1
Q
What is acne rosacea?
A
Episodic or persistent facial flushing, with a notable predisposition towards women aged between 30 and 60 who have fair skin.
2
Q
Epidemiology of rosacea?
A
Middle aged women with fair complexion are commonly affected
3
Q
Aetiology of rosacea?
A
Genetic and environmental
Immune response to demodex mite
4
Q
Presentation of rosacea?
A
Erythemato- telangiectatic; facial flushing, exacerbated by heat, alcohol, sun exposure, warm baths, stress, spicy food, cosmetic products
Papulo- pustular; red bumps (papules) and pus filled pimples (pustules)
Rhinophymatous rosacea; swollen, bulbous nose with enlarged sebaceous glands and prominent hair follicles. Erythematous, thickened, scarred and exhibits a rough waxy surface
Ocular rosacea; red irritated and watery eyelids
5
Q
Differentials for rosacea?
A
Seborrheic dermatitis
Acne vulgaris
Lupus erythematosus
6
Q
Management of rosacea?
A
Camouflage cream, sun protection, avoid triggers and using soap substitutes
Reduce flushing; topical brimonidine/ oral propanolol
Telangiectasia; laser therapy
For papulopustular variants: Topical azelaic acid, topical metronidazole, topical ivermectin, oral antibiotics (such as tetracyclines); systemic retinoids may then be used if these measures fail.
For ocular rosacea: Warm compress, massage, and lubricants. Referral to ophthalmology may be necessary.
For rhinophyma: Surgical debulking (dermabrasion, cryotherapy, or cautery) or laser debulking. Oral antibiotics (such as doxycycline) and retinoids may also be useful.
7
Q
What is acne vulgaris?
A
A a chronic disorder of the skin affecting the pilo-sebaceous unit, in which there is blockage of the follicle leading to comedones and inflammation
8
Q
Epidemiology of acne vulgaris?
A
Most common dermatological condition affecting individuals of all ethnicities and ages
Highest prevalence in adolescents and young adults affecting upto 80% of the population
9
Q
Risk factors for acne vulgaris?
A
Hormonal changes (e.g. during puberty, menstrual cycle, polycystic ovary syndrome)
Increased sebum (oil) production
Blockage of hair follicles and sebaceous glands by keratin and sebum
Bacterial colonization (Propionibacterium acnes)
Family history of acne
Certain medications (e.g. corticosteroids, hormonal treatments)
10
Q
Pathophysiology of acne vulgaris?
A
In normal skin, skin cells in the stratum corneum of the epidermis (corneocytes) desquamate successfully without blocking pilo-sebaceous units.
In acne, the corneocytes are excessively cohesive. They do not detach successfully.
Because of this, the keratin rich corneocytes accumulate and block off hair follicles causing follicular hyperkeratinisation.
Sebum is trapped in the hair follicle since it cannot be drained away. Androgens may also contribute to this causing sebaceous gland hyperplasia and increased sebum production.
This combination of sebum and keratin forms micro-comedones - the earliest feature of acne vulgaris. This is only visible under a microscope.
Gradually, the follicle becomes more distended with keratin and sebum, and the micro-comedone enlarges to become a comedone.
Initially, these are closed comedones, referred to as whiteheads. The contents are not exposed to the skin surface or oxygen, and therefore appear as fleshy/white papules.
Eventually, closed comedones become open comedones. As their contents become exposed to oxygen, they oxidise which causes black discolouration. Open comedones are therefore referred to as blackheads.
Comedones are then colonised with a gram positive bacillus called Propionibacterium (Cutibacterium) acnes. This is a commensal organism (part of the normal skin flora) but leads to an inflammatory response in the right conditions of the comedone, in a predisposed patient.
The comedone is subsequently transformed into an inflammatory papule, which is now associated with erythema. A papule is a solid, raised lesion less than 0.5cm in diameter.
As things progress and more neutrophils accumulate, the inflammatory papule becomes a pustule; this is a lesion less than 0.5cm in diameter that contains pus.
Eventually, the inflammatory papule or pustule becomes so distended that it ruptures into the dermis, triggering a marked and deep seated inflammatory response.
This leads to the formation of nodules/cysts, which are painful and red. A nodule is a solid lesion larger than 0.5cm, and cysts are walled off fluid containing structures.
11
Q
Classification of acne vulgaris?
A
Non-inflammatory: blackheads and whiteheads.
Inflammatory: inflammatory papules, pustules, and nodules (cysts.)
Mild acne: predominantly non-inflammatory lesions.
Moderate acne: predominantly inflammatory papules and pustules.
Severe acne: nodules (cysts), scarring, acne fulminans, and acne conglobata.
12
Q
Presentation of acne vulgaris?
A
Open/ closed comedones, inflammatory papules and pustules, nodules and cysts
Face, neck, chest and back are commonly affected
Scarring
Post inflammatory hyperpigmentation/ erythema
Acne fulminans
Acne conglobata
13
Q
Management of acne?
A
Mild-moderate acne is treated with any 2 of the following in combination:
Topical benzoyl peroxide.
Topical antibiotics (clindamycin)
Topical retinoids (tretinoin/adapalene)
Moderate-severe acne is treated with a 12-week coures of the following first line options:
Topical retinoids (tretinoin/adapelene) + topical benzoyl peroxide.
Topical retinoids + topical antibiotics (clindamycin)
Topical benzoyl peroxide + topical retinoid (tretinoin/adapelene) + oral antibiotic (lymecycline/doxycycline.)
Topical azelaic acid + oral antibiotic (lymecycline/doxycycline)
Second line oral antibiotics: trimethoprim and erythromycin e.g. in pregnant/breast-feeding women where tetracyclines are contra-indicated.
Combined oral contraceptives (COCPs) (if not contraindicated) in combination with topical agents can be considered as an alternative to systemic antibiotics in women
14
Q
When should patients be referred to dermatology for acne?
A
Acne fulminans
Mild to moderate acne not responding to 2 12 week courses of treatment
moderate to severe acne not responding to 12 week courses of treatment
Psychological distress
Acne with scarring
Persistent pigmentary changes
15
Q
Complications of acne?
A
Post inflammatory erythema
Post inflammatory hyperpigmentation
Scarring
16
Q
What is actinic keratosis?
A
Pre-malignant skin condition that preceeds cutaneous SCC
17
Q
Epidemiology of actinic keratosis?
A
Higher in those with fair complexion
Those exposed to higher levels of solar radiation
18
Q
Pathophysiology of actinic keratoses?
A
Sun exposure leading to DNA damage within keratinocytes
19
Q
Presentation of actinic keratoses?
A
Thickened papules or plaques , surrounding erythematous skin and keratotic, rough, warty surface
20
Q
Risk factors for actinic keratoses?
A
Type I or II skin (fair, burns easily)
History of sunburn or extensive sun exposure
Outdoor occupation or hobbies
Immunosuppression
21
Q
Differentials for actinic keratoses?
A
Seborrheic keratosis
Cutaneous horns
Psoriasis
Basal cell carcinoma
22
Q
Investigations to diagnose actinic keratoses?
A
Dermatoscopy: useful for visualizing the surface and vascular structures of the skin lesion.
Skin biopsy: performed if there is diagnostic uncertainty or if malignancy is suspected.
23
Q
Management of actinic keratosis?
A
Cryotherapy, curettage or surgical excision
5-FU creams, NSAIDs, Imiquimod
24
Q
What is alopecia?
A
Loss of hair from areas where hair normally grows.
25
Classification of alopecia?
Scarring; destruction of underlying hair follicle
Discoid lupus erythematosus
Localised scleroderma
Burns/ injury
Infection
Lichen planopiliaris
Folliculitis decalvans
Non- scarring; hair follicle remains intact
Autoimmune
SLE
Hypothyroidism
Androgenic alopecia
Telogen effluvium
Traction alopecia
26
Management of alopecia?
Camouflage; wig, hairpiece, mesh
False lashes, tattoo
Topical steroid
Topical immunotherapy
Minoxidil; dilates local blood vessels to scalp
Dithranol; stains hair darker colour
Systemic steroids
JAK inhibitors; baricitinib
27
Complications of alopecia?
Psycho-social; poor quality of life, depression and anxiety
Other illness may co-exist
28
What is eczema?
Chronic disorder of the skin characterised by dermal inflammation with resultant spongiotic change in epidermis histologically with chronic features including epidermal acanthosis, hyperkeratosis, parakeratosis
29
Classification of eczema?
