Term
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Definition
Acne Vulgaris Comedones
Propionibacterium acnes. Altered keratinization leads to follicular plugging. Tyrosine-fatty acids react. Once pilosebaceous unit is plugged get closed environment, stimulation of inflammatory mediators, local inflummation, pain, itching. Androgens and oral steroids can cause. Upregualtion of TRL-2, MMP's breakdown collagen, T-lymphs increased in perilesional infiltrate of lesions that scar. P acnes activates TLR-2 and TLR-3 which activates cytokines, disrupting keratinization.
Blackhead = Open comedone
Whitehead = Closed comedone |
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Definition
Papulopustular Acne Vulgaris
Crust forms as part of inflammatory process.
Treat with topical antibiotic- Benzyl peroxide, Erythromycin/Clindamycin, Azaleic acid-least irritating and slowest working/Retinoic acid, Tazotene/Adapalene-less irritating than retinoids (To prevent follicular plugging). Sinus tracts can form in the dermis as well as scaring. Nasal labial fold involvement.
Oral antibiotics:TTC, Minocycline, Doxycycline
Creams>Lotions>Solutions>Gels>Foams |
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Definition
Nodulocystic Acne Vulgaris
Follicular opening extrudes contents. Can be painful and cause systemic like symptoms such as fatigue and lethargy. Intense and aggressive inflammatory response to follicular plugging. Genetic predisposition. T-lymphs and cytokines being activated.
Tream with Oral Isotretinoin |
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Definition
Erythematous rosacea
No comedones, Aberrant innate immune system, UVR, Vascular changes, Epidermal barrier dysfunction, neurogenic inflammation, microbes (Demodex mites). Inc cytokines and antimicrobial peptides cause symptoms. Genetic predisposition. No nasal-labial fold involvement.
Treat with azoleic acid (targets calcecedins and calcerdin cascade) to stop inflammatory mediators and decrease erythema. Avoid triggers, titanium dioxide and zinc oxide to block sunrays, avoid UVR, topical mediations- metronidazole, azaleic acid, brimonidine gel, oxymetazoline hydrochloride cream |
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Definition
Rosacea, erythema, telangiectasia, red papules, tiny pustules
Barrier dysfunction and vascular dysfunction. Redness due to vasodilation of blood vessels |
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Definition
| Rosacea, Telangiectasia, papules and pustules, some swelling |
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Rosacea with rhinophyma
Nose disfiguration, end result of uncontrolled sebaceous gland growth in nose, bulbous appearance or dark deep purple blue discoloration. Use pulse light treatment, plastic surgeon for restructuring of nose |
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Definition
Hidradenitis suppurativa with paired black comedones
-Can affect apocrine glands
-Follicular opening of PSB becomes plugged with sebum and an acute-chronic inflammatory response occurs (axilla, anogenital area, inguinal fossa, lower abdominal skin flaps)
-Can have sinus tracts, fistulae formation, hypertrophic scars
Tell patient's to avoid tight clothing to prevent friction on skin, prescribe topical antibiotic erythromycin/clindamycin, wash with soap and water 2x day, allow as much air to get to the region, encourage nothing is wrong can treat but need surgical intervention |
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Definition
| Hidradenitis suppurativa with bulging and depressed scars, draining sinuses and larger ulcer in the axilla |
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Definition
| Hidradenitis suppurativa. Severe scarring on the buttocks, inflammatory painful nodules with fistulas and draining sinuses |
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Definition
| Hidradenitis suppurativa with considerable inflammation and purulent exudate from multiple sinuses |
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Definition
| Rubella with Erythematous macules and papules |
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Definition
A: Rubeola, Measles with exanthem. Erythematous macules and papules B: Measles with Koplik spots (2-3mm gray-white raised lesions) (Measles Virus)
Viral illness that can be immunized against. Maculopapular rash that begins on the head (ears/hairline) and spreads to the trunk and extremities. Child won't want to play or eat. Skin manifestations, rash preceded by fever, cough, conjunctivitis. Virus that is inhaled, affects the respiratory and cutaneous system. Rash becomes confluent and begins to fade after day 6 leaving a faint-brown stain. |
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Definition
Hand-foot-and-mouth disease
Coxsakievirus A16 or Enteroviruses. Viral illness associated with vesicles in the mouth, palms of hands, feet, oral mucosa. Supportive care using oral topical treatments and good hygiene. Older child, more painful the lesions are (can be misinterpreted as mono in older kids but EBV won’t give lesions on palms and soles of feet). Spread by direct contact. |
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Definition
| Hand-foot-and-mouth disease oral lesions (macules->grayish vesicles that erode to painful ulcers) |
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Definition
Varicella. Multiple, pruritic, erythematous papules, vesicles on face and neck, some vesicles have crusted
Lesions look like dewdrops (small raised vesicle-smooth raised <1cm, clear fluid) on a rose petal (red). Also the virus that gets reactivated when someone has shingles. VZV (HHV-3) . Initially vesicular lesions on erythematous base that progress to paupules, vesicle ruptures to form a crust. 2 week duration. Vaccine is VARIVAX in 2 doses. |
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Definition
| Molluscum contagiosum umbilicated papules |
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Definition
Roseola Exanthum Subitum Sixth Disease
Morbiliform erythematous popular rash with some clearing centers, pinpoint, raised, generalized, covers the trunk and spreads to the neck and legs (can last hours or days). Very high fever with no other symptoms for 3-5 days then rash. Human herpesvirus (HHV-6). 6months-4 years (90% prior to age 2). Incubation 5-15 days |
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Definition
Erythema infectiosum Fifth's Disease, Slapped Cheek Rash
Parovirus B19. Fever and rash. Arthritis in older children. Transmission through respiratory secretions. 4-14 day incubation. Winter,spring epidemics. 60% children 5-15. Fiery red maculopapular rash on cheeks. Palms/soles usually spared. Trunk, neck and buttocks involved. Prevent child from being around pregnant women. |
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Definition
A. Cellulitis after puncture trauma. The forearm is swollen, erythematous, and tender; there is abscess formation. B. Cellulitis arising at the site of a surgical excision: Staphylococcus aureus. Note discharge of pus.
Measure, document, describe (size, shape, color), take picture, check perfusion to distal tips of finger, draw a line if monitoring to see if progressing to necrotizing fasciitis. If you treat with antibiotics use a good broad spectrum gram pos antibiotic |
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Definition
Impetigo
Honey-colored crust. Eval for neuropathic sensation to differentiate from herpes simplex. Often caused by Staph aureus or group A Strep pyogenes. Treat with systemic antibiotics and topics. . Use Cephalexin (Keflex), dicloxacillin (Diclox), TMP/SMZ (Bactrim, Septra), Mupirocin, Gentle debridement of crusts using antibacterial soap and a washcloth |
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Definition
Erythrasma. Well-demarcated reddish-brown patches in the axilla (A) and groin (B). The potassium hydroxide preparations were negative; the Wood's lamp examination showed a bright coral red fluorescence.
Tream with clindamycin in solution IV for 2 weeks. In intertriginous and hair bearing areas. |
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Definition
Lyme Disease rash (Erythema migrans) with tick bite visible
Borrelia burgdorferi. White-tailed deer is "host" to adult tick, white-footed mouse gets spirochete into the host. Spirocetes replicate and migrate after tick bite causing targetoid rings. Correlate geographic area. Deer tick is Lxodes dammini. Can also cause althragias and CNS symptoms. Looks like furnuncle, open punctuate lesion, order titers, use doxycycline, do IND |
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Definition
Rocky Mountain Spotted Fever
Rash on medial aspect of foot and hands. Fever, lethargy, low appetite, elevated wbc count, don't always have rash. Rickettsia rickettsi. Small pink macules that blanch -> deep red papules that do not blanch -> hemorrhagic papules/macules. incubation about 7 days. IFA IgG and IgM anti-rickettsia antibody |
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Definition
Erythema multiforme target lesions
-Idiopathic, can be caused by NSAIDs, anticonvulsants, anti-tubercular drugs, allopurinol, carbamazapine, HSV, VZV, Parapoxvirus, adenovirus, hepatitis, HIV |
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Definition
Toxic Epidermal Necrolysis Syndrome
SJS/TENS-Mucus membranes can be involved. Urethra- burns with urination. After new drug ask are you able to eat, do you ahve sores on lips, does it burn when you pee. Split of skin at dermal/epidermal junction so mortality is much higher.
TENS-Higher percentage body surface involvement than SJS. Desquamation of skin, 90% mortality rate. nNkolsky sign
SJS or TENS
Epidermis splitting from dermis and losing all attachment, can have massive fluid loss and hypotension within hours
-life threatening
-SJS= 5-12% of body surface infolvement
-TENS= >20% body surface involvement (rare to survive)
->100 drugs can cause SJS and TENS
-understand it is a blistering disease, check for Nikolosky sign, if positive get to hospital
-can be caused by sulfa antibiotics (sulfasalazine), allopurinol, tetracyclines, anticonvulsants (carbamazepine, lamotrigine, phenobarbital, phenytoin), NSAIDs, Nevirapine, Thiacetazone
-clinically begins within 8 weeks after onset of drug exposure- fever, headache, rhinitis, myalgias may precede mucocutaneous lesions by 1-3 days
-skin eruption initially symmetric-distributed on face, upper trunk, proximal extremities, rapidly extends to rest of body
-initial skin lesions are erythematous, irregularly shaped, dusky-red to purpuric macules which progressively coalesce into patches that desquamate- the dark center of lesions may blister
-can see targetoid lesions on hands, desquamation, violaceous lesions |
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Term
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Definition
Staphylococcal scalded-skin syndrome
Prior to skin desquamation have sandpaper rash and also involves perioral area. Staph aureus produces an exfoliative exotoxin. Newborns to age 2/6. Endotoxin A&B destroys cell adhesion molecules. Serine proteases bind to cell adhesion molecules. Epidermolysis occurs at the stratum corneum and stratum granulosum |
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Definition
Tinea capitis. alopecia
Itchy scalp with patchy hairloss (not always). Remove 1 hair in the center of patch of alopecia, the bulb of the hair follicle gives the greatest yield
Griseofulvin (Fulvicin PG) (also iatroconizole and lamacil)
-fungistatic (but can effect a cure if used properly in children w tinea capitis)
-effective for dermatophytes
-take w fatty foods for adsorption
-Monitor LFTs and CBC
-treat child for up to 12 weeks and have come back and reculture hair |
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Term
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Definition
Tinea corporis.
Fungal infection of skin on a body (not food, hand or head). Do KOH,m looking for hypae. Looks similar to nummular eczema
Miconazole (Micatin)(Monistat), Econazole(Spectazole), Terbinafine (Lamsil), Naftifine (Naftin) |
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Term
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Definition
| Tinea cruris. Groin Advancing border with satellite lesions, take scraping from advancing edge without satellite lesions. |
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Definition
Tinea pedis, athlete's foot
Mocassin type (along medial aspect of foot). Plantar moccasin type (has maceration between toes. Interdigital type (look between D5 and D4). Vesiculobullous type (secondary to aggresive t-cell response to fungal elements, blisters, bullae) |
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Definition
Tinea mannum and Tinea pedis
Uniformly one hand only. Accentuated skin lines, white scale, majority treated as if hand eczema and treatment hasn’t helped. 2 foot 1 hand disease. Look at the feet, inbetween toes and bottom of feet. Tinnea mannum when just one hand orboth hands |
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Definition
Tinea unguium. Onchomycosis. Fungal element evades keratin of nails. On fingers usually involves all 10 but on foot can be fewer. If on foot first strep is to treat tinea pedis. Topical antifungals can take 12 months to see results. Probiotics can be applied topically. Commonly Dermatophytes and candida.
Ciclopirox Sol (Penlac)- topical antifuncal 5.5-8.5% cure rate
Gisieofulvin for 12-18 months 50% cure rate,, 50% relapse at 1 year
Terbinifine 250 mg daily treat 3 months, safer than Sporonix, rare hepatitis
Itraconazole (Sporonox) can pulse dose 1 week per month, lots of drug interactions/hepatitis risk (oral drug). Dug can be found in nail bed 9months after pt has taken dose
-topical probiotics w good efficacy OTC, less expensive |
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Definition
Tinea Versicolor/Pityriasis
Always oval-shaped. On chest, neck or back. Malassezia furfur. Hypogigmentation. Overgrowth allowed by innate immune system, particularly in hot humid weather, people who do lots of exercise with close fitting clothing. Takes 4-6 weeks to re-pigment. KOH skin scraping- characteristic spaghetti and meatballs, broad hyphae with budding clusters of cells, can be salmon colored
Topical azoles (Miconazole=Micatin, Monistat) effective. Lamsil and other allylamines are not effective
-topical ketoconazole or selenium sulfide lotion- selenium sulfide lotion-leave on for few hours. Ketoconazole shampoo-leave 10-15 min, Exercise
-oral ketoconazole 400mg single dose, repeat in 2-4 weeks
-treat the family (varies)
-sunscreens
-never a cure, can lower fungal element count then encourage UV light exposure but risks w that too |
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Definition
Stevens-Johnson Syndrome
Begins with vesicles that look like target lesions of EM but they crust in the center. See vesicle in middle after erythema forms where fluid ruptures to form a crust. Patient will say their skin hurts. Can be caused by lamictal |
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| Seborrheic keratosis. benign |
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| Acanthosis nigrans. benign |
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Definition
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| Sebaceous hyperplasia. benign |
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| Epidermal inclusion cyst. benign |
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Alopecia Areata
Compare and contrast surrounding skin and hair follicle appearance in this and other pictures. (fungal infections had exclamation point hairs in middle) not fungal bc well circumscribes area w loss of hair follicles. The body has now rec the hair follicle itself as ag and host immune response is destroying the follicle. White functate lesions,smooth on palpation. Immunologically mediated. Growth of hair follicle is antigenic process (viewed as). Can be early sign of other autoimmune diseases |
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Definition
| Nonscarring Alopecia. Male pattern baldness (misnomer). Hairloss is eather scarring or nonscarring alopecia. Only ones nonscaring are those ass w fungal disease or male pattern baldness..receding hair line, patch of hairloss at crown of scalp. Genetically determined. Passed from male offspring from mother’s side of family |
