Skin Flashcards
What are the features of Basal cell carcinoma?
Elevated or rolled border with central ulceration
How nodular BCC presents?
Pearly or translucent nodule with pink, red, or white color (nodular BCC)
How Superficial BCC presents?
Reddish patch or irritated area (superficial BCC)
Histological pattern of BCC
Invasive clusters of spindle cells surrounded by palisading basal cells
How to manage Low-risk BCC lesions on the trunk or extremities?
electro-dessication and curettage (ED&C).
How to manage Low-risk superficial BCC?
managed with topical therapy using either 5-fluorouracil or imiquimod.
How to t/m BCC on face?
Mohs micrographic surgery
How to manage Nodular BCC on the trunk or extremities?
standard surgical excision, typically with 3-5 mm margins.
Important point of BCC
Radiation therapy rarely used for pts who are unable to undergo surgery
What are the risk factors of SCC?
UV and ionizing radiation
Immunosuppression
Chronic scar or wound Or burn injuries
How SCC clinically present?
Scaly plaques / nodule
With or without hyperkeratosis Or ulceration
Neurologic sign with perineural invasion results paresthesias and numbness
Histological pattern of SCC
invasive cords of squamous cells with keratin pearls
How to confirmed SCC?
or excisional)
Skin biopsy (punch, shave or excisional)
How to manage Small or low-risk lesion SCC?
surgical excision or local destruction (e.g cryotherapy, electrodessication)
How to manage High risk lesion or lesion SCC located in cosmetically sensitive area?
Mohs micrographic surgery
How keratoacanthoma presents?
Rapidly growing, “volcano-like” nodule with a central keratotic plug.
How to treat keratoacanthoma?
May regress spontaneously, many are treated as well-differentiated squamous cell carcinomas.
What are the risk factors for the melanoma?
fair skin types,
h/o blistering sunburns,
prior personal or Fx H (>/=2 members) of melanoma
dysplastic nevus syndrome, atypical nevi and greater than 100 (>10 in one explanation) typical nevi.
What is the 1st step to approach melanoma?
excisional biopsy that removes the entire lesion with narrow margins and depth through the subcutaneous fat.
Important point of Melanoma
Don’t Perform shave biopsy—
won’t determine depth of tumor which is main prognostic factor
What are the signs of DELIBERATE SCALD INJURY ?
Linear demarcation with no splash marks
Doughnut pattern
Sparing of flexures creases (Zebra pattern)
Extensive burns to back and buttocks
How plaque psoriasis presents?
Most common well defined erythematous plaques with scales typically over extensor surface
How Guttate Psoriasis presents?
Erythematous macules with scaling typically following an acute strep infection
Triad of INTERTRIGO
Due to infection with Candida species
presents as well-defined, erythematous plaques with satellite vesicles or pustules in intertriginous
Occur at occluded parts of body viz axilla or groin
How to t/m Intertrigo?
Topical nystatin is used for Candidal skin infections
How tinea Capitis presents?
Scaly erythematous patch on scalp
Hair loss with residual black dot
With or without LAD seen in african american
How to dx tinea Capitis?
KOH examination of hair shaft to document spores
How to t/m Tinea Capitis?
Oral Griseofulvin as first line
Otherwise terbinafine / Itraconazole / fluconazole
What is the MCC type in US?
black dot tinea capitis—caused by Trichophyton tonsurans.
What are the risk factors for tinea Corporis?
Athletes who have skin to skin contact
Humid environment
Contact with infected animal
How tinea Corporis rash presents?
Scaly erythematous prurtic patch with centrifugal spread
Followed by central clearing with raised annular border
How to dx the Tinea Corporis?
clinical but skin scrapings and microscopic examination using KOH is confirmatory for atypical and refractory cases—> reveal the presence of hyphae.
How to t/m Tinea Corporis?
First line used of topical antifungal—>terbinafine / cotrimazole
2nd line as extensive oral meds—>Terbinafine / Griseofulvin
Name the organism which causes tinea Corporis
Trichophyton rubrum is the most frequent culprit
How Tinea Versicolor rash presents?
Hyper/Hypo pigment lesion on face if children Or Upper Extremity in adolescent and adult With Or without pruritus and fine scale
How to dx Tinea Versicolor?
KOH preparation shows hyphae and yeast cells in a spaghetti and meatballs pattern
How to t/m Tinea Versicolor?
