Revise Notes Derm

Question 1

Acanthosis Nigricans
Pathophysiology

Insulin resistance leads to increased insulin secretion,

which stimulates proliferation of fibroblasts and keratinocytes via IGFR-1
Causes: T2DM, GI malignancy, PCOS

Answer 1

Clinical features

Symmetrical dark, brown or black, velvety patches of skin develop in the axillae, groin, neck.

Question 2

Acne Vulgaris
Pathophysiology

A chronic skin condition, usually affecting the face, which is characterised by obstruction and inflammation of the pilosebaceous units.

Lesions include
Comedones - non-inflamed blackheads/whiteheads
Papules - inflamed dome-shaped bumps
Papules may develop into pustules - filled with white/yellow pus

Severity - the severity of acne influences its management - NICE defines acne as:
Mild - Mostly non-inflammatory (comedones)

Moderate - more widespread, with papules and pustules

Severe - widespread inflammation, with large burden of papules, pustules and deeper nodules/cysts. There may be areas of scarring.

Answer 2

Management of mild-moderate acne

1st line - Prescribe a 12 week course of a combined topical treatment. Options:

Topical adapalene with benzoyl peroxide
Topical tretinoin with clindamycin
Topical benzoyl peroxide with clindamycin

Question 5

Management of moderate-severe acne

1st line - Prescribe a 12 week course of:
Topical adapalene with benzoyl peroxide (as per mild-mod)

Topical tretinoin with clindamycin (as per mild-mod)

Topical adapalene with benzoyl peroxide AND oral tetracycline (lymecycline/doxycycline)

Topical azelaic acid BD AND oral tetracycline (lymecycline/doxycycline)

Answer 5

Note - tetracyclines are contraindicated in pregnancy - erythromycin can be used as an alternative.

Combined oral contraceptives in combination with topical agents should be considered as an alternative to PO antibiotics in women in the absence of contraindications.

Referral to dermatology

Mild-Moderate acne has not responded to 2 x complete course of treatment

Moderate-Severe acne has not responded to treatment which included PO ABx

Scarring, pigmentary changes, or psychological distress

Secondary care treatments include: PO Isotretinoin (contraindicated in pregnancy)

Question 6

Benign Skin Lesions
Seborrhoeic Keratosis

A benign, warty spot which occurs as part of ageing

Clinical features

Flat or raised lesions which can be several cm
May have a “stuck-on” appearance
Can appear in groups - e.g. under the breasts, in the groin, or across the back

Answer 6

Solar Lentigo

A benign, patch of pigmented skin which occurs secondary to sun exposure

Clinical features

Flat, well-circumscribed patch of hyperpigmentation
Often occur in groups on sun exposed sites e.g. dorsum of hands.

Question 7

Keratoacanthoma

A rapidly growing, locally destructive epithelial tumour

Clinical features

Initially a smooth, dome-shaped nodule on sun exposed sites (face/upper limbs)
Later undergoes rapid growth
Characterised by a central

hyperkeratotic plug (crater filled with keratin - removal of the plug leaves the lesion “volcano-like”)

Answer 7

Management

Surgical excision due to local invasion, and indistinguishability from SCC

Question 8

Dermatofibroma

A benign fibrous nodule caused by the abnormal proliferation of dermal dendritic histiocyte cells

Often occurs following a precipitating injury (e.g. insect bite, a rose thorn injury).
Commonly affects gardeners who sustain thorn injuries

Answer 8

Clinical Features

Solitary firm nodules or papules (0.5-1cm in size)

Pink, light brown, or flesh-coloured lesions
Button hole sign - overlying skin dimples on pinching the lesion

Question 9

Dermatitis
Atopic Dermatitis (Eczema)

A chronic inflammatory skin condition characterised by chronic dermatitis with episodic acute flares

Clinical Features

Most commonly manifests in early childhood (< 5 yrs)
Itchy, dry skin often affecting the hands, or flexor surfaces of the limbs (such as elbow and knee creases)

Nb. In Asian/African-Caribbean patients, eczema may affect extensor surfaces > flexor

Acute flares - increased pruritus, erythema, vesicles

Personal or family history of atopy - asthma, hayfever etc.

Weeping or pustules and systemic symptoms (pyrexia) - may suggest bacteria infection

Answer 9

Management

Generous use of emollients/ointments are the mainstay of management

Steroids should be prescribed during acute flares to achieve remission - aim to use the weakest cream to control symptoms, continue for 48hrs after resolution

Mild - hydrocortisone 0.5-2.5%
If areas of dry skin and occasional itch

Moderate - Betnovate RD (0.025%) or Eumovate (0.05%)
If dry skin with frequent itching, and erythema

Potent - Cutivate (0.05%) or Betnovate (0.1%)
If widespread dryness, severe itch, erythema and oozing/cracked skin

Very potent - Demovate (0.05%)
NICE also recommends topical tacrolimus (e.g. Pimecrolimus 1%

(Elidel)) as a second-line option for the treatment of moderate-severe atopic dermatitis in adults and children aged two years and over that has failed to respond to topical corticosteroids,

where there is a risk of adverse effects (such as irreversible skin atrophy) from further topical steroid use.

Question 11

Pompholyx (Dyshidrotic) Eczema

Eczema affecting the fingers, palms of the hands and soles of the feet
Characterised by intense pruritus and small 1-2 mm vesicles/blisters

Classically precipitated by moisture - e.g. humidity/sweating/high temps.
Management: Potent steroids are usually required

Question 12

Seborrhoeic Dermatitis

Pathophysiology

A chronic skin condition occurring due to the over proliferation of normal skin fungus (Malassezia Furfur), with resultant inflammation.

Associations with HIV and Parkinson’s disease
Clinical features

Symmetrical eczematous lesions occurring most commonly on skin areas which are rich in sebaceous glands, including the:

Eyebrows, nasolabial folds
Periorbital and behind the ears
Upper chest and back

SD is characterised by erythematous patches of skin with, flaking and scales.
Dandruff - desquamation of scales from scalp

Otitis externa
Blepharitis - red, swollen eyelids with flaking/scaly skin

Answer 12

Management

Scalp and Beard:
1st line: Ketaconazole 2% shampoo
Alt: Zinc pyrithione containing shampoo, coal tar

2nd line: If severe itching of scalp - consider topical steroid - betnovate 0.1%

Face and Body:
1st line: Ketoconazole 2% OR imidazole cream (clotrimazole/miconazole)

Nb. ketoconazole is not licensed in children
Consider adding mild steroid (hydrocortisone) for flares

In infants, seborrhoeic dermatitis most commonly affects the scalp, and usually resolves spontaneously after a couple of months.

