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Cell Injury-4
Cell Injury-4
1
TYPES OF PIGMENTS
Two Types:
• Exogenous – Coming from outside the cell
body. e.g. Carbon.
• Endogenous – Synthesized within the
body itself.
2
EXOGENOUS PIGMENTATION
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EXOGENOUS PIGMENTATION (Contd.)
ANTHRACOSIS:
• Carbon or coal dust- most commonly found
air pollutant.
• Enters the body through inhalation.
• Picked up by macrophages within the lungs.
• Transported through lymphatic channel to the
regional lymph nodes.
• Causes chronic obstructive lung disease.
4
EXOGENOUS PIGMENTATION (Contd.)
TATTOOING:
• Localized exogenous pigmentation of the skin
• Various coloured substances are injected into
the skin.
• Phagocytosed by the dermal macrophages.
• Reside for the remainder of life.
• Does not elicit any inflammatory response.
5
ENDOGENOUS PIGMENTATION
• Deposition of endogenously produced pigments.
• Endogenous Pigments:
Two types:
Non-Haemoglobin derived
Lipofuscin
Melanin
Haemoglobin derived
Haemosiderin
Bilirubin
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ENDOGENOUS PIGMENTATION (Contd.)
LIPOFUSION PIGMENTATION:
• Derived from Latin word FUSCUS meaning brown.
• Also known as wear and tear or Aging pigment.
• Formed as a result of lipid peroxidation of poly
unsaturated lipids.
• Seen in cells undergoing slow regressive changes.
• Practically prominent in:
Liver and hearts of aging person.
Patients with severe malnutrition.
Cancer patients.
• Appears microscopically as yellow brown fine
intracytoplasmic granules. 7
ENDOGENOUS PIGMENTATION (Contd.)
MELANIN PIGMENTATION:
• Derived from Greek word Melas meaning black.
• Produced in melanocytes.
• Oxidation of tyrosine by tyrosinase.
• Appears brown black.
• CONGENTIAL:
Peutz-Jegher’s Syndrome
Albright’s Syndrome
Melanocytic Naevi
• ACQUIRED:
Pregnancy – Melasma
Lentigo senilis
Lentigo maligna
8
ENDOGENOUS PIGMENTATION (Contd.)
HAEMOSIDERIN PIGMENTATION:
• A Hb derived Iron containing pigment.
• Appears golden yellow to brown.
• Produced as a result of Iron excess.
• Haemosiderosis
• Two forms:
Local
Systemic
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ENDOGENOUS PIGMENTATION (Contd.)
HAEMOSIDERIN PIGMENTATION:
Local Haemosiderosis:
• Results from gross haemorrhages or
rupture of small vessels.
• Macrophages take up haemoglobin and
lysosomal enzymes convert it to
haemosiderin.
• Best example is local Bruise.
10
ENDOGENOUS PIGMENTATION (Contd.)
HAEMOSIDERIN PIGMENTATION:
Systemic Haemosiderosis:
• Due to systemic overload of Iron as seen in:
Increased absorption of dietary Iron.
Impaired use of Iron.
Excessive breakdown of RBCs.
Multiple blood transfusion.
• Deposited in many organs and tissues like
lever, bone marrow, spleen, pancreas,
kidneys.
• Small amount – No damage.
• Large amount – Parenchymal damage
• Haemochromatosis. 11
ENDOGENOUS PIGMENTATION (Contd.)
BILIRUBIN PIGMENTATION:
• Hb derived pigment.
• Metabolized and detoxified in liver.
• Breakdown products are re-utilized in
RBC Synthesis.
• When liver function is disturbed due to
disease excess Bilirubin deposits.
• Jaundice.
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PATHOLOGIC CALCIFICATION
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PATHOLOGIC CALCIFICATION (Contd.)
DYSTROPHIC CALCIFICATION:
• Occurs in nonviable or dying tissues
in the presence of normal serum
Calcium level.
• Pathogenesis involves two steps
Initiation
Propagation
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PATHOLOGIC CALCIFICATION (Contd.)
DYSTROPHIC CALCIFICATION:
Pathogenesis – Initiation
• Occurs extracellularly & intracellularly
• Extracellularly in membrane bound
vesicles derived from dead or dying cells.
• Acidic phospholipids in their membranes
attract Calcium salts.
• Phosphates accumulate as a result of
action of membrane bound phosphatases.
15
PATHOLOGIC CALCIFICATION (Contd.)
DYSTROPHIC CALCIFICATION:
Pathogenesis – Initiation (Contd.):
• Normal cell membrane ensures low
concentration of Ca and PO4 in the cytosol.
• Following membrane damage Ca and PO4
enter cells.
• Taken up by mitochondria.
• Formation of hydroxyapatite crystals.
• Formation of Ca-Salts – reliable indicator of
impeding cell death.
16
PATHOLOGIC CALCIFICATION (Contd.)
DYSTROPHIC CALCIFICATION:
Pathogenesis – Propagation:
• Facilitated by structural components of the
extracellular matrix.
• Matrix protein available in the dying tissue
as a result of cell injury and death also
contribute.
Osteopontin – An acidic Ca binding
phosphoprotein
Osteonectin – Ca binding protein that inhibits
cell spreading and migration 17
DYSTROPHIC CALCIFICATION (Contd.):
Examples:
• In the Caseous material of TB lesions.
• Areas of fat necrosis in the breast and mesentery.
• Haematomas.
• Old Scars.
• Atheroma.
• Degenerate colloid goiters.
• Degenerate tumours.
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DYSTROPHIC CALCIFICATION (Contd.):
MORPHOLOGY:
• Macroscopic:
Appears as fine, white granules or clumps often
felt as gritty deposits.
• Microscopic:
Appears as a basophilic, amorphous sometimes
clumped material intracellularly or extracellularly.
Psammoma bodies – lamellated configuration.
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METASTATIC CALCIFICATION
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METASTATIC CALCIFICATION (Contd.)
CAUSES:
• Increased secretion of PTH.
Parathyroid tumour.
Ectopic secretion by other malignant tumours
like lung cancer.
• Destruction of bone tissue.
Primary tumours of bone marrow – multiple
myeloma.
Metastatic deposits of other tumours in bone.
Vitamin D Excess
Renal failure- Secondary hyperparathyroidism.
21
METASTATIC CALCIFICATION (Contd.)
ORGANS INVOLVED:
• Kidneys – around the tubules.
• Lungs – in the alveolar walls.
• Stomach – around the fundal glands.
• Blood Vessels – internal elastic lamina.
• Ca deposits appear as amorphous
basophilic densities.
22
Psommoma Bodies
Dystrophic calcification in skeletal muscle