0% found this document useful (0 votes)
524 views10 pages

Dermatology USMLE Step 1, 2 Notes

This document discusses several dermatological conditions including systemic lupus erythematosus (SLE), psoriasis, cellulitis, dengue, and bullous diseases. It provides information on taking medical histories for these conditions and examining patients, including symptoms to ask about. For psoriasis and bullous diseases specifically, it describes classifications, precipitating factors, clinical findings, and comparisons between pemphigus vulgaris, bullous pemphigoid, and dermatitis herpetiformis. The document also provides guidance on managing cellulitis and questions to ask patients.

Uploaded by

itzjuliia
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
524 views10 pages

Dermatology USMLE Step 1, 2 Notes

This document discusses several dermatological conditions including systemic lupus erythematosus (SLE), psoriasis, cellulitis, dengue, and bullous diseases. It provides information on taking medical histories for these conditions and examining patients, including symptoms to ask about. For psoriasis and bullous diseases specifically, it describes classifications, precipitating factors, clinical findings, and comparisons between pemphigus vulgaris, bullous pemphigoid, and dermatitis herpetiformis. The document also provides guidance on managing cellulitis and questions to ask patients.

Uploaded by

itzjuliia
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 10

Dermatology

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

Epidemiology ● Peak incidence: > 60 ● Peak incidence: 40–60 ● Peak incidence:


years of age years of age 15–40 years
● Most ● ♂>♀
common bullous autoimmun
e disease

Etiology ● Autoantibodies directed ● IgG antibodies directed ● Most likely


against bullous against desmoglein 3 and d genetic
pemphigoid antigen of esmoglein 1 (mediate kerati predisposition
the epithelial basement nocyte adherence) to autoimmune
membrane ● Exacerbating factors: drugs , reaction
viruses, UV radiation, diet (associated
with HLA-
DR3 and HLA-
DQ2)
● Associated
with celiac
disease;
sensitivity
to potassium
iodide (e.g.,
contrast
medium)

Clinical findings ● A prodromal stage with ● Progression in stages ● Tense, grouped


formation of urticarial ● Spontaneous subepidermal v
lesions may occur weeks to onset esicles(herpetif
months before onset of painful flaccid orm
of blistering. , intraepidermal appearance)
● Large, tense, blisters → ● Intense pruritus
subepidermal blisters on lesions rupture ● Bilateral,
and become symmetrical
normal, erythematous, or confluent distribution, co
erosive skin → mucosal mmonly over
● Intensely pruritic lesions, erosions and elbows, knees,
possibly hemorrhagic, heal crusts → re- buttocks,
without scar formation epithelialization shoulders, scalp
● Distributed on palms, soles, with hyperpigme ● No mucosal
lower legs, groin and axillae ntation but involvement
without scarring
● Oral involvement rare
● Pruritus is typically absent.
● nikolsky sign negative
● Lesions typically first
present on the oral
mucosa (> 50% of
cases), then on body parts
exposed to pressure
(e.g., intertriginous areas)

foliaceous is more similar to this one.

Diagnostics Autoant ● BPAg1 (BP230) ● Desmoglein 3 and desmogl ● Tissue


ibodiesa ● BPAg2 (BP180) ein 1 transglutaminas
gainst e
● bullous pemphigoid antigen
must be hemidesmosome. ● Epidermal trans
(bullow the dermis) glutaminase
● Endomysium

Tzanck ● Negative ● Positive ● Negative


test

Nikolsky ● Negative ● Positive ● Negative


's sign

Histolog ● Subepidermal clefting ● Intradermal suprabasal ● Subepidermal


y and blistering clefting and blistering just clefting
and im ● Eosinophil-rich infiltrates above the basal layer of and blistering
munohi in blisters seen on biopsy the epidermis ● IgA and
stochem ● Separated complement C3
istry
● Deposition of linear IgG and
C3 along standing acantholytic cells deposits
the dermoepidermal on the floor of the blister, in dermal
junction, similar in appearance to a papillae
row of tombstones
● Acantholysis seen in biopsy
● Deposition of IgG in
the intercellular spaces of
the epidermis (esp.
early lesions)

Treatment ● First-line: High-dose ● First-line: High- ● First-


topical steroids(clobetasol, b dose systemic steroids (pre line: Dapsone
etamethasone dnisone) ● Gluten-
● Second-line: ● Immunosuppression (e.g., a free diet
Systemic glucocorticoids and zathioprine, IVIG, rituximab) ● Topical steroids
immunosuppressants (e.g., may be
methotrexate, azathioprine) ● Topical treatment adjunctively
used to control
Immunosuppressive therapy for life severe pruritus
● Low dietary
intake of iodine

Prognosis ● Benign disease, usually ● Often fatal without ● Usually a


responds well to treatment treatment! lifelong
condition
requiring
continuous
treatment and
dietary
adjustments
Variant forms of pemphigus vulgaris: Pemphigus foliaceus
Etiology: autoimmune disease (only antibodies against desmoglein 1 detectable)
Acantholysis at layer of stratum granulosum
Clinical presentation
Formation of bullae in the epidermis, which burst spontaneously because of their (superficial) location
Localized mainly on the face, head, stomach, and back
Almost never with mucosal involvement (unlike pemphigus vulgaris)
Treatment
First-line: systemic steroids
Dapsone
Topical steroids

Variant forms of bullous pemphigoid: Gestational pemphigoid


Definition: bullous, pemphigoid-like dermatosis during pregnancy of unknown cause (most likely immunological)
Epidemiology: 1:50,000 pregnancies (in the US)
Linear deposition of IgG and complement
Type 17 collagen. Dermal-epidermal fissure
● Neutrophil, eosinophil
Clinical presentation
Commonly starts in the periumbilical region during the 2nd and 3rd trimester
Intensely pruritic, mostly non-blistering lesions (eczema, urticarial or papular lesions) on extremities and mucous membranes
Grouped vesicles with herpetiform appearance (“gestational herpes”) usually occur as the disease advances.
Diagnostics: The diagnosis is confirmed via biopsy and immunofluorescence.
Prognosis
Usually self-limiting; heals spontaneously after delivery, but associated with complications (e.g., premature labor, increased lifetime risk
of autoimmune disease)
Likely to recur at future pregnancies

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)

Nonbullous impetigo (∼ 75% of cases) Bullous impetigo (∼ 25% of cases)


Lesions Lesions
papules → small vesicles surrounded by erythema, coalescent Vesicles that grow to form large, flaccid bullae, which go on to
with red halo → pustules that rupture → oozing secretion that rupture and form thin, brown crusts
dries→ honey-colored crusts → heal without scarring Lateral traction causes sloughing of the skin (positive Nikolsky
Negative Nikolsky sign sign)
Localization Localization
Face (most common), especially around the nose and mouth trunk and upper extremities (more extensive than nonbullous)
Extremities Ecthyma: ulcerative impetigo that extends into the dermis (coin-
May be pruritic but is rarely painful sized, superficial ulcer, with a 'punched-out' appearance)
Systemic signs: possible in severe cases (e.g., fever, malaise,
weakness, adenopathy)

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

You might also like

pFad - Phonifier reborn

Pfad - The Proxy pFad of © 2024 Garber Painting. All rights reserved.

Note: This service is not intended for secure transactions such as banking, social media, email, or purchasing. Use at your own risk. We assume no liability whatsoever for broken pages.


Alternative Proxies:

Alternative Proxy

pFad Proxy

pFad v3 Proxy

pFad v4 Proxy