USMLE Step 1

Dermatology
Rahul Damania, MD, FAAP
 Dermatology

• These will comprise some of your

imaging questions on Step 1

Welcome! Dermatological skin conditions

• Also focus on systemic diseases that can

cause rashes
• Bacterial & viral lesions
Skin Histology
• Epidermis layers full of keratinocytes:
– What cell layer has anucleate cells rich with are rich in
keratin?
• Corneum
– What cell layer that has cells involved in process of
keratinization?
• Granulosum
– What cell layer is full with desmosomes?
• Spinosum (desmodomal separation causes spines)
– What cell layer is the regeneration layer?
• Basalis
• Dermis:
– Sebaceous glands, blood vessels, and connective tissue
• Dermatophyte infections can occur here
Skin Histology
• A 27-year-old Caucasian female presents with
weight loss and weakness. She feels dizzy and
lightheaded. Physical exam reveals several areas of
her skin including her elbows and knees are more
tan than other areas. The cells which are stimulated
are derived from which embryological layer?
– Neural crest  melanocytes
• Adrenal insufficiency (primary)  POMC is a precursor for
three hormones:
– ACTH, MSH, beta-endorphin
Mnemonic Neural Crest Derivative
M Melanocytes
O Odontoblasts
T Tracheal cartilage
E Enterochromafin like cells
L Laryngeal cartilage
P Parafollicular C cells of Thyroid
A All ganglia and Adrenal medulla
S Schwann Cells
S Septum (aorticopulmonary)
Melanin
• Biochemistry review: What amino acid is the
precursor to melanin?
– Tyrosine
• Phenylalanine is a precursor to tyrosine. What is the
pathology related to the lack of an enzyme which
converts phenylalanine to tyrosine?
– PKU – patients present pale and fair, blue eyes and
characteristic, musty body odor

Dopamin
Phenylalanine Tyrosine Dopa NE Epi
e
TH DDC DH SAM
Dermatological Terms
• Blister containing pus.
– Vesicle
• Dried exudate from vesicle, bulla, or pustule.
– Crust
• Elevated skin lesion <1 cm
– Papule
• Flat skin lesion <1 cm
– Macule
• Elevated skin lesion > 1 cm
– Plaque
• Flat skin lesion > 1 cm
– Patch
 • Vesicle containing puss?
• Pustule
USMLE
Dermatology • Transient papule or plaque?
(Basic Terms) • Hives or urticaria

Fluid
Flat lesion Raised lesion containing
lesion

<1 cm >1cm <1 cm >1 cm <1 cm >1 cm

Macule Patch Papule Plaque Vesicle Bullae

Birthmark
Chickenpox, Bullous
Freckle (congenital Acne Psoriasis
shingles pemphigoid
nevus)
 Viral Skin Lesions
• An unimmunized child presents with fever to
102 F, runny nose, and eye discharge. Patient on
exam has a benign lung exam however is
coughing frequently. White spots on oral
mucosa are present. What is the likely
diagnosis?
– Measles (rubeola)  what are the oral lesions?
• Koplik spots on buccal mucosa
• Begins on head
and then spreads
to trunk and
extremities
• Darker than
rubella and can
coalesce
 Viral Skin Lesions
• An umminized child presents with fever to 102
and a pinkish red eruption. The patient on exam
has lymphadenopathy behind the hear that is
tender. What is the morphology of the likely
etiology?
– RNA Toga-virus  Rubella
• What is the difference between Koplik spots and
the oral lesions seen in rubella?
– Forchheimer spots are on the posterior soft palate
• Rubella the rash
is a pinkish
maculopapular
eruption that
does not coalesce
• Begins at hairline
and spreads
cephalocaudally
 Viral Skin Lesions
• A 2 year old child presents with 6 days of high
fevers to 102.5 F. He has cervical lymphadenopathy.
Mother notes several seizures in relation to the
fevers. Today was the first day he does not have a
fever, and characteristically has a maculopapular
rash on exam. What is the likely morphology of this
etiology?
– HHV-6 (DNA virus)  Roseola
• Rash develops after the fevers and
lymphadenopathy is different than rubella
 Viral Skin Lesions
• A woman presents with joint pain and low grade fevers.
She has joint pain that is transient in upper and lower
extremities. History is notable for febrile contacts
throughout the child care center which she is
employed. What is the characteristic rash description
behind the likely etiology?
– Slapped cheek rash --> Erythema infectiousum
• Caused by parvovirus B19 (DNA virus)
• The patient comes for follow-up continues to have
chronic arthritis and on routine blood work is found to
be anemic and thrombocytopenic with low reticulocyte
count. What is the likely diagnosis?
• Aplastic anemia
 Viral Skin Lesions
• A male presents with a pruritic rash that is
prominent on the trunk. He presents to you as he
now has tingling. The rash has various macules,
vesicles and pustules and is near the umbilicus
extending to the posterior left flank. What is the
likely anatomic sensory area which is affected?
– T10  Herpes Zoster (shingles)
 Viral Skin Lesions
• A 4 year old male presents with fevers and
decreased PO. On exam you note small vesicles on
the ventral surfaces of the hands. He has had
multiple children in daycare having similar
symptoms. What is the likely morphology of the
likely etiology?
– Coxsackievirus  picorna-virus (RNA virus)
• What are other Picorna viruses?
– Polio virus
– Echovirus – aseptic meningitis
– Rhinovirus – common cold
– Hepatitis A
Mnemonic Rash on Palms and Soles

