This document provides an overview of pathological physiology, focusing on hyperbiotic and hypobiotic processes, neoplasia (tumors), and tumor characteristics. It discusses disorders of tissue growth during prenatal and postnatal development. Hyperbiotic processes include hyperplasia, hypertrophy, and regeneration, while hypobiotic processes involve atrophy. Neoplasia is defined as non-controllable cell proliferation leading to tumor formation, which can be caused by oncogenic mutations, carcinogenic factors, or viruses. Tumors are characterized by atypical cell and tissue growth, invasion and metastasis potential, and relapse. The document also briefly outlines tumor diagnosis and treatment approaches.

1. DEPARTMENT OF PATHOLOGICAL PHYSIOLOGY- 2019

2. The Plan of Lecture
1. Hyperbiotic and hypobiotic processes
2. Neoplasia. Tumor
3. Nomenclature of tumor
4. Carcinogenic factors
5. Pathogenetic mechanisms of tumors
6. Protooncogenes
7. Tumor suppressor genes
8. Genes of apoptosis
9. DNA repair genes
10.Atypicalness.
11.Metastases
12.Mechanisms of anti-blastomic resistance

3. Disorders of the tissue growth may occur at all periods of the individual
(intrauterine as well as postnatal) development of the organism:
PRENATAL PERIOD
a) gametopathies- occur at the period of maturation of gametes (spermatozoon and
ovum ) and fertilization
b) blastopathies- occur from the moment of fertilization up to the 15th day of
pregnancy
c) embryopathies - occur from the 16th up to the 75th day of pregnancy;
d) fetopathies – occur from the 76th up to the 280th day of the pregnancy (up to
the birth);
POSTNATAL PERIOD
1.Hypobiotic processes- inhibition of the tissue growth
2. Hyperbiotic processes- acceleration of the tissue growth

5. Hyper- and hypobiotic processes
nucle
us
Normal cell
Disaplasia
Hyperplasia
Hypertrophy
Atrophy
Metaplasia

7. Atrophy- is the pathological process which is
characterized by diminution of the volume of
cells, tissues or organs.
-Physiological and pathological forms
-General and local forms
Reasons:
-disfunctional
-neurogenic
-mechanical compression
-physical, chemical factors and etc .

9. Hypertrophy – increasing of the volume of
tissue due to increasing of each cell volume .
- Increased work load
-Physiological and pathological hypertrophy
-Compensatory or vicarious hypertrophy
-Regeneration hypertrophy
-Correlation hypertrophy
-True and false (pseudo-) hypertrophy

10. Hyperplasia – increasing of the
volume of tissues as a result of an
increase in the number of cells (division
of cells).
-Physiological and pathological forms
-Hormonal and
-Compensator types of hyperplasia

11. Regeneration – is the restoration
of destructed or lost tissue.
-physiological regeneration
-reparative regeneration
-pathological forms:
-hyperregeneration
-hyporegeneration
-metaplasia
- dysplasia

12. • Metaplasia — means replacement of one
type of the cell by other one derived from the
same tissue.
• Dysplasia — is the proliferation and
formation of different sized, shaped and
structured cells in the tissue due to genetic
reprogramming.

13. Neoplasia — non-controllable,
uncoordinated, unlimited, excessive, rapid,
abnormal proliferation of cells that leads to
the formation of tumor. This typical
pathological process arise under influence of
carcinogenic factors.

14. The reason for development of
Neolasia is oncogenic mutations
• 1.Protooncogenes
• 2.Tumor-supressor genes
• 3.Genes of apoptosis
• 4. DNA repair genes

15. C
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Chemical
Action of soot and tar, chrome, nickel,
arsenic compounds, cobalt, asbestos,
benzol, polycyclic and aromatic
hydrocarbons, aromatic amins, aflatoksin,
hormons (estrogen)
Physical
Ionizing radiation, ultraviolet rays , X-rays,
burns , mechanical trauma and etc.
Biological
Oncogenic -viruses:
DNA-included oncoviruses : human
papilloma virus (HPV), herpes virus (HHV-
8), Epstain-Barr virus (EBV), hepatitis B and
C virus (HBV and HCV)
RNA-included oncoviruses: HIV (AIDS),
HTLV-1 and etc.

17. Nomenclature of tumors
vThe name of tumors are usually formed by adding the suffix “-oma” to the
names of tissue from which they develop. Malignant tumors of the epithelial
tissue are called cancer or carcinoma, and malignant tumors of connective
tissue- sarcoma.
BENIGN
Fibroma – tumor of connective tissue. It
frequently is observed in brest, uterus and
etc.
Myoma — tumor developed in the muscle
tissue.
Leiomyoma ― tumor developed from
smooth muscles.
Rabdomyoma ― tumor developed from
striated muscles.
Hemangyoma — tumor of vascular origine.
Lymphangyoma ― tumor developed from
the lymph vessel.
Lipoma — tumor of fat tissue.
Osteoma – tumor developed from bones.
Хоndroma ― tumor developed from
cartilages.
MALIGNANT
Fibrosarcoma - malignant tumor of
connective tissue.
Myosarcoma — malignant tumor
developed in the muscle tissue.
Liposarcoma – malignant tumor of fat
tissue.
Angiosarcoma — malignant tumor of
vascular origin.
Оsteosarcoma - malignant tumor
developed from bones.
Хоndrosarcoma. – malignant tumor
developed from cartilages

