dermatology Flashcards
cyst types
Epidermoid cyst - ‘Blackhead’
Sebaceous cyst - ‘Whitehead’
Dermoid cyst - Can contain hair (or teeth/other abnormal growths within -dependent on the location [ovaries])
what is tinea capitis
fungal infection of the scalp (scalp ringworm), which is a key cause of scarring hair loss in children
well-demarcated hair loss on the scalp
kerion- which are raised, pustular, boggy masses appearing as numerous bright yellow areas with the skin surface surrounded by regions of hair loss and flakiness.
what is Tinea corporis
dermatophyte fungal infections of the trunk / arms / legs
i.e ringworm
what is eczema
chronic atopic condition caused by defects in the normal continuity of the skin barrier, leading to inflammation in the skin
different types e.g. atopic dermatitis, contact dermatitis
how to dx atopic dermatitis
an itchy skin condition plus 3/+ of:
- hx of involvement of the skin creases (eg. folds of elbows/behind knees)
- personal hx of asthma or hay fever (/hx atopic dis in 1st deg rel if < 4)
- hx of general dry skin in last yr
- visible flexural eczema (elsewhere if <4)
- onset < 2 yrs (not if <4)
acute changes in atopic dermatitis
erythema
swelling
crusting
erosions
fissuring
scaling
unclear boarders
hyper/hypopigmentation in darker skin
chronic changes in atopic dermatitis
scaling
lichenification (thick skin)
prurigo like lesions (nodules from scratching)
xerosis (v dry)
atopic stigmata in dermatitis
dennie morgan folds (under eyes)
keratosis pilaris
peri-orbital darkening
xerosis
what is eczema herpeticum
viral skin infection in patients with eczema caused by the herpes simplex virus (HSV) or varicella zoster virus (VZV)
presentation eczema herpeticum
patient who suffers with eczema that has developed a widespread, painful, vesicular rash with systemic symptoms such as fever, lethargy, irritability and reduced oral intake
- there will usually be lymphadenopathy
mx eczema herpeticum
ADMIT FOR IV ACICLOVIR ASAP
opthal if near eye
quantity of emollients needed per week in <12s
250-500g (500g is one big tub)
oitments are thicker creams are thinner
emollient safety advice
they are flammable (careful in px who smoke)
slip risk in bath
steroid ladder
Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)
how to use topical steroids
use the weakest steroid for the shortest period required to get the skin under control
don’t use more than once daily
finger tip unit needed for area size of 2 palms
topical steroid SEs
skin thinning - can make the skin more prone to flares, bruising, tearing, stretch marks and telangiectasia
systemic absorption of the steroid
excessive hair growth
other options to steroid tx
topical calcineurin inhibitors
2dary care referral
- phototherapy
- systemic therapies (e.g. pred course, methotrexate, ciclosporin, axathioprin)
- biologics
2 types of contact dermatitis
irritant contact
allergic contact
what is irritant contact dermatitis
direct chemical / physical irritation to the skin
not a hypersensitivity reaction
do not need sensitisation
anyone affectedw
what is allergic contact dermatitis
type IV hypersensitivity reaction (delayed)
prior sensitisation needed
only ppl w allergy react
- patch testing done (not prick testing - that is done for type I immediate reactions)
what is nummular dermatitis
a pruritic eczematous dermatosis characterized by multiple coin-shaped lesions
what is stasis dermatitis
type of eczema that develops in people who have poor blood flow
often near ankles
older ppl, venous insuff
tx w compression
what is seborrheic dermatitis
chronic form of eczema - appears on the body where there are a lot of oil-producing (sebaceous) glands like the upper back, nose and SCALP
what is psoriasis
T cell mediated abnormal immune response resulting in keratinocyte proliferation
- dry, flaky, scaly, faintly erythematous skin lesions that appear in raised and rough plaques, over the extensor surfaces of the elbows and knees and on the scalp.
- clear borders
Plaque psoriasis
thickened erythematous plaques with silver scales, commonly seen on the extensor surfaces and scalp. The plaques are 1cm – 10cm in diameter.