Men drive Meningococcus

Kawasaki Kawasaki disease

C Coxsackievirus A
All others
A (Toxic Shock syndrome, Janeway lesions,
Oslers nodes, Reiter’s syndrome)
R Rocky Mountain Spotted Fever

S Secondary Syphilis
 Bacterial Skin Lesions
• A patient with recurrent nose bleeds presents to the ICU
with a desquamating rash on palms and soles, fever,
vomiting, rash, hypotension, multiorgan failure, elevated
AST, ALT, and direct bilirubin. Nasal packing is seen on
exam. What is the mechanism behind this toxin?
– TSST-1 Super antigen  bridges MHC II to TCR. What
particular region of TCR?
• V-beta region  causing massive lymphocyte release
– Causes desquamation of the hands/soles
– Remember this is not an endotoxin
 Bacterial Skin Lesions
• Immunology review:
• In gm negative sepsis what is a major virulence
factor?
– Endotoxin
• What is the other name?
– LPS
• What portion is antigenic?
– Lipid A toxin
• LPS – activates macrophages, cytokine release, and actives
coagulation cascade
• Exotoxin how is it different?
– Protein based  A-B (A active toxin, and B binds to cellular receptor)
 Bacterial Skin Lesions
• An infant presents with fever and hypotension
diffuse blisters are seen which disappear upon
slight pressure. What is the likely physical exam sign
seen described in this patient?
– Staphylococcal Scalded Skin Syndrome 
Nikolsky sign (+). What other path?
• Pemphigus vulgaris
– Mechanism of A+B toxin?
• Epidermolytic toxins A+B bind to desmoglein 1
of desmosomes  skin splits at the stratum
granulosum.
 Bacterial Skin Lesions
• A toddler presents with recurrent runny nose. Mother is
frustrated because she notices that his nose is constantly
runny to the point where he has now non-itchy pustules
surrounding his nose and peri-oral region. He has vesicles
with characteristic yellow-tinged hue. What is the likely
organism?
– Staph aureus – second is Streptococcus pyogenes
– Imetigo
• What is the treatment?
– Mupirocin
• MOA: inhibits t-RNA synthetase
• True or false:
– Patients who develop nonbullous impetigo caused by
Streptococcus pyogenes can progress to having PSGN.
• True
 Cellulitis
• A patient presents with redness and pain to his
calf. He was running away from a neighbor’s dog
which bit him. Exam shows slight purulence with
significant erythema around the calf site, bit
mark is visible. What is the likely organism?
– Pasteurella multocida
 Scarlet Fever
• A young child is brought to the peds by his mom
who reports the boy has had a sore throat for two
weeks. She noticed he has developed a red flush in
the skin with a bright red tongue. He is increasingly
agitated and the rash appears to be spreading to his
trunk. What is the likely VF behind this diagnosis?
– Scarlet Fever (S.Pyogenes)  Erythrolysin, Streptolycin
• Patients who develop scarlet fever caused by Streptococcus
pyogenes can progress to having PSGN
• TRUE
• A teenager presents with the
following on his forehead. What
is the diagnosis?
– Comedonal acne
• White heads and blackheads
– Mechanism?
• Androgen related increase in sebum
and excess keratin block follicles 
blockage of tube
• A teenager presents with the
following on his cheek. What is
the diagnosis?
– Pustular/inflammatory acne
• Pimples
– Organism?
• Propionibacterium acne  sebum
converted to FA  irritation 
pimple
• A teenager presents with
the following on his chin.
What is the diagnosis?
– Nodular acne.
• Scarring and tract formation.
Acne Treatment
• A woman comes in with mild acne. She has a few comedones with
an occasional inflamed papule or pustule. What is the treatment?
– Topical benzoyl peroxide
– Topical antibiotic
• Clindamycin or erythromycin.
• A man has failed initial therapy for acne and has numerous
papules and pustules with mild scarring. What is the treatment?
– Topical benzoyl peroxide
– Topical Vitamin A (isotretinoin). Adverse effect?
• Photosensitivity and IIH
• Teen very depressed as she has numerous large cysts on her face
and neck. Nothing has worked and she is severely scarred. What is
the treatment?
– Oral antibiotic: tetracycline. MOA?
• Binds to 30S ribosomal subunit; prevents attachment of aminoacyl-tRNA
– Oral isotretinoin  decreases sebum production.
• Adverse effect?
– Extremely teratogenic
Fungal skin infections
• A wrestler presents with a rash with a rash on his body. He
states that it is not itchy however on exam you note a central
clearing with raised borders. What is the likely diagnosis?
– Tinea corporis
• Superficial mycoses. What is the most common tinea infection?
– Tinea pedis
• A patient who presents with hair loss in a patchy distribution.
He has multiple black dots on the occipital area. Areas of
circular hair loss are seen on exam. How does the treatment
of this etiology differ from tinea corporis?
– Oral/systemic therapy is needed for tinea capitus and tinea
unguinum
• Treatment oral griseofulvin or oral terbinafine. MOA?
– Griseofulvin – microtubule formation inhibitor, has disulfiram-like reaction with
ethanol, teratogenic, induces CYP metabolism
– Terbinafine -- inhibit synthesis of ergosterol, found in the fungal cell membrane via
inhibition of squalene epoxidase
 Microtubule
High Yield USMLE points
inhibiting drug
Mebendazole Anti-helminthic
Griseofulvin Anti-fungal
Colchicine Used for gout and peri-carditis

