Week 2 - H - Pruritus (Pruritoceptive/Neuropathic/genic/Psychogenic), Dermatitis (contact, atopic, seborrhoeic, venous)

Question 1

What is the definition of pruritus?

Answer 1

Pruritus aka itch is defined as

A usually unpleasant, poorly localised, non-adapting sensation that provokes the desire to scratch

Question 2

There are different classifications for the causes of itch * pruritoceptive * neuropathic * neurogenic * psychogenic Define these classifications of itch and give an example of a condition

Answer 2

* Pruritoceptive itch - something (usually inflammation or dryness) within the skin that triggers itch - eg eczema

* Neuropathic itch - damage to central or peripheral nerves causing itch eg the all over itch some people with multiple sclerosis get or the itch instead of pain some people get following herpes zoster

* Neruogenic itch - no evident damage to nerve tissue but itch caused by CNS effects - eg after opiates

* Psychogenic itch - psychological causes eg itch in delusions of infestation

Question 3

There are different mediators of itch * Chemical mediators * nerve transmission * central nervous system mediators

What are examples from each of these three?

Answer 3

Chemical mediators eg histamine and tryptase

Nerve transmission mediatiors - unmyelinated C fibres

Central nervous system mediators - opiates

Question 4

Time to identify different itchy conditions from a picture

Answer 4

Scalp psoriasis -pruritoceptive itch

Question 5

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Answer 5

This is lichen planus

Pruritic purple planar, poly-angular papules (itchy violaceous flat-topped papules)

Can see the horizontal line showing Koebner’s phenomenon - when lesions arise ina site of trauma

Question 6

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Answer 6

This patient has a scabies infection

To be exact has Norwegian scabies -the highly infectious chronic crusted form of scabies where thousands of mites embed

Question 7

Define hypekeratosis, parakeratosis, acanthosis?

Answer 7

* Hyperkeratosis is the increased thickness of the keratin

* Parakeratosis- persistence of nuceli in the keratin layer

* Acanthosis is the increased thickness of the epidermis

Question 8

What condition discussed in a different set of cards are both hyperkeratosis and parakeratosis seen in?

What else is seen histologically in this condition?

Answer 8

Hyperkeratosis and parakersotis are are seen in the stratum corneum in psoriasis - along wth munro microabscesses (small collections of leucocytes which attract complement causing inflamamtion)

Also there is a thickened stratum spinosum and large capillary vessels within the papillary dermis

Question 9

What is oedema between keratincoytes known as? - this can occur in eczema

Answer 9

Spongiosis - oedema between keratinocytes

Question 10

What is another word for dermatitis? - there are many different types

Try and define eczema (not atopic eczema - just eczema in general)

What are the clinical features?

Answer 10

Dermatitis is also known as eczema

Eczema is an inflammatory skin reaction characterized histologically by spongiosus (oedema) with varying degrees of acanthosis

The clinical features are mainly due to the spongiosus

* The main clinical feature is itching - a rash that is never itchy is unlikely to be dermatitis.

* Other features caused by the spongiosus include redness, scaling and papulo-vesicles

Question 11

Two main classification schemes for eczema are * Time course - acute and chronic * Aetiology based There is an acute phase and a chronic phase in dermatitis

What is seen in acute dermatitis? (histology and clinically)

Answer 11

Acute phase

Definite spongiosus on histology- fluid separating the epidermal cells

ITCH

Papulovesicular rash

Erythematous lesions

Oooze or scaling

Question 12

What is seen in the chronic phase of dermatits?

Answer 12

Chronic dermatitis

Orthokeratotic hyperkeratotis - thickening of the stratum corneum of the epidermis (hyperkeratosis) with non-nucleated keratinocytes retained in this layer.

(Hyperkeratosis with parakeratosis seen in psoriasis)

Also elevated plaques and scaling

Question 13

Discussed the acute and subacute symptoms that can occur in eczema There are many different types of eczema and they can be classified as endogenous or exogenous

What is the difference between endogenous and exogenous eczema and give examples?

Answer 13

Endogenous eczema - due to conditions within the body - eg

* atopic dermaitis or

* seborrhoeic dermatitis or

* stasis dermatitis (venous/varicose eczema)

Exogenous eczema - due to external factors * eg contact dermatitis (irritant or allergic)

Question 14

CONTACT DERMATITIS

The main four types of eczema we shall discuss * Contact dermatitis - exogenous * Atopic dermatitis * Seborrhoeic dermatitis * Stasis dermatitis

What is the difference in the mechanism of irritant and allergic contact dermatitis?

Answer 14

Allergic contact dermatitis is an immune mediated dermatitis due to a delayed (type IV) hypersensitivty reaction to a previously encountered allergen

Irritant contact dermatitis is due to the direct irritant action of a substance on the skin and is common in eg hospital works due to frequent hand washing

Question 15

What is the immunopathology of allergic contact dermatitis?

Answer 15

In allergic contact dermatitis, the langerhans cells in epidermis process the antigen and present it to the lymph nodes in the dermis containing T-helper cells

The T-helper cells then become sensitised and Th1 mediated reaction happens upon re-exposure to the antigen - typically 24-48 hours after reaction

Question 16

What are common allergens causing contact dermatitis and what are the symptoms of the condition?

Answer 16

Common allergens include nickel as seen in trouser buckle, jewellery, watches, chromates in cement and leather, susbtances in gloves

Symptoms usually involved a red itchy rash with papulovesicle formation and oozing/crusting (symptoms replicate acute phase of dermatitis)

Question 17

How do we investigate patients with suspected allergic contact dermatitis?

Answer 17

Gold standard for allergic contact dermatitis is patch testing

Allergens are applied to special chambers and applied to the patients back for 48 hours then removed

Readings are taken at 48 and 96 hours looking for dermatitis-type changes

Question 18

What is the management of allergic contact dermatitis?

Answer 18

Avoidance of the causative allergen

Regular emollients

Topical steroids

Question 19

Irritant contact dermatitis as discussed is due to the direct irritant action of a substance on the skin and is not-immune mediated

What are examples of this? What are the symptoms?

Answer 19

Soap/detergent/cleaning products

Water

Oil

Nappy rash - irritant to urine

Symptoms include erythema, pupulovesicular rash + ozzing/crusting

Difficult to distinguish from allergic contact dermatitis based on clinical features alone

Question 20

What can occur in both irritant and allergic contact dermatitis if prolonged untreated exposure?

Answer 20

The eyrthema and papulovesicles can lead to eventual lichenification (thickening of the skin) and fissuring

Question 21

What is the management of irritant contact dermatitis? What may irritant contact dermaittis often overlap with?

Answer 21

Avoidance of irritants

Use soap substitutes eg dermol 500

Regular emollients

Topical steroids for flare-ups

May overlap with atopic dermatitis

Question 22

ATOPIC DERMATITIS

Multifactorial cause - genetic and environmental factors resulting in inflammation

What other conditions is eczema commonly linked to?

Answer 22

The atopic triad aka the atopic March

* Atopic eczema - usually begins in infancy

* Asthma - usually after 2 years old

* Allergic rhinitis - hayfever - usually later in late child / teen years

Question 23

Atopic eczema is the most common inflammatory skin disease in children

Where does the conditions often start in children vs in older children?

Answer 23

In children, it often starts on the face and extensor surfaces

In older children, it starts in the typical flexural pattern (ante-cubital fossa, popliteal fossa and flexor aspect of wrists)

Question 24

The diagnosis of eczema is a clinical one The diagnostic criteria comes from the symptoms

What is the diagnostic criteria?

Answer 24

ITCH + 3 or more

* Visible flexural rash

* History of flexural rash

* Dry skin

* Onset at less than 2 years old

* Personal history of atopy or first degree relative

* Rash on cheeks and extensor surfaces in infant

Question 25

How would describe the acute lesions as seen in atopic eczema?

Answer 25

Erythematous pruritic rash indicating inflammation

Can also cause the small vesicular rash that oozes and may crust increasing likelihood of pathogenic skin infection

Question 26

Chronic in scratching in atopic eczema can cause different signs What are these?

Answer 26

Excoriations may be seen - scratch marks

Lichenification may occur - exaggeration of normal skin creases caused by thickened skin due to chronic scratching

Also habit scratching

Secondary infection

Question 27

Atopic eczema can affect both the child (keeping awake at night) and the parents (having to wake a night due to child)

Secondary infection in eczema is common What would indicate this? What is the common pathogen? What is the treatment?