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Definition
Scarring Alopecia
Diff from alopecia areata. More rare. Has scale and solitary patch well circumscribed no exclamation pt hairs, can scrape and KOH, punch biopsy is best though can indicate more severe derm disorders like lichen planopilaris. Can also find perifollicular erythema, patch and hair follicles w surrounding erythema, inflammatory process, never hair that will grow back here again. Clue to other systemic diseses |
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Definition
SLE
SLE, ex of systemic lupus erythemetosous. One sign of SLE, 5 varients, hair loss may or may not be associated w. scarring hair loss. Even treatment for sle w immunosuppressive drugs will not bring ahair back. |
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Definition
Discoid Lupus
perifollicular erythema and hair loss, red patch (indicitave of discoid lupus) that only attacks skin not rest of body like SLE |
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Definition
Trichotillomania
Secondary to the patient themselves or someone else, physically, and using trauma removing hair. Have new hairgrowth coming, not permenant, manifestation of anxiety disorder. Cognitive behavioral therapy and dermatological therapy |
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Definition
Clubbing
Actually a form of nail bed destruction. Occurs bc the vacular system to the nail bed itself is highly, highly vascular and sens to low levels of oxygen, raised area occurs at nail bed bc in response to low oxygen levels in blood, the tissue that forms that nail bed responds to hypoxia by hypertrophying (making itself bigger to try to get more oxygen). Sign of pulmonary diease, usually mesophilioma or any of the interstitial lung diseases |
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Habit-Tic Deformity
Very common. Manifestation of anxiety. The reason the nail plate itself looks like it does with all the riges it bc of repetitive tauma at bottom, unconscious pressing of cuticle repeatedly over time so the nail that grows out is deformed bc the nail plate is forming under the small layer of skin at bottom. Everything that comes out is leftowver dead stuff, keratin attached to nail bed. Damage to nail fold damages subsequent keratin |
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Definition
angioedema (A larger edematous area that involves the dermis and subcutaneous tissue. Person has difficulty breathing and itching.) and urticarial (Transient edematous papules and plaques, usually pruritic and caused by edema of the papillary body)
Causes- something ingested, pressure on skin, psychological stress, physical stress, idiopathic
IgE and IgE receptor dependent, involves mast cell degranulation, for C1-esterase deficiency give C1-esterase IV
Immunological causes: Autoimmune (autoantibodies against FceRI or IgE), IgE dependent (allergic), immune complex (vasculitis), kinin-complement dependent (C1 esterase inhibitor deficiency)(genetic inherited)
Nonimmunologcial causes: Direct mast cell-releasing agents (opiates), vasoactive stimuli (stings), drugs (ASA, NSAIDs, ACE inhibitors, and others)
Treat with epinephrine, Benadryl, sometimes Iv steroids |
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Definition
Cholinergic urticarial
different than dermatographism, comes from exposure of the skin so the epidermis and dermis have to be exposed to vigorous exercise, runners and athletes can get, small urticarial wheels that feel like papules, don’t require treatment, mast cells degranulate in response to something else going on in body but doesn’t progress into angioedema and doesn’t require treatment other than stopping the exercise, |
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Definition
Dermatographism
Most common form of urticarial you will see, Dermatographism, hives that came as a result of someone marking on their skin, sign that someone could be atopic |
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Definition
Urticarial vasculitis
A form of vasculitis that is visualized on the skin surface, requires biopsy and referral to a dermatologist, will not blanche
manifestation of many different systemic diseases, if youwere to palpate these lesions they would feel slightly raised and they would not blanch, fist key it could be vasculitis and not hives |
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| Papule. raised, solid <1cm |
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| Nodule. Raised, solid >1cm |
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Definition
| Purpura. Blood in skin, 2mm |
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Definition
| Plaque. Raised, plateau superficial |
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Definition
| Pustule. Pus filled lump <1cm |
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Definition
| Petechiae. Pin-head purpura |
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Definition
| Crust: Dried exudates of body fluids that may be either yellow ( i.e serous crust) or red ( i.e hemorrhagic crust) |
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Definition
| Scale: Excessive accumulation of stratum corneum. |
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Definition
| Erosion: Loss of epidermis without an associated loss of dermis |
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Definition
| Ulcer: Loss of epidermis and at least a portion of the underlying dermis |
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Definition
| Excoriation: Linear, angular erosions that may be covered by crust and are caused by scratching. |
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Definition
| Atrophy: An acquired loss of substance. In the skin, this may appear as a depression with intact epidermis ( i.e loss of dermal or subcutaneous tissue) or as sites of shiny, delicate, wrinkled lesions ( i.e epidermal atrophy) |
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Definition
| Lichenification: A distinctive thickening of the skin that is characterized by accentuated skin fold markings. |
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| Anatomy and layers of skin |
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Definition
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Term
| Anatomy and components of skin |
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Definition
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Definition
| Shingles. VZV virus remains dormant in dorsal root ganglia of spinal cord where it lives quietly until a trigger that stimulates the acquired immune system to be suppressed (flu, illness, car accident) (lowers normal immune mechanism of skin and causes reactivation and spreading along dermatome/cutaneous part of body where virus was)(lesions begin as in chicken pox then bc virus travels along nerve root get pain like aching /burning dull pain (neuropathic pain) (lesions distributed in a dermatomal pattern) |
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Definition
| Erysipelas. St. anthony's fire. Usually Strep A. Is bright red and has induration (can palpate and feel swelling). Enlarged lymph nodes. Systemic and local inflammatory response. Treat with 1st-generation cephalosporin, TMP/SMZ, Dicloxacillin, Erythromycin. Often need admission and IV antibiotics. Can occur anywhere on body. Often times develops in patients in the hospital. |
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Definition
Candidiasis/Monilla. Satellite lesions at border of patch. Light pink to dark red. No fluorescence with wood's light
Found in intertriginous areas |
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Definition
| Tinea faciei. Face. Take #15 blade and scrape stratum corneum |
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Term
| Fitzpatrick Skin Phototype Classification |
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Definition
-classify based on questions about do you burn, how long does it take
1.white skin, always burns, never tans
2.white skin, always burns, minimal tan
3.white skin, burns minimally, tans moderated and gradually
4. light brown skin, burns minimall, tans well
5.brown skin, rarely burns, tans deeply
6.dark brown/black skin, never burns, tans deply |
