Pathology Flashcards
What is the visual presentation of hyperkeratosis
A scaly skin rash
Build up of keratin layer
What are the 4 main reaction patterns of inflammatory skin diseases
Spongiotic-intraepidermal oedema e.g. eczema
Psoriasiform- elongation of the rete ridges e.g. psoriasis
Lichenoid-basal layer damage e.g. lichen planus and lupus
Vesiculobullous- blistering e.g. pemphigoid, pemphigus
What is the characteristic of lichenoid disorders
Damage to basal epidermis - between epi and dermis
Most common condition is lichen planus
Can be a lichenoid drug reaction
How does lichen planus present
Itchy flat topped pink/purple papules
Very ithcy
Affects wrists, forearms, shins and ankles
May get lacy, white streaks in cheeks or on papules- Wickham’s striae
what is the main feature of immunobullous diseases
Blisters
vesicles and bullae
What is pemphigus
Rare autoimmune bullous disease
Autoantibodies cause damage to the junctions between skin cells - intrepidermal
Loss of junction integrity causes severe blisters
How can you treat pemphigus
Responds to steroids
What is the most common subtype of pemphigus
Pemphigus vulgaris
80% of cases
Describe the cause of pemphigus vulgaris
IgG autoantibodies made against desmoglein 3 which forms the desmosomes
Immune complexes form and complement is activated
Proteases are released and dissolve the attachments between cells - leads to acantholysis
Occurs within the epidermis itself
what is acantholysis
Breakdown of intercellular adhesion sites
common to all types of pemphigus
What causes bullous pemphigoid
IgG antibodies attack the hemidesmosomes that attach the basal cells to the basement membrane
This breaks down the DEJ and causes separation of dermis and epidermis
Complement is activated and the surrounding tissues are damaged
How does bullous pemphigoid present
Can present with itchy red plaques and papules before the blisters develop
Subepidermal blisters - deep
Large, tense blisters on normal, red or urticarial base
When they burst, they leave erosisons but do not scar
Unlikely to affect mucosa (mouth only if at all)
typically localised to one area or widespread on trunk/ limbs
Nikolsky sign negative
What would show up if you did immunofluorescence on a bullous pemphigoid sample
Linear pattern of IgG antibodies would show up along the basement membrane - solid typically green line alone BM
Would also pick up complement
What condition is dermatitis herpetiformis associated with
Coeliac disease
Personal or family history
How does dermatitis herpetiformis present
Extremely itchy lesions - typically preceeds blisters
Small blisters on erythematous urticarial base - often scratched off leaving crusts or excoriation
Symmetrical
Often affects the elbows, extensor forearms, knees, buttocks, face and scalp
The hallmark is papillary dermal microabscesses
Which HLA group is dermatitis herpetiformis associated with
HLA-DQ2 haplotype
What would a dermatitis herpetiformis sample look like under immunofluorescence
IgA deposits seen at the tips of the dermal papillae
Granular IgA deposits
What is the aetiology of acne
It is a chronic inflammatory disease of the pilosebaceous units.
Increased androgens during puberty cause increased activity of sebaceous glands
Keratin and sebum plugs the pilosebaceous unit
Glands get blocked, inflamed then rupture
Infection with other bacteria (p acnes) causes further inflammation
What is the normal distribution of acne
face, upper back, anterior chest
High concentration of sebaceous glands
What is the clinical presentation of rosacea
Recurrent facial flushing - exacerbated by sudden change in temperature , alcohol & spicy food
Erythema
Visible blood vessels
Pustules and papules
Thickening of skin Rhinophyma - enlarged red nose
Affects nose, chin, cheeks and forehead
How can you differentiate between acne and rosacea
Rosacea does not have comedones - black/white heads
Also normal sebum excretion rates
What are some triggers of rosacea
Sunlight Alcohol Spicy foods Stress Sudden temperature changes
List some topical treatments for acne
Bezoyl peroxide
Antibiotics
Retinoids
How do topical retinoids work
Dry skin up by shrivelling the sebaceous glands and reducing secretion
Anticomedonal
Describe the presentation of acne vulgaris
Comedones - black/white heads
Pustules and papules
cysts
erythema
What is a potential complication of acne
Scarring
Can be atrophic (shallow/ice pick) or hypertrophic (keloid)
Usually after deep lesions
Where on the body does rosacea normally appear
Nose, chin, cheeks and forehead
How can you treat rosacea
Reduce exposure to triggers - diet, wear suncream Topical = metronidazole, ivermectin Oral tetracycline - long term Roacccutane if severe Vascular laser for telengectasia Rhinophyma - surgery
How do you treat lichen planus
Symptomatically
Usually burns out after 12-18 months
Can use topical steroids
Oral if very severe
what is Nikolsky’s sign
When the top layer of skin slips away from the lower ones when rubbed slightly
Positive in pemphigus
Which areas of the body are typically affected by pemphigus vulgaris
Scalp, face, axillae, groins Mucosal involvement (eyes, genitals) is very common May also appear on pressure points
Which condition has higher risk, pemphigus or pemphigoid?
