Dermatology Flashcards
Atopic Dermatitis and Eczema
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Inflammatory skin condition characterised by dry, pruritic/itchy skin with a chronic relapsing course.
Usually in childhood, men and women equally
Cause:
Genetics → polygenetic inheritance- predisposition for increased IgE formation and sensitisation aka type 1 hypersensitivity
triggers
- Dust mites
- Heat
- Humid climate
- Stress
- Skin irritation
RF:
- Allergic rhinitis (hayfever)
- Age <5 years
- Family history of eczema
- PMH/FH of atopy (food allergies, asthma)
Contact Dermatitis: type of eczema after exposure to a causative agent, e.g. new occupation, change of hobby
Eczema herpeticum: emergency where theres infection of skin by HSV 1 or 2. In children with atopic eczema, is a rapidly progressing painful rash with punched out erosions. Life threatening so IV acyclovir
CLINICAL FEATURES
- Pruritis- may have excoriations (scratch marks)
- Dry skin
- Sites of skin involvement:
- Infants- cheeks, forehead, scalp, extensor surfaces
- Children- flexures esp wrists, ankles and antecubital and popliteal fossa
- Acute flares:
- Erythema
- Scaling
- Vesicles
- Papules
- Lichenification (thick leathery skin due to constant scratching)
- hyperpigmentation if chronic
INVESTIGATIONS
Clinical diagnosis
Elevated IgE levels
Contact dermatitis: skin patching for type 4 sensitivity, skin prick for type 1 (food allergies, urticaria)
MANAGEMENT
Give emollients to improve skin barrier function
Topical corticosteroids i.e. hydrocortisone
If severe: immunosuppressive agent - oral ciclosporin
PROGNOSIS
chronic disease with a varying course. Approximately 60% of children will have symptom resolution as they enter puberty, but relapse may occur in 50%
COMPLICATIONS
- Psychological stress
- Adverse effects of drugs
Ciclosporin side effects
- Hypervolaemia
- Hypertension
- Hyperkalaemia
- hair growth
- gum hyperplasia
- Hyperglycaemia
Cellulitis
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Infection of deep dermis and subcutaneous tissue. Develops when micro organisms gain entry to dermal and subcutaneous tissues via disruptions in cutaneous barrier e.g. minor skin injury
Most common:
- Staphylococcus aureus (catalse +ve)
- Streptococcus pyogenes (catalse -ve)
RF
- Diabetes
- Obesity
- Oedema
- Venous insufficency
- Eczema
CLINICAL FEATURES
- Diabetes
- Obesity
- Oedema
- Venous insufficency
- Eczema
- Systemic: fever, chills, nausea, headache
Erysipelas: more superficial, limited version of cellulitis. well defined lesion, due to strep pyrogenes. Flucloxacillin treatment
INVESTIGATIONS
Diagnosis: clinical: only do further test if systemic signs or septicaemia
Septic signs: high HR, RR, low BP, low GCS
Bloods: high WCC, high CRP
Skin swab MCS
If suspect sepsis(or significant systemic upset and/or comorbidities), admit patient do blood culture and sensitivities
MANAGEMENT
Flucloxacillin
Severe systemic: septic, tachy, hypo: Hospital admission + IV co-amoxiclav/cefuroxime/clindamycin/ceftriaxone
If penicillin allergy: Clarithromycin/erythromycin/doxycycline
COMPLICATIONS
- Sepsis
- Chronic oedema in affected extremity
- Necrotising fasciitis
- Periorbital/orbital cellulitis
PROGNOSIS
excellent
Pressure sores
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Damage to skin, usually over bony prominence as a result of pressure. Due to constant pressure limiting blood flow to skin and causing damage.
Common in hospitals and the elderly
RF
- Immobility
- Recent surgery or intensive care stay
- Diabetes
- Malnutrition
Risk screening: Waterlow score- takes BMI, nutritional status, skin type, mobility and continence into account
CLINICAL FEATURES
- Location- over bony prominences, typically sacrum or heel
- Focal area of nonblanchable erythema
- Evidence of decreased skin perfusion (increased CRT)
- Painful (unlike neuropathic ulcers which are painless)
- Signs of wound infection- purulent drainage, foul smell
Four stages of pressure sores:
- Stage 1 ⇒ nonblanchable erythema of intact skin
- Stage 2 ⇒ loss of dermis +/- epidermis. Superficial ulcer
- Stage 3 ⇒ loss of all skin layers (full thickness)
- Stage 4 ⇒ extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures
INVESTIGATIONS
risk factor assessment: blood glucose, HbA1C, serum albumin (malnutrition)
Screen for infection: WCC and CRP
MANAGEMENT
- Pressure relief over affected area
- Frequent position changes (every 2 hrs) for immobile patients
- Moist wound environment (encourages ulcer healing)
- Ensure good nutrition
Analgesia (paracetamol, ibuprofen)
If stage 3 or 4 sore:
- Surgical debridement and reconstruction with flap formation (if suitable for sugery)
- Debridement of necrotic tissue (if not suitable for surgery)
PROGNOSIS
good with prompt care
COMPLICATIONS
sepsis, cellulitis, osteomyelitis → if pressure ulcer becomes infected, infection can spread → all can be treated with systemic antibiotics
Psoriasis
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Chronic inflammatory skin disease characterised by erythematous circumscribed scaly papules
Plaques caused by hyperproliferation of keratinocytes stimulated by abnormal T cell activity.
