Dermatology Flashcards
Long term use of immunomodulator meds increases the risk of developing?
Lymphoma
Atopic dermatitis (eczema)
chronic inflammatory skin condition that starts in infancy and persists into adulthood. characterized by puritis leading to lichenification.
Atopic triad
asthma, eczema, allergic rhinitis
Patients with eczema are at increased risk for?
2ndary infections with staph aureus and viral HSV or molluscum due to itch/scratch cycles
Triggers for eczema?
climate, food, stress, skin irritants, allergens
Manifestation of eczema in
Infants: Children: Adults:
Infants: red, edematous, weeping, puritic papules and plaques on face, scalp, extensor surfaces (diaper usually spared)
Children: dry, scaly, pruritic, excoriated papules/plaques in flexural areas and neck
Adults: lichenification and dry, fissured skin in flexural areas. hand or eyelids too
How to diagnose eczema?
Clinical.
KOH prep can help distinguish eczema from tinea
Eosinophilia and IgE may be seen in some patients with eczema but not used to diagnose
Treatment for Eczema
Topical corticosteroids- 1st line (use intermittently to avoid skin atrophy)
Other pharm therapy to treat eczema and avoid steroids?
Immunomodulators- Tacrolimus
Erythema toxicum neonatorum
begins 1-3 days after delivery and resembles eczema, presenting with red papules, pustules, vesicles with surrounding erythematous halos. Eosinophils present in the pustules or vesicles.
Treatment for erythema toxicum neonatorum?
Bening. usually resolves in 1-2 weeks without treatment.
Contact dermatitis
Type IV hypersensitivity reaction. results from contact with an allergen that patient has previously been exposed to (nickel, poison ivy, perfume/deodorant, neomycin)
Contact dermatitis description
“linear” “angular”
can spread over body if hands spread it or via transfer via circulating T lymphocytes.
Is latex a contact dermatitis reaction?
NO- type 1!
Type I hypersensitivity reaction
Mechanism
Antigen cross-links IgE on presented mast cell and basophils triggering release of vasoactive amines (histamine). develops rapidly due to preformed antibody.
What types of hypersensitivy reactions are antibody mediated
I, II, III
Asthma is what type of hypersensitivity reaction?
Type I
Type II hypersensitivity reaction
IgM and IgG bind to antigen on enemy cell- lead to lysis by complement or phagocytosis -> leading to MAC
goodpasture syndrome is a ___ hypersensitivity reaction?
Type II
Rheumatic fever is ___ hypersensitivity rxn?
type II
Autoimmune hemolytic anemia, erythroblastosis fetalis are type ____ hypersensitivity rxn?
II
Type III hypersens rxn
antigen/antibody complexes activate complement. complement attracts PMNs which release lysosomal enzymes.
What is an immune complex?
Antigen-antibody-complement
Glomerulonephritides and vasculitides are often type ____ hypersens rxn?
Type III
Arthus reaction
Type III: local reaction to antigen by preformed antibodies (vascular necrosis and thrombosis)
when might an arthus reaction occur?
rarely 4-12 hours post vaccination
hypersensitivity pnemonitis is what type of hypersensitivity reaction?
Type III (Arthus reaction)
Serum sickness
antibodies to foreign proteins are produced in 5 days. Immune complexes form and deposit in membranes- lead to tissue damage by fixing to complement.
Ex: drug reaction
type IV hypersensitivity
Delayed cell mediated. sensitized T lymphocytes encounter antigen, release lymphokines and lead to macrophage activation
TB skin test is what type hypersens rxn?
Type IV
transplant rejection is what type hypersens?
type IV
How do you diagnose contact dermatitis
Patch testing (after acute phase eruption is treated)
Treatment
topical corticosteroid and allergen avoidance (systemic corticosteroid in severe cases)
Seborrheic dermatitis
common. chronic inflammatory skin disease caused by hypersensitivity to (Malassezia furfur, a generally harmless yeast found in sebum and hair follicles)
Malassezia furfur
yeast found in sebum, hair follicles, around sebaceous glands- can lead to seborrheic dermatitis reaction
Presentation of seborrheic dermatitis
Infants:
Children/Adults:
Infants: severe, red diaper rash with yellow scale, erosions, blisters. scaling and crusting (cradle cap) on scalp
children/adult: red, scaly, patches seen around ears, eyebrows, nasolabial fold, midchest, scalp.
