IRISH DERM TUTOR

This section of the website aims to cover topics at the level that could come up in either the MRCGP exam (UK), MICGP exam (Ireland) for GPs and hopefully the MRCP for non-consultant hospital doctors.

Please contact me if you can identify anything else useful that I could add.

Topics covered in order:

• Psoriasis

• Eczema

• Acne

• Rosacea

• Lichen planus

• Erythema nodosum

• Pyoderma gangrenosum

• Acanthosis nigricans

• Erythema multiforme

• Stevens-Johnson syndrome/Toxic epidermal necrolysis

Video 1: Psoriasis to TEN

• Henoch-Schonlein purpura

• Alopecia

• Dermatitis herpetiformis

• Bullous pemphigoid

• Pemphigus vulgaris

• Porphyria cutanea tarda

• Necrobiosis lipoidica

• Dermatomyositits

• Lupus (chronic discoid, subacute, acute)

• Systemic sclerosis

• Pretibial myxoedema

Video 2: Henoch-Schonlein purpura to Pretibial Myxoedema

• Bacterial infections- impetigo, erysipelas

• Fungal- Dermatophytes/candida

• Viral infections- HSV, Eczema herpeticum, VAricella, Zoster, Whitlow, Molluscum

• Genital ulcers- Syphilis, chnacroid

• Tumours- SCC, Keratoacanthoma, BCC, Melanoma

Video 3: Bacterial infections- Tumours

• Other tumours- Mycosis fungoides, Kaposi's sarcoma

• Pityriasis rosea

• Scabies

• Erythroderma

• Behcet's

• Reactive arthritis

• Pigmentary disorders-morphoea, vitiligo, melasma, albinism

• Pityriasis versicolor

• Seborrheic dermatitis

• Geneoderamatoses- Tuberous sclerosis, Neurofibromatosis

Vid 4: Other tumours- neurofibromatosis

Affects 1-3% population

Peak onsets 15-25 years and 50-60 years

Characterized by abnormally excessive and rapid growth of cells in the epidermis called keratinocytes which go through a much quicker lifecycle then usual

The underlying pathology is complex but in part due to immune dysregulation (different profile of immune cells and cytokines in skin)

Psoriatic arthritis in up to 40%- inflammatory type of arthritis. DRAMA

DIP joints affected

Rheumatoid-like arthtirtis

Asymmetric oligoarthritis

arthritis Mutilans

Ankylosing spondylitis like arhritis

Often have nail changes also (pitting - small pinprick holes, onycholysis - separation of nail plate from nail bed)

Chronic plaque psoriasis

Characterised by pink red (‘salmon pink”)hyperkeratotic plaques which often occur on extensor surfaces such as knees and elbows

Other areas that may provide clues it is psoriasis: natal cleft, behind ears, umbilicus, nape of the neck, the scalp and the hands/feet

New plaques may occur at areas of skin trauma (kobnerisation)

Guttate psoriasis: (guttate is latin for “raindrop”)

Follows URTI.

Symptoms:

Rash appears around 2 weeks after infection and it appears very acutely with multiple papules/small plaques appearing within a very short time

Palms and soles are usually spared and the diagnosis is a clinical one

Treatment:

Usually resolves over course of a few weeks.

Simple emollients (moisturisers)

For resistant causes: topical steroids or phototherapy (narrow band uvb - come in to clinic about 3 times per week for a period of about 8-10 weeks)

Pustular psoriasis

Can be generalized and this is a dermatology emergency

Get a widespread erythematous rash with pustule throughout it

Patient can be very unwell with fevers, elevated inflammatory markers, tachycardia, dehydration and electrolyte abnormalities

Patient should be admitted if have this for stabilisation of skin and may need to commence a systemic agent

Certain triggering factors can cause this:

• Sudden withdrawal of steroids

• Infection

• Pregnancy

Localised palmoplantar pustulosis:

A chronic pustular condition affecting the palms and soles

It is a localised variant of psoraisis (about 1/4 of patients will have psoraisis elsewhere)

Almost exclusively seen in smokers

Pustules are superficial and dry out leaving a brown adherent scale which peels off

Erythrodermic psoriasis:

Erythroderma means widespread erythema of the skin with >90% body surface area affected

This is just one of the caues of erythroderma

May or may not be preceded by usual type psoriasis

Patient can be quite stable with this or can be systemically unwell

Flare ups of psoriaiss can be due to – streptococcal sore throat, trauma (koebner phenomenon), beta blockers, antimalarials, lithium

Treatment psoriasis:

 Mild to moderate disease:

Topical steroids

Topical calcipotriol (vit D derivative) - eg calcipotriol (dovonex)

Often use a combination strong steroid and calcipotriol (Dovobet, Enstilar foam)

Phototherapy - narrowband uvb safer long term than pUVA so would be first choice

With more severe disease systemic treatment - eg significant body surface area affected, psoriasis in particularly troublesome areas (eg face, hands, scalp, genitals) or if it is significantly affecting the patient’s quality of life

Systemic agents:

Methotrexate

Cyclosporin

Others - Acitretin (a retinoid much like roaccutane), Apremilast, Fumaric acid Esters

Biological immune modifying agents:

TNFa inhibitors tend to be first line - adalimumab usually first agent of choice

There are increasingly more biologics becoming available to dermaotlogists for treating psoriasis

Very common

Prevalence:

• Approx 25% (15-44%) < 5 years olds have it incidence of up to 5% in children

• Approx 5-10% of adults

Co-association with asthma or allergic rhinitis in up to 50%

Lesions typically occur on flexural surfaces

Is a “barrier defect”- so lets water out of skin and the skin is very dry

Irritants/allergens can easily get into skin causing inflammation

This combination leads to constant itch which makes the inflammation worse and you get a worsening itch scratch cycle

Chronic itching and inflammation can lead to hypo/hyperpigmentation and lichenification (thickened skin with exaggerated skin lines)

It is an itchy condition and patients present with dry skin and an associated red,scaly rash

Often have secondary changes such as scratch marks and excoriations

Can get secondarily infected and can look impetiginised (golden crust) or weepy

With chronic scratching the skin can become thickened with exaggerated skin markins (lichenification) - more noticeable darker skin types

May manifest differently depending on age:

Infants (< 1 year old): often effects face first but can be widespread

School age: flexural pattern, especially elbows and knees

Adults: often localized eczema (such as hands, eyelids, flexures)

Discoid eczema

A common type of eczema in which the patches are roundish (annular/disc shaped). This type can be stubborn to treat and may require stronger topical steroids.

Treatment:

Use of regular emollients extremely important to repair barrier and maintain water in the skin

Topical corticosteroids to decrease inflammation

Oral antihistamines don’t help at all with itch

Sedating antihistamines (eg piriton) should only be used to aid sleep in circumstance that infant is not sleeping

(Topical treatments is obviously a very important thing to be aware about in GP so for more information, click here)

Chronic disorder of pilosebaceous apparatus

Get increased cells building up at infundibulum

Overproduction and build up of sebum

Good haven for colonisation and proliferation of Propionibacterium acnes leading to inflammation

Can enlarge and rupture leading to marked inflammation and scarring

Characterised in order of increasing severity by:

1/comedones (whiteheads and blackheads)

2/Papules and pustules

3/Cysts and nodules

4/Scarring- the endpoint we wish to avoid

Treating acne:

First line therapy: topical antibiotics (eg tetracyclines), benzyol peroxide or topical retinoids

2nd line: 4-6 months of low dose oral antibiotics such as tetracyclines or erythromcyin.

OCP such as dianette in females (if no contraindication)

Spironolactone occasionally used

3rd line: use of oral retinoids [isotretinoin-only prescribed by specialists]

Isotretinoin (Roaccutane) for acne has many adverse effects but is very effective, SEs include:

Causes marked dryness of skin and mucous membranes (especially lips)

Teratogenic- must exclude pregnancy during treatment as well as at 1 month intervals and should be on 2 forms of contraception

Mood issues. Difficult topic- scattered case reports of suicide with people on roaccutane in the past. Studies difficult to find causal link of roaccutane with mood issues. Risk is low but caution applied if significant personal or family history of depression.

Abnormalities of lipids and LFTs may occur (exclude before treatment and check again at maybe 8 weeks)

Other S.E- paronychia (infection at base of nail), contact lens problems, fragile skin (no waxing during treatment)

Acne fulminans: A rare, systemic disease in which severe and often ulcerating acne is accompanied by fever, arthralgia and occasionally arthritis

Chronic skin condition

Tends to affect cheeks, forehead, chin and nose

Characterised by redness, dilated blood vessels, papules and pustules and often a tendnecy to blush easily

Women more often affected

30-60s

Symptoms/Subtypes:

1/Erythema and telangiectasia of skin

2/Acneform papule and pustule formation are present especially covering cheeks, nose, chin and glabella regions (absent commedones)

3/Rhinophyma (irrregular thickening of skin of nose)

4/Conjunctivitis and blepharitis may be associated (ocular rosacea)

5/Granulomatous rosacea- persistent larger papules and nodules

Exacerbations: sunlight, heat, alcohol, consuming spicy food, hot drinks.

To distinguish from acne: absent comedones, distribution of rash (is wider in acne), effect of sunlight, age (acne not as common above 30 but can still occur)



Autoimmune disease: chronic inflammatory condition.

Immune attack targeted against basal kertinocytes.

All the Ps: Pruritic, purple, polygonal, flat topped papules/plaque often over wrists and ankles. Genitalia also affected often.

Wickham's striae present- fine, white, lacy pattern over the papules

Often get oral involvement- lacy white membrane on buccal surface of cheeks (up to 50%)

Can get nail invovlement (10%)

If affects scalp can get scarring alopecia (called lichen planopilaris)

Like psoriasis shows koebnerisation (eg trauma caues new lesions in that area)

Often idiopathic

Some associations:

Autoimmune liver disease (eg PBC)

Systemic viral disease (eg hep C)

Drugs (Thiazides, ACEi, Antimalarials)

Resolves in 12-18 months.

If mild may give topical steroids to treat symptoms. Could also consider phototherapy (eg uvb)

If more widespread and severe may give course of prednisolone or use another immunosuppressive agent of which there are many.

Acute panniculitis (inflammation of fat layer) that produces painful nodules or plaques usually on the shin.

Commonly seen in:

Infections: eg Streptococcal infections/TB

Inflammatory conditions: Sarcoidosis, IBD

Pregnancy

Medications: Penicillin/OCP/Tetracyclines/sulphonamide/sulphonylureas

Often idiopathic

Treatment:

Treat underlying cause if found

Bed rest

Compression stockings

Anti inflammatories for pain

Tends to go away over a few weeks-months



Autoinflammatory disorder

Called a neutrophilic dermatosis because lots of neutrophils are seen in the dermis on biopsy

Starts as inflammatory pustules/papules that appear on limbs and trunks

Enlarge rapidly to produce large necrotic ulcers with sloughy base- which undermines a raised purplish prominent rim. Can double size in a week

Biopsy: Intense neutrophilic infiltration in dermis, necrosis of overlying epidermis

Can show pathergy- exaggerated skin injury occuring after minor trauma (eg ulceration occuring at site where bloods were taken)

Associations:

GI- IBD

Rheum- RA, AS

Liver- Chronic hepatitis, PBC, PSC

Haem- Leuk, Lymph, myeloproliferative disorders( PRV, myeloma)

Others- DM, Sarcoid

Treatment:

Medical emergency

High dose Prednisolone to stop rapid growth

Ciclosporin when taper prednisolone

[other regimes may be used sometimes]



Get velvety thickening and pigmentation of major flexures (axilla, groin, neck)

Associations-

Stomach cancer [often more florid and late manifestation]

Insulin resistant DM

Obesity

PCOS

Drugs: NODES: nicotinic acid, OCP, dilantin (phenytoin), estrogens, steroids

Old way of thinking: Erythema multiforme- Steven Johnson- TENs were a spectrum of the same disease

This classification can cause alot of confusion

Recent consensus meeting:

E multiforme is one disorder and the Steven johnsons/TEN spectrum is a completely distinct clinical disorder.

1/E multiforme (minor and major): caused by infection or drugs

2/Steven-Johnson/TEN: almost always caused by drugs

E multiforme typical target or raised edematous papules distributed acrally usually. But can be more widespread and involve mucous membranes

SJS/TEN: widespread shallow blisters and erosions  and one or more mucous membrane erosions

SJS vs TENS:

Epidermal detachment:

 <10% Body surface area Steven-johnson

10-30% SJS/TEN spectrum

>30% TEN

Now into each in more detail:

Erythema multiforme:

Acute self limiting and recurrent condition affecting skin and mucosal surfaces.

Hypersensitivity reaction due to circulating immune complexes (often occurs 7-14 days after initial insult)

Urticaria (hive) like rash with purpura or vesicles in the centre ('target lesion' or 'bull's eye')

Target leisons not always clear cut

Often seen on back of hands, palms and forearms

Erythema multiforme minor: usually acral rash

Erythema multiforme major: involvement of larger body surface area and mucous membranes also

Associated with:

HSV

Mycoplasma pneumonia

Other infection:  Hep B, HIV, EBV, Psittacosis, Ricketts, Mumps, Orf

Drugs: Sulfa drugs, Barbiturates, Penicillin

Internal malignancy

Steven Johnson is a severe reaction in which there is sheet-like skin and mucosal loss (mucous membranes of mouth, eyes, genitalia)

Nearly always caused by medications

100 times more common in association with HIV infection.

Medical emergency

Toxic epidermal necrolysis:

More severe variant of Steven-Johnson (>30% surface area)

Rash rapidly spreads over body

Begin as large, painful, burning macules- eventually epidermis sheds to reveal a moist dermis layer underneath.

Skin biopsy aids in diagnosis

Management:

Withdraw offending agent, manage them in specialist plastics/burns unit for very careful and skin,oral and eye care

Treat any infections with antibiotics

Use of steroids/other agents is controversial

Causes: [usually occur within first 8 weeks of starting the drug]

Anbibiotics:

-Suflonamides (cotrimoxazole) [often HIV patients on this as PCP prophylaxis]

-Beta-lactams

Anticonvulsants (lamotrigine, carbamazepine, phenytoin, phenobarbitone)

Allopurinol

Anti-inflammatories- NSAIDs

[AAAA]



Palpable Purpura in dependent areas (buttocks and lower legs)

Form of small vessel vasculitis

4-15 years of age most frequently (can occur at any age) 

Male 2:1

Triggers- Streptococcal sore throat, drugs (ACEi,NSAIDs)

Get IgA depostiiton in blood vessel walls

Joint pain

Renal impairment (Severe kidney impairment in 5% of cases)

Abdo pain and minor GI bleeds 

IgA elevated in 50%. May be leucocytosis or eosinophilia.

Treatment and recovery:

Prednisolone only for severe GI or renal involvement.

Usually recovery in 4 weeks. 

 

Alopecia areata:

Autoimmune condition.

Patchy alopecia:Loss of hair that leaves single or multiple, discrete, often round, areas of shiny baldness on the scalp, beard area or any hair bearing part of body.

Alopecia totalis: all or nearly all of scalp hair gone

Alopecia univeralis: all or nearly all hair from scalp and body gone

Signs:

Disease may be active if see broken hairs at the advancing edge of lesion that look like exclamation marks= these are very short hairs, thicker distally and thinner proximally

Autoimmune associations:

Vitiligo

Thyroid disease

P anaemia

RA

DM

1/3 have positive family history

Many patients experience hair regrowth in 9-12 months, may initially be white hair when comes back.

No scarring occurs with this form of hair loss

Treatment:

Topical steroids, minoxidil, PUVA

[Trichotillomania: self inflicted pulling out of ones hair. Often arises in people with obsessive compulsive disorder. May develop as coping mechanism for stress or anxiety. Exam may reveal irregularly-shaped patches of alopecia.]

[Teloegen effluvuium- generalized hair loss that can occur after an insult ('shock to the system') such as an infection, general anaesthetic. Can occur 2 months after initial insult.]

Causes of hair loss with scarring:

Discoid lupus erythematous

Lichen planus

Scleroderma

Radiodermatitis

Hair follicle destroyed  in all above. Regrowth never occurs.

Blistering conditions

Extremely itchy condition associated with gluten-sensitive enteropathy (which may be asymptomatic)

Most common in 3rd or 4th decade

Get erythematous rash on extensor surfaces (elbow, buttocks, shoulder, scalp)

Small vesicles present

Mucous membranes may be affected.

Skin biopsy shows IgA deposits in unaffected skin

Treatment- dapsone (for itch-works almost immediately) and gluten free diet.

Less then 10% have symptoms of gluten senisitive enteropathy

Greater then 90% have abnormalities on endoscopy with 2/3 show villous atrophy on biopsy

Disease of the elderly (over 60)

Presnts with TENSE blisters with surrounding urticarial rash

Autoimmune blistering disorder characterised by presence of IgG autoantiboides to components ofthe basement membrane.

Split is deep occuring between epidermis and dermis so that blisters are tense and do not spontaneously rupture

Mouth involved in only 10%

Treatment: high dose oral steroids and taper down to dose that keeps blisters at bay.



Flaccid blisters, often present as erosions

Large areas of body can be affected and mortality without treatment is high

Mucosal involvement with ulceration (presenting sign in up to 50%)

Get soreness from blisters as they rapidly denude(appearance often one of weeping erosions)

Blisters can be extended with gentle pressure (Nikolsky's sign)

Due to deposition of IgG in epidermis, desposition higher then in bullous pemphigoid

Skin biopsy- intraepidermal split above basal layer

Treatment- high dose steroids and azathioprine (as long term maintenance)

May have increased risk of skin malignancy



Clinical effects due to increased porphyrins in blood stream. [porhyrins are part of metabolic pathway to produce haem]

Can be inherited

Usually acquired due to liver damage: get acquired decreased activity of liver enzyme uroporphyrinogen decarboxylase which blocks the pathway leading to increased porphyrins in bloodstream

    [Predisposing factors- Alcohol, smoking, oestrogens, Hep C, Haemochromatosis]

Porphyrins enter into the skin and are activated by UV light causing damage locally and giving the clinical effects

Classic example is person that is away on holiday and drinking alot. The liver damage releases porphyrins into the blood and the skin. The UV light activates them causing the damage

Presents with bullous eruptions (blisters) on exposure to sunlight.

These heal with scarring and milia (small cysts)

Also get hypertrichosis (excess hair)

Diagnosis: increased levels of plasma AND urinary porphyrins!!!

Treatment:

Sun protection, cut down alcohol

Repeated venesection

Chloroquine

Diagnosis depends on increased levels of plasma and urinary uroporphyrins

[In clinic if examine urine with Wood's lamp- urine shows pink fluorescence (shows urine porphyrins)]

[If have similar clinical features but porphyrin levels are normal it could be pseudoporphyria which is often a reaction to medications eg NSAIDs]



Unusual complication of DM (may also occur in non diabetics)

Due to small vessel damage leading to partial necrosis of dermal collagen

Skin appears thinned

More commonly seen in young/middle aged females

Skin over shins most commonly affected (often presents as erythemaous plaques that gradually develop a yellow-brown waxy discolouration with visible telangiectasia)

Treatment-  support bandaging. Low dose aspirin helps healing.

When develops over 40 years- 1/3 of patients have a carcinoma

More common in females.

Rash affects face and often extensor bony prominences of shoulder and limbs and back of hands.

Puffy, red, upper outer eyelids often seen (heliotrope rash)

Rash can be seen on knuckles and dorsal fingers (Gottron's papules)

Gross dilatation of the posterior nail fold capillaries.

