derm Flashcards
how to describe a skin lesion
SCAM
size (widest diameter) and shape
colour
associated secondary change
morphology and margin (border)
what is the ABCDE relating to pigmented skin lesions
increases likelihood of melanoma if any of these features are present
asymmetry
irrecular border
two or more colours within the lesion
diameter over 6mm
evolution (hx change in size, shape or colour)
what is a comedone
a plug in a sebaceous follicle containing altered sebum, bacteria and cellular debris, can present as either open (blackheads) or closed (whiteheads)
what is koebner phenomenon
a linear eruption arising at site of trauma
what is purpura
red or purple colour (due to bleeding into the skin or mucous membrane) which does not blach on pressure
petechiae (small pinpoint macules) and ecchymoses (larger bruise like patches)
what is a macule
a flat area of altered colour
what is a papule
solid raised lesion <0.5cm in diameter
what is a nodule
solid raised lesion >0.5cm in diameter with a deeper component
what is a plaque
palpable scaling raised lesion >0.5cm in diameter
what is a vesicle
raised, clear fluid-filled lesion <0.5cm in diameter
what is a bulla
large blister
raised, clear fluid filled lesion >0.5cm in diameter
what is a pustule
pus containing lesion <0.5cm in diameter
what is an abscess
localised accumulation of pus in the dermis or subcut tissue
what is a wheal?
transient raised lesion due to dermal oedema
e.g. urticaria
what is a boil/furuncle
staph infection around or within a heair follicle
what is a carbuncle
staph infection of adjacent hair follicles (multiple boils/furuncles)
what does excoriation mean
loss of epidermis following trauma
what is lichenification
well defined roughening of skin with accentuation of skin markings
what is hirsutism
androgen dependent hair growth in a femalw
what is hypertrichosis
non androgen dependent pattern of excessive hair growth
what is clubbing
loss of angle between the posterior nail fold and nail plate
suppurative lung disease, cyanotic heart disease, IBD
what is koilonychia
spoon shaped depression of nail plate
iron deficiency anaemia, congenital
what is oncholysis
separation of the distal end of the nail plate from the nail bed
trauma, psoriasis, fungal nail infection and hyperthyroidism
what is pitting of the nail
punctate depressions of the nail plate
psoriasis, eczema, alopecia areata
functions of normal skin
proteacitve barrier against environmental insults
temp regulation
sensation
vit D synthesis
immunosurveillance
appearance/cosmesis
what are the skin appendages
structures formed by skin derived cells
hair, nails, sebaceous glands, sweat glands
cell types in the epidermis
keratinocytes
langergans cells
melanocytes
merkel cells
function of keratinocytes
produce keratin as a protective barrier
functions of langerhans ells
present antigens and activate T-lymphocytes for immune protection
functions melanocytes
produce melanin, which gives pigment to skin and protects the cell nuclei from UV radiation induced DNA damage
function merkel cells
contain specialised nerve endings for sensation
layers of the epidermis
stratum basale: basal cell layer - cells actively dividing, deepest layer
stratum spinosum: prickle cell layer - differentiating cells
stratum granulosum: granular cell layer - cells lose nuclei and contain granules of keratohyaline, secrete lipid into the intercellular spaces
stratum corneum: horny layer - layer of keratin, mose superficial
in thick skin e.g. sole also the stratum lucidum (palyer compact keratin) beneath stratum corneum
what makes up the dermis
mainly collagen
also elastin, glycosaminoglycans
also immune cells, nerves, skin appendages and lymphatic and blood vessels
types of hair
lanugo: fine long hair in fetus
vellus: fine short hair on all body surfaces
terminal hair: coarse long hair on scalp, eyebrows, eyelashes and pubic areas
structure of hair
each hair consists of modified keratin and is divided into the hair shaft (keratinised tube) and hair bulb (actively dividing cells and melanocytes)
growth cycle of hair follicle
anagen: long growing phase
catagen: short regressing phase
telogen: resring/shedding phase
structure of nails
nail plate (hard keratin) which arises from the nail matrix at the posterior nail fold and rests on the nail bed
nail bed contains blood capillaries - give pink colour
function of sebaceous glands
produce sebum via hair follicles (pilosebaceous unit). secrete sebum onto skin surface which lubricates and waterproofs
stimulated by the conversion of androgens to dihydrotestosterone therefore activated in piberty
types of sweat glands
eccrine: universally distributed in skin
apocrine: in axillae, areolae, genitalia and anus. only function from puberty and produce odour
phases of wound healing
haemostasis
inflammation
proliferation
remodelling
what happens in haemostasis
vasoconstriction and platelet aggregation
clot formation
what happens in inflammation stage healing
vasodilation
migration of neutrophuls and macrophages
phagocytosis of cellular debris and invading bacteria
what happens in proliferation stage of healing
granulation tissue formation (fibroblasts) and angiogenesis
re-epithelialisation (epidermal cell proliferation and migration)
what happens in the remodelling stage of healing
collagen fibre re-organsiation
scar maturation
what are the emergency presenations in derm
anaphylaxis and angiodema
toxic epidermal necrolysis
stevens-johnson syndrome
acute meningococcaemia
erythroderma
eczema herpeticum
necrotising fasciitis
common causes urticaria, angiodema, anaphylaxis
Idiopathic, food (e.g. nuts, sesame seeds, shellfish, dairy
products), drugs (e.g. penicillin, contrast media, non-steroidal antiinflammatory drugs (NSAIDs), morphine, angiotensin-converting
enzyme inhibitors (ACE-i)), insect bites, contact (e.g. latex), viral or
parasitic infections, autoimmune, and hereditary (in some cases of
angioedema)
features urticaria
Urticaria is due to a local increase in permeability of capillaries
and small venules. A large number of inflammatory mediators
(including prostaglandins, leukotrienes, and chemotactic factors)
play a role but histamine derived from skin mast cells appears to
be the major mediator. Local mediator release from mast cells can
be induced by immunological or non-immunological mechanisms
presentation urticaria
(swelling involving the superficial dermis, raising the
epidermis): itchy wheals
presentation angioedema
(deeper swelling involving the dermis
presentation anaphylaxis
bronchospasm,
facial and laryngeal oedema, hypotension; can present initially
with urticaria and angioedema
mx urticaria/angiodema/anaphylaxis
Corticosteroids for severe acute urticaria and angioedema
Adrenaline, corticosteroids and antihistamines for anaphylaxis
what is erythema nodosum
A hypersensitivity response to a variety of stimuli
what causes erythema nodosum
Group A beta-haemolytic streptococcus, primary tuberculosis,
pregnancy, malignancy, sarcoidosis, inflammatory bowel disease
(IBD), chlamydia and leprosy
presentation erythema nodosum
Discrete tender nodules which may become confluent
● Lesions continue to appear for 1-2 weeks and leave bruise-like
discolouration as they resolve
● Lesions do not ulcerate and resolve without atrophy or scarring
● The shins are the most common site
what is erythema multiforme
often of unknown cause, is an acute self-
limiting inflammatory condition with herpes simplex virus being
the main precipitating factor. Other infections and drugs are also
causes. Mucosal involvement is absent or limited to only one
mucosal surface.
what is stevens-johnson syndrome
characterised by
mucocutaneous necrosis with at least two mucosal sites involved.
Skin involvement may be limited or extensive. Drugs or
combinations of infections or drugs are the main associations.
Epithelial necrosis with few inflammatory cells is seen on
histopathology. The extensive necrosis distinguishes Stevens-
Johnson syndrome from erythema multiforme. Stevens-Johnson
syndrome may have features overlapping with toxic epidermal
necrolysis including a prodromal illness
what is toxic epidermal necrosis
usually drug-induced, is
an acute severe similar disease characterised by extensive skin and
mucosal necrosis accompanied by systemic toxicity. On
histopathology there is full thickness epidermal necrosis with
subepidermal detachment
mx Erythema multiforme, Stevens-Johnson syndrome and Toxic epidermal necrolysis
Early recognition and call for help
● Full supportive care to maintain haemodynamic equilibrium
what is acute meningococcaemia
A serious communicable infection transmitted via respiratory
secretions; bacteria get into the circulating blood
cause accute meningococcameia
Gram negative diplococcus Neisseria meningitides
presentation acute meningococcaemia
Features of meningitis (e.g. headache, fever, neck stiffness),
septicaemia (e.g. hypotension, fever, myalgia) and a typical rash
● Non-blanching purpuric rash on the trunk and extremities, which
may be preceded by a blanching maculopapular rash, and can
rapidly progress to ecchymoses, haemorrhagic bullae and tissue
necrosis
mx acute meningococcaemia
Antibiotics (e.g. benzylpenicillin)
● Prophylactic antibiotics (e.g. rifampicin) for close contacts (ideally
within 14 days of exposure)
what is erythroderma
Exfoliative dermatitis involving at least 90% of the skin surface
what causes erythroderma
Previous skin disease (e.g. eczema, psoriasis), lymphoma, drugs
(e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol,
captopril) and idiopathic
presentation erythroderma
● Skin appears inflamed, oedematous and scaly
● Systemically unwell with lymphadenopathy and malaise
mx erythroderma
● Treat the underlying cause, where known
