This document provides information on evaluating dermatologic lesions and summarizes common macular skin conditions. It describes primary and secondary skin lesions, noting characteristics like papules, plaques, nodules, vesicles, bullae and more. Common bacterial causes of macules discussed include Neisseria meningitidis, which presents as progressively worsening erythematous macules and can lead to necrosis. Rocky Mountain spotted fever presents as a maculopapular rash that becomes petechial or purpuric, with potential for neurologic involvement. Epidemic typhus causes a maculopapular rash with meningoencephalitis, delirium and coma.
This document provides information on evaluating dermatologic lesions and summarizes common macular skin conditions. It describes primary and secondary skin lesions, noting characteristics like papules, plaques, nodules, vesicles, bullae and more. Common bacterial causes of macules discussed include Neisseria meningitidis, which presents as progressively worsening erythematous macules and can lead to necrosis. Rocky Mountain spotted fever presents as a maculopapular rash that becomes petechial or purpuric, with potential for neurologic involvement. Epidemic typhus causes a maculopapular rash with meningoencephalitis, delirium and coma.
This document provides information on evaluating dermatologic lesions and summarizes common macular skin conditions. It describes primary and secondary skin lesions, noting characteristics like papules, plaques, nodules, vesicles, bullae and more. Common bacterial causes of macules discussed include Neisseria meningitidis, which presents as progressively worsening erythematous macules and can lead to necrosis. Rocky Mountain spotted fever presents as a maculopapular rash that becomes petechial or purpuric, with potential for neurologic involvement. Epidemic typhus causes a maculopapular rash with meningoencephalitis, delirium and coma.
This document provides information on evaluating dermatologic lesions and summarizes common macular skin conditions. It describes primary and secondary skin lesions, noting characteristics like papules, plaques, nodules, vesicles, bullae and more. Common bacterial causes of macules discussed include Neisseria meningitidis, which presents as progressively worsening erythematous macules and can lead to necrosis. Rocky Mountain spotted fever presents as a maculopapular rash that becomes petechial or purpuric, with potential for neurologic involvement. Epidemic typhus causes a maculopapular rash with meningoencephalitis, delirium and coma.
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Lecture – Evaluation of the Dermatologic Patient
Return to this lecture to review cases/images before exam
Lesion Morphology o Primary Lesion – the initial or principle lesion when the disease begins Types of Primary Lesions Papule – superficial, elevated, solid lesion less than 1 cm in diameter o Pustule – papules filled with white blood cells (pus) Plaque – superficial, raised lesion that’s bigger than 1 cm o Well demarcated o Example includes psoriasis Nodule – deep, solid lesion usually bigger than 1 cm o Usually located in dermis or subcutaneous fat o Three dimensional growth Cyst – contains fluid, keratin, or mucin Macule – nonpalpable, not raised, lesion less than 1 cm in diameter Patch- bigger version of a macule Vesicle – superficial, fluid-filled lesion less than 1 cm o If grouped vesicles surrounded by erythematous ring, think Herpes Simplex o If not grouped, and still surrounded by erythematous ring, thing VZV “dewdrop on rose petal” Bullae – vesicle that’s bigger than 1 cm Wheal (hive) – transient, edematous papule, plaque, or nodule o Round, clear in the center o Annular in nature Burrow – linear or serpentine tunnel in the epidermis o Usually caused by scabies mite o Scabies love the creases between fingers, the butt, and the axilla Comedo – specialized lesion resulting from an impaction within the pilosebaceous (hair follicle/sebaceous gland) unit o Black heads – open comedons o White heads – closed comedons o Solar comedons – caused by sun; found in the elderly o Secondary Lesion – develops from a primary lesion An example would be if a patient scratches off the papule, and then the excoriation (scraped off area) of the scratch is the secondary lesion Types of Secondary Lesions Crust/Scab – dried exudate of blood/plasma on the surface of the skin Scale – thickened stratum corneum o Common in psoriasis Scar – visible alteration in the skin following the repair of injury o Ulcers – fastigial scars Atrophy – loss of tissue