• 1.
  

  a) T b) T c) T d) F e) T

A clinical yeast infection not responsive to an initial course of fluconazole would likely merit a repeat evaluation for a non-albicans Candida species, azole resistance, or another infectious cause. Repeat microscopy or yeast culture collection would be preferable to OTC medication administration without a physical examination to help determine a root cause. Additional treatment with a first line agent may be considered.

• 2.
  

  a) F b) T c) T d) T e) T

While BV is sexually associated and bio-typing may reveal similar species for both partners, randomized-controlled trials have shown no benefit to partner treatment to date. Swidsinski et al. have demonstrated the ability of G. vaginalis and other organisms to form biofilms that may be difficult to penetrate with antibiotics. Pathogenicity may be a factor of biofilm density and virulence of the involved organisms. Recurrent episodes of BV have a higher likelihood of exhibiting metronidazole resistance. Treatment with clindamycin may be required. Presence of A. vaginae may also be related to poor treatment outcomes. Thirty percent of women with an initial response to BV treatment will relapse within 3 months and almost 60% within 12 months. Maintenance therapy with twice weekly metronidazole gel for 4 months may be warranted.

• 3.
  

  a) F b) T c) F d) F e) F

The CDC recommends partner testing and treatment for trichomoniasis as partner infection rates may be as high as 70–80%. The diagnosis of trichomoniasis in a male sexual partner may require a combination of urine, urethral culture or urine PCR. A single dose of metronidazole or tinidazole may also be used for partner treatment. Of the three most common causes of vaginitis, partner testing has only been recommended for trichomoniasis. Partner testing should be considered in the presence of infections such as chlamydia or gonorrhea.

• 4.
  

  a) F b) T c) F d) T e) T

Vulvar scarring (loss of the contours of the labia minora, burying of the clitoris, synechiae of the labia minora) is not specific to VLS. Erosive or atrophic conditions (lichen planus, dermatologic autoimmune disorders, caustic vulvitis, post-menopausal atrophy) may induce similar modifications of the vulvar architecture. In addition VLS is not always associated with scarring. When a patient treated by UPCS for VLS has symptoms, compliance should be evaluated and an associated condition requiring a specific treatment should be searched for before concluding to a (very unlikely) “resistance” to topical corticosteroids. These associated conditions are mainly infection (most frequently candidiasis) and vulvodynia, or much more rarely, differentiated VIN or acanthotic lichen sclerosus. There is no evidence so far that treatment of VLS prevents transformation into squamous cell carcinoma. Patients with VLS should be informed that the risk of transformation is very low and that a precursor stage usually precedes the transformation. The patient will be advised to see her doctor in case of symptoms resisting to UPCS or palpation of a thickened, ulcerated or infiltrated area. Differentiated VIN defined by cytological and architectural atypia localized at the basal and suprabasal layers of the epidermis is associated with lichen sclerosus or lichen planus. As opposed to usual VIN characterized by full thickness atypia, differentiated VIN does not contain HPV. One study showed that the percentage of prior synchronous or subsequent vulvar squamous cell carcinoma in women with differentiated VIN was 85.7 % compared with 25.7 % in women with usual VIN. Multifocal pigmented vulvar patches are mainly post inflammatory and most frequently result from lichen sclerosus. Clinical features of lichen sclerosus should be searched for in patients with multiple pigmented vulvar patches. The diagnosis of benign post inflammatory pigmentation should be histologically confirmed because rarely, melanocytic proliferation is associated with lichen sclerosus.

• 5.
  

