Dermatology Flashcards
What are the components of a derm hx?
1) Name/Age Occupation
2) PC
3) Background risk factors/severity markers
4) HPC
5) PmH
6) SH (hobbies/travel) + FH
7) Drug history
8) RS
Rash Hx?
1) When, where, evolution
2) Duration, symptoms - is it itchy?
3) Previous episodes
4) exacerbating/relieving factors
5) Other areas affected?
6) Severity markers ie. psoriasis
7) Impact on life/work/psychosocial
Severity markers?
Previous treatments eg. UV/Systemic drugs
Hospitilisation
Missing work/School
Social/personal life
Lesional History
Different as cancer until proved otherwise:
HPC lesion:
- How it started, how it’s evolving, symptoms, D/C, Bleeding etc
Risk factors:
- Sun, country of residence, occupation
- Previous episodes
- Family Hx
Flat non-palpable lesion
Small - Macule
Large - Patch
Raised lesions
0.5cm: Nodule
Palpable patch
Elevated, flat lesion = Plaque
Can also get an atrophic sunken/flat lesion = plaque
Other descriptive derm terms
Circumscription Colour Consistency (soft/hard/firm) Distribution = Localised vs generalised. Clustered (HSV) Dermatomal Peripheral vs centripetal Symmetrical? Flexor vs extensor surfaces Photodistribution Monomorphic/pleomorphic Annular --> Serpiginous Discoid (Solid) Koebnerisation - Psoriasis, LP, viral warts
Fluid filled lesions?
Small = Vesicle
Large = Blister
Pus filled = Pustule
Surface characteristics: Scale? Warty? Ulcerated? Crusty? Excoriated? Lichenification?
Scale = Keratotic surface
Warty = Rough/papillomatous surface
Ulcerated = Loss of epidermis (full thickness), partial thickness = erosion
Crusty = Dried Exudate
Excoriated = superficial ulceration secondary to scratching
Lichenification = Flat surfaced epidermal thickening secondary to rubbing
Post-inflam hyperpig.
Ulcer Description?
Size, Shape, Location
Edge:
1) Punched out
2) Raised & rolled
3) Sloped
4) Overhanging
Base: Clean, necrotic, sloughy, granulation tissue
Surrounding tissue eg. thick woody hard sclerotic skin = lipodermatosclerosis
Derm investigations?
Dermoscopy Mycology (scrapings) Swabs - Microbiology/viral Biopsy: - History - Stains - Immunofl. studies
3 layers of skin?
1) Epidermis: Keratinised stratified squamous epithelium
2) Dermis: collagenous connective tissue
3) Subcutis: Fat layer, nerve endings and blood vessels
Basal cell function?
Sit on basement memebrane and produce keratinocytes, which rise to the top as squamous cells. Also produce keratin
Causes of Non-Scarring Alopecia?
Male/Female Pattern alopecia Telogen Effluvium Low iron reserves Alopecia Areata (AI hairloss) Hyper/hypothyroid
–> follicles still there, so may regrow
Causes of Scarring Alopecia?
Lichen Planus Lupus Traction/Traumatic Folliculitis Other
Follicles destroyed, so chance of regrowth. Irreversible so need to manage pt expectation!
How to differentiate scarring from non-scarring alopecia?
Non Scarring:
- Speed of loss, stress, anaemia, Previous episodes, FH, other diseases
Scarring:
- Itch, redness/scale, previous sclap damage, pain, suppuration
Examination:
Pattern of hair loss
Scarring?
Visible active disease of scalp?
Alopecia Ix?
Blood tests - hair loss screen: biotin, ferritin levels etc
Skin biopsy: H&E & Immunoflorence. Biopsy - transverse and longitudinal
What is psoriaris?
A common, chronic hereditary condition where you get an inflammatory hyperproliferation of the epidermis. It is a pustular disease and in some forms may be life-threatening
Bimodal age of onset - youth/middle life
T-cell mediated
Psoriasis triggers?
Infection: Strep Psychological: Stress Drugs: Steroid withdrawal, B blockers, lithium, antimalarials (chloroquine/hydroxychloroquine), NSAIDs and Ace inhibitors Trauma : Koebnerisation Sunburn HIV
Psoriasis types?