Who is at higher risk for severe seborrheic dermatitis?
HIV/AIDS and Parkinson disease patients
Diagnosis of seborrheic dermatitis?
clinical
Treatment of seborrheic dermatitis?
Selenium sulfide or Zinc Pyrithione shampoo
Topical antifungal (ketoconazole cream) or topical corticosteroid for other areas.
Stasis dermatitis
Lower extremitity dermatitis due to venous hypertension (forcing blood from deep to superficial venous system)
Venous htn is often a result of?
Venous valve incompetence or flow obstruction
Where does stasis dermatitis usually occur?
medial ankle. stasis ulcers may develop
treatment for stasis dermatitis?
leg elevation, compression stockings, emollients, topical steroid
Eczema herpeticum
medical emergency. grouped vesicles. emergency due to propensity for systemic spread- potentially to brain.
treatment for eczema herpeticum?
IV acyclovir
A rash involving extensor surfaces think?
psoriasis
Flexor surface rash think?
atopic dermatitis (unless infant- located on extensor)
Psoriasis
T-cell mediated inflammatory dermatosis characterized by erythematous plaques with silver scale (dermal inflammation and epidermal hyperplasia)
Koebner phenomenon
lesions of psoriasis can be provoked by local irritation or trauma
What medications may worsen psoriatic lesons?
B-blockers, lithium, Ace-Inh
finding is psoriatic arthritis
small joints in hands and feet affected. “sausage digits” and pencil in cup on xray
Diagnosis of psoriasis
Clinical. Biopsy if diagnosis uncertain.
Auspitz sign?
Pinpoint bleeding when scale of psoriasis is scraped
histology for psoriasis shows?
thickened epidermis, elongated rete ridges, absent granular cell layer, preservation of nuclei in stratum corneum (parakeratosis), neutrophil infiltrate in stratum corneum (munro microabscess)
parakeratosis
nuclei in stratum corneum in psoriasis
munro microabscess
neutrophil infiltrate in stratum corneum in psoriasis (sterile)
Treatment for psoriasis
Topical steroids
Calcipotriene (Vit D)
Tazarotene (Vit A)
If you have severe psoriasis or psoriatic arthritis treat with?
Methotrexate or anti-TNF biologics
UV light therapy can also be used for patients with lots of skin involvement
Urticaria (hives)
Result from release of histamine and prostaglandins from mast cells in type I hypersensitivity response
Dermal edema
urticaria/ wheals
Most common cause of chronic urticaria
idiopathic
Treatment for urticaria?
Systemic antihistamines
treatment for anaphylaxis?
epinephrine, antihistamine, IV fluid, airway maintenance
morbilliform rash should make you think of
drug reaction
Patients with drug reactions often have what on histology?
eosinophilia
When do drug reactions usually take place?
7-14 days after starting a new drug
IF a patient reacts within 1-2 days of starting a new drug is it likely the causative agent?
NO
Extreme complications of drug eruptions include?
Erythroderma, SJS, TEN
erythroderma
intense, wide spread reddening of the skin with exfoliation
treatment for drug reaction
stop drug. antihistamines for symptoms. topical steroids for itching if needed
Erythema multiforme
Cutaneous reaction with targetoid lesions that have many triggers (often recurrent)
Presentation of erythema multiforme
Lesions start as erythematous macules that become centrally clear and develop a blister. may have systemic symptoms (fever, myalgias, arthralgias, HA)
What characteristic part of body is often affected with erythema multiforme?
PALMS AND SOLES
Erythema multiforme major involves?
mucous membranes
Nikolsky sign
Push on rash and it exfoliates
Nikolsky (+) or (-) in EM, SJS, TEN?