Generalized photosensitive rash

Weakness of the major proximal muscle groups is also commonly seen.

Rarely involuntary muscles affected (swallowing or breathing difficulties)

Calcification in deep muscle plains occurs in childhood

Diagnosis:

Raised CPK

Muscle biopsy confirms

Most ANA positive

Presence of anti-Jo1 associated with pulmonary involvement.

Chronic discoid lupus erythematous:

Most patients with discoid lupus just have skin involvement (but 5-25% can develop SLE)

Affects sun-exposed areas

Affects face, neck, scalp and hands (female:male 2:1)

Well-demarcated plaques of scaling erythema that progress to atrophy

Plaques heal with scarring, pigment change (tend to look darker on caucasian skin/pale on black skin) and telangiectasia

Scalp lesions destroy hair bulbs leading to scarring alopecia

Diagnose often made by skin biopsy

Small proportion have circulating ANA which may indicate risk of progression to systemic lupus.

Treatment- topical sun-block and steroid creams

Systemic therapy- hydroxychloroquine (aka plaquenil)

Subacute Lupus:

Precipitated by sun exposure

Can look like psoriatic type papulosquamous rash or get annular (circular) plaques that are clear centrally. No scarring.

Medium assocaition with SLE

Anti-Ro positivity high in this population

Can be due to drugs (anti seizure meds, anti-TNF, PPIs)

 Acute cutaneous lupus:

Highest association with a SLE

Classic presentation is the malar eruption or 'butterfly rash'

Other variants of acute lupus: photosensitivity, bullous lupus, chelitis and mouth ulcers, papular rash on arms which can form large plaques

Features include-

Firm skin which may be discoloured sometimes with 'salt and pepper discolouration' 

Microstomia

Facial telangiectasia

Beaking of the nose.

Raynaud's is seen in 90-95% with systemic scloerosis (colour change: white to blue to red

Male:female SS 1:3

Usually divided into 2 subsets: limited and diffuse.

Limited: Skin affected below elbows and knees (can involve the face)- associated with features of CREST sydnrome. Anti-centromere antibody strongly associated with limited and CREST.

CREST syndrome (calcinosis, raynaud's, esophageal dysmotility, sclerodactyly, telangiectasia) 

Diffuse: Skin affected can be above elbows and knees on the body. This subtype more likely to have kidney, heart and joint problems.

Scl-70 is unique to systemic sclerosis and is more likely to be associated with severe disease affecting the lungs. Commoner in diffuse subtype.

ANA positive in majority of subtypes of systemic sclerosis.

Lung involvement can occur in systemic scleorsis:

1/Pulmonary vascular disorder evolving over time into pulmonary hypertension

2/Interstitial lung disease.

Transfer factor is reduced with pulmonary fibrosis - this is the earliest sign of fibrosis in systemic sclerosis;

Lupus Pernio:

Due to sarcoid disease. Can get diffuse bluish plaque on nose and on closer insepction small red papules in lesion , can also get on ear lobes.

[will aim to get picture of this]

Is a rare complication of Grave's disease.

Get raised indurated pinkish patches.

Can occur anywhere but typically occurs on the shins and dorsum of the feet.

High titre of TSH receptor antibodies would be expected



Impetigo:

Impetigo is a common bacterial skin infection. 

Usually due to Staph aureus but can be due to beta haemolytic strep also (eg strep pyogenes)

Can get pustules and the classic honeycomb coloured crusted erosions. 

One subtype is bullous impetigo in which you can get blisters which occurs due to staph exfoliative toxins

Local- topical antibiotics (eg mupirocin)

Widespread- oral flucloxacillin

Erysipelas:

More superficial form of cellulitis

Unlike cellulitis almost all cases are casused by Group A beta haemolytic strep (strep pyogenes)

Get distinctive warm, red, tender skin lesion with induration and sharply defined, raised, rapidly advancing border

Vesicles or bullae may develop. 

legs and face are comonly affected

Raised WCC, blood cultures positive in 5% of patients

Treatment is with IV antibiotics such as benzylpenicillin and erythromycin.

Ddx:

DVT, necrotising fasciitis, contact dermatitis

The infection can cause damage to the surrounding lymphatics leaving the patient prone to lymphoedmea and recurrence of hte infection

Dermatophytes:

Diagnosis made by microscopy of scrapings taken from lesion.

Clinical: Get erythematous plaques with scaling border and area of healing in the centre

Dermatophytes named tinea. Then named depending on the location of the infection irregardless of the type of microorganism.

Tinea Coroporis: body

Tinea Pedis: feet

Tinea cruris- more common in men and also during hot and humid seasons. It may extend to the inner thighs and backwards to the perineum and anus. Most often the infection spreads from the toe webs to the groin.

Tinea manum: Can get a dry and scaly form which commonly affects only one hand. The feet should be examinesd as they are often infected.

Tinea pedis: Commonest fungal infection. Primary lesions consist of maceration, scaling, occasional vesicles and fissures between and underneath the toes. Any or all of the toe webs may be affected although the most affected web space is the fourth.