Atopic eczema
Allergic contact dermatitis (see separate section on contact dermatitis)
Irritant contact dermatitis (see separate section on contact dermatitis)
Seborrheic dermatitis
Venous eczema (stasis dermatitis)
Asteatotic dermatitis (eczema craquele)
Erythrodermic eczema
Pompholyx eczema
30
Pathophysiology of eczema?
Lymphocytic infiltration of the dermis
Keratinocytes in the epidermis start detaching from one another resulting in widening of intracellular space
31
What is seen on histology in eczema?
Epidermal acanthosis: thickening of the epidermis due to hyperplasia.
Hyperkeratosis: thickening specifically of the stratum corneum.
Parakeratosis: retained nuclei in the stratum corneum indicating problems with the usual differentiation process.
32
Presentation of eczema?
Childhood predominance
Atopic phenotype; asthma, hayfever, raised eosinophils
Flexor surface distribution; ACF, posterior knee
Itchy, erythematous skin
Erythrodermic eczema:
This is a dermatological emergency and may complicate atopic eczema.
It is syndrome characterised by widespread redness (>90%)
There is often skin exfoliation too, which leads to exfoliative dermatitis.
Seborrhoeic dermatitis:
This common condition is thought to happen due to Malassezia Furfur, a commensal organism on the skin. A predisposed individual due to genetic and environmental factors may develop an inflammatory response to the organism.
The skin is flakey with a fine scale, oily, and erythematous. There is usually minimal pain or stinging or itch.
The scale may coalesce into thicker plaques.
It tends to affect the face (especially hairline, nasolabial fold, and brow area) in adults.
Stasis dermatitis:
Also known as venous eczema.
This is eczema associated with chronic venous insufficiency (venous hypertension), usually affecting the gaiter area.
There may be associated skin changes therefore, including: venous ulcers, lipodermatosclerosis, and hemasiderosis.
Pompholyx eczema:
This is a subtype of eczema associated with intensely itchy vesicles that erupt in the hands.
It is also referred to as dishydrotic eczema.
Eczema craquele:
Eczema associated with dry skin.
33
Risk factors for seborrhoeic dermatitis?
Family history
Oily skin
Immunosuppression (such as HIV)
Neurological and psychiatric diseases (such as Parkinson's Disease or Depression)
Stress
34
Investigations to diagnose eczema?
Clinical diagnosis
Patch test
Swab
Skin biopsy
35
Severity classification of eczema?
Mild - areas of dry skin, and infrequent itching (with or without small areas of redness)
Moderate - areas of dry skin, frequent itching, and erythema (with or without excoriation and localized skin thickening)
Severe - widespread areas of dry skin, incessant itching, and erythema (with/without excoriation, extensive skin thickening, bleeding, oozing, cracking, and alteration of pigmentation)
Infected - if eczema is weeping, crusted, or there are pustules, with fever or malaise
36
Management of eczema?
Avoid triggers; soaps, perfumes, biological detergents or synthetic fabrics, allergens
Topical treatment for eczema:
Mild eczema - liberal emollient usage + mild topical corticosteroid (such as hydrocortisone 1%) for areas of red skin.
Moderate eczema - liberal emollient usage + moderate topical corticosteroid (such as clobetasone butyrate 0.5% - Eumovate) for 5 days. Hydrocortisone 1% should be used for the face and flexures. Consider prescribing maintenance topical corticosteroids to control areas of skin prone to frequent flares.
Severe eczema - liberal emollient usage + potent topical corticosteroid (for example betamethasone valerate 0.1% - Betnovate) to be used on inflamed areas. For the face and flexures, use a moderate potency corticosteroid (such as Eumovate).
Light therapy
Systemic steroids
Systemic retinoids
DMARDs; methotrexate, ciclospoin, azathioprine
Biologicals;
Dupilumab: IL-4Rα inhibitor
Baricitinib: JAK inhibitor
37
When to refer to dermatology for eczema?
Severe and not responding to topical treatment after 1 week
Uncertainty surrounding diagnosis
Control over diagnosis is not satisfactory
treatment resistant facial eczema
38
Complications of eczema?
Poor sleep
Poor mood
Skin breakdown
Itchiness
Psycho-social insecurities
Eczema herpeticum
39
What is eczema herpeticum?
Disseminated herpes simplex virus in eczema resulting in vesicles and punched out erosions.
There may be multiorgan involvement
Diagnosis can be confirmed with a swab & Tzanck test.
Admission to hospital and IV aciclovir
40
What is basal cell carcinoma?
Skin cancer originating from basal keratinocytes within epidermis, commonly secondary to DNA damage from UV radiation
There is invasion of the basement membrane
41
Epidemiology of BCC?
Most common skin cancer
Incidence is rising due to increased exposure to UV radiation
Incidence increases with age, common over age of 40
More common in areas with intense UV radiation
42
Risk factors for BCC?
Family history
Genetic syndromes; naevoid basal cell carcinoma syndrome; autosomal dominant loss of function of the PTCH tumour suppressor gene
Pale skin
Light hair
High levels of sun/ UV exposure
Immunosuppression
Chronic inflammation
Old age
Male sex
43
Pathophysiology of BCC?
Genetic mutations leads to uncontrolled proliferation of basal cells
Activation of the hedgehog signaling pathway
Local tissue invasion and destruction as BCC grows
Typically does not metastasize to other organs
44
Classification of BCC?
Nodular - the most common subtype, characterized by a raised, shiny, pink or translucent nodule with central ulceration or crusting
Morphoeic (sclerosing) - presents as a firm, scar-like plaque with indistinct borders, making it challenging to diagnose and treat
Keratotic - presents with horn cysts within well-circumscribed basal nodules
Pigmented - rare, and typically presents with brown or black pigmentation within the lesion
Superficial - presents as scaly, red patches or plaques, often mistaken for eczema or psoriasis
45
Signs and symptoms of BCC?
Very slow growing
Local destruction can occur but metastasis is rare
Usually asymptomatic (pain/bleeding rare)
Flesh coloured nodules with central depression, pearly surface, rolled edge, and telangiectasia
They can can necrose and ulcerate in the centre ('rodent ulcer)
In sun-exposed areas. There may be background sun-damage such as actinic keratoses
46
Differentials for BCC?
Squamous cell carcinoma
Melanoma
Seborrheic keratosis
Actinic keratosis
Dermatofibroma
47
Investigations to diagnose BCC?
Excision biopsy with 4mm margin, 6mm margin for high risk lesions defined as;
2cm diameter
Location on the ear, lip, face, hands, feet, or genitals
Immunosuppressed
Recurrent disease
Sentinel lymph node biopsy
48
Management of BCC?
Almost always treated surgically with excision using a 4mm margin (6mm for high risk lesions)
Mohs micrographic surgery
Radiotherapy
Curettage and cautery, topical 5-FU, topical imiquimod, cryotherapy
Immunotherapies
49
Complications of BCC?
Local tissue invasion
Recurrence of tumour
Metastasis is very rare
Psychological distress due to disfigurement
50
What is cellulitis?
Bacterial soft tissue infection of the dermis and subcutaneous tissue
51
Pathophysiology of cellulitis?
Bacterial entry through breaks in skin barrier leading to infection and inflammation
Bacteria multiply in subcutaneous tissue triggering immune reaction
52
Risk factors for cellulitis?
Breaks in the skin, such as cuts, abrasions, insect bites, or surgical wounds
Chronic conditions that compromise skin integrity - venous insufficiency or lymphedema, pressure sores, ulcers, recent trauma
Obesity
Diabetes
Immunosuppression
Intravenous drug use
Recent history of cellulitis
53
Clinical features of cellulitis??
Erythema
Calor (heat)
Swelling
Pain
Poorly demarcated margins
Systemic upset: fever, malaise
Lymphadenopathy
Rarely blisters and pustules (severe disease)
Often evidence of breach of skin barrier e.g. trauma, ulcer etc.
54
Aetiology of cellulitis?
Streptococcus pyogenes
Group A beta haemolytic streptococci
Staphylococcus aureus
55
Differentials for cellulitis?
DVT
Erysipelas
Allergic reactions/ contact dermatitis
Necrotising fasciitis
56
Eron classification to grade severity of cellulitis?
Class I — there are no signs of systemic toxicity and the person has no uncontrolled comorbidities.
Class II — the person is either systemically unwell or systemically well but with a comorbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection.
Class III — the person has significant systemic upset, such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable comorbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize.
Class IV — the person has sepsis or a severe life-threatening infection, such as necrotizing fasciitis.
57
Investigations to diagnose cellulitis?