1) Chronic plaque psoriasis (commonest)
2) Flexoral psoriasis
3) Psoriatic arthritis/ nail psoriasis (nail dystrophy)
4) Guttate
5) Erythrodermic
6) Pustular
7) Sebo-psoriasis
Chronic plaque psoriasis findings
Chronic, well demarcated (distinguishes from eczema) Red/pink plaques Silvery-white scale Extensor surfaces and scalp Accounts for 80-90%
Types of psoriatric arthropathy?
1) Asymmetric (60-70%)
2) Symmetrical polyarthtropathy (15%)
3) DIP (5%)
4) Destructive (5%) - arthritis mutilans
5) Axial arthritis (5%)
Guttate psoriasis?
Post-strep throat
young adults
Shower of scattered discrete lesions
3mm to 1cm lesions, round or slight oval
Pustular psoriasis?
1) Localised:
- Palmoplantar common - sterile pustules on erythematous base
- chronic relapsing remitting condition
2) Generalised:
Life threatening - abrupt onset + fever GOOGLE IMAGE. Likely to be secondarily infected
Mx of generalised pustular psoriasis?
1) resuscitate ABC
2) Admit
3) Greasy emollients
4) IV support
5) Systemic therapy
6) Avoid or treat concurrent infection
7) ITU if necessary
Complications of erythrodermic psoriasis?
Derm emergency:
1) Fluid loss
2) hypothermia
3) infection
4) hypercatabolic state
5) SHOCK
Mx same as generalised pustular psoriasis
Mx Psoriasis?
1) Emollients/bath oil/soap substitutes
2) Topical agents:
- Vitamin D
- Tar
- Dithranol
- Steroids
3) Phototherapy
UVA + psoralen = pUVA
4) Systemic agents
5) Biological agents
Topical agents in psoriasis?
1) Vitamin D
2) Tar (anti-proliferatives)
3) Dithranol
4) Steroids
Only useful in localised disease
Systemic agents in psoriasis?
1) Retinoids (acitretin)
2) Fumaric acid
3) Hydroxycarbamide
4) Immunosuppression:
- Methotrexate (especially if joint involvement)
- Ciclosporin
Biologic agents in Psoriasis?
Anti TNF:
- Etanercept
- Infliximab
- Adalimumab
Anti IL-12/23:
- Ustekinemab
5 P’s of Lichen Planus
Purple (violacious) Planar = flat Polished = Shiny Papular Pruritic
(polygonal/pigmented)
What is Wickham’s striae?
Reticulated lace like lichen planus usually in the mouth, but can be anywhere
Lichen planus treatment?
Emollients/soap substitutes
Topical:
- Super potent steroids
- UVB
Systemic:
- Oral steroids (CF psorarisis - never oral)
- Hydroxychloroquine
- Immunosuppression
Actinic Lichen Planus?
Sun-induced (photodistributed) lichen planus eg. dense hyperpigmentation of face
What is the herald patch. What condition is it seen in.
Initial lesion in pityriasis rosea post infection.
A week later, several other reactive lesions arise. Browny/orange, lines up down the back ‘christmas tree’ with some scale.
Acute exanthematous eruption
Common in children/young adults
? Viral cause - seasonal variation
What is Eczema?
An inflammatory dermatosis characterised by erythema and itching.
Histologically shoes spongiosis (fluid building up under skin) + inflammation
Causes of eczema?
Atopic Contact allergic Contact irritant Seborrhoeic (dandruff) Varicose Asteototic (elderly - dry out) Drug
Different morphology in eczema?
Pompholyx Discoid Lichen Simplex - thickening due to rubbing Lichen Amyloid Nodular prurigo Erythroderma
What is Atopic eczema?
- A chronic itchy relapsing dermatitis
Atopy: phenotypic predisposition to develop asthma, allergic rhinitis and atopic eczema
Increase IgE response and eosinophilia
Increased sensitivity to pruritic stimuli
Exacerbating factors for atopic eczema?
Topical irritants Soap Secondary infection: - Staph, viral herpes, tinea House dust mite Animal Moulds Food allergies
Atopic eczema prognosis?
50% clear by 3 years
66% clear by 6 years
90% clear by 20 years
What is pityriasis Alba?
