Dermatology

Any atophy in PMH: astham, eczema, hayfever
Childhood skin problems

SH: ask about sun exposure, occupation, regular burn, going abroad

DH: any new medications started, new creams / cosmetics

chronic inflammatory dermatosis notable for open / closed comedones [black and whiteheads], and papules / pusutles / nodules

+ve FHx [genetic]
Androgens [testosterone and DHEAS] stimulates sebaceous gland activity and sebum production
Adolescence age
External factors like diet, stress, pollutant exposure

Increased sebum production from increased androgens. This provides a lipid rich environment which favours the proliferation of skin microorganisms and leads to follicular occlusion

Hyperkeratinisation leads to keratinous plugs / microcomedones

Inflammation with interleukins and TNF-alpha

comedones like whiteheads [closed] and blackheads [open]

Papules and pustules formation leading to nodules and cysts = leads to scarring

a very severe acne form associated with systemic upset

mild: white / blackheads +/- sparse inflammatory lesions

moderate: widespread non-inflammatory lesions + papules and pustules

severe: extensive inflammatory lesions including nodules, pitting and scarring

mild-moderate: 12 weeks course of topical combination therapy [topic adapalene + benzoyl peroxide OR topical tretinoin + clindamycin]

moderate to severe: 12 weeks cause of same as above + / - oral doxycycline

COCp can be used as an alternative to oral ABx in women

Use either 1 highly effective methods like an IUD or 2 complementary user dependent like barrier + oral contraceptives.

this is because Isoretinoin is a potent teratogen and strict adherence to the pregnancy prevention programme (PPP) is needed.

px with acne conglobata [v severe form]

px with nodulo-cystic acne

consider referall: if not responding to 2 completed courses, OR if not responding to previous Tx that has an oral ABx, OR acne with scarring OR acne causing significant psychological distress

bacterial infection of the dermis and deeper subcutaenous tissue

causes: staph aureus, group A / C strep, MRSA

Usually via a breach in the skin barrier which provides an entry. Breach via trauma, eczema, fungal, ulcers

usually on shins unilaterally

Erythema is reasonably well defined. Blisters / bullae in more severe cases

Swelling and if golden yellow crust seen, indicates staph aureus

systemic: fever, malaise, nausea

clinical, no further investigations needed

if px is admitted and speticaemia is suspected, do bloods and cultures

Eron classification

class 1: no systemic signs and no uncontrolled co-morbidities

class 2: systemically unwell or well with co-morbidities like obesity or PAD which may complicated Tx

class 3: significant systemic upset or unstable co-morbidities

class 4: sepsis syndrome or severe life threatning infection like necrotising fasciitis

Eron class 3 and 4
severe / rapidly deteriorating cellulitis
very young px < 1yr, or frail
immunocompromised
significant lymphoedema
facial / periorbital cellulitis

oral flucloxacillin first line

ALT: give clarithromycin / erthryomcin or doxycycline

admission may not be necessary, check local guidelines

oral / IV co-amoxiclav or clindamycin

IV cefuroxime / cefriaxone

form of cellultis caused by group A strep pyogenes. Usually sharp demarcated borders from normal skin and affects the upper dermis and extends into the superficial cutaneous lymphatics

same management as cellulitis

the most common subtype. Well demarcated red, scaly patches affecting extensor surfaces, sacrum and scalp

will see smoother skin compared to plaque psoriasis

transient psoriatic rash frequently triggered by strep infection. Multiple red / tear drop lesions on the body

usually resolves spontaneously within 2-3 months. Otherwise treat like psoriasis

Tonsillectomy may be necessary with recurrent episodes

commonly on palms / sores. Not infectious pus but the px are systemically unwell. Treated as a medical emergency and requires admission to hospital

rare severe form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin. Will see large patches of exfoliation resulting in raw exposed areas.

Medical emergency and needs admission

skin changes are caused by the rapid generation of new skin cells, resulting in an abnormal buildup and thickening of the skin.

Genetic associations: HLA B-13 / 17

worsened by skin trauma and stress. Triggered by strep infection

generally, dry / red / scaly patches on the skin, usually over the extensor surfaces of elbows / knees / scalp

think about psychosocial implications: low mood, low self-esteem, depression

Auspitz, Koebner

residual pigmentation of skin after lesions resolve

small bleeding where the plaques are scraped off

development of psoriatic lesions to areas of skin affected by trauma

1st line: potent topical steroid [beclamethasone] + vitamin D analogue [cholecalciferol], daily

2nd line: if no improvement after 8 weeks, double the vit D to BD

3rd line: no improvement after 12 weeks, potent corticosteroid BD for 3 weeks OR coal tar preparation applied OD / BD

phototherapy: narrow UVB light given

Photochemotherapy: psoralen + UVA light [PUVA]

Systemic therapy: methotrexate, ciclosporin, systemic retinoids, biologic agents

potent topical steroids OD / 4 weeks

if no improvement, use a different combination of topical agents

mild-moderate potency corticosteroid applied OD / BD daily for 2 weeks

can cause skin atrophy / striae / depigmentation and rebound sx

should not be used for more than 1-2 weeks

recommend a 4 week break between topical steroids if starting a new regime

causes less cell division leading to less epidermal proliferation. adverse effects are uncommon and these can be used long term.

Avoid in pregnancy, max dose is 100g for adults

chronic atopic condition caused by defects in the normal continuity of the skin barrier [irritants, allergens, microbes], leading to inflammation of the skin

coin shaped eczema patches that are itchy. Treat via moderately
potent corticosteroid + emollients like betamethasone

usually present in infancy with dry / red / itchy / sore patches of skin over the flexor surfaces and on the face / neck

eczema gives bacteria an opportunity to cause cellulitis, usually staph aureus

treat via flucloxacillin

avoid hot water baths, scratching / scrubbing skin, using soaps / body washes that remove the natural oils in the skin

reduce environmental triggers that can make sx worse like temperature changes, certain foods, washing powders, emotional event

artificial barrier over the skin via an emollient, used after washing and before bed

ex) E45, Aveeno, Cetraben

thicker emollients + topical steroids + wet wraps

treat any bacterial / viral complications

finger tip units. 1 FTU = 0.5g

severe primary infection of the skin by HSV 1 / 2. more common in children. Will see monomorphic, punched out erosions, 1-3mm in diameter

admit and give IV aciclovir

Lund & Bowder Chart Or Wallace’s rule of 9

head + neck = 9%
each arm, each anterior / post part of the leg = 9%
ant / post chest = each 9 %
ant / post abdomen = each 9 %

superifical epidermal: red and painful, no blisters

partial thickness. pale pink painful, blistered. Slow CRT

partial thickness to the deep dermal. typically white but may have patches of non-blanching erythema. Reduced sensation , painful to pressure

full thickness. white / leathery brown / black in colour. no blisters, no pain [no sensation]

all deep dermal and full thickness burns [2nd and 3rd degree]
any 1st degree over 3% of total body surface area [2% in children]
any second degree involving face / hands / feet / genitalia / limbs
Any inhalation injury
Any electrical / chemical burn injury
Suspicion of non-accidental injury

ABC. remove appendage from source, irrigate heat burn with cool water and cover burn.

Electical burns: turn off the power supply

Chemical burns: brush off any powder and irrigate with water. Neutralising attempts are NOT recommended

inflammatory response to burn area. Will see systemic CVS effects due to fluid loss and sequestration of fluid into the third space.

Immunosuppression is common with large burns and sepsis is a common cause of death following major burns. [commonly bacterial translocation from the gut lumen]

early intubation for smoke inhalation or injury to face / neck

IV fluids via Parkland formula, give half of the amount in the first 8hrs

insert catheter, give analgesia and transfer to burns unit

Escharotomy may be needed to divide burnt tissue. Skin grafting is considered.

