Dermatology [HYPERSENSITIVITY RXNS]

Urticaria
Urticaria aka hives is a Type I Hypersensitivity Reaction.
Caused by exposure to an antigen, it crosslinks IgE on mast cells
causing Histamine to be released. This causes leaky capillaries, Anaphylaxis = shortness of breath and hypotension with
producing an annular, blanching red papule of varying size. exposure to allergen. Give epinephrine. Follow with
That antigen can be anything: bee stings, pressure, heat, food, systemic steroids, H1 blocker and H2 blocker.
contact dermatitis. If there’s no anaphylaxis a clinical diagnosis
may be made; use anti-histamines to decrease the rash. Since
any antigen can cause urticaria it’s critical to identify the agent
and avoid using it again. Send them to RAST to identify the
culprit antigen.

Drug Reaction
These are commonly a pink, morbilliform rash (though any rash
may be the case) occurring 7-14 days after exposure (so new
drugs are not culprits) in hospitalized patients. They’re generally
widespread, symmetric, and pruritic. Always stop the
offending agent. Give diphenhydramine for mild symptoms,
corticosteroids for severe symptoms.

A fixed drug eruption is any rash or blister that occurs in the

same one spot in reaction to one drug every time it’s administered.
It occurs within 24 hours of exposure. Avoid the drug. It’s never
life-threatening.

Erythema-Multiforme Steven-Johnson Syndrome + Toxic Epidermal Necrolysis

This is primarily a cutaneous drug reaction to medication (Sulfa, Both diseases are the same disease that exist as a continuum in
Anticonvulsants, NSAIDs, and PCN) that appears as a target severity commonly occurring from drug reactions (sulfa,
shaped lesion that can occur on the palms and soles. It’s benign anticonvulsants, NSAIDs, PCN). Each causes widespread loss of
and self-limited. Remove the drug and watch. Two other sheets of skin with a Nikolsky Sign. Two things differentiate
possibilities to consider: 1 – It can be caused by chronic HSV the diseases: Body Surface Area + Biopsy. SJS involves <10%
and refractory cases need acyclovir and 2 – if it’s spreading or BSA and has basal cell degeneration on biopsy. TEN involves
involving the oral mucosa get ready for Steven-Johnson >30% BSA and shows full-thickness epidermal necrosis.
Syndrome. Syphilis may also present with Targetoid lesions on Removal ALL meds (including steroids) and admit to the burn
the palms and soles and might be present as a distractor on the unit (heat, electrolytes, fluid, infection risk). The biopsy is critical
tests. to differentiate between the SJS / TEN (which responds to
removal of antibiotics) and Staphylococcus Scalded Skin
Syndrome (which responds to the administration of antibiotics),
as well as separating severity of SJS versus TEN. SSSS doesn’t
have mucosal involvement.

Dz Pt Tx Bx
Urticaria IgE-Mast Cell mediated release of histamine after Diphenhydramine, N/A
exposure to any antigen, blanching red papule Epinephrine if Anaphylaxis
Drug Reaction Widespread Symmetric pruritic rash OR Stop the drug, monitor N/A
Any One rash at One spot in reaction to One Drug
Erythema Targetoid lesion on palms and soles caused either by Acyclovir and/or Remove Drug N/A
Multiforme HSV or will progress to Steven Johnson
Steven <10% BSA affected Admit to the burn unit, fluids, electrolytes, Basal Cell
Johnson Nikolsky’s, Oral Mucosal Involvement supportive care. Degeneration
Toxic >30% BSA affected Steroids AREN’T helpful and may Total epidermal
Epidermal Nikolsky, Oral Mucosal Involvement exacerbate the condition thickness necrosis
Necrolysis

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 Dermatology [PAPULOSQUAMOUS RXNS]

Seborrheic Dermatitis (NOT Seborrheic Keratosis) You know what’d be sweet over here? Images! Unfortunately, we
Think of this as super-dandruff. Dandruff is flaking of the scalp. can’t swipe off Google; we’re currently developing our own
It’s treated with selenium shampoo. Seborrheic Dermatitis is a dermatology atlas. Derm is a very visual field, so make sure YOU
Google the dz until then (some imgs already in the qbank).
fungal infection that causes an inflammatory reaction in areas
rich in sebaceous glands. That means hair. Look for a rash on the
scalp and eyebrows that spares other areas of the face and ears.
Treat with selenium shampoo. Topical steroids can be used as
well if the inflammation doesn’t settle with selenium. Low-yield
test associations include: HIV infection, cradle cap (infants),
and Parkinson’s disease.

Psoriasis
Psoriasis is an autoimmune disease which causes proliferation of
keratinocytes with excessive accumulation of the stratum
corneum. It’s thought to be caused by dysregulation of T-Helper
cells. The patient will have symmetric, well-demarcated silvery
scales that bleed when picked that commonly affect the scalp,
gluteal fold, elbows, and knees. Nail pitting and onycholysis
(detachment of the nailbed) are common. If joint pains are
present, consider Psoriatic Arthritis (see rheumatology –
seronegatives). The first step is UV light (sunlight or artificial
exposure). Topical steroids are used in flares. Other agents, both
topical and systemic, are beyond the scope of a med student
(methotrexate, calcineurin-inhibitors, Anti-TNF-alpha). There
MAY be the need to biopsy to rule out lymphoma if the diagnosis
is in question.

Pityriasis Rosea
A benign and self-limiting condition that resolves on its own (~6
weeks). We don’t know what causes it. The disease begins with a
flat, oval, salmon-colored macule (hyperpigmentation in darker
skinned races) called the herald patch. The disease then
progresses to several salmon-colored scaling lesions with a
trailing scale (the scale does not reach the border of the salmon-
colored lesion). This will always spare the palms and soles.
While it is self-limiting, it may be the presentation of syphilis;
rule it out with an RPR. Involvement of the hands and soles
greatly increases the chance of syphilis.

Lichen Planus
Lichen Planus is an inflammatory disorder of unknown etiology.
It causes an intensely pruritic pink or purple flat topped
papules (you can feel them) with a reticulated network of fine
white lines. It usually involves the wrists and ankles but may
involve the trunk, the oral mucosa or the vaginal mucosa.
Treatment is similar to psoriasis. Topical steroids are the
mainstay of therapy, but should not be continued long term. UV
light can be used as an adjunct (as opposed to psoriasis where it’s
more effective). Topical and systemic immune modulators are
beyond the scope of this text. Be aware that a lichenoid drug
eruption (drug-induced lichen planus) can occur with Ace-I,
thiazides, furosemide, and Beta-blockers.

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 Dermatology [BULLOUS DISEASES]

Pemphigus Vulgaris
Pemphigus is an autoimmune disorder against desmoglein. It’s
present in desmosomes that interconnect the epithelial cells of the
Basement Membrane
epidermis. Because the destruction is between epithelial cells
(intra-epidermal), the blister is thin and tears easily (
Nikolsky’s Sign). Diagnosis is made by biopsy showing a Weak Barriers with lots of gaps
tombstone effect as basement membrane cells remain attached ( Nikolsky’s)
while epithelial cells split apart from each other. X Desmosome Destroyed
Immunofluorescence reveals antibodies on epithelial cells Hemidesmosome Intact
throughout the skin lesion. Because it’s an autoimmune disease,
treatment starts with systemic steroids. Once controlled, swap to
steroid sparing immune modulators when possible IF lights up the epidermis
(mycophenolate mofetil, rituximab). This disease is life- around the cells where the
threatening, does involve mucosa, and occurs in people ages 30- antibodies are
50.

Bullous Pemphigoid
Pemphigoid is another autoimmune disorder, this time against Strong barrier
the hemidesmosomes that attach basement membrane cells to the
( Nikolsky’s)
basement membrane (sub-epidermal lesion). The detachment
causes a blister but the intact epithelium results in a tense, rigid
bullae ( Nikolsky’s). Again, a biopsy is used for diagnosis X Hemidesmosome Destroyed
showing intact epithelium that’s detached from the basement Desmosome Intact
membrane. Immunofluorescence shows antibodies at the
dermal-epidermal junction. Treatment is with steroids during
acute attacks – topical for limited disease, systemic for severe. IF at the dermal epidermal
This ISN’T life threatening and DOESN’T involve the mucosa.
junction
It’s most commonly found in ages 70-80.