Topical terbinafine / Ketoconazole Or Selenium sulfide
Triad of Seborrheic dermatitis
Erythematous plaques/ yellow Greasy scale on d/f parts of face, scalp, umbilicus and diaper area
Associated with Parkinson disease and HIV
T/m via topical antifungal agents Ketoconazole Or Selenium sulfide
Triad of Erythema NODOSUM
Subcutaneous fat cells inflammation present as red, tender discrete pretibial nodules
Multiple, tender, erythematous subcutaneous nodules/plaques on lower extremities—arthralgia and malaise can develop alongside nodule
Associated with Systematic disorder
Triad of Behcet syndrome
Recurrent painful ulcer in mouth and in Genital area
Thrombosis
Uveitis with Erythema NODOSUM
How to Dx Behcet syndrome?
Pethargy—>Exaggerated skin ulceration with minor trauma
Biopsy—> non specific vasculitis of different size vessels
Histopathologic findings of Pemphigus vulgaris
Intra epidermal cleavage Detached kertinocytes (Acantholysis) Tomestone cells along basal layer
Immunofluorescence finding of Pemphigus vulgaris
Netlike Or chicken wire pattern intra cellular IgG
How the SJS/TEN presents?
Prodromal symptoms like influenza
Rapid onset reddish macules / vesicles / bullae
Necrosis with sloughing of epidermis with mucosal involvement
Name the medication which could lead to SJS/TEN
Allopurinol
Anti epileptics / Abx like sulfonamides
NSAIDs
Sulfasalazine
Name the bugs which could lead to SJS/TEN
Mycoplasma pneumonia
Vaccination
Host VS graft disease
How to t/m SJS/TEN?
FLUID resuscitation
Wound care similar to that for burns and often done in burn unit
How to t/m Bullous pemphigoid?
High potency topical glucocorticoid (e.g. clobetasol)—1st line also effective against extensive disease
How the rashes of DERMATITIS HERPETIFORMIS presents?
Grouped and pruritic erythematous papules, vesicles, and bullae on the extensor surface of body like elbow
Skin biopsy—of Dermatitis herpetiformis
DH shows subepidermal microabscesses (blisters) at the tips of the dermal papillae
Name the medicine given in Dermatitis herpetiformis
Dapsone
How and where warfain induced skin necrosis?
breast / buttock, thighs / abdomen
pain Followed by bullae and skin necrosis
How the rashes of PORPHYRIA CUTANEA TARDA Present?
painless blisters with increased skin fragility on the dorsal surfaces of the hands,
facial hypertrichosis and hyperpigmentation.
How to manage PORPHYRIA CUTANEA TARDA ?
Phlebotomy or hydroxychloroquine may provide relief, as can interferon-alpha, in patients simultaneously infected with Hepatitis C virus.
Hyperkeratotic, hyperpigmented plaques with a classic velvety texture is feature of which skin condition?
ACANTHOSIS NIGRICANS
Triad Of Actinic keratosis
Occur on Sun exposed parts of body
Erythematous papules with a central scale due to hyperkeratosis. A “sandpaper-like” texture on palpation— typical.
T/m is fluorouracil cream
Name the other indication of fluorouracil cream besides actinic keratosis
Bowen disease
How the rashes of Pityriasis Rosacea develop?
pink or brown scaly plaque with central clearing (crinkled, cigarette-paper like appearance) and a collarette of scale (herald patch)
followed by development of maculopapular rash classically in a “Christmas tree”
Occur on the trunk, neck or flexural surfaces of extremities
Triad of ICHTHYOSIS VULGARIS (lizard skin)
hereditary or acquired and worse in winter
normal skin at birth with gradual progression to dry scaly skin—typical feature
skin is usually dry and rough with horny plates over the extensor surfaces of the limbs
How the rashes of EXFOLIATIVE DERMATITIS (erythroderma) presents?
Widespread, scaly eruption of the skin
drug-induced, idiopathic, or secondary to an underlying dermatological or systemic disease
Sun exposure topic
Read it from uworld
How HIDRADENITIS SUPPURATIVA/ ACNE INVERSA occurs?
chronic inflammatory occlusion of folliculopilosebaceous units —> prevents keratinocytes from properly shedding from the follicular epithelium—> HS
Triad of HIDRADENITIS SUPPURATIVA/ ACNE INVERSA
intertriginous areas and hair bearing area
solitary, painful, inflamed nodules which regress or Converts into abscess
usually made clinically without the need for biopsy or cultures.
What are the complications of HIDRADENITIS SUPPURATIVA/ ACNE INVERSA?
Sinus tracts
Comedones
Scarring— Severe scarring can lead to dense, rope-like bands in the skin with strictures and lymphedema
How to t/m keloid?