in either the epidermal, dermal, or subcutaneous regions o The skin becomes and feels thin in epidermal o In dermal atrophy, you can feel a depression Caused by genetic or traumatic incidents o Subcutaneous – due to injections, such as cortisol Lichenification – epidermal thickening characterized by thickening and accentuation of skin markings Excoriations – oval or linear depressions in the skin with a complete removal of epidermis Ulcer – defect devoid of epidermis extending deep into the dermis or subcutaneous tissue o Common in diabetics Fissure – in between excoriation and ulcer in depth; linear, wedge-shaped breaks in the epidermis extending down to the dermis o Perleche – corners of the mouth dry out Erosion – moist circumscribed depressed area limited to the epidermis o Common with candida infection o Note the difference between intact and damaged blood vessels If the redness on the body blanches upon compression, this indicates intact blood vessels If the redness does NOT blanche, this indicates damage to the blood vessels Results in petechial vs purpura vs ecchymosis (small to large redness) o Note turgor pressure of skin Important in determining hydration of patient Macules – Pathology, Clinical Lecture, and Microbiology General Terms o Macule – flat, non-palpable lesion smaller than 1 cm in diameter Lesion with color change or subtle texture change, without elevation above skin surface o Patch Bigger version of macule Normal Skin Flora o Coagulase-negative staphylococci Staph epidermidis Catalase + Can inhabit anywhere on the skin o Corynebacterium – located in the groin, skinfolds, and armpits o Brevibacterium – located in the webs of the toes o Propionibacterium – located in the hair follicles and sebaceous glands; can cause body odor o Micrococcus – located in the stratum corneum and the upper part of the hair o Candida – fungus; colonizes oral and vaginal mucous membranes; can also be in the GI mucous membranes o Transient Colonizers that may or may not be on the body include Strep pyogenes Staph aureus Factors affecting skin infections o Balance of host defense and microbial virulence o Alterations in microenvironment Temperature – increases can ward off infectious agents Humidity – changes in dampness Drops in dampness (drying out) can cause cracking of the skin, which allows for entry sites for pathogens pH- great defense against microbes; typically the skin has an acidic pH if this pH changes, it can allow different organisms to colonize on the skin o As we age, cracks in the skin occur which allows pathogens to enter o Antibiotic treatment can kill normal flora and allow opportunistic pathogens to grow Bacterial Causes of Macules o Neisseria meningiditis Etiologic Agent/Bacteriology Gram-negative, non-motile diplococcus Asymptomatically carried by 10-20% of people in the nasopharynx Transmission occurs via respiratory droplets Pathogenesis Antigenic polysaccharide capsule, which prevents phagocytosis IgA protease, which degrades IgA and evades immune response Pili Endotoxin, which produces LPS, which is highly inflammatory Presentation Initially presents as erythematous macules o Start off as petechiae and progress to purpura Starts on the extremities and progresses to the trunk Final evolution of the infection includes the development of gun-metal grey, hemorrhagic necrotic patches May develop into symmetrical peripheral gangrene Diagnosis CSF or blood gram stain Culture on Thayer-Martin or Chocolate agar Hallmarks/Giveaways/Unique Features The progression is the giveaway o Rocky Mountain Spotted Fever Etiologic Agent/Bacteriology Rickettsiae rickettsii Obligate intracellular, gram-negative bacterium Vertebrate reservoir – dogs/rodents Arthropod vector – dog tick Causes Multiplication of bacteria at the site of the tick bite, and then the bacteria spreads to the blood and vascular endothelium Presentation Fever, severe headache, myalgia, cough, runny nose Maculopapular rash that becomes petechial or purpuric o The macules are flat and red Typical Patients Typical geographic distribution; can be on east coast Hallmarks/Giveaways/Unique Features Splenomegaly and neurologic involvement Can have disseminated intravascular coagulation and death Note that R. akari causes Rickettsiae pox, while R. conorii causes Mediterranean spotted fever o Epidemic Typhus Etiologic Agent Rickettsiae prowazekii Vertebrate reservoir – human Arthropod vector - louse Presentation Maculopapular rash with sever meningoencephalitis with delirium and coma Infection can reside in lymph nodes and reactivate years later