19. Fibroma
Hemangioma

20. BENIGN
1. Consist of differentiated cells.
2. Tissue atypicalness is observed.
3. Moderate rate of growth is characteristic.
4. Expansive pathway of growth is
characteristic.
5. Don’t metastasize.
6. Enveloped into capsule.
7. Metabolism in benign tumors does not
differ from that of in normal tissue.
MALIGNANT
1. Consist of undifferentiated cells
2. Tissue and cell atypicalness are observed.
3. Invasive pathway of growth and excess
rapid growing are characteristic.
4. Metastases are frequent.
5. Recidivating is frequent.
6. Don’t poses capsule.
7. Inverts metabolism in the organism,
intoxication and cachexia are observed

21. •Epigenomic mechanism
•Mutation mechanism

22. Steps of Virus Cancerogenesis
• Cytoreception of virus
• Internalization
• Integration
• Persist replication of viruses inside the cell
• Transformation of cell
• Promotion
• Progression.

23. Mutated gens in oncogenesis
1.Protooncogenes
2.Tumor-supressor genes
3.Genes of apoptosis
4.DNA repair genes

24. Protooncogen Tumor
ERB-1 Lung cancer, glyoma
ERB-2 Brest cancer, ovarian cancer
K-RAS Lung Cancer , cancer of pancreas
and intestine
H-RAS Cancer of kidneys
N-RAS Melanoma
Abl Chronic mieloleukosis
C-myc Burkitt limfoma
N-myc Neuroblastoma
L-myc Small cellular cancer of lungs

25. Antioncogen Tumor
E-kadherin Brest and stomach cancer
NF-1 Neurofibromatosis I-type
NF-2 Neurofibromatosis II-type
APC Cancer of stomach, pancreas
and intestine
Rb Retinoblastoma
p53 Li-Fraumeny syndrome
WT-1 Willms tumor
BRCA-1 Brest and ovarian cancer
BRCA-2 Brest cancer in women and
men

26. Mutation of p53 gen

28. Steps of chemical
carcinogenesis
• Initiation (transformation of normal cell
into the neoplastic)
• Promotion (action of promoters
stimulate the rapid proliferation of
neoplastic cells)
• Tumor progression (due to additional
mutations tumor cells undergo to
malignisation)

29. Characteristic features of tumor

30. • Atypicalness. The tumor cells differ from
the normal, also from the cells that are
observed in other pathological processes.
As distinct from the proliferative
inflammation, hyperplasia, regeneration,
etc., in tumors reproduction of cells does
not depend on regulative mechanisms of
the organism.
• Morphological, biochemical, functional,
immunological and growth atypycalnesses are
observed.

31. vMorphological atypicalness:
• Cellular: Hyperchromic, enlarged nuclei,
chromosomal abnormality, multinuclear
cells are observed. The volume of
cytoplasm decreases, the number of
ribosome's increases. The form and
volume of mitochondria changes.
Membrane surface larger than in the tumor
cells and weakening of the intercellular
connections are observed.
• Tissue atypicalness: atypical structural
changes in the tumor growing tissue

32. Stages of neoplasia

33. vAnomaly of division (unlimited,
noncontrollable division, immortality of cells).
v Anomaly of differentiation (lack of
differentiation).
Characteristic features of tumor
vAtypicalness of growth - anomalies of cell
division, lack of differensation, ability of
invasion and metastasis, relapse.

35. Mechanism of invasion

36. Metastasis by hematogenic pathway

37. Biochemical atypicalness
Accelerated consumption of amino acids,
glucose, cholesterol by tumor cells and
activation of anaerobic glycolysis.
Tumor cell is a "trap" for nitrogen-containing
compounds
Tumor cell is a "trap" for carbohydrates
Tumor cell is a "trap" for lipids

38. Functional atypicalness
Hypofunction
Hyperfunction
Dysfunction

39. Tumor antigens recognised by
T-lymphocytes (CD8+)

40. Mechanisms of antiblastomic resistance
Anticancerogenic
Antimutation
Anticellular (specific,
non-specific)

41. Diagnosis and general principles for the treatment of neoplasia.
TNM system (T - tumor, N - lymph node, M - metastasis).
T - indicates the size of the tumor,
N - involvement of regional lymph nodes in the process,
M - indicates the presence of metastases.
PI- proliferation index is the criteria to verify the
degree of histological and biological malignancy of the
tumor. The marker for determining PI is the
expression of Ki-67.
Ki-67 is a nuclear antigen, which is an indicator of the
cell being in the stage of division (proliferation) stage.
Classical triad for the treatment of cancer:
Surgical → chemotherapy → radiotherapy.
Immunotherapy (monoclonal antibodies)
is also used.