Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Dermatology > PATHOLOGY; Classification of skin conditions > Flashcards

PATHOLOGY; Classification of skin conditions Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

How many (main) reaction patterns are there?

A

4.

  1. Spongiotic intraepidermal oedema (eczema)
  2. Psoriasiform-elongation of the rete ridges (psoriasis)
  3. Lichenoid-basal layer damage (liche plants and lupus) - damage to basal epidermis.
  4. Vesiculobullous-blistering (pemphigoid, pemphigus and dermatitis herpetiformis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathogenesis of psoriasis

A

> Epidermal hyperplasia and increased epidermal turnover

> Hereditary factors?

> New lesions can arise at sites of trauma

> Complement mediated attack on keratin layer.

COMPLETE PATHOGENESIS IS UNCLEAR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Psoriasis presentaiton

A

Well defined scaly plaques

Red shiny scale

Picking flakes

Auspitz sign

Extensor surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Psoriatic nail dystrophy

A

Atypical nail growth and subungual hyperkeratosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Elongation of the rete pegs

A

Psoriasis

Become club shaped - bulbous at base

Some fusion of the rete pegs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lichenoid disorders

A

Conditions characterised by damage to basal epidermis

Lichen planus

Itchy flat topped violaceous papule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lichen plans - histology

A

Irregular sawtooth acanthosis

Hypergranulosis and orthohyperkeratosis

Band-like upper dermal infiltrate of lymphocytes

Basal damage with formation of cytoid bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Range of other lichenoid disorders

A

I> Some resemble lichen planus

  • discoid lupus
  • some drug rashes

> Others have more marked vacuolar interface change

  • examples are erythema multiforme, toxic epidermal necrolysis
  • severe EM/ TEN may be life threatening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In lichen planus - what shape does the epidermis form?

A

Saw toothed.

Keratosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Buccal mucosa sign of lichen planus

A

Wickham’s striae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Immunobullous disorders

A

Vesicles and bull occur as a secondary phenomenon in many skin diseases e.g. eczema, herpes virus infection, burns

BLISTERS as primary feature.

Pemphigus
Bullous pemphigoid
Dermatitis herpetiformis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bullous Pemphigus

A

> Rare autoimmune bullous disease

> Sex incidence is equal, usually middle age

> Loss of integrity of epidermal cell adhesion

> Variable severity

> Responds to steroids

4 distint subtypes

majority PEMPHIGUS VULGARIS

LYMPHOCYTES present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is happening in pemphigus?

A

Body is making antibody that are damaging the points of adhesion between the keratinocytes

Can involve oesophagus - can slough their oesophageal lining.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pemphigus vulgaris?

A

Autoimmune condition

IgG auto-antibodies made against DESMOGLEIN 3

Desmoglein 3 maintains desmosomal attachments

Immune complexes form on cell surface

Complement activation and protease release

Disruption of desmosomes

Blisters are fragile and burst

End result is ACANTHOLYSIS

Presentation//

  • Produces fluid filled blisters which rupture to form shallow erosions
  • involves skin esp. scalp, face, axillae, groin, trunk
  • may affect mucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Desmoglein 3

A

Maintains desmosomal attachments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is common to all variants of pemphigus?

A

Process of acantholysis.

Lysis of intercellular adhesion sites

Desmosomes are cleaved.

17
Q

Basal layer of epidermis is intact/broken in pemphigus vulgarise?

A

Preserved as they have different types of attachment

18
Q

Bullous pemphigoid

Which inflammatory cells are present

A

> Subepidermal blister
No acantholysis
“Tense” blisters

React with hemidesmosomes that are sticking basal layer to the basal membrane.

Circulating antibodies (IgG) react with a major and or/minor antigen of the HEMIDESMOSOMES anchoring basal cells to basement membrane.

Result is local complement activation and tissue damage.

EOSINOPHILS

19
Q

Immunofluorescence in Bullous pemphigoid

A

Linear IgG + complement deposited around basal membrane

Send EARLY lesions for histology

20
Q

Older lesions of pemphigoid

A

These show re-epithelialisation of their floor, mimicking pemphigus vulgaris.

21
Q

Dermatitis herpetiformis

A

> Rare condition
Autoimmune bullous disease
COELIAC disease

> HLA-DQ2 haplotype
Intensely itchy lesions
- symmetrical
Elbows, knees, buttocks often excoriated
Hallmark is papillary dermal micro abscesses

IgA deposition 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

22
Q

Dermatitis herpetiformis is associated with with GI disease?

A

Coeliac disease

23
Q

Hallmark of dermatitis herpetiformis

A

Papillary dermal micro abscesses

Sub epidermal bull formation

24
Q

Which type of immunoglobulin is deposited in dermatitis herpetiformis

A

IgA in dermal papillae

25
Q

What component of gluten does IgA react with?

A

Gliadin

But cross reacts with connective tissue proteins.

26
Q

Which antibody is present in pemphigus and pemphigoid?

A

IgG

27
Q

Acne vulgaris

A

Distribution reflects sebaceous gland sites

- face, upper back, anterior chest

28
Q

Aetiology of acne

A
  1. ↑ Androgens at puberty
  2. ↑ androgen sensitivity of sebaceous glands
  3. Keratin and sebum plugging of pilosebaceous units (Comedones)
  4. Infection with anaerobic bacterium, corynebacterium acnes
  5. Rupture of keratin and sebum build up causes inflammation and foreign body granulomas
29
Q

Rosacea

A

Recurrent facial flushing

Commoner in females

Visible blood vessels (eurasia)

Pustules, yellow heads

Perifollicular granulomas

Follcular demodex mites noted

Thickening of skin - rhinophyma

TRIGGERS

  • sunlight
  • alcohol
  • spicy foods
  • stress

NOT A TYPE OF ACNE

30
Q

Is rosacea a type of acne?

A

NO

31
Q

Which mite is commonly noted in Rosacea?

A

Demodex mites

Live in hair follicles

32
Q

Munro’s micro abscesses

A

An abscess (collection of neutrophils) in the stratum corneum of the epidermis due to the infiltration of neutrophils from papillary dermis into the epidermal stratum corneum.

They are a cardinal sign of psoriasis

Dermatology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions