Lecture 7 Part 2 PDF

Tinea Cruris (Jock Itch) T cruris is more common in men. It is rare prior to puberty and uncommon before the 20s. T cruris presents as chronic, brown to red patches in the groin folds (Figure 7.24). Scale may be present, but is frequently absent. There may be mild pruritus, but it is often asymptom...

Tinea Cruris (Jock Itch) T cruris is more common in men. It is rare prior to puberty and uncommon before the 20s. T cruris presents as chronic, brown to red patches in the groin folds (Figure 7.24). Scale may be present, but is frequently absent. There may be mild pruritus, but it is often asymptomatic. It spares the scrotum, penile shaft, and glans penis. It should be differentiated from Candidiasis, which is typically bright red in color, typically involves the glans penis and scrotum, and usually shows satellite pustules or papules. T cruris is caused by the same fungi that commonly cause T pedis and T corporis (Trichophyton rubrum, Trichophyton mentagrophytes, and Epidermophyton floccosum). T cruris should be treated with a topical antifungal cream. If patients complain of itching, they can also use hydrocortisone 1% cream for the first several days of treatment. Patients with T pedis should be examined for T cruris, and vice versa, as the two commonly co-exist. When cured, patients should use an antifungal powder (miconazole 2% powder) at least once a week to prevent recurrence, as without this type of prophylaxis, the rate of recurrence is extremely high. If T cruris does not respond as expected to treatment, the patient should be referred to a dermatologist, as several rare dermatoses that mimic T cruris can be serious if not diagnosed. Nail Dystrophy Abnormal appearance of the toenails and fingernails due to trauma is quite common. Chronic low grade trauma is probably the most common cause of fingernail dystrophy. For toenails, this is usually due to exercise (jogging) causing repetitive impact between the shoe and the nail tissue. For fingernails, the trauma is usually due to habits, such as picking the cuticles (Figure 7.25). Acute trauma to the nail itself may lead to the nail falling off. As long as there was no damage to the nail matrix, the nail should grow back normally. Acute trauma to the distal finger which damages the matrix can cause temporary nail dystrophy if the matrix heals properly. If the matrix heals with a scar or with any abnormality, the dystrophy may be permanent (Figure 7.26). The nail matrix is a tightly regulated tissue which forms the nail plate. Any disruption in the normal anatomy of the matrix leads to abnormalities of the nail plate. For acute traumatic injuries, no treatment is necessary or effective. The plate dystrophy will grow out with the nail if the matrix heals. If the matrix doesn’t heal, the dystrophy will be permanent, and will be extremely difficult, if not impossible, to surgically repair. For chronic injuries, resolving the source of chronic injury (ill-fitting shoes or picking habit) will usually lead to resolution of the plate abnormalities. Vitiligo Vitiligo most commonly presents in darkly pigmented individuals in the first three decades of life. There is a familial predisposition. It is also weakly associated with other autoimmune diseases, such as autoimmune thyroid disease and alopecia areata. Vitiligo presents as asymptomatic, completely depigmented patches. There may be minimal erythema, but this is actually uncommon. The patches are very white. Hairs within the depigmented areas are also usually depigmented. (Figure 7.27) (Figure 7.28) (Figure 7.29) There are commonly multiple depigmented areas. The most frequent sites are the hands, elbows, knees, perioral, periocular, and genital areas. Some patients will only have one patch of vitiligo, while other patients may have 80 – 100% of their body involved. While the pathogenesis of vitiligo is unclear, the current leading hypothesis is that it most likely represents an autoimmune disease in which a specific immune response against melanocytes develops. Besides the association with other autoimmune diseases, it should also be noted that rare patients who develop vitiligo will also develop immune reactions against ocular melanocytes (retina and iris) and meningeal melanocytes (leads to encephalitis). One thing that argues against this hypothesis is that on biopsies of vitiligo, it is rare to find any inflammatory or immune cells (lymphocytes, macrophages, etc); however, this may be due to the timing of biopsies. Other hypotheses are that there is a primary abnormality of melanocytes, and they die because they are unable to detoxify the reactive metabolites that accumulate during melanin production. It has also been hypothesized that there is a primary abnormality of the cutaneous innervation. Vitiligo is difficult to treat. Facial vitiligo responds best to treatment, while vitiligo on the hands is the most resistant. First line treatment is with topical steroids and topical immunomodulators, such as tacrolimus (Protopic). The most effective treatments involve use of ultraviolet light, either narrowband UVB or PUVA (both discussed under psoriasis). Alopecia Areata (AA) Alopecia areata affects 2% of people at some point in their lives. At any given moment, 0.2% of the population has alopecia areata. Young adults