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Definition
15 or higher blocks 90% of UV rays, numbers above pick up 2 or 3 % more, more about how often you apply and how completely
Sunscreen: -chemical vs physical blocks
-benefit most effective <25yrs age
-benefits of SS use not seen until 10 years after use |
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Definition
Sun and exposure to UV light
-chronic uv exposure and multiple genetic mutaions
-p53 protects our skin from abnormal cells and this gene is altered w chronic uv exposure |
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Definition
| UV light implicated but have to have the gene that causes the mutation in the melanocyte that gives us melanoma- especially intense short term exposure and burn is implicated |
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Term
| The ugly duckling approach |
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Definition
| Many nevi, do all the lesions look the same? Same color? Do any stand out? Looking for the ugly duckling in the family of nevi (moles) |
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Definition
Asymmetry-shape/color
Border-irregulat/notched
Color-very dark or variegated, blue,black,brown,red,pink,white
Diameter->6mm, or larger than pencil eraser, rapidly changing
Evolving-evolution or change in any of the ABCD features |
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Definition
BCC (cancer of the epidermis)
-most common NMSC in humans
-can develop de nove/spontaneously or in a lesion that was already there
-middle ages, fair skin, M>F w F incidence rising
-intense UV exposure/episodes of burning
-can occur in non-sun-exposed areas
-clinical variants-varied presentations- nodular, superficial, pigmented, morpheaform, others-cystic, basosquamous, fibroepithelioma of pinkus, categorized based on histologic subtypes
-skin type 1-4 more likely to get
-tanning booths has exponentially increased
-will disfigure your skin
superficial (clearing center in some parts but not all)(a totally clearing center would be a tinea)(no hyphae could be exzema)(do biopsy)
-if not 100% sure, biopsy a lesion to rule of BCC
2-noduloulcerative basal cell w pigment (biopsy right infront of ear) nice advancing rolled border w ulcerative center, invading anterior conchi of ear, refer to dermatologist)
3-pigmented BCC lesion uniform in shape and size, punch biopsy not sure if melanoma
4-pearly nodule w telangiectatic border-mostly on face can be most cosmetically disfiguring bc on cheek near nasal labial fold, if this area of face is distorted has large impact on how pt looks
5-inner canthus of eye and lower eyelid, ulcerative center, acrotic in middle, rolled border
6-basal cell- biopsy anywhere in this lesion, adequate to get a quality diagnosis, don’t need a lot of tissue bc all of these lesions would be treated by Mohn micrographic surgery |
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Definition
AK
-precursor of squamous cell carcinoma
-abnormal keratinocytes at the lower portion of the epidermis
-gritty papule w an erythematous base
-yellow-white scale
-rough texture
-visual inspection + palpation
-areas of highest sun exposure: dorsum of hands, scalp, shins, ears, face
-can become hyperkerotolic (thick)
-photodamaged skin->AK->SCC in situ/localized/Bowen’s disease->invasive SCC
-subtypes:hyperkeratotic, pigmented, atrophic, actinic chelitis
-bowen’s disease (SCC in situ)-arise from a preexisting AK, arise de novo, arise from oncogenic strains of HPV, keratinocyte atypia is seen throughout all layers of the epidermis
-bowenoid papulosis- term used when there are histopathologic changes of SCC in situ found within genital warts- secondary to oncogenic strains of HPV-16 and 18
-red rough spots that sting when you rub your hand over them, thickened plaques that look like psoriasis, big thick cutaneous horns
-can be prevented with sunscreen
Treatment:
-consider the number, location, thickness of lesions
-treat the individual lesion, or treat mult AKs in one area
-consultation with a dermatologist to guide therapy may be useful
-liquid nitrogen cryotherapy, topical 5-fluorouracil, topical imiquimod cream
-patients w AKs are at increased risk of developing other nonmelanoma and melanoma skin cancers
-sunscreen use everyday
-UV-blocking clothing
B-AK in center, need to move fingertips over lesion to identify. Pt would say it feels like you’re poking me
C-hyperkeratotic/hypertrophic AK on scalp w many other benign lesions (sebborheic keratosis)
D-diffuse AK on sordum of arm
A-multiple AK on central face, sun-exposed areas from UV radiation before age 25 |
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Term
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Definition
| Squamous can spread inside the body and kill you (basal cell can never progress past the bony plate, will never kill you) |
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Term
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Definition
Keratocanthoma, variation of AK
-well circumscribed, ulcerative border on nose, aggressive form of AK
-need to biopsy and treat
-needs to be referred to dermatologist who does mohs micrographic surgery, biopsying it will destroy the topography of the nose |
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Definition
SCC
-A-looks like patch of eczema
B-looks like patch of eczema or fungal infection
-need to get history of sunscreen exposure, family history, sunscreen use
D-bowen’s disease/localized on finger, person treated for hand eczema, didn’t clear (follow-up apt to check if lesion cleared)
B-be sure to make follow-up apt
D-person who has been treated for AK, causes crusting intense inflamed areas-drug working, once healed skin will be smooth
A-impt to look at oral mucosa and lip line (intense uv exposure) actinic chelitis (on lips/vermillion border), refer to dermatologist |
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Term
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Definition
| Increases as you move closer to equator |
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Term
| Primary functions of the skin |
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Definition
Immunologic function, langerhaans cells are the first step in the innate immune system. Skin also communicates w the acquired immune system
Langerhans cells reside Just above the basal cell layer (first layer). Over course of 28 days these cells differential leading to stratum corneum (what you feel, piece of seran wrap, if hydrated look right thru it into the dermis)
The dermis contains BVs, touch receptors, lymphatics and the subcutaneous tissue is a cushion for the rest of the skin |
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Term
| skin's antimicrobial response |
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Definition
| Defensins, cathelicidins/psoriasin, reactive oxygen intermediates |
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Term
| Skin’s inflammatory response |
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Definition
| Cytokines, chemokines, neuropeptides, eicosanoids |
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Term
| skin's influence on adoptive immune response |
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Definition
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Term
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Definition
| Protecting us from outside agents, self-esteem, psychological makeup, prevents fluid loss, maintains internal homeostasis, protects us from UV radiation |
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Term
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Definition
| what the disease process begins with |
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Term
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Definition
| Most commonly seen in psoriasis also contact dermatitis. The lesion was scratched, production of another psoriatic lesion. Trauma induced replication of the original lesion. |
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Term
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Definition
Benign melanocytic neoplasms
Not a danger to the patient, allow the patient to decide if they want to do anything about them
-describe what you see: size, shape, color’s,location, are there other lesions that look similar?
-clinical decision: observe, document, follow up, refer to dermatologist, biopsy-always do punch biopsy or excisional biopsy (has to go down into subcutaneous tissue- if you remove only part of this dermatologist can’t give a prognosis to the pt) , pigmented lesions require depth for diagnosis
-multiple nevi
-ABCDEs, >6mm?, family history of melanoma, history of burns prior to age 18? Esp burns that blistered. Has mole changed, is it itching |
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Term
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Definition
A-Junctional nevous- melanocytes sitting at the junction of the epidermis and dermis giving the darkly pigmented color, B- compound nevous- raised a little bit when you palpate, brown papule, uniformly brown, has melanocytes not just at the dermal-epidermal junction but also deeper down into the dermis giving the raised appearance, C- intradermal nevous- skin-colored, has nests of melanocytes in there but they’r not as close to the surface, as far up into the keratinocytes as in the other 2 types, no ansymmetry in color, no history of sunburns (all normal)
-in some derm offices will use dermatoscopes to magnify and look for specific characteristics of even normal moles |
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Term
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Definition
Freckles
-small, red or light-brown macules that are promoted by sun exposure and fade during the winter months
-key features of skin-type 1 or 2, can come or go, protective from uv light
-they are usually confined to the face, arms, back
-the number varies from a few spots on the face to hundreds of confluent macules on the face and arms
-they occur as an autosomal dominant trait and are most often found in individuals w fair complexions
-they use of good sunscreen spf 30+ prevents the appearance of new freckles and helps prevent the darkening of existing freckles that typically accompanies sun exposure |
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Term
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Definition
Café au lait macules
-may be associated w neurofibromatosis, tuberous sclerosis, but when there’s only 1 or 2, they’re really normal and of no concern to the pt
-found in 10-20% of the normal population
-usually start to form in infancy or in early childhood |
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Term
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Definition
Becker’s nevus
-hematoma, pt’s don’t like the large discoloration
-can’t do anything except lasers can dec pigmentation
-involves other tissues including CT
-color will still come back after getting rid
-reassure
-more deep (involves dermis and subcutaneous tissues) than café au lait macules |
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Term
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Definition
Halo Nevus
-dermatoscope can be used to see halo
-lesion losing it’s color along periphery
-halo affect during adolescence
-most common in teenagers and most common on back, commonly seen w junctional nevi
-lymphocytes are infiltrating that nevus and they’re destroying the melanocytes to the nevus essentially goes away, but the whole area remains hypopigmented
-dermascopy view, characteristics to determine if nevus becoming melanoma or junctional nevus undergoing evolution and forming a halo |
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Term
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Definition
Solar Lenigines
-brown spots as we age, UV, lentigo (macular, well-circumscribed, brown)
-brown spots on face of adult
-form commonly on arms and dorsum of hands in men and women, but more often women come in
-tell pt they are age spots
-a generation refers to them as liver spots
-from chronic uv exposure |
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Term
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Definition
-Peutz-Jeghers Syndroime
-(inspect for brown macules on lower lip(not a problem but inspect further)—if brown macules on buccal mucosa, tongue, lower and upper eyelids, evert the upper eyelid—refer for eval, will see lesions within facial area but can also be seen in palms of hand) |
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Term
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Definition
Congenital Dermal Menalocytosis/Mongolian spot
-dark bluish brown marks on babies, very common
-usually seen in ppl w Asian descent but not always, not dangerous, resolve in childhood
-nothing more than superficial discoloration
-superficial collection of melanocytes in the dermis that haven’t had a chance to migrate up to the keratinocytes
-normal melanocyte function requires that the melanocyte migrates from the basal layer up to the stratum corneum and as it does that, it gets rid of melanosomes, which is the organelle in the melanocytes that houses the pigment, problem w this coloration, hasn’t had time to deposit melanosomes into epidermis, refelecxtion of light into dermis gives blue color |
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Term
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Definition
Nevus of Ota (Oculodermal Melanocytosis)
-blue-brown unilateral or occasionally bilateral facial patch
-more common in Asians and Blacks
-more dermal dendritic melanocytes than in congenital dermal melanocytosis but less than in blue nevus
-first noted in teenage or young adult years
-melanocytes w greyish blue discoloration bc melanocytes very deep in structural components of the skin
-always unilateral, favors the distribution of the first two branches of the trigeminal nerve
-blue slera
-discoloration comes from an embryologic development where the melanocytes are derived rom the neural crest and then migrat to the leptomeninges, the uveal tract of the eye, and the inner ear, can help understand why some pts get melanoma of the eye (melanocytes deposited there in embryologic development) |
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Term
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Definition
Spitz Nevus
-erythemytous papule, can be flesh-colored
-always seen in children
-in adult would be compound nevi
-dome shaped but not dangerous
-could be juvenile melanoma but no consensus
-should be removed, biopsied and confirmed
-melanocyte deposition near it |
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Term
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Definition
Congenital Melanocytic Nevus
-nevi that are present when child comes out of uterus, was this seen on your newborn exam? Much higher incidence of changing into melanoma (developed after leaving uterus or when in?) |
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Term
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Definition
Nevus Spilus (Speckled Lentiginous Nevus)
-very common
-involves whole discolored lesion, measure all the way across
-solitary areas of increased pigmentation
-melanocytic lesions that don’t’ require intervention but require education and possible referral to a dermatologist |
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Term
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Definition
-malignant tumor that arises from melanocytes- commonly cutaneous in origin, can arise on mucosal surfaces (or underneath tongue, or on soft/hard palate)
-abnormal growth w abnormal genetic material
-can be in genital skin, uveal tract of eye (encourage to see opthamologist)
-hallmarks of cancer: produces growth signals(can be measured in tissue, how much mitotic regeneration is going on, limitless replicative potential, all cancer cells can grow in hypoxic conditions and create their own blood supply-sustained angiogenesis), insensitive to antigrowth signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, invasion of adjacent tissues, metastasis (apply to melanoma)(helps to understand pathology report)
-activation of oncogenes and/or inactivation of tumor-suppressor genes
-complex genetic abberrations, FDA approved drug, advocate that pt get into center where trials are
being done to treat different stages of melanoma
-educate, prevent, screen, biopsy (if melanoma make referral)
-drug targets KIT and BRAF- cytokine-signalling chemicals that are genetically encoded and either the oncogenes produce or the tumor suppressor genes aren’t suppressing any longer. Acral and mucosal are locations of melanoma and genetic studies have shown which signaling molecules found inspecific origin of that melanocyte
-monoclonal ab for treatment of stage 3 melanoma, drug can prolong life and improve survival rates, must be started as soon as possible. Melanoma has complex development. Drug interacts w BRAF and tyrosine kinase receptor and KIT signaling molecule
Host immune response:
-determines how pt shows melanoma and progresses with it, not just genetics and UV light, also immune system
-melanoma is an immunogenic tumor
-host can respond to a melanoma cell: melanoma cells are recognized as an antigen, antigen is processed and presented to the host’s CD8 cytotoxic T cells, if the CD8 T cell recognizes this Ag and if activated, the T cell can kill tumor cells, CD4 helper T cells and Ab’s are also involved
