Dermatology Flashcards
define acne vulgaris
chronic inflammatory skin condition
mainly affects face, back and chest
blockage and inflammation of pilosebaceous unit
presents with lesions - non inflammatory (comedones), inflammatory (papules, pustules) or mixture
what are some complications of acne?
scarring, post inflammation hyperpigmentation or depigmentation and anxiety or depression
what advice should be given for acne?
avoid over cleaning skin
avoid non alkaline synthetic detergent
avoid oil based products - make up, sunscreen
avoid picking
tx are effective but can take 6-8 wks to work
how should mild to moderate acne be managed?
12 week course of one of:
topical adapalene with topical benzoyl peroxide
topical tretinion with topical clindamycin
topical benzoyl peroxide with topical clindamycin
how should moderate to severe acne be managed?
12 week course of one of:
topical adapalene with topical benzoyl peroxide
topical tretinion with topical clindamycin
topical benzoyl peroxide with topical clindamycin + either oral lymecycline or oral doxy
topical azelaic acid with oral lymecycline or oral doxy
when should urgent referral for acne vulgaris be made?
acne fulminans - same day on call hospital dermatology team within 24 hrs
when should referral to consultant dermatologist team be made for acne?
not responded to tx
acne with scarring or persistent pigmentation
contribution to mental health
what are the layers of the skin?
epidermis (outer - stratum corneum) + langerhans cells
dermis - collagen, fibrinogen, nerve endings, hair follicles, blood vessels
subcut tissue, protective padding
pathophysiology of psoriasis
increased cell turnover - hyperproliferation of epidermis…scaling, dilation of blood vessels - erythema
history
PC - rash v lesion, site, evolution, duration- acute/chronic, distribution - symmetrical/asymmetrical, flexors/extensors, mucous membranes, sun exposed sites
hx - sx - itching, soreness, exacerbating, relieving, PMH, personal and family hx of skin disease including atopy, drug hx, social, occupation and travel hx +/- sexual hx, psychosocial impact of skin disease, previous and current treatments, hx of skin cancer, sun bed use, occupation - UV exposure
examination
good light and magnifying glass
INSPECT, PALPATE, DESCRIBE, SYSTEMATIC CHECK of whole skin/nails etc
should include hair/scalp, nails, mucous membranes
palpate - ear gloves if infection suspected
comment on morphology - look, distribution, sites, dermatomal
examine other systems if appropariate -joints, LN’s
Site (rash) or size/shape (lesion) Colour Associated changed Morphology
Asymmetry, Border, Colour, Diameter for pigmented lesions
distribution - generalised, flexural, extensor, photosensitive
configuration - discrete, confluent, linear, target
colour - erythematous, purpuric, brown/black, hypopigmented
surface - scale, crust, excoriation, erosion/ulceration
morphology - macule, papule, patch, plaque, nodule, vesicle, pustule, bulla
papule
small lump <5mm
nodule
larger lump 5-10mm
erythema
redness
vesicle
small water blister
bulla
large water blister
pustule
pus filled vesicle
telangiecta
thread vein
alopecia
hair loss/thinning
hirsutism
hairiness
excoriations
scratch marks
striae
stretch marks
pruritus
itching
macule
non palpable area
patch
discoloutation
plaque
macule >2cm
erosion
palpable, flat topped area >1-2cm
ulcer
2cm
lichenification
loss of epidermis, loss of epidermis and dermis, thickening of skin with exaggerated skin markings
how are skin types defined?
fitzpatrick skin types
white - 3 types from always burns to sometimes burns
moderate brown
dark brown
black
annular
ring shaped
wheal
urticaria
discoid
shape
comedone
open or closed
hypertrichosis v hirscuitism
both excess hair growth - latter in males
nail findings
koilonychia
pitting
oncholysis
clubbing
what are the sx to ask for in a dermatology hx?
pigmentation
dry skin
open sores, lesions, ulcers
peeling
rashes
itchiness
pain
red,white or pus filled bumps
scaly or rough skin
changes in mole colour size
loss of skin pigment
excessive flushing
bleeding or discharge
systemic sx - pyrexia, malaise, joint pain, swelling, weight loss
tenderness
history
PC - rash v lesion, site, evolution, duration- acute/chronic, distribution - symmetrical/asymmetrical, flexors/extensors, mucous membranes, sun exposed sites
hx - sx - itching, soreness, exacerbating, relieving, PMH, personal and family hx of skin disease including atopy, drug hx, social, occupation and travel hx +/- sexual hx, psychosocial impact of skin disease, previous and current treatments, hx of skin cancer, sun bed use, occupation - UV exposure, improvemenet of lesions when away from work
what are the psychosocial aspects of a hx which are important?
impact on ADL’s
embarassment
pain
chronic conditions
what are the thinnest sites of the skin?
scrotum and eyelids
what is the normal pH of the skin and why is this?
