Dermatology Flashcards
Parvovirus causes…
Fifths disease aka erythema infectiosum
CP: Fever, HA, maculopapular rash (lacy reticular pattern) on back & abd (recurs with heat/sunlight) & “slapped red cheeks”
Tx = symptomatic
Prog = self limiting with excellent prognosis
Parvo-virus - 5 letters & = fifth disease
Coxsackie virus causes…
Hand foot & mouth disease
Poxvirus causes…
Molluscum contagiosum & other diseases - 9 different pix viruses
SARS is caused by…
Coronavirus
All ages
CP: Atypical one
Koebner’s phenomenon - what is it? What diseases does it happen in?
New lesions at site of trauma
Seen in psoriasis and lichen planus
Wickham straie
Fine white lines on the skin lesions or on the oral mucosa of people w/ lichen planus
Salmon-colored papule with white colarette scaling along cleavage lines
Pityriasis Rosea
Confined to trunk & proximal ext, face spared
Pityriasis rosea - thought to be idiopathic but has some relation to which infection?
viral infections, especially human herpes virus 7 (HHV7)
Pustular psoriasis - MC location, description
Location
Description
A/w?
Deep, yellow, non-infected pustules that evolve into red macules on palms/soles
Most severe variant (von Zumbusch type) – can be deadly. Acute onset widespread erythema, scaling, sheets of superficial pustules (WHOLE BODY). Assoc w/ systemic symptoms: malaise, fever, diarrhea, leukocytosis, hypocalcemia. Caused by: pregnancy, infection & withdrawal of glucocorticoids.
FAM HX of psoriasis (genetic component) - 2/2 keratin hyperplasia cells in the stratum basale due to T-cell activation & cytokine release
Guttate psoriasis
Location
Description
A/w?
Small, erythematous papules with fine scales, discrete leisons & confluent papules
Trunk & extremities most affected. Child/young adult w/ no hx psoriasis. Strong assoc w/ recent strep infection.
Plaque psoriasis
Location
Description
A/w?
Most common variant (>50%), symmetrically distributed cutaneous plaques on scalp, extensor elbows, knees & gluteal cleft – may be asymptomatic, pruritis common
Inverse psoriasis
Location
Description
A/w?
Inverse p = intriginous areas affected (inguinal, perineal, genital, intergluteal, axillary, inframammary), D/dx = fungal/yeast/bac inf under breast folds – given anti-fungal, not better, come back = inverse psoriasis
Erythrodermic psoriasis
Uncommon, acute or chronic, generalized erythema/scaling head to toe (whole body), complications = loss of adequate skin barrier (first line innate immune defense → abscess, cellulitis) & electrolyte abnl). NOvesicles/pustules.
Psoriasis is called a multi-systemic disease - Which other systems are involved frequently?
Nail beds - nail pitting
Joints - psoriatic arthritis - rheum issue
Mild to moderate psoriasis treatment
Mild to Moderate:
Emolients (like eucerin) to keep skin moist
Topical corticosteroids - HIGH DOSE
Hydrocortisone, Triamcinolone, fluocinonide, betamethasone dipropionate, clobetasol
Alternatives:
Vitamin D analogs → calcitriene, calcitrol, tacalcitol)
Tar-T/Gel, Topical retinoids, anthralin shampoo, tacrolimus or pimecrolimus for face
Moderate to severe psoriasis treatment
Moderate to Severe Disease:
Phototherapy (good for widespread disease), UVB (alone or w/ topical tar), Narrow band UVB @ sub-erythrmogenic doses, home phototherapy UVB machines
Systemic for severe → Methotrexate, Cyclosporine, Apremilast Biologics (TNF-alpha inhib) Entarecept, Infliximab, Adalimumab, Ustekinumab, secukinumab, ixekizumab, brodalumab, guselkumab
Pityriasis (tinea) versicolor etio
KOH?
Woods lamp?
Tx?
Malassezi furfur (part of normal skin flora)
KOH - spagetti & meatball from hyphae & spores
Woods lamp - yellow-orange fluorescence
Tx - topical anti-fungal (selenium sulfinde, sodium sulfacetamide, “azoles”
Tx options seborrheic dermatitis, textbook description
“Erythematous plaques with fine white scales” over areas of high sebaceous gland secretion (nasolabial fold, forehead, beard muscache, eyelids, chest, scalp (dandruff)
Tx: Topical selenium sulfide, sodium sulfacetamide, ketoconazole, or ciclopirox, steroids
Type I hypersensitivity reaction
IgE mediated reaction - Immediate
Ex: urticaria, angioedema, bronchospasm, hypotension, anaphylaxis
Type II hypersensitivity rxn
Cytotoxic, antibody-mediated (drugs in combination with cytotoxic antibodies cause cell lysis)
A type II hypersensitivity is said to occur when damage to the host tissues is caused by cellular lysis induced by the direct binding of antibody to cell surface antigens. While the antibodies involved in type I HS are of the IgE isotype, those involved in type II HS reactions are mainly of the IgM or IgG isotype.
Ex - Autoimmune hemolytic anemia, Immune thrombocytopenia, neutropenia
Ab = CELL destruction - why examples are low CELL counts
Type III hypersensitivity reaction
Type III hypersensitivity occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and attraction of leukocytes. Such reactions may progress to immune complex diseases.
Examples - Drug-mediated vasculitis Serum sickness Arthus reaction Reactive arthritis IgA Berger, HSP PSGN
Type IV hypersensitivity reaction
Type IV hypersensitivity is often called delayed or cell-mediated hypersensitivity
This is because antigen exposure activates T cells, which then mediate tissue injury. Depending upon the type of T cell activation and the other effector cells recruited, different subtypes can be differentiated (ie, types IVa to IVd).
Ex: Erythema multiforme
Allergic contact dermatitis, some morbiliform reactions (erythema multiforme), severe exfoliative dermatoses (SJS/TEN), DRESS, AGEP, interstitial nephritis, drug-induced hepatitis etc
Types of hypersensitivity reactions
● Type I – Immediate in onset and caused by immunoglobulin (Ig)E-mediated activation of mast cells and basophils
● Type II – Delayed in onset and caused by antibody (usually IgG-mediated) cell destruction
● Type III – Delayed in onset and caused by immune complex (IgG:drug) deposition and complement activation
● Type IV – Delayed in onset and T cell-mediated
Erythema multiforme
Causes Type of rxn A/w? CP Tx
Acute, self-limited type IV Hypersensitivity rxn
Lesions evolve over 3-5 days, last 2 weeks
MC in young adults 20-40 YO
A/w HSV (MC), mycoplasma, S. pneumo, DRUGS (sulfa, BL, phenytoin)
CP:
TARGET (iris) lesions that are dull, “dusty-violet” red purpuric macules/vesicles or bullae in the CENTER surrounded by pale edematous rim & a peripheral red halo
EM minor - NO mucosal membrane lesions . Lesions distributed acrally (peripherally).
EM major - involves > 1 mm (oral, genial ocular) - cover more central BSA, NO epidermal detachment
Tx:
Symptomatic, d/c offending drug, antihistamines, analgesics, topical steroids, oral STEROIDs if severe
SJS/TEN occurs most commonly after ?
Sulfa and anticonvulsant meds, nsaids, allopurinol
SJS - what percent body surface area sloughs off vs TEN?
SJS < 10%
TEN > 30% +/- skin necrosis
Clinical manifestations SJS/TEN
Fever
URI sx
Widespread blisters begin on trunk/face
Erythematous/pruritic macules > 1 mucous membrane involvement with epidermal detachment (+Nikolsky’s sign)
Tx: like severe burns - burn unit admission, pain control, stop offending med, fluid & electrolyte replacemet, wound care
Thrombosed capillaries are pathognomonic for what skin lesion?
Verruca vulgaris (common wart) Verruca plantis (plantar wart)
55 YO male comes in concerned about 10 mm velvety warty plaque on his back - what is most likely dx?
Seborrheic keratosis = “Seb ker”
Also described as a “greasy, stuck-on” appearance sometimes
I think they look warty but book also describes them as “velvety” as the front of this card.
MC in fair-skinned elderly w/ prolonged sun exposure.