Onychomycosis: Tinea affecting nails represents about 30% of all superficial fungal infections. Nails are usually discoloured soft, brittle and may loosen away from the nail bed . Commonest form starts distally in the nail plate.

Tinea incognito:

The name given to tinea when appearance has been altered by inappropriate treatment (usually topical steroid cream)

Original infection slowly extends

Often doctors thinks its a dermatitis instead of fungal infection

The steroid cream dampens down inflammation but when cream is stopped for a few days the rash gets worse and has altered appearance

Tinea capitis (infection of scalp) due to T. Tonsurans, M. Canis, T. Rubrum or T. Verrucosum

M canis is zoophilic (derived from animals)

Favus:

A type of tinea capitis. Is rare in the UK and USA but get in middle east, south east europe, mediterranean and africa. Cup shaped crusts called scutulae form around loose hairs. Scarring alopecia is common.

Due to Trichophyton schoenleinii

When the lesions fall off the portion of scalp affected is usually hairless.

Tinea diagnosis:  Microscopy of scrapings in potassium hydroxide

Tinea management:

Topical preparation such as miconazole (daktarin) or ketoconazole

More severe- oral antifngals (eg itraconazole)

[prolonged treatment for up to 4-6 weeks is usually required for body/scalp lesion, up to 6 months for nail infections]

Candida:

A group of yeasts

Particularly affects moist areas such as flexural areas like the groin and under the breast

Commonly seen under occluded surfaces so often in nappy rash

Often see satellite lesions extending beyond the main rash

More common in immunosuppressed patients (eg DM/HIV/Steroids)

Can get oral candida and vaginal candida infection

Herpes family:

Herpes Simplex Virus:

Localized vesicles and blistering.

Oral involvement more frequently due to HSV 1

Genital ulcers: herpetic ulcers are the commonest cause of genital ulcerations in the developed world. 80% are caused by HSV 2 and 20% by HSV 1. Primary lesions are painful and associated with enlarged lymph nodes.

Treat with antiviral (eg aciclovir, valciclovir)

Eczema herpeticum- patients with atopic eczema are prone to infections with HSV which become disseminated throughout the eczematous areas (aka Kaposi's varicelliform eruption)

Patient can be unwell and is medical emergency

If affects eye can cause blindness if not treated appropriately

Treatment with acyclovir required

Suspect when get severe flare of eczema with punched out lesions.

Chicken pox (varicella): distributed centripetally with trunk affected more than extremities. Individual lesions are in various stages of development (macules, papules, vesicles, crusted and healed lesions).

Classical lesion that is often cited is the dew drop on a rose petal appearance.

Chickenpox in adults:

More serious then in children.

Varicella pneumonia occurs in up to 20% of adults with chickenpox occuring 3-5 days into the course of the illness.

Symptoms include

Tachypnoea, cough, dyspnoea, fever.

Cyanosis, pleuritic chest pain and haemoptysis are common

Treat with aciclovir

Zoster (shingles): more common in elderly and immunosupressed. It is caused by activation of dormant virus which has been living in dorsal root ganglia nerve cells in the spine after previous exposure to chicken pox. When reactivated it migrates down the sensory nerves to cause herpes zoster lesions. Pain preceding the characteristic vesicular lesions is typical.

Special cases Zoster infection:

Post herpetic neuralgia- can persist for years. Treatment is challenging and patients may require antidepressants, carbamazepine or ablation of the affected ganglion.

Ramsay Hunt- get reactivation of the zoster virus in the geniculate ganglion (collection of sensory neurons of the facial nerve) resulting in pain and vesicles in the ear, ipsilateral facial palsy and sometimes impairment of taste on the same side.

If  the opthalmic branch of the trigmeninal nerve is affected - may cause corneal ulcers and blindness.

Herpes simplex infection of the eye in general often affects the cornea (keratitis) and can lead to corneal ulcers ('dendritic'-branching ulcers). Recurrences are common and may result in blindness.

Herpetic whitlow: was commonly seen in dentists, dental hygienists and other health workers before universal use of gloves. Now more common in children. Get pain and vesicles/blistering in pulp of finger. Can get tenderness, erythema and deep seated blisters in nail fold.

 Molluscum Contagiosum:

Umbillicated, pearly papules 2-5mm in diameter

Often seen in childhood

Caused by a DNA pox virus called molluscum contagiosum virus (MCV)

Commonly occur on face, especially near the eyelids; also occur on genitals and trunk

Treat with cryotherapy, liquid nitrogen or curretage.

Can be seen in patients with advanced HIV/AIDs

Syphillis:

Primary syphillis:

Chancre: Small, firm and painless ulcer

Can get lympadenopahty close to ulcer.

Secondary syphillis:

Develops 4-12 weeks after primary infection.

Characterised by :

Macular or papular rash which is symmetrical on the trunk and limbs as well as the palms and soles

Rash is pale pink and non itching

Confluent plaques (conylomata lata) may form in moist flexures (eg groin, around buttocks)

Small grey or white erosions may be seen on buccal mucosa

Patients may get muscle and joint pains, headaches and fevers

Generalized lymphadenopahty is common.