● Emollients and wet-wraps to maintain skin moisture
● Topical steroids may help to relieve inflammation
what is kaposis varicelliform eruption
eczema herpticum
what is eczema herpeticum
Widespread eruption - serious complication of atopic eczema or
less commonly other skin conditions
cause eczema herpticum
HSV
presentation eczema herpeticum
Extensive crusted papules, blisters and erosions
● Systemically unwell with fever and malaise
mx eczema herpeticum
Antivirals (e.g. aciclovir)
● Antibiotics for bacterial secondary infection
what is necrotising fascitis
● A rapidly spreading infection of the deep fascia with secondary
tissue necrosis
causes necrotising fasciitis
Group A haemolytic streptococcus, or a mixture of anaerobic and
aerobic bacteria
● Risk factors include abdominal surgery and medical co-morbidities
(e.g. diabetes, malignancy)
presentation necrotising fasciitis
● Severe pain
● Erythematous, blistering, and necrotic skin
● Systemically unwell with fever and tachycardia
● Presence of crepitus (subcutaneous emphysema)
● X-ray may show soft tissue gas (absence should not exclude the
diagnosis)
mx necrotising fasciitis
● Urgent referral for extensive surgical debridement
● Intravenous antibiotics
what is cellulitis
● Spreading bacterial infection of the deep subcutaneous tissue
what is erysipelas
acute superficial form of cellulitis and involves
the dermis and upper subcutaneous tissue
causes Erysipelas and Cellulitis
● Streptococcus pyogenes and Staphylococcus aureus
● Risk factors include immunosuppression, wounds, leg ulcers,
toeweb intertrigo, and minor skin injury
presentation erysipelas and cellulitis
● Most common in the lower limbs
● Local signs of inflammation – swelling (tumor), erythema (rubor),
warmth (calor), pain (dolor); may be associated with lymphangitis
● Systemically unwell with fever, malaise or rigors, particularly with
erysipelas
● Erysipelas is distinguished from cellulitis by a well-defined, red
raised border
mx erysipelas and cellulitis
● Antibiotics (e.g. flucloxacillin or benzylpenicillin)
● Supportive care including rest, leg elevation, sterile dressings and
analgesia
what is the cause of staph scalded skin syndrome
● Production of a circulating epidermolytic toxin from phage group
II, benzylpenicillin-resistant (coagulase positive) staphylococci
presentation staph scalded skin syndrome
● Develops within a few hours to a few days, and may be worse over
the face, neck, axillae or groins
● A scald-like skin appearance is followed by large flaccid bulla
● Perioral crusting is typical
● There is intraepidermal blistering in this condition
● Lesions are very painful
● Sometimes the eruption is more localised
● Recovery is usually within 5-7 days
mx staph scalded skin syndrome
● Antibiotics (e.g. a systemic penicillinase-resistant penicillin,
erythromycin or appropriate cephalosporin)
● Analgesia
3 main groups of superficial fungal infection
dermatophytes (tinea/ringworm), yeasts (e.g.
candidiasis, malassezia), moulds (e.g. aspergillus)
presentation tinea corporis
(tinea infection of the trunk and limbs) - Itchy,
circular or annular lesions with a clearly defined, raised and scaly
edge is typical
presentation tinea cruris
s (tinea infection of the groin and natal cleft) – very
itchy, similar to tinea corporis
presentation tinea pedis
s (athlete’s foot) – moist scaling and fissuring in
toewebs, spreading to the sole and dorsal aspect of the foot
presentation tinea manuum
Tinea manuum (tinea infection of the hand) – scaling and dryness
in the palmar creases
presentation tinea capitis
(scalp ringworm) – patches of broken hair, scaling
and inflammation
presentation tinea unguium
(tinea infection of the nail) – yellow discolouration,
thickened and crumbly nail
presentation tinea incognito
(inappropriate treatment of tinea infection with
topical or systemic corticosteroids) – Ill-defined and less scaly
lesions
presentation candidiasis
(candidal skin infection) – white plaques on mucosal
areas, erythema with satellite lesions in flexures
presentation pityriasis
Tinea versicolor (infection with Malassezia furfur) – scaly
pale brown patches on upper trunk that fail to tan on sun
exposure, usually asymptomatic
mx superficial fungal infections
● Establish the correct diagnosis by skin scrapings, hair or nail
clippings (for dermatophytes); skin swabs (for yeasts)
● General measures: treat known precipitating factors (e.g.
underlying immunosuppressive condition, moist environment)
● Topical antifungal agents (e.g. terbinafine cream)
● Oral antifungal agents (e.g. itraconazole) for severe, widespread,
or nail infections
● Avoid the use of topical steroids – can lead to tinea incognito
● Correct predisposing factors where possible (e.g. moist
environment, underlying immunosuppression)
main divisions of skin cancer
non-melanoma (basal cell carcinoma and
squamous cell carcinoma) and melanoma (malignant melanoma).