EM: (-) SJS: (+) TEN: (+)
Treatment of erythema multiforme
symptomatic treatment (systemic corticosteroids have no benefit)
SJS and TEN
2 diff points on spectrum of life-threatening exfoliative mucocutaneous diseases often caused by drug induced immune reaction
Epidermal separation of SJS involve < ___ % of body surface area whereas TEN involves > _____ % of BSA.
SJS < 10%
TEN > 30%
Common drugs that may cause SJS/TEN
Sulfa, penicillins, seizure meds, quinolones, cephalosporins, steroid, NSAIDs
Diagnosis of SJS
Biopsy: degeneration of basal layer of epidermis
Diagnosis of TEN
Full-thickness eosinophilic epidermal necrosis
With (+) Nikolsky sign, what should be on differential?
SJS, TEN, SSSS, graft vs. host (after bone marrow transplant), radiation therapy, burns)
SSSS is usually seen in? etiology?
kids < 6 (infectious etiology)
SJS/TEN usually seen in? etiology?
adults, drugs
Treatment of SJS/TEN
early diagnosis. discontinue drug
cover skin, manage fluids and electrolytes like you would for burn victim
Erythema nodosum
panniculitis process of subcu adipose tissue caused by infection wth strep, coccidiodes, yersinia, TB, drug rxns (sulfa, abx, OCPs) and chronic inflammatory diseases (sarcoid, crohn, ulcerative colitis, behcet)
panniculitis
process of subcu adipose tissue
erythema nodosum presents as?
painful, red nodules on anterior shins. slowly spread- turning brown or gray. Present with fever and joint pain
Patients with erythema nodosum may have what false (+) test
VDRL
Work up for erythema nodosum?
ASO, PPD in high risk patients, CXR (sarcoid), IBD work up?
Treatment for erythema nodosum?
underlying disease. cool compress, NSAID, potassium iodide
BULLOUS PEMPHIGOID location of blisters: autoantibodies: blister appearance: nikolsky sign: mucosal involvement: patient age: med triggers: mortality: diagnosis: treatment:
location: basement membrane zone
autoantibodies: hemidesmosomes
appearance: firm, stable blisters, can be preceded by urticaria
Nikolsky: (-)
Mucosal involve: no rarely
Patient age: > 60
Trigger: idiopathic
Mortality: rare, and milder course
Diagnosis: clinical. skin biopsy with direct immunoflorecense is best test or ELISA
Treatment: prednisone
PEMPHIGOUS VULGARIS location of blisters: autoantibodies: blister appearance: nikolsky sign: mucosal involvement: patient age: med triggers: mortality: diagnosis: treatment:
location of blisters: intraepidermal
autoantibodies: desmoglein (keratinocye adhesion)
blister appearance: erosion more common bcz no keratinocyte adherence
nikolsky sign: +
mucosal involvement: common
patient age: 40-60
med triggers: ACE-in, penicillamine, phenobarb, penicillin
mortality: possible
diagnosis: clinical. skin biopsy with direct immunoflorecense is best test or ELISA
treatment: high dose therapy or immunomodulators
HSV1 vs HSV2
HSV1- oral-labial
HSV2- genital
Recurrent HSV-1 often triggered by?
sun and fever
Diagnosis
Clinical. Viral culture of lesion is most accurate test.
Positive Tzanck smear will show?
Multinucleated giant cells
If no multinucleated giant cells on Tzanck smear is it herpes?
NO
Treatment of herpes in immunocompromised patient
need to start antiviral (acyclovir, famciclovir, valacyclovir) within 72 hours of start of outbreak
Treatment for herpes if severe frequent recurrences- more than 6 outbreaks/year?
Daily prophylaxis with acyclovir, famciclovir, valacyclovir
Symptomatic HSV lasting > 1 month can be a sign of
AIDS defining illness
In adults, varicella zoster infections can be more severe and have associated systemic complications like
pneumonia and encephalitis
Treatment for varicella in kids?
self-limited
Treatment for varicella in adults?
acyclovir
pain control for adults with varicella?
neuropathic agents: gabapentin. TCAs
If immunocompromised, pregnant or newborn is exposed to varicella zoster how do you treat?
WIthin 10 days they should be given varicella immunoglobulin
Immunocompetent adults should receive a varicella vaccine within ____ days of exposure?
5
If you see giant molluscum contagiosum think:
HIV and decreased cellular immunity
Molloscum is spread by?
direct skin to skin contact
Diagnosis of molluscum
clinical. best test is large inclusions (molluscum bodies) seen under microscope
What subtypes of HPV lead to squamous malignancies?
16 and 18
Spread of HPV is by?
direct contact
Condyloma accuminatum - genital warts are caused by HPV subtypes
6,11
How do you visualize mucosal HPV lesions?
acetic acid
most accurate test to diagnose HPV?
PCR
Bullous impetigo is almost always caused by?
staph aureus
Impetigo affects what skin layers?
Epidermis
Cellulitis affects what skin layers?
Dermis and subcu fat
Erysipelas affects what skin layers
dermis
Nec fasc affeccts what skin layers
subcu and fascia and muscle
Rash of salmonella typhi
small pink papules on trunk “rose spots” in groups of 10-20
For chronic carrier state of salmonella typhi what operation should be considered?
cholecystectomy
Treatment for impetigo
mild:
severe non-MRSA
severe MRSA likely
mild: mupirocin topical
severe non MRSA: cephalexin, dicloxacillin, erythromycin
severe MRSA: TMP-SMX, clinda, doxy
Erysipelas
typically raised, indurated, well demarcated area confined to dermis and typically caused by strep
Treatment for cellulitis
5-10 days of oral antibiotics. IV antibiotics if evidence of systemic tox, comorbid conditions, DM, extremes of age, hand or orbital involvement
Nec Fasc
Mixed infection of anaerobic and aerobic bacteria that includes S. aureus, E.coli, C.perfringens
Presentation of nec fasc
erythema quickly spreads over course of hours to days and skin becomes dusky or purple leading to necrosis
physical exam signs suggesting nec fasc
gas production, crepitus, putrid discharge, bullae, severe pain
Treatment
immediate surgery and debridement and broad spectrum antibiotics (penicillin G is drug of choice for strep)
Why is clindamycin helpful in nec fasc
used to decrease toxin production by bacteria
for anaerobic coverage for nec fasc use?
metronidazole or 3rd gen cephalosporin
Ludwig angina
bilateral cellulitis of submental, submaxillary, sublingual spaces that results from an infected tooth.
How does ludwig angina present?
dysphagia, drooling, fever, red, warm mouth and can lead to death from asphyxiation
Does erythromycin cause photosensitivity?
No! Its doxy and tetra
Treatment for superficial folliculitis?
mupirocin
Treatment for more severe folliculitis?
cephalexin, cloxacillin and clinda if MRSA is suspected
Most effective treatment for comedonal (black head) acne
Topical retinoid cream
What kills p.acnes?
Topical benzoyl peroxide
If retinoids and benzoyl peroxide are inadequate, what can you use for comedonal black head acne?
topical clindamycin or erythromycin
General progression of pharmacotherapy for acne treatment?
topical benzoyl peroxide/retinoid/antibiotic/oral antibiotic/oral isoretinoin
isoretinoin (oral) contraindications
teratogen
elevates LFTs
patients require periodic blood tests to check LFTs, cholesterol, triglycerides
Pilonidal cysts
abscesses in the sacrococcygeal region. starts as folliculitis then becomes infected with perineal microbes like bacteroides (most common in 20-40 year old men)
Pilonidal cysts can develop into?
perianal fistulas
Risk factors for pilonidal cyst?
deep and hairy natal clefts, obesity, sedentary lifestyle
Treatment for pilonidal cyst?
Incision and drainage and sterile packing of wound
Tinea versicolor
Caused by malassezia furfur- yeast that is part of normal skin flora (humid conditions and oily skin can make organism pathogenic
risk factors for tinea versicolor
cushing syndrome. immunosuppression
presentation of tinea versicolor
small scaly patches of varying color on chest or back. patches can be hypopigmented or hyperpigmented
Diagnosis
clinical. best test is KOH prep of scale revealing “spaghetti and meatball” (hyphea and spores)
Treatment for tinea versicolor
ketoconazole cream or selenium sulfide cream
Candidiasis presents in what areas?
moist areas like groin, skin folds, vagina, below breast
Oral thrush is common in infancy?