Chancroid:

Caused by H ducreyi and is commonest cause of genital uclers in Africa (4-7 day incubation period)

Erythemaous papule breaks down into a painful ulcer and several ucler merge to form giant lesions

See ulcers on prepuce and freunulum and vaginal entrance and perineum i women

Get inguinal lymphadenopathy which is usually unilateral and can suppurate

Diagnosis: isolating organism from swabs and culturing on chocolate based media

Treatment- co-trimoxazole or tetracycline.

 SCC:

SCC spectrum:

Actinic (solar) keratosis-----SCCis (aka Bowen's disease)-----SCC

Actinic keratosis (scaly erythematous areas)- dysp

SCC in situ (aka Bowen's disease)- thicker plaques, often seen on legs in elderly patients

SCC (tips that is invasive: tenderness and induration under skin)

Squamous cell carcinoma: malignancy of keratinocytes

Seldom seen in people aged under 45.

Usually occurs in sun exposed areas such as the face and lower lips. It is the second most common type of non-melanoma skin cancer (after BCC)

On exam is often tender and often indurated

Mets- spreads to distant sites by lymphatic channels

Risk of mets- depends on size and location. (ears and lips high risk of mets)

Diagnosis and treatment:

Biopsy for diagnosis

Radical surgery and sometimes radiotherapy. (95% cure rate if prompt and complete excision carried out)

40% risk of developing additional SCC in next 2 years.

Prognosis:

5 year survival 73%

Keratocanthoma-

Low grade malignancy that resembles squamous cell carcinoma pathologically. It is seen mostly on sun exposed sites.

Develops from hair follicle, more common in males.

It is usually solitary but may be multiple. It presents as a fleshy, elevated and nodular lesion with a central hyperkeratotic core.

Most significant feature is its rapid growth.

Short history and rapid increase in size suggest kerathoacanthoma rather than squamous cell carcinoma.

Don't spread elsewhere.

Basal cell carcinomas:

Commonest cutaneous neoplasm in humans (85% are on head and neck)

Major RF BCC is sun exposure

Nodular basal cell carcinoma:

Commonest facial BCC

Prominent telangiectasic vessels on surface of lesion

Border of lesion is translucent, looks pearly white and is slightly raised

Superficial BCC occur more frequently on trunk and extemities and present with scaling, irregular plaque. Again have pearly-white raised border.

Morphoeic BCC (aka sclerosing BCC)

Waxy, scar-liiek plaque with indistinct borders

Get wide and deep subclinical extension so need to be very careful with these

Rare compared to other BCCs

Treatment and prognosis:

Excision surgery for large and deep tumours (nodular, morephoeic)

For superficial BCCs can consider cryotherapy, certain topical agents and photodynamic therapy

Cure in more than 90%

Moreaphorm BCCshave highest recurrence

Melanoma: malignancy of melanocytes

ABCDE criteria for diagnoisis

Asymmetry

Border irregularity

Colour variability

Diameter >5mm

Evolving lesion with changes over time

(also look for bleeding, itching, satellite lesions)

Excision biopsy is key for diagnosis and determining prognosis with Breslow's thickness

Acral lentiginous melanoma:

Normally seen on sole of foot and occasionally or palm of hand
Seen often in darkly skinned races

Poor prognosis

Lentigo maligna

Represents increased number of atypical looking melanocytes at dermo-epidermal junction

Is a type of malignant melanoma in situ

Occurs on facial or sun-exposed skin of patients in their 60s or older

Often very slow growing over years-decades

If invades the dermis is then a lentigo maligna melanoma and behaves like a melanoma (suspect if get thick, darker or get discrete nodules)

Mycosis fungoides (cutaneous T cell lymphoma)

Atypical lymphocytes seen in epidermis and dermis

Usually has low grade clinical course and can remain in one stage (patch-plaque-tumour) for a number of years

Initially presents as a pruritic eczematous rash (pre malignant). Can get an appearance of "cigarette paper" atrophy on the surface. Lesion slowly progresses to thick plaque.

As more lymphocytes infiltrate it progresses from a patch to a plaque to a thick tumour

As malignancy develops nodular lesions appear and proceed to become necrotic.

Kaposi's sarcoma:

Associated with HHV 8

Is a reactive hyperplasia of the vascular endothelial cells. Not really a neoplastic lesion

Lesions are blue-red, firm, warty and neither painful nor itchy.

Nowadays usually seen in young HIV positive men (lesions found here on tip on nose,neck and buccal mucosa)

Prior to AIDs epidemic- a rare tumour of elderly men affecting the legs usually and associated with lymphoedema

Likely viral cause

First clinical lesion in pityriasis rosea- “herald patch” which is an isolated erythematous patch appearing on the trunk surrounded by ring of scaling skin

A number of oval macules appear on the upper arms, remainder of trunk and upper thighs about 2-4 days later. Tend to spread out along rib cage in a 'fir tree' type pattern

Involvement of hands, feet or scalp is rare

Severe itch uncommon

Usually remits within 4-8 weeks.

