DERMATOLOGY Flashcards
skin
largest organ in body
contains adnexal structures - hair, nails, glands, sensory structures
important role in protection, homeostasis and transmission of sensations
3 stages of hair cycle
anagen
catagen
telogen
anagen phase of hair cycle
active growing phase
80-90% of hair
catagen phase of hair cycle
2-3wk phase growth stops/follicle shrinks
1-3% of hairs
telogen phase of hair cycle
resting phase for 1-4months
up to 10% of hairs in a normal scalp
functions of skin
thermoregulation
skin immune system
barrier
Vit D synthesis
interpersonal communication
why skin disease is important
disfigurement
discomfort
disability
depression
death
external causes of skin disease
temp
UV
chemical
infection
trauma
internal causes of skin disease
systemic disease
genetics
drugs
infection
morphology
appearance of skin lesions
how big is “small”
usually means less than 5mm
small and large flat circumscribed areas
macule - small
patch - large
small and large raised areas
papule - small
plaque - large
small and large fluid filled
vesicle - small
bulla - large
small and large pus filled
pustule - small
abscess - large
loss of epidermis (& dermis)
erosion - loss of epidermis
ulcer - loss of epidermis & dermis
macule & patch
non-palpable change in skin colour with distinct borders
papule and plaque
papule - solid lesion < 1cm diameter
plaque - solid lesion > 1cm in diameter
nodule
palpable lesion > 1cm diameter which is taller than it is wide
vesicle & bulla
vesicle - fluid-containing, superficial, thin-walled cavity < 1cm
bulla - fluid-containing, superficial, thin-walled cavity > 1cm
erosion and ulcer
erosion - skin defect where there has been loss of the epidermis only
ulcer - skin defect where there has been loss of the epidermis and dermis
pustule and abscess
pustule - pus containing, superficial, thin-walled cavity
abscess - thick-walled cavity containing pus
most common skin conditions (give 5 examples)
psoriasis
acne
eczema
urticaria
leg ulcers
cutaneous signs
erythema nodosum
sarcoidosis
vasculitis
malignancy
autoimmune conditions
acanthosis nigricans
associated with insulin resistance, obesity, malignancy
flexural distribution
hyperkeratosis and hyperpigmentation, papules
‘velvety’ appearance
investigations in derm (if bacterial inf suspected)
charcoal swab
ask for MC&S
- microscopy
- culture
- sensitivities
investigations (if viral inf suspected)
viral swab for PCR
can swab vesicle/bulla if vesicular eruption
if systemic illness, can take throat swab
investigations (if fungal inf suspected)
skin scraping
nail clipping
hair sample
fungal cultures
skin biopsy
punch biopsy
homeothermic
tightly regulate temperature (37 +/- 0.5)
temperature varies with…
external temp
activity
circadian rhythm
menstrual cycle
location of peripheral thermoreceptors
skin, especially in face and scrotum
location of central thermoreceptors
spinal cord, abdominal organs, hypothalamus
response to cold stress - how is heat production within body increased?
general metabolism - oxidative phosphorylation and other chemical reactions are not 100% efficient
voluntary muscular activity - “futile” muscular activity
shivering thermogenesis - involuntary muscular activity
non-shivering thermogenesis - only significant in infants due to brown adipose tissue
response to cold stress - how is heat loss from body reduced?
vasomotor control - sympathetic arteriolar constriction reduces delivery of blood to the skin
behavioural responses - adding clothing, moving to warmer environment, reducing surface area
hypothermia - response to cold stress
a fall in deep body temp to below 35
who is at risk of hypothermia
neonates
elderly
homeless people
cold store workers
outdoor pursuits
treatment of cold stress
dry/insulate to prevent further heat loss
slow re-warming with bag/blankets
internal re-warming with hot drinks and/or warm air
rapid re-warming by immersion in water, extracoporeal circulation
frost bite: vascular component
vasoconstriction
increase in viscosity
promotes thrombosis
causes anoxia
frost bite: cellular component
ice crystals form in extracellular space
increases extracellular osmolality
causes movement of water from intracellular space
cell dehydration and death
how is heat production minimised? response to heat stress
decreased physical activity and food intake
as a response to heat stress, how is heat loss from the body increased?