Volume = TBSA of burn in % * kg * 4

a local / generalised superficial swelling of the skin. Can be acute or chronic

usually allergies to food / medication / animals
contact with chemicals / latex / stinging nettles
insect bites
viral infections
dermatographism [rubbing of skin]

Idiopathic
Inducible by: sunlight, temp change, exercise, strong emotions, hot / cold weather, pressure
Autoimmune like SLE

small itchy lumps on skin ~ associated with patchy erythematous rash. Can be localised to a specific area or widespread. Angioedema and flushing of the skin may be seen

non-sedating antihistamine [Fexofenadine]

for flare ups, oral steroids can be considered

refer to specialist for problematic cases with Tx like cyclosporin and LTRAs

severe systemic reaction of skin / mucosa due to a drug reaction

RF: HIV

penicillins, sulphonamides [cotrimoxazole], anti-psychotics [phenytoin, carbamazepine, lamtrogine], allopurinol, NSAIDs, COCp

Non-drug causes: infection, vaccination

maculopapular rash with large lesions, may later develop into vesicles / bullae

+ve Nikolsky sign

Mucosal involvement, systemic sx [fever, arthralgia]

scalp / palms / soles spared

+ve sign is when blisters / erosions appear when skin is rubbed gently

clinical but skin biopsy can be done to confirm diagnosis

will see epithelial necrosis with few inflammatory cells

admit for supportive tx, refer to dermatology / burns unit for tx

specialist guided steroids, immunoglobulins, immunosuppressants

seen secondary to a drug reaction, will see a scalded appearance over an extensive area.

A more severe SJS

phenytoin, sulphonamides, allopurinol, penicillins, carbamazepine, NSAIDs

pyrexia / tachycardia

+ve Nikolskys sign

biopsy will show: full thickness epidermal necrosis with subepidermal detachment

stop precipitating factor. ICU + IV fluids

1st line: IV immunoglobulins

SJS < 10% TBSA, TEN is > 30%

between the two, is an overlap

pruritus seen in the last trimester

lesions are often on abdominal striae, sparing the periumbilical area

management depends on severity: emollients, mild topical / oral steroids

acute, self-limiting rash affecting young adults. Thought to be linked to herpes hominis virus 7

resolves after around 6 weeks

majority have no prodrome, might see a viral infection beforehand

Herald patch on trunk, followed by erythematous / oval / scaly patches which follow a characteristic distribution parallel to the line of Langer = fir tree appearance

when >95% of the skin is involved in a rash of any kind

eczema, psoriasis, drugs, lymphomas, leukaemias, idiopathic

Results from progression of chronic plaque psoriasis. Associated with mild systemic upset and can be triggered by many things such as withdrawal of systemic steroids. Need to be admitted for management

hypersensitivity reaction triggered by infection. divided into major and minor

HSV virus, idiopathic, streptococcus, drugs [penicillins, sulphonamides, allopurinol, NSAIDs, carbamezepine], CT disease like SLE sarcoidosis, malignancy

target lesions initially on dorsal hands / feet before spreading to torso. mostly on UL. + mild pruritus

more severe form and is associated with mucosal involvement

infection [strep, TB], systemic disease [sarcoid, IBD, Behcets], Malignancy, drugs [penicillins, sulphonamides, COCp], pregnancy

inflammation of subcutaneous fat usually causing tender, erythematous, nodular lesions. Usually on shins / forearms

resolves within 6 weeks , no scarring

autoimmune condition causing sub-epidermal blistering of the skin. Secondary to development of antibodies against hepidesmosomal proteins BP 180 and 230

itchy, tense blisters around flexures. usually heals w / o scarring

Type 4 hypersensitivity drug reaction with eosinophilia and systemic sx

anti-epileptics, allopurinol, olanzapine, sulphonamide ABx

high fever / tachycardia. Morbilliform [rash that looks likes measles] eruption. Haematological abnormalities, high WCC count, inflammation of internal organs

stop suspected causative medication. monitor + supportive care. consider systemic steroids

vascular birthmarks seen on half of newborn babies, often called stork marks / bites. Usually on forehead / eyelids / nape of neck

