Dermatology Flashcards
(147 cards)
1
Q
What are the benefits of sun exposure?
What are the risks of sun exposure?
A
Emotional/psychological health
Vitamin D production- bone health and cancer protection
Cardiac health- treat HTN
UV-B- sunburn, direct DNA damage and carcinogenesis.
UV-A- photoaging (wrinkles), potentiates UV-B carcinogenesis, immunological effects
2
Q
How is a diagnosis of skin cancer achieved?
A
Awareness of GP/well trained (dermatoscope) 2ww referral Dermatoscope AI technology Surgical biopsy
3
Q
What is an acquired naevus?
A
Nevi refer to moles/birthmarks.
Moles
Flat- junctional naevus (above epidermis)
Raised- Compound naevus (@ epidermis)
Large crusty- Intradermal naevus (@dermis)
Halo naevus- nevi with ring of lightened skin surrounding it.
Premalignant- dysplastic naevus
Growing naevus in pregnancy- normal
Benign acral naevus- on hands and feet
Congenital naevus birthmark- large have a higher risk of melanoma
4
Q
What is superficial spreading malignant melanoma?
A
Most common subtype.
Black-brown-grey-blue.
Superficial to deep invasion.
Stratify with Breslow thickness.
5
Q
What is lentigo melanoma
A
More in head and neck
Premalignant
Invasion of sebaceuous glands with melanocytes
can progress to lentigo maligna melanoma
6
Q
Malignant Melanoma mimics
A
Multi component hemangioma- collection of BV.
Intracorneal haemorrhage- blood under stratum corenum- turns brown in colour- scrape off wiht blade reomval.
Subungual haematoma- bleeding udner the nail plate- take serial images if unsure of diagnsis.
benign longitudianl melanonychia.
sebhoerric keratosis.
7
Q
What are some differentials of BCC?
A
Xanthelsma
Pickers nodule- psychiatry, around the body may have other picked areas.
Benign fibrous papules- on nose usually- young women
Spitz naeuvus
Sebaceous hyperplasia- multiple, yellow
Dermatofibroma- young females, secondary to shaving or insect bites.
intradermal nevus
8
Q
What are some differentials of SCC?
A
Inflamed squamous papilloma/viral wart
Regressing keratoacanthoma- painless, ulcerated, crater form; arising from hair follicles, may heal on its own.
Traumatised/rapid growing/inflamed SK
SK
Lymphedema nodules
Giant comedones; in acne, elderly, large keratin plugs in the middle.
Viral warts; nodular, looped vessels, keratin.
9
Q
What is the importance of sunscreen?
A
Protection against sun harmful UV
Apply 15-30 mins before
Reapply every 2hrs
Apply in large amounts
10
Q
What are the surgical excision margins for the different skin cancers?
A
Pigmented- 2mm
Melanoma- WLE- In siut-5mm, <2mm deopth 1cm, >2mm depth then 2cm
SCC 4+mm excision
BCC 4mm excision
11
Q
What is impetigo?
A
Superficial bacterial infection which can be either non bullous (common) or bullous.
Non bullous- Mainly Staph aureus, but can also be Strep pneumonia or a mix of both.
Bullous- Staph aureus.
Common in younger children but can still occur in adults.
12
Q
What are the signs and symptoms of impetigo?
A
Non bullous- small vesicles/pustules, usually around the mouth/nose area. Usually asymptomatic but may be itchy.
Bullous- Larger flaccid fluid filled vesicles/blisters for 2-3 days, appearing on flexures, face, trunk and limbs. May also have systemic features if large area involved, i.e. fever/lymphadenopathy.
13
Q
How is impetigo investigated/diagnosed?
A
Usually a clinical diagnosis.
Take swab for MCS from a moist lesion or deroofed blister, in the case of recurrence, resistance or widespread disease.
14
Q
How is impetigo managed?
A
Encourage hygiene to stop spread of infection.
Stay at home until lesions are dry/crusted over. If still crusted or weeping then stay at home until 48hrs after Abx treatment.
Ensuring pre-existing skin conditions (such as eczema) are optimally treated.
Non-bullous- Hydrogen peroxidase for 5 days; alternative topical Abx.
More extensive, severe or bullous infection may require oral antibiotics (flucloxacillin or clarithromycin if allergic to penicillin) for five days (or seven days depending on clinical judgment).
15
Q
What is folliculitis?
A
Refers to inflammation of the hair follicle, commonly due to staph aureus.
Can be either superficial or deep- where deep leaves scars.
This is due to obstruction of the pilosebaceous glands +/- inefction.
16
Q
What are the RF associated with folliculitis?
A
Uncut beard. Shaving 'against the grain'. Particularly thick hair. Excessive friction from clothing. Overly tight-fitting clothing. Excessive sweating and hyperhidrosis. High external humidity. Pre-existing dermatitis. Reduced host immunity - eg, poorly controlled diabetes, immunosuppression. Nasal carriage of infecting strains of S. aureus. Skin abrasion/wound/abscess. Occluded skin - particularly for dermatological treatment with topical corticosteroids.
17
Q
What are the signs and symptoms of folliculitis?
A
Often appears as a small rash or area of red bumps over hairy area (painful/painless).
Pruritic
If mild and left alone, the rash usually resolves without scarring.
Pustules at the centre of lesion
Affects axilla, beard, face, scalp, thighs and inguinal regions.
Erythematous papules form in a relatively regular, sometimes ‘grid-like’, pattern.