What is it a sign of in adults?
Yes common in infants!
Sign of immunocompromise in adults
Oral candidiasis presents as
painless white plaques that can be easily scraped off
Candidiasis of the skin
erythematous patches with occasional erosions and satellite lesions often seen in skin folds and diapers of infants
Diagnosis of candida?
clinical. KOH- candidal spores and psuedohyphea. Best test is fungal culture
Treatment for oral candidiasis
oral fluconazole tablets
nystatin swish and swallow
clotrimazole
treatment for superficial skin candidiasis
topical antifungal
treatment for candidiasis diaper rash
topical nystatin
Dermatophyte infections occur only in
cells with keratin (skin, hair, nails)
Causative dermatophyte organisms
trichophyton, microsporum, epidermophyton
Risk factors for dermatophyte infection
DM, decrease peripheral circulation, immune compromise, chronic maceration of skin (athletic activity)
Types of dermatophyte infections
tinea corporus, tinea pedis/manuum, tinea cruris, tinea capitis
tinea corporis
scaly, pruritic eruption with sharp irregular border and with central clearing (ringworm like rash)
tinea pedis/manuum
chronic interdigital scaling with erosions between toes or as thickened scaly skin on soles of feet and involvement of 1 hand is typical in 1 hand/2 feet syndrome
tinea cruris
jock itch. typically spares scrotum.
tinea capitis
fungal scalp infection causing scaling and hair loss.
keroin
large inflammatory, boggy mass caused by tinea capitis
Diagnosis of tinea
clinical. Best initial test: KOH showing hyphea. Most accurate. fungal culture
Treatment of tinea?
Exception?
topical antifungal. escalate to oral if infection is widespread.
Tinea capitis must be treated with oral medications to penetrate into hair follicles.
Pubic lice bites often turn what color? why?
blue. contain anticoagulant in their saliva.
Treatment of head lice:
topical permethrin. pyrethin. benzoyl alcohol. mechanical removal
body lice treatment
wash body, clothes, bedding. rarely may need topical permethrin
pubic lice
permethrin, pyrethin, benzoyl alcohol, mechanical removal
can scabies be seen with naked eye?
no
diagnosis of scabies.?
history of itching in several family members is suggestive
treatment of scabies
5% permethrin from neck down. (head to toe in infants) and contacts should be treated as well.
Ivermectin can also be used
clothing and bedding should be thoroughly washed
3 types of gangrene
Dry, wet, gas
dry gangrene
due to insufficient blood flow to tissue- typically from atherosclerosis. early signs are dull ache, cold, pallor. necrosis sets in and tissue becomes blue/black
(DM, vasculopathy, smoking are risk factors)
wet gangrene
bacterial infection with skin flora. tissue appears bruised, swollen, blistered with pus
gas gangrene
c.perfringes infection (med emergency!)
associated with dirty wounds contaminated with dirt or fecal matter
subcu injection of black tar heroin is a risk factor for?
gas gangrene
Skin finding for paraneoplastic sign of GI adenocarcinoma
Acanthosis nigricans
lichen planus 6 P’s
planar, purple, polygonal, pruritic, papules, plaques
What drugs can induce lichen planus?
thiazide, quinolone, b-blocker
lichen planus is associated with what infection?
HCV
Wickham striae
lacy white lines present on lichen planus lesions
Koebner phenom
lesions that appear at site of trauma (can occur in lichen planus)
Treatment of mild lichen planus
topical corticosteroids
Rosacea
chronic disorder of pilosebaceous units without a clear etiology
Central facial erythema with telangiectasias is an early sign of?
rosacea
rhinophyma
longstanding facial rosacea can lead to severe overgrowth of nasal connective tissue
Treatment for rosacea
topical metronidazole
for severe or ocular disease- oral doxycycline
How can you differentiate pityriasis rosea from 2ndary syphillus?
pityriasis spares palms and soles
Pityriasis roseA
acute dermatitis reaction best hypothesized to result from viral infection with human herpesvirus
herald patch
initial lesion of pityriasis rosea. erythematous with peripheral scale.
differential for pityriasis
secondary syphilis. tinea corporis.
