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The Skin > Changes In Skin Colour > Flashcards

Changes In Skin Colour Flashcards

1
Q

Determinants of skin colour

A

Exogenous pigments
- introduced from outside (injection/ingestion)
Endogenous pigments
- produced within (melanin & breakdown of Hb)

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2
Q

Exogenous pigments

A

Carotenoderma
- consumption of large amounts of fruit/ veg high in beta-carotene eg: carrot, sweet potato & pumpkin
Tattoos
Ingestion of certain heavy metals eg: blue/black pigment at gum margin

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3
Q

Endogenous pigments

A

Melanin
- determinant = skin colour
- brown pigment produced by melanocytes (pigment producing cells)
- skin, choroid of eye, hair, mucous membranes & meninges
Pigments from haemaglobin breakdown
- bilirubin
- haemosiderin

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4
Q

Melanocytes

A
  • dendritic cells in basal layer of epidermis
  • intracytoplasmic organelles = melanosomes
  • melanosomes = site of melanin synthesis, deposition & transportation to keratinocytes
  • Epidermal melanin unit = association of 1 melanocyte with 30-40 surrounding keratinocytes to which transfers melanosomes
  • darkly & lightly pigmented skin = same number of melanocytes
    Dark = increased melanocytes activity, larger melanosomes - more melanin
    Light = decreased melanocytes activity, smaller melanosomes - less melanin
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5
Q

Melanin bio synthetic pathway

A
  1. Tyrosine (amino acid) (=metabolized by enzyme tyrosinase to = DOPA, further metabolised form DOPAquinone
    TYROSINASE (key regulatory enzyme = controls initial biochemical reactions , no = no melanin)
  2. Dihydroxyphenylalanine
    TYROSINASE
  3. DOPAquinone
    SERIES OF REACTIONS
  4. melanin
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6
Q

Immediate pigmentary darkening

A
  • follows exposure to UVA radiation
  • Within minutes & fades over 20-30min
  • oxidation of pre-existing melanin/ melanin precursors
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7
Q

Delayed tanning

A
  • follow exposure to UVB & UVA radiation
  • visible within 24-72hrs of exposure to UVB/UVA
  • new pigment formation via increase in tyrosinase activity
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8
Q

Single exposure to UVR (cellular level)

A
  • increase size of melanocytes observed
  • increased tyrosinase activity
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9
Q

Repeated exposure to UVR (cellular level)

A
  • increase number of melanosomes transferred to keratinocytes
  • increased number of active melanocytes
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10
Q

Vitiligo

A
  • acquired multifactorial disorder = autoimmune destruction of melanocytes
  • depigmented macules & patches in localized/ generalized distribution
  • areas of skin affected = absence of functional melanocytes
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11
Q

Vitiligo Pathogenesis

A
  • multi factorial
  • autoimmunity
  • genetics
  • oxidative stress
  • environmental factors (exposure to chemicals)
  • melanocytes detachment from BM
  • neural hypothesis (nerve ending near pigment cells in epidermis, release cytotoxic neurochecmical mediators = melanocyte destruction)
  • “convergence theory” (multiple mechanisms = melanocyte destruction & loss)
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12
Q

Autoimmunity (vitiligo Pathogenesis)

A
  • associated autoimmune diseases: Hashimoto’s thyroiditis, Graves’ disease, TiDM, RA, Alopecia areata, Addison’s disease
  • immune system = central role in Pathogenesis
  • numerous activated cytotoxic T lymphocytes = perilesional area of vitiligo skin (mainly cytotoxic CD8 lymphocytes)
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13
Q

Autoimmunity process(vitiligo Pathogenesis)

A
  1. Genetic factors, environmental exposures
  2. Melanocytes stress
  3. Melanocyte stress signals sent via exosomes to APCs in skin
  4. Antigen presentation leads to T cell activation in lymph nodes & production of chemokines
  5. Recruitment of cytotoxic CD8 T cells which attack melanocytes
  6. Depigmented skin
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14
Q

