Dermatology Flashcards
(54 cards)
What are the 3 main layers of the skin?
-epidermis
-dermis
-subcutaneous tissue
What is the function of the skin?
Epidermis acts a protective barrier, protects from bacteria etc
What is the stratum corneum?
Outer keratin layer of the epidermis
Where is stratum corneum thicker?
Palms of hand
Soles of feet
Why does psoriasis present with plaques?
Increased cell turnover
Hyper proliferation of epidermis
How can acne vulgaris be classified?
mild: open and closed comedones with or without sparse inflammatory lesions
moderate acne: widespread non-inflammatory lesions and numerous papules and pustules
severe acne: extensive inflammatory lesions, which may include nodules, pitting, and scarring
What’s the treatment for mild-moderate acne vulgaris?
-12wk topical combination therapy:
-a fixed combination of topical adapalene with topical benzoyl peroxide
-a fixed combination of topical tretinoin with topical clindamycin
-a fixed combination of topical benzoyl peroxide with topical clindamycin
topical benzoyl peroxide may be used as monotherapy if these options are contraindicated
What’s the treatment for moderate to severe acne vulgaris?
12-week course of one of the following options:
-a fixed combination of topical adapalene with topical benzoyl peroxide
-a fixed combination of topical tretinoin with topical clindamycin
-a fixed combination of topical adapalene with topical benzoyl peroxide + either oral lymecycline or oral doxycycline
-a topical azelaic acid + either oral lymecycline or oral doxycycline
tetracyclines should be avoided in pregnant or breastfeeding women and in children younger than 12 years of age
What is the pathophysiology of acne vulgaris?
-follicular epidermal hyperproliferation, leading to formation of keratin plug, causes obstruction of pilosebaceous follicle.
Colonisation by anaerobic bacterium Propionibacterium acnes
Inflammation
Activity of sebaceous glands controlled by androgen, why acne often starts during puberty
What is actinic keratoses?
premalignant skin lesion that develops as a consequence of chronic sun exposure
What is the typical appearance of actinic keratoses?
small, crusty or scaly, lesions
may be pink, red, brown or the same colour as the skin
typically on sun-exposed areas e.g. temples of head
multiple lesions may be present
What are some management options for actinic keratoses?
Sun avoidance and sun cream
fluorouracil cream: typically a 2 to 3 week course
topical diclofenac
cryotherapy
curettage and cautery
What is Acanthosis nigricans?
Describes symmetrical, brown, velvety plaques that are often found on the neck, axilla and groin
What is the pathophysiology of acanthosis nigricans?
insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)
What are some causes of acanthosis nigricans?
obesity
type 2 diabetes mellitus
polycystic ovary syndrome
Cushing’s syndrome
acromegaly
hypothyroidism
familial
Prader-Willi syndrome
gastrointestinal cancer
drugs
combined oral contraceptive pill
nicotinic acid
Whats an example of a sedating anti-histamine?
chlorpheniramine
Give example of non sedating anti-histamine?
loratidine
cetirizine
What should be done if BCC if suspected?
Routine referral to dermatology, 2wk wait isnt required
What are some management options for BCC?
surgical removal
curettage
cryotherapy
topical cream: imiquimod, fluorouracil
radiotherapy
What are some features of BCC?
sun-exposed sites, especially the head and neck account for the majority of lesions
initially a pearly, flesh-coloured papule with telangiectasia
may later ulcerate leaving a central ‘crater’
What is thr character of BCC?
slow-growth and local invasion
Metastases are extremely rare
What type of hypersensitivity is allergic contact dermatitis?
Type VI
What is dermatitis herpetiformis?
an autoimmune blistering skin disorder associated with coeliac disease
deposition of IgA in the dermis
What are some features of dermatitis herpetiformis and how is it diagnosed?
itchy, vesicular skin lesions on the extensor surfaces (e.g. elbows, knees, buttocks)
skin biopsy: direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis