Lecture 10 – 60s and Above - PDF

Lecture 10 – 60s and Above Cherry Angioma Essentially all individuals over age 60 have cherry angiomas. These lesions may start to appear as early as the 20s. They affect all races, but are more noticeable in lightly pigmented patients. Cherry angiomas are small, bright red papules (Figure 10.1)....

Lecture 10 – 60s and Above Cherry Angioma Essentially all individuals over age 60 have cherry angiomas. These lesions may start to appear as early as the 20s. They affect all races, but are more noticeable in lightly pigmented patients. Cherry angiomas are small, bright red papules (Figure 10.1). Early lesions may be flat. Large lesions may reach 5 mm in diameter. Lesions are partially compressible. If traumatized, they often bleed significantly, but the bleeding is typically easy to stop. Cherry angiomas are small proliferations of superficial blood vessels. They are occasionally hormone responsive, showing increased growth in high estrogen states (pregnancy, OCP use). Cherry angiomas do not require treatment, but can be electrocauterized if desired. Seborrheic Keratosis (SK) SKs are extremely common lesions. They typically start to develop after age 30. A given patient may have anywhere from one SK to hundreds. Having many SKs is a familial trait. SKs are waxy, “verrucous” brown-to-black plaques and papules (Figure 10.2) (Figure 10.3). The surface is often slightly scaly. They can typically be easily removed with the fingernail, but will recur. They range is size from 1-2 mm up to 5-6 cm in diameter. They are most common on the trunk, proximal extremities, and face. A given patient may have hundreds of SKs (Figure 10.4). Flat SKs can very closely mimic moles. Clues such as slight scaling or waxiness can be helpful, but sometimes a biopsy is necessary to determine if a given lesion is an atypical nevus or an SK. SKs are completely benign and do not require treatment. They occasionally become irritated and can be quite itchy in this setting. If the patient desires treatment, they can be treated with liquid nitrogen or they can be scraped off and the base treated with electrocautery. Chondrodermatitis Nodularis Helicis (CNH) CNH is fairly common in older individuals. It is rare prior to age 50. CNH presents as a tender papule on the helix of the ear. The center of the papule is often hyperkeratotic (Figure 10.5). The papule is usually skin colored, but can be red. CNH usually occurs on the ear on the side that the patient sleeps on. CNH is likely due to ischemia of the skin and cartilage secondary to pressure from sleeping on the ear. Pathologically, cartilage is often seen being extruded through the central keratotic area. CNH can be treated surgically. The papule can be shaved flat with the surrounding skin, and this is often curative. In addition to being effective treatment, shaving the papule off is often diagnostically useful, as it can be difficult to differentiate CNH from an actinic keratosis or squamous cell carcinoma clinically. Additionally, patients may purchase a “CNH pillow”, which has a central hole for the patient’s ear to relieve the pressure on the affected ear. Basal Cell Carcinoma (BCC) BCC is by far the most common skin cancer. There are approximately 4 BCCs for every 1 SCC, and approximately 10 BCCs for every 1 melanoma. BCCs are related to sun exposure, occurring mainly on sun exposed skin and being more common in patients with significant sun exposure. Intermittent, intense exposure early in life seems most relevant to BCCs. In addition, individuals with lighter pigmentation are at greater risk. There are several clinical types of BCC: Nodular BCCs are most common. These have a very typical pearly appearance, are usually dome-shaped and have sharp borders (Figure 10.6). In addition to the pearly appearance, there are typically prominent telangiectasias on the surface of nodular BCCs (Figure 10.7). This type is most common on the head and neck. Superficial BCCs are most common on the trunk. They present as slightly pink, scaly patches or thin plaques (Figure 10.8) (Figure 10.9). Morpheaform and infiltrating BCCs often present as firm plaques that are ill-defined with no clinically obvious borders. They are often difficult to diagnose clinically, and a biopsy may be required. Dysfunction of the PTCH gene is the most important genetic alteration in BCCs. The product of this gene (called “patched”) binds to another protein called “smoothened”. When patched is bound to smoothened, smoothened is deactivated. When patched is mutated, it cannot bind smoothened, and smoothened signals for cell proliferation. PTCH mutations are seen in most BCCs in the general population. The next most common mutation in sporadic BCCs is in the p53 gene, another tumor suppressor. In a specific disease called “Basal Cell Nevus Syndrome”, there is a germline deactivation of the PTCH gene. When a mutation occurs in the one remaining functional copy of the gene, a BCC develops. These patients develop hundreds of BCCs all over their body. Treatment of BCCs is surgical – lesions are excised. Other accepted techniques include curetting and electrodessication, imiquimod treatment for superficial BCCs, and in selected circumstances, treatment with liquid nitrogen, although this modality is seldom used. Untreated, a BCC can be locally