and children are most commonly affected. AA typically presents with sharply circumscribed areas of complete hair loss which develop suddenly. Typically the areas are 1-5 cm in diameter. There may be a few, fine depigmented hairs present in the areas of hair loss, and these are often called exclamation point hairs because the distal portion of the hair shaft is thicker than the proximal portion. The scalp is most commonly involved, but the beard area, eyelids, eyelashes, or any other hair bearing area can be affected. (Figure 7.30) (Figure 7.31) Variants are alopecia totalis, where the entire scalp is affected, and alopecia universalis, where all hair on the entire body is affected. Only pigmented hairs are affected, and this explains cases of patients going “white overnight” – if a patient has mixed gray hair and pigmented hair and develops alopecia totalis, they will lose all the pigmented hairs and only the gray hairs will remain. The natural history of the disease varies depending on the severity of the disease. Essentially, the more widespread the disease, the less likely it is to spontaneously resolve. Patients with a few small patches of hair loss are very likely to have the disease spontaneously resolve within 2 years, while patients with alopecia universalis are very unlikely to ever get better. AA, alopecia totalis, and alopecia universalis are autoimmune diseases in which CD4 and CD8 cells attack hair bulbs. The inciting events and causes of remission are unknown. Localized disease is effectively treated with injections of steroids directly into areas of hair loss. This obviously is not practical for patients with widespread disease. Widespread disease can be treated with immunosuppressive medications, but treatment is usually not very effective. Patients should be asked questions about symptoms of thyroid disease, diabetes, and lupus, as these autoimmune diseases are weakly associated with AA. Pattern Baldness, Male and Female Both are extremely common. MPB can begin anytime from the mid-teens onward. FPB typically doesn’t begin until peri-menopause or menopause, although rare women may have onset of FPB during puberty. There is a familial predisposition, but inheritance is unclear and likely involves multiple genes. MPB involves the bi-temporal areas and the vertex of the scalp. It may lead to nearly complete loss of scalp hair on the anterior scalp, crown, and vertex. The far lateral parietal scalp and the occipital scalp are typically spared. (Figure 7.32) FPB involves the vertex and the crown. Women can have their hair become quite thin, but it is very rare for a woman to have complete loss of scalp hair in any area. (Figure 7.33) MPB is related to the enzyme 5-alpha-reductase, type 2, which converts testosterone to dihydro- testosterone (DHT). DHT has more potent effects on the hair follicle, causing progressive miniaturization of the follicle. 5α-reductase, type 2 is distributed unevenly throughout the scalp, with increased expression in MPB-affected areas and decreased expression in other areas. FPB is related to relative increases in circulating androgenic hormones. MPB can be treated with oral finasteride, which blocks DHT. It can also be treated with topical minoxidil, for which the mechanism of action is unknown. These agents can be used in combination for increased effect. They are much better at halting progression of balding than they are at regrowing hair. Treatment is effective in about 2/3 of patients. FPB can be treated with topical minoxidil. In post-menopausal women, anti-androgen agents, such as spironolactone, can also be beneficial. Finasteride and its derivatives have been used to treat FPB in post menopausal women with some efficacy. Hair transplant is effective in both MPB and FPB. In this procedure, hair follicles from unaffected portions of the scalp (parietal and occipital scalp) are surgically harvested and re- implanted in affected portions of the scalp, where they continue to grow. Telogen Effluvium Telogen effluvium is most common in young adult females, although it can affect anyone. Telogen effluvium presents with increased shedding of hair. Patients will usually complain of finding excess hair in the shower drain after washing their hair. The patient may note that their hair is thinner, but other people typically don’t notice any difference. Telogen effluvium typically occurs 3 months after a severe physiologic or psychologic stress. If the stress was acute, the increased shedding will last several months and then resolve. If the stress is ongoing, the increased shedding will continue until the stress resolves. The most common stress to cause telogen effluvium is labor and delivery. On the normal scalp, 90% of hairs are in anagen, 9% in telogen, and 1% in catagen. In telogen effluvium, the stress causes an abnormal number of anagen hairs to suddenly switch into telogen. After spending 3 months in telogen, these hairs are shed. This is why there is a three month delay between the stress and the shedding. Telogen effluvium will resolve spontaneously, as long as the stress resolves. In cases of chronic psychologic stress (job loss, marital stress, etc.), the increased shedding may become chronic. Regardless, the prognosis is excellent – no patient goes bald from telogen effluvium. Melasma Melasma