Pathology of the Skin Flashcards

(33 cards)

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?

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
How dos pemphigus vulgaris present?
Produces fluid filled blisters which rupture to form shallow erosions
26
On fluorescent staining of the skin with pemphigus vulgaris, what is it said to resemble?
chicken wire
27
What is bullous pemphigoid?
Subepidermal blister with no evidence of acantholysis
28
What do the auto-antibodes in bullous pemphigoid react with?
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
How would you describe bullous pemphigoid?
discrete fluid filled blisters due to breaking of the DEJ
30
What is the hallmark of dermatitis herpetiformis?
papillary dermal microabscess
31
where and how does dermatitis herpetiformis present?
Symmetrical intensely itchy lesions on the elbows, knees and buttocks (often excoriated)
32
What is dermatitis herpetiformis associated with?
coeliac disease and HLA-DQ2 haplotype
33
Explain the autoimmunity aspect of dermatitis herpetiformis.
- 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.