Skin Flashcards
Skin most common conditions:
They are all inflammatory chronic conditions
-Excema
-Psoriasis
-Acne Vulagairs
Skin ?
It acts as a barrier and is impermeable to water
-prevents the loss of moisture and ingress of substances
-protects tissue against thermal and mechanical damage
-shields tissues from UV radiation and infection
-functions as part of thermoregulation
-synthesises vitamin D3 via UV exposure and is a sensory organ
Layers of skin:
1.)Epidermis: formed of multiple layers, contain keratinocytes
2.)Dermis: where sweat glands, hair, air follicles, muscles, sensory neuron’s and blood vessels are. Formed of the papillary layer and reticular layer
3.) Hypodermis: formed by adipose, lobules and ski appendages such as hair follicles, sensory neurones and blood vessels.
Looking inside the eperdermis
STRATUM CORNEUM
The upper most layer, consisting of 20-30 cell layers.
Consists of keratin and horny scales made up of dead keratinocytes.
STRATUM LUCIDUM
Present in skin found in the palms and soles, consisting of 2-3 cells.
STRATUM GRANULOSUM
Containing keratohyalin granules and lamellar granules.
Keratohyalin granules contain a keratin precursors, which aggregate and form bundles.
STRATUM SPINOSUM
8-10 cell layers, containing cells with cytoplasmic processes, such as Langerhans cells (a dendritic cell).
Langerhans cells engulf microorganisms and foreign bodies.
STRATUM BASALE
Consists of mitotically active stem cells that constantly produce keratinocytes.
Cells of the eperdermis:
-Keratinocytes: - originate from the basal layer, produce keratin and responsible for the formation of the epidermal water barrier
- Melanocytes: found in the stratum basal, produce melanin giving skin pigment
-Langerhans cells: found in the stratum spinosum, a dendritic cell, playing a significant role in antigen presentation
-Merkles cells- found in the stratum basal, a mechanoreceptor used in light touch
What is Excema?
A chronic, pruritic, inflammatory skin condition known as atopic dermatitis
Common features of Excema:
generalised skin dryness, early years disease onset, personal or family history and atopic disease (asthma, allergic rhinitis).
Commonly develops in the first year of life but can occur at any age
Eczema and how it can occur
It can occur in one of three ways
1.) genetic- family history, loss of function of filaggrin, variation in phenotypical expression of cytokines
2.)microbiome- S aureus colonisation
3.) epidermal barrier dysfunction- elevated trans epidermal water loss of pH, physical damage and allergic inflammation
Function of keratinocytes:
Become disrupted/reduced presence of natural moisturising factors
Function of corneocytes
This is differentiated keratinocytes, they shrink due to water loss
Function of eperdermis:
It dehydrates, gaps between keratinocytes allow inclusion of irritants
Inflammation occurs propagating pruritis and further disruption of the eperdermis
Management of eczema:
Triggers, complete emollient therapy and flare up therapy
Non pharmacological treatments: education and risk management
Patients need to be educated about the pathophysiology of eczema and factors that provoke it, how to recognise flare up of the condition and how to recognise symptoms and signs of bacterial infections
Give lifestyle advice: consider psychosocial difficulties, avoid extreme hot or cold weather/humidity and irritating clothing like wool, keep nails short and dont use potent soaps and detergents and make sure skin hydration is maitained
Non pharmacological treatments: hydration complete emollient therapy
This is clinically proven to largely reduce the number and severity of Excema flare ups, reduces amount of treatment to stop a treatment by 75%
Topical application of lotions, cream, gels, ointments and oils.
Emollients occlude the disrupted epidermal barrier, therefore reducing dehydration of the epidermis.
Occlusion impedes ingress of irritants and pathogens into the epidermis.
Specific emollients nourish the epidermis with humectants, a synthetic replacement of NMF.
Humectants draw and hold moisture in the epidermis.
The occlusion of complete emollient therapy:
Emollients efficacy dependent on products richness
-depends on patients and richness describes the ratio of aqueous and organic/greasy excipients of a formulation
Richness of complete emollient therapy :
Low richness
Least greasy.
Shorter-lived occlusion time.
Greater patient acceptability.
High richness
Most greasy.
Long lasting occlusion time.
Less patient acceptability.
Humecrants:
Humectants: substance, especially a skin lotion or a food additive, used to reduce the loss of moisture.
Examples of them are; glycerine, glycolic acid, lactic acid, propylene glycol, hyaluronic acid, urea, pantheons, gelatine, sorbitol
Complete emollient therapy process:
1.)Emollient as leave-on product:
4-6 applications per day (every 3 hours)
Emollients should be wiped onto the skin, in the same direction as the hair grows.
Emollients should not be rubbed into the skin.
Patient should use 0.5 Kg – 1 Kg per week, depending on age and severity of their condition.
2.)Emollient as ‘soap’ substitute:
Instead of any soap, handwash or shower gel.
Infers and additional 0.5 Kg of emollient use per month.
3.) Emollient as a bath additive:
Added directly to bath water, or lightly applied and rinsed from the skin during bathing.
Patients should be advised to pat dry, rather than rub dry, their skin after washing.
Infers and additional 0.5 Kg of emollient use per month.
Pharmacological treatments:
It is the management of flares of eczema; topical corticosteroids and calcineurin inhibitors
About topical corticosteroids:
Main stay of treatment for flare-ups of eczema:
Effective
Cheap
Vast clinical experience
Widely used for inflammatory and hyperproliferative disorders.
Different potency treatments available.
Long term use (especially high potency) on large body areas can lead to adrenal suppression.
Other side effects- skin thinning, telangiectasias, folliculitis and contact dermatitis.
Topical corticosteroids inflammation:
Swelling, redness, pain and the later proliferative changes in chronic inflammation.
Mast cells, present in the dermis, are activated in response to inflammation and therefore release histamine.
Lymphocytes in the dermis also generate an inflammatory response.
Following an inflammatory response the genes of the keratinocyte cell produce mRNA which is translated into inflammatory cytokines to further propagate the inflammatory response.
Mechanism of action of topical corticosteroids:
Corticosteroids exert their effects via the glucocorticoid receptor
Glucocorticoid receptors can be present in several forms:
Corticosteroids exert their effect via the α-isoform (interacts with endogenous cortisol) of the glucocorticoid receptors.
High presence of the glucocorticoid receptor β-isoform (regulatory roles) can result in resistance.
Glucocorticoid receptors can be found in most of the cells in of the body.
Glucocorticoid receptors are specifically expressed in the keratinocytes and fibroblasts of the epidermis.
When unoccupied, glucocorticoid receptors are usually present in the cytoplasm.