Pemphigus
Very high mortality if untreated - 75-99%
How do you treat pemphigus
First line - oral steroids (pred)
Typically start steroid as inpatient – may be IV
Then can add another immunosuppressive agent - usually azathioprine
Topical steroids and anaesthetics are symptomatic treatment only
List physical causes of skin blistering
Insect bites
Burns
Friction - particularly in elderly as friable skin
List infectious causes of skin blistering
HSV – cold sores, eczema herpeticum
VZV – chickenpox, zoster
Coxsackie virus – hand-foot-and-mouth disease
Staph aureus – bullous impetigo, SSSS
Strep pyogenes – bullous cellulitis
List genetic causes of skin blistering
Epidermolysis bullosa (EB)
Which drug reactions can cause skin blistering
EM / Stevens-Johnson syndrome
Toxic epidermal necrolysis (TEN)
Fixed drug eruption
What is the role of desmosomes
Hold adjacent epidermal cells together
What is the role of the hemidesmosomes
Hold the epidermis to the dermis at the DEJ
How would you investigate suspected bullous disease
History and examination
Bloods – Usual set with inflammatory markers – ESR/CRP
May do swabs to rule out infection
Biopsy with IMF - this will be your diagnostic test
which age group is most affected by bullous pemphigoid
Age >60 years in majority
How do you treat bullous pemphigoid
Topicals: emollients, topical antisepsis / hygiene measures
First-line – topical steroid + doxycycline for localised disease
Second line – oral steroid + steroid sparing like doxy for generalised disease
May use doxy alone if disease is not severe
Rest are 3rd line onwards that isn’t responding - azithioprine, dapsone, biologics
Bullous pemphigoid is typically self limiting - true or false
True
However it is chronic and can take months to years to resolve without treatment
Treatment reduces recovery to 3-6 months
which age group is most affected by pemphigus vulgaris
Usually a disease of middle age
How does pemphigus vulgaris present
Flaccid vesicles/bullae
Includes oral, throat and genital lesions
They rupture easily leaving raw, denuded erosions
Nikolsky sign positive
How would pemphigus vulgaris present on immunofluorescence
Would see IgG deposits outlining epidermal cells
Looks like chicken wire
Which age group is most affected by dermatitis herpetiformis
Mainly young adults
Can affect all ages though!
How would you investigate dermatitis herpetiformis
Coeliac serology – IgA antibodies to tissue transglutaminase (tTG)
Histology of lesion- subepidermal blisters, microabscesses in dermal papillae
Biopsy uninvolved skin for detection of granular deposits of dermal papillary IgA on immunofluorescence
Small intestinal scope + biopsy
How do you treat dermatitis herpetiformis
Gluten-free diet - mainstay
Drugs: dapsone, Tetracyclines
How do you treat mild acne
Topical treatment only
e.g. Benzoyl peroxide
Topical antibiotics, retinoids
Range of anti-comedonal, inflammaotry and microbial effects
What are comedones
Blocked pores bascially
If closed - whitehead
If open - blackhead
What can cause an increase in sebum production
Androgen effect as sebaceous unit had androgen receptors
Increased androgen production - seen in puberty or androgenic hormone imbalance in females
Increased availability - decreased SHBG
Increased androgen receptor responsiveness
The more bacteria present in acne, the worse it is - true or false
False!
No relationship between # of bacteria and acne severity
More related to amount of sebum and ductal cornification
Which bacteria commonly colonise acne
Propionobacterium acnes
Staph. epidermidis
Malassezia furfur
How do you grade acne
Mild- scattered papules and pustules
Moderate- numerous papules, pustules and
mild atrophic scarring
Severe - as above, cysts, nodules and significant scarring
What factors can aggravate acne
Poor diet Being pre-menstrual = common to flare Sweating UV Steam or oil in environment Stress
How do you treat moderate acne
Topical treatment and oral antibiotics or Dianette® (females)
How do you treat severe acne
Isotretinoin (Roaccutane®)
What are the side effects of benzoyl peroxide for acne
Erythema and peeling
Bleaches clothes, hair, bedlinen and towels
Retinoids should be avoided in pregnancy - true or false
True
Systemic absorption of topicals not significant but still avoid
What are the side effects of topical retinoids for acne
Stinging, irritation, erythema and peeling
Which antibiotics are used for acne
Topical:
Erythromycin
Tetracycline
Clindamycin
Oral: Erythromycin Oxytetracycline Doxycycline Minocycline - needs LFT monitoring
What is the main skin side effect of tetracyclines
Photosensitivity
If antibiotic therapy isnt working for acne should you try another
Yes
Try a second antibiotic after 3-6 months
Can contraception be used to treat acne
Yes - combined pills
Typically use dianette
Oestrogen decreases androgen production
Takes 6 months to lower sebum though
Progesterone rich / Only contraceptives may exacerbate acne
What are the indications for starting someone on roaccutane
Nodulo-cystic acne
Inadequate response to conventional therapy
Relapse after adequate antibiotics
Significant scarring
Severe psychological impairment (dysmorphophobia)
post-inflammatory hyperpigmentation
How does roaccutane work
Reduces sebaceous gland activity
List side effects of roaccutane
Dry skin, lips, eyes, nose Skin fragility Hyperlipidaemia Abnormal liver function Teratogenesis- contraception Mood alteration Arthralgia Acne fulminans Hair thinning Benign intracranial hypertension
How does tuberous sclerosis present in the skin
Multiple hamartomas Angiofibromas Peri-ungual fibromas Shagreen patches Ash leaf macules
What causes tuberous sclerosis
Autosomal dominant mutation
2/3 are de-novo
What causes neurofibromatosis
Autosomal dominant
Mutation in neurofibromin gene (tumour suppressor) on chromosome 17
How does neurofibromatosis present in the skin
Neurofibromas
Cafe au lait macules
Axillary freckling
Lisch nodules
List skin manisfestations of diabetes
Infections
Leg ulcers and other complications
Some specific disease related to diabetes - Necrobiosis Lipoidica etc
What is erysipelas
skin infection in upper dermis - typically strep
Seen in diabetics
Confluent erythema
Well demarcated
Not raised, scaly or crusty
Would be tender, hot, painful, patient may feel unwell
How do you treat erysipelas
Need oral or IV antibitoics as deep
Would probably use IV if on the face/periorbital
Candida is common in diabetes - true or false
True
Occurs in warm moist areas
Also seen around nails
Hyperglycaemia favours growth
Describe the appearance of Necrobiosis Lipoidica
Bilateral lesions - tyipcally on shins
Smooth skin surface = deeper issue
Epidermal issue will typically be dry and scaly
Erythema and yellowing seen - subcutus peeks through
What causes Necrobiosis Lipoidica
Technically unknown
Most patients are diabetics - ?microvascular cause
Granulomatous inflammatory reaction around destroyed collagen
How do you treat Necrobiosis Lipoidica
Inject steroids around lesion
Can use tacrolimus - calcineurin inhibitor
How might psoriasis present in the nails
Pitting
Onycholysis (lifting of the nail plate off the nail bed)
Subungual hyperkeratosis– keratin build up below the nail
Longitudinal ridging
Thickening
Crumbling
Colour changes
How can you treat psoriatic nail disease
Topical steroids
Intralesional if a few nails affected
Calcipotriol
PUVA - systemic psoriasis treatment
How do you diagnose fungal nail disease
Take clippings
Assess for skin involvement
How do you treat fungal nail disease
Topical or oral antifungals
How does fungal nail disease present
Thickened nails
Brittle
Yellow discoloration
What is a subungual haematoma
Bleeding under the nail
Typically after obvious trauma but repeated microtrauma can be enough
What must be ruled out before diagnosing simple subungal haematoma
Subungual melanoma
They can bleed too
Dermoscopy can help clarify
How does subungal melanoma present
Irregular pigmentation under nail Typically a brown/black stripe down nail Extends to involve proximal nail fold May bleed, ulcerate, Abnormalities of the nail plate
How do you manage subungal melanoma
