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
Roughly what % of Bowen’s disease lesions go on to develop into invasive squamous cell carcinoma
About 5% of intraepidermal SCC lesions
Basal cell carcinoma (BCC) - state the following:
- Pathophysiology
- Presentation
- Diagnosis
- Management
Originating layer and area found:
- DNA damage
- Originates from basal cells in the deep epidermis (stratum basale)
- Locally destructive but minimal risk of metastasis
Presentation:
Slow growing
- Often a waxy, pink pearl-like nodule with rolled edges
- Telangiectasia
- Can seem to be a scab that doesn’t heal / can have spontaneous bleeding
Found in sun exposed areas e.g. face, ears
Diagnosis:
- Biopsy
Management:
- Excision / Moh’s micrographic surgery if in poor location e.g. near eye
- Shave, curettage, and cautery
- Cryotherapy
- UV phototherapy
- 5-FU or Imiquimod cream
+/- radiotherapy
List some different subtypes of basal cell carcinoma
- Nodular (most common)
- Superficial
- Morphoeic
- Pigmented
- Mixed BCC and SCC (basosquamous)
Describe the basic prognosis for basal cell carcinoma
Most BCCs are cured by treatment
However ~ 50% develop a second BCC within 3 years of the first
Also increased risk of other skin cancers, especially melanoma
List some risk factors for basal cell carcinoma (non-modifiable and modifiable)
Non-modifiable:
- Age (and male)
- Previous BCC or other form of skin cancer (squamous cell carcinoma, melanoma)
- Type 1 or 2 skin type
Modifiable:
- Sun damaged skin / repeated prior episodes of sunburn
- Immunocompromised
- Inherited syndromes e.g. Gorlin syndrome
- Exposure to radiation / arsenic
Squamous cell carcinoma (SCC) - state the following:
- Pathophysiology
- Presentation
- Diagnosis
- Management
Pathophysiology:
- Originates from keratinocytes in the middle epidermis (stratum spinosum)
- Found in UV exposed areas e.g. face, ears
- Potential to metastasise
Presentation:
Rapidly growing
- Mostly a scaly appearance, irregular raised and rough (ulcerating)
- Can be sore or tender
In sun exposed areas
Diagnosis:
- Skin biopsy 4mm margin (following excision mostly)
Management:
- Surgical excision (rarely use Moh’s micrographic surgery)
- For small / low risk tumours: cryotherapy or shave, curettage, and cautery
- Local radiotherapy
List some risk factors for developing squamous cell carcinoma
Non-modifiable:
- Age (and male)
- Previous SCC or other form of skin cancer, esp. actinic keratosis
- Type 1 or 2 skin type
Modifiable:
- Sun damaged skin / repeated prior episodes of sunburn
- Immunocompromised
- Smoking
- Inherited syndromes e.g. xeroderma pigmentosum
- Exposure to radiation / arsenic
- Organ transplant recipients
Melanoma - state the following:
- Originating layer and area found
- Typical appearance
- Diagnosis method
- Prognosis
- Type of referral and management
- Safety netting advice
Originating layer and area found:
- Originates from melanocytes in the deep epidermis
- Found in UV exposed areas e.g. face, ears but can appear anywhere on the body
Typical appearance:
- Generally a darker colour (due to melanin production) like a mole
- Use ABCDE assessment method to assess for risk of melanoma
Diagnosis:
- Dermoscopy
- Biopsy = 2mm margin
- Consider staging CT is suspicion of metastasis
Management:
- Surgical excision with 2mm margin initially, establish breslow thickness then further excision based off this
- Sentinel node biopsy
- In metastatic disease = adjuvant immunotherapy / chemotherapy
+ radiotherapy in some cases
List some risk factors for melanoma
Non-modifiable:
- Age (and male)
- Previous melanoma or other form of skin cancer e.g. BCC or SCC
- Strong family history of melanoma
- Type 1 or 2 skin type
- Many melanocytic naevi (moles)
- >5 atypical naevi (moles)
Modifiable:
- Sun damaged skin / repeated prior episodes of sunburn
- Immunocompromised
Impetigo - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Highly contagious superficial epidermal infection of the skin
- Mainly caused by staph aureus or group A strep
- Most common in infants and school-aged children, commonly infecting the skin after cuts / abrasions or insect bites
Presentation:
- Superficial erosion with a characteristic golden crust
- Erythematous macule transforms into vesicles or pustules (also can be bullous or non-bullous)
Investigations:
- Often clinical diagnosis
- Consider swab if recurrent or resistant to treatment
Management:
- Topical Fusidic acid or Mupirocin (both antibiotics) over affected areas 5-7 days
- Consider oral antibiotics e.g. Flucloxacillin if widespread infection
- Patients should avoid sharing items
- Avoid school or work until completed 48 hours of antibiotic treatment (limit spread)
Folliculitis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Inflammatory condition of the hair follicles, forming papules or pustules (commonly neck, armpit or groin but sparing palms and soles)
- Caused by various factors, but staph aureus is most common causative organism
- Subtype of eosinophilic folliculitis, is non-infective type associated with immunosuppression
Presentation:
- Pustules and papules surrounding hair follicles
Investigations:
Usually clinical diagnosis
- Skin biopsy if eosinophilic folliculitis is suspected
Management:
- Topical antibiotics and consider antibacterial scrubs e.g. chlorhexidine (oral antibiotics if severe or resistent)
Cellulitis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Bacterial infection of dermis and subcutaneous layers (through break in the skin barrier)
- Most commonly caused by staph aureus or strep pyogenes / group A step
Presentation:
- Poorly demarcated erythematous patch
- Associated calor, dolor and rubor
+/- systemic symptoms e.g. fever and malaise
Investigations:
- Blood tests: FBC (high WCC), CRP, U+E (may be AKI if severe infection),
- Blood cultures
- Wound swab
Management:
- Consider admission if severe / risk factors e.g. immunocompromised
- Mark the area of erythema in pen
- Elevate leg if possible
Class 1: oral Flucloxacillin
Class 2: consider oral or IV
Class 3-4: IV Flucloxacillin
List some risk factors for cellulitis
- Previous / recent history of cellulitis
- Breaks in the skin e.g. surgical wounds
- Chronic skin conditions e.g. chronic venous insufficiency, pressure sores
- Diabetes
- Immunosuppression
- Obesity
- IV drug use
Outline how cellulitis and erysipelas are different and how they present
Cellulitis is a deep bacterial infection involving dermis and subcutaneous layers, whereas erysipelas is form of superficial cellulitis
Cellulitis = poorly-demarcated margins
Erysipelas = well-demarcated margins
Outline the criteria used to classify the severity of cellulitis and roughly the 4 categories
Eron classification = categorise severity and guide treatment decisions
Class 1 = no systemic symptoms and no comorbidities / risk factors
Class 2 = systemic symptoms OR no systemic symptoms but with comorbidities / risk factors
Class 3 = the person has significant systemic symptoms e.g. confusion
Class 4 = septic or a severe infection
Herpes simplex virus (HSV) - state the following:
- Pathophysiology (including mode of transmission)
- Presentation
- Investigations
- Management
Pathophysiology:
- Infection by the herpes simplex virus of either: eyes, oral cavity or genital area
- Usually HSV-1 or HSV-2
- First contact with the virus is usually asymptomatic
- Usually transmitted during childhood via direct contact with infected secretions
Presentation:
- Prodrome of pain, burning, tingling, itching, and paraesthesia preceding lesions
- Crops of vesicles that rupture, leaving superficial ulcers
Investigations:
- Mainly clinical diagnosis
- Take swab for anogenital lesions
Management:
ORAL
Reassurance that they are usually self-limiting
- Analgesia
- Avoid kissing and oral sex until all lesions have fully healed
ANOGENITAL
- Attend a specialist sexual health service for diagnosis, treatment, STI screen
- Analgesia
- Avoid sexual activity until all lesions have fully healed
- If ophthalmic involvement, see ophthalmologist
Herpes zoster virus (singles) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Reactivation of the varicella zoster virus, from lying dormant in nerve ganglia following primary infection with chickenpox
- Predominantly affects elderly but can affect immunocompromised young adults
Presentation:
- Vesicular rash in dermatomal distribution (starts as erythematous papules)
- Exquisitely painful in dermatomal distribution (nerve pain)
- May have systemic symptoms e.g. fever, headache, malaise
Investigations:
- Mainly clinical diagnosis
Management:
- Analgesia with NSAIDs (or nerve pain anaglesia e.g. Gabapentin)
- Oral antiviral within 72h of rash onset
- IV antivirals if severe or immunocompromised, ophthalmic symptoms or suspicion of meningitis etc.
