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Summary30 annotations on 6 pages by Alan Campbell x19 x11
19/08/2015
6
eg nickle, fragrance, preservatives
Photosensitive dermatitis
Also called chronic actinic dermatitis
> 50 year old, more common in men
Exposure to sunlight (ultraviolet radiation), worse in summer
How to make the diagnosis?
Clinical diagnosis
Endogenous: IgE, RAST (radioallergosorbent testing – not specific)
Exogenous: patch test
Skin Biopsy
Skin pathology -glossary
HyperkeratosisIncrease in thickness of the stratum corneum for the site
Due to:
Reduced shedding
Ichthyoses, squamoproliferative lesions
Increased proliferation
Inflammation, excoriation, squamoproliferative lesions
#1 p. 6
19/08/2015
7
ParakeratosisNucleated cells in the stratum corneum
Increased proliferation, abnormal maturation
Excoriation, chronic inflammation, HPV infection, dysplasia
May be a diagnostic clue
Psoriasis (confluent), pityriasis rosea (mounds), seborrhoeic dermatitis (perifollicular)
Acanthosis
Epidermal hyperplasia
Increased proliferation for any reason
Different patterns e.g:
Psoriasiform
Pseudoepitheliomatous
#2 p. 7
19/08/2015
7
ParakeratosisNucleated cells in the stratum corneum
Increased proliferation, abnormal maturation
Excoriation, chronic inflammation, HPV infection, dysplasia
May be a diagnostic clue
Psoriasis (confluent), pityriasis rosea (mounds), seborrhoeic dermatitis (perifollicular)
Acanthosis
Epidermal hyperplasia
Increased proliferation for any reason
Different patterns e.g:
Psoriasiform
Pseudoepitheliomatous#3 p. 7
19/08/2015
8
SpongiosisIntercellular oedema of the epidermis
Separation of the keratinocytes
Desmosomes (prickles) become easily visible
Eventually result in collections of intraepidermal fluid (vesicle)
Typical of spongiotic dermatitis:Contact dermatitis
eczema
ExocytosisMovement of inflammatory cells through the epidermis
Usually associated with spongiosis
Generally lymphocytes but also eosinophils and others
No associated epidermal damage
NOT:
Interface dermatitis (keratinocyte cell death)
Epidermotropism (lymphocytes homed to basal epidermis)
Spongiotic dermatitisIntraepidermal intercellular oedema
Neutrophilic
acute contact dermatitis
Eosinophilic
Contact dermatitis
Atopic eczema
Follicular
Seborrhoeic dermatitis
Miliarial (acrosyringial)
Miliaria rubra
Spongiotic dermatitisAcute
Spongiosis
Vesiculation
Acute on chronic inflammation
Subacute
Hyperkeratosis, parakeratosis
Mild hyperplasia
Focal spongiosis
Lymphocyte exocytosis
ChronicLichen simplex chronicus
•Hyperkeratosis, parakeratosis
•Psoriasiform hyperplasia
•Papillary dermal fibrosis
•Perivascular chronic inflammation
#4 p. 8
19/08/2015
8
SpongiosisIntercellular oedema of the epidermis
Separation of the keratinocytes
Desmosomes (prickles) become easily visible
Eventually result in collections of intraepidermal fluid (vesicle)
Typical of spongiotic dermatitis:Contact dermatitis
eczema
ExocytosisMovement of inflammatory cells through the epidermis
Usually associated with spongiosis
Generally lymphocytes but also eosinophils and others
No associated epidermal damage
NOT:
Interface dermatitis (keratinocyte cell death)
Epidermotropism (lymphocytes homed to basal epidermis)
Spongiotic dermatitisIntraepidermal intercellular oedema
Neutrophilic
acute contact dermatitis
Eosinophilic
Contact dermatitis
Atopic eczema
Follicular
Seborrhoeic dermatitis
Miliarial (acrosyringial)
Miliaria rubra
Spongiotic dermatitisAcute
Spongiosis
Vesiculation
Acute on chronic inflammation
Subacute
Hyperkeratosis, parakeratosis
Mild hyperplasia
Focal spongiosis
Lymphocyte exocytosis
ChronicLichen simplex chronicus
•Hyperkeratosis, parakeratosis
•Psoriasiform hyperplasia
•Papillary dermal fibrosis
•Perivascular chronic inflammation
#5 p. 8
19/08/2015
9
Subacute spongiotic dermatitis
Lichen simplex chronicus
Treatment
Triggers
Infection
Emollients
Steroids
Emollients
Aim to retain barrier function
water in
pathogens and irritants out
#6 p. 919/08/2015
10
Emollients
Moisturising bath oil
Soap substitute
Moisturising cream (contains preservatives) or ointment at least twice daily
Topical steroids
Reduce inflammation & itch
Anti-inflammatory
Immunosuppressive
Vasoconstrictive
Topical steroids: 4 strengths
MildModerate
Potent
V. PotentHydrocortisone 1%
Eumovate
BetnovateElocon
Dermovate
Side effects
Skin thinning
Striae
(Systemic absorption)
Pruritus, soreness
Sleep
Growth
Development
Social functioning, school absence, low self esteem, family impact
Infection
How to use
Safe if used appropriately
Need to use enough to control eczema
1 finger tip unit = area of 2 palms
Pro-active vs reactive treatment
Intermittent/ once daily use
#7 p. 10
19/08/2015
10
Emollients
Moisturising bath oil
Soap substitute
Moisturising cream (contains preservatives) or ointment at least twice daily
Topical steroids
Reduce inflammation & itch
Anti-inflammatory
Immunosuppressive
Vasoconstrictive
Topical steroids: 4 strengths
MildModerate
Potent
V. PotentHydrocortisone 1%
Eumovate
BetnovateElocon
Dermovate
Side effects
Skin thinning
Striae
(Systemic absorption)
Pruritus, soreness
Sleep
Growth
Development
Social functioning, school absence, low self esteem, family impact
Infection
How to use
Safe if used appropriately
Need to use enough to control eczema
1 finger tip unit = area of 2 palms
Pro-active vs reactive treatment
Intermittent/ once daily use
#8 p. 10
19/08/2015
11
Treatments
If infected:
Anti-Staph oral antibiotic
Combination of topical steroid & antibiotic (e.g. Fucidin H / Fucibet)
Should be used < 2 weeks to prevent bacterial resistance
Treatments Bandages :
Prevent scratching & retain moisture. Increase steroid penetration.
Exacerbate infection
Sedative antihistamines: help sleep (?itch)
Complementary therapies: “natural” or “herbal” are not necessarily safe
Habit reversal
Topical calcineurin inhibitors
Immunomodulators : block inflammatory cascade by pathologic T cells
2 available (tacrolimus, pimecrolimus)
Not licensed <2 years old
Do not cause skin thinning
Main side effect: burning
Long term safety still awaited
Treatments
• If severe:
• Hospital treatments:
Ultra-violet light treatment
Immuno-suppressants (e.g. methotrexate, azathioprine, ciclosporin)
Summary
Common and significant impact
Control not cure
Are there allergens/ irritants
Is it infected
Emollients and appropriate topical steroid
Free advice / informationNational eczema society
Website: www.eczema.org
E-mail: [email protected]
Helpline: 0870 241 3604
#9 p. 11
19/08/2015
1
Eczema Dr Julia Gass, Consultant Dermatologist
Dr Ed Rytina, Consultant HistopathologistAddenbrooke’s Hospital, Cambridge
OutlinePathophysiology
Different types of eczema
Exacerbating factors
Management
What is eczema?Eczema = dermatitis
Dry
Itchy
Inflamed/ red
Skin barrier abnormality/ susceptibility to infection
Who gets eczema?20% people have eczema at some time
All age groups can be affected; atopic eczema usually starts in early childhood
Eczema is not contagious
Pathophysiology
Inflammatory skin reaction
Immunologically mediated (increased Th2 cells and interleukins)
Decreased skin barrier molecules (eg ceramide lipids)
What happens in eczema?
