Pigments

Pigments are colored substances

Endogenous-

Synthesized within the body

Exogenous coming from outside

Endogenous pigments:

Melanin, lipofuscin and derivatives of hemoglobin

Exogenous pigments:

Anthracosis, siderosis, silicosis and plumbism.

Endogenous
pigments
1. Melanin
2. Lipofuscin
3. Derivatives of haemoglobin

Melanin

1. Melanin

Melanin is a brown-black pigment found in the

form of fine brown granules in the skin, choroids
of the eye, hair and adrenal medulla.

Synthesis occurs in melanosomes present in

melanocytes- present in basal layer of epidermis.

Tyrosine is the precursor of melanin and

tyrosinase is the enzyme involved in its formation.

Melanochromes formed from tyrosine polymerizes

to form melanin polymers

Melanin
Melanin appears as black, brown or red pigment
depending upon the amount and its distribution in
the skin.
Local melanin pigmentation e.g. pigmented nevus,

melanoma.
Generalized melanin pigmentation e. g. Addisons

disease.

Melanin

Black, brown, red color of skin due to

amount and distribution of melanin.
Protects against UV rays in sunlight.

Microscopic appearance: Melanin granules

are small, uniform, dirty brown, round
granules.

Foci of melanocytes may be located in

intestine, heart, kidney etc called melanosis
usually harmless

Melanin

Metabolism of Tyrosine
PHENYLALANINE

Phenylalanine
hydroxylase
TYROSINE
DOPAMINE
NOREPINEPHRINE
EPINEPHRINE
THYROXINE
MELANINE

Tyrosine (Hydroxyphenylalanin, a.a)

Tyrosinase

Dopamine
Leucodopachrome

Cysteine

5,6-Dihydroxyindole
Indole 5-6-quinone
melanochrome

Melanin polymers

Abnormal accumulation of melanin

Hormonal
disturbances
hyperpigmentation

may

cause

acanthosis nigricans due to lesions in adrenal.

Pathological amounts
associated with tumors of melanocytes, melanomas
and melanocarcinomas

Local melanin pigmentation

Melanoma

Melanoma

Pigmented naevus (Skin mole)

Nevus is a small accumulation of melanocytes in
the skin.

Acanthosis nigricans
Brown to black, poorly defined, velvety hyperpigmentation of the skin. It is usually
found in body folds, such as the posterior and lateral folds of the neck, the armpits,
groin, navel, forehead, and other areas.
Increased amount of melanin within the skin.

Albinism
Complete absence of melanin in an individual

Xeroderma Pigmentosum

Inherited disorder
Lack enzyme to repair DNA mutation
Usually autosomal recessive, but may be
inherited as autosomal dominant
Propensity to develop skin cancer
Cannot stand any sun exposure
Children of the Moon

Leukoderma
Local loss of the pigment

Vitilago
Characterized by partial or complete loss of
melanocytes in epidermis

Importance

The pigment itself is not harmful.

The importance of melanin depend on the

alterations such as
Adrenal

diseases

Hormonal

imbalances

Neoplasia

which cause the disease.

Lipofuscin

2.

Lipofuscin

Insoluble, yellow or brown

pigment granules.
Sometimes evident in
hepatocytes,
especially
those toward the centers
of lobules.
It represents complexes
of lipids and protein that
are
derived
from
polyunsaturated lipids of
subcellular membrane

Lipofuscin

Represents the presence of lysosomes that have

accumulated a noticable amount of indigestible
residue.

Lipofuscin is sometimes called "wear-and-tear

pigment", since the amount increases over time
(i.e., with advancing age) in cells like
hepatocytes and neurons which are both
permanent (not routinely replenished) and
metabolically active

Importance

The pigment itself is not harmful.

It is an important marker that indicates that

whether the cell has suffered free radical
injury.

Derivatives of hemoglobin

1.

Haemosiderin

2.

Porphyria

3.

Bilirubin

Erythrocyte Destruction

Breakdown of the RBC

Toward the end of 120 day life span of the RBC, it begins to break
down.
The membrane becomes less flexible.
The concentration of cellular hemoglobin increases.
Enzyme activity, especially glycolysis, diminishes

Removal
Aging RBCs or senescent RBCs are removed from the circulation
by the reticuloendothelial system (RES) which is a system of
fixed macrophages.
These cells are located all over the body, but those in the spleen
are the most efficient at removing old RBCs.

