Dermatology Flashcards
Functions of the skin
- Barrier to infection
- Thermoregulation
- Protection against trauma
- Protection against UV (melanin from tyrosine)
- Vit D synthesis
- Regulate H2O loss
What is the epidermis
Outermost layer of the 3 layers of the skin
What are langerhans cells of the skin
- present in the epidermis and dermis
- antigen presenting cells- travel to lymph nodes
what are merkel cells
- mechanoreceptor and tactile sensation
- make contact with specilised nerve ending
- found in basal layer of epidermis
- merkel tumour is fatal
what are the deepest layers of the skin
dermis , then hypodermis deeper (ie SC)
What are the layers of the skin
Epidermis
Basement membrane
Dermis
Hypodermis
Where is Type 1 collagen found
Skin tendons vasculature organs bone
Where is Type 2 collagen found
Cartilage
Where is Type 3 collagen found
Reticular layer of the dermis- commonly found alongside type 1
What are eccrine glands
sweat glands
help regulate body temp
What are Apocrine glands
- accompany hair follicles
aporine secretion
what are sebaceous glands
degradation of cells causes secretions which lubricate and waterproof hairs
what are meissener’s corpuscles
found in papillary dermis, detect light touch
what are pacinian corpuscles
foudn in wt bearing areas in deep dermis and SC
deep pressure and vibration detection
What are cavernous haemangiomas/strawberry marks
- Benign
- present in first few days of life
- raised
- resolves around ~1 year, +- scarring
Management of cavernous haemangiomas
- generally resolved around 18m of age
- may leave scarring
- if near mouth, nose, eye (impairing eating, nasal breathing, vision), betablockers can stop their growth
What is a complication of a massive cavernus hemangioma
Kasabach-merrit syndrome:
- decreased platelet count- thrombocytopenia
- DIC
What is a port wine stain
nevus flammeus
- benign
- present at birth
- flat
- stays for life
When may a port wine stain not be benign
when over the eye
do CT
-sturge- weber syndrome– abnormal vasculautre in the brain ft eye abnormalities eg glaucoma
What is a nevus
mole
- small dark spot
- san damage can cause them to become malignant
- more in Tunernes syndrome
What is a mongolian blue spot
- looks like bruising
- often around bakc or buttocks
- innolculus
- stay ofr life
- more prevalent in dark-skinned populations
- may be mistaken for NAI
What are cafe au lait
- brown, flat patches
- on most people
- if >5 of them and wid ein diamtere- may be sign of neurofibromatosis
What is erythema toxicum neonatum
- angry looking, red spots surrounded by red area
- normal
- if child is unwell (off feet, not settling)– make sure of diagnosis and rule out staph infection
What is the mechnism of an abscess
bacterial infection on minor wound, hair follicle, blocked oil/sweat gland
most commonly S.areus
sometimes parasites in developing countries
Management of an abscess
- inscision and drainage
- abx
what would you treat an abscess of the belly button with
co-amox
is in confined area so may be caused by an anaerobe or an aerobe
What are the types of cysts
- sebaceous- rare, sebum filled
- pilar- around hair follicles, often on scalp, run in families, middle aged adults
- epidermoid- face, neck, chest, shoulder, genitals. young.middle aged adults. PMHX- acne
tx of skin cyst
- do not burst
- warm compress
- excision
- Abx- fluclox
What are boils
- deep folliculitis
- staph areus
- looks like big, spots, filled with exudate
What are carbuncles
- colleciton/cluster of boils
- red, filled with purulent exudate
- Staph areus, Strep pyogens
- contagious
- most common on back and neck
- may be itchy and painful
- +- systemic sx- feever, chills
presentation of contact dermatitis
- infammation
- blistering
- dry
- thickened- red/dark brown
- cracked
- sore, stinging, itchy
- normlly on hands/face
management of contact dermatitis
- avoid irritant or allergen
- emollient
- topical steroid- hydrocortisone, beclamethason
- oral steroids
- *- phototherapy
- immunosupression
- *- alitretinoin- retinoid
– if occupational- need to report it to OH department
Causes of itchy skin
