Dermatology Flashcards
Bacteria that proliferate immediately after a burn
Gram-positive skin flora (Staph Aureus)
> 5 days after a burn, most infections are caused by
Gram-negative organisms (Pseudomonas)
Fungi (Candida)
Early signs of wound infection
Change in appearance (partial thickness becomes full thickness)
Loss of viable skin graft
Burn wound sepsis
Can develop rapidly
Findings: Temperature < 36.5 (97.7) or > 39 (102.2) - Low temperature counts too! Weird! Progressive tachycardia (>90) Progressive tachypnea (>30) Refractory hypotension (SBP < 90)
Also common: Oliguria Unexplained hyperglycemia Thrombocytopenia AMS
Diagnosis of Burn Wound Sepsis
Quantitative Wound Culture (> 10^5 bacteria/g tissue)
Biopsy (determine tissue invasion depth)
Treatment of Burn Wound Sepsis
Empiric broad spectrum IV antibiotics
Pip/Taz
Carbapenem
Potentially include Vanc for MRSA coverage
Potentially include Aminoglycoside for MDR Pseudomonas
Local wound care & debridement
Definition of a large burn
> 20% of body surface area
You see a pediatric burn patient with uniformity of burned skin, sharp lines of demarcation & flexor surface sparing. What do you do?
Call child protective services
Child with: Recent infection Hematuria Abdominal Pain Lower extremity purpuric rash No thrombocytopenia
Vasculitis (probably HSP)
Treat with hyrdation & NSAIDS
Major risk factor for Actinic Keratosis
Chronic sun exposure
Surrounding skin often shows features of solar damage (telangiectasias, hyperpigmentation)
Clinical significance of Actinic Keratosis
Potential progression to squamous cell carcinoma
Likelihood of malignant progression of an individual lesion is low
When is a biopsy of Actinic Keratosis indicated?
> 1cm diameter Indurated Ulceration Rapidly growing Fail appropriate treatment (Cryotherapy or fluorouracil if large)
Histopathology of Actinic Keratosis
Acanthosis (Thickening of epidermis)
Parakeratosis (Retention of nuclei in stratum corneum)
Nuclear atypia
Abnormal keratinization w/ thickening of stratum corneum
Treatment for Actinic Keratosis
Cryotherapy
Large area may require field therapy (Fluorouracil)
Characteristics of Allergic Contact Dermatitis
Erythematous papules or vesicles
Lichenification in chronic cases
Triggers of Allergic Contact Dermatitis
Toxicodendron Plants (Poison Ivy)
Nickel
Rubber
Topical medications
Characteristics of Pityriasis Rosea
Numerous
Oval
Scaly
Plaques
Follow cleavage lines of the trunk
Begins with initial lesion (“Herald Patch”) larger than later lesions
Characteristics of Psoriasis
Well-circumscribed
Plaques
Silvery scales
Predominantly extensor surfaces & scalp
Characteristics of Seborrheic Dermatitis
Scaly
Oily
Erythematous rash
Skinfolds around: Nose Eyebrows Ears Scalp
Characteristics of Seborrheic Keratosis
Benign
Pigmented
Well-demarcated border
Velvety / Greasy surface
“Stuck On” appearance
Mongolian Spot
Benign
Flat
Blue-grey patches
Usually over lower back & buttocks
Can be seen elsewhere
Look like bruises, but are nontender. Document them so future providers know.
Nonwhite children have them at birth, spontaneously fades during first decade. So benign. Reassure.
When does colic (prolonged periods of inconsolable crying) peak?
2 months
Parents get exhausted, increases risk of abuse
Cafe-au-lait macules are associated with
Neurofibromatosis
Ash-leaf spots are associated with
Tuberous Sclerosis
Port-wine stains are associated with
Sturge-Weber syndrome
Cafe-au-lait macules
Ash-leaf spots
Port-wine stains
These skin findings make you want to look for
Intracranial lesions
Epilepsy
They are all associated with neurocutaneous syndromes
When is Babinski reflex normal?
< 1 year
When are Seborrheic Keratoses not benign?
When several appear all at once, they may indicate occult internal malignancy (Leser-Trelat sign).
Usually, they’re benign AF, though.
Treatment for Seborrheic Keratoses
Observation
If bothersome, excision, cryosurgery or electrodessication may be performed.
Acrochordon
Skin Tag
Seen in regions subjected to friction (neck, axilla, inner thigh)
Most common presentation of Basal Cell Carcinoma
Slow- growing papule or nodule
Pearly, rolled border
Overlying telangiectasias
Ulceration common
Bleeding following minor trauma common
Cutaneous warts
Most common in children & young adults
Seen on hands, elbows & feet
Not usually pigmented
Biopsy findings of Seborrheic Keratosis
So rarely done
Small cells (resembling basal cells)
Variable pigmentation
Hyperkeratosis
Keratin-containing cysts
Differentiating Melanoma from Seborrheic Keratosis
Melanoma has:
Indistinct or irregular border
Smooth or nodular surface
Changing appearance over time
Predilection for sun-exposed areas
Biopsy is occasionally required to tell the difference.
