1
Q
What is the pathophysiology of acne?
A
- Narrowing of hair follicles due to hypercornification – corneodesmosomes block the entrance to hair follicles
- Results in increased serum production
- Sebum becomes trapped in the hair follicles and stagnates in the pit due to lack of oxygen
- Creates anaerobic conditions to allow propionobacerium acnes to multiply
- P.acne breaks down the triglycerides in serum into free fatty acids, resulting in irritation, inflammation and the attraction of neutrophils
- Results in pus formation and further inflammation
2
Q
What is the clinical presentation of acne?
A
- Whiteheads – closed comeodones
- Blackheads – open comedones
- Skin-coloured lesions
- Inflammatory lesions (when the closed wall of comedones ruptures)
- Papules (small red bumps)
- Pustules (white/yellow spots)
- Nodules (large red bumps)
- Commonly found on face, chest and upper back
3
Q
How is acne diagnosed?
A
- Usually a clinical diagnosis
- Skin swabs for microscopy and culture
- Hormonal tests in females
4
Q
How is mild acne managed?
A
- Benzyl peroxide gel/cream (increases skin turnover, clears pores and reduces bacterial count)
- Topical antibiotics e.g. clindamycin or erythromycin gel
- Topical retinoids e.g. tazarotene gel (inhibit formation and reduce number of microcomedones, but s/e include burning, stinging and scaling)
5
Q
How is severe acne managed?
A
- Above topical therapy with oral therapy
- Oral tetracyclines e.g. oral doxycycline then minocycline (4m minimum treatment)
- Hormonal treatment when standard antibiotics have failed (anti-androgens suppress sebum production)
6
Q
What is endogenous eczema?
A
Atopic eczema due to hypersensitivity
7
Q
What is exogenous eczema?
A
Contact dermatitis precipitated by chemicals, sweat and abrasives
8
Q
What is the aetiology of eczema/ dermatitis?
A
- Damaged filaggrin
- Exacerbated by chemicals, detergents and woollen clothes
- Infection in skin or systemically can cause an exacerbation
9
Q
What is the pathophysiology of eczema/ dermatitis?
A
- Breakdown of skin due to thinning of the stratum corneum, leading to an increased risk of inflammation
- Initial T helper 2 CD4 lymphocyte activation resulting in inflammation
- Loss of natural moisturising factor leads to dry skin and development of cracks
- Abnormal lipid bilayer that provided an inadequate permeability barrier
10
Q
What are the risk factors of eczema/ dermatitis?
A
- Family history
- Faulty gene that codes for filaggrin
11
Q
What is the clinical presentation of eczema/ dermatitis?
A
- Commonly found on the face and flexure surfaces of limbs
- Itchy, erythematous and scaly patches, especially in the flexure of the elbows, knees, ankles, wrists and around the neck
- Increased skin dryness
- Acute lesions may weep or exude and show small vesicles
- Recurrent S.aureus infections
12
Q
How is eczema/ dermatitis diagnosed?
A
Atopic dermatitis
- Clinical diagnosis
- High serum AgE in 80%
- Must have a itchy skin condition in the past 6m
Plus 3+ of:
- History of involvement of skin creases
- Personal history of asthma or hay fever (or FHx)
- History of generally dry skin
- Onset of childhoods
13
Q
How is eczema/ dermatitis managed?
A
- Education and explanation
- Avoid irritants e.g. soaps and furry animals, don’t get too hot
- COMPLETE EMOLLIENT THERAPY e.g. E45 cream – artificial restoration of lipid barrier above the stratum corneum that prevents water loss between corneocytes (apply every 4h 3-4 times a day)
- TOPICAL THERAPY – first line topical corticosteroids e.g. hydrocortisones (inhibits pro-inflammatory cytokines), second line calcineurin inhibitors e.g. pimecrolimus ointment (less effective but less s/e and good for sensitive areas)
- MODERATE TO SEVERE OR NON-RESPONSIVE – oral immune-modulators (e.g. ciclosporin), oral steroids (prednisolone), antibiotics (flucloxacillin), phototherapy, antihistamines (e.g. chlorphenamine – no clinical effect but sedate patient so they can sleep)
14
Q
What is the aetiology of psoriasis?
A
- Polygenic
- Dependent on environmental triggers (group A strep infection, drugs, UV lights, high alcohol intake, stress)
- Family history
15
Q
What is the pathogenesis of psoriasis?
A
- T-lymphocyte driven to an unidentified antigen
- T cell activation results in upregulation of Th1 cells e.g. interferon-gamma, interleukins, growth factors and adhesion molecules
- Upregulation of cytokines results in increased uncontrolled hyperproliferation of the keratinocytes in the epidermis with an increase in the epidermal cell turnover rate
16
Q
What are the risk factors of psoriasis?
A
- Family history
- Group A strep infection
- Drugs e.g. lithium
- UV light
- High alcohol intake
- Stress
17
Q
What is the clinical presentation of chronic plaque psoriasis?