If required, prescribe emollients 1st line to loosen scalp scale.

If necessary, topical imidazole creams can be used.

Question 13

Contact Dermatitis

There are two main types of contact dermatitis - irritant, and allergic
Irritant dermatitis

Common, non-allergic inflammation of the skin secondary to contact with irritants such as acids/alkalis (often within cleaning products/detergents)

Features: erythema, crusting.
Allergic dermatitis

Answer 13

Allergic dermatitis
A T-cell mediated type 4 hypersensitivity reaction

Often occurs on the scalp following application of hair dye, skin exposed to nickel

Features: Blistering, weeping eczema (e.g. more on the hairline, following hair dye) 24-48 hrs after exposure to sensitized allergen.

Diagnosis: Skin patch testing
Management: Potent topical steroids

Question 15

Dermatitis Herpetiformis
Pathophysiology

IgA deposition in the dermis, most commonly occuring in patients with coeliac disease (90%)

Clinical features

An intensely itchy, papular rash with vesicles affecting the extensor surfaces - especially the elbows, buttocks, shoulders and knees

Answer 15

Investigations

Anti-TTG/EMA antibodies

Biopsy of lesions confirm IgA deposition in dermis

Management

Dietary management: Elimination of dietary gluten

Question 16

Dermatological Emergencies
Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

Pathophysiology

Severe mucocutaneous reactions. SJS and TENs are considered variants of the same disease.
Aetiology: Usually caused by a drug reaction. Common causative medications include:

Sulfonamide antibiotics - sulfasalazine, co-trimoxazole
Penicillins
AEDs - lamotrigine, carbamazepine, phenytoin

Allopurinol - increased risk in East Asian population (HLA-B*58:01 genotype screening can reduce this risk)
COCP
NSAIDs

Answer 16

Clinical features

There is usually a history of flu-like prodrome, sore throat, fever, arthralgia
Rash begins as a macular (flat) rash with target lesions (lighter around outside, dark inside)

The rash typically begins on the upper torso and then rapidly spreads to the arms, legs and face over hours to days

Blisters later develop which may burst, the exposed sores are painful

There is subsequently desquamation of sheets of skin - Nikolsky’s sign is positive (gentle lateral rubbing on skin separates the epidermis and causes desquamation

Mucosal involvement - oral ulceration, lip involvement - a key feature

Pruritus is uncommon - not usually itchy
Eye involvement - eye pain, conjunctivitis, corneal ulcers

Question 17

Investigations

Diagnosis is clinical. Skin biopsy can be confirmative.
SJS vs TEN

As above, SJS/TEN are widely considered to be variants of the same disease - the conditions are differentiated by the proportion of body surface area involvement as follows:

SJS: < 10%
SJS/TEN: 10-30%
TEN: > 30%

Answer 17

Management

IV fluids - risk of dehydration
Stop causative medications

Generous creams/emollients/dressings to maintain skin moisture

IV immunoglobulin/plasmapheresis can be used

Question 18

Drug Hypersensitivity Syndrome (DRESS)

Pathophysiology

Also known as Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS),

DHS is a severe, cutaneous and systemic reaction to a new medication
T-cell mediated reaction

Answer 18

Clinical features

Symptoms usually begin > 2 weeks after commencing AED, allopurinol
Triad of:
High pyrexia > 38 degrees

Extensive rash - usually morbilliform, often featuring target lesions or blisters - may later develop into an exfoliative dermatitis with skin shedding

Organ involvement - e.g. hepatitis is most common, AKI
Other features:

Bloods - Eosinophilia, leukocytosis, thrombocytopenia, anaemia
Lymphadenopathy
Mucosal involvement in 1/3rd patients

Question 19

Drug Hypersensitivity Syndrome (DRESS)

Pathophysiology

Also known as Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS),

DHS is a severe, cutaneous and systemic reaction to a new medication
T-cell mediated reaction

Answer 19

Causative drugs

AEDs - carbamazepine, phenobarbital and phenytoin
Allopurinol
Olanzapine
Sulfonamide antibiotics

Diagnosis

Skin biopsy

Management

Stop causative drug
Corticosteroids - prednisolone
Supportive treatments - emollients, antihistamines, fluids etc.

Question 20

Erythroderma

Pathophysiology

Any rash which involves at least 90% of the skin surface area

Most commonly occurs secondary to an exacerbation of chronic skin disease

such as psoriasis or atopic dermatitis (often triggered in psoriasis after withdrawal of steroids)

Answer 20

Clinical features

Widespread erythematous, pruritic rash over > 90% of body surface area
Systemically unwell, fever, malaise, lethargy

History of chronic skin disease
May be signs of desquamation

Management

Emollients, creams, wet dressings
Consider topical steroids
Replace fluid/electrolytes

Question 21

Eczema herpeticum

Pathophysiology

Herpes simplex 1 or 2 infection of skin, on a background of eczema

Usually occurs in infants/children, or patients with severe eczema
Clinical features

Rapidly progressive painful rash in a patient with a history of eczema is highly suspicious

Lesions are itchy and painful
On examination - monomorphic ‘punched-out’ erosions (circular, depressed ulcer appearance), blisters, crusted papules. Usually 1-3mm each.

Answer 21

Diagnosis

Clinical +/- swabs (for HSV, or may show superadded infection with strep/staph)

Management

Urgent admission for IV aciclovir and dermatology review
Ophthalmology review if eye involvement

Question 23

Erythema multiforme
Clinical features

Target lesions, commonly on the hands/feet initially, and subsequently on the limbs and torso

There may be mucosal involvement - referred to as erythema multiforme major

Answer 23

Causes

Typically the result of a hypersensitivity reaction in response to an infection (or drugs/malignancy). Common causes include:

Viral - Herpes simplex virus most common, orf
Bacterial - streptococcal or mycoplasma infection

Drugs - antibiotics (penicillin, sulfonamides), allopurinol, carbamazepine
Sarcoidosis, SLE, malignancy

Question 24

Folliculitis
Key learning

Acute pustular infection
Most commonly due to S.aureus, fungal infection also common

Present as pustules or papules with erythema around hair follicles

Can be itchy or painful and can occur anywhere on body

Often self resolve, if severe/recur can use topical or oral antibiotics/antifungals

Pathophysiology

Inflammation of hair follicles, usually caused by bacterial or fungal infection
Most common organism= S.aureus

Answer 24

Epidemiology

Common, affecting all ages
More prevalent in warm and humid climates, athletes, and those with compromised immune systems

including diabetics
History

Itching, burning, or tenderness around hair follicles.

