Dermatology Flashcards

1
Q

What is acanthosis nigricans?

Causes of acanthosis nigricans

A

Symmetrical, brown, velvety plaques on the neck, axilla and groin

Seen in: GI cancer, DM, obesity, PCOS, Cushings disease, acromegaly, hypothyroidism, familial, prader willi
Drugs: OCP, nicotinic acid

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2
Q

Features of acne rosacea

A
nose, cheeks and forehead
Flushing
Telangiectasia
Later develops into persistent erythema with papules and pustules
Rhinophyma
Blepharitis
Sunlight may exacerbate symptoms
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3
Q

Management of acne rosacea

A

Topical metronidazole for mild symptoms
Abx (oxytetracycline) for more severe disease
Laser therapy for telangiectasia

High factor sunscreen
Concealer

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4
Q

Pathophysiology of acne vulgaris

A

Follicular epidermal hyperproliferation -> keratin plug formation -> obstruction of pilosebaceous follicles -> colonisation by anaerobic bacteria (Proprionibacterium acnes) -> inflammation

Activity of sebaceous glands are controlled by androgen

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5
Q

Features of acne vulgaris

A

Comedones due to dilated sebaceous follicle (closed = whitehead, open = blackhead)

Papules and pustules (follicle bursts -> releases irritants -> inflammation)

Excessive inflammation -> nodules and cysts

Eventually leads to scarring -> ice-pick scars and hypertrophic scars

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6
Q

Classification of acne vulgaris

A

Mild - open and closed comedones +/- sparse inflammatory lesions

Moderate - widespread non-inflammatory lesions and numerous papules and pustules

Severe - extensive inflammatory lesions, nodules, pitting, scarring

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7
Q

Management of acne vulgaris

A
  1. Single topical therapy (topical retinoids, benzoyl peroxide)
  2. Topical combination therapy (topical abx, benzoyl peroxide, topical retinoid)
  3. Oral abx: tetracyclines (limecycline, doxycycline, oxytetracycline), erythromycin
    Oral abx should be coprescribed with a topical retinoid or benzoyl peroxide.
    COCP is an alternative in women
  4. Oral isotretinoin under specialist supervision (C/I in pregnancy)
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8
Q

Features of actinic keratosis

A

Premalignant skin lesion as a result of chronic skin exposure

Small, crusty, scaly lesions
Pink/red/brown or same colour as skin
Typically on sun-exposed areas
Multiple lesions may be present

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9
Q

Management of actinic keratosis

A

Prevention of further risk: sun avoidance, sun cream

Fluorouracil cream
Topical diclofenac
Topical imiquimod
Cryotherapy
Curettage and cautery
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10
Q

Features and treatment of alopecia areata

A

Features - autoimmune condition, localised well de-marcated patches of hair loss with small broken exclamation mark hairs at the edge of the hair loss

Management - explanation is often sufficient as majority will regrow, other treatment includes topical/intralesional corticosteroids, topical minoxidil, phototherapy, dithranol, contact immunotherapy, wigs

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11
Q

Basal cell carcinoma features

A

Sun-exposed sites
Pearly, flesh-coloured papule with telangiectasia
May later ulcerate leaving a central crater
Slow growing and local invasion
Metastasis is rare

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12
Q

Management for basal cell carcinoma

A
Surgical removal
Curettage
Cryotherapy
Topical cream: imiquimod, fluorouracil
Radiotherapy
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13
Q

Bowen’s disease features and management

A

Squamous cell carcinoma in situ

More common in elderly females
Red, scaly patches
Often occurs on sun-exposed areas (eg. lower limb)

Management - topical 5-fluorouracil or imiquimod, cryotherapy, excision

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14
Q

Features of bullous pemphigoid

A

Autoimmune condition causing sub-epidermal blistering of the skin, secondary to antibodies against hemidesmosomal proteins

More common in elderly patients
Itchy, tense blisters typically around flexures
Blisters usually heal without scarring
Mouth is usually spared

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15
Q

Management of bullous pemphigoid

A

Referral to dermatologist for biopsy and confirmation of diagnosis
Oral corticosteroids are mainstay of treatment
Topical corticosteroids, immunosuppressants and abx are also used

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16
Q

Investigations for bullous pemphigoid

A

Skin biopsy -> immunofluorescence shows IgG and C3 at the dermoepidermal junction

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17
Q

Immediate management of burns (inc. heat burns, electrical burns and chemical burns)

A

A-E, analgesia

Heat burns: remove person from source, irrigate the burn with cool water for 10-30min, cover burn with clingfilm

Electrical burns: switch off power supply, remove person from source

Chemical burns: brush any powder off then irrigate with water

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18
Q

Assessing the extent of burns

A

Wallace’s rule of nines: Head+neck 9%, each arm 9%, each anterior leg 9%, each posterior leg 9%, anterior chest 9%, posterior chest 9%, anterior abdomen 9%, posterior abdomen 9%

The palmar surface is roughly equivalent to 1% of total body surface area

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19
Q

Different depths of burns and their features

A

Superficial epidermal = red and painful

Partial thickness (superficial dermal) = pale pink, painful, blistered

Partial thickness (deep dermal) = typically white, may have patches of non-blanching erythema, reduced sensation

Full thickness = white/brown/black in colour, no blisters, no pain

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20
Q

Burns referral to secondary care

A
  • Deep dermal and full thickness burns
  • Superficial dermal burns of more than 3% total body surface area (adults) or 2% (children)
  • Superficial dermal burns involving face, hands, feet, perineum, genitalia, or any flexure, circumferential burns of the limbs, torso or neck
  • Any inhalation injury
  • Any electrical or chemical burn injury
  • Suspicion of NAI
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21
Q

Calculating amount of fluids required following burns

A

Parkland formula:
Vol of fluid = total body surface area of the burn (%) x weight (kg) x 4

Half of the fluid should be administered in the first 8 hours

Urinary catheter inserted

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22
Q

What is an escharotomy and what are the indications

A

careful division of the encasing band of burn tissue to potentially improve ventilation, or relieve compartment syndrome and oedema

Indications: circumferential full thickness burns to the torso or limbs

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23
Q

Contact dermatitis two different types

A

Irritant contact dermatitis: common, non-allergic due to weak acids/alkalis, often on hands. Erythema is typical, crusting and vesicles are rare

Allergic contact dermatitis: type IV hypersensitivity. Uncommon, seen on the head following hair dye. Topical treatment with potent steroid is indicated

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24
Q

Features of dermatitis herpetiformis

A

Autoimmune blistering skin disorder, associated with coeliac disease
Caused by deposition of IgA in the dermis

Itchy, vesicular skin lesions of the extensor surfaces

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25
Q

Diagnosis and management of dermatitis herpetiformis

A

Diagnosis: skin biopsy -> direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis

Management: gluten-free diet, dapsone

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26
Q

Eczema herpeticum

  • Cause
  • Risk factor
  • Presentation
  • Examination finding
  • Management
A

Severe primary infection of the skin caused by herpes simplex virus 1 or 2

Commonly seen in children with atopic eczema

Often presents as a rapidly progressing painful rash

O/E: monomorphic punched out erosions (circular, depressed, ulcerated lesions), usually 1-3mm in diameter

Potentially life-threatening, so children should be admitted for IV aciclovir

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27
Q

Management of eczema

A

Emollients and soap substitutes
Topical steroids
UV radiation
Immunosuppressants (ciclosporin, antihistamines, azathioprines)

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28
Q

Topical steroids ranked by potency

A

Mild: hydrocortisone
Moderate: betnovate RD, eumovate
Potent: betnovate, cutivate
Very potent: dermovate

1 finger tip (0.5g) should treat a skin area about twice that of the flat of an adult hand

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29
Q

Features of erythema multiforme

A

Hypersensitivity reaction commonly triggered by infections
Divided into minor and major forms

Target lesions
Initially seen on the back of hands/feet before spreading to torso
Upper limbs more commonly affected than lower limbs
Pruritus occasionally seen and usually mild

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30
Q

Causes of erythema multiforme

A
Viruses (herpes simplex virus)
Idiopathic
Bacteria (mycoplasma, streptococcus)
Drugs (penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, OCP)
Connective tissue disease (SLE)
Sarcoidosis
Malignancy
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31
Q

Causes of erythema nodosum

A

Infection (streptococci, TB), systemic disease (sarcoidosis, IBD, Behcets), malignancy/lymphoma, drugs (penicillins, sulphonamides, COCP), pregnancy

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32
Q

Erythema nodosum features

A
inflammation of subcut fat
Typically causes tender, erythematous, nodular lesions
Usually occurs over shins
Usually resolves within 6 weeks
Lesions heal without scarring
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33
Q

What is erythroderma?

Causes of erythroderma

A

A term used when more than 95% of the skin is involved in a rash of any kind

Eczema, psoriasis, drugs (gold), lymphomas, leukaemias, idiopathic

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34
Q

Causes and risk factors of fungal nail (onychomycosis)

A

Causes: dermatophytes (Trichophyton), yeasts (candida), non-dermatophyte moulds

Risk factors: DM, increasing age

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35
Q

Features of onychomycosis (fungal nail)

A

Unsightly nails

Thickened, rough, opaque nails

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36
Q

Investigations of fungal nail (onychomycosis)

A

Nail clippings

Scrapings of the affected nail

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37
Q

Management of fungal nail (onychomycosis)

A

No treatment required if asymptomatic

Dermatophyte infection: oral terbinafine first line, oral itraconazole second line. 6wks-3m for fingernails, 3-6m for toenails

Candida infection: topical antifungal (amorolfine) for mild disease, oral itraconazole for 12 weeks for more severe infection

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38
Q

Guttate psoriasis features

A

2-4 weeks after streptococal infection

Tear drop papules on trink and limbs

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39
Q

Management of guttate psoriasis

A
Most cases resolve spontaneously in 2-3 months
Regular emollients
Potent topical corticosteroid
Topical vitamin D analogue
UVB phototherapy
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40
Q

Hereditary haemorrhagic telangiectasia

  • inheritance pattern
  • diagnostic criteria
A

Autosomal dominant

If the patient has 2 then they are said to have a possible diagnosis of HHT, if they have 3+ then they are said to have definite diagnosis of HHT

  1. Spontaneous recurrent epistaxis
  2. Telangiectases at the lips/oral cavity/fingers/nose
  3. Visceral lesions (eg. GI telangiectasia, pulmonary arteriovenous malformations, hepatic AVM, cerebral AVM, spinal AVM)
  4. Family history (first degree relative with HHT)
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41
Q

What is herpes zoster?

Features and cause
Management of herpes zoster

A

Shingles.
Acute, unilateral, painful blistering rash caused by reactivation of varicella zoster virus

Management: oral aciclovir

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42
Q

Shingles vaccine

  • who is it offered to?
  • what type of vaccine is it?
  • vaccine contraindication
A

Offered to all patients aged 70-79 yrs
Live-attenuated and given subcutaneously

C/I in immunosuppression as it is live-attenuated

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43
Q

Causes of hirsutism

A

Cushing’s syndrome, congenital adrenal hyperplasia, androgen therapy, obesity (insulin resistance), adrenal tumour, androgen secreting ovarian tumour, drugs (phenytoin, corticosteroids)

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44
Q

Management of hirsutism

A

Weight loss if overweight
Waxing/bleaching
COCP

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45
Q

Management of hyperhidrosis

A

Topical aluminium chloride is first line (S/E = skin irritation)

Iontophoresis

Botulinum toxin (for axillary symptoms)

Surgery

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46
Q

Causes and spread of impetigo

A

Superficial bacterial skin infection - Staphylococcus aureus or Streptococcus pyogenes

It can be a primary infection or a complication of an existing skin condition (eg. eczema, scabies, insect bite)

Common in children, particularly during warm weather
Spread by direct contact with discharges from the scabs

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47
Q

Features of impetigo

A

Golden crusted skin lesions typically found around the mouth

Very contagious

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48
Q

Management of impetigo

A

Limited, localised disease:

  • Topical fusidic acid is first line
  • Topical mupirocin if MRSA

Extensive disease:
-Oral flucloxacillin first line
Oral erythromycin is pen-allergic

Children should be excluded from school until the lesions are crusted and healed, or 48hrs after starting abx

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49
Q

Adverse effects of isotretinoin

A

Teratogenicity (use two forms of contraception)
Dry skin, eyes, lips/mouth (most common side effect)
Low mood
Raised triglycerides
Hair thinning
Nose bleeds
Photosensitivity
Intracranial hypertension (avoid prescribing with tetracyclines)

50
Q

Features and management of a keratocanthoma

A

Looks like a volcano/crate
Initially a smooth dome-shaped papule
Rapidly grows to become a crater centrally-filled with keratin

Spontaneous regression within 3 months usually, however should be excised urgently as it is clinically difficult to exclude form a SCC

51
Q

What is the Koebner phenomenon? What conditions is it seen in?

A

Skin lesions which appear at the site of injury

Seen in: psoriasis, vitiligo, warts, lichen planus, lichen sclerosus, molluscum contagiosum

52
Q

Leukoplakia

  • features
  • diagnosis
  • management
A

Premalignant condition, presents as white, hard spots on mucous membranes in the mouth
Common in smokers
Diagnosis of exclusion, rule out candidiasis and lichen planus
Biopsies often performed to exclude SCC
Regular follow up to exclude malignant transformation into SCC

53
Q

Lichen planus features

A

Itchy, papular rash most common on palms, soles, genitalia and flexor surfaces of arms
Rash is polygonal in shape, with a ‘white-lines’ pattern on the surface (Wickham’s striae)
Koebner phenomenon (new lesions at the site of trauma)
Oral involvement (white lace pattern on buccal mucosa)
Thinning of nail plate, longitiduinal ridging

54
Q

Management of lichen planus

A

Topical steroids
Benzydamine mouthwash/spray for oral lichen planus
Oral steroids/ immunosuppression for extensive lichen planus

55
Q

Lichen sclerosus features

A

Inflammatory condition usually affecting the vagina
More common in elderly females
Leads to atrophy of the epidermis with white plaques forming
Very itchy

56
Q

Lichen sclerosus diagnosis and management

A

Diagnosis is usually clinical, but biopsy may be done it atypical features are present

Management - topical steroids and emollients
Follow up due to increased risk of vulval cancer

57
Q

Features, diagnosis and management of lipoma

A

Smooth, mobile, painless lump
Generally found in the subcutaneous tissues

Clinical diagnosis

Mx: observation. Remove if diagnosis uncertain or if compressing surrounding structures

58
Q

4 main types of malignant melanoma (frequency, typically affected body part, appearance)

A

Superficial spreading: Commonest. Affects arms, legs, back and chest in young people. Growing moles with change in size/ shape/ colour/ discharge

Nodular: second commonest. Sun-exposed skin in middle-aged people. Red or black lump which bleeds/ oozes

Lentigo maligna: less common. Chronically sun-exposed skin in older people. Growing mole with change in size/shape/ colour/ discharge

Acral lentiginous: rare. Nails, palms, or soles in african-americans or asians. Subungal pigmentation (Hutchinsons sign) or on palms/ feet

59
Q

Margins of excision

A
Breslow thickness
0-1mm thick = 1cm margin
1-2mm thick = 1-2 cm
2-4mm thick = 2-3 cm
>4 = 3 cm
60
Q

Management of malignant melanoma

A

Suspicious lesion -> excision biopsy (remove lesion completely with a 2mm margin)
Once diagnosis is confirmed, Breslow thickness should be assessed to determine whether further re-excision of margins is required

61
Q

Malignant melanoma risk factors

A

Increased UV exposure, sunburn, fair complexion, lots of moles, positive family history, previous melanoma, elderly

62
Q

Signs of malignant melanoma

A
ABCDEF
Asymmetry
Border irregularity or blurring
Colour variation
Diameter >6mm
Evolution of mole
Funny looking mole
63
Q

Prognosis of malignant melanoma

A
Depends on Breslow thickness
<1mm = 95-100% 5-yr survival
1-2mm = 80-96%
2.1-4mm = 60-75%
>4 mm = 50%
64
Q

Cause of molluscum contagiosum

A

Skin infection caused by molluscum contagiosum virus
Transmission occurs directly by close personal contact, or indirectly via contaminated surfaces

Majority of cases occur in children (esp children with atopic eczema), often 1-4 yrs

May occur around the genitals in adults as a result of sexual contact

65
Q

Features of molluscum contagiosum

A

Characteristic pink/pearly white papules with a central umbilication which are up to 5mm in diameter
Lesions appear in clusters anywhere on the body, with sparing of the palm and sole

66
Q

Management of molluscum contagiosum

A

No treatment usually, as it is self limiting
Spontaneous resolution within 18 months
Contagious so avoid sharing towels/clothing/baths
Encourage not to scratch lesion
If lesions are troublesome then use cryotherapy or squeeze the lesion following a bath
No need to exclude form school/swimming

Prescribe an emollient and a mild topical corticosteroid if itchy
Prescribe a topical abx (fusidic acid) if skin looks infected

67
Q

Causes of nail pitting

A

Psoriasis

Alopecia areata

68
Q

Causes of leuconychia

A

Hypoalbuminaemia
Fungal disease
Lymphoma

69
Q

Features of pellagra

Causes of pellagra

A

Dermatitis, diarrhoea, dementia (3 Ds)
Also depression, and death if not treated

Caused by nicotinic acid deficiency, may occur as a consequence of isoniazid therapy. More common in alcoholics

70
Q

Cause of pemphigus vulgaris

A

Autoimmune disease caused by antibodies ageinst desmoglein 3

More common in Ashkenazi jewish population

71
Q

Features of pemphigus vulgaris

A

Mucosal ulceration, oral involvement
Skin blistering - flaccid, easily ruptured vesicles and bullae
Lesions are painful but not itchy

72
Q

Diagnosis and management of pemphigus vulgaris

A

Acantholysis on biopsy

Management - steroids first line, immunosuppressants

73
Q

What is pityriasis rosea? Who does it tend to affect? What causes it?

A

Acute, self-limiting rash
Tends to affect young adults
Thought to be due to Herpes hominis virus 7 (HHV 7)

74
Q

Features of pityriasis rosea

A

Majority of patients have no prodrome, but some patients give a history of a recent viral infection

Pruritus

Herald patch usually on trunk
Herald patch is followed by erythematous, oval, scaly patches

Oval patches follow a characteristic distribution with the longitudinal diameters of the oval patches running parallel to the line of Langer (fir-tree appearance)

75
Q

Management of pityriasis rosea

A

Self-limiting, usually disappears after 6-12 weeks so no treatment needed

76
Q

Pityriasis versicolor

  • what is it
  • cause
  • predisposing factors
A

Superficial cutaneous fungal infection caused by Malassezia furfur

Predisposing factors: occurs in healthy individuals, immunosuppression, malnutrition, Cushing’s

77
Q

Pityriasis versicolor features

A
Most commonly on the trunk
Hypopigmented, pink or brown patches
May be more noticeable following a suntan
Scale is common
Mild pruritus
78
Q

Management of pityriasis versicolor

A

Topical antifungal (ketoconazole shampoo)

If failure to respond, consider alternative diagnoses (send scrapings) + oral itraconazole

79
Q

Causes of pruritus

A
Liver disease
Iron deficiency anaemia
Polycythaemia
Chronic kidney disease
Lymphoma
Other causes:
Hyper/hypothyroidism
DM
Pregnancy
Urticaria
Skin disorders: eczema, scabies, psoriasis, pityriasis rosea
80
Q

Subtypes of psoriasis

A

Plaque psoriasis: most common. typical well demarcated red scaly patches on the extensor surfaces

Flexural psoriasis: smooth skin

Guttate psoriasis: transient psoriatic rash triggered by Strep infection. Red teardrop lesions

Pustular psoriasis: usually on palms and soles

81
Q

Features and complications of psoriasis

A

Raised red plaques with silver scaling, typically on extensor surfaces
Nail signs: pitting, onycholysis
Arthritis

Complications: 
Psoriatic arthropathy
Metabolic syndrome
Cardiovascular disease
VTE
Psychological distress
82
Q

Exacerbating factors of psoriasis

A

Trauma
Alcohol
Drugs (beta blockers, lithium, antimalarials, NSAIDs, ACEI, infliximab)
Withdrawal of systemic steroids

Streptococcal infection may trigger guttate psoriasis

83
Q

Management of psoriasis

A

Regular emollients to reduce scale loss and pruritus

First line: potent topical corticosteroid and topical vit D analogue OD for up to 4 weeks as initial treatment

Second line: if no improvement after 8 weeks then offer vit D analogue BD

Third line: if no improvement after 8 weeks then offer either: potent topical corticosteroid BD for up to 4 weeks, or a coal tar preparation OD/BD

Short acting dithranol may be used

Secondary care:

  • Phototherapy
  • Systemic therapy (oral methotrexate first line)
84
Q

Advice for using topical corticosteroids in psoriasis

A

Aim for a 4 week break between courses of topical corticosteroids
Use potent topical corticosteroids for no longer than 8wks at a time

85
Q

Vitamin D analogues

  • examples
  • MoA
  • Side effects
A

Examples: calcipotriol, calcitriol, etc
MoA: reduce cell division and differentiation. they tend to reduce the scales and plaque thickness but not the erythema
SE: uncommon. Avoid in pregnancy

Unlike corticosteorids they may be used long term
Unlike coal tar prep and dithranol they do not smell or stain

86
Q

Systemic therapy used in secondary care for the management of psoriasis

A

Methotrexate - first line
Ciclosporin
Systemic retinoids
Biological agents: infliximab, etanercept

87
Q

Phototherapy for psoriasis

  • type of phototherapy
  • how often
  • side effects
A

Narrow band UV B light is now the treatment of choice
Can be given 3 times a week
Adverse effects include skin ageing and squamous cell carcinoma

88
Q

Childhood causes of purpura

A
Meningococcal septicaemia
Acute lymphoblastic leukaemia
Congenital bleeding disorders
Immune thrombocytopenic purpura
Henoch-Schönlein purpura
NAI
89
Q

Adulthood causes of purpura

A

Immune thrombocytopenic purpura
Bone marrow failure
Senile purpura
Drugs (quinine, antiepileptics, antithrombotics)
Nutritional deficiency (vit B12, C, folate)

90
Q

Pyoderma gangrenosum features

A

Typically on lower limbs
Initially small red papules
Later deep, red, necrotic ulcers with a violaceous border
May be accompanied with systemic symptoms (fever, myalgia)

91
Q

Causes of pyoderma gangrenosum

A
Idiopathic (50%)
IBC
RA, SLE
Myeloproliferative disorders
Lymphoma, myeloid leukaemias
Monoclonal gammopathy
Primary biliary cirrhosis
92
Q

Management of pyoderma gangrenosum

A

Oral steroids are first line

Ciclosporin and infliximab have a role in difficult cases

93
Q

Features of pyogenic granuloma

A

Most common sites: head/neck, upper trunk and hands (oral mucosa is common in pregnancy)
Initially small red/brown spot
Rapidly progresses within days/weeks forming raised red/brown lesions which are often spherical in shape
Lesions may bleed profusely and ulcerate

94
Q

Management of pyogenic granuloma

A

If pregnancy-related they often resolve spontaneously post-partum
Other lesions usually persist

Removal methods: curettage and cautery, cryotherapy, excision

95
Q

Scabies pathophysiology

A

Caused by the Sarcoptes scabiei mite and is spread by prolonged skin contact
Scabies mite burrows into the skin, laying its eggs in the stratum corneum
Intense pruritus due to a delayed type 4 hypersensitivity reaction to the mites/eggs about 30 days after initial infection

96
Q

Features of scabies

A

widespread pruritus
Linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist

Secondary features due to itching: excoriation, infection

97
Q

Management of scabies

A

Permethrin 5% is first line
Malathion 0.5% second line
Pruritus persists for up to 4-6 weeks post eradication

Avoid close contact with others
All household and close contacts should be treated
Launder, iron and tumble dry clothing, bedding and towels on the first day of treatment

98
Q

Seborrhoeic dermatitis in adults

  • cause
  • features
  • associated conditions
A
  • cause: chronic dermatitis thought to be caused by an inflammatory reaction related to proliferation of a normal skin inhabitant, Malassezia furfur
  • features: eczematous lesions on sebum-rich areas (scalp-> dandruff, periorbital, auricular, nasolabial folds), otitis externa, blepharitis

0Associated with HIV and parkinsons disease

99
Q

Management of adult seborrheic dermatitis

A

Scalp disease:
First line: OTC preparations containing zinc pyrithione (head and shoulders) and tar (neutrogena T gel)
Second line: ketoconazole shampoo

Selenium sulphide and topical corticosteroid may be useful

Face and body management:
Topical antifungals (ketoconazole)
Topical steroids

Difficult to treat, recurrence is common

100
Q

Seborrhoeic keratoses

  • what is it
  • features
  • management
A

benign epidermal skin lesions seen in older people

Features: stuck-on appearance, large variation in colour from flesh colour to light brown or black, keratotic plugs on the surface

Management: reassurance (benign), may remove (curettage, cryotherapy, shave biopsy)

101
Q

Polymorphic eruption of pregnancy

  • what is it
  • features
  • management
A

Pruritic condition associated with last trimester
lesions often first appear in abdominal striae
Management: emollients, mild potency topical steroids, and oral steroids depending on severity

102
Q

Pemphigoid gestationis

  • features
  • when does it develop
  • management
A

Pruritic blistering lesions, often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms
Usually presents in 2nd or 3rd trimester and rarely seen in first pregnancy
Management: oral corticosteroids

103
Q

5 types of basal cell carcinoma

A

Nodular BCC - commonest. Raised translucent papule, usually on face

Superficial BCC - superficial erythematous macule on the trunk, may show spontaneous regression

Morpheaform BCC - flat, slightly atrophic lesion or plaque without well-defined borders, high recurrence rate

Cystic BCC - clear or blue-grey appearance, may resemble nodular BCC

Basosquamous carcinoma - atypical, features resemble BCC and SCC, biologically more aggressive and more destructive, metastatic disease may occur

104
Q

Skin types

A

Fitzpatrick classification
1 - never tans, always burns (red hair, freckles, blue eyes)
2 - burns easily, tans poorly
3 - may burn, tans poorly
4 - burns minimally, tans easily (olive)
5 - rarely burns, always tans (asian)
6 - never burns, tans darkly (black african)

105
Q

Spider naevi

  • what are they
  • where are they found
  • vs. telangiectasia
  • associated conditions
A

Central red papule with surrounding capillaries which blanch upon pressure

Almost always found on upper part of body

Can be differentiated from telangiectasia by pressing on them and watching them fill - spider naevi fill from the centre, telangiectasia fill from the edge

Associations - liver disease, pregnancy, COCP

106
Q

Squamous cell carcinoma risk factors

A
Excessive exposure to sunlight
Actinic keratosis/ bowens disease
Immunosuppression
Smoking
Long standing leg ulcers
Genetic conditions
107
Q

treatment of squamous cell carcinomas

A

Wide local excision for diagnostic biopsy, then repeat surgery to gain adequate margins
Surgical excision with 4mm margin if lesion <20mm in diameter, and 6mm margin if lesion >20mm diameter

Moh’s micrographic surgery used in high-risk patients and in cosmetically important sites

108
Q

Poor prognostic factors of squamous cell carcinoma

A

Poorly differentiated
>20mm in diameter
>4mm deep
Immunosuppression

109
Q

Invasive SCC features

A

Erythematous keratotic papule or nodule on a background of sun exposure
Ulceration may occur
Regional lymphadenopathy may be present

May metastasise

110
Q

Tinea capitis

  • features
  • cause
  • diagnosis
  • management
A
Scalp ringworm (dermatophyte fungal infection)
Scarring alopecia, mainly seen in children
If untreated, a raised, pustular, spongy/boggy mass (kerion) may form

Most common cause: Trichophyton tonsurans)

Diagnosis: scalp scrapings

Management: oral antifungal (terbinafine), topical ketoconazole shampoo for the first two weeks to reduce transmission

111
Q

Tinea corporis

  • causes
  • features
  • management
A

Ringworm (dermatophyte fungal infection)
Causes: Trichophyton rubrum and Trichophyton verrucosum (contact with cattle)

Well-defined annular, erythematous lesions with pustules and papules

Management: oral fluconazole

112
Q

Tinea pedis features

A
Athletes foot (dermatophyte fungal infection)
Itchy, peeling skin between toes
Common in adolescence
113
Q

Toxic epidermal necrolysis (TEN)

  • causes
  • features
A

Potentially life-threatening skin disorder, commonly seen secondary to a drug reaction
Examples: phenytoin, sulphonamides, allopurinol, penicillins, carbamazepine, NSAIDs

Scalded appearance over an extensive area
Systemically unwell (pyrexia, tachycardia)
Positive Nikolsky sign (epidermis separates with mild lateral pressure)

114
Q

Toxic epidermal necrolysis management

A

Stop precipitating factor
ITU supportive care
IV Ig first line
Other options: ciclosporin, cyclophosphamide, plasmapharesis

115
Q

Venous ulceration

  • features
  • risk factors
  • investigations
  • management
A

features: medial malleolus, shallow ulcer with granulated base
risk factors: varicose veins, DVT, venous insufficiency, poor calf muscle function, AV fistulae, obesity, leg fracture, trauma over medial malleolus
Ix: Duplex USS, ABPI normal (0.9-1.2)
Mx: compression bandaging (four layers)
Oral pentoxifylline (peripheral vasodilator)

116
Q

Features of vitiligo and associated conditions

A

Autoimmune
Well-demarcated patches of depigmented skin
Peripheries tend to be most affected
Trauma may precipitate new lesion (koebner phenomenon)

T1DM, Addisons, autoimmune thyroid disease, pernicious anaemia, alopecia areata

117
Q

Management of vitiligo

A

Sunblock
Camouflage makeup
Topical corticosteroids may reverse changes if applied early
Topical tacrolimus and phototherapy may be helpful

118
Q

Arterial ulceration

  • features
  • ix
  • mx
A

Features: small deep lesions, well-defined borders, evidence of arterial insufficiency, found at distal sites
Ix: ABPI either reduced (<0.9) or raised (due to calcification, >1.2), duplex USS, CT angiography
Mx: lifestyle advise, statin, aspirin, optimise BP and DM, angioplasty or bypass grafting, amputation

119
Q

Neuropathic ulceration

  • features
  • ix
  • mx
A

Features: painless, over areas of abnormal pressure, often secondary to joint deformity in DM
Ix: blood glucose levels, ABPI normal, duplex USS, swab if ?Infection, X-ray if ?osteomyelitis, neuro foot exam
Mx: optimise DM control, improve diet, increase evercise, regular chiropody, abx for any infection, surgical debridement, amputation

120
Q

What is Charcot’s foot?

A

Neuroarthropathy whereby a loss of joint sensation results in continual unnoticed trauma and deformity
Neuropathic ulcers can be seen alongside Charcot’s foot

Patients present with swelling, distortion, pain, and loss of function