Typical Patients Africa and South America Hallmarks/Giveaways/Unique Features Location is the giveaway Delirium and coma o Endemic Typhus Etiologic Agent Rickettsiae typhi Vertebrate reservoir – rodent Arthropod vector – fleas Presentation Less sever version of epidemic typhus Typical Patients Found worldwide o Scrub Typhus Etiologic Agent Orientia tsutsugamushi Vertebrate reservoir – rodents Arthropod vector - mites Typical Patients Far east Fungal Causes of Macules o Tinea versicolor – see later o Dermatophytes – fungal infections Tinea Capitis – infection of scalp Tinea barbae – beard region Tinea faciei – fungus on the face Tinea corporis – fungus on the trunk/extremities Tinea cruris – jock itch; fungus in the groin Tinea pedis – athlete’s foot o Candida Mycology Dimorphic yeast Epidemiology Part of normal flora of skin, mouth, and intestine Pathogenesis Produces infections in immunosuppressed, diabetics, and those using antibiotics Rapidly colonized damaged skin May overgrow in oral (thrush) and vaginal mucosa (vaginitis) Manifestations Candidiasis – diaper rash/vaginitis o See on groin and satellite spots elsewhere Satellite spots are the hallmark of diaper rash caused by candida o Satellite spots can be pustules if they have white spots Thrush – macules on surface of the tongue Erythematous Macules o Viral Exanthems General Information Viral infections are frequently associated with cutaneous manifestations, esp. in children Types Epstein-Barr Virus (Infectious Mononucleosis) o Etiologic Agent Human Herpes Virus 4 o Causes Primary EBV infection o Presentation Faint, non-specific erythematous exanthem in ~70% of mono patients Develops on day 4-6 of infection and can last for a week First appears on trunk/upper arms, then spreads to face and forearms In patients with hypersensitivity, seen as pruritic, copper-colored macular eruption over extensor surfaces, and then spreads to trunk and extremities o Typical Patients Young Adults from 17 to 25 o Hallmarks/Giveaways/Unique Features Ampicillin, penicillin, etc. are given to patients with infectious mononucleosis (b/c misdiagnosed as bacterial infection) and causes a hypersensitivity eruption Occurs 7-10 days after start of antibiotic Scarlet Fever o Etiologic Agent Group A- Strep pyogenes o Presentation Occurs as a rash The fever is present up to two days prior to the rash appearing Patients may present with a temperature o Typical Patients Young patients/children o Hallmarks/Giveaways/Unique Features Roseola Infantum/ Sixth Disease/ Exanthem Subitum o Etiologic Agent Herpes Virus 6 Enveloped, double stranded DNA Replicated in the T and B cells and the tonsils of the oropharynx Virus persists in the saliva o Presentation Rapid onset of high fever, followed by eruption of rash as fever subsides Lasts 24-48 hours and may occur before temperature returns to normal Lesions are discrete, circular, erythematous, rose-red macules Macules occasionally surrounded by white halo o Typical Patients Common in infants and young children 6 months to 3 years o Hallmarks/Giveaways/Unique Features Common in spring, summer, and fall Fever then rash AGE – any patient with HHV under 3 has HHV 6, not HHV7 Pityriasis Rosea o Etiologic Agent Human Herpes Virus 7 Enveloped, double stranded DNA o Presentation Acute, benign, self-limited Over a few days/weeks, crops of smaller, thin macules and patches form on the trunk and proximal extremities o Typical Patients HHV-7 is present in children older than 3 into early childhood o Hallmarks/Giveaways/Unique Features Herald Patch – the very first, and largest macule Remains throughout the course of the disease Can be visualized and is often obvious “Christmas Tree” pattern on trunk/back can be common Rubeola (Measles) o Etiologic Agent/Virology Paramyxovirus Single stranded, non-segmented, negative sense RNA Enveloped Helical nucleocapsid Humans are the natural host and reservoir of the virus Starts with replication of the virus in the epithelial cells of the respiratory tract, with subsequent spread to the lymphoid tissue and blood, resulting in viremia Incubation period of 10-14 days o Causes Transmission via respiratory droplets Enters via respiratory tract and spreads to subepithelial and lymphatic tissues o Presentation Prodrome of fever, cough, nasal congestion, and rhinoconjunctivitis Exanthema appears over 2-4 days and consists of erythematous macules and papules that begin on the forehead, hairline, and spreads cephalocaudad Begins behinds the ears following a fever 9-10 days after infection, develop runny nose, fever, and cough o