Breakdown of skin barrier
Moisture escapes
Skin becomes dry and brittle
Irritants and bacteria can penetrate
Red, inflamed, itchy
19/08/2015
2
Why does eczema happen?• Complex
Genetic: loss of function mutation in Filaggrin gene (skin barrier function)
Environmental triggers
Combination/ interaction of above
Types of eczema
Endogenous (internal factors)
Atopic eczema
Discoid eczema
Pompholyx eczema
Asteatotic eczema
Seborrhoeic dermatitis
Gravitational eczema
Exogenous (external factors)
•Contact dermatitis
•Photosensitive dermatitis
Types of eczema
Atopic Eczema
Why is atopic eczema important?Most common inflammatory disease of early childhood
Affects 20% of children under 5 (UK); 2% adults
Serious effect on QoL/ sleep/ schooling/ family
First step in the atopic march (followed by food and respiratory allergies)
Associations
Often a family history of atopy (hayfever, asthma, rhinitis)
Associated personal atopy- risk of eczema 30-50%
Affected parent(s)- risk 60-80%
19/08/2015
3
• face and scalp (infants) Trunk (crawlers)
Distribution with age
flexures (child)lichenification and excoriation
Natural History
Flares up intermittently
50% spontaneous remission by school age
70% spontaneous remission by puberty
50% flare as adult
What can worsen it?Soaps/ preservatives/ wool/ detergents/ perfumes
Create inflammation, irritation
1. Contact Irritants
HDM, pollen, animal dander
Cause peripheral eosinophilia and raised IgE
Increased release of vascular mediators stimulating cutaneous inflammation
Seasonal flares
Associated asthma or seasonal rhinitis
2. Aeroallergens 3. Scratching
Vicious cycle
19/08/2015
4
4. Bacterial Infection
Staph Aureus
Yellowish crust, weepy, sore
5. Viral infectionsHSV (eczema herpeticum)
Sore; punched out erosions; unwell
6. Diet
Role in infants: egg/ cow’s milk protein
Food allergy may co-exist, without causality
Associated gut dysmotility (colic, vomiting, bowel habit)
Failure to thrive
7. Other
Stress
Temperature
Discoid eczemaAny age
Equal gender incidence
May occur in children as part of atopic eczema
Round, well defined
Very itchy. Tends to relapse
Seborrhoeic dermatitis
Any age group
Yellowish oily scale, scalp often affected
Babies: -cradle cap
-skin creases
19/08/2015
5
Adults- eyebrows, around nose, blepharitis, hairline
- Inflammatory reaction to yeast (Malassezia furfur)
Gravitational eczema(=varicose/ stasis eczema)
Occurs with venous stasis and blood pooling
On legs, associated with leg ulcers
Chronic course
Pompholyx eczema
Blistering (vesicles) affecting hands & feet
Initially tiny deep vesicles- crack- crust
Intensely itchy
Intermittent flares
Aggravated by irritants
Asteatotic eczema
Common in winter, elderly
Legs, arms, (trunk)
Dry cracked skin (crazy paving)
Contact dermatitis• Irritant
Very common
Quick onset
No previous exposure
Any age group
Allergic
•Less common
•Slow onset (48hrs)•Previous (multiple) exposure•Often after teenage
19/08/2015
6
eg nickle, fragrance, preservatives
Photosensitive dermatitis
Also called chronic actinic dermatitis
> 50 year old, more common in men
Exposure to sunlight (ultraviolet radiation), worse in summer
How to make the diagnosis?
