Here is the list of the diseases that start with letter “V“:
- Van Der Woude syndrome (VDWS)
- Varicella zoster virus (VZV)
- Vernal keratoconjunctivitis (VKC)
- Vogt–Koyanagi–Harada syndrome (VKH syndrome)
- Von Willebrand disease (vWD)
- Vaginitis / Vulvovaginitis
Vaginismus, sometimes anglicized vaginism, is the German name for a condition that affects a woman’s ability to engage in any form of vaginal penetration, including sexual intercourse, insertion of tampons and/or menstrual cups, and the penetration involved in gynecological examinations. This is the result of a reflex of the pubococcygeus muscle, which is sometimes referred to as the “PC muscle”. The reflex causes the muscles in the vagina to tense suddenly, which makes any kind of vaginal penetration—including sexual intercourse—painful or impossible.
A woman suffering from vaginismus does not consciously control the spasm. The vaginismic reflex can be compared to the response of the eye shutting when an object comes towards it. The severity of vaginismus, as well as the pain during penetration (including sexual penetration), varies from woman to woman.
A woman is said to have primary vaginismus when she has never been able to have penetrative sex or experience vaginal penetration without pain. It is commonly discovered in teenagers and women in their early twenties, as this is when many young women in the Western world first attempt to use tampons, have penetrative sex, or undergo a Pap smear. Women with vaginismus may be unaware of the condition until they attempt vaginal penetration. A woman may be unaware of the reasons for her condition.
Secondary vaginismus occurs when a woman who has previously been able to achieve penetration develops vaginismus. This may be due to physical causes such as a yeast infection or trauma during childbirth, while in some cases it may be due to psychological causes, or to a combination of causes. The treatment for secondary vaginismus is the same as for primary vaginismus, although, in these cases, previous experience with successful penetration can assist in a more rapid resolution of the condition. Peri-menopausal and menopausal vaginismus, often due to a drying of the vulvar and vaginal tissues as a result of reduced estrogen, may occur as a result of “micro-tears” first causing sexual pain then leading to vaginismus.
Van Der Woude syndrome (VDWS) is a genetic disorder and congenital malformation. People with VDWS have cleft lip with or without cleft palate, pits or mucous cysts on the lower lip, hypodontia, a hypernasal voice, cleft or bifid uvula, syngnathia, narrow high arched palate, and ankyloglossia. Extraoral manifestations include limb anomalies, popliteal webs, accessory nipples, congenital heart defects, and Hirschsprung disease. However, Van der Woude syndrome has variable phenotypic expression. For example, some individuals affected by Van der Woude syndrome have isolated lip pits without any cleft syndrome. Affected individuals have normal intelligence. Ongoing research is being conducted to discover the genes involved in causing Van der Woude syndrome. A mutation in the gene IRF6 (interferon regulatory factor 6) has recently been discovered to be strongly associated with the disorder.
VDWS is the most common syndromic form of cleft lip and palate (CLP), accounting for 2% of all cleft lip and palate cases. Approximately 70% of cases of CLP are isolated, meaning that there are no other health issues present. However, cases of CLP with Van der Woude syndrome are considered syndromic because the individuals exhibit other abnormalities in addition to the cleft lip/palate. Van der Woude syndrome was first characterized in 1954.
Varicella zoster virus (VZV) is one of eight herpes viruses known to infect humans (and other vertebrates). It commonly causes chicken-pox in children and Herpes zoster (shingles) in adults and rarely in children. Varicella-zoster virus is known by many names, including: chickenpox virus, varicella virus, zoster virus, and human herpes virus type 3 (HHV-3). Primary VZV infection results in chickenpox (varicella), which may rarely result in complications including encephalitis or pneumonia. Even when clinical symptoms of chickenpox have resolved, VZV remains dormant in the nervous system of the infected person (virus latency), in the trigeminal and dorsal root ganglia. In about 10–20% of cases, VZV reactivates later in life producing a disease known as shingles. Serious complications of shingles include postherpetic neuralgia, zoster multiplex, myelitis, herpes ophthalmicus, or zoster sine herpete.
Within the human body it can be treated by a number of drugs and therapeutic agents including acyclovir for the chicken pox, famciclovir, valaciclovir for the shingles, zoster-immune globulin (ZIG), and vidarabine. VZV immune globulin is also a treatment.
A live attenuated VZV Oka/Merck strain vaccine is available and is marketed in the United States under the trade name Varivax. It was developed by Merck, Sharp & Dohme in the 1980s from the Oka strain virus isolated and attenuated by Michiaki Takahashi and colleagues in the 1970s. It was submitted to the U.S. Food and Drug Administration for approval in 1990 and was approved in 1995. Since then, it has been added to the recommended vaccination schedules for children in Australia, the United States, and many other countries.
Vernal keratoconjunctivitis (VKC) or Spring catarrh is a recurrent, bilateral, and self limiting inflammation of conjunctiva, having a periodic seasonal incidence. Predisposing factors include: age & sex- 4–20 years – more common in boys than girls; Season- more common in summer, hence the name Spring catarrh is a misnomer; recently it is being labelled as Warm weather conjunctivitis; climate – more prevalent in the tropics.
