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Y2 - Dermatology > Rashes > Flashcards

Rashes Flashcards

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Dermatology Board Prep flashcards
1
Q

What is hyperkeratosis?

A

Increased thickness of the keratin layer

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2
Q

What is parakeratosis?

A

Persistence of nuclei in the keratin layer

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3
Q

What is acanthosis?

A

Increased thickness of the epithelium

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4
Q

What is papillomatosis?

A

Irregular epithelial thickening

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5
Q

What is spongiosis?

A

Intercellular oedema develops in the epidermis

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6
Q

What are the 4 main reaction patterns of inflammatory skin diseases?

A

Spongiotic
Psoriasiform
Lichenoid (basal layer damage)
Vesiculobullous (blistering)

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7
Q

What are examples of each reaction pattern of inflammatory skin disease?

A

Spongiotic - interaepidermal oedema
Psoriasiform - psoriasis
Lichenoid - lichen plan’s, SLE
Vesiculobullous - pemphigoid, pemphigus, dermatitis herpetiformis

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8
Q

What is psoriasis?

A

A common chronic inflammatory dermatosis

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9
Q

What is the pathology of psoriasis?

A

Unclear

Complement attracts neutrophils to the keratin layer

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10
Q

What is the clinical presentation of psoriasis?

A

Symmetrical bilateral well-demarcated silvery or erythematous plaque
Nail changes - onycholysis, pitting, hyperkeratosis
Extensors, scalp, etc

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11
Q

What is acute psoriasis?

A

Covering body
Underlying cutaneous lymphoma, drug reaction or psoriasis
Manage as if severe widespread burn

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12
Q

What is the histological appearance of psoriasis?

A

Elongation of ridges, which become club-shaped and fuse with neighbouring ridges
Few lymphocytes in dermis
Neutrophil polymorphs
Abscesses

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13
Q

What are lichenoid disorders?

A

Conditions characterised by damage to basal epidermis

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14
Q

What is the most common lichenoid disorder?

A

Lichen planus

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15
Q

What is the clinical presentation of lichenoid disorders?

A

Itchy flat-topped raised papules

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16
Q

What is the histological appearance of lichenoid disorders?

A

Irregular sawtooth acanthuses (thickening of epidermis)
Hypergranulosis (thickened granular layer) and hyperkeratosis (thickened keratin later)
Infiltrate of lymphocytes
Basal damage with formation of cytoid bodies

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17
Q

What is pemphigus?

A

A group of rare autoimmune bullous diseases
Loss of integrity of epidermal cell adhesion
All involve acantholysis
Intraepidermal

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18
Q

What is acantholysis?

A

Lysis of intercellular adhesion sites

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19
Q

What patients usually present with pemphigus?

A

Middle aged

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20
Q

What is the treatment for pemphigus?

A

Steroids

21
Q

What is the most common variant of pemphigus?

A

Pemphigoid vulgaris

22
Q

What is the pathophysiology of pemphigoid vulgaris?

A

IgG auto-antibodies attack desmoglein 3, the protein that maintains desmosome attachments
Immune complexes form on cell surface and activates complement, causing protease release
Disruption of desmosomes causes acantholysis

23
Q

What is the clinical presentation of pemphigoid vulgaris?

A

Fluid filled blisters which rupture to form shallow erosions
Involves skin, especially scalp, face, axillae, groin, trunk
May affect mucosa

24
Q

How is diagnosis of pemphigoid vulgaris done?

A

Immunofluorescence - chickenwire pattern

25
Q

What is bullous pemphigoid?

A

Sub-epidermal blister

No acantholysis

26
Q

What is the pathophysiology of bullous pemphigoid?

A

IgG antibodies attack the hemidesmosomes anchoring basal cells to the basement membrane
This causes local complement activation and tissue damage

27
Q

How is diagnosis done for bullous pemphigoid?

A

Immunofluorescence - linear pattern

Histology for early lesions

28
Q

What is dermatitis herpetiformis?

A

Rare autoimmune bullous disease

Associated with coeliac, 90% have gluten sensitive enteropathy

29
Q

What is the clinical presentation of dermatitis herpetiformis?

A

Intensely itchy symmetrical lesions
Elbow, knees and buttocks
Papollary dermal microabscesses

30
Q

What is the pathophysiology of dermatitis herpetiformis?

A

IgA antibodies target gliadin component of gluten and cross react with connective tissue matrix proteins
Immune complexes form in dermal papillae and activate complement and generateneutrophil chemotaxins

31
Q

How is dermatitis herpetiformis diagnosed?

A

Immunofluorescence - granular IgA deposits in dermal papillae

32
Q

Where are the common sites for acne?

A

Sebaceous gland sites - face, upper back, anterior chest

33
Q

What is the aetiology of acne?

A

Androgens are released in puberty
Sebaceous glands are sensitised to androgen
Keratin plugging of pilosebaceous units
Infection with anaerobic bacterium corynebacterium acnes

34
Q

What does keratin and sebum build up produce?

A

Comedones (black and whiteheads)

35
Q

How does rosacea present?

A

Recurrent facial flushing
Visible blood vessels
Pustules
Thickening of the skin

36
Q

Who tends to get rosacea?

A

10% in caucasian adults
Commoner in females
Aged 30-60

37
Q

What are some factors that can trigger rosacea?

A 
Sunlight
Alcohol
Spicy foods
Stress
Tetracyclines
38
Q

What is the pathology of rosacea?

A

Vascular ectasia
Patchy inflammation with plasma cells
Pustules
Perifollicular granulomas

39
Q

What are risk factors for psoriasis?

A

15-25 y/os, 50-60 y/os
Environmental factors - stress, drugs (beta blockers), previous infection
Family history

40
Q

What are common comorbidities in psoriasis?

A 
Psoriatic arthritis
Metabolic syndrome
Crohn's disease
Cancer
Depression
Uveitis
41
Q

What is the management for psoriasis?

A 
Emollients
Vitamin D analogues
Coal tar
Dithranol
Steroid ointments
Phototherapy
Immunosuppression
42
Q

What is the management for acne?

A

Benzoyl peroxide
Vitamin A derivatives
Antibiotics
Isotretinoin

43
Q

What are the morphological features of acne?

A

Comedones (black and white heads)
Pustules and papules
Cysts
Erythema

44
Q

What is the management for rosacea?

A

Reduce aggravating factors (dietary triggers, sun exposure, topical steroids)
Metronidazole
Oral tetracycline

45
Q

What is the management for lichenoid disorders?

A

Emollients
Symptomatic treatment (steroids)
Phototherapy

46
Q

What is the difference between bullous pemphigoid and pemphigus?

A

BP - split is deeper, through the derma-epidermal junction

P - split is more superficial, intra-epidermal

47
Q

What are the investigations for bullous pemphigoid and pemphigus?

A

Skin biopsy and immunofluorescence

48
Q

What is the management for bullous pemphigoid and pemphigus?

A

Systemic steroids
Immunosuppression
Emollients
Tetracycline antibiotics in pemphigoid

Y2 - Dermatology (12 decks)

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