Oxidative stress (vitiligo Pathogenesis)

A
  • melanocytes from vitiligo patients have intrinsic defects = reduce capacity to manage cellular stress
  • melanocytes respond to stress by releasing reactive oxygen species (ROS)
  • production & accumulation of ROS triggers DNA damage & compromises cellular function
  • oxidative stress tiggers immune response & recruitment of T cells = destruction of melanocytes
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15
Q

Examples of exogenous stressors

A
  • UV radiation
  • trauma
  • cytotoxic compounds
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16
Q

Examples of endogenous stressor

A
  • Melanin synthesis itself
  • melanogenesis can be toxic to melanocytes itself = energy consuming process performed by melanocytes
17
Q

Oculocutaneous Albinism (OCA)

A
  • group of genetic disorders = hypopigmentation due to partial / total absence of melanin in skin, hair follicles & eyes
  • multiple subtypes of OCA: OCA1 & OCA2 = 90% of cases
  • almost always inherited in autosomal recessive manner
18
Q

OCA Pathogenesis

A
  • defect in melanin biosynthesis pathway
  • mutations in genes that encode proteins involved in pathway
  • normal number of melanocytes
  • reduction in amount of melanin present in each melanosomes
19
Q

OCA 2

A
  • mutations in OCA2 gene encodes the P-protein
  • “tyrosinase-positive” OCA (tyrosinase normal, p protein problem)
  • P-protein is involved in the biogenesis of melanosomes & processing & transport of melanosomal proteins & pH-regulation that supports melanogenesis
  • without p protein = melanin synthesis impaired
20
Q

OCA1A

A
  • OCA1 = TYR (gene mutation) * tyrosinase (gene product)
  • severe gene mutation of TYR
  • absent tyrosinase activity
  • inability to produce pigment throughout life
  • absent melanin in hair, skin, eyes
21
Q

OCA1B

A
  • milder gene mutation of TYR
  • reduced tyrosinase activity
  • low level of pigment production throughout life
  • variable dilution in hair & skin pigment
22
Q

Melasma

A
  • acquired disorder of hyperpigmentation
    = brown to grey macules & patched on sun exposed areas of skin
  • common, chronic & recurring disorder
  • mostly commonly affects females with darker skin types
23
Q

Risk factors & triggers of melasma

A
  • multifactorial
  • genetic predisposition (familial, 1st degreee relatives)
  • sunlight exposure (UVR & visible light) NB
  • skin phototype (skin phototype III-IV, medium pigmented)
  • hormonal factors (pregnancy, oral contraceptives, hormone therapy, hyperestrogenic states)
  • medications (photosentizing drugs, anti-epileptics eg: phenytoin)
24
Q

Melasma Pathogenesis

A
  • hyperpigmentation arises from hyper functional melanocytes that deposit an excess amount of melanin in dermis & epidemis
  • normal number of melanocytes, larger number of melanosomes is affected skin
    UVR plays NB role in Melasma pigmentation
  • induces production of alpha-melanocyte stimulating hormone
  • directly stimulate melanocytes & increase melanin production
  • chronic UVR = damage to BM of epidermis: penetration of melanocytes & melanin into dermis
    Increased number of mast cells in skin - UVR triggers release of histamine from mast cells & histamine bind to H2 receptors in skin = activating tyrosinase pathway = melanogenesis
    Chronic UV exposure increases vascularisation of Melasma lesions = pigmentation within skin
25
Q

Pityriasis versicolor

A
  • common, benign, superficial fungal infection of skin
  • Malassezia spp, dimorphic lipophilic fungus (grow both in yeast form & mycelial form) which forms part of normal skin flora
    = dyspigmentation of skin
  • presents multiple oval-round macules/ patches/ plaques with fine scale
    — brown/ hyperpigmentation
    — white-tan/ hypopigmented
    — pink/ erythematous
26
Q