usually fade over a few months but can persist

superficial cutaneous fungal infection caused by Malassezia furfur

RFs: healthy individuals, immunosuppression, malnutrition, cushings

mostly trunk. Hypopigemented pink / brown patches. Mild pruritus and scale is common

topical antifungal: ketoconazole shampoo

if this fails, consider alternative diagnoses and give oral itraconazole

rare, non-infectious, inflammatory disorder. A very uncommon cause of very painful skin ulceration. Usually on LL

idiopathic, IBD, rheumatological, haematological [myeloproliferative], granulomatosis with polyangiitis, primary biliary cirrhosis

neutrophilic dermatoses: dense infiltration in the affected tissue, seen on biopsy

on LL. initially, a sudden small pustule / red bump / blood blister. Later the skin breaks down and ulcerates. Borders of ulcer is purple. Systemic features

clinical, histology only really useful to rule out other causes of an ulcer

oral steroids first line.

Immunosuppressive therapy via ciclosporin and infliximab.

Surgery once disease process is controlled on immunosuppression

chronic dermatitis thought to be associated with fungus malassezia furfur. Associated with HIV and Parkinsons

Eczematous lesions on the sebum rich areas like scalp / periorbital / auricular / nasolabial fold.

Salmon pink, scaly, ill defined plaques seen

otitis externa [common] and blepharitis may develop

for scalp: ketaconazole 2% shampoo

for face and body: topical ketoconazole, steroids

Seborrhoeic dermatitis seen in nappy area / scalp / face / limb flexures of babies. Will see erythematous rash with coarse yellow scales

reassure, topical emollient on scalp. Imidazole if persists. will resolve spontaenously by around 8 months of age

non-allergic, due to weak acids or alkalis from detergents

will be seen on hands with erythema and crusting. more painful than itchy

type 4 hypersensitivity reaction. often seen after dyeing hair. will see intense pruritus.

give topical potent steroid and avoid offending agent

autoimmne disease caused by antibodies directed against desmoglein 3, a cadherin type epithelial cell adhesion molecule. Common in Jewish population

will see mucosal ulceration. .skin blistering and easily rupturing vesicles and bullae. lesions are painful but no itchy. +ve Nikolskys sign

acantholysis on biopsy

most common type of cancer in the West. Lesions are also known as “rodent ulcers”. Characterised by slow-growth and local invasion

UV exposure
Hx of sunburn in childhood
Skin type 1 [always burns, no tanning]
increasing age
Male
Immunosuppression

occurs mostly in sun-exposed sites like head / neck. Initially pearly, flesh-coloured papule with telangiectasia. Can later ulcerate, leaving a central crater

Routine derm referral. 2WW if concerned that delay will have significant impact

Medical: topical imiquimod / fluorouracil, cryotherapy, radiotherapy, curettage

Surgical removal is also an option

excessive sun exposure / PUVA therapy
Acitinic keratoses and Bowens disease
Immunosuppression
Smoking
Long-standing leg ulcers
Genetic condition [xeroderma pigmentosum]
Associated with HPV

typically on sun exposed sites such as head / neck OR dorsum of hands / feet

Rapidly expanding, painless, ulcerating nodules
Cauliflower like appearance, there may be areas of bleeding

Surgical excision with 4mm margins IF lesion is less than 20mm in diameter

If larger than 20mm, margins increase to 6mm

Mohs micrographic surgery is used in cosmetically important sites or in high risk px

sun exposure, fair skin, FHx, naevi count, immunosuppression

Asymmetry, Border irregularity, colour variation, diameter of 7mm or more, evolving

70% of cases. typically in young people’s arms / legs / back and chest. Will see a growing mole with changes in size / shape / colour with perhaps oozing or bleeding

second most common. usually in middle aged people’s sun exposed areas.

will see a red / black lump that bleeds or oozes

seen in older people, chronically sun exposed skin

will see a growing mole that is evolving and oozing / bleeding

will see in nails / palms / soles of people with darker skin tone.

Subungual pigmentation [Hutchinsons sign] or on palms / feet

Major criteria: change in size / shape / colour

Minor criteria: diameter of 7mm or more, inflammation, oozing / bleeding, altered sensation

if suspicious: excision biopsy with lesion removed completely. Then review biopsy to see if further re-excision of margins is needed [usually 1-3cm].

Further tx include: sentinel lymph node mapping, isolated limb perfusion, block dissection of regional lymph node groups

measured using Breslow Thickness. if less than 0.75mm, survival is 95-100%. If more than 4mm, 5yr survival is 50%

a common premalignant skin lesion that develops as a consequence of chronic sun exposure

small, crusty, scaly lesions. Will be pink / red / brown / flesh colour. On sun exposed areas.

conservative: prevent further risk via sun avoidance / sun cream

Medical: 2-3 weeks of fluorouracil cream + topical hydrocortisone, topical diclofenac, topical imiquimod, cryotherapy, curettage and cautery

caused by fungi in the genus Trichophyton. Will see scaling / flaking / itching between the toes.

Management is topical imidazole or terbinafine

common skin condition caused by molluscum contagiosum virus. Mostly occurs in children with atopic eczema [1-4yr olds].

Transmission via direct close personal contact OR indirectly via fomites [contaminated surfaces] like shared towels / flannels

Typical small, flesh coloured papules that have a central dimple. Typically appears in “crops” of multiple lesions in a local area.

Commonly on trunk / flexures but anogenital lesions may also occur

conservative: reassure px that it is self-limiting within 18months. Explain it is contagious so avoid sharing towels / clothing / baths. Encourage not to scratch the lesions. self isolation is not needed

medical: treatment is not recommended but cryotherapy can be done

people who are HIV +ve with extensive lesions = urgent HIV specialist referral

for px with eyelid / ocular lesions = refer to opthalmologist

adults with anogenital lesions = refer to GUM for STI screening

tumour like lesions that arise from the connective tissue of a scar, and extend beyong dimensions of original wound

ethnicity [dark skin], young adults, commonly on sternum, shoulder, neck, faces

keloid scar image

if early, intralesional steroids can be used [triamcinolone]

excision can be considered but can cause further scarring

superficial bacterial skin infection caused by staph aureus OR strep pyogenes

Can be primary OR a secondary complication of an existing skin condition like eczema / scabies / insect bites

direct contact with discharge from the scabs of an infected person
Invasion via minor abrasions / scratching
Mainly via hands / indirectly via toys / clothing / equipment

Incubation period is 4-10 days

if staph infection, will see a golden crust. can be anywhere but usually on face, flexures, limbs

can see presence of bullous / vesicles with pus, which burst to form a golden crust. These will eventually heal without scarring but will be painful / itching

it is common to have systemic sx

exclude from school until lesions are crusted OR post 48hrs after ABx tx

Hydrogen peroxide is used if not systemically unwell OR not at high risk of complication. If ABx is needed, fusidic acid can be used.

if extensive, use oral flucloxacillin

Mite Sarcoptes scabies is the cause and is spread by prolonged skin contact.

Scabies mite will burrow into skin, laying its eggs which causes a delayed type 4 hypersensitivity reaction which will cause intense pruritus.

It can take up to 8 weeks for any sx or rash to appear after the initial infestation

Intensely itchy small red spots with track marks where the mites have burrowed. Will see widespread pruritus but can be localised to finger webs

Will see excoriation from scratching

avoid close physical contact. Need to hot wash all clothes / bedding / towels with scabies + hoovering of carpets and furniture. Need to treat all household / close physical contacts even if ASx

1st line med: permethrin 5% is applied to the whole body for 8-12 hours.

