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Immuno > Immuno 5: Inflammatory dermatoses > Flashcards

Immuno 5: Inflammatory dermatoses Flashcards

1
Q

Outline important structural features of skin microanatomy

A

Basement membrane between epidermis and dermis

Underlying the fat is fascia then muscle

Within the dermis there are ADNEXAL structures hair follicles and sebaceous glands, sweat glands. Also matrix

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2
Q

What is a pilosebaceous unit

A

Hair follice + sebaceous gland + pioerecti muscle

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3
Q

T/f sebaceous gland= sweat gland

A

F…. sebaceous associated with hair follice

The sweat glands are eccrine and apocrine

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4
Q

Distributin of each sweat gland

A

Eccrine= all over the body

Apocrine= axilla and groins (smelly sweat), drains into hair follice

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5
Q

What is the rest of the dermis made of aside from the pilosebaceous unit

A

Collagen, elastin, connective tissue, fibroblasts and immune cells, GAGs, blood vessels

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6
Q

What is all the pink on H&E in the dermis

A

Collagen.

The cells in the dermis are mostly fibroblasts

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7
Q

What is the difference in the substance produced by sweat glands and sebaceous glands

A

Sweat obs sweat

Sebaceous produces sebum which is a oil that lubricates the hair and also kills bacteria and fungi

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8
Q

Where are langerhans cell, merkel cell mostly located

A

Langerhans= in the stratum spinosum

Merkel=stratum basale

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9
Q

What happens to keratinocytes after production in the stratum basale from stem cell

A

They differentiate as they move up,

eventually to become the keratines stratified epithelim in the stratus corneum to perform barrier function

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10
Q

Outline differentiation of keratinocytes

A

Basal cell

Prickle cell

Granular cell

Keratin

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11
Q

What is contained within the granules of cells of the granular layer

A

Keratin

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12
Q

What is the difference between cells in the granular and the corneum layer

A

In the corneum has no nucleus (effectively dead cells)

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13
Q

Outline the structure of the straum corneum

A

BARRIER

Corneocytes bound together in a glue which is rich in lipids and proteins

Dead cells flaking off the top

Filagrin part of this glue

Defects in the barrier lead to eczema

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14
Q

What gene mutation is common in eczema patients

A

Filgarin gene mtutation

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15
Q

Define atopy

A

tendency to develop hypersensitivity

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16
Q

What are the 2 atopic diseases

A

Eczema, asthama, allergic rhinitis (hayfever)

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17
Q

What is the pattern in atopic eczema

A

Common

Relapsing and remitting

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18
Q

What is the problem in atopic eczema

A

Related to the reduced barrier function of the skin

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19
Q

What is the atopic march

A

People tend to develop

Eczema, then food allergy, then asthma and then rhinitis

(the initial eczema allows sensitisation to allergens which then manigest in other atopic disease later in life)

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20
Q

Outline the basic pathology in eczema

A

Reduce barrier function of skin and dryness(i.e. due to filagrin or other polymoprhism)

Infiltration of bacteria (S. Aureus) or other irritants (soap etc), further drying skin and reducing barrier function.

Immune response activated. APC (langerhans) leads to activation of CD4+ lymphocytes in a Th2 response. IgE production, mast cells degranulate

If it persists from acute to chronic, then it changes to Th1 response, in which CD4+ and CD8+ T cells are activated and produce INFa

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21
Q

Signs of a filagrin gene mutation

A

Hyperlinearity (more prominent lines) … so more likely eczema

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22
Q

What does acute eczema often look like

A

Red, raw, weepy, vesicles, food likely to get in contact with it and lead to food allergies later due to sensitisatin

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23
Q

What sites are most affected in infantile atopic eczema

A

The most affected areas are those that the baby can access easily (face, arms, elbows, knees).

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24
Q

Common site of eczema outbreak in infant vs child

A

From infant to child:
Infant: arms, face, knee etc. wherever they can access

child now affects: antecubital fossa, the popliteal fossa, hands, face and neck, legs and feet (flexural areas, and areas where there is build up of sweat).

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25
Q

Differentiate acute and chronic eczema

A

Acute is when it is very red and raw and weepy

Chronic is when it now looks more skil coloured:

appear excoriated and lichenified

Lichenification: the skin looks thickened and there is accentuation of the skin lines

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26
Q

What is erythrodermic eczema

A

The redness is all oer and the patient is systemically unwell

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27
Q

What can be consequence of inflammed skin in eczema

A

S. Aureus can colonise on the skin and activate immune response to perpetuate the eczema

Can also cause infections

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28
Q

What other infection are eczema patient more likely to get

A

Herpes Simplex Virus

Punched out blisters which break down to form ulcers

=Eczema herpeticum

Patient can become very unwell, and virus can spread into blood and this can cause herpes encepalitis.