Blood tests - FBC (high WCC), CRP, U+E (may be AKI if severe infection), blood cultures
Wound swab if there is an open wound, penetrating injury, drainage, or an obvious portal for microbial entry, exposure to water borne-organisms, an infection acquired outside the UK or in severe cellulitis
Ultrasound scan - for distinguishing nonpurulent cellulitis from cellulitis with underlying abscess and for identifying drainable fluid collection
58
Indications for admission to hospital with cellulitis?
Class III - Class IV cellulitis
Rapidly deteriorating cellulitis
Under 1 year of age or frail
Immunosuppression
Significant lymphoedema
Facial cellulitis (unless very mild)
Suspected orbital or periorbital cellulitis (admit to ophthalmology)
Class II cellulitis (systemically unwell or systemically well but with a comorbidity)
59
Treatment for cellulitis?
Mark the area of erythema to aid in detection of rapidly spreading cellulitis, and to monitor treatment response
Elevate if possible
Review if wound debridement is required
Class I - high-dose oral flucloxacillin (clarithromycin/doxycyline if penicillin allergic and erythomycin if pregnant)
Class II - admit systemically unwell patients or those systemically well but with a comorbidity. May be able to ambulate with IV antibiotics.
Class III-IV - admit for IV antibiotics
60
Complications of cellulitis?
Abscess formation
Lymphangitis (infection of lymphatic vessels)
Systemic spread of infection (sepsis)
Recurrence of cellulitis
Chronic or recurrent lymphedema
Scarring and changes in skin texture
61
What is an arterial ulcer?
Ischaemic ulcer that develops due to insufficient blood supply
Associated with peripheral arterial disease
62
What is a venous ulcer?
Stasis ulcer due to insufficient blood return from the lower limbs
Associated with chronic venous insufficiency
63
Epidemiology of venous and arterial ulcers?
Arterial ulcers and venous ulcers are more prevalent in older populations
Arterial ulcers are more common in men
Venous ulcers are more common in middle age women
64
Aetiology of vascular ulcers?
Peripheral arterial disease; atherosclerosis
Venous insufficiency; valve malfunction
65
Presentation of arterial ulcers?
Occur distally (e.g. at the heel or toe tips)
Are small and deep
Have a 'punched out' margin
Do not bleed or ooze
Associated with other features of peripheral arterial disease (weak distal pulses, skin/hair atrophy)
66
Presentation of venous ulcer?
Occur in the gaiter area (more often on the medial side)
Are large and shallow
Have sloping edges
Bleed or ooze
Associated with features of chronic venous insufficiency (haemosiderin deposition, lipodermatosclerosis, atrophie blanche)
67
Differentials for venous ulcers?
Diabetic ulcers
Vasculitis ulcers
Malignant ulcers
68
Investigations to diagnose vascular ulcer?
Physical examination
Doppler USS
Ankle Brachial pressure index
Angiography
69
Interpretation of ABPI?
More than 1.4: suggests abnormal thickening of vascular walls (typically in diabetes due to calcification)
1 - 1.4: Normal
0.91 - 0.99 — peripheral arterial disease may be present. Further investigation is necessary if there is significant clinical suspicion.
< 0.9: suggests peripheral arterial disease present
<0.5: Severe disease, Patients will require an urgent referral to a vascular surgery centre.
70
Management of Arterial and venous ulcers?
For arterial ulcers, this could involve improving arterial circulation through a combination of lifestyle changes, medications, and, in severe cases, surgical interventions. Medications can include antiplatelet drugs (such as aspirin or clopidogrel), statins to reduce cholesterol levels, and possibly antihypertensives to control blood pressure. In cases where these measures are not sufficient, angioplasty or bypass grafting may be considered. NB: compression stockings are contraindicated here as they will worsen the ischaemia.
Venous ulcers are managed through compression therapy to reduce venous hypertension, alongside wound care and possibly surgical intervention for severe or refractory cases.
71
What is neurofibromatosis?
NF1 is due to a loss-of-function mutation in the neurofibromin gene on Chromosome 17.
NF2 arises from a loss-of-function mutation in the Schwannomin (Merlin) tumour suppressor gene on Chromosome 22
72
Features of NF1?
Cutaneous features
Cafe-au-lait spots: Oval-shaped, coffee-coloured patches that continue to grow throughout life. Presence of 6 macules >5mm (or >15mm if post-pubertal) is a feature of NF1.
Axillary or inguinal freckling
Neurofibromas: Small nodular tumours in the skin.
Non-cutaneous features
Lisch nodules: Hamartomas on the iris appearing as brown patches/mounds, typically visible by age 6.
Optic glioma
Scoliosis and other bone malformations
Learning difficulties
Hypertension
Gastrointestinal issues: Bleeding or obstruction due to tumours in the bowel.
Epilepsy: Due to tumours in the brain.
73
Features of NF2?
Bilateral vestibular schwannomas (acoustic neuromas), causing sensorineural hearing loss, tinnitus, and vertigo.
Meningiomas
Spinal ependymomas
Posterior lens opacities
Cerebral calcification
Astrocytomas
Glial hamartomas
74
Differentials for NF?
Legius syndrome
Segmental NF
McCune- Albright syndrome
Genetic syndrome; bloom syndrome, fanconi anaemia
75
What is porphyria cutanea tarda?
group of disorders affecting the enzymes involved in the porphyrin pathway, which synthesises haem. In PCT, there is a deficiency in the enzyme uroporphyrinogen decarboxylase, leading to a buildup of precursors or intermediate molecules
76
Epidemiology of porphyria cutanea tarda?
PCT can be either genetic (approximately one-third of cases) or acquired, typically due to exposure to certain triggers.
77
Aetiology of porphyria cutanea tarda?
Alcohol consumption
Estrogen-containing medications such as hormone replacement therapy or oral contraceptive pills
Infections such as Hepatitis B and C, HIV
Conditions causing iron overload
Renal dialysis due to inadequate excretion
78
Presentation of porphyria cutanea tarda?
Photosensitivity
Blister/bullae formation that easily rupture to form erosions
Healing blisters may leave scars and milia (cysts)
Skin may become thick and resemble scleroderma
Hyperpigmentation and hypertrichosis (especially on the top of the cheek)
79
Differentials of porphyria cutanea tarda?
Dermatitis herpetiformis
Bullous lupus erythematosus
Epidermolysis bullosa
80
Management of porphyria cutanea tarda?
Conservative measures: avoidance of sunlight and known drug triggers
Phlebotomy: to reduce iron levels
Medication: Chloroquine may help by increasing excretion
81
Investigations to diagnose porphyria cutanea tarda?
Skin biopsy
Urinoporphyrinogen III/ uroporphyrin
Urine may appear tea coloured
Assessments for underlying causes are crucial, such as kidney function, iron studies, Hepatitis B and C. Antinuclear antibody (ANA) tests are often positive in PCT.
82
Cutaneous presentation of streptococcus pyogenes infection?
Acute or Chronic Rheumatic Fever: Migrating polyarthritis, mitral valve regurgitation or stenosis, Sydenham chorea, erythema marginatum
Post-Streptococcal Glomerulonephritis: Haematuria, hypertension, and proteinuria, following 1-3 weeks after a streptococcal throat infection.
Erythema Nodosum: Painful nodules, primarily on the shins, caused by immune complex deposition.
Post-streptococcal Reactive Arthritis: Arthritis in one or more joints in patients who do not meet the criteria for Rheumatic Fever.
Toxic Shock Syndrome: Supertoxin mediated, causing a widespread erythematous rash and fever, with potential for rapid progression to multi-organ failure and coma if untreated.
Scarlet Fever: Fever, desquamating rash, 'strawberry' tongue often accompanied by abdominal pain and vomiting, caused by erythrogenic toxin.
83
Presentation of tuberous sclerosis?
Angiofibromas: Dome-shaped, firm papules in a butterfly distribution across the face.
Ashleaf macules: Oval patches of hypopigmented skin that fluoresce under a Wood's light.
Shagreen patch: Leathery, cobbled plaque, often on the sacrum, that is dimpled like orange peel.
Ungal fibromas: Smooth, fleshy tumours that grow from the nail folds either around or under the nail.
Café Au Lait patches: Hyperpigmented macules on the body.
Retinal hamartomas: These can lead to visual disturbances.
Cardiac rhabdomyomas: These are benign heart tumours and may cause cardiovascular complications.
Lung and renal involvement: Can lead to further systemic complications.
Epilepsy: The most common neurologic manifestation, often with onset in infancy or childhood.
Learning difficulties: Cognitive impairments are common, with varying severity.
Behavioural abnormalities: This may include autistic features, ADHD-like symptoms, and other behavioural problems.
84
Differentials for tuberous sclerosis?
Neurofibromatosis
Sturge weber syndrome
Von Hippel- Lindau disease
85
Aetiology of tuberous sclerosis?