Most common form of psoriasis in adults
Guttate psoriasis
commonly occurs in children.
- many small raised papules across the trunk and limbs - mildly erythematous and can be slightly scaly.
- RAINDROPS
- over time the papules -> plaques.
- often triggered by a STREPTOCOCCAL THROAT INFECTION, stress or medications.
- resolves spontaneously within 3 – 4 months.
Pustular psoriasis
rare severe form of psoriasis where pustules form under areas of erythematous skin. The pus in these areas is not infectious. Patients can be systemically unwell.
Medical emergency -> admission to hx
psoriasis triggers
infection (espesh guttate)
local skin injury - Koebner phenomenon (KP) = is the appearance of new skin lesions on previously unaffected skin secondary to trauma
obesity
smoking
alcohol
stress
HIV
drugs that can induce psoriasis
BBs
lithium
antimalarials
abx
NSAIDs
ACEi
Anti TNFs
systemic steroid withdrawal
Auspitz sign
small points of bleeding when plaques are scraped off
nail changes in psoriasis
nail pitting
leukonychia (white nails)
thickening, discolouration, ridging
onycholysis (separation of the nail from the nail bed)
flexural psoriasis
ie. inverse psoriasis - in axilla, groin, breasts etc
well demarcated shiny smooth plaques often lacking scale
fissuring
co-morbidities assoc w psoriasis
things that increase the risk of CVD -particularly obesity, hyperlipidaemia, HTN and DMT2
tx psoriasis
topicals =
emollients
steroids
coal tar
vitamin D analogues
calcineurin inhib
phototherapy
conventional systemics =
ciclosporin
methotrexate
acitretin
biologics =
all the -umabs
how long break in between courses of topical corticosteroids in patients with psoriasis
4 weeks
what is Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis
where a disproportional immune response causes epidermal necrosis
-> blistering and shedding of the top layer of skin.
Generally SJS affects <10% of body surface area + TEN affects >10%
causes of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis
Medications =
Anti-epileptics
Antibiotics
Allopurinol
NSAIDs
Infections =
Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV
presentation of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis
spectrum of severity
px start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin.
then develop a purple or red rash that spreads across the skin and starts to blister.
a few says after this skin starts to break away + shed leaving the raw tissue underneath
pain, erythema, blistering to lips + mucus membranes
irritates + ulcerated eyes
can also affect the urinary tract, lungs and internal organs
Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis mx
medical emergencies - admitted to a suitable dermatology or burns unit for treatment.
Supportive care - nutritional care, antiseptics, analgesia and ophthalmology input.
Treatment options include steroids, immunoglobulins and immunosuppressant medications guided by a specialist.
what is uticaria
hives - small itchy lumps that appear on the skin (maybe w rash, angioedema and flushing of the skin)
caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin (type 1 reaction - exaggerated IgE mediated immune responses)
- may be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.
causes of acute uticaria
triggered by something that stimulates the mast cells to release histamine. This may be:
Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications (common culprit drugs are the ‘As’: anticonvulsants, antibiotics, anti-inflammatories (NSAIDs), and allopurinol)
Viral infections
Insect bites
Dermatographism (rubbing of the skin)
types of chronic uticaria
an AI condition where autoantibodies target mast cells and trigger them to release histamines and other chemicals
Chronic idiopathic urticaria
Chronic inducible urticaria
Autoimmune urticaria (w other condition)
how can chronic inducible urticaria be triggered
Sunlight
Temperature change
Exercise
Strong emotions
Hot or cold weather
Pressure (dermatographism)
mx uticaria
non-sedating antihistamines (e.g. loratadine or cetirizine) - for up to 6 weeks following an episode
a sedating antihistamine (e.g. chlorphenamine) may be considered for night-time use (in addition to day-time non-sedating antihistamine) for troublesome sleep symptoms CKS
prednisolone is used for severe or resistant episodes
what is cellulitis
an infection of the skin and the soft tissues underneath
will be breach in skin barrier
cellulitis presentation
Erythema
Warm or hot to touch
Tense
Thickened
Oedematous
Bullae (fluid-filled blisters)
A golden-yellow crust indicates a staph aureus infection
systemically unwell - sepsis?