- xerosis (dry)
- exposure to heat, sun, wind
- eczema, psoriasis, ichthyosis vulgaris
- bacterial
- fungal
- parasites
Non derm causes:
- *- polycythemia
- liver cirrhosis/cholestasis
- CKD
- *- thyroid disease
- *- leukaemia, hodgkins
- *- pregnancy/menopause
- neuropathic
- psychosomatic
who is xerosis more common in
elderly
redcued sebum production, loss of collagen and elastin
Management of xerosis in elderly
- inspect regulalry for damage
- emollients regularly
- OTC products containing menthol- creates cold burn sensation that can relieve itching– eg tiger balm , capsacin
What types of ichthyosis vulgaris are there
Genetic (auto dom/xlinked)
- rate at which skin regenerates is affected-
- either shedding is too slow or skin cells reproduce too fast
Acquired
- Kidney disease
- hypothyroidism
- *- sarcoidosis
- *- Hodgkin’s
- *- HIV
A baby has persistently dry, very thickened rough skin. Her mother states her skin looks ‘fish-scaly’. It has gotten worse in the winter. Her father had a similar issue. What is your main diagnosis
Ichthyosis vulgaris
What are some causes of pruritis ani
- idiopathic
- psychological
- anorectal dysfunction
- secondary skin conditions- eczema, psoriasis
- infections- S.aureus, **scabies
- anal pathology- fissures, haemorrhoids
- colorectal cancer
- *- drugs- corticosteroids, colchicine
- *- food- spicy, nuts, alcohol
Ix for itchy anus
- DRE
- swab
management of pruritis ani
- coping techniques
- diet
- meds- laxatives, abx
- soothing topical preparations containing bismuth subligate, ZnO
- midly potent corticosteroids if inflamed
- sedating antihistamines if nocturnal
Causes of pruritis vulvae
- dermatological conditions- eczema psoriasis
- infections, infestations
- neoplasia- lichen sclerosis/VIN/carcinoma
- hormones- atrophic vaginitis
- GI disease and urinary incontinence
management of pruritis vulvae
- shower rather than bathe
- clean vulval area once a day with soap substitute (not soap)
- dab dry
- avoid feminine hygiene products
- avoid tight fitting clothes/synthetics
- avoid fabric conditioner and biological wash powder
- avoid spermicide- lubricated condoms
- management underlying cause
- sx- emollient plus mildly anxiolytic antihistammine
- consider 2 w trial of hydrocortisone 1%
- antifungal/antibacterial if co-existing infection
- 2ww if unexplained lump or ulcer
What is urticaria
Type 1 hypersensitivity
swelling involving superficial dermis, raising the epidermis
itchy wheals
prostaglandins, leukotrienes, chemotactic factors, mostly– histamine (skin mast cells)
What is angioedema
- Type one hypersensitivity
- deeper swelling than urticaria involving dermis and SC tissue
- tongue, lips
What is anaphylaxis, sx
- type 1 hypersensitivity (igE , histamine from mast cells and basophils)
- bronchospasm, facial and laryngeal oedema, wheeze, SOB, hypotension, tachycardia, light-headedness, collapse
Management of urticaria
- Avoid trigger
- Antihistammines- cetirizine, fexofenadine, loratadine
- oral pred if severe
Tx of angioedema
- corticosteroids (pred)
tx of anaphylaxis
IM Adrenaline (1mg/mL, 1:1000)
- <5yrs 150mcg/0.15mL
- 6-11yrs 300mcg/0.3mL
- 12-17yrs 300 or 500mcg depending on size of child and whether they are prepubertal
- >18yrs 500mcg/0.5mL
repeat every 5 mins if needed for all ages
High flow O2
IM/IV Chlorphenamine maleate
IV hydrocortisone
A patient complains he has been suffering from the flu in the past few weeks and is worried about his rash. He states red patches that were painful came up on his shins and have now turned into bruises. PMHx- sarcoidosis, TB. What is this rash called, what causes it
Erythema Nodosum
Causes- TB!!, sarcoidosis, IBD, chlamydia, group A beta haemolytic strep
most commonly found on shins
tender nodules–> bruises
Management of erythema nodosum
painkillers
self limiting
A man presents with a red rash consisting of small red spots a few cm in size. They looks like targets/bulls-eye, with a dark red centre with a crusty ring around it. They started suddenly on his hands and feet then spread to his limbs and chest. PMHX- HSV. What is the diagnosis- causes?
