Pathophysiology Assessment 7
Dermatology Professor Hints
Be familiar with the basic vocab in the handouts
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See handout from Dr. Skinner
Estimate how long it has been since an acute illness by exam of the nails
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Rate of growth of fingernails: 3mm/month
Rate of growth of toenails: 1mm/month
Use these to relate to when the acute illness happen and calculate length of time.
Distinguish among the clinical presentations of bullous pemphigoid, pemphigus vulgaris, porphyria
cutanea tarda, impetigo, contact dermatitis, urticaria, dermographism, and fungal infection. Know
antigens responsible for various blistering diseases
Disease
Bullous Pemphigoid
Clinical Presentation
Elderly, pruritic, bullous
“Blistering” lesion
1st part of disease is urticarial
phase with eosinophlia
Pemphigus Vulgaris
Large blisters “bullae” , if you
push on blister it moves
laterally
Prophyria Cutanea Tarda
Hypertrichosis (excessive hair
growth) of face,
photosensitivity,
hyperpigmentation
Impetigo
“Golden and honey crusted
scabs”, acute onset, usually
peri-oral
“outside rash”
Contact Dermatitis
Key Points
Autoantibodies to BPAg1 &
BPAg2 (this is the part of the
protein within the
hemidesmosome of basement
membrane)subepidermal
lesion
Linear band of IgG at
basement membrane upon IF
IgG attacking desmoglein III
(between keratinocytes)
causing acantholysis and
suprabasal epidermal
separation
Defect in heme production
(uroporphyrinogen
decarboxylase) , can see
fluorescence of urine under
wood’s lamp
Skin infection, typically S.
aureus (less often Strep)
Type IV hypersensitivity
Poison ivy is prototype, can be Allergen picked up by
contact with nickel, jewelry,
langerhans cell, taken to
etc.
lymph node and presented to
T cells (takes time)
Redness, bumps, thickened
skin, blisters, oozing scrusts,
Epidermal edema (contrast
thick scaly skin
Pathophysiology Assessment 7
Dermatology Professor Hints
with urticaria)
Urticaria
“inside rash”, transient, itchy,
edematous, lightly
erythematous, papules or
wheals with central clearing.
*Streaks and blisters are
characteristic of plant
dermatitis (teacher said to
know this for exam)
Dermal edma, Type 1
hypersensitivity, IgE
mediated, hives, etc.
Can be due to drugs, foods,
malignancy, etc.
Dermographism
Complaint of itching, when
skin is scratched hives show
up
Fungal Infection
(dermatophyte)
Tinea’s
Don’t order random lab tests,
maybe a CBC, ESR, and
relevant chemistry panel
Normal skin, but when
scratched produces hives (we
perform this and we have the
diagnosis)
Tinea pedis: Athletes foot
Tinea cruris: Jock itch
Tina corpora: Ringworm of
body
Tinea capitis: infected hair
shafts on scalp
Tinea unguium: Nails
Know dx criteria for atopic dermatitis
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Pruiritic skin disease of uknown origin typified by pruitus, eczematous lesions, xerosis
“The itch that rashes”
Acute, eczematous, crusted scaly plaques, marked by excoriation
Facial and extensor involvement in infants, flexor involvement in adults (very testable)
Major criteria
o Pruitis
Pathophysiology Assessment 7
Dermatology Professor Hints
o Morphology & Distribution
 Flexor adults
 Extensor/facial in infants
o Relapsing dermatitis
o History of dermatitis
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Minor criteria
o Dennie morgan folds under eyelid
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o
o
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Pityrasis alba (ill defined patches on cheeks and skin)
Icthyosis (fish scaled appearance on lower extremities)
Hyperlinear palms (marked skin lines on palms)
Keratosis pilaris (lateral aspect of arms and legs are hyperkeratotic, papules
around hair follicles)
Know causes (and clinical presentations thereof) of alopecia
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Androgenic Alopecia
o Common baldness
o Gradual miniaturization of hairs with transformation of large terminal follicles
into small ones
o Dependent on DHT
o Men: Frontotemporal recession, women at the crown of scalp
o Treat with minoxidil or fenasteride
o Propecia inhibits Type 2 5-alpha reductase
Telegen Effluvium
o Excess of hair shunted into telogen phase from anagen
o Pregnancy is the prototype
Anagen Effluvium
o Drugs can cause, effects 80-90% of hair
Alopecia Areata
o Circular areas of complete hair loss with normal scalp
o Nail pitting associated with this (know this)
o Lymphocytic infiltrate, immunological process
Traction alopecia
o Use or rollers, combs, etc.
Folliculitis
o S. Aureus is main cause (know this)
o Inflammation of opening of hair follicle
o Less often caused by pityrosporum
Pathophysiology Assessment 7
Dermatology Professor Hints
Know epidemiology of squamous cell, basal cell and melanoma. Distinguish among them by appearance
(description). Know common sites for metastasis, genetic and viral associations
Cancer
Squamous Cell
Carcinoma (SCC)
Epidemiology
Associated with cumulative
sun exposed,
Appearance/Description/Associations
Associated with stratum spinosum
keratinocytes
Risk factors:
p53 mutation
UV, HPV, chronic
inflammation, burns,
arsenic, radiation,
leukoplakia
Metastasis to lymph nodes
and lung*
Nests of tumor cells, keratin pearls
Basal Cell carcinoma
(BCC)
**Most common neoplasm
in United States
PCTH Mutation (SHH /SMO
pathway)
Risk factors:
“Pearly border and telangiectasia”
UV, fair complexion,
sunburns, FH,
immunosuppression (10x
increase)
Metastasis is rare*
Histologically can have different
subtypes (looks more basophilic
histologically (purple), palisading
Pathophysiology Assessment 7
Dermatology Professor Hints
basal cells form nests with clefting)
Melanoma
Environment and genetic
predispositions
Nodular: no radial growth phase,
superficial: more radial growth,
pigmented has dark spots,
mopheaform has flatter more
sclerotic appearance
CDK2N (more familial), BRAF
mutation
Acral lentiginous melanoma
most common in dark
skinned patients
melanoma under nails
and on soles of feet
Assymetric
Lentigo
malignamelanoma in situ
in older individuals
(remember lentigo is just
liver spots, lentigo maligna
is melanoma in situ
transposed on a lentigo)
Diameter >6mm
Border Irregularity
Color Irregularity
*Ugly duckling sign is buzzword for
melanoma according to Dr. Kennedy
(one mole looks different than rest)
Nodular melanoma (starts
off in vertical phase)
According to PaPh 50% develop
from nevi, does not correlate to all
sources I’ve read.
First radial growth phase, then
vertical (vertical has poor prognosis
based on depth)
Lymph node involvement is #1
prognostic factor, based on initial
Pathophysiology Assessment 7
Dermatology Professor Hints
biopsy however it is depth of vertical
growth
Know pathophys of warts, treatment thereof
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Caused by HPV, virus inoculated by defects in epithelium
Condylomata accuminata
o HPV 6,11 (low risk for cancer), 16 and 18 high risk
Flat warts can be spread by shaving
Treatment
o Duct tape, salicyclic acid, liquid nitrogen, TCA, cantharidin, podophylin, laser,
imiquimod (promotes innate immunity), oral cimetidine, intralesional candida
antigen
Know exacerbating factors of acne
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Disorder of pilo-sebaceous units
Plugging of follicular hole
Exacerbating factors
o Increased testosterone causing increased sebum secretion (androgen receptors on
sebaceous glands)
o Mechanical irritation
o Greasy occlusive products
o Hyperandrogenic states
 Polycystic ovarian disease
 Virilizing tumors
 Congenital adrenal hyperplasia
o Steroids can induce acne (especially on back/upper trunk)