Dermatology Flashcards
Macule
< 1 cm, non-palpable
Ex: petechiae
Patch
> 1 cm, non-palpable Ex: fixed drug eruption, - annular scaly erythematous patch of tinea, - subacute lupus - melanoma
Papule
< 1 cm, circumscribed solid/cystic elevation which can be follicular or non-follicular
- Follicular:
- Equidistant: Fox-Fodyce disease
- Ostia
- Flat-topped papules of lichen
- Verruca vulgaris
- Seborrheic keratosis
- Umbilicated of molluscum contagiosum - Pustule: light head on top
Plaque
> 1 cm
Mesa-like elevation
- Papules may coalesce to form plaque
Ex: psoriasis, eczema
Nodule
1-2 cm: solid or cystic elevation
- Extensive involvement of the dermis
Tumor
2+ cm: solid or cystic elevation
- Extensive involvement of the dermis
Vesicle
< 1 cm: usually tense
Ex: herptiform vesicles (Herpes Zoster)
Bullae
> 1 cm: may be tense or loose collection of fluid
Ex: Bullous pemphigoid
- Bullous Herpes Zoster
Erosion
Partial loss of epidermis
- Does not bleed
- All blisters, whether vesicles or bullae, eventually form ulcers or erosions
Ex: bullous impetigo (typically staph-mediated exfoliatoxin)
- Pemphigus follaceous
Ulcer
Complete loss of epidermis
- Often bleeds
- All blisters, whether vesicles or bullae, eventually form ulcers or erosions
- Accompanied by fibrin deposition
Ex: shallow ulcerations in Herpes Zoster
- Calciphylaxis (high mortality, seen in dialysis patients)
- Pyoderma gangrenosum (gun-metal gray border)
Depression
Formed when there is atrophy of subcutis
Ex: too much cortisone or anabolic steroids injected into skin (often iatrogenic)
- Lupus profundus (panniculitis)- loss of fat under skin)
Color of skin
Red: dilation of vessels modified by density of erythrocytes and inflammatory cells, melanin in epidermis, altered epidermis
Yellow: exogenous pigment, carotene, bile, lipids, solar elastosis, mast cells, altered collagen
Blue: melanin in reticular dermis
Brown/black: hemosiderin, melanin
White: loss of melanin or melanocytes or both
Burrow
Linear, serpiginous lesions of skin
- Formed when tunnel is formed in epidermis
Ex: scabies
Cord
Linear/serpiginous lesion of skin
- Formed when pathologic process involves linear/elongated structure
Ex: thromophlebitis
Risk factors for Melanoma
Familial melanoma: B-K mole syndrome
- Giant congenital nevus > 20 cm
- Bathing trunk nevus
UV radiation: intermittent blistering sunburns early in life
Atypical/dysplastic nevus syndrome patients with multiple clark/dysplastic/atypical nevi
Hereditary Melanoma
VERY rare (< 1% of all melanomas)
Germline mutations
- CDKN2A (p16): cyclin-dependent kinase inhibitor 2A
- High association with pancreatic carcinoma (15% lifetime risk)
- Don’t necessarily need to genetically test, most revealed through pedigree
Sporadic melanoma
MUCH more common than hereditary melanoma
Somatic mutations
1. BRAF= serine/threonine kinase mediating pathway of RAS signaling
- Mutation in BRAF–> turns on growth signal
- Seen in 73-82% of melanocytic nevi
- cKit: associated with acral, mucosal melanomas
Large congenital nevi
“Bathing trunk nevi”
~10% risk of developing melanoma
Skin phototypes
1-6: 1 and 2 most at risk
Type 1: fair skin, hair, freckles
Risk factors for melanoma
UV exposure–> blistering lesions (history of multiple burns in early life)
- One blistering sunburn–> doubles risk
- Intermittent exposure hypothesis (infrequent, heavy sun exposure)
Skin phenotypes:
- light skin
- Blond/red hair
- Blue/green eyes
- Prominent freckling
Clark/dysplastic/atypical melanocytic nevi
- Larger than 5 mm with irregular borders
Family history:
- 10-15% melanoma patients have positive family history
- Younger first-degree relative ex: 40 year old brother (not 85-year old grandmother)
Diagnositc tools for melanoma
Light source, magnification, polarization (dermatoscopy)
Immunohistochemistry:
Useful adjunct to H&E diagnosis of melanoma
- Poorly differentiated tumors
- Little or no pigment
- Spindle cell tumors
- + pagetoid spread –> not clearly melanoma
Stains: MART-1 (Melan-A) - Most sensitive and specific HMB-45 S-100
Superficial spreading melanoma
Most common subtype:
- Account for 70% of all melanomas
- Diagnosed most often between the ages of 30 and 50 years
Occurs at any site, most frequently:
- Trunk of men
- Legs of women
Pathogenesis:
- Asymptomatic
- Slowly changing from months-years
- Brown to black macule with color variegation and irregular, notched borders
- Best fits the ABCD criteria
- When enters radial growth phase–> papule or nodule
- Can arise de novo or in a pre-existing nevus
Nodular melanoma
Second most common type of cutaneous melanoma:
- Accounts for 15-30% of all melanomas
- Believed to arise as a de novo vertical growth phase tumor without the pre-existing horizontal growth phase
Epi:
- Mean age of onset is 53 years
- More common in men
Appearance:
- Occurs most frequently on the trunk
- Blue to black, or pink to red-colored, nodule
+/- ulceration
- Tend to be diagnosed at a thicker, more advanced stage with an associated poorer prognosis
Lentigo maligna melanoma
Represents up to 15% of cutaneous melanomas
- Diagnosed most frequently in the 7th-8th decade of life
- Arises in a precursor lesion termed lentigo maligna
- 5% of lentigo malignas progress to invasive melanoma
Pathogenesis: cumulative sun exposure
- Found on chronically sun-damaged skin
- Head and neck
- Preference for the nose and cheek
- Slow growing
Appearance: Ill-defined, asymmetric, brown to black macule with color variegation and an irregular border
- Both LM and LMM more difficult to excise because of ill-defined margins
Least association with nevi
Acral Lentiginous melanoma
5-10% of all melanomas:
- Most common subtype in darker-pigmented individuals
- 60-72% in African Americans
- 29-46% in Asians
Median age of onset being 65 years old
- Most common site is the sole
- Not all palmar or plantar melanomas are ALMs (minority are SSMs or NMs)
Appearance:
- Variegation in color and irregular borders
- May be mistaken for plantar wart or hematoma
More advanced lesion upon diagnosis associated with poorer outcomes
** ALM is not thought to be associated with sun exposure
Subungual melanoma
Variant of ALM:
- Generally arises from the nail matrix
- Most commonly on the great toe or thumb
- A widening, dark, or irregularly pigmented longitudinal nail streak (melanonychia striata)
+/- Nail dystrophy
Hutchinson sign=
- Pigmentation of the proximal nail fold
- Poor prognosis, associated with advanced subungual melanoma
ABCDE of melanoma
A: Asymmetry – one half is not identical to the other half
B: Border – irregular, notched, scalloped, ill-defined
C: Color – Varying shades from one area to the next
D: Diameter – > 6 mm or pencil eraser
E: Evolving
- Other reasons for changes in mole:
- Inflammation
- Folliculitis
- Trauma
- Hormonal influence
- Natural evolution
Histopathology of melanoma
Cytologic atypia:
- Cellular enlargement
- Nuclear enlargement
- Nuclear pleomorphism
- Hyperchromasia of nuclei
- Nucleolar variability
- Mitoses
Architectural disorder:
- Asymmetry
- Poor circumscription
- Variation in size of nests of melanocytes in the lower epidermis and dermis
- Lack of maturation of nests with descent into the dermis
- Pagetoid spread
Desmoplastic melanoma
AKA Neurotropic melanoma
Indurated papule, plaque, nodule
Pigmentation absent in at least 40% of cases (i.e. amelanotic)
Typical locations:
- Head and neck (53.2%)
- Extremities (26.2%)
- Trunk (20.6%)
Mean age 63 years old
Diagnosis is delayed due to non-specific clinical features
Histopathologically, it may simulate fibrosis/scar or a neural neoplasm leading to misdiagnosis and inappropriate treatment
Amelanotic melanoma
Pink/skin colored raised bump- harder to ID as nevi
Prognostic factors of melanoma
Most important= Breslow thickness
- Measured from the granular cell layer to the deepest penetration of the neoplasm
- Survival decreases with increasing tumor thickness
Melanoma ulceration
- Marker for aggressive nature of lesion
- Nodular lesions
- Up stage equivalent to one T level
Mitosis
- New prognostic factor as of 2009
- Proliferation of the primary melanoma
- Threshold considered significant is greater than 1 mitosis per mm2
- Adversely influences survival
