Dermatology Flashcards
Outline the Fitzpatrick scale for skin
- Always burns, does not tan (pale, blue/green eyes, blonde/red hair)
- Burns easily, tans poorly (fair skin, blue eyes)
- Tans after initial burn (darker white)
- Burns minimally, tans easily (light brown)
- Rarely burns, tans darkly easily (brown)
- Never burns, always tans darkly (dark brown/black)
Describe the 2 main types of UV rays
UVA
- Longer wavelength
- Mainly causes skin aging and damage
- Can travel through windows
UVB
- Shorter wavelength
- Mainly causes burning
- Can’t travel through windows
Can use Altruist suncream - great UVA protection
Outline the ABCDE assessment for pigmented lesions
Asymmetry
Border (regular/irregular)
Colour
Diameter
Evolution
State the minor and major criteria (Glasgow 7-point checklist) for pigmented lesions, how much they score and when to refer (what number)
Major= 2 points each:
- Irregular shape
- Irregular colour
- Change in size
Minor = 1 point each:
- Diameter > 7mm
- Inflammation
- Oozing
- Change in sensation
Refer on urgent cancer pathway if:
>3 points
Suspected nodular malignant melanoma
Dermoscopy suggests melanoma
Scabies - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Infection by Sarcoptes scabiei mite
- Causes an intensely itchy rash
- Highly contagious (spread by direct contact)
Presentation:
- Intensely itchy rash usually affecting webs in-between fingers, flexures of the wrist, armpits, abdomen and groin
- Symptoms often worse at night
- Rash is papular or vesicula, +/- superficial burrows
Investigations:
- Clinical diagnosis based on symptoms and appearance
Management:
- Topical permethrin 5% (apply to cool dry skin over WHOLE body and leave for 12 hrs before washing off then repeat 7 days later)
- Treat all family members ON THE SAME DAY
Acne vulgaris - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management (dependant on severity)
Pathophysiology:
- Blockage and inflammation of follicle in the skin (pilosebaceous unit)
- Failure of the stratum corneum layer of the epidermis to fully detach causes a buildup and blockage of the pilosebaceous unit
- Leads to formation of open/closed comedones
- Comedones can become colonised propionibacterium (cutibacterium) acnes, leading to inflammation
Overall = formation of comedones and inflammation
Presentation:
- Presence of open/closed comedones
- Presence of inflammatory papules, pustules, nodules or cysts
- Face most commonly affected (but also neck, chest and back)
Investigations:
- Clinical diagnosis based on symptoms and appearance
- However may need to swab if diagnosis uncertain
Management (dependant on severity):
Mild-moderate acne = 2 of the following in combination in 12 week course:
- Topical benzoyl peroxide
- Topical retinoids (Tretinoin/Adapalene)
- Topical antibiotics (clindamycin)
Moderate-severe acne = 12 week courses of the following first line options:
- Topical benzoyl peroxide
- Topical retinoids (tretinoin/adapalene)
- Topical antibiotics (clindamycin)
- Combined oral contraceptives (COCPs)
+ Isotretinoin as a final line
- Psychological support / mental health screen
List some side effects of Isotretinoin medication for acne
- Teratogenic
- Association with mood disturbance / depression
- Drying of skin, mouth, eyes, lips
- Hair thinning
- Photosensitivity
- Nose bleeds
List some risk factors for acne vulgaris
- Family history of acne
- Naturally oily skin (increased sebum production)
- Hormonal disturbance e.g. during puberty, menstrual cycle, PCOS
- Certain medications (e.g. corticosteroids, hormonal treatments)
- Smoking (more in adults)
State when to refer a patient with acne to Dermatology
- Acne of any severity which is contributing to poor mental health
- Mild-moderate unresponsive to 2 completed courses of treatment
- Moderate-severe acne unresponsive to treatment
- Acne with scarring / persistent pigmentary changes
Rosacea - state the following:
- Pathophysiology
- Common demographic
- Presentation
- Investigations
- Management
Pathophysiology:
- Episodic or persistent facial flushing
- Exact cause unknown, suspect genetic and environmental factors
Common demographic:
- Women
- Aged between 30-60
- Fair skin
Presentation:
Different subtypes!
- Facial flushing (exacerbated by heat, alcohol, sun exposure, warm baths, stress, spicy foods etc.)