5.5
creates acid mantle…acidic substances such as amino acids, lactic acids and fatty acids in perspiration, sebum and horones
there are resident protective microflora and acididc cond repel pathogens and reduce body odour
haemosiderin
colour - red brown
where is melanin found?
epidermis
what are the key components of the skin?
epidermis -stratum basale, stratum spinosum, stratum granulosum, stratum corneum — keratinocytes, langerhans cells, melanocytes, merkel cells present
dermis - collagen, elastin, glycosaminoglycans, immune cells, nerves, blood vessels, lymphatics
which skin conditions affect particular components of the skin?
pathology in epidermis -
change in epidermal turnover time - psoriasis (reduced turnover time)
change in surface of skin/loss of epidermis - scales, crusting, exudate, ulcer
changes in pigmentation - hypo or hyper
pathology in dermis -
change in contour of skin/loss of dermis - papules, nodules, skin atrophy, ulcers
disorders of skin appendages - hair disorders, acne
changes related to lymphatics and blood vessels- erythema, urticaria, purpura
what are the main physiological functions of the skin?
protective barrier
temp regulation
sensation
vit d synthesis
immunosurveillance
appearance
what are the 3 types of hair?
lanugo - fine long hair on foetus
vellus - fine short hair on body surfaces
terminal - coarse long hair - scalp, eyebrow, pubic
how can pathology of hair occur?
reduced or absent melanin production - grey or white hair
change in duration of growth cycle - hair loss
shaft abnormalities
what do pathologies of the nail involve?
nail matrix - pits, ridges
nail bed - splinter haemorrhage
nail plate - discoloured nails, thickened nails
what do pathologies of the sebaceous glands involve?
increased sebum production and bacterial colonisation - acne
sebaceous gland hyperplasia
what do pathologies of the sweat gland involve?
inflammation of apocrine lgand - hidradenitis suppuravita
overactivity of eccrine glands - hyperhidrosis
allergic rashes/urticaria
skin cancers
definition, cause and tx of erysipelas
Erysipelas is localised skin infection caused by Streptococcus pyogenes. In simple terms, it is a more superficial, limited version of cellulitis.
The treatment of choice is flucloxacillin.
definition, cause, sx and tx of athletes foot
Athlete’s foot. It is usually caused by fungi in the genus Trichophyton.
Features
typically scaling, flaking, and itching between the toes
topical imidazole, undecenoate, or terbinafine first-line
how is eczema treated?
avoid irritans
simple emollients
Use weakest steroid cream which controls patients symptoms
from hydrocortisone to betamethasone to fluticasone to clobetasol
1 finger tip = 0.5 g - for 2x size of flat hand
wet wrapping (emollinet under wet bandages)
if severe - ciclosporin
what is the natural history of eczema?
It typically presents before 2 years but clears in around 50% of children by 5 years of age and in 75% of children by 10 years of age
fx of eczema
itchy, red rash
in infants face and trunk
younger child - extensor sufaces
older - flexor surfaces and creases of face and neck
define urticaria
local or generalised superficial swelling
fx - pale, pink raised skin - described as hives, pruritic
how is urticaria managed?
non sedating antihistamines
prednisolone is severe or resistant
what are the 2 main types of contact dermatitis?
irritant - non allergic reaction due to weak acids/alkalis like detergents or cement. often on hands, erythema typical
allergic - type 4 hypersensitivity reaction, usually following hair dyes. pc acute weeping eczema, topical steroid if severe
define dermatitis herpetiformis
an autoimmune blistering skin disorder associated with coeliac disease, caused by deposition of IgA in the dermis.