A
- Most common type
- Well-demarcated disc-shaped, salmon-pink silvery plaques on the exterior surface of limbs (esp. elbows and knees)
- Scalp involvement is common and most seen at the hair margin
- Thickened epidermis
- New plaques at the site of skin trauma
18
Q
What is the clinical presentation of flexural psoriasis?
A
- Tends to occur later in life
- Well-demarcated red, glazed, non-scaly plaques
- Confined to flexures e.g. groin, natal cleft and sub-mammary areas
19
Q
What is the clinical presentation of guttate psoriasis?
A
- Most commonly in children and young adults
- Generalised, concentrating on the trunk, upper arms and legs
- Explosive eruption of small circular plaques on the trunk 2w after strep core throat
20
Q
What is the clinical presentation of palmoplantar psoriasis?
A
Thickening of palms and soles
21
Q
How is chronic plaque psoriasis managed?
A
- Emollients e.g. E45
- Topical vit D analogues
- Topical corticosteroids
- Topical retinoids
- Ultraviolet B
- Coal tar
- Anti-mitotic for large plaques e.g. dithranol cream
- UV A phototherapy for extensive plaques with DMARDs and immunosuppressants
22
Q
How is flexural psoriasis managed?
1st and 2nd line
A
- 1st line – topical mild-moderate corticosteroid e.g. hydrocortisone
- 2nd line – topical vit D analogue e.g. calcipotriol cream
23
Q
How is guttate psoriasis managed?
A
- Topical mild-moderate corticosteroid
- Ultraviolet B
- Coal tar
24
Q
How is palmoplantar psoriasis managed?
A
- Emollients
- Keratolytic agents e.g. salicylic acid
- Potent topical corticosteroids e.g. glucinonide
- Phototherapy with UV A
- Oral retinoid e.g. acitretin
25
What is the pathophysiology of squamous cell carcinoma?
Locally invasive, malignant tumour of the squamal keratinocytes
26
What are the risk factors of squamous cell carcinoma?
- UV exposure
| - Chronic inflammation (e.g. wound scars and immunosuppression)
27
What is the clinical presentation of squamous cell carcinoma?
- Most common on sun-exposed sites in later life
- Lesions are often keratonic, ill-defined nodules that may ulcerate
- Can grow very rapidly
- Ulcerates lesions on the lower lip or ear are often more aggressive
- Examination of regional lymph nodes to look for metastases
28
How is squamous cell carcinoma managed?
- Surgical excision with a minimal margin of 5mm
| - Radiotherapy (esp. if non-resectable)
29
What is basal cell carcinoma?
Tumour of basal keratinocytes
30
What is the clinical presentation of basal cell carcinoma?
- Border of ulcerated lesions is raised with a pearly appearance
- Slowly enlarging. Shiny nodule on the head and neck area which bleeds following minor trauma and doesn’t heal
- Slowly causes local tissue destruction if not treated
31
How is basal cell carcinoma managed?
- Surgically excised with wide borders and histology
- Superficial BCCs can be managed with non-surgical treatment (cryotherapy and photodynamic therapy)
- Radiotherapy is used in those unable to tolerate surgery
32
What are the types of malignant melanoma?
- Superficial spreading (SSMM)
- Nodular – most aggressive type
- Lentigo maligna – usually on the face
- Acral – restricted to palms/ soles
33
What are the risk factors of malignant melanoma?
- UV exposure e.g. suntanning and sunbed use
- Red hair
- High density freckles
- Skin type 1
- Atypical moles
- Multiple melanocytic naevi
- Sun sensitivity
- Immunosuppression
- Family history
- Pale skin
34
What is the clinical presentation of malignant melanoma?
| location in men, location in women, colour, minor signs, major signs
- Men: back/chest
- Women: lower legs
- Very dark colour (black or almost black in part of the lesion)
- Minor signs: inflammation, crusting or bleeding, sensory change, itching
- Major signs: change in size, shape or colour (usually darkening)
35
What are the differential diagnoses of malignant melanoma?
- Benign pigmented naevus
- Seborrhoeic wart (most common pigmented lesion in the elderly)
- Pyogenic granuloma (presents as a small warty lesion that bleeds easily, non-pigmented and occurs where there is minor trauma e.g. shaving)
36
How is malignant melanoma diagnosed?
| 5 criteria
ABCDE symptoms and criteria for diagnosis:
- Asymmetrical shape
- Border irregularity
- Colour irregularity
- Diameter > 6mm
- Elevation/ evolution
37
How is malignant melanoma managed?
- Surgical excision is curative in early cases
- Very wide excision doesn’t improve survival
- Limited sensitivity to radiotherapy
- For metastatic disease: removal of regional lymph nodes, isolated limb perfusion, radiotherapy, immunotherapy and chemotherapy
38
What is the prognosis of malignant melanoma?
- Thin lesions have best prognosis
- If over 60y, then <5y survival
- Female advantage in prognosis
- Ulceration is usually a late-stage sign
- Poor prognosis if present on trunk vs limbs
Phase 2a high tier list content
flashcards
Decks in class (10)
# Cards
