Week 10 Dermatology Flashcards
Necrobiosis Lipoidica
Diabetic skin change
Waxy, yellow
Usually on shins
Can ulcerate and scar
Diabetic dermopathy
Small, round, brown, atrophic skin
Usually shin
Scleredema
Diabetic skin change
Progressive, thickening of skin
Upper back, shoulders
Diabetic ulcers
Open sores/wound
Bottom of foot
Granuloma Annulare
Diabetic skin change
Smooth, discoloured plaque
“Ring” (annular) shaped
Cushings disease
Increased cortisol
Signs:
- acne
- central adiposity
- moon face, buffalo hump
- global skin atrophy
- striae on abdomen, thighs
- pupura (reduced connective tissue)
Addison’s disease
Decreased cortisol
- Hyperpigmentation
- Acanthosis Nigricans
Malignancy
- Necrolytic migratory erythema
- Erythema gyratum repens
- Acanthosis nigricans
Necrolytic migratory erythema
Glucagonoma syndrome (tumour causing excess glucagon)
Erythematous, scaly plaques
Acral, intertriginous (areas where skin rubs against each other) areas
Assoc. with pancreatic islet cell tumours
Other signs: hyperglycaemia, weight loss
Treatment: remove tumour
Erythema gyratum repens
Red, concentric band with whorled pattern
(Gyratum “gyrate” - moving in circular motion)
Severe itch and peripheral eosinophilia
Strongly assoc with lung cancer
Assoc with breast, cerval cancer
Treatment: underlying malignancy
Acanthosis nigricans
Smooth, velvet like, hyperkeratotic (thickening of outer layer of skin) plaque
Intertriginous areas (e.g. groin, axilla)
3 types:
Type I: malignancy (most common: adenocarcinoma of GI)
Type II: autosomal dominant
Type III: obesity, insulin resistance. Most common
Sweet’s syndrome
Small, red, bumps, can ulcerate
Assoc. with leukaemia
Sister Mary, Joseph nodule
Nodule bulging into umbilicus
Mestatic cancer in abdomen, pelvis
Erythema Annulare
Red, ring shaped, skin rash
Assoc. with haemotoglical cancers e.g. Hodgkin’s Lymphoma
Cutaneous (affecting skin, nails etc.) features associated with nutritional deficiency
Vitamin B
Vitamin C
Zinc
Vitamin B deficiency
Vit B6: pyridoxine - Dermatitis
Vit B12: cobalamin - Angular cheilitis
Vit B3: niacin - Pellagra (3Ds: dermatitis, dementia, diarrhoea)
Zinc deficiency
Acrodermatits Enteropathica
Pustules, bullae, scaling
Acral, perioral
Inherited - mutation in SLC39A (Zn transporter in intestines)
In infants can occur with breast feeding, when breast milk contains low amounts of Zn
In adults, can occur: alcoholism, malabsorption, IBD
Treatment: Zn supplement
Vitamin C deficiency
Scurvy
- Punctate purpura (non-blanching rash)
- dry curly hair
- dry skin
- inflamed gums-
non-healing wounds
Features of Erythema nodosum and some diseases it may be associated with
- Inflammatory condition
- Red nodules/lumps on skin due to inflammation of fat cells under skin
- Both shins
Associated with: Streptococcal infection, TB, IBD, infectious mononucleosis, sarcoidosis
Describe features of Pyoderma gangrenosum and some diseases it may be associated with
- Inflammatory skin condition
- Small, red blisters that form deep ulcers (with purple edges)
(“pyoderma” infection of skin with pus)
- Usually legs
Associated with: IBD (Chron’s, UC), Rheumatoid Arthritis, Myeloma
Describe hair and nail changes associated with systemic disease
- Alopecia areata (autoimmune)
- Hair thinning: B12, iron deficiency, hypothyroidism
Male pattern baldness - androgen excess
Nail clubbing - Lung Ca, IE, Liver cirrhosis, IBD, Interstitial pulm. fibrosis
Nail fold telangectasia (widened venules) - Scleroderma, SLE
Changes in skin are markers of what diseases?
