This document discusses intracellular accumulation of substances within cells (dystrophy) and the morphological changes that occur. It notes that substances accumulate due to disturbances in metabolism, including nutrients stored for later use, degraded products from membrane turnover, and substances not metabolized due to enzyme deficiencies or as foreign materials. The pathological process of dystrophy is described as being based on metabolic disturbances in tissues leading to structural changes. Various mechanisms of dystrophy are provided, including infiltration of substances, transformation of one substance to another, decomposition, and perverse synthesis. Specific examples of parenchymal, stromal-vascular, and mixed dystrophies are summarized.

1. Morphology of pathological
intracellular accumulation of
endogenous and exogenous
products(dystrophy)

2. Substances that accumulate within cells may be :
 Nutrients- such as fat, glycogen, vitamins and minerals,
are stored for later use.
 Degraded phospholipids ,from the turnover of endogenous
membranes, are engulfed in lysosomes and may be recycled.
 Substances that are not metabolized accumulate in
cells. These include:1) endogenous substrates that are not
further processed because a key enzyme is missing (hereditary
storage diseases), 2) insoluble endogenous pigments (e.g.,
lipofuscin, melanin), 3) aggregates of normal or abnormal
proteins, 4) foreign particulates, such as inhaled silica or
carbon or injected tattoo pigments.
Overload of normal body constituents including iron,
copper and cholesterol, injures a variety of cells
Abnormal form of proteins may be toxic if they are retained
within cells (e.g., Lewy bodies in Parkinson disease and mutant α1-antitrypsin)

3. Dystrophy
pathological process, which is
based on a disturbance of the
tissue (cell) metabolism,
leading to structural changes

4. Etiology of dystrophy :
 Hypoxia,
toxic substances,
drugs,
physical and chemical agents
genetic damage,
acquired or hereditary defects of enzymes
(fermentopathy),
 viruses,
nutritional imbalance,
diseases of the nervous or endocrine systems,
 disorders of the blood and urine tests
for diseases of the internal organs

5. Morphogenetic mechanisms of
dystrophies
1.Infiltration. Excessive penetration of
substances or metabolic products of the cells,
blood vessels, intercellular substance (protein
infiltration of kidney proximal tubule epithelium by
increasing its number of primary urine or
metastatic calcification of due to hypercalcemia).
2.Transformation. The transition from one
substance to another (transformation of
carbohydrates into fat in diabetes mellitus).

6. Morphogenetic mechanisms of
dystrophies
3. Decomposition (Phaneros). The disintegration of
cell ultrastructure and intercellular substance or
complex chemical substances, leading to disruption of
metabolism and accumulation of products of disturbed
metabolism in the cell. (The collapse of the
polysaccharide-protein complexes is at the heart of
fibrinoid changes in the connective tissue in rheumatic
diseases).
4.Perverse synthesis. Formation in cells and tissues
of substances not found in normal. (The formation of
glycogen in the narrow tubules Henle in diabetes)

7. Сlassification of dystrophies
1. Depending on the prevalence of morphological
changes in the specific cells or stroma and vessels:
a) parenchymal;
b) stromal-vascular;
c) mixed.
2. Depending on the type of disturbance exchange:
a) protein (disproteinosis);
b) fat (lipidosis);
c) carbohydrate;
d) mineral.

8. Сlassification of dystrophies
3. Depending on the distribution
process:
a) local;
b) systemic
4. Depending on the origin:
a) acquire;
b) hereditary.

9. Parenchymal dystrophy
(Parenchymal disproteinosis):
1. Hyaline droplet degeneration
2. Hydropic
3. Hornу

10. Hyaline droplet degeneration
This type of dystrophy is most often found in the kidneys and liver
Kidneys
Disease(glomerulonephritis, renal amyloidosis, paraproteinemic
nephrosis)
Macroscopically organs do not have the characteristics, the type of
authority determined by the characteristics of the underlying disease
(glomerulonephritis, amyloidosis)
Microscopically - in the cytoplasm of nephrocytes appear large
hyaline droplet protein, merging and fills the entire cell.
 Ultrastructure : destruction of mitochondria, EPS, brush border
Hyaline droplet degeneration nephrocytes associated with the
mechanisms of infiltration (in high porosity of the glomerular filter)
and subsequent decomposition – lack of vacuolar-lysosomal apparatus
nephrocytes providing reabsorption of protein;
Result- irreversible process leading to cell necrosis