- Telangiectasia (if chronic)
- Can have papules
- Can affect nose (rhinophyma)
Investigations:
- Clinical diagnosis based on symptoms and appearance
Management:
- Avoid triggers
- Topical brimonidine or oral propranolol (reduce flushing)
- Laser therapy if telangiectasia
List some subtypes of rosacea and more specific treatments for these subtypes
Erythematous / telangiectasia = laser therapy for telangiectasia
Papulo-pustular = topical azelaic acid, topical Metronidazole
Rhinophyma = surgical or laser debulking
Ocular = warm compress and massage, may need referral to ophthalmology
Psoriasis - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Autoimmune disease characterised by erythematous, scaly plaques
- Caused by uncontrolled proliferation of keratinocytes, leading to areas of hyperkeratosis
Presentation:
- Well-demarcated erythematous scaly plaques (symmetrical, usually over extensor surfaces)
- Pruritus surrounding plaques
+ associated nail changes (50%)
+ joint involvement
Management:
Lifestyle advice e.g. weight loss, smoking cessation
- Topical emollients
- Topical corticosteroids (reduce inflammation)
- Topical Vitamin D (reduce keratinocyte proliferation)
- Topical calcineurin inhibitors
- UV phototherapy
- Systemic e.g. Methotrexate or biologic therapy e.g. Infliximab
Atopic dermatitis (eczema) - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Chronic inflammation of the dermis, leading to changes in the epidermis
- Leads to thickening of the epidermis and stratum corneum
- Extremely common, affecting up to 20% of children
- Strongly associated with asthma and hayfever (as well as family history)
Presentation:
- Highly pruritic erythematous rash (symmetrical, usually over flexor surfaces)
+ excoriations
+/- lichenification if chronic
Management:
Avoid triggers / allergens, keep areas cool and dry
- Soap substitutes
- Topical emollients
- Topical corticosteroids (continued for 48hrs after the flare is controlled)
- If severe, can consider oral steroids
+ topical fusidic acid if areas of secondary infection or oral antibiotics
List some common triggers for a psoriasis flare
- Stress
- Infection e.g. streptococcus (guttate)
- Alcohol + smoking
- Cold/dry weather
- Withdrawal of treatment e.g. steroids
- Skin trauma (Koebner phenomenon)
- Medications e.g. oral steroids!, Aspirin, NSAIDs, beta-blockers, Lithium, antimalarials e.g. Quinine
List some examples of different strength topical steroids
- Mild / low
- Moderate
- Potent
- Very potent
How Educators Brilliantly Finessed Dermatology…
H: Hydrocortisone (least potent)
E: Eumovate
B: Betnovate
F: Fluticasone
D: Dermovate (most potent)
Mild / low:
- Hydrocortisone
Moderate:
- Eumovate (Clobetasone)
- Mometasone
Potent:
- Betnovate (Betamethasone)
- Fluticasone
Very Potent:
- Dermovate (Clobetasol)
Outline how a finger tip unit is used for topical steroid use
One finger tip unit is the amount of cream on one finger tip and corresponds roughly to the surface area of two palms
List some common side effects of topical steroid use
- Skin thinning
- Skin striae
- Skin discoloration (hypo or hyperpigmentation)
- Tachyphylaxis (effectiveness may decrease with prolonged use)
- Telangiectasia
Risk of systemic absorption with very potent steroids or extensive application
Dermatofibroma - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Slow-growing benign nodule
- Caused by proliferation of fibroblasts, commonly triggered by trauma
- Multiple dermatofibromas can be seen in some immune conditions e.g. SLE, HIV
Presentation:
- Small, firm nodule (usually <1 cm), often reddish-brown
- Positive dimple sign (dimple forms when pinched)
- Asymptomatic or mild tenderness upon pressure
Investigations:
- Mainly clinical diagnosis
- Can biopsy if clinical uncertainty
Management:
- Observation unless they bothersome or cosmetically undesirable
- If removal needed = surgical excision, cryotherapy or laser therapy (less scarring)
Briefly state the difference between pemphigus vulgaris and bullous pemphigoid
Both autoimmune blistering disorders
pemphiguS vulgaris = superficial blisters
- superficial fragile painful blisters
- positive Nikolsky’s sign
- mucosal involvement
bullous pemphigoiD = deep blisters
- more robust, dense blisters
- negative Nikolsky’s sign
What is Nikolsky’s sign
Skin finding = top layers of the skin slip away from the lower layers when rubbed
Outline the general management for both pemphigus vulgaris and bullous pemphigoid
Steroids
- High-potency topical corticosteroids if local disease
- Oral corticosteroids if extensive involvement
Immunosuppressive medications for severe or refractory cases e.g. Azathioprine
Stevens-Johnson syndrome - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Immune-mediated hypersensitivity disorder
- Often triggered by adverse drug reactions but less commonly infections (viral, bacterial or fungal)
- Ranges from mild to severe forms (TEN)
