Dermatology Flashcards
(35 cards)
Psoriasis
What? Rash characterised by scaling, red plaques which favours extensor surfaces, nails and scalp
Epidemiology: 2% european population
Onset:
Peak onset either in 10-20s or 50-60s.
Aetiology:
Inheritance - Non-mendelian but highly heritable (1 parent = 12-20% risk, 2 parents = 40-50% risk)
Triggering events:
- Strep throat (*guttate psoriasis)
- HIV
- Drugs (Lithium, BB, TNF-alpha, chloroquine, antimalarials, oral steroids)
- Bone marrow transplant
- Lifestyle (Smoking esp for PPPP, alcohol, obesity, stress)
- Koebner phenomenon
Pathology
2 processes: Epidermis hyperkeritanisartion and inflammatory infiltration to the dermis and epidermis (forming munro micro-abscesses)
Presentation:
Progression - fluctuating course from onset
Symptoms: Itch, skin discomfort, pain, irritation
Sub-syndromes: Stable chronic plaque psoriasis, guttate, erythrodermic, Pustular (PPPP or generalised), nail, scalp, palmoplanatar.
Systemic aspects: Joints (e.g. RA, Ank Spon, Psor A), CV( Metabolic syndrome, MI, PVD), Psychological
Diagnosis: Clinical
Management:
General - Recurrent guttate consider long term pen or tonsillectomy), PPPP quite smoking, Treat HIV and Drug avoidance
1st line: TOP emollients, TOP corticosteroids, TOP vit D analogues
2nd line: UVR (1st UVB, 2nd PUVA. PUVA carries SCC risk)
3rd line: Methotrexate, ciclospirin, retinoids
4th line (specialised clinics) : IV or Inf biologics
Prognosis:
- Increased risk of metabolic syndrome and CV disease
Acne
Definition: Disorder of the pilosebacious gland, common in adolescence and early adult life
Epidemiology
M>F
Aetiology:
- Genetics
- Teenage year
- Drugs: No comedones (corticosteroids, anti-epileptics, lithium, EGF receptor inhibitors) , with comedones (anabolic steroids)
- Endocrine
Pathology
- Comedones due to deranged keratinisation of follicular epithelium
- P acne infection
- Sebum
Presentation Distribution: Face + torso Features: - Comedones (whitehead or blackhead) - Pustules - Papules - Cysts - Scars (ice pick, keloids, hypo/ hyperpigmentation)
Sub-types of acne:
- Comedonal acne
- Papulopustular acne
- Acne fulminans
- Acne excoriee
- Acne conglobata
- Mechanical acne
- Chloracne
Management:
*Duration: Must trial meds for >2 months to assess effectiveness
Options:
- Target comedones - TOP retinoids e.g. Isotretinoin
- Kill the bugs! - Benzyl Peroxide (BPO), TOP ABx (Tetracyclines, clindamycin, erythromycin), Systemic Abx (Tetracyclines or erythromycin)
- Reduce the sebum - Systemic retinoids, COCP
1st line: TOP retinoids + BPO +/- Abx +/- COCP
2nd line: Systemic retinoids
Contraception consideration: If using systemic retinoids must be on two modes of birth control until 5 weeks post-treatment
Atopic Dermatitis
Epidemiology:
20-30% of children
Age 2-4yrs
Progression:
Onset in childhood with recurrence in adolescence (facial eczema) or in adulthood *(hand dermatitis)
Pathogenesis
- Atopy
- Abnormal barrier (due to filaggrin mutation)
- Infections (Increase colonisation of staph a)
Also… Non-medellian genetic predisposition and “hygiene hypothesis”
Presentation:
Typical patient: 6-12month olf child , itchy rash with scaling on face and scalp. Patent scratches the rash. Rash spreads to extensor surfaces, and other time to flexor surfaces. Skin is weepy in acute episodes and lichenification develops over time. Worsened by soap and detergent.