Occurs more in Spring and Autumn

Treatment:

No specific treatment

Systemic antihistamines, moisturisers may help with itch.

Topical steroids don't shorten duration of disease.

Due to parasitic mite Sarcoptes scabiei

Itchy excoriated papules on finger webs, elbows, ankles, axilla and genitalia

Rarely causes blistering

Burrows of the scabies mite are seen and patchy excoriated fissured eczema occurs

Adult males develop itchy penile nodules. Infants get nodules on palms or soles

Treatment: Permethrin cream (lyclear) to whole body at day 0 and day 7.

Any inflammatory skin disorder covering in excess of 90% of the body surface leading to skin failure.

In adults most common is eczema followed by psoriasis, leukaemia/lymphoma, drugs and a condition called pityriasis rubra pilaris

Sequelae include high output cardiac failure, hypothermia, loss of fluid and albumin and increased susceptibility to infection.



Classic triad- recurrent oral ulcers, recurrent genital ulcers, iritis.

Recurrent oral ulceration. Can effect eyes causing blindness. Also can get genital ulceration. Diagnosed aided by a positive skin pathergy test (development of pustules at venepuncture sites)

Other features- fever, abdo pain, diarrhoea, episcleritis, polyarteritis, arterial and venous thrombosis, pericarditis.

HLA B5 associated with ocular disease; HLA B12 with reurrent oral ulcers.

Treatment is with steroids or colchicine.

Autoimmune reaction to an infectious agent [bacteria- genitals (chlamdiya), bowel (campylobacter, shigella, salmonella)]

Classic triad of:

1/Non-suppurative polyarthritis

2/Inflammatory eye disease (Conjunctivitis early and may be followed by iritis)

3/Urethritis

[can't see, can't pee, can't climb a tree (arthritis usually affects lower limbs)]

Skin lesions often occur on the feet with pustules and hyperkeratosis (keratoderma blennorhagicum) May also get erosive lesions affecting penis (circinate balanitis) or mouth

Rare complications- heart block, aortic incompetence, pericarditis.

Melasma:

Hormonally stimulated increase in melanin pigment that mainly appears on face (affects both pregnant women and those taking the OCP)

Get hyperpigmentation which is augmented by sunlight.

Takes many months to resolve after delivery

MSH levels are normal

Affects women with darker skin tones

Morphoea (aka localised scleroderma)

Firm, white or violaceious patch of thickened skin on any body site (usually thighs, trunk and upper arms)

Affects kids and young adults

Developing lesions have well demarcated red or violet peripheral edge

As activity burns out- the edge assume the same colour as the central lesion and lesion itself becomes very firm with atrophic glazed surface appearance

A linear variant of morphoea may be seen on scalp and face of kids (en coup de sabre)

Vitiligo:

Autoimmune condition

Acquired areas of skin depigmentation due to loss of melanocyte function

Associated with type 1 DM, coeliac disease, autoimmune thyroid and Addison's

Biopsy- epidermal melanocytes lost from basal layer of epidermis

Treatment generally unsatisfactory

Condition also occurs in darker skinned races

Albinism:

Group of inherited abnormalities of melanin synthesis charcterised by congenital reduction/absence of melanin pigment in association with specific developmental changes in the optic system resulting from hypopigmentation.

At much increased incrased risk of skin cancers due to lack of protective pigmen

Oculocutaneous albinism involves 2 regions of body:

Skin and hair

Optic system including eye and optic nerves.

Ocular albinism- just optic system affected

Caused by yeast malassezia furfur (normal commensal but causes this reaction in some people)

White untanned skin: pale brown/pink macules which are often hardly visible

Tanned skin: appears pale, white and slightly scaly (yeast affects tanning)

Diganosis:

Wood’s light: yellow green fluorescence

Microscopy: hyphae and yeast cells (spaghetti and meatballs)

Treatment:

Topical antifungals (clotrimazole, terbinafine)

Systemic antifungals rarely required

Condition can recur.

Caused by a yeast infection (malassezia furfur)

Is very  common in immunosupressed patients and neuro patients (parkinson’s)

Treat with topical antifungal (eg miconazole)

Tuberous sclerosis

AD with variable expression

Epilepsy in infancy or childhood

Mental reatardation often seen

Angiofibromas

Elevated hypopigmented macules (ash leaf pathces) often seen

Periungal fibromas arise as pink projections from nail folds

Shagreen patch is angiofibromatous raised plaque usually on back

Fundoscopy may reveal white streaks along fundal vessels

Neurofibromatosis:

Type 1: mixture of skin features: cafe au lait spots (>6), axillary freckling, cutaneous neurofibromas, lisch nodules (multiple brown deposits in the iris of the eye), optic nerve gliomas.

Develop over years but pace may increase with puberty and pregnancy.

Many other features:

HTN

Learning difficulties/behavior problems

Type 2:

Not as many skin features

More CNS tumours (acoustic neurofibromas common)

Juvenile cataracts