24. Pathology of lipidogenic pigments: types, causes of formation, examples of diseases. Macro- and microscopic changes in organs with lipofuscinosis, outcomes.

Types of lipopigments:

1. - Lipofuscin,

2. - vitamin E deficiency pigment ,

3. - ceroid,

4.- lipochromes.

The first three pigments are considered varieties of lipofuscin and differ only in the place of formation: lipofuscin and vitamin E deficiency pigment - in parenchymal cells, ceroid - in mesenchymal cells.

Lipofuscin is an aging pigment - a glycoprotein in the form of golden-brown grains. It is formed by autophagy: primary granules containing fragments of mitochondria and ribosomes are formed perinuclearly in the cell in the zone of the most active metabolic processes.

Ceroid, a type of lipofuscin, is formed by macrophages by heterophagy of lipid-containing material in the tissue necrosis zone, especially if lipid oxidation is enhanced by hemorrhage or if there are so many lipids that their autooxidation begins earlier than digestion. In pathological conditions, the formation of ceroid is most often noted with tissue necrosis, especially with increased lipid oxidation by hemorrhage, or in the presence of lipids in such quantities that their autooxidation begins earlier than digestion.

Lipochromes - lipids with carotenoids - normally give a yellow color to adipose tissue, adrenal cortex, blood serum, and the yellow body of the ovaries; in pathology, they occur in the case of:

a) DM (accumulation of lipochromes in the skin and bones due to a sharp violation of lipid-vitamin metabolism).

b) sharp and rapid weight loss (ochre-yellow fatty tissue due to condensation of lipochromes).

Lipofuscinosis: In pathological conditions, the content of lipofuscin in cells is increased - lipofuscinosis, which can be secondary and primary (hereditary).

1. Primary (hereditary) - selective accumulation of L. in the cells of certain organs:

benign hyperbilirubinemia with selective hepatocyte lipofuscinosis (Dabin-Johnson, Gilbert, Krieger-Nayyar syndromes)

neuronal lipofuscinosis with selective lipofuscinosis of neurons, decreased intelligence, vision, seizures (Kafa syndrome)

2. Secondary lipofuscinosis is observed in the following cases:

1. old age ("aging pigment").

2. cachexia (brown atrophy of the myocardium, liver).

3. an increase in the functional load on the organ (myocardial lipofuscinosis in heart disease).

4. abuse of analgesics, vitamin deficiency

Pathogenesis of secondary lipofuscinosis:

• The synthesis of redox enzymes in the cytochrome chain is disrupted

• Switching cell metabolism to a more "economical" lipofuscin pathway

• "Brown atrophy of organs": liver, myocardium, striated muscles.

25. Pathology of tyrosinogenic pigments: types, role in normal and pathological conditions. Violation of melanin metabolism: melanin metabolism is normal, classification.

1. Types and origin of proteinogenic (tyrosinogenic) pigments:

1. Melanin is formed by menalocytes of neuroectodermal origin from DOPA

2. pigment of enterochromaffin cells - is formed by enterochromaffin cells of the gastrointestinal tract from tryptophan

3. adrenochrome is formed by the cells of the adrenal medulla by the oxidation of adrenaline