Diagnosis Course of disease is very predictable, no diagnosis needed o Typical Patients Common exanthema in children o Hallmarks/Giveaways/Unique Features Koplik spots – appears during the prodrome Gray-white papules on the buccal mucosa Rubella o Etiologic Agent/Virology Togaviridae Enveloped, positive sense, single stranded RNA Spread via respiratory droplets Incubation period of 16-18 days o Causes Primary site of infection is the nasopharynx, followed by spread to the lymph nodes and a subsequent viremia Spreads to spleen as well o Presentation Mild, self-limited disease in children and adults Major complications when transmitted to a fetus in utero, including congenital malformations, miscarriage, stillbirth Mild prodrome of fever, headache, and upper respiratory symptoms 1-5 days after prodrome, an eruption of erythematous macules and papules appears on the face, spreading cephalocaudad o Diagnosis Tender lymphadenopathy, especially occipital, posterior auricular, and cervical Virus is detectible in the respiratory tract, skin, joints, and kidneys o Hallmarks/Giveaways/Unique Features Forchheimer’s Spots - Erythematous petechial macules present on the soft palate Erythema Infectiosum/Fifth’s Disease/Slapped Cheek Disease o Etiologic Agent/ Virology Parvovirus B19/ Eryhtrovirus B19 Transmission via respiratory secretions, blood products, and vertical (mom to fetus) Very small, single stranded DNA virus o Causes Note that this disease affects red cells, causing diseases like aplastic anemia Grows in the hematopoietic cells in bone marrow o Presentation Mild prodromal symptoms before exanthema Bright red macular erythema of the cheeks, with sparing of the nasal bridge and circumoral (around mouth) region 1-4 days after erythema, the second stage appears in the form of erythematous macules and papules occurring mostly on the extremities o Diagnosis Detection of serum-specific IgM o Typical Patients Seasonal pattern, with a peak incidence in winter and spring Most common in children between 4 and 10 o Hallmarks/Giveaways/Unique Features Cheeks first, then macules on the extremities o From here on are not exanthems Drug Eruptions Exanthematous Drug Reactions o Timeframe Occurs 7-14 Days after starting medication o Presentation Erythematous macules or sometimes papules Symmetric, beginning on trunk and extremities Becomes confluent o Treatment Resolves spontaneously 1-2 weeks after stopping drug o Medications that Cause EDRs: Penicillins Sulfonamides Cephalosporins Anticonvulsants Allopurinol Primary Syphilis Etiologic Agent/Bacteriology o Treponema pallidum pallidum Note that Treponema pallidum pertenue causes yaws Yaws is common in the warm, tropical regions of Africa, Asia, etc. Note that Treponema carateum causes pinta Pinta occurs in Mexico, Central, and South America o Regularly coiled spirochete o Cork-screw shaped bacteria o Flagellum o Highly susceptible to heat and drying o Can be normal flora of the mouth Causes o Inoculation occurs on mucosal surfaces and injured skin o Transmission via very close contact Presentation o Chancre Nontender, small, red papule or crusted superficial erosion Develops 2-6 weeks after infection Occurs as a single lesion, although can occur in multiples In men, occurs in the coronal sulcus or sides of frenulum of the penis In women, occurs within the vagina or on the cervix Extragenital sites include the lips, tongue, breasts, and anus o Regional lymphadenopathy occurs 1-2 weeks after the chancre o Enlargement of the inguinal lymph nodes is present Diagnosis/Treatment o Untreated heals within a few weeks o Diagnosed via microscopic examination o Assay o Antibody test for Treponema pallidum Secondary Syphilis Etiologic Agent o Treponema pallidum pallidum Causes o Hematogenous and lymphatic dissemination after weeks or months Presentation o Prodromal symptoms of fever, malaise, sore throat, adenopathy, weight loss, myalgia o Generalized, non-pruritic (not itchy), roseola-like macules Looks like pytriasis rosea o Presents two to six weeks after primary syphilis Hallmarks/Giveaways/Unique Features o Hallmark presentation on the palms and soles; symmetrical papules found here Tertiary Syphilis Etiologic Agent o Still Treponema pallidum pallidum Causes o Consequence of untreated syphilis Presentation o Gummas – nodular lesions that involute with scarring Found in bones, skin, and testes o Cardiovascular manifestations of coronary disease, aortic insufficiency, aortic aneurysm o Neurological symptoms including meningitis, headache, stiff neck, seizures Later on, see Tabes dorsalis