Hyaline change

Hyaline change

Is various histological or cytological alterations characterized by glassy homogeneous material appear as eosinophilic in H&E staining section . It may be intracellular or extracellular .
Intracellular hyaline change
mainly seen in epithelial cells e.g
1- hyaline droplets in proximal convoluted epithelial cells in case of excessive re absorption of plasma protein.
2- hyaline degeneration of rectus abdomenalis muscle called zenker s degeneration ,occurring in typhoid fever

3-Mallory s hyaline is aggregates of intermediate filaments in the hepatocytes in case of alcoholic liver
4- Russell s bodies excessive accumulation of immunoglobulin's in plasma cells.

Intracellular hyaline as Russell s bodies in cytoplasm of plasma cells

Extracellular hyaline is seen in connective tissues.
Examples of extracellular hyaline change as :-
1- Hyaline degeneration in leiomyomas of the uterus.
2- Hyalinised old scar of fibro- collagenous tissues.
3- Hyalinised glomeruli in chronic glomerulonephritis.
4- Hyaline arteiosclerosis in renal vessels in hypertension and diabetes mellitus.

Extracellular hyaline deposit in leiomyoma uterus

Hyaline arteriolosclerosis. The arteriolar wall is hyalinized and the lumen is markedly narrowed

Mucoid degeneration

There is a change characterized by accumulation of mucin in intracellular and extracellular loci.
Mucin is a glycoprotein secreted by mucous glands .
Epithelial mucin examples
1- Catarrhal inflammation of mucous membrane of respiratory tract ;alimentary tract ;and uterus .
2- Obsruction of duct leading to mucocele in the oral cavity and gall bladder .
of ovary ;stomach ;and large bowel. tumors Secreting 3- mucin
4- fibrosis of the pancreas .

intra cytoplasmic Mucinous material in epithelial cell of ovary

Connective tissue mucin
Examples of disturbance of connective tissue
mucine :-
1- mucoid degeneration in some tumours e.g. myxomas ; neurofibroma; fibroadenoma; and soft tissue sarcoma.
2- dissecting aneurysm of the aorta.
3- myxomatous change in the dermis.

Myxoid change in neurofibroma

Amyloid degeneration
amyloidosis is a condition associated with a number of inherited and inflammatory disorders in which extracellular deposits of fibrillar proteins are responsible for tissue damage and functional compromise. These abnormal fibrils are produced by the aggregation of misfolded proteins (which are soluble in their normal folded configuration). The fibrillar deposits bind a wide variety of proteoglycans and glycosaminoglycans, including heparan sulfate and plasma proteins . The presence of abundant charged sugar groups in these adsorbed proteins give the deposits staining characteristics that were thought to resemble starch (amylose). Therefore, the deposits were called amyloid . .

Schematic diagram of an amyloid fiber showing fibrils (4 shown, may be up to 6)

Classification of Amyloidosis
Amyloid may be systemic (generalized), involving several organ systems, or it may be localized, when deposits are limited to a single organ, such as the heart. On clinical grounds, the systemic, or generalized, pattern is sub classified into primary amyloidosis when associated with some immunocyte dyscrasia, or secondary amyloidosis when it occurs as a complication of an underlying chronic inflammatory or tissue destructive process.

Morphologic feature of amyloidosis

-Grossly
1- the affected organ enlarged ;pale ; and rubbery.
2- cut surface show firm ;waxy ; and translucent parenchyma.
- Microscopically
1- the deposits of amyloid are found in extracellulr locations initially in the wall of small blood vessels.
2- the deposits are in large amount causing microscopic changes and effects of pressure atrophy .

Classification of amyloidosis

A- based on cause
1- primary
2- secondary
B- based on extent of amyloidosis
1- generalized involving multiple organs
2- localized involve one or two organs or sites
C-based on clinical location
1- pattern I involving tongue ;heart bowel ;skeletal muscle ; skin and nerve
2- pattern II involving liver; spleen ;kidney ; and
adrenals.
3- mixed pattern involved of both pattern I and II.



D- based on tissue in which amyloid is deposited
1- mesenchymal organs derived from mesoderm.
2- parenchymal organs derived from ectoderm and endoderm .
E- based on precursor biochemical protein in to spicific serum amyloid protein.

Amyloidosis of kidneys shows small ;pale ; waxy kidneys

Amyloid deposits are seen in glomerular capillry tuft and in peri tubular connective tissue cause atrophy of tubules of kidney

The spleen appear as pale and waxy appearance

Amyloid material seen in red pulp causing atrophy of white pulp

Amyloid deposits cause pressure atrophy of hepatocytes

Pathologic pigments
Pigments are colored substances that are either
exogenous, coming from outside the body, or endogenous, synthesized within the body itself.
Endogenous pigments include lipofuscin, melanin, and certain derivatives of hemoglobin.
1-Lipofuscin, or "wear-and-tear pigment," is an insoluble brownish-yellow granular intracellular material that accumulates in a variety of tissues (particularly the heart, liver, and brain) as a function of age or atrophy.

2-Melanin is, brown-black pigment produced in melanocytes. It is synthesized exclusively by melanocytes located in the epidermis and acts as a screen against harmful ultraviolet radiation.
3- Hemosiderin is a hemoglobin-derived granular pigment that is golden yellow to brown and accumulates in tissues when there is a local or After lysis of the erythrocytes at the site of hemorrhage, the red cell debris is phagocytosed by macrophages; the hemoglobin content is then catabolized by lysosomes with accumulation of the heme iron in hemosiderin.

exogenous pigment

The most common exogenous pigment is
1- inhaled pigments :-
A- pneumoconiosis.
B-anthracosis deposition of coal.
2- injected pigments (tattooing ):-
Indian ink and carbon deposit in dermis.