Buzzwords in MCQs:
Recent skin trauma
Hot tub use
Sharing contaminated items i.e. razors

Question 25

Clinical Features/examination findings Pustules or papules with erythema around hair follicles Lesions may be discrete or coalesce into larger areas of inflammation May be pruritic or painful and can occur anywhere on the body Often occur in recently shaved or occluded areas

Answer 25

Investigations Clinical diagnosis Swab MCS if atypical features or severe infection are present. Management Often self-resolve Symptomatic relief with warm compresses and analgesics Avoidance of shaving or friction may prevent recurrence If recurrent/severe 4-6 week course of topical (mupirocin/fusidic acid) or oral (flucloxacillin) antibiotics/antifungals Complications Rare Cellulitis Folliculitis decalvans (chronic folliculitis leading to hair loss)

Question 26

Fungal Skin Infections Tinea Fungal skin infection is most commonly caused by dermatophyte fungi including trichophyton rubrum Clinical Features Fungal Infections on the body - tinea corporis/ringworm Annular erythematous lesions with have a scaly edge and a clear centre Fungal infections of groin - tinea cruris In the groin, the inguinal skin folds and medial thighs are most commonly affected with red-brown plaques with uniform scaling Fungal foot infections - tinea pedis/ athletes foot Interdigital infection is most common - white/erythematous, cracked and fissured skin which has scale. Fungal scalp infection - tinea capitis / scalp ringworm Scaling of the scalp with pruritus, erythema, crusting. . May be patches of alopecia - risk of scarring alopecia without treatment Kerion - a bogy, puss filled, crusty mass - urgent referral required

Answer 26

Investigations Skin scrapings for microscopy and culture Management Mild, non-extensive disease: 1st line: Topical antifungal (terbinafine or imidazole cream) Add a mild topical steroid (hydrocortisone) - if marked inflammation Severe/extensive disease: Oral antifungal - 1st line: Terbinafine (alt: itraconazole/griseofulvin) Scalp infection Kerion present - urgent referral to dermatology 1st line Tx of scalp infection is oral antifungal - griseofulvin or terbinafine

Question 27

Pityriasis Versicolor Pathology A superficial fungal infection of the epidermis caused by the overgrowth of Malassezia yeasts which are part of the normal skin flora Clinical features Multiple oval or confluent patches gradually appear on the trunk/ back Patches can be scaly and are sometimes itchy Patches appear ‘fawn’ coloured, pink or white and are more apparent in summer when the healthy skin becomes more tanned MCQs may mention that the rash was noticed during/after holiday

Answer 27

Management Small area involved: topical clotrimazole cream Extensive area involved: 1st line - Ketoconazole 2% shampoo 1st line OD for 5 days

Question 28

Erythrasma Pathology A chronic superficial skin infection caused by the overgrowth of the diphtheroid corynebacterium minutissimum Clinical features Slowly enlarging, well-circumscribed, flat, pink-brown patches of skin which typically occur in the inner thighs, groins or axillae Investigations Scrapings for MCS. Appears coral-red when assessed under Wood’s lamp

Answer 28

Management 1st line: Topical miconazole or clotrimazole BD for 2 weeks for localised infection Oral antibiotics (erythromycin, clarithromycin or doxycycline) if extensive disease

Question 29

Hair & Scalp Disorders Alopecia Areata Pathophysiology A chronic condition of non-scarring alopecia characterised by sudden hair loss, where hair follicles are preserved. The aetiology is thought to be autoimmune. Clinical features A sudden patch/patches of hair loss affecting the scalp or beard Patches are well-circumscribed, with normal underlying skin is normal Exclamation mark hairs might be seen - short hairs which narrow at the base

Answer 29

Management If there is evidence of hair re-growth - no treatment is needed If there is no hair regrowth - consider topical potent steroids (e.g. Betnovate)

Question 30

Hirsutism Pathophysiology Androgen dependent hair growth in women Causes include PCOS - accounts for 70% cases Others: idiopathic, adrenal hyperplasia, cushing’s syndrome, acromegaly, hyperprolactinaemia

Answer 30

Investigations Measure serum total testosterone levels Management 2WW referral if concern re. adrenal/ovarian neoplasm - suggested by sudden onset hair growth or virilisation Conservative measures - weight loss, cosmetic/hair removal If additional treatment is required Facial hirsutism - topical eflornithine 1st line COCP - can be used in premenopausal women

Question 31

Hereditary Haemorrhagic Telangiectasia An autosomal dominant condition characterised by the presence of telangiectasia on the skin and mucous membranes Clinical features 2/4 = probable diagnosis, 3/4 = definite diagnosis History of epistaxis Presence of telangiectasia Visceral lesions (e.g. within the GI tract → GI bleed) Family history of similar signs/symptoms

Answer 31

Figure 169: Hereditary haemorrhagic telangiectasia. Michael Sand, Daniel Sand, Christina Thrandorf, Volker Paech, Peter Altmeyer, Falk G Bechara, HereditaryHemorrhagicTelangiectasia, CC BY 2.5

Question 32

Lichen Planus A chronic inflammatory skin condition of autoimmune aetiology Clinical features Very itchy rash which affects the palms of the hands/wrists, soles of the feet and ankles, lower back or flexural surfaces The rash may be papular or polygonal in shape Often violaceous in colour Wickham’s striae (fine white lines) run across the surface of the rash. Patients may have oral involvement, with a white lace pattern on buccal mucosa or tongue

Answer 32

Management Potent topical steroids, benzydamine mouth wash if oral lichen planus

Question 33

Lichen sclerosus A chronic, inflammatory skin condition which afffects the perianal and genital skin, of unknown aetiology. Possibly an autoimmune process. Clinical features Women 10 x more frequently affected than men White, cracked plaques affecting the: Anal/perianal skin Vagina - labia majora/minora/clitoral hood - but NOT vaginal mucosa Penis - glans (referred to as BXO) Pruritus ++ May be associated dysuria, dyspareunia etc.