TSC is caused by loss-of-function mutations in the Tuberous Sclerosis Complex 1 (TSC1) and Tuberous Sclerosis Complex 2 (TSC2) tumour suppressor genes. These mutations lead to hamartoma formation across various body systems.
86
Management of tuberous sclerosis?
Seizure control: Antiepileptic drugs are used, and in refractory cases, ketogenic diet, vagus nerve stimulation, or epilepsy surgery may be considered.
Learning support: Including special education services and behavioural therapies.
Surveillance for associated complications: Regular ophthalmologic, cardiac, pulmonary, and renal assessments are recommended.
Dermatologic treatments: Options include topical treatments, laser therapy, and surgical removal for severe skin lesions.
87
What is scleroderma?
autoimmune disorder characterized by abnormal fibrosis of the skin and internal organs
88
Epidemiology of systemic sclerosis?
Rare, 10-30 cases per million
Affects women more than men, 3:1 ratio
Peak age between 30 and 60 years
Genetic predisposition and environmental triggers
89
Pathophysiology of systemic sclerosis?
Dysregulation of the immune system, leading to autoimmune responses
Abnormal activation of fibroblasts, resulting in excessive collagen production and fibrosis
Vascular abnormalities, including endothelial cell damage and microvascular dysfunction
Immune complex deposition and inflammation in affected tissues
89
Features of limited systemic sclerosis?
Disease is limited to hands/ feet/ face
Calcinosis
Raynauds
Oesophageal dysmotility
Sclerodactyly
Telangiectasia
90
Features of diffuse systemic sclerosis?
Widespread skin thickening affecting trunk, upper arms and legs
Early involvement of internal organs
Raynaud's phenomenon
Dysphagia
Gastroesophageal reflux disease (GORD)
Digital ulcers
Joint pain and inflammation
Pulmonary involvement, including interstitial lung disease
Cardiac manifestations
91
Differentials of systemic sclerosis?
Dermatomyositis
Eosinophilic fasciitis
Morphea (localized scleroderma)
Sarcoidosis
Systemic lupus erythematosus (SLE)
92
Investigations to diagnose systemic sclerosis?
Antinuclear Antibody (ANA) Test: commonly positive in SSc
Anti-centromere antibodies are positive in 80% in limited SSc
Anti-topoisomerase-1 (Scl-70) and anti-RNA polymerase antibodies may be present in diffuse SSc
93
Management of systemic sclerosis?
Skin care: Emollients and moisturizers to manage dryness and minimize skin complications
Raynaud's Phenomenon: Calcium channel blockers and lifestyle modifications
Immunosuppressants: In cases of severe skin or systemic involvement
Physiotherapy: to maintain joint mobility.
Gastrointestinal Management: Medications and dietary adjustments for GORD and dysphagia
94
Complications of systemic sclerosis?
Digital ulcers leading to gangrene
Restrictive lung disease
Pulmonary hypertension
Renal crisis
Cardiac involvement
Joint contractures and disability
95
Epidemiology of cutaneous manifestations of SLE?
Up to 85% of individuals with SLE experience some form of cutaneous involvement during the course of the disease
SLE predominantly affects women of childbearing age, with a higher prevalence among individuals of African, Asian, or Hispanic descent
Certain cutaneous manifestations may be more common in specific ethnic groups
Skin changes are often associated with the overall SLE disease activity and may occur at any time during the course of SLE
96
Pathophysiology of cutaneous manifestation of SLE?
multifactorial and may involve immune complex deposition, autoantibody production, and inflammation. The immune system's abnormal response to self-antigens leads to tissue damage, including skin lesions
97
Cutaneous manifestations of SLE?
Malar Rash (Butterfly Rash): A characteristic erythematous rash across the cheeks and bridge of the nose, resembling a butterfly's wings.
Discoid Lupus Erythematosus (DLE): Coin-shaped, scaly, and erythematous plaques that may lead to scarring and dyspigmentation.
Photosensitivity: Exaggerated skin sensitivity to ultraviolet (UV) light, leading to skin rashes upon sun exposure.
Alopecia: Hair loss or thinning, often in patches.
Subacute Cutaneous Lupus Erythematosus (SCLE): Annular, papulosquamous, or psoriasiform lesions often triggered by UV exposure.
Ulcers and Vasculitis: Painful skin ulcers or vasculitic lesions resulting from inflammation of blood vessels.
98
Differentials for cutaneous manifestation of SLE?
Rosacea
Psoriasis
Allergic dermatitis
99
Management of cutaneous manifestations of SLE?
Topical Treatments: Corticosteroid creams or ointments for local control of skin symptoms
Sun Protection: Sunscreen and protective clothing to minimize photosensitivity
Systemic Therapy: in severe cases, systemic corticosteroids, antimalarials, or immunosuppressive medications may be necessary
Disease-Modifying Anti-Rheumatic Drugs (DMARDs): to control overall disease activity
Patient Education: emphasizing sun protection measures and regular follow-up for disease monitoring
100
Complications of cutaneous manifestation of SLE?
Scarring and dyspigmentation
Chronic skin changes
Progression to more severe systemic disease
101
What is a wart?
Benign cutaneous proliferation due to infection with HPV
Wart is on non plantar skin
Verrucae is a plantar wart on soles of feet
102
Aetiology of warts/ verruca?
HPV type 1, 2, 4, 27, 57
The virus enters the skin via microabrasions and induces hyperplasia of the epidermis. Spread occurs through direct contact (person-to-person or autoinoculation) or via fomites in moist environments. The host immune response plays a significant role in resolution or persistence.
103
Presentation of warts?
Common warts: Firm, rough, skin-coloured papules or nodules, typically on hands, fingers, or knees.
Plantar warts (verrucae): Occur on the soles; may be painful on pressure, sometimes with black punctate dots (thrombosed capillaries).
Plane (flat) warts: Smooth, flat-topped papules, usually on the face or hands.
Filiform warts: Long, slender projections, often found on the face or neck.
Generally asymptomatic but may cause discomfort or cosmetic concern.
104
Differentials for warts?
Callus
Molluscum contagiosum
Basal cell carcinoma
Seborrhoeic keratosis
Actinic keratosis
105
Investigations to diagnose warts?
Diagnosis is clinical and based on appearance.
No investigations are usually required.
Consider referral or biopsy if:
Lesion is atypical or growing rapidly.
Lesion fails to respond to treatment.
Immunosuppression is present, or skin cancer is suspected.
106
Management of warts?
Reassurance and watchful waiting: First-line, especially in children — 65% of warts resolve within 2 years.
Do not treat unless lesions are:
Painful
Affecting function (e.g., walking)
Causing significant distress
Recurrent or spreading
Topical salicylic acid:
Apply daily to the wart after soaking and paring down.
Continue for up to 12 weeks.
Most effective when used consistently with mechanical removal of surface debris.
Cryotherapy (liquid nitrogen):
May be used if salicylic acid is ineffective or not tolerated.
Typically administered every 2–3 weeks for up to 3–4 sessions.
Not routinely used in children due to pain.
Referral to dermatology if:
Warts/verrucae are extensive, recalcitrant, or disfiguring.
Lesions are atypical or suspicious of malignancy.
Immunocompromised patients with poor response to standard treatment.
107
What is dermatitis herpetiformis?
Chronic blistering skin disorder characterised by intensely itchy, grouped vesicles and papules
Cutaneous manifestation of gluten sensitivity
108
Epidemiology of dermatitis herpetiformis?
10 per 100000
Northern european descent particularly scandinavian or celtic origin
Peak origin 30 to 40 years
109
Risk factors for dermatitis herpetiformis?
Coeliac disease
HLA-DQ2, HLA-DQ8
110
Pathophysiology of dermatitis herpetiformis?
DH is triggered by an autoimmune response to dietary gluten (found in wheat, barley, and rye) in genetically predisposed individuals
There is formation of IgA antibodies against tissue transglutaminase (tTG) in the small intestine
Circulating immune complexes containing IgA-tTG deposit in the skin's papillary dermis
Activation of the complement cascade and recruitment of neutrophils, leading to the characteristic skin lesions
111
Signs and symptoms of dermatitis herpetiformis?
Intense itching, often preceding the appearance of skin lesions.
Grouped vesicles (small fluid-filled blisters) and papules (small raised bumps) on the elbows, knees, buttocks, shoulders and lower back.
Lesions are symmetrically distributed.
Scratching may lead to excoriations (scratch marks) and secondary bacterial infections.
112
Differentials for dermatitis herpetiformis?