- Melanoma measuring < 1mm in thickness
Anatomic site
- Worse prognosis: Head and neck, Trunk, Hand and feet; Five-year survival 84%
- Better prognosis: Arms and legs; Five-year survival 93%
Age
- Increasing age–> decreasing survival
- Patients older than 50 years of age have a 84% five-year survival vs. 90% for younger patients
Gender
- Female patients have a better survival
- Female five-year survival 90%
- Men five-year survival 83%
Prognostic factors in regional metastases
Status of regional lymph nodes most powerful prognostic factor for survival
- Presence of regional lymph nodes portends a worse prognosis
- Number of lymph nodes involved is the most significant risk factor
The second most important risk factor is tumor burden
- Micrometastatic disease (SLN Bx) vs. macrometastatic disease (clinically palpable disease)
Worse prognosis:
- Ulceration
- Satellites
- Both clinical and microscopic metastasis around a primary melanoma
- In-transit metastasis: Intralymphatic metastases between the primary tumor and its nodal basin
Prognostic factors in distant metastases
Site of metastasis – most important factor
- Visceral metastases poorer prognosis than non-visceral (skin, subcutaneous tissue, distant lymph nodes) sites
- Number of metastases
- Amenable to surgical resection
Psoraisis Vulgaris
Pathophys:
- Multifactorial disorder with genetic predisposition
- New immune cell recognised: TH17 cell–> increased IL 17 causing increased keratinocyte proliferation–> chemokine release–> skin defense
Risk factors:
- Strep pharyngitis
- Stress
- Skin trauma (scratches): Koebner phenomenon
Features:
- Nail pitting (v. difficult to treat)- increased risk of psoriatic arthritis
- Morning stiffness
Psoriasis Inversa
Skin fold regions (inverse of expected region)
Does not have silver plaques
Erythroderma
Defined by erythema and desquamation involving more than 90% of skin surface
Differential:
- Skin eruption
- Infection
- Allergic reaction
Pustular psoriasis
May be systemically ill
- Need to be followed/assesed for: hypocalcemia, hypotension, fever
Care must be given with systemic steroids as taper–> pustular flare
Psoraisis treatment
Local:
- Corticosteroids
- Vit D analogues
- Tar
Phototherapy:
- PUVA
- Narrowband UVB
Systemic:
- Retinoids (push cell differentiation)
- Methotrexate
- Cyclosporine
- Mycophenolate mofetil
- TNF-alpha inhibitors for psoriatic arthritis
Atopic dermatitis
3/4 major features:
- Prutitus
- Typical morphology and distribution
- Chronically relapsing
- Personal or family history of atopy
Usually not before 3 months of age
- Relies on patient sratching it
In infancy:
- face= common site
- sites where they can rub against bed, reach easily
- May see failure to thrive
Childhood/adulthood
- Flexural surfaces= common sites
- Chronic involvement can lead to lichenification (skin thickens)
Features:
- White dermatographism (not red wheal, but white wheal)
Theory behind pathophys:
- Immunologic abnormalities (humoral immue, t-cell mediated immune response)
- Structure of skin abnormal (BAD skin)
- Defect in humoral immune response: high levels of serum IgE, binding to langerhaans cells
- Antigen-induced activation of IgE-bearing cells (mast cells, macrophages)
- Decrease in cyclic AMP–> hyperreactive mast cells, Langerhans’ cells
Exacerbating factors:
- Anxiety, stress
- Climatic factors: temps, humidity
- Irritants: detergents, solvents, wool/rough material
- Food, contact, inhaled antigens
Itch-scratch cycle
Pruritis precedes visible eruption
- C-fibers transmit itch first
Scratching–> increased release of histamine from mast cells–> pruritis
Differential diagnosis of Atopic dermatitis
Differential diagnosis:
- Psoraisis, scabies, eczema
- Wiskott-Aldrich (eczema, thrombocytopenia, immunodeficiency)
- Hyper-IgE (cold staph abscesses- not painful/hot, eczema-like rashes, lung infections)
- Cutaneous T-cell lymphoma
Seborrheic Dermatitis
Earlier onset=typical
Absent pruritis
Limited distribution on face, groin
- Greasy scaly macules and patches on the central part of the face (nose, mouth, and eyebrows).
