Macules - Week 1

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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

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