-aggressive immune response, lots of CD8,CD4, T cells-innate immune system
-melanocyte overwhelms innate immune system
-juvenile melanoma in children, not as aggressive as melanoma after 20
-can get at any age in life
-cutaneous melanoma w regression, host’s response causes variation in color
-Risk factors: family history of cutaneous melanoma, lightly pigmented skin, tendency to burn, red hair color, intense intermittent sun exposure, chronic sun exposure, residence in equatorial latitudes, PUVA (Psoralen Ultraviolet Light Treatment- wonderful treatment for psoriasis but increases pt’s risk of developing melanoma), tanning bed use esp under age 35, iatrogenic or acquired immunosuppression (someone this is on drugs for any of the collagen vascular diseases or autoimmune diseases such as Enbrel, Imuran, normal immune system is suppressed so at higher risk of developing melanoma)
-Melanocytic nevi and solar lentigines: increased total number of acquired melanocytic nevi (MN), >100 MN, relative risk ~8-10 fold increased, atypical melanocytic neve (AMN) >5 relative risk ~4-6 fold inc, multiple solar lentigenes (SL) relative risk ~3-4 fold increased, relative risks (RR) are multiplicative-a person w >100 MN +>5 AMN +mult SL has relative risk ~10x5x3, 150-fold
-personal history of cutaneous melanoma, be seen by dermatologist
-types of primary melanoma: superficial spreading melanoma, nodular melanoma, lentigo maligna melanoma, acral lentiginous melanoma(palms of hands, soles of ft), amelanotic melanoma, ocular melanoma(uveal tract in utero), others
Melanoma key concepts
-common and deadly cancer
-physicians should integrate a skin exam into the routine visit
-pt education is crucial component to skin cancer prevention
-if doing a biopsy- punch biopsy or excisional biopsy
-melanoma has high cure rates if diagnosed and treated early
-key prognostic factors for primary tumor: thickness or depth of tumor invasion is the single-most important prognostic factor for survival and clinical management—survival decreases with increasing Breslow’s depth
-immunologically targeted drug: venflurmab?-monoclonal ab, before this only interferon for stage 3 or higher, had to take for 1 year-terribly sick, quality of life poor |
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Term
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Definition
Lentigo Maligna Melanoma
A-solar lentigo on face in sunexposed are but variation/varigation in color- hyperpigmented blue, violaceous areas, form within a lentigo that was just a brown spot but it’s changed
-better prognosis but needs to be treated just as aggresively
-punch biopsy
-B-starting to erode |
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Term
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Definition
Superficial Spreading Melanoma
-most common but also very obvious
2-formed within a preexisting nevi, 10 years ago just a normal nevus, abn melanocyte proliferation-varigated in color >6cm, irregular border
1-began on its own, denovo, scarring from host response trying to deal w abnormal melanocytes
-2 growth phases of melanoma growth, horizontal (better to diagnose here) then vertical |
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Term
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Definition
Melanoma in situ
-localized but can spread
-look closer and can see dark pigment much different than rest of nevi on back (ugly duckling)
-biopsy needs to be deep enough down to subcutaneous tissue so proper prognosis and treatment
-can remove w 6mm punch biopsy |
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Term
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Definition
Acral Letiginous Melanoma
-bad mole on sole of feet
-never should be hyperpigmentation on soles of feet or soles of hand, have to presume it’s melanoma until proven otherwise, can be less obvious than this- press and no blanching, ask if exposed to chemicals w bare feet, try to remove physically or w alcohol wipes, if pigment remains-biopsy, want to catch before get this large |
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Term
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Definition
Amelanotic Melanoma
-morphologic appearance is variable and the clinical appearance of pigment is subtle or often absent
-lesion may be confused w a variety of benign lesions such as psiasis or dermatitis
-may be confused w a variety of malignant lesions- SCC in situ or BCC
-difficult diagnosis to make, important to biopsy when unsure of diagnosis
-melanocyte still the abnormal cell, not controlled by host immune response
-ulceration, irregular border
-punch biopsy
-shave biopsy or saucerization biopsy will destroy prognosis, Breslow’s depth cannot be determined, treatment and staging of illness can never be done |
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Term
| Pt’s w a history of skin cancer |
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Definition
| Need to have a skin examination every 6-12 months and/or referral to a dermatologist |
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Term
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Definition
Atopic Dermatitis
-spans the lifetime
-genetic predisposition to being affected by environmental factors that can affect your skin, upper airways, nasal mucosa, conjunctiva of eyes (epigenetic modifications)
-#1 priority=education
[image]
-itching- sensitization to allergens
-4 associated conditions: eczema, food allergy, asthma, rhinitis ask about family history of these (to find predisposition)
[image]
-Atopic dermatitis: accurate term for a specific genetic predisposition to “eczema” in a specific pattern for life
-eczema “to boil over”-someone who has poison ivy also has, too broad term
-atopic- unusual, wheezing, rashes, runny nose/itching eyes/dennie folds
-they will have an IgE mediated response to environmental sensitisors (dryer sheets, scented lotions ect)
-barrier function of the skin is dysfunctional- you’re skin can’t control water loss as well as someone without atomic dermatitis, best way to do that is w petroleum jelly
-prevent exposure to a lot of UV light, use a physical blocking sunscreen- zinc oxide/titanium oxide (less likely to cause sensitization)
-tell person they might develop eye symptoms or asthma later on in life, education-helps them to control
B-cheek of 3-4 yr old-keratosis pylaris genetically encoded disorder, <1mm lesions, if palpate feel rough sandpaper surface, lesions come and go but in early childhood primarily on cheeks as age, upper lateral aspects of arms and anterior thighs, nasal polyps
-itch is so intense that see excoriations and crusting from repetitive scratching
-3mo-2/3yo itching on face, 5-12/13 mostly antecubital fossa and popliteal fossa
-itch precedes the rash (itching more noxious to brain than pain)- scratch until skin is broken open, feel relief once dermis is broken open- crust and exudate=secondary lesions
-primary treatment goal: treat the itch(oral antihistamine, give at night bc itching is unconscious), then use barrier cream that will enable skin to repair itself (emollients) and topical corticosteroid for inflammation |
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Term
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Definition
-allergic contact dermatitis (ACD)-caused by an ag that elicits a type 4 cell mediated hypersensitivity rxn (t cells). Same distribution as ICD but is secondary to skin exposure to airborne particles that cause the rx-burning poison ivy or poison oak (must have has previous sensitization to get this)
-acute allergic contact dermatitis
-otc cream rxn, bullae, well-demarcated area, massive erythema with visiculation and bullae formation
-treat w topical corticosteroids and avoidant of the chemical
-patch testing to determine what is causing the reaction
-allergic contact dermatitis in periocular area w repetitive exposure to something person has been sensitized to –edema, crusting from secondary excoriations-makeup or eyedrops, topical antibiotic
-nickel dermatitis in person w earings who is sensitive to nickel-jewlery, cosmetics |
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Term
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Definition
-irritant contact dermatitis (ICD)- caused by a substance that will come in contact w skin, doesn’t require sensitization, immediate rxn will be seen as a bilster or patch well demarcated showing where substance hit the skin (ash come in contact w skin)
-varied presentation
-bleeding, vesicular, almost blisters on digits
-1st severe contact dermatitis, 2nd more chronic, less intense, scaling
-seen in ppl who work in construction
-acute exposure to offending agent |
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Term
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Definition
Chronic irritant contact dermatitis
-not cell-mediated allergic rxn, consistent exposure to chemical or water or product, breaking down epidermal barrier function, skin can’t heal
-usually seen on distal tips of fingers
-up close would see small fissures and peeling of skin
-recurrent damaging of the epidermal barrier
