Dermatology USMLE Step 1, 2 Notes
Dermatology USMLE Step 1, 2 Notes
Cellulitis
History taking
● Malar rash
● Discoid rash
● Photosensitivity
● Alopecia, dry eyes and mouth, oral ulcers
● Gangrene of fingers, Raynaud’s phenomenon
● Chest pain, dyspnoea
● Joint pain
● Seizures
● Change in urinary frequency and volume, haematuria, frothy urine, loin pain
● Anaemia = pallor, chest pain, palpitation, fatigue, giddiness, dyspnoea, jaundice Leukopenia = susceptibility to infections
Thrombocytopenia = gum bleeding, easy bruising, menorrhagia
APLS = history of recurrent spontaneous abortion, DVT/PE, AMI, CVA
● Constitutional (fever, LOA, LOW, malaise)
Examination
“This patient most likely has SLE as evidenced by the butterfly rash affecting the nose bridge but sparing the nasolabial folds.”
Proceed with the following:
General appearance
• Weight loss (due to chronic inflammation)
• Cushingnoid appearance (due to steroid therapy) Hands
Management
Start antibiotics
for patients who have cellulitis, need to find underlying trigger. some patients have tinea pedis→ skin breakdown, facilitating bacterial
entry. treat for interdigital intertrigo
if prophylactic antibiotics - probably would be penicillin
Cellulitis mimickers
Near medial malleolus with erythematous background → stasis dermatitis
gout → colchicine instead of antibiotics!
Psoriasis
a polygenic disorder, aetiology is multifactorial - environmental and genetic
Classification
5 or 6 clinical presentations of psoriasis (depends on resource)
1. Chronic plaque psoriasis.
2. Guttate psoriasis (small, symmetrical and superfi cial papular lesions scattered over the body, especially the trunk).
3. Erythrodermic psoriasis (generalized erythema and scaling, with risk of sepsis and cardiovascular compromise in severe
cases).
4. Pustular psoriasis (either limited to the palms and soles or generalized).
5. Inverted
6. Hyperkeratotic palmo-plantar psoriasis.
7. Flexural psoriasis (mainly affecting intertriginous areas).
From a clinical perspective, psoriasis can be regarded as a spectrum of different cutaneous manifestations. At any one point in
time, different variants can coexist in a particular individual.
Precipitating factors
● Physical trauma (Koebner phenomenon).
● Infections (classically beta-haemolytic Streptococcus ).
● Drugs (e.g. beta-blockers, antimalarials, lithium, NSAIDS and steroids).
● Psychological stress (although hard evidence for this is lacking).
● Alcohol.
● Tobacco.
● Climate (psoriasis tends to fl are in cold climates, although some facial psoriasis is worsened by exposure to sunlight).
History taking
HOPC- rash? joint pain?
● Duration, distribution, progression of skin lesion
• when did the rash start? (chronic with acute exacerbation vs acute)
● Description of lesion - (small vs large plaque, scaly, pink, blistering, vesicle, pustule, discharge)
• how has it changed since onset? ever had it before?
• distribution
• itch? pain? bleed?
● Exacerbated by - alc, drugs, NSAIDs
● A/W
• nail
• joint pain, stiffness (aka back pain) → loss of function
• pruritus
• HLA B27 related sx - IBD
● PMHX
• skin: UV light tx. current medication/management
• atopy - hayfever, asthma, eczema
• skin reaction to sunlight/ use of sunblock?
● meds
• topical, oral, etc
• TCM
• OCP (erythema nodosum)
● Fam HX
• HLA B27 disorders (+ in 30% pt)
● Social HX
● cosmetic concerns, psychological burden
Examination
“This patient most likely has psoriasis as evidenced by te raised erythematous plaques with silvery scale”
Proceed with the following:
Nail
● pitting
● onycholysis
● subungal hyperkeratosis
Joint
● mobility aids around bed
● tender swollen joints , deformities
Management
Questions
What is the Koebner phenomenon? Psoriasis appearing at the sites of trauma to the skin (e.g. surgical scar, site of phlebotomy,
microtrauma to knees etc.).
How can you establish the severity and functional status of these patients?