May require excision of the entire nail apparatus if not amputation
What is a myxoid pseudocyst
A benign, painless cyst (though lacks capsule) at the edge of the nail
Treat by draining - may recur
What causes lichen planus
T cell mediatedautoimmunedisorder
Inflammatory cells attack an unknownproteinwithin the skin and mucosalkeratinocytes
How does lichen planus present in the nails
Thinning Onycholysis Pterygium(fusion of nail with nail bed) Loss of nail Ridges
What are Beau’s lines
Transverse lines secondary to nail growth arrest, usually at a time of severe illness, chemotherapy
Deep grooved lines horizontal on nail
What is paronychia
Infection in the skin around a nail
Acute may be due to trauma, nail biting and usually bacterial
Chronic is typically a fungal infection
How do you differentiate between scarring and non-scarring alopecia
Non-scarring alopecia’s demonstrate visible follicular units on dermoscopy, while scarring alopecia’s are devoid of follicular units
What is androgenic alopecia
Typical male or female pattern baldness
Likely due to androgen sensitivity and genetics
How can you manage androgenic alopecia
Monoxodil 5%(vasodilatory effects)
Males – finasteride (stops testosterone being converted to DHT)
Spironolactone
Hair transplant
Camoflage: nanogen fibres, hair piece, wig
Psychological support
What is telogen effluvium
Hair loss related to stressful events
Hair suddenly moves from the anagen to telogen phase causing mass hair shedding
Can be due to pregnancy, surger, illness, stress
Usually corrects itself with time
What causes alopecia areata
Autoimmune condition
T-cell mediated
How does alopecia areata present
May have preceding tingling, ‘trichodynia’
Focal patches of confluent hair loss.
Exclamation mark hairs - thinner at base, thicker at top
How do you manage alopecia areata
Potent topical steroids Intralesional steroids DCP JAK inhibiors Camoflage
What is traction alopecia
Hair loss caused by traction
Usually due to tight hairstyles or headgear
What is trichotillomania
Irresistible urge to pull at hair
Associated with OCD, stress and anxiety - treat these to treat
How does trichotillomania present
Temples and vertex common sites - often on side of dominant hand
Irregularly shaped patches of hair loss
Varying lengths
Tinea capitis can lead to alopecia - true or false
True
Can even scar if extensive + chronic (called kerion - highly inflamed TC lesion)
List 3 main causes of scarring alopecia
Discoid SLE
Lichen planopilaris
Folliculitis decalvans and Dissecting Cellulitis of the scalp
How does discoid lupus present on the scalp
Persistent, scaly, discoid lesions on the head and neck area
Inflammatory plaques present
Can cause scarring, discolouration
May be triggered by sunlight
How do you treat discoid lupus
High potency steroids
Intralesional steroids
Protopic
Systemic treatment: hydroxychloroquine, oral pred, methotrexate, other immunosuppressives
Sun protection
How does Lichen planopilaris present
Symptoms: itch, pain, tenderness, burning
Significant loss of hair - scarring/permanent
Common sites: forehead, nape of neck, sides of scalp
Slow to progress
Trichoscopyreveals absentfollicles, white dots, tubularperifollicularscale and perifollicularerythema
How does folliculitis decalvanspresent
Follicular pustules and scarring alopecia
Characteristically, several or many hairs can be seen coming out of a single follicle, so the scalp looks”tufted”
How does dissecting cellulitis of the scalp present
Perifollicular and follicular pustules Nodules and pseudocysts, often with purulent exudate Abscess Hair loss - scarring/permanent Keloid scars
What is hirsutism
Male pattern of secondary or post-pubertal hair growth occurring in women
May develop thicker hairs, across the moustache and beard area, lower abdomen etc
What can cause hirsutism
PCOS
Cushings
Congenital adrenal hyperplasia
Caused by increased androgens or stronger response to them
How do you manage hirsutism
COCP
Spironolactone
Metformin
Hair removal - many types
What is hypertrichosis
Non-hirsute excessive hair growth over and above the normal for the age,sexand race of a male or female
Can be congenital, associated with naevi or spina bifida
Aquired - malnutrition, malignancy and certain drugs
Which drugs can cause hypertrichosis
Ciclosporin
Phenytoin
Minoxidil - used for hair loss
What is DRESS
Drug exanthem with eosinophilia and systemic symptoms
Red rash skin reaction with additonal symptoms
Facial swelling Lymphadenopathy Liver involvement - check LFT Morbilliform rash Fever
May even go on to need organ transplant if multiple organ involvement
What is a drug exanthem
Erthematous macular + papular rash in response to medication
Usually then becomes confluent
Usually blanches
Axillae, groins hands and feet often spared.