  a) F b) T c) F d) F e) T

In vulval clinics, contact dermatitis represents 15 to 30% of the conditions seen, whereas lichen sclerosus and vulvodynia are the two most frequent reasons for consultation. There are two types of contact vulvar dermatitis which may have similar clinical features. Irritant contact dermatitis is the most frequent. It results from a loss of the barrier function related to moisture, enzymes, friction, heat and oestrogen deficiency. Urinary incontinence is one of the main causes of irritant dermatitis. Allergic contact dermatitis is an immunologically mediated inflammatory cutaneous reaction (type IV hypersensitivity) to an allergen in a sensitized individual. The main allergens are topical anaesthetics, perfumes, topical antibiotics and corticosteroids. Patch tests are performed to confirm the diagnosis of allergic contact dermatitis. The suspected allergen should be searched for by a careful investigation looking for all topical products that had been applied on the vulva, knowingly or not (products carried by the hands and not intentionally applied on the vulva). The results of the patch tests should be interpreted with caution. They can be false-negative because they are classically applied on the back, a site that does not reproduce the humid environment of the vulva. On the other hand, the relevance of a positive patch test should always be discussed. The diagnosis of vulvar contact dermatitis mainly relies on a careful history taking and clinical examination and on the regression of the dermatitis after withdrawal of the suspected agent. Biopsy helps to rule out differential diagnosis such as lichen simplex chronicus, vulvo-vaginal candidiasis and psoriasis. Topical steroids help to reduce itch and inflammation but the treatment mainly relies on the suppression of the irritant or allergenic products and on the restoration of the cutaneous barrier.

• 6.
  

  a) F b) F c) F d) T e) F

Many women have a delay in diagnosis of vulvar cancer, dystrophy or vulvar intraepithelial neoplasia (VIN) because of the assumption that vulvar pruritus is caused by fungal infections such as Candida. Vulvar pruritus, especially when it is persistent or seen in the elderly, can be the only manifestation of a vulvar cancer and should be carefully worked up with a full pelvic exam and directed biopsy. If a mass of this size is completely excised prior to evaluation by a cancer specialist then the correct diagnosis as well as options for evaluation of the lymph nodes and size of the tumor as well as the status of the margins can be compromised. The first step in management is a biopsy. Because of the patient’s discomfort in the office an evaluation under anesthesia or sedation is recommended so that more biopsies can be taken of the lesion to confirm the diagnosis for proper treatment planning. MRI may assist in evaluation for some patients diagnosed with vulvar cancer. However, this patient does not have a cancer diagnosis yet.

• 7.
  

  a) T b) T c) T d) T e) T

Women at increased risk for invasive vulvar carcinomas are those with HPV infection, which mediates cellular transformation and can result in premalignant and malignant cellular changes. Carcinogens in tobacco smoke can potentiate these changes and further increases the risk of vulvar cancer. Immunosuppression results in a decreased ability to spontaneously clear the HPV virus. Lastly, lichen sclerosis and other chronic inflammatory conditions of the vulva confer an increased risk of vulvar cancer which is independent of HPV infection.

• 8.
  

  a) T b) T c) F d) T e) F

A study by Elmerstig et al. found women report guilt, sacrifice, resignation, and the motivation to behave in a manner consistent with the notion of an ideal woman as reasons for why women continue to have sex despite the presence of pain.

• 9.
  

  a) F b) F c) T d) F e) F

Epidemiological results indicate that only 60% of women who report chronic vulvo-vaginal pain seek treatment, and 40% of these never receive a formal diagnosis.

• 10.
  

  a) F b) T c) F d) T e) F

Research conducted in laboratory settings indicates that there are no significant differences between women with vulvo-vaginal pain and non-afflicted women relative to their physiological level of sexual arousal when exposed to an erotic stimulus, although women with pain tend to report more negative feelings toward the stimulus.

• 11.
  

  a) T b) T c) T d) F e) F

Following application of 5% lidocaine ointment nightly for a mean of 7 weeks, 57% (of 61 patients) with localized provoked vulvodynia reported a significant (>50%) decrease in dyspareunia and 40% more women were able to have intercourse. Peteresen et al. performed the only randomized, double blinded, placebo-controlled trial using Botulinum toxin A and demonstrated no improvement with use of 20 units over placebo in 64 women with vulvodynia. A randomized, double-blinded, placebo-controlled trial by Foster et al. compared use of oral desipramine and topical lidocaine as both monotherapy and combination therapy. The aim was to target both peripheral and central neuronal pathways which could also potentially elucidate the origin of the neuropathic component of this diagnosis. All arms of the study, including the double placebo arm, demonstrated a decrease in vulvar pain. There was no significant difference in pain reduction between patients treated with placebo vs topical lidocaine monotherapy (33% vs 20%). Oral gabapentin has not been studied in a placebo controlled trial although observational studies have suggested an improvement in patient’s pain using this medication. A critical review of the literature to date suggests that vestibulectomy is successful in 60–90% of cases, whereas other non-surgical therapies are 40–80% effective. However, there is no consensus or standardized definition for evaluation of outcomes between studies. While there are no studies comparing surgical management with placebo, some approaches appear to be more successful than others. Vestibulo-plasty has been noted to be ineffective.

