This document provides an overview of pathology and inflammation. It defines pathology as the scientific study of disease and outlines its main classifications. It also describes the core components of pathology including etiology, morphological changes, clinical significance, and pathogenesis. Different types of cell injuries, necrosis, and cellular adaptations such as atrophy, hypertrophy, hyperplasia, and metaplasia are discussed. The document concludes with a definition and causes of inflammation.

1. PATHOLOGY
Dr/ Ammar Omar
Assistant professor of Histopathology
Department of Pathology and Histology
Thamar university

2. INTRODUCTION TO PATHOLOGY
PAHOLOGY: the scientific study of disease is
called pathology. It is the study of who the
organs and tissues of a healthy body changes to
those of a sick person.
CLASSIFICATION:
• General and special pathology
• Clinical and anatomical pathology

3. General pathology:-
It is the study of basic reactions of cells and tissues to
abnormal stimuli that underlay all diseases i.e it
describes basic principles and mechanisms of diseases
productions, for examples, inflammations.
Special pathology:-
It is the study of specific responses of specialized
organs and tissues to more or less well-defined stimuli
i.e. special pathology deals with diseases of specific
organs or system of the body, for example,
inflammation in lung or kidney.

4. Core of pathology
Core of
pathology
Etiology
Morphological
changes
Clinical
significance
Pathogenesis

5. Etiology-course of disease
Etiology
Genetic
Acquired

6. Genetic:-
Abnormalities of chromosomes called mutations or defect
in genes.
Acquired:-
• Physical agents
• Chemical poisons
• Nutritional deficiencies
• Infections
• Abnormal immunological reactions
• Psychological factors

7. Pathogenesis
Pathogenesis means the sequences of events in the cells or tissues
or the whole organism in response to the causative agent- from
the initial stimulus to the ultimate expression of the
manifestations of the diseases.
Morphological changes
This refers to the structural and associated functional
changes in the cells or tissues that are either characteristics
of the diseases or diagnostic of the etiological process.

8. Clinical significance
It refers to sings, symptoms, course and prognosis of the
disease.

9. Cell injury
When the limits of adaptive capacity are
exceeded or when no adaptive response is
possible, a consequences of events follows,
termed as cell injury.

11. Reversible cell injury
It donates pathological changes
that can be reversed when the
stimulus (or stress) is removed
or if the cause of injury is mild.
Irreversible cell injury
It donates pathological changes
that are permanent and cause
cell death.

12. Causes of cell
injury
Hypoxia
Physical
agents
Chemical
agents
Immunological
reactions
Genetic
defects
Microbiologi
cal agents
Nutritional
imbalance

13. Mechanisms of cell injury
1. Impaired cell membrane function by
• Production of free radicals
• Loss of calcium homeostasis
• Activations of complements
• Lysis of enzymes
• Direct membrane Lysis by viruses, heats, cold
and chemicals

14. 2. Decrease ATP production due to
• Hypoxia
• Hypoglycemia
3. Genetics alterations
4. Metabolic derangements
• Exposure to exogenous injurious agents
• Accumulation of some endogenous substances

15. Features of irreversible cell injury
Nuclear changes
Nucleus may show one of the three patterns of
changes.
• Pyknosis
• Karyolysis
• Karyorrhexis

16. Cytoplasmic changes
• Irreversible damage to mitochondria manifested by
sever vacuolization
• Extensive damage to the plasma membrane
• Massive calcium influx acting as a poisons for
mitochondria
• Loss of enzyme and proteins due to increased
membrane permeability
• Lysosomal swelling and leakage of enzymes

17. Necrosis
Definitions
1- Necrosis refers to a sequence of morphological
changes that follow cell death in livening tissue.
2- The morphological changes caused by progressive
degradative actions on dead cells is called necrosis.
3- Necrosis is the sum of intracellular degradative
reactions occurring after the death of individual cell
within a living organism.
Necrosis = cell death + morphological changes.

18. Mechanism of necrosis
Mechanism
of necrosis
Enzymatic
degradation of cell
Denaturation
of protein

19. Types of Necrosis
Types of
necrosis
Liquefactive
necrosis
Gangrenous
necrosis
Fat necrosis
Fibrinoid
necrosis
Coagulative
necrosis

20. Coagulative necrosis
• in this type of necrosis, the necrotic cell retains
in cellular outline for several days. Coagulative
necrosis typically occur in solid organ, such as
kidney, heart, and adrenal gland as a result of
deficient blood supply and anoxia.