Answer 27

Secondary infection would be indicated by crusting of the skin

Usually caused by a staph aureus infection

Treatment is usually topical fusidic acid or oral flucloxacillin

Question 28

What is the infection known as when the herpes simplex virus affects previous areas of eczema? How are the lesions described here?

Answer 28

This is known as eczema herpeticum

Rememeber monomoprhic punched-out lesions

Question 29

Mutation in which gene increases the likelihood of atopy? What is the purpose of this gene?

Answer 29

Mutations in the filaggrin gene are linked to an increase in atopy (atopic eczema, asthma and hayfever)

Filaggrin is a protein found in the granaular layer of the epidermis and is very important in helping the terminal differentation of the keratinocytes

This is allows the stratum corneum to form which is the main outer cutaneous barrier

Question 30

If there is a mutation in the filagrin gene preventing terminal differentiation of the keratinocytes therefore impairing the function of the stratum corneum, how can this cause eczema?

Answer 30

Normal barrier function

* Prevents water loss - therefore impaired function results in dry skin

* Prevents entry of infectious agents, irritants and allergens - impaired function results in likelihood of eczema

Question 31

What is the allergic response that causes the IgE production as seen in atopic individuals?

Answer 31

Atopic individuals may have overactive Th2 lymphocytes which releases different inflammatory cytokines

IL-4 released from TH2 cells causing B cell maturation into IgE cells

Question 32

What tests can be done to test for immediate hypersensitivityes that are linked to eczema? (eg due to food allergic or latex allergy) What type of hypersensitivty is atopic eczema?

Answer 32

Tests for immediate hypersensitivity (type 1) is usually skin prick testing followed by RAST (radioallergosorbent testing) testing if skin prick fails

Atopic eczema is type IV hypersensitivity reaction - T cell mediated

Question 33

What is the management of eczema?

Answer 33

Cotton clothes and bedding

Emollients (moisturisers) used at least twice a day are advised to prevent drying and itchy of the skin

Daily steroids for active sites

• * Hydrocortisone 1% for mild eczema
• * Clobetasone butyrate 0.05% for moderate (eumovate)
• * Bethametasone valerate 0.1% for severe (betnovate)
• * Clobetasol proprionate 0.05% for very severe (dermovate)

Question 34

If the emollients and steroids fail to treat eczema What is second line therapy? - paritcularly used if having to use potent/very potent sterois for prolonged periods of time

Answer 34

Calcineurin inhibitors eg tacrolimus

Phototherapy - mainly UVB or immunosuppresants are usually last line options given by dermatologists

Question 35

What is seborrhoeic dermatitis? How does it present? (where is affected) What causes it?

Answer 35

Seborrhoeic dermaitits is a common long-term skin disorder affecting areas of the sin that are rich in sebaceous glands

Typically causes red, scaly rash affecting the scalp (dandruff), eyebrows, nasolabial folds, cheeks and flexures

It is caused by the overgrowth of skin yeasts (eg malassezia)

Question 36

What is the treatment of seborrhoeic dermatitis?

Answer 36

Mild topical steroid creams/antifunggals are usually given to treat seborrhoeic dermatitis eg daktacort (hydrocortisone and miconaole) or ketaconazole

Question 37

What is one of the common causes of severe seborrhoeic dermatitis presentations?

Answer 37

HIV

Question 38

What is venous dermatitis also known as? Who does it typically present in?

Answer 38

Venous dermatitis aka stasis eczema aka varicose eczema

Typically occurs in patients with a chronic venous insufficiency

Question 39

What is the presentation of venous eczema and why does chronic venous insufficiency cause it?

Answer 39

Chronic venous insufficiency causes an increase in hyrodstatic pressure (pressure pushing out of the veins) causing the vens to leak causing oedema

This can lead to the dry, flaky and itchy skin seen in venous eczema

Question 40

Photosensitive eczema is a condition where a subject’s skin becomes inflamed due to a reaction to sunlight or artificial light. What is this also known as? What is the typical feature where the eczema stops known as?

Answer 40

Photosensitive eczema is also known as chronic actinic dermatitis aka photodermatitis

There is a typical ccut-off at the patients collar as this is not exposed to the sunlight