what is basal cell carcinoma
A slow-growing, locally invasive malignant tumour of the
epidermal keratinocytes normally in older individuals, only rarely
metastasises
● Most common malignant skin tumour
causes basal cell carcinoma
● Risk factors include UV exposure, history of frequent or severe
sunburn in childhood, skin type I (always burns, never tans),
increasing age, male sex, immunosuppression, previous history of
skin cancer, and genetic predisposition
presentation basal cell carcinoma
● Various morphological types including nodular (most common),
superficial (plaque-like), cystic, morphoeic (sclerosing), keratotic
and pigmented
● Nodular basal cell carcinoma is a small, skin-coloured papule or
nodule with surface telangiectasia, and a pearly rolled edge; the
lesion may have a necrotic or ulcerated centre (rodent ulcer)
● Most common over the head and neck
mx basal cell carcinoma
● Surgical excision - treatment of choice as it allows histological
examination of the tumour and margins
● Mohs micrographic surgery (i.e. excision of the lesion and tissue
borders are progressively excised until specimens are
microscopically free of tumour) - for high risk, recurrent tumours
● Radiotherapy - when surgery is not appropriate
● Other e.g. cryotherapy, curettage and cautery, topical
photodynamic therapy, and topical treatment (e.g. imiquimod
cream) - for small and low-risk lesions
what is squamous cell carcinoma
● A locally invasive malignant tumour of the epidermal
keratinocytes or its appendages, which has the potential to
metastasise
what causes squamous cell carcinoma
● Risk factors include excessive UV exposure, pre-malignant skin
conditions (e.g. actinic keratoses), chronic inflammation (e.g. leg
ulcers, wound scars), immunosuppression and genetic
predisposition
presentation squamous cell carcinoma
● Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate
mx squamous cell carcinoma
● Surgical excision - treatment of choice
● Mohs micrographic surgery – may be necessary for ill-defined,
large, recurrent tumours
● Radiotherapy - for large, non-resectable tumours
what is malignancy melanoma
● An invasive malignant tumour of the epidermal melanocytes,
which has the potential to metastasise
what causes malignant melanoma
● Risk factors include excessive UV exposure, skin type I (always
burns, never tans), history of > 100 moles or atypical neavus
syndrome moles, family history in first degree relative or previous
history of melanoma
presentation malignant melanoma
● The ‘ABCDE Symptoms’ rule (major suspicious features):
Asymmetrical shape
Border irregularity
Colour irregularity*
Diameter > 6mm
Evolution of lesion (e.g. change in size and/or shape)*
Symptoms (e.g. bleeding, itching)
● More common on the legs in women and trunk in men
what is superficial spreading melanoma
common on the lower limbs,
in young and middle-aged adults; related to intermittent high-
intensity UV exposure; around 70% of all melanomas are superficial
spreading melanomas
what is nodular melanoma
common on the trunk, in young and middle-
aged adults; related to intermittent high-intensity UV exposure
what is lentigo maligna melanoma
common on the face, in elderly
population; related to long-term cumulative UV exposure
what is acral lentiginous melanoma
common on the palms, soles and nail
beds, in elderly population; no clear relation with UV exposure
mx malingnat melanoma
● In general, surgical excision is the definitive treatment (often a
second surgery, wide local excision is needed after the initial excision biopsy). Radiotherapy may sometimes be useful.
Chemotherapy is used for metastatic disease.
causes atopic eczema
● Not fully understood, but a positive family history of atopy (i.e.
eczema, asthma, allergic rhinitis) is often present
● A primary genetic defect in skin barrier function (loss of function
variants of the protein filaggrin) appears to underlie atopic eczema
● Exacerbating factors such as infections, allergens (e.g. chemicals,
food, dust, pet fur), sweating, heat, occupation and severe stress
presentation atopic eczema
● Acute presentation consists of itchy papules and vesicle often
weepy (exudative)
● Chronic lesions : dry scaly itchy patches can be erythematous in
paler skin or grey/ brown in richly pigmented skin
▪ More common on the face and extensor aspects of limbs in infants,
and the flexor aspects in children and adults
● In richly pigmented skin eczema may present as
brown, grey or purple bumps (papular eczema or follicular
eczema)
● Chronic scratching/rubbing leads to lichenification
● Across of skin types eczema can lead to
pigmentary changes such as hypopigmentation (reduced
pigmentation) and hyperpigmentation (increased pigmentation)
● Nail may show pitting and ridging of the nails
mx atopic eczema
● General measures - avoid known exacerbating agents, frequent
emollients +/- bandages and bath oil/soap substitute
● Topical therapies – topical steroids for active areas; topical
immunomodulators (e.g. tacrolimus, pimecrolimus) for
maintenance therapy as steroid-sparing agents
● Oral therapies - antihistamines for symptomatic relief, antibiotics
(e.g. flucloxacillin) for secondary bacterial infections, and
antivirals (e.g. aciclovir) for secondary herpes infection
● Phototherapy and immunosuppressants (e.g. azathioprine,
ciclosporin, methotrexate) for severe non- responsive cases, biologic
therapy
complications atopic eczema
● Secondary bacterial infection (crusted weepy lesions)
● Secondary viral infection - molluscum contagiosum (pearly
papules with central umbilication), viral warts and eczema
herpeticum
what is acne vulgaris
An inflammatory disease of the pilosebaceous follicle
causes acne vulgaris
● Hormonal (androgen)
● Contributing factors include increased sebum production,
abnormal follicular keratinization, bacterial colonization
(Propionibacterium acnes) and inflammation
presentation acne vulgaris
● Non-inflammatory lesions (mild acne) - open and closed
comedones (blackheads and whiteheads)
● Inflammatory lesions (moderate and severe acne) - papules,
pustules, nodules, and cysts
● In richly pigmented skin:
1. Inflammatory lesions’ may not be so apparent, instead
hyperpigmented lesions (‘acne hyperpigmented
macules’) are seen.
