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 Pigments are coloured substances present in most
living beings including humans.
 2 broad categories of pigments are :
 Endogenous pigments are either normal constituents
of cells or accumulate under special circumstances eg
– melanin , ochronosis , haemopoetin – derived
pigments and lipofuscin.
 Exogenous pigments are those which are introduced
into the body from outside such as by inhalation ,
ingestion or inoculation.
Melanin
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 Melanin is the brown – black , non-haemoglobin –
derived pigment normally present in the hair , skin ,
choroid of the eye , meninges , adrenal medulla.
MELANOCYTES
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Neural crest derived cells located in the basal layer of skin..
Their function is to produce an insoluble pigment , melanin using
Tyrosine as a substrate and to transfer this product to adjacent
epithelial cells.
Ratio of melanocytes
to basal keratinocytes varies from
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1 : 4 to 1 : 10 depending on the site of the body
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EPIDERMAL MELANIN UNIT
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The functional unit
composed of a
melanocyte and the
adjacent keratinocytes
receiving melanin from
it is referred to as
epidermal melanin
unit
Generalised hyperpigmantation
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 Addison’s disease – seen in areas exposed to light
and of buccal mucosa.
 Chronic arsenical poisoning – characteristic rain-
drop pigmentation of the skin.
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MELASMA / CHLOASMA
Blotchy
hyperpigmentation of the
face , especially cheeks ,
forehead and chin ,which
is caused by both hormones
( pregnancy ) and
sunlight.
HPE : Incresed amount of
basal layer pigment.
Focal hyperpigmentation
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 Café-au-lait spots – are pigmented patches seen in
neurofibromatosis and albright’s syndrome.
 Peutz – Jeghers syndrome – characterised by focal
peri-oral pigmentation
 Melanosis coli - pigmentation of the mucosa of the
colon.
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 Melanotic tumors – both benign such as pigmented
naevi , and malignant such as melanoma , are
associated with increased melanogenesis.
 Lentigo is a pre-malignant condition in which there
is focal hyperpigmentation on the skin of hands ,
face , neck and arms.
MALIGNANT MELANOMA
Rapidly spreading
malignant tumor of
skin
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Occurs at all ages
but is rare before
puberty.
ETIOPATHOGENESIS
 UNKNOWN
 EXCESSIVE EXPOSURE TO SUN
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RISK FACTORS
 Large numbers of benign naevi
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 Freckles
 Clinically atypical naevi
 Severe sunburn
 Early years in a tropical climate
 Family history of Malignant Melanoma
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RISK FACTORS
 Persistent change in appearance of a mole
 Presence of pre-existing naevus (Dysplastic Naevus)
 Family history of melanoma
 More than 50 moles , 2mm or more in diameter.
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HPE :
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Epidermis is markedly hyperplastic
Intraepidermal melanocytes tend to be bizarre.
Papillary dermis may be widened and inflamed.
Junctional activity
Prominent melanin pigmentation
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Invasion of surrounding tissues
Marked cytologic atypia
Nuclear grooves , folds and pseudoinclusions.
Large eosinophilic nucleoli
Abundant mitotic figures ,some of them atypical.
Immunohistochemical features
i.
Vimentin
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ii.
S – 100
iii.
HMB-45
iv.
Melan-A
v.
Tyrosinase
vi.
Microphthalmia Transcription Factor
Spread and metastasis
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Along the dermoepidermal junction and upper dermis .
Later invades deep dermis
Subcutis and deeper structures.
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HYPOPIGMENTATION/ LEUKODERMA/
HYPOMELANOSIS /
DEPIGMENTATION/
AMELANOSIS
Decrease in the number of melanocytes / melanin
VITILIGO
 Disfiguring , patchy total loss of
skin pigment.
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 Patches have an irregular border
but are sharply demarcated
from the surrounding skin.
 Hairs in patches of vitiligo
usually become white.
 Scalp and eyelashes are rarely
affected.
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HPE :
 Absence of melanocytes
 Vacuolated keratinocytes may
be seen
 Melanophages may be found
in the dermis
 Negative for Masson- Fontana
and Dopa reaction.
PIEBALDISM / PATTERNED LEUKODERMA/
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 Autosomal dominant , permanent stable
leukoderma.
 Irregularly shaped depigmented patches
present from birth and are associated in
about 85% cases with a white forelock
arising from a depigmented area in the
center of forehead.
 Depigmented areas have a predilection for ventral skin.
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 Small islands of hyperpigmentation ,1-5cms in diameter ,
are present within depigmented area .
HPE : Skin has no / few melanocytes and is normal in all
other aspects.
ALBINISM
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Absence of melanin secondary to a variety of enzymatic
defects that interfere with melanin synthesis.
It is not one disease but many.