Local therapy- Topical steroids are effective. Commonly used solutions are of fluorometholone, medrysone, betamethasone or dexamethasone. Mast cell stabilizers such as sodium cromoglycate (2%) drops 4-5 times a day are quite effective in controlling VKC, especially atopic ones. Azelastine eyedrops are also effective. Topical antihistamines can be used. Acetyl cysteine (.0.5%) used topically has mucolytic properties and is useful in the treatment of early plaque formation. Topical Cyclosporine is reserved for unresponsive cases.
Treatment includes: Systemic therapy – Oral antihistamines and oral steroids for severe cases. Treatment of large papillae – Cryo application, surgical excision or suupratarsal application of long acting steroids. General measures include use of dark goggles to prevent photophobia, cold compresses and ice pack for soothing effects, change of place from hot to cold areas. Desensitization has also been tried without much rewarding results.
Vitiligo is a condition that causes depigmentation of sections of skin. It occurs when melanocytes, the cells responsible for skin pigmentation, die or are unable to function. The cause of vitiligo is unknown, but research suggests that it may arise from autoimmune, genetic, oxidative stress, neural, or viral causes. The incidence worldwide is less than 1%. The most common form is non-segmental vitiligo, which tends to appear in symmetric patches, sometimes over large areas of the body.
The most notable symptom of vitiligo is depigmentation of patches of skin that occurs on the extremities. Although patches are initially small, they often enlarge and change shape. When skin lesions occur, they are most prominent on the face, hands and wrists. Depigmentation is particularly noticeable around body orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus. Some lesions have hyperpigmentation around the edges. Patients who are stigmatised for their condition may experience depression and similar mood disorders.
There are a number of treatments that treat vitiligo. Treatment options generally fall into four groups:
Exposing the skin to UVB light from UVB lamps is the most common treatment for vitiligo.
The treatments can be done at home with a domestic UVB lamp or in a clinic. Normally a small lamp is needed if the spot is small.
Treatment can take a few weeks if the spots are on the neck and face and if they existed not more than 3 years. If the spots are on the hands and legs and have been there more than 3 years, it can take a few months.
In a clinic the treatments are done 2-3 times a week, and at home every day, which makes the home treatments more effective.
If the spots are on a large area of the body, full body treatment in a clinic or hospital will be needed.
Both UVB Broadband and UVB Narrowband lamps can be used. However these treatments are unreliable at best. There is no treatment that totally repigments the skin.
Ultraviolet light (UVA) treatments are normally carried out in a hospital clinic. Psoralen and Ultraviolet A light (PUVA) treatment involves taking a drug which increases the skin’s sensitivity to ultraviolet light. The skin is then exposed to high doses of ultraviolet A light (UVA). Treatment is required twice a week for 6–12 months or longer. Because of the high doses of UVA and the Psoralen, PUVA may cause side effects such as ‘sunburn’ type reactions or skin freckling.
Narrowband ultraviolet B (UVB) phototherapy is now used more commonly than PUVA as it is less damaging to the skin. As with PUVA, treatment is carried out twice weekly in a clinic or every day at home, and there is no need to use a Psoralen.
The traditional treatment is the application of corticosteroid cream.
In cases of extensive vitiligo the option to de-pigment the unaffected skin with topical drugs like monobenzone, mequinol or hydroquinone may be considered to render the skin an even colour. The removal of all the skin pigment with monobenzone is permanent and vigorous sun-safety must be adhered to for life to avoid severe sun burn and melanomas. Depigmentation takes about a year to complete.
Vogt–Koyanagi–Harada syndrome (VKH syndrome) is a condition seen in humans and dogs involving various melanocyte-containing organs, characterized by uveitis (inflammation of the inside of the eye), poliosis (whitening of hair), vitiligo (loss of pigment in the skin), and meningitis, although dogs with this syndrome rarely develop meningitis. It is also known as uveodermatologic syndrome.
VKH syndrome is an immune-mediated disease. The mechanism of the disease is thought to be T helper cell mediated autoimmune attack of melanocytes in the skin and uvea of dogs and humans, and in the central nervous system and inner ear of humans.
In dogs VKH syndrome (often called VKH-like syndrome) most commonly affects young animals and is seen most commonly in the Akita Inu, but also in the Siberian Husky and Samoyed. Uveitis usually occurs first and is often severe enough to cause blindness. VKH syndrome can also cause retinal detachment, cataracts, and glaucoma. Pigment partly disappears from the retinal pigment epithelium and iris. Skin lesions include loss of pigment and hair on the eyelids, nose, and lips. Symptoms and biopsy will confirm the diagnosis.
