Pathology

Question 1

Aconthosis

Answer 1

Thickening of the epithelial layer

Question 2

Parakeratosis

Answer 2

Keratin layer has persisting nuclei

Question 3

Hyperkeratosis

Answer 3

Thickening of the keratin layer

Question 4

Papillomatosis

Answer 4

Irregular epithelial thickening

Question 5

Spongiosis

Answer 5

Oedema fluid between squames increasing prominence of intercellular prickles.

Question 6

4 Classes of inflammatory skin diseases

Answer 6

Psoriaform
Vesiculobullous
Spongiotic
Lichenoid

Question 7

Describe psoriaform inflammatory diseases

Answer 7

Involve elongation of rete ridges (downward thickening of the epidermis between the dermal pappillae)

Question 8

Describe spongiotic inflammatory diseases

Answer 8

Intraepidermal oedema

Question 9

Describe lichenoid disorders

Answer 9

Damage to the basal layer of the epidermis

Question 10

Describe vesiculobullous disorders

Answer 10

Blistering

Question 11

What is the dermis made up of?

Answer 11

Type 1 and Type 3 collagen in a matrix.
Ground substance
Elastic fibres

Question 12

What are the two regions that the dermis is divided into?

Answer 12

The papillary dermis- thin, bundles of type 1 collagen

The reticular dermis- contains appendage structures, sweat glands, pilosebaceous units.

Question 13

Pathological features of psoriasis

Answer 13

Unknown cause- however thought to be partly hereditary
Neutrophils gather in the upper layer of the epidermis- complement mediated due to no infection causing this.
Parakeratosis
Aconthosis
Blood vessels from the dermis come close to the surface- (Ausfitz sign, when scab is picked they bleed)
Dystrophic nails.

Question 14

Pathological features of lichen planus

Answer 14

Irregular saw tooth aconthosis
Orthokeratosis- parakeratosis without the persisting of nuclei
Hypergranulosis (increased thickening of the stratum granulosum)
Band like upper dermal infiltrate of lymphocytes
Basal damage with formation of cytoid bodies.

Question 15

What other pathological diseases resemble lichen planus?

Answer 15

Drug rashes

Discoid lupus

Question 16

How can you distinguish between lichen planus and other similar pathological diseases?

Answer 16

Lichen planus generally involves the oral cavity.

Question 17

What is an immunobullous disorders?

Answer 17

Blisters are the PRIMARY feature unlike in most disorders where they are a secondary feature of disease.

Question 18

Pemphigus

Answer 18

Rare, autoimmune disease.
Loss of integrity of epidermal cell adhesion (they don’t stick together as well as they should)
Has 4 distinct subtypes- majority are pemphigus vulgaris.

Question 19

What does pemphigus respond to?

Answer 19

Steroids.

Question 20

Pathology of pemphigus vulgaris

Answer 20

Autoimmune disorder.
IgG antibodies attack desmoglien 3 (maintains desmosomal attachments. Immune complexes form on cell surface causing complement activation and protease release)

Question 21

Appearance of pemphigus vulgaris

Answer 21

Fluid filled blisters which rupture to form shallow erosions.

Question 22

Pathology of bullous pemphigoid

Answer 22

Sub-epidermal blister

No evidence of acantholysis (lysis of intercellular adhesion sites)

Question 23

Pathology of bullous pemphigoid

Answer 23

IgG antibodies react to the major/minor antigen on hemidesmosomes. Hemidesmosomes attach basal cells to the basement membrane. This means the basal cells can detach and blisters can form in the space left (sub-epidermally).
Also local complement activation and tissue damage.

Question 24

Dermatitis herpetiformis

Answer 24

Strong association with coeliac disease.

Rare, autoimmune bullous disease.

Question 25

Presentation of dermatitis herpetiformis

Answer 25

Intensely itchy symmetrical lesions. | Elbows, knees and buttocks often excoriated (skin has been removed)

Question 26

Pathology of dermatitis herpetiformis

Answer 26

Papillary dermal microabscesses Neutrophil rich microabscess develop just below the epidermis IgA mediated- target gliadin component of gluten Granular lumpy deposits in tip of dermis.

Question 27

Pathological process of acne vulgaris

Answer 27

Increased androgen at puberty Increased sensitivity of sebaceous glands to androgen Keratin and sebum block the pilosebaceous units (causing black heads) Rupture causes acute inflammation.

Question 28

Rosacea

Answer 28

Recurrent facial flushing Visible blood vessels Pustules forming Thickening of the skin (rhinophyma)

Question 29

Pathology of rosacea

Answer 29

Vascular dilation (ectasia) Patchy inflammation with plasma cells Pustules Perifollicular (around the hair follicle) granuloma formation.

Question 30

Causes of rosacea. | What can stop rosacea

Answer 30

Sunlight, alcohol, spicy foods, stress | Sometimes they respond to tetracyclines