Tx:
1st line: Skin care (Acute- Creams, antiseptics. Chronic - emollients. Both - Bandaging) + TOP corticosteroids (Risk of skin atrophy and systemic absorption) + Sedative anti-histamines
2nd line: Phototherapy, Systemic immunosuppressives (Pred / azathioprine / ciclosporin / methotrexate / biologic)
Prognosis
- If uncomplicated, no scarring
- Many children grow out of it
- Antigen removal is only effective if patient skin in not intact and antigen is causal
Contact irritant dermatitis
Pathophysiology: Irritants break down of lipids in stratum corneum, leads to Type 1 HS and final common pathways dermatitis
Epidemiology:
Who’s at risk? Healthcare workers washing hands and wearing gloves, kitchen workers and incontinent patients
Risk factors:
- Repeated irritant exposure
- Atropic dermatitis Hx
Clinical features
- On site exposure to irritant
- Timing depends of irritant exposure
- Dose dependent reaction (not all or nothing)
- Erythema
- Scaling
- Spongiosis and eventual skin hypertrophy as in all dermatitis
DDx
- Contact allergic dermatitis (Requires sensitisation time and reaction is all or nothing)
Ix:
Diagnosis: Skin pricking testing and Specific IgE serology
Management
1st line: Minimise exposure and lifestyle measures( wear gloves in cold weather)
If symptomatic and lichenification : Steroids
Contact allergic dermatitis
Pathology: Type 4 HS reaction (Sensitisation takes 1-3 weeks to develop. 2nd exposure leads to reaction in 24 to 96 hours)
Common agents
- Nickel
- PPD (henna)
- Hairdressers
Clinical features
- Erythema
- Reactions matched chemic exposure
- Spongiosis when acute. If chronic then epidermal hypertrophy in hyperkeratosis and acanthosis
- Delayed reaction
DDx
-Contact urticaria
Ix
Diagnosed on patch testing (Suspected antigen + other applied to back and left for 24 hours. Antigen removed and patients skin examined after 48-96 hours)
Mx
1st line- Avoidance of allergic substance
Urticaria
Presentation:
Features - Triple response (Erythema, flare, weal).
Duration - Weal should last <24 hours
Symptoms - Pain, ithch
Different types:
- Acute urticaria
- Chronic systemic urticaria (CSU)
- Contact urticaria
- Physical urticaria
- Angioedema
- Angioedema without urticaria
ACUTE URTICARIA
What - Urticarial episode <6 weeks
Cause - Recent infection, drugs (aspirin, NSAIDs, Penicillins, contast dyes), insect bites, foods (shellfish)
Ix - Clinical diagnosis
Mx - Remove precipitants, anti-histamine and consider short PRED course. If severe reaction, refer to derm. If anaphylaxis, O2 + IVF + adrenaline IM
CHRONIC SYSTEMTIC URTICARIA (CSU)
What - Urticaria >6 weeks
Cause - Either IgE or IgG mediated. Associated with autoimmune disorders (Thyroid, RA, Pernicious anaemia)
Ix -
Mx - 1st line H1 blockage +/- H2 blockage. 2nd line immunosuppressives.
CONTACT URTICARIA
Classification: Immunological or non-immunological
PHYSICAL URTICARIA Examples: - Solar - Aquagenic - Dermographism - Cold - Cholinergic
ANGIOEDEMA
What - Swelling in the deep dermis or subcutis
Location: Lips, eyes, tongue >
Mx - Treat as urticaria
ANGIOEDEMA W/O URTICARIA
Pathology - No primary mast cell involvement
Types:
1. ACEi induced angiooedema
2. C1 esterase inhibitor deficiency (Presents with large airway obstruction. Manage with C1 esterase inhibitor or SC icatibants)
Acne inversa
Pathogenesis: Occlusion of the follicular infundibulum and rupture into the surrounding dermis –> Sterile abscess formation and eventually sinus tract formation downwards
Epidemiology
Women>
Young>
Presentation
Location: Axillae, perianal, perineum, groin
Features: Malodrous discharge, pain and systemic malaise
Mx:
1st line - Systemic retinoids + systemic Abx
Flare ups - Systemic retinoids
Prognosis: SCC risk in chronic disease. Be aware of depression and suicide risk
Dermatitis
Aetiology:
Two central processes….
1. Immune system dysregulation (Type 1 or 4 HS reaction)
2. Compromise of the skin carrie function
Pathology:
- Acute –> Spongiosus (intercellular epidermal oedema) –> Blisters or weepy skin
- Chronic –> Acanthosis (epidermal thickening) and hyperkeratosis (thickening of stratum corneum)
Presentation
Acute - Erythema, induration, weeping skin, blisters, itch
Chronic - Skin is thick and tough, dry. Itch +/- fissures +/- lichenification
Dermatitis
Aetiology:
Two central processes….
1. Immune system dysregulation (Type 1 or 4 HS reaction)
2. Compromise of the skin carrie function
Pathology:
- Acute –> Spongiosus (intercellular epidermal oedema) –> Blisters or weepy skin
- Chronic –> Skin hypertrophy by acanthosis (epidermal thickening) and hyperkeratosis (thickening and stratum corneum)
Presentation
Acute - Erythema, induration, weeping skin, blisters, itch
Chronic - Skin is thick and tough, dry. Itch +/- fissures +/- lichenification
Seborrhoeic dermatitis
This is better understood as a response to the yeast Pityrosporum (Malassezia species) that is found on skin.