21. Liquefactive necrosis
Liquefactive necrosis:- Liquefactive necrosis is
characterized by digestion of tissue. It shows
softening& liquefaction of tissue. It
characteristically results from ischemic injury to
the CNS. It also occurs in superlative infections
characterized by formation of pus.

23. Caseous necrosis
• Caseous necrosis has a cheese-like (caseous,
white) appearance to the naked eye. And it
appears as an amorphous eosinophilic
material on microscopic examination. Caseous
necrosis is typical of tuberculosis.

24. Fat necrosis
• Fat necrosis can be caused by trauma to tissue with high fat
content, such as the breast or it can also be caused by acute
hemorrhagic pancreatitis in which pancreatic enzymes diffuse
into the inflamed pancreatic tissue & digest it. The fatty acids
released from the digestion form calcium salts (soap formation
or dystrophic calcification). In addition, the elastase enzyme
digests the blood vessels & cause the hemorrhage inside the
pancreas, hence the name hemorrhagic pancreatitis.

25. Fibrinoid necrosis
• Fibrinoid necrosis is a special form of necrosis
usually caused by immunemediated vascular damage.
It is marked by complexes of antigen and antibodies,
sometimes referred to as ―immune complexes‖.

26. Gangrenous necrosis
Gangrenous
necrosis
Dry Gangrenous Gas Gangrenous
Wet Gangrenous

27. Dry Gangrenous
. Commonly occur in limbs due to ischemia leading to
Coagulative necrosis involving multiple tissue layers.
. The organ is dry, shrunken and limited putrefaction.
. Not complicated with bacterial infection.

28. Wet Gangrenous
• occurs due to ischemia ( see in moist tissue e.g
intestine).
• The organ is moist, ,soft, swollen, and dark
with marked putrefaction.
• Coplicated with bacterial infections.

29. Gas Gangrenous
• Caused by bacteria (clostridium perferingens.
• commonly occur in muscles tissues.

30. Apoptosis
• Definition: apoptosis is a distinctive morphologic pattern of cell death affecting a
single or small group of cell. Apoptosis is energy- dependent programmed cell
death for removal of unwanted individual cell. Apoptosis in Greak means
*dropping off*
• Death by apoptosis is a normal phenomenon that serve to eliminate cell that are no
longer needed and to maintain a steady number of cells in tissue.
• The main event in apoptosis is the activation of enzymes called caspases

32. Comparison between necrosis and apoptosis
Necrosis Apoptosis
Stimuli Hypoxia & toxins Physiological &
pathological
Histological detection Easy Difficult
Cell affected Large group Single cell or small group
Nucleus Pyknosis,
karyorrhexis&karyolysis
Condensation &
fragmentation of chromatin
Cytoplasm Cytomegaly Shrinkage
Tissue reaction Inflammation No inflammation

33. Cellular Adaptations

34. • Adaptations are reversible changes in the
number, size, phenotypes, metabolic activity,
or function of cells in response to changes in
their environment.

35. Following are the important adaptive changes:
 Atrophy: decrease in cell size.
 Hypertrophy: increase in cell size.
 Hyperplasia: increase in cell number.
 Metaplasia: change in cell type.

37. Atrophy
• Shrinkage in the cell size by loss of cell substances is
known as atrophy. Atrophic cells may have
diminished function.

38. Atrophy
Disuse
atrophy
Denervation
atrophy
Pressure
atrophy
Atrophy due
to endocrine
deficiency
Atrophy due
to lack of
nutrients
Senile
atrophy
Ischemic
atrophy

39. Hypertrophy
• is increase in the size of cells resulting in size of organ.
1. Physiologic hypertrophy e.g increased functional
demand (striated muscle cells in skeletal muscles and
heart) or hormonal stimulations (enlargement of
uterus during pregnancy).
2. Pathologic hypertrophy e.g cardiac enlargement due
to hypertension or aortic valve diseases.

40. Hyperplasia
• is an increase in the number of cells. It can
lead to an increase in the size of the organ. It is
usually caused by hormonal stimulation. It can
be physiological as in enlargement of the
breast during pregnancy or it can pathological
as in wound healing.

42. Metaplasia
• Transformation of differentiated mature cells
into another type of cells of the same group.
• Metaplasia occurs in cells to adapt them to the
change in their environment or their function.
Metaplasia may be a precancerous lesion.

43. Ciliated columnar cells
Stratifiied squamous cells

44. Dysplasia
• disordered epithelial cellular proliferation commonly
in association with chronic irritation or chronic
inflammation.

