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Year 2 - MCD - Immunology > 5 - Inflammatory Dermatoses (27.02.2020) > Flashcards

5 - Inflammatory Dermatoses (27.02.2020) Flashcards

1
Q

Stats re skin disease

A
  • 20% consultations in GP
  • Under represented in curriculum
  • Overlaps with many specialties
  • Largest organ (16% body mass, 1.8m2 surface area)
  • Clinical skills paramount in diagnosis
  • Over 2000 diseases affect the skin
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2
Q

Skin histology basics

A
  • stratum cornea
  • epidermis (basal cell layer, spinous cell layer, granular layer)
  • papillary dermis
  • reticular dermis
  • hypodermis
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3
Q

Skin microanatomy

A
  • epidermis
  • dermis (reticular dermis underlies the papillary dermis)
  • hypodermis/subcutis
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4
Q

Difference between hair bearing and non-hair bearing skin

A
  • look similar but one has hair follicles as well as sebaceous glands and sweat glands.
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5
Q

Sweat gland types

A

Eccrine:

  • occur over most of the body and open directly into the surface of the skin
  • not smelly

Apocrine:

  • open into the hair follicle, leading to the surface of the skin.
  • apocrine glands develop in areas abundant in hair follicles such as scalp, armpits and groin
  • smelly
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6
Q

How do keratinocytes change as they move up the membrane?

A
  • at the stratum basale there are dividing keratinocytes (stem cells)
  • stratum spinosim: there are connections between the cells
  • stratum granulosum: keratin granules in cells-
  • on top there are dead, nuclear keratinocytes
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7
Q

How do keratinocytes change as they move up the membrane?

A
  • at the stratum basale there are dividing keratinocytes (stem cells)
  • stratum spinosim: there are connections between the cells
  • stratum granulosum: keratin granules in cells
  • on top there are dead, nuclear keratinocytes

basal cell -> prickle cell -> granular cell -> keratin

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8
Q

Structure of the stratum corneum

A
  • there is ‘‘glue’’ between the cells (lipid between keratinocyte)
  • very important for the barrier function of the skin
    Defects lead to eczema
  • Filagrin gene mutation common in eczema patients
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9
Q

Atopic eczema

A
  • Atopy – tendency to develop hypersensitivity
  • Atopic diseases - eczema, asthma, hayfever
  • Atopic eczema – common, relapsing and remitting
  • there is a defective barrier of the skin.
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10
Q

What are the main atopic diseases?

A
  • eczema
  • asthma
  • hayfever
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11
Q

Atopic march

A
  • develop specific atopies at different times of their life (see slide 14)
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12
Q

Pathophysiology of atopic eczema

A
  • intrinsic factors lead to defects in the epidermal skin barrier (e.g. filargrin gene mutation)
  • extrinsic factors: penetration of exogenous agents e.g. allergens such as HDM, irritants such as detergents in soaps or pathogens e.g. staphylococcus
  • this causes recognition by CD4+ T-cells
  • there is mast cell degranulation and histamine release

Acute AD: CD4+ T-cells and the Th2 immune response

Chronic AD: CD4+ and CD8+ T-cell activation and Th1 response.

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13
Q

What is palmar hyper linearity a sign of?

A
  • sign of filagrin gene mutation
  • of someone has this and itchy skin they are quite likely to have eczema
  • quite common, a lot of people with eczema will have this.
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14
Q

What is a sign of filagrin gene mutation?

A

palmar hyperlinearity

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15
Q

Infantile atopic eczema

A
  • reddish, crusty skin
  • poorly defined, eroded, inflamed eczema
  • often not immediately around the mouth
  • pattern of eczema changes with age
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16
Q

Common sites of eczema outbreaks

A
  • changes with age
  • infants: face, elbows, knees
  • children: feet, posterior leg, hands and arms, neck, face, scalp
  • adults: neck, cubital region, behind the knees, hands, face, torso, legs but anterior knee spared also gluteal region and feet spared
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17
Q

Chronic eczema

A
  • Eczema with lichenification (chronic changes) -> thick, leathery skin usually as a result of scratching and rubbing -> this causes hypertrophied skin
  • cut off between healthy and involved skin is not clear
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18
Q

severe eczema

A
  • might be febrile

- there is a range in eczema, sometimes it is mild and sometimes it is quite severe

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19
Q

What pathogens are eczema patients vulnerable to?

A
  • staph aureus

- herpes simplex

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20
Q

Eczema herpeticum

A
  • herpes simplex virus can enter and spread around the skin (usually in humans without eczema only in mouth and genital region)
  • > give steroids
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21
Q

Name the types of eczema

A
  • acute (CD4+ Th2 reaction)
  • chronic (CD4+ and CD8+, Th1 reaction)
  • eczema with lichenification (associated with chronic changes due to scratching and rubbing that cause hypertrophy of the skin and make it leathery)
  • infantile (in children)
  • ## seborrhoeic eczema
22
Q

Seborrhoeic eczema

A
  • microorganisms such as yeast, that live naturally on the skin, contribute to it
  • like dandruff
  • around the nose, around the eyebrows, chest, back
  • tends to come back at times of stress
  • papers on the body where there are a lot of oil-producing (sebaceous) glands.
  • most commonly affects adults between 30-60 as well as infants under 3 months.
23
Q

Allergic contact dermatitis

A
  • patient sensitised to particular antigens (e.g. cosmetics, hairdye (contains PPD) can also be found in henna)
24
Q

Discoid eczema

A
  • disk like pattern of eczema
  • e.g. on legs.
  • in people that overwash (e.g. shower every day)
  • especially adults that get older, skin gets drier, not as much lipid
  • avoid soap
25
Q

Psoriasis

A
  • plaque like lesions
  • well defined, there is a clear cut-off between involved and not involved skin
  • salmon pink colour
  • patient needs to have genetic susceptibility (there are many genes)
  • may be genetic susceptibility and triggers (e.g. stress, alcohol, smoking, certain drugs (lithium, antimalarial medication, beta blockers) and also infections e.g. streptococcus -> removing tonsils can help with psoriasis
26
Q

Pathogenesis of psoriasis

A
  • too rapid proliferation of keratinocytes- top layer has nuclei in it even though it should not have any
27
Q

Histological features of Psoriasis

A
  • Hyperkeratosis (thickening of the stratum corneum)
  • Parakeratosis (retention of nuclei in the stratum corneum)
  • Acanthosis (thickening of the stratum spinosum in the epidermis)
  • Inflammation (neutrophils in the epidermis, lymphocytes in the dermis)
  • Dilated blood vessels
28
Q

Where does psoriasis occur

A
  • scalp
  • around umbilicus
  • sometimes genital area
  • armpit
  • knees
  • buttocks
  • groin and genitals
  • often quite symmetrical
29
Q

Symmetry in dermatology

A

suggests that it is inflammatory and not e.g. infectious

30
Q

Nails affected by psoriasis

A
  • Subungual hyperkeratosis
  • Dystophic nail and loss of cuticle
  • onycholysis
  • onycholysis and pitting (not many conditions cause this, psoriasis is the main one)
31
Q

What body parts do you inspect in psoriasis?

A
  • look at scalp
  • look at nails
  • where it itches?
32
Q

Guttate psoriasis

A
  • many papules
  • each papule is salmon coloured and small
  • often exacerbated by streptococcal infections

=> gutter, like raindrops, psoriasis

33
Q

Palmoplantar pustulosis

A
  • little postures on hands and/or feet
  • caused by a different set of genes
  • often exacerbated by smoking, stress and obesity
34
Q

Generalised pustular psoriasis

A
  • extensive involvement of the skin with little postules
  • here you have to think: is it infectious, drug reaction or psoriasis?
  • contain neutrophils but are sterile, there is no infection inside
  • febrile, malaise,
35
Q

What are the main causes of pustules?

A

infection
drug reaction
psoriasis?

36
Q

Acne

A
  • common condition (especially in teenagers)

- disorder of the hair follicle

37
Q

Acne formation

A
  • buildup of debris/keratin in the pore
  • there is a buildup of dead cells and sebum below it
  • there is also proliferation of bacteria
  • a pimple on the skin surface is formed
  • rupture of the follicular canal
  • pus goes into dermis
  • inflammatory reaction
38
Q

Acne cause

A
  • Comedone formation
  • Genetic predisposition
  • Propionibacteria acnes
  • Androgenic stimulation (mostly happens at puberty)
39
Q

Blackhead vs whitehead

A

blackhead = open comedome

whitehead = closed comedome

40
Q

What are the different forms of acne

A
  • whitehead
  • blackhead
  • papule
  • nodule
  • pustule

=> usually there is a combination of these different thing.

41
Q

Treatment for acne

A

Ladder:

  • things to sterilise the skin
  • topical antibiotics, also have a direct anti-inflammatory cells
  • OCP in females can help reduce testosterone effects
  • oral ABs
  • the one drug that can cause depression in some (isotretinoin) -> very effective for severe acne
42
Q

Bullous Pemphigoid

A
  • causes blistering
  • the split is the skin is slightly deeper
  • tense blisters (bullae, can grow quite big and may have a reddish/purpleish colours they may contain blood)
  • B-cell make AB, causes splitting of the level above the BM
  • occurs in elderly patients (above 60)
  • needs to be treated with systemic steroids (less AB production)
  • dangerous if not treated
43
Q

Basement membrane zone

A
  • specialised area
  • epidermis is derived from ectoderm
  • dermis is derived from mesoderm
  • > 2 structures from different embryological origins are stuck together
  • there are specialised proteins involved sticking them together.
  • e.g. tonofilaments and anchoring fibers
  • if any of these proteins are genetically defected or there are autoantibodies against them, this causes problems.
44
Q

Epidermolysis Bullosa

A
  • there is a number of different forms
  • this is a genetic condition
  • if any of the proteins is defective (from slide 48) the skin shears off.
  • ranges from very severe to relatively mild.

= group of rare inherited skin disorders causing fragile skin. Any trauma or friction may cause painful blisters.

45
Q

Pemphigus vulgaris

A
  • slightly superficial
  • intercellular connections between keratinocytes
  • autoantibody against proteins that connect keratinocytes
  • rarer
  • more likely to occur in people with asian heritage than caucasians
  • different age group
  • treatment: oral steroids = systemic immunosuppression
  • without treatment risk of death is around 80-90%
  • with treatment around 10%
46
Q

What is the subcutis?

A
  • it is a different name for the hypodermis

- adipose rich tissue beneath the dermis

47
Q

How does the terminology for the keratinocyte change as it moves up the epidermis?

A

basal cell -> prickle cell -> granular cell -> keratin

48
Q

Psoriasis vulgaris

A

soles Well-demarcated, erythematous plaques with thick, yellowish scale and desquamation on sites of pressure arising on the plantar feet; similar lesions were present on the palms.

Not fungal because it is so symmetrical.

49
Q

Name some subclassifications of psoriasis

A
  • psoriasis vulgaris
  • guttate
  • palmoplantar
  • generalised pustular
  • nail psoriasis
50
Q

autoantigen in pemphigus vulgaris

A

Desmogleins autoantigen in PV

Year 2 - MCD - Immunology (5 decks)

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