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: helpline@eczema.org

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: helpline@eczema.org

Helpline: 0870 241 3604