Hyperpigmented lesions may also signify ongoing
inflammation
2. Non erythematous nodules may be present and detected by
palpation
● Commonly affects the face, chest and upper back
mx acne vulgaris
● General measures - no specific food has been identified to cause
acne, treatment needs to be continued for at least 6 weeks to
produce effect
● Topical therapies (for mild acne) - benzoyl peroxide and topical
antibiotics (antimicrobial properties), and topical retinoids
● Oral therapies (for moderate to severe acne) - oral antibiotics, and
anti-androgens (in females)
● Oral retinoids (for severe acne)
complications acne vulgaris
● Post-inflammatory hyperpigmentation, scarring, deformity,
psychological and social effects
what is psoriasis
● A chronic inflammatory skin disease due to hyperproliferation of
keratinocytes and inflammatory cell infiltration
types of psoraisis
● Chronic plaque psoriasis is the most common type
● Other types include guttate (raindrop lesions), seborrhoeic
(naso-labial and retro-auricular), flexural (body folds), pustular
(palmar-plantar), and erythrodermic (total body redness)
causes psoriasis
● Complex interaction between genetic, immunological and
environmental factors
● Precipitating factors include trauma (which may produce a
Köebner phenomenon), infection (e.g. tonsillitis), drugs, stress,
and alcohol
presentation psoraisis
● Well-demarcated erythematous scaly plaques
● in richly pigmented skin psoriasis can
present as dark brown, grey or purple patches or plaques
● Lesions can sometimes be itchy, burning or painful
● Common on the extensor surfaces of the body and over scalp
● Auspitz sign (scratch and gentle removal of scales cause capillary
bleeding)
● 50% have associated nail changes (e.g. pitting, onycholysis)
● 5-8% suffer from associated psoriatic arthropathy - symmetrical
polyarthritis, asymmetrical oligomonoarthritis, lone distal
interphalangeal disease, psoriatic spondylosis, and arthritis
mutilans (flexion deformity of distal interphalangeal joints)
mx psoriasis
● General measures - avoid known precipitating factors, emollients
to reduce scales
● Topical therapies (for localised and mild psoriasis) - vitamin D
analogues, topical corticosteroids, coal tar preparations,
dithranol, topical retinoids, keratolytics and scalp preparations
● Phototherapy (for extensive disease) - phototherapy i.e. UVB and
photochemotherapy i.e. psoralen+UVA
● Oral therapies (for extensive and severe psoriasis, or psoriasis
with systemic involvement) - methotrexate, retinoids,
ciclosporin, mycophenolate mofetil, fumaric acid esters,
and biological agents (e.g. etanercept, adalimumab, ustekinumab)
complications psoriasis
● Erythroderma, psychological and social effects
common causes of blisters
impetigo , insect bites, herpes simplex
infection, herpes zoster infection, acute contact
dermatitis, pompholyx (vesicular eczema of the hands and feet, see below) and
burns.
what is bullous pemphigoid
A blistering skin disorder which usually affects the elderly
causes bullous pemphigoid
● Autoantibodies against antigens between the epidermis and
dermis causing a sub-epidermal split in the skin
presentation bullous pemphigoid
● Tense, fluid-filled blisters on an erythematous base
● Lesions are often itchy
● May be preceded by a non-specific itchy rash
● Usually affects the trunk and limbs (mucosal involvement less
common)
mx bullous pemphigoid
● General measures – wound dressings where required, monitor
for signs of infection
● Topical therapies for localised disease - topical steroids
● Oral therapies for widespread disease – oral steroids, combination
of oral tetracycline and nicotinamide, immunosuppressive agents
(e.g. azathioprine, mycophenolate mofetil, methotrexate, and
other)
what is pemphigus vulgaris
● A blistering skin disorder which usually affects the middle-aged
cause pemphigus vulgaris
● Autoantibodies against antigens within the epidermis causing an
intra-epidermal split in the skin
presentation pemphigus vulgaris
● Flaccid, easily ruptured blisters forming erosions and crusts
● Lesions are often painful
● Usually affects the mucosal areas (can precede skin involvement)
mx pemphigus vulgaris
● General measures – wound dressings where required, monitor for
signs of infection, good oral care (if oral mucosa is involved)
● Oral therapies – high-dose oral steroids, immunosuppressive
agents (e.g. methotrexate, azathioprine, cyclophosphamide,
mycophenolate mofetil, and other)
what is vitiligo
● An acquired depigmenting disorder, where there is complete loss
of pigment cells (melanocytes)
cause vitiligo
● Thought to be an autoimmune disorder, where the innate
immune system causes destruction or loss of melanocytes, leading
to loss of pigment formation in the skin
presentation vitiligo
● Presentation at any age
* A single patch or multiple patches of depigmentation (complete loss
of pigment), often symmetrical
● Common sites are exposed areas such as face, hands, feet, as well
as body folds and genitalia
● Favours sites of injury and this phenomenon is called the Koebner
phenomenon
mx vitiligo
● Minimise skin injury as a cut, graze, or sunburn can potentially
trigger a new patch of vitiligo
● Topical treatments such as topical steroids and calcineurin
inhibitors (such as topical tacrolimus and pimecrolimus)
● Phototherapy such as UVB therapy, excimer laser
● Oral immunosuppressants such as methotrexate, ciclosporin and
mycophenolate mofetil
what is melasma
● An acquired chronic skin disorder, where there is increased
pigmentation in the skin
cause of melasma
● Thought to be due to genetic predisposition, and triggered by
factors such as sun exposure, hormonal changes such as pregnancy
and contraceptive pills
● The pigmentation is caused by an overproduction of pigment
(melanin) by pigment cells (melanocytes)
presentation melasma
● Brown macules (freckle-like spots) or larger patches with an
irregular border
● Symmetrical distribution
● Common sites are forehead, cutaneous upper lips and cheeks,
rarely can occur on neck, shoulders and upper arms
mx melasma
● Lifelong sun protection
● Discontinuation of hormonal contraceptive pills
● Cosmetic camouflage
● Topical treatments that aim at inhibiting the formation of new
melanin such as hydroquinone, azelaic acid, kojic acid (a chelating
agent) and vitamin C
● Laser treatments need to be used with caution as the heat
generated by lasers can potentially cause post-inflammatory
hyperpigmentation.
