Pathology of the cell and its details including cell injury and its descriptions.

1. Pathology of the cell: cell injury.
Intracellular and Extra-cellular
accumulation of substances.

2. Alteration. Cell injury.
Alteration is the pathological change of cells
structure, intercellular material, tissue and
organs which is accompanied by violation of
their vital functions.
Cell injury can be:
1. Reversible injury is characterized by the
ability of the cell to return to its normal state.
2. Irreversible cell injury leads to cell death
– necrosis or apoptosis.

3. Reasons of alteration development
1. hypoxia that leads to ischemia
2. chemicals and drugs
3. physical agents
4. microbiological agents (bacteria, viruses,
fungi's)
5. immune mechanisms
6. genetic defects (apoptosis)
7. nutritional imbalances
8. aging
All causes of cell injury can be divided into :
Hereditary causesHereditary causes
Acquired causesAcquired causes

4. Morphogenesis of cell and intercellular matrix injury
1. Iinfiltration – redundant accumulation of
metabolites into the cells and intercellular matrix.
2. Decomposition (phanerosis) – disintegration of
membranous structures of the cells and
intercellular matrix.
3. Perverted synthesis - synthesis of abnormal
substances in the cells and tissues, that are not
meeting in a norm.
4. Transformation – formation of one type of
metabolism’s products from common initial
substances for proteins, fats and carbohydrates.

5. The cellular morphologic changes induced by
various stimuli can be divided into:
1. patterns of acute cell injury — reversible and— reversible and
irreversible cell injury leading to necrosis orirreversible cell injury leading to necrosis or
apoptosis,apoptosis,
2. sub-cellular alterations that occur as responsethat occur as response
to more chronic or persistent injurious stimuli,to more chronic or persistent injurious stimuli,
3. intracellular accumulations of a numberof a number
substances — lipids, carbohydrates, proteins—substances — lipids, carbohydrates, proteins—
as a result of derangements in cell metabolismas a result of derangements in cell metabolism
or excessive storage.or excessive storage.

6. PATTERNS OF ACUTE CELL INJURY
1. Cellular swelling appears if cells are incapable of maintaining
ionic and fluid homeostasis. Macroscopically, organ is pallor,
increased density and in weight. Microscopically, small clear
vacuoles may be seen within the cytoplasm.
The ultra-structural changes:
(1) plasma membrane - blebbing, blunting, and distortion of
microvilli; creation of myelin figures;
(2) mitochondrial changes - swelling, rarefaction, and арpearance
of phospholipid-rich amorphous densities;
(3) dilatation of the endoplasmic reticulum with detachment and
dis-aggregation of polysomes;
(4) nucleolar alterations.
2. Fatty change is appearance of small or large lipid vacuoles in the
cytoplasm that occurs in hypoxic and various forms of toxic injury.

7. Patterns of acute cell injury
Cellular swellingCellular swelling
Outcomes:Outcomes: a process is reversible, but ata process is reversible, but at
protracted hypoxia can be seen necrosisprotracted hypoxia can be seen necrosis
of cellof cell
(total or focal colliquative necrosis).(total or focal colliquative necrosis).

8. CELLULAR ACCUMULATIONS
Cellular dystrophy is the morphological
display of the broken exchange of cell’s
organelles, attended with the change of
cell’s structure.

9. 1.A normal endogenous substance is produced
at a normal or increased rate, but the rate of
metabolism inadequate to remove it. Such as:
water, lipid, protein, and carbohydrates;
2. A normal or abnormal endogenous, either
exogenous, substance accumulates because it
cannot be metabolized. Such as mineral, or a
products of abnormal metabolism;
3. An abnormal exogenous substance is
deposited (pigments or an infectious products)
Categories of stockpiled substances::

10. INTRACELLULAR ACCUMULATIONS
Can represented by accumulation of:
Lipids (fatty changers)
Cholesterol and cholesterol esters
Proteins
Glycogen
Complex Lipids and Carbohydrates
Pigments

