between the layers (like rubbing or pressure) will create blisters and painful sores. Sufferers of EB have compared the sores to third-degree burns.[1]

Epidemiology

An estimated 50 in 1 million live births are diagnosed with EB, and 9 in 1 million are in population. Of these cases, approximately 92% are EBS, 5% are DEB, 1% are JEB, and 2% are unclassified. Carrier frequency ranges from 1 in 333 for Junctional, to 1 in 450 for Dystrophic. Carrier frequency for Simplex is not indicated in this article, but is presumed to be much higher than JEB or DEB.

The disorder occurs in every racial and ethnic group throughout the world and affects both genders. [2]]