- Advise avoiding contact with pregnant women, babies, immunocompromised until the lesions fully crusted over
Herpes zoster virus (chicken pox) - state the following:
- Pathophysiology (including mode of transmission)
- Presentation
- Investigations
- Management
Pathophysiology:
- Highly contagious disease caused by the varicella virus (herpes virus 3)
- Predominantly seen in children (peak 1-9 years)
- Transmission: airborne and direct contact with the rash
Presentation:
- Raised itchy spots which transform into vesicular rash, typically starting on face and spreading to rest of body
- Systemic symptoms e.g. mild fever, fatigue, loss of appetite
- Eventually crusts over and heals
Investigations:
- Mainly clinical diagnosis
Management:
Primarily conservative (usually self-limiting)
- Keep child’s fingernails short (prevent scratching and subsequent infection)
- Cooling measures e.g. calamine lotion
- Analgesics and antipyretics
- Isolation until rash has fully crusted over (approx. 5 days after rash onset)
Viral warts - state the following:
- Pathophysiology (including mode of transmission)
- Presentation
- Investigations
- Management
Pathophysiology:
- Caused by human papilloma virus (HPV), leading to proliferation of the keratinocytes and hyperkeratosis = wart
- Common in school aged children or immunocompromised
- Spread by direct skin-to-skin contact
Presentation:
- Hard, keratinous surface (cauliflower appearance)
Investigations:
- Mainly clinical diagnosis
Management:
No treatment may be required, wait for spontaneous resolution (50% disappear within 6 months)
Consider treatment if immunocompromised, or patient preference
- Cryotherapy
- Topical salicylic acid
Ringworm (dermatophytosis) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Superficial fungal infection of the skin, caused by dermatophytes (fungi which grow in dead keratin)
Presentation:
- Red, scaly patch that often has an area of central clearing (crusted edge)
- Pruritus over affected area
Investigations:
- Skin scrapings
Management:
- Topical antifungal Clotrimazole or Ketoconazole
- For tinea capitis or onychomycosis, systemic agents e.g. Terbinafine or Itraconazole
State the locations for different tinea infections:
Tinea barbae
Tinea capitis
Tinea corporis
Tinea cruris
Tinea faciei
Tinea manuum
Tinea pedis
Tinea unguium
Beard = Tinea barbae
Head = Tinea capitis
Body = Tinea corporis
Groin = Tinea cruris
Face = Tinea faciei
Hand = Tinea manuum
Foot = Tinea pedis
Nail = Tinea unguium
List soem factors which make someone more vulnerable to developing ring worm
- Poor hygiene
- Immunocompromised
- Close contact with other infected individuals
- Close contact with animals
Outline the management for oral candidiasis
Topical antifungal treatment for 14 days
- Miconazole oral gel
(2nd line = Nystatin suspension)
Outline the management for genital candidiasis
- Oral Fluconazole 150mg capsule single dose
(2nd line = Clotrimazole 500mg intravaginal pessary)
+ use of topical Imidazole
Outline the management for cutaneous candidiasis infection
Topical Imidazole (Clotrimazole, econazole, miconazole, or ketoconazole) or Terbinafine
Consider prescribing a mildly potent corticosteroid cream if itch / inflammation is problematic
Outline the management for fungal nail infection
May not need to treat if asymptomatic
Oral terbinafine (6 weeks for fingernails, 12-24 weeks for toenails)
Head lice - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Infestation by parasitic insects of hairs of the human head, feeding on scalp blood
Presentation:
- Intensely itchy scalp
- Visual lice in the hair (sesame seed sized)
Investigations:
- Live louse must be seen to confirm active head lice infection (use fine tooth comb)
**Itching scalp is not sufficient to make a diagnosis
ALL members of the household / close contacts should also be checked
Management:
- Systematic wet combing
- Physical insecticide (suffocation) e.g. Dimeticone 4% gel
- Chemical insecticide e.g. Malathion 0.5% aqueous liquid
Intertrigo - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Inflammatory skin condition, predominantly in skin folds (friction)
- Common in infants, obese, poor hygiene, diabetes or malnutrition