45. • Loss of normal arrangement. Cell show pleomorphism, hyperchromatism
and occasional mitosis.
• Pleomorphism: cells variable in size and shape in the tissue.
• Dysplasia may be:
• -Mild (basal third of the epithelium).
• Moderate (lower two third).
• Severe (whole epithelial thickness).
• Mild dysplasia is commonly reversible, severe dysplasia is a precancerous
lesion.

46. Anaplasia
• Cells differentiate to a more IMMATURE or
embryonic form.
• Malignant tumors are characterized by anaplastic cell
growth.
• Ovarian cancer cells dividing

47. INFLAMMATION
Definition:
Inflammation is a protective involving host cells,
B.V, proteins and other mediators that is intended
to:
Eliminate the initial cause of cell injury.
Removal of the necrotic cells and tissue.
Initiate the process of repair.

48. Nomenclature:
The Nomenclature of inflammatory lesion are
usually indicated the suffix (itis).
Examples:
Inflammation of appendix appendicitis
Inflammation of pancreas pancreatitis
Exception
Inflammation of the lung pneumonia

49. Causes of inflammation
1. Biological injury by infection of bacteria, viruses and
parasites.
2. Physical injury by severe cold, heat and radiation.
3. Chemical injury by acids, alkalis and others.
4. Mechanical injury by trauma, friction and foreign
bodies.
5. Immunological injury e.g. antigen-antibody cell
reaction.
6. Any tissue damage leading to necrosis.

50. Cardinal signs of inflammation:
1. Heat (calor)
2. Redness ( rubor)
3. Pain (dolor)
4. Loss of function ( functio lesa)
5. Swelling (tumor)

51. Types of inflammation
Acute inflammation
is an inflammation of short duration characterized by
formation of inflammation exudate.
Chronic inflammation
which is an inflammation of prolonged duration
characterized by tissue destruction and healing of the
tissue.

53. Acute inflammation
• In acute inflammation the tissue response is
rapid i.e. sudden onset. It lasts for days of few
weeks and is characterized by the presence of
fluid exudate, fibrin threads and
polymorphonuclear leucocytes (neutrophil).

54. ACUTE INFLAMMATION:
The classical signs are: REDNESS (rubor)
HEAT (calor)
SWELLING (tumour)
PAIN (dolor)
LOSS OF FUNCTION (functio laesa).
These gross signs are explained by changes occurring at
microscopic level. Three essential features are:
1. HYPERAEMIA
2. EXUDATION OF FLUID
3. EMIGRATION OF LEUCOCYTES.

55. • HYPERAEMIA: The hyperaemia in inflammation is
associated with the well known microvascular changes.

56. EXUDATION: Exudation is the increased passage of protein-rich
fluid through the vessel wall into the interstitial tissue.

58. • EMIGRATION OF LEUCOCYTES :
Neutrophils and mononuclears pass between the endothelial cell
junctions by amoeboid movement through the venule wall into
the tissue spaces. In this process both neutrophils and endothelial
cells are activated and both express cell adhesion molecules,
initially SELECTINS and then INTEGRINS.

61. CHEMOTAXIS:
The initial margination of neutrophils and mononuclears
is potentiated by slowing of blood flow and by
increased ‘stickiness’ of the endothelial surface. After
penetration of the vessel wall, the subsequent movement
of the leucocytes is controlled by CHEMOTAXIS. The
cell moves in response to an increasing concentration
gradient of the particular chemotactic agent, usually a
protein or polypeptide

63. • Important examples of chemotactic agents are:
Fractions of the COMPLEMENT SYSTEM (esp. C3a) Factors
derived from arachidonic acid by the neutrophils –
LEUKOTRIENES (e.g. LTB4) Factors derived from pathogenic
BACTERIA Factors derived from sensitised lymphocytes –
CYTOKINES (e.g. IL-8). The leucocytes move by extension of
an anterior pseudopod with attachment to extracellular matrix
molecules such as fibronectin using cell adhesion molecules. The
cell body is then pulled forward by actin and myosin filaments.

64. PHAGOCYTOSIS:
This is the process by which neutrophils and
macrophages clear the injurious agent. It is an
important defence mechanism in bacterial
infections particularly.

66. There are 3 families of OPSONIN.
1. Immunoglobulin, especially IgG – recognized by Fc receptors
on neutrophil surface.
2. Complement, especially C3b – recognized by C3b receptors on
neutrophil surface.
3. Carbohydrate binding proteins, or lectins – bind sugar residues
on bacterial cell walls. The opsonic activity