vasomotor control - arteriolar dilation increases delivery of blood to the skin
sweating - sympathetic cholinergic fibres increase evaporative heat loss
behavioural responses - removing clothing, moving to shaded area, increasing surface area
heat exhaustion is a consequence of heat stress (heat illness) - explain
body temp raised in range 37.5-40
results in vasodilation and drop in central blood volume
caused by a disturbance of the body’s fluid/salt balance due to excessive sweating
symptoms include
headache
confusion
nausea
profuse sweating
clammy skin
tachycardia
hypotension
weak pulse
fainting and collapse
heat stroke (heat injury) - consequence of heat stress explain
body temp raised above 40
body’s temp control mechanisms fail
symptoms include hot dry skin (sweating stops) and circulatory collapse
who is most at risk of heat stress
neonates
elderly
people doing physical work in hot, humid environments
workers wearing non-breathable protective clothing
treatment of heat stress
move to cool environment
remove clothing
fan
sponge with tepid water
give fluids (oral, IV)
fever
part of body’s mechanism for fighting infection
caused by endogenous pyrogens (IL-1, IL-6)
concept of ‘set point’ controlled by hypothalamus
- endogenous pyrogens shift set point
- caused by local production of prostaglandins by cyclo-oxygenase in the hypothalamus
- explains why aspirin and paracetamol reduce fever
what agencies to meds have to be approved/licensed by
MHRA - Medicines and Healthcare Products Regulatory Agency
EMA - European Medicines Agency
SMC - Scottish Medicines Consortium
unlicensed
not approved for use in UK
‘off-label’
a licensed medication that is being used for an unlicensed indication
‘specials’
unlicensed dermatological preparations
long history of use, no strong evidence base but clinically effective
causes of prescription errors
lack of knowledge - about patient, meds or allergies
mistake writing/generating prescription
poor communication
no local/national guidelines
pharmacy/medicine info service
factors associated with poor adherence
psychiatric co-morbidities
slower acting agents
multiple applications per day
lack of patient education
cosmetic acceptability of treatments
unintentional non-adherence
the NHS spends £100 million annually on unused medicine
pharmacology
branch of medicine concerned with uses, effects and modes of action of drugs
define pharmacokinetics
effect of body on drug
define pharmacodynamics
effect of drug on body
pharmacokinetics
need to think about route of administration - topically where possible, if oral, optimal absorption important
distribution - where drug goes
metabolism - esp in liver disease
excretion - esp in renal disease
pharmacodynamics
individual variation in response
think about
- age of patient
- pregnancy risk
- drug interactions
- pharmacogenetics
topical therapy
medication applied to skin
vehicle + active drug
vehicle
pharmacologically inert, physically and chemically stable substance that carries the active drug
factors affecting topical absorption
concentration
base/vehicle
chemical properties of drug
thickness and hydration of stratum corneum
temperature
skin site
occlusion
examples of vehicle
solution
cream
lotion
gel
foam
tape
paste
spray powder
shampoo
ointment
paint
examples of topically used drugs (give 6 examples)
corticosteroid
antibiotic
antiviral
chemo
antiinflam
salicyclic acid
topical steroids - anti-inflam and immunosuppressive properties
regulate pro inflam cytokines
suppress fibroblast, endothelial and leukocyte function
vasoconstriction
inhibit vascular permeability
topical steroids
range of potencies
used appropriately - very safe
prescribe enough - see BNF , can use finger-tip units - 0.5g , should treat area double size of one hand - useful in young children , charts available for age
6 examples of side effects of topical steroids
thinning/atrophy
bruising
telangiectasia
acne/rosacea
glaucoma
cataracts
systemic treatments in derm
retinoids
traditional immunosuppressants
biologics (also immunosuppressive)
retinoids
vit A analogues
- normalise keratinocyte function
- anti inflam and anti cancer effects
teratogenic - careful patient selection
side effects of retinoids
cheilitis and xerosis
increase transaminases and triglycerides
