Pathology Flashcards

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1
Q

What are the four main inflammatory skin patterns?

Give an example of each.

A
  1. Spongiotic - intraepidermal oedema e.g. eczema (see Dr Brown’s eczema lecture)
  2. Psoriasiform - elongation of the rete ridges e.g. psoriasis
  3. Lichenoid - basal layer damage e.g. lichen planus and lupus
  4. Vesiculobullous-blistering e.g. pemphigoid, pemphigus and dermatitis herpetiformis
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2
Q

What are the two main pathological problems in psoriasis?

A

Acanthosis of the epidermis

Parakeratosis (nuclei persist in the surface keratin)

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3
Q

What is the Koebner phenomenon?

A

New lesions of psoriasis arise at sites of trauma

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4
Q

What is the genetic influence in psoriasis?

A

Unclear - associated with specific HLA types

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5
Q

Which inflammatory cells are there in psoriasis?

A

No infection, but neutrophils gather in the epidermis, suggests that complement is activated in psoriasis which draws the neutrophils.

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6
Q

What is the problem in erythrodermic psoriasis?

A

Patients die from oozing fluid from the skin which causes metabolic problems

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7
Q

What is psoriasiform?

A

Histology – the ridges are elongated and fused; often become clubbed at the base – known as psoriasiform. May also get neutrophils in the corneal layer.

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8
Q

Which layer of the skin is affected in lichenoid disorders?

A

Basal layer of epidermis

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9
Q

What is the main clinical feature in lichen disorders?

A

Itchy flat topped violaceous papules

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10
Q
  • Irregular sawtooth acanthosis
  • Hypergranulosis and orthohyperkeratosis
  • Band-like upper dermal infiltrate of lymphocytes
  • Basal damage with formation of cytoid bodies
    Which disease is this?
A

Lichenoid disorder

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11
Q

Immunobullous disorders

  • Main clinical feature?
  • Give three examples
A

Blisters

  1. Pemphigus
  2. Bullous pemphigoid
  3. Dermatitis herpetiformis
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12
Q

Pemphigus

  • What type of disease?
  • Epidemiology?
  • Histology?
  • Severity?
  • Treatment?
  • Types?
  • Most common type?
A
  • Rare autoimmune bullous disease
  • Sex incidence is equal, usually middle -age
  • Loss of integrity of epidermal cell adhesion
  • Variable severity - occasionally fatal
  • Responds to steroids
  • Pemphigus has four distinct types which are separable clinically and histologically.
    The most common is pemphigus vulgaris.
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13
Q

Pemphigus vulgaris

  • Which antibody?
  • What forms on cell surface?
  • Disruption of which structures?
  • End result?
A
  • IgG auto-antibodies made against desmoglein 3
  • Immune complexes form on cell surface
  • Disruption of desmosomes
  • End result is ACANTHOLYSIS
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14
Q

Pemphigus vulgaris

- Which areas of the body are affected?

A

Scalp, face, axillae, groin, trunk. It may affect mucosa e.g. mouth, resp.tract. Extensive mucosal involvement may be fatal. It produces fluid filled blisters which rupture to form shallow erosions.

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15
Q

What pathology is common to ass variants of pemphigus?

A

Acantholysis = lysis of intercellular adhesion sites

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16
Q

What causes the bulla is pemphigus vulgaris?

A

Basal cells stick onto the basement layer, but above this they fall apart, causing a bulla

17
Q

What test is used for pemphigus vulgaris and what does it show?

A

An anti-IgG antibody with a fluorescent tag locates bits of IgG in the skin. When UV light is shone on the skin, IgG shows up

18
Q

Bullous pemphigoid

  • Which layer of skin is affected
  • Immunology?
  • Clinical sign?
  • Pathology difference from PV?
A

Bullous is SUB EPIDERMAL, and attacks the hemidesmosomes. Complement is activated between basal layer cells and basement membrane – epidermis floats off, causing a blister.
There is no evidence of acantholysis.

19
Q

What is the pathophysiology of bullous pemphigoid?

A

Circulating antibodies (IgG) react with a major and/or minor antigen of the hemidesmosomes anchoring basal cells to basement membrane. The result is local complement activation and tissue damage.

20
Q

What does immunofluorescence show in bullous pemphigoid?

What do older lesions show?

A

Immunofluorescence shows linear IgG + complement deposited around the BM.
Older lesions of pemphigoid show re-epithelialisation of their floor, mimicking pemphigus vulgaris.

21
Q

Dermatitis herpetiformis

  • What type of disease
  • Associated with which disease?
  • Genetics?
  • Clinical signs?
  • Hallmark feature?
A
  • Autoimmune bullous disease
  • Strong association with coeliac disease
  • Associated with HLA-DQ2 haplotype
  • Intensely itchy lesions-symmetrical
  • Elbows, knees and buttocks-often excoriated
  • Hallmark is papillary dermal microabscesses
22
Q

Which antibody is dermatitis herpetiformis associated with?

A

IgA

23
Q

Describe the pathology of acne

A
  • Androgens at puberty
  • Androgen sensitivity of sebaceous glands
  • Keratin plugging of pilosebaceous units
  • Infection with anaerobic bacterium corynebacterium acnes