Treatment of pityriasis rosea
heals in 6-8 weeks without treatment. skin lube, antipruritics, antihistamine for symptoms
Vitiligo often presents on?
hands, face, genitals
treat vitiligo with?
topical steroids, tacrolimus ointment, UV and laser therapy
eyelid lesions types
xanthelasma, hordeolum, chalazion
xanthelasma
soft, yellow plaques on medial aspects of eyelids associated with hyperlipidemia and primary biliary cirrhosis
hordeolum
painful acute eyelid gland infection (stye) (usually staph aureus located on edge of lid)
Chalazion
painless cyst due to blocked eyelid gland
Seborrheic keratosis
very common skin tumor that appears in almost all people after age 40. no malignant potential.
presentation of seborrheic keratosis
exophytic, waxy brown papule and plaque with superficial keratin cysts. “stuck on appearance”
Treatment
cryotherapy, shave excision, currettage. Some may appear similar to melanoma so biopsy may be needed
Actinic keratosis
flat areas of erythema and scale caused by exposure to sun. need to be treated to prevent transformation into squamous cell carcinoma
Treatment actinic keratosis
cryosurgery, topical 5-FU, topical imiquimod
Cutaneous squamous cell carcinoma
2nd most common skin cancer. sun exposure most common cause. chemical carcinogens, radiation therapy, burns or trauma (draining infection sinuses in osteomyolitis), chronic immunosuppression (transplant recipient) all dispose patients to SCC
Presentation of SCC
erythematous, ulcerated, papule or nodule
Marjolins ulcer
type of rare SCC that arises in sites of scars, burns, ulcers
Arsenic exposure
rare cause of multiple SCC in palmoplantar distribution
SCCs that rise from actinic keratosis are more or less likely to metastasize than those on lips and those that form ulcers?
less likely if from actinic keratosis
Diagnosis
confirm with shave biopsy
Treatment of SCC
surgical excision. Mohs surgery (very thin slices excised and examined). lesions with high metastatic potential may need radiation or chemo.
basal cell carcinoma
most common malignant skin cancer. slow growing and locally destructive but has VIRTUALLY NO METASTATIC POTENTIAL.
inherited basal cell nevus syndrome
multiple BCCs appearing early in life and on non-sun exposed areas
Melanoma
most common life threatening derm disease.
Risk factors for melanoma
fair skin, tendency to burn, intense burst of sun exposure (especially in childhood and with intermittent exposure), presence of large congenital melanocytic nevi, increased number of nevi or dysplastic nevi. Immunosuppression increases risk.
FAM-M syndrome
familial atypical mole and melanoma syndrome (inherited predisposition to melanoma)
ABCDEs of melanoma
asymmetric, irregular border, color variation, diameter >6, evolution (change)
Diagnosis
excisional biopsy on any suspiciuos lesionq
itching in a changing skin lesion is suspicious for?
malignancy
Staging of malignant melanomas?
Breslow thickness (depth of invasion in millimeters) and by tumor-node-metastasis (TNM)
poor prognostic sign for melanoma?
ulceration
Name the 5 types of melanoma
- superficial spreading
- nodular
- acral lentiginous
- lentigo maligna
- amelonotic
superficial spreading melanoma
60% of all. Can occur at any age. most common in young adults. presents on trunk in men. legs in women. Prolonged horizontal growth allows for early diagnosis when still confined to epidermis
Nodular
Lesions have rapid vertical growth phase and appear as fast growing red-brown nodules with ulcerations
acral lentiginous
begins on palms, soles, nail beds as slowly spreading pigmented patch. most common in asian and black
lentigo meligna
arises in a solar lentigo. common on sun damaged areas of face
amelanotic
lesion without clinical pigmentation. difficult to identify. can be further classified into any above type
Patients with early melanoma are at high or low risk of recurrence? high or low risk of subsequent melanomas?
low risk of recurrence.
high risk of subsequent melanomas.