Bullous pemphigoid
Erythema multiforme
Scabies
Herpes simplex virus infection
Contact dermatitis
113
Investigations to diagnose dermatitis herpetiformis?
Skin biopsy
Serological testing
Endoscopy and small bowel biopsy
114
Management of dermatitis herpetiformis?
Gluten free diet
Dapsone cream
115
Complications of dermatitis herpetiformis?
Secondary bacterial skin infection
Scarring
Post inflammatory hyperpigmentation
Side effects of dapsone;
116
What is a dermatofibroma?
Slow growing skin lesion that presents as a firm, raised nodule on the skin surface caused by proliferation of fibroblasts triggered by trauma
117
Epidemiology of dermatofibroma?
Prevalence increases with age
More common in women
More common in adults
118
Presentation of dermatofibroma?
A small, firm nodule that is typically less than 1 cm in diameter
Variable coloration, often brown or reddish-brown
A dimple or central depression (known as the "dimple sign") when the lesion is squeezed or pinched
Asymptomatic or mild tenderness upon pressure
Slow growth over time
119
Management of dermatofibroma?
Observation: Many dermatofibromas are asymptomatic and require no treatment unless they become bothersome or cosmetically undesirable
Surgical Excision: If necessary for cosmetic or symptomatic reasons, surgical removal of the lesion is a viable option. This is often performed by a dermatologist or dermatologic surgeon
Cryotherapy: Freezing the dermatofibroma with liquid nitrogen is another option for removal
Laser Therapy: Some dermatofibromas may be treated with laser therapy to minimize scarring
120
What is dermatomyositis?
Autoimmune rheumatic disease. It is characterised by myositis leading to proximal muscle weakness, and distinct cutaneous manifestations. This condition can manifest as a para-neoplastic phenomenon, indicating an underlying malignancy.
121
Presentation of dermatomyositis?
Muscle weakness; proximal weakness
Skin manifestations:
Heliotrope rash: a bilateral lilac discolouration around the eyes, particularly around the upper eyelid, with associated skin swelling.
Gottron's papules: purple nodules and plaques appearing over the knuckles in the hands.
Shawl rash or Shawl sign: a fixed erythematous rash affecting the back, shoulders, and chest.
V Sign: a photosensitive rash appearing on the anterior chest (sun-exposed area.)
Nailfold erythema: Evident by dilated nailfold capillary loops, particularly visible on dermoscopy.
122
Differentials for dermatomyositis?
Polymyositis
SLE
Scleroderma
123
Investigations to diagnose dermatomyositis?
Muscle biopsy
Anti-antibody screen; anti- Mi2, anti-Jo1, anti-SRP
Plasma muscle enzymes; CK, ALT, AST, LDH
124
Management of dermatomyositis?
Oral corticosteroids
Malignancy screening as dermatomyositis can be a paraneoplastic phenomenon
125
What is erythema nodosum?
panniculitis, or inflammation of the subcutaneous fat, which manifests as tender, raised, erythematous nodules predominantly affecting the shin area.
126
Epidemiology of erythema nodosum?
More common in women
Typically affects 20-30 year olds
127
Causes of erythema nodosum?
Idiopathic
Sulphonamide, dapsone
Oral contraceptive pill
Sarcoidosis
Ulcerative collitis
Crohn's disease
Tuberculosis, streptococcus, toxoplasmosis
128
Presentation of erythema nodosum?
Tender, raised, red or violet nodules, usually located on the anterior surface of the legs.
Accompanied by systemic symptoms such as fever, malaise, and arthralgia in some cases.
129
Differentials for erythema nodosum?
Cellulitis
DVT
Necrobiosis lipoidica
Vasculitis
130
Investigations to diagnose erythema nodosum?
FBC, ESR, CRP,
CXR
Throat culture
Test for IBD
131
Management of erythema nodosum?
NSAIDs
Rest and leg elevation
Potassium iodide
Colchicine
Corticosteroids
132
What is erythema multiforme?
immune-mediated condition characterised by typical or atypical target lesions and potential blistering
bulls-eye-like formations with two (atypical) or three (typical) colours. These lesions may have central vesicles or blisters that eventually erode and crust over
133
Aetiology of erythema multiforme?
HSV
Mycoplasma
EBV
CMV
HIV
VZV
134
Pathophysiology of erythema multiforme?
Delayed T-cell-mediated skin reaction, meaning the reaction may not appear until several weeks after the initial insult, which may have already resolved
Two main categories;
Erythema multiforme minor, which does not involve mucous membranes and is usually triggered by an infection
Erythema multiforme major, which includes mucous membrane involvement and is more commonly drug-induced
135
Presentation of erythema multiforme?
Target lesions
Burning, painful skin lesions
Oral lesions are extremely painful
136
Differentials for erythema multiforme?
Steven Johnson syndrome
Toxic epidermal necrolysis
Urticaria
Fixed drug eruption
137
Investigations to diagnose erythema multiforme?
Clinical
Swabs
Skin biopsy can be taken
138
Management of erythema multiforme?
Treat underlying cause
Steroids
Chlorhexidine
Burrows solution
Ensure hydration is maintained
139
Skin conditions that can present with itch?
Lichen planus
Lichen simplex
Dermatitis herpetiformis
Atopic dermatitis (eczema)
Venous eczema
Asteatotic eczema
Scabies
Urticaria
Psoriasis
140
Systemic conditions which present with an itch?
Renal failure
Liver disease
Iron deficiency anaemia
Polycythaemia
Hyper/hypothyroidism
Lymphoma
Diabetes mellitus
HIV infection
Drugs: opiates, statins, ACE-inhibitors, chloroquine
Paraneoplastic syndromes
141
What are genital warts?
type of sexually transmitted infection (STI) characterised by small, skin-coloured or grey growths in the genital area. They are typically painless and present in regions traumatised during sexual intercourse
142
Risk factors for genital warts?
Unprotected sex
Multiple sexual partners
Immunosuppression
Starting sexual activity at a young age
143
Aetiology of genital warts?
Caused by HPV
90% of cases are due to serotypes 6 and 11
144
Presentation of genital warts?
Painless lumps on the genitals or anal area
Lumps that are either keratinised (hard) or non-keratinised (soft)
Areas of the body that are traumatised during sexual intercourse are commonly affected
145
Differentials for genital warts?
Molluscum contagiosum
Condyloma lata
Genital herpes
Skin tags
Mpox
146
Management of genital warts?
Podophyllotoxin: a plant-based antiviral that can destroy wart tissue
Imiquimod: an immune response modifier that stimulates the body's immune system to fight the virus
Cryotherapy (a process that freezes the wart using liquid nitrogen) or ablative therapy can be used to treat keratinised warts
Sinecatechin ointment: a plant-based treatment that can reduce wart volume with regular use
147
What is a haemangioma?
benign, but proliferative tumour of blood vessels that commonly presents in infancy where most of these tumours will spontaneously regress during childhood
Infantile haemangiomas that are high-risk (e.g. near the eye, have potential to compromise the airway) are managed with propranolol in the first instance. Surgical options can also be considered
148
Differentials for head lice?
Dandruff (seborrheic dermatitis)
Allergic reactions to hair products
Psoriasis
Folliculitis
Scabies
Impetigo
Fungal infections
149
What is impetigo?
Impetigo is a highly contagious superficial epidermal infection of the skin primarily caused by Staphylococcal and Streptococcal bacteria
150
Epidemiology of impetigo?
Most common in infants and school age children
Affects girls and boys equally
151
Aetiology of impetigo?
Staphylococcus aureus
Group A beta haemolytic streptococcus
152
Risk factors for impetigo?
Pre-existing skin conditions (i.e. eczema, cuts, burns, scabies)
Immunosuppression
Direct contact with an infected individual
Environmental factors such as crowding, humidity and poor hygiene.
153
Classification of impetigo?
Bullous: The child will have fluid filled lesions greater than 1 cm in diameter
Non-bullous: This is more common, and the child will not have bullae
Primary: Infection occurs in otherwise normal skin.
Secondary: Infection is related to an underlying skin condition (i.e. eczema) or breach to the skin barrier (i.e. bite or cut).
154
Presentation of impetigo?
Erythematous macule that vesiculates or pustulates
Superficial erosion with a characteristic golden crust
Impetigo may be bullous (causing large blisters) or non-bullous (causing sores)
Patches may be itchy or painful
155
Differentials for impetigo?
Eczema herpeticum
HSV
Contact dermatitis
Tinea corporis
156
Investigations to diagnose impetigo?
Clinical
Skin swab
157
Management of impetigo?
Localised, non bullous;
Hydrogen peroxide 1% cream
2% fusidic acid
Mupirocin
Widespread non bullous impetigo;
Topical fusidic acid
Oral flucloxacillin for 5 days
Bullous impetigo;
Oral flucloxacillin for 7 days
Refer to hospital if;
Suspected complications of impetigo (sepsis, glomerulonephritis, or deeper soft tissue infection)
The patient is immunocompromised and infection is widespread
158
Complications of impetigo?
Cellulitis
Septic arthritis
Sepsis
Scarring
Acute post streptococcal glomerulonephritis
159
What is intertrigo?
Inflammatory skin condition the skin folds resulting from skin-on-skin friction, often exacerbated by heat, moisture, maceration, and lack of air circulation. It is frequently complicated by secondary bacterial or fungal infections.
160
Epidemiology of intertrigo?
More common in obese patients
Infants, due to short necks, relative chubbiness, and flexed posture. Intertrigo in infants may be exacerbated by drooling.
Closed toe and tight clothing
Predisposing factors, including urinary and faecal incontinence, hyperhidrosis, diabetes, poor hygiene, and malnutrition.
161
Aetiology of intertrigo?
Bacterial infection: Staphylococcus aureus, group A beta-haemolytic streptococcus
Fungal infection; candida
162
Presentation of intertrigo?
Commonly seen in groin, axillae, inframammary folds
Erythematous patches, symmetrical and may progress to more severe inflammation with erosions, fissures, exudation, crusting, and maceration.
Candidal intertrigo, there may be satellite macules, papules, or pustules. Toe web intertrigo can range from mild and asymptomatic to severe with erythema, desquamation, erosions, malodour, maceration, and possibly purulent discharge.
163
Differentials for intertrigo?
Seborrhoeic eczema
Psoriasis
Tinea cruris
Erythrasma, atopic eczema, irritant contact dermatitis, allergic contact dermatitis
Hailey hailey disease
164
Investigations to diagnose intertrigo?
Fungal culture to rule out fungal infection
Bacterial culture to identify secondary bacterial infection
Skin biopsy for histopathological examination in unclear or refractory cases
165
Management of intertrigo?
Minimise moisture and friction
Promote skin hygiene
Topical agents: Application of topical antifungal (clotrimazole, miconazole, topical terbinagine), antibacterial (fusidic acid), or corticosteroid agents (hydrocortisone), depending on the causative organisms and severity of inflammation.
Topical steroids
Systemic therapy: In severe or refractory cases, systemic antibiotics, antifungal agents, or immunosuppressive therapy may be required.
Common antifungals; terbinafine, itraconazole
166
What is juvenille dermatomyositis?
Juvenile dermatomyositis (JDM) is the paediatric variant of dermatomyositis, a systemic autoimmune disease primarily affecting the skin and muscles.
167
Epidemiology of juvenile dermatomyositis?
Rare disease with 20 new cases per year
More common in females
More common in ages 4-10 years
168
Presentation of JDM?
Fatigue
Joint pain
Proximal muscle weakness, particularly in the neck, shoulder, and hip girdle
Malar rash, a red or purple rash on the cheeks and across the bridge of the nose
Heliotrope rash, a violet rash over the eyelids
169
Differentials for JDM?
Polymyositis
Lupus
Scleroderma
Muscular dystrophies
170
Investigations to diagnose JDM?
Bloods; raised ESR, CK
Antibodies; ANA, myositis specific antibodies
MRI
Muscle biopsy
171
Management of JDM?
Acute flare management with steroids
Long-term maintenance with steroid-sparing immunosuppressive agents (including azathioprine, tacrolimus, and biologics such as rituximab and anti-TNF)
172
Complications of JDM?
Muscle contractures
Arthritis
Interstitial lung disease
Calcinosis
Thrombocytopaenia
173
Prognosis of JDM?
Not associated with underlying malignancy
Overall mortality of 3%
174
Risk factors for keloid scar?
Darker skin, especially those of African, Hispanic or Chinese ethnicity
Age between puberty and 30 years old
Previous history of a Keloid scar
175
What is a keratoacanthoma?
Rapidly growing skin lesion which develops from hair follicles in skin exposed to the sun.
Rapid growth over several weeks, followed by spontaneous regression in many cases. Does not deeply invade or metastatize
Rapidly enlarging dome-shaped nodule with a central keratin-filled crater or horn
Well-differentiated keratinocytes, often has a distinct cup-shaped appearance
176
What is Koebner phenomenon?
Aberrant skin response in which new skin lesions appear at sites of physical or mechanical trauma, such as scratching, friction, burns, or surgical incisions, in individuals who have certain predisposing skin conditions.
177
Triggers for koebner phenomenon?
Psoriasis - patients with psoriasis are particularly susceptible to the Koebner phenomenon.
Vitiligo
Lichen Planus
Atopic Dermatitis (Eczema)
Excessive scratching or rubbing of the skin
Friction from tight clothing or straps
Burns, including sunburns
Insect bites or stings
Surgical incisions or wounds
178
What is lichen planus?
Chronic inflammatory disorder mediated by T cells, manifesting as pruritic, polygonal, planar, purple papules or plaques
179
Aetiology of lichen planus?
Autoimmune
Recognised triggers include Hepatitis C infection, allergic contact dermatitis, localised skin injury or infection, and certain medications, causing a lichenoid eruption.
180
Presentation of lichen planus?
Cutaneous lichen planus: Characterized by pruritic, polygonal, planar, purple papules or plaques, often with white lacy lines (Wickham's striae) on the surface. Lesions typically appear on the flexor aspects of the wrist and ankles, and nail involvement may present as longitudinal ridging.
Oral lichen planus: Features mucosal ulceration and Wickham's striae in a reticular pattern on the gums and tongue, causing a burning sensation on eating. The striae cannot be wiped off, unlike oral candida.
Lichen planopilaris: Presents as scarring alopecia characterized by follicular papules.
Lichenoid eruption: Similar to lichen planus but usually affects the trunk, and oral mucosa is typically spared. Wickham's striae are usually absent.
181
Differentials for lichen planus?
Psoriasis
Oral candidasis
Drug eruption
Eczema
Pityriasis rosea
182
Investigations to diagnose lichen planus?
Hepatitis C testing
Patch testing
Biopsy; immunoglobulin deposition at the base of the epidermis
183
Management of lichen planus?
Conservative measures: Avoiding trauma to prevent Koebnerisation, and abstaining from alcohol or smoking due to the elevated risk of oral squamous cell carcinoma.
Topical therapy: Potent corticosteroids, tacrolimus, or ciclosporin mouthwash.
Systemic therapy: Steroids, methotrexate, acitretin, or hydroxychloroquine can be used
Light therapy: UV-B therapy may be beneficial
184
What is lyme disease?
Infectious condition caused by the spirochaete Borrelia burgdorferi, transmitted via the bite of Ixodes ticks predominantly found in wooded areas.
185
Epidemiology of lyme disease?
Progressively increasing, with a significant proportion of cases originating from the northeastern regions of the USA and northern-eastern Europe.
186
Aetiology of lyme disease?
Borrelia burgdorferi via the bite of an infected Ixodes tick.
187
Presentation of lyme disease?
Stage 1: Localised disease, lasting several weeks.
Tick bite (recalled in approximately 75% of cases)
Flu-like symptoms
Regional lymphadenopathy
Erythema chronicum migrans (circular, target-shaped lesion observed in 80% of cases within 30 days)
Borrelia lymphocytoma - blue patch on the earlobe, nipple or scrotum (predominantly seen in children)
Stage 2: Early disseminated disease, lasting from days to months.
Continued flu-like symptoms
Neuroborreliosis: facial nerve (single or bilateral) and other cranial nerve palsies, aseptic meningitis, encephalitis, polyradiculitis, and Bannwarth's Syndrome, peripheral mononeuritis
Cardiovascular involvement: myocarditis, heart block and other arrhythmias, pericarditis
Early painful arthritis
Stage 3: Late disseminated disease, lasting from months to years
Arthritis: recurrent attacks, usually affecting large joints such as the knee, typically non-destructive
Late neurological disorders: polyneuropathy, chronic encephalomyelitis, dementia, psychosis
Acrodermatitis chronica atrophicans: blue-red discoloration and swelling at extensor surfaces, may be associated with peripheral neuropathy
Controversial association with fibromyalgia and chronic fatigue syndromes
188
Differentials for lyme disease?
Borrelia recurrentis
Leptospirosis
Treponema infections
Rickettsia
Babesiosis
Tularaemia
Tick borne relapsing fever
Q fever
189
Investigations to diagnose lyme disease?
Serology
ELISA
190
Management of lyme disease?
