Basics

Describing a lesion
o Type of lesion
o Colour
o Texture
o Site
o Distribution/Symmetry
o E.g. Maculopapular lesions which is red, smooth, and grouped only on the right wrist

Colour, Site + Symmetry + Distribution... Type of lesion + SSSCCCTTT

Type of Lesion
o Macule circumscribed change in skin colour without elevation

o Papule solid, elevated lesion which is <0.5cm in diameter

o Nodule solid, elevated lesion which is >0.5cm in diameter

o Vesicle circumscribed elevated lesion which contains free fluid and is <0.5cm
E.g. Herpes (HSV1, HSV2, Varicella Zoster)
o Bulla circumscribed elevated lesion which contains free fluid and is >0.5cm
o Cyst Sac containing liquid or semisolid material, usually in dermis
o Pustule Circumscribed, elevated lesion containing pus

o Plaque raised lesion which has greater surface area compared to elevation
o Scale Heaping up of stratum corneum or keratin
o Lichenification Accentuation of skin markings associated w/ thickening of epidermis

o Ulcer Loss of epidermis and part of dermis (leaving depressed, moist lesion)
o Erosion Loss of epidermis ONLY (shallow ulcer)
Distribution of Lesion
o Discrete Individual lesion
o Grouped Multiple, individual lesions on one area
o Generalised Most of skin of a particular area covered (e.g. generalised over the back)
o Disseminated Multiple, widespread lesions
o Linear Forming a line
o Dermatomal Confined to a dermatome
o Annular Forming a ring
o Polycyclic Formic interlinking circles

Pattern of Lesion
o Symmetrical
o Assymetrical
o Sun-exposed

Colour of Lesion
o White (depigmented)
o Pale (hypopigmented)
o Dark (hyperpigmented)
o Red (erythematous)
o Brown
o Black
Skin Layers
o Epidermis 95% keratinocytes which move up from the Stratum Germinativum (in 4wk)
Stratum Corneum
Stratum Lucidium (only in areas of thick skin e.g. sole of foot)
Stratum Granulosum
Stratum Spinosum
Stratum Germinativum/Basale

Epidermis is avascular; blood supply is from dermal capillaries

Cells include:
Keratinocytes 95%
Melanocytes
Langerhans cells (immune function)
Merkel cells (sensory function)

Pathology of epidermis:
Changes in turnover time (e.g. psoriasis [5d vs normal 28d] rapid turnover)
Changes in surface or loss of epidermis (e.g. scales, crusting, ulcers/erosions)
Changes in pigmentation (e.g. hyper melanoma; hypo vitiligo)
o Dermis
Stratum Papillare (highly vascular for dermis + epidermis)
Stratum Reticulare (highly collagen for structure of skin)

Pathology of dermis:
Changes in contour or loss of dermis (e.g. papules, nodules, ulcers)
Disorders of skin appendages (e.g. hair, sebaceous glands [acne])
Disorders of blood vessels (e.g. urticaria, purpura)

o Sub-cutaneous tissue

Can Liars Get Skin Grafts (with) Prior Rejection

Hair:
o Types: All hair is modified KERATIN w/ shaft + hair bulb (dividing cells + melanocytes for pigment)
Lanugo fine, long fetal hair
Vellus fine, short hair on all body surfaces
Terminal coarse, long hair on scalp, eyebrows, eyelashes, pubic)
o Pathology of hair:
Reduced or absent melanin pigment (e.g. grey/white hair)
Changes in growth cycle duration (e.g. hair loss)

Sebaceous glands (Sebum producing gland which exits with hair follicle)
o Function: Lubricate + waterproofing of skin
o Pathology of sebaceous glands:
Increased sebum + bacterial colonisation (acne)
Sebaceous gland hyperplasia

Sweat glands:
o Types:
Eccrine everywhere in skin, active pre-puberty
E=everywhere
APocrine post-puberty sweating in axilla, genitalia, anus; react w/ bacteria = odor
A=axillary, P=pubertal areas
o Pathology of sweat glands:
Inflammation/infection of APOCRINE glands (e.g. hidradenitis suppurativa)
Overactivity of eccrine glands (e.g. hyperhidrosis Rx: Topical aluminium chloride)

Functions of skin**:
o Appearance/cosmesis

o Protection :
From: UV, mechanical/chemical insult, pathogens, dehydration
How: Quick turnover + avascularity + Langerhans cells

o Thermal regulation
How: When cold hair + adipose; When hot sweat glands + vascular dilation

o Sensation

o Metabolic function
Vit D synthesis
Triglyceride energy storage

When skin is compromised**:

o Appearance Plastic surgery or cosmesis
o Protection + Thermal regulation Wrap in wet cloth or bandaging or other materials to cover
up access for infection
o Sensation Nil
o Metabolic function Supplements if necessary
Stages of wound healing**:
o Hemostasis Vasoconstriction + Platelet aggregation = Clot formation

o Inflammation:
Vasodilation
Migration of neutrophils + macrophages
Phagocytosis or debris + bacteria

o Proliferation Angiogenesis, re-epithelialisation, granulation tissue formation (via fibroblasts)

o Remodeling Collagen reorganisation + scar tissue formation

Bullous and Blistering Diseases
Pemphigus

Background
o What is it?
Bullous (a large vesicle [>0.5cm]) and blistering disease

Location of bulla varies upon which disease is present

o Causes
Autoimmunity to
Vulgaris Mainly Desmoglein 3 (more severe disease)
Foliaceus Mainly Desmoglein 1 (less severe disease)
NB: Bullous pemphigoid not autoimmune; many causes including
drugs (e.g. ibuprofen, ACE-I, penicillamines)

Diseases
o Pemphigus Vulgaris (suprabasal acantholytic vesicle)
Characteristics
Numerous blisters and few bullae, not itchy

o Light finger pressure causes sloughing of skin

Symptoms
****Mouth lesions (90%)****
o NB: SJS needs two mucous membranes +
infection/drug as cause
Dehydration (fluid leaking out)
Infection + Sepsis (bacteria leaking in)

Mortality!

o Pemphigus Foliaceus (subcorneal acantholytic vesicle)

Characteristics
Few bullae which are centered around hair follicles

o Bullous Pemphigoid (subepidermal oedema/blister w/ IgG + C3 deposition)

Characteristics
Many bullae due to thick wall, hence breakage ( dehydration
+ sepsis!); itchy, pre-bullous urticarial rash
Caused by starting new drugs
*****NO oral mucosal involvement/mouth lesions*****
NEGATIVE-
 Diagnosis for ALL
o Best Test: Biopsy

Treatment for ALL

o Initial: Steroids
o Pemphigus vulgaris: Consider immunosuppressants

Pemphigus Vulgaris Pemphigus Foliaceus Bullous Pemphigoid

Cause Antibodies to Antibodies to Desmoglein 1 Many including drugs
Desmoglein 3
Antibodies to
Hemidesmosomal BP
antigens
Location Suprabasal Subcorneal Subepidermal
(epiderm + derm junction)
IgG + C3 deposition
Characteristics Numerous blisters Few bullae Many bullae
Few bullae Centered around hair follicles
90% oral lesions
Positive Negative
Diagnosis Biopsy
Treatment IV Fluid, Topical Steroids, (Sometimes Abx + PO steroids)

Other Bullous + Blistering

Pemphigoid Gestations Pruritic blistering lesion in pregnancy often peri-umbilical but spreading to
trunk, back, buttocks, arms; 2nd + 3rd trimester; rarely in 1st pregnancy; Rx = corticosteroids (oral)
Porphyrias**

Definition: Group of inherited metabolic disorders which should be considered in any patient presenting
with an atypical medical, psychiatric or surgical history

Pathogenesis:
o Pathway starts with Glycine and Succinyl CoA
o Enzyme deficiencies result in overproduction and increased excretion of toxic haem precursors

o Normally when haem is made, inhibits enzyme ALA synthase to stop production of haem
o Haem is broken down in liver
o Low haem can precipitate porphyrias:
Inducing liver enzymes breaks down haem CRAP GPS (hence if epileptic, will need to
take Gabapentin + Benzos to prevent seizures since all others interact with CP450)
Blood loss results in loss of haem

o Haem mainly synthesised in liver + erythroid cells used in haemoglobin + cytochrome P450
o Giving high carbohydrate diet
Succinyl CoA to reduce the haem pathway and hence stop the buildup of toxic metabolites
Types:

Classification:
o Acute porphyria producing neuropsychiatric features
ADP (very rare)
AIP (most common neuropsychiatric porphyria; auto dom; NOT photosensitive)

o Cutaenous porphyria mostly affecting skin

PCT (this is the most common porphyria 1/25000 in UK)
EPP
CEP

o Mixed porphyrias with cutaneous and neuropsychiatric features

VP
HCP
Types: Age 20-40
o Neuropsychiatric (acute attacks, e.g. AIP)
Enzyme deficiency: Porphobilinogen deaminase

Precipitating factors: Drugs, fasting, smoking, alcohol, emotional distress, infection

NB: One of these are present in >90%! NOT photosensitive!

