Pathology of the Skin Flashcards

1
Q

What is hyperkeratosis?

A

Increased thickness of keratin layer

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2
Q

What is parakeratosis?

A

persistence of nuclei in the keratin layer (pre-malignant or inflam)

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3
Q

What is acanthosis?

A

Increased thickness of epithelium

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4
Q

What is Papillomatosis?

A

Irregular epithelial thickening

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5
Q

Spongiosis?

A

oedema fluid between cells

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6
Q

What are the 4 classifications of inflam skin diseases?

A

spongiotic
psoriasiform
lichenoid-basal layer damage
vesiculobullous- blistering

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7
Q

What is the aetiology of acne?

A

Increased androgens at puberty
increased androgen sensitivity of sebaceous glands
keratin plugging of pilosebaceous units - then rupture
infection with anaerobic bacterium

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8
Q

What is the bacteria that infects pilosebaceous units in acne vulgaris?

A

corynebacterium acnes

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9
Q

What is a comedone?

A

Follicules impacted and distended by incompletely desquamated keratinocytes and sebum

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10
Q

What is a blackhead?

A

open comedone

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11
Q

What is a whitehead?

A

closed comedone

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12
Q

Is Rosacea more common in females or males?

A

Females

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13
Q

Give the clinical features of rosacea

A
recurrent facial flushing (erythema)
scaling
visible blood vessels 
small pustules 
thickening of the skin (rhinophyma)
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14
Q

What can trigger/aggravate rosacea?

A

sunlight
alcohol
spicy foods
stress

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15
Q

What is the pathology of rosacea?

A
Vascular ectasia
Patchy inflammation with plasma cells
Pustules
Perifollicular granulomas
Follicular Demodex mites often noted (possibe allergic reaction to mites)
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16
Q

What are the primary features of immunobullous disorders?

17
Q

What is pemphigus?

A

Loss of integrity of epidermal cell adhesion

18
Q

What does pemphigus respond to?

19
Q

Which subtype of pemphigus make sup 80% of cases of pemphigus?

A

Pemphigus vulgaris

20
Q

Describe what happens in pemphigus vulgaris?

A

Desmoglein 3 maintains desmosomal attachments
Immune complexes form on cell surface
Complement activation and protease release
Disruption of desmosomes
End result is ACANTHOLYSIS – epithelium dissolves
Intraepidermal bulla

21
Q

What are the auto-antibodies in pemphigus vulgaris directed against?

A

desmoglein 3

22
Q

Where does pemphigus vulgaris affect?

A

skin esp. scalp, face, axillae, groin, trunk

23
Q

Where can pemphigus vulgaris affect? Not usually.

A

Mucoa - mouth and respiratory tract

Extensive mucosal involvement may be fatal

24
Q

What is common to all variants of pemphigus?

A

the process of acantholysis = lysis of intercellular adhesion sites

25
Q

How dos pemphigus vulgaris present?

A

Produces fluid filled blisters which rupture to form shallow erosions

26
Q

On fluorescent staining of the skin with pemphigus vulgaris, what is it said to resemble?

A

chicken wire

27
Q

What is bullous pemphigoid?

A

Subepidermal blister with no evidence of acantholysis

28
Q

What do the auto-antibodes in bullous pemphigoid react with?

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

29
Q

How would you describe bullous pemphigoid?

A

discrete fluid filled blisters due to breaking of the DEJ

30
Q

What is the hallmark of dermatitis herpetiformis?

A

papillary dermal microabscess

31
Q

where and how does dermatitis herpetiformis present?

A

Symmetrical intensely itchy lesions on the elbows, knees and buttocks (often excoriated)

32
Q

What is dermatitis herpetiformis associated with?

A

coeliac disease and HLA-DQ2 haplotype

33
Q

Explain the autoimmunity aspect of dermatitis herpetiformis.

A
  • 90% with DH have gluten sensitive enteropathy (may be asymptomatic)
  • DIF shows deposits of IgA in dermal papillae
  • IgA antibodies target gliadin component of gluten but cross react with connective tissue matrix proteins
  • Immune complexes form in dermal papillae and activate complement and generate neutrophil chemotaxins.