Answer 33

Management Very potent or potent topical steroids - if no response, biopsy must be performed to rule out malignancy (e.g. vulval cancer)

Question 35

Melasma Melasma is a common acquired hyperpigmentation disorder, mainly affecting sun-exposed areas, particularly the face. It predominantly occurs in women, often linked to hormonal changes, and is more prevalent in individuals with darker skin tones. Pathophysiology Melasma results from overproduction of melanin by melanocytes, leading to excess pigmentation. Key factors include UV radiation, hormonal influence (elevated oestrogen levels - hence association with pregnancy), genetic predisposition.

Answer 35

Clinical Features Symmetrical hyperpigmented macules: Brown or grey-brown patches on the face, commonly on the cheeks, forehead, upper lip, and chin. Butterfly distribution: Central facial involvement is typical, but melasma can also affect the forearms or neck.

Question 36

Melasma mng

Answer 36

Management Sun protection: Broad-spectrum sunscreen (SPF 30 or higher) is crucial to prevent worsening. Topical treatments: Hydroquinone: First-line depigmenting agent. Tretinoin: Often combined with hydroquinone for better efficacy. Triple therapy: Combines hydroquinone, a corticosteroid, and tretinoin.

Question 37

Milia Pathophysiology Originate from maldeveloped sweat /sebaceous glands. Very common in newborn babies, affecting up to 50%.

Answer 37

Clinical Features Small (1–2 mm) whitish yellow papules that commonly occur over the nose and face. Milia are transient - they usually rupture and disappear within a few weeks. No treatment is required

Question 38

Nail Infections Acute Paronychia Pathology Localised, superficial infection of the folds of tissue surrounding the nail Causative organisms: Staphylococcus aureus - most common Clinical features Painful swelling of the skin tissue at the base of the nail bed On examination - lateral/proximal nail folds are erythematous, painful and swollen. There may be pus present.

Answer 38

Management Warm soaks If collection present - incision and drainage is required Topical antibiotics are appropriate for minor, localised infection - fusidic acid Oral antibiotics if - I&D not performed, cellulitis, fever or extensive area of infection

Question 39

Onychomycosis (Fungal nail infection) Pathology Fungal infection of all or any part of the nail, characterised by unsightly, thickened, rough/flakey and discoloured nails. Toenails much greater risk than fingernails Causative organisms: Dermatophyte fungi - cause > 75% of cases Trichophyton rubrum Trichophyton mentagrophytes Non-dermatophyte fungi account cause a minority of cases Moulds (10%) - Scopulariopsis, aspergillus etc. Yeasts - candida albicans

Answer 39

Clinical features Part or all of one or more nails may be affected with an abnormal appearance, with some of the following features: Discolouration of nail - may look white, green, yellow Nail may appear flaky or crumbling Dystrophy of nail - thickening and hyperkeratosis Investigations Nail clippings/scrapings for fungal microscopy and culture Management If dermatophyte or candida nail infection is confirmed: Topical antifungal - if very early, distal, minimal nail involvement Amorolfine 5% nail lacquer - tx for 6 months, once weekly - high failure rate If topical measures are not successful or appropriate: Dermatophyte - 1st line - oral terbinafine Candida - 1st line - oral itraconazole

Question 40

Nappy rash Pathophysiology Inflammation of the skin in the nappy area Irritant contact dermatitis The presence of urine and faecs contributes to maceration of the skin from overhydration, and increases the local pH. Friction from the nappy contributes to irritation Secondary infection can occur - candida albicans, staph aureus/streptococci

Answer 40

Clinical features Well-defined erythematous rash, oedema and dryness affecting the skin which is in contact with the nappy - buttocks, proximal thighs, suprapubic region May be papular changes present There is typically sparing of the skin folds including the inguinal creases and subgluteal creases Candida is suggested by well-defined bright red patches, the presence of papules or pustules, scale and satellite lesions

Question 41

Nappy rash

Answer 41

Management Conservative measures - high absorbency nappies, clean skin regularly & frequently change nappies Mild erythema but asymptomatic - barrier cream at each nappy change Evidence of inflammation or discomfort - topical hydrocortisone 1% OD for one week If candidal infection is suspected or confirmed on swabs - topical imidazole cream (clotrimazole, miconazole etc.) Bacterial infection - oral flucloxacillin

Question 42

Pellagra Pathophysiology Deficiency in vitamin B3 (Niacin/nicotinic acid) 1. Niacin Deficiency, caused by inadequate dietary intake of vitamin B3 or tryptophan, a niacin precursor. 2. Results in impaired NAD and NADP synthesis (essential coenzymes in cellular metabolism) 3. Which results in...Dermatitis, Diarrhea, Dementia; the "3 Ds" due to disrupted energy metabolism in skin, gastrointestinal, and nervous tissues.

Answer 42

Clinical features: 3D’s Diarrhoea Dementia Dermatitis (particularly affects sun exposed site - OE: Casal’s collar - see image below) Management Niacin supplementation: oral or intravenous nicotinamide (niacinamide) or nicotinic acid Balanced diet: increased intake of niacin-rich foods such as poultry, fish, meat, peanuts, and enriched cereals Manage underlying causes: chronic alcoholism, malabsorptive disorders etc.

Question 43

Bullous Pemphigoid Pathophysiology Autoimmune aetiology - autoantibodies vs hemidesmosomal proteins BP180 and BP230 results in sub-epidermal blistering Clinical features Typical age of onset 60-80 yrs May be a history of non-specific rash before blisters Large, tense bullae. Some rupture and form crusted erosions. Most commonly involves the flexor aspects of limbs No mucosal involvement (key feature for exam purposes vs pemphigus vulgaris)

Answer 43

Investigations Biopsy - IgG antibodies + C3 at the dermo-epidermal junction Management Dermatology referral, oral steroids are mainstay of treatment

Question 44

Pemphigus Vulgaris Pathophysiology Autoimmune aetiology with autoantibodies vs Desmoglein 3 (cell adhesion molecule) Clinical features Typically 40-60 yrs More common in Jewish and Indian populations Commonly starts with lesions on the mucous membranes, inside the mouth, or affecting the genitals. Tense blisters may later develop on the skin - can be painful

Answer 44

Investigations Biopsy - acantholysis - loss of coherence between epidermal cells due to destruction of desmoglein molecules Management Dermatology referral, oral steroids

Question 45

Porphyria Cutanea Tarda Pathology Enzyme Deficiency: Reduced activity of uroporphyrinogen decarboxylase (UROD) Often in the context of liver injury - alcohol excess, HepB/C are typical clues in questions, haemochromatosis, oestrogens can exacerbate the condition . This results in porphyrin accumulation in the liver Porphyrins accumulate in the skin, causing sensitivity to sunlight/photosensitivity This results in the typical skin manifestations - blisters, erosions, and hyperpigmentation on sun-exposed areas.

