Dermatology Diagnosis+management Flashcards
(342 cards)
Skin layering
Epidermis: outermost layering made of thin sheet of stratified squamous epithelium. As cells differentiate and migrate upwards in strata their nuclei are replaced by keratin. outermost layer is called the stratum corneum.
Dermis: deep to epidermis. Thicker and made up largely of connective tissue. Contains papillary (upper) and reticular (lower) layer as well as network of nerves and nerve endings for sensation of pain, pressure, touch and temperature. Also muscle fibres (erector pili), hair follicles, sweat glands and sebaceous glands and many blood vessels.
Papillary layer: upper region of dermis with rows of dermal papillae. Help bind skin layers together and also form ridges on fingertips and skin on palms of hands and feet forming your footprint and fingerprint. Patterns are unique to each individual.
Reticular layer: lower dermis filled with network of interlacing fibres (mostly collagen making skin tough) and also elastin fibres (reduce with age causing wrinkles)
Hypodermis: subcutaneous layer supports layers of skin: made of loose connective tissue and fat. Helps regulate temperature and serves as a store for energy sources. Also acts as a shock absorbing pad helping protect underlying tissue areas.
Outer layer dead dry cells sloughed off
External dead cells constantly separating from skin (desquamation) 4kg/year!
Each surface cell lasts 28 days then sheds and is replaced
Functions of skin
protective barrier; temp regulation; sensation; Vit D synth; immunosurveillance; UV protection; prevents moisture loss
Skin cell types and functions
Keratinocytes
Produce keratin as protective barrier
Langerhans cells
Present antigens and activate T lymphocytes for immune protection
Melanocytes
Produce melanocytes for skin pigmentation and protection from UV radiation damage
Merkel cells
Contain specialised nerve endings for sensation
Epidermal layers
Stratum basale (Basal cell layer) Actively dividing cells, deepest layer
Stratum spinosum (Prickle cell layer) Differentiating cells
Stratum granulosum (Granular cell layer) So called as they lose their nuclei and contain granules of keratohyalin. Secrete lipid into intracellular spaces
Stratum corneum (Horny layer) Layer of keratin, most superficial layer
Dermal neoplasia types
Non-malignant (BCC; SCC)
malignant melanoma
Actinic keratoses (premalignancy)
Identifying skin cancers
BCC: pearly/waxy bump or flat brown lesion; most easily treated and unlikely to spread
SCC: firm red pimple/nodules or scaly patch NOT SHIN. easily treated if detected early but more likely to spread than BCC
Melanoma: existing mole that bleeds, itches or changes shape/colour with large brownish patches or smaller spot with black/red or white patches. most serious form needs immediate diagnosis as later is difficult to treat and spreads easily
BCC and cause
> 75% skin cancers UK
Locally invasive but rarely metastasize due to slow growth
Slow and irregular growth (subclinical finger-like outgrowths)
Metastases can occur in larger tumours: 2% if diameter >3cm; 50% if diameter >10cm
Aetiology:
Unknown
More common on areas of chronic sun exposure such as face, head and neck
Thought to arise from hair follicles
EPIDEMIOLOGY:
Uncommon in dark skin
Most common cancer in EU, australia and US
BCC risk factors
Genetics UV exposure esp. In childhood Previous BCC Increasing age Male sex: this gap increases with age also Skin types I and II
BCC presentation and types
Usually head, neck area
Nodule with indurated edge (pearl), telangiectasia and ulcerated centre (rodent ulcer)
Types:
Nodular: classic. Solitary shiny red nodule. Can be cystic or ulcerated
Superficial: often multiple on upper trunk and shoulders
Morphoeic: sclerosing or infiltrative BCC
Pigmented: brown, blue or greyish in colour
Baso-squamous
BCC investigations and diagnosis
Refer all suspicious lesions
Biopsy must be done to confirm before treatment commences
CT/MRI for larger or deeper cases where bony involvement is suspected or where tumour may have invaded major nerves, orbit or parotid gland
Diagnosis:
Clinical exam
Exisional biopsy
BCC differentials
Intradermal naevus Sebaceous hyperplasia Fibrous papule Molluscum contagiosum Keratocanthoma
BCC management
Surgical removal (excision + 4mm margin)
Curettage and cautery/electrodesiccation
Cryotherapy/cryosurgery
Imiquimod 5% cream
Fluorouracil (5FU) 5% cream
PDT (light therapy + a topical photosensitising agent»_space; to destroy cancer cells)
Radiotherapy (RT): incomplete excision, recurrent BCC, nodular BCC of the head and neck under 2 cm, and BCC with invasion of bone or cartilage
Prognosis:
Recurrence rate about 5%
Actinic keratosis
Keratoses: thickened skin
Solar/Actinic: sunlight induced
Pathophysiology:
Sun damaged skin over years
UV induced DNA damage leads to dysplastic intra-epidermal proliferation of atypical keratinolcytes
Non- contagious
Epidermiology:
Rare in UK <40 years
More common in elderly, fair skinned, blue eyed red/blonde haired individuals
More common in men
More common in those working outdoors, sunbathers, sunbed use, recreational activities
AK presentation
Sun exposed areas: face, ears, lips, bald scalp, forearms, back of hands, lower legs
Variable appearance even with multiple lesions on same individual
Rough sandpaper like feel
Skin coloured, pink, reddish brown colour
Thick scaly, warty layer (yellow white scaly crust)
Can be itchy
Grade:
Slightly palpable (better felt than seen)
Moderately thick (easily felt and seen)
Very thick, hyperkeratotic and/or obvious
May also be field damage: large areas of multiple AKs on background of erythema and sun damage
AK progression
Small risk of SCC
Generally more risk of all skin cancer types
Increased risk in pts. Who have numerous AK patches or those on immunosuppresive drugs for other conditions
AK may not convert to SCC or cancers
May regress but may also recur
2WW dermal referral red flags and non urgent referral
Recent growth Recent tenderness Recent inflammation Nodular lesion/lump Bleeding Ulceration Lesions on lips
Non-urgent referral: Diagnostic uncertainty Widespread or numerous patches Severe actinic damage Immunosuppressed pts. Very young pts presenting with AK (xeroderma pigmentosum)
AK diagnosis and differentials
Diagnosis:
Clinical exam; ideally with dermatoscope
Biopsy if in doubt
Differentials:
BCC; SCC (indurated nodular lesions but more rapid growth tend to be eroded or ulcerated)
Seborrhoeic keratosis (greasy brown crusts with sharply demarcated borders and non-erythematous base, areas not exposed to sun)
Bowen’s disease
Amelanotic melanoma
Discoid lupus erythematosus (abnormal pigmentation, dilated follicles and atrophy)
Psoriasis
AK management
Advise: limit sun exposure; sun protection all day all times of year; pre-canceous lesion; safety net vigilance and report skin changes
Creams: 5-fluorouracil, 5FU (cytotoxic)
Imiquimod (CMI↑)
Diclofenac (unknown mechanism)
Retinoic acid (regulate the differentiation and growth of keratinocytes, anti-aging, …)
Cryotherapy: causes no scarring, but is painful Photodynamic therapy (PDT) >> better than cryo., but useful for single lesions
Surgical excision»_space; assessment of the whole lesion but leaves scar, may recur in surrounding damaged tissues
Prevention
Education ›››› Hats - Long sleeves – Sunscreens (SPF>30)
SCC
Malignant tumour of skin
Arises from keratinising cells of epidermis or it’s appendages
Locally invasive and metastasis often (fast growing)
Epidemiology:
2nd most common skin cancer (after BCC)
20% non melanoma skin cancers caused by SCC and 80% by BCC
Incidence is rising worldwide
SCC risk factors
Chronic UV exposure
Susceptibility to sun exposure: fair skin, blonde/red hair
Ionising radiation exposure
Chemical carcinogens: arsenic and chromium, soot, tar and pitch oils
HPV infection
Immunodeficiency
Chronic inflammation: near chronic ulcers, around chronic sinuses etc.
Premalignant conditions such as Bowen’s disease or Actinic keratoses
SCC presentation
Variable appearance
Typically non-healing ulcer or growth in sun exposed areas of head and neck
Indurated keratinising or crusted nodule with/without ulceration
Slow growing ulcer without keratinisation
Slow growing reddish plaque
SCC may make local metastases or spread to local lymph nodes
SCC differentials
Keratoacanthoma (can be difficult to differentiate even histologically).
BCC.
Malignant melanoma (particularly amelanotic malignant melanomas).
Solar keratosis.
Pyogenic granuloma.
Seborrhoeic warts (especially if traumatised or infected).
Plantar warts or Verrucas (Periungual SCC)
SCC investigations/ diagnosis
Clinical exam
Excisional biopsy (+safe margin) in small lesions, not cosmetically sensitive areas or near to vital structures
Incisional biopsy (punch biopsy) for large lesions in cosmetically sensitive areas or near vital structures
Enlarged nodes LAP: FNA or excisional biopsy
CT/ MRI bone or soft tissue spread, cervical lymph nodes, perineural invasion
TNM staging for SCC
Stage 0/Tis: primary tumour carcinoma is in situ; no regional LN metastases or distant
Stage 1/T1: tumour <2cm; no regional or distant metastases
Stage 2/T2: tumour between 2-5cm; no local or distant metastases
Stage 2/T3: tumour >5cm
Stage 3/T4: tumour invading deeper extradermal structures OR any stage with regional lymph node spreading
Stage 4: any stage with distant metastases