skin inflammation conditions

Acne vulgaris

• chronic conditions of the pilosebaceous unit

• Affects 80- 90% of adolescents

• It affects the face, chest and back

Onset of acne’s

• hormonal trigger- during adolescence, increased testosterone production

• Genetic influence: overproduction of 5a reductase enzyme in the skin, converting testosterone

Non inflammation stage

• keratin and sebum clog the hair follicles

• Further hyperkeratinisation, and sebum production enlarge the follicle → microcomedone evolves into comedomes

Inflammation and infection stages

• clogged follicles ruptures → triggers inflammatory response

• Sebum overproduction → fuels acne overgrowth

Severity degrees of Acne vulgaris

• fibrous healing: new collagen is deposited to repair deep acne lesions

• Scarring risk: excess or uneven collagen leads to permanent scars

• Early and effective treatment minimise scar formation

Treatment of acne vulgaris- aims and option

• reduce the number and severity of skin lesions and preventing complications

Desired molecular effects

• inhibit follicular hyperproliferation

• Reduced sebum production

• Inhibit C acne’s overgrowth

• Control inflammation and prevent

• Prevent/ clear clogged pores

Treatment

• Adapalene and benzoyl peroxide

• Tretinoin and clindamycin

• Benzoyl peroxide and clindamycin

Benzoyl peroxide

• penetrate the epidermis → converted into benzoin acid and hydrogen peroxide

• Has comedolytic and anti- inflammatory effects

• Hydrogen peroxide release free radicals, damaging and killing C acne’s cells

Retinoids

• penetrate epidermis and slightly the dermis

• Enter keratinocytes → binds to intracellular retinoids acid receptor → acts as transcription factor modulating gene expression to

Topic oral antibiotics

• clindamycin or erythromycin

  • Combined with topical retinoids or benzoyl peroxide

• Oral antibiotics

  • Lymecycline

Azelaic acid

• normalise keratinisation

• Antimicrobial activittt

• Modest anti inflammatory

Psoriasis

• chronic inflammatory skin disease → accelerated skin turnover leading to scaling

  • Immune mediated

  • Not communicable

• Clinical manifestation

  • Well demarcated raised plaques with silvery scales

Over activate keratinocytes

• increased proliferation

• Defective differentiation

• Accelerated keratinocyte turnover

Amplified persistent inflammatory cascade

• abnormal infiltration and activation of T cells

• Abnormal release a leading to chronic inflammations → psoriasis skin lesions

• Formation of new capillaries closer to the surface

Topical emollients and salicylic acid

• moisturise dry skin

• Reduce scaling

• Increase absorption of other topical treatment

Topical vitamin D analogues

• bind to vitamin D intracellular recpetor on keratinocytes

• Reduce keratinocyte proliferation

• Regulate the keratinocytes differentiation turnover

• Mild immunosuppression effect to reduce the relase of inflammatory cytokines

Topical coal tar

• anti proliferative

• Anti inflammatory

• Anti pruritic

Topical dithranol

• penetrates damaged skin and psoriatic lesions faster than healthy skin

• Intracellular drug oxidation- generate in stable free radicals in keratinocytes

• Reducing mitotic activity to regulate the hyperproliferation of keratinocytes

Methotrexate

• a folic aciiiid antagonist inhibits the human dihydrofolate reductase enzyme as suuubstrate analogue the respective bacterial enzyme is targeted by trimethoprim

• It has anti proliferative effects as folic acid is essential to produce purines

• Immunosuppresssive effect on activated T cells