Erythrocyte Destruction

Two Paths
Extravascular
Intravascular
R.B.Cs

Haemoglobin

Globin

Haeme

Iron

Extravascular Destruction

The RES cells lyse the RBCs and digest them. Components of the
RBC are recycled.
Iron is transported by transferrin to the bone marrow to be
recycled into hemoglobin.
Amino acids from globin are recycled into new globin chains.
The protoporphyrin ring from heme is broken and converted
into biliverdin
Biliverdin is converted to unconjugated bilirubin and carried
to the liver by albumin, a plasma protein.
Bilirubin is conjugated in the liver and excreted into the
intestine, where intestinal flora convert it to urobilinogen.
Most urobilinogen is excreted in the stool, but some is picked
up by the blood and excreted in the urine.
Conjugated (indirect) and unconjugated (direct) bilirubin can
be used to monitor hemolysis.

recycled into new globin chains

(Haemeoxygenase)

Formed in
mononuclear
phagocytes
(Biliverdinreductase)
In blood

Transport to liver

Bilirubin Glucuronosyle

To be recycled into haemoglobin

Intravascular Destruction
free hemoglobin and dimers that are released
into the bloodstream is picked up by a protein carrier
called haptoglobin.

The

The

haptoglobin-hemoglobin complex is large and

cannot be excreted in the urine. It is carried to the liver
where the RES cells are and the breakdown process
occurs as in extravascular destruction.

If

there is an increase in intravascular destruction, the

haptoglobin is used up and free hemoglobin is excreted
in the urine (hemoglobinuria).

Hemosiderin
Local breakdown of red cells in tissues, e. g.
in internal haemorrhage.
Extravasated red cells

Phagocytosis of red cells

by macrophages

Haemosiderin (yellow)
(Prussian Blue reaction)

Iron free pigments

3.

Haemosiderin

Hemoglobin derived, golden yellowish to brown

granular pigment in which iron is stored.

Under normal conditions small amounts of

hemosiderin can be seen in mononuclear
phagocytes of the bone marrow

Excess of iron causes hemosiderin to accumulate

in the cells either as localized or as a systemic
derangement.

Hemosiderin laden macrophages are called as

heart failure cells.

HE Stain

Prussian blue reaction.

Hemosiderin granules in liver cells

From ROBBINS BASIC PATHOLOGY2003

Localized Haemosiderosis

Local accumulation of haemosiderin results from

haemorrhage.
Best example
icommon bruise.

Localized Haemosiderosis

The area is first red-blue. With the lysis of R.B.Cs

the haemoglobin is transformed to hemosiderin

Local macrophage phagocytosed the red cell

debris, and then lysosomal enzyme convert the
haemoglobin, through the sequence of events.

The play of colours through which passes reflects

these changes.

The red blue color of haemoglobin is transformed

to green-blue, indicating the formation of biliverdin
(green bile)

Then bilirubin (red bile)

Localized Haemosiderosis
Thereafter iron moiety of haemoglobin is deposited as
golden yellow haemosiderin.

Systemic Haemosiderosis

Haemosiderin is deposited in many organs

and
tissues,
a
condition
called
hemosiderosis.

Associated with haemolytic anaemia and

transfusion.

4.Porphyrin

Porphyrins are pigments normally present

in hemoglobin and myoglobin.

Jaundice/Icterus
1.

Pre-hepatic

2.

Intra-hepatic

3.

Post-hepatic

Exogenous
pigments

Exogenous pigments
1.Carbon

Anthracosis: deposition of carbon or coal

dust

Mainly in lungs.

Macroscopically-Anthracosis

Carbon
particles
appears
as
black
pigment in the tissue.

In lungs carbon
appears as focal
accumulation.

Anthracosis

Pulmonary anthracosis

Bronchial anthracosis

Microscopically-Anthracosis

Carbon particles are present in macrophages.

2. Iron

Siderosis:
Deposition of iron in the lungs .

Macroscopically:
Iron dust causes a brown or rusty red
pigmentation due to local accumulation of
macrophages having iron dust.
Only slight fibrosis.

Microscopically:
Brown or black irregular shaped granules in
macrophages.

3.Silicon
Silicosis: deposition of silicon in the lungs.
Causes extensive fibrosis.
Increased macrophages and lymphocytes
in the alveoli.
Macroscopically : Nodules formation on
lungs.
Fibrotic lesions in the regional lymph
nodes.
Microscopically: nodular lesion contain

Silicosis

Silicosis

Silicosis

Silicosis

4.Lead

Plumbisim:
Presence of both lead and hydrogen sulphide.

Macroscopically:
Pigmentation occurs only in those areas
where hydrogen sulphide is present.
Lead with hydrogen sulphide form a black
pigment, seen at the gum line.