Dermatitis Herpetiformis
This isn’t a true blistering disease but is commonly tested against
them. It’s another autoimmune disease caused by IgA Papillae
Rugae
antibodies against transglutaminase. It’s the cutaneous
manifestation of celiac sprue and has the same pathology. The Epidermis
antibody-antigen complex gets deposited at the dermal papillae Basement Membrane
Dermis
and causes an extension of the epidermis. It manifests as multiple
small vesicular eruptions that are pruritic and found on the
buttocks / legs or extensor surfaces. A biopsy is not needed, IgA Deposition
though if performed it’ll show “neutrophilic abscess.” Make the @ Papillae
diagnosis instead by diagnosing the Sprue with anti-endomysial
Papillae enlarge
or anti-transglutaminase antibodies and an endoscopy. Treat the
skin manifestation by treating the underlying disease: remove
gluten from diet entirely.

Porphyria Cutanea Tarda

The most common porphyria disease, it’s the lowest yield of the
four. Bullae on sun-exposed areas is highly suspicious for the
disease. The diagnosis is made with coral red urine under
Wood’s Lamp caused by accumulation of urinary uroporphyrins.
The underlying etiology is a deficiency of uroporphyrinogen
decarboxylase but can be brought on by OCPs, alcohol, Hep C, or
Hemochromatosis. Avoid the sun.

Disease Age Mucosa Blisters Target Dx IF Tx

Pemphigus 40-50 Involved Nikolsky Dermatomes Bx Within Epidermis Steroids à MM
Vulgaris Thin, Tears (intracellular)
Bullous 70-80 No Nikolsky Hemidesmosomes Bx On Basement Membrane Steroids
Pemphigus Tense, Tough (to BM) Epidermal-Dermal
Junction
Dermatitis 20-30 No Nikolsky IgA Deposition Antibodies Deposition at the papillae Remove Gluten from
Herpetiformis @ papillae (though this is not needed) Diet
Porphyria Any No Nikolsky N/A Wood’s Don’t do it Avoid the sun
Cutanea Tarda Tense, Tough Lamp

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 Dermatology [ECZEMATOUS REACTIONS]

Atopic Dermatitis (Eczema)
Eczema presents as a dry, red, and itchy rash. In infants, it You know what’d be sweet over here? Images! Unfortunately, we
presents as papules, vesicles, and crusts (careful with impetigo) can’t swipe off Google; we’re currently developing our own
dermatology atlas. Derm is a very visual field, so make sure YOU
that presents on cheeks and extensor surfaces. It’s almost always
Google the dz until then (some imgs already in the qbank).
part of the “3As,” Asthma, Allergies, and Atopy. For infants, de-
escalate food additions and slowly add food back. Avoid food that

triggers a reaction. In adults, where the condition has been more
chronic, there’s symmetrical lichenification induced by a
chronic itch-scratch cycle. Again, avoidance of triggers (as with
infants) is crucial. Topical emollients can avoid the need for
steroids. If topical steroids are prescribed, they may be used only
for a brief time as they can lead to skin atrophy. The goal is to
break the itch-scratch cycle and allow the skin to heal.

Contact Dermatitis
There are two forms of contact dermatitis: irritant and allergic.
Irritant is caused by direct toxic effect of a chemical on the skin:
i.e. excessive hand-washing, rubbing on leather boots, or some
occupation-related chemical. Avoid those irritants and the patient
should be fine. Allergic contact dermatitis is caused by a Type
IV hypersensitivity reaction in response to some allergen.
Common causes are metals like Nickel (on clothing or jewelry),
latex, or plants (poison ivy / oak). Look for a red rash in the shape
of an object (like a glove, bracelet, or shoe strap). Treat by
avoiding contact with triggering agents and with topical
diphenhydramine or aloe creams.