relapsing and symptom free intervals
20-40yrs old
Causes:
- Genetic predisposition- important
- Immunology
- Infection
- Mechanical irritation
Exacerbating factors:
- Drugs e.g. beta blockers, lithium, antimalarials, NSAIDs, ACEi, infliximab
- Trauma
- Alcohol
- Withdrawal of systemic steroids
Four main types:
1) Plaque psoriasis: Raised inflamed plaque lesions with a superficial silvery white scale eruption. Drugs like ACEi, B blockers, NSAIDs, Lithium make it worse. Exposure to sun makes better
2) Flexural psoriasis: skin is smooth, occurs on skin creases or flexures (groin, armpit)
3) Guttate psoriasis: Widespread erythematous fine scaly papules (Water drop appearance) on trunk, arms, legs. After URTI (usually streptococcal). Phototherapy (topical if lesions are symptomatic)
4) Psoriatic arthritis: Inflammatory damage and deformity to joints- often proceeds development of skin lesions. HLA-B27. asymmetrical polyarthritis of hands and feet, DIP swelling and dactylitis, pencil in cup deformity of DIP. NSAIDs and DMARDs (methotrexate), avoid steroids as can flare skin lesions
CLINICAL FEATURES
1) Skin lesions- erythematous, well demarcated scaly papules and plaques on scalp and extensor surfaces of knees and elbows- purple/silver plaques
2) Joint swelling or pain (psoriatic arthritis occurs in 20% of psoriasis patients)-
- Symmetric polyarthritis (quite similar to RA)
- Asymmetrical oligoarthritis: typically affects hands and feet (20-30%)
- sacroiliitis
- DIP joint disease(10%)
- arthritis mutilans (severe deformity fingers/hand, ‘telescoping fingers’)
- X ray findings
- New bone forming yet also erosive changes
- Pencil in cup
- Periostitis
3) Nail changes- pitting and onycholysis (separation of nail from nail bed)
INVESTIGATIONS
clinical diagnosis
if unsure: skin biopsy
Koebner Phenomenon: physial stimuli or skin injury leads to skin lesions
Auspitz sign: small pinpoint bleeding when scales are scraped off
MANAGEMENT
Topical potent corticosteroid (e.g. betamethasone) to reduce inflammation & topical vit D analogue (calcipotriol) to reduce keratiocyte proliferation
- if no improvement after 8 weeks: Vitamin D analogue 2x daily
- if no improvement after 8-12 weeks with vit d analogue: potent corticosterois + coal tar preparation
- Use milder topical steroids for flexural than plaque because skin is thinner and more sensitive to steroids in flexural regions
- dont use steroids fo over 8 weeks as risk of skin atrophy, rebound symptoms and striae (basically cushings)
2nd: Phototherapy- narrowband UVB light
3rd/systemic: Oral methotrexate is first line- useful in psoriatic arthritis
COMPLICATIONS
- Cardiovascular disease
- Psoriatic arthritis
- Depression
PROGNOSIS
chronic and fluctuating, long term with topical or systemic meds necessary for most
Urticaria/Hives
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Erythematous, blanching, oedematous, non-painful, pruritic lesions that develop rapidly, usually over mins
Typically less than 24 hours and leaves no residual skin markings upon resolution
Acute urticaria: Mainly allergy related- IgE mediated
Chronic urticaria: heat, cold, pressure, sunlight, vibration, acetylcholine release, water
Drug causes of urticaria: Aspirin, penicillin, NSAIDs, opiates
CLINICAL FEATURES
- Erythematous oedematous lesions- pale, pink, smooth raised skin (wheals)
- Pruritus
- Resolution within 24 hours
- Swelling of face, tongue or lips (up to 40% of urticaria cases have angio-oedema too)
- Lesions blanch when palpated
INVESTIGATIONS
clinical
If suspect urticarial vasculitis then ESR and CRP
MANAGEMENT
1st Antihistamines- loratadine
Severe or recurrent: prednisolone
Prevent: avoid trigger
PROGNOSIS
good
COMPLICATIONS
- Excorations
- Sedation (side effect of antihistamines)
- Skin infections
