Dermatology Flashcards
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