What causes Molluscum Contagiosum?
Poxvirus
Characteristics of Molluscum Contagiosum
Small, pruritic, skin-colored papules
Umbilicated centers
Diagnosis is clinical
Affects mostly children
Adults & adolescents can develop them too
How is Molluscum Contagiosum transmitted?
Skin-to-skin
Contaminated fomites
Autoinoculation to additional sites
Where do Molluscum Contagiosum lesions appear in kids?
Extremities
Face
Trunk
Where do Molluscum Contagiosum lesions appear in adults?
Anogenital region (sexxxxxx)
Molluscum Contagiosum treatment
Self-limited illness (6 - 12 months)
To prevent further spread, reduce symptoms or for cosmetic reasons, you can do:
Curettage
Cryotherapy
Topical agents (podophyllotoxin)
Who has a prolonged course with Molluscum Contagiosum?
Patients with impaired cellular immunity
Poorly controlled HIV patients can have hundreds of lesions.
If Molluscum Contagiosum has excessively large, numerous or widespread lesions, what do you do?
HIV Test
Hypersensitivity rash with blisters or bullae
Type 2 (Antibody-dependent cellular cytotoxicity)
Erythematous maculopapular hypersensitivity rash
Type 3 (Immune complex deposition)
C3 deficiency predisposes you to
Pyogenic bacterial respiratory tract & sinus infections
C5 - C8 deficiency predisposes you to
Recurrent Neisseria infections
Disorders of Phagocytosis
Chronic Granulomatous Disease
Chediak-Higashi
Job Syndrome
Defective leukocyte adhesion proteins)
Present with severe pyogenic bacterial infections
Selective IgA deficiency predisposes you to
Recurrent respiratory infections
Chronic giardiasis
Most common form of Tinea Capitis in the USA
Black Dot Tinea Capitis
Most common in African Americans
Trichophyton Tonsurans is the cause, but other dermatophytes can cause TC as well
Transmission of Tinea Capitis
Human-to-human
Fomites (shared combs)
Characteristics of Tinea Capitis
Scaly, erythematous plaque on the scalp
Progresses to patchy alopecia w/ residual black dot (broken hair)
Other findings: Inflammation Pruritus Occipital or postauricular lymphadenopathy Scarring
Diagnosis of Tinea Capitis
Clinical diagnosis
Can confirm with KOH exam of hair stubs
Treatment of Tinea Capitis
PO Griseofulvin or Terbinaine
Many experts recommend household contacts be treated with Selenium Sulfide or Ketoconazole Shampoo
Alopecia Areata
Smooth circular areas of hair loss
No scaling
Discoid Lupus Erythematosus
Well-demarcated inflammatory plaques Hypo- or Hyperpigmented lesions Scarring Photosensitivity Alopecia
Cutaneous candidiasis
Erythematous
Vesiculopapular rash
Warm, moist areas (Skin folds)
Pressure-induced alopecia
From prolonged pressure on scalp during surgical procedures
Transient hair loss develops a few weeks postop
Regrowth ensues without significant residual alopecia
Hair pattern of trichotillomania
Irregular pattern
Broken hair strands of varying length
Seborrheic Dermatitis of the Scalp
Dandruff
Etiologies of Urticaria
Infections (Viral, bacterial, parasitic)
IgE Mediated (Antibiotics, insect bites, latex, food, blood products)
Direct mast cell activation (Narcotics, muscle relaxers, radiocontrast medium)
NSAIDs
Idiopathic (up to 50% of patients)
Most commonly affected sites for atopic dermatitis in adults
Flexural areas (neck, antecubital, popliteal)
Face
Wrist
Forearms
Timeline of Contact Dermatitis
Symptoms develop over hours-to-days
Symptoms resolve within several days
Erythema Multiforme
Target lesion Erythematous, iris shaped macules Can also contain vesicles or bullae Can be painful or pruritic Symmetrically distributed on extensor surfaces of extremities. Also palms and soles
Etiology of Pityriasis Rosea
Likely viral
Self-limited
Difference between Stevens-Johnson Syndrome & TEN
SJS is when it affects < 10% of body surface area
TEN is when it affects > 30% of body surface area
Anything in between is an overlap
Onset of SJS / TEN
4 - 28 days after exposure to trigger (2 days after repeat exposure)
Acute flu-like prodrome
Rapid onset erythematous macules, vesciles, bullae
Necrosis & sloughing of epidermis
Mucosal involvement
Drug triggers of SJS/TEN
Allopurinol Antibiotics (Sulfonamides) Anticonvulsants (Carbamazepine, Lamotrigine, Phenytoin) NSAIDs (Piroxicam) Sulfasalazine
Non-drug triggers of SJS/TEN
Mycoplasma Pneumoniae
Vaccination
Graft vs. Host Disease
Clinical features of Stevens Johnson Syndrome
Coalescing erythematous macules
Bullae
Desquamation
Mucositis
Systemic signs of Stevens Johnson Syndrome
Fever Tachycardia Hypotension AMS Seizures Coma
When does Erythema Multiforme typically present?
After herpes simplex infection