Depending on the biochemical defect , melanin may be
lacking in the skin , eyes / CNS to produce variety of
defects.
CHEDIAK HIGASHI SYNDROME
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Autosomal recessive inherited disorder of pigmentation ,
immunity and haematologic function.
Patients may be described as having pigmentary dilution .
Thus white patients may appear totally white , while darker
skinned patients may have a grayish tinge.
Their hair has a metallic colour .
Melanin – like pigments
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 Ochronosis
 Rare autosomal recessive disorder
 Deficiency of an oxidase enzyme required for
breakdown of homogentisic acid which then
accumulates in the tissues and is excreted in the
urine.
 Urine , if allowed to stand for some hours in air ,
turns black due to oxidation of homogentisic acid.
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 Pigment is deposited both intracellularly and
intercellularly , is termed ochronosis.
 Commonly affected tissues – cartilages , capsules of
joint , ligaments and tendons.
Haemopoetin – derived pigments
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 Haemopoetins are most important endogenous
pigments derived from haemoglobin , cytochromes ,
and their breakdown products.
 In disordered iron metabolism and transport ,
haemopoetin – derived pigments accumulate in the
body .
 These pigments are haemosiderin , acid haematin ,
bilirubin , porphyrins.
Haemosiderin
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 Hemoglobin-derived, golden yellow-to-brown,
granular or crystalline pigment that serves as one of
the major storage forms of iron.
 Excessive storage of haemosiderin occurs in
situations when there is increased breakdown of red
cells, or systemic overload of iron due to primary
(idiopathic, hereditary) haemochromatosis , and
secondary causes such as in thalessemia ,
sideroblastic anaemia , multiple blood transfusions.
Local haemosiderosis
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 Haemorrhage into the tissues.
 With lysis of red cells , haemoglogin is liberated
which is taken up by macrophages where it is
degraded and stored as haemosiderin.
 Eg – changing colors of a bruise or a black eye .
Generalised haemosiderosis
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 Systemic overload with iron may result in
generalised haemosiderosis.
 Two types of pattern are:
 Parenchymatous deposition of haemosiderin occurs
in paenchymal cells of the liver , kidney , pancreas
and heart.
 Reticuloendothelial deposition occurs usually
following repeated blood transfuions .
Idiopathic haemochromatosis
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 Autosomal dominant disease characterised by
excessive absorption of iron.
 Triad of pigmentary liver cirrhosis , pancreatic
damage resulting in diabetes mellitus , and skin
pigmentation.
Haematin
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 Haemopoetin-derived brown-black pigment
containing haem-iron in ferric form.
 Seen most commonly in chronic malaria .
Bilirubin
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 Normal non-iron containing pigment present in the
bile.
 Derived from porphyrin ring of the haem moeity of
haemoglobin.
 Normal level of bilirubin in blood is less than
1mg/dl.
 Excess of bilirubin causes jaundice.
Porphyrins
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 Are tetrapyrrols which exist in 3 forms :
 Haem contains iron
 Chlorophyll contains magnesium
 Cobalamin contains cobalt.
 Porphyria results from genetic deficiency of one of
the enzymes required for synthesis of haem so that
there is excessive production of porphyrins.
 Precipitated by intake of some drugs.
Lipofuscin
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 Insoluble pigment, also known as lipochrome or
wear-and-tear pigment. It appears as a yellowbrown, finely granular cytoplasmic, often
perinuclear, pigment.
 found in atrophied cells of old age
 Seen in myocardial fibres , hepatocytes , cells of
testis and neurons.
Exogenous Pigments
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 Inhaled pigments
 The most common exogenous pigment is carbon
(coal dust), a ubiquitous air pollutant of urban life.
Accumulations of this pigment blacken the tissues
of the lungs (anthracosis) and the involved lymph
nodes.
 In coal miners the aggregates of carbon dust cause
a serious lung disease known as coal worker's
pneumoconiosis.
Injected pigments
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Tattooing is a form of localized, exogenous
pigmentation of the skin.
Intentionally produced by professional artists.
Pigments like india ink ,cinnabar and carbon are
introduced into the dermis where the pigment is
taken up by macrophages and lies permanently
in the connective tissue.
Egs- prolonged use of ointments containing mercury ,
tattooing by pricking the skin with dyes.
Ingested pigments
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 Chronic ingestion of certain metals may produce
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
pigmentation ;
Argyria – chronic ingestion of silver compounds
results in brownish pigmentation in the skin , bowel
, kidney.
Chronic lead poisoning – produce characteristic blue
lines on teeth at the gumline.
Melanosis coli results from prolonged ingestion of
certain cathartics.
Carotenaemia – yellowish red coloration of skin
caused by excessive ingestion of carrots.
THANK YOU
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