Pathology of Rashes 1 Flashcards

You may prefer our related Brainscape-certified 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of cell is mainly the epidermis?

A

Stratified keratinising squamous epithelium

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

Where are melanocytes found?

A

Dermo-epidermal junction

Basal layer

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

Where are langerhan cells?

A

Located in upper and mid-epidermis

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

What do langerhan cells act as?

A

Sentinels monitoring environment for antigens

Important in initaiting inflammation

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

What is the dermis?

A

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

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

Where does papillary dermis lie?

A

Just under epidermis, it is thin

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

What does reticular dermis contain?

A

Sweat glands

Pilosebaceous units

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Epidermal Basal membrane made of?

A

Laminin and collagen IV

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

What is hyperkeratosis?

A

Increased thickness of keratin layer

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

What is parakeratosis?

A

Persistence of nuclei in the keratin layer

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

What is acanthosis?

A

Increased thickness of epithelium

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

Why is there no nuclei in keratin layer usually?

A

Because the cells are dead and ready to fall off

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

What is papillomatosis?

A

Irregular epithelial thickening

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

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

How many main reaction patterns of inflammatory skin disease?

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where psoriasis can develop?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is psoraisis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Histology of psoraisis?

A

Elongation of rete ridges

Epidermis is elongated and plumped and fuses with neighboring ridges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Psoriasis is not hereditary. True or False?

A

FALSE

Can be partly hereditary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are lichenoid disorders?

A

Conditions characterized by damage to basal epidermis

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

Histology of lichen planus?

A
  • Irregular sawtooth acanthosis
  • Hypergranulosis and orthohyperkeratosis
  • Band like upper dermal infiltrate of lymphocytes
  • Basal damage with formation of cytoid bodies
26
Q

Other lichenoid disorders?

A

Discoid lupus
Drug rashes
Toxic epidermal necrolysis

27
Q

What occurs as a secondary phenomenon in many skin diseases? eg eczema, HPV, burns

A

Vesicles and bullae (blisters)

28
Q

Primary feature of immunobullous diseases?

A

Blisters

29
Q

Important examples of immunobullous disorders?

A

Pemphigus
Bullous pemphigoid
Dermatitis herpetiformis

30
Q

Pemphigus is rare. True or false?

A

True

Rare autoimmune disease, usually middle age

31
Q

What histologically is pemphigus?

A

Loss of integrity of epidermal cell adhesion

32
Q

What does pemphigus respond to?

A

Steroids

33
Q

How many distinct sub types of pemphigus?

A

4

34
Q

80% of cases of pemphigus are sub type?

A

Pemphigus vulgaris

35
Q

What immune response happens in pemphigus vulgaris?

A

IgG auto-antibodies made against desmoglein 3

36
Q

What is the role of desmoglein 3?

A

Maintains desmosomal attachments

37
Q

Process pf auto-antibodies against desmoglein 3?

A

Immune complexes dorm on cell surface
Complement activation and protease release
Disruption of desmosomes
END RESULT= Acantholysis

38
Q

What parts of body does pemphigus vulgaris involve?

A

Skin esp scapl, face, axillae, groin, trunk

May affect mucosa of resp tract, mouth

39
Q

What does pemphigus produce?

A

Fluid filled blisters which rupture to form shallow erosions

40
Q

What is acantholysis?

A

Lysis of intercellular adhesion sites

41
Q

What is bullous pemphigoid?

A

Subepidermal blister

-No evidence of acantholysis

42
Q

What do antibodies do in bullous pemphigoid?

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

43
Q

What do antibodies attack in bullous pemphigoid?

A

Hemidesmosomes

Basal membrane

44
Q

What can older lesions of bullous pemphigoid mimick?

A

Show re-epithelialization of their floor mimicking pemphigus vulgaris

45
Q

What generally is dermatitis herpetiformis?

A

Relatively rare condition Autoimmune bullous disease

-associated with celiac disease

46
Q

Haplotype of coeliacs?

A

HLA-DQ2

47
Q

Symptoms of dermatitis herpetiforms?

A

Intensely itchy lesions, symmetrical

-knees, elbows, buttocks

48
Q

Hallmark of dermatitis herpetiformis?

A

Papillary dermal microabscesses

49
Q

90% of patients with dermatitis herpetiformis have?

A

Gluten sensitive enteropathy

50
Q

What does distribution of acne vulgaris reflect?

A

Sebaceous gland sites

51
Q

Aetiology of acne?

A

Increased androgens at puberty
Increased androgen sensitivity of sebaceous glands
Keratin plugging of pilosebaceous units
Infection with anaerobic bacterium- corynebacterium acnes

52
Q

Process of acne?

A
  • 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
Q

What is rosacea?

A

Recurrent facial flushing
Visible blod vessels
Pustules
Thickening of skin (rhinophyma)

54
Q

Triggers of rosacea?

A

Sunlight
Alcohol
Spicy foods
Stress

55
Q

Pathology of rosacea?

A
  • Patchy inflammation with plasma cells
  • Pustules
  • Perifollicular granulomas
  • Follicular demodex mites often noted
  • Allergic reaction to mites?
56
Q

Antibody reaction in dermatitis herpetiformis?

A
  • 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