- Frequently accompanied by secondary bacterial (staph aureus, group A strep) or fungal infections (candida)
Presentation:
- Erythematous patches in skin folds (commonly axilla, groin), often symmetrical
- Severe inflammation can occur with fissures, exudation, crusting
- If candida, satellite lesions
Investigations:
Largely clinical diagnosis
- Consider fungal culture
- Consider bacterial culture
Management:
- Barrier creams (reduce skin-on-skin friction and moisture)
- Topical agents e.g. antifungal, antibacterial
- Consider topical corticosteroids if severe inflammation
- Minimise moisture and friction e.g. loose fitting clothing, weight loss
Patient education and promote skin hygiene for prevention
List some complications of cellulitis
- Systemic spread (sepsis)
- Abscess
- Scarring and changes in skin texture
- Lymphangitis (infection of lymphatic vessels)
- Recurrence of cellulitis
Outline who is eligible for the shingles vaccination and some benefits
One off vaccination for:
- Over > 65
- 70-80 if not previously vaccinated
- > 50 and immunocompromised
- Helps reduce risk of developing shingles
- If do develop shingles, symptoms are less severe
List some potential complications from chickenpox infection
- Secondary bacterial infection
- Pneumonia
- Encephalitis (rare)
- Reye’s syndrome (primarily in children)
- Shingles later in life
Congenital varicella syndrome (if early pregnancy)
List some potential complications from shingles
- Corneal ulcers, scarring and blindness (if ophthalmic involvement)
- Chronic neuropathic pain (post-herpetic neuralgia)
- Secondary bacterial infection
Molluscum contagiosum - state the following:
- Pathophysiology (including mode of transmission)
- Presentation
- Contagious?
- Management
Pathophysiology:
- Common viral infection of the skin, caused by molluscum contagiosum virus (member of Poxvirus family)
- Particularly prevalent among children and adolescents, commonly present on genitals
- Normally resolves within a few months, but can > 18 months
- Direct skin-to-skin contact
Presentation:
- Multiple firm, flesh coloured, dome-shaped umbilicated nodules
Investigations:
- Mainly clinical diagnosis
- Consider STI screen (if anogenital involvement in adults)
- Consider HIV testing (if extensive lesions)
- Urgent referral to ophthalmology if ocular lesions AND red eye
Management:
- Majority of cases are self-resolving and no treatment is required
- Children do NOT need to be kept off school but minimise contact and sharing of personal items
- Further steps if unresolving: cryotherapy, topical Imiquimod 5% cream
Staphylococcal scalded skin syndrome (SSSS) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Severe desquamating rash, caused by staph aureus
- Staph aureus released exotoxins leading to destruction of epidermis
- Primarily affects infants (under 5)
- KEY = Nikolsky sign positive
Presentation:
- Superficial fluid-filled blisters
- Erythroderma
- Desquamation of epidermis = positive Nikolsky sign
- Perioral crusting or fissuring (but oral cavity unaffected)
- Fever
- Irritability
Investigations:
- Mainly clinical diagnosis
- Consider blood cultures (staph aureus) or skin biopsy
Management:
Mainly supportive
- Regular monitoring
- Analgesia
- Careful wound management (prevent secondary infections)
- IV fluids
- IV antibiotics (IV Flucloxacillin = inhibit toxin synthesis)
Steven-Johnson syndrome - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Immune-mediated hypersensitivity disorder
- Often triggered by adverse drug reactions (less commonly infections: viral, bacterial or fungal)
- Range of severity, with toxic-epidermal necrolysis at the most severe end (SJS < 10% of body surface, TEN > 30%)
Presentation:
Often presents within 1 week of medication intake
- Initially URTI symptoms e.g. cough, cold, fever, sore throat
- Erythematous macules (later become target-shaped)
- Flaccid blisters develop = Nikolsky sign is positive
- Mucosal ulceration
Investigations:
Largely clinical
- Bloods (FBC, CRP, U&Es, LFTs, glucose, magnesium, phosphate and bicarbonate)
- Supported by a skin biopsy
- Wound swab if suspected infection
Management:
Largely supportive
- Stop drug suspected of causing SJS