causes cellulitis
Staphylococcus aureus
Group A streptococcus (mainly streptococcus pyogenes)
Group C streptococcus (mainly streptococcus dysgalactiae)
consider MRSA
Eron classification cellulitis
Class 1 – no systemic toxicity or comorbidity
Class 2 – systemic toxicity or comorbidity
Class 3 – significant systemic toxicity or significant comorbidity
Class 4 – sepsis or life-threatening infection
mx cellulitis
class 3/4/v old/v young/immunocomp/near face= admission for IV abx
abx = FLUCLOXACILLIN (oral or IV)
alts = Clarithromycin
Clindamycin
Co-amoxiclav (the usual first choice for cellulitis near the eyes or nose)
what is melanoma
malignant neoplasm of melanocytes
RFs melanoma
age
UV exposure
skin type (paler)
>100 melanocytic naevi (having lots of moles)
>5 atypical naevi
multiple solar lentigines
FHx
personal hx
familial melanoma
CDKN2A
red flags skin lesion
asymmetry
irregular border
multiple colours
>7mm diameter
evolution
7 pt weighted checklist for skin lesions
need 3+ for referral
major features (2 pts each)
change in size
irreg shape
irreg colour
minor features (1)
largest diameter >7mm
inflam
oozing or crusting
change in sensation (inc itch)
what is acral lentiginous melanoma
palms soles or nails
no connection to UV
equal incidence in all skin (so most common for darker skin to get)
presents late so worse prog
what is lentigo maligna melanoma
elders
chronic accum sun exposure
on face
on sun damaged skin
(darkened bits)
what is nodular melanoma
red/black lump which bleeds/oozes
early vertical growth phase
most aggressive
males
trunk, head, neck
(can seem more symm w reg borders but is pigmented + growing)
what is superficial spreading melanoma
most common
prolonged radial growth phase
trunk in males
legs in females
what is amelanotic melanoma
hx rapid growth
residual pigment
look pink and stick out
what is used to help stage melanoma
breslow thickness
stage 0 melanoma
in situ
stage 1 melanoma
thinner tumours confined to skin (almost 100% 5+ yr survival)
stage 2 melanoma
thicker tumours confined to skin (80%)
stage 3 melanoma
lymph node involvement (70%)
stage 4 melanoma
distant mets (30%)
mx melanoma
GP 2 wk wait referral
diagnostic excision of pigmented skin lesion w 2mm peripheral margin
wide local excision
test for BRAF mutation (causes it to grow more aggressively)
what is a sentinel lymph node biopsy
take out nearest draining lymph node as well (use dye to see)
tx stage 3/4 melanomas
Targeted therapy:
BRAF (protein that helps control cell growth) inhibitors
- dabrafenib
MEK inhibitors
- trametinib
Immunotherapy
Anti CTLA4 antibody
Anti PD1 antibody
rarely use radio or chemo
RFs for non-melanoma skin cancer
UV exposure
- SCCs = chronic cumulative
- BCCs = intermittent intense
pale skin
age
immune suppression (SCC)
ionising radiation
chronic wounds (SCC)
smoking (SCC)
HPC (SCC)
genetic syndromes
what is actinic keratosis
dry, scaly patches of skin that have been damaged by the sun
partial thickness dysplasia of epidermal keratinocytes
begins in basal layer
no BM invasion
flesh-coloured, irregularly shaped, small macules/plaques
small
devs over yrs at sun exposed sites
v small no progress to SCC
no reg flag sx
tx actinic keratosis
prev further risk
topical tx
-fluorouracil cream
- diclofenac
- imiquimod
Photodynamic therapy (PDT)
discrete lesions:
cryotherapy
C&C
refer if does not resolve/unsure dx
what is bowen’s disease
precancerous dermatosis
SCC IN SITU
full thickness dysplasia of epidermal keratinocytes