-persistent chronic exposure
-chronic exposure to product
-hands are most often involved due to chronic exposure to offending agent
-must ask about exposure to al contactants
-treatment: avoid offending agent/stop exposure, repair epidermal barrier, treat inflammation w topical steroid |
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Term
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Definition
-dermatitis on dorsum of foot
-between D1 and D2- maceration- tale tell sign of eczema |
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Term
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Definition
| face, neck, arms-secondary to volatile chemicals |
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Term
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Definition
| - exposure of chemical + UV = the dermatitis. Limes in margaritas in the Bahamas, lime juice + highly intense UVA = dermatitis (don’t have to be sensitized) |
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Term
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Definition
Seborrheic Dermatitis
-common, look for scale (many types), primarily characterized by redness and scaling, affects all ages, sebaceous glands-scalp, face-posterior auricular, anterior chest wall
-Malassezia furfur? (not direct relationship but antifungal helps)
-genetic predisposition(family history), flares w seasonal changes, males worse than females, improves w topical treatment, exceptions- immunosuppressed patients
-3mo old in diaper period, adolescence/puberty, 50-60 year olds (peak incidence)
-thick micaceous scale, can also be thin
-cradle cap on a child
treatment: remove scales with mineral oil-based product and calm down erythema and inflammation caused by the overactive sebaceous glands by using a topical corticosteroid. Topical antifungal shampoos can help too
-posterior auricular area- involves skin fold areas
-severe form of faxial seborrheic dermatitis, involves nasal-labial fold (area w high conc of sebaceous glands), look closely at where erythema and scaling is
-M.furfur doesn’t play a role w diaper rash age group- treat w topical corticosteroids, beefy red shiny appearance |
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Term
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Definition
Pityriasis Rosea (PR)
-acute exanthematous eruption w scale and unique distribution (if scale associated, termed pityriasis)
-self-limited course +/1 pruritis-over a 6 to 12-week period
-herald plaque/patch (solitary lesion that occurs 2-3 weeks before eruption of rash, usually on neck or trunk)(2-5cm patch that can be thickened from the scale, erythematous w distinctive collarette of scale, inside can be salmon-colored)
-rest of lesions not that big form over 7-10 days and fade slowly
-lines of cleavage (Christmas tree pattern), linear distribution
-seasonal pattern
-associated w reactivations of HHV-6, HHV-7, other vial etiology
-large Harold patch, collarette of scale- collar that goes around the inside of the lesion
-oval salmon colored patches
-treatment:
-spontaneous remission in 6-12 weeks, rare to have recurrence
-oral antihistamines for itch
-topical antipruritic lotions
-topical steroid creams (class 4-7) (improve appearabnce)
-UVB light or natural sunlight can give relief to persistent pruritis
-oral glucocorticoids in some cases
-resolves on its own |
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Term
| Differential diagnosis to consider when looking at Pityriasis Rosea |
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Definition
-Drug eruptions (esp captopril and barbituates)
-secondary syphilis (evaluate w RPR to rule out)
-guttate psoriasis (uniform scale)
ismall plaque parapsoriasis
-erythema migrans w secondary lesions
-erythema multiform
-tinea corporis |
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Term
| Psoriasis lecture details |
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Definition
Pathogenesis:
-genetic predisposition, immune mediated, t cell disorder (CD8 and CD4 T cells, TNF-a and IFN-a) NK cells, systemic
-Environmental triggers: Koebnar phenomenon, psychogenic stress (worrying and scratching), infections (primarily Streptococcus), HIV, hypocalcemia, drugs, alcohol consumption, smoking, obesity, beta blockers, lithium, antimalarial drugs
Types:
-varies by site, morphology is different
Diagnosis:
-PASI score, Cardiff Dermatology Life Quality Index
Joint Disease- destroys the joints at the synovial membrane
30-40% of pts have nonevident joint disease
-if one parent has psoriasis, 8% of offspring have predisposition, if both parents 41% of offspring
Epidemiology: ~1.5-2% of pop in western countries, psoriatic arthritis occurs in 10-25% of patients with cutaneous psoriasis. 22 is peak incidence in adult population. If not managed at 8 will severely affect self-esteem in adolescence
Pathogenesis:
-alternation of the keratinocyte differentiation from 27/28 days to 10/15 days and keratinocytes are made at 28 times the normal rate, too many keratinocytes being produced at the basal layer and differentiating too fast- get plaques
-cytokines interleukin-17 and interleukin-23, TNF-a—immune modulating drugs target these
Diagnosis:
-based on morphology of lesions
-may have 1 or 2 lesions or no lesions just joint destruction, may have entire body surface involved or just parts of the body surface involved
-should also include seborrheic dermatitis in differential if scale on scalp
-plaque tends to occur on extensor surfaces-elbows,knees-but can affect any part of body including periocular area, posterior auricular area, palms and soles of feet, intriginous zones (w/o plaques, beefy red erythematous patch called inverse psoriasis)
-look in all skin folds and intergluteal fossa
-look at scalp and flexural areas of skin, exterior aspects of arms and legs, palms + soles of feet
-assess severity w PASI- psoriasis area and sensitivity index—based on redness, thickness, location of lesions, scaling, for assessing severity and treatment efficacy
-chronic, no cure, treatment is ongoing and varies depending on lifestyle and season
Treatment:
-Vitamin D3 analogs (Dovonex)
-corticosteroids (class 1-3)-need super potent (for no more than 2 weeks at a time. will suppress the hypothalamic pituitary adrenal access after two weeks of use, consider as strong as giving oral corticosteroids. Psoriatic patients should never take oral corticosteroids-side effect of developing pustular psoriasis)(preferably class 1 or 2- stratum corneum may act as a reservoir so corticosteroid will work even after being placed on skin)
-anthralin- messy and difficult
-topical retinoids – acetylene retinoid (Tazarotene)—selectively binds retinoic acid receptor (RAR)-B and RAR-y, decreases epidermal proliferation, inhibits psoriasis-associated differentiation
-pulse therapy for high-potency drugs decreases side effects—ex 2 weeks on, 2 weeks off when using class 1-4 topical corticosteroids. Ex of using 2 modalitites to clear plaque psoriasis- combination therapy w dovonex/ultravate
-use ointement on palms and soles of feet and creams anywhere else, scalp sprays shampoos oil based vehicles (corticosteroids)
-usually don’t use vit d analogs or topical retinoids on own-alter keratinocyte proliferation but don’t do anything for erythema and disfiguration
-see pt back every 2-4 weeks, make sure not overusing topical corticosteroiod, can have tachyphylaxis if topical corticosteroid used longer than it should be- skin develops resistance, will no longer be effective
-photo(chemo)therapy w psorolin -UVB , photochemotherapy w UVA
-methotraxate- oral medication that’s used as well as cyclosporine (systemic side effects, monitor closely)
-systemic retinoids (acitretin)-oral, diff than isotretinoin in follicular disorders, never use in women (stays in body rest of life)
-targeted immune modulators-biologic therapies, 2,000 immune modulators targeting T cells and cytokines (TNF-a, IL-12/13, monoclonal antibodies, TNF inhibitors)
-ongoing research: antagonism of IL17,IL-20, IL-22; oral inhibitors of JAK, protein kinase C, p38 kinase; inhibitors of STAT-3; topical STA-21 ochromycinone |
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Term
| psoriasis vulgaris 2 types |
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Definition
Psoriasis vulgaris
-eruptive, inflammatory type
-chronic stable (plaque) type |
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Term
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Definition
Chronic plaque psoriasis
-classic plaque seen w silvery scale
-assess the lesion and check for pinpoint bleeding
-do KOH and evaluate for any fungal elements
-scrape lesion at advancing edge, scale is going to go onto slide, put potassium hydroxide on it and look closely for hyphae or any of the other elements that are seen in fungal diseases of the skin. If that’s neg and you elicit pinpoint bleeding, that’s a pos auspitz sign-pathomneumonic for a plaque of psoriasis
-numular 1cm erythematous lesions with a silvery scale
-can form on trunk and extensor surfaces
-most common type
-lichen planus has a silvery scale but no auspitz sign and usually not greater than 2-4mm in size |