Stasis Dermatitis
When fluid sits in a place for a long time chronic skin changes
develop. So, for whatever reason, people with chronic lower
extremity edema will develop stasis dermatitis. It’s characterized
by edema, erythema, brown discoloration, and scaling (flaking
of skin). It’s a clinical diagnosis; biopsy should be avoided as a
non-healing ulcer may develop. Venous stasis ulcer (medial
malleolus) can accompany stasis dermatitis. Early stasis
dermatitis may mimic cellulitis, but is often the diagnosis when
symmetrical and bilateral. Treatment is correcting volume
overload (diuretics only when overloaded) and using
compression stockings and leg elevation to facilitate drainage of
fluid from the legs.

Hand Dermatitis
Resulting from excessive hand-washing (look for the food-
industry or health-care worker). The dermatitis is on the hands
only. The goal is to avoid frequent hand washing and wear
protective gloves instead. Harsh hand soaps should be avoided.
Moisturizers should be used frequently.

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 Dermatology [HYPERPIGMENTATION]

Nevi (Moles)
Nevi are benign hyperplasia of melanocytes. Use the ABCDE
mnemonic to ensure a benign lesion. (A)symmetric, irregular ABCDE = Cancer
Border, mixed Color, a large Diameter (>5mm), or Evolving Asymmetric
(changing over time) is suspicious of cancer and requires biopsy. Irregular Border
If anyone is positive, biopsy. If ALL are negative, offer Mixed Colors
reassurance. There are three kinds of nevi depending on the layer Large Diameter > 5mm
the melanocytes are growing in. They’re often a subject of Evolving (changes in ABCD)
Qbanks rather than actual test questions. Be more concerned
about whether it’s ABCDE or not. What you care about is You need ANY 1 to suspect cancer
melanoma. Do a wide excisional biopsy and refer to the surgery
skin cancer topic for more details.

Seborrheic Keratosis (NOT Seborrheic Dermatitis)

This is an ugly looking mole here to remind you that not all Is it Cancer?
ABCDE is melanoma. These are often large, brown, greasy
looking, and crusted. They look, “stuck on” the face of an old Nevi Seborrheic Keratosis Actinic Keratosis
person. Here’s the thing - it’s a cosmetic mark of aging, but it can
look an awful lot like melanoma. If it’s been present for a long
time and is unchanged, leave it be; it’s Seborrheic Keratosis. If
Benign Mole Benign, Ugly Mole Bowen’s DZ
it’s new or changing, do the biopsy to rule out melanoma. Board
exams can get tricky about this, so be careful. (no) (no)

Actinic Keratosis Squamous Cell

A premalignant condition appearing as erythematous with a Carcinoma
sandpaper-like yellow to brown scale. This is squamous cell
carcinoma in the making and carries all the same risk factors.
Look for the sun-exposed patient (farmer, sailor, burns early in
childhood) and the sun-exposed area (face, arms, hands).
Primary prevention is key (wide-brimmed hats, sunscreen,
avoidance of sun). Local ablation with cryosurgery is first line
treatment. 5-FU cream is used for diffuse lesions not amenable to
cryosurgery. Actinic Keratosis, Bowen Disease (carcinoma in
situ), and Invasive Sqaumous Cell Carcinoma are the same
disease along a common spectrum.

Squamous Cell Carcinoma

SCC is a locally invasive malignancy of keratinocytes that can
metastasize (unlike basal cell). Risk factors are sun exposure (see
Actinic Keratosis). If it involves the lip, the lesion is almost
always on the lower lip. The lesion itself will be fleshy,
erythematous, and crusted or ulcerated. Biopsy the lesion, then
perform surgical excision.

Keratoacanthomas look and sound like squamous cell

carcinoma but grow more rapidly and regress spontaneously.
Because of their similarities to SCC, if found they’re resected
like SCC. If a patient describes a SCC that “went away on its
own” it was keratoacanthoma.

Kaposi Sarcoma
Malignancy of vascular endothelial cells that occurs with co-
infection of HHV-8 and Immunosuppression (AIDS). It’s a
purple lesion. Treat the AIDS and the tumors go away. Failure to
resolve with HAART (rising CD4) implies the need for local or
systemic chemotherapy. Also, they can be anywhere.