Clinical diagnosis
Endogenous: IgE, RAST (radioallergosorbent testing – not specific)
Exogenous: patch test
Skin Biopsy
Skin pathology -glossary
HyperkeratosisIncrease in thickness of the stratum corneum for the site
Due to:
Reduced shedding
Ichthyoses, squamoproliferative lesions
Increased proliferation
Inflammation, excoriation, squamoproliferative lesions
19/08/2015
7
ParakeratosisNucleated cells in the stratum corneum
Increased proliferation, abnormal maturation
Excoriation, chronic inflammation, HPV infection, dysplasia
May be a diagnostic clue
Psoriasis (confluent), pityriasis rosea (mounds), seborrhoeic dermatitis (perifollicular)
Acanthosis
Epidermal hyperplasia
Increased proliferation for any reason
Different patterns e.g:
Psoriasiform
Pseudoepitheliomatous
19/08/2015
8
SpongiosisIntercellular oedema of the epidermis
Separation of the keratinocytes
Desmosomes (prickles) become easily visible
Eventually result in collections of intraepidermal fluid (vesicle)
Typical of spongiotic dermatitis:Contact dermatitis
eczema
ExocytosisMovement of inflammatory cells through the epidermis
Usually associated with spongiosis
Generally lymphocytes but also eosinophils and others
No associated epidermal damage
NOT:
Interface dermatitis (keratinocyte cell death)
Epidermotropism (lymphocytes homed to basal epidermis)
Spongiotic dermatitisIntraepidermal intercellular oedema
Neutrophilic
acute contact dermatitis
Eosinophilic
Contact dermatitis
Atopic eczema
Follicular
Seborrhoeic dermatitis
Miliarial (acrosyringial)
Miliaria rubra
Spongiotic dermatitisAcute
Spongiosis
Vesiculation
Acute on chronic inflammation
Subacute
Hyperkeratosis, parakeratosis
Mild hyperplasia
Focal spongiosis
Lymphocyte exocytosis
ChronicLichen simplex chronicus
•Hyperkeratosis, parakeratosis
•Psoriasiform hyperplasia
•Papillary dermal fibrosis
•Perivascular chronic inflammation
19/08/2015
9
Subacute spongiotic dermatitis
Lichen simplex chronicus
Treatment
Triggers
Infection
Emollients
Steroids
Emollients
Aim to retain barrier function
water in
pathogens and irritants out
19/08/2015
10
Emollients
Moisturising bath oil
Soap substitute
Moisturising cream (contains preservatives) or ointment at least twice daily
Topical steroids
Reduce inflammation & itch
Anti-inflammatory
Immunosuppressive
Vasoconstrictive
Topical steroids: 4 strengths
MildModerate
Potent
V. PotentHydrocortisone 1%
Eumovate
BetnovateElocon
Dermovate
Side effects
Skin thinning
Striae
(Systemic absorption)
Pruritus, soreness
Sleep
Growth
Development
Social functioning, school absence, low self esteem, family impact
Infection
How to use
Safe if used appropriately
Need to use enough to control eczema
1 finger tip unit = area of 2 palms
Pro-active vs reactive treatment
Intermittent/ once daily use
19/08/2015
11
Treatments
If infected:
Anti-Staph oral antibiotic
Combination of topical steroid & antibiotic (e.g. Fucidin H / Fucibet)
Should be used < 2 weeks to prevent bacterial resistance
Treatments Bandages :
Prevent scratching & retain moisture. Increase steroid penetration.
Exacerbate infection
Sedative antihistamines: help sleep (?itch)
Complementary therapies: “natural” or “herbal” are not necessarily safe
Habit reversal
Topical calcineurin inhibitors
Immunomodulators : block inflammatory cascade by pathologic T cells
2 available (tacrolimus, pimecrolimus)
Not licensed <2 years old
Do not cause skin thinning
Main side effect: burning
Long term safety still awaited
Treatments
• If severe:
• Hospital treatments:
Ultra-violet light treatment
Immuno-suppressants (e.g. methotrexate, azathioprine, ciclosporin)
Summary
Common and significant impact
Control not cure
Are there allergens/ irritants
Is it infected
Emollients and appropriate topical steroid
Free advice / informationNational eczema society
Website: www.eczema.org
E-mail: [email protected]
Helpline: 0870 241 3604