What bacterial infection can mimic kaposi sarcoma?
bacillary angiomatosis caused by bartonella henselae.
how do you treat bacillary angiomatosis?
erythromycin
Treatment for Kaposi’s?
HAART therapy if HIV. small local lesions can be treated with radiation or cryotherapy. Systemic spread to GI tract or lung requires systemic chemo.
Mycosis fungoides
slow progressive neoplastic proliferation of T cells. More common in men.
Presentation of mycosis fungoides?
non-specific psoriatic appearing plaques or patches that are itchy and on trunk and butt. later lesions are skin tumors with palpable lymph nodes.
Sezary syndrome
Leukemic phase of cutaneous T-cell lymphoma characterized by circulating sezary cells in peripheral blood- erythroderma and lymphadenopathy
Diagnosis of mucosis fungoides
clinical features, histology, sezary cells on microscopy (ceribriform lymphocytes)
treatment for mycosis fungoides
phototherapy. electron beam radiation.
cherry angiomas (hemangiomas)
small, vascular, red papule that appear anywhere on body. most common benign vascular tumor. no treatment needed.
Immediately after a burn injury, what organisms predominate?
Gram positive
S.aureus
After more than 5 days, which organisms predominate in wound infections?
gram negative or Fungi
Pseudomonas, Candida
Who is at highest risk of a wound infection after a burn?
patients with >20% surface area burns
What is the first sign of burn wound infection?
change in appearance- partial thickness burns turn into full thickness injury or wound loses loss of viable skin graft
Burn wound sepsis findings for vital signs
temp <36.5 (97.7), >39 (102.2)
Progressive tachy >90
Progressive tachypnea >30
Refractory hypotension <90 systolic
In burn patients oliguria, unexplained hyperglycemia, thrombocytopenia, mental status changes are concern for?
wound infection
how do you diagnose wound infection in burn patients
quantitative wound culture and biopsy for histopathology
Treatment for burn infections?
empiric broad spectrum antibiotics IV (Pip/tazo, carbapenem) with possible Vanc for MRSA coverage or an aminoglycoside for multidrug resistant pseudomonas
delayed neuropsychiatric syndrome
carbon monoxide poisoning due to fire exposure can lead to mental status change
why does metabolic rate increase after large surface area burns?
release of inflammatory mediators
signs of increased metabolic rate with surface area burns?
increased temp to 38.5 (101.3), tachycardia, tachypnea, hyperglycemia
Signs of deliberate burn injury and child abuse?
Linear demarcation with no splash marks, extensive burns to back and butt with sparing of flexural creases (due to dipping in boiling water)
Compare erysipelas vs cellulitis
erysipelas: superficial dermis, raised and sharply demarcated edges, rapid spread, fever early in course
cellulitis: deep dermis and subcu fat, flat edges poor demarcation, slow spreading, fever later in course
Tinea corporis (ringworm) risk factors, presentation, treatment
Risk factors: athletes who have skin-to-skin contact, humid environment, contact with infected animals (rodents)
Presentation: scaly, red, itchy patch with centrifugal spread and later central clearing with a raised annular border
treatment: topical antifungal (clotrimazole, terbinafine) oral antifungals (terbinafine, griseofulvin)
nummular eczema
presentation
treatment
red, itchy patch with some scale. can be confused with tinea corporis
treatment- topical corticosteroid and moisture
Porphyria cutanea tarda presentation
blisters, bullae, scarring, hypo/hyperpigmentation on sun-exposed skin (back of hands, forearms, face)
scarring and calcifications like with scleroderma
Conditions associated with porphyria cutanea tarda
Hep C HIV Excessive alcohol Estrogen use Smoking
Testing for porphyria cutanea tarda diagnosis
elevated liver enzymes and iron overload
elevated plasma or urine porphyrin
porphyria cutanea tarda leads to photosensitivity due to accumulation of?
porphyrinogens that react with oxygen by UV light
porphyria cutanea tarda is due to deficiency of
uroporphyrinogen decarboxylase
Treatment for porphyria cutanea tarda
Phlebotomy or hydroxychloroquine
Allergen induced delayed type hypersensitivity
contact dermatitis
bacterial invasion of superficial skin infection
impetigo
subepidermal anti-transglutaminase IgA autoantibody?