Pityriasis versicolor Pathogenesis

A

clinical disease occurs when round yeast of Malassezia transforms to mycelial form (hyphae)
Factors may promotes conversion
- high temp & humid climate
- oily skin
- excessive sweating
- immunodeficiency
- poor nutrition
- pregnancy
- corticosteroids use
- bath oils/skin lubricants = Malassezia growth (yeast lipophilic)
- not poor hygiene
- “spaghetti & meatball”
- organism found both yeast (spore) & filamentous (hyphal) form

27
Q

Brown/ hyperpigmentation in PV

A
  • yeasts induce enlarged melanosomes within melanocytes = increases melanin production
  • Underlying mechanism not known
28
Q

White-tan/ hypopigmentation in PV

A
  • chemicals (dicarboxylic acids) = produced by Malassezia (metabolism of surface lipids)
    = diffuses into epidermis & impairs function of melanocytes & synthesis of melanin
29
Q

Pink in PV

A
  • secondary to mild inflammation of epidermis caused by Malassezia or its metabolites
30
Q

Post-lesional changes in skin colour

A
  • secondary to variety of insults to skin: cutaneous inflammation, physical/chemical injuries
  • hyperpigmentation = inflammatory causes, eg: acne vulgaris, atopic dermatitis, impetigo, insect bites, lichen simplex chronicus
  • Hypopigmentation = iatrogenic causes, eg: medical procedures such as biopsies, cryotherapy, intralesional steroids, laser therapies, surgical procedures
  • depigmentation = injury type cause, eg: thermal/chemical burns, lacerations (physical/chemical injury)
31
Q

Variations in post-lesional changes in skin colour

A
  • same insult, but one patient presents with hypo & hyper
  • variation in individual response to trauma/inflammation = not well understood
  • individual’s genetic tendency or inheritable traits
  • thought = robust melanocytes react with increased melanin production= hyperpigmentation
  • less robust melanocytes = susceptible to damage = hypopigmentation
  • greater frequency, severity, duration of PIH (post inflammatory hypo/hyperpigmentation) is darkly pigmented skin
32
Q

Post-lesional hyperpigmentation Pathogenesis

A
  • acquired excess of melanin pigment following cutaneous inflammation/ injury
  • inflammatory mediators (eg: prostaglandins) enhance pigment production
    Epidermal = increased melanin production &/ transfer keratinocytes
    Dermal = melanin enters dermis via damaged basement membrane, phagocytosed & subsequently resides within dermal macrophages (melanophages)
    (Grey to blue/brown discoloration of skin)
33
Q

Post-lesional hypopigmentation & depigmentation

A
  • cutaneous inflammation may inhibit melanogenesis & inhibit transfer of melanosomes to keratinocytes
  • severe inflammation = loss of functional melanocytes/ melanocyte death = depigmentation & permanent pigmentary changes
34
Q

Leprosy

A
  • slowly progressive infectious disease = Mycobacterium leprae
  • granuloma formation in nerves & skin
  • primary skin lesions = hypopigmented/ erythematous & often anaesthetic (lack sensation)
  • cutaneous hypomelanotic macules = earliest expression of leprosy
  • lepromatous & tuberculoid
    3 things
    1. Contagious person
    2. Close/intimate contact
    3. Susceptible person (genetic)
35
Q

Leprosy Pathogenesis

A
  • M.Leprae: intracellular acid-fast bacillus = predilection for macrophages & Schwann cells
  • grows best in cooler temps = predilection for skin & peripheral nerves close to skin
  • spread nasal & oral droplets
  • inoculation via nasal mucosa or less commonly through breaks in skin barrier
  • Average incubation period: 4-10 years (ranges 6months-20years)
  • majority of exposed individuals do not develop disease = genetic factors increase susceptibility to develop disease
  • certain animals are environmental reservoir of leprosy
36
Q

Hypopigmentation due to leprosy

A
  • mechanism of hypopigmentation in leprosy not well understood
  • hypothesized that patients with leprosy = lack tyrosine cause by overuse of amino acid by M. leprae
  • alternative hypothesis for hypopigmentation is disruption in transfer of melanosomes to keratinocytes

The Skin (9 decks)

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