Dermatology Flashcards
Diaper Dermatitis etiologies
- wearing diapers: contact dermatitis, miiaria (heat/sweat rash, blockage of eccrine sweat glands), candida (moist conditions)
- rash in diaper area as well as other areas: atopic dermatitis, seborrheic dermatitis
- affects diaper area irrespective of diaper use: scabies, bullous impetigo
management of diaper dermatitis
- frequent diaper changes every 2 hours or when soiled
- open air exposure
- topical zinc oxide or petroleum jelly
- 1% hydrocortisone cream (< 2 wk use)
- may need topical Abx
Perioral Dermatitis Clinical Manifestations
MC seen in young women; may have a history of topical corticosteroid use
papulopustules on erythmetous base which may become confluent into plaques and scales
classically spares the vermillion border
Management of Perioral Dermatitis
topical metronidazole or erythromycin
oral tetracyclines
avoid topical corticosteroids
Types I - IV of Cutaneous Drug Reactions
- Type I: IgE-mediated, ex: urticaria and angioedema. IMMEDIATE
- Type II: cytotoxic, Ab-mediated (drugs in combo with cytotoxic antibodies cause cell lysis)
- Type III: immune antibody-antigen complex. Ex: drug mediated vasculitis and serum sicness
- Type IV: DELAYED (cell-mediated) – morbilliform reactions, Ex: Erythema Multiforme
Clinical Manifestations of Cutaneous Drug Reactions
-
exanthematous/morbilliform rash: MC skin eruptions. (type IV delayed) generalized distribution of bright red macules and papules that coalesce to form plaques. Rash typically begins 2 - 14 days after medication initiation
ex: antibiotics, NSAIDs, allopurinol, thiazide diuretics -
Urticarial: (type I immediate) occurs within minutes to hours after drug administration
ex: antibiotics, NSAIDs, opiates and radiocontrast media - Erythema Multiforme (Type IV delayed) target lesions may not always be present in drug-induced EM
MC Drugs: Sulfonamides, penicillins, phenobarbital, dilantin
fever, abdominal pain, and joint pain may accompany the cutaneous drug reaction
Management of Cutaneous Drug Reactions
- dicontinue offending medication
- Exanthematous/Morbiliform: oral antihistamines
- Drug-induced urticaria/angioedema: systemic corticosteroids, antihistamines
- Erythema Minor: symptomatic therapy
- Anahylaxis: intramuscular epi
What is Lichen Planus?
idopathic cell-mediated immune response
increased incidence with Hepatitis C
Clinical Manifestations of Lichen Planus
5 Ps: Purple, Polygonal, Planar, Pruritic Papules with fine scales and irregular borders
can develop Koebner’s Phenomenon: new lesions at sites of trauma (also seen in psoriasis)
Wickham Striae: fine white lines on the skin lesions or on oral mucosa. nail dystrophy
Management of Lichen Planus
topical corticosteroids 1st line
2nd line: PO steroids, UVB therapy, retinoids. rash usually resolves spontaneously in 8 - 12 months
What is Pityriasis Rosea?
maculopapular rash with uncertain etiology (possibly associated with viral infections – HHV7)
primarily older children/young adults
increased incidence in the spring/fall
can mimic syphillis so order RPR if the patient is sexually active
Clinical Manifestations of Pityriasis Rosea
Herald Patch** (solitary salmon-colored macule) on the trunk 2 - 6 cm in diameter
general exanetham 1 - 2 weeks later: smaller, very pruritic 1 cm round/oval salmon-colored papules with white circular (collarette) scaling along cleavage lines in a Christmas Tree Pattern
(confined to trunk and proximal extremities (face usually spared)
resolves in 6 - 12 weeks
Management of Pityriasis Rosea
none needed
pruritus: PO antihistamines, topical corticosteroids, oatmeal baths
possible UVB therapy if severe
What is the most common cause of Stevens-Johnson Syndrome/TEN?
MC after drug eruptions: especially sulfa and anticonvulsant meds
also NSAIDs, Allopurinol, antibiotics
infections are a less common cause; Ex: Mycoplasma, HIV, HSV
What is the difference between Stevens-Johnson Syndrome and TEN?
SJS = sloughing < 10% BSA
TEN = sloughing > 30% BSA, may develop skin necrosis
clinical manifestations of SJS and TEN
fever and URI Sx ► widespread blisters begin on trunk/face, erythematous/pruritic macules >= 1 mucous membrane involvement with _epidermal detachment*_ (+ Nikolsky sign)
Management of SJS and TEN
treat like severe burns: burn unit admission, pain control, withdrawal of offending med, fluid and electrolyte replacement, wound care
What is Erythema Multiforme?
acute self-limited Type IV hypersensitivity reaction
MC in young adults 20 - 40 yo
skin lesions usually evolve over 3 - 5 days and persist for about 2 weeks
Associations: Herpes Simplex Virus MC**, Mycoplasma, S. pneumo
meds: sulfa drugs, beta-lactams, Phenytoin, Phenobarbital
Clinical Manifestations of Erythema Multiforme
TARGET lesions classic**
dull, “dusty-violet” red, purpuric macules/vesicles or bullae in the center surrounded by pale edematous rim and peripheral red halo. often febrile
What is the difference between EM minor and EM major?
EM Minor: target lesions distributed acrally (distal portion of limbs–hands and feet–and head–ears and nose); no mucosal membranes involved
EM Major: target lesions with involvement of >= 1 mucous membrane (oral, genital, or ocular mucosa) < 10% BSA acrally → centrally (no epidermal detachment)
Management of Erythema Multiforme
Symptomatic
discontinue offending drug
antihistamines
analgesics
skin care
steroid/lidocaine/diphenhydramine mouthwash for oral lesions
systemic corticosteroids if severe
What are the main pathophysiological factors of Acne Vulgaris?
- increased sebum production: î androgens increase sebaceous gland activity
(MC after puberty, î androgens PCOS and Cushing’s Disease)
- Clogged sebaceous glands: due to increased proliferation of follicular keratinocytes
- Propionbacterium acne overgrowth: P. acne is part of the normal flora that overgrows in blocked pores ⇒ lipase production by P. acne which converts sebum into inflammatory fatty acids that damage healthy cells
- inflammatory response
Clinical Manifestations of Acne Vulgaris
commonly seen in areas with î sebaceous glands (face, back, chest, upper arms)
- comedones: small, non-inflammatory bumps from clogged pores
– open comedones: (blackheads) – incomplete blockage
– closed comedones (whiteheads) – complete blockage
2. inflammatory: papules or pustules surrounded by inflammation
3. nodular or cystic acne: often heals with scarring
Diagnosis of Acne Vulgaris (mild, moderate, severe)
Mild: comedones (+- small amounts of papules &/or pustules)
Moderate: comedones, larger amounts of papules and pustules
Severe: nodular (>5 mm) or cystic acne
Management of Mild Acne Vulgaris
Mild Acne Treatment
topical retinoids, benzoyl peroxide, topical Abx, OCPs
Topical Retinoids: (Retin-A, Adapalene) may be used alone or in combo with other meds
Benzoyl Peroxide: decreases Propionbacterium concentration and reduces inflammation (SE: erythema, dermatitis)
Topical Abx: (Clindamycin) MC used with benzoyl peroxide to reduce resistance
OCPs: reduce androgen production reducing sebum production
Management of Moderate Acne
Moderate Acne Treatment
Tx for mild acne + oral Abx, +/- anti-androgen agents
oral antibiotics: tetracyclines such as minocycline or doxycycline
spironolactone: anti-androgen effects. spironolactone is a K+ sparing diuretic
Management of Severe Acne
Treatment of Severe Acne
Isotretinoin: affects all of the 4 pathophysiologic mechanisms of acne
SE: psych side effects, hepatitis and increased TGs/cholesterol, arthralgias, leukopenia, premature long bone closure, dry skin.Highly Teratogenic***** (must obtain at least 2 pregnancy tests prior to initiating treatment and then monthly), must committ to at least two forms of contraception (beginning one month prior to initiation and one month after disconinuation)
What is pediculosis?
lice
What is the term for head lice?
body lice?
pubic lice?
pediculosis humanus capitus
pediculosis humanus corporis
phthirus pubis
Clinical Manifestations of Pediculosis capitus/corporis/phthirus pubis
intense itching* (especially occipital area) and papular urticaria near lice bites
nits* white oval-shaped egg capsules at the base of the hair shaft, removed with a comb
Management of pediculosis (lice)
permethrin topical drug of choice** (anti-parasite) capitus: permethrin shampoo left on x 10 minutes
pubis/corporis: permethrin lotion at least 8 - 10 hours (safe in children 2 years and older)
2nd line: lindane: neurotoxic (headaches, seizures – do not use after showering)
Bedding/clothing are laundered in hot water with detergent and dried in hot drier for 20 minutes. toys that cannot be washed should be placed in air-tight plastic bags x 14 days
Where do scabies like to burrow?
intertriginous zones including web spaces between fingers/toes (where 2 skin areas may touch or rub together), scalp
What causes the hypersensitivity reaction with scabies?
female mites burrow into the skin to lay eggs, feed, and defecate (scybala are the fecal particles that precipitate a hypersensitivity reaction in the skin)
How long can scabies survive off the human body?
scabies cannot survive off the human body for more than 4 days
Clinical Manifestations of Scabies
intensely pruritic lesions* papules, and vesicles and LINEAR BURROWS – commonly found in intriginous zones. usually spares the neck and face. intense pruritus with minimal skin findings _increased intensity at night**_
How do you diagnose scabies?
- often a clinical diagnosis
- skin scraping of the burrows with mineral oil to identify mites or eggs under microscopy
Management of Scabies
- Permethrin topical (Elimite, Nix) is the drug of choice**. Applied topically from the neck to the soles of the feet for 8 - 14 hours before showering. Repeat application after 1 week is recommended.
- Lindane is cheaper but DO NOT use after showering (causes seizures* due to increased absorption through open pores)
CI: teratogenic–not used in breastfeeding women, children < 2 yo
- 6 - 10% sulfur in petroleum jelly for pregnant women/infants. Oral ivermectin if extensive
- All clothing, bedding, etc. should be placed in plastic bag for at least 72 hours then washed and dried using heat
What is androgenetic alopecia?
progressive loss of the terminal hairs on the scalp in a characteristic distribution
What is the key androgen leading to androgenetic alopecia?
DHT (dihydrotestosterone)
Management of Androgenetic Alopecia
Minoxidil: best used if recent onset alopecia involving a smaller area
Oral Finasteride: 5 alhpa reductase inhibitor – androgen inhibitor (inhibits the conversion of testosterone to dihydrotestosterone)
SE: decreased libido or ejaculatory dysfunction
What is another name for Roseola Infantum?
Sixth’s Disease (Human Herpes Virus 6 or 7)
Clinical Manifestations of Roseola
Prodrome of HIGH FEVER* 3 - 5 days ⇒ fever resolves before the onset of a rose, pink maculopapular, blanchable rash on the trunk/back and spreads to the face
(only childhood viral exanthem that starts on the trunk** and spreads to the face)
Child appears well and alert during febrile phase*. may be a little fussy
Management of Roseola
supportive, anti-inflammatories, antipyretics (to prevent febrile seizures)
What is the coxsackie virus?
virus part of the enterovirus family
MC in children < 5 yo
spread feco-oral and oral-orally
MC in late summer/early fall
two types – Coxsackie A & B
Clinical manifestations of herpangina
sudden onset of high fevers
stomatitis: small vesicles on the soft palate, uvula & tonsillar pillars that ulcerate before healing, sore throat
3 - 5 days
MC in children 3 - 10 yo
What virus causes Mumps?
paramyxovirus
Clinical Manifestations of Mumps
low-grade fever, myalgia, HA ⇒
parotid gland pain & swelling
What are some complications of Mumps?
MC seen in older patients
Orchitis in males* (usually unilateral)
oophoritis, encephalitis, aseptic meningitis
Mumps is the MC cause of acute pancreatitis in children. Deafness, arthritis, infertility
Clinical Manifestations of Rubeola (Measles)
URI prodrome: high fever
3 C’s: cough, coryza, conjunctivitis
Koplik Spots* (small red spots in buccal mucosa with pale blue/white center) precedes rash by 24 - 48 hours ⇒
morbiliform (maculopapular) brick-red* rash on face beginning @ hairline ⇒ extremities (palms and soles involvement usually seen last if it occurs) that darkens and coalesces
Rash usually lasts 7 days fading from top to bottom. Often febrile along with rash
To which virus family does Rubella belong?
Togavirus
Compare/Contrast Rubeola (measles), Rubella (German Measles) and Roseola (6th disease)
Clinical Manifestations of Rubella (German Measles)
- low-grade fever, cough, anorexia, lymphadenopathy (posterior, cervical, posterior auricular) ⇒
pink, light-red spotted maculopapular rash on face ⇒
extremities (lasts 3 days)
Compared to Rubeola, rubella spreads more rapidly & does not darken or coalesce
Forchheimer spots: small red macules or petechiae on soft palate (also seen in Scarlet fever)
2. Transient photosensitivity and joint pains may been seen (especially in young women)*
Possible Complications of Rubella
generally no complications in children with Rubella as compared to Rubeola
Teratogenic esp 1st trimester*: congenital syndrome* - sensorineural deafness, cataracts, TTP (“blueberry muffin rash), mental retardation, heart defects (part of the TORCH syndrome)
What is another name for Erythema Infectiosum?
Fifth Disease
Clinical Manifestations of Erythema Infectiosum (Fifth Disease)
coryza, fever ⇒
“slapped cheek”* rash on face with circumoral pallor 2 - 4 days ⇒
lacy reticular rash on extremities (especially upper). spares the palms and soles. resolves in 2 - 3 weeks
arthropathy, arthralgias: older children & adults**
What could happen if a woman were to contract an infection of Erythema Infectiosum during pregnancy?
associated with î fetal loss in pregnancy (fetal hydrops, CHF, spontaneous abortion)
Diagnosis of Erythema Infectiosum (Fifth Disease)
serologies
What can Erythema Infectiosum cause in sickle cell patients?
aplastic crisis or G6PD deficiency
What is Erythema Toxicum?
thought to be due to immune system activation. seen in up to 70% of neonates
Clinical Manifestations of Erythema Toxicum
small, erythematous macules or papules ⇒
pustules on erythematous base 3 - 5 days after birth
does not involve the palms or soles. individual lesions may spontaneously disappear
Management of Erythema Toxicum
self-limited
usually resolves spontaneously in 1 - 2 weeks
What is Miliaria?
Blockage of eccrine sweat glands (especially in hot and humid conditions)
this leads to sweat seeping into the epidermis and dermis. increased counts of skin flora (S. epidermis, S. aureus)
There are different types of Miliaria (sweat rash). How does Miliaria crystallina manifest?
1. Miliaria crystallina: tiny, friable clear vesicles (due to sweat in the superficial stratum corneum) MC in neonates (especially in 1 week old neonates)
There are different types of Miliaria. How does Miliaria rubra manifest?
Miliaria rubra: severely pruritic papules (may develop pustules). Deeper in the epidermis
There are different types of Miliaria. How does Miliaria profunda manifest?
Miliaria profunda: flesh-colored papules (due to sweating in the papillary dermis)
What is Milia and how does in manifest?
keratin retention within the dermis of immature skin
1 - 2 mm pearly white-yellow papules especially seen on the cheeks, forehead, chin and nose
Milia develop when tiny skin flakes become trapped in small pockets near the surface of the skin. Although milia can develop at any age, they’re most common among newborns.
What are café au lait macules?
uniformly hyperpigmented macules or patches with sharp demarcation. either present at birth (or developing early in childhood). varying colors from light brown to chocolate brown
due to increasde number of melanocytes & melanin in the epidermis
Children with >= 6 Café Au Lait macules (especially when accompanied with axillary or inguinal freckling) should be evaluated for…
Neurofibromatosis type I
nerve sheath tumors
What are Port Wine Stains? (aka Nevus Flammeus)
vascular malformations of the skin (due to dilated dermal capillaries)
Clinical Manifestations of Port Wine Stains
pink-red sharply demarcated, blanchable macules or papules in infancy
Over time, they grow & darken to a purple (port-wine) color and may develop a thickened surface
- They occur most commonly on the head and neck. Usually unilateral or segmental.*
- MC seen on the face but can occur anywhere (can be associated with other abnormalities such as glaucoma and spinal abnormalities)*
Management of Port-Wine Stains
pulse dye laser treatment (best if used in infancy)
What is Sturge-Weber Syndrome?
