Advance Skin Analysis - Quick Reference Notes

Melanogenesis

  • Melanocytes produce melanin in melanosomes.
  • Tyrosine in melanosome is converted to melanin by the enzyme tyrosinase.
  • Melanin diffuses through the epidermis, giving skin its colour.

UVR influences in skin, cells and system

  • Increases free radicals.
  • Increases keratinocytes.
  • Increases number of melanosomes.
  • Not increase melanocytes.
  • Oxidises pheomelanin pigment granule.
  • Damages dermal proteins by increasing MMPs.
  • Oxidises vitamin C.
  • Damages DNA.

Post-inflammatory hyperpigmentation (PIH)

  • Result of injury that breaks the dermal/epidermal junction, inflammation, and UV exposure.
  • Pigmentation often follows trauma (infection, allergic reaction, medication, burns, eczema/dermatitis).
  • Common in Fitzpatrick 3-4.
  • Pigmentation can darken with UV exposure or medication.

Dermal vs Epidermal pigmentation

  • Dermal pigment:
    • Inflammation + UV disrupt basal cell layer.
    • Melanin released and trapped by macrophages in the papillary dermis.
    • Pigment remains in dermal area; difficult to remove.
  • Epidermal pigment:
    • Inflammation leads to oxidation of essential fatty acids.
    • Immune cells and melanocytes altered; increased transfer of pigment to keratinocytes.
    • Increased stimulation and transfer of melanin leads to epidermal pigmentation.

Peri-orbital pigmentation

  • Dark circles around the eye area.
  • Common in Asian/Indian/Mediterranean skin; often genetic.

Lipofuscin

  • Brownish pigment with a yellow tinge.
  • Result of breakdown/absorption of damaged blood cells, cellular waste, toxins, free radical activity, and lipid/protein oxidation.
  • Known as aging spots/pigment.
  • Indicates lifestyle and health history.

Poikiloderma

  • Combination of elastin loss, telangiectasia, and pigmentation loss.
  • Affects sides of neck, under chin, and sides of cheek toward ear.
  • Common around 40 years old.
  • Caused by photosensitivity from chronic sun exposure, hormonal imbalances, and possibly fragrances.

Pityriasis rosea

  • Herald patch is the initial lesion.
  • Scaly patches develop 2 weeks later.
  • Rash subsides in 6-14 days.
  • Unknown cause; linked to Herpes virus.
  • More common with seasonal changes (cooler temperatures).
  • Common sites: thighs, trunk, upper arms, neck.
  • Itchiness increases with overheating; treatment includes anti-itch meds, steroids, or UV light therapy.

Essential fatty acid deficiency (EFAD)

  • EFAs produce Prostaglandins, hormone-like substances that regulate body functions.
  • Prostaglandins are vital for immune function and maintain heart rate, blood pressure, blood clotting, and fertility.
  • EFAs/prostaglandins are involved in repair of cell membranes.

EFAD continued

  • Healthy keratinocyte membranes consist of Phospholipids, cholesterol, and glycolipids.
  • Membranes regulate transport of nutrients, waste, and oxygen.
  • Unhealthy membranes accelerate ageing; EFAs are needed to repair membranes.

Secretions: Essential fatty acid deficiency

  • Ceramides (Ceramide-1) support healthy barrier function.
  • Ceramides are key components of the lipid bilayer in the stratum corneum.
  • Ceramide-1 can be obtained from Linoleic acid (Omega-6).
  • Lack of EFAs reduces lipid phase, increasing TEWL.

Identification of EFAD

  • Causes: fat ext{-}free ext{ diets}.
  • Menopausal women may require more EFAs.
  • Skins unresponsive to treatments; eczema; psoriasis; alipidic skins.
  • Review diet and supplementation.

Impaired acid mantle

  • Hydrolipidic film covers skin (water/oil).
  • Oil sits on top of water due to physics.
  • Acid mantle formed by secretions from sweat glands, sebaceous glands, epidermal lipids, and NMF.
  • Microflora in the emulsion form the first line of defense.
  • Fluid intake and ambient humidity influence TEWL.

Advantages of intact acid mantle

  • Microflora maintain low skin pH.
  • Inhibits growth of harmful bacteria.
  • Limited nutrients on skin surface hinder bacterial establishment.
  • Prevents toxin absorption into skin.
  • Primary skin lubricant.
  • Regulates water movement through the epidermis (TEWL).

Dermal enzymes (MMP & MME)

  • MMPs (Matrix Metalloproteinases) / MME (Macrophage Metalloelastase): collagenase and elastase digest proteins.
  • Prevent dermal degradation; healthy dermis requires turnover of collagen/elastin.

TIMPs and balance

  • TIMP (Tissue Inhibitors of Matrix Metalloproteinases) keep MMPs in check.
  • TIMPs decline with age or low free water.
  • UVR increases MMPs, leading to dermal matrix breakdown.
  • Low TIMPs fail to control MMPs; repair slows.

Impaired enzyme activity

  • Identification: epidermal excess keratinization; dermal premature ageing; water phases.
  • Water regulates most enzymatic/chemical reactions.
  • Enzymes are catalysts for minerals/vitamins to enable metabolism.
  • Enzyme activity linked to TEWL; enzymes are pH-sensitive.
  • Skin pH is more acidic near the stratum corneum; optimal enzyme function supports cell shedding.

Causes of impaired enzyme activity

  • Check client fluid intake and humidity.
  • Medications with diuretic effects.
  • Alcohol and coffee increase water needs.
  • Prolonged air conditioning exposure can speed TEWL.

Impaired lymphatic circulation

  • Lymph movement aided by body movement.
  • Balanced hydration supports lymphatic function.
  • Steady lymph flow supports balanced metabolism.
  • Lymphatic and circulatory systems work together.

Lymphatic implications and symptoms

  • Interstitial fluid reaches dermis via circulation.
  • Water is drawn to hyaluronic acid in the dermis.
  • Free water moves to epidermis from the basal layer.
  • Impaired lymph flow harms renewal/repair; wounds heal poorly; waste products poison tissue.
  • Puffy eyes and dark circles indicate poor lymph flow.
  • Hydration and fluid intake (approx. 6-8 glasses daily) support lymph flow.
  • Common causes: jet lag, illness, medications, menopause, fatigue, cold, over-exertion, tension.

Medications affecting the skin

  • Antibiotics: sensitivity, redness, rash, photosensitivity.
  • Antidepressants: sensitivity, redness, rash, photosensitivity, flaking.
  • Thyroid meds: increased photosensitivity.
  • Sleeping tablets: increased sensitivity/reactivity, allergic reactions, swelling.
  • Cortisone: acne/congestion, thinner skin, easy bruising, poor healing; diffuse redness.
  • Insulin: changes in skin feel, thickening.
  • Contraceptive pill: increased sensitivity, breakouts, congestion.
  • Pain killers: reduced barrier function due to lower hydration.
  • Retinoids: thinning, sensitivity.
  • Sinus meds: redness, dehydration.
  • Hydroquinone: increases breakdown of melanosomes as a tyrosinase inhibitor.
  • Roaccutane: slower healing, barrier disruption, photosensitivity.
  • Blood pressure meds: increased photosensitivity; redness, easy bruising.
  • Diuretics: low potassium.

Diagnostic tools

  • Skin analysis equipment: magnifying lamp, Wood’s lamp/black light/Visia skin scanner, digital camera (pictography).
  • Consultation card for progressive use.
  • Your eyes, ears, and fingers as part of assessment.