rarely psychiatric, eye, bone side effects
4 diff molecules used orally in derm
acne - isotretinoin
psoriasis - acitretin
cutaneous T cell lymphoma - bexarotene
hand eczema - alitretinoin
immunosuppressants
treatment of inflam skin disorders
oral steroids
azathioprine
ciclosporin
methotrexate
mycophenolate mofetil
risk of malignancy and serious infection
need regular blood test monitoring
- FBC
- renal and liver function (ciclosporin and methotrexate)
biologics in derm
next generation in treatment of inflam conditions
- genetically engineered proteins derived from human genes
- designed to inhibit specific components of the immune system
- very effective, but expensive
‘cept’ suffix
indicates it is a receptor fusion
‘mab’ suffix
used to denote monoclonal antibodies
risk of infection with biologics
TB reactivation
serious infection
avoid line vaccines
malignancy
TNF inhibitors - risk of demyelination
how can we make a diagnosis of a skin inf
history
examination
investigations
signs of an infection
erythema
hot
tender
pus
exudate
fever
impetigo
superficial skin condition - most common bacterial skin inf in children
can be bullous
staph aureus, strep pyogenes
treatment for impetigo
always check local formulary
if localised: fusidic acid 2% cream 3-4times daily for 5 days
mupirocin 2% cream up to 3x daily for 5 days
if widespread, severe, bullous:
flucloxacillin 500mg oral 4x daily for 7 days
erythromycin 500mg oral 4x daily for 7 days
likely organism of cellulitis/erysipelas
streptococcus pyogenes
staphylococcus aureus
1st choice antibiotic for cellulitis/erysipelas
flucloxacillin 1g IV every 6hrs
plus benzylpenicillin 1.8g IV every 6hrs
differential diagnosis of cellulitis
DVT
venous eczema
allergic contact dermatitis
necrotising fasciitis
oedema blisters
acute exacerbation of oedema
dorsum of feet
often erythematous
can feel hot
lipodermatosclerosis
if acute can be hot and tender
- look for signs of venous disease
- bilateral (often misdiagnosed as cellulitis)
treatment
- treat underlying venous disease
- topical steroids
fungal infections
tinea - infection by a dermatophyte
candidiasis
tinea on body
ringworm or tinea corporis
tinea on head
tinea capitis
tinea on feet
tinea pedis (athlete’s foot)
tinea on groin
tinea cruris
tinea on nails
onychomycosis
treatment of tinea
topical treatment - terbinafine or clotrimazole cream
requires antifungals - if affecting scalp or nails
check and treat other family members
treatment for candida
nystatin
miconazole
ketoconazole cream
acne vulgaris
disease of pilo-sebaceous unit (PSU) - face, chest, back
causes “sticky” keratinocytes + increased sebum viscosity
blocked follicles = COMEDONES
change in commensal bacteria behaviour (propionobacterium) = INFLAMMATION
papules, pustules, nodules, cysts, scars
comedones
blocked follicles
topical treatment for acne vulgaris
benzoyl peroxide
antibiotic: clindamycin, dalacin T lotion, erythromycin
retinoids: adapalene
combination: duac (BPO and clindamicin)
treclin (tretinoin and clindamicin)
epiduo gel - adapalene and BPO
others - azaleic acid, nicatinamide gel
systemic treatment for acne vulgaris
antibiotics: tetracyclines, erythromycin, trimethoprim
anti-androgens: combined oral contraceptive pill
isotretinoin (roaccutane)
UVB
dapsone
isotretinoin
retinoid medication - vit A derivative
most effective treatment - reserved for treatment failure, evidence of scarring, severe acne, acne fuminans
prescribed by dermatologists and dispensed by hospital pharmacy
weight based treatment - aim to achieve total cumulative dose 120mg/kg
can have multiple treatment courses if needed
multiple side effects - dry skin, lips, epistaxis, dry brittle hair, myalgia
counselling required prior to treatment -risk of low mood
teratogenic
can raise triglycerides
acne fulminans
sudden onset acneform eruption
feverish and unwell
joint pains
start low dose isotretinoin but cover with prednisolone
treatment for scarring
treat inflam first
if had isotretinoin usually should wait for 1yr before looking into treatment for scarring
- depends on type of scarring
- intralesional steroid
- excision of ice pick scars
- laser
- dermabraison
- chemical peels
acne rosacea
chronic inflam
- PSU
- cutaneous vasculature
ace of clubs distribution