Post-inflammatory hypopigmentation
Often in black skin & children
What is Pomphoylx?
Episodic visculobullous disorder. A type of eczema
Causes tiny blisters on fingers/palms/soles
Who gets discoid eczema?
Females aged 15-25 yrs
Females and males 55-65 yrs
Increased incidence in winter
What is lichen simplex chronicus?
Chronic eczema itch-rub cycle leads to lichenification and pigmentation
Some excoriation, some scale
What is Lichen Amyloid?
same process as Lichen simplex, but leads to deposition of amyloid under skin.
Tend to get a hyperpigmented cobblestone type appearance
What is Nodular prurigo?
Chronic-itch rub cycle in eczema characterised by very itchy firm lumps, often excoriated to the point of erosion
Complications of Atopic eczema?
1) Secondary staph infection
2) Eczema herpeticum
Eczema mx?
1) Emollients/soap substitutes/bath oils
2) Topical anti-inflammatories (Steroids/Tacrolimus)
3) phototherapy:
- pUVA
- UVB
4) Systemic agents:
- Systemic steroids
- Azathioprine
- Ciclosporin A
5) other agents
(treat infection)
+ avoid provoking factors
+ Anti-histamines for itching
Steroid hierarchy
Mild: hydrocortisone
Moderate: Clobetasone (Eumovate)
Beclomethasone (Propaderm)
Potent: Bethametasone (Betnovate)
Super potent: Clobetasol (dermovate)
nb. Start at appropriate level - DO NOT have to start at bottom and work way up
Topical Steroids SE?
1) Potential systemic absorption - only complication is addisonian crisis on stopping
2) Tachyphylaxis
3) Skin Atrophy
4) Tinea incognito - red scaly plaque mistaked for eczema
5) May cause acne or perioral dermatitis
6) Skin changes eg. telangiectasia
nb. Steroid sparing alternative - topical tacrolimus
Investigation of atopic dermatitis?
Clinical diagnosis so very rarely investigate
Biopsy
Swab (bacterial/viral)
Specific IgE (RAST) testing
Classification of nappy rash?
Seborrhaeic dermatitis - sparing of skin folds
Seborrheic dermatitis Mx
1) antifungal shampoo
2) corticosteroid scalp application
3) topical steroids
4) Oral ketoconazole/itraconazole
What is contact dermatitis?
Inflammation due to interaction of external agent and skin
- Non-immunological irritant in 80% (would irritate most people)
- Immunological allergic in 20% (only in those with sensitivity)
What type of allergic reaction is allergic contact dermatitis
Type IV - delayed cell mediated hypersensitivity
Allergic contact dermatitis Dx & Tx
Dx:
- History of allergen exposure
- Clinical features
- Patch testing (2 days with wells on back)
Tx:
- Allergen avoidance
What are the different types of melanocytic naevi?
Junctional naevus - band of melanocytes clumped together. Relatively Flat
Intradermal naevus - Melanocytes migrate down into dermis, so tend to be deeper, pushing up, often with hair follicles. Shiny, dome shaped, but no surface changes. Can be any colour (pink/black/blue)
Compound naevus - combination of junctional and intradermal + epidermal changes - rough warty appearance because of epidermal involvement
Congenital melanocytic naevi
Beckers Naevus
Epidermal naevus - Warty change, often swirling following embryological growht lines
Congenital melanocytic naevi
There from birth, and tend to grow with the person.
Not likely to become malignant unless greater >20cm (risk greatly increases)
What is Beckers Naevus?
stippled/reticular patches of pigmentation, often hairy. Not actually melanocytic- actually a hamaratomatous.
Subungal naveus - Linear nail change vs deltoid nail change?
Linear = benign
Triangular = melanoma until proved otherwise
What is a Spitz Naevus?
Look dark/irregular so easily confused for melanoma. Almost always not cancerous. Normally biopsied to confirm
What are seborrhoeic keratosis?
Benign, warty/papillomatous lesion.
- Age >30
- Pale to dark brown
- ‘stuck on’ appearance
- Waxy/greasy
- Keratin cysts within
What is a dermatofibroma?
- Insect bite/pimple fibroses into a hard/firm papule.
- Palpate to feel. press from either side and centre with dimple ‘dimple sign’
Often mistaken for melanoma
What are the indicators of sun damage?
1) Actinic keratosis
2) Solar Lentigines
3) Freckles
4) Favre-Racouchot - sun dmg so bad you start forming cysts and blackheads over face
5) Solar elastosis (histological thickened skin) - whitening of collagen
6) Freckles
Risk factors for Skin cancer?
1) Sun exposure/Occupation
2) Fitzpatrick Skin type 1-3
3) Radiotherapy
4) Phototherapy
5) High risk pt groups:
- 100 moles
- Immunosuppressed
6) FH
Features SCC?
Subtypes?
SCC produce keratin therefore abnormal keratotic lesions (dyskeratotic)
Well/moderately/poorly differentiated
What is Actinic (solar) keratosis
Dysplasia - redness, ill defined clumps of dyskeratotic keratin caused by sun dmg. Premalignant SCC.
Full thickness = CIS = bowen’s disease
What is Bowen’s disease?
SCC in situ. Full thickness dysplasia
well circumscribed erythematous scaly plaque.
Differentials include eczema and psoriasis.
Solitary/few
Asymptomatic
BCC subtypes?
Nodular
Superficial
Morphoeic/infiltrative (most dangerous subtype - ill defined therefore poorly defined borders)
Pigmented
BCC features
Arise from basal layer (produce other cells) so not very keratotic. Commonest human cancer
Rarely invades
Pearlescent
Telangiectasia
Rolled border
AKA rodent ulcer
Nodular BCC
classical BCC - Raised, rolled edge with central ulceration. Pearlescent. Sometimes has overlying telangiectasia
Infiltrative BCC
Slightly pearlescent. Difficult to see when tumour ends and skin begins. Need to biopsy
High risk tumour
SCC features
Keratotic/Ulcerated Rapid growth \+- Painful Increased risk in transplant recipients Metastatic potential higher on head and neck
What is Lentigo Maligna?
Irregular mole/freckle
In-situ melanoma
Pre-malignant
Face, elderly, sun damaged skin
Irregular pigmented macules, variagation in pigment, blurring of border
Lentigo maligna Mx?
Surgical Excision IS best option.
Topical: 5-FU Immiquimoid Cryotherapy Photodynamic therapy
Malignant Melanoma features
ABCD Asymmetrical (in 2 plains) Border (irregular, growing) Colour (>2 colours, odd colours, variagation of pigment) Diameter (anything growing)
Skin markings lost
Rapid growth
May Ulcerate
What is Hutchingson’s sign?
Sub-ungal melanoma coming through skin fold
Prognostic factors in melanoma?
1) Breslow thickness
2) Ulceration (bad)
3) Mitotic index
4) Sentinal Node Biopsy (if Breslow > 1mm)
What is Breslow thickness?
Depth from top to bottom in mm. 5 yr survival:
4mm = 25%
surrogate marker for how active the tumour is (mitotic rate)
How do you do a sentinel node biopsy
WLE of melanoma + biopsy.
If melanoma >1mm, sentinel node biopsy. Radioactive blue dye around scar, then WLE, then geiger counter to find sentinel node + send to lab to see if tumour is in there or not. If tumour in there, has already metastasised, so has gone from stage I to stage III.
Melanoma Tx
Surgical: Narrow excision and Histology Then Wide local Excision Plus: Breslow >1mm sentinal node Breslow
Tx of non-melanoma skin cancer
Non-surgical (superficial disease)
1) Topicals
- Imiquimoid
- 5-FU
2) Photodynamic therapy - Cream soaks into tumour, light activates into toxin
3) Cryotherapy
Deeper disease
4) Radiotherapy
5) Surgery:
- Excision
- Curettage and cautery
- Mohs Surgery (Gold standard)
What is Moh’s surgery?
A surgical procedure used to treat non-melanoma skin cancer.
Has the best cure rate with good tissue preservation.
Used for high risk BCC; those which are infiltrative, in high risk areas(head/neck/near eye) and recurrent. In young patients etc.
Not used much for SCC as harder to visualise under microscope
1) Anaesthetise + slice out tumour and freeze
2) look at biopsy straight away under microscopy and check margins
3) If cut margins encroaches on tumour, go back and excise some more + check again
Aetiology of acne?
- Androgens
- Sebacious gland over-activity
- Comedome and cyst formation
- Colonisation of follicle with Propinobacter.acnes
- Inflammation
Blackheads = Open comedones (Oxidised)
Whiteheads = Closed
What is Acne Rosacea?
Acne + redness
–> vasodilation of blood vessels + telangiectasia
- Tx: Metronidazole cream
- Oral tetracycline
- Oral retinoid (at a lower dose than for acne)
Acne Classification?
Mild
Moderate
Severe –> Scarring is straight away severe
Comedonal
Inflammatory
Mixed
Acne Treatments:
Topical:
- Benzoyl peroxide
- Antibiotics
- Retinoids (normal desquamation + reduce inflammatory response
Systemtic:
- Antibiotics
- Anti-androgens (in women)
- Isotretinoin
Tx of comedomal acne?
1st choice usually topical retinoids:
- Adapalene, Tretinoin, Isotretinoin
Tx of mild papular-pustular acne?
Combine topical retinoids and topical Antimicrobials
- Adapalene/isotretinoin
- Benzoyl peroxide/antibiotics eg. clindamycin
Tx of moderate inflammatory acne
Oral abx + topical retinoids
Eg. Tetracyclines, minocycline, lymecycline
Alternative oral tx for females with moderate acne?
Co-cyprinderol (dianette) - should be reserved for moderate to severe acne +- evidence of androgenisation (hirsutism, adiposity, irregular menses)
nb. Spironolactone also has anti-androgen effects and can be used in both men and women
Tx of severe Acne?
Oral Isotretinoin
Sx: Dry skin, dry eyes Hoarse Voice Cheilitis Headache Arthritis/Myalgia TERATOGENICITY Adverse psychiatric effects - mood swings, depression, suicide
NEED to make sure they are not pregnant (pregnancy test), informed about and taking contraception
What is a blister?
A cicumscribed skin lesion containing fluid
Blister/Bulla >5mm in diameter
Vesicle
Causes of blistering?
1) Inflammatory eg. Pompholyx Eczema
2) Immunobullous diseases eg. Pemphigoid/pemphigus
3) Infectious: bullous Impetigo/varicella, bullous cellulitis
4) Extrinsic causes: Trauma/burns
5) Other causes. eg. Drugs, metabolic (porphyria)
Pemphigoid?
DEEP Autoimmune bullous disease caused by antibodies against cells that holds epidermis to basement membrane
Common in older pts May begin with urticarial plaques Later, Tense, round blisters Oral mucosa rarely involved May be widespread
Course and complications of bullous pemphigoid
Course: Usually self-limiting and treatment (minimal immunosuppressive therapy) can be stopped around 2 years
Complications: discomfort, loss of fluid from ruptured bullae
Pemphigus vulgaris?
Chronic SUPERFICIAL autoimmune bullous disorder.
- Highly aggressive (100% mortality without Tx)
- Begins in oral mucosa
- Flaccid vesicles and superficial EROSIONS
- +ve Nikolsky (describes the spread of bullae following application of horizontal, tangential pressure to the skin). Pull the skin next to a blister and the epidermis comes off
Antibodies in Pemphigus vs Pemphigoid
Pemphigus: antibodies directed against desmoglein 3, a cadherin-type epithelial cell adhesion molecule that holds cells to EACH OTHER.
Pemphigoid: antibodies against hemidesmosomal proteins BP180 and BP230 that hold epidermis to BASEMENT MEMBRANE. Immunoflorescence shows IgG and C3 at the dermoepidermal junction
Immunoflorescence: Pemphigus : Ab all around epidermis (Chicken wire)
Pemphigoid : Ab on basement membrane
Pemphigus vulgaris Tx and complications
Tx:
- Aggressive immunosuppression eg. Pred, mycophenolate
Complications:
- Overwhelming sepsis
- Drug side effects
- Fluid loss/heat loss etc.
What is Dermatitis Herpetiformis?
AI blistering condition associated with coeliac disease formed by depositoon of IgA in dermis
Intensely pruritic vesicular eruption. Begins in early adult life, affecting mostly whites.