Deep folliculitis tends to cause more erythema, becoming more confluent between the lesions, with no noticeable surface pustules and intense irritation of the skin. It can cause scarring, keloid formation and hair loss.
Regional draining lymph nodes should be checked for adenitis, which is rare in simple or mild folliculitis. Folliculitis of the eyelash is known as a stye.
18
Q
How is folliculitis investigated?
A
Clinical diagnosis.
Swab required if recurrent or treatment resistant.
Also consider punch biopsy if atypical response to treatment.
19
Q
How is folliculitis managed?
A
Conservatively; Reduce shaving, use clean shaving equipment, shave within the grain of the hair, use moisturiser after shaving, don’t share shaving towel/equipment with anyone in the house. Maintain good skin hygiene.
Doesn’t usually require pharmacological treatment.
Superficial; use antiseptics i.e. triclosan.
Deep; topical/oral Abx, preferred are flucloxacillin or erythromycin.
If recurrent use Abx for 4-6 weeks.
20
Q
What is cellulitis?
What are the RF?
What are the complications?
A
- Acute bacterial infection of dermis and subcut tissues
- Typically due to strep pyogenes or staph aureus
- Risk factors- skin trauma, ulceration, obesity
- Complications- necrotising fasciitis, sepsis, persistent leg ulceration, recurrent cellulitis
21
Q
What are the signs and symptoms of cellulitis?
A
- Commonly occurs on shins- lower limb
- Erythema, pain, swelling, warm to touch
- Blisters and bullae may form
- Systemic upsets eg fever
22
Q
How is cellulitis investigated?
A
- Clinical- no further investigations in primary care
- In secondary care- swab for culture, ultrasonography, skin biopsy
- Bloods, BP - septicaemia
23
Q
How is cellulitis classified?
A
Eron Classification:
Class I- No signs of systemic toxicity and Px has no other comorbidities.
Class II- Px has comorbidity which may delay recovery +/- systemic infection.
Class III- Px has significant systemic upset i.e. acute confusion, tachycardia, hypotension or unstable comorbidities.
Class IV- Px has sepsis or necrotizing fasciitis.
24
Q
How is cellulitis managed?
A
Needs hospital admission if; Eron 3/4, rapidly deteriorating, lymphoedema, facial/peri-orbital cellulitis, child <1yrs or immunocompromised.
Other Px give:
- First-line mild-moderate cellulitis: flucloxacillin
- Penicillin allergy: clarithromycin, erythromycin (in pregnancy), or doxycycline
- Severe cellulitis: co-amoxiclav, cefuroxime, clindamycin, ceftriaxone
25
What is chicken pox?
Caused by varicella-zoster virus
Transmission: personal contact or droplets
- Incubation period 1-3 weeks
- Infectious from 1-2 days before the rash appears until the vesicles are dry or have crusted over, usually 5 days after rash onset
Avoid school during the highly infectious period
- The virus persists in sensory nerve ganglia of the dorsal root. Years later, it can reactivate and cause herpes zoster (shingles)
26
What are the signs and symptoms of chicken pox?
- Prodromal symptoms such as nausea, myalgia, anorexia, headache, general malaise, and loss of appetite.
- Small, erythematous macules which appear on the scalp, face, trunk, and proximal limbs, and progress over 12–14 hours to papules, clear vesicles (which are intensely itchy), and pustules. Vesicles can also occur on the palms and soles, and mucous membranes, with painful and shallow oral or genital ulcers. Vesicles appear in crops. Crusting occurs usually within 5 days, and crusts fall off after 1–2 weeks
27
How is chicken pox managed?
- Usually a self-limiting disease in healthy children
- Keep short nails (to avoid causing damage by scratching)
- Treating symptoms:
- Paracetamol
- Topical calamine lotion
- Chlorphenamine (avoid in certain groups, for example pregnant and breastfeeding women, and children less than 1 year of age)
- Aciclovir can be considered for an immunocompetent adult or adolescent (aged 14 years or older) who presents within 24 hours of rash onset, particularly for people with severe chickenpox or those at risk of complications
- Don't use NSAIDs, could cause cellulitis of the lesions
28
What are the complications of chicken pox?
- Bacterial skin infection, most common in young children
- Lung involvement, more common in adults
- In pregnancy, severe maternal chickenpox and fetal varicella syndrome
In later pregnancy, varicella can result in neonatal chickenpox infection
- In immunocompromised people, severe disseminated chickenpox with varicella pneumonia, encephalitis, hepatitis, and haemorrhagic complication
29
What is shingles?
Shingles (herpes zoster) is a viral infection of an individual nerve and the skin surface that is served by the nerve (dermatome). It is caused by the reactivation of the varicella-zoster virus, the virus which causes chicken pox.
30
How is shingles investigated?
Clinical diagnosis.
Abnormal skin sensations and pain, followed by a unilateral vesicular rash in the affected dermatome.
The location of symptoms depends on the affected nerve.
Immunocompetent people, the infection usually occurs on the thorax, with dermatomes T1 to L2 most commonly affected. In immunocompromised people, symptoms can be more widespread and affect multiple dermatomes (disseminated disease).
Rash may be atypical in older/immunocompromised
31
How is shingles managed?
Hospital admission if; young child, severely immunocompromised, ophthalmic involvement, widespread or systemically unwell.
Prescribe oral anti viral
Manage pain
Offer self care advice; i.e keep the rash clean, stay away from children, pregnant, immunocompromised etc.
32
What is a wart?
Infection of keratinocytes by HPV.
Usually found on the hands and feet, if at the base of the feet then considered a verruca.