Management If you kill the yeast, the rash goes.
BCC
Definition: Keratinocyte tumours that resemble basal cells histologically
Incidence
Most common skin cancer
Epidemiology
European / australian populations>
Mean age = 67
Aetiology
UVR related
RF: Immunosuppression, organ transplantation, Hx of skin cancer
Pathology
- True cancer
- Rarely metastasise
- Destructive by local invasion e.g. to the eye, cranium or nose
Presentation
Location: Middle 1/3 of the face, 30% in sun exposed areas (scalp, back, legs and arms)
Progression: Over months-year
Classic features: Pearly + ulceration + telangiectasia + areas of translucency
Subtypes
- Nodular (well demaracated)
- Morphoeic (not well demarcated)
- Superficial (@ back and limbs >)
DDx
- Melanoma?
- Appendageal tumour?
Investigation
1st line - Biopsy and histology
Management 1st line SURGERY +/- adjuvant RT - Nodular BCC = Excision with 4mm margin - Morphoeic BCC = Mohs surgery - Superficial Bcc = Cryotherapy or chemotherapeutics
SCC
Definition
Keratinocyte tumours whose cells are histologically more differentiated than basal cells
Incidence
Less common than BCC
M>
Aetiology
- Precursor lesions (actinic keratoses or IEC)
- UVR
- Xeroderma pigmentosum
- Immunosuppression
- PUVA+++ (e.g. psoriasis)
Pathology
- Able to metastasise (3-5%)
Presentation Location: Areas of cumulative UVR exposure (backs of hands, tops of ears, faces, bald heads) Features: - Keratinising nodule - Varied size - ? ulceration - ?Keratin "volcano"
Management
1st line: SURGERY by excision with 4-6mm margin of normal tissue ?grafts/flaps
2nd line: Added RT for “large and thick” high risk tumours
Melanoma
Epidemiology
Common
F>
Mean age -53
Aetiology *UVR Immunosuppression PUVA FH (large number of nevi and 2/3 melanomas)
Pathology
Melanocytes are derived from neural crest cells
Metastasise early
Classification by morphology: Lentigo, nodular, acral, amelanotic
Risk stratification by Breslow Thickness
- Method: Distance in mm from the granule layer to the deepest part of the tumour
- Use: Risk of metastases
- Results= 4mm gives worse prognosis, 1mm gives better prognosis
Presentation
Location: Legs and trunk>
Clinical subtupes:
- Superficial spreading melanoma (SSM) - Flat with appearance of lateral spread of clones. DDx: freckles or lentigines
- Nodular - Raised pigmented dark lesions. DDx: melanocytic nevi or angiomas
-In situ
-Lentigo maligna melanoma - @ continuously UVR exposed skin
- Amelanotic melanoma
- Acral melanoma
DDx
- Seborrheic keratoses
- Angioma
- Talon noir
Investigation
Suspected melanoma? Excision with 2mm diameter for URGENT histology and breslow thicknss
Mx
1st line: Histology confirmed melanoma –> WLE (Breslow thickness <1mm, then 1cm margin. BT >1mm then 2cm margin)
Follow-up
Monitor for recurrence
Prognosis
Breslow thickness dependent
More fatal skin cancer
SCC Precursor lesions
1. Actinic keratosis Features: - Erythema -Rough scale -Varied size - Multiple - Focal and smaller than IEC
Risk: Less risky than IEC
Tx: - Cryotherapy OR curette and cautery +/- TOP chemotherapeutics
- Intraepithelial carcinoma / “Bowen’s disease”
Features:
Macular, roughened, erythematous, Keratic/ scaled/ telangiectasia
Larger and more plaque like than AK
Bowen’s disease tends to be isolated and well demarcated.