How do you treat drug exanthems
Stop the offending drug
Treat symptoms - antihistamine & topical steroids, regular emollient
If DRESS give oral steroids
Which drugs often cause exanthem reactions
Antibitoics - penicillins, cephalasporins
Allopurinol
Anti-epileptics
NSAIDs
What is the main difference between SJS and TEN
SJS – mucosal involvement more likely <10% skin involved
TEN - >30% skin involved
Describe the presentation of SJS
Characteristic prodrome of respiratory symptoms, followed up to 14 days later by erosions of at least 2 mucosal surfaces with variable skin involvement
Pyrexia, systemic upset especially in children
May be dehydrated
Target like lesions, blisters etc
Epidermal detachment - desquamation affecting up to 10% of body
Nikolskys sign – positive, detachment of epidermis on light lateral pressure
How do you treat SJS and TEN
Stop any offending drug or treat underlying cause
Needs HDU or ICU as very dangerous
May have burns unit input
Supportive treatment:
Fluid management, thermoregulation, regular emollient, dressing care etc
Prevent secondary infection
Which drugs can cause urticaria
Can be any drug if patient is truly IgE allergic
NSAIDs and aspirin can induce a pseudourticaria
Describe erythema multiform
Hypersensitivity reaction to some drugs or infection
Forms target lesion on skin
Usually acute and self limiting
Can involve mucosa and lead to fever
List causes of erythema multiform
Idiopathic
Drugs - sulphonamides, penicillin, phenytoin
Viral infections – common with HSV in children
What is a fixed drug eruption
A T cell mediated reaction to a specific drug
Recurrent and fixed site when exposed to offending drug.
Erythema, oedema, bruised appearance, blistering
Which drugs commonly cause a fixed drug eruption
Tetracyclines
Paracetamol
Sulphonamides
NSAIDS
Which drugs commonly cause a phototoxic drug reaction
Quinine
Doxycycline
NSAIDS
Retinoids
Describe the appearance of erythema nodusum
Tender nodules usually on shins
Deep - nodules felt on palpation, may not be visible
Which drugs can cause eryhtema nodusum
Sulfonamide Amoxicillin Oral contraceptive Non-steroidalanti-inflammatorydrugs Bromide Salicylate
Which drugs can induce bullous pemphigoid
Frusemide, penicillamine, penicillin, sulphonamides
Younger demographic compared to BP
How can amiodarone affect the skin
Can cause blue/black discoloration
How does pityriasis rosea present
Solitary lesion appears 2-4 days before onset of rash – herald patch
Truncal eruption – small pink oval lesions with peripheral “micca” scale
How do you treat pityriasis rosea
Self-limiting - likely viral cause
Can use topical steroids
What causes vitiligo
Loss of melanocytes from affected areas
May be assoc with other autoimmune conditions
Around 30% have a family history
How can you treat vitiligo
Topical steroids / phototherapy may help
Consider cosmetic camouflage
Which skin conditions often have a psychological component
Urticarias
Pruritis
Flushing reactions
Sweat gland disorders
Stress can also trigger flare of many skin diseases - it is an inflammatory process
What are salmon patches
Very common birthmark - 50% of babies
Either on face or back of neck
Thought to be due to persistant foetal circulation rather than a malformation. Tend to resolve
Neck lesions more persistant, around 10% into adulthood
What are haemangiomas
Vascular tumours confined to children - benign
They occur during early childhood and most will regress and disappear
Describe the appearance of a port wine stain
Macular red birthmark They don’t extend outwith the initial area but may thicken These lesions persist for life Common on the face Typically unilateral
What causes a port wine stain
Vascular malformation of capillaries
When is a port wine stain associated with epilepsy
If their PWS is in the distribution of CN V1 - nose
Associated with ipsilateral vascular malformation in brain
Called Sturge Weber syndrome