• 12.
  

  a) F b) T c) T d) T e) T

Hyperkalemia has not been proposed as a cause for vulvodynia. Hyperoxaluria has been proposed based on a single case report of one woman with vulvar pain refractory to usual medical management who had complete resolution of symptoms following use of a low oxalate diet and calcium citrate supplementation. Subsequent studies have not been able to corroborate this theory and thus this is not generally thought to be a cause of vulvodynia. The pain described by patients with vulvodynia is similar in nature to that described by patients with neuropathic pain such as post-herpetic neuralgia and diabetic neuropathy. Patients most often describe a burning pain which can be constant, but may be exacerbated by certain triggers. Studies suggest both central and peripheral responses to neuro-modulating agents further supporting this etiology. Additionally, patients with vulvodynia have an increase in number and caliber of nerves, specifically pain sensing nociceptors, which may lend to increased sensitivity. Genetic features may predispose women to the development of neuropathic pain secondary to inflammation. Specifically, allele 2 of interleukin 1 beta (IL-1 beta) receptor antagonist (an inflammatory mediator) may be associated with an exaggerated inflammatory response due to decreased ability to down regulate the inflammatory activity. Based on the presence of vulvar erythema, older terminology referred to vestibulitis signifying inflammation. This was initially corroborated by tissue samples of patients with localized vestibulodynia who were noted to have an inflammatory infiltrate. However, subsequent studies noted the presence of an inflammatory infiltrate in asymptomatic controls.

• 13.
  

  a) F b) F c) T d) T e) F

The prevalence of vulvodynia has been estimated by various studies ranging from 4–16% of women. In a population base study including over 2200 women, Reed et al. found that about half of women meeting vulvodynia criteria sought treatment for their symptoms and only 1.4% were diagnosed with vulvodynia. Caucasian and African American women have a similar prevalence, whereas Hispanic women are 80% more likely than either Caucasian or African American women to experience vulvar pain. A prospective study involving 239 women with provoked vestibulodynia noted significant improvement in pain ratings, sexual satisfaction, sexual function and depressive symptoms over two years, regardless of treatment modality. Vulvodynia has been associated with younger age, earlier menarche, and pain with first tampon use in one study.

• 14.
  

  a) F b) T c) T d) T e) F

Douching can alter the pH in the vagina and introduces irritating substances, at times making symptoms worse. White cotton underwear is preferred as it allows the vulvar skin to breathe and avoid moisture, which can predispose to irritation. In the same vein, we also recommend avoiding nylons and tight fitting clothing. We do recommend a daily skin barrier such as zinc oxide, Vaseline, various cooking oils (e.g. Crisco, bland vegetable oil). These prevent irritation from the many substances and materials that come into contact with the vulvar skin. Dryer sheets contain perfumes and chemicals that can cause contact irritation. All people sharing a dryer should abstain from using dryer sheets as the chemicals coat the drum of the dryer and can contaminate the patient’s clothing even if used in a previous load. Waxing and shaving of the vulva are discouraged as these methods can cause folliculitis, predisposing patients to contact irritation and development of secondary infection.

• 15.
  

  a) F b) F c) T d) F e) F

HS is not acute; it is chronic. HS is not due to bacterial pathogens, although it may be secondarily infected. HS is a disorder of the folliculo-pilos-ebaceous unit, not the apocrine glands. The apocrine glands may be involved secondarily. It may occur in non-sweating areas and in lean individuals.

The rupture of the folliculo-pilo-sebaceous unit (FPSU) is caused by a combination of hormonal stimulation and a physical defect in the FPSU. The rupture appears to occur at an area that has less collagen support. The material from within the duct that is released into the dermis includes bacteria, yeast, hair fragments, follicular ductal cell lining, fatty acids, and other debris. This causes extensive acute, chronic and granulomatous inflammatory reaction that variably proceeds to the development of sinus tracts, scarring, and an unpleasant discharge. The immune systems are triggered as a secondary reaction to the foreign material released into the dermis. HS is not rare. It occurs in men, in childhood and in seniors.

• 16.
  

  a) F b) F c) F d) T e) F

The dietary choices that lead to obesity are those that also predispose to HS. Lean patients also have HS. There is no direct correlation between obesity and the severity of HS. Female HS patients commonly flare before their periods. This is believed to be due to the androgenic effect of ovarian progestins. Thus, the androgenic progestin medroxyprogesterone acetate can both precipitate HS de novo and worsen pre-existing HS. It is not a good choice for a contraceptive. Smoking is a well-recognized factor in the development of follicular occlusion, neutrophil chemotaxis, and TNF production by keratinocytes. It is important to recognize that HS is not usually associated with elevated levels of androgen in the blood. The effect of androgens in this disease is mediated at the nuclear androgen receptor in the various parts of the folliculo-pilo-sebaceous unit, areas not susceptible to measurement. HS is seldom secondarily infected. Cellulitis is rare, and septicemia is almost unheard of.

• 17.
  

  a) T b) F c) F d) F e) F

While a is the classic description, HS can occur anywhere on the body surface where folliculo-pilo-sebaceous units exist. The primary lesion in acne vulgaris is the comedo. The comedones in HS represent residual follicular portions of the folliculo-pilo-sebaceous unit that have had their hair and sebaceous glands destroyed by the disease but are still being stimulated by androgens, producing chronic plugging in the follicular stump. This is an end stage lesion, so it has earned the name “tombstone comedo”. Only 4% of patients with HS have Hurley III, but because of the severity of their disease they are overrepresented in clinics. In the general population, about 75% of patients with HS are in Hurley Stage I. Sinus tracts are persistent and become inflamed intermittently. They can be difficult to identify. During de-roofing, care must be taken to explore all sinuses and de-roof each one sequentially until all areas are clear. Only by de-roofing all sinuses and clearing all inflammatory debris will recurrence be prevented. Some inflammatory lesions of HS heal with no scarring. This represents success of the healing part of the inflammatory response, with reconstitution of a functional folliculo-pilo-sebaceous unit. Only when the lesion proceeds to the development of a sinus will scarring almost always occur. The earlier the lesion is de-roofed, debrided and allowed to heal by secondary intention, the less scarring will occur.

• 18.
  

  a) T b) F c) F d) T e) F

Atopic vulvitis is the term given when atopic eczema affects the female genital area. It occurs as part of a more widespread complaint of eczema (and often atopy) in the patient and is not localised solely to the genital area. Atopic disease has a strong personal and family history. Individuals will often suffer from the atopic triad of eczema, asthma and hayfever/atopic rhinitis. There is a genetic component to the inheritance of atopic disease and therefore it is important to ascertain if there is a positive family history, especially when individuals do not have an obvious history of other atopic disease. Ecchymoses (bruising caused by superficial telangectasiae) are the hallmark of lichen sclerosus, not eczema. If topical corticosteroids are abused and overused, one of the side effects can be skin thinning and bruising. However, if used according to instruction, topical corticosteroids are safe and effective and should not cause such problems. Soap substitution with an emollient and regular use of an emollient to moisturise are fundamental principles of management of inflammatory skin conditions as they help to restore the skin’s barrier function. This should be in conjunction with an appropriate topical corticosteroid regimen. Topical corticosteroids are necessary to relieve inflammation caused by inflammatory conditions such as eczema. It is a common misconception that topical corticosteroids should not be used on sensitive (e.g. flexural) sites and there is a general phobia amongst non-specialists and the public about using these topical agents. Prolonged use of superpotent or potent corticosteroids can cause side effects, especially if applied to skin adjacent to the inflamed area. If an area of eczema does not respond to topical steroid use, it is important to check for compliance, rule out infection or other pathology and ensure irritants are not inadvertently being applied to the skin. If poor response is still seen after taking these precautions, topical calcineurin inhibitors may be used as a second-line therapy.

• 19.
  

  a) F b) F c) T d) F e) T

Two peaks of presentation occur; these are in pre-pubertal girls and post-menopausal women. Lichen sclerosus is not uncommon in girls and the prevalence is estimated to be 1 in 900. It is therefore not classified as a rare disease. Lichen sclerosus is an autoimmune condition although the exact pathogenesis and the trigger for the disease is unknown. Due to the appearance of the condition, the possibility of sexual abuse is often queried. The presence of lichen sclerosus does not rule out abuse as it does have a predilection for traumatised surfaces, however, there are certain features that should be looked for that make sexual abuse more likely. These are lichen sclerosus presenting in older pre-pubertal girls, poor response to treatment and co-existing sexually transmitted infections. Well-demarcated white plaques in a figure of eight distribution surrounding the vulva and perianal areas, wrinkled skin, telangiectasia and ecchymoses are all classical signs of lichen sclerosus. Extra genital lichen sclerosus can occur, although it is rare. It presents as well-demarcated atrophic plaques on the trunk and limbs. It is essential that any child presenting with such lesions undergoes a vulvar examination to check for genital lichen sclerosus. Expert opinion, evidence extrapolated from randomised controlled trials in adults and a few case-series in girls suggests that superppotent or potent topical corticosteroids are first line treatment for lichen sclerosus in pre-pubertal girls. These should be applied daily to the affected areas for 2–3 months and then on an ‘as and when’ basis. Soap substitution and regular use of an emollient to moisturise are fundamental principles of management of inflammatory skin conditions.

• 20.
  

  a) F b) T c) F d) T e) T

Haemangiomata usually appear within the first month of life and may be very subtle at first. They typically undergo a period of rapid growth, followed by a slower period of involution. Haemangiomata in general are the most common pediatric skin tumor and affect girls more frequently than boys, especially those who are born prematurely or with a low birth weight. Vulvar capillary hemangiomata do not always require treatment, but being in a sensitive site they may affect function or become ulcerated and infected. In these circumstances treatment is necessary to restore function, promote development of the child and alleviate the symptoms and sequelae of secondary complications. Haemangiomata at any site may ulcerate, especially those that grow rapidly. However, those situated on flexural surfaces have a higher chance of ulceration as they are subject to increased friction and become ulcerated/macerated much more easily. Rapidly growing haemangiomata causing secondary complications were traditionally treated with high dose oral corticosteroids. However, in recent years oral beta blockers have been recognised as an even more effective treatment. The exact mechanism of action is unknown, however, this is an area that is undergoing intense research at present. Oral steroids or beta blockers should only be instigated under specialist supervision.

• 21.
  

  a) F b) T c) T d) F e) F

Absence of normal vaginal lactobacillus morphotypes in patients with DIV and the presence on culture of an abnormal vaginal flora with frequent growth of group B streptococci and E coli led to the assumption that the etiology was infectious in origin. The favorable response to 2% clindamycin (cream) strengthened the hypothesis that the etiology is a bacterial infection. Despite these findings, failure of other antibiotics especially metronidazole, with a spectrum of antibacterial activity similar to clindamycin, to treat the condition argues against an infectious etiology. Moreover, studies demonstrating that steroids are as effective as clindamycin undermined the theory of a bacterial cause for DIV. Symptoms and signs are non-specific and other etiologies of purulent vaginitis need to be excluded before confirming diagnosis, predominantly atrophic vaginitis and Trichomonas vaginitis. A wet mount (office based microscopy of vaginal discharge) is essential to confirm diagnosis. Definition includes the presence of markers that necessitates evaluation of vaginal secretion with microscopy (wet mount). Per definition it is mandatory to show an increase in inflammatory cells and para-basal epithelial cells (immature squamous cells). Vaginal flora is abnormal and pH is always elevated above 4.5. From the author’s point of view, one cannot make a diagnosis of DIV without including a description of wet mount microscopy. Although the peak age diagnosis is peri menopausal, 50% of women diagnosed with DIV will be in their reproductive ages. It is unnecessary to perform a biopsy of the vaginal wall to confirm the diagnosis of DIV. The conditions necessitating a biopsy are a group of multi-mucosal erosive disease including erosive lichen planus, cicatricial pemphigoid and pemphigus vulgaris that are rare and usually have external-genital involvement.