Patient would also need to be admitted for antiretroviral treatmet e.g. acyclovir

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29
Q

Other types of eczema than atopic

A

Seborrhoeic

Allergic contact dermatitis

Discoid

30
Q

Outline seborrhoeic eczema

A

Greasy scaly skin with redness around nasal labial folds, forehead and eyebrows or scalp

The overgrowth of yeast and the dermatitis occur at the same time(includes dandruff)

Not as itchy

  • It can be treated with anti-dandruff/anti-fungal shampoo, antifungal cream and topical steroid
  • This gets worse in times of stress, staying up late or drinking too much alcohol
31
Q

What is allergic contact dermatitis

A

Reaction to an individual product

Common: makeup, perfume, fragrance, nickel, rubber, PPD in henna

32
Q

Why is S Aureus called super antigen

A

• Often, there is colonisation of the skin with staphylococcus aureus
• S. aureus acts as a super antigen  activates the eczema  worsening of eczema
in a topic eczema

33
Q

What is discoid eczema

A
  • This is descriptive of the pattern
  • It occurs in discoid areas (often on the legs, but can be anywhere
  • Each individual disc looks like eczema
  • But the intervening skin may look normal

Over washing can cause it

34
Q

Cause of discoid eczema and treatmnet

A 
•	The cause of this is often just dry skin with secondary dermatitis
•	Treatment involves: 
o	Emollient use
o	Topical steroid 
o	Avoidance of soap/shower gel
35
Q

What is psoriasis

A

Psoriasis is another inflammatory dermatoses, in which patients present with psoriatic plaques.

There are a number of patterns that allows us to identify this. Patients have salmon pink coloured plaques, with a silvery scale.

36
Q

T/f psoriasis is a monogenetic confition F

A

F Psoriasis is a genetic condition, but it is polygenetic – a number of different genes can cause it

37
Q

Environmental triggers of psoriasis

A

Psoriasis has environmental triggers as well as genetic susceptibility. This may include an infection, stress or certain drugs or alcohol .

38
Q

Histology of psoriasis

A
  • The epidermis becomes thicker – this is called acanthosis
  • The stratum corneum also becomes thicker – this is hyperkeratosis
  • The individual cells are not losing their nuclei – this is parakeratosis
  • There’s dilatation of blood vessels in the dermis so red colour

Scaling

39
Q

What immune cells are involved in psoriasis

A
  • There are lymphocytes within the dermis
  • This immune reaction is being driven by T cells and excess cytokines/TNF-alpha

-neutrophils recruited to epidermis and over production of keratinocytes….. thickening of epidermis

40
Q

Common sites of psoriasis

A 
Psoriasis is commonly seen at the 
scalp, 
elbows, 
knees, 
and genital areas, 
around the umbilicus and
 at the natal cleft of the buttocks. It is also seen on the hands and feet

Note the difference to eczema, which was on inside of elbow and knees and psoriasis is on the outside

41
Q

Differentiate the skin lesions in atopic eczema and psoriasis

A

Atopic eczema not well defined skin lesions

In psoriasis

, the plaques are very well defined

Generally, it is rare for someone to have BOTH atopic eczema and psoriasis.

42
Q

Triggers for psoriasis

How can it be distinguished from athletes foot on the feet

A

It can be triggered by pressure and trauma to areas of skin.

I.e. in the feet on sites of pressure and symmetrical whereas fungal infection would not be

43
Q

Pattern of psoriasis

What are the nail signs for psoriasis. How do you differentiate them from fungal infection nail signs

A

Well defined plaques

Psoriasis is also a very symmetrical condition

NAIL:
Subungual hyperkeratosis

Dystophic nail and loss of cuticle

Onycholysis and pitting

In fungal infection just one or two nails, in psoriasis all of most of them, and these patterns

44
Q

What is guttate psoriasis

A

lots of little, raindrop like lesions on the skin

45
Q

When is guttate psoriasis affecting patients

A
  • This generally affects young people (teenagers), and can occur after a streptococcal sore throat
46
Q

How long does rash last in gutate psoriasis

How is pateint treated

A
  • The rash can persist for weeks or

- We can treat the patient with antibiotics and topical steroids to clear the psoriasismonths

47
Q

T/f there is no relationship between guttate psoriasis and later development of chronc plaque psoriasis

A

F - These patients have a genetic susceptibility – they are more likely to develop chronic plaque psoriasis

48
Q

What is palmoplantar pustolosis

A

This is where, instead of plaques forming on the body, pustules form on the palms of the hands and soles of the feet. The patients are otherwise well, however this can be itchy and sore.