Erythema Multiforme
can be
- idiopathic
- triggered by medications (penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapineor)
- infections (HSV)
How can you differentiate between steven johnsons syndrome, toxic epidermial necrolysis and erythema mulitforme
Erythema multiforme- no mucosal involvement/limited to one mucosal surface
SJS- at least 2 mucosal sites involved
Toxic epidermal necrolysis- involves mucosal surfaces
what is steven johnsons syndrome
mucocutaneous necrosis with at least 2 mucosal surfaces involved
sx of steven johnsons syndrome
- prodromal illness- sore throat , runny nose, sore eyes, pyrexia
Rash
- abrupt onset
- painful lesions starting on trunk
- spreads rapidly
- sheet like skin loss
- epidermal/mucosal loss
sx of erythema multiforme
target like/bulls eye spots
red spots with dakr centre
start on hands/feet- spread up limbs and trunk
sudden onset
tx of erythema multiforme
- self resolving in couple of weeks
- does not progress to SJS or toxic epidermial necrolysis
- pain killers
- tx cause eg hsv-1- oral aciclovir
- itch- antihistamines, topical corticosteroids
recurrent
- dapsone
- hydrochloroquine
- azathioprine
Causes of steven johnson syndrome
drugs
infections
Management of steven johnson syndrome
- stop causative agent analgesia, fluids debridement of necrotic skin dressings and emollients ophthalmological review (iris, conjunctival scarring, conjunctivitis, corneal blisters)
What is Toxic Epidermal Necrosis
Acute
- skin and mucosal necrosis (over 30%)
- with systemic toxicity
causes of toxic epidermal necrosis
usually drug induced
- abx- -sulphonamide, penicillins
- allopurinol
- carbamazepine, phenytoin
- NSAIDs
presentation of toxic epidermal necrosis
prodromal illness
abrupt onset rash
- painful lesions starting on trunk and rapidly spreading
- sheet like skin loss
- epidermal/mucosal loss
- Nikolsky’s sign- epidermal separates with mild lateral pressure- ie skin tears
Management of toxic epidermal necrosis
- stop causative agent
- full supportive care- analgesia, fluids
- *- debridement of necrotic skin
- dressings
- emollients
- *- ophthalmological review
What is bullous pemphigoid
elderly
Autoimmune
attacks antigens between epidermis and dermis, causing sub-dermal split in the skin
Presentation of bullous pehmphgoid
tense, fluid filled blisters on an erythematous base
- large blisters
- itchy
- may be preceded by a non specific itchy rash
- trunk and limbs
Management of bullous pemphigoid
- wound dressings
- topical steroids
- oral steroids, tetracycline, nicotinamide
- azathioprine/methotrexate- immunosups
What is pemphigus vulagris
midle-aged/older
autoantibodies against antigens within epidermis
intra-epidermal split
blistering and erosion of skin and mucosal membranes
presentation of pemphigus vulgaris
- flaccid, easily ruptured blisters
- form erosions and crusts
- painful
- usually affects mucosal areas
Management of phemphigus vulgaria
- dressings
- oral care
- hgih dose steroids
- immunosups- metho, azathioprine, cyclophosphamide
Two main subdivisions of skin cancer
- melanocytic (melanoma)
- non melanocytic (keratinocyte carcinomas, cancers of the epidermis, eg BCC, SCC,
What are melanocytic naevi
- moles, skin tags
- raised or flat
how to check if mole is malignant
- ABCDE
Asymetry Boarder- irregular Colour - multi Diamtere >6mm Evolving
What si seborrheic keratosis, appearance
benign warty spot
- not pre-cancerous
- can be assoc with BCC
- common sign of skin aging
appearance
- stuck on
- well demarcated brown plaque
- only 1st layer of epidermis
Management of seborroeic keratosis
- leave it
- if irritating- cryotherapy, curettage
What is actinic keratosis
- precancerous- 20% chance of turning into SCC
appearance
- red or white flat plaques
- mostly seen on scalps
- feel rough, dry
Causes/RFs of actinic keratosis
- UV- sunbeds, sunbathing
- P53 mutation
- *- HPV
- *- immunosupression
Ix for actinic keratosis
look out for IDRBEU (BCC)
- induration/inflam
- Diamtere >1cm
- rapidly growing
- bleeding
- erythema
- ulceration
biopsy/excision
What is Bowen’s disease, appearance
- non invasive SCC
- precancerous
irregular, well defined red,scaly lesion
slow growing
sun-distributed, often on shins
Management of Bowen’s disease
- topical 5-flurouracil (cytotoxic)
- cryotherapy, excision
- pt education- UV protection
- FU- 3m
What is a malignant melanoma
- highly malignant
melanocyte tumour
1/4 progress from moles
RFs for malignant melanoma/SCC
- UV exposure
- prev skin ca
- > 5 melanocytic naevi
- immunosupression
- genetic skin conditions
presentation of malig melanoma
asymmetrical irregular border multi-pigmented lesion diameter >6mm evolving
ix for malignant melanoma
- dermatoscpoy- ABCDE
- excision biopsy
METS
**- lactate dehydrogenase (mets liver) - XR
-CT - MRIs, PET
- USS
Management of malig melanoma
- surgical excision with 0.5cm safety margin
- CT
- Immunotherapy
- if large, nearby lymph node biopsy
Site of mets malig melanoma
- brain
liver
bones
abdo
Cell type of SCC
epidermal keratinocytes
presentation of SCC
- grow over weeks or months
- pink or hyperpigmented /brown lesion
- hyperkaratotic
- may be ulcerated, nodular, warty
- crusting
- will not heal
ear, lips, genitals, mucosal sites
sore/tender
Management of scc
- Surgical excision
- Cryotherapy, curettage, or cautery
- RT
what cell type is bcc
- epidermal keratinocytes
presentation of bcc
- shiny pearly nodule with umbilical centre - rolling edges - telangiectasias - face/head/neck - slow growing
ix for bcc
dermatoscopy
biopsy
tx of bcc
- Surgical excision
- Cryotherapy, curettage, or cautery
- RT
What is paget’s disease of the nipple
- skin condition indicative of malignanct- HER-2
- Eczemoid changes- itching, flaking, flattened nipple, ulceration
ix for Pagets disease of the nipple
punch biopsy
mammogram
tx for pagets disease of the nipple
- excision
- CT
- RT
What is Kaposi sarcoma, RF
endothelial cell cancer, caused by HPV 8 virus
RF- AIDS, immunosupression
ix kaposis
biopsy of the skin
endoscopy , colonoscopy, FIT if suspected in digestive tract
CXR, bronchosocpy
tx of kaposis
tx cause- eg HAART retrovirus for HIV
CT or RT
excise big lesions
What is neurofibromatosis
genetic condition causes tumour (usually benign) to grow along the nerves
Sx of kaposis
painless red/purple papules/nodules anywhere on skin or mucous membranes
with N+V, SOB, chest pain, haemoptysis, abdo pain, diarrhoea if affecting internals
What genes are affected in neurofibromatosis
NF1 chromosome 17/NF2 chromosome 22
Presentation of neurofibromatosis
- cafe au lait spots- pale, coffee coloured flat patches
- soft tumours under the skin
- cluster of freckles in unusal places- armpits, groin, under breast
- problems with bnoes, eyes, nervous system
What is the difference between neurofibromatosis 1 and 2
NF1- schwannomas on nerves throughout nervous system- impaired hearing, vision, dizziness, balance, discoordination, headaches
NF2- less common, neurofibromas on peripheral nerves. Pain, neurological sx
tx of acne vulgaris
topical
- benzoyl peroxide
- topical abx - eg clindamicin
- retinoid- comedolytic and antinflam
oral 1. - tetracyclines- doxy, lymecycline, oxytetracycline, 2. erythro, trimetho Antiandrogens (for females) - spironolactone - COCP, POP - Cyproterone - metformin
Isotretinoin (systemic retinoid)-sebaceous gland function, keratinization)- accutain/roaccutane/rizuderm
laser therapy for scarring
what advice do you need to give after giving isotreinoin
teratogenic- need to use 2x contraception
How to evaluate unconscious , burnt pt
- ABCDE
- look- mechanism, depth, % coverage
- monitor NV status of extremities to detect compartment syndrome
Mechanism of burns and how deep they tend to affect
scalds- hot liquids
- superficial, superficial dermal
Flash burns
- high voltage, but current did not enter the body
- superficial
sunburn
- UVA- dermis, SC fat
- UVB- potent, erythema, epidermis
- epidermis, if severe may reach dermis and blister
Contact Burns
- touching hot object directly
- deep dermal, full thickness
Electrical
- small, deep burns at entry and exit points
Muscles tetany- arrhythmias, resps, spinal cord injury, transient paralysis, pareasthesia,
Chemical
- acids, alkalis
- deep dermal, full thickness
- formation of eschar (thick dead skin) more common
What are the degree of burns
1. superficial epidermal later o/e- red, no blistering cap refill fast painful heals within a week
2a. Superficial dermal/partial thickness
- epidermis and upper dermis
o/e- red/pale pink, blistering
cap refil- slow, blanches
v painful
heals within 2 weeks
2b. Deep dermal/partial thickness
- epidermis and full dermis
o/e- red, blotchy +- blistering
no blanching, absent/sluggish cap refill
sensation absent or present
- full thickness (3rd degree)
- epidermis, full dermis and SC
O/e- dry.waxy/white/leathery/brown
no blisters, blanching, cap refill or sensation
burns- what is the rule of 9 for calculating % coverage
each arm- 9% head 9% entire chest 9% entire abdo 9% Entire back 18% each leg 18% groin 1% palm 1%
What is a more precise way of calculating % burns
Lund and Browder diagram
Immediate general management of burns
- stop burning process
- do not remove anything stuck to the skin
- 20-30min under cold water
- layer with clingfilm- dont wrap!
- no wet dressings or creams
- elevate, NSAID, opiate
Immediate management of chemical burns
- 1 hour irrigation ASAP
- elemental metals- soaked with mineral oil instead of above
- topical abx- 1% silver sulfadiazine cream, 0.5% silver nitrate solution and mafendine acetate 10% cream
Immediate management of electrical burn
- rush to ED (not much 1st aid)
- topical abx- 1% silver sulfadiazine cream, 0.5% silver nitrate solution and mafendine acetate 10% cream
Immediate management of scald
- run affected areas under running cold water for at least 20min
- avoid icy water as causes vasocontriction
- lightly wrap with towel dipped in cold water
Immediate management of sunburn
- avoid sun
- protective clothing
- sunscreen SPF 50%
- oral food supplement polupodium
- 2 aspirin, then 2 every 4 hours, topical steroid B for 2-3 days
- cool baths
- Aloe vera
- keep hydrated
- if severe- electrlyte correction
- abx if signs of infection
SMART prevention - shade 11am-3pm aim to cover up remember to take extra care with children then use sun protection SPF 30+
Non-immediate management of burns in general
- debridement
- moisturisation
- broad spec abx
- escharotomy
what is an escharotomy
- for full thickness, circumferential burns
- skin dies, tought and leathery
- this contrcits the swelling internal tissues– compartment syndrome
- plus poor breathing if arounf torso
- procedure to relive pressure, done in ED
Where do u cut in an escharotomy
- along ulnar surface of upper limbs
- midline of neck
- horizontally on upper chest
- lateral sides of chest
- horizontal across abdo
- medial and lateral surfaces of lower limb and feet
A pt who suffered a chemical burn 3 days ago develops a progressive reddening of the intact skin around the burn- what is you main differential, causative agent and tx
burn wound cellulitis
strep pyogens
penicillin
What is the difference between cellulitis and erysipelas
cellulitis- involves deep SC tissue
erysipelas- acute, suerficial form of cellulitis, involves dermis and upper SC tissue
What are 2 main bacterial causes of cellulitis
- strep pyogens
staph areus
sx of cellulitis
most commonly in lower limb
- inflammation- swelling, eythema, warmth, pain
- lymphangitis
- systemically unwell
erysipelas- more well defined, raised borders
tx of cellulitis
abx- fluclox, benzylpenicillin rest leg/limb elevation sterile dressings analgesia