11. Intracellular accumulations of lipids
In the cytoplasm of cells lipids forms moveable lipoprotein
complexes, lipids with proteins – lipoproteids. They make
basis of cell membranes.
Reasons:
1. anoxaemia at:
а) diseases of the cardio-vascular system
b) chronic diseases of lungs
c) anemia’s
2. diabetes mellitus
3. obesity
4. protein malnutrition
5. hepatotoxins (alcohol abuse)
The most frequent localization: myocardium, liver, kidney

12. Liver: organ enlarges and becomes yellow, soft
and greasy - “goose liver”.
Microscopically there are small fat vacuoles in
the cytoplasm of hepatocytes around the
nucleus.
Heart. Lipid is found in heart muscle-cells in the
form of small droplets. It occurs in two patterns:
1. prolonged moderate hypoxia, which create
grossly apparent bands of yellow myocardium
with bands of darker, red-brown, un-involved
myocardium - “tiger’s heart”.
2. fatty change produced some forms of
myocarditis

13. Intracellular accumulations of proteinsIntracellular accumulations of proteins
Any disorder producing proteinuria leads to
pinocytotic reabsorption of the protein in
kidney tubules. When these pinocytotic
vesicles in the epithelial cells fuse with
lysosomes, hyaline cytoplasmic droplets,
which appear pink in hematoxylin and eosin
stains, are formed.
Mechanism: infiltration.
Accumulations of immunoglobulins
synthesized in the cisternae of the RER of
plasma cells may create rounded, acidophilic
Russell bodies.

14. Liver - Mallory bodies (the red globular material)
composed of cytoskeletal filaments in liver cells
chronically damaged from alcoholism.
Intracellular accumulations of proteinsIntracellular accumulations of proteins
Keratoid (horny) – characterized by increase
production of keratin substance in epithelium
of skin, squamous epithelial cells of cervix,
esophagus

15. Intracellular accumulations of pigmentsIntracellular accumulations of pigments
Pigments can be:
1. exogenous, coming from outside the body,
2. endogenous, synthesized within the body itself.
Exogenous pigment is carbon or coal dust, which is
air pollutant of urban life. When inhaled, it is picked
up by alveolar macro-phages and transported
through lymphatic channels to the regional
tracheobronchial lymph nodes (anthracosis).

16. Violations of pigments exchanging consist of:
1. increase of its quantity
2. stopping of pigment’s synthesis
3. violation of further metabolism
4. the appearance of pigments that are not meeting
at norm.
Intracellular accumulations of pigmentsIntracellular accumulations of pigments
Endogenous pigments are:
1. hemoglobin-derived – derivative of hemoglobin;
2. protein-derived – derivative of amino acid;
3. lipopigments – lipofuscin.

17. Hemoglobin-derived pigments
From fragments of hemoglobin the following
pigments are appeared :
in norm - ferritin , hemosiderin, billirubin
in pathology – hematin, hematoidin, porfirin
Hemosiderin is a hemoglobin-derived, golden-
yellow granular pigment,
in such form iron is stored in cells.

18. Hemosiderin accumulate in cells as:
1. a localized process - result from hemorrhages
2. a systemic hemosiderosis – it is deposited in many
organs and tissues. It is seen at:
(1) increased absorption of dietary iron,
(2) impaired utilization of iron,
(3) hemolytic anemias,
(4) transfusions, (5) poisons, (6) infections

19. It is derived from hemoglobin but does not contain iron.
Its normal formation and excretion are vital to health,
and jaundice is a common clinical disorder due to
excesses of this pigment within cells and tissues.
Pathology of billirubin exchange
According to the mechanism of development
jaundice is subdivided into three types:
1. before-hepatic (hemolytic)
2. hepatic (parenhimatosis)
3. sub-hepatic (mechanical)
They are differentiate:
-on the billirubin concentration in blood,
-on the tint (color) of skin,
-on the color of urine and excrement.

20. Pathology of billirubin exchange
Hereditary hyperbilirubinemias reflect defects in bilirubin
conjugation or excretion, or both.
Hepatocellular changes are most pronounced in the
Dubin-Johnson syndrome.
The liver appears brown-black on gross examination
and the hepatocytes contain large amounts of
cytoplasmic brown pigment

21. Intracellular accumulations of pigments
Melanin it is an endogenous, brown-black tyrosin-derived
pigment formed in melanocytes.
Classification of changers:
1. system increasing – in norm (sunburn), in pathology:
a) vices of ectoderm development (hereditary)
b) destruction of cortex or all adrenal gland (innate)
2. local increasing of melanin - pigment nevus (innate
vice of skin development)
3. general de-pigmentation - albinism (genetic pathology)
it is characterized by white skin and hairs, red eyes
4. local de-pigmentation – autoimmune local destruction
of melanogenic cells of skin – white spots (vitiligo), or
destruction of nerves, which innervate melanocytes – at
Syphilis (leykoderma).