What conditions are seen in Sturge Weber syndrome
Causes seizures, intellectual impairment, hemi-paresis and glaucoma
Will have a port wine stain in V1 distribution
What is Klippel-Trenauney
syndrome
Port wine stain on limb
The associated vascular malformation involves many vessels
Leads to progressive limb overgrowth and thickening
Where do most infantile haemangiomas appear
Commonest on head and neck
Which babies are at higher risk of infantile haemangiomas
Commoner in prems & females
What are some of the complications of infantile haemangiomas
Can be very painful if they become ulcerated
Risk of infection
Bleeding
Compression
Obstruction of vision if around the eye or airway if near it
What does a tumour type lesion over the spinal cord in an infant suggest
Spina bifida
May have an overlying haemangioma - rare
How would you treat a serious infantile haemangioma
Topical or Intra-lesional corticosteroids
Systemic corticosteroids
Propranolol @ 2-3 mgs /Kg for several months
Used if in a high risk area
What is a mongolian blue spot
Blueish birthmark
Common over buttock but can be seen anywhere
Common in black and asian skin
Can be confused with NAI - need to document when you find one
Congenital Melanocytic Naevi have a risk of developing into melanoma - true or false
True
Around 4 fold risk
Higher for larger lesion
What is a Congenital Melanocytic Naevus
A melanocytic (pigmented) mole
Aquired in childhood
May become warty or hairy
When would you consider an underlying cause of cafe au lait macules in a child
If they have 2 or more under the age of 2 then you would consider neuroectodermal disease
Which type of cell is primarily responsible for the development of urticaria, angioedema and anaphylaxis
Mast cells
Found in the dermis
Histamine release from mast cells can have which cutaneous effects
Urticarial lesions or wheals due to superficial dermal oedema
Angioedema due to deep dermal or subcutaneous swelling
Meningococcal meningitis is associated with what type of rash
Non-blanching purpuric rash
Caused by damage of the dermal vessel walls by bacteria in the endothelial cell walls
Check with glass test
How do you treat suspected meningococcal disease in primary care
IV / IM Benzylpenicillin as soon as possible
Transfer to hospital ASAP
How do you treat suspected meningococcal disease in secondary care
Ceftriaxone or Cefotaxime are the antibiotics of choice
What can cause SJS
Most commonly drugs - NSAIDs, sulphonamides, anticonvulsants and other antibiotics
Typically occurs 2-8 weeks after ingestion
May be caused by infections in some
How long does SJS typically last
4 - 6 weeks
Describe the presentation of TEN
May have initial fever, sore eyes
Rapidly spreading skin lesions, initially dusky-red macules which coalesce, leading to necrosis and detachment
Large areas of epidermal and mucosal detachment affecting >30 % body surface area
Nikolskys sign – positive, detachment of epidermis on light lateral pressure
Pain is major feature
May be resp / GI epithelial involvement
Rapidly progressing
What causes TEN
Almost always due to drugs
Develops 1-3 weeks after taking the drug
What is erythroderma
Defined as erythema, often with scale, of at least 90% of the body surface area
Descriptor not diagnosis
What can cause erythroderma
Can be idiopathic Dermatitis Psoriasis Drug reactions Cutaneous T-cell lymphoma - may have overlying ulcerating tumours
Though to be due to reduced cell transit time and increased mitotic rate
Which drugs are common causes of erythroderma
Allopurinol
Antibiotics
Carbamazepine
PPIs
How do you manage erythroderma
Initial management supportive and symptomatic - fluids, temp regulation etc
Emollients +++
May need antihistamines for associated pruritus
Specific treatment for underlying condition
List some complications of erythroderma
Tachycardia and enter high output cardiac failure - due to increased blood flow to skin
