Dermatology

Question 1

What parasite causes scabies?

Answer 1

Sarcoptes scabiei

Question 2

What causes scabies?

Answer 2

Sarcoptes scabiei burrow into the stratum corneum and deposit eggs & faeces

Question 3

What would you see in a history of scabies?

Answer 3

Generalised intense pruritis that is worse overnight

Question 4

What causes pruritis in scabies?

Answer 4

Hypersensitivity reaction to mite saliva, eggs and faeces that occurs 4-6 weeks after infestation

Question 5

Explain the pathogenesis of pruritis in scabies

Answer 5

Th2 response with raised IL-4 and IgE

Question 6

What are three risk factors for scabies?

Answer 6

Overcrowding, poverty, extremes of age, new sexual partner and immunosuppression

Question 7

What three examination findings would you see in scabies?

Answer 7

Burrows, erythematous papules and vesicles, excorations of web space, axilla and peri-umbilical areas

Question 8

How would you investigate scabies?

Answer 8

Ink burrow test, dermatoscopy, biopsy and skin scrape

Question 9

How would you manage scabies?

Answer 9

Insecticide cream (permethrin and ivermectin), antihistamines and antibiotics for secondary infection

Question 10

Define urticaria

Answer 10

Itchy, blotchy rash caused by swelling of the epidermis - lasts less than 24 hours

Question 11

Explain the pathogenesis of urticaria

Answer 11

Mast cell activation degranulates histamine, leukotrienes and prostaglandins. This causes vasodilation, oedema & pruritus or angioedema in the dermis & subcutaneous tissue (tongue + lips)

Question 12

What are the features in a history for urticaria?

Answer 12

Pruritus resolving in 24 hours, leaving no mark

Question 13

What are the two risk factors for urticaria?

Answer 13

Food or drug exposure, family history of angioedema

Question 14

What examination findings would you see in urticaria?

Answer 14

Blanching, erythematous, oedematous lesion, angioedema

Question 15

What would be a red flag examination finding in urticaria?

Answer 15

Angioedema and or stridor

Question 16

What investigations would you perform for urticaria?

Answer 16

Clinical diagnosis, immunological tests if it occurs for longer than 6 weeks

Question 17

What is the management of urticaria?

Answer 17

High-dose antihistamines, steroids (if severe), trigger avoidance

Question 18

What is eczema?

Answer 18

Inflammatory skin condition of the epidermis causing dry, pruritic skin with chronic relapse

Question 19

Where would you most commonly find eczema?

Answer 19

Presents on cheek, forehead, scalp, extensor and flexor surfaces

Question 20

What causes eczema?

Answer 20

Caused by genetic and environmental factors with defect in skin barrier & immune dysregulation post-allergen exposure

Question 21

Explain the four phases of eczema pathogenesis

Answer 21

1. Sensitisation – antigen exposure causes IgE production, sensitising mast cells
2. Acute phase – re-exposure causes degranulation and skin inflammation, oedema and erythema
3. Sub-acute phase – dries and crusts due to water loss through porous skin
4. Chronic phase – cycles of itching, drying & re-introducing allergen leading to skin thickening (lichenified)

Question 22

What would you see in a history of eczema?

Answer 22

Pruritis & dry skin (xerosis)

Question 23

What examination findings would you see in eczema?

Answer 23

Erythema, scaling, vesicles, papules, keratosis pilaris, excoriation and lichenification in chronic cases

Question 24

How would you investigate eczema?

Answer 24

Itchy skin plus history of itchy skin in creases, atopy, dry skin, flexural eczema, an onset less than 2 years

Consider allergy testing, IgE levels and skin biopsy

Question 25

How would you manage eczema?

Answer 25

Emollients (moisturise, improve barrier and reduce allergens), topical steroids (hydrocortisone), antibiotics if infected, antihistamines

Question 26

What is the pathogenesis of pruritis in an insect bite?

Answer 26

Chemicals from the sting or mouth parts enter body, causing a release of histamine (vasodilator) in response to venom. This leads to swelling, oedema and pain. Anaphylaxis can also occur – IgE hypersensitivity to antigen in pre-sensitised people causes mast cell degranulation

Question 27

What features would be present in a history of insect bites?

Answer 27

Bite or sting markings, oedema, pain, warmth, pruritis, wheal and flare

Question 28

What are the risk factors for pruritis with insect bites?

Answer 28

Exposure to insects, history of anaphylaxis

Question 29

Describe the investigations performed for insect bites

Answer 29

Clinical diagnosis, consider FBC (raised WCC) or sensitivity testing

Question 30

How would you manage insect bites?

Answer 30

1. Ice, clean, remove sting (if present) 2. Corticosteroid (prednisolone) 3. Antihistamine (cimetidine)

Question 31

What is dermatitis herpetiformis?

Answer 31

Autoimmune blistering skin disease associated with coeliac disease

Question 32

Explain the pathogenesis of dermatitis herpetiformis

Answer 32

Autoantibodies are produced againsttissue transglutaminase (TTG), this leads to anti-epidermal deposits in papillary dermis. Neutrophils and complement mediate the immune response resulting in vesicular or bullous erythematous pruritic rash.

Question 33

What would feature in a history of dermatitis herpetiformis?

Answer 33

Itchy, red skin with papules and vesicles in clusters

Question 34

What risk factors can lead to dermatitis herpetiformis?

Answer 34

Coeliac disease, male gender, 30-50 year age rang, white ethnicity

Question 35

What examination findings would be seen in an insect bite?

Answer 35

Pustules, bulls-eye rash (Lyme disease), bite markings

Question 36

What examination findings would be seen in dermatitis herpetiformis?

Answer 36

Symmetrical papules, vesicles & blisters on scalp, shoulder, buttocks, elbow & knees Blisters can erode and crust, leaving hypo/hyperpigmentation

Question 37

What are the investigations for dermatitis herpetiformis?

Answer 37

Coeliac screen (anaemia, anti-tissue transglutaminase, anti-endomysial antibody), skin biopsy (granular IgA deposits in dermal papillae)

Question 38

How would you manage dermatitis herpetiformis?

Answer 38

Gluten-free diet, NSAIDs, steroids or topical steroids if oral is contraindicated

Question 39

What is lichen planus and where can it be seen?

Answer 39

Pruritic, chronic inflammatory dermatosis resulting from keratinocyte apoptosis. It affects the skin, mucous membranes, genitals, scalp and nails.

Question 40

Describe the autoimmune pathogenesis of lichen planus

Answer 40

Activated T cells induce apoptosis of basal keratinocytes at dermal-epidermal junction, causing hyperkeratotic epidermis with irregular acanthosis

Question 41

What would you see featured in a history of lichen planus?

Answer 41

Pruritis

Question 42

What are the risk factors associated with lichen planus?

Answer 42

Female gender, hepatitis C infection, 20-60 year old age range

Question 43

What examination findings can be seen in lichen planus?

Answer 43

Shiny, flat-topped papules or plaques (mainly on extremities, wrists, ankles, vulva), mucosal erosion (vulval), Wickham’s striae (overlying white lacy networks)

Question 44

How would you investigate lichen planus?

Answer 44

Consider a biopsy – lymphocytic infiltrate at dermo-epidermal junction, necrotic keratinocytes, hyperkeratosis

Question 45

How would you treat lichen planus?

Answer 45

Corticosteroids (topical - betamethasone), antihistamines (chlorphenamine), phototherapy