The2 2 major screening test for pulmonary embolism is the perfusion scan purchase 100mg kamagra gold otc impotence journal, which involves the injection of aggregates of human serum albumin labeled with a radionuclide into a peripheral vein cheap kamagra gold 100 mg visa erectile dysfunction is often associated with quizlet. These albumin aggregates (~10 to 50 μm wide) travel through the right side of the heart cheap 100mg kamagra gold mastercard erectile dysfunction differential diagnosis, enter the pulmonary vasculature, and lodge in small pulmonary vessels. Only lung areas receiving blood flow will manifest an uptake of the tracer; the nonperfused region will not show any uptake of the tagged albumin. Because pulmonary arterioles, capillaries, and venules have little structural support, they can be easily distended or collapsed, depending on the pressure surrounding them. It is the change in transmural pressure (pressure across the capillaries) that influences vessel diameter. From a functional point of view, pulmonary vessels can be classified into two types: extra-alveolar vessels (pulmonary arteries and veins) and alveolar vessels (arterioles, capillaries, and venules). The extra-alveolar vessels are subjected to pleural pressure-any change in pleural pressure affects pulmonary vascular resistance in these vessels by changing the transmural pressure. The transmural pressure in the extra- alveolar vessels increases, and they become distended (Fig. However, alveolar diameter increases at high lung volumes, causing the transmural pressure in alveolar vessels to decrease. As the alveolar vessels become compressed, pulmonary vascular resistance increases. At low lung volumes, pulmonary vascular resistance also increases, as a result of more positive pleural pressure, which compresses the extra-alveolar vessels. Because alveolar and extra-alveolar vessels can be viewed as two groups of resistance vessels connected in series, their resistances are additive at any lung volume. However, alveolar vessels are compressed, causing a rise in pulmonary vascular resistance. At low lung volumes, alveolar vessels are distended, but the extra-alveolar vessels are compressed from the rise in pleural pressure, which results in a rise in pulmonary vascular resistance. Because smooth muscle plays a key role in determining the caliber of extra-alveolar vessels, drugs can also cause a change in resistance. Serotonin, norepinephrine, histamine, thromboxane A, and2 leukotrienes are potent vasoconstrictors, particularly at low lung volumes when the vessel walls are already compressed. Drugs that relax smooth muscle in the pulmonary circulation include adenosine, acetylcholine, prostacyclin (prostaglandin I ), and isoproterenol. Although the pulmonary circulation is2 richly innervated with sympathetic nerves, surprisingly, pulmonary vascular resistance is virtually unaffected by autonomic nerves under normal conditions. Although changes in pulmonary vascular resistance are accomplished mainly by passive mechanisms, resistance can be increased by low oxygen in the alveoli, alveolar hypoxia, and low oxygen in the blood, hypoxemia. Recall from Chapter 17 that hypoxemia causes vasodilation in systemic vessels, but in pulmonary vessels, hypoxemia or alveolar hypoxia causes vasoconstriction of small pulmonary arteries. This unique phenomenon is called hypoxia-induced pulmonary vasoconstriction and is accentuated by high carbon dioxide and low blood pH. The exact mechanism is not known, but hypoxia can directly stimulate pulmonary vascular smooth muscle cells, independent of any agonist or neurotransmitter released by hypoxia. Two types of alveolar hypoxia (regional hypoxia and generalized hypoxia) are encountered in altered lung function, with different implications for pulmonary vascular resistance. In regional hypoxia, pulmonary vasoconstriction is localized to a specific region of the lungs and diverts blood away from a poorly ventilated region, which minimizes the effect on gas exchange (Fig. Regional hypoxia has little effect on pulmonary arterial pressure, or resistance, and when alveolar hypoxia no longer exists, the vessels dilate and blood flow is restored. Generalized hypoxia, on the other hand, causes vasoconstriction throughout both lungs, leading to a significant rise in resistance and pulmonary artery pressure (Fig. Generalized hypoxia can lead to pulmonary hypertension (high pulmonary arterial pressure), which leads to pathophysiologic changes (hypertrophy and proliferation of smooth muscle cells, narrowing of arterial lumens, and a change in contractile function). Pulmonary hypertension causes a substantial increase in workload of the right heart, often leading to right heart hypertrophy. Low oxygen tension in the alveoli (alveolar hypoxia) is the major mechanism regulating blood flow within normal lungs. In the fetus, pulmonary vascular resistance is extremely high as a result of generalized hypoxia: <15% of the cardiac output goes to the lungs, and the remainder is diverted to the left side of the heart via the foramen ovale and to the aorta via the ductus arteriosus. When alveoli are oxygenated on the newborn’s first breath, pulmonary vascular smooth muscle relaxes, the vessels dilate, and vascular resistance falls dramatically. The foramen ovale and the ductus arteriosus close and pulmonary blood flow increases enormously. Net fluid transfer across the pulmonary capillaries depends on the difference between hydrostatic and colloid osmotic pressures inside and outside the capillaries. In the pulmonary circulation, two additional forces play a role in fluid transfer-surface tension and alveolar pressure. The force of alveolar surface tension (see Chapter 19) pulls inwardly, which tends to lower the interstitial pressure and draw fluid into the interstitial space. By contrast, the alveolar pressure tends to compress the interstitial space and the interstitial pressure is increased (Fig. Fluid movement in and out of capillaries depends on the net difference between hydrostatic and colloidal osmotic pressures. In the lung, two additional factors (alveolar surface tension and pressure) are involved in fluid exchange. Alveolar surface tension enhances filtration, whereas alveolar pressure opposes filtration. The relatively low pulmonary capillary hydrostatic pressure helps keep the alveoli “dry” and prevents pulmonary edema. Mean pulmonary capillary hydrostatic pressure is normally 8 to 10 mm Hg, which is lower than the plasma colloid osmotic pressure (25 mm Hg). This is functionally important because the low hydrostatic pressure in the pulmonary capillaries favors the net absorption of fluid. Alveolar surface tension tends to offset this advantage and results in a net force that still favors a small continuous flux of fluid out of the capillaries and into the interstitial space. This excess fluid travels through the interstitium to the perivascular and peribronchial spaces in the lungs, where it then passes into the lymphatic channels (see Fig. The lymphatic vessels are not found in the alveolar–capillary area but are strategically located near the terminal bronchioles to drain off excess fluid. Lymphatic channels, like small pulmonary blood vessels, are held open by tethers from surrounding connective tissue. Pulmonary edema occurs when excess fluid accumulates in the lung interstitial spaces and alveoli and usually results when capillary filtration exceeds fluid removal. Pulmonary edema can be classified as cardiogenic pulmonary edema (due to heart dysfunction) or noncardiogenic pulmonary edema (due to lung injury). Cardiogenic pulmonary edema is caused by an increase in capillary hydrostatic pressure or by a decrease in plasma colloidal osmotic pressure. Increased capillary hydrostatic pressure is the most frequent cause of pulmonary edema and is often the result of an abnormally high pulmonary venous pressure (e. The second major cause of pulmonary edema is noncardiogenic and is due to increased alveolar surface tension and/or increased permeability of the alveolar–capillary membrane.

The length–tension curve represents the effect of initial resting length generic kamagra gold 100 mg online valium causes erectile dysfunction, or preload cheap 100 mg kamagra gold with amex erectile dysfunction nofap, on the isometric contraction of skeletal muscle proven 100 mg kamagra gold top erectile dysfunction pills. At initial lengths less than and up to L, such a curve represents theO maximum force that can be generated at any given preload. No shortening occurs in these situations, and the curve depicts muscle contraction as if all its energy was channeled into the development of force only. The bottom graph shows that, for contractions B, C, and D, the initial portion is isometric (the line moves upward at constant length) until the afterload force is reached. The muscle then shortens at the afterload force (the line moves to the left) until its length reaches a limit determined (at least approximately) by the isometric length–tension curve. The dotted lines show that the same final force/length point can be reached by several different approaches. Relaxation data, not shown on the graph, would trace out the same pathways in reverse. Although the length–tension curve depicts isometric contraction of muscle, it also represents the limit of shortening of any isotonic contraction of that muscle. Isotonic contractions involve an initial isometric phase during which force is generated up to the point it equals the load the muscle is trying to move (i. Once that point is reached, the muscle then shortens while moving that load (the isotonic phase). Note that during an isotonic contraction, the muscle will eventually reach a length where the maximum isometric force capable by the muscle matches the afterload the muscle is trying to move (see dashed lines in Fig. At this point, the muscle cannot shorten anymore; to do so would place the muscle at a length where its maximum isometric force-generating capability was less than the load it was trying to move-an impossibility. In other words, isotonic contractions of a muscle moving any afterload cannot move past a limit defined by the isometric length–tension curve for that muscle. Also note that if the muscle begins its shortening from a reduced initial length, its subsequent extent, or amount, of shortening will be reduced because the muscle starts closer to the limit imposed by the isometric–length tension curve. The following constraints apply to the extent of shortening of an isotonic contraction of skeletal muscle: (1) increasing preload up to L increases the extent of shortening (the distance the afterload is moved); (2) at any giveno preload, increasing the afterload decreases the extent of shortening; (3) at any given preload, the final length of the muscle at the end of an isometric contraction is proportional to the afterload; and (4) the isometric length–tension curve sets the limit to the extent of shortening of any isotonic contraction of skeletal muscle. The example above demonstrates that the distance a muscle can move an object is progressively reduced as the muscle tries to move increasingly heavy loads. One might postulate that skeletal muscle could move a heavy load as far as it could a light load if there was some way to change (enhance) the intrinsic contractile ability of the muscle cell itself. Such intrinsic enhancement would reveal itself as a shift of the ascending limb of the length–tension curve upward and to the left relative to its original position. Such a shift would move the limit to extent of shortening to the left, thereby letting the muscle move the heavy load as far as it could move the light load in its original state. Unfortunately, such intrinsic or cellular/molecular enhancement of the contractile mechanism is not possible under any normal physiologic conditions for skeletal muscle fibers. In essence, skeletal muscle shortening is constrained by its loading conditions; it cannot modify its cellular contractile capabilities independently of preload and afterload. Such is not the case with cardiac muscle, however, which can shift its length–tension relationship (see Chapter 13). Anatomic location also places restrictions on muscle function by limiting the amount of shortening or determining the kinds of loads encountered. Skeletal muscle is generally attached to bone, and bones are attached to each other. In most cases, the system works at a mechanical disadvantage with respect to the force exerted. For example, curling the forearm requires muscles that are attached near the fulcrum of the arm “lever” rather than at the more mechanically advantageous position near the hand. This means that in order to pull the forearm toward the upper arm while holding a weight in the hand, the muscle must exert a much greater force than the actual weight of the load being lifted (the muscle force is increased by the same ratio that the length change at the end of the extremity is increased). In the case of the human forearm, the biceps brachii, when moving a force applied to the hand, must exert a force at its insertion on the radius that is approximately seven times as great. However, the shortening capability of skeletal muscle by itself is rather limited. The benefit of the skeletal lever system is that it multiplies the distance over which an extremity can be moved. Consequently, it is possible to create large distances moved by the end of the limb with only small actual shortening of the muscle responsible for moving the limb. In this forearm example, the resulting movement of the hand is approximately seven times as far and seven times as rapid as the shortening of the muscle itself. Contraction of the biceps muscle lifts the lower arm (flexion) and elongates the triceps, whereas contraction of the triceps lowers the arm and hand (extension) and elongates the biceps. The bones of the lower arm are pivoted at the elbow joint (the fulcrum of the lever). Thus, the hand will move seven times as far (and fast) as the biceps shortens (lever ratio, 7:1), but the biceps will have to exert seven times as much force as the hand is supporting. Force must be used to relengthen the muscle, and this force must be provided externally. However, in the body, muscles are often arranged in antagonistic pairs of flexors and extensors. In this manner, for example, a shortened biceps can be relengthened by the action of the triceps; the triceps, in turn, is relengthened by contraction of the biceps. Cellular processes within skeletal muscle cells must supply biochemical energy to the contractile mechanism because contracting muscles perform work. Additional energy is required to pump the calcium ions involved in the control of contraction and for other cellular functions as well. Creatine phosphate is the most important storage form of high-energy phosphate; together with some other smaller sources, this energy reserve is sometimes called the creatine phosphate pool. Glycolysis, an anaerobic pathway, and oxidative phosphorylation, an aerobic pathway, are the two major metabolic paths that supply energy to the energy-requiring reactions in the cell and to the mechanisms that replenish the creatine phosphate pool. Glucose for the glycolytic pathway may be derived from circulating blood glucose or from glycogen, which is the polymer storage form of glucose in skeletal muscle and liver cells. Glucose is the preferred fuel for skeletal muscle contraction at higher levels of exercise. At maximal work levels, almost all the energy used is derived from glucose produced by glycogen breakdown in muscle tissue and from blood-borne glucose from dietary sources. Muscle has performance limitations based on its structure and energy-conversion processes; as such, its efficiency is much <100%, and it produces relatively large quantities of heat, which must be dealt with by the organism that it is serving (see Chapter 28). Metabolic differences among muscle fibers affect their ability to sustain contraction. Although the basic structural features of the sarcomeres and the thick–thin-filament interactions are essentially the same among skeletal muscles, the chemical reactions that supply the contractile system with energy vary. A typical skeletal muscle usually contains a mixture of fiber types with different metabolic properties.

The postoperative patient is seen within the first 48 hours of surgery-preferably within 24 hours order generic kamagra gold impotence following prostate surgery. Typical postoperative medications include (1) antibiotic solutions for infection control and (2) steroids and/or nonsteroidal anti-inflammatory drugs for controlling the inflammation order generic kamagra gold on line men's health erectile dysfunction causes. Important hardware and software advances in ultrasound technology will include new phaco needles generic kamagra gold 100 mg with visa erectile dysfunction treatment germany, improved fluidics, and improved instrumentation, which will allow safer, more efficient removal of cataracts. In addition, nonultrasound methods for cataract removal will reduce incision size even further, including the mechanical approach (Catarex, which is in preclinical development, uses a rotating blade and whorl-like fluidics to remove lens material through a 1-mm capsulorrhexis; AquaLase, now available, uses fluid micropulses to emulsify the lens) and the laser approach, as previously discussed. Both nonultrasound methods are expected to eliminate the risk of thermal injury to the wound site. American Academy of Ophthalmology: Cataract in the Otherwise Healthy Adult Eye (Preferred Practice Patterns). Blood collects in the retrobulbar space, often causing proptosis of the involved eye and a tense orbit. The risk of this complication is greatest in highly myopic eyes with long axial lengths. It may result in a secondary central retinal vein and/or central retinal artery occlusion. Peribulbar injections given with a shorter needle have become more popular recently, as has topical anesthesia for cataract surgery. Blood collecting in the retrobulbar space may cause a secondary increase in intraocular pressure from the pressure of the blood on the globe. When a retrobulbar hemorrhage occurs, intermittent pressure is applied initially to the globe to tamponade the bleeding. Most wound leaks require repair in the operating room with additional sutures to achieve a watertight closure. If a wound leak is present, the iris often becomes incarcerated in the wound and may prolapse through the wound, which leads to increased inflammation and increased risk of infection. Blood vessels in the base of the cataract wound or possibly from the iris are usually the source of the blood. The intraocular pressure needs to be monitored closely because secondary elevation may occur. The rupture causes a rapid rise in intraocular pressure with loss of the anterior chamber, iris prolapse, and possible prolapse of the entire intraocular contents if not recognized and treated promptly. What is the incidence of posterior capsule rupture for an experienced surgeon during cataract surgery? Patients with advanced age, systemic hypertension, arteriosclerosis, glaucoma, and long axial-length eyes are at greater risk. The wound must be closed as quickly as possible; the surgeon maytamponadethewoundwithhisorher thumb until a suture is ready. In this performing posterior sclerotomies to case nearly the entire lens ‘‘dropped’’ following a releaseaccumulatedblood. Theprognosis circumferential extension of a radial tear during for visual outcome is usually quite poor. All eyes show some postoperative uveitis, characterized by cell and flare reaction in the anterior chamber. Despite individual variation, the degree of inflammation is usually proportionate to the degree of trauma induced by the surgical procedure. Fragments of lens material-either nucleus or cortical remnants- may cause inflammation. Nuclear fragments may become a source of chronic inflammation that leads to macular edema. This is more common when implants are poorly positioned and specifically when they are in contact with uveal tissue. The classic presentation includes severe ocular pain, decreased vision, eyelid swelling, conjunctival chemosis, and hypopyon. This condition must be suspected in any patient who presents with more inflammation than expected postoperatively. What are the common organisms cultured from the vitreous of endophthalmitis patients? In the Endophthalmitis Vitrectomy Study the most common causative pathogens were gram-positive, coagulase-negative organisms (e. Corneal edema frequently occurs adjacent to the cataract wound and usually resolves spontaneously. Surgical trauma, preexisting endothelial corneal dystrophy, and elevated intraocular pressure may cause central corneal edema. Treatment of elevated intraocular pressure and topical steroids, as necessary for inflammation, are important. Corneal or epithelial transplantation may be necessary for patients when corneal Figure 23-3. It is more commonly seen in patients with preexisting endothelial cell loss (Fuchs’ loss during cataract surgery? Vitreous loss may result from rupture of the posterior lens capsule or weakness or dehiscence of lens zonular apparatus. Vitreous loss increases risk of retinal detachment, cystoid macular edema, and endophthalmitis. The additional surgical trauma also may lead to an increase in corneal trauma and secondary central corneal edema. Patients predisposed to retinal detachment because of high myopia, lattice degeneration, and a history of retinal detachment in the fellow eye are at greatest risk. The risk of retinal detachment after cataract surgery has decreased with the advent of extracapsular cataract extraction, which has replaced intracapsular extraction. Cystoid macular edema after cataract surgery (Irvine-Gass Syndrome) has historically been documented with fluorescein angiography (left), where it has a classic petaloid appearance in late frames of the angiogram. More recently, optical coherence tomography is increasingly being used to diagnose and follow macular edema (right). Cystoid macular edema is more common after intracapsular than extracapsular cataract extraction. It is also more common when vitreous loss occurs, especially if vitreous or iris becomes incarcerated in the wound. Initial treatment often includes topical steroids or nonsteroidal anti-inflammatory medications (Acular). Acetazolamide (Diamox) has been shown to reduce edema in some cases and is often used as an oral medication. More recently, intravitreal triamcinolone has been shown to help cystoid macular edema, although the improvement may be transient. A secondary or ‘‘after-cataract’’ membrane develops after extracapsular cataract surgery. The posterior capsule opacifies when persistent lens fibers adhere to the capsule, or the remaining lens fibers undergo metaplasia. Patients typically present with progressive decrease in vision or problems with glare after surgery.

It is most frequently described as a topical and/or systemic imidazoles is usually curative; burning sensation buy kamagra gold 100 mg amex erectile dysfunction doctor manila, although itch cheap 100mg kamagra gold erectile dysfunction treatment california, stinging discount 100 mg kamagra gold erectile dysfunction treatment with diabetes, pain, or recurrence is common, however. Further reading neoplastic disease Royal College of Obstetricians and Gynaecologists. Vulval pain afects a signifcant number of women Lesions should be biopsied to make a defnitive and can negatively impact quality of life and sexual diagnosis and to rule out underlying invasive malig- function. Previously used reduced impact on sexual activity and psychological terms such as vestibulitis should be avoided. Long-term specialist follow-up is needed, as there is a risk of progression to invasive malignant disease. Assessment Women may present with vulval pain alone or in Extramammary Paget’s disease conjunction with other symptoms such as vulval skin Vulval extramammary Paget’s disease is character- changes, itching, or vaginal discharge. Surgical excision to assessing the nature of the pain, one should also of the lesion is both therapeutic and diagnostic, determine: allowing the identifcation and treatment of asso- any triggers (e. If invasive malignancy is precipitating events (including physical or psychological ruled out, alternative non-surgical treatments, such trauma); as photodynamic therapy and imiquimod, may be the impact of the pain on the patient’s function and considered. It is most fre- infectious (see vulval itching and vulval ulceration) quently characterised as a burning sensation, but Sexually transmitted ● may be described as pain, stinging, or irritation over herpes simplex virus ● lymphogranuloma venereum a prolonged period of time (months or years). It can ● granuloma inguinale be classifed based on the area of the vulva afected ● chancroid and factors provoking the pain (Box 1). Alternatively ● syphilis women may repeatedly report developing and treat- Non-sexually transmitted ing thrush or a urinary tract infection, with no or ● candidiasis partial response to therapy. Examination of the vulva ● tuberculosis does not usually reveal any architectural or skin ● fununculosis changes, but does allow the site of pain to be elic- ● diphtheria ited and the pelvic foor muscle tone to be assessed. Management usually Lichen sclerosus requires a combination of conservative and pharma- Immunobullous disorders cological measures. All patients are likely to beneft Crohn’s disease from education, support groups (e. Other conservative measures include counselling, pelvic foor physio- neoplastic (see vulval swellings) therapy, and chiropractic. Topical anaesthetics, such Squamous cell carcinoma Basal cell carcinoma as 5% lidocaine ointment and gel can ofer temporary Melanoma pain relief. Pharmacological treatments include tri- Sarcoma cyclic antidepressants (typically amitriptyline) and Bartholin’s glands adenocarcinomas gabapentin. Vulval intraepithelial neoplasia Extramammary Paget’s disease Undifferentiated tumours infection Possible secondary tumours A number of infections, both sexually and non- neurological sexually transmitted (Box 1), may result in pain, Herpes neuralgia usually from ulceration or suppuration. Tese are Spinal nerve compression discussed in detail elsewhere (see Vulval ulceration). Pudendal nerve entrapment Pudendal neuralgia vulvodynia infammatory disease Generalised Infammatory skin disease and systemic disease can Provoked (sexual, nonsexual, or both) both cause vulval pain, ofen through ulceration (see Unprovoked Vulval ulceration) and excoriation (see Vulval itching). Mixed (provoked and unprovoked) Localised (vestibulodynia: previously known as vulval vestibulitis, clitorodynia, hemivulvodynia, etc. Tese are discussed in detail elsewhere (see Mixed (provoked and unprovoked) Vulval swellings). Neurological complications causing both sensory and motor symptoms in the of herpes simplex virus type 2 infection. Neururol results in herpes zoster (shingles), a painful vesicular Urodyn 2008; 27(4): 306–10. British Post-herpetic neuralgia describes persistent pain fol- Journal of Dermatology. J Reproductive Med antidepressants or gabapentin may be used to treat 2004; 49(10): 772–77. Treatment depends on includes not only tumours of the vulva itself, but the cause of the sacral nerve root irritation or com- also swellings that appear at the vulva as a result pression and is usually undertaken by the patient’s of the displacement of other structures, as in cases general practitioner or an orthopaedic surgeon. Infammatory lesions and ulceration of the obstetric trauma vulva may be accompanied by swelling of the vulva Perineal pain is a common complaint in the post- owing to oedema. Tese conditions are considered partum period following vaginal delivery and under Vulval ulceration. Conditions presenting may persist beyond this in a signifcant number of with itching of the vulva as the main complaint are women. Following surgical repair, post-operative manage- Tey may be benign or malignant, which can be ment includes laxatives and broad-spectrum anti- further divided into primary and secondary. Sebaceous cyst Mucous cyst Implantation cyst Dermoid cyst Hydrocoele of the canal of Nuck vestigial cyst Benign Fibroma Lipoma Fibromyoma Hidradenoma Papilloma Lymphangioma Myxoma Angioma Melanoma benign Neuroma Caruncle Malignant Figure 2 Vulval cyst following female circumcision; the content was Squamous cell carcinoma old blood. Rodent ulcer – basal cell carcinoma Adenocarcinoma The cyst tends gradually to increase in size, caus- Sarcoma ing local discomfort, until marsupialisation is per- Melanoma – malignant formed. Choriocarcinoma Sebaceous cysts are fairly common, afecting the labia majora as a rule. The true nature of these cysts Cystic swellings is usually known only through histological examina- Bartholin’s cyst. It is essentially a type of hernia and Hydrocoele of the canal of Nuck vestigial cyst. Tis is caused by the duct opening of the Bartholin’s gland infective swellings becoming blocked, thus producing a swelling in the Bartholin’s abscess. It is not particularly ten- Bartholin’s abscess presents as an extremely painful der unless it becomes infected and forms an abscess. Varicocoele must be distinguished from an inguinal hernia extending into the labium majus and from a cyst of the canal of Nuck (the processus vaginalis, which has failed to become completely obliterated). Both of the latter tend to involve only the anterior parts of the labium majus, but all these conditions extend to the groin. Inguinal hernias usually dis- appear as pregnancy progresses, but varicocoeles become worse. A strangulated hernia will not be reducible, but the accompanying acute symptoms and the history should make the diagnosis clear. A haematoma of the vulva may follow delivery or occur as the result of direct trauma. It is recognised as a bluish swelling, which is painful and tender, and spreads up into the pelvis by the side of the vagina. An endometrioma is a rare cause of a blood-containing cyst on the vulva and is occurs at the entrance to the vagina. The duct of the gland has become blocked Benign new growths and the secretions within the gland infected. Tis situation can be problematic in pregnancy and in patients who As the vulva comprises skin, any swelling that can are immunocompromised (e. Tey may occur at any age, are sof and oval or rounded, and are covered by vulval skin. Tey are usually solitary and small (about Varicocoele of the vulva occurs mainly in pregnancy 1 cm in diameter) and their nature is confrmed by and can become worse with successive pregnancies. A papilloma is a sessile benign tumour of Tey give a typical varicose appearance in the labia the skin of the labia in women of middle or old age. Less commonly, fbromyoma, myxoma, angioma, lym- phangioma, benign melanoma, and neuroma are found, each distinguished by microscopic examina- tion of the excised lesions.

J. Silvio. University of Evansville.