• 22.
  

  a) F b) T c) F d) F e) T

Fifty percent of patients with DIV are diagnosed in post-menopausal women, suggesting that lack of estrogen deficiency may play a role in DIV. Unfortunately, there is no predictable response to local or systemic vaginal estrogen treatment in women with DIV. This phenomenon serves as a critical diagnostic step in differentiating the two entities since they both can present with similar symptoms of vulvo-vaginal irritation and dyspareunia. Experts agree that a treatment trial with topical estrogen is a useful method to differentiate between DIV and atrophic vaginitis. Although the etiology and pathogenesis remain unknown, symptoms and signs overlap with other immune mediated vaginal disease including erosive lichen planus and benign membrane pemphigus. There is a favourable response to anti-inflammatory agents (corticosteroids) suggesting that the etiology is immune mediated. Both topical vaginal clindamycin and local vaginal corticosteroids are useful treatments for DIV. Both have anti-inflammatory affects. There has been no randomized controlled study comparing these two treatment options. Either local vaginal 2% clindamycin or vaginal corticosteroids are adequate treatment. Choice of treatment should consider the availability and cost of these medications which are differently distributed worldwide. Initial therapeutic response is extremely encouraging, after an initial 3 week treatment course with 86% of patients experiencing dramatic improvement. But 35% will relapse after cessation of initial treatment. It is important to recognize that DIV is a chronic condition in the majority of cases and to continue maintenance treatment as needed for some women. The major adverse outcome from the treatment with topical clindamycin or corticosteroids is developing a symptomatic yeast infection necessitating treatment. This occurs in 25% of patients. Adding fluconazole to the treatment regimen in patients prone to develop such an infection is recommended.

• 23.
  

  a) F b) F c) T d) F e) T

In 2004 the ISSVD abolished the VIN grading system (VIN 1, 2 and 3). The term VIN is used only for high grade lesions, without grading specification. Three diagnostic terms are recommended to describe squamous VIN: VIN, usual type (the more common VIN type, generally related to HPV), VIN, differentiated type (the less common type, generally not related to HPV) and VIN unclassified type (or VIN, NOS). Classification is made on the basis of morphologic criteria only and not HPV type. Significantly higher incidence of VIN is reported among white women than among black, Asian/Pacific Islander, or Hispanic women. In the last 30 years the incidence of VIN increased with a peak at ages of 40 to 49 and a second peak in women older than 55. In difficult cases, diagnosis of VIN type may be aided by p53 and p16 immunohistochemistry. Although there are exceptions, the p53− p16+ phenotype supports VIN, usual type diagnosis and p53+ p16− supports VIN differentiated type. In most cases VIN differentiated type is characterized by unifocal lesions, especially in post-menopausal women. Sometimes, whitish plaques with roughened surface are difficult to distinguish from associated dermatoses. Lichen sclerosus often affects the adjacent skin. The most recent multi-centre study on HPV genotype distribution in VIN and vulvar cancer found HPV-DNA in 86.7% VIN and 28,6% vulvar carcinomas examined. Patients with usual type VIN (91% of VIN) were significantly younger than patients with differentiated type VIN (48.5 years vs 60.0 years) and had a higher prevalence of HPV (90.3% vs 48.9%).

• 24.
  

  a) F b) T c) F d) F e) F

No substantial differences have been reported among different techniques; all seem to have a similar efficacy. Treatment must be individualized, taking into account the age, general condition and psychological issues of the patient, localization, size and focality of the lesion and multi-centricity of intraepithelial neoplasia through the lower genital tract. A 5-mm peripheral margin is appropriate for the management of VIN, though there are no definitive studies evaluating the safety margins in resections, as positive margins do not predict the development of recurrence. Resection depth varies in pilous areas where atypical cells can compromise skin appendages up to 4 mm and in hairless areas where sebaceous glands do not exceed not exceed 1mm of depth. CO2 laser vaporization is very useful in mucous areas, but surgical excision, performed with a scalpel, electrosurgery or laser, is still considered the treatment of choice. As no surgical specimen for histological evaluation is obtained with CO2 laser vaporization it is of the utmost importance to perform several biopsies in order to rule out possible invasive disease. The results of randomized–controlled studies show that topical Imiquimod can be an effective treatment for VIN usual type, but up to now Imiquimod has not been approved by the FDA for treatment of VIN and its use must be limited to clinical controlled studies. The optimal duration and frequency of application has not been determined. There are only two possible antigenic targets for therapeutic vaccines, namely E6 and E7, since they constitute the only proteins that are expressed both in precancerous and cancerous lesions. The aim of HPV prophylactic vaccination is to generate neutralizing antibodies against the HPV capsid L1 proteins.