Features
itchy, vesicular skin lesions on the extensor surfaces (e.g. elbows, knees, buttocks)
define erythema nodosum
inflammation of subcut fat
what are the sx of erythema nodosum?
tender, erythematous, nodular lesions
typically over shins but can be anywhere
usually resolves within 6 weeks without scarring
what are the causes of erythema nodosum?
infection -streptococci, tuberculosis, brucellosis
systemic disease - sarcoidosis, inflammatory bowel disease, Behcet’s
malignancy/lymphoma
drugs- penicillins, sulphonamides, combined oral contraceptive pill
pregnancy
what are the causes of fungal nail infection?
causative organisms - dermatophytes (90% of cases) such as Trichophyton rubrum
yeasts (5-10% of cases) e.g. Candida
non-dermatophyte moulds
what are the risk fx for fungal nail infections?
> age
DM
psoriasis
repeated nail trauma
what are the fx of fungal nail infections?
unsightly nails
thickened, rough, opaque nails
which investigations are performed for fungal nail infections and tx?
nail clippings for M+S
tx - not treated if asx
if dermatophyte or candida - topical tx, if more extensive oral terbinafine if dermatophyte or oral itraconazole if candida
define stevens johnson syndrome
severe systemic reaction affecting skin and mucosa
what are the causes of SJS?
penicillin
sulphonamides
lamotrigine, carbamazepine, phenytoin
allopurinol
NSAIDs
oral contraceptive pill
what are the clinical fx of SJS?
maculopapular rash with target lesions
may develop into vesicles or bullae
Nikolsky sign is positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently
mucosal involvement
systemic symptoms: fever, arthralgia
how is SJS managed?
hospital admission for supoortive tx
what are the sx of psoriasis?
red, scaly patches
can get nail signs - pitting, oncholysis
arthritis
what is the pathophysiology behind psoriasis?
multifactorial
genetic
immunological - abnormal T cell activity stimulates keratinocyte proliferation
environmental - exacerbated by skin trauma, stress, infection or improved by sunlight
what are the subtypes of psoriasis?
plaque psoriasis: the most common sub-type resulting in the typical well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp
flexural psoriasis: in contrast to plaque psoriasis the skin is smooth
guttate psoriasis: transient psoriatic rash frequently triggered by a streptococcal infection. Multiple red, teardrop lesions appear on the body
pustular psoriasis: commonly occurs on the palms and soles
what are the complications of psoriasis?
psoriatic arthropathy (around 10%)
increased incidence of metabolic syndrome
increased incidence of cardiovascular disease
increased incidence of venous thromboembolism
psychological distress
define alopecia areata
Alopecia areata is a presumed autoimmune condition causing localised, well demarcated patches of hair loss. At the edge of the hair loss, there may be small, broken ‘exclamation mark’ hairs
what is the natural hx of alopecia areata?
Hair will regrow in 50% of patients by 1 year, and in 80-90% eventually. Careful explanation is therefore sufficient in many patients
what can be offered as management for alopecia areata?
topical or intralesional corticosteroids
topical minoxidil
phototherapy
dithranol
contact immunotherapy
wigs
define keloid scars
Keloid scars are tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound
what are the predisposing fx of keloid scars?
ethnicity: more common in people with dark skin
occur more commonly in young adults, rare in the elderly
common sites (in order of decreasing frequency): sternum, shoulder, neck, face, extensor surface of limbs, trunk
how are keloid scars treated?
early keloids may be treated with intra-lesional steroids e.g. triamcinolone
excision is sometimes required but careful consideration needs to given to the potential to create further keloid scarring
define vitilligo
Vitiligo is an autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin. It is thought to affect around 1% of the population and symptoms typically develop by the age of 20-30 years.
what are the associated conditions of vitiligo
type 1 diabetes mellitus
Addison’s disease
autoimmune thyroid disorders
pernicious anaemia
alopecia areata
what are the clinical fx of vitiligo?
well-demarcated patches of depigmented skin
the peripheries tend to be most affected
trauma may precipitate new lesions (Koebner phenomenon)
how is vitiligo managed?
sunblock for affected areas of skin
camouflage make-up
topical corticosteroids may reverse the changes if applied early
there may also be a role for topical tacrolimus and phototherapy, although caution needs to be exercised with light-skinned patients
what are the characteristics of basal cell carcinoma and is it likely to metastasise?
lesions known as rodent ulcers
characterised by slow growth and local invasion
mets rare
most common type of cancer in western world
what are the clinical fx of basal cell carcinoma?