unusual on non-facial sites
subtypes of acne rosacea
erythemato-telangiectatic
papulo-pustular
phymatous (M»>F)
ocular
no comedones
topical treatment for acne rosacea
metronidazole - rosex, metrogel
azeleic acid - finacea
ivermectin - soolantra
brimonidine - mirvaso
systemic treatment for acne rosacea
oral antibiotics - tetracyclines and erythromycin
isotretinoin - low dose
light based treatments
laser
atopic eczema
aka atopic dermatitis
inflammatory skin condition
commonly affects flexural areas
multiple types and a spectrum of severity
wide range of external or internal factors can induce condition
definition of atopic eczema
an itchy skin condition in the last 12 months
plus 3 of following:
- onset before age 2
- history of flexural involvement
- history of generally dry skin
- history of other atopic disease - history in 1st degree relative if under 4yrs
pathogenesis of atopic eczema
genetics
- many genes implicated
- key role for filaggrin gene
- atopic FH - atopic eczema, asthma, hay fever (allergic rhinitis), food allergy
- epidermal barrier dysfunction
- environmental factors
- immune system dysregulation
pathology of atopic eczema
spongiosis (intercellular oedema) within the epidermis
acanthosis - thickening of epidermis
inflammation - superficial perivascular lymphohistiocytic infiltrate
clinical features of atopic eczema
itch
distribution - flexures, neck, eyelids, face, hands and feet
tends to spare nappy area
acute changes - pruritus, erythema, scale, papules, vesicles
exudate, crusting, excoriation
chronic changes - lichenification, plaques, fissuring
exogenous (external) types of eczema
contact dermatitis - irritant and allergic
lichen simplex
photoallergic or photoaggravated eczema
endogenous (internal) types of eczema
atopic
discoid
venous
seborrhoeic dermatitis
pompholyx
juvenile plantar dermatitis
asteatotic
allergic contact dermatitis
type 4 hypersensitivity
delayed hypersensitivity - 48-72hrs to develop reaction
antigen presenting cells take hapten/allergen to LN and present to naive T cells
clonal expansion of these T cells, released into blood stream
when these T cells next encounter hapten
- mast cell degranulation, vasodilatation and neutrophils
irritant contact dermatitis
skin injured by…
1. friction - microtrauma, cumulative
2. environmental factors - cold, over-exposure to water, chemicals such as acids, alkalis, detergents and solvents
patch testing
potential allergens applied (no needles involved)
baseline/standard series - applied to all patients
applied monday - removed wednesday - re-assess friday
seborrheic dermatitis - infants
distinctive pattern
predilection for scalp, proximal flexures
<6months age usually
often clears within weeks of treatment
seborrheic eczema - adults
chronic dermatitis
malassezia yeast increased in the scaly epidermis of dandruff and seborrheic dermatitis
red, sharply marginated lesions covered with greasy looking scales
distinctive distribution - areas rich in supply of sebaceous glands (scalp, face, upper trunk)
discoid eczema
circular plaques of eczema
cause often unknown
may develop at sites of trauma/irritation
asteatotic eczema
very dry skin
cracked scaly appearance
most commonly shins affected
climate - heat
excessive washing/soaps
venous eczema
stasis eczema or varicose eczema
increased venous pressure
oedema
ankle and lower leg involved
resolution of oedema can help - compression stockings
treatment of eczema
patient education
avoid causative/exacerbating factors
emollients (moisturisers)
- ointments - greasy but effective
- creams - lighter
- lotions - more watery
soap substitutes
intermittent topical steroids - different potency - hydrocortisone, betamethasone
sometimes need antihistamines or antimicrobials
calcineurin inhibitors - topical pimecrolimus and tacrolimus
treatment of severe eczema
UV light
immunosuppression
- azathioprine
- ciclosporin
- mhycophenolate mofetil
- methotrexate
biologic - dupilumab (IL-4/IL-13 inhibitor)
what is psoriasis
chronic, immune mediated disease
sharply demarcated erythematous plaques with micaceous scale
3% of UK pop
20-30yrs and 50-60yrs
75% before 40yrs
systemic disease
- 5-30% develop psoriatic arthritis
- psychosocial implications
- metabolic syndrome
pathogenesis of psoriasis