Symmetrically distributed papules and vesicles
Mx;
gluten free diet
Dapsone
Erythema multiforme? Causes?
Features
target lesions
initially seen on the back of the hands / feet before spreading to the torso
upper limbs are more commonly affected than the lower limbs
pruritus is occasionally seen and is usually mild
If symptoms are severe and involve blistering and mucosal involvement (eye/mouth) the term Stevens-Johnson syndrome is used.
Causes
viruses: herpes simplex virus (the most common cause),
idiopathic
bacteria: Mycoplasma, Streptococcus
drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
connective tissue disease e.g. Systemic lupus erythematosus
sarcoidosis
malignancy
Erythema multiforme causes
Causes
viruses: herpes simplex virus (the most common cause),
idiopathic
bacteria: Mycoplasma, Streptococcus
drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
connective tissue disease e.g. Systemic lupus erythematosus
sarcoidosis
malignancy
what is toxic epidermal necrolysis?
Features?
Toxic epidermal necrolysis (TEN) is a potentially life-threatening skin disorder that is most commonly seen secondary to a drug reaction. In this condition the skin develops a scalded appearance over an extensive area. Some authors consider TEN to be the severe end of a spectrum of skin disorders which includes erythema multiforme and Stevens-Johnson syndrome
Features
systemically unwell e.g. pyrexia, tachycardic
positive Nikolsky’s sign: the epidermis separates with mild lateral pressure
Drugs known to induce TEN phenytoin sulphonamides allopurinol penicillins carbamazepine NSAIDs
Management
stop precipitating factor
supportive care, often in intensive care unit
intravenous immunoglobulin has been shown to be effective and is now commonly used first-line
other treatment options include: immunosuppressive agents (ciclosporin and cyclophosphamide), plasmapheresis
Drug causes of TEN
Drugs known to induce TEN phenytoin sulphonamides allopurinol penicillins carbamazepine NSAIDs
Mx of TEN
Stop precipitating factor Nurse on burns unit Supportive care Fluid balance Nutrition temperature Prevent infection IV IG
Golden Crust?
Tx?
Impetigo (Staph aureus)
Tx
Topical Potassium permanganate Soaks
Topical Fusicidic/ Flucloxacillin
Commonest cause of abscess
Staph - another form of impetigo
Cellulitis causes?
Tx
Staph OR Strep pyogenes
Therefore IV Fluclox
Clari in pen allergic
If severe: IV benpen + fluclox
Single infectious bullae?
staph toxin blistering
Staph scalded skin syndrone aka Staph toxic shock syndrome
Superficial desquamation caused by staph infection
Tinea diagnosis + Tx
Ix: Card scrapings + look under microscope for hypae
Woods lamp - tinea lights up under lamp
Tx: Topical antifungal eg.. Terbinafine, ketoconazole, itraconazole
Topical ketoconazole shampoo should be given for first 2 weeks to reduce transmission
Systemic:
eg. Griseofulvin, terbafine
Tinea incognito
Hidden serpiginous edge Tinea + steroid –> Swells up and expands, filling up with pustules
Tinea in feet? Head? Trunk, legs/arms? Groin?
Tinea pedis
Tinea capitis (get very rampant occipital lymph nodes with scalp infection)
Tinea corporis
Tinea Cruris
What is a kerion?
A large raised, pustular, spongy/boggy mass eg. on the scalp, formed by untreated tinea capitis.
Skin fold lesions - some erosion
Cutaneous candidiasis
–> INTERTRIGO
but also:
- Genital
- Folliculitis
- Nappy dermatitis
- Nails
- Chronic mucocutaneous candidiasis
Hyperpigmented lesions around chest, young man just back from holiday. Worse in sunshine
Pityriasis versicolor,
is a superficial cutaneous fungal infection caused by Malassezia furfur
Features most commonly affects trunk patches may be hypopigmented, pink or brown (hence versicolor) scale is common mild pruritus
Predisposing factors occurs in healthy individuals immunosuppression malnutrition Cushing's
Management
topical antifungal. NICE Clinical Knowledge Summaries advise ketoconazole shampoo as this is more cost effective for large areas
if extensive disease or failure to respond to topical treatment then consider oral itraconazole
scabies tx?