Chemotherapeutic: Bind Tubulin and inhibit

Vincristine its polymerization into microtubules,
Vinblastine preventing mitotic spindle formation
(M-phase arrest)

Chemotherapeutic: Hyper-stabilizes
polymerized microtubules in M phase so that
Paclitaxel mitotic spindle cannot breakdown
(A-phase arrest)
Fungal skin infections
• A patient presents after vacation to the dermatologist.
It is noted across her body that there are patches of
hypopigmentation, and she is distraught that her whole
body did not tan. KOH preparation is positive. What is
the likely morphology of this etiology on KOH
preparation?
– Spaghetti (hyphae) and meatballs (yeast) appearance 
Tinea versicolor
• What is the likely organism?
– Malessezia furfur
• What is the mechanism behind the hypopigmentation?
– Inhibition of tyrosinase in the synthesis of melanin
» DOPA to melanin
• Patient is given ketoconazole for treatment. MOA?
– Inhibit ergosterol synthesis
Terbinafine

“Azoles”
Fungal skin infections
• An obese patient presents with skin fold hyperemia.
White patches are seen within the erythematous
skin folds. What is the likely infectious etiology?
– Candida  intertrigo
• KOH shows pseudohyphae and yeast
• Candida infections on USMLE:
– Thrush in diabetic or asthmatic on inhaled
corticosteroids
– Vulvovaginitis in female with curd like discharge and >
4.5 vaginal pH
– Diaper rash in baby with satellite lesions
– Esophagitis in a patient with HIV infection <100 CD4
 Fungal skin infections
• An elderly male presents with forgetfulness and
inability to balance his check books. He has a
tremor at rest and has a flat affect when he is
answering questions. On exam you note a greasy
appearing rash on his scalp. You note scales on his
eyebrows and nasal creases as well. What is the
likely diagnosis?
– Seborrheic dermititis  caused by M. furfur
• Another USMLE presentation:
– Cradle cap in newborns
• Treatment?
– Selenium sulfide
 Vitiligo
• A 24-year-old African-American man presents to
your office complaining of irregular depigmented
patches on his hands and around his mouth. He has
recently been diagnosed with Hashimoto
thyroiditis.
• Mechanism?
– Autoimmune destruction of the melanocytes  Vitiligo
• What are associations with Vitiligo?
– Hashimoto’s thyroiditis
– Addison’s disease
 Albinism
• Inability to synthesize
Vitiligo melanin.
• Defect in tyrosinase.
• Acquired loss of
melanocytes. • Can involve skin, hair,
or eyes.
• Patchy involvement.
• Skin protection 
melanoma chance
increases.

• Freckle. Mechanism:
• Increased number of
melanosomes.
• No increased melanocytes.
 Nevus
• A patient presents with an elevated, dome shaped
lesion that is tan-brown. The dermatologist
measures the lesion as 5 mm with smooth edges.
What is the likely diagnosis?
– Nevus  benign neoplasm of the skin
• How do you classify nevi – based on where the
melanocytes are located
– Dermal epidermal region, flat, and non-hairy 
junctional
– Within dermis, raised, hairy, common in adults  dermal
 Dysplastic Nevus
• A child presents with multiple 10 mm brown-
black lesions surrounding an erythematous
background. Biopsy shows no invasion of
basement membrane. There is a family history
of melanoma. What is the likely diagnosis?
– Dysplastic Nevus Syndrome
 Melanoma
• A 54 year old female presents with a growing skin
lesion. She has a history of sun sensitive lesions and
blisters. This runs in the family and a genetic etiology
has been suspected. Exam shows blisters on mucosal
surfaces and tanned regions of skin. On her back you
notice a raised, 7 mm dark lesion with irregular
borders. What is the likely predisposing factor behind
the likely diagnosis?
– History of Xeroderma Pigmentosum  risk factor for
melanoma
• Xeroderma Pigmentosum. What is the mechanism?
– Defect in repairing pyrimidine dimers which can overtime
progress to melanoma
 Melanoma
• What is the difference between radial growth phase and
vertical growth phase?
– Radial growth phase – no malignant potential, lateral spread in
epidermis and papillary dermis
– Vertical growth phase – malignant potential, penetration of
malignant cells into the underlying reticular dermis
• What histological characteristic determines prognosis?
– Depth of invasion into the dermis
• What clinical features make you suspect melanoma?
– Asymmetry
– Border irregularities
– Color variation
– Diameter greater than or equal to 6 mm
– Evolving
Type of Melanoma High Yield USMLE points

