General Flashcards
What are the causes of acnathosis nagricans?
type 2 diabetes mellitus
gastrointestinal cancer
obesity
polycystic ovarian syndrome
acromegaly
Cushing’s disease
hypothyroidism
familial
Prader-Willi syndrome
What drugs cause acanthuses nagricans?
OCP
Nictonic
Mechanism of acanthuses nagricans?
insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)
What is the pathophysiology of acne vulgaris?
- Follicular epidermal hyperproliferation resulting in the formation of a keratin plug.
- Obstruction of the pilosebaceous follicle.
- Activity of sebaceous glands may be controlled by androgen, although levels are often normal in patients with acne
- colonisation by the anaerobic bacterium
- Propionibacterium acnes
Features of mild acne?
mild: open and closed comedones with or without sparse inflammatory lesions
Features of moderate acne?
widespread non-inflammatory lesions and numerous papules and pustules
Features of severe acne?
extensive inflammatory lesions, which may include nodules, pitting, and scarring
Management of acne vulgaris?
- single topical therapy (topical retinoids, benzoyl peroxide)
- Topical combination therapy (topical retinoids + benzoyl peroxide)
- Oral therapy:
- Tetracyclines
- If pregnant –> erythromycin - If women: Oral contraceptive pill
- Oral isotretinoin
If a gram negative folliculitis is found from acne treatment, how is this managed?
This is a complication of long term antibiotics
High dose trimethoprim
Features of actinic keratosis?
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
Management of actinic keratosis?
- Sun avoidance
- fluorouracil cream: typically a 2 to 3 week course.
- topical chemotherapy, inflames skin - Topical diclofenac
- Topical imiquidmod
Causes of scarring alopecia?
trauma, burns
radiotherapy
lichen planus
discoid lupus
tinea capitis*
Causes of non-scarring alopecia?
male-pattern baldness
drugs: cytotoxic drugs, carbimazole, heparin, oral contraceptive pill, colchicine
nutritional: iron and zinc deficiency
autoimmune: alopecia areata
telogen effluvium
- hair loss following stressful period e.g. surgery
trichotillomania
What is alopecia areata?
autoimmune condition causing localised, well demarcated patches of hair loss. At the edge of the hair loss, there may be small, broken ‘exclamation mark’ hairs
Management of alopecia areata?
topical or intralesional corticosteroids
topical minoxidil
phototherapy
dithranol
contact immunotherapy
wigs
What can be seen in alopecia areata?
edge of the hair loss, there may be small, broken ‘exclamation mark’ hairs
In alopecia areata how often does hair regrow?
In 50% of cases in 1 year, 80-90% in one year
Sedating anti-histamine?
Chlorpheniramine
Non-sedating anti-histamine?
Loratidine
Cetirizine
Features of BCC?
rodent ulcers and are characterised by slow-growth and local invasion. Metastases are extremely rare. BCC is the most common type of cancer in the Western world.
What is the most common type of cancer in the western world?
BCC
Morphology of BCC?
Sun exposed site
initially a pearly, flesh-coloured papule with telangiectasia
may later ulcerate leaving a central ‘crater’
In bulls pemphigoid, what do the antibodies target?
Hemidesmosomes BP180
BP230
Features of bullous pemphigoid?
itchy, tense blisters typically around flexures
the blisters usually heal without scarring
there is usually no mucosal involvement (i.e. the mouth is spared)*
Features of skin biopsy in bullous pemphigoid?
immunofluorescence shows IgG and C3 at the dermoepidermal junction
what type of hypersensitivity type of pemphigoid?
Type 2
What type of hypersensitivity is contact dermatitis?
Type 4
What are the two types of dermatitis?
Irritant contact dermatitis
Allergic contact dermatitis
What is dermatitis artefacta?
self-inflicted skin lesions
Patients often deny they are self inflicted
linear/geometric lesions that are well-demarcated from normal skin.
- depends on mechanism of injury
Skin lesions “suddenly appear overnight”
Patient may be not phased - “ la belle difference”
Diagnostic approach to dermatitis artefacta?
exclusion of other dermatological conditions
Biopsy
Psychiatry assessment
Mechanism behind dermatitis herpetiformis?
deposition of IgA in the dermis.
Common areas affected by dermatitis herpetiformis?
Knee
Elbows
Buttock
Papules and vesicles
Diagnosis of dermatitis herpetiformis?
Skin biopsy
Management of dermatitis herpetiformis?
Gluten free diet
Dapsone
Causes of eczema herpeticum?
Herpes simplex 1
Herpes simplex 2
CMV!!! - uncommon
Features of eczema herpeticum?
monomorphic punched-out erosions (circular, depressed, ulcerated lesions) usually 1–3 mm in diameter are typically seen.
Management of eczema herpeticum?
admitted for IV aciclovir.
Mild topical steroid?
Hydrocortisone 0.5-2.5%
Moderate topical steroid?
Betamethasone valerate 0.025% (Betnovate RD)
Clobetasone butyrate 0.05% (Eumovate)
Potent topical steroid?
Fluticasone propionate 0.05% (Cutivate)
Betamethasone valerate 0.1% (Betnovate)
Very potent topical steroid?
Clobetasol propionate 0.05% (Dermovate)
Mechanism of erythema ab igne?
caused by over exposure to infrared radiation. Characteristic features include reticulated, erythematous patches with hyperpigmentation and telangiectasia
What can erythema ab igne turn into ?