11. Hyaline droplet protein in the epithelium of the
proximal convoluted tubules

12. Hyaline droplet degeneration
Liver
Disease (acute alcoholic hepatitis , rarely in
primary biliary cirrhosis, cholestasis )
Microscopically - the study of the light
microscope resemble hyaline droplet
degeneration .
In the electron microscope are presented
fibrillar protein appear in hepatocytes and are
called alcoholic hyaline, or Mallory bodies.

13. Alcoholic hepatitis. A, groups of cells in the stage of necrosis.
B, eosinophilic bodies Mallory

14. Нydropic dystrophy
Which is the advent of the cell vacuoles filled with cytoplasmic fluid.
Disease Observed more frequently in the epithelium of the skin (
herpes simple, windy pox), renal tubular epithelium
(glomerulonephritis, amyloidosis), hepatocytes (viral and toxic
hepatitis ) reflects a perversion of protein-synthetic function of
hepatocytes due to viral replication;
Hydropic degeneration nephrocytes associated with the mechanisms
of infiltration and decomposition.
Macroscopically: organs are not changed;
 Microscopically: the cells increased in volume, the cytoplasm is
filled vacuoles containing transparent liquid. Cell nucleus is displaced
to the periphery. Of ultrastructural cell components decompose. Cell
turns into a fluid-filled vacuole in which floats nucleus. It is the focal
Liquefactive necrosis. He called –ballonn dystrophy.
 Result- unfavorable because often turns into a balloon dystrophy

15. Hydropic degeneration in the
epithelium of the proximal
convoluted tubules of the kidneys

16. Hydropic degeneration in the epithelium of the
proximal convoluted tubules of the kidneys

17. Hydropic degeneration of hepatocytes and the intralobular
limfo-makrofagal infiltrate. Viral chronic hepatitis B.
.

18. Нorny dystrophy
Pathological keratinization it is excessive
formation of the horny substance in the stratum
epithelium (hyperkeratosis, ichthyosis) or the
formation of horny substance, where normally it
does not occur (on mucous membrane- leukoplakia)
Cause: developmental disorders of the skin
(ichthyosis- "fish scales“), chronic inflammation,
vitamin deficiency, viral infections.
May be local and systemic.
The result is favorable. Removing the cause leads to
tissue repair.

19. ICHTHYOSIS "fish scales"

20. ICHTHYOSIS "fish scales"

21. ICHTHYOSIS

22. а б
Hairy (soft) leukoplakia in AIDS (at the root of the tongue (a),
on the side surface of the tongue (b).
.
Leucos is white, Plaka-plate

23. leukoplakia

24. Parenchymal lipidoses
1. Characterized by impaired metabolism cytoplasmic
fat.
2. Morphologically manifest accumulation of drops of
neutral lipids (triglycerides) in the cytoplasm of cells.
3.To identify the color of the lipids used by Sudan III or
Sudan IV frozen sections; the usual methods of
manufacturing in histological preparations in place of the
dissolved fat droplets (fat soluble in alcohol, xylene) are
visible vacuole.
4. Frequently fatty degeneration develops in the liver,
kidney and myocardium.

25. Fatty dystrophia of myocardium
The causes of steatosis: 1) hypoxia - the most common cause (with
anemia, chronic cardiovascular disease); 2) intoxication (diphtheria,
alcohol poisoning phosphorus, arsenic, and others.).
The mechanism of the development of steatosis in hypoxia: 1) lack
of oxygen leads to a decrease in oxidative phosphorylation in
cardiomyocytes; 2) switching to anaerobic glycolysis is accompanied
by a sharp decrease in ATP synthesis; 3) damage to the mitochondria;
4) disturbance of the beta-oxidation of fatty acids; 5) accumulation of
lipids in the form of small droplets in the cytoplasm (pulverized
obesity).
The mechanism of the development of steatosis with intoxication
associated with reduced beta-oxidation of lipids in connection with the
destruction of mitochondria.
Electron-microscopic picture: fat inclusions having the characteristic
striations are formed in the collapse of the mitochondrial cristae.