- Endocrine disorders
- Internal malignancies
- Nutritional deficiencies
- Systemic infection
- Systemic inflammatory conditions
Endocrine skin changes
- Thyroid
- Diabetes
- Steroids
- Sex hormones
Endocrine:
Skin changes assoc with thyroid disorders
Thyroid:
- dry skin (hypothyroidism)
- thyroid dermopathy/pretibial myxoedema (Grave’s) - waxy, discoloured skin on anterior lower leg
- thyroid acropathy (Grave’s) - swelling of soft tissue of hands, clubbing of fingers
Endocrine:
Diabetic skin changes
Necrobiosis lipoidica
Sclerederma
Diabetic dermopathy
Diabetic ulcers
Granuloma annulare
Endocrine:
Skin changes in steroid imbalance
Cushing’s disease (excess steroids)
Addison’s disease (insufficient steroids)
Cutaneous signs that may indicate internal malignancy
Necrolytic migratory erythema
Erythema gyratum repens
Acanthosis nigricans
Erythema annulare
Sweet’s syndrome
Sister Mary Joseph nodule
Skin changes in systemic infection
Erythema nodulosum
Skin changes in systemic inflammatory disease
Pyoderma gangrenosum
Effects of UV light on skin
DNA damage on keratinocytes causing neoplastic transformation
Damages host’s immune system
Main type of skin cancer
- Basal cell carcinoma (BCC)
- Squamous cell carcinoma (SCC)
- Malignant melanoma
Basal cell carcinoma
- Most common
- Basal cells’s DNA control formation of new skin cells
- Mutation in DNA causes basal cells to proliferate rapidly and eventually form a tumour
- PTCH gene mutation associated
- 80% BCC found on head/neck/UV exposed sites
- Rarely metastises
Types:
Nodular -
Raised lesion/nodule, shiny, telangectasia (dilated blood vessels), uclerate centrally
Superficial -
Scaly, flat
Pigmented
Morpheic/sclerotic
Treatment:
Surgical excision: 2-3 mm margin
Cutterage and cautery
Cryotherapy
Mohs micrographic surgery
Squamous cell carcinoma
Most often on skin that has been regularly exposed to sunlight or UV radiation
Originates from keratinocytes
Pre-malignant types: Actinic keratoses
Bowen’s disease (SCC in situ)
Risk of metastasis
- Appeares keratinized, crusty, scaly
Treatment:
- Surgical excision: 4mm margin
Cautery and cutterage
Pre malignant/SCC in situ:
Cryotherapy
Topical imiquimod (immune repsonse modifier)
Malignant melanoma
Differentials:
Melanocytic nevi (moles), seborrhoiec keratoses (warts), actinic keratoses, bowen’s disease
Malignant melanoma: Irregular pigmented lesions on sun exposed area
Aietiology:
Due to UV damage
2 phases: radial growth phase - vertical growth phase
Risk factors: Genetic, UV radiation, Sun exposure, skin type I and II, immunosuppression, genetic CDK2NA
Appearence
Asymmetrical
Borders (unveven)
Colour (lots of different ones)
Diameter (more than 6mm)
Evolution (size, colour has changed)
Prognostic factors:
Clinical appearence - size, depth (blue/grey colour means it is deeper), location, ulceration
Histological appearence: Breslow’s depth (<1mm good prognosis), Clark level (anatomical level in skin) high mitotic rate
Types:
Superficial spreading malignant melanoma
Nodular melanoma
Acral melanoma (hands and feet)
Subungal melanoma (nail)
Amelanotic melanoma
Lentigo melanoma (pre-malignant form) (arises in a lentigo - flat brown lesion)
Melanoma in situ
Treatment:
Surgical excision - margin based on Breslow thickness (1cm margin: <1mm Breslow)
Chemotherapy - BRAF inhibitors, MEK inhibitors
Immunotherapy - Nivolumab, ipilimumab
Assess lymph node spread
Imaging - CT, MRI
Describe some tumour syndromes with cutaeneous presentations
Gorlin’s syndrome - multiple BCC, jaw cysts
Cowden syndrome - multiple harmartomas (benign growth that looks like neoplasm), thyroid, breast cancer
Severe drug reactions
Erythema multiforme
Stevens Johnson syndrome
Toxic epidermal necrolysis (TEN)
AGEP/pustular drug rash
Acute blistering conditions
Drug induced:
- Steven Johnson Syndrome
- Toxic epidermal necrolysis
Immunobullous:
- Bullous pemphigoid
- Bullous pemphigus
- Linear IgA disease
- Adult varicellar
Steven Johnson Syndrome
Affects skin and mucous membranes
Flu-like symptoms followed by red/purple rash that forms blisters
Less severe form of TEN
Drug induced - antivulsants e.g. carbamepazine
Toxic epidermal necrolysis
- Dermatological emergency
- Flu like symptoms, skin blisters and epidermis peels off forming painful, raw areas
- Mostly drug induced e.g. anticonvulsants or antibiotics
- Forms a spectrum of disease with Steven Johnson Syndrome (<10% = SJS, TEN more severe)
- SCORTEN severity scale