Symptoms:
Prodrome (25%) Anxiety, restlessness, insomnia

Abdominal pain (95%)

Psychiatric features Mania, agitation, depression (any of these)
Neuro features Seizures, motor neuropathies, areflexia (any of these)
Dark/red urine, especially on standing
Sympathetic overdrive Tachycardia, HTN, arrhythmia (rare)
Sensory neuropathy in bathing trunk distribution

Ix:
First: Urine colour
Best: Elevated porphobilinogen in fresh urine protected from light
o Often raised BETWEEN attacked, and markedly raised DURING attacks
o Do not measure enzyme activity (Porphobilinogen deaminase) as can
be normal in 10% - measure porphobilinogen even BETWEEN attacks
(eMedicine and Doctor UK)
Other: DNA analysis, bloods (hyponatraemia)

Rx:
Admit, remove precipitating factor, pain relief
N+V+Anxiety+Restlessness: Chlorpromazine (do NOT use benzos)
Tachy + HTN: Beta-blockers
Definitive management: High carbohydrate load (oral or IV dextrose 10% - up
to 3L in 24hr, but watch for hyponatraemia)
o , hence
pathway cannot be started

Severe attacks: IV Haem arginate/haematin (inhibits ALA synthase)

o Cutaenous Porphyria (e.g. PCT auto dom)

Cause PCT
Inherited (20%) Deficiency of uroporphyrinogen decarboxylase (UROD)
Sporadic (80%) Associated with liver disease chronic HepC, iron overload
(haemochromotosis), alcohol

Symptoms:
Bullous and blistering of dermis in sun-exposed areas due to photosensitivity
(build-up of porphyrin A/B/E in CEP/PCT/EPP respectively)
o Mostly forehead, cheeks, ears, back of hands
Red urine
Splenomegaly
Hypertrichosis (abnormal hair growth over body)
o Hirsutism = Excessive androgen-dependent hair growth (e.g.
moustache, pubic hair, etc); only diagnosed in women + children

Ix PCT
Urine sample analysed under
24hr urine uroporphyrins

Between attacks: Specific enzyme activity (uroporphyrinogen decarboxylase

AKA UROD)

Treatment
All: Avoid sunlight, avoid precipitants (e.g. alcohol, high iron food)
Best medication: Chloroquine (used also in P vivax + ovale)
o Anti-malarial drug which mops up uroporphyrin
Consider: Phlebotomy/venesection (for iron overload from liver disease)
Lead Poisoning (as presents similarly to Porphyrias)

Background:
o Accumulates slowly in body, hence even low doses over time can cause poisoning
o 95% deposited in bones + teeth; and whatever is in blood 99% of that is in RBCs
o Affects CNS, kidneys, bone marrow issues

Risk:
o Children <3 (lead ingestion, e.g. lead-based make up)
o Adults in smelting/refining/alloying/casting/battery industry/scrap industry

Features: Symptoms are CONTINUOUS (unlike porphyria which is intermittent)

o Abdominal pain
o Psychiatric + neuro features (e.g. behaviour issues, aggression, motor and sensory neuropathy)
o Blue gums (specific to lead!)

Ix:
o FBC Microcytic anaemia
o Film Basophilic stippling of RBCs
o Lead levels
<10 = normal
>10 = impaired cognitive development in children
>45 = abdominal pain
>70 = CNS symptoms
>100 = life threatening

o Other
XR of bones bone growth arrest in children
XR of abdomen ingestion of lead
X-ray fluorescence detect overall lead in body
CT/MRI brain consider if CNS symptoms

Rx:
o Level <45 Remove source of lead, conservative Mx
o Level >45
First: Dimercaprol/Dimercaptosuccinyc acid (DMSA)
If not effective of level >100: ADD Calcium disodium edetate
CaNa2 edetate does NOT cross BBB
This allows for lead neurotoxicity of it was to be used alone
Must ALWAYS be used with dimercaprol
Drug Eruptions + Hypersensitivity
Urticaria, Angioedema, Anaphylaxis

Common causes
o Acute urticaria, angioedema, anaphylaxis:
Bugs/Insect Stings
Foods Nuts, sesame seeds, shellfish, dairy)
Drugs Penicillins, Sulfa Drugs, Allopurinol, Rifampin, Contrast, ACE-I
o Chronic Urticaria:
Pressure
Cold
Vibration
Characteristics:
o Acute Urticaria COMING AND GOING RASH!
Rash:
Wheal Cutaneous mast cell release of histamine = leaky capillaries
Redness Inflammatory mediators (e.g. prostaglandins, leukotrienes,
chemotactic factors)
Itchiness
Renal Allergic interstitial nephritis (eosinophiluria)
Blood Drug-induced Haemolysis

o Angioedema Deep swelling involving dermis + subcut (e.g. lip + tongue swelling)

o Anaphylaxis Bronchospasm, laryngeal edema, BP ± ANY signs of urticaria/angioedema

*Fixed drug reaction: Hypersensitivity to drugs causing rash only in one specific area

Treatment:
o Acute and Chronic Urticarial Reactions: Antihistamines (non-sedating AKA 2nd gen)
Loratadine
Fexofenadine
Cetirazine
NB: Rx of anaphylaxis is with diphenhydramine or hydroxyzine (which are sedative)
NB: If refractory, rarely use oral steroid course

o Severe acute urticaria OR angioedema (without resp distress): Antihistamines + Corticosteroids

o Anaphylaxis:
First:
Secure airway + High flow O2
IM Adrenaline (500mcg 0.5mL of 1:1000) repeat every 5min
IV fluid

IV Hydrocortisone
IV Chlorphenamine (sedating)

ITU Support, Salbutamol + Ipratropium nebulisers

Discharge: 2x epi-pens at all times

Erythema Multiforme + Steven-Johnson Syndrome + Toxic Epidermal Necrolysis

Cause
o EM ONLY Infection (*HSV* [main culprit in 50%], Mycoplasma, Strep)

o EM, SJS, TEN Drugs (Penicillins, Sulfa [ , Allopurinol, Rifampicin, AEDs)

All caused by all of these drugs except MH exclusively by sulfa

Characteristics (Spectrum of disease)

o Morbilliform Hypersensitivity (mild) -
Diffuse, red maculopapular rash
o EM Minor (mild)
Erythematous ring surrounded by pale center
Starts symmetrically on extremities (back of hands + feet; arms > legs)
Itchy (mild)
Self-limiting
o EM Major + Stevens-Johnson Syndrome (moderate-severe) dermatological emergency
EM minor characteristics but more severe (+ blistering + mucous membranes)
Mucous membrane x2 (minimum) involvement... e.g. mouth/lips, conjunctiva, resp
Respiratory epithelium involvement (causing pulmonary lesions)
o NB: People with SJS die of respiratory failure
o Toxic Epidermal Necrolysis (severe) Dermatological emergency
ITIVE in >30% skin + SJS characteristics
Biopsy shows full thickness epidermal necrosis + subepidermal detachment

Rx: Remove offending drug, clear infection, supportive care (e.g. fluids, Abx/IVIG if necessary)
o Acyclovir may be used in EM
o IVIg for TEN (first line)
o NB: Death is most often due to sepsis, electrolyte imbalance, multi-system organ failure
Infections
Fungal Infections (a.k.a dermatophyte, tinea _____, superficial fungal infection) ANY asymmet rash
o Causes
Candida
Dermatophytes (fungus inside epidermal keratin OR hair follicle)
Trichophyton
o Trichophyton rubrum , Tinea unguium
(nails)
o Trichophyton tonsurans Tinea capitis

Epidermophyton
o

Microsporum
o

o Diagnosis
Initial Test: KOH Preparation (is it fungal?)
Melts away epidermal cells leaving behind only fungal hyphae/filament
Next test:
Best Test: Fungal Culture (what type of fungus?)
Takes 4-6 weeks to grow in many cases, hence treat empirically first

o Treatment
Hair/nails/scalp NOT INVOLVED Any topical/oral antifungal (e.g. clotrim, oral flucon)
Hair/scalp/nails INVOLVED Terbinafine or Itraconazole
Oral/systemic to penetrate hair + nails
6 weeks fingers, 12 weeks toes 80% cure
Adverse effect of Terbinafine: LFTs
CNS/Heart/Systemic Amphotericin B

o Notes
Tinea ( superficial fungal ):
Capitis Scalp
Faciei Face
Corporis Body/Arms/Legs (RINGWORM)
Manuum Hand
Pedis Food (aka A s Foot)
Unguium Nail (aka Onychomycosis)
Cruris Groin
Specific Fungal Infections
o Tinea Capitis AKA Scalp Ringworm (most com = Trichophyton tonsurans)
Features: Scaling + hair loss (NB: alopecia areata has NO scaling), ± redness
Ix: Scrape + send for MCS
Microscopy may diagnose in 24hr, cultures take 2-3wk
Rx: Griseofulvin, terbinafine, itraconazole, ketoconazole shampoo

o Tinea Unguium/Onychomycosis
Definition: Fungal infection of any part of nail (bed, matrix, plate)
Risk: DM, Immunosuppression
Cause: Trichophyton rubrum (70% of cases), Candida
Features: White crusty/crumbly lesion under nail, cosmetic problem mainly, rare pain
Ix: Scrapings + MCS (micro takes 24hr, culture takes 4-6wk)
Rx: Observe
Very limited: TOPICAL
o Dematophyte (e.g. T rubrum): Topical antifungal
o Candida: Amorolfine nail laquer (1x/wk x12mo)
More than one digit: ORAL
o First: Terbinafine 250mg OD for 2wk
o Second: Itraconazole 100mg BD for 1wk

o Pityriasis Versicolor AKA Tinea Versicolor

Definition: Superficial fungal infection caused by Malassezia furfur

Features: Occurs AFTER sunbathing abroad

Truncal patches which may be hypopigmented, pink, or brown
o If white Often hyperpigmented or pink
o If black Often depigmented

Hence versicolor
Scaling of lesion (common)
Pruritus (mild)

Ix: -green)

Rx:
First: Topical antifungal (e.g. miconazole, terbinafine, selenium sulphide)
Refractory: Oral itraconazole
Bacterial
o Staph Aureus
Impetigo
Types:
o Non-bullous (70%)
o Bullous (30%)

Features:
o Small pustules to start which then develop into:
Honey coloured plaques (yellow, golden)
Crusty
Oozing
Itching