Risk: 10% progression to SCC
Tx:Cryotherapy / curette and cautery OR Excision + histology
SJS
Milder version of TEN
body area <10%
mucosal involvement
Lower morbidity and mortality
Mx: Stop drugs, supportive care, skin care, ophthalmic review
TEN
THIS IS A MEDICAL EMERGENCY
Potentially fatal skin and mucosal adverse drug reaction
Arising from drug administered between 7-28 days
Clinical features
Sheets of skin undergoing necrosis
Wrinkling and blisters between sheets is seen
Rubbing apparently normal skin will cause the epidermis to come away(bonus- what is this called^)
Macular deep red/blue areas are seen (quite similar to target lesions)
exquisitely painful
Pathology
Full thickness epidermal death due to Fas mediated cell apoptosis
Management
- Stop all relevant drugs ASAP
- Allopurinol
- Sulphonamides
- Phenytoin
- Penicillin
- Carbamazepine
- NSAIDs - Manage in a high dependency unit
- Pharmacological management
- Steroids
- IVIG
- Anti-TNF Infliximab
Mimics of Skin Cancer: Pigmented lesion
Keratoacanthoma: VV rapid growth of volcano like lesion. Treat as SCC
Seborrhoeic keratoses: Flat/raised, warty surface, greasy apperaance, irregular shape, numerous, itch/bleed, varied pigmentation, comodone like opening, milia. @ trunk, limbs, face
Lentigo: Flat brown marks with sun damaged skin surrounding
Melanocytic nevi: Appearance in childhood and peak in 30-40s. Progress from flat and dark –> Raised pigmented –> lost pigment by remain raised. The skin creases are remained and there is irregular boarder.
Campbel de Morgan spots
Aka cherry angiomas
Vascular lesions
Rarely causing concerns
Ix: You can remove the blood by pressure – only diagnostic if positive
Risk factors for non-melanoma
- Exposure to natural sunlight or artificial sunlight over long periods of time
- Blistering sunburns in childhood are especially associated with melanomas and BCC
- SCC are caused by cumulative UVR - Fair complexion, which includes:
- Fair skin that freckles and burns easily, does not tan, or tans poorly
- Blue or green or other light-colored eyes
- Red or blonde hair - Actinic keratosis
- Past treatment with radiation.
- Weakened immune system
- Exposure to arsenic
*Smoking is not a known risk factor for BCC
SSSS
Who?
Usually seen in children under 5
Features: Does not affect the mucosae Onset- scarlet fever like rash around mouth and nappy area and perioral crusting and furrowing \+Nikolskys Scalded skin
Ix:
Clinical diagnosis
Superficial biopsy (excludes TEN)
Swab the throat and eyes (not skin)
Mx
IV anti-staphylococcal drugs (flucloxacillin, vancomycin)Barrier nursing
DRESS
Meaning: Drug Reaction with Eosinophilia and Systemic Symptoms Precipitants: - Carbamazepine - Phenytoin - Dapsone - Allopurinol Presentation: Cutaneous features- - Widespread rash (possibly erythrodermic) - ?eczematous - ?facial oedema Potential systemic features- - Lymphadenopathy - Pyrexia - Hepatitis - Nephritis
Progression
Reaction persists for several weeks
Mortality rate of 10% (due to hepatitis)
Management
Supportive care is important and stop drugs. Systemic steroids can be used
Erythema Multiforme
Cause: Infections (HSV or mycoplasma) > Drugs (e.g. allopurinol)
Features: Target lesion Annular lesion with a red/dusky cyanotic centre and a bright erythematous outer ring separated by a slight paler zone (3 colours) Haemorrhage/blistering may occur. Usually acral in distribution
Ix:
1st line clinical
2nd line biopsy
Mx:
Basic skin care with antiseptics
If markedly symptomatic, use topical steroids
If eye involvement –> Ophthalmoscopy REFERRAL
Prevention is caused by recurrent HSV = LONG TERM ACICLOVIR
Scabies
Intensely itchy infestation with sarcoptes scabei Mite
Features:
- Worse at night
- Burrows are linear structures in which female mite burrows before laying eggs
- Nodules common around nipples/ genitals
- Widespread excoriation
- Can only be caught from close physical contact- parent-child or child-child
- Rash features- pimple-like (papular) itchy rash, can include tiny blisters (vesicles) and scales.
DX: clinical identification of mite
TX: permethrin/malathion- applied after a warm bath and left on overnight. Repeat after 7 days. AND Treat contacts
MOLLUSCUM CONTAGIOSUM
Epidemiology
More common in children (often assoc with atopic eczema)
If in adults think Immunosuppression (inc HIV)
Pathology
Small pox infection spread by direct contact
Caused by MCV (virus)
Transmission by close personal contact or indirectly via fomites (contaminated surfaces)
Px:
Pinkish, pearly white papules with umbilication
Lesions occur in clusters everywhere except palms of hands and soles of the feet.
- Lesions / papule / nodules
- Shiny white centre *
- Central umbilication *
- Surrounding eczema
Mx:
Self limiting, don’t share towels