Disturbed thermoregulation - hyperthermia
Compensatory hypermetabolism due to loss of heat
Describe the appearance of eczema herpeticum
Multiple, monomorphic crusted vesicles are seen
Often haemorrhagic,
May be associated bacterial infection
May also have fever, malaise, lymphadenopathy
What is eczema herpeticum
Widespread infection with Herpes Simplex
Most commonly seen in children and young adults with atopic eczema
How do you treat eczema herpeticum
Prevention - avoid contact with friends and family with H Simplex infection
Severe cases – IV antiviral ASAP
Less severe cases – oral Rx
How does pustular psoriasis present
Sterile pustules on skin surface
Often surrounded by red, inflamed skin
May be localized, usually to the hands and feet
Can be widespread - this is life threatening
Usually an acute presentation
What can trigger pustular psoriasis
Pregnancy Withdrawal of corticosteroids Infections Hypocalcaemia Other drugs eg salicylates, lithium
List potential complications of pustular psoriasis
Can be fatal! Hypoalbuminaemia Hypocalcaemia Acute renal tubular necrosis Liver failure Secondary infection
How do you treat pustular psoriasis
Remove any triggers if possible
Supportive treatment
Most cases require systemic therapy - Acitretin or Methotrexate
Consider PUVA
What is necrotising faciitis
Infection in the deep dermis, subcutaneous fat and fascia
Group A strep is a common aetiological agent but often multiple organisms involved
Which factors can predispose to necrotising fasciitis
Trauma
Diabetes
Surgery
How does necrotising fasciitis present
painful, hot skin which is erythematous / dusky
Bullae and necrosis develops
Rapidly progressive cellulitis and necrosis
Patient is generally severely ill
How do you treat necrotising fasciitis
Urgent management with surgical debridement and high dose IV antibiotics is essential
How do you differentiate between venous and arterial ulcers
Venous – malleolus, superficial
Arterial – distal, deeper
How can you treat acanthosis nigricans
Can try topical retinoids / vit D analogues, sal. acid
What can cause acanthosis nigricans
Insulin resistance is the main cause - seen in diabetes
Can be paraneoplastic
What causes pretibial myxoedema
Graves disease
Auto-antibodies cross-react with the fibroblasts and cause thickening of the skin and fluid accumulation
How do you treat pretibial myoedema
Treat underlying Graves
Correct circulation – compression stocking
What skin signs may be seen in hyperthyroidism
Warm, moist smooth skin Hyperhidrosis Facial flushing, palmar erythema Fine, thin hair. Diffuse alopecia Pruritus Pretibial myoedema seen in Graves
What skin signs may be seen in hyperthyroidism
Cold, dry pale skin
Dry, coarse brittle hair, diffuse alopecia
Loss of lateral 1/3 eyebrow
Periorbital oedema and generla puffiness
Thickened brittle nails
What skin signs may be seen in Addison’s
Increased pigmentation - due to MSH release alongside the ACTH
Seen all over but especially in palmar creases and buccal mucosa
Which tumours can cause increased pigmentation in the skin
Pituitary
Lung
Due to MSH release
Which tumours can cause hirsutism
Ovarian
Other androgenic effects like acne and baldness may be seen
What are the 3 types of lupus skin disease
Cutaneous / Chronic Discoid LE - only in skin
Subacute cutaneous LE
Systemic LE - typical CTD with skin signs
How do you treat Cutaneous / Chronic Discoid LE
Reduce sun exposure - can be a trigger
Use potent topical steroids – only condition where you start with potent in the face due to scarring risk and high inflammation
Then Hydroxycholroquine – oral
Also true for subacute type
How does Cutaneous / Chronic Discoid LE present
Erythematous indurated plaques on sun exposed sites
Heals with scarring
If on hairy site will lead to permanent hair loss
How does subacute cutaneous LE present
Usually ring-shaped erythematous scaly plaques, not indurated
Symmetrical.