Ix: Clinical (rarely, swabs)

Rx:
o Conservative:
Wet dressings, crust removal, hygiene
No school until 48hr post-Abx or all lesions crusted

o Medical: Antihistamines for all

Small localised: Topical fuscidic acid
If MRSA suspected Topical mupirocin

Wider spread: Oral flucloxacillin

Pen allergic: Erythromycin

SSSS (see below)

Erysipelas + Cellulitis (less common than Strep pyo)

o Strep Pyogenes (AKA Group A Beta-Haemolytic Strep synonymous terms)

Dermis (+ superficial lymphatics) Erysipelas

Definition: Spreading infection of dermis/upper subcut tissue

Features: Red, hot, swollen, painful lower limb

o WELL-DEFINED, RAISED BORDER
o FEVER, MALAISE, RIGORS

Rx: Abx
o Empircal: Fluclox
o Known MSSA: Continue Fluclox
o Strep pyo: Stop fluclox, start Pen V (phenoxymethylpenicillin)
o Pen allergic: Clarithromycin
o Failed therapy: Clindamycin
Complication: Local necrosis, abscess, septicemia

Subcutaneous tissue Cellulitis or Necrotizing Fasciitis

Cellulitis
o Definition: Spreading infection of deep subcut tissue

o Features: Red, hot, swollen, painful lower limb

Border is NOT well-defined or raised
NO fever, malaise, rigors

o Ix: ERON criteria

o Rx: As above for erysipelas
o Complication: Local necrosis, abscess, septicemia

Necrotizing/Necrotising Fasciitis (Nec Fasc):

o Definition: Rapidly spreading infection in deep fascia with 2ndary
tissue necrosis

o Types:
Type 1 = mixed anaerobes + aerobes (often post-op in DM)
Type 2 = Strep pyogenes

o Features: Red, hot, painful, necrotic skin; fever; extremely tender

o Ix: X-ray Soft tissue gas

o Rx: Extensive debridement (most important) + IV Abx

Notes
Staph aureus can also cause cellulitis + erysipelas, but S pyo more common
Can RARELY cause glomerulonephritis (Group A BH Strep AKA Strep Pyogenes)

Cellulitis severity assessment +

management
o Syphillis
Characteristics
Primary Syphilis Contact point (~3wks post-exposure)
o Classically: Single, firm, painless skin ulcer
May be multiple and painful in some cases
o Painless lymph nodes

Secondary Syphilis Skin (~4-10wks post-exposure)

o Rash (diffuse macular)
o Alopecia
o Condylomatum Latum/Lata (NOT accuminata as per HPV)

Tertiary Syphilis CNS/Cardiac (~3-15yrs post-exposure)

Investigations
Primary Syphilis
o First: Dark field microscopy
A type of microscopy which allows spirochaetes to light up
NB: VDRL/RPR only ~75%+ (sensitivity) as chancer/ulcer can
resolve prior to antibody formation

Secondary + Tertiary Syphilis

o First: VDRL/RPR 100%+ (sensitivity)
o Confirm with: Fluorescent Treponemal Antibodies (FTA)
Antibodies against Treponema pallidum (syphilis spirochete)

Treatment
Primary + Secondary Syphilis IM Penicillin (Allergy: Doxycycline)
Tertiary IV Penicillin (Allergy: Desensitize)??
Viral
o Herpes Simplex Virus (HSV)
Characteristics
Multiple, small vesicular lesions (mouth, genitals)
o Can present w/ more severe gingivostomatitis (multiple mouth ulcers)
Can ulcerate (which consequently changes management plan)

Management
If clear lesions:
o First: Acyclovir (or any other antiviral) topical if single lesion, oral if
multiple lesions or gingivostomatitis
o If resistant: Foscarnet (antiviral which does not act via thymidine
kinase)

o Second - Investigations:
Best test: Viral culture

If ulcerated lesions:
o Investigate first, then treat

o Varicella/Herpes Zoster (Chickenpox reactivates to form Shingles; HZ = reactivation) HHV3

Characteristics
Dermatomal distribution of dense vesicular lesions on erythematous bed
o Across chest
o Trigeminal
Whole of trigeminal nerve Cover half of face
Zoster opthalmicus Covers V1 distribution REFER
May start on tip of nose
o Oticus (Ramsay-Hunt)
Burning, tingling, itching (NB: Pain PRECEDES rash by 2-3d)
Can ulcerate (which consequently changes management plan)

Management
Identical to HSV except in duration and dosage!
o Acyclovir [5x daily, cheap] or famciclovir [OD, $$] within 72hr of onset
o OTC pain meds (paracetamol)
o Antihistamine (itching)

Safety net ?rash not getting better, ?post-herpetic neuralgia

Pregnancy:
Risk for mum Varicella pneumonia, encephalitis
Risk for baby:
o 0-28wk = fetal varicella syndrome
o 28-36 = shingles first few yrs
o 36+ = shingles when born

NB: Varicella zoster is one of eight herpes viruses and though Varicella zoster causes
chickenpox and shingles, VZ is synonymous with chickenpox and HZ with shingles
 o Human Papilloma Virus See GUM

o Ulcer Review
HSV Vesicle then painful ulcer
Chancroid
Painful ulcer + painful lymph nodes
Soft

Syphilis
Painless ulcer + painless lymph nodes
Firm + indurated
Lymphogranuloma Venereum (LGV)
Painless ulcer + painful nodes

Parasites
o Scabies**
Cause Sarcoptes scabiei

Pathology Subcorneal feces deposit causing Type IV hypersens 30d later

Characteristics
Linear burrows found on:
o Web spaces
o Fingers
o Flexor aspect of wrist
Itchy (reaction to scabies stool)

Diagnosis Clinical; or scrape + look for scabies mites or fecal pellets

Treatment
Initial: Permethrin 5%
o 1st dose left on for 8-12hr (if removed in <8hr, reapply)
o Repeat in 7d
o Pruritus may persist for 6-8wk further

Second line: Malathion 0.5% (leave on for 24hr + repeat in 7d)

Household contacts: Treat at same time, even if asymptomatic

At home: Clean all clothes + sheets on 1st day of treatment

If HIV+ and crusted scabies: Ivermectin + isolation

Toxin Mediated Diseases (Nikolsky Diseases)
Staphylococcal Scalded Skin Syndrome (SSSS) + Toxic Epidermal Necrolysis + Toxic Shock
o Characteristics of ALL
(desquamation of rash on light pressure)
Hypovolaemia
Diffuse erythematous rash

NB: If shock BP, HR, Creat, LFT) present toxic shock syndrome
o Cause
SSSS Staphylococcal toxi Rx: Abx
TEN Drug (penicillin, sulfa, allopurinol, rifampin, phenytoin) Rx: Steroids, Abx,
Remove drug, IVIg (first line)
ToxShock Staphyloccocal toxin
Treat: Penicillin
If Allergy To Penicillin: 1st gen Cephalosporin

SSSS TEN Tox Shock

POSITIVE (SSSS alone = less common)
(+ rash/skin changes)
Hypovolaemia YES
Shock No No **YES**
( BP, HR, Creat, LFT) Bacteria ONLY in skin May be pyrexial + high HR Also high fever
but NOT shocked
Cause Staphylococcal Toxin **Drug** Staphylococcal Toxin
Penicil, Sulfa, Allopur, Rifamp (complication of SSSS)
Rx Abx IVIg Abx

SSSS
o Definition: Staph toxin causing widespread rash/scalding usually in infants/children
o Features: Identical to TEN but different cause!! TEN has mucosal involvement + EM target lesion
Face, neck, axilla, groin affected most
(in some), highly painful
Recovery in 5-7d
o Rx: Abx, analgesia
Benign and Precancerous Skin Lesions
Seborrheic Keratosis AKA Senile Wart (NB: Keratosis = excessive keratinocytes)
o BENIGN
o Hyperpigmented, well- lesions of the skin
o Large variety of size, shape, colour
o Does not progress

o Ix: Biopsy ONLY if uncertain

o Rx: NONE, unless cosmesis then curettage/cryo

Actinic/Solar Keratosis** - keratosis = build-up of keratin

o PRECANCEROUS Squamous Cell Carcinoma
Low risk 1/1000 AKs turn to SCC

o Features:
Erythematous papules/plaques (often multiple)
Sand-paper/gritty presence on palpation
ONLY on areas of sun exposure (e.g. face [temples common])

o Ix: Biopsy ONLY if uncertain or refractory to initial therapy

o Treatment: Can observe, but safe to remove

Topical 5-FU (2-3wk) will induce skin inflammation
Topical diclofenac gel (for mild AK only mod effic but few S/E)
Liquid nitrogen/cryotherapy

Imiquimod
Curettage + cautery
Photodynamic therapy

If refractory, hyperkeratotic, or nodules: Refer for BIOPSY

Keratoacanthoma
o BENIGN epithelial tumour more frequent in middle age (does NOT get more common with age)
o Features: Smooth dome shaped red papule which rapidly grows central crater forms w/
yellow-brown keratin
o Rx: Conservative spontaneous regression in 3mo is common
These lesions are usually excised, however, as ?SCC
Malignant Lesions of Epidermis
Do NOT do shave biopsy as need to assess true thickness; do a PUNCH BIOPSY

Basal Cell Carcinoma (10x more com than SCC; most com cancer in west world) keratinocyte cancer

o Definition: Slow-growing locally invasive malignant epidermal skin tumour which is thought to
arise from hair follicles

o Risk
UV exposure + past sunburns + low skin types (e.g. 1 = ginger always burn, never tan)
Age (common in elderly)

o Characteristics of nodular (most common type)

