Pathology of Rashes 1 Flashcards

1
Q

Functions of skin?

A
  • Strong barrier to antigens and organisms
  • Thermoregulation
  • Fluid and electrolyte balance sweat glands
  • Fluid and electrolyte balance sweat glands
  • Endocrine function - UV stimulation of Vit D
  • Protection of UV rays
  • Immune function - Langerhans
  • Sensory function touch, temp, pressure
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2
Q

What type of cell is mainly the epidermis?

A

Stratified keratinising squamous epithelium

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3
Q

Where are melanocytes found?

A

Dermo-epidermal junction

Basal layer

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4
Q

Where are langerhan cells?

A

Located in upper and mid-epidermis

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5
Q

What do langerhan cells act as?

A

Sentinels monitoring environment for antigens

Important in initaiting inflammation

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6
Q

What is the dermis?

A

Matrix of type 1,2 & 3 collagen
Elastic fibres
Ground substances

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7
Q

Where does papillary dermis lie?

A

Just under epidermis, it is thin

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8
Q

What does reticular dermis contain?

A

Sweat glands

Pilosebaceous units

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9
Q

Epidermal Basal membrane made of?

A

Laminin and collagen IV

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10
Q

What is hyperkeratosis?

A

Increased thickness of keratin layer

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11
Q

What is parakeratosis?

A

Persistence of nuclei in the keratin layer

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12
Q

What is acanthosis?

A

Increased thickness of epithelium

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13
Q

Why is there no nuclei in keratin layer usually?

A

Because the cells are dead and ready to fall off

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14
Q

What is papillomatosis?

A

Irregular epithelial thickening

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15
Q

What is spongiosis?

A

Oedema fluid between squames appears to increase prominence of intercellular prickles
If severe vesicles filled by oedema fluid develop

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16
Q

How many main reaction patterns of inflammatory skin disease?

A

4

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17
Q

4 main inflammatory skin disease reaction patterns?

A
  • Spongiotic-intraepidermal oedema e.g. eczema
  • Psoriasiform-elongation of the rete ridges e.g. psoriasis
  • Lichenoid-basal layer damage e.g. lichen planus and lupus
  • Vesiculobullous-blistering e.g. pemphigoid, pemphigus and dermatitis herpetiformis
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18
Q

Where psoriasis can develop?

A

-Epidermal hyperplasia
: increased epidermal turnover
Hereditary factors
New lesions can arise at sites of trauma

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19
Q

What is psoraisis?

A

Complement mediated attack on keratin layer, complement attracts neutrophils to keratin layer

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20
Q

Histology of psoraisis?

A

Elongation of rete ridges

Epidermis is elongated and plumped and fuses with neighboring ridges

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21
Q

Psoriasis is not hereditary. True or False?

A

FALSE

Can be partly hereditary

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22
Q

What are lichenoid disorders?

A

Conditions characterized by damage to basal epidermis

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23
Q

What is a common lichenoid disorder?

A

Prototypic condition is lichen planus

24
Q

Symptoms of lichenoid disorder?

A

Itchy flat topped Violaceous papules

25
Histology of lichen planus?
- Irregular sawtooth acanthosis - Hypergranulosis and orthohyperkeratosis - Band like upper dermal infiltrate of lymphocytes - Basal damage with formation of cytoid bodies
26
Other lichenoid disorders?
Discoid lupus Drug rashes Toxic epidermal necrolysis
27
What occurs as a secondary phenomenon in many skin diseases? eg eczema, HPV, burns
Vesicles and bullae (blisters)
28
Primary feature of immunobullous diseases?
Blisters
29
Important examples of immunobullous disorders?
Pemphigus Bullous pemphigoid Dermatitis herpetiformis
30
Pemphigus is rare. True or false?
True | Rare autoimmune disease, usually middle age
31
What histologically is pemphigus?
Loss of integrity of epidermal cell adhesion
32
What does pemphigus respond to?
Steroids
33
How many distinct sub types of pemphigus?
4
34
80% of cases of pemphigus are sub type?
Pemphigus vulgaris
35
What immune response happens in pemphigus vulgaris?
IgG auto-antibodies made against desmoglein 3
36
What is the role of desmoglein 3?
Maintains desmosomal attachments
37
Process pf auto-antibodies against desmoglein 3?
Immune complexes dorm on cell surface Complement activation and protease release Disruption of desmosomes END RESULT= Acantholysis
38
What parts of body does pemphigus vulgaris involve?
Skin esp scapl, face, axillae, groin, trunk | May affect mucosa of resp tract, mouth
39
What does pemphigus produce?
Fluid filled blisters which rupture to form shallow erosions
40
What is acantholysis?
Lysis of intercellular adhesion sites
41
What is bullous pemphigoid?
Subepidermal blister | -No evidence of acantholysis
42
What do antibodies do in bullous pemphigoid?
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
43
What do antibodies attack in bullous pemphigoid?
Hemidesmosomes | Basal membrane
44
What can older lesions of bullous pemphigoid mimick?
Show re-epithelialization of their floor mimicking pemphigus vulgaris
45
What generally is dermatitis herpetiformis?
Relatively rare condition Autoimmune bullous disease | -associated with celiac disease
46
Haplotype of coeliacs?
HLA-DQ2
47
Symptoms of dermatitis herpetiforms?
Intensely itchy lesions, symmetrical | -knees, elbows, buttocks
48
Hallmark of dermatitis herpetiformis?
Papillary dermal microabscesses
49
90% of patients with dermatitis herpetiformis have?
Gluten sensitive enteropathy
50
What does distribution of acne vulgaris reflect?
Sebaceous gland sites
51
Aetiology of acne?
Increased androgens at puberty Increased androgen sensitivity of sebaceous glands Keratin plugging of pilosebaceous units Infection with anaerobic bacterium- corynebacterium acnes
52
Process of acne?
- Sebum produced by sebaceous gland plugs pilo-sebaceuos unit - Keratin and sebum build up to produce comedones (blackheads / whiteheads) - Rupture causes acute inflammation + foreign body granulomas
53
What is rosacea?
Recurrent facial flushing Visible blod vessels Pustules Thickening of skin (rhinophyma)
54
Triggers of rosacea?
Sunlight Alcohol Spicy foods Stress
55
Pathology of rosacea?
- Patchy inflammation with plasma cells - Pustules - Perifollicular granulomas - Follicular demodex mites often noted - Allergic reaction to mites?
56
Antibody reaction in dermatitis herpetiformis?
- Shows deposits of IgA in dermal papillae - IgA ABs 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