Photosensitive - on sun exposed sites
Heal without scarring
Which conditions is more associated with the development of SLE - Cutaneous / Chronic Discoid LE or subacute cutaneous LE
Subacute
Also more likely to be antibody positive
What skin signs are seen in SLE
Butterfly ‘malar’ rash is classic - spares nasolabial folds
Photosensitive
Nail fold capillaries prominent
May have widespread DLE type rash
Describe the skin changes seen in systemic sclerosis
Scleroderma
No surface change - deeper in dermis
Very hard and no give in skin – can be very restrictive
Common in fingers - sclerodactyly
Will also see telengectasia and Raynaud;s
List the skin features of dermatomyositis
Photosensitivity rash like that of L.E
Shawl like pattern
Heliotrope oedema of eyelids
Linear finger rash with Gottron’s papules
Describe the appearance of erythema multiforme
Target lesions
Often affects knees, elbows, palms, soles and mucosal areas
What can cause erythema multiforme
90% due to infection – HSV
Often follows a coldsore
Some meds - sulphonamide
Describe the appearance of erythema nodusum
Red, tender, diffuse nodules
Will be able to feel nodules deep in skin
Typically on shins
What can cause erythema nodusum
Infections – Strep, TB, EB, fungal
Drugs – OCP, sulphonamides
Inflammatory bowel disease
Sarcoidosis
Describe the appearance of cutaneous vasculitis
Non-blanching, purpuric rash ± bullae and necrosis.
Lower legs usually worst
What is livedo reticularis
Mottled cyanotic network exacerbated by cold - purple/blue lines of veins
Can be caused by hot water bottle exposure!
Also heart failure, emboli, drugs etc
What is Mycosis Fungoides
A cutaneous T cell lymphoma
Presents first with a reddish patch and then becomes a plaque
Can then erupt and cause erythroderma
Which cancers often met to the skin
Breast, lung, colon, stomach, uterus, kidney,, lung, colon
What is a sister mary joseph nodule
A malignant metastatic nodule found around the umbilicus
Sign of advanced cancer
Which primary cancer is associated with generalised pruritis
lymphoma
What is pityriasis versicolor
A common yeast infection of the skin which can affect melanocyte function leading to variable pigmentation
What is urticaria
A transient (individual lesions last <24 hours) eruption of erythematous and oedematous swellings of the dermis, usually associated with itching
Also called hives or wheals
What is angioedema
Transient (24 to 48 hours at most) swellings in the deeper dermal, subcutaneous and submucosal tissues.
Often seen in lips and tongue
Urticaria is seen in which autoimmume disease
SLE
Which drug is associated with angioedema
ACE inhibitors
What can cause urticaria and angioedema
Allergy Drugs - salicylates Physical urticarias - solar, cold, water etc. SLE Infections Idiopathic - chronic type
How do you treat urticaria
Allergen avoidance if trigger identified
If no trigger then suppressive therapy
- antihistamines (H1 and H2)
- leukotrine antagonists
- serotonin antagonists
- UV phototherapy
How do antihistamines work
Reversible competetitive inhibitors of histamine - bind to histamine receptors
Reduces the action of histamne
How do you differentiate anaphylaxis from urticaria and angioedema
Will also present with respiratory compromise and hypotension - they will be shocked
What are the 4 main types of itch
Pruritoceptive - triggered by something in skin
Neuropathic - damage to C or P nerves
Neurogenic - no C/PNS damage but still nerves that are triggering itch
Psychogenic - psychological cause with no CNS damage
Which nerve fibres transmit the sensation of itch
unmyelinated C fibres
Which chemical mediators in the skin can trigger itch
Histamine
Tryptase
Interleukin 2
Substance P
What treatments are available for non-specific itch
Sedative anti-histamines
Emollients - with menthol or cooled in fridge
Antidepressants can work for neuropathic itch
Photo therapy
Opiate antagonists, serotonin (5HT3 receptor) antagonists
Which type of antihistamines are good for treating itch - sedative or non-sedative
Sedative
non-sedative antihistamines useless for most itch except in urticaria and insect bites