Symptomatic keloid treated with intralesional glucocorticoids
Triad of DERMATOFIBROMA
Occurs lower extremities.
nontender & appear as discrete, firm, hyperpigmented nodules
dimpling in the center when the area is pinched (“dimple” or “buttonhole” sign) due to fibrous component
How to t/m and dx the DERMATOFIBROMA?
Dx —-> made clinically based on the appearance of the lesion.
T/m—-> cryosurgery or shave excision is usually not required unless change in size color or symptomatic and cosmetics reasons
Triad of Epidermal INCLUSION CYST/EPIDERMAL CYST
discrete benign nodule containing normal epidermis that produces keratin.
dome-shaped, firm, freely movable cyst or nodule with a central punctum (small, dilated, pore-like opening).
Larger and more inflamed lesions can have a thick, yellowish-white, cheesy, and malodorous discharge.
How to manage Epidermal Inclusion cyst / Epidermal cyst?
usually resolve spontaneously but can often recur.
Excision is typically reserved for patients who desire removal of the lesion for cosmetic reasons.
Incision and drainage is usually needed for infected and fluctuant cysts that are painful and erythematous
Important point of PRESSURE NECROSIS/DECUBITUS ULCER
Do not massage—as it will further damage skin overlying bony prominences
Triad of PYODERMA GANGRENOSUM
Starts as inflammatory papule, pustule, vesicle, or nodule—> rapidly progresses to form expanding ulcer with a purulent base and ragged violaceous borders—painful
Dx with skin biopsy
T/m is steiod
Triad of ECTHYMA GANGRENOSUM
Hemorrhagic nodule with surrounding erythema—>necrotic ulcer
Caused by P. aeruginosa
occurs in setting of profound neutropenia
What is the main cause of sepsis on burns?
main causes are pneumonia and wound infections (from Staphylococcus aureus or Pseudomonas aeruginosa)
Burn topic
Read it from skin chapter
Burn topic
Read it from skin chapter
Name the medicine causing HTN Type 1
beta lactam drugs,
NM blocking agents,
quinolones
platinum containing chemotherapeutic agents and foreign proteins (e.g. chimeric proteins)
How to manage type 1 HTN?
Urticarial and pruritus without systemic Sx: antihistamines discontinue offending drug and if Systemic give IM epi and steroids
Name the COMMON DRUGS ASSOCIATED WITH PHOTOSENSITIVE REACTION
Tetracycline
Antipsychotic like chlorpromazine /prochlorperazine
Diuretics like lasix and thiazide
Amiodarone / Promethazine / piroxicam
How drugs causing photo sensitive Rxn?
By producing oxidants
How PHOTOALLERGIC REACTION occurs?
UV light alter the configuration of Topical (eg, sunscreens) and systemic medications—->induces a delayed hypersensitivity reaction.
Name the condition which causes multiple skin tags
Insulin resistance
Pregnancy
Crohn disease (Perianal)
Name the condition which shows explosive onset of multiple itchy Seborrheic keratosis
GIT malignancy
Name the condition which shows Seborrheic Dermatitis
Parkinson disease
And
HIV infection
Triad of Vitiligo
Autoimmune destruction of melanocytes
Depigmentation macules on acral areas and extensor surface
If limited topical steroids / If extensive and unresponsive—> oral steroids / topical calcineurin inhibitor and PUVA
Skin condition which shows positive nikolsky sign
Pemphigus vulgaris
SJS / TEN
Triad of PIEBALDISM
Inherited absence of melanocytes
Usually noticed at birth
Confined to head and trunk
how Congenital dermal melanocytosis presents?
Neonate blue-grey macule on sacrum and buttocks.
Benign birthmarks fade spontaneously during 1st decade
Name the types of Acne Vulgaris
Acne inflammatory
Acne comedones
Acne (cystic) nodular
Triad of Acne comedones
Comdones on forehead / chin / nose
Progress to inflammatory pustules / Nodules
T/m retinoid / salicylic / glycolic acid and if fail, give benzoyl peroxide if inflammatory acne
Triad of Inflammatory acne
Inflamed pustules / papule / Erythema
If mild—> topical retinoid + benzoyl peroxide
If moderate—> add topical ABx ( clindamycin/ erythomycin) and
And add oral ABx if severe
Triad of Nodular cystic (acne)
Large nodules which appear cystic
Nodules change into sinus tract
If moderate give topical retinoid + benzoyl peroxide + topical ABx
If severe oral ABx and if unresponsive oral isotretinoin
Important point of benzoyl peroxide
cause photosensitivity reaction Common S/E are irritation, contact dermatitis, dryness, erythema, peeling and stinging
How STEROID-INDUCED ACNE OR STEROID INDUCED FOLLICULITIS presents?
Characterized by monomorphous pink papules on face, trunk and extremities
absence of comedones
How acne Rosacea presents?
Papule and pustules on face With flushing
Dilated capillaries
Redness in conjunctivia and lid margin dilated vessel
Occur when body temperature increases
How to t/m acne Rosacea?
Topical metronidazole for papulopustular type
Laser or Topical Brimonidine for Erythema telangiectasia
How SEBACEOUS HYPERPLASIA presents?
small pale/yellow papules at the central face.
Lesions are stable in size and appearance
Triad of SEBORRHEIC KERATOSIS
waxy, “stuck on,” warty, and well-circumscribed appearance.
Occur on face and trunk. But not occur on the palms and soles.
removal by snip/shave excision, cryosurgery, and electrodessication
Triad of Atopic Dermatitis in children
Itchy red Scaly crusted lesion
Underlying allergic disorder
Topical emollient with or without steroid ointment
Location of Atopic Dermatitis
Child / adult—-> lichenified plaques in flexural creases
In infants—–> Extensor surface / cheek / scalp / Trunk
Name the complications due to Atopic Dermatitis
Cellulitis/abscess Eczema herpeticum Impetigo Tinea Corporis Molloscum contagiosum
How Eczema Herpeticum presents?
Due to Atopic Dermatitis
Painful vesicular rash with punch out erosion & Hx crusting
Systemic acyclovir—>give asap
Name the metals causing Allergic contact Dermatitis
nickel
chromium / cobalt, beryllium
zinc.
Important point of allergic contact Dermatitis
Rash appears days after exposure
frequently form linear streaks where skin has brushed against plant leaves
How the rash of uritricaria presents?
Well circumscribed raised reddish plaques
Lesions can be oval / round / serpiginous
Important point of Uritricaria
Acute less than 6 wks
And
Chronic more than 6 wks
Important point of Mast cell degranulation
If occurs in deeper layers—-> Angioedema with or without Uritricaria / typically presents as non-pitting and nonpruritic edematous swelling
If occurs in Superficial layers—-> pruritis and localized swelling in upper layers of skin
Triad of Serum Sickness like condition
Prodromal Sxs with pain in joints / Uritricaria / no mucosal involvement
Occur after use of ABx like
Low complement with increased inflammatory markers
Triad of Blue Nevi
Smooth-surfaced, dome-shaped melanocytic papules that develop from macules
tend to be less than 1cm in diameter
blue color due to the depth of the melanin in the skin.
Important point
MELANOCYTIC NEVI follows the ABCDe rules
How Nevus simplex presents?
Macular stain with salmon patch and stork bite /Angel kiss
Blanchable pink red patches occur at head and neck region
Fades away by 1-2 years of age but persist at back of neck
How LENTIGO SIMPLEX presents?
characterized by a round or oval macule with even pigmentation
Due to intraepidermal melanocyte hyperplasia
Important point of ACROCHORDON
Skin tag occurs in regions of body which causing friction
Triad of SENILE PURPURA (solar or actinic purpura)
Due to loss of elastic fiber in perivascular CT
Seen in elderly using anticoagulants / steroids / NSAIDS
ecchymosis due to rupture of blood vessels
Triad of STRAWBERRY (SUPERFICIAL INFANTILE) HEMANGIOMA
Composed of capillaries separated by connective tissue—superficial, well demarcated and lanch with pressure
grow rapidly during 1-2 yrs and then frequently regress spontaneously by age 5-8yrs
BB If complications
Triad Of CHERRY ANGIOMA OR SENILE HEMANGIOMA
Seen in adults
sharply circumscribed areas of congested capillaries and post-capillary venules in the papillary dermis.
Dont regress spontaneously and may bleed if disrupted
Triad of CAVERNOUS HEMANGIOMA OR CAVERNOUS MALFORMATIONS
Consist of dilated vascular spaces with thin-walled endothelial cells.
Cavernous hemangiomas of the brain and viscera are associated with von Hippel-Lindau disease
soft blue, compressible masses
Triad of Pyogenic granuloma
small red papule that pedunculated or sessile shiny mass.
Grows rapidly over weeks / months
lip and oral mucosa and can bleed with minor trauma
What are the d/f Neonatal rashes?