Pearly + shiny looking nodule/bump, usually on head and neck
Sometimes/rarely plaque, cystic, pigmented
appearance (rather than nodular)
Telangiectasia
Rarely metastasises
(sometimes necrotic/ulcerated centre if large

o Complications: BCCs around eyes, nasolabial folds, around ear + in post-auricular sulcus
All have tendency to form deep BCCs with chance for recurrence accurate margins
must be taken (i.e. must ENSURE removal of BCC)

Squamous Cell Carcinoma (10x more common than malignant melanoma) keratinocyte cancer
o Risk
UV exposure, skin type, Sun burns in past
Immunodeficiency
(pre-malig), Actinic Keratosis (may see some still on patient with SCC)
Chronic inflammation (ulcers, wound scars

o Characteristics
Hypopigmented (NB: Melanoma is HYPERpigmented) on head and neck
Scaly/crusty lesion, ulcerated but NOT healing
CAN metastasise, must check local lymph nodes

BCC (superficial type, resembles plaque, may have pearly rolled up edge)

BCC with pearly rolled edges surround central

crater
Malignant Melanoma** (least common) melanocyte cancer
o Risk: MMRISK
Moles (atypical)
Moles (multiple)
Red hair
Inability to tan
Sunburns
Kin w/ melanoma

o Characteristics - ABCDEFGHI
Asymmetry
Border (irregular)
Colour irregularity (hyperpigmented, non-consistent)
Diameter >6mm (size of pencil eraser) Most important
Evolves over time
(Firm)
(Gushing blood)
(Heightened/raised)
(Itchy)

Common on legs in women (skirts), trunk in men (no shirts)

o Types:
Superficial spreading (70%) Usually stay local, grow horizontally

Nodular (15%) Black bump on skin, bleeds/ulcerates, grows vertically (most

aggressive)

Lentigo maligna (5%) Penetrates deeply but rarely past BM, stays in-situ, papule on
surface, can remain asymptomatic for a fair while (even >1yr)

Acral lentiginous Melanoma of palm of hand, sole of foot or under nails

Worried about penetration of epidermal basement membrane once enters dermis then spread
to other tissue via local lymph nodes or blood stream

Mets are often to LNs, liver, lung, bone, brain

Diagnosis for ALL
o BCC + SCC:
Clinical examination: Visual inspection + Nodal involvement (this is enough if nodes
NOT palpable can begin Rx)

If diagnosis is uncertain: Punch biopsy

If Rx is by cryo/ablating: Punch biopsy FIRST (so histology known)

If nodes positive, or signs of mets (e.g. bony involvement): CT/MRI

o Melanoma:
First: Full thickness excisional biopsy (w/ 2mm margins) acts as treatment also

If >1mm Breslow depth: Sentinel lymph node biopsy

If inadequate margins taken: Wide margin excision
Stage: Liver USS, CT CAP

Other: S-100 tumour marker

Treatment for ALL EXCISION

o Other options if surgery not possible/low-risk lesions:
BCC Surgical excision w/ 3-4mm margin (gold standard treatment)
Other: Cryotherapy, Curettage + cautery, Topical imiquimod, Radiotherapy

SCC Surgical excision

Other: Curettage + cautery, Cryo, Imiquimod, 5-
surgery, radio (if large), chemo (for mets)

MM Narrow first then wide local excision (gold standard)

First: NARROW margin (2mm) excision
o Look to see if all margins adequately resected
o Determine breslow depth

Inadequate margins taken: WIDE margin excision (margin based on Breslow)

Other Radiotherapy, chemotherapy, lymphadenectomy

Prognosis of MM Breslow depth single most important factor

o
o HIV+ CD4 <100
o Characteristics
Cuboidal epithelium
Blood oozing through lesions
o Diagnosis Clinical (HIV+ with T-cells <100; KS-looking lesion)
o Treatment Anti-retrovirals
KS disappears after CD4 raises as it is caused by Human Herpes Virus 8
Fix immunosuppression Inhibit HHV8 infection KS disappears
DDx For Melanoma - ABCDE

Atypical Nevus
Blue Nevus
Congenital Nevus

Epidermal Nevus
Eczemas/Dermatitis**
Eczema Inflammation of the epidermis/dermatitis
o Types
Common Atopic, Contact, Xerotic, Seborrheic
Rarer Discoid, Venous, Dermatitis Herpetiformis (NOT same as eczema herpeticum)
o Characteristics Papules or vesicles on an erythematous base, pruritus, pain

Atopic Eczema MOST IMPORTANT/MOST COMMON (20% <12y/o)

o Risk FH atopy (eczema, asthma, hayfever/rhinitis, allergies)

o Pathophysiology: Abnormal TH2 cell response

o Characteristics
Itchy, dry scaly papules on erythematous base in flexural regions w/ FH Atopy, 2y/o
Scratching perpetuates itchiness Excoriation/Lichenification
May be weepy lesions in acute phase (i.e. not dry, but exudative)
Infection can ensue after breaching enough skin (e.g. eczema herpeticum)

Infants: FACE + TRUNK

<18mo: EXTENSOR
>18mo: FLEXURAL SITES + FACE

o Diagnostic Criteria
Itchy skin (or parental reported scratching) for >1yr + 3 of the following...
Onset <2
Flexural site involvement REPORTED
Flexural site involvement VISUALISED
Generally dry skin in last year
Hx of atopy

Skin prick test (or RAST test if cannot do skin prick test)
House dust mite (50-60%)
Grass (75%)
Birch pollen (65%)
Cat dander (50%)

NB: Skin prick test = T1 response (read in 15min)

NB: Patch test for contact dermatitis = T4 response (read in 48hr)
o Treatment
First General: Avoid exacerbat facs/stop soap, emollients, soap substitute, bandages
Diprobase Best emollient for eczema
Dermol 500 Best soap substitute for eczema (contains anti-bacterial)

Second: Topical steroids AND/OR Oral antihistamines (e.g. sedating - chlorphenamine)

Use eumovate for mild/moderate flares
Antihistamines have NO benefit on mast cells, but can help sleep loss via their
sedating properties (i.e. do NOT use non-sedating antihistamine) [syst review]

Steroid-sparing: Topical Immunosuppressants Tacro, Siro, Pimecro (-limus)

o T-cell inhibitors (like steroids, without adverse effects!)
o Use when worried about steroid overuse (esp on face)
o Cause burning + stinging

Refractory to all + severe:

Phototherapy
Oral prednisolone or Immunosuppressants (tacro)

Secondary infection:
Antibiotics (e.g. Staph)
Antivirals (e.g. eczema herpeticum) Also stop any topical steroids + Start
fluclox for extra coverage
 Contact Dermatitis/Eczema
o Cause Most commonly METAL (esp nickel), but could be anything (soap, oil, poison ivy, etc)
Irritant Chemicals (non-immune) e.g. soaps, alkali/acidic agents
Allergic E.g. peanuts immune mechanism (type IV hypersensitivity)
o Characteristics
Irritant
Acute quick reaction, sharp margins; Chronic poorly defined margins
Palmar surface of hand w/ increase skin linearity (i.e. more skin lines)
Allergic
Papulovesicular eruption, swelling, itching
Dorsum of hand, head following dye (around hairline, not so much scalp)
o Ix: Patch testing determine allergens (do not do patch testing in other eczema)

o Treatment
Initial: Remove source
If severe: Topical steroids

Xerotic Eczema/Dry Skin (Asteatotic Eczema No fat in skin)

o Characteristics Dry, cracking skin which starts in fall and worst in winter
o Treatment Lotion/lubrication

Skin prick Food allergies, pollen

Do not use in widespread eczema (use RAST instead)
OKAY to use in anaphylaxis as long as allergen is diluted (often 1:10 dilution)

RAST Measure IgE to specific allergen

Use when cannot use skin prick

Skin patch Only for contact dermatitis

Seborrhoeic Dermatitis/Eczema
o Cause Hypersensitivity to fungus (Malassezia furfur) on face + scalp

MF also causes P versicolor

o Epidemiology 2% of population (common)

o Characteristics T-Zone involvement, auricular, scalp

Localised in areas rich with sebaceous glands (i.e. all areas where hair is)
Redness, oily and flaking of face and scalp (which results in dandruff)
Erythematous rash w/ yellow flaky scales

o Treatment
Face + body: Topical steroid (hydrocortisone) AND anti-fungal (ketoconazole)
Scalp:
First: Head + Shoulders (zinc pyrithione) OR Neutrogena T/Gel (tar shampoo)
Second: Ketoconazole (shampoo, oral)

NB: Limited role for emollients compared to other conditions in dermatology!

Venous/Varicose Eczema (Stasis)

o Cause Inflamed skin of legs from venous stasis
o Characteristics
Inflamed skin of legs
o Treatment Emollients, Topical steroids, Leg elevation, Compression stockings
o Complication Venous ulcers

Discoid (Nummular) Eczema Fx: Coin shaped eczema-like lesions; Rx: Emollients, topical steroids
Dermatitis Herpetiformis
o Associations Coeliac (in nearly EVERY patient)
o Pathology IgA deposition in dermis
o Features Intensely itchy papular/vesicular/blistering/bullous rash, affects
EXTENSOR surfaces (esp scalp, bum, elbows, knees)
o Ix: Skin biopsy, Coeliac work-up
o Rx: Gluten free diet, Dapsone (does NOT resolve without treatment)
Dapsone also used in Rx of leprosy; can be used in PJP
Dapsone S/E Methaemoglobinaemia (SOB, Cyanosis, Normal PaO2)

Pompholyx
o Definition: Hand and feet eczema (cheiropompholyx + pedopompholyx, respectively)

o Features: Small blisters on palms + soles, dry cracked skin also, pruritus

o Rx: Cool compresses, emollients, topical steroids

Pityriasis Rosea (NOT an eczema, but similar looking) Pityriasis means flaking
o Characteristics
Diffuse red rash
Oval plaques/patches w/ central scale which does NOT extend to edge of lesion
Herald patch First lesion which appears a few weeks prior to other lesions

NB: Similar to secondary syphilis BUT...