• 25.
  

  a) F b) T c) F d) T e) T

Partner notification, as it is usually done in bacterial STI and HIV, is not recommended in the presence of AGW. Preventive interventions for partners of patients with AGW who do not present lesions themselves have not been evaluated and would theoretically be of limited value other than offering quadrivalent HPV vaccine. Counseling of AGW index cases on using condoms consistently is warranted at least until all lesions have cleared. The quadrivalent HPV vaccine has been shown to offer protection for vaccine types that the AGW patient has not been exposed to and for prevention of recurrences or lesions at new sites. The bivalent vaccine has not been studied in the context of AGW as it does not readily protect against HPV found in AGW. It has not been studied in men. Regulatory authorities have not issued recommendations in the context of AGW. Patient home-applied therapies are first line treatments and can be recommended to be used in the privacy of a patient’s home. There is no evidence that this kind of treatment is less effective than office administered therapies. Office administered therapy can be first line treatment for some patients especially if there are bulky lesions or multiple sites are affected.

• 26.
  

  a) F b) F c) T d) F e) F

The vulval lymphatics do not cross the genitocrural folds. There are no lymph nodes located beneath the femoral fascia and lateral to the femoral artery outside the opening of the fossa ovalis. Statement c is true, but there is still no consensus on the definition of laterality, the role of the tumour diameter and localisation and the depth of invasion. A free pathologic margin not less than 8 mm is safe. This can be obtained with a clinical free margin of 1–2 cm. Groin metastases are absent only when stromal invasion is ≤1 mm (stage Ia)

• 27.
  

  a) F b) F c) F d) F e) T

Inguinal lymphadenectomy is never indicated when the vulval tumour has a stromal invasion ≤1 mm; that is Stage Ia. The indication for inguinal lymphadenectomy is not based on the vulval tumour diameter, but on stromal invasion >1 mm. When sentinel lymph node dissection is positive for metastasis total or radical groin lymphadenectomy is mandatory. Groin lymph node assessment is only surgical; clinical negative palpation of the groin has been demonstrated to be unreliable. Superficial inguinal lymphadenectomy has no more indication in the surgical treatment of invasive vulval carcinoma since the GOG study published in 1992 by Stehman et al.

• 28.
  

  a) F b) T c) F d) T e) T

Today, total or radical groin lymphadenectomy does not necessarily require the removal of the femoral fascia along with the sartorius and adductor longus muscle fascias in order to be sure that all the inguino-femoral lymph nodes have been excised. The femoral fascia can be preserved because no lymph nodes are present beneath or outside the opening of the fossa ovalis. The en-bloc skin incision has been replaced by the triple incision since there is no need to remove a large skin portion in order to be oncologically radical. Three separate incisions, one for the vulva and two for the groins, reduces the local morbidity (less wound breakdown, better cosmetic results with psychological benefits) without impairing oncologic radicality (same local recurrence rate compared with en-bloc incision). When groin lymphadenectomy is performed it must be total or radical, which means excision of all the inguino-femoral lymph nodes. Except sentinel lymph node dissection, today, there is no consideration of other types of conservative groin surgery.

• 29.
  

  a) F b) T c) T d) F e) T

Genital herpes is not a notifiable disease in most countries. Partner disclosure is recommended so that informed negotiation about safer sexual practices can take place. Actual partner or last partner should be informed of the diagnosis, so they may be evaluated for potential unrecognized genital herpes. Type-specific serology can be performed to assist in securing the diagnosis of genital herpes, particularly in circumstances when differentiating an initial from recurrent disease is difficult. Viral identification tests should be performed when there is a lesion, either via viral culture, DFT or PCR. Topical antiviral treatment is not helpful in either initial or recurrent disease. Psychosexual counselling may be offered since rapid adaption to a diagnosis of genital herpes can help recovery.

• 30.
  

  a) F b) F c) T d) F e) F

Pap smear cervical cytology is not definitive for HSV infection; however, cytology may show giant cells typical of herpes viral infections, including HSV. Clinical diagnosis is not definitive. Other causes of ulcerative diseases may manifest similarly. Viral culture will give a definitive answer plus provide the genotype of the infection. It is important in collecting the sample appropriately to break a FRESH vesicle first, and then swab the base of the lesion or ulcer firmly to collect cells for culture or DFT. If the lesion is crusting over the culture may be falsely negative. Rapid herpes assays have recently become available, but are not yet validated to give an accurate sensitivity. PCR is the most sensitive assay, although not available in all laboratories. It also defines typing of the HSV.