Answer 45

Clinical features Dorsum of hands and neck most commonly affected Fragile, bruised skin Photosensitive Fluid or blood-filled blisters may be present Skin may become sclerosed/ thickened and hard Milia may be present. Management Venesection if ferritin is raised Hydroxychloroquine are an alternative - aid porphyrin excretion

Question 46

Pressure Sores Key learning Localised damage to skin/underlying tissue due to pressure/sheering forces Most common over bony prominences Occurs in 6% of admitted patients Risk assess via Waterloo assessment and grade 0 to 4 Prevention with regular turning, pressure mattress, regular monitoring Management via tissue viability input for dressings Complicated by infection- consider specialist dressings, antibiotics and surgery if indicated

Answer 46

Definition Areas of skin necrosis usually over bony prominence Causes Pressure forces- i.e. person’s own weight if in bed Shear forces- sliding down bed or chair Moisture - sweat, urine faeces- increases shear forces transmitted to deeper tissues and cause dermatitis Friction Risk factors Waterlow risk assessment Used when patient admitted to a ward to stratify risk to patients. Score includes: Sex Age Weight Mobility Continence Smoking Appetite Tissue malnutrition Neurological deficit Peripheral blood supply- peripheral vascular disease, diabetes, anaemia Visual assessment skin quality Major surgery Medications (Steroids, Cytotoxics, Anti-inflammatories)

Question 47

Clinical Features & Grading 0- Skin hyperaemia 1- Skin discolouration + non-blanching erythema 2- Partial thickness skin loss or blistering with ulceration not involving subcutaneous tissue 3- Full thickness skin loss with damage and necrosis (ulcer) down to subcutaneous fat 4- Full thickness skin loss (ulcer) down to bone, joint or tendon → very difficult to heal and predisposes to fatal infection

Answer 47

Management: Prevention - continence measures, turning, nutrition. Incident report- mandatory for any pressure sore in admitted patients Healing: Led by tissue viability team Healing helped by: Pressure re-distribution- pressure relieving equipment Good nutrition Wound management- specialised dressings Hydrocolloid dressings can improve healing- moist environment VAC (negative pressure) dressings 2nd line: Maggot therapy Surgery (usually under plastics)

Question 48

Primary Hyperhidrosis Excessive sweating which can be focal or generalised, and idiopathic (primary) or secondary to another cause. Primary focal hyperhidrosis: Focal, visible, excessive sweating for at least 6 months duration , plus at least 2 of: Bilateral, symmetrical distribution Impairment of daily activities due to symptoms At least one episode per week Age of onset <25 years Family history Cessation of focal sweating during sleep.

Answer 48

Management 1st line: Aluminium chloride hexahydrate (20%) preparations (OTC) If ongoing symptoms, refer to dermatology for specialist treatments

Question 49

Psoriasis Pathophysiology A chronic, inflammatory skin condition, of autoimmune aetiology, which occurs due to hyperproliferation of abnormal keratinocytes. 2 peak ages of onset: 20-30 and 50-60 years of age Subtypes and clinical features Chronic plaque psoriasis (CPP) The most common subtype Characterised by well demarcated, erythematous patches with white/silver scale - usually on extensor surfaces such as elbows/knees Lesions may appear cracked/fissured if overlying a joint. In patients with dark skin, the lesions may have a grey appearance The scalp is usually affected too

Answer 49

Flexural psoriasis Itchy, well-demarcated erythematous patches affecting flexures, normally smooth with little to no scale Most common sites include the inguinal folds, axillae, inframammary fold, perianal region and umbilicus. The surface of the rash is smooth and shiny, with little to no scale in contrast to CPP. Pustular psoriasis Affects the palms of the hands, and soles of the feet Can become generalised and rapidly spread across the entire body

Question 50

Psoriasis Pathophysiology A chronic, inflammatory skin condition, of autoimmune aetiology, which occurs due to hyperproliferation of abnormal keratinocytes. 2 peak ages of onset: 20-30 and 50-60 years of age

Answer 50

Associated features Psoriatic arthropathy - 10% Nail involvement - onycholysis, pitting

Question 51

Management Management differs according to the subtype and distribution of disease

Answer 51

Management of Chronic Plaque Psoriasis Step 1 - Steroid AND Vit D analogue (apply at different times of the day) Offer a potent topical steroid (Cutivate (0.05%) or Betnovate (0.1%)) OD AND topical vitamin D analogue OD (e.g. calcipotriol) Step 2 - Review after 4 weeks If improvement - continue until lesions clear/almost clear If no improvement - Stop steroid and escalate topical vitamin D analogue to TWICE daily Step 3 - Review after 4 weeks If no improvement Treat with a potent corticosteroid (cutivate/betnovate) twice daily for 4 weeks OR Coal tar once or twice daily Secondary care management options include Phototherapy - UV B Systemic treatment - Methotrexate

Question 52

Management of Scalp Psoriasis

Answer 52

Step 1 - Prescribe one of: Potent corticosteroid OD for 4 weeks OR Vitamin D analogue OD OR Coal tar shampoo Step 2: Combined potent steroid and vitamin D

Question 53

Management of Flexural Psoriasis

Answer 53

Step 1: Use a mild to moderate steroid OD-BD for 2 weeks maximum E.g. hydrocortisone, eumovate, betnovate RD

Question 54

VIT D analogues

Answer 54

Vitamin D analogues Examples: Calcipotriol, tacalcitol, calcitriol Mechanism: Reduce keratinocyte proliferation Avoid in pregnancy

Question 55

Guttate Psoriasis Clinical Features Red, teardrop shaped lesions all over the body, with overlying scale History of sore throat/URTI - commonly precipitated by strep throat infection

Answer 55

Management Reassure patients that lesions usually self-resolve within 2-3 months If > 10% of body affected, refer urgently to dermatologist for consideration of UVB phototherapy Offer topical treatments as per chronic plaque psoriasis algorithm Step 1: OD potent steroid plus OD calcipotriol

Question 56

Pyogenic granuloma A benign lesion which results from the proliferation of capillary blood vessels. Causes Pregnancy Post-trauma

Answer 56

Clinical features A small fleshy, red lesion with a smooth surface - over the next few weeks rapidly grows into a raised, spherical nodule which may bleed or ulcerate. May feature a keratinised border which a white collarette

Question 57

Rosacea Pathology A chronic, inflammatory skin condition of unknown aetiology Clinical features Rosacea typically affects the face - specifically the cheeks, nose, chin and forehead There is often persistent or transient skin erythema/redness Recurrent episodes of facial flushing- often triggered by sun exposure, alcohol, temperature changes Papules and pustules may be present Facial skin thickening can occur, which often affects the nose - patients may develop rhinophyma

Answer 57

Management Management depends on the clinical phenotype/ main symptoms Facial erythema - topical brimonidine Papules/pustules Mild-Moderate: topical ivermectin (alt: metronidazole) If no improvement, escalate to mod-sev tx. Moderate-Severe: Topical ivermectin PLUS oral tetracycline (doxycycline/oxytetracycline) Erythromycin - alternative in pregnancy/breastfeeding If no improvement - refer to dermatology Skin thickening - doxycycline

Question 58

Shin Lesions Erythema Nodosum A panniculitis caused by iInflammation of the subcutaneous fat of the shins Clinical features Painful, erythematous, nodular lesions on the shin Usually self-resolve in 6 weeks without leaving scarring

Answer 58

Causes Infection - TB, streptococci IBD Sarcoidosis Pregnancy Drugs - COCP, penicillin, sulfonamides

Question 59

Pyoderma Gangrenosum Clinical features Initially PG starts as a small red papule/lesion Papule then progresses into a deep, expanding ulcer which becomes necrotic Ulcer classically has a violaceous border

Answer 59

Causes Idiopathic - majority AI disease - IBD/RA/SLE/PBC Haematological malignancy - leukaemia/lymphoma

Question 60

Necrobiosis Lipoidica Diabeticorum A granulomatous skin disorder which occurs as a complication of diabetes Clinical features NLD appears initially as small red papules on the shins, usually bilaterally The papules then enlarge into shiny, yellowy-red patches Lesions may have telangiectasia Usually painless but can be tender

Answer 60

Pretibial myxoedema A feature of Grave’s thyrotoxicosis Clinical features Symmetrical erythema of the shins, with swelling and shiny skin Other features of thyrotoxicosis - acropachy, exophthalmos etc.

Question 61

Skin Cancers Basal Cell Carcinoma Pathology The most common skin malignancy - a locally invasive of keratinocyte cancer Clinical features

Answer 61

Clinical features Nodular BCC is the most common subtype Pearly, pink/flesh coloured papule with telangiectasia May ulcerate in the centre or bleed Often have rolled edges due to the presence of central depression/ulceration

Question 62

Squamous Cell Carcinoma Pathology Locally invasive malignancy of keratinocytes 5% rate of metastatic disease Clinical features Enlarging crusty or scaly lumps, usually appearing over several weeks to months Typically arise from premalignant lesions - actinic keratosis/Bowen’s - usually in areas that have been exposed to sun (face, hands etc.) May ulcerate Often painful Risk factors: Immunosuppression (renal transplant, HIV), smoking, sun exposure

Answer 62

Management Surgical excision most commonly

Question 63

Malignant Melanoma Pathology Malignant skin cancer arising from melanocytes There are four common subtypes of melanoma with different clinical characteristics 1. Superficial spreading melanoma The commonest subtype - 60% - peak incidence 70-80yrs. Slow-growing, flat pigmented lesions which spread horizontally (radial-growth) Lesions may be asymmetrical or have irregular borders

Answer 63

2. Nodular melanoma The second commonest Usually appear as an atypical, dome-shaped nodule which grows rapidly over a few weeks to months Lesions may bleed spontaneously or ulcerate Can be pigmented or nonpigmented, might be red, black or fleshy pink 3. Lentigo maligna melanoma Typically present as a slow growing, pigmented/ brown macule The macule may be asymmetrical/ irregular in shape with atypical pigmentation which might be irregular, and feature different shades of brown, black, red etc.

Question 64

Acral lentiginous melanoma Usually occur on the soles of the feet, or palms of hand. Can also occur on the nail bed. Slowly enlarging pigmented lesions which may bleed or ulcerate

Answer 64

Acral lentiginous melanoma Usually occur on the soles of the feet, or palms of hand. Can also occur on the nail bed. Slowly enlarging pigmented lesions which may bleed or ulcerate

Question 65

Assessment ABCDE - Be suspicious of lesions which feature.. Asymmetry Border irregularity Colour variability Different - to the other naevi “the Ugly Duckling sign” Evolving - in colour, shape, size or structure

Answer 65

NICE advises using the following 7-point checklist for assessment of pigmented lesions Major criteria - score 2 points each Change in size Irregular colour Irregular borders/ shape Minor criteria - score 1 point each Diameter > 7mm Oozing Abnormal sensation - itchiness etc Inflammation NICE advised to refer urgently anyone with 3 or more points, and to consider urgent referral for any single major feature/any ABCDE features Management If there is any clinical uncertainty or suspicion of melanoma, refer the patient urgently for specialist assessment via the 2 week wait suspected cancer pathway Excision biopsy is usually performed +/- further re-excision of margins depending on Breslow thickness.

Question 66

Actinic Keratosis (Solar Keratosis) Pathophysiology Premalignant skin lesions which occur secondary to chronic sun exposure The presence of AK suggested that the patient is at an increased risk of SCC AK lesions can evolve into squamous cell carcinomas - suggested by thickened, ulcerated lesions which are enlarging

Answer 66

Clinical features Flat or thickened papules or plaques which may be scaly or crusty Vary in colour and may be pink, red or brown in colour Usually occur on sun exposed sites - hands, head, lips, ears Management Topical - fluorouracil, diclofenac, imiquimod Cryotherapy, curettage, cautery

Question 67

Xeroderma Pigmentosum Genetics: A rare, autosomal recessive disorder of DNA repair which results in impaired ability to repair DNA damage caused by UV light following sun exposure. Risk factor: It is six times more prevalent in Japanese people than in other ethnicities

Answer 67

Clinical manifestation: XP leads may present with multiple BCCs and other skin malignancies at a young age. In severe cases, it is necessary to avoid sunlight completely. The two most common causes of death in XP are metastatic melanoma and squamous cell carcinoma.