polygenic predisposition + environmental triggers
35-90% have FH
infection
drugs
trauma
sunlight
histology of psoriasis
hyperkeratosis
neutrophils in stratum corneum
psoriasiform hyperplasia : acanthosis with elongated rete ridges
dilated dermal capillaries
T cell infiltration
subtypes of psoriasis
chronic plaque psoriasis
guttate psoriasis
palmo-plantar psoriasis, or pustulosis
scalp psoriasis
nail psoriasis
flexural/inverse psoriasis
pustular psoriasis
erythodermic psoriasis
diagnosis of psoriasis
clinical
skin biopsy if atypical
differential diagnosis of psoriasis
seborrheic dermatitis
lichen planus
mycosis fungoides
Bowens disease, drug eruption, infection, secondarry syphillis, contact dermatitis
management of psoriasis
primary care
- emollients
- soap substitutes
- vit D3 analogues
- coal tar creams
- topical steroid - with care
- salicylic acid
secondary care
- optimise topical therapy
- crude coal tar
- dithranol
- UVB phototherapy
- oral retinoids - acitretin, teratogenic
seborrheic keratoses
benign
warty growths, “stuck on appearance”
can have variable appearance
patients often have multiple +/- cherry angiomas
generally left untreated, but if troublesome - cryotherapy and curettage
cryotherapy
liquid nitrogen
pros - cheap and easy to perform “on the day”
cons - can scar, failure/recurrence, no pathology result
sign of leser-trelat
paraneoplastic phenomenon
abrupt onset of widespread seborrheic keratosis, particularly in a younger individual
SKs remain benign but may indicate underlying solid organ malignancy - GI adenocarcinoma
viral warts
due to HPV
rough hyperkeratotic surface
difficult to treat
will clear when immunity developed to virus
cryotherapy or wart paints can stimulate immune system slightly
can curette in severe cases
what is a cyst
encapsulated lesion containing fluid or semi-fluid material
usually firm and fluctuant
different types of cysts
epidermoid cyst
pilar cyst
steatocystoma
dermoid cyst
hidrocystoma
ganglion cyst
how to treat cysts
excision
if inflamed/infected
- antibiotics
- intralesional steroid
- incision & drainage
dermatofibroma
benign, fibrous nodule, often on limbs - proliferation of fibroblasts
cause is unknown
firm nodule, tethered to skin but mobile over fat
pale pink/brown , often paler in centre
dimple sign positive
usually asymptomatic - can be itchy or tender
excision if concern or symptomatic
lipoma
benign tumour consisting of fat cells
common
cause unknown
smooth and rubbery subcutaneous mass
usually asymptomatic
if tender - angiolipoma, liposarcoma - rare malignancy
angioma
vascular lesion
explain angiomas
overgrowth of blood vessels in the skin due to proliferating endothelial cells
generally asymptomatic - can be unsightly or bleed
occur in all age groups , both sexes
pregnancy and liver disease
excision or laser
explain pyogenic granulomas
rapidly enlarging red/raw growth, often at a site of trauma
bleed easily
cause unknown
occur in up to 5% of pregnancies
common on head and hands
removed by curettage and cautery
Bowen’s disease
aka intraepidermal squamous cell carcinoma
- full thickness dysplasia, entirely contained within the epidermis, no metastatic potential
- potential to become malignant
irregular, scaly erythematous plaque
how to treat Bowen’s
cryotherapy
curettage - lesion scraped off and heat applied to seal vessels and destroy residual cancer cells
photodynamic therapy
imiquimod
what is photodynamic therapy
photochemical reaction to selectively destroy cancer cells
topical photosensitising agent applied - concentrates in cancerous cells
red light applied (light colour dependant on which agent is used)
photodynamic reaction occurs between light, photosensitiser and oxygen causing inflammation and destruction of cells
pros and cons of photodynamic therapy
pros :
done for patient by hosp staff
can treat multiple areas including those which would be hard to reach by patient
1 or 2 treatments
cons: requires hosp appts
can be painful and scar
imquimod
aldara
immune response modifier - stimulates cytokine release
actinic keratoses
rough scaly patches on sun damaged skin
low risk of transformation to SCC
treatment
- cryotherapy
- curettage
- diclofenac gel
- imiquimod
melanoma in situ
melanoma cells entirely confined to epidermis