Most common with predominant radial

Superficial spreading phase

Occurs in elderly and on face, good

Letigo maligna prognosis

Nodular melanoma Only vertical phase, no radial phase

Located on palm, sole, or nail, poor

Acral lentiginous prognosis
Not related to sun exposure
 Seborrheic
Keratosis
• What is the most benign tumor found in older
people over 50?
– Seborrheic Keratosis  Benign pigmented epidermal
tumor
• A 55 year old male presents with multiple verrucoid
stuck on lesions. He has them on the face, and at
first they were countable however now they have
increased in number and size. What is the likely
next best step?
– CT scan  Leser Trelat sign
• Underyling malignancy like stomach adenocarcinoma
 Acanthosis
Nigracans
• An obese 5 year old patient presents with increased
amounts of bed wetting. He on exam has velvety
hyperpigmented skin changes in his neck fold and
under his arm pit. His mother states she has been
trying to scrub them clean. What is the likely next
best step in management?
– Obtain glucose level  screen for insulin resistance with
Acanthosis Nigracans
• High association with obesity and metabolic
syndrome  down regulation of insulin receptors
causing insulin resistance
 Keratoacanthoma
• Patient presents with a lesion on his hands; it
has been growing for the past month and has a
distinct umbillication in the center. He had this
lesion before which regressed spontaneously.
Biopsy shows a dysplastic cells with a central
keratin plug. What is the likely diagnosis?
– Keratoacanthoma 
• “Cup shaped tumor filled with keratin debris”
• Pathology will show a “well differentiated SCC”
• Develops rapidly and regresses
 Actinic Keratosis
• Patient is a farmer and has a scaling lesion on the
head. Dysplastic cells are noted in the epidermal
region. Hyperkeratosis is noted as well on biopsy.
What is the likely progression of this lesion if not
treated?
– Squamous cell carcinoma of the skin  actinic keratosis
• Actinic keratosis, acts like squamous cell carcinoma
• Can use agents such as – 5 flourouracil. MOA?
– Antimetabolite, forms 5-F dUMP, inhibiting thymidylate
synthase, decreasing dTMP
 Basal Cell
Carcinoma
• What is the most common malignant skin tumor?
– Basal cell carcinoma
• What anatomical lesion does it preferentially affect?
– Upper lip and inner canthus of eye in sun exposed areas
• A 59 year old male presents with a raised papule on
the upper surface of his lip. The sides of the crater-
like lesion has multiple spiraled blood vessels. What
may histological biopsy of this lesion reveal?
– Cords of basophilic-staining dysplastic basal cells in
infiltrating the underlying dermis
Squamous Cell Carcinoma
• A 49 year old female who was a victim of a burn
presents for discharge from her skin. She has been
having this drainage from the site of her burn, and
has felt as if she never was able to heal the lesion.
Biopsy shows malignant cells invading the dermis.
What is the likely diagnosis?
– Squamous cell carcinoma
• Risk factor: chronic draining sinus, burn, or sunlight
• Favors lower lip
• What precursor lesion can progress to squamous
cell carcinoma?
– Actinic Keratosis
 Icthyoses Vulgaris
• A 20-year-old man presents to his primary care
doctor complaining that his skin looks "scaly." He
notes that his skin has become progressively dry
and itchy over the past several years, and he is
embarrassed about its appearance and doesn not
want his skin to progress to the "lizard skin" his
father had growing up. Past medical history is
significant for asthma. What is the likely
mechanism?
– Increased stratum corneum with absent granulosum
causing increased hyperkeratosis/dry skin
 Eczema
• A 1 yo infant has a itchy red scaly rash on her face. She
has a FMH of asthma and allergies, and was recently
diagnosed with cow’s milk protein allergy. What is the
immunological mechanism?
– Type 1 HS  Eczema
• Acute flairs may have spongiosis. What is the
mechanism?
– Inflammation causes fluid within the epidermis
• Infants: face and extensor surfaces  adults/kids:
flexural creases
• Relate to atopic features
• A patient with eczema and vesicles on top?
– Eczema herpeticum
 Job Syndrome
• A patient with recurrent abscesses + eczema
with absence of neutrophils on biopsy of
abscess. What would the likely immunologic E
level be?
– High  hyper Ig-E syndrome
• Deficiency of Th17 cells
• What other immunodeficiency has high IgE and
eczema?
– Wiskott Alrich Syndrome
• Thrombocytopenia + recurrent infections + eczema
 H.S. Mechanism USMLE High Yield