more of a well defined plaque
cant met
develop over yrs at sun exposed sites
bowen’s disease tx
INITIAL = 5-flurouracil
cryotherpy
C&C
PDT
what is squamous cell carcinoma (SCC)
2nd most common skin cancer
abnormal, accelerated growth of squamous cells
now invasion past BM
potential to met
features of SCC
rapid growth - wks/mths
raised base
keratotic/scaly lesions
may ulcerate/bleed
may be painful
sun exposed sites - face, lips, ears, hands, forearms, lower legs
tx SCC
surgery - standard excision, Mohs surgery (removes skin layers at a time)
radiotherapy
what is basal cell carcinoma (BCC)
most common type of skin cancer
abnormal, accelerated growth of basal cells
features BCC
slowly growing plaque/nodule
skin coloured, pink/pigmented, often shiny / pearly
rolled edges
telangiectasia
ulceration + spontan bleeding
rarely mets
BCC tx
surgery
radiotherapy
what to do Mohs surgery
if high risk :
tumour site = central face, eyes, nose, ears
size (>2cm)
histology sub type (morphoetic, infiltrative, micronodular, basosqaumous)
poor clinical definition of tumour margins
recurrent lesions
perineural/perivascular involvement
tx of superficial BCC
C&C
Cryotherapy
Topical - imiquimod, 5-flurouracil
Photodynamic therapy
what is polymorphic eruption of preg
pruritic condition associated with last trimester
lesions often first appear in abdominal striae
mx depends on severity: emollients, mild potency topical steroids and oral steroids
what is atopic eruption of pregnancy
is the commonest skin disorder found in pregnancy
it typically presents as an eczematous, itchy red rash.
no specific tx needed
what is pemphigoid gestationis
pruritic blistering lesions
often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms
usually presents 2nd or 3rd trimester and is rarely seen in the first pregnancy
oral corticosteroids are usually required
how long does it take a pityriasis rosea rash to resolve
6-12 weeks
presentation of pityriasis rosea
Minority may give a hx of a recent viral infection
herald patch (single larger pink/red oval 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 = ‘fir-tree’ appearance
how is acne caused
chronic inflammation, with or without localised infection, in pockets within the skin known as the pilosebaceous unit (tiny dimples on skin that contain hair follicles + sebaceous glands - produce sebum)
There is increased sebum production, trapping of keratin + blockage -> swelling + inflam
Swollen and inflamed units are called comedones.
acne tx
explore the psychosocial burden
No tx may be acceptable if mild
TOPICAL BENZOYL PEROXIDE reduces inflammation, helps unblock the skin and is toxic to the P. acnes bacteria
TOPICAL RETINOIDS (chemicals related to vitamin A) slow the production of sebum (women of childbearing age need effective contraception)
- e.g. ADAPALENE
TOPICAL antibiotics such as CLINDAMYCIN (prescribed with benzoyl peroxide to reduce bacterial resistance)
ORAL antibiotics such as LYMECYCLINE
use erythromycin in pregnancy
DONT USE ABX AS MONOTHERAPY
Oral contraceptive pill can help PX stabilise their hormones and slow the production of sebum
tx severe acne
oral retinoid e.g. isotretinoin ie roaccutane (TERATOGENIC)
- only prescribed by specialist after other methods fail
SEs isotretinoin ie roaccutane
Dry skin and lips
Photosensitivity of the skin to sunlight
Depression, anxiety, aggression and suicidal ideation. Patients should be screened for mental health issues prior to starting treatment.
Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
what are viral warts
common benign lesion caused by HPV
spread through direct skin contact
specialist dermatology referral for acne
Severe acne (scarring, hyperpigmentation and widespread pustules)
tx viral warts
none
soaking/paring
chemicals -salicyclic acid
cryotheraoy
c&c
laser
what is molluscum contagiosum
a viral skin infection caused by the molluscum contagiosum virus, which is a type of poxvirus
self-resolving but can take yrs
spread through direct contact
features of molluscum contagiosum
small, flesh coloured papules (raised individual bumps on the skin) that characteristically have a central dimple. They typically appear in “crops” of multiple lesions in a local area
what is an epidermoid cyst
benign cyst derived from infundibulum of hair follicle
have a central punctum
what is a pilar cyst
benign keratin filled cyst derived from outer hair root sheath
often runs in fams - AD
what is seborrhoeic keratosis
+ how does it look
v common benign lesion
well-circumscribed plaques or papules with a ‘stuck on’ appearance
brown, black or light tan.
look waxy or scaly and slightly raised
They appear gradually, usually on the face, neck, chest or back
a sign of Leser-Trélat disorder
asx
what is solar lentigo
from cumulative sun exposure on back of hand + face
what is dermatofibroma
common benign lesion usually on legs
get at middle age
has a tethering/pinch sign
can get from mild trauma
what is a lipoma
common benign tumour made of fat cells
soft/smooth dome shaped subcut lesion
what is a pyogenic gruanuloma
acquired proliferation of BVs
what is allergic rhinitis
inflammation of the inside of the nose caused by an allergen, such as pollen, dust, mould, or flakes of skin from certain animals
causes cold-like sx
tx w salt water rinsing/antihistamines
what parasite are head lice
pediculus humanus capitis parasite
tx head lice
dimeticone 4% lotion can be applied to the hair and left to dry. This is left on for 8 hours, then washed off. This process is repeated 7 days later to kill any head lice that have hatched since treatment.
fine combs
what are scabies
tiny mites called Sarcoptes scabiei that burrow under the skin causing infection and intense itching
lay eggs in the skin
can take 8 wks to get sx/rash from initial infestation
scabies presentation
incredibly itchy small red spots, possibly with track marks where the mites have burrowed.
The classic location of the rash is between the finger webs, can be whole body
does anyone they live w have similar rash?
scabies tx
PERMETHRIN cream - apply to whole body when cool, leave for 8 – 12 hours then wash off
repeat 1 wk later
Oral IVERMECTIN as a single dose that can be repeated a week later is an option for difficult to treat or crusted scabies.
tx household + close contacts in the same way
wash clothes + bedding on hot, hoover carpets
still itching after scabies tx?
Itching can continue for up to 4 weeks after successful treatment
Crotamiton cream and chlorphenamine at night at night can help with the itching.
what is crusted scabies
serious infestation with scabies in px that are immunocompromised.
- may have over a million mites in their skin
- extremely contagious
- patches of red skin that turn into scaly plaques - can be misdiagnosed as psoriasis
- may not have an itch as they do not mount an immune response to the infestation
- may need admission for tx as an inpatient with oral ivermectin and isolation.
what is impetigo
superficial bacterial skin infection, usually caused by the staphylococcus aureus bacteria
contagious
non-bullous or bullous
non-bullous impetigo presentation
typically occurs around the nose or mouth. The exudate from the lesions dries to form a “golden crust”. Do not usually cause systemic symptoms or make the person unwell.
non-bullous impetigo tx
Antiseptic cream (hydrogen peroxide 1% cream) first line
Topical fusidic acid (abx)
Oral flucloxacillin is used to treat more wide spread or severe impetigo
what is bullous impetigo
always s. aureus
this bacteria can produce epidermolytic toxins that break down the proteins that hold skin cells together -> 1–2 cm fluid filled vesicles to form on the skin. These vesicles grow in size and then burst, forming a “golden crust”. Eventually they heal without scarring. These lesions can be painful and itchy.
more common in neonates + <2yrs
more likely to get systemic sx
tx bullous impetigo
Swabs of the vesicles can confirm the diagnosis, bacteria and antibiotic sensitivities.
Tx w antibiotics, usually flucloxacillin. This may be given orally or intravenously if they are very unwell or at risk of complications.
The condition is very contagious and patients should be isolated where possible.
what is staphylococcal scalded skin syndrome (SSSS)
a condition caused by a type of s. aureus bacteria that produces epidermolytic toxins (they are protease enzymes that break down the proteins that hold skin cells together).