Complete removal of tick Doxycycline
In cases of complicated infection or Lyme disease affecting the central nervous system, or Lyme carditis with haemodynamic instability, IV Ceftriaxone is recommended as first-line therapy
191
What is Jarisch-Herxheimer reaction?
Develops in first 24 hours of treatment with any antibiotic for lyme disease
This is a systemic reaction thought to be caused by the release of cytokines when antibiotics kill large numbers of bacteria, resulting in worsening of fever, chills, muscle pains and headache
192
What is malignant melanoma?
skin cancer that arises from the melanocytes, the cells responsible for producing the skin pigment melanin.
193
Risk factors for melanoma?
Family history or prior personal history of melanoma
Genetic syndromes, such as Familial Atypical Multiple Mole Melanoma Syndrome
Skin type prone to burning and not tanning (Fitzpatrick type I or II)
Immunosuppression
High levels of sun or UV exposure
Presence of atypical melanocytic naevi
Smoking
Advanced age and male sex
194
Pathophysiology of melanoma?
Originate from a melanocyte that begins to divide uncontrollably, leading to a localised cluster of melanocytes that may eventually become invasive and metastasise. Most melanomas arise de novo from normal skin, but about a third may develop from pre-existing melanocytic naevi
195
Presentation of melanoma?
Asymmetry of the lesion
Border irregularity
Colour variegation
Diameter >6mm
Elevation/evolution over time
196
Types of melanoma?
Superficial spreading (Pagetoid) - this has a long radial phase, and is the most common type
Lentigo maligna melanoma (Hutchinson's melanotic freckle) - this has a very long radial phase, existing as the pre-malignant lesion lentigo maligna before it starts invading the basement membrane
Nodular ab initio - this has no radial phase, and is the most aggressive type
Acral lentiginous - this has a short radial phase, and occurs in patients with darker skin tones at higher frequency, involves the palms/soles
Subungual - growing under the nail
Amelanotic
197
Differentials for malignant melanoma?
BCC
SCC
Seborrheic keratosis
Dysplastic nevus
198
Investigations to diagnose melanoma?
Excisional biopsy of the lesion with a 2mm margin
Sentinel lymph node biopsy if the Breslow thickness is >1mm
PET or CT scans may be necessary in the presence of clinical suspicion for metastases
199
Management of melanoma?
Excision with a 2mm margin and further excision depending on the Breslow thickness;
Melanoma in situ: 5 - 10 mm
Melanoma < 1 mm: 10 mm
Melanoma 1-2 mm: 10 - 20 mm
Melanoma > 2 mm: 20 mm
Lymph node clearance if lymph nodes involved
Radiotherapy in some cases
Adjuvant Immunotherapy/chemotherapy in metastatic disease (Stage III/IV), such as pembrolizumab (PD-1 blocking drug)
Mole-mapping and lifestyle advice to prevent recurrence in those at risk
200
What is Breslow thickness?
The Breslow thickness is determined histologically, and is the most important prognostic indicator.
It is measured in mm, from the top of the granular layer in the epidermis to the deepest point that the tumour extends.
201
What is melanocytic naevi?
benign skin lesion due to a local proliferation of pigment cells (melanocytes).
202
Pathophysiology of melanocytic naevi?
Junctional: flat + pigmented (due to melanocytes at the basal layer of the epidermis)
Compound: raised + pigmented (due to melanocytes at the basal layer of the epidermis + deep in the dermis)
Intradermal: raised + pale (due to melanocytes deep in the dermis)
203
What is a dysplastic naevus?
An atypical naevus that may resemble a melanoma, by having 'ABCDE' features.
They may be part of a syndrome called Familial Atypical Multiple Mole-Melanoma (FAMMM) syndrome, where there are multiple naevi (>50) many of which are atypical and an increased risk of melanoma.
204
What is a blue naevus?
A naevus that is blue in colour because the melanocytes are very deep in the skin.
205
What arethe features of a Becker's naevus?
Irregular hyperpigmented patch affecting shoulders of males
Darkens during puberty and becomes hairy
206
What is a halo naevus?
Melanocytic naevus that is surrounded by a white halo.
207
What is a spitz naevus?
A red, dome-shaped papule that is commonly found on the face of children.
208
What is molloscum contagiosum?
Common, contagious skin infection caused by molluscum contagiosum virus, a member of the poxvirus family.
209
Aetiology of molluscum contagiosum?
molluscum contagiosum virus (MCV), a virus from the poxvirus family
210
Presentation of molluscum contagiosum?
Small, smooth, pearly-colored papules with a central area of umbilication
These lesions can occur anywhere on the body, but they are most commonly found on the genitals
In immunocompromised patients, lesions can be extra-genital and particularly prevalent on the face
When the lesions are present on the eyelid margin, they can cause irritation, redness and follicular conjunctivitis, characterised by small lymphoid tissue elevations on the tarsal conjunctiva.
211
Differentials for molluscum contagiosum?
Basal cell carcinoma
Genital warts
HSV infection
Keratoacanthoma
212
Investigations to diagnose molluscum contagiosum?
Visual inspection
Swab
213
Management of molluscum contagiosum?
Cryotherapy
Topical treatment; salicylic acid, imiquimod, potassium hydroxide
Curettage
214
What are Papulosquamous eruptions?
Rashes consisting erythematous papules and scale
215
Differentials for Papulosquamous eruptions?
Psoriasis
Lichen planus
Pityriasis rosea
Tinea
Pityriasis versicolor
Discoid eczema
Mycosis fungoides
216
What is Bullous Pemphigoid?
One of the autoimmune blistering disorders characterised by tense subepidermal blisters
217
What is pathophysiology of bullous pemphigoid?
Autoantibodies targeting the hemidesmosomes that bind the basal keratinocytes of the epidermis to the basement membrane. The antigens are the BP180 and BP230 components of hemidesmosomes
This causes the development of tense, sub-epidermal blisters that are not readily deroofed
218
Risk factors for bullous pemphigoid?
Other associations include drugs (PD-1 inhibitors in melanoma, ACEi and penicillamine), psoriasis treatment (phototherapy), injury to skin, neurological disease, and genetics
219
Presentation of bullous pemphigoid?
Usually affects older people
Prodrome of itch, irritation, erythematous, eczematous, urticarial skin changes, followed by tense subepidermal blisters
Nikolsky's sign is negative
The mucous membrane's are spared, except for the cicatrial variant (characterised by marked scarring and predilection for the mucous membranes)`
220
Investigations to diagnose bullous pemphigoid?
Biopsy for immunoflouresence from lesion edge
Anti BP180/BP230 antibodies circulating
221
Treatment of bullous pemphigoid?
Topical potent steroids at onset of symptoms e.g. itch
Doxycycline for anti-inflammatory effect
Systemic steroids (0.5-1mg/kg of prednisolone), continued until no further lesions for one year.
Azathioprine and mycophenolate if relapse during steroid withdrawal
222
What is pemphigus vulgaris?
One of the autoimmune blistering skin conditions characterised by flaccid intra-epidermal blisters.
223
Pathophysiology of pemphigus vulgaris
IgG autoantibodies are targeted against desmosomes, structures that link keratinocytes to other keratinocytes within the epidermis
The specific antigens are desmoglein 1 and desmoglein 3
This leads to the development of blisters within the epidermis, which are flaccid and often deroofed
224
Presentation of pemphigus vulgaris
Flaccid, thin walled blisters leading to erosions across the body
Mucous membranes may be involved
Nikolsky's sign is positive
Patients can be quite unwell with pemphigus vulgaris and mortality is high without treatment
225
Investigations to diagnose pemphigus vulgaris
Biopsy for immunoflouresence from the edge of the lesion
Detection of autoantibodies against desmoglein 1 and desmoglein 3 using indirect immunofluorescence (IIF) or enzyme-linked immunosorbent assay (ELISA)
226
Management of pemphigus vulgaris?
Oral prednisolone
Antibiotics for secondary bacterial infection
227
What is pityriasis rosea
A self-limiting rash that resolves after 10 weeks characterised by a herald patch and subsequent fir-tree pattern eruption
228
Aetiology of pityriasis rosea?
Viruses: such as HHV6/7, COVID-19, and Flu
Drugs: such as gold, ACEi, penicillamine, and biologics.
Many vaccines: BCG, hepatitis B, and pneumococcal.
229
Presentation of pityriasis rosea?
Usually, a few days after a viral infection e.g. an URTI, the patient presents with a 'herald patch.'
This is a red-pink oval/discoid plaque with a peripheral colarette of scale on the trunk or upper arm/thigh. It may be misdiagnosed as ringworm.