PR has NEGATIVE VDRL/RPR
PR is NOT on hands and feet (as with secondary syph)
PR has a herald patch

PR has generally larger lesions

PR scales do NOT extend to edge of lesion
PR on skin tension lines, not extensor surfaces
PR has herald patch

o Rx: Nil spontaneously clears in 6-12wk; can use topical steroids

Decubitus Ulcers
Definition: Ulcers which occur over any pressure point
o Heel
o Sacrum (on bed)
o Elbows
o Knees
Cause
o Pressure
o Shear force (deep fascia and muscle pulling away from skin)
o Friction (external stimuli against skin)
Mechanism Necrosis or Reperfusion Injury
Treatment
o Prevention: Movement
o Ulcerated: Debride
Hair
Alopecia Areata (hair loss in particular areas)
o Cause
Autoimmune antibodies to hair follicles
Syphilis (secondary)

o Features: Complete hair loss in specific patch w/o any obvious skin lesion

o Investigate: VDRL/RPR
o Treat: Conservative, IV Steroids

o Prognosis Regrowth in 50% @ 1yr, 80-90% eventually

o NB: If complete hair loss Alopecia Areata Totalis

Telogen Effluvium (Telogen = Hair follicle; Effluvium = Flowing away from)

o Cause Severe/overwhelming illness which shuts off hair production
o Features Hair falling out/coming out on hair brush/thinning of hair on head
o Treatment Treat severe illness, hair comes back

Alopecia
Scarring
Trauma, Burns
Radiotherapy
Lichen planus
Discoid lupus
Tinea capitis

Non-Scarring
Male-pattern baldness
Drugs (e.g. chemo, carbimazole, COCP)
Iron deficiency
Alopecia areata
Telogen effluvium
Trichotillomania
Acne Vulgaris**
Definition: Scaly, red skin with comedones (black and whiteheads), pimples, and possibly scarring
o Comedone: Impacted hair follicle within the acne
o Blackhead: Open comedone
o Whitehead: Closed comedone

Pathophysiology:
o Hyperkeratinization of follicle blocks sebum release
o Androgens = sebum
o Propionibacterium acnes converts sebum to fatty acid = pro-inflammatory

Types: C P P NC
o I Comedones, sparse, no scarring
o II Comedones, papules, moderate ± minimal scarring
o III Comedones, papules, pustules, scarring
o IV Nodulocystic, extensive, severe scarring

Treatment

NON-DRUG TREATMENT
o Wash face 2x/day with soap (not more)
o Reduce sugars + dairy products if using in excess
o Laser or blue light phototherapy (both proven benefit)

o TOPICAL MEDICATION B, A, Ab
o First: Topical Benzoyl Peroxide (OTC topical antibiotic start 5%, work up to 10%)
Burning
o Second: Topical Retinoic Acid (vit A derivatives Adapalene, isotretinoin)
Avoid strong sunlight,
o Third: ADD topical antibiotic erythromycin, clindamicin
Can come in combination treatment with Benzoyl Peroxide

ORAL MEDICATION (take 3-4mo to work) Ab, C, Depression-drug

o Fourth: Oral lymecycline OR minocycline (for deep penetration) AND ONE TOPICAL Rx
o Fifth for women: Dianette (COCP w/ cyproterone anti-androgen)
o Sixth: SWITCH to oral retinoic acid (e.g. Roaccutane/Isotretinoin)
HIGHLY TERATOGENIC, depression, psychosis, mood swings

Precautions:
Must use one, but ideally two, forms of contraception
Monthly pregnancy tests
Continue contraception for 1mo after ending treatment

o TREATMENT OF SCARRING
o Laser resurfacing, dermabrasion, chemical peels

If developing scarring, MUST start on ONE oral and ideally with a topical to maximise efficacy
e.g. benzoyl peroxide + lymecycline
e.g. Adapalene + COCP (dianette)

DDx Acne, acne rosacea, folliculitis

Acne Rosacea**
Definition: Disease of face characterised by episodes of facial flushing, persistent erythema,
telangiectasia, papules and pustules

Cause: Unknown, made worse by ALCOHOL

Features: Facial flushing, acne-like papules WITHOUT COMEDONES (black/whiteheads)

o Intermittent-constant facial flushing ± burning senstation in a 30-50y/o

Forehead
Nose
Cheeks

o Papules + pustules (occur AFTER flushing; similar to acne)

o DRY skin (NB: Acne usually greasy)

o Telangiectasia (common)

o Complications:
Rhinophyma (nose swelling)
Eye disease Blepharitis, conjunctivitis, keratitis (w/ peripheral
vascularisation of cornea)

Ix: Nil

Rx:
o First: Avoid precipitants, sunscreen (high factor), cosmetics (camouflage cream)
Do NOT use topical steroids thinning of face

o Refractory to conservative, mild/moderate: Topical metronidazole

o Severe (papulopustular) or refractory: Oral Abx (doxycycline, erythromycin)

o Refractory to ALL: Oral Isotretinoin (Roaccutane), laser therapy

Acne Young, comedones, no flushing

Rosacea 30-50, no comedones, flushing
Personal Notes Start Here
Psoriasis**
Definition: Chronic inflammatory non-contagious condition caused by hyperproliferation of keratinocytes
with inflammatory cell infiltration
o DDx: Eczema (atopic, seborrheic), fungal/tinea, pityriasis rosea, t-cell lymphoma

Types:
o Chronic plaque Most common (90%)
Round/oval, Well-demarcated, red w/ silvery scale, Elevated, Itchy, Symmetrical
Eczema is NOT well-demarcated

On extensor surfaces + scalp + sacrum

Nail changes (50%):

Pitting (COMMONEST)
Onycholysis (nail detachment from bed)
Oil-drop sign (yellow-red discolouration under nail)
Ridges

Auspitz sign Bleeding from scale after scratching

Plaques at injury sites 1-2wk later

Also seen in vitiligo, warts, mollusum contagiosum, lichen planus + sclerosus

Consider differentials:
If Hx atopy + flexural Eczema
If scaly + WHITE + asymmetrical Tinea
If guttate-like, no Hx, Herald patch Pityriasis rosea
If asymmetrical + not scaly T-cell lymphoma

o Guttate (raindrop/small lesions) CHILDREN (40% develop chronic plaque) (?pityriasis rosea)
Often on TRUNK and PROXIMAL EXTREMITIES (palms and soles rarely affected)
Nail changes typically ABSENT
Often secondary to URTI from S pyo/GABHS (2-4wk later; if recurrent ?tonsillectomy)
Remits with or without Rx (spontaneously in most in 2-3mo); but use Rx!

o Flexural (body folds/skin-on-skin) (?eczema)

Any flexural site including skin folds and genital area
Lesions often smoother than plaque psoriasis
Not always exclusively flexural if flexures involved then classified as this

o Seborrhoeic (naso-labial and retro-auricular) First affects SCALP

Similar to Seborrhoeic Dermatitis
Face typically spared but scalp and behind ears present with plaques

o Pustular (palmar-plantar) 90% females, 90% smokers

Affecting the soles of the feet and the palms
Different to Palmar-Plantar Pustulosis
o Erythrodera/Erythrodermic (total body redness [>95%])
Causes of erythroderma:
Psoriasis
Eczema
Drugs (e.g. Gold, vancomycin)
Haematological malignancy (lymphoma, leukaemia)
Idiopathic

Features Total body redness (>90%)

Rx
Bed rest in a warm room (30-32 C)
Cool, wet dressings
Emollients

First lines:
o Ciclosporin + infliximab Fastest acting
o Methotrexate Slower acting

No topical steroids as high absorption

Causes:
o Initial cause: Genetic (HLA Cw6 + B17 + B13), immunological and environmental factors
Type 1 Helper T-cell mediated disease (cytokine release hyperproliferation)

o Precipitants:
Trauma (which can give Koebner phenomnenon rash within linear lesion)
Infection, Stress, Alcohol, Drugs (inc NSAIDs, Beta Blockers, Lithium, Interferon)
LOW sunlight (psoriasis BETTER in summer)

Epidemiology:
o Affects 2% of population

o Initial presentation in:

Type I (75%): (65% associated with HLA Cw6)
Type II (25%): (15% associated with HLA Cw6)

o Associated conditions:
Iritis + Uveitis
IBD (11% of those with IBD get psoriasis)
Psoriatic arthritis (10% of those with psoriasis get PA)
Asymmetrical, DIP involvement, seronegative
Cardiovascular risk (psoriasis increases risk of metabolic syndrome; 3x risk MI @ 60y/o)

Investigations: Rarely needed, but can do BIOPSY

o Biopsy features
Epidermal hyperplasia
Dilated blood vessels in dermis (correlation to Auspitz sign)
Leukocytes in mainly dermis
Neutrophils can also be found in epidermis
Management: (no cure, just suppress)
o Localised/Mild: Topical therapies Emollient, steroids, Vit D, Coal tar, Dithranol, Retinoids,
Keratolytics, Scalp preparations (e.g. salicylic acid)

Emollient (skin softner) E.g. diprobase

Reduces scale and itchiness
Bath with soap substitute (E.g. dermol 500) Dry Apply emollient

Scalp preparations First line still topical steroids, but 2nd line:
Salicylic acid (keratolytic) Thins and sheds thickened epidermal layer
Coal tar (high viscosity black solution) Shampoo, cream, ointment
Oils

