Degeneration
ACUTE CELLULAR SWELLING
? Excessive entry of free fatty acids into the liver
(starvation,corticosteroid therapy).
? Enhanced fatty acid synthesis.
? Decreased fatty acid oxidation.
? Increased esterification of fatty acid to
triglycerides (alcohol).
? Decreased apoprotein synthesis (CCl4).
? Impaired lipoprotein secretion from the liver
(alcohol).
FATTY CHANGE
?Morphology of fatty change
Sudan III,Oil red O,Osmic acid
?Liver
?Heart
?Kidney
?Intracellular hyaline changes
?Hyaline degeneration of arterioles
?Hyaline degeneration of connective tissue
Hyaline changes (degeneration)
? Absorption of protein causing hyaline
droplets in proximal epithelial cells in
the kidney.
? Russel bodies in plasma cells.
? Viral inclusions in the cytoplasm or
the nucleus.
? Masses of altered intermediate filaments
(Mallory bodies).
Intracellular hyaline changes
? A heterogeneous group of pathogenic
fibrillar proteins accumulating in tissues
and organs.
? Excess synthesis
? Resistance to catabolism
AMYLOIDOSIS
Chemical nature of amyloid fibrils
Two major forms:
AL (amyloid light chain protein)
AA (amyloid-associated protein):
Derived from serum AA (12kd)
synthesized in liver and elevated in
inflammatory states.
Minor forms of amyloid fibrils:
Transthyretin (TTR),A mutant form of a
serum protein in familial amyloid
polyneuropathy.
A variant of TTR in aging.
Beta-2-microglobulin (the component of
class I MHC molecules) in long-term
hemidialysis.
Minor forms of amyloid fibrils:
Beta-2-amyloid protein forms the core of
cerebral plaques and deposits within
cerebral vessel walls in Alzheimer
disease,deriving from a transmembrane
glycoprotein precursor.
Minor forms of amyloid fibrils:
Transthyretin (TTR),A mutant form of a
serum protein in familial amyloid
polyneuropathy.
A variant of TTR in aging.
Beta-2-microglobulin (the component of
class I MHC molecules) in long-term
hemidialysis.
Minor forms of amyloid fibrils:
Beta-2-amyloid protein forms the core of
cerebral plaques and deposits within
cerebral vessel walls in Alzheimer
disease,deriving from a transmembrane
glycoprotein precursor.
? primary (B-cell dyscrasia,AL)
? Secondary or reactive (AA),
Collagen diseases,bronchiectasis,chronic
osteomyelitis.
? Hemodialysis-related,Beta-2-microglobulin
deposition.
? Hereditary (AA)
Clinical forms of amyloidosis Systemic
amyloidosis:
? Nodular (tumor-forming deposits,
B-cell dyscrasia,AL)
? Endocrine amyloidosis (procalcitonin)
? Amyloidosis of aging,Heart,lung,
pancreas,spleen,brain.
Localized amyloidosis
? Exogenous:
Carbon
Tattooing
?Endogenous:
Lipofuscin
Melanin
Hemosiderin
Bilirubin
Pigmentation
? Dystrophic calcification
? Metastatic calcification
Pathologic calcification
? Necrotic tissues
? Atheroma
? Damaged heart valves
Dystrophic calcification
? Fig 2-13
? Increased secretion of parathyroid
hormone
? Destruction of bone tissue
? Vitamin D-related disorders,
Sarcoidosis
? Renal failure
Metastatic calcification
Hypercalcimia
Metastatic calcification Affecting
Interstitial tissue of gastric mucosa
Kidneys
Lungs
Pulmonary veins
Systemic arteries
ACUTE CELLULAR SWELLING
? Excessive entry of free fatty acids into the liver
(starvation,corticosteroid therapy).
? Enhanced fatty acid synthesis.
? Decreased fatty acid oxidation.
? Increased esterification of fatty acid to
triglycerides (alcohol).
? Decreased apoprotein synthesis (CCl4).
? Impaired lipoprotein secretion from the liver
(alcohol).
FATTY CHANGE
?Morphology of fatty change
Sudan III,Oil red O,Osmic acid
?Liver
?Heart
?Kidney
?Intracellular hyaline changes
?Hyaline degeneration of arterioles
?Hyaline degeneration of connective tissue
Hyaline changes (degeneration)
? Absorption of protein causing hyaline
droplets in proximal epithelial cells in
the kidney.
? Russel bodies in plasma cells.
? Viral inclusions in the cytoplasm or
the nucleus.
? Masses of altered intermediate filaments
(Mallory bodies).
Intracellular hyaline changes
? A heterogeneous group of pathogenic
fibrillar proteins accumulating in tissues
and organs.
? Excess synthesis
? Resistance to catabolism
AMYLOIDOSIS
Chemical nature of amyloid fibrils
Two major forms:
AL (amyloid light chain protein)
AA (amyloid-associated protein):
Derived from serum AA (12kd)
synthesized in liver and elevated in
inflammatory states.
Minor forms of amyloid fibrils:
Transthyretin (TTR),A mutant form of a
serum protein in familial amyloid
polyneuropathy.
A variant of TTR in aging.
Beta-2-microglobulin (the component of
class I MHC molecules) in long-term
hemidialysis.
Minor forms of amyloid fibrils:
Beta-2-amyloid protein forms the core of
cerebral plaques and deposits within
cerebral vessel walls in Alzheimer
disease,deriving from a transmembrane
glycoprotein precursor.
Minor forms of amyloid fibrils:
Transthyretin (TTR),A mutant form of a
serum protein in familial amyloid
polyneuropathy.
A variant of TTR in aging.
Beta-2-microglobulin (the component of
class I MHC molecules) in long-term
hemidialysis.
Minor forms of amyloid fibrils:
Beta-2-amyloid protein forms the core of
cerebral plaques and deposits within
cerebral vessel walls in Alzheimer
disease,deriving from a transmembrane
glycoprotein precursor.
? primary (B-cell dyscrasia,AL)
? Secondary or reactive (AA),
Collagen diseases,bronchiectasis,chronic
osteomyelitis.
? Hemodialysis-related,Beta-2-microglobulin
deposition.
? Hereditary (AA)
Clinical forms of amyloidosis Systemic
amyloidosis:
? Nodular (tumor-forming deposits,
B-cell dyscrasia,AL)
? Endocrine amyloidosis (procalcitonin)
? Amyloidosis of aging,Heart,lung,
pancreas,spleen,brain.
Localized amyloidosis
? Exogenous:
Carbon
Tattooing
?Endogenous:
Lipofuscin
Melanin
Hemosiderin
Bilirubin
Pigmentation
? Dystrophic calcification
? Metastatic calcification
Pathologic calcification
? Necrotic tissues
? Atheroma
? Damaged heart valves
Dystrophic calcification
? Fig 2-13
? Increased secretion of parathyroid
hormone
? Destruction of bone tissue
? Vitamin D-related disorders,
Sarcoidosis
? Renal failure
Metastatic calcification
Hypercalcimia
Metastatic calcification Affecting
Interstitial tissue of gastric mucosa
Kidneys
Lungs
Pulmonary veins
Systemic arteries