26. Fatty dystrophia of myocardium
Microscopic picture: fatty degeneration of the
myocardium (pulverized obesity) often has a focal
character; containing fat cardiomyocytes are located mainly
along the knee venous capillaries and small veins, where
the hypoxic factor is most pronounced.
Macroscopic picture: myocardium flabby, pale yellow,
chambers of the heart are stretched, the size of the heart
slightly enlarged; from the endocardium, especially in
papillary muscles, visible yellow and white striations
("tiger heart"), due to focal lesions. Myocardial
contractility decreases with steatosis.

27. Fatty degeneration of the myocardium
("tiger heart")

28. Fatty degeneration of the
myocardium ("tiger heart")

29. Fatty degeneration of the myocardium

30. Fatty liver
 1. Characteristic accumulation of neutral lipids (triglycerides) in the liver
cells.
 2. Is the result of an imbalance between the supply, utilization and excretion
of lipids liver cells.
 3.Due to the following mechanisms:
 a) excessive intake of fatty acids and triglycerides in the cell for
hyperlipidemia - alcoholism, diabetes, general obesity;
 b) reduction of waste - oxidation of fatty acids in the mitochondria cristae -
during hypoxia, anemia, toxic effects;
 c) reduction of liver lipid excretion cells, mainly due to a decrease in
production of apoprotein necessary to transport lipids in the form of
lipoproteins:
 d) with malnutrition due to lack of protein in the diet, or diseases of the
gastrointestinal tract
 e) action of toxic substances (ethanol, carbon tetrachloride, phosphorus,
et al.);
 f) inherited defects of enzymes involved in fat metabolism.

31. Fatty liver
Macroscopic picture:
• liver is enlarged, flabby, the cut with a touch of yellow fat («goose
liver») .
Microscopic picture
• when stained with hematoxylin-eosin staining in the cytoplasm of
hepatocytes vacuoles are seen at the site of the solution at processing
fat droplets; when stained with Sudan III fat droplets are colored
orange-red color, Sudan IV - black;
prevalence of fatty degeneration in the peripheral regions of the liver
lobule evidence of infiltration mechanism of its development, which
is characteristic of hyperlipidemia;
 development of steatosis mainly in the central parts of the liver
lobule associated with the mechanism of decomposition and occurs
with increasing hypoxia liver.

32. Hepatic steatosis («goose liver»)

33. Globular hepatic steatosis

34. Globular hepatic steatosis

35. Fatty liver
Result:
 fatty liver is reversible;
the function of the liver in fatty degeneration over
time remains normal;
joining necrosis leads to organ dysfunction and
development of hepatic insufficiency.

36. Fatty dystrophia of the kidneys
Lipids appear in the epithelium of the tubules of the nephron main
departments (proximal and distal) most often in the nephrotic
syndrome.
 Fatty dystrophia of associated with developing nephrotic syndrome
and hyperlipidemia аnd lipiduriey.
Fatty dystrophia nephrocytes joins hyaline droplet and hydropic
degeneration in the nephrotic syndrome.
Macroscopic picture: of the kidneys are enlarged, flabby (when
combined with amyloidosis - dense), cortex swollen, gray with yellow
specks, visible on the surface and cross section.
Result: the outcome of fatty degeneration depends on the degree. If
not accompanied by a large damage to the structure, the process is
reversible.

