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Immunology Y2 > Inflammatory Dermatoses > Flashcards

Inflammatory Dermatoses Flashcards

1
Q

What do eccrine glands produce and where are they found?

A

Eccrine sweat glands make watery sweat glands and are all over

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2
Q

What do apocrine glands produce and where are they found?

A

Apocrine sweat glands make more viscous sweat and are mainly concentrated in the axilla and groin

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3
Q

The matrix of the dermis is made out of what? (8)

A

collagen, elastin, glycosaminoglycans, connective tissue, fibroblasts, immune cells, blood vessels and nerves

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4
Q

5 layers of the skin? Top to bottom

A

Stratum cornea, stratum granulosum, stratum spinosum, stratum basale and dermis

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5
Q

Purpose of Merkel cells and where are they found?

A

Involved in sensation, they sit on the basement membrane

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6
Q

Purpose of dendritic cells?

A

APCs

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7
Q

Purpose of melanocytes? How to spot a melanocyte under histology?

A

 Make melanin and protect nuclei of keratinocytes from UV damage, they look like cells with a bit of white in under histology slides

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8
Q

What is the stratum corneum composed of?

A

Dead keratinocytes

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9
Q

Describe the life of a keratinocyte, mention which lawyer of th e

A
  • Keratinocytes start off in the stratum basale and proliferate, moving up the epidermis and differentiating
  • Eventually they produce keratin which makes up most of the stratum corneum
  • By the time they reach the stratum corneum, keratinocytes have lost their nuclei and died They form the barrier of the skin
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10
Q

What do defects of the stratum corneum lead to

A
  • Defects lead to eczema
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11
Q

What protein glues corneocytes together

A

Filagrin

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12
Q

Filagrin does what?

A

glues corneocytes together

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13
Q

Atopy is…

A

tendency to develop hypersensitivity

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14
Q

Order that these atopic diseases tend to present in life:

food allergy, eczema, rhinitis, asthma

A

eczema, food allergy, asthma, rhinitis

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15
Q

Describe how atopic eczema can occur, starting with mutations in skin

A

skin has intrinsic factors such as filaggrin gene mutations that allow extrinsic factors such as allergens (dust mites), pathogens and irritants in.
These are taken in by APC and stimulate an immune response (activate CD4 cells and TH2 response). Produces IgE causing mast cells to degranulate and atopic eczema.

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16
Q

What does palmar hyper linearity suggest

A

a sign of a filagrin gene mutation and can be used to assess risk of eczema

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17
Q

What is a sign of a filagrin gene mutation and can be used to assess risk of eczema

A

palmar hyper linearity

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18
Q

Describe acute eczema

A

very red, weepy, blistery, colonised with bacteria

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19
Q

Describe chronic eczema

A

will look less red, excoriated (scratched) and lichenified (thickened looking skin and accentuation of skin lines)

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20
Q

Describe erythrodermic eczema

A

means red all over – can be used to describe severe eczema

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21
Q

Describe Eczema HERPETICUM

A

where herpes simplex proliferates on the skin in someone with eczema – this can become serious and even lead to an encephalitis

22
Q

SEBORRHOEIC eczema, aka…

A

dandruff

23
Q

PSORIASIS causes?

A

Genetics and environmental triggers such as stress

24
Q

How does thickening of skin occur in psoriasis? Why does this lead to scaling (what cells remain in the top layer)

A

Genetic/environmental triggers occur. T cells then accumulate in the dermis and stimulate cytokine release especially TNF-α, this leads to neutrophils going into the epidermis and overproduction of keratinocytes leading to thickening of the skin.

The top layer is immature and hasn’t lost its neutrophils so you get lots of scaling, also leads to blood vessels dilating.

25
Q

What is acanthosis

A
  • Epidermis becomes thicker in psoriasis
26
Q

What is hyperkeratosis

A
  • Stratum corneum becomes thicker in psoriasis
27
Q

What is parakeratosis

A
  • Individual cells aren’t losing nuclei in psoriasis
28
Q
  • Stratum corneum becomes thicker in psoriasis is known as ….
A

hyperkeratosis

29
Q
  • Epidermis becomes thicker in psoriasis is known as ….
A

acanthosis

30
Q
  • Individual cells aren’t losing nuclei in psoriasis is known as ….
A

parakeratosis

31
Q

Explain what happens in psoriasis, mention what forms pustules, and what causes the red colour and what changes are driven by lymphocytes

A
  • Epidermis becomes thicker (acanthosis)
  • Stratum corneum becomes thicker (hyperkeratosis)
  • Individual cells aren’t losing nuclei (parakeratosis)
  • Influx of neutrophils within epidermis – can form pustules
  • Dilatation of blood vessels in the dermis (gives the red colour)
  • Lymphocytes within the dermis that drive this immune reaction (there are also exess cytokines and TNFalpha)
32
Q

Describe CHRONIC PLAQUE psoriasis

A

Salmon pink plaques with a silvery scale, very well defined

33
Q

Describe psoriasis VULGARIS

A

Well-demarcated, erythematous plaques with thick, yellowish scale and desquamation on sites of pressure arising on the plantar feet and palms

34
Q

3 SIGNS OF NAIL PSORIASIS:

A

PITTING
SUBUNGUAL HYPERKERATOSIS Build-up of keratin under the nail – leads to dystrophic nail and loss of cuticle
ONYCHOLYSIS Nail plate lifts off the nail bed

35
Q

Describe GUTTATE psoriasis

A

pattern of psoriasis is ‘rain drop’, usually found on the trunk and occurs after streptococcus infection (throat/blood test) – usually affects young people and can persist for weeks or months

36
Q

What infection does guttate psoriasis often occur after

A

streptococcus

37
Q

Describe PALMOPLANTAR PUSTULOSIS

A

Psoriasis where, instead of plaques on the body, someone gets pustules on the palms of the hands and soles of the feet

38
Q

Describe GENERALISED PUSTULAR psoriasis

A

Patients are febrile, malaise, tachycardic, toxic (high pulse rate, low BP etc.). Cause could be infections or psoriasis or drug reaction.

39
Q

What is ACNE disease of in the skin

A
  • Disease of the pilosebaceous unit
40
Q

what is the 2ndary infection in acne?

A

PROPIONIBACTERIA ACNES

41
Q

What causes comedone formation

A

caused by hyperkeratinisation of the neck/infundibulum of a follicle

42
Q

4 things that contribute to acne?

A

genetic predisposition
- Increased sebum production
hyperkeratinisation leading to Thickening of the infundibulum (forms blackheads)

43
Q

What is BULLOUS PEMPHIGOID

A
  • Autoimmune condition with production of an auto-antibody that acts against a protein in the basement membrane (BM between epidermis and dermis)
44
Q

What is the skins basement membrane between

A

Epidermis and dermis

45
Q

What antigens are attacked by autoantibodies in bullies pemphigoid

A

BPAg1 and BPAg2 (bullous pemphigoid antigen 1 and 2)

46
Q

Bullous pemphigoid usually affects people of what age

A

elderly patients, starts off as rash and then blisters develop and progress

47
Q

How does bullous pemphigoid Start and how does it cause mortality

A
  • Tense blisters
  • Usually in elderly patients, starts off as rash and then blisters develop and progress
  • Without treatment, the blisters get infected and cause death by sepsis
48
Q

What causes EPIDERMOLYSIS BULLOSA:

A

Genetic condition causing a problem with the basement membrane zone

49
Q

What causes PEMPHIGUS VULGARIS

A
  • Auto-antibody directed against a component of the hemi-desmosome within the epidermis
50
Q

Target of the antibody in pemphigus vulgaris?

A

DESMOGLEIN 1 and 3

51
Q

What does pemphigus vulgarisms cause

A
  • Blisters are superficial

- Blisters break down, causing erosions

52
Q

What is the desmosome

A

The connection between keratinocytes

Immunology Y2 (5 decks)

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