SCC
Features of erythema multiform?
target lesions
initially seen on the back of the hands / feet before spreading to the torso
upper limbs are more commonly affected than the lower limbs
pruritus is occasionally seen and is usually mild
Causes of erythema multiform?
viruses: herpes simplex virus (the most common cause), Orf*
idiopathic
bacteria: Mycoplasma, Streptococcus
drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
connective tissue disease e.g. Systemic lupus erythematosus
sarcoidosis
malignancy
What is erythema multiform major?
Erythema multiform, with mucosal involvement
What is the pathophysiology behind erythema nodosum?
Inflammation of subcutaneous fat
Nodular lesions
Causes of erythema nodosum?
infection
- streptococci
- tuberculosis
- brucellosis
systemic disease
sarcoidosis
inflammatory bowel disease
Behcet’s
malignancy/lymphoma
drugs
- penicillins
- sulphonamides
- combined oral contraceptive pill
Pregnancy
What is erythrasma and what is its cause?
flat, slightly scaly, pink or brown rash usually found in the groin or axillae
overgrowth of the diphtheroid Corynebacterium minutissimum
How should erythrasma be investigated?
Examination with Wood’s light reveals a coral-red fluorescence.
Management of erythrasma?
Topical miconazole or antibacterial are usually effective. Oral erythromycin may be used for more extensive infection
What is the definition of erythroderma?
95% body coverage rash
Causes of erythroderma?
eczema
psoriasis
drugs e.g. gold
lymphomas, leukaemias
idiopathic
Most common causes of fungal nail?
dermatophytes - mainly Trichophyton rubrum, accounts for 90% of cases
yeasts - such as Candida
non-dermatophyte moulds
Other causes of unsightly nails?
Differential diagnosis
psoriasis
repeated trauma
lichen planus
yellow nail syndrome
How to investigate nail fungus?
nail clippings
- high false negative rate
If nail fungal dermatophyte, management?
dermatophyte infection:
oral terbinafine is currently recommended first-line with oral itraconazole as an alternative
6 weeks - 3 months therapy is needed for fingernail infections whilst toenails should be treated for 3 - 6 months
treatment is successful in around 50-80% of people
If nail fungus is candida, management?
mild disease should be treated with topical antifungals (e.g. Amorolfine) whilst more severe infections should be treated with oral itraconazole for a period of 12 weeks
How long should topical agents for nail fungus be used for toes?
9-12 months
How long should topical agents for nail fungus be used for fingers?
6 months
Features of granuloma annulare?
papular lesions
slightly hyperpigmented and depressed centrally
dorsal surfaces of the hands and feet, and on the extensor aspects of the arms and legs
Associated with T2DM
When do you get guttate psoriasis?
Precipitated by a streptococcal infection 2-4 weeks prior to the lesions appearing.
Features of guttate psoriasis?
Tear drop papules on the trunk and limbs
- gutta is Latin for drop
- pink, scaly patches or plques of psoriasis
tends to be acute onset over days
How does the rash of guttate psoriasis differ from pityriasis rosea?
Guttate psoriasis: Sclary tear drop
raised oval lesions with a fine scale confined to the outer aspects of the lesions.
PR: Herald patch, followed by rest of rash 1-2 weeks
distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer.
Fir tree appearance
Management of guttate psoriasis?
most cases resolve spontaneously within 2-3 months
there is no firm evidence to support the use of antibiotics to eradicate streptococcal infection
topical agents as per psoriasis
UVB phototherapy
Features of hereditary haemorrhage telengectasia?
Autosomal dominant
epistaxis : spontaneous, recurrent nosebleeds
telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)
visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM
family history: a first-degree relative with HHT
Most common cause of hirsutism?
PCOS
Causes of hirsutism?
PCOS
Cushing’s syndrome
congenital adrenal hyperplasia
androgen therapy
obesity: thought to be due to insulin resistance
adrenal tumour
androgen secreting ovarian tumour
drugs: phenytoin, corticosteroids
Difference between hirsutism and hypertrichosis?
androgen-dependent hair growth in women,
hypertrichosis being used for androgen-independent hair growth
Causes of hypertrichosis ?
drugs: minoxidil, ciclosporin, diazoxide
congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis
porphyria cutanea tarda
anorexia nervosa
Best OCP for hirsutism?
co-cyprindiol (Dianette)
ethinylestradiol and drospirenone (Yasmin)
Management of facial hirsutism?
Topical eflornithine
CANNOT BREAST FEED / BE PREGNANT*
Management of hyperhidrosis?
- Topical aluminium chloride
- iontophoresis: particularly useful for patients with palmar, plantar and axillary hyperhidrosis
- botulinum toxin: currently licensed for axillary symptoms
Causes of impetigo?
Staph aureus
Strep pyogenes
Features:
‘golden’, crusted skin lesions typically found around the mouth
very contagious
Management of impetigo?
- hydrogen peroxide 1% cream for ‘people who are not systemically unwell or at a high risk of complications’
Other:
topical antibiotic creams:
topical fusidic acid
topical mupirocin should be used if fusidic acid resistance is suspected
MRSA is not susceptible to either fusidic acid or retapamulin. Topical mupirocin should, therefore, be used in this situation
Risk factors for keloid scars?
ethnicity: more common in people with dark skin
common sites (in order of decreasing frequency): sternum, shoulder, neck, face, extensor surface of limbs, trunk
What is a keratocanthoma?
benign epithelial tumour
What are the features of a keratocanthoma?
Features - said to look like a volcano or crater
initially a smooth dome-shaped papule
rapidly grows to become a crater centrally-filled with keratin
Management of keratocantoma?
Urgent excision for ? SCC
What is the koebner phenomena?
skin lesions that appear at the site of injury