Dermatology Week 1 Flashcards
What is psoriasis?
Chronic papulosquamous skin disease of unknown etiology
How does psoriasis present?
Psoriasis presents as well defined red plaques with silvery scale
At what age is psoriasis most likely to be seen? Sex predominance?
20s and 50s. Although it can be found in individuals of any age. M=F
What form of psoriasis is the most common in children?
Guttate psoriasis - appears as little dots as like a paint brush
Describe the pathogenesis of Psoriasis
T cells are the driving force (mostly Th1 more than Th2) and significant amount of T cells are present in the dermis and epidermis. Also immune dysregulation leads to increase in inflammatory mediators leading to epidermal proliferation, differentiation and angiogenesis
What are the triggers of psoriasis?
external trauma (Koebner phenomenon), infections (esp strep pharyngitis), HIV disease, hypocalcemia, stress, drugs, alcohol, smoking
Sharply demarcated thick skin + silvery scale are characteristics of what dermatological lesion?
Psoriasis
What is Auspitz sign?
This is when bleeding is present after you scrap a psoriasis lesion. It shows that presence of angiogenesis in the disease
What are the symptoms of Psoriasis?
Frequent itch, occasionally painful. Improved in the summer and worse during the winter.
What is atopy?
Tendancy towards allergic diseases like allergic rhinits, asthma, atopic dermatitis
What’s the atopic march and what are the steps
atopic dermatitis –> asthma –> allergic rhinitis
“DAR” - Dermatitis-Asthma -allergic Rhinitis
What is involved in the pathogenesis of atopic dermatitis? Key players
1) T cells activation leading to increased IgE
2) Hyperresponsive dendritic cells aka langerhan cells (these are antigen presenting cells) – they meet the allergen and present it to the T cells leading to increased IgE
3) Defective epidermal barrier
What type of T cells are produced in acute vs chronic atopic dermatitis
In acute dermatitis there is increaed Th2 cells –> increased IL-4 which triggers B cells to make IgE –> increased IgE (seen during disease flares)
In chronic atopic dermatitis there is increased Th1 cells
What are the characteristic features of the defective barrier seen in Atopic dermatitis?
The epidermis has decreased CERAMIDES - affecting barrier function and inflammatory response
Dry skin
Increased transepidermal water loss
Increased penetration of irritants, allergens and microbes
What are some of the triggers of Acute Dermatitis?
Food allergens, aeroallergens
Infection (Staph aureus, cutaneous viruses)
Animal dender
Pollen
Dust mites
Why is there increased cutaneous infections in patients with Atopic dermatitis?
Loss of the epidermal barrier
There is also lack of innate antimicrobial peptides in skin like beta defensins and cathelicidines that are produced by keratinocytes
What is the the classic clinical history or presentation characteristics of a patient with atopic dermatitis
Pruritis
Usually in the first two years of life
Dry skin
Personal or family hx of atopy
Give examples of things that can worsen the itch in acute dermatitis?
Temperature, wool, stress, soap
In a histopathologic section of atopic dermatitis, what are the key characteristics of atopic dermatitis?
Spongiosis (intra-epidermal edema) and acanthosis
What’s the prognosis of atopic dermatitis?
It exacerbates and remitts. Improves by 3-4 years. An infant unlikely to have AD as an adult
What are the general skin care principals for Acute Dermatitis
Hydration is very important
Avoid long hot showers
Avoid soap, especially fragranced
Apply think emollients to help with barrier - some of these replace absent ceramides
Bleach baths reduce staph infection and help with atopic dermatitis
What is the standard treatment of atopic dermatitis?
Address sleep issues
Nutritional advice
topical steroid
topical or oral antibiotics
Oral antihistamines
What type of a reaction is allergic contact dermatitis?
Type 4 hypersensitivity reaction
What are the two phases of allergic contact dermatitis?
1) Sensitization phase
2) Elicitation phase
What are the key facts about clinical history of allergic contact dermatitis?
Presence of pruritis or burning
Acutely lasts days to weeks, and chronically lasts months to years
First exposure - takes 7-10 days to react
Second exposure - takes 12 horus or more to react
What are the histopathologic features of:
acute contact dermatitis?
subacute dermatitis?
chronic dermatitis?
Acute - Spongiosis and vesicles in the epidermis, and lymphocytes in the dermis
Subacute - spongiosis but no vescicles, acanthosis, scale/crust
Chronic - psoriasiform, epidermal hyperplasia, parakeratosis, fibrosis
How do you treat contact dermatitis?
identify irritant or allergen
topical/oral corticosteroids
antihistamines
antipruritic lotion
What are the findings on a physical exam of an individual with Urticaria?
Wheals and dermographism
What is the histopathology of urticaria/angioedema
Edema of dermis and subcutanous tissue
Mixed inflammatory cell infiltrate around dermal blood vessels
What is the pathophysiology of urticaria/angioedema?
It is a type 1 immediate hypersensitivity reaction
Antigen binds to IgE on the surface of mast cells and basophils
This leads to activation, degranulation, release of vasoactive amines like histamine, leukotrienes and prostaglandins
Urticaria treatment
Antipruritic lotions
Antihistamines
Epinephrine if there is anaphylaxis
What is the site of disease for acne vulgaris?
The pilosebaceous unit (hair follicle and attached sebaceous gland)
What is the clinical findings distribution of acne vulgaris?
face, neck, ears, upper chest, back and arms
What is the “beard distribution” about and what causes it?
This is acne that appears around the jaw line. It is found in women who are in a hyperandrogenic state
What are the four types of rosacea and describe them?
1) Erythematotelangiectasis - redness, telangiectasias (dilated blood vessels)
2) Papulopustular - pimples, pustules, redness
3) Occular - eye irritation, conjuctival injection / bloodshot look
4) Rhinophymatous - thickening of the skin of the nose. Can also affect chin
What causes warts?
Warts are caused by HPV (Human Papilloma Virus)
What type of a virus is HPV? And describe its class
HPV is a papovirus - slow growing, double stranded, naked (lack envelop) DNA virus
Where do warts occur?
Warts occur anywhere on skin or on mucous membranes. Genital HPV is associated with sexual activity
How does HPV cause damage to the skin or lead to warts?
It infects the epidermis or dermis layer only.
It infects cells in the upper epidermal layers - causing proliferation and hyperkeratosis (accumulation of keratin)
What are the three presentation levels in HPV infection?
Clinical - infection is visible to the naked eye
Subclinical - infection is visible with the aid of diagnostics tools like acetic acid which causes whitening
Latent - virus present in apparently normal skin
List the types of warts?
Verruca valguris - common warts
Verruca plana - flat warts
Verruca plantaris - plantar warts
Condyloma accuminata - genital warts
Verruca plana
In what age group is it mostly seen?
Described the kind of lesion and what places of the body it is commonly found?
Flat warts
Often found in kids and yound adults
Described as small flat topped papules
Commonly seen on the face, legs and arms
What is a plantar wart?
This is a wart seen on the feet. It often appears at pressure points
What is a mosaic wart?
This is a coalesced group of warts
What is a myrmecia?
This is a deep, dome shaped, often inflammed wart
Which HPV subtypes are associated with Genital warts?
HPV 16 and 18
The HPV high risk subtypes are associated with genital warts and also……………?
dysplasia that may progress to malignancy –>Example - cervical cancer
Periungual squamous cell carcinoma
Describe the wart pathology?
Hyperkeratosis and parakeratosis
Increased stratum granulosum layer
Increased capillaries in the papillary dermis
What’s the treatment for warts?
Some spontaneouly regress
Topical tx - cryotherapy (freezing), cantharadin (blistering), imiquimod - Aldara (topical immune modulator
Surgery
Laser
Oral cimetidine, ranitidine
Duct tape
What causes molluscum contagiosum?
It is caused by molluscum contagiousum virus - a poxvirus
How is molluscum contagiosum trasmitted?
Molluscum contagiosum is transmitted by skin to skin contact
Who is most commonly affected by molluscum contagiosum?
Children - face, trunk extremeties
Sexually active young adults - genital lower abdomen, upper thighs
Immunocompromised CD4<100 - face, eyelids, genitals –> “giant mollusca”
4th group less likely than the groups above is eczema compromised skin
What is the clinical appearence of molluscum contagiosum?
Dome-shaped, flesh colored papules
Central umbilication
Crusting and erythema if irritated
Molluscum dermatitis - surrounding erythema like reaction
What is the pathology of molluscum contagiosum?
Epidermal thickening - Acanthosis
Cup shaped
Molluscum bodies present in spinous layer of epidermis - cytoplasmic inclusions in the spinous cells
What is the function of melanocytes and where do they originate?
Melanocytes produce pigment and they originate from the neural crest and migrate to epidermis, dermis, retina, inner ear, leptomeninges
What is a junctional nevi and what are its characteristics?
A type of benign nevi
These are flat and brown characterized by melanocytic nests present to the dermo-epidermal junction
What is an intradermal nevi and what are its characteristics?
This is a raise, tan colored lesion
Made up of nests of melanocytes ONLY in the dermis.
Nests become smaller as you go down deeper into the dermis
What is a compound nevi and what are its characteristics?
This is a raised lesion (papule or plaque), light to medium brown
Nests of melanocytes are at the junction of the epidermis and dermis, and also in the dermis
What type of congenital melanocytic nevi has the higherst melanoma risk?