This can be done using the PASI and DLQI: PASI: the Psoriasis Area and Severity Index is an objective assessment of the severity of
psoriasis. It takes into consideration redness, scaling, thickness and area of involvement. Maximum score is 72. Whilst the PASI
score is routinely measured in dermatology clinics and for clinical research purposes, this evaluation during PACES would not be
expected.
Dengue
IgM, NS1 antigen
supportive treatment
IV hydration
trend platelet
monitor for bleeding manifestations
daily FBC
KIV TXA if heavy bleeding
Bullous Diseases
Pemphigus (Inflamm disorders): Blistering/bullous disorders
Bullous pemphigoid Pemphigus vulgaris Dermatitis herpetiformis
Impetigo
Pathogens
Staphylococcus aureus: ∼ 80% of cases
Causes both bullous and nonbullous impetigo
S. aureus strains that produce exfoliative toxins A and B are responsible for bullous impetigo.
Streptococcus pyogenes (GAS): ∼ 10% of cases: causes nonbullous impetigo only
S. aureus and GAS coinfection: ∼ 10% of cases
Predisposing factors
Warm and humid climate
Crowded, unsanitary living conditions; poor personal hygiene
Medical conditions
Atopic dermatitis and other skin conditions
Diabetes mellitus
Immunodeficiency (e.g., HIV, post-organ transplantation, systemic corticosteroids)
Route of infection
Primary impetigo: bacterial infection of previously healthy skin
Secondary impetigo (impetiginization): secondary infection of pre-existing skin lesions (e.g., scabies, insect bites, abrasions, eczema)
Skin cancer
basal cell carcinoma
pink, flesh coloured, pearly papule. +/- necrosis (rodent ulcer), talengiectasia noted over the lesion.
- not dermal nevus bc it would have no talengiectasia, hair growing over it, not pearly
excisional biopsy with NARROW (not wide) margin (3-5mm)
SCC: crusting, ulceration
Leukoplakia vs SCC
62 YO man with 20-pack-year smoking hx and recently began chewing tobacco. drinks 6-10 beers each weekend. pmhx significant for
T2DM and HTN. last HbA1c was 8.3%. BMI 27.5%. on oral examination, white patch is seen on buccal mucosa. the lesion appears to have
a granular texture, is not indurated, and is not removed by scraping with a tongue depression. no regional LAD, no ulceration or erosion,
and no surrounding erythema or induration.
- this points toward Leukoplakia more than SCC. if it were SCC, expect LAD, erosion, etc
Scabies
itching in nursing patient is scabies until proven otherwise
can treat immediately if high dose
isolate pt
staff nurse to kindly weigh patient
ivermectin x stat dose
permethrin x 3 days (3 bottles) - dose is weight based.
next day - call nursing home ensure env is cleaned, everything washed in 40c water. all healthcare staff and neighbor have to undergo
scabies regime as well.
Others
Lichen planus
a lot of P's - purple/pink, polygonal papules, plaques
often associated with hep C
treatment: high potency steroid (betamethasone). self-limited, goes away in 2 years
Rosacea
Classified into 3 types: papulopustular, phymatous, and ocular
Unknown mech. Most likely a chronic inflammatory response to cutaneous microorganisms, UV light damage, vasomotor dysfunction
Present with: erythema, facial flushing, telangiectasias
Typically precipitated by heat, hot drinks, alcohol, emotion
Treatment:
avoid the sun
if papulopustular: topical metronidazole, azelaic acid, ivermectin. PO tetracyclines if severe
prognosis: usually intermittent, but can lead to permanently flushed skin too
erythematous papules & pustules in central face: acne (papulopustular) rosacea
not acne vulgaris, no comedones
Erythema multiforme
cell-mediated immune process
trigger: HSV (hx of painful sores/ genital ulcers), sulfonamide, collagen vascular disease
appearance: targetoid lesion on the palms
self limiting
vs SJS would have nikolsky positive, and DRESS would come with end organ damage
vs Lyme disease - lyme targetoid lesion less raised, on tracks rather than extremities
Drug chart
how long has pt been on a drug/herbal med/ tcm
Why is drawing a drug chart impt? because knowing the time interval may help you identify the pathology
Chronology of reactions
Herpes Zoster
Allergic Contact Dermatitis