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 Dermatology [HYPOPIGMENTATION]

Introduction
Finding a lesion on someone that’s Hypopigmented isn’t a big
deal, but it’s often the subject of board examinations. There isn’t
one algorithm to follow - just a loose group of associations to
remember – which is perfect for building a summary table.

Tinea Versicolor
When there’s a patchy depigmentation one of the things to
consider is a fungal infection with Malassezia globosa. A normal
fungus present in skin flora, it’s unclear what causes it to
overgrow, though Cushing’s and Immunosuppression are risk
factors. Hypopigmentation is a result of inhibited melanin
production. Patients present with small scaly patches of varying
color (typically in summer, as these spots don’t tan). Diagnosis is
made by KOH prep of the scale that reveals hyphae + spores
that looks like “spaghetti and meatballs.” Treat with topical
selenium sulfide.

Vitiligo
An autoimmune disease that causes small sharply demarcated
depigmented macules or patches with irregular borders that can
coalesce. They’re usually found on the extremities, face, and
genitalia. Lesions can be picked up by the Wood’s Lamp Test
(no pigment at all), but definitive diagnosis is confirmed by the
absence of melanocytes on histology. It’s associated with
autoimmune disorders such as hypothyroidism and lupus.
Treatment is often ineffective. Steroids and UV light have been
attempted.
Piebaldism is inadequate melanocyte migration with a
white forelock on the scalp)
Albinism
If a patient is completely white with pale hair and pale eyes they
Albinism is inadequate tyrosinase activity, total
likely have albinism. It’s a genetic disorder of tyrosinase
depigmentation in all surfaces
(normal melanocytes, deficient enzyme) so there is no treatment;
the diagnosis is clinical. Simply protect these people from UV PKU is a deficiency in phenylalanine hydroxylase, causing
exposure and educate on preventing skin cancer. Albinism is a relative deficiency of tyrosine. Screened for at birth.
tested against Piebaldism and PKU, which can result in pale- Intellectual disability, seizures follow if not for a special diet
skinned kids.

Ash Leaf
A child with a single hypopigmented (NOT depigmentation) Shagreen patches (elevated fleshy collagen plaques)
spot that’s positive on Wood’s Lamp is an Ash Leaf Spot and
pathognomonic for Tuberous sclerosis. Watch for early onset Adenoma Sebaceum (hyperplastic blood vessels)
seizures. Get a CT scan to visualize the tubers in the brain. Look
for Shagreen patches and adenoma sebaceum.

Dz Patient Diagnosis Biopsy Treatment Path Risk Factors

Tinea Small Patchy Scales KOH Prep Topical Overgrowth of Cushing’s
Versicolor of varying color “spaghetti and Ø selenium Sulfide fungus (normal flora) Immuno↓
Back and Chest meatballs”
Vitiligo Macule or Papule on Wood’s Lamp Absent Melanocytes Ø tx Autoimmune Other
Hands and Face enhances lesion on histo prep Ppx vs Sun Autoimmune
Albinism All body Genetic Testing Ø tx
Ppx vs Sun
Ash Leaf Hypopigmented Wood’s Lamp Ø See Peds
lesion from birth then CT

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 Dermatology [SKIN INFECTIONS]

Impetigo
Commonly seen in children, this is caused by an infection with
Strep pyogenes. Bullous impetigo is increasing in incidence and
is caused by Staph aureus. Look for a child with honey-crusted
lesions on the face. Impetigo can lead to post-strep
glomerulonephritis but NOT rheumatic fever. Diagnosis is
clinical, often in response to therapy if not just by the lesion itself.
Treat topically (mupirocin) or with systemic antibiotics. Any
Beta-Lactam antibiotic (amoxicillin or 1st gen cephalosporins)
is sufficient for the initial treatment of non-bullous impetigo. If
bullous or there is no response, switch to clindamycin.

Erysipelas
Commonly seen in adults, this is caused by an infection with
Strep pyogenes. Erysipelas infects the lymphatics, so it’ll be easy
to see a dark red, well-demarcated, indurated lesion that
outlines the lymphatics, appearing to “climb up the extremity.”
Treatment, like impetigo, starts with Beta-Lactams against strep
(Amoxicillin) and escalates if there’s no improvement.