destructive. This is especially concerning when the tumor is near a vital structure, such as the eye, ear, or mouth. Morpheaform and infiltrating BCCs are the most locally destructive. It is extremely rare, essentially unheard of, for a BCC to metastasize, regardless of the size of the tumor. Squamous Cell Carcinoma (SCC) As noted above, SCCs are significantly less common than BCCs. About 30-50% of SCCs arise from actinic keratoses, while the rest arise de-novo. SCCs are related to chronic, cumulative sun exposure. Light pigmentation is a greater risk factor for SCCs than it is for BCCs. In addition, SCCs are dramatically more common in immunosuppressed patients, especially organ transplant recipients. Finally, there is also an increased risk of SCC in individuals who smoke. SCCs present as keratotic papules, plaques or nodules. There is usually a dense, firm, adherent scale on top of the lesion. Beneath the scale, it is often erythematous, but in some cases, the scale may be the major or only feature. There are several subtypes of SCC: SCC-in-situ is also called Bowen’s Disease. These tumors are typically erythematous plaques with a moderate amount of scale on the surface (Figure 10.10) and very sharp borders. They are indolent, and typically will remain in-situ for years before becoming invasive tumors. Of special note, SCC-in-situ on the penis is called Erythroplasia of Queyrat and is more likely to become invasive than other forms. Invasive SCC is the most common form. It can present as a plaque with a very dense scale, as an erythematous papule or nodule with or without scale (Figure 10.11) (Figure 10.12), or as a non-healing cutaneous ulcer. The borders are typically relatively ill-defined clinically, regardless of the morphology of the lesion. Keratoacanthoma (KA) is the other distinctive type of lesion. KAs start suddenly and grow rapidly. They are erythematous, keratotic, dome-shaped nodules (Figure 10.13). Untreated, many of these lesions will grow rapidly, plateau, and then spontaneously regress. However, there is no way to know which lesions will regress spontaneously, so all lesions should be treated as potentially aggressive malignancies. Finally, an SCC can present as a chronic ulcer arising in a scar. This is called Marjolin’s ulcer. In addition, SCC can develop in chronic ulcers of any type. The precursor lesions to SCCs are actinic keratoses. AKs show keratinocyte atypia in the deeper parts of the epidermis. In SCC-in-situ, the atypia extends through the full thickness of the epidermis. In invasive SCC, in addition to full-thickness epidermal atypia, atypical keratinocytes invade through the basement membrane into the dermis. Most SCCs, however, develop de-novo. As in AKs, the most common genetic alterations in SCCs are mutations in the p53 gene. Similar to BCCs, SCCs are treated with surgery. More tissue must be removed to treat SCCs, as the borders are less obvious in SCC and the sequelae of treatment failure are more significant. Although it is uncommon, SCCs do have the ability to metastasize. Lesions located on the lip and the ear are the most likely to metastasize. Other high risk lesions are SCCs arising in scars (Marjolin’s ulcer), SCCs arising in chronic ulcers, and SCCs in immunosuppressed patients. Dermatoheliosis Dermatoheliosis becomes more common with increasing age. It is more common in individuals who live in areas of intense sun. The more lightly pigmented an individual, the earlier dermatoheliosis becomes apparent, and the more severe it is. Dermatoheliosis is the medical term for skin aging due to sun exposure. The main characteristics are wrinkling (Figure 10.14), altered pigmentation (hypo- and hyperpigmentation), and altered texture (roughness). Other characteristics include actinic keratoses, enlarged comedones (Figure 10.15), and atrophy of the skin. It affects the face and dorsal hands most significantly, but also affects the chest and back. Dermatoheliosis affects both the epidermis and dermis. Wrinkles are due to alterations in the dermal collagen. Pigmentation abnormalities are due hyperplasia of the melanocytes, and damage to the keratinocytes that affects their ability to take up melanin. Textural alteration is due to damage to keratinocytes. The damage that leads to dermatoheliosis is caused by ultraviolet radiation. Ultraviolet light is divided in ultraviolet A (UVA), B (UVB), and C (UVC). No UVC reaches the surface of the earth; it is blocked by the ozone layer. Of the UV light that reaches the earth, 95% is UVA and 5% is UVB. UVB is higher energy than UVA, but is unable to penetrate beyond the epidermis. UVA is lower energy and is able to penetrate into the dermis. UVB causes most epidermal damage, while UVA is responsible for most dermal damage. Dermatoheliosis is mainly of cosmetic concern. It is a marker of risk for skin cancer. Treatment of dermatoheliosis reduces the risk of skin cancer and improves the cosmetic appearance of the skin. Treatment is almost exclusively directed at facial dermatoheliosis. The most important aspect of treatment is to stop further damage through aggressive use of sun protection. Without aggressive sun protection, damage will quickly recur regardless of the treatment employed. Tretinoin is the best studied treatment. Tretinoin normalizes the maturation of the epidermal