features venous ulcer
- Often painful, worse on standing
- History of venous disease e.g. varicose veins, deep vein thrombosis
- Malleolar area (more common over
medial than lateral malleolus) - Large, shallow irregular ulcer
- Exudative and granulating base
- Warm skin
- Normal peripheral pulses
- Leg oedema, haemosiderin and melanin deposition (brown pigment),
lipodermatosclerosis, and atrophie
blanche (white e scarring with dilated
capillaries) - Normal ankle/brachial pressure index
mx venous ulcers
- Compression bandaging
(after excluding arterial insufficiency)
features arterial ulcers
- Painful especially at night, worse when legs are elevated
- History of arterial disease e.g.
atherosclerosis - Pressure and trauma sites e.g. pretibial, supramalleolar (usually lateral), and at distal points e.g. toes
- Small, sharply defined deep ulcer
- Necrotic base
- Cold skin
- Weak or absent peripheral pulses
- Shiny pale skin
- Loss of hair
ix for arterial ulcers
- ABPI < 0.8 - presence of arterial
insufficiency - Doppler studies and angiography
mx arterial ulcer
- Vascular reconstruction
- Compression bandaging is
contraindicated
features neuropathic ulcer
- Often painless
- Abnormal sensation
- History of diabetes or neurological
disease - Pressure sites e.g. soles, heel, toes,
metatarsal heads - Variable size and depth
- Granulating base
- May be surrounded by or underneath a
hyperkeratotic lesion (e.g. callus) - Warm skin
- Normal peripheral pulses*
*cold, weak or absent pulses if it is a
neuroischaemic ulcer - Peripheral neuropathy
ix neuropathic ulcers
- ABPI < 0.8 implies a neuroischaemic
ulcer - X-ray to exclude osteomyelitis
mx neuropathic ulcer
- Wound debridement
- Regular repositioning, appropriate
footwear and good nutrition
causes itchy eruption
inflammatory condition (e.g. eczema), infection (e.g. varicella), infestation (e.g. scabies), allergic
reaction (e.g. some cases of urticaria) or an unknown cause, possibly autoimmune (e.g. lichen planus)
features lichen planus
- Family history in 10% of cases
- May be drug-induced
- Forearms, wrists, and legs
- Always examine the oral
mucosa - Violaceous (lilac) flat-topped
Papules or hyperpigmented
papules (in darker skin) - Symmetrical distribution
- Nail changes and hair loss
- Lacy white streaks on the oral
mucosa and skin lesions
(Wickham’s striae)
mx lichen planus
- Corticosteroids
- Antihistamines
features melanocytic naevi
- Not usually present at birth but develop
during infancy, childhood or adolescence - Asymptomatic
- Congenital naevi may be large,
pigmented, protuberant and hairy - Junctional naevi are small, flat and dark
- Intradermal naevi are usually dome-shape
papules or nodules - Compound naevi are usually raised, warty,
hyperkeratotic, and/or hairy
mx melanocytic naevi
- Only if symptomatic
Shave or complete excision
features seborrhoeic wart
- Tend to arise in the middle-aged or elderly
- Often multiple and asymptomatic
- Face and trunk
- Warty greasy papules or nodules
- ‘Stuck on’ appearance, with well-defined
edges
mx seborrhoeic wart
- Only if symptomatic
Curette and cautery
Cryotherapy
causes purpuric eruption
thrombocytopenic (e.g. meningococcal septicaemia, disseminated intravascular coagulation, idiopathic
thrombocytopenic purpura) or non-thrombocytopenic e.g. trauma, drugs (e.g. steroids), aged skin, vasculitis (e.g. Henoch-Schönlein
purpura).