most common type is nodular
sun exposed site especially head and neck
initially a pearly, flesh-coloured papule with telangiectasia
may later ulcerate leaving a central ‘crater’
how is BCC managed?
routine referral if suspected
management - surgical removal, curettage, cryotherapy, topical cream - imiquimod, flurouracil, radiotherapy
what are the 3 common types of skin cancer?
basal cell
squamous cell
melanoma
how common is squamous cell carcinoma and is it likely to metastasise?
common
mets rare
what are the risk factors for squamous cell carcinoma?
excessive exposure to sunlight / psoralen UVA therapy
actinic keratoses and Bowen’s disease
immunosuppression e.g. following renal transplant, HIV
smoking
long-standing leg ulcers (Marjolin’s ulcer)
genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism
what are the clinical fx of squamous cell carcinoma?
on sun exposed sites
rapidly expanding painless, ulcerate nodules
cauliflower like appearance
may be areas of bleeding
what is the tx of squamous cell carcinoma?
surgical excision with 4mm margins if <20mm
if tumour >20mm 6mm margins
Mohs micrographic surgery may be used in high-risk patients and in cosmetically important sites.
what gives good and poor prognosis in squamous cell carcinoma?
good - well differentiated, <20mm, <2mm, deep, no associated conditions
poor - poorly differenitated, >20mm, >4mm, immunosuppression
what are the 4 main subtypes of melanoma?
superficial spreading - majority - growing mole
nodular - second commonest - red or black lump which bleeds/oozes
lentigo maligna - less common - growing mokes
acral lentiginious - rare - subungual pigmentation
what are the main diagnostic features of melanoma?
change in size, shape, colour - major
diameter >7mm, inflammation, oozing/bleeding, altered sensation
how is melanoma treated?
if suspicious - excision biopsy with histopathological assessment
once diagnosis is confirmed - pathology determines whether further re excisision of margins is required
margins related to Breslow thickness- 0-1mm thick = 1cm, 1-2mm thick = 1-2cm, 2-4mm = 2-3cm, >4mm = 3cm
what is the prognostic factor of malignant melanoma?
according to breslow thickness
if <0.75 mm = 95-100% survival
if >4mm = 50%
how is psoriasis managed?
stepwise approach
regular emollients - reduce scale loss and reduce pruritus
1st line - potent corticosteroid once daily + vit D for 4 weeks
if no improvement after 8 weeks - vit D analogue twice daily
if no improvement 8-12 weeks - potent corticosteroid 2x daily for 4 weeks or a coal tar preparation once or twice daily
short acting dithranol can be used
secondary care - phototherapy or systemic therapy such as oral methotrexate
side effects of topical corticosteroid therapy
as we know topical corticosteroid therapy may lead to skin atrophy, striae and rebound symptoms
the scalp, face and flexures are particularly prone to steroid atrophy so topical steroids should not be used for more than 1-2 weeks/month
face, flexural and genital psoriasis management
NICE recommend offering a mild or moderate potency corticosteroid applied once or twice daily for a maximum of 2 weeks
scalp psoriasis management
NICE recommend the use of potent topical corticosteroids used once daily for 4 weeks
what nail changes can be seen in psoriasis?
around 80-90% of patients with psoriatic arthropathy have nail changes.
Nail changes that may be seen in psoriasis
pitting
onycholysis (separation of the nail from the nail bed)
subungual hyperkeratosis
loss of the nail
what are the exacerbating fx of psoriasis?
trauma
alcohol
drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACE inhibitors, infliximab
withdrawal of systemic steroids
Streptococcal infection may trigger guttate psoriasis.
steroid tx eczema
Mild - Hydrocortisone 0.1–2.5%
Moderate- Betnovate-RD
Potent - Beclometasone dipropionate 0.025%
Betamethasone valerate 0.1%
stronger - body, weaker - face and creases
emollient tx eczema
liquid- E45
cream - epaderm
define pityriasis rosea
acute, self-limiting rash which tends to affect young adults. The aetiology is not fully understood but is thought that herpes hominis virus 7 (HHV-7) may play a rol
clinical fx pityriasis rosea
a minority may give a history of a recent viral infection
herald patch (usually on trunk)
followed by erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance
prognosis pityriasis rosea
self limiting - 6-8 weeks