Treatment:
- Analgesia, fluids, special matresses, infection control, non adherent dressings
Differential: Staphylococcal scalded skin syndrome
Nodular melanoma
Acral melanoma
Subungal melanoma
Amelanotic melanoma
Melanoma in situ
Nodular BCC
Superficial BCC
Pigmented BCC
Morphoeic/sclerotic BCC
Erythema multiforme
- Self-limiting allergic reaction
- Multiple erythematous rash and bullae
- Due to HSV, EBV, sometimes drug
- Target lesions
Acute generalized exanthematous putulosis
- Sudden skin euruptions that appear a few days after medication
- Antibiotics
Cutaneous vasculitis
- inflammation of blood vessels in skin
Triggers: infection, drugs, connective tissue disease e.g. RA
- Need to check for systemic vasculitis (inflammation of blood vessels in body)
- Often localised, not progressive
- Less unwell than in meningococcal rash
Acute pupura (meningococcal sepsis)
- Pupura (red spots that are non-blanching) rash
- Fever, nausea/vomiting, joint pain, cold hands and feet, tachycardia, tachypnoea, hypotension
- Nisseria meningitidis
Dermatomyosistis
- Inflammation of muscles
- Affects muscles and skin
- Presents with itchy, red/[urple rash, usually on sun-exposed surfaces
- Muscle weakness
Immunobullous disordes
Bulluos pemphoid
Mucous membrane pemphigoid
Paraneoplastic pemphigoid
Pemphigus vulgaris
Autoimmune blistering disease due to autoantiodies against basement membrane proteins
Dermatitis herpetirformis (itchy vesicles grouped together, assoc. with coeliac) - treated with topical streoids, gluten free diet
Difference between bullous pemphigoid and pemphigus
Bullous pemphigoid
Autoantibodies destruction of hemidesmosomes (attached to basement membrane, causes epidermis to separate from dermis blister forms under epidermis)
Tense fluid filled blisters, subepidermal so does not rupture easily
On flexures
Bullous pemphigus/pemphigus vulgaris
Autoantibodies against proteins involved in desomosomes
Mucosal erosions early sign
Erythematous macules become flaccid blisters
Blisters are intraepidermal so burst earily becoming erosions
On chest, back
Treatment for both:
- oral steroids
Immunosuppressive agents - azothioprine
Burst blisters
Dressings
Check for oral/mucosal involvement
Adult varicella
VZV
Acute blistering condition
Complications in adults: pneumonia, neurogical complications
Linear IgA disease
- Blistering condition
- IgA antibodies deposited in the epidermis in a line
- Itchy rash with small blisters
Chronic skin disease
Erythoderma, Acute pustular psoriasis
Erythoderma
Descriptive term
80-90% erythema
Causes: psoriasis, eczema, drug reaction, cutaneous lymphoma
Treatment: treat underlying disorder
Acute pustular psoriasis
- Red paiunful skin with white, pus-filled bumps
Treatment: ciclosporin, methotrexate
Uticaria
Itchy, wheals
Lesions last <24 hours
Non-scarring
Commnest skin condition presenting at AandE
Immune mediated: Type I allergic IgE repsonse
Non-immune mediated: mast cell degranulation e.g. opiates
Causes: viral infectios, parasitic infections, NSAIDs, physical stimulants - cold
Treatment: antihistamines, steroids
:
Venous dermatitis with venous ulcer
Purple, brown discolouration both lower legs (due to leaky valves in legs, leading to fluid accumulation and haemosiderin deposition)
Risk factors: Multiple pregnancies, varicose veins, obesity, history of DVT, amlodipine (as causes peripheral oedema)
Investigations:
Ankle Brachial Pressure Index (compared blood pressure between upper and lower limbs) - normally equal, >0.8 indicates occlusion and needs vasuclar arterial assessment
Treatment:
Compression - 3 layer bandaging, class II/III stockings
Emoillent
Topical steroid
Investigations if ulcer didn’t heal:
- Vacular surgery assessment - arterial circulation e.g. MRI angiography
Skin biopsy - exclude inflammatory skin disease
Bacterial swabs
Other causes of leg ulceration:
Diabetes
Drug induced - nicorandil
Pressure sores
Skin cancer
Venous vs. Arterial ulcer
Venous: more superficial, diffuse with surrouding skin changes, usually on ankle
Arterial: Deep, punched out, usually toes, feet, heel
Acne vulgaris
Clinical features: Pustules, papules, comedones
Other features: open comedones (white heads), closed comedone (blackheads), ice pick scars
Differentials:
Rosacea, iatrogenic: due to steroids, folliculitis
Pathophys:
Increaesed androgens cause increased sebum production and viscosity. Sebaceous glands become blocked with keratin and oil.