Question 68

Skin Infections & viral exanthem Nb. Some of the below conditions are discussed in more detail within the infectious disease notes Chickenpox Causative organism Varicella zoster virus Clinical features Itchy rash which begins on the face/head and trunk, then spreads to the limbs Small, erythematous macules which progress into papules, vesicles and pustules. Vesicles are often in crops. Old lesions then crust after 5 days-ish Exclusion/quarantine period Until all vesicles have crusted over, usually about 5 days after the rash appears.

Answer 68

Chicken pox

Question 69

Shingles Causative organism Post-chicken pox, VZV remains dormant in the dorsal root ganglia (DRG) Shingles results from reactivation of dormant VZV in the DRG, often when the immune system is weakened (e.g. with advancing age) The viral infection affect the dermatome that is supplied by the affected nerve root Clinical features Prodrome - dermatomal burning pain or abnormal sensation, headache, malaise Dermatomal rash then develops - begins as a maculopapular lesions, before clusters of vesicles then form. Itchy, painful. Lesions later burst and crust over. Does NOT cross the midline T1-L2 are the most commonly affected dermatomes - rash on thorax.

Answer 69

Management Admit if: Severely immunocomp’d, immunocomp’d child, ophthalmic involvement (Hutchinson’s sign), complications (meningo-encephalitis etc.) Oral antiviral medications within 72 hours of rash if: Immunocompromised Non-truncal shingles Moderate-severe rash or pain Age > 50 years - to reduce post-herpetic neuralgia Herpetic pain/neuralgia: 1st line: Paracetamol plus either NSAID or codeine If not effective - consider amitriptyline/gabapentin/pregabalin/duloxetine If severe pain - consider prednisolone within first 2 weeks (if immunocompetent), in combination with antiviral Tx.

Question 70

Measles Causative organism RNA Paramyxovirus Clinical features Prodrome: Irritable, tearful, conjunctivitis Koplik spots on buccal mucosa - 'grain of salt' appearance Morbilliform rash - Starts behind the ears then spreads to the rest of the body. Initially maculopapular then becomes more 'blotchy'.

Answer 70

Exclusion/quarantine period 4 days after the onset of the rash. Measles is highly contagious from the start of symptoms.

Question 71

Rubella Causative organism Togavirus Clinical features Pink maculopapular rash begins on the face, and spreads to the rest of the body The rash fades rapidly - and resolves by day 3-5 Lymphadenopathy - commonly suboccipital and postauricular

Answer 71

Exclusion/quarantine period Stay away from school/nursery for 6 days after the rash appears

Question 72

Erythema Infectiosum (Slapped cheek syndrome) Causative organism Parvovirus B19 Clinical features Rose-red rash on cheeks (slapped cheeks) - later spreads to the arms and body Rash may reappear after resolution when bathed in warm water - can last for months Management

Answer 72

Management Supportive measures - paracetamol, hydration Inform pregnant women who have been exposed to see their GP/midwife Infection of non-immune pregnant women with parvovirus B19 may result in complications including foetal anaemia, hydrops fetalis or foetal death. If a pregnant woman has been exposed - perform blood tests including parvovirus IgM and IgG antibodies. Recent or current infection is indicated by IgM positive - refer to specialist for close foetal monitoring, growth scans to observe for the above complications. IgG and IgM both negative - not immune and therefore susceptible to infection IgG positive & IgM negative - immune - reassure of immunity Exclusion/quarantine period Isolation from nursery/school is NOT necessary once the rash has developed, as child is no longer infectious.

Question 73

Scarlet Fever Causative organism Streptococcus Pyogenes (group A beta-haemolytic streptococci), releases erythrogenic toxins. Most common in children from 2-8 years. Clinical features - the 4 S’s of Scarlet fever:

Answer 73

Sore throat Strawberry tongue - swollen and covered in small bumps Sandpaper rash - a pinhead, punctate rash which starts on the torso, then spreads to the palms and soles. Skin then desquamates. Sircumoral (circumoral) pallor Pastia’s lines - accentuated redness in the flexor creases - axilla, inguinal folds, elbows etc. Diagnosis Throat swab Management Phenoxymethylpenicillin (Pen V) for 10 days Exclusion/quarantine period Until 24 hours after starting antibiotics.

Question 74

Hand, foot and mouth disease Causative organism Picornavirida family (coxsackie A16, enterovirus 71) Clinical features Sore throat, fever, anorexia Macular lesions on the palms and soles which evolve into red blisters, and peel 7-10 days later Painful mouth ulcers

Answer 74

Management Conservative, no school exclusion is required

Question 75

Impetigo Causative organisms Most common - staphylococcus aureus. Streptococcus pyogenes. Clinical features Most commonly on the face, around the mouth or on the extremities Macule develops into pustule/vesicle which then ruptures. The fluid dries forming a golden, honey-coloured crust, referred to as ‘cornflake lesions' Lesions are itchy, sometimes painful Impetigo can be bullous with blisters/vesicles Management

Answer 75

Management Non-bullous impetigo 1st Line: Hydrogen Peroxide 1% If unsuitable: Fusidic acid 2% or mupirocin 2% topical Extensive disease: Topical OR oral antibiotics (as below) Bullous impetigo OR systemically unwell/high risk 1st line: Oral antibiotics Flucloxacillin Pen all: Clarithromycin or erythromycin (in pregnancy Exclusion/quarantine period Exclude from school for 48hrs or until lesions have crusted

Question 76

Molluscum Contagiosum Causative organism Mollusum contagiousm virus Clinical features Dome-shaped, pearly-white or fleshy papules with central umbilication Lesions usually occur in clusters, and can affect any part of the body - often the trunk/flexures in children.

Answer 76

Management Conservative - should self-resolve within 12-18 months Exclusion from school, gym, or swimming is not necessary.