is almost exclusively a disease of young adult females. Melasma presents as flat, asymptomatic areas of hyperpigmentation on the face. Most commonly, it involves the forehead, nose, central cheeks, and/and perioral areas. It frequently involves only the cheeks (Figure 7.34), or it may involve the jawline only. Melasma occurs in the setting of increased estrogen and increased sun exposure. Women typically present during or after pregnancy or while taking oral contraceptives. Melanocytes have estrogen receptors, which cause increased melanin production when activated. Ultraviolet radiation also stimulates melanin production. Excess estrogen stimulation and ultraviolet exposure must both be addressed if melasma is going to be treated effectively. For women who are pregnant and develop melasma, treatment should be limited to effective sunscreen use until the pregnancy is over. For women who develop melasma while taking oral contraceptives, they should be counseled that the melasma is unlikely to resolve if they continue the OCP. In addition to treating the causes of melasma, topical medications can be helpful in accelerating improvement in the pigmentation. Standard treatment includes tretinoin cream every other night, combined with a bleaching cream (hydroquinone 4%) which inhibits melanin production. Dermatofibroma Dermatofibromas are more common in women. Dermatofibromas present as small (3-6 mm) firm, slightly raised papules. Squeezing a dermato- fibroma between the fingers causes it to sink deeper into the skin (“dimple sign”). Most dermato- fibromas are either brown (Figure 7.35) or pink with a rim of hyperpigmentation (Figure 7.36). The pathogenesis of dermatofibromas is unknown. They are probably an abnormal scarring response to minor trauma (insect bite, inflamed hair follicle). Pathologically, there is a proliferation of benign, fibroblastic cells. Dermatofibromas do not require treatment. If there is any question about the diagnosis, the lesion should be excised for diagnostic purposes. Angiofibroma (Fibrous Papule) Angiofibromas are more common than dermatofibromas. They occur from puberty onward. Angiofibromas present as very small (1-3 mm) skin colored to pink papules. They occur almost exclusively on the nose (Figure 7.37). Occasional patients will also have angiofibromas on the glans penis, and in this setting they are called pearly penile papules (Figure 7.38). Patients with tuberous sclerosis will often have hundreds of facial angiofibromas which become confluent on the central face and nose (Figure 7.39). The pathogenesis of angiofibromas is unknown. In normal individuals they are thought to be an abnormal scarring response to minor trauma, such as a squeezed pimple. In patients with tuberous sclerosis, they are a manifestation of the abnormalities in tuberin or hamartin. Angiofibromas require no treatment. If excessive numbers of angiofibromas are noted, tuberous sclerosis should be considered. Cysts Cysts are extremely common. Cysts on the trunk are more common in men, while cysts on the scalp are more common in women. Cysts on the trunk are usually infundibular cysts (epidermal inclusion cyst, epidermoid cyst, sebaceous cyst). They are usually 1-3 cm in diameter and often have a central punctum from which foul smelling white material can be expressed with pressure on the lateral aspects of the cyst. They may slowly enlarge with time, and they may rupture in the skin, suddenly becoming extremely painful, red, and swollen. Cysts on the scalp are usually isthmic cysts (pilar cyst). On average they are smaller than infundibular cysts. They do not have a central punctum, and they do not discharge the material which fills them. There is no potential to rupture and become inflamed like an infundibular cyst. Cysts develop when hair follicles become blocked and the usual secretions accumulate in the follicle causing it to dilate. In infundibular cysts, the blockage occurs in the more superficial, infundibular portion of the follicle, and this is why there is a visible punctum which may express the contents of the cyst. In isthmic cysts, the blockage is in the deeper, isthmic portion of the follicle, which is why the opening is not visible and material cannot be expressed. Cysts do not require treatment. If a patient desires treatment for cosmetic purposes, because the cyst is expressing smelly material or is becoming repetitively inflamed, the cyst can be excised. It is important to excise the cyst completely, because if any fragments are left in the skin, the cyst is very likely to recur. Lipoma Lipomas are extremely common. They occur on the trunk and extremities, usually not manifesting before age 20. They are more common in overweight individuals. Lipomas present as deep tumors. They are relatively well defined, but the edges are usually not sharp. They may slowly enlarge with time (Figure 7.40). They are typically asymptomatic, but may be tender or painful if they press on a nerve. Predisposed individuals may develop multiple lipomas (Figure 7.41). Lipomas are benign neoplasms of the subcutaneous fat. Lipomas do not require treatment. If there is a question about the diagnosis, the lesion is symptomatic, or if the patient wishes a lesion removed for cosmetic purposes, they can be easily excised by a dermatologist or surgeon.