IgE, mast cells, Anaphylaxis,

Type 1
and basophils eczema, allergies
IgM and IgG AIHA, Good
Type 2
autoantibodies pasteur’s
Antigen-Ab Serum sickness,
Type 3 complex PSGN, SLE
deposition nephritis
TB test
T cell delayed
Type 4 Contact
response
dermatitis
 Contact
Dermatitis
• A patient presents with a periumbilical skin
reaction after a recent pair of jeans. What is the
immunological mechanism?
– Type 4 hypersensitivity
• Also watch for a camper who comes back with a
linear, excoriated vesicular lesion
• What are the primary effector cells?
– CD8 positive T cells
 Pemphigus
Vulgaris
• A 51-year-old man presents to your clinic complaining of
painful blisters over his entire body. He notes that he
currently has several ulcers in his mouth as well. Physical
examination reveals severe bullae. You note that a blister
disappears when you rub his skin with your finger. What is
the mechanism behind the diagnosis?
– IgG antibodies against desmoglein at intercellular junctions
between epidermal keratinocytes  Pemphigus vulgaris
• Occurs at what layer?
– Stratum spinosum
• Acantholysis = separation of keratinocytes at spinosum
• USMLE point: PV affects the ORAL mucosa
 Bullous
•
Pemphigoid
A 64 year old man presents to your clinic complaining
of painful blisters over his entire body. Physical
examination reveals severe bullae that are tense. You
note that a blister does not dissapear when you rub his
skin with your finger. What is the mechanism behind
the diagnosis?
– IgG antibodies against hemidesmosomes of the epidermal
basement membrane  Bullous pemphigoid
• Occurs at what layer?
– Basement membrane
• Linear band of Ab along the basement membrane
• USMLE point: BP does NOT affect the oral mucosa
Dermatitis Herpetiformis
• A patient presents with diarrhea and abdominal pain. She has
a history of recurrent infections, and now is having weight
loss. She has an erythematous rash that is pin-point and
vesicular on the extensor regions and in the gluteal area.
They are pin-point, vesicular lesions that are non-painful but
itchy. Her anti-tissue transglutaminase is positive. What is the
likely treatment?
– Dietary modification  Dermatitis Herpetiformis
• What is the etiology of her abdominal pain?
– Celiac disease  autoimmune intolerance of gliadin
• What is the pathological finding in this rash?
– IgA-anti-IgA complexes in the dermal papillae
– Type 3 HS
• What other pathology has IgA deposits in the skin?
– Henoch-Schloein purpura
 Lichen Planus
• A 40 year old male with chronic hepatitis C presents
with a itchy rash that is on his legs. It is papular and
extends throughout his shin and ankle region. He has
subtle white oral lesions as well. What is the
pathological finding of this rash?
– Inflammation at the dermal epidermal junction (‘sawtooth’
appearance)  Lichen planus
• What are the oral lesions?
– Wickham striae
• The P’s of LP: Pruritis
• Purple
• Polygonal
• Planar
• Papule
 Psoriasis
• 34 yo woman with chronic skin rash. Shows well
demarcated coral colored plaques with silvery scales
over the scalp, elbows and knees. You remove the
scales and see pinpoint bleeding. What is the clinical
sign just observed?
– Auspitz sign  Psoriasis
• Mechanism: extension of the papillary dermis to
surface epithelium and elongation of dermal papillae
– Rete ridges
• Scaling lesion that has HLA relationship +
environmental factors
• Immune cells in the stratum corneum are called:
– Munro abscesses
Psoriasis
• A woman has a pruritic silver scaly lesion on her
elbows. What is the best therapy for localized disease?
– Psoriasis  Topical steroids (triamcinolone)
• Prevent skin atrophy with calcipotriene (Vit D analog)
– Medications used to decrease IL-2 release?
• Tacrolimus and pimecrolis  NFKB inhibitors  inhibit calcineurin
• Widespread disease treatment:
– UV light.
– Methotrexate.
– TNF-alpha antagonists  examples?
• Infliximab, Etanercept, Alefacept, & Efalizumab
– Monoclonal antagonist of IL-12 and IL-23?
• Ustekinumab.
 TNF Inhibitors
• When are they the correct answer?
– Crohn’s patients with fistula formation or mod IBD
– Rheumatoid patient that is unresponsive to methotrexate
– Psoriatic arthritis patients
– Ankylosing spondylitis patients unresponsive to NSAIDs
• Remember, all are monoclonal antibodies except
etanercept (protein receptor complex binding TNF)
• Adverse effect?
– Worsen bacterial infections  inhibits the immune system.
What is the next best step?
• PPD test
– Developing lymphoma
 Pityriasis Rosea
• Patient has a rose colored patch that started 3
weeks ago. He now presents with a central
clearing maculopapular rash that is intensely
pruritic. It is around his truncal region. What is
the likely diagnosis?
– Pityriasis rosea
• Herald patch  Christmas tree (follows lines of skin
cleavage)
• Differential: tinea corporis
 Erythema
Multiforme
• Teenager has SOB and low grade fever. X-ray shows
interstitial lung markings consistent with pneumonia.
He begins azithromycin. One-week into treatment he
presents with a dusky targetoid rash on his abdomen
and legs. What is the likely immunological mechanism?
– Type IV HS  underlying etiology: Mycoplasma infection
• What virus can cause you to have recurrent EM rashes?
– HSV
• Medications: Sulfa, PCN, barbiturates, phenytoin
Stevens Johnson Syndrome
• A patient with epilepsy presents to the physician
with fever, and blisters. He has oral erythema and
small macular skin eruption. His medication recc:
carbamazepine, phenytoin, and recently
lamotrigine. What rash can be the most severe
progression of this presentation?
– Toxic Epidermal Necrolysis
• < 10 % body surface area = SJS
• > 30% body surface area = TEN
• USMLE point: watch for a drug trigger
 Prodrome
4-28 days after
Sloughing of trigger > 30 % BSA
epidermis
< 10 % BSA TEN
Mucosal
SJS
involvement
 Erythema
Nodosum
• A 26 yo female presents with abdominal pain and
diarrhea. She has been having fatty stools
chronically. Barium enema shows narrowing at the
level of the jejunum. Patient undergoes EGD and
biopsy shows non-caseating granulomas. A rash on
her lower legs is seen which she reports as mildly
painful. What is the likely diagnosis?
– Erythema nodosum  Chron’s disease
• TYPE 4 HS characterized by subcutaneous nodules on pretibial
area
• What infectious etiologies can cause this rash?
– Coccidiomycosis, histoplasmosis, TB, and leprosy
 UC
Crohn’s • Begins in rectum and
extends to cecum.
• Anywhere from mouth
to anus (MCC terminal arthritis, • Mucosa and submucosa,
ileum) erythema crypt abscesses.
• Transmural, granulomas. nodosum, • Loss of haustra “lead
pyoderma pipe sign”, pseudopolyps
• Cobblestone mucosa, gang
strictures, fistula. • Associate with PSC, and
p-ANCA
• Associate with aphtous
ulcers. • Increased risk for colonic
carcinoma and toxic
megacolon.
Necrotizing noninfectious and inflammatory disease with painful necrotic ulcers
Presentation: sharply demarcated ulcer with raised and violaceous border
purulent base
Porphyria Cutanea Tarda
• A male with chronic hepatitis C presents with
abdominal pain and blistering lesion on his neck and
arms. He has had a history of RBC + urine dipsticks, and
he complains of increased hair growth in areas
surrounding his rash. What is the likely mechanism
underlying this presentation?
– Deficiency of uroporphyrinogen decarboxylase  PCT
• Photosensitivity + blisters + red urine
• What is the amino acid precursor in heme synthesis?
– Glycine
 Glycine + succinyl
coA
Delta ALA synthase: Sideroblastic Anemia, basophilic
stippling with remnants of rRNA, X-linked
Delta ALA ALAD: Lead poisoning, child with dev delay, abd pain,
and microcytic anemia
Porphobilinogen
PROD: AIP, abd pain, port-wine urine, precipitated by
drugs
Hydroxymethylbilane

Uroporphyrinogen UROD: PCT, blisters, red urine, hypertrichosis,

photosensitivity
Corporophyrinogen

Protoporphyrin
Ferrochetalase: lead poisoning –cannot incorporate
iron into heme in the mitochondria
Heme
 Serum Sickness
• A child presents with low-grade fever, hives and refusal
to walk. He has mild lymphadenopathy. His mother
states he was just put on amoxicillin for an ear
infection 7 days prior. What is the likely immunological
mechanism?
– Type 3 HS  serum sickness
• Antibodies to foreign proteins
• An Arthus reaction is similar Type 3 HS however
different:
– AgAb deposition in vascular walls, serosa, and glomeruli
– Activates compliment cascade
– Pain, swelling, hemorrhage and necrosis can be present
– Usually in experimental setting when Ag are injected (Td)
 Mastocytosis
• A patient presents with recurrent plaques,
flushing, and dermal edema. When the skin is
stroked, the examiner is able to see the lines
created. He has been having nasal bleeding and
analysis of his skin shows excessive histamine
granules and +KIT tyrosine kinase gene. What is
the likely diagnosis?
– Mastocytosis
• What medication may be helpful?
– Cromolyn
 Mycosis
• Fungoides
A patient presents with red-brown patches throughout his
body that are raised and scaling. He has been having these
lesions for many year and now he has diffuse skin
involvement with nodular growth. T helper cell markers are
positive on skin scraping. What is the likely diagnosis?
– Mycosis fungiodes  erythroderma + lymph + atypical
T cells
• Sezary syndrome: large, nodules that form with systemic
spread and full body scaling + malignant T-cells in the
blood
• Tennis racket shaped organelles on EM in dermal cells:
– Langerhan’s histiocytosis
 Erythema High Yield USMLE Association

painful subcutaneous nodules

Erythema Nodosum
on shins in IBD patient

Dusky, targetoid rash after

Erythema Multiforme
infection or drug

Rheumatic fever part of the

Erythema Marginatum
JONES criteria

Lyme disease Ixodes tick bite

Erythema Chronicum Migrans
with bulls-eye appearance

Fifth disease caused by Parvo

Erythema Infectiosum Virus B 19, slapped cheek rash
and fever
Thank You for Attending!