22. MELANIN
Increasing
Decreasing
Innate Hereditary
Innate Hereditary
Local Systemic
Local
Systemic
Local Systemic
Local Systemic
vitiligo albinism
leucoderma
vitiligo
pigmentalnevi pathologic physiologic

23. Extracellular accumulations
The four major components, best seen in connective
tissue, are:
1. Collagen fibers (non-branching)
2. Elastic fibers (branching)
3. Proteoglycans (a gel)
4. Basement membranes (sheets)
Extracellular pathology includes changes in quantity
and quality of normal components, as well as the
appearance of abnormal materials.
The mechanisms: - a congenital defect
- acquired pathology

24. Extracellular accumulations
Types of stored substances in extra-cellular
matrix:
1. Lipids
2. Proteins
3. Minerals
4. Pigments
5. Glycogen
6. Complex Lipids and Carbohydrates

25. Mucoid swelling
It is disorganization and swelling of
perivascular intercellular matrix
(disorganization of connective
tissue).
Microscopic research:Microscopic research: there is the phenomenon of meta-there is the phenomenon of meta-
chromatic changers. That is - basophyl color of basicchromatic changers. That is - basophyl color of basic
substances. Collagen fibers don’t change the structure,substances. Collagen fibers don’t change the structure,
but swell and undergo fibrillar destruction. A process isbut swell and undergo fibrillar destruction. A process is
often accompanied by the cellular reactions - there areoften accompanied by the cellular reactions - there are
lymphocytes, plasma cells and histyocytes.lymphocytes, plasma cells and histyocytes.
Macroscopic researchMacroscopic research:: tissue or organ is stored.tissue or organ is stored.
Process is convertible at the removal of reason.Process is convertible at the removal of reason.

26. Fibrine changes
Microscopic research: the collagen fibers are saturated
with the proteins of plasma and become
homogeneous, forming insoluble durable connections
with a fibrin; they eozynophyl,
SHYK-“+” .
Macroscopic research: tissue or organ is stored.
Outcomes: 1. fibrinoid necrosis,
2. hyalinosis,
3. sclerosis

27. Fibrin changes
It is deep and irreversible disorganization of connective
tissue, in basis of which destruction of basic substances
and fibers lies. It is accompanied by the acute
increasing of permeability of vessels and formation of
fibrinoid.
It is characterized byIt is characterized by
swelling of intercellularswelling of intercellular
matrix and collagen fibers,matrix and collagen fibers,
their destruction withtheir destruction with
formation of fibrin in placeformation of fibrin in place
of the blasted fibers.of the blasted fibers.

28. Hyaline change
It is an alteration within cells or in the extracellular
space, which gives a homogenous, glassy, pink
appearance in routine histological sections stained
with hematoxilin and eosin.
It is characterized by
accumulation in tissue of
pathological albumens of dense
consistency, reminding a hyalin
cartilage.
Hyaline consists of plasma
albumens, lipids, carbohydrates
and AB.
Extracellular accumulations of proteinsExtracellular accumulations of proteins

29. Types of hyalinosis according to
mechanisms of formation:
1. hyaline in the finale of fibrinoid changers – arises up in
damaged perivascular stroma of organs or in the wall of the
damaged arteries or arterioles
2. hyaline in the finale of plasmatic impregnation of vascular
wall – in the vessel’s wall after protracted angio-spasm at
patients with hyperglycemia and hyperlipidemia
3. local hyalinosis in the finale of inflammation – after
calming down of process in the hearth of inflammation
appears local hyalinosis
4. hyaline in the finale of necrosis and 5. sclerosis
Outcomes: A process is irreversible, is completed by
structural deformation of organs (at rheumatism – hyalinosis
of heart valves)