Question 77

Scabies Causative organism Sarcoptes scabiei mite Clinical features Intensely itchy rash Worse at night, disturbing sleep May be a history of family members with same symptoms/ living in overcrowded conditions (nursing home, care facilities, prisons) On examination Erythematous papules most commonly distributed in the interdigital spaces, periumbilical area, hands, wrists, axilla, buttocks etc. Thin, grey lines 0.5-1.0cm may be seen - the mites burrows

Answer 77

Management 1st line: Permethrin 5% - once weekly to all areas of the body, for two doses. All close contacts also require treatment 2nd line: Malathion Exclusion/quarantine period Children can return to school/nursery after first treatment has been completed.

Question 78

Head lice Causative organism Pediculus humanus capitis Clinical features Scalp itch Investigation Detection combing - to identify live lice Management

Answer 78

Management Wet combing removal Dimeticone 4% gel/spray Malathion No exclusion period

Question 79

Pityriasis Rosea Causative organism Viral infections (HHV-7), but evidence lacking Clinical features A herald patch appears first - a single pink/red patchy with scale 1-2 weeks later, a more widespread rash develops, characterised by well demarcated oval lesions which are pink-red in colour, and usually have slight scaling Lesions are usually on the trunk and proximal limbs

Answer 79

Management Self-limiting - should resolve in 6-12 weeks Memory aid - exclusion criteria MMR - Measles, Mumps, Rubella = 4, 5, 6 Measles - 4 days after rash Mumps - 5 days after swelling Rubella - 6 days after rash

Question 80

Urticaria Key learning Acute- < 6 weeks- often caused by viral infection or medications- penicillin, aspirin, NSAIDs, vaccines, ACEi (angio-oedema) Chronic- > 6 weeks- spontaneous, consider autoimmune /vasculitic if painful Clinical diagnosis- red itchy rash with pale centre Management- treat underlying cause, trial and titrate antihistamine, consider short term steroid course Pathophysiology Superficial swelling epidermis and mucous mumbranes Angio-oedema- deeper form- swelling in dermis and submocosal/subcutaneous tissues Mast cell-driven causing pruritus, vascular permeability and oedema

Answer 80

Epidemiology 10% prevalence Peak 20-40s Female predominance Acute more common than chronic Causes Acute Viral infection Food/other non-drug allergy Drug allergies- penicillin, aspirin, NSAIDs, vaccines, ACEi (angio-oedema) Chronic Commonly spontaneous NSAIDs Viral infections and H pylori Autoimmune including thyroiditis Extreme temperatures

Question 82

Toxic Shock Syndrome Key learning Results from bacterial toxins triggering a widespread systemic inflammatory response Most commonly Staphylococcus aureus Associated with prolonged tampon use, recent surgery and skin wounds Presents with fever, rash, hypotension, and multi-organ dysfunction. Diagnosis is clinical Managed with antibiotics and supportive care including involvement of critical care Pathophysiology Caused by toxins produced by bacteria, commonly Staphylococcus aureus or Streptococcus pyogenes. Toxins trigger a systemic inflammatory response, leading to widespread tissue damage and organ dysfunction.

Answer 82

Epidemiology Any age Commonly associated with menstruation in women using tampons (prolonged tampon use) Also associated with skin wounds, nasal packing and surgical procedures Clinical Features Often rapid onset Fever Hypotension Sunburn-like rash Headache Diarrhoae and vomiting Signs of multi-organ dysfunction (hypoxia, AKI, confusion)

Question 83

Urticaria Clinical Features Red (initially pale centre), raised and extremely itch rash Angio-oedema often affects face, tongue, genitals, hands and feet Consider vasculitic cause if painful and persists despite initial management Management

Answer 83

Management Acute often self-limiting Treat underlying cause If chronic Consider non-sedating antihistamine once a day for up to 6 weeks- can increase if treatment inadequate Severe symptoms- oral steroid course for up to 7 days 50% of chronic go into remission Refer to dermatology if above fail for consideration of long term immunosuppressants Complications Skin infection from excoriation Scarring Psychological- poor sleep, social isolation, anxiety and depression

Question 84

Venous Eczema Pathophysiology A breakdown in the skin occurring secondary to venous disease Clinical features Occur in the gaiter region (middle of the calf down to just below the malleoli) Wound edges are sloping and irregular (in contrast to the well-defined, punched out erosions seen in arterial disease) Signs of venous insufficiency - pitting oedema, hyperpigmentation secondary to haemosiderin deposition, varicose veins, lipodermatosclerosis (hardened skin, red colour, champagne bottle leg due to constriction).

Answer 84

Investigations Arrange a doppler US of both legs with ABPI to rule out peripheral arterial insufficiency ABPI of 0.8-1.3 is normal < 0.5 - severe arterial disease (compression is contraindicated) 0.5-0.8 - arterial disease (compression should be avoided) > 1.3 - suggests arterial calcification - unreliable readings (compression use with caution) Management Compression bandaging - high compression multilayer bandaging is recommended (strongest that patient can tolerate) Pentoxifylline (400mg TDS) can aid ulcer healing - increases microcirculatory blood flow Treat infection if required with antibiotics - 1st line: Flucloxacillin (pen. All: clari/doxy)

Question 85

Vitiligo Pathophysiology A chronic skin disorder characterised by areas of depigmentation, secondary to loss of melanocytes. Thought to be of autoimmune aetiology.

Answer 85

Clinical features Strongly associated with thyroid disease 10-15% of pts with vitiligo (or other AI diseases) Well demarcated macules of hypopigmentation with a “chalky” or “milky” white colour Management High SPF sun protection to areas of hypo/depigmentation Potent topical steroids OD for 1-2 months if localised vitiligo affecting < 10% of the body and not the face (not appropriate for pregnant women)

Question 90

Toxic shock syndrome Examination Findings Diffuse erythroderma Mucosal hyperemia Signs of shock- tachycardia, hypotension, reduced GCS Investigations Diagnosis is based on clinical presentation and supported by laboratory investigations i.e. positive blood cultures, raised WCC/CRP and deranged kidney or liver function

Answer 90

Management Early involvement of critical care Aggressive supportive care with intravenous fluids, vasopressors for hypotension, antibiotics targeting the causative bacteria (e.g. clindamycin, vancomycin) Management of complications such as renal failure or respiratory distress. Complications Multi-organ failure Septic shock High morbidity and mortality if not recognised and treated promptly