- Scalp is a common site of involvement, which the patients complain of bad “dandruff.” The condition is seen in neonates (e.g. cradle cap), which resolves when the maternal hormones are washed out.
- The condition is usually not seen in prepubescent age. In adults, the condition is more common in patients with neurologic diseases such as Parkinson’s disease.
Cause: belief that condition is caused by a commensal fungus, namely, Malesezzia furur.
Treatment: antifungal creams and shampoos are often recommended such as ketoconazole cream and shampoo. Other treatments include zinc based soaps and shampoos, immunomodulators such as pimecrolimus, and low potency steroid.
Scabies
Papules, burrows, nodules
Distribution:
- Infants= generalized
- Adults: finger webs, wrists, exillae, groin
Pruritis in patient and contacts
Mite debris on microscopic examination
Eczema herpes
Disseminated Herpes Simplex Virus (HSV)
Painful umbilicated pustular vesicles
Fever, malaise, lymphadenopathy
Significant morbidity and mortality (risk of systemic herpes infection)
Seen in patients with atopic dermatitis or other chronic skin conditions:
- dissemination of the cutaneous herpes simplex virus into the eczematous skin may lead to the eruption of clusters of umbilicated pustular vesicles known as eczema herpeticum or Kaposi’s varicelliform eruption
Impetigo
Pustular vesicles with straw-colored discharge
- Due to staph aureus infection
Treatment for atopic dermatitis
- Topical steroids or immune modulators: tacrolimus, pimecrolimus
- Antihistamines
- Wet wraps
- Coal tar in ointment base, anthralin
- Antibiotics (topical, oral)
- Leukotriene antagonist
Flares:
- PUVA, UVB
- Systemic steroids
- Immunomodulators (cyclosporine, tacrolimus, azathioprine)
Lichen planus
Pruritic disorder of skin, mucous membranes
Appearance: violaceous polygonal papulaes, plaques on penis
- Hypertrophic or erosive
Oral mucosa with typical white reticulated plaque
- Associated with HCV
Erosive lichen planus= increased risk of squamous cell carcinoma in oral/mucosal lichen planus
- v. painful, can cause scarring/disfigurement
Lichen Nitidus
Variant of lichen planus
Seen in children
- non-pruritic
Acne keloidalis nuchae
Chronic folliculitis–> scarring ressembling keloids in darker-skinned individuals
Abscesses
Cause: Staph
- Furuncle= single follicle
- Carbuncle= multiple follicles
Treatment with I&D and antibiotics
- Chronic abscesses due to carriage
Hidradenitis Suppurativa
Inflammatory non-infectious process
Multi-focal and symmetric involving 2+ locations
- Treatment is difficult, scarring results
Epidermal cysts
Firm, mobile nodules
Treatment: I&D
Scarlet Fever
More common in kids, caused by Group A strep erythrogenic exotoxin
- 24-48 hours after sore throat
- Sandpaper-like papules
- Pastia lines, desquamation of palms and soles
Diagnosis: strep culture, ASO
Treatment: antibiotics