Natural bacteria on skin (proprionibacterium acnes) becomes trapped in sebum, leading to inflammation and formation of acne.
Types:
Acne vulgaris can be split into:
papulonodular, nodulocystic, comedonal
Agressive types: Ance fulminans (quick onset, painful)
Leeds Acne Score
Treatments:
Topical Retinoids (isotretinoin), OCP - reduces sebum production
Retinoids, benzyl peroxide - reduces occulsion of oil glands
Antibiotics (clindamycin, erythromycin) - reduces build up of bacteria (P. Acnes)
Oral isotretinoin - conc Vit A, reduces sebum production, plugging, bacteria
- Side effects: dry skin, liver dysfucntion, mood changes, teratogen. Females need to be on Pregnancy Prevention Program - require regular pregnancy tests, 4 wk drug dispensing only
Eczema
Inflammatory skin condition characterised by dry, itchy skin that is chronic and relapsing.
Aetiology:
Mutation for filaggrin - abnormal filaggrin causing barrier defect (increased permeability so bacteria can enter)
Types:
Endogenous: Atopic eczema, Seborrhoeic
Exogenous: Contact, Photoreaction
Atopic eczema - itchy, inflammatory condition, assoc with astha, hayfever (atopy), high IgE levels. Type I HS
Clinical features: Red dry symmetrical patches on face, flexor surfaces e.g. behind knees (between fingers suggest contact dermatitis)
Symptoms: tiredness, psychological impact, growth reduction
Causes atopic eczema: baterial - staph. aureus, viral: molluscum, eczema herpeticum
Investigations:
Bacterial swab (if skin broken)
Fungal mycology skin scrape
IgE RAST test
Skin prick testing - used more in children, detects food allergies
Allergic contact dermatitis - patch test
Treatments:
- Irritant avoidance
- Emoillents
- Steroids (mild, moderate, potent, super potent)
SE: perioral dermatitis, thinnning of skin
- Anti histamines
- Oral retinoid
- UV therapy
- Immunosuppressive agents - Methotrexate, Ciclosporin
Biologics - Dupilumab (anti-IL4/13)
Contact dermatitis
Due to exogenous agent
Irritant - direct noxious effect
Allergy - Type IV hypersensitivty (delayed T cell)
Common allergens: Nickle, fragrance
Seborrhoeic dermatitis
- Chronic, scaly inflammatory condition
- Usually face, eyebrows
- Mistaken for dandruff, facial psoriasis
- Overgrowth of Pityropsorum ovale (yeast)
- Severe in HIV
Management:
Anti-yeast shampoo: ketoconazole
Improves with UV
Venous/varciose dermatitis
Underlying venous disease
Affects lower legs, can look brown (due to haemosiderin accumulation)
Valve incompetence, leading to increased hydrostatic pressure, fluid leaks out leading to skin to stretch and inflammation
Symmetrical
Treatment: Emoillents, Steroids, Compression
Psoriasis
Chronic inflammatory relapsing skin disease characterised by scaly papules and plaques
Peak onset: 20-30, 50-60
Aetiology:
T cell immune mediated.
Abnormal infiltration of T cells - release of inflammatory cytokines and TNF - increased keratinocyte proliferation
20% pts develop psoriatic arthritis, assoc with metabolic syndrome
Types:
Plaque
Guttate (looks like rain drops)
Pustular
Clincal features : symmetrical, salmon pink, scaly, well demarcated, extensor surfaces (elbows, knees), pitting nails, onycholysis (separation of nail from nail bed)
Risk factors:
Genetics, infection e.g. streptococcal infection (provokes guttate psoriasis, drugs e.g. lithium
Treatments:
Topical creams - moisterisers, steroids, vit D analogues, coal tar, dithranol, retinoid
Phototherapy (immunosuppressant, decreases T cell proliferation, increaeses Vit D)
Acitretin (oral retinoid/vit D)
Immunotherapy - methotrexate, ciclosporin
Biologics - adalimumab (anti - TNF)
(in order of increasing effectiveness/toxicity)
Alopecia areata
Autoimmune disease against hair follciles and follicular melanocytes
Affects scalp, eyelashes, eyebrows, facial hair, pubic hair
Types:
Alopecia totalis (whole scalp)
Alopecia universalis (whole body)
Treatments:
Super potent corticosteroid e.g. clobetasol
Others:
- Corticosteroid injections
- High does orals corticosteroids
- Allergic contact immunotherapy: DCP treatment
Biologics: JAK2 inhibitors
- Minoxidil (vasodilator to treat hair loss)
Other causes hair loss:
Primary skin conditions:
- psoriasis, eczema,
- scarring skin diseases: cutaneous discoid lupus, frontal fiborsing alopecia
- fungal infection
- syphilis
Secondary causes:
- Thyroid disease
- Iron/B12 deficiencies
- Androgen excess
- Chemotherapy
- Trichotillomania
Investigations:
- Dermoscopy (exclamation hairs (top is wider than bottom)
- Bloods - thyroid
- Fungal mycology
- Syphilis test
- Skin biopsy including hair follicles
Classifications of hair loss and conditions
Non scarring:
- alopecia areata
- telogen effluvium
- drug induced - chemo
- syphilis
Scarring:
- cutaenous discoid lupus
- frontal fibrosing alopecia
- lichen planus
- fungal infection
Localised: alopecia areata, fungal infection. Rest generalised
Which layer of skin do hair and sweat glands grow?
Epithelial growth down to dermis
Immunobullous disorders
Bullous pemphigoid
Paraneoplastic pemphigoid
Bullous pemphigus
Dermatitis herpetiformis (treat: topical steroids, (gluten free diet, oral dapsone)
Impetigo
Golden encrusted leisions with inflammation of dermis
Staph. aureus
Usually children
Treatment: Fusidic acid
Tinea
Fungal infection of skin/nails
Usually feet
Microsporum
Terbinafine cream
Cellulitis
Infection invading dermis
Usually lower limbs, travels through lymphatics
Group A strep, Staph. aureus
Assoc. systemic upset
Enron Classification
- Pt not systemically unwell
- Pt systemicall unwell
- Pt moderately systemic unwell
- Pt septic, severe life threatning complications
Treatments:
- Oral Flucoxacillin (1st line), Doxy (2nd line)
- IV Flucoxacillin (1st line), Doxy (2nd line)
- IV abx + Surgical debridement
Streptococcal toxic shock
Presents as localised infection, fever, shock, diffuse rash
Group A Strep
Treatment: Surgery, penicillin + clindamycin, immunoglobulins
Nec fasc
Life treatening soft tissue infection spreads to deep tissues
Signs/symptoms: pain out of proportion, rapidly progressive, necrotic tissue
Imaging - XR: fasical oedema, gas in tissues
Type 1 - polymicrobial (synergystic action of aerobes and anaerobes). Exsisting wounds.
Type 2 - Strep pyogenes. Healthy tissue.
Type 3: vibrio vulnificus
Typr 4: fungal
Psoariatic arthritis
Usually one joint, involves DIP (distal interphalangeal joint), dactylitis
XR: erosion around DIP, pencil in cup deformity (if advanced)
Pathophysiology:
T cell mediated. Activation of TNF leading to activation RANKL, activating OCs and erosion of bone.
Investigations:
Exclude other inflammatory conditions e.g. RA (rheumatoid blood factor), Autoantibodies - ANA
Treatment:
Psoriasis and psoriatic arthritis: methotrexate, apremilast, adalimumab