no metastatic potential
treated with excision
lentigo maligna
type of melanoma in situ
usually facial
sun protection
cover up
avoid sun at peak hours - 10am-4pm
don’t burn and try not to tan
avoid sunbeds
sunscreen
- UVA and UVB radiation
- at least SPF 30/4 star
- need to apply 2tbsps every 2hrs
risk factors for non-melanoma skin cancer
UV radiation
photochemotherapy (PUVA)
chemical carcinogens
ionising radiation
human papilloma virus
familial cancer syndromes
immunosuppression
basal cell carcinoma
slow growing
locally invasive
rarely metastasise
nodular
- pearly rolled edge
- telangiectasia
- central ulceration
- arborising vessels on endoscopy
treatment of BCCs
excision is gold standard
- ellipse with rim of unaffected skin
- curative if fully excised
- will leave scar
curettage in some circumstances
imiquimod if superficial
indications for Mohs surgery
site
size
subtype
poor clinical margin definition
recurrent
perineural or perivascular involvement
squamous cell carcinoma
derived from keratinising squamous cells
usually on sun exposed sites
can metastasise, up to 16% depending on study
faster growing, tender, scaly/crusted or fleshy growths
can ulcerate
treatment of SCC
excision
+/- radiotherapy
follow up if high risked
immunosuppressed
>20mm diameter
>4mm depth
ear, nose, lip, eyelid
perineural invasion
poorly differentiated
keratoacanthoma
varient of squamous cell carcinoma
erupts from hair follicles in sun damaged skin
grows rapidly, may shrink after few months and resolve
surgical excision
risk factors for melanoma skin cancer
UV radiation
genetic susceptibility - fair skin, red hair, blue eyes, and tendency to burn easily
familial melanoma and melanoma susceptibility genes
ABCDE rule
Asymmetry
Border
Colour
Diameter
Evolution
7 point checklist
major features:
change in size, shape, colour
minor features:
diameter >5mm, inflammation, oozing/bleeding, mild itch or altered sensation
cutaneous lymphoma
secondary cutaneous disease from systemic/nodal involvement
primary cutaneous disease - abnormal neoplastic proliferation of lymphocytes in the skin
- cutaneous T cell lymphoma (65%)
- cutaneous B cell lymphoma (20%)
cutaneous T cell lymphoma
counts for 65%
mycosis fungoides
sezary syndrome
CD30+ lymphoproliferative disorders
subcutaneous panniculitis like T cell lymphoma
cutaneous CD4+ lymphoma
extranodal NK/T cell lymphoma
cutaneous B cell lymphoma
counts for 20%
cutaneous follicle centre lymphoma
cutaneous marginal zone lymphoma
cutaneous diffuse large B cell lymphoma
mycosis fungoides (MF)
most common CTCL & accounts for around 50% of all primary cutaneous lymphomas
incidence 6 per 1 mil pop
cause unknown
more common in older patients and more common in men than women
indolent course
stages of MF
patch
plaque
tumour
metastatic
sezary syndrome
CTCL affecting skin of entire body
lymph node involvement
sezary cells in peripheral blood
poor prognosis - median survival 2-4yrs
treatment of cutaneous lymphoma
dependent on stage
topical steroids
PUVA or UVB
localised radiotherapy
interferon
bexarotene
low dose methotrexate
chemotherapy
total skin electron beam therapy
extracorporeal photophoresis
bone marrow transplantation
total skin electron beam therapy
type of radiotherapy consisting of very small electrically charged particles
delivers radiation primarily to superficial layers
extracorporeal photophoresis
step 1 - patients blood drawn and leukocytes collected
step 2 - collected white cells mixed with psoralen which makes T cells sensitive to UVA radiation
step 3 - exposed to UVA radiation, damaging diseased cells
step 4 - treated cells reinfused back to patient
cutaneous metastases
can be secondary to primary skin malignancy such as melanoma or due to primary solid organ malignancy
- most commonly breast, colon and lung
management of cutaneous metastases
treat the underlying malignancy
local excision
localised radiotherapy
symptomatic
consequences of skin failure
sepsis
hypo and hyper thermia
protein and fluid loss
renal impairment
peripheral vasodilation
erythroderma
descriptive term rather than diagnosis
“any inflam skin disease affecting >90% of total skin surface”
causes of erythroderma
psoriasis
eczema
drugs
cutaneous lymphoma
hereditary disorders
unknown