ERYTHEMA TOXICUM NEONATORUM
Neonatal HSV
Neonatal Varicella
SSSS
Triad of ERYTHEMA TOXICUM NEONATORUM
Generalized reddish macules / papaules / pustules
No involvement of palms and soles
T/m is reassurance only
Important point of Neonatal rashes
VSV and HSV both t/m with acyclovir
HOW SSSS presents?
Neonatal rashes start with fever/ irritability / diffuse Erythema
Followed by blistering and exfoliation
T/m is vancomycin / nafcillin / oxacillin
Triad of non Bullous Impetigo
Due to S.aureus / S.pyogenes
Painful non itching pustules
Honey crusted lesion without Prodromal Sxs
Triad of Bullous Impetigo
Due to S.aureus
Flaccid bullae with yellow fluid without Prodromal Sxs
Collarette of scale at periphery of rupture lesions
How to t/m Impetigo?
)
If limited —-> Topical ABx mupriocin
If extensive—-> Oral ABx (cephalexin / Dicloxacillin / clindamycin
Triad of ERYSIPELAS
Prodromal Sxs early with superficial skin involvement
Raised, sharply demarcated margin is a classic feature.
T/m is Oral amoxicillin Or IV ceftriaxone
Name the bacteria causing ERYSIPELAS
Strept pyogenes
What are the risk factors of Cellulitis?
obesity / venous insufficiency
disruption of skin (e.g. Tinea pedis infection).
Chronic fungal foot infection can serve as a nidus of bacterial cellulitis
Triad of Non purulent Cellulitis
S.pyogenes / MSSA with prodrome SxS later in course
Inflammation involve deep dermis & sub cutanous fat
Flat edges with poor demarcation
Triad of Purulent Cellulitis
Due to MSSA / MRSA
Purulent drainage
Folliculitis—> furnucle—>Carbuncle (if multiple furnucle
How to t/m Cellulitis?
If mild and without Systemic Sxs—->oral dicloxacillin
Severe Cellulitis with Systematic Sxs—-> IV nafcillin or cefazolin are DOC
In areas with high prevalence of MRSA, vancomycin can be used as 1st line agent.
Surgical Drainage if abscess Or necrotizing fasciitis
Name the Bacteria causing Necrotizing fasciitis
Strep.pyogenes /Staphy aureus
C.perferingens
Triad of Necrotizing fasciitis
Positive hx of trauma
Pain with Systematic Sxs
Erythema / Swelling / edema of Skin /Crepitus
How to d/f polymyositis from Necrotizing fasciitis?
Polymyositis localise to only one muscle and without air on imaging
And
Necrotizing fasciitis is Generalized and with air on imaging
How the patient of SSSS presents?
Start with Fever and Prodromal Sxs
Erythema starts on face and then Generalized
Superficial flaccid bullae with +ve Nikolsky sign
Scaling / desquamation /extensive exfoliation of skin continue for about 5 days
Name the bacteria causing Scarlet Fever
group A β-hemolytic streptococcus that produce erythrogenic exotoxin
How Scarlet Fever presents?
Pharyngitis with Prodromal Sxs
fine, pink blanching papular rash (rough, sandpaper like) initially
And desquamation begins in the face, progresses down the trunk and finally extends to hand and feet
What is the characteristic of Scarlet Fever?
punctate or finely papular texture which is sometimes palpable, hence sandpaper like
Cheeks extremely red and area around moth appears pale—“circumoral pallor”
How to t/m Scarlet Fever?
penicillin V (drug of choice) Erythromycin,clindamycin, and 1st generation cephalosporins—good alternatives for penicillin allergic pts
Triad of FELON
Due to needle INJURY and common in tailors
tense abscess (non-purulent vesicle in whitlow) and intense throbbing pain.
Incision and drainage with appropriate antibiotic (e.g cephalosporins) is the treatment of choice.
Triad of CONDYLOMATA LATA
Due to Secondary syphilis
Flattened pink or gray velvety papules
Seen in mucous membranes and moist skin of the genital organs, perineum, and mouth
Important point MOLLUSCUM CONTAGIOSUM
Do HIV testing if genelised rashes and hundred in number
Dx is clinical
Self limiting with 6 to 12 months otherwise curettage, cryotherapy, or topical agents (e.g. podophyllotoxins)
Triad of CONDYLOMATA ACCUMINATA
anogenital warts
verrucous, papilliform, and either pink or skin-colored.
Usually Dx is clinical otherwise biopsy if atypical
How to t/m CONDYLOMATA ACCUMINATA (anogenital warts)?
Chemical or physical agents (eg, trichloroacetic acid, podophyllin)
Immune therapy (eg, imiquimod)
Surgery (eg, cryosurgery, excision, laser treatment)