- IV fluids
- Analgesia
- Good skin care precautions (clean with saline soaked gauze)
+ potential treatment of secondary infections
For Steven-Johnson syndrome, list some drugs that are more likely to cause a reaction (as well as viral infections)
Drugs:
- Sulfonamides
- Beta-lactams (penicillins and cephalosporins)
- Antiepileptics
- Allopurinol
- NSAIDs
Viral (less common):
- Herpes simplex virus
- EBV
- HIV
- Influenza
- Hepatitis
List some SKIN conditions commonly presenting with an itch
Non-infective:
- Eczema
- Venous eczema
- Urticaria
- Psoriasis
- Dermatitis herpetiformis (seen in coeliac disease)
- Lichen planus
- Lichen simplex
Infective:
- Scabies
List some systemic conditions commonly presenting with an itch
Disease:
- Thyroid problems (hypo or hyper)
- Diabetes
Haematological:
- Iron deficiency anaemia
- Polycythaemia
- Lymphoma
Organs / medication:
- Renal failure
- Liver disease
- Medications e.g. opiates, statins, ACE-inhibitors, chloroquine
+ psychogenic
List the 4 most common drugs to cause drug-induced urticaria
- Penicillin antibiotics
- NSAIDs
- Aspirin
- Opiates
Outline the difference between acute and chronic urticaria
Acute urticaria:
- Sudden onset of wheals
- Associated with triggers e.g. infection or medication
- Often self-limiting
- Symptoms resolving within a few hours to days
- Can last up to 6 weeks
Chronic urticaria:
- Persistent or recurrent wheals
- Can be spontaneous (idiopathic) or inducible (caused by a known trigger)
- Symptoms lasting for > 6 weeks
Urticarial lesions (wheals) are transient and move about
Outline the pathophysiology of urticaria
Mast cell driven disease
Leads to release of histamine ((triggered by cytokines or autoantibodies)
Increased permeability of local capillaries and small venules, leading to leaking of fluid = oedema
List some potential triggers for urticaria
- Contact with certain substances
- Food
- Temperature change
- Exercise
- Pressure
- Dermatographism
- UV radiation
- Medications
Outline the management of urticaria
Aim: control symptoms, improve QOL and reduce recurrence
- Avoidance of aggravating factors
- Stop any offending medications or avoid any likely triggers
- Non-sedating antihistamines e.g. Cetirizine, Fexofenadine or Loratidine
- If symptoms are severe, give a short course of oral corticosteroids e.g. oral Prednisolone
List some risk factors for urticaria
- Female
- Young-middle aged (20 – 40)
- History of atopy
- Family history
- Chronic stress
When should a person with urticaria be referred to a dermatologist/immunologist?
- Painful and persistent symptoms
- Poorly controlled on antihistamines (able to add other options e.g. Cyclosporine, Tacrolimus
- Acute severe urticaria thought to be due to food / latex allergy
- Some forms of chronic inducible urticaria, difficult to manage in primary care e.g. cold urticaria
Necrotising fasciitis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Severe, life-threatening infection involving the subcutaneous tissue and fascial planes
- Typically caused by infection with toxin-producing bacteria (Group A Strep or Staph aureus)
- Rare but very high mortality rate
Presentation:
- Pain disproportionate to clinical signs
- Visible skin changes: dark discoloration, blistering
- Crepitus on palpation
- Systemically unwell: fever, tachycardia, tachypnoea, hypotension
Investigations:
- Blood tests: FBC (raised WCC, CRP, evidence of organ dysfunction)
- Blood cultures
- Plain x-ray or CT/MRI (visualise gas in the tissue)
*investigations should not delay treatment
Management:
- Urgent surgical debridement
- IV broad spectrum antibiotics e.g. Gentamicin, Clindamycin
- General support e.g. IV fluids, vasopressors if needed
Emollients:
- Describe how they work
- Type of formulation / products
- Where they can be used
- Adverse effects
Describe how they work:
- Protect and moisturise outer layer of the skin
- Help skin retain water and prevent dryness
Type of formulation / products:
- Ointments
- Gels
- Creams
- Sprays
- Lotions
Where they can be used:
- Anywhere on the body
- Try and avoid ointment use on scalp as it will make hair greasy
Adverse effects:
- Sometimes sting / cause rash
- Flammable!!