Topical steroids + Vit D analogue (e.g. **Dovobet [betamethasone + calcipotriol]**)

Short-term therapy, but MOST IMPORTANT OF ALL TOPICAL AGENTS
Cochrane review found steroid + Vit D analogue is best (i.e. Dovobet)
o Vit D reduces scale + plaque thickness by reducing cell division (but
not erythema); can be used long-term
o Steroids reduce skin irritation (e.g. pruritus); cannot be used long-
term; they are best for facial psoriasis though (less irritation than VitD)
o Steroids better in flexural areas (dovobet a bit irritant here)

Cannot be used for extensive psoriasis as systemic steroid absorption

o Get rebound effect leading to Erythroderma or Pustular Psoriasis
Used only in low-moderate dose in flexural psoriasis as:
o Flexural sites have thin skin already
o Higher absorption in hot, sticky areas

Vit D analogues (e.g. Dovonex/calcipotriol)

Excellent longer-term therapy
Side effects: irritation of face, hypercalcaemia in high amounts

Topical vitamin A analogues/retinoids (e.g. Tazarotene)

Teratogenic, not to be given in pregnancy even in topical form

Dithranol Consider when Dovobet failed

Short contact regime: 30min 1hr dose on affected area only; higher dose
0.1% - 2% formulations
keratinocyte proliferation by inhibiting DNA synthesis
Burns normal skin, stains clothes/sheets
 o Extensive or Resistant (Second Line): Phototherapy (Uses: Psoriasis mainly, also eczema + vitiligo)
PUVA (Psoralen + UVA; photochemotherapy) Can be combined with oral retinoid
Psoralen Has high UV absorbance
PUVA is a stronger therapy but higher incidence of SCC (NOT melanoma),
photoageing, hence USED AFTER UVB
Less time commitment

UVB (Narrow band) Often combined with a topical agent

Often USED FIRST as less risk of skin cancer, also used FIRST for GUTTATE
Bigger time commitment (3x/wk), however

o Extensive AND Severe: Oral therapy (may have to start here in PUSTULAR psoriasis)
First: Methotrexate (especially useful if associated psoriatic arthropathy)
2.5mg + 10mg pills; taken weekly
Hepatotoxicity, neutropenia, nausea
Monitoring:
o Pre-treatment assessment (FBC, U+E, LFT)
o Post-treatment BIWEEKLY blood tests until 6 weeks stable
o Post-stable MONTHLY blood tests until 1 year stable
o Then at least once every two months

Others:
Ciclosporin
o Fast acting immunosuppressant (within 1 week) Erythroderma
o Side effects: HTN, nephrotoxicity

Oral retinoids (e.g. Roaccutane/isotretinoin)

Mycophenolate mofetil
Fumaric Acid Esters

Failure with MTX, DLQI >10, PASI >10: Biological agents (monoclonal antibodies)
Example: infliximab, adalimumab, etanercept, efalizumab
Infliximab
o 90% improvement in 80% of patients by 10 wks
o Excellent for nail psoriasis by 6 months (otherwise hard to treat)
o NB: Oral steroids should NEVER be used (very, very few exceptions)
Notes:
o Complication Psoriatic ERYTHRODERMA, Psoriatic Arthritis (10%), increased cardio risk
o Epidermis turnover is 4 days from usual 28 days
o DLQI = Dermatology Life Quality Index; PASI = Psoriasis Area and Severity Index
ndary
o (managed by GPs); care)
BUT no correlation between body coverage and QoL
Terminology:
o ximab = chimeric monoclonal Ab
Part mouse, part human
Avoids rejection, still provides response
o zumab = humanised monoclonan Ab
Non-
o umab = human monoclonal Ab
None of the side-effects of chimeric or humanised
o cept = receptor antibody
Erythrodermic Psoriasis - emergency

Definition: Generalised (>90%) redness of skin commonly caused by psoriasis, but also by eczema, drug
eruptions and malignancy

Causes: Psoriasis, eczema, drug eruptions, malignancy

Types:
a. Worsening chronic plaque psoriasis
b. Precipitated by infection, drugs, or withdrawal of steroids

Features:
a. >90% of skin is hot + red
b. Pain + itching
c. Systemically unwell
d. Psoriatic characteristics are NOT present (have FINE scales [rather than normal coarse])

Ix: FBC, U+E, LFT, CRP/ESR, Blood cultures (ensure no renal failure)

Rx:
a. Bed rest in warm room (30-32 deg C Much higher than room temp)
b. Emollients + cool/wet dressings
c. Nutritional support
d. Monitor

e. Ciclosporin Fast-acting immunosuppression

Keloid Scars

Epidemiology: Most common in dark skinned people + young (rare in adults), if incisions made along
relaxed
Features: Most often found on the STERNUM > shoulder > neck > face > extensor surfaces > trunk
o Firm, shiny, skin-coloured/red scar often arising from injury (piercing, scar, acne)
o Extend BEYOND initial scar (NB: Hypertrophic scar CONFINED to original scar/injury)
Can continue to expand for years
Claw-like projections extend from main scar

o Caused by randomly organised collagen

Rx: Intralesional corticosteroid injection (in early keloid), Cryo, Excision
 Itchy Eruption/Pruritus/Pruritic Eruption

Eczema Scabies Urticaria Lichen Planus

History FH atopy Hx contact with Exacerbating of Planus
symptomatic person factors (e.g. food, Purple, Pruritic, Peripheral, Papules, Penis
Exacerbating factors drugs, contact)
Pruritus worse @ nt
Common Typically FLEXOR Fingers (webs, sides) Nil Forearms
Sites surfaces (esp Wrists Wrists
ATOPIC) Elbows Legs
Oral (50%)
Can be variable Ankles
Feet (webs) Flexural

Scalp NEVER affected

Lesion Dry Papular/vesicular Linear burrows Pink wheals Violaceous papules
Erythematous base (tortuous sometimes)
Symmetrical
Exudate if acute Rubbery nodules Koebner phenom
Associated 2° bac/vir infection 2° eczema/impetigo Angioedema Nail changes (thinning + longitudinal ridging)
Features Anaphylaxis
Hair loss

White streaks in oral mucosa 50%

Striae)
Ix Patch test (contact) Skin scrape + Bloods (infectn, IgE) Biopsy
Serum IgE microscopy Urine dip (AIN)
Skin swab (infection)
Rx Emollients Permethrin Antihistamines Antihistamines
Soap substitutes Malathion Corticosteroids
Topical steroids Antihistamines Non Severe
Antihistamines O2 Topical Steroids
Phototherapy HIV+ = Ivermectin Adrenaline
Immunomodulators IV fluid Severe
Oral Steroids Immunosuppression
Abx/Antivirals
Notes Lichenoid drug eruptions (gold, quinine, thiazides)

Lichen sclerosis elderly women, vulval lesions

(quite itchy), inner thigh lesions; Ix biopsy to R/O
other pathology; Rx emoll + steroid; Risk vulval Ca
More Worrying Causes of Pruritus
A Changing Pigmented Lesion

BENIGN MALIGNANT
Melanocytic Nevi Seborrheic Malignant Melanoma
Wart/Keratoses
History Develops in infancy, Middle-aged or elderly Middle aged or elderly
childhood or adolescence
Often multiple ABCDE
Asymptomatic Symptoms (itchy, bleed)
Asymptomatic
Risk factors UV, skin
type, #moles
Common Sites Variable Face + trunk Women legs
Men trunk
Lesion Dark lesion of various size Warty/nodular Asymmetrical
+ shape in child Border irregularity
Well-defined edges Colour irregularity
Diameter >7mm
Evolving
Management Rarely necessary Rarely necessary Excision
Purpuric Eruption

Meningococcal DIC Vasculitis Senile Purpura

Septicemia (e.g. HSP, others)
History Acute onset Hx trauma, Painful lesions Elderly, sun-
Meningism malignancy, sepsis, damaged skin
Sepsis liver failure,
obstetric
complications
Common sites Extremities Spontaneous Dependent areas Extensor surfaces of
bleeding from ENT, (legs, sacral, hand/forearm
GI, Resp, Wound buttocks, flanks)
Lesion Petechiae Petichiae Palpable Non-palpable
Ecchymoses Ecchymoses Painful
Surrounding skin is
thin/atrophic
Associated Features Unwell Unwell Unwell WELL
Ix Bloods Bloods (clotting Bloods, urinalysis Nil
NP aspirate screen) Skin biopsy
LP
Rx Abx, steroids Rx underlying cause Rx underlying cause Nil

Transfuse for Steroids

coagulation deficits Immunosuppress

Anticoagulate for
thrombosis

Red Swollen Leg

Cellulitis/Erysipelas DVT Chronic Venous Insufficiency

History Painful, spreading rash Pain w/ swelling, redness Heavy leg, worse on standing +
Hx trauma walking
Hx immobility, clotting
tendency Hx DVT
Lesion Ery well-defined edge Discoloured (blue/purple)
Cel diffuse edge Edema
Varicose veins
Assoc Features Fever, malaise Usually well Lipodermatosclerosis
?PE SOB (erythematous induration
causing champagne bottle)

Stasis dermatitis/venous eczema

Venous ulcers
Ix ASO titre D-dimer Doppler USS or Venography
Skin swab Doppler USS or Venography
Rx Abx Anticoagulation Leg elevation
Compression stockings
Sclerotherapy for VV
Vitiligo**

Definition: Loss of melanin in the tissues, including possibly the hair (white hair)

Pathophysiology: Unknown - ?autoimmune ?other (can be part of polyendocrine syndrome 1 or 2)

Features:
o Presents any age, usually 20-30yr
o Patchy + symmetrical depigmented macules on skin which may be well-demarcated