features DIC
- History of trauma,
malignancy,
sepsis, obstetric
complications,
transfusions, or liver failure - Spontaneous bleeding from
ear, nose and throat,
gastrointestinal tract,
respiratory tract or wound
site - Petechiae, ecchymoses,
haemorragic bullae and/or
tissue necrosis - Systemically unwell
ix DIC
- Bloods (a clotting screen is
important)
mx DIC
- Treat the underlying cause
- Transfuse for coagulation
deficiencies - Anticoagulants for thrombosis
features vasculitis
Painful lesions
- Dependent areas (e.g. legs,
buttocks, flanks)
- Palpable purpura (often
painful)
- Systemically unwell
ix vasculitis
- Bloods and urinalysis
- Skin biopsy
mx vasculitis
- Treat the underlying cause
- Steroids and
immunosuppressants if there
is systemic involvement
features actinic purpura
- Arise in the elderly population
with sun-damaged skin - Extensor surfaces of hands
and forearms - Such skin is easily traumatised
- Non-palpable purpura
- Surrounding skin is atrophic
and thin - Systemically well
mx actinic purpur
nonw needed
differentials ofr a red swollen leg
cellulitis, venous thrombosis, chronic venous insufficiency
skin changes inchronic venous insufficeincy
- Discoloured (blue-purple)
- Oedema (improved in the morning)
- Venous congestion and varicose veins
- Lipodermatosclerosis (erythematous
induration, creating ‘champagne
bottle’ appearance) - Stasis dermatitis (eczema with
inflammatory papules, scaly and
crusted erosions) - Haemosiderin deposition
- Venous ulcer
what are keloid scars
An overgrowth of scar tissue, which tends to be larger than the original wound itself
cause keloid scars
● Thought to be due to overproduction of collagen during wound healing after minor injuries, skin surgery, insect bites and acne
spots in genetically predisposed individuals
● More commonly seen in darker skin types
presentation keloid scars
● Firm, smooth, hard nodule which can be itchy or painful
● Common sites are chest and shoulders
mx keloid scars
● Avoidance of further trauma to the skin such as scratching
● Topical treatments such as topical steroids and silicone gel can potentially flatten the scar, and improve the symptoms
● Intralesional steroid injection if topical treatments are not effective
● Surgery such as excision needs to be carried out only as the last resort and with caution as the new wound may cause a larger
keloid scar
what is an emollient
● Aqueous cream, emulsifying ointment, liquid paraffin and white soft
paraffin in equal parts (50:50)
indications for emollients
● To rehydrate skin and re-establish the surface lipid layer
● Useful for dry, scaling conditions and as soap substitutes
e.g. topical steroids in derm
classified as mildly potent (e.g, hydrocortisone),
moderately potent (e.g. clobetasone butyrate (Eumovate)), potent
(e.g.betamethasone valerate (Betnovate)), and very potent (e.g. clobetasol
propionate (Dermovate))
e.g. oral steroids derm
● Oral steroids: prednisolone
indications steroids in derm
● Anti-inflammatory and anti-proliferative effects
● Useful for allergic and immune reactions, inflammatory skin conditions,
blistering disorders, connective tissue diseases, and vasculitis
SE steroids
● Local side effects (from topical corticosteroids): skin atrophy (thinning),
telangiectasia, striae, may mask, cause or exacerbate skin infections,
acne, or perioral dermatitis, and allergic contact dermatitis.
● Systemic side effects (from oral corticosteroids): Cushing’s syndrome,
immunosuppression, hypertension, diabetes, osteoporosis, cataract, and
steroid-induced psychosis
indications oral aciclovir in derm
● Viral infections due to herpes simplex and herpes zoster virus
SE aciclovir
● Gastrointestinal upsets, raised liver enzymes, reversible neurological
reactions, and haematological disorders
classes of oral antihistamines
● Classified into nonsedative (e.g. cetirizine, loratadine) and sedative
antihistamines (e.g. chlorpheniramine, hydroxyzine)
inidcations oral antihistamines derm
● Block histamine receptors producing an anti-pruritic effect
● Useful for type-1 hypersensitivity reactions and eczema (especially
sedative antihistamines for children)
SE oral antihistamines
● Sedative antihistamines can cause sedation and anticholinergic effects
(e.g. dry mouth, blurred vision, urinary retention, and constipation)
topical abx derm
fusidic acid, mupirocin (Bactroban), neomycin
oral abx derm
penicillins, cephalosporins, gentamicin, macrolides,
nitrofurantoin, quinolones, tetracyclines, vancomycin, metronidazole,
trimethoprim
indications abx derm
● Useful for bacterial skin infections, and some are used for acne
topical antiseptics derm
Chlorhexidine, cetrimide, povidone-iodine
indications topical antiseptics derm
● Treatment and prevention of skin infection
oral retinoids derm
Isotretinoin, Acitretin
indications oral retinoids derm
● Acne, psoriasis, and disorders of keratinisation
SE oral retinoids
● Mucocutaneous reactions such as dry skin, dry lips and dry eyes,
disordered liver function, hypercholesterolaemia, hypertriglyceridaemia,
myalgia, arthralgia and depression
● Teratogenicity: effective contraception must be practised one month before, during and at least one month after isotretinoin, but for two years
after Acitretin (
biological therapy derm
Monoclonal antibodies (eg. Infliximab, Adalimumab, Ustekinumab,
Certolizumab, Gorlilumab), Fusion antibody proteins (eg. Etanercept),
Recombinant human cytokines and growth factors (eg. Interleukins)
ndications biological therapy derm
psoriasis, atopic dermatitis and hidradenitis suppurativa
SE biological therapy
● Local side effects: redness, swelling, bruising at the site of injection
● Systemic side effects: allergic reactions, antibody formation, flu-like
symptoms, infections, hepatitis, demyelinating disease, heart failure, blood
problems, rare reports of cancers (eg. non-melanoma skin cancers,
lymphoma)
how to use emollients
● Apply liberally and regularly
how to use corticosteroids
● Apply thinly and only for short-term use (often 1 or 2 weeks only)
● In general, use 1% hydrocortisone or mild-moderate potent topical
steroids on the face and thin skin areas eg. neck and flexures.