When a skin infection occurs and these toxins are produced, the skin is damaged and breaks down.
affects children under 5 years (older have developed immunity to the toxins)
staphylococcal scalded skin syndrome (SSSS) presentation
- generalised patches of erythema on the skin
- then skin gets thin + wrinkled.
- then the formation of fluid filled blisters (bullae) - burst + leave v sore, erythematous skin below
similar appearance to a burn or scald.
Nikolsky sign = v gentle rubbing of the skin causes it to peel away
Systemic sx = fever, irritability, lethargy + dehydration.
If untreated it can lead to sepsis and potentially death.
Staphylococcal scalded skin syndrome (SSSS) tx
admission + tx with IV abx.
Fluid and electrolyte balance is key to management as patients are prone to dehydration.
When adequately tx, usually make a full recovery without scarring.
causes of erythema nodosum
infection
- streptococci
- tuberculosis
- brucellosis
systemic disease
– sarcoidosis
- inflammatory bowel disease
- Behcet’s
malignancy/lymphoma
drugs
- penicillins
- sulphonamides
- COCP
pregnancy
features of rosacea
typically affects nose, cheeks and forehead
flushing is often first symptom
telangiectasia are common
later develops into persistent erythema with papules and pustules
rhinophyma (large bulbous nose)
ocular involvement: blepharitis
SUNLIGHT exacerbates symptoms
what to avoid in rosacea
direct sunlight
oil based products
alcohol
spicy food
hot drinks
sudden temp changes
excessive exercise
rosacea tx for:
predominant erythema/flushing:
mild-to-moderate papules and/or pustules:
moderate-to-severe papules and/or pustules:
daily application of a high-factor sunscreen
predominant erythema/flushing:
topical BRIMONIDINE gel
brimonidine (topical alpha-adrenergic agonist) - ‘as required basis’
mild-to-moderate papules and/or pustules:
topical IVERMECTIN is first-line
alternatives include: topical METRONIDAZOLE or topical azelaic acid
moderate-to-severe papules and/or pustules:
combination of topical ivermectin + oral DOXYCYCLINE
laser therapy may be appropriate for patients with prominent telangiectasia
avoid topical steroids
what is shingles
(herpes zoster infection) is an acute, unilateral, painful blistering rash caused by reactivation of the varicella-zoster virus (VZV).
RFs shingles
increasing age
HIV: strong risk factor, 15 times more common
other immunosuppressive conditions (e.g. steroids, chemotherapy)
most common affected dermatomes in shingles
T1-L2
shingles features
prodromal period
- burning pain over the affected dermatome for 2-3 days
rash
- initially erythematous, macular rash over the affected dermatome
- quickly becomes vesicular
- well demarcated by the dermatome and does not cross the midline. However, some ‘bleeding’ into adjacent areas may be seen
shingles tx
infectious (avoid preg women + immunocomp ppl) until vesicles crusted over
analgesia - paracetamol + NSAIDs first line
- then neuropathic agents
- consider oral steroids in first 2 wks if immunocomp + no res
antivirals within 72 hours, unless the px is < 50 years and has a ‘mild’ truncal rash associated with mild pain and no underlying risk factors
- aciclovir, famciclovir, or valaciclovir
what constitutes as severe acne + what do you do if a patient has it
scarring, hyperpigmentation and widespread pustules
requires specialist dermatology referral
which bacteria contributes to dev of acne
Propionibacterium acnes
what is a keloid
tumour-like lesions that arise from the connective tissue of a scar and extend BEYOND the dimensions of the original wound
predisposing factors to keloid
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
keloid tx
early keloids may be treated with intra-lesional steroids e.g. triamcinolone
what is a hypertrophic scar
an grow following trauma and can present similarly to keloid, they do not extend past the margins of the damaged skin.