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Term
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Definition
Plaque psoriasis on scalp
-looks like seborrheic dermatitis
-requires aggressive treatment w topical corticosteroids
-erythema more pronounced than scale
-not cured |
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Term
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Definition
Childhood plaque psoriasis
-usually occurs on scalp or trunk
-lack of white silvery scale
-advancing border
-children’s skin still developing into a unified cutaneous system so the lesions of rapid keratinocyte proliferation and rapid production of keratinocytes are going to look different
-if develop plaque psoriasis at this age, likelihood of having severe psoriasis for rest of life is quite high
-plaque around ear different than seborrheic dermatitis bc SD would be lower in the posterior auricular fossa |
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Term
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Definition
Guttate Psoriasis
-unique form that gives much smaller lesions w much less scale
-commonly in children and young adults
-almost uniformaly secondary to a streptococcal infection
-can draw ab titers to prove recent strep infection
-more salmon colored lesions
-koebner phenomemon possible from scratching-get linear form
-exposure from uv light can cause it to form too |
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Term
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Definition
Palmoplantar Psoriasis
-can be pustular
-scaling much more intense and thicker than tinea pedis or irritant contact dermatitis
-difficult to treat w only topical corticosteroids
-refer to derm or psoriatic center |
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Term
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Definition
Erythrodermic Psoriasis
-determine if drug rxn or psoriasis, refer to dermatologist
-redness always generalized, no discrete plaques |
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Term
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Definition
Pustular Psoriasis
-can be formed from a koebner phenomenon
-immediate referral to dermatologist
-can occur when intralesional steroids are used on plaque psoriasis to improve the appearance |
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Term
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Definition
Nail Psoriasis
-bc psoriasis is systemic can affect the nails
-nail pitting
-look at all of the digits
-if has progressed to more intense rxn to t lymph disease get acxrodermatitis, looks like fungal infection of nails
-look at skin to see if any other manifestations of psoriasis |
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Term
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Definition
Flexural (Inverse) Psoriasis
-beefy red looks like fungal or candida but well demarcated border, also satellite lesions
-always in intrigenous zones
-best treated by dermatologist, danger w corticosteroids |
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Term
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Definition
Psoriatic Arthritis
-where the immunologic drugs geared to treat psoriatic arthritic cannot be done w any topical medications
-looks like fungal infection or cellulitic infection of hands
-but can see plaques here of psoriasis where if this was an infection of the digit, wouldn’t see the dorsum of the hand being involved |
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Term
| Different sites of involvement in psoriatic arthritis and reactive arthritis |
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Definition
[image]
-assess the hand for joint disease and rule out psoriatic arthritis |
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Term
| Psoriasis drug treatment chart |
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Definition
[image]
drug, target, what its made of |
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Term
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Definition
| appearance of small bleeding points after successive layers of scale have been removed from the surface of psoriatic papules or plaques |
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Term
| Drug rxn signs, diagnosis, treatment |
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Definition
-cutaneous signs are inflammatory, generalized, symmetric (except FDE)
-diagnosis: clinical features of rash, morphology, timing of onset of rash
-take picture
-may need a biopsy: punch, refer to dermatologist
-always document the specific drug name and a clear description of the cutaneous reaction |
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Term
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Definition
-occur <1 hr of the last administered dose
-IgE mediated, mast cell degranulation, liberation of massive amnt of cytokines
-urticaria, angioedema, anaphylaxis
-carry an epipen |
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Term
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Definition
-occur >1 hr but usually >6hrs after the start of taking the drug-may even occur weeks after the start of taking the drug
-exanthematous erupitons (look like papulosquamous rash on trunk)
-solid lesions anywhere on body, usually in same place, same color over interval of time
-fixed drug erupitons (FDE), systemic reactions (DISH, SJS,TENS)
-vasculitis (inflammation of inner lining of any blood vessel, primarily arteries)(requires intensive workup)(document supplements, herbals)
-varies in appearance-light brown macule to dark brown/purple lesion
-fixed-might not be able to see on pt when they are asking you about it, pt will look okay just don’t like lesion |
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Term
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Definition
-family history of drug reactions
-history of URI, EBV (mono) (if pt given antibiotic, usually penicillin derivative and have EBV will get rash)(doen’t mean allergic if get rash need special allergy testing to prove)
-remember 7 I’s, Instilled(eye drops, sublingal drops), inhaled(steroids, beta adrenergic inhalers, albuterol not likely to cause bc pure beta agonist), ingested (capsules, tablets, syrup, herbal supplements), inserted(suppositories, vaginally, rectally), injected(IM, sub0Q, IV), incognito(non-traditional mediations/hiding-homeopathic, vitamins, OTC), intermittent (Tylenol, Motrin, Advil, etc)
-create a drug timeline- day of onset of rash is day 0 and work backwards and forwards. Usually the medication starting the rash was started 7-10 days before onset of rash. Repeated exposure will be much shorter |
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Term
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Definition
Exanthematous drug eruption
-most common cutaneous drug eruption (~90%)
-rash that covers lots of body surface
-lesions begin on the trunk and spread centrifugally to the extremities in a symmetric fashion
-erythematous macules and infiltrated papules
-intense itching, fever
-systemic symptoms of malaise, responding to ag and creating plasma proteins (body working overtime and mounting inflammatory response)
-most intense erythema in center, central fugal distribution
-tends to peel/desquamate, stratum corneum will shed off in about 2 weeks (central to periphery)
Treatment
-stop the drug, treat parietus and symptoms of itching w oral antihistamines and sometimes topical corticosteroids |
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Definition
Fixed drug eruptions
-often affects the mouth, genitalia, face, and acral areas
-might see bullae, check for nekolsky sign to make sure not SJS or TENS
-lesions usually resolve over a few days or weeks after drug is discontinued
-3 types: hand most common, genitalia area can also be affects
-mucus membrane involvement at the urethra and different types- squamous cell and columnar cells meet at junction-get erosions
-hand picture-reaction to acetaminophen
-genitalia picture-reaction to doxycycline
-body lesion-reaction to Bactrim (not sure if EM, TENS, SJS- check for N sign, complete skin exam |
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Term
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with systemic involvement |
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Definition
drug-induced hypersensitivity syndrome (DIHS)
-any skin eruption w systemic symptoms: fever, malaise, lymphadenopathy, facial swelling, systemic signs of inflammation
-rash: macular exanthema, erythematous centrofacial swelling
-caused by many drugs: allopurinol, antibiotics(sulfonamide, penicillin, minocycline, metronidazole), anti-TB(isoniazid), anticonvulsants(phenytoin, carbamazepine, lamotrigine), NSAIDS(sulindac, diclofenac, meloxicam), anti-HIV(abacavir)
-medical history
-complete skin exam-eval for blistering lesions, check for Nikolsky sing
-CBC, LFTs, BUN- this drug rxn will target bone marrow, liver and kidney
->70% of patients have an eosinophilia (allergic rz)
-consult dermatology |
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