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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.
Pigments
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
hydroxylase
MELANINE
PHENYLALANINE
TYROSINE
DOPAMINE
NOREPINEPHRINE
EPINEPHRINE
THYROXINE
Tyrosine (Hydroxyphenylalanin, a.a)
Dopamine Leucodopachrome Cysteine
5,6-Dihydroxyindole
Indole 5-6-quinone melanochrome Melanin polymers
Tyrosinase
Abnormal accumulation of melanin
Hormonal disturbances may cause
hyperpigmentation
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
Haeme
Haemoglobin
R.B.Cs
Globin 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.
(Haemeoxygenase)
(Biliverdinreductase)
Formed in mononuclear phagocytes
Transport to liver
In blood
Bilirubin Glucuronosyle
To be recycled into haemoglobin
recycled into new globin chains
Intravascular Destruction
The free hemoglobin and dimers that are released into the bloodstream is picked up by a protein carrier
called haptoglobin.
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).
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
Hemosiderin
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.
In lungs carbon
appears as focal
accumulation.
Macroscopically-Anthracosis
Carbon particles
appears as black
pigment in the tissue.
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
concentric layers of hyalinized collagen.
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.
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