Usually asymptomatic and will resolve spontaneously w/o treatment.
33
Describe the appearance of a wart.
Raised, rough, firm surfaces. May resemble a cauliflower.
May spread by direct skin-skin contact or via indirect contact.
May persist for years, resolution is faster in children.
34
How are warts treated?
Usually not treated unless Px insists, cosmetically unsightly, numerous.
Treat with topical salicylic acid, cryotherapy or both. Don't tend to use cryotherapy in young children.
35
What is oral herpes simplex?
Viral infection causing vesicles/crusting/ulceration around the lips, cheeks or nose.
Caused often by HSV-1.
36
What are the signs and symptoms of oral HSV?
May present with a prodrome of fever, sore throat and lymphadenopathy.
Initial symptoms of pain, burning, tingling, and itching may precede visible lesions and typically last 6–48 hours.
Immunocompromised Px may have more serious manifestations of the virus.
37
How is oral HSV managed?
Non IC Px-
Analgesics for pain and fever relief
Oral acyclovir
Encourage good self care and trigger avoidance (sunlight, stress, trauma, fever)
IC Px-
Need hospital admission if unable to swallow, has serious complication, dehydrated or troublesome infection.
38
What is genital HSV?
Common STI caused by HSV 1 / HSV 2.
| Spread via direct contact with an infected person.
39
How does genital HSV present at first exposure?
Multiple painful blisters on external genitalia, bursting to leave erosions and ulcers.
Usually bilateral lesions appearing 4-7 days after HSV exposure.
Px may present with dysuria, vaginal or urethral discharge, and systemic symptoms such as fever and malaise.
Primary episodes can last 20 days.
Following primary infection, the virus becomes latent in local sensory ganglia.
40
How does recurrent genital HSV present?
Occurs after a reactivation of HSV.
Unilateral blistering, prodromal tingling and burning symptoms hrs to days before.
Less common and less severe systemic symptoms lasting 5-10 days.
41
How is genital HSV investigated?
Take Hx and examination.
Take a swab for viral culture/PCR.
Screen for other STIs, HIV, pregnancy and immunosuppression.
All suspected genital herpes should be referred to the genitourinary clinic.
42
How is genital initial HSV managed?
Oral acyclovir 200mg five times a day started within 5 days of the start of the episode or while new lesions are forming.
This should be continued for 5-10 days, or longer if new lesions are still forming while on treatment.
43
How is recurrent genital HSV managed?
Self care management
Episodic antiviral treatment- 200mg 5DS for 5 days (infrequent attacks).
Suppressive oral acyclovir 400 mg twice a day for 6–12 months). This is an option if attacks are frequent (six or more attacks per year), causing psychological distress, or affecting the person's social life.
Px with HIV may need double dose of treatment or extended period.
Refer Px with HIV, pregnancy or non resolving disease.
44
What is molluscum contagiosum?
Viral skin infection appearing pinkish/pearly white appearance up to 5mm in diameter. Can appear in clusters and anywhere in the body besides palm and soles.
Usually in children or immunocompromised.
Spent by direct contact or indirect through use of towels.
45
How is molluscum contagiosum managed?
Self limiting- resolving within 18 months.
| Eczema/inflammation may appear before resolution; in which case treat with emollients if itching or Abx if infected.
46
What is dermatophytosis?
| What are the RF?
'Ringworm'/tinea corporis/tinea cruris (body/groin).
| RF include humid environment, sweating, obesity, tight fitting clothing etc.
47
How is dermatophytosis diagnosed?
Clinical diagnosis- itchy, scaly skin.
| Single/multiple lesions, red/pink, flat/raised annular patches with red scaly exterior and clear towards the centre.
48
How is dermatophytosis managed?
Advice with self care
If mild/non-extensive then topical terbinafine or imidazole.
If marked inflammation then hydrocortisone.
If severe or extensive then oral terbinafine. If not tolerated or contraindicated then itraconazole.
If still persists after topical anti fungal then identify underlying reason (i.e. non compliance, reinfection etc) send skin sample for fungal microscopy and culture.
49
What is candidiasis?
Yeast skin infection, occurring mainly where two surfaces of skin meet, i.e. in the folds where there is a lot of moisture.
Usually asymptomatic, unless the Px is immunocompromised or mucosa is infiltrated.
50
How is candidiasis diagnosed?
It is a clinical diagnosis.
| Investigations are not needed, response to treatment confirms diagnosis, otherwise take a swab for MCS.
51
How is candidiasis managed?
1) If immunocompromised or systemic infection then hospital admission.
2) Otherwise; Topical terbinafine or imidazole.
If itchy then also give 1% hydrocortisone for 7 days. If it resolves with these then continue for 7 more days, otherwise review the diagnosis.
3) If not responsive to topical then give oral fluconazole for >16yrs, <16yrs see specialist.
52
What self care management would you advice a Px with candidiasis?
Hygiene
Dry thoroughly after a shower
Lose weight- if obesity is the problem
Avoid skin occlusion where possible
53
What is scabies?
Intensely itchy parasitic skin infestation.
Px usually infected with 10-15 mites.
Spread by direct skin contact.
Common in closed spaces with large groups i.e. schools, prisons etc.
If immunocompromised can have crusted scabies- hyper infestation with thousands to millions of mites. Need hospital.
54
How is scabies investigated?
Diagnosis of Hx of Px and family.
| Examination of Px and family.
55
How is scabies treated?
Topical insecticide to be applied once and then again a week later- permethrin 5%.
For itching can take topical crotamiton.
Should encourage washing all clothes and bed sheets, also treat family members with the insecticide even if asymptomatic.
Untreated can develop a bacterial infection which can lead to impetigo, folliculitis, boils, cellulitis.
56
What are lice infestations?
Head lice are a parasitic infestation of hair, where the lice feed off blood from the scalp.
57
How are head lice diagnosed?
Detection combing.
Only active head lice is a live louse is found, despite the presence of hatched/unhatched eggs.
Should treat the Px only if they have active headlice, treat close contacts on the same day.
58
How are head lice managed?
Treat with either of the following;
Physical insecticide dimeticone (Hedrin).
Traditional insecticide malathion.
Wet combing with fine tooth head louse comb.
Detection combing is useful to see if the treatment is effetive.
Lifespan of lice is 1-2 days so no need to wash bedding/clothes.
59
What is eczema?
| What are the features?
Chronic itchy inflammatory skin infection, affecting all ages.
Episodic exacerbations
Fx/Personal Hx of atopy
Itching- mainly at flexure regions; scalp, extensor regions in infants.
Adults primary manifestation may be generalised dry and itchy hands.
60
How is eczema diagnosed?
Clinical diagnosis.
61
How is eczema managed?
1) Emollients for acute flares and remissions.
2) Red/inflamed- topical steroids.
3) Persistent itch- 1 month of non-sedating anti-histamine i.e. certizine.
4) If sleep affecting sleep- sedating anti-histamine chlorphenamine.
5) Severe extensive eczema- short course oral corticosteroids.
6) Weeping/crusting/malaise/fever- Secondary bacterial infection need Abx.
62
When is a dermatology referral needed in eczema?
Unclear diagnosis
Uncontrolled eczema
Bandaging techniques/treatment advice
Recurrent secondary infection
63
What are the different types of steroid cream increasing in potency?
Mild- Hydrocortisone 0.25-0.5%
Moderate- Betnovate/Eumovate
Potent- Cutivate/Betnovate(0.1%)
Very potent- Dermovate
One FTU (fingertip unit)- 0.5g is sufficient to cover the palm of an adult hand twice.
64
What is acne vulgaris?
Chronic inflammatory skin condition of adolescence.
| Obstruction of the pilosebaceous unit leading to comedones, pustules and inflammation.
65
What are the features of acne vulgaris?
Comedones- closed top is whitehead, open top blackhead can form.
Follicle can burst and release irritants- inflammatory lesions with pustules/papules.
XS inflammatory response can lead to nodules/cysts.
Can get drug induced acne.
Acne fulminans- systemic upset with acne, requiring hospital admission- responds to oral steroids.
66
How is acne vulgaris diagnosed?
Clinically diagnosed then classified.
Mild- Open and closed comedones +/- sparse inflammation.
Moderate- Widespread non inflammatory lesions + papules and pustules.
Severe- Extensive inflammatory lesions with scarring, pitting and nodules.
67
How is acne vulgaris managed?
1) Single topical therapy- retinoids/benzoyl peroxide.
2) Topical combination therapy- topical Abx/benzoyl peroxidase/retinoids.
3) Abx- Tetracycline (avoid in pregnancy/breastfeeding/<12yrs- use erythromycin here). Oral Abx should be used for 3 months and should be used in combination with topical BP or retinoid to avoid resistance.
3) Women can use COCP as an alternative to oral Abx.
4) Oral isoretinoin (Roaccutane)- needs specialist monitoring, Vitamin A analogue, SE- dry eyes, dry skin, fragile skin.
68
What is psoriasis?
| What are the drug triggers for psoriasis?
Chronic remitting and relapsing condition.
Systemic immune mediated inflammatory condition.
Erythematous, circumscribed scaly papules, and silvery-white plaques.
Affects extensor regions, scalp, knees. Less commonly nails, ear and umbilical region.
Exacerbated by genetic, infectious, emotional, and environmental factors.
Anti-malarials, BB, lithium, NSAIDs, potentially oral steroids.
69
What are the RF for psoriasis?
| What are the differentials of psoriasis?
- Infection
- Hormonal changes eg postpartum
- Medications
- FHx
- Trauma
- Alcohol and smoking worsens symptoms
- Sunlight improves
Tinea capitis, eczema, seborhoeic dermatitis.
70
How does psoriasis present?
Monomorphic erythematous plaques
Covered with silvery white scales
Occasionally halo affect around the plaque
Affecting scalp, lower back, extensor surfaces- elbows, knees, shins
Lesions can join to form larger lesions
Clear well circumscribed
Can affect nails too- pitting onycholysis, pitting, subungual hyperkeratosis, complete nail dystrophy.
71
How is psoriasis managed in priamry care?
Regular emollient use to reduce irritation.
1) Potent corticosteroid OD, Vit D analogue OD (at different times) for 4 weeks.
2) Vit D analogue BD
3) Potent corticosteroid for 4 weeks or coal tar preparation 1-2 times a week.
Refer to dermatologist if extensive, severe, uncertain diagnosis, resistant to primary care treatment, refer to rheumatologist if psoriatic joints.
72
How is psoriasis managed in secondary care?
Phototherapy 2-3 times a week for 10-12 wks targets immune cells and keratinocytes to encourage epidermal remodelling.
If unresponsive then;
Methotrexate- folic acid antagonist and works as anti-proliferative and anti-inflammatory.
Ciclosporin (not used unless want a fast response since SE)
Aciretin- systemic oral retinoid- very teratogenic.
Phosphodiesterase inhibitors
Biologics- infliximab
73
What is urticaria?
Superficial swelling of epidermis and mucosa- leads to raised, red, tichy skin.
Deeper urticaria of the submucosa and dermis is known as angioedema and resolves in 72hrs.
Acute urticaria <6 weeks
Chronic urticaria >6weeks
74
What are the causes of urticaria?
```
Acute-
Drug allergy
Acute viral/bacterial infection
Food allergy
Widespread reaction following local i.e. latex allergy
Bee/wasp sting
```
Chronic-
Mainly idiopathic
Autoimmune condition associated i.e. thyroid, SLE, coeliac
Underlying infection i.e. H.pylori
75
How is urticaria managed?
Mild is self limiting.
Treat with upto 6 wks of NS antihistamine i.e. cetirizine, upto QDS for initial response.
If severe symptoms then consider prednisolone.
Can give S antihistamine if interring with work/sleep i.e. chlorphenamine at night.
Refer to dermatology if not resolving with antihistamines, painful/persistent, food/latex allergy causing acute severe urticaria.
76
What are the RF for developing skin cancer?
Exposure to UV light
Severe sun burn in childhood (e.g. blistering)
Immunosuppression
Multiple (>100) or giant (>20 cm) naevi
Skin type (Fitzpatrick Skin types I & II)
Family history (cyclin-dependent kinase mutations are linked to 20-40% of familial melanoma)
Genetic mutations (CDK4, xeroderma pigmentosum, melanocortin 1 receptor)
77
What is BCC?
What are some characteristic features of BCC?
What are the differentials for BCC?
Most common type of cancer
Basal cell carcinoma.
Slow growing
Locally invasive
Malignant epidermal (basal layer) skin tumour
Months- years
Sun-exposed areas of the body- 80% head and neck
Differentials include sebaceous hyperplasia, amelanotic melanoma, SCC.
78
What are the RF for BCC?
```
Skin type
Male sex
Increasing age
Genetics- albinism, Gorlin's syndrome, xeroderma pigmentosum (sensitivity to UV light)
Previous skin cancers
Immunosuppression
Carcinogens- ionising radiation
```
79
How does BCC present?
```
Long history
Slowly enlarging
Appears initially as new scab which bleeds easily but not healing or a new lump.
Can be itchy
Commonly of the head/neck
Pearl like rim surrounding a crater
Arborizing telangiectasia
```
80
How is BCC investigated?
```
Dermoscopy
Hx
Examination
Excision biopsy- almost always.
If superficial/flat or in a very structural location (and planning for Mohs surgery) can do curettage biopsy (scrapings) or incisional biopsy.
```
81
How is superficial BCC managed?
| How is nodular BCC managed?
Can choose to not treat.
Superficial-
-Creams: 5FU OD for 4 wks. Initially have a bad reaction then will resolve. OR Aldara (Imiquimod) take Mon-Fri for 6wks. Works on TOL like receptors
-Cryotherapy
-Curettage and cautery/excisional biopsy.
Photodynamic therapy: Apply cream, then follow with specific wavelength of light which kills the cells.
Nodular/papular-
- Excisional biopsy with a margin of 4mm- unless severe.
- Mohs surgery- very microscopic to minimise tissue loss and maximise cancer removal. Remove part of the BCC and immediately look through the microscope to see if all is removed, if not then can excise further. Good for recurrent/infiltrative BCC.
- If Px high risk for surgery then do a punch biopsy for diagnosis followed by radiotherapy.
- If rare then chemotherapy- Vismodegib.
82
What is SCC?
| What are the clinical features of SCC?
NMSC- Derived from the epidermal layer which makes keratin.
2nd common skin cancer after BCC.
It can metastasise.
Slow growing, can ulcerate, tender/painful, appearing in sun exposed areas.
83
What are the RF for SCC?
Immunosuppressed Px
Px with organ transplants- requires immunosuppression.
Cumulative UV light exposure
Px with skin conditions such as Xeroderma pigmentosum, albinism.
84
How does SCC present?
Scaly or crusty raised area of skin with red/inflamed base.
Can be sore/tender, may bleed.
Can appear as ulcer.
Can appear anywhere but mainly sun exposed areas head, neck, skin, ears.
85
How is SCC investigated?
Hx
Examinations
Dermoscopy
Excisional biopsy
High risk- need to check if any metastasis to LN. Image with USS, X-Ray, CT, MRI or with LN biopsy.
86
How is SCC managed?
Surgical excision with 4mm margin for low risk and upto 10mm margin for more high risk.
Can use radiotherapy.
May use curettage and cautery but less likely.
Mohs surgery
Aggressive cryotherapy.
87
What is amelanotic melanoma?
Type of melanoma
| Malignant cells have little to no pigment
88
What are the RF for amelanotic melanoma?
Increasing age
| Sun exposed/sun damaged areas
89
How does amelanotic melanoma present?
Classically they are skin coloured
Can appear red/pink/erythematous
Early presentation includes asymmetrical macular lesion
90
How is amelanotic melanoma investigated?
Hx
Examination
Dermoscopy- Irregular pigmentation (with irregular dots/globules), polymorphous vascular patterns including reticular pigmentation, linear/dotted irregular vessels, white lines etc.
2-3mm of excision biopsy.
Differentials include BCC, seborrheic keratosis, actinic keratosis etc.
91
How is amelanotic melanoma managed?
Surgical excision with the depth being related to the Breslow thickness, as with malignant melanoma.
92
What is melanoma?
| What are the clinical features of melanoma?
Common skin cancer
Asymmetry
Border irregularities
Colour variations
Diameter>6mm
Evolving
93
What are the RF for melanoma?
Intermittent intense exposure to sunlight/UV
Early childhood sunburns
```
Skin which doesn't tan easily- more likely to burn
Indoor tanning beds
Navi
Personal Hx of melanoma
FHx of melanoma
```
94
How does melanoma present?
```
Asymmetrical
>Irregular border
>2 colours
>6mm diameter
Evolution of the lesion
```
95
How is melanoma investigated?
Hx
Physical ABCDE
Biopsy
Lab tests
Imaging- USS for LN metastasis, CXR for lung metastasis.
96
How is melanoma managed?
Wide margin local excision is recommended (if localised)
Resectable stage 3/4- usually drain to LN then treat via resection and adjuvant therapy.
Advanced unresectable disease- systemic treatment is the mainstay, unless if brain metastasis then need resection.
LN metastasis- needs complete LN dissection.
Do sentinel LN to help guide treatment- more treatment options available and will increase survival rate.
Adjuvant therapy- chemo does not work so use immunotherapy.
97
What is the pathophysiology of BCC?
Exact aetiology is unknown
| Relationship between pilosebaceous unit and BCC
98
What is the pathophysiology of SCC?
DNA gene mutations of the p53 tumour suppression gene, due to UV light damage. Also damage may be related to smoking, ageing and immune suppression.
99
What is the pathophysiology of melanoma?
Benign naevus (typical mole) - controlled proliferation of melanocytes
Dysplastic naevus (atypical mole) - abnormal proliferation of melanocytes resulting in a pre-malignant lesion with atypical cellular structure.
Radial growth phase - melanomas tend to extend superficially and outwards initially. Melanocytes acquire the ability to proliferate horizontally in the epidermis, but few cells invade the papillary dermis.
Vertical growth phase - malignant cells invade the basement membrane and proliferate vertically downwards into the dermis.
Metastasis - malignant cells may spread to other areas of body. Typically they travel to regional lymph nodes first; but they may spread to other areas of the skin / soft tissue, or to solid organs (such as the lungs, liver, bone or brain).
100
What is Breslow thickness?
| How does it relate to excision of melanoma?
Breslow thickness refers to the depth of vertical invasion of the melanoma.
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Melanoma in situ (Tis): 5–10 mm
Melanoma < 1 mm (T1): 10 mm
Melanoma 1–2 mm (T2): 10–20 mm
Melanoma 2–4 mm (T3): 20 mm
Melanoma > 4 mm (T4): 20 mm
```
101
What is actinic keratosis?
| What are the RF?
Precancerous scaly lesion found on sun burned skin.
Fair skin
Hx of sun exposure
Defective immune system
Hx of sun burned
102
How does actinic keratosis present?
```
Starts off like dry skin.
A flat or thickened papule, or plaque
White or yellow; scaly, warty, or horny surface
Skin coloured, red, or pigmented
Tender/itchy or asymptomatic
```
If grows very fast or into a lump, any bleeing/ulcerating then needs medical attention since can develop into SCC.
May also develop in cutaneous horns.
103
How is actinic keratosis investigated?
Dermoscopy
104
How is actinic keratosis managed?
```
Some can resolve themselves.
Creams- 5FU, Imiquimod
Curettage
Cryotherapy
Photodynamic therapy
Laser treatment
```
105
What is seborrhoeic keratosis?
| What are the RF?`
Harmless, pigmented 'senile' warts that most Px will develop. They are not infectious and non cancerous nor do they develop into cancer.
Due to the build up of skin cells; sign of skin ageing.
106
How does seborrhoeic keratosis present?
Flat or raised papule or plaque
1 mm to several cm in diameter
Skin coloured, yellow, grey, light brown, dark brown, black or mixed colours
Smooth, waxy or warty surface
Solitary or grouped in certain areas, such as within the scalp, under the breasts, over the spine or in the groin
Looks like a 'stuck on' wart.
107
How is seborrheic keratosis investigated?
On examination
Can confirm with dermoscopy
If in doubt do biopsy
108
How is seborrheic keratosis managed?
Very common and so not usually treated.
Treatment may only be on NHS if single lesion, unsightly or gets caught so uncomfortable.
Cryotherapy
Curettage
109
What is Bowen's disease?
| What are the RF?
SCC in situ i.e. confined to the outer skin layer, not serious but can progress to SCC very occasionally.
Long term sun exposure/UV light
Immunosuppression
Ionising radiation
HPV
110
How does Bowen's disease present?
Scaly plaque (can look like psoriasis but not symmetrical distribution)
Orange/red
Often found on sun exposed areas
May grow under nail as a red streak then later ruin the entire nail bed
111
How is Bowen's disease investigated?
Observation
| Dermoscopy- Reveals crops of rounded and coiled blood vessels.
112
How is Bowen's disease managed?
```
Observation- no treatment.
Cryotherapy
Curettage
Excision
5FU cream
Imiquimod cream
Photodynamic therapy
Radiotherapy and laser
```
113
What are the secondary infections common to eczema?
-Bacterial:
Staph aureus- impentiginisation.
Strep pyogenes- Impetigo
Viral:
Molluscum contagiosum
Eczema herpeticum
Eczema coxsakium
Fungal:
Dermatophyte
Yeast
114
What are the secondary infections common to eczema?
-Bacterial:
Staph aureus- impentiginisation.
Strep pyogenes- Impetigo
Viral:
Molluscum contagiosum
Eczema herpeticum
Eczema coxsakium- eczema with hand, foot and mouth exacerbations.
Fungal:
Dermatophyte
Yeast
115
What is eczema herpeticum?
| What are the common causes?
Fever and malaise with clusters of itchy blisters or punched out erosions.
Commonly caused by Herpes simplex type 1 or 2. Usually after a primary episode.
Can affect many organs including lung, eyes, brain and liver.
116
How does eczema herpeticum present?
Monomorphic blisters
Could be filled with clear yellow fluid or thick purulent material.
Often blood-stained i.e., red, purple or black.
New blisters have central dimples (umbilication).
They may weep or bleed.
Older blisters crust over and form sores (erosions)
Lesions heal over 2–6 weeks.
In severe cases where the skin has been destroyed by infection, small white scars may persist long term.
117
How is eczema herpeticum investigated?
Hx of eczema and presenting complaint.
Viral swab by scraping base of fresh blister.
Viral culture
PCR
118
How is eczema herpeticum managed?
Not fatal
Treat with aciclovir 400-800mg 5 times daily for 10-14 days or until healed.
If bacterial infection also then systemic Abx.
119
What is necrotising fasciitis?
Bacterial infection of soft tissue and fascia. Bacteria release toxins leading to thrombosis of BV and so destruction of soft tissue and fascia.
Type I- Polymicrobial (>1 bacteria): In older Px or DM.
Type II- Haemolytic strep A or MRSA caused: 'Flesh eating', affecting any age group.
Type III- Gas gangrene: Following surgery or injury, causing subcut gas.
120
What is the pathophysiology of necrotising fasciitis?
Can affect any age group.
An opening in the skin leading to bacterial invasion.
If cervicofascial- due to mandibular fracture or dental infection.
Direct contact with a person with the bacteria.
In children type II can be due to chicken pox.
Starts in the fascia and initially spreads horizontally without clinically appearing, then spreads vertically.
121
What are the RF for developing necrotising fasciitis?
```
Aspirin and non-steroidal anti-inflammatory drugs
Advanced age
Diabetes mellitus
Immune suppression
Obesity
Drug abuse
Severe chronic illness
Malignancy
```
122
How does necrotising fasciitis present?
Initially (within 24hrs of injury)- Px will develop severe worsening pain, fever, malaise, intense thirst (dehydration), nausea.
3-4 days after- Swelling, dark fluid filled blisters, wound becomes necrosed (black), oedema, crepitus, pain continues until the peripheral nerves are destroyed.
Towards the end the infection may spread to the bloodstream, Px develops shock, low BP, high fever.
123
How is necrotising fasciitis investigated?
Hx and examination- immunocompromised Px will have atypical presentation.
Positive finger test- Make a 2mm vertical incision in the affected skin, then push the index finger through- +ve if no resistance through the subcut tissue.
Typically no bleeding
Fluid oozes out of the skin
Raised Cre and urea, WBC, Na and CRP.
Imaging can also indicate any gas within the skin.
124
How is necrotising fasciitis managed?
Hospitalise the Px, may need ITU.
Identify the causative agent then treat with high dose IV Abx- initially treat with penicillin, metronidazole, clindamycin etc.
Urgent debridement- removal of necrotic tissue.
Oxygen, fluids etc to increase BP.
May need skin graft after resolution.
125
What is Staphylococcal scalded skin syndrome (SSSS)?
| What is the pathophysiology of SSSS?
Staph aureus infection causing red blistering skin- resembling a scald/burn.
Caused by a release of epidermolytic toxins A and B which bind to desmosomes causing skin cells to separate.
Since we develop lifelong protective antibodies to these toxins, this is a disease of neonates-5yrs old.
126
What are the signs and symptoms of SSSS?
Starts with irritability, fever and widespread redness. Within 24-48hrs blisters form and then erupt to look like scalded skin.
Tissue paper-like wrinkling of the skin- large bullae in groin, armpits and body orifices.
Rash spreads to other parts of the body including the arms, legs and trunk.
Top layer of skin starts to peel off.
127
How is SSSS investigated/diagnosed?
Hx and examination
Tzanck smear- Scrape off base a new vesicular lesion after deroofing then view under microscope. Useful for rapid detection or herpes infection or distinguishing between SJS/TEN from SSSS.
Skin biopsy, which shows intraepidermal cleavage at the granular layer
Bacterial culture from skin, blood, urine or umblical cord sample (in a newborn baby)
128
How is SSSS managed?
Needs hospitalisation for IV flucloxacillin. If MRSA then give vancomycin.
After a few days discharge with oral Abx.
Supportive: Paracetamol, skincare/moisture (Vaseline), neonates in incubator, monitor fluids and electrolytes.
Usually resolves within 5-7 days of treatment.
If untreated can develop cellulitis, sepsis and pneumonia.
129
What are the dermatological manifestations of some systemic diseases?
Hyperlipidaemia- xanthelasma (around eye), xanthoma (anywwhere else).
IBD- pyoderma gangrenosum and erythema nodusum (shin).
DM- Fungal infection and granuloma annulare (around feet).
Liver disease- jaundice, pruritis, purpura, erythema of palms, spider navie.
Sarcoidosis- erythema nodusum
130
What is Steven Johnson syndrome and Toxic epidermal necrolysis?
What are the RF?
Both overlap.
Nearly always a drug induced acute skin reaction leading to sheet like skin and mucosal loss.
```
Anyone on medication
Female>Male
High risk if HIV
More common with systemic drugs than topical
Medication with a longer t1/2
Some genetic association (HLA group)
```
131
Which drugs are commonly associated with SJS/TEN?
1) Antibacterial sulfonamides: cotrimoxazole
2) NSAIDs
3) Allopurinol
4) Anti-convulsants: lamotrigine, carbamazepine, phenytoin, phenobarbitone
5) Nevirapine (non-nucleoside reverse transcriptase inhibitor)
Less commonly:
Beta-lactam: penicillins, cephalosporins
Paracetamol/acetaminophen
132
Which cells are involved in SJS/TEN?
Natural killer cells lead to the mass destruction of the epidermis.
SJS <10% skin loss
TEN >30% skin loss
133
How does SJS/TEN present?
Can present within 1-3 wks of medication, 2 months of anti-convulsant.
```
Prodromal illness few days before:
Fever > 39 C
Sore throat, difficulty swallowing
Runny nose and cough
Sore red eyes, conjunctivitis
General aches and pains
```
Then abrupt tender/red skin rash starting at the trunk and then moving to face and limbs (no scalp, palm or soles). Maximum effect by day 4.
```
Skin lesions can involve:
Macules — flat, red and diffuse (measles-like spots) or purple (purpuric) spots
Diffuse erythema
Targetoid — as in erythema multiforme
Blisters — flaccid (ie, not tense).
```
Blisters then merge to leading to sheet detachment. If skin is rubbed and outermost layer peels off this is Nikolsky sign +ve.
134
What are the mucosal manifestations of SJS/TEN?
No blisters, prominent and severe. At least two mucosal surfaces are involved.
Eyes (conjunctivitis, less often corneal ulceration, anterior uveitis, panophthalmitis) — red, sore, sticky, photosensitive eyes
Lips/mouth (cheilitis, stomatitis) — red crusted lips, painful mouth ulcers
Pharynx, oesophagus — causing difficulty eating
Genital area and urinary tract — erosions, ulcers, urinary retention
Upper respiratory tract (trachea and bronchi) — cough and respiratory distress
Gastrointestinal tract — diarrhoea.
135
How is SJS/TEN investigated/diagnosed?
Elevated serum granulysin within the first few days.
Skin biopsy for diagnosis and exclusion of SSSS.
Histopathology will show keratinocyte necrosis, minimal inflammation, full thickness epithelial/epidermal necrosis.
Also map out their drug history to identify likely cause.
136
How is SJS/TEN managed?
Cessation of drug
Hospitalise- ideally ITU/burns unit
Temperature control (since skin can't do that)
Pain relief
Nutritional support
General management and monitoring of skin and other mucosal surfaces involved.
Can give prophylactic Abx.
Although drugs not used to treat, ciclosporin is proving effective.
137
What are the complications of SJS/TEN?
```
Dehydration
Infection
GI perforation/ulceration
Thrombosis/DIC
Shock
```
138
What is acute generalised exanthematous pustulosis (AGEP)?
Exanthematous- Widespread rash associated with systemic symptoms, often viral or drug in origin.
Severe cutaneous adverse reaction (SCAR) to a drug
Rare
Leads to superficial pustules
Anyone can develop AGEP
139
Which drugs cause AGEP?
1) Antibacterial sulfonamides
2) Oral antifungals, particularly terbinafine
3) Aminopenicillins
4) Calcium channel blockers such as diltiazem
5) Allopurinol
```
Less commonly:
Hydroxychloroquine
Carbamazepine
Paracetamol
Tetracyclines
```
In children EBV is a common cause of AGEP.
140
How does AGEP present?
Starts off in face/armpits/groin.
Soon becomes widespread, may get facial oedema.
Red skin with studded sterile pustules.
Px usually well but may have fever/malaise.
Persists for 1-2 wks then skin peels off.
141
How is AGEP investigated?
Usually a clinical diagnosis but can also do clinical investigations to confirm.
Blood tests show increased neutrophils, skin biopsy will have neutrophils in the pustules.
142
How is AGEP treated?
| What are the complications of AGEP?
Discontinue the offensive drug.
Can be treated at home if well enough.
Otherwise Px goes into hospital and treated with analgesics, topical corticosteroids, moisturisers, oral antihistamines etc.
Complications include:
Organ dysfunction, SJS/TEN, DRESS.
143
What is Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)?
Specific, severe reaction to a drug affecting multiple organs at one time.
Classified as a SCAR and may overlap with SJS/TEN.
Affects all ages and genders equally.
144
Which drugs cause DRESS?
1) Allopurinol
2) Antibacterial sulfonamides
3) Anti convulsants (carbapemezine)
4) Nevirapine
145
How does DRESS present?
Morbilliform (measles like) eruption including target lesions (lasting many weeks)
Erythroderma (>90% skin red)
Facial oedema
High fever
Haematological abnormalities
Lymphadenopathy
Inflammation of one or more internal organs (hepatitis, myocarditis, pericarditis, meningitis, encephalitis, seizures, coma etc)
146
How is DRESS investigated/diagnosed?
Needs clinical triad of:
1) High fever
2) Extensive skin rash
3) Organ involvement
Supported by deranged LFTs and eosinophilia.
Skin biopsy may be useful
Patch test prove useful in anticonvulsants
Do tests to check organ damage i.e. bloods, urinalysis, ECG etc.
147
How is DRESS managed?
Immediate withdrawal of medication followed by close monitoring.
In severe cases with organ damage- systemic corticosteroids can be used.
Supportive; Dressings, topical steroids, emollients, oral antihistamines.
Most Px recover within the month but it is common for them to have a relapse.