Presentation:
- If medication = within a week of medication intake
- Can result after recent history of URTI
- Erythematous macules, later become target-shaped
- Flaccid blisters develop and Nikolsky sign positive
- Mucosal involvement (ulceration)
- Affects <10% of body surface
Investigations:
- Usually clinical but can be supported by skin biopsy
Management:
- Largely supportive (fluids and analgesia), focus on skin and eye care
- Treat any secondary infections
Actinic keratosis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Also known as ‘solar keratosis’
- Pre-malignant condition, with a low potential to transform into squamous cell carcinoma
- Thought to arise as a result of sun exposure, leading to DNA damage in keratinocytes
Presentation:
- Thickened papules / plaques with surrounding erythematous skin
- Keratotic, rough, warty surface
- Generally asymptomatic, occuring on sun-exposed areas of body only
Investigations:
- Dermatoscopic examination
- Biopsy for histology if needed
Management:
Main aim = prevention of progression into SCC
For localised lesions = cryotherapy, curettage or surgical excision
For larger lesions = topical agents e.g. 5-Fluorouracil, Imiquimod or NSAIDs
+ patient education on sun-protective measures (prevent further formation)
List some risk factors for the development of actinic keratosis
- Type 1 or 2 skin (fair, burns easily)
- History of sunburn
- Prolonged sun exposure e.g. outdoor occupation or hobbies
- Immunosuppression
Outline the prognosis for actinic keratosis if left untreated (in terms of risk of progression)
Rare for a solitary actinic keratosis to evolve to squamous cell carcinoma
But the risk with more than 10 actinic keratoses is thought to be about 10 to 15% (if left untreated over time)
Also because skin is sun damaged, at risk of developing other types of skin cancer e.g. BCC, SCC, melanoma
Erythroderma - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
Dermatological emergency
- Widespread erythema affecting over 90% of the skin surface
- Most commonly triggered by pre-existing skin condition e.g. eczema, contact dermatitis, psoriasis but can be drug allergy or idiopathic
Presentation:
- Significant skin erythema affecting over 90% of the skin surface
- Pruritus
- Oedema
- Potential systemic symptoms e.g. fever/chills, hypovolaemia, tachycardia (due to heat and fluid loss)
Investigations:
Mainly clinical diagnosis
- Bloods (FBC, CRP, U&Es)
- Skin biopsy (confirm diagnosis and identify underlying cause)
Management:
- Supportive care e.g. IV fluids
- Emollients (soothe skin)
- Treat underlying skin condition
- Hospitalisation for severe cases
List 2 conditions associated with erythema nodosum
Over 50% cases of idiopathic
- IBD
- Sarcoidosis
Erythema nodosum - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Inflammation of the subcutaneous fat
- Often idiopathic, but can be associated with IBD or sarcoidosis
- Often occurs in patients in 20-30’s
Presentation:
- Tender, raised, erythematous nodules over anterior shins
- Can be associated with systemic symptoms e.g. fever, malaise, arthralgia
Investigations:
Mainly clinical diagnosis
- Bloods (FBC, CRP, ESR)
- Consider chest x-ray (sarcoidosis) or calprotectin bloods (IBD)
Management:
Primarily focused on treating underlying cause
- Rest and leg elevation
- NSAIDs for pain and inflammation
- Colchicine / corticosteroids for severe, refractory cases
Lichen planus - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Chronic T-cell mediated inflammatory disorder
- Idiopathic, or
Presentation:
6Ps
- purple papules or plaques
- pruritic
- polygonal
- planar
- Lesions typically appear on the flexor aspects of the wrist and ankles
- Can have mucosal involvement / ulceration with candida like appearance
Investigations:
- Usually clinical
Management:
- Avoiding trauma to prevent Koebnerisation
- Avoid alcohol or smoking (risk of oral SCC)
- Topical therapy: topical corticosteroids, Tacrolimus, or Ciclosporin mouthwash
- Systemic therapy: oral steroids, methotrexate, acitretin, or hydroxychloroquine can be used
- Phototherapy
Bowen’s disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Carcinoma in situ or intraepidermal squamous cell carcinoma
- UV radiation damages DNA
Presentation:
- One or more irregular scaly plaques (can be several cm in diameter
- Orange-red in colour
- Often in sun exposed areas of skin
Investigations:
- Dermoscopy (coiled blood vessels)
- Biopsy (full thickness dysplasia of the epidermis, but in-situ)
Management:
Consider observation if elderly or low risk of transformation
- Cryotherapy
- 5-FU / Imiquimod
- Excision
- Shave, curettage and electrosurgery
- Photodynamic therapy
+ sun protection advice to limit further lesions
List some risk factors for development of bowen’s disease
- Chronic sun exposure
- Immunocompromised
- Exposure to radiation
- Arsenic ingestion
- HPV