2nd line is malathion

Pruritus can persist for up to 4-6 weeks post-eradication

Will see crusting skin that will be teeming with hundred of thousands of organisms. will be extremely contagious and there will be scaly plaques just like psoriasis

admission may be needed for treatment with oral ivermectin and isolation

immunocompromised px may not notice pruritus as they do not mount an immune response to the infestation

trichopyton tonsurans OR microsporium canis from cats / dogs

scarring alopecia in children. if untreated a raised / pustular / spongy mass called a kerion can form

scalp scrapings. lesions from microsporium canis will see a green fluorescence under Wood’s lamp

Give topical ketoconazole shampoo for first 2 weeks to reduce transmission

oral antifungals like terbinafine for Trichophyton tonsurans OR griseofulvin for Microsporium infections

caused by trichophyton rubrum and trichophyton vervucosum [contact with cattles]

well defined annular erythematous lesions with pustules / papules

oral fluconazole

arises from the use of steroids to treat an initial fungal infection. Usually caused by a misdiagnosis of ringworms for dermatitis, so a steroid is prescribed.

the steroid improves sx BUT accelerates the growth of the fungal infection by immune suppression.

caused by coxsackie A16 virus and enterovirus 71

illness starts with typical viral URTI sx: tiredness, sore throat, dry cough, raised temp

after 1-2 days, small painful mouth ulcers will appear, followed by blistering red spots across the body [hands / feet / mouth].

no medical management. give fluids / analgesia. will resolve after 10 days. contagious so should avoid sharing towels / bedding

viral spread via RNA paramyxovirus. done through aerosol transmission. rash starts 4 days after infection. rarely seen now due to immunisation programmes

prodromal phase: irittable, conjunctivitis, fever

Koplik spots: white spots on buccal mucosa

diarrhoea seen in 10% of px

IgM antibodies can be detected within a few days of rash onset

supportive. admit if immunosuppressed or pregnant. inform public health as it is a notifiable disease

otitis media [most common], pneuomonia is the most common cause of death.
Encephalitis, diarrhoea, keratoconjunctivitis, myocarditis

usually affects children under 6yrs old

infection caused by staph, producing epidermolytic toxins, causing widespread painful blisters and desquamation

lesion is initially superficial and crusted. in 24hrs, the surrounding skin will become painful and scarlet. Skin will become tender / paper like = forms blisters and desquamotus [peels off].

looks like scalded skin.

erythema, bullae / blisters, desquamation

admit for IV flucloxacillin and analgesia.

monitor and maintenance via fluid and electrolytes

infection of the skin and soft tissue of the proximal and lateral nail fold, caused by staph aureus. usually seen in the tx of wound infection

swelling, erythema, tenderness, pussy discharge

recent wound history

wound swab if discharge is present

flucloxacillin 500mg QDS, seek advice if MRSA is suspected.

if wound does not improve, refer to surgeons

HPV via direct contact

papules with rough, papillomatous and hyperkeratotic surface, ranging from 1mm to 1cm.

will see plantar warts [localised to soles which are painful], plane warts on hands / face, and filiform warts [on a long stalk]

topical tx with salicyclic acid OD. most px will resolve with 12 weeks.

cryotherapy is also an option

presumed autoimmune condition, causing localised well demarcated patches of hair loss. There may be “exclamation mark” hairs at the borders.

No signs of inflammation / erythema / atrophy

1st line: topical steroids OR intralesional corticosteroids

Minoxidil to stimulate hair growth

psychological support

immune mediated skin disorder that has an unknown aetx but drug causes include: gold, quinine, thiazides

itchy, papular rash mostly on palms / soles / genitalia and flexor surfaces of arm

rash is often polygonal in shape with “white lines” pattern on surface [Wickhams striae]. Will see Koebner phenomenon.

Oral involvement of white lace pattern on the buccal mucosa in 50% of cases

1st line: topical steroids

Benzydamine mouthwash for oral lichen planus

autoimmune skin disorder associated with coeliac disease. Caused by deposition of IgA in the dermis. 90% of px will have small bowel biopsy findings consistent with glutent sensitive enteropathy

Blistering, itchy, vesicular skin lesions on the extensor surfaces

Skin biopsy of direct immunoflourescence will show deposition of IgA in a granular pattern in the upper dermis. Will also see the presence of anti-tTG antibodies consistent with coeliac disease

gluten free diet

Dapsone for severe pruritus [SE of haemolytic anaemia]

autosomal dominant condition that presents with multiple telangiectasia over the skin and mucous membranes

forms telangiectasia and arteriovenous malformations [AVM]. This lead to significant bleeding, epistaxis and GI bleeding

need 3 out of the 4:
epistaxis [spontaneous or recurrent]
Telangiectasia
FHx: 1st degree relative
Visceral lesions: GI bleeding or AVM seen on CT / CXR [pulmonary nodules]

if blood loss is severe: blood transfusion

if IDA, give iron supplements

Embolisation of AVMs within organs can help manage the condition

chronic painful inflammatory skin disorder, characterised by the development of inflammatory nodules, pustules, sinus tracts and scars in intertriginous areas

should be suspected in pubertal / post pubertal px who have a diagnosis of recurrent furuncles and boils

areas where two skin surfaces rub each other, like the axilla or inner thighs

FHx, smoking, obesity, diabetes, PCOS, mechanical stretching of skin

initial manifestation involves recurrent painful inflamed nodules usually on intertriginous skin.

Nodules can rupture, leading to purulent discharge, malodorous material [foul smelling]

nodules can result in plaques, sinus tracts, “rope like” scarring

good hygiene, loose clothing, stop smoking, lose weight

give steroids / flucloxacillin for acute flares. Longer term, give topical clindamycin / oral rifampicin

surgical excision and drainage is also an option

autoimmune condition which results in the loss of melanocytes = depigmentation of the skin

associated with T1DM, addisons, autoimmune thyoid disorders, pernicious anaemia, alopecia areata

genetics involving tyrosine enzyme
immune destruction of melanocytes
Associated with treatments like transdermal patches of methylphenidate for ADHD and immune checkpoint inhibitors like pembrolizumab

Triggered by stress
Correlates with metastatic melanoma, stem cell transplants

vitiligo clinical features

sun block for affected areas of skin, camouflage make up

topical corticosteroids can reverse changes if early enough

Tacrolimus / phototherapy

typically nose / cheeks / forehead

will see flushing as the first sx. Telangiectasia and development into persistent erythema with papules and pustules

Rhinophyma / blepharitis

associated with rosacea where the nose enlarges and becomes red / bumpy / bulbous

apply daily sunscreen, camouflage creams to hide redness

topical brimonidine gel [alpha adrenergic agonist]

topical ivermectin 1st line

alt: topical metronidazole

topical ivermectin + oral doxycycline

when the sx are not improved with primary care = laser therapy

any px with rhinophyma

symmetrical, brown velvety plaques found on neck / axilla / groin

T2DM, GI cancer / malignancy, obesity, PCOS, acromegaly, cushings disease, hypothyroidism, familial, prader-willi syndrome, COCp or nicotinic acid

insulin resistance leads to hyperinsulinaemia. this stimulates keratinocytes and dermal fibroblast proliferation via interaction with IGFR1

androgen dependent hair growth in women

PCOS

cushings, CAH, androgen therapy, obesity, adrenal tumour, phenytoin / corticosteroids

Ferriman-Gallwey scoring system

9 body areas scored from 0-4. More than 15 total is moderate / severe

weight loss, waxing / bleaching, COCp use

topical eflornithine for facial hirsutism [CI in pregnancy and breast feeding]

androgen dependent hair growth

minoxidil, ciclosporin, diazoxide

Congenital hypertrichosis terminalis / lanuginosa

anorexia nervosa

skin lesions that appear at the site of injury

purplish, non-blanching, reticulated rash caused by obstruction of the capillaries, leading to swollen venules

idiopathic, polyarteritis nodosa, SLE, antiphospholipid syndrome, Ehlers Danlos syndrome, homocystinuria

acute, unilateral painful blistering rash caused by reactivation of VZV. follows primary VZV infection which lies dormant in dorsal root or cranial n ganglia

increasing age, HIV [strongest RF], other immunosuppressive conditions [steroids, chemotherapy]

Prodrome: burning pain over affected dermatome for 2-3 days. Pain is severe and can interfere with sleep. Systemic sx like fever, headache, lethargy