keratinocytes, thereby improving the textural and pigmentary abnormalities. It improves wrinkling by increasing dermal collagen production. It takes about 6 months of tretinoin use to see significant benefit. Continued use probably also decreases the risk of skin cancer. The major side effects are skin redness, dryness, and irritation, which occur during the first week of use, then peak and begin to resolve by 6 weeks of use. There will always be some redness and scaling, but these side effects become minimal after several months of use. Other treatments include skin resurfacing with lasers, chemical peels, and dermabrasion. Each of these methods causes destruction of the epidermis and superficial dermis. After treatment, the acute wounds heal over several weeks with complete healing occurring after several months. During the acute wound phase, patients can have significant pain with oozing and weeping. The chronic healing phase takes several months, and the skin essentially looks normal during this phase, except for being pink. Once healed, the skin quality is dramatically improved from the pre-treatment phase, with normalization of the texture, pigmentation, and wrinkling. These physical modalities are more effective treatments than tretinoin, but are also dramatically more risky, costly, and painful. Rhinophyma Rhinophyma occurs almost exclusively in men. It becomes more common with age, and is rare prior to age 50. It occurs only in patients with rosacea. Rhinophyma is chronic enlargement of the skin of the nose. Typically, the enlargement is lumpy and nodular (Figure 10.16). There is also significant enlargement of the pores. Rhinophyma is mainly due to enlargement of the sebaceous glands. In addition, there is fibrosis of the skin. Rhinophyma occurs exclusively in patients with rosacea and may represent a form of “lymphedema” of the skin, related to the repeated vascular flushing associated with rosacea. The only effective treatment for rhinophyma is surgical removal of excess skin. While prevention is likely through proper treatment of rosacea, this has not been formally studied. Necrobiosis Lipoidica Diabeticorum (NLD) and Diabetic Dermopathy (DD) NLD and DD occur mainly in patients with diabetes. NLD is rare, and DD is fairly common. NLD can be seen in patients of any age with diabetes, but DD occurs mainly in older patients with diabetes. Both diseases can occur in patients without diabetes. NLD occurs almost exclusively on the shins. It presents as large, yellow-brown, sharply bordered, hard, shiny plaques (Figure 10.17). In active lesions, there is often a red to violaceous, inflamed border to the plaques. The plaques are sometimes painful or itchy and may ulcerate. DD also occurs mainly on the shins. It presents as small, sunken, soft, brown patches (Figure 10.18). When pressing on the patches, the finger often sinks slightly into the skin. NLD and DD are both probably due to micro-angiopathy associated with diabetes. In NLD, this leads to ischemic damage to dermal collagen, and an inflammatory reaction against the damaged collagen then leads to the clinical disease. In DD, there is no inflammatory reaction, and the clinical disease is probably due exclusively to the ischemic damage to the dermis. Two treatment modalities are employed for NLD, but neither is very effective. Topical, intra- lesional, and systemic steroids are often used if the plaques have active, inflamed borders. In addition to steroids, anticoagulants (aspirin) or other agents intended to improve microcirculation (pentoxifylline, ticlodipine) are often used. If there is no inflammatory border, then agents intended to improve microcirculation are usually used alone. Diabetic dermopathy is rarely treated. In general, better glucose control doesn’t affect the course of NLD or DD once they have developed. Whether onset of either of these diseases is related to poor glucose control is unknown. In patients with suspected NLD or DD who are not known to have diabetes, HbA1C should be checked. If normal, HbA1C should be rechecked annually to monitor for diabetes development. Xanthelasma Xanthelasma becomes more common with age, especially in individuals with hyperlipidemia. Xanthelasma are smooth, slightly raised, yellow to white papules near the medial canthi. They are not symptomatic. Xanthelasma represent deposits of lipid within macrophages in the superficial dermis. Xanthelasma are significant mainly for cosmetic reasons. They can be removed surgically. Importantly, 50% of patients with xanthelasma have hyperlipidemia that should be treated; therefore, patients with xanthelasma should have their serum lipid profiles monitored. Eruptive Xanthomas (EX) EX are uncommon, but tend to occur in patients with known hypertriglyceridemia and diabetes. EX present as a sudden eruption of small (1-4 mm) yellow, orange, or pink papules that are slightly itchy. They are usually most prominent on extensor areas, although flexor areas can also be involved (Figure 10.19). EX appear when serum triglyceride levels become so great that triglycerides are deposited in the skin. An inflammatory reaction occurs to the deposited triglycerides, resulting in the pink-red- orange color and the itch. With EX, triglyceride levels are at least 1000 mg/dl and are often as high as 3000-4000 mg/dl (normal is