Dermatitis herpetiformis (autoimmune reaction triggered by dietary gluten)
vasculitis due to cryoglobulin immune complexes
mixed cryoglobulinemia
(associated with hep C)
palpable purpura, arthralgias, glomerulonephritis
cherry angiomas (hemangiomas) are also known as
senile hemangiomas
cavernous hemangiomas
dilated vascular spaces with thin-walled endothelial cells. present as soft, blue, compressible masses growing up to a few cm. appear on skin, mucosa, deep tissues, viscera
cavernous hemangiomas of brain and viscera are associated with?
Von Hippel-Lindau disease
spider angiomas
bright red arterioles surrounding by outwardly radiating vessels. they blanch with pressure. blanch with pressure. estrogen dependent and seen in preg, OCP use, and cirrhosis related hyperestrogenemia
strawberry (infantile) hemangiomas
appear during first weeks of life. grow rapidy and then regress spontaneously by 5-8
SCC typically present as
enlarging nodule in sun exposed areas with thick rough skin surface or ulceration
Is it typical for SCC to cause numbness and paresthesias
Yes- can invade perineural area early
Seborrheic dermatitis
common inflammatory disease that affects the scalp (dandruff), face (eyebrow, nasolabial folds, external ear, chest and intertriginous areas.
What disorders can seborrheic dermatitis be associated with?
Parkinson disease
HIV
itchy red plaques with fine, loose, yellow greasy looking scale?
seborrheic dermatitis!
Treatment for seborrheic dermatitis?
topical antifungals
dermatofibroma
fibroblast proliferation causes isolated or multiple lesions- most commonly on lower extremities.
lesions are non-tender and can be triggered by trauma in area or insect bite.
“dimple or buttonhole” sign
dermatofibroma with a firm fibrous component that may cause dimpling in the center when its pinched
Treatment of dermatofibroma
cryosurgery or shave excision
pyogenic granuloma
benign vascular skin tumor that presents as small red papule and grows rapidly over weeks-months to a pedunculated or sessile shiny mass. most commonly occur on lip or oral mucosa and can bleed with minor trauma
skin infection caused by poxvirus?
molluscum contagiosum
treatment for molluscum
its self limited and lesions usually resolve in 6-12 months
SSSS
caused by exfoliative toxin-producing strains of S.aureus
why are cultures from bullae in SSSS usually sterile?
because its a toxin mediated process
HSV is the most common infectious agent associated with what acute-self limited skin eruption?
erythema multiforme
what adults can be affected by SSSS?
kidney disease or immunocompromised
if you biopsy erythema toxicum neonatorum- you will find
eosinophils and sterile pustule
initial management of comedonal acne ?
topical retinoid with organic acid preparations (salicylic, azelaic, glycolic acid)
when should you use benzoyl peroxide for acne?
inflammatory pustular acne
histopathology “tombstone cells”
pemphigous vulgaris
netlike itercellular IgG and C3 on immunoflourescence?
pemphigous vulgaris
autoantibodies against desmogleins 1+3
pemphigous vulgaris
acantholysis
detached keratinocytes
linear IgG deposits at basement membrane and tense bullae?
bullous pemphigoid
Flaccid bullae and mucocutaneous blisters with biopsy showing intraepidermal cleavage
pemphigous vulgaris
Two types of contact dermatitis
allergic (type IV hypersensitivity)
irritant (physical or chemical contact)
A rash typically beginning as small papules that become confluent and evolve into vesicles or bullae and eventually crust in 7-10 days. Rash is limited to single dermatome but may involve adjacent dermatomes
Herpes Zoster
Widely scattered, red, scaly papules and plaques that often follow strep infection or can occur in patients with RA (on TNF-a)
Guttate Psoriasis
Treatment for guttate psoriasis
UV phototherapy
Topical glucocorticoids
Vitamin D