Topical permethrin/malthione
- Head to toe, wash 24 hrs later, repeat a week later to kill eggs when they hatch
Treat contacts
Can also use systemic (immunocompromised) ivermectin
Viral wart cause?
HPV
Cold sore organism + Ix?
HSV
–> blister fluid PCR
Tx with acyclovir
Eczema herpeticum optic risk?
Stellate ulcer of eye –> blinds you
Molluscum cause + characteristic finding?
Pox virus
- self limiting
- Central dimpling
- Often clustered
Tx:
Cryotherapy
Immiquimod
Kaposi’s sarcoma cause?
HHV-8
Granulomatous infectious papular erythematous rash
Mycobacteria
also Lupus vulgaris TB
Annular erythematous plaque which keeps growing, in a man who has just returned from philiipines. Stick a pin in it and he feels no pain. What is it?
M.leprii
Eczema distribution in 10 month old?
Young Children?
Older Children?
Face & trunk
Extensor surfaces
Typical distribution: flexor surfaces + creases of face and neck
Causes of acantosis nigricans?
gastrointestinal cancer diabetes mellitus obesity - Most common caused. linked to inuslin resistance polycystic ovarian syndrome acromegaly Cushing's disease hypothyroidism familial Prader-Willi syndrome drugs: oral contraceptive pill, nicotinic acid
Where are Keloid scars most likely to form?
Keloid scars are tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound
Predisposing factors
ethnicity: more common in people with dark skin
occur more commonly in young adults, rare in the elderly
common sites (in order of decreasing frequency): STERNUM, shoulder, neck, face, extensor surface of limbs, trunk
Keloid scars are less likely if incisions are made along relaxed skin tension lines*
Treatment
early keloids may be treated with intra-lesional steroids e.g. triamcinolone
excision is sometimes required
Acne rosacea Tx?
Acne rosacea treatment:
mild/moderate: topical metronidazole
severe/resistant (if plaques): oral tetracycline
What is a Rhinophyma?
Rhinophyma is a condition causing development of a large, bulbous, ruddy nose associated with granulomatous infiltration, commonly due to untreated rosacea
NICE first line tx of psoriasis?
Emolliants, bath oils, soap substitutes
first-line: NICE recommend a potent corticosteroid applied once daily plus vitamin D analogue applied once daily (applied separately, one in the morning and the other in the evening) for up to 4 weeks as initial treatment
second-line: if no improvement after 8 weeks then offer a vitamin D analogue twice daily
third-line: if no improvement after 8-12 weeks then offer either: a potent corticosteroid applied twice daily for up to 4 weeks or a coal tar preparation applied once or twice daily
short-acting dithranol can also be used
What is a keratoacanthoma?
Keratoacanthoma is a benign epithelial tumour. They are more frequent in middle age and do not become more common in old age (unlike basal cell and squamous cell carcinoma)
Features - said to look like a volcano or crater
initially a smooth dome-shaped papule
rapidly grows to become a crater centrally-filled with keratin
Spontaneous regression of keratoacanthoma within 3 months is common, often resulting in a scar. Such lesions should however be urgently excised as it is difficult clinically to exclude squamous cell carcinoma. Removal also may prevent scarring.
Organism in fungal nail infections?
Trichophyton rubrum
Onychomycosis is fungal infection of the nails. This may be caused by
dermatophytes - mainly Trichophyton rubrum, accounts for 90% of cases
yeasts - such as Candida
non-dermatophyte moulds
What is lichen sclerosis?
sclerosus: itchy white spots typically seen on the vulva of elderly women
Erythema nodosum causes
Causes
infection: streptococci, TB, brucellosis
systemic disease: sarcoidosis, inflammatory bowel disease, Behcet’s
malignancy/lymphoma
drugs: penicillins, sulphonamides, combined oral contraceptive pill
pregnancy
Athlete’s foot cause and treatment
Athlete’s foot is also known as tinea pedis. It is usually caused by fungi in the genus Trichophyton.
Features
typically scaling, flaking, and itching between the toes
Clinical knowledge summaries recommend a topical imidazole (eg. topical miconazole), undecenoate, or terbinafine first-line
eg. topical miconazole
Verrucas?