tx seborrheic dermatitis
scalp = ketoconazole 2% shampoo
Face and body = topical antifungals: e.g. ketoconazole
topical steroids: best used for short periods
red flags for drug reactions
mucosal involvement
blistering/skin peeling off
pain (common to be itchy but not usually pain)
lymphadenopathy
systemic upset - fever, abnormal LFTs, U&Es
what to document in drug reaction
documentation of all drugs + dates administered (inc OTC + complementary)
dates of eruption
create a drug time-line
response to removal of suspected agent
response to re-challenge (only if mild reaction + unsure of cause)
tx of mild drug eruption
withdraw drug
emollients
topical corticosteroids in short term for sx relief
antihistamines if urticaria
what are steven johnson syndrome (SJS) + toxic epidermal necrolysis (TEN)
almost always caused by drugs
- drug eruption
TEN more severe
distinct from erythema multiforme (normally caused by infections - HSV / mycoplasma )
more common in px w HIV
most common causes of SJS + TEN
allopurinol
carbamazepine
lamotrigine
phenobarbital
phenytoin
sulfasalazine
sulfur abx
NSAIDs
nevirapine (HIV tx - ART)
presentation of SJS/TEN
new drug 7-21 days prev
prodrome of resp tract sx
fever
PAIN
dusky red lesions
atypical targets (ie not 3 concentric rings)
erythematous plaques
difference between SJS + TEN
percentage of detachment of epidermis (which becomes necrotic + starts peeling off)
SJS <10%
TEN >30% - more likely to have systemic sx that are worse
10-30 = SJS-TEN crossover
both have mucosal involvement
how to find prognosis in SJS + TEN
SCORTEN calc
mx SJS/TEN
ABCDE
stop medication (all non-essential if don’t know)
admit to ICU / burn unit
correct fluid + electrolytes
caloric replacement
protect from 2ndary infections w topical abx ointments (but not routine)
ophthalmology consult + eye care
urology consult if urethral inflam
oral antacids + mouth care
pulmonary hygiene if resp syndrome
periodic cultures of mouth, eyes, skin, sputum
physical therapy to prev contractures
topical paraffin (50/50), non adherent dressings
don’t prescribe any meds w/o discussion w senior
get lots of specialists involved
drug reaction with eosinophilia + systemic sx (DRESS)
15-40 days after exposure (anticonvulsants, sulfonamides etc)
high fever
rash: morbilliform eruption (measles-like) sometimes w oedema (espesh on face), infiltration, purpura and scaling
lymphadenopathy
atypical lymphocytes
eosinophilia
internal organ involvement
mx DRESS
withdrawal of drug
systemic steroids for severe cases
supportive tx
- dressings
- topical steroids
- emollients - 50/50 (50% white soft paraffin 50 % liquid paraffin - v greasy!)
- oral antihistamines
- address: fluid status, electrolytes, temp, nutrition
- tx 2ndary infection
acute generalised exanthematous pustulosis (AGEP)
<4 days after medication exposure - usually beta lactam abx
high fever
small sterile pustules arise within larger areas of oedematous erythema
oedema hands + face, purpura, vesicles, bulla, target lesions, mucosal involvement
marked leukocytosis w elevated neutrophils
(can look similar to acute pustular psoriasis)
mx AGEP
withdraw the drug (sld be enough)
topical steroids
emollients
antihistamines
systemic therapy rarely indicated
what is erythroderma
generalised erythema affecting >90% skin surface
due to rapid epidermal cell turnover
causes of erythroderma
eczema - espesh topical dermatitis
psoriasis
drug eruption - sulphonureas, isoniazid, sulfonamide
cutaneous T cell lymphoma
idiopathic
what comps do px w erythroderma need to be monitored for
dehydration, infection and high-output heart failure
Erythrodermic psoriasis
may result from progression of chronic disease to an exfoliative phase with plaques covering most of the body. Associated with mild systemic upset
more serious form is an acute deterioration. This may be triggered by a variety of factors such as withdrawal of systemic steroids. Patients need to be admitted to hospital for management
what is staphylococcal scalded skin syndrome (SSSS)
rare, severe, superficial blistering skin disorder which is characterised by epidermal detachment (more superficial than SJS/TEN)
triggered by exotoxin release from specific strains of s.aureus
normally in children <5
presentation SSSS
- usually starts with generalised patches of erythema on the skin
- then the skin looks thin and wrinkled
- then formation of fluid filled blisters called bullae, which burst and leave very sore, erythematous skin below.
Nikolsky sign (where very gentle rubbing of the skin causes it to peel away)
Systemic sx: fever, irritability, lethargy and dehydration.
If untreated -> sepsis, death.
what is bullous pemphigoid
an AI condition causing sub-epidermal blistering of the skin
more common in the ELDERLY
a result of an attack on the BM of the epidermis by IgG +/- IgE immunoglobulins + activated T lymphocytes
target is protein BP180
features of bullous pemphigoid
itchy, tense intact blisters typically around flexures
the blisters usually heal without scarring
there is stereotypically no mucosal involvement
dx bullous pemphigoid
Skin biopsy
- immunofluorescence shows IgG and C3 at the dermoepidermal junction
what is pemphigus vulgaris
AI blistering skin disease, painful blisters of the skin + mucus membranes
ages 30-60
jews + indians
antibodies directed against desmoglein 3 found on desmosomes
features pemphigus vulgaris
mucosal ulceration is common and often the presenting symptom (often oral)
skin blistering - flaccid, easily ruptured vesicles and bullae
Lesions are typically painful but not itchy. These may develop months after the initial mucosal symptoms.
Nikolsky’s = spread of bullae following application of horizontal, tangential pressure to the skin
dx pemphigus vulgaris
acantholysis on biopsy
tx pemphigus vulgaris
steroids are first-line
immunosuppressants
tx bullous pemphigoid
referral to a dermatologist for biopsy and confirmation of diagnosis
oral corticosteroids are the mainstay of treatment
topical corticosteroids, immunosuppressants and antibiotics are also used
hyperhydrosis tx
Topical aluminium chloride
cause of lichen planus
T-cell mediated AI disorder
where wld you see lichen planus
mucus membranes of mouth + vagina (inside vagina)
nails
wrists
characteristic feature of lichen planus
white lines on surface of the rash
- Wickham’s striae
is otherwise flat-topped, purple, polygonal papules and plaques
itchy
histology of lichen planus
saw-tooth pattern of epidermal hyperplasia
t-cell infiltration of dermis
reduced melanocytes
globular deposits of IgM
Lichen planus tx
potent topical steroids are the mainstay of treatment
e.g. betnovate
presentation acanthosis nigricans
symmetrical, brown, velvety plaques that are often found on the neck, axilla and groin
pathophysiology of acanthosis nigricans
insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)
causes of acanthosis nigricans
T2DM
GI cancer
obesity
PCOS
acromegaly
Cushing’s disease
hypothyroidism
familial
Prader-Willi syndrome
drugs
- COCP, nicotinic acid
tx pityriasis versicolor
topical antifungal - ketoconazole shampoo
presentation pityriasis versicolor
pale white/brown/pink patches
well-demarcated
dry scaly
usually on trunk
cause of pityriasis versicolor
fungal infection caused by Malassezia furfur
what is dermatitis herpetiformis
autoimmune blistering skin disorder associated with coeliac disease
caused by deposition of IgA in the dermis
Dermatitis herpetiformis features
itchy, vesicular skin lesions on the extensor surfaces (e.g. elbows, knees, buttocks)
skin bipsy for dermatitis herpetiformis
direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis
Hereditary haemorrhagic telangiectasia diagnostic criteria
epistaxis : spontaneous, recurrent nosebleeds
telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)
visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM
family history: a first-degree relative with HHT
side effect of ketoconazole
gynecomastia
sx in neonate who has got VZV from mother
dysfunc of bladder + bowel
eye defects - cataracts, chorioretinitis
limb hyperplasia
cortical atrophy
microcephaly
1 + = foetal varicella syndrome
tx dermatophyte nail infections
oral terbinafine