Von Willebrand disease (vWD) is the most common hereditary coagulation abnormality described in humans, although it can also be acquired as a result of other medical conditions. It arises from a qualitative or quantitative deficiency of von Willebrand factor (vWF), a multimeric protein that is required for platelet adhesion. It is known to affect humans and dogs (notably Doberman Pinschers), and rarely swine, cattle, horses, and cats. There are three forms of vWD: inherited, acquired and pseudo or platelet type. There are three types of hereditary vWD: vWD Type I, vWD Type II and vWD III. Within the three inherited types of vWD there are various subtypes. Platelet type vWD is also an inherited condition.
vWD Type I is the most common type of the disorder and those that have it are typically asymptomatic or may experience mild symptoms such as nosebleeds although there may be severe symptoms in some cases. There are various factors that affect the presentation and severity of symptoms of vWD such as blood type.
vWD is named after Erik Adolf von Willebrand, a Finnish pediatrician who first described the disease in 1926.
The various types of vWD present with varying degrees of bleeding tendency, usually in the form of easy bruising, nosebleeds and bleeding gums. Women may experience heavy menstrual periods and blood loss during childbirth. Severe internal or joint bleeding is uncommon (which mostly occurs in type 3 vWD).
Vulvodynia is a chronic pain syndrome that affects the vulvar area and occurs without an identifiable cause or visible pathology categorized in the ICD-9 group 625—specifically ICD-9 625.7, which is for pain and other disorders of the female genital organs. It refers to pain of the vulva unexplained by vulvar or vaginal infection or skin disease.
The term “vulvodynia” simply refers to “vulvar pain”, and does not imply a specific cause.
Pain is the most notable symptom of vulvodynia, and can be characterized as a burning, stinging, irritation or sharp pain that occurs in the vulva, including the labia and entrance to the vagina. It may be constant, intermittent or happening only when the vulva is touched, but vulvodynia is usually defined as lasting for years.
Symptoms may occur in one place or the entire vulvar area. It can occur during or after sexual activity, when tampons are inserted, or when prolonged pressure is applied to the vulva, such as during sitting, bike riding, or horseback riding. Some cases of vulvodynia appear random where no particular cause can be determined.
A wide variety of possible causes and treatments for vulvodynia are currently being explored. The condition is one of exclusion and other vulvovaginal problems should be ruled out.
Possible causes include: genetic predisposition to inflammation, allergy or other sensitivity (for example: oxalates in the urine), an autoimmune disorder similar to lupus erythematosus or to eczema or to lichen sclerosus, infection (e.g., yeast infections, bacterial vaginosis, HPV), injury, and neuropathy–including an increased number of nerve endings in the vaginal area. Some cases seem to be negative outcomes of genital surgery, such as a labiectomy.
The condition is one of exclusion and other vulvovaginal problems should be ruled out. The diagnosis is based on the typical complaints of the patient, essentially normal physical findings, and the absence of identifiable causes per the differential diagnosis. A cotton “swab test” is used to delineate the areas of pain and categorize their severity. Patients often will describe the touch of a cotton ball as extremely painful, like the scraping of a knife.
Vaginitis is an inflammation of the vagina. It can result in discharge, itching and pain, and is often associated with an irritation or infection of the vulva. It is usually due to infection. The three main kinds of vaginitis are bacterial vaginosis (BV), vaginal candidiasis, and trichomoniasis. A woman may have any combination of vaginal infections at one time. The symptoms that arise vary with the infection, although there are general symptoms that all vaginitis infections have and infected women may also be asymptomatic. Testing for vaginal infections is not a part of routine pelvic exams; therefore, women should neither assume their health care providers will know of the infection, nor that they will provide appropriate treatment without their input.
Vaginal infection are often (varies between countries between 20 to 40% of vaginal infections) a mix of various etiologies, which present challenging cases for treatment. Indeed, when only one cause is treated, the other pathogens can gain in resistance and induce relapses and recurrences. The key factor is therefore to get a precise diagnosis and treat with broad spectrum anti-infective (often also inducing adverse effects).
Further, either a change in pH balance or introduction of foreign bacteria in the vagina can lead to infection known as vaginitis. There are physical factors that can contribute to development of infection, such as constantly wet vulva due to tight clothing, chemicals coming in contact with the vagina via scented tampons, antibiotics, birth control pills, or a diet favoring refined sugar and yeast. There is also psychological and emotional dimension to vaginitis. Dr. Christiane Northrup argues, “some women respond to a perceived boundary violation with a vaginal infection”. The two dimensions of vaginitis have important implications regarding treatment.
The cause of the infection determines the appropriate treatment. It may include oral or topical antibiotics and/or antifungal creams, antibacterial creams, or similar medications. A cream containing cortisone may also be used to relieve some of the irritation. If an allergic reaction is involved, an antihistamine may also be prescribed. For women who have irritation and inflammation caused by low levels of estrogen (postmenopausal), a topical estrogen cream might be prescribed.
Prevention of candidiasis, the most common type of vaginitis, starts with good hygiene: drying completely after bathing, wearing fresh undergarments, and wiping from front to rear after defecation all help to prevent contamination of the vagina with harmful bacteria. Douching is never recommended, as it often does more harm than good, by upsetting the normal balance of yeast in the vagina. Prevention of bacterial vaginosis includes healthy diets and behaviors as well as minimizing stress as all these factors can affect the pH balance of the vagina. Consuming good bacteria in products with live-culture, such as yogurt, sauerkraut and kimchi, or simply through probiotic supplements, one can reduce the likelihood of developing vaginitis due to antibiotics.