The large or giant type (>20cm) especially if it is a midline lesion
Why is a blue nevi blue and where on the body is it commonly found?
It is blue because of the Tyndall effect (the transmission through the skin causes that color)
Most often found on the dorsal hands, feet, scalp, face
What kind of nevi has a “fried egg” appearence - raised center with macular border
Dysplastic nevi - irregular border and color, greater than 6mm
What is Familial atypical mole-melanoma syndrome?
This is a syndrome associated wth increased risk of dysplastic nevi and melanoma - it has numerous nevi (>50), melanoma in 1 or more relatives, nevi’s are histologically dysplastic
High risk for developing melanoma - 100% by 80 years
What genes are associated with Familial Atypical Mole-Melanoma Syndrome?
CDKN2a - a tumor suppresor. Mutation causes abnormal proliferation of melanocytes. Certain mutations are also associted with PANCREATIC CANCER
CDK4
Two relatives with melanoma, dysplastic nevi, Fhx of pancreatic cancer. What are you most likely worried about?
This person possible inheritedthe CDKN2A mutation –> Familial Atypical Mole-Melanoma syndrome
What is the most commonly found somatic mutation in melanoma?
What is the treatment for melanomas positive for this mutation
BRAF
Verumafinib
What are the subtypes of melanoma?
Superficial spreading
Nodular
Lentigo maligna
Acral lentiginous
Amelanotic
What are the characteristics of superficial spreading melanoma
most common type
median age 50
upper back in both sexes, but women additionally found on legs
Radial (Horizontal) growth phase then veritcal growth phase with appearence of a nodule
Can show regression
Nodular melanoma
Usually only a papulle - friable, fungating or ulcerated. Bleeding seen later in course
Common in men
Seen in sun-exposed areas
What subtype of melanoma is most common in dark or Asian patients?
And common site on the body
Metastasis?
Acral lentiginous melanoma - its incidence is the same as whites with other melanomas
Median 50 yes, M=W
Growth is junctional, later vertical growth
In blacks, #1 site is the foot. Thumb and hallux are most often affected digits
Can metastasize to axillary and epitrochlear nodes - due to delayed diagnosis
What is a subungual melanoma
This is a melanoma of the nail bed
Can mimick wart, traumatic hematoma, KS(?)
Hutchinson’s sign
What is Hutchinson’s sign?
This is pigmentation of proximal nail bed fold at the end of a pigmented band, suggestive of melanoma
What are the characteristics of Lentigo maligna
What is the common site
This is a IN SITU melanoma - resultof lentiginous proliferation of atypical melanocytes extending over at least 3 rete ridges in chronic sun damaged skin
Most commonly found in old patients with chronic sun exposure
Head is the common site
Slow growing with radial phase that can last 5-20 years
Proliferation is at the dermo-epidermal junction and the lesion can have indistinct borders (often larger than appears)
What is Lentigo maligma melanoma
Lentigo maligna that has developed an invasive component
Amelanotic melanoma
Doesnt really look like a melanoma - can mimick PG(?) and BCC(?)
Differs in its lack of color
Seen in patients with albinism
What are the factors considered in staging and prognosis of melanoma?
Lymph node status (most important prognostic factor)
Organ metastases
Mitoses in the lesion on histology
Thickness of the tumor
What is Breslow’s depth?
It says how deeply tumor cells are going in the skin (thickness of the tumor). Used as part of prognosis
In melanoma, what indicates an increased risk of metastasis?
Lymph nodes are enlarged and felt by touch
Tuumor is thicker than 1mm
Advanced tumor or patient has indicating symptoms
What is a sentinel lymph node?
This is the first lymph node that is draining a cancer. Highest probability of finding metastases
What is the most important prognostic factor in melanoma?
Lymph node status
Describe the pathogenesis of acne? Include the 4 main factors that are involved in the development of acne
1) Epidermal proliferation
2) Increased sebum production
3) Proprionibacterium acnes bacteria (P. acnes)
4) Inflammation
What stimulates sebum production?
Androgens stimulate sebum production
Androgens are highest during first 6 months of life and during puberty
High androgens are found in infants, adrenarche (9-10 years), women with hyperandrogenic states “beard area”
What are the histologic features of a dysplastic nevi?
Assymetric and broad
“Shoulder” phenomenon
Lentiginous melanocytic hyperplasia
Irregular shape and distribution of epidermal nests
Bridging of rete
Dermal fibrosis
Inflammatory infiltrate
Cytologic atypia of melanocytes
Describe the shoulder phenomenon and in what type of lesions is it found?
The bridging phenomenon is found in compound dysplastic lesions
Epidermal component extends beyond the lateral border of the dermal nevus cells in compound lesions
Which subtype of melanoma has no radial growth phase?
Nodular melanoma
Other melanomas have a radial in situ growth phase before they develop into an invasive tumor