Hallmarks/Giveaways/Unique Features o Cardiovascular and neurological symptoms Erythema Marginatum Causes o Cutaneous manifestation of acute rheumatic fever Presentation o Erythematous macules that spread peripherally and become patches and plaques o Located in the trunk, axilla, and proximal extremities Hallmarks/Giveaways/Unique Features o Associated with active phases of rheumatic fever o Precede joint manifestations of the disease o Seen in conjunction with carditis Non-palpable Bleeding in Skin (Bruises) o Tends to be related to a problem with clotting This is NOT a vasculitis disease Note that vasculitis can lead to end-organ disease; worry about lung and kidney Vasculitis – palpable bleeding *NOT A MACULE* o Petechiae – less than 3 mm in diameter Often associated with a platelet problem o Purpura – less than 1 cm but more than 3 mm o Ecchymosis – greater than one cm in diameter Related to coagulation problems Photo-Distributed Macules o Pathologic Classifications of Photo-Distributed Macules Type I – IgE Dependent Reactions Deals with insulin and proteins associated with type I reactions Histamine release occurs from basophils and mast cells o Results in macular (typical) or papular (rare) hives (urticaria) o There is lots of fluid present in the urticaria Type II – Direct Antibody Cytotoxicity Penicillins, cephalosporins, sulfonamides, and rifampin Type III – Immune Complex Disease Quinine, salicylates, chlorpromazine, sulfonamides Type IV- Delayed hypersensitivity Lymphocyte dependent Requires prior exposure Most common mechanism of drug eruptions Topical or systemic Often NOT dose dependent, while types 1-3 tend to be Occur 7-20 days after taking the drug o Phototoxic Drug Reactions Occur in patients who receives a sufficient amount of phototoxic drug with UV light Appears to be an exaggerated sunburn Limited to sun-exposed areas Drugs include: Tetracyclines NSAIDs Fluoroquinolones Amiodarone Psoralens Phenothiazines Sulfonamides o Photoallergic Reactions Cell-mediated hypersensitivity reaction to an allergen activated or produced by the effect of light on a drug Pruritic and primarily in sun-exposed sites Can spread to non-sun-exposed sites Longer lasting than phototoxic reactions Drugs include: Thiazide diuretics Sulfonamides Sulfonylureas Phenothiazines Quinine/quinidine TCAs Anitmalarials NSAIDs o Collagen Vascular Disease Cutaneous Lupus Erythematosus Multisystem disorder that prominently affects the skin The cutaneous lesions may be associated with internal diseases such as: o Arthritis o Nephritis o Serositis o Hematologic disease o Neurologic disease Subtypes: o Acute Cutaneous Lupus Commonly associated with systemic disease Butterfly malar rash on the face Macular eruption Transient erythema following sun exposure Spares the nasolabial folds Can be associated with anti-double stranded DNA antibodies and lupus nephritis Ranges from mild erythema to intense edema Can last hours to weeks o Subacute Cutaneous Lupus Majority of patients do not have systemic disease o Chronic Cutaneous Lupus/Discoid Lupus Majority of patients do not have systemic disease Dermatomyositis o General information Connective tissue vascular disorder of uncertain etiology Bimodal age distribution – juvenile and adult Proximal extensor muscle weakness (hip/shoulder) Distinctive rash near scalp, around eyes, and extensor areas Can be associated with malignancy in adults Especially ovarian cancer, breast cancer, lung cancer, and GI cancers o Associated With: Poikiloderma- hyper and hypopigmentation, telangiectasia (dilation of capillaries), and epidermal atrophy Basically, thinning of skin with white, brown, and red areas Telangiectasia is common in patients with basal cell carcinoma Heliotrope Sign – purple poikiloderma around the eyes Gottron’s Sign – red papules, plaques, and poikiloderma on the knuckles Ragged cuticles with telangiectasia Hypopigmented Macules o Tinea Versicolor Etiologic Agent Malassezia furfur – fungus Lipid dependent Human only Causes Overgrowth of normal flora; not a true infection Not contagious Presentation Sharply demarcated, hypopigmented, pink, or hyperpigmented macules and patches over the trunk with very fine scale Diagnosis Potassium Hydroxide test- under a microscope, appears to have a spaghetti and meatball appearance o These fungal elements are present in the stratum corneum Wood’s Lamp – yellow/green fluorescence Typical Patients Chronically recurs during warmer months and in warmer climates Patients with sun exposure makes the hypopigmented spots more prominent Hallmarks/Giveaways/Unique