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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

7 Pigmentation

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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.