Dermatology Flashcards

1
Q

What parasite causes scabies?

A

Sarcoptes scabiei

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2
Q

What causes scabies?

A

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

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3
Q

What would you see in a history of scabies?

A

Generalised intense pruritis that is worse overnight

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4
Q

What causes pruritis in scabies?

A

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

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5
Q

Explain the pathogenesis of pruritis in scabies

A

Th2 response with raised IL-4 and IgE

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6
Q

What are three risk factors for scabies?

A

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

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7
Q

What three examination findings would you see in scabies?

A

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

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8
Q

How would you investigate scabies?

A

Ink burrow test, dermatoscopy, biopsy and skin scrape

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9
Q

How would you manage scabies?

A

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

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10
Q

Define urticaria

A

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

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11
Q

Explain the pathogenesis of urticaria

A

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

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12
Q

What are the features in a history for urticaria?

A

Pruritus resolving in 24 hours, leaving no mark

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13
Q

What are the two risk factors for urticaria?

A

Food or drug exposure, family history of angioedema

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14
Q

What examination findings would you see in urticaria?

A

Blanching, erythematous, oedematous lesion, angioedema

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15
Q

What would be a red flag examination finding in urticaria?

A

Angioedema and or stridor

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16
Q

What investigations would you perform for urticaria?

A

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

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17
Q

What is the management of urticaria?

A

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

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18
Q

What is eczema?

A

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

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19
Q

Where would you most commonly find eczema?

A

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

20
Q

What causes eczema?

A

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

21
Q

Explain the four phases of eczema pathogenesis

A
  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)
22
Q

What would you see in a history of eczema?

A

Pruritis & dry skin (xerosis)

23
Q

What examination findings would you see in eczema?

A

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

24
Q

How would you investigate eczema?

A

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

25
Q

How would you manage eczema?

A

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

26
Q

What is the pathogenesis of pruritis in an insect bite?

A

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

27
Q

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

A

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

28
Q

What are the risk factors for pruritis with insect bites?

A

Exposure to insects, history of anaphylaxis

29
Q

Describe the investigations performed for insect bites

A

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

30
Q

How would you manage insect bites?

A
  1. Ice, clean, remove sting (if present)
  2. Corticosteroid (prednisolone)
  3. Antihistamine (cimetidine)
31
Q

What is dermatitis herpetiformis?

A

Autoimmune blistering skin disease associated with coeliac disease

32
Q

Explain the pathogenesis of dermatitis herpetiformis

A

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.

33
Q

What would feature in a history of dermatitis herpetiformis?

A

Itchy, red skin with papules and vesicles in clusters

34
Q

What risk factors can lead to dermatitis herpetiformis?

A

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

35
Q

What examination findings would be seen in an insect bite?

A

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

36
Q

What examination findings would be seen in dermatitis herpetiformis?

A

Symmetrical papules, vesicles & blisters on scalp, shoulder, buttocks, elbow & knees

Blisters can erode and crust, leaving hypo/hyperpigmentation

37
Q

What are the investigations for dermatitis herpetiformis?

A

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

38
Q

How would you manage dermatitis herpetiformis?

A

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

39
Q

What is lichen planus and where can it be seen?

A

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

40
Q

Describe the autoimmune pathogenesis of lichen planus

A

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

41
Q

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

A

Pruritis

42
Q

What are the risk factors associated with lichen planus?

A

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

43
Q

What examination findings can be seen in lichen planus?

A

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

44
Q

How would you investigate lichen planus?

A

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

45
Q

How would you treat lichen planus?

A

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