Acne Vulgaris
The most common dermatologic condition, it’s caused by an
infection by Propionibacterium acnes. It causes zits. Acne is a
product of increased sebum production, follicular
hyperkertinization, and colonization. It’s a clinical diagnosis. The
type of acne determines the approach to treatment.

See this as “the worse the acne or the more refractory, the higher
up the ladder you go.” That ladder is topical retinoids, benzoyl Disease State Treatment
peroxide, oral antibiotics, and isotretinoin. It is truly an escalation Comedones Topical retinoids
approach: (whiteheads,
- Not bad acne = retinoids blackheads)
- Teen cares about acne = benzoyl + retinoids Inflamed Comedones or Topical Retinoids +
- Acne won’t go away = doxycycline Pustules Benzoyl Peroxide
- Scarring, nothing else has worked, severe = isotretinoin Severe Pustular or Oral Antibiotics
Nodulocystic disease (Doxycycline, erythromycin)
Severe Inflammatory or Isotretinoin (UPT first)
On the test, though, they’ll give buzzwords that you should link
Resistant
with certain treatments. Rather than escalate, jump right to the
treatment (see to the right).

Tinea Infections
Tinea corporis is infection on the body. Look for a round
expanding plaque with moderate scaling and central clearing. It
responds to topical antifungals

Tinea pedis is infection of the foot. Look for interdigital

maceration and scaling between toes. Treat with topical
antifungals.

Tinea cruris is “jock itch” and is a fungal infection of the groin.

Treat with topicals.

Tinea unguium (onychomycosis) is treated with oral

antifungals. Terbinafine is best, itraconazole is ok. Make sure you
confirm the diagnosis with a KOH prep.

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 Dermatology [ALOPECIA]

Male Pattern Baldness – Androgenic Alopecia
Hair follicles are programmed to miniaturize under post-pubertal
androgens. This is a common disease in men; it’s largely
considered cosmetic. The top of the head (the crown) begins to
thin. Eventually, hair loss predominates. 5-DHT is implicated in
the pathology. Initial therapy is with Minoxidil topically and
finasteride orally. Women with hyperandrogenism can suffer as
well; they’re treated with OCPs (suppress ovarian production of
hormones) and spironolactone.

Alopecia Areata
A systemic autoimmune disorder against hair follicles. It
creates a well-defined circular bald spot. Also look for the
exclamation point sign - small hairs within the bald-spot that
appear to be floating because the hair shaft gets progressively
narrower and loses pigment close to the scalp. The disease is
treated with steroids – topical, intralesional, and systemic
depending on severity.

Tinea Capitis
A superficial fungal infection caused most commonly by
Trichophyton tonsurans. It also causes a circular bald spot with
all hairs at equal length. A KOH prep must be ordered to
visualize the fungus; Trichophyton doesn’t fluoresce under
Wood’s Lamp. Treat with oral Griseofulvin (note NOT topical)
– failure to do so will result in permanent hair loss.

Trichotillomania
A psychiatric disease whereby the patient compulsively pulls out
hair one strand at a time. There is a high association with anxiety
disorders (PTSD, OCD, MDD). The vignette will always give you
a woman. Since she pulls hair out in different regions at different
times, there’ll be patchy alopecia with hair regrowth at different
lengths. Diagnosis is made by shaving a “window” into her scalp
and assessing equal hair growth within the window; the
regrowing hair is too short to be plucked, hence it’s allowed to
grow. Treatment is to treat the compulsion (see psychiatry).

Traction Alopecia
Permanent scarring resulting in permanent alopecia that’s
secondary to keeping the hair pulled tightly (extreme braiding)
that puts excessive traction on the root. This is preventable but
irreversible once it occurs. RIP man buns.

Chemo
Chemotherapy targets rapidly dividing cells. This means the
cancer (yay!) but also the gut (diarrhea), bone marrow (anemia,
infection), and hair. Hair loss is expected, anticipated, and
without treatment. Anagen-effluvium is when chemo disrupts
growth, producing thin fragile hairs that shed with light touch,
effectively skipping from anagen to exogen. Telogen-effluvium
shifts anagen hairs to telogen; thinning the hair as the hair follicles
exit growth phase too early.

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