Features Spaghetti and meatball microscopy Distribution is more in the trunk area Treatment Topical and oral antifungals o Vitiligo Causes Unknown, but three following theories: Autoimmune destruction of melanocytes o Due to increased cell-mediated immunity o Melanocyte destruction may be directly mediated by autoreactive CD8+ T-cells Intrinsic Defects of Melanocytes o Early apoptosis of melanocytes Disturbance in oxidant-antioxidant system o Accumulation of oxidized pteridines These pteridines fluoresce in clinically-affected skin Increased superoxide dismutase and catalase is present in the lesioned and normal skin of affected patients Presentation Depigmented sharply demarcated macules and patches with no surface changes Diagnosis Accentuated bright white under Wood’s Lamp Typical Patients Associated with other autoimmune diseases such as hypo/hyperthyroidism, pernicious anemia, Addison’s Hallmarks/Giveaways/Unique Features Pam Hoover and Michael Jackson o Pityriasis Alba Causes Post-inflammatory pigment changes from mild eczema Presentation Poorly demarcated, hypopigmented, lightly scaling plaques Found on lateral arms and cheeks Diagnosis NOT accentuated by wood’s lamp Typical Patients Found in patients with atopic dermatitis Hallmarks/Giveaways/Unique Features NOT A DEPIGMENTATION LIKE VITILIGO; only hypopigmentation o Halo Nevus Presentation Central pigmented melanocytic nevus (mole) and surrounding depigmented halo Typical Patients Common, benign neoplasm in children and young adults Patients with vitiligo might be at higher risk to develop halo nevus Hallmarks/Giveaways/Unique Features Yeah, it’s just a mole with a depigmented (white) ring around it o Hypopigmented Sarcoidosis Causes Sarcoidosis is a systemic granulomatous disorder o Commonly involves the lungs (90%) o Cutaneous manifestations in 1/3 of patients Presentation Occurs on extremities mostly Spontaneous repigmentation may occur Red-brown to violet papules and plaques on face, lips, neck, upper back, and extremities Diagnosis Histological display of naked granulomas Typical Patients Occurs in 6% of sarcoid patients o Carry no prognostic significance o Tuberous Sclerosis Causes Autosomal dominant disorder Spontaneous mutation (75%) Presentation Hamartomas (benign, focal neoplasms of multiple tissues) in multiple organs o Such as skin, brain, eye, heart, and kidney Hypomelanotic macules are often the first sign and are present at birth or neonatal period Ash-leaf macule – characteristic white macule rounded at one end and pointed at other Confetti macule – many small hypopigmented macules especially on arms and legs Typical Patients Adenoma sebaceum occurs on face within first two years of life Hallmarks/Giveaways/Unique Features Classic triad: o Adenoma sebaceum Papules on the central face around the nose and mouth Facial angiofibromas – red to pink bumps More show up as you get older o Seizures o Mental retardation Koenen tumors – periungual papules or nodules developing later in childhood o Occur around or on top of the nail and can mess up nail growth o Hypopigmented Mycosis Fungoides Etiologic Agent Mycosis fungoides; most common type of cutaneous T-cell lymphoma Presentation Hypopigmented lesions on trunk and extremities Typical Patients Common in dark-skinned patients Typical age range is 30-40 years o Hypopigmented Lesions in Leprosy Lepromatous Leprosy Presentation o Small, multiple, subtle, ill-defined o Located on the face, extremities, and buttocks Hallmarks/Giveaways/Unique Features o No anhidrosis or loss of sensation Tuberculoid Leprosy Presentation o Discrete edges, may be quite large o Asymmetrically distributed on posterolateral aspects of extremities, back, buttocks, and face Hallmarks/Giveaways/Unique Features o Loss of sensation, alopecia, and anhidrosis occurs within the patches Hyperpigmented Macules o Melanocytes Usually so dispersed, that they can be difficult to find, except when the form freckles For example, patients with vitiligo exhibit less melanin in fewer melanocytes A freckle is a location of more melanin A lentigo is a location of more melanocytes o Café-au-lait Spots Hyperpigmented macules and patches Diseases that these spots are common in include: Neurofibromatosis o Large, bilateral patches o Multiple tumors usually exist in the skin, brain, and organs McCune-Albright Fractures and Precocious Puberty o Small spots that don’t cross the midline o Non-Palpable, Macular Purpura Causes Often associated with mild trauma plus one predisposing factor: o Procoagulant defect This includes anticoagulant use, hepatic insufficiency, Vitamin K deficiency, and disseminated intravascular coagulation o Poor dermal support of blood vessels This can be solar macular purpura Caused by sun exposure and aging combined with trauma Common in elderly individuals Corticosteroid synthesis Vitamin C deficiency (scurvy) Presentation Visible hemorrhage into skin or mucous membranes Hallmarks/Giveaways/Unique Features This purpura is not palpable, meaning it’s not raised. Palpable purpura is due to vasculitis This purpura is very apparent. It’s something you have noticed on old people before, but never knew what it was. o Pigmented Purpura Causes Extravasation of RBCs leading to iron deposition Chronic venous insufficiency of the lower legs leading to hemosiderin deposition Presentation Clustered, yellow-brown or reddish-brown petechial hemorrhages o Color is due to hemosiderin deposition Most commonly found on lower legs, but can be found elsewhere Hallmarks/Giveaways/Unique Features Considerably lighter than macular, non-palpable purpura o Post-Inflammatory Hyperpigmentation Causes Acne Atopic dermatitis (eczema) Drug reactions Herpes Zoster (Shingles) Burns Presentation Can occur at any site of previous inflammation Typical Patients Patients with darkly pigmented skin are particularly prone Hallmarks/Giveaways/Unique Features Note that this is hyperpigmentation o Melasma Causes Increased pigment in summer months, due to sun exposure There may be a hormonal component to this, as it is common during pregnancy and when taking oral contraceptives Presentation Irregular hyperpigmented macules and patches on face, neck, and forearms Typical Patients Mostly women, especially Hispanic and Asian women Hallmarks/Giveaways/Unique Features Lasts for years Pregnancy/hormonal changes o Melanoma Causes Malignant tumor arising from melanocytes Presentation Asymmetry of nevus Irregular border of a nevus Varying color throughout the nevus Mole diameter that is larger than a pencil eraser Evolving nevus over time Diagnosis Early detection is very important Typical Patients One of the most common cancers in young adults Hallmarks/Giveaways/Unique Features ABCDE diagnosis Subtypes Superficial Spreading Melanoma o Causes 1/3 come from a pre-existing nevus generally observed to change via the ABCD mnemonic o Presentation Trunk of men Legs of women Begins as an asymptomatic brown to black macule, with color variations and irregular borders After a slow horizontal (becomes wider) growth phase, a rapid vertically oriented (becomes deeper) growth phase occurs with development of a popular nodule Regression (hypo/depigmentation) of part of lesion is common (2/3) o Typical Patients Most common type of cutaneous melanoma in fair-skinned individuals Lentigo Maligna Melanoma o Causes Occurs on chronically sun-damaged skin, mostly on the face o Presentation Slowly growing asymmetric brown to black macule with color variations and irregular, indented borders o Diagnosis Minority of cutaneous melanoma o Hallmarks/Giveaways/Unique Features Lentigo maligna is used to mean melanoma in situ of sun-damaged skin (radial growth only), and lentigo maligna melanoma is used for those with dermal invasion (vertical growth) Acral Lentiginous Melanoma o Presentation Occurs on the palms and soles or in and around the nail Presents as an asymmetric brown to black macule with color variation and irregular borders o Typical Patients This is more common in fair-skinned patients, but these pigmented races experience this melanoma more often than the other types 70% of melanomas in dark skinned patients 45% of melanomas in Asians Prognostic Factors for Melanoma Breslow Depth of Invasion o Measured in millimeters from the top of the granular cell layer to the deepest point of tumor penetration Clark’s Level of Invasion o Level 1 – Epidermis only o Level 2 – invasion of the papillary dermis o Level 3 – filling of the papillary dermis to the junction of the superficial reticular dermis o Level 4 – invasion of the reticular dermis o Level 5 – invasion of the fat Factors associated with unfavorable outcomes o Ulceration o No tumor infiltrating lymphocytes o Increased mitoses o Regression o Vascular invasion o Satellites o Fixed Drug Eruptions Causes NSAIDs, barbiturates, tetracyclines, carbamazepine Presentation Lesion develops 1-2 weeks after first exposure Subsequent exposures occur within 24 hours at exactly the same site as the original exposure One or few round, well-demarcated red patches Occurs on the lips, hands, feet, and genitalia Fade over several days with post inflammatory brown pigmentation