49
Q

What is palmoplantar pustolosis often linked to

A

This must be driven by a different genetic susceptibility. These patients are often smokers, but cessation of smoking doesn’t seem to make it better.

50
Q

What is generalised pustular psoriasis

A

Pustules on a background of inflammation

the condition makes patients very unwell. They are febrile and toxic. They have a high HR, and low BP. They are so unwell that they cannot function.

High mortality without treatment

51
Q

How is generalised poustular psoriasis treated

A

They are treated with immunosuppressants. Patients are also given emollients and topical steroid treatment

52
Q

What does acne affect

A

Pilosebaceous unit

53
Q

Acne development

A

Comedone caused by build up of keratin (hyperkeratinisation, thickening of infundibulum of hair follice), creating a plug

Increased sebum production due to androgenic stimulation

Growth of propionibacteria acnes causing inflammation

Turns into cyst

Inflammatory cells spilling into the dermis (out of the follice), causing even more inflammation

54
Q

Why does acne happens

A

Genetic factors + hormones

55
Q

Differentiate white head and black head

A

White head is teh comidone covered with skin

Blackhead is where there is no skin and you can see dead follicl cells within it

Papules and Nodules and pustules are inflammatory nodules

56
Q

Outline hormonal basis of acne

A

It is driven by hormones (androgenic stimulation causes hypertrophy of sebaceous glands  excess production of sebum).

57
Q

What can be the result of lesion healing

A

Scarring

58
Q

Where is acne most common

A

Where the sebaceous glands are present:

Face neck upper chest

59
Q

What is bullous pemphigoud

A

AI condition… antibody against component of basement membrane… often in elderly

blister forms

60
Q

Why are special proteins required for the epitdermis and the dermis

A

BECAUSE the epitdermis is derived from the ecoderm and the dermis is derived from the mesoderm so you need proteins to hold them toegether via the basement membrane

61
Q

Which proteins are found between the epidermis and the dermis

A

Tonofilaments from epidermis linking to the basement membrane

anchoring fibrils in the dermis linking to basement membrane too

lots of proteins involved

62
Q

Which anitgens are involved in bollous pemphigoid

A

BPAg 1 and BPAg 2

Involved in hemidesmosome

B cells produce produce ABs against them

63
Q

Pathology of bollous pemphigoid

A
  • The BPAg proteins are located on the basement membrane
  • This AI disease has autoantibodies against these proteins. Causes inflammation at the BM zone, and splitting of the epidermis from the dermis
  • This is a deep blister, where the deep blister split is at the location of the basement membrane

(subepidermal blister)

64
Q

Treatment for bollous pemphigoid

A

high dose oral steroids, and other immunosuppressant drugs (methotrexate)

Suppresses formation of autoantibodies and allows skin to recover

Must be maintained for number of years

65
Q

Who does bollous pemphigoid often occur in adn what is the effect

A

In bullous pemphigoid, you get tense blisters.

It is usually an elderly patient in their 70s/80s/90s.

The condition begins with a rash (looks like eczema), followed by the development of blisters.

The blisters progress, and without treatment, they become infected.

Patients can then die from sepsis.

66
Q

What is epidermolysis bullosa

A

IN BULLOUS PEMPHIGOID AND PEMPHIGUS, THERE IS AN AUTO-ANTIBODY ATTACKING THE BP PROTEIN. IF SOMEONE HAS A MUTATION IN ONE OF THE GENES FOR THESE PROTIENS, THEY GET A GENETIC BLISTERING CONDITION, CALLED EPIDERMOLYSIS BULLOSA.

67
Q

Differentiate the blisters in bollous pemphigoid and pemphigus

A

In bullous pemphigoid, the blisters are deep. In pemphigus, the blisters are superficial.

68
Q

What is the protein affected in pehmphigus vulgaris and what is the consequence

A

There is an auto-antibody, but this time it is directed at a component of the desmosomes within the epidermis called DESMOGLEINS 1&3 (especially between stratum spinosum.. the spinous processes in the stratum spinosum are desmosomes)

It causes blisters, but these are much more superficial. Because of this, they break down and flake off ….erosions of skin.

69
Q

Differentite where the split occurs in pemphigoi and pemphigus

A

In pemphigus within the epidermis

In pemphigoid it is between epidermis and dermis

70
Q

What are the causes of pustules on the skin

A

Infection
Psoriasis
Drug reaction

Immuno (5 decks)

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