Rash itself is erythematous and macular. Well demaracated by the dermatome

Infectious so avoid pregnant / immunocompromised until vesicles have crusted over. Cover the lesions to reduce risk and one-off vaccine for shingles is offered in px over 70yrs old

NSAIDs / paracetamol for neuropathic pain. Corticosteroids given if immunocompetent and NSAIDs is not working

Antivirals [aciclovir] within 72hrs unless px is younger than 50 AND has a mild rash with no RFs.

if severe, admit to hospital for IV antivirals [or if suspecting opthalmic or meningitis]

post herpetic neuralgia, herpes zoster ophthalmicus [Hutchinsons nose]

Ramsay Hunt syndrome

pediculus capitis is organism. feeds on human blood and lays eggs [grey / brown]. Nits are the empty egg shells [white] that have hatched

via direct HEAD-HEAD CONTACT

nits cannot jump / fly / swim

fine-toothed combing of wet / dry hair

only give meds IF living lice is indicated like malathion, isopropyl myristate, dimeticone

household contacts DO NOT need to be treated unless also affected

bleeding into skin from small blood vessels: leads to non-blanching rash

typically seen in low platelets BUT also in bleeding disorder like vWf

ADMIT for meninogoccal septicaemia or Acute lymphoblastic leukaemia

give parenteral ABx prior to transfer

live attenuated vaccine [varivax]

indicated in healthcare workers and contacts of immunocompromised px

shingles vaccine for all px aged over 70yrs. Live attenuated, SC route

SEs: injection site reactions, chickenpox development

FBC, Ferritin and TFT

caused due to the change in androgen levels

reassure px

causes include infection, SLE, lichen planopilaris

will see atrophy / tufting of hairs and the loss of follucular opening

there will be destruction and loss of follicular opening in scarring. This is not seen in non-scarring

benign epidermal skin lesions seen in older people

large variation in colour from flesh to light borwn to black. Stuck on appearance and keratotic plugs may be seen on surface

reassure that it is benign. Remove via curettage, cryotherapy

common benign fibrous skin lesions, caused by the abnormal growth of dermal dendritis histiocyte cells, often preceded by an injury

mostly on legs and arms. Found in immune conditions like HIV / SLE

solitary firm papule / nodule, 5-10mm in size

dimple / crusting depression when lesion is squeezed and picked. Slow growth over time

if asx, no Tx unless bothersome or cosmetically undesirable

surgical excision, cryotherapy, laser therapy

benign tumour of adipocytes, found in subcutaenous tissues

malignant transformation into liposcarcoma is very rare

lipoma features

observe, if diagnosis is uncertain OR compressing on surrounding structures = removal

size over 5cm
increasing size
pain
deep anatomical location

trauma, pregnancy, young adult women

common on head, neck, upper trunk, hands

initial small red brown spots that develop into raised spherical red / brown lesions. can bleed and ulcerate

lesions in pregnancy usualy resolve spontaneously post partum

removal via curettage + cauterisation, cryotherapy, excision

encompasses epidermal cysts and pilar cysts [outer root of the hair follicle]

excision of cyst wall is needed to prevent reoccurence

spider naevia fill from the centre but telagiectasia fill from edges, when pressing on them and watching them fill

liver disease, pregnancy, COCp

spider naevi

ASx, flat, slightly scaly pink / brown rash found on groin / axilla. Caused by an overgrowth of the diphtheroid Corynebacterium Minutissum.

Will see coral-red fluorescence on Wood’s light.

Treat via oral erythromycin

Acute gastric ulcers tht develop in response to severe physiological stress such as burns. Involves an increase in gastric acid secretion and a decrease in mucosal blood flow folowing severe burns

Precancerous dermatosis that is a precursor to SCC. More common in elderly px.

Will see red / scaly patches in sun-exposed areas

Manage via topical 5-fluorouracil BDS / 4 weeks

loss and thinning of hair in response to severe stress

Acrodermatitis which are red, crusted lesions around the perianal / periorificial region. Can also lead to hypogonadism, alopecia, cognitive impairment, short stature