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
2
Q
Skin histology basics
A
- stratum cornea
- epidermis (basal cell layer, spinous cell layer, granular layer)
- papillary dermis
- reticular dermis
- hypodermis
3
Q
Skin microanatomy
A
- epidermis
- dermis (reticular dermis underlies the papillary dermis)
- hypodermis/subcutis
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.
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
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
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
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
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.
10
Q
What are the main atopic diseases?
A
- eczema
- asthma
- hayfever
11
Q
Atopic march
A
- develop specific atopies at different times of their life (see slide 14)
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.
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.
14
Q
What is a sign of filagrin gene mutation?
A
palmar hyperlinearity
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
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
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
18
Q
severe eczema
A
- might be febrile
- there is a range in eczema, sometimes it is mild and sometimes it is quite severe
19
Q
What pathogens are eczema patients vulnerable to?
A
- staph aureus
- herpes simplex
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
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
Psoriasis
- 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
Pathogenesis of psoriasis
- too rapid proliferation of keratinocytes- top layer has nuclei in it even though it should not have any
27
Histological features of Psoriasis
- 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
Where does psoriasis occur
- scalp
- around umbilicus
- sometimes genital area
- armpit
- knees
- buttocks
- groin and genitals
- often quite symmetrical
29
Symmetry in dermatology
suggests that it is inflammatory and not e.g. infectious
30
Nails affected by psoriasis
- Subungual hyperkeratosis
- Dystophic nail and loss of cuticle
- onycholysis
- onycholysis and pitting (not many conditions cause this, psoriasis is the main one)
31
What body parts do you inspect in psoriasis?
- look at scalp
- look at nails
- where it itches?
32
Guttate psoriasis
- many papules
- each papule is salmon coloured and small
- often exacerbated by streptococcal infections
=> gutter, like raindrops, psoriasis
33
Palmoplantar pustulosis
- little postures on hands and/or feet
- caused by a different set of genes
- often exacerbated by smoking, stress and obesity
34
Generalised pustular psoriasis
- 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
What are the main causes of pustules?
infection
drug reaction
psoriasis?
36
Acne
- common condition (especially in teenagers)
| - disorder of the hair follicle
37
Acne formation
- 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
Acne cause
- Comedone formation
- Genetic predisposition
- Propionibacteria acnes
- Androgenic stimulation (mostly happens at puberty)
39
Blackhead vs whitehead
blackhead = open comedome
whitehead = closed comedome
40
What are the different forms of acne
- whitehead
- blackhead
- papule
- nodule
- pustule
=> usually there is a combination of these different thing.
41
Treatment for acne
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
Bullous Pemphigoid
- 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
Basement membrane zone
- 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
Epidermolysis Bullosa
- 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
Pemphigus vulgaris
- 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
What is the subcutis?
- it is a different name for the hypodermis
| - adipose rich tissue beneath the dermis
47
How does the terminology for the keratinocyte change as it moves up the epidermis?
basal cell -> prickle cell -> granular cell -> keratin
48
Psoriasis vulgaris
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
Name some subclassifications of psoriasis
- psoriasis vulgaris
- guttate
- palmoplantar
- generalised pustular
- nail psoriasis
50
autoantigen in pemphigus vulgaris
Desmogleins autoantigen in PV