Secondary to the human papilloma virus
Firm, hyperkeratotic lesions
Pinpoint petechiae centrally within the lesions
May coalesce with surrounding warts to form mosaic warts
Corn and calluses
A corn is small areas of very thick skin secondary to a reactive hyperkeratosis
A callus is larger, broader and has a less well defined edge than a corn
Keratoderma
May be acquired or congenital
Describes a thickening of the skin of the palms and soles
Acquired causes include reactive arthritis (keratoderma blennorrhagica)
Pitted keratolysis
Affects people who sweat excessively
Patients may complain of damp and excessively smelly feet
Usually caused by Corynebacterium
Heel and forefoot may become white with clusters of punched-out pits
Palmoplantar pustulosis
Crops of sterile pustules affecting the palms and soles
The skin is thickened, red. Scaly and may crack
More common in smokers
Juvenile plantar dermatosis
Juvenile plantar dermatosis Affects children. More common in atopic patients with a history of eczema
Soles become shiny and hard. Cracks may develop causing pain
Worse during the summer
What is Pemphigoid gestationis?
pruritic blistering lesions
often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms
usually presents 2nd or 3rd trimester and is rarely seen in the first pregnancy
oral corticosteroids are usually required
What is Polymorphic eruption of pregnancy
Polymorphic eruption of pregnancy
pruritic condition associated with last trimester
lesions often first appear in abdominal striae
management depends on severity: emollients, mild potency topical steroids and oral steroids may be used
NOT associated with blistering - think pemphigoid gestationis
Pyoderma gangrenosum?
initially small red papule, often on shin
later deep, red, necrotic ulcers with a violaceous border
idiopathic in 50%, may also be seen in inflammatory bowel disease, connective tissue disorders and myeloproliferative disorders
Vitiligo? Features, assoicated conditions and management
Vitiligo is an autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin. It is thought to affect around 1% of the population and symptoms typically develop by the age of 20-30 years.
Features
well demarcated patches of depigmented skin
the peripheries tend to be most affected
trauma may precipitate new lesions (Koebner phenomenon)
Associated conditions type 1 diabetes mellitus Addison's disease autoimmune thyroid disorders pernicious anaemia alopecia areata
Management
sun block for affected areas of skin
camouflage make-up
topical corticosteroids may reverse the changes if applied early
there may also be a role for topical tacrolimus and phototherapy, although caution needs to be exercised with light-skinned patients
Causes of Steven’s Johnson
Causes idiopathic bacteria: Mycoplasma, Streptococcus viruses: herpes simplex virus, Orf drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill connective tissue disease e.g. SLE sarcoidosis malignancy
Causes of hirsuitism
Polycystic ovarian syndrome is the most common causes of hirsutism. Other causes include: Cushing's syndrome congenital adrenal hyperplasia androgen therapy obesity: due to peripheral conversion oestrogens to androgens adrenal tumour androgen secreting ovarian tumour drugs: phenytoin
Causes of hypertrichosis?
Causes of hypertrichosis drugs: minoxidil, ciclosporin, diazoxide congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis porphyria cutanea tarda anorexia nervosa
Granuloma anulare?
Idiopathic, annular plaque, raised purple/red/nodular edge
Tx:
- Emolliant soap substitutes
1) Topical steroids/ Intralesional steroids
2) photo therapy
3) Systemic medications eg. methotrexate
Differentiating feature between acne and acne rosacea?
Acne will have comedomes (blackheads)
Cutaneous vasculitis?
Purple/pruritic patches/plaques
Central vesiculation and necrosis
DISTRIBUTION is the defining feature
Ix:
1) Urinalysis (blood/protein)
2) BP (rule out kidney involvement)
3) (Skin biopsy - not always necessary)
4) Vaculitis screen
To differentiate primary from secondary causes?
- FBC, LFT, U+E
- Urinalysis
- ESR CRP
- Autoantibodies - ANA, ENA, RhF, ANCA, dsDNA , C3 C4, Pr3, MPo
- Infection (Hep B, C) , ASOT, mycoplasma
2 most common cause of vasculitis:
- Drugs
- Sepsis
How to differentiante TEN from staph scalded skin syndrome
Mucosal involvement - Pts with scalded syndrome never have mucosal involvement