37. Fatty dystrophia of the kidneys

38. Parenchymal carbohydrate
dystrophy:
 1.Associated with glycogen metabolism disorders (Disease - Diabetes
mellitus).
 2. Associated with metabolic disorders of glycoproteins(mucus dystrophy.
Disease -Mucoviscidosis).
1. Diabetes mellitus: in this disease, hyperglycemia, and glucosuria
observed. Tissue glycogen decreases. In the liver, fatty degeneration
develops. In the renal tubular epithelium, especially narrow and distal
segments of glycogen infiltration occurs. Tubular epithelium becomes
high with a light frothy cytoplasm. In the lumen of the tubules visible
granules of glycogen. Suffer and glomeruli, their basement membrane is
more permeable to sugars and plasma proteins. In the kidney develops
intracapillary glomerulosclerosis.
2. Mucoviscidosis: is a hereditary disease which is based on the mucous
degeneration. Change the quality of mucus, it becomes thick, viscous,
poorly displayed, which leads to the development of cysts and sclerosis.
Affects the pancreas, glands of the bronchial tree, and all other exocrine
gland.

39. Tubules of the kidneys in diabetes

40. Stromal-vascular dystrophy
Stromal-vascular (mesenchymal) dystrophy develop as a
result of metabolic disturbances in the connective tissue and
are identified in the stroma of organs and blood vessel walls.
Stromal vascular disproteinozy:
1.Mucoid swelling
2.Fibrinoid swelling
3.Hyalinosis.
Mucoid swelling, fibrinoid swelling and hyalinosis
may be successive stages disorganization of
connective tissue (eg in rheumatic diseases).

41. Mucoid swelling
 Surface and reversible disruption of connective tissue.
 Characterized by the accumulation in the fundamental substance of
connective tissue glikozoaminoglikan (preferably hyaluronic acid), which
leads to increased vascular permeability and release of tissue fine plasma
proteins - albumin.
 Infiltration is the mechanism of development. Mucoid swelling is more
common in the walls of arterioles and arteries, heart valves, parietal
endocardium.
 Macroscopic picture: organ or tissue is usually not changed.
 Microscopic picture: metachromasy detected phenomenon, especially with
toluidine blue: focus on the accumulation of mucoid swelling seen
glikozoaminoglikann m giving metahromatic (purple) staining.
 Electron-microscopic picture: identified advanced interfibrillar spaces
containing granular protein mass; collagen fibers are preserved only in places
revealed some of their damage.
 Result: Mucoid swelling - a reversible process, but often turns into an
irreversible process of profound disorganization of connective tissue -
fibrinoid swelling.

42. Fibrinoid swelling
This type of dystrophy is accompanied by a significant
increase in vascular permeability. Of the vessel lumen
out large-molecular proteins -fibrinogen.
The mechanism of development - infiltration and
decomposition.
Electron-microscopic picture: in the area of fibrinoid
changes detected degradation of collagen fibers and
fibrin.
Result: An irreversible process, completed fibrinoid
necrosis, hyalinosis, sclerosis.

43. Hyalinosis.
1. It is characterized by the accumulation in the tissues translucent
dense masses resembling hyaline cartilage.
2.There is the outcome of fibrinoid swelling plasmorrhages, sclerosis,
necrosis.
3. Hyaline is fibrillar protein complex.
4.The mechanism of formation is composed of hyaline fibrous
structures destruction and impregnating them with fibrin and other
plasma components (globulins, beta-lipoproteins, immune complexes,
and so forth.).
5.Divide: a) hyalinosis proper connective tissue b) vascular
hyalinosis;
6.Both of these species may be: a) common hyalinosis b) local
hyalinosis.

44. local hyalinosis proper
connective tissue
that hyalinosis developed in the outcome of
mucoid swelling and fibrinoid changes is
hyalinosis heart valve leaflets for rheumatism
(rheumatic heart disease).
Macroscopic picture: heart enlarged
ventricular cavity enlarged. Mitral valve dense,
whitish, spliced together and greatly deformed.
Atrioventricular opening narrowed. Chordal
strands thickened and shortened.

45. Hyalinosis heart valve leaflets for
rheumatism

46. There are 3 types of vascular hyaline:
a) simple hyaline - arises from plasmorrhages
unaltered plasma components (more common in
hypertension disease, atherosclerosis);
b) lipogialinе - contains lipids and beta-
lipoproteins (most typical for diabetes);
c) complex hyaline - constructed from immune
complexes, fibrin and destroys the structure
(typical for diseases with immunological
disorders, such as rheumatic diseases).

47. Hypertensive heart disease(A).
Hyalinosis arterioles in kidney (B).

48. Hyalinosis
1.A common hyalinosis arterioles occurs in
hypertension and diabetes as an outcome
plasmorrhages.
•2.In hypertensive due to arteriolar hyalinosis
develops arteriolosklerotic nephrosclerosis, or
primary shrunken kidneys: small dense of the kidney
with fine-grained surface and dramatically thinned
cortical layer.
•3.A common hyalinosis small vessels (mostly
arterioles) is the basis of diabetic microangiopathy.
Result: More unfavorable outcome

49. Stromal vascular lipidoses
1. Increase of fat in adipose tissue
2. Metabolic disorders of fat (cholesterol and its esters) on the walls of the
aorta and large arteries
1. Increase of fat in adipose tissue is called obesity
 Depending on the mechanism of the following types of obesity:
 a) alimentary; b) cerebral (trauma, brain tumors);
c) endocrine (Cushing's syndrome, hypophyseal syndrome, hypothyroidism,
etc.); d) hereditary.
 Outward manifestations are distinguished:
 a) a balanced type (uniform fat distribution);
 b) the upper (face, head, neck, upper body); c) Intermediate (abdominal);
 g) lower (in the hips and legs)
 Depending on the percentage of excess body weight:
 Grade I - 20-29%;
 Grade II - 30-49%;
 Grade III - 50-59%;
 Grade IV - more than 100%.

50. The heart general obesity
Macroscopic picture:
 increase the size of the heart, under the
epicardium determined accumulation of large
amounts of fat,
Microscopic picture: fatty tissue grows into
the stroma of the myocardium, cardiomyocyte
atrophy;
Result: the development of heart failure;
possible rupture of the right ventricle, where
obesity is more pronounced.

51. The heart general obesity

52. The heart general obesity

53. Stromal vascular lipidoses
2. Metabolic disorders of fat (cholesterol and its
esters) on the walls of the aorta and large arteries
Macroscopic picture: in the intima of the aorta
visible yellow spots and stripes, as well as towering
above the white-yellow plaques, some of them
ulcerated.
 Microscopic picture: when stained by Sudan III in
the thickened intima of the aorta visible lipid deposits
in the form of droplets and needle-like crystals of
cholesterol, painted in orange color; inclusion of fat
found in foam cells (macrophages, smooth muscle
cells); among lipid deposits - proliferation of
connective tissue.

54. Lipidoses in the intima of the aorta
stained by Sudan III

55. Mineral dystrophy
Breach calcium metabolism
It may be: 1.Dystrophic 2. Metastatic 3. Metabolical (the
formation of calcium-containing stones)
1.Dystrophic calcification.
1.The calcium level in blood does not vary.
2. Calcium salts are deposited locally in areas of necrosis and sclerosis
having more alkaline environment than the surrounding tissue.
3. Foci of calcification become stony density and called petrifikates.
4. Calcification occurs: in fibrous plaques with the collapse
(atheromatosis) of atherosclerosis, in the lungs during the healing foci
of caseous necrosis in tuberculosis.
5. Dystrophic calcification does not usually cause abnormalities in the
body, but in some cases (calcified heart valves, with atherosclerosis)
aggravates the course of the disease and may contribute to the
formation of blood clots on the wings of valves and vessels.

56. Net cardiosclerosis. Focal
petrifikaty in the thickness of the
myocardium

57. Calcificatio atherosclerotica

58. Mineral dystrophy
2.Metastatic calciication relects deranged calcium
metabolism and is associated with increased serum
calcium concentrations (hypercalcemia). I Almost any
disorder that increases blood calcium levels can lead
to calciication in pulmonary alveolar septa, renal
tubules and blood vessels. Metastatic calciication is
seen in various disorders, including chronic renal
failure, vitamin D intoxication and hyperparathyroidism.
3. Metabolical ( the formation of calcium-containing
stones in sites such as the gallbladder, renal pelvis,
bladder and pancreatic duct.

59. The formation of stones
Stones - very dense formations, lying freely in the abdominal
organs or excretory ducts of glands.
Classification of stones:
Structurally
1. Crystalloid (radiant)
2. Colloidal (layered)
Chemical composition:
 Gallstones can be:
 1. Pigment
 2.Calcareous
 3.Cholesteric
 Urinary stones may be:
 • urate
 • phosphates
 • oxalates, etc.

60. The formation of stones
Localization stones varied, but most often in the
urinary system and biliary tract.
Reasons for development:
• Common factors: a metabolic disorder congenital
or acquired character
• Local factors: impaired secretion stagnation
secretion, inflammatory processes in the body
Complication of gallstones is often mechanical
(obstructive) jaundice, kidney stones -
hydronephrosis.

61. Endogenous pigments: lipofuscin, melanin and
some derivatives of hemoglobin
 lipofuscin- yellow-brown insoluble pigment, also known as lipohrom or
aging pigment. It consists of polymers, lipids and phospholipids, associated
with the protein. Lipofuscin not interfere with the function of the cell.
 Lipofuscinosis - metabolic disturbance characterized by excessive
accumulation of lipofuscin, this condition can be primary (hereditary) and
secondary.
 Primary (hereditary) lipofuscinosis characterized by selective
accumulation of lipofuscin in the cells of a particular organ. Examples of
primary lipofuscinosis: hereditary steatosis (Dubin-Johnson syndrome) with
selective accumulation of lipofuscin in hepatocytes, neuronal lipofuscinosis
(Sjogren's syndrome-Spielmeyer), which is characterized by the
accumulation of pigment in the nerve cells, which is accompanied by a
decrease in intelligence, seizures, visual impairment.
 In secondary lipofuscinosis pigment found in cells undergoing slow
regressive changes, more often in older people and in patients with
malnutrition or cancer exhaustion. Usually seal body and reduce its size
(brown atrophy). The most distinctive changes occur in the liver,
myocardium, striated muscle

62. Lipofuscin in cardiomyocytes

63. Lipofuscin in cardiomyocytes

64. Melanin (from the greek. Melas -
black)
 .
Melanin is an insoluble, brown-black pigment found principally in epidermal
cells of the skin, but also in the eye and other organs. It is located in
intracellular organelles known as melanosomes and results from
polymerization of certain oxidation products of tyrosine. The amount of
melanin is responsible for the differences in skin color among the various
races, as well as the color of the eyes. It serves a protective function owing to
its ability to absorb ultraviolet light. In white persons, exposure to sun-light
increases melanin formation (tanning).
Strengthening melanogenesis - hyperpigmentation (melanosis).
The process can be : congenital and acquired, local and common .
● Acquired common melanosis - Addison's disease. Cause of the disease in a
bilateral lesion of the adrenal gland (autoimmune lesions, tuberculosis,
tumors, metastases, amyloidosis), leading to a decrease in blood levels of
cortisol and ACTH increased synthesis having melanin stimulating effect,
which causes the activation of tyrosinase and increased synthesis of melanin
in the skin and mucous shells.

65. Metabolic disturbance of melanin
.
● Congenital common melanosis - xeroderma pigmentosum.
The disease is inherited in an autosomal recessive manner
and is associated with impaired ability of the DNA of skin cells
to repair after exposure to UV light. After exposure to sunlight
appears small spotty pigmentation, also marked the area of
depigmentation, telangiectasia, skin cracks.
Focal acquired hypermelanosis - melanosis colon (people
suffering from chronic constipation). Local hyperpigmentation
include freckles, melasma, lentigines, intraepidermal nevus
(mole). Focal hyperpigmentation of the skin occurs in pituitary
adenomas, hyperthyroidism, diabetes mellitus.

66. Metabolic disturbance of melanin
Decrease in melanin synthesis appears albinism and vitiligo.
● Albinism -a hereditary disease for which, characterized by the
absence or reduction of the enzyme activity of tyrosinase.
Melanocytes are present in the body.
● Vitiligo - local manifestation of hypopigmentation,
characterized by a lack of melanocytes in the clearly limited and
often symmetrical parts, from single spots to almost complete
surface of the skin. The disease can be familial or develop after
injury, due to endocrine disorders or autoimmune, inflammatory
or necrotic after the processes in the skin (cystic dermatitis,
burns, syphilitic lesions).

67. Intraepidermal nevus

68. Intraepidermal nevus

69. Intradermalny nevus

70. Group of pigments associated with
the metabolism of hemoglobin
 1. Detect in the norm ((hemoglobin, ferritin, hemosiderin, bilirubin)
 2. Detect under pathological conditions (hematoidin, hematin, porphyrins).
 3. Containing iron (hemoglobin, ferritin, hemosiderin, hematin)
 4. Does not contain iron (bilirubin, hematoidin, porphyrins)

 Hemoglobin is a high chromoprotein contains iron and is composed of
heme and protein. The collapse of red blood cells and splitting off of
hemoglobin is called hemolysis. At physiological disintegration erythrocytes
formed pigments: ferritin, hemosiderin and bilirubin
 Hemosiderin - ferritin polymer formed mainly in macrophages of the spleen,
liver, lymph nodes, and bone marrow, as well as in almost any organ and
tissue. These cells are called sideroblasts, at their death already
synthesized pigment can be phagocytosed by other macrophages, called
siderofagami. Hemosiderin detected in cells when stained with hematoxylin
and eosin as grains of golden-yellow or golden brown, with Perls reaction,
these beads are greenish-blue color is due to formation of ferricyanide iron

71. Hemosiderin
Hemosiderin - ferritin polymer formed in macrophages
of the spleen, liver, lymph nodes, bone marrow and
any organ and tissue. These cells are called
sideroblasts, at their death already synthesized
pigment can be phagocytosed by other macrophages,
called siderofages. Hemosiderin detected in cells
when stained with hematoxylin and eosin as grains of
golden-yellow or golden brown. With Perls reaction,
these beads are greenish-blue color is due to
formation of ferricyanide iron
Excessive accumulation of hemosiderin called
hemosiderosis.
Hemosiderosis is local and general

72. Hemosiderosis
● Local hemosiderosis. Occurs when the
extravascular hemolysis in the foci of hemorrhage.
Hemosiderin accumulation does not damage tissue or
organ, but if combined with hemosiderosis sclerosis,
function is impaired.
● General hemosiderosis. Develops an excess of
iron for intravascular (intravascular) hemolysis or
increase absorption of iron from food. In these cases,
hemosiderin deposited mainly in the hepatocytes of
the liver macrophages, spleen, bone marrow and
other organs. In most cases, the pigment does not
damage the parenchymal cells and causes organ
dysfunction.

73. Brown induration of the lung

74. Hemosiderin liver cells

75. Hemochromatosis
If the high content of iron is accompanied
by tissue injury with atrophy of the
parenchyma, multiple sclerosis,
decreased organ function. This condition
is called hemochromatosis.
Hemochromatosis occurs when total
body iron content of more than 15 g
It may be primary or secondary

76. Hemochromatosis
Primary hemochromatosis. Caused by a genetic defect that
leads to increased absorption of dietary iron, usually inherited as
an autosomal recessive trait. Typical manifestations: liver
cirrhosis, diabetes, bronze skin color (bronze diabetes),
cardiomyopathy with cardiomegaly, mucous and serous
membranes, lack of exo- and endocrine glands. The brownish
color of the skin caused by an excess of melanin due to bilateral
adrenal lesions, similar to Addison's disease.
Secondary hemochromatosis. Reason: The iron-saturation of
the organism (for parenteral or intramuscular administration to
drugs, blood transfusions, overdosing of vitamin C, as well as
anemia with erythroid hyperplasia).

77. Metabolic disturbance of bilirubin
(jaundice)
At infringement of bilirubin metabolism occurs jaundice
(yellowish staining of the skin, mucous membranes,
internal organs).
Classification of jaundice.
●Overhepatic (hemolytic). Occurs when intravascular
hemolysis.
● Enterohepatic (parenchymal). Observed in cases
involving damage to hepatocytes.
● Underhepatic (mechanical or obstructive). Formed
in violation of the outflow of bile.

78. Thank you for your
attention!