1-20 days later, a similar widespread eruption (but the individual lesions may be smaller) occurs on the body that follows a fir tree (Christmas tree) pattern appears, with the long axis of the lesions sweeping from back to front as if following Langer's lines.
In most cases, there are virtually no symptoms except for the rash.
230
Management of pityriasis rosea?
Antihistamines, emollients, and topical steroids may be of use in these patients
231
What is psoriasis?
Psoriasis is a chronic autoimmune disease characterised by well-demarcated, erythematous, scaly plaques.
232
Types of psoriasis?
Chronic plaque psoriasis- this is the commonest type and causes symmetrical plaques on the extensor surfaces of the limbs (knees + elbows), scalp and lower back.
Flexural (inverse) psoriasis- smooth, erythematous plaques without scale in flexures and skin folds.
Guttate psoriasis- multiple small, tear-drop shaped, erythematous plaques occur on the trunk after a Streptococcal infection in young adults.
Pustular psoriasis- multiple petechiae and pustules on the palms and soles.
Generalised/erythrodermic psoriasis- this is rare but serious form characterised by erythroderma and systemic illness.
233
Risk factors for psoriasis?
Skin trauma (Koebner phenomenon)
Infection: Streptococcus, HIV
Drugs: B-blockers, Anti-malarials, Lithium, Indomethacin/NSAIDs (BALI)
Withdrawal of steroids
Stress
Alcohol + smoking
Cold/dry weather
234
Differentials for psoriasis?
Pityriasis rosea
Tinea
Seborrhoeic dermatitis
Bowen's disease
Discoid eczema
Mycosis fungoides
Discoid lupus
Scabies
235
Presentation of plaque psoriasis
Itchy, well-demarcated circular-to-oval bright red/pink elevated lesions,overlying white or silvery scale, distributed symmetrically over extensor body surfaces and the scalp.
Nailbed pitting: superficial depressions in the nailbed
Onycholysis: separation of nail plate from nailbed
Subungual hyperkeratosis: thickening of the nailbed
236
Management of psoriasis?
Betnovate
Topical vitamin D
Phototherapy
Methotrexate
Ciclosporin
Acitretin
Biologics; infliximab, entanercept, adalimumab
237
Aetiology of pyoderma gangrenosum?
Myeloma and myeloproliferative disorders
Liver disease e.g. autoimmune hepatitis
Inflammatory arthritides
Autoimmune thyroid disorders
Diabetes
Inflammatory bowel disease
Sarcoidosis
Granulomatosis with polyangiitis
PAPA syndrome (pyogenic arthritis, pyoderma gangrenosum, and acne)
Idiopathic (50%)
238
Pathophysiology of pyoderma gangrenosum?
Autoimmune/ autoinflammatory
Dysregulation of the immune system leads to excessive inflammation and tissue damage, resulting in ulcer formation.
239
Presentation of pyoderma gangrenosum?
Painful ulcerating lesion violaceous, undermined edge, healing with a characteristic cribriform scar. Pus is sterile
Histologically, there is a neutrophilic infiltrate within the dermis
Blood blister, pustule, or papule at the site of a minor trauma. This rapidly expands into a painful ulcer
240
Investigations to diagnose pyoderma gangrenosum?
Skin biopsy
Lab tests; ESR, CRP, FBC
USS
MRI
241
Management of pyoderma gangrenosum?
Topical steroids
Immunosuppression; prednisolone, cyclosporin, azathioprine
Wound care
Debridement
Pain management
242
What is a pyogenic granuloma?
single, shiny, red nodule of up to 1cm, often described as ""raspberry-like". This nodule will have grown rapidly from a painless, small, discoloured spot. Pyogenic granulomas are most commonly located on the fingers and hands
243
Aetiology of pyogenic granuloma?
Minor trauma, such as a pin prick
Infection, commonly Staphylococcus aureus
Pregnancy
Some medications, such as oral retinoids
244
Management of pyogenic granuloma?
Surgical excision
Laser surgery
Curettage and cautery
Cryotherapy
245
What is scabies?
Scabies is caused by the mite Sarcoptes scabei, a highly contagious infestation spread by direct contact.
246
Pathophysiology of scabies?
A delayed type IV hypersensitivity reaction results in symptoms around 30 days after the initial infection.
247
Presentation of scabies?
It presents with an intensely itchy rash that usually affects the inter-web spaces, flexures of the wrist, axillae, abdomen and groin.
The itch is classically worse at night.
The rash is usually papular or vesicular and superficial burrows may often be seen.
248
What is Norwegian scabies?
Norwegian (or crusted) scabies is where an individual is affected by millions of mites causing a generalised scaly rash- it is seen in immunocompromised patients (eg those with HIV).
249
Management of scabies?
Permethrin 5%
Crotamiton cream can be used to relieve the itching
Malathion 0.5% should be used 2nd line
250
What is seborrheic dermatitis?
chronic or relapsing skin condition predominantly affecting sebum-rich areas of the skin, primarily in young adults and the elderly
caused by an inflammatory reaction to the proliferation of Malassezia furfur
251
Presentation of seborrheic dermatitis?
Ill defined greasy, flaky scales on an erythematous background
252
Risk factors for seborrheic dermatitis?
Family history
Oily skin
Immunosuppression (such as HIV)
Neurological and psychiatric diseases (such as Parkinson's disease or depression)
Stress
253
Management of seborrheic dermatitis?
Ketoconazole shampoo
Zinc pyrithione shampoo
Short course of topial corticosteroids
In infants try topical emollient and olive oil
254
What is Seborrhoeic keratoses?
benign, warty, epidermal growths which occur commonly with skin aging
255
Presentation of seborrhoeic keratosis?
Warty plaque with a fissured keratin surface
They can occur anywhere on the body with the exception of the palms, soles and mucous membranes.
256
Management of seborrhoeic keratosis?
Cryotherapy
Curettage
Laser ablation
257
What is SCC?
Locally invasive malignant tumour of epidermal keratinocytes
258
Risk factors for SSC?
Fhx
Genetic syndromes, for example Xeroderma Pigmentosum
Pale skin
Light hair
High level of sun exposure
Immunosuppression
Chronic inflammation
Actinic keratosis
Bowens disease
Smoking
Old age
Male sex
259
Features of SCC?
Keratinised, scaly, irregular nodules
Ulcerating everted edge
Polyploid lesion
Pain, tenderness, bleeding
260
Investigations to diagnose SCC?
Excision biopsy with 4mm margin
261
Management of SCC?
Excision with 4-6mm margin
Mohs micrographic surgery
Radiotherapy
Other options include curettage and cautery, topical 5-flourouracil, topical imiquimod, and cryotherapy if the lesion appears low risk
262
What is vitiligo?
Autoimmune dermatological disorder where there is loss of melanocytes, the pigment-producing cells in the skin's epidermis. This results in a loss of pigmentation, manifesting as white patches on the skin.
263
Epidemiology of vitiligo?
It has a similar prevalence across genders and ethnic groups, typically presenting in young adulthood, but it can occur at any age.
264
Aetiology of vitiligo?
Genetic factors affecting tyrosinase enzyme
Transdermal methylphenidate patches
Pembrolizumab and nivolumab.
Stress
Other autoimmune diseases such as thyroid disease, Type I diabetes, rheumatoid arthritis, myasthenia gravis, pernicious anaemia, autoimmune hepatitis, alopecia areata, psoriasis, and lichen planus.
265
Differentials of vitiligo?
Pityriasis alba
Post inflammatory hypopigmentation
Tinae versicolor
Albinism
Lichen sclerosus
Idiopathic guttate hypomelanosis
266
Investigations to diagnose vitiligo?
The diagnosis of vitiligo is primarily clinical, with investigations seldom required.
Skin biopsies may be employed where the diagnosis is uncertain.
Fluorescence under a Wood's lamp may be observed.
Screening for concomitant autoimmune diseases such as thyroid dysfunction, B12 deficiency, or diabetes may be necessary.
267
Management of vitiligo?
Conservative measures:
Avoidance of trauma.
Use of cosmetic camouflage techniques.
Sun-protection due to increased risk of sun-damage and spreading of vitiligo
Pharmacological;
Topical steroids
Phototherapy
Systemic treatments like oral steroids, methotrexate, ciclosporin, and mycophenolate may also be used.
268
Complications of vitiligo?
Psycho- social
Associated autoimmune diseases:
Thyroid disease.
Type I diabetes.
Polyendocrine genetic conditions.
Rheumatoid arthritis.
Myasthenia gravis.
Pernicious anaemia.
Autoimmune hepatitis.
Alopecia areata.
Psoriasis.
Lichen planus.
PassMed
flashcards
Decks in class (17)
# Cards