congenital disorder associated with classic triad:
1. facial port wine stain (especially along trigeminal distribution area & around eyelids)
2. leptomeningeal angiomatosis (typically benign growth consisting of small blood vessels)
3. ocular involvement (glaucoma)
May develop hemiparesis contralateral to the facial lesion, seizures or intracranial calcification & learning disabilities
What are Mongolian Spots?
congenital dermal melanocytosis due to mid-dermal melanocytes that fail to migrate to the epidermis from the neural crest
may be seen in > 80% of Asians and East Indian infants. increased in African Americans
Clinical Manifestations of Mongolian Spots
blue or slate gray pigmented lesions MC seen in presacral/sacral-gluteal area (may be seen on the shoulders, legs, back, and posterior thighs as well) with indefinite borders. May be solitary or multiple
Management of Mongolian Spots
spots usually fade over the first few years of life (before 10 years)
What is a Nevus Simplex? (aka “stork bite” or “salmon patch”)
Areas of surface capillary dilation. MC seen on the nape of the neck, eyelids & forehead.
Management of a Nevus Simplex (aka “stork bite” or “salmon patch”)
- observation: most will resolve spontaneously by age 2 & don’t usually darken over time
- laser therapy: will reduce the appearance of lesions
(those on eyelids and glabella usualely disappear by 2 - 3)
(can deepen in color with vigorous activity or changes with ambient temperature)
Pathophysiology of Staphylococcal Scalded Skin Syndrome (aka Ritter Disease)
MC seen in infants or children < 5 yo
Disseminated exfoliated exotoxins produced by Staphylococcus aureus (esp strains 71 & 55)
These toxins may cause proteolysis & destruction of the intraepidermal desmosomes of the skin
Clinical Manifestations of Staphylococcal Scalded Skin Syndrome (SSSS aka Ritter Disease)
- Malaise, fever, irritability, extreme skin tenderness ⇒
cutaneous, blanching erythema - bright skin erythema often starting centrally & around the mouth before spreading diffusely. Erythema is worse in the flexor areas and around orifices - especially the mouth. After 1 - 2 days ⇒
- develop sterile, flaccid blisters esp in the areas of mechanical stress (hands, feet, flexural areas & buttocks) ⇒*
- Nikolsky Sign** separation of the dermis & rupture of the fragile blisters when gentle pressure is applied to the skin ⇒*
_Desquamative phase_ – skin that easily ruptures, leaving moist, denuded skin before healing
2. inflamed conjunctiva may be seen (may become purulent) but mucous membranes are NOT involved
Diagnosis of Staphylococcal Scalded Skin Syndrome (SSSS aka Ritter Disease)
- clinical diagnosis. intact bullae are sterile
- cultures from urine, blood & nasopharynx. skin biopsy: lower stratum granulosum layer splitting.
Complications of Staphyloccal Scalded Skin Syndrome (SSSS aka Ritter Disease)
secondary infection: sepsis, pneumonia, cellulitis
excessive fluid loss; electrolyte imbalances
What is Scarlet Fever? (Scarlatina)
diffuse skin eruption that occurs in the setting of GABHS (Streptococcal pyogens) infection
Due to Type IV (delayed) hypersensitivity reaction to a pyrogenic (erythrogenic toxin A, B or C)
Clinical Manifestations of Scarlet Fever
- Fever, chills, pharyngitis (“strep throat”)
- Rash: diffuse erythema that blanches with pressure plus many small (1 - 2 mm) papular elevations that feels like “SANDPAPER” when palpated
“sunburn with goosebumps”
MC starts in the groin & axillae then rapidly spreads to the trunk and then the extremities. The rash often desquamates over time (usually spares the palms & soles)
– often associated with a flushed face with CIRCUMORAL PALLOR & STRAWBERRY TONGUE
– Pastia’s Lines = linear petechial lesions seen at pressure points, axillary, antecubital, abdominal or inguinal areas
Key Characteristics of Scarlet Fever
Management of Scarlet Fever
Same as strep pharyngitis. May return to school 24 hours after Abx initiation
- Penicillin G or VK 1st line**. Amoxicillin, Amoxicillin/clavulanic acid (Augmentin)
- Macrolides if PCN allergic. other alternatives include Clindamycin, cephalosporins