● Fingertip unit (advised on packaging) – strip of cream the length of a
fingertip
preventing pressure sores
● Pressure sores are due to ischaemia resulting from localised damage to
the skin caused by sustained pressure, friction and moisture, particularly
over bony prominences.
● Preventative measures involve frequent repositioning, nutritional support,
and use of pressure relieving devices e.g. special beds
how to prevent sun exposure
Spend time in the shade between 11am-3pm
Make sure you never burn
Aim to cover up with a t-shirt, wide-brimmed hat and sunglasses
Remember to take extra care with children
Then use Sun Protection Factor (SPF) 30+ sunscreen
fitzpatrick skin phototype
I Always burns, never tans
II Always burns, sometimes tans
III Sometimes burns, always tans
IV Never burns, always tans
V Tans very easily, very rarely burns
VI tans very easily, never burns
bowens disease
=in situ SCC
full thickness dysplasia epidermal keratinocytes
acitinic keratoses
partial thickness dysplasia epidermal keratinocytes
sun exposed sites=scaly erythema
Derm red flags
Need urgent referral
Blistering/skin peeling
Pain
Lymphadenopathy
Mucosal involvement
Systemic upset: fever, abnormal LFTs/U&E
Mx mild drug rxn
Stop drug
Emollients
Topical corticosteroids
Antihistamines if urticarial
SJS and TEN
Steven Johnson syndrome and toxic epidermal necrolysis are on a scale
SJS less severe, TEN more
Cause SJS AND TEN
DRUGS
Sx SJS and TEN
sx 7-21d after med given
Prodrome=resp infection, fever, pain
Dusky red lesions, atypical targets, erythematous plaques, mucosal involvement, systemic symptoms, detachment epidermis
Mx SJS and TEN
stop med
Dressings and emollient/paraffin
ICU/burns unit
Fluid and electrolytes
Supportive: eyes, mouth, swabs for infection, physio
DRESS
Drug rxn with eosinophilia and systemic sx
Sx DRESS
15-40D after drug exposure- anticonvulsant and sulfonamodes
Fever, oedema
Rash=morbilloform, purpura, scaling
Lymphadenopathy
Eosinophilia
Effects organs-LFTs
Mx DRESS
Stop drug cause
Systemic steroids if severe
Supportive: dressings, topic steroids, emollients, oral antihistamines, fluids, tx secondary infection
AGEP
Acute generalised exanthematous pustulosis
Sx AGEP
Less than 4d after drug exposure - beta lactam abx
Fever
Small sterile pustules and oedematous erythema
Increased WCC
purpura
Vesicles
Target lesions
Mucosal involvement
Mx AGEP
Stop drug cause
Topical corticosteroids, emollients, antihistamines
What is erythroderma
Erythema over 90% skin surface
Causes erythroderma
Dermatitis
Psoriasis
Drug eruption
Cutaneous t cell lymphoma
Features erythroderma
Hx: atopy, steroid withdrawal
Clues underlying diagnosis=psoriasis, eczema
Ix erythroderma
FBC
U&E
LFT
CRP
total IgE
Blood film
+/- skin biopsy, lymph node ix
Mx erythroderma
Stop causative drugs
Monitor vitals and fluid
Dressings and emollients
Tx cause
Topical corticosteroids
Symptoms bullous pemphigoid
Sub dermal blistering
Usually elderly
Tense intact blisters
Bullous pemphigoid cause
AI
drug eruption
Attack on BM by IgE
Diagnosis bullous pemphigoid
Skin biopsy and direct immunofluroescence
Mx bullous pemphigoid
Specialist!
Systemic and topical steroids
Features staph scalded skin syndrome
Usually children
Superficial skin blistering and crusting, often flexural
No mucosal involvement
Mx staph scalded skin
Tx infection
Supportive- fluid, skin care
Cause staph scalded skin
Staph aureus exotoxins
Cause pemphigous vulgaris
AI
IgG auto Ab
Sx pemphigous vulgaris
Intra epidermal blisters=non tense, erosion
Painful blisters skin and mucous membranes
30-60y, Jews, indians
Mx pemphigous vulgaris
Specialist
Topical and systemic steroids
what is an acral distribution
distal areas- hands and feet
cause dermatitis herpetiformis
coeliac and IgA defieincy
biologic used in eczema
tacrolimus
associations psoriasis
arthritis
IBD
uveitis
coeliac
T2DM
gout
prognosis melanoma
breslow depth >3mm = poor prognosis
pathology psoriasis
autoimmune: T cell mediated keratinocyte proliferation