Ix: Check for evidence of other autoimmune disease (e.g. , hypothyroid, diabetes, pernicious
anemia, alopecia areata)

Rx:
o Cosmetics (e.g. make-up, or bleach normal areas if vitiligo widespread [M Jackson])
o Sunscreen
o Topical steroids (potent)
o Topical tacrolimus
o Phototherapy (caution with light skinned patients)
o Psychological therapy

DDx:
o Post-inflammatory HYPOpigmentation
o Pityriasis vericolor + leprosy (both give SCALY HYPOpigmentation in vitiligo SMOOTH
Depigmentation)

Molluscum Contagiosum

Cause: Pox Virus

Epidemiology: In children and HIV+ adults
Features: Wart with umbilicated centre
Treat: Freeze/chop it out

Itch (from Dr Topham lecture) Rx: Stop soaps; Start emollient + topical steroids

Emollients

Prescribe 500g, use as much as you need

E.g.
o 50/50 LP:WSP Very greasy (better but less acceptable for patients for severe disease)
NB: Paraffin is flammable patient should NOT be smoking
o Diprobase Not greasy

o Dermol 200 Only for using in shower

o Dermol 500 Antiseptic added for leaving on OR using in shower!
o Dermol 600 Only for adding to bath
Steroids HMEBED

Class I (weak) Hydrocortisone, Modrasone (bit stronger)

Class II (intermediate) Eumovate
Class III (strong) Betnovate, Elacon (even stronger)
Class IV (very strong) Dermovate (up to 600x more potent than hydrocortisone)

Reassure they are safe, limited systemic absorption

Prescribe 100g usually
Use 1-2x/day
Use only in areas with active lesions or was active in last 48hr
Only use weak or intermediate on face, and use sparingly if no good, swap to topical tacrolimus
Use ideally only for short-term (BD for 2wk), then stop
DLQI 30 point questionnaire for ALL derm disease and how it affects QoL
Dermatofibroma Nodule which is HARD on palpation

**

Definition: Recurrent oral ulcers caused by vasculitis targeting venules (can also give vulvar ulcers)

Epidemiology: More common in men, eastern Mediterranean, 20-40y/o

Features:
o 2 of 4 features necessary:
Oral ulcers (95%)
Genital ulcers w/ scarring afterwards (70%)
Anterior uveitis
Erythema nodosum (tender, red, raised lesions on both legs)

o Also:
Neuro (memory loss, aseptic meningitis)
Cardio (vasculitis, MI)
Rheum (large joint arthritis in 10%)
GI (abdo cramping)

Vascular 25% are anti-phospholipid syndrome POSITIVE (risk for MI, clots)

Diagnostic criteria: RECURRENT ORAL ULCERS and two of following:

o Recurrent genital aphthous ulcers (or scarring)
o Skin lesions (e.g. erythema nodosum)
o Eye involvement (e.g. anterior/posterior uveitis)
o Positive pathergy test (using 21g needle) turns to pustule in 48hr then large wound

Ix: Basic tests + pathergy test (needle prick inflamed + small pustule formation); HLA-B51

Rx: NSAIDs (colchicine), Topical steroids, oral steroids, if severe then infliximab... Warfarin if get arterial
thrombosis
Burns

Definition of BURN: Injury caused by thermal, electrical chemical or radiation energy

o Scald: Specific to a burn by hot liquid or steam

Epidemiology: Risk = <5 + >75; 50% occur in kitchens

o Head + neck = 9%
o Each arm = 9%
o Anterior leg = 9%
o Posterior leg = 9%
o Anterior chest = 9%
o Posterior chest = 9%
o Anterior abdomen = 9%
o Posterior abdomen = 9%

Assessment:
o ABCDE
Fluid resuscitation (patient may be HYPERkalemic)
Prevent hypothermia
Assess for associated injuries

o Depth of burn: (Refer deep dermal onwards to 2ndary care)

Epidermal (1st degree) Red, glistening, NO BLISTERS, brisk cap refill, heals in 1wk
without scarring

Superficial dermal (2nd degree) Pale, pink, SMALL BLISTERS, brisk cap refill, heal in 2-
3wk/minimal scarring

Deep dermal (2nd degree) Dry, cherry red, BLISTERS, no cap refill, reduced or absent
sensation

Full thickness epidermal and dermal (3rd degree) Absent sensation

Sub-cut/Muscle/Bone (4th degree) Requires reconstruction and often amputation

o Assess neurovascular status

o Assess for inhalation burns Hoarse voice, singeing of eyebrows, face/neck burns, stridor ( )

Ix:
o ECG
o Blood FBC, U+E, LFT, G/S + X-match
o ABG (?CO2 poisoning)
o CXR
Rx: Analgesia, cool then prevent hypothermia, transfer to burns centre

o Minor
Analgesia
Clean burns w/ soap and water, leaving any blisters intact (prevent infection)
Non-adhesive dressing
?Tetanus prophylaxis

o Major ABCDE (100% oxygen, IV fluid, ECG)

Remove clothes
Rinse body with cool tap water, then cover with dry linens (to prevent hypothermia)

If inhalation burns: ?intubate/mechanical ventilate + transfer to burns centre

Pyoderma Gangrenosum**

Definition: Painful nodules or pustule breaks down to form progressively enlarging ulcer
o Pyoderma Purulent surface
o Gangrenosum Blue/black or violaceous edge

Associations: Idiopathic in 50%

o GI IBD (mostly UC), PBC
o Rheum (Polyarthritis RA [particularly RF+], )
o Haem disease (leukaemia, lymphoma, IgA monocloncal gammopathy [e.g. myeloma])

Risk of developing: Biopsies, injections, insect bites, venesection, surgery... etc

Features:
o Non-healing ulcer/wound usually in lower limbs (NB: in IBD can be around stoma site)
Deep, red, necrotic ulcer w/ violaceous border
o pimple-to- with violaceous border Pathergy
o May have fever + myalgias

Ix: Urgent referral is required

o Blood FBC, U+E, LFT, CRP/ESR, p-ANCA)
o Swab + Culture of ulcer
o Biopsy

Rx:
o All patients: Wound care (moist dressings is necessary)
o Non-Severe: Immunosuppression (potent topical steroids, topical tacrolimus, intralesional
injection of corticosteroids, oral steroids)
o Severe: Consider IV methylpred, ciclosporin, infliximab, skin graft

o NB: Surgery may WORSEN condition due to pathergy

Ulcers***

RISK/CAUSE LOCATION FEATURES Rx

ARTERIAL Severe PAD Trauma sites Hx of cardiovascular disease Wound dressings +
(ABPI <0.5) e.g. pre-tibial bandages
L trauma sites
SUPRAmalleolar B pale, dry Vascular
Toes, top of foot E punched out, defined reconstruction (as
NB: If ABPI normal, then Between toes D deep per peripheral
disease is within small S cold skin, weak peripheral vascular disease
vessels (e.g. vasculitis) pulses (+other signs art dis) above)
ateriorgram will be
normal, hence useless
Various shaped borders, Dry NB: Compression
stockings are
Cardiovascular risk
Cold/shiny/pale skin CONTRAINDICATED
Weak/absent periph pulses
Loss of hair

ABPI <0.8

Very painful
VENOUS Varicose veins Medial malleolar MOST Hx of venous disease e.g. Graduated
Prior DVT COMMON varicose veins/DVT compression
Venous insufficiency bandages
Sometime lateral L medial gaiter
Previous fracture, malleolus B red, moist Debridement +
trauma, surgery E large, irregular cleaning
Anywhere mid-calf to D shallow
just below malleoli S warm skin, normal Dressing
peripheral pulses
Abx
Leg edema, hemosiderin + Topical steroids
melanin deposition, Oral pentoxifylline
lipodermatosclerosis
Treat underlying
ABPI 0.8-1 cause (e.g. varicose
veins, DVT)
Mild-moderate pain
NEUROPATHIC Alcohol Plantar foot (soles, Hx of diabetes Control BM
B12 heels, metatarsal head)
CKD Surrounding callus Clean ulcer
DM, Drugs (Isoniazid) Weight bearing areas Often deep base (debridement)
Every vasculitis
Peripheral neuropathy Elevate
Peripheral neuropathy Diminished/No pain
Do not use affected
foot

Orthotics

Last resort:
Amputation

Marjolin Ulcer SCC which develops within ulcer as heaped up tissue; typical after chronic recurrence of ulcer
Ix: Biopsy... Rx: Resect ± lymph nodes
Comment on BEDS (base, edge [width + irregularity], depth, surround tissue), +take photo
Ix for all ulcers: ABPI, bloods, swab, duplex USS, biopsy if not healed for 12mo
Lyme Disease**

Definition: Tick-borne spirochete disease caused by Borellia burgdorferi

Epidemiology: Most common tick-borne disease in northern hemisphere; can be anywhere in North
America or Europe (e.g. Connecticut in US, Norwich in UK)

Features: Fever, headache, erythema chronicum migrans, arthralgia

(asymmetrical oligoarthritis), cranial neuropathy (common cause of bilateral
facial nerve palsy), lymphocytic meningitis, AV block
o Erythema chronicum migrans: Early Lyme disease, circular rash at
tick bite which radiates for 2-40d creating ring with raised border,
starts as red macule/papule (pathognomonic for Lyme)
Large in size than EM (if seems like target lesion, but most
cases of Lyme are homogenous red lesions)
Larger + not flaky like Tinea Corporis/Ringworm

Ix: Serology (ELISA antibody titre to Borellia burgdorferi), rarely LP (if CNS involve)

Rx:
o Uncomplicated: Doxycycline (Amoxicillin of doxy is contraindicated)
o Disseminated disease (E.g. CNS/cardiac): Ceftriaxone

Complications: Jarisch-Herxheimer reaction (after Abx) symptoms like endotoxinaemia

o Also seen in Leptospirosis, Syphilis (both of which are also spirochaetes)
Pregnancy + Skin Conditions

Polymorphic eruption of pregnancy

o 3rd trimester pruritic lesions
o Often appear IN abdominal striae
o Rx emollients, mild topical steroids, oral steroids

Pemphigoid gestations
o 2nd or 3rd trimester pruritic blistering lesions (but ONLY in 2nd or more pregnancy, not first)
o Often peri-umbilical, then spreads to back, arms, etc
o Rx Oral steroids usually required
Other Dermatology

Shin Lesions
o Erythema Nodosum
Causes SORE SHINS (strep, Oral contra pill, Rickettsia, Eponymous (Behcet),

by Streps (most common), sarcoid, IBD, drugs (penicillins,

COCP)
Symptoms Symmetrical, red/purple, tender, raised nodules without scarring
Ix CXR most important (as sarcoid + TB two very important causes)
Prognosis Resolves within 6wk in most

o Pretibial myxoedema

Shiny, orange peel skin, symmetrical + erythematous lesions

o Pyoderma gangrenosum (as above)

o Necrobiosis lipodica diabeticorum

Shiny, painless area of yellow/red skin on shin of diabetics

Erythema Ab Igne
o Cause Over-exposure to infrared radiation
o Associations Hypothyroidism
o Features
Reticular, erythematous rash with HYPERpigmentation +
telangiectasia

Patients often feel cold (due to hypothyroidism)

o Complications SCC

Levido Reticularis (due to capillary spasm)

o Vasculitis
o Hyperviscosity syndromes
o APLS
o Cholesterol atheremboli
o RA
Hirsutism + Hypertrichosis
o Definition:
Hirsutism Androgen DEPEDNENT hair growth
Hypertrichosis Androgen INDEPENDENT hair growth

o Causes:
Hirsutism
Ovarian issues (PCOS = most common overall; ovarian tumour [andro secrete])
Over-active adrenal gland (Cu
Androgen therapy
Obesity (peripheral conversion of oestrogen to androgens)
Drugs Phenytoin

Hypertrichosis
Drugs Minoxidil, ciclosporin
Porphyria cutanea tarda
Anorexia
Congenital hypertrichosis:
o Lanuginosa
o Terminalis

Skin disorders in malignancy (due to paraneoplastic syndromes)

Acanthosis Nigricans Causes:
o Endocrine
o Obesity
o GI cancer

Skin lesions associated with DM

o Necrobiosis lipodica
o Infection
o Neuropathic ulcers
o Vitiligo
o Lipoatrophy
o Granuloma annulare (popular hyperpigmented lesion with central depression)

Skin lesions associated with TB

o Lupus vulgaris (50% of cases with TB) Face, nose, mouth
o Erythema nodoum
o Scarring alopecia
o Scrofuloderma Breakdown of skin overlying TB focus
o Verrucosa cutis Red brown wart most often in hands
o Gumma

Erythrasma
o Asymptomatic, flat, slightly scaly, pink/brown/red rash in groin or axilla
o Caused by overgrowth of Corynebacterium mintissimum
o Ix
o Rx Topical miconazole
Dermatology Revision

Pruritus
o Dermatological or...
Liver, Thyroid, Renal

o Drug rashes:
Maculopapular rash Type 4 hypersens (7-14d)
Urticarial rash Type 1 hypersens (1-2d)

o DDx: TULIPES (Tinea, Urticaria, Lichen, Impetigo, Psoriasis, Eczema, Scabies)

o Psoriasis Raised, scaly, extensor, symmetrical, well demarcated, red

o Eczema Flexural, scaly, lichenified, erythematous base
o Urticaria Itchy rash + comes and goes every few hours = PATHOGNOMONIC of URTICARIA (this
could easily come up in OSCE)

o Rx Stop soap, start aqueous cream (as soap substitute; dermol 2/5/600), start emollient for
after showers (certraben, diprobase), topical steroid (unless infection)
Steroids:
Hydrocortisone
Eumovate
Betnovate
Elacon (AKA mometasone)
Dermovate

History taking:
o Remedies When did start? What happened?
o Impact on life?
o DHx When did you start these meds?

Topical steroids:
o 100g for body
o 30g for face

o Use mildest steroid that will be effective (mild ONLY on face, start mild-mod for body, mod for
hands/feet) NB: Flexural sites absorb steroid so use less
o Max 2x daily
o Use sparingly
o Use on areas affected inc last 48hr
o Prescribe 2-4wk then R/V
o Must explain patient difference between emollient and steroid (or else they will use steroid as
emollient)
o Reassure safe + atrophy not an issue with short-term use

Emollients:
o Large quantity, 500g, use liberally, at least 2-3x/day, use on sites affected and even sites not

Urticaria:
 o Symmetrical wheals, well demarcated
o Must ask about lip + eye swelling (angioedema) + SOB

o Antihistamines Loratadine, cetirazine (if fails, increase dose even though not licensed for this)
Ensure using anti-histamine by the clock, not PRN (reduces flares)
Switch antihistamine
Monteleukast
Oral steroids (sometimes as reduce dose, urticaria comes back )

o Food diary
o Allergy testing ONLY if clear history to support it is related to some specific trigger

o TYPES:
Acute >6wk Drugs, food, venom
Chronic <6wk Cold, vibration, pressure, exercise, dermatographism (scratching or
rubbing skin causes wheal)

Eczema:
o Atopic:
Itchy + 3:
Flexural
Hx of flexural
Hx dry skin
Hx atopy
Onset <2

Relative sparing of nappy area in children

Hyperlinearity of palms in adults + lichenification (increased skin folds, thickening)

Ix: Patch testing used for CONTACT allergy (Type 4 hypersens)

Skin prick testing for endogenous allergens

Rx: Stop soaps, start emollient, mild-mod steroid, pimecro/tacro (may burn/sting), PUVA
Wear gloves if on hand + consider hand PUVA + Alitretinoin (same precautions
as per isotret)

Hand eczema:
Atopic
Irritant (water + soap most common)
 Pompholyx (potassium permanganate, topical steroids)

o Seborrheic:
T portion of face, Dandruff, Malassezia furfur
If severe consider HIV

Use anti-fungal (e.g. miconazole), then tacro

Ketoconazole shampoo helpful

o Discoid eczema:
Intensely itchy

o Asteatotic
o Venous eczema (not bilateral cellulitis!)... cellulitis does NOT give scaly appearance, skin is still
flat and intact
Cellulitis Unilat, acute, pain + fever, red/hot/tender (not the case in venous eczema)

Rx VE:
Soap sub, emollient, top steroid, Compression bandage + elevate end of bed,
?surgery for varicosities

Lichen Planus:
o ae
o High potency topical steroids (as lichenified)

>10% skin involvement of PASI (0-72) high Marker of moderate-severe disease

Guttate psoriasis Phototherapy useful as widespread
Plaque psoriasis Many Rx
Flexural psoriasis NO Scaling, well-defined patch (eczema is slightly scaled and poorly defined)
Erythroderma (>90% skin is red) Emollients, low potency topical steroids, some oral Rx

Rx psoriasis:
o Emollient, Dovobet, Coal tar, Salicylic acid, Dithranol
o UVB, PUVA
o MTX, Ciclosporin

Complications psoriasis:
o Metabolic syndrome (cardiac risk)

o Psoriatic arthritis
DIP
RA
Ank Spon
Mutilans

Ciclosporin Nephrotoxicity (monitor creatinine)

Acitretin Teratogenicity
Anti-TNF TB reactivation

Scabies
o Permethrin for 12hr repeat after 7d
Tinea
o Unilateral
o Annular
o Active edge

o Rx: Terbinafine cream, Oral terbinafine/itraconazole... etc

Drug rash (penicillins, allopurinol, rifampicin, sulfa drugs, NSAIDs) Rx emollient, topical steroid,
antihistamine

Bullous pemphigoid Oral steroids, Abx if 2nd infect, Potassium permanganate soap

Red face:
o Rosacea
Rx:
Avoid irritants (alcohol, curry)
Topical metro, Oral tetracyclines/erythromycin (6-12wk), Isotretinoin

o Acne:
Rx: Benzoyl perox, Topical retinoids, topical Abx, COCP (dianette), Oral Abx, Oral
retinoids, Isotretinoin monthly preg test, 2x
forms contraception... unless sign pregnancy waiver form)
Isotretinoid DRYNESS = everyone gets

White heads = use topical retinoids (peel skin)

ACNE vs ROSACEA Acne = comedones, scars, young; Rosacea = telangiectasia,

flushing, no comedones, rhynophyma

Changing lesions:
o Describing:
SSSCCCTTT
ABCDE

o Types:
Freckles
Benign nevus
Dysplastic nevus
Melanoma
Seb keratoses
Dermatofibroma
Pigmented BCC
Hemangioma

o Atypical nevus May flag up several ABCDE but benign.. the key is HISTORY OF CHANGE... these
will NOT be changing

Atypical nevus
Blue nevus
Congenital nevus
Dermal nevus
 Epidermal nevus

Malignant melanoma
o Superficial spreading (spread radially before vertically)
o Lentigo maligna (rarely invade BM)
o Acral lentiginous (can include sub-ungual melanoma under nail bed)
o Nodular (worst prog, grow vertically from outset)

Seb Keratoses Greasy, stuck on, horns, on old people

BCC Rolled edge, pearly, telangiectasia (stretching skin helps to see)

o Nodular
o Ulcerating (still has rolled edge + telangiectasia!)
o Morphoeic (can see stretch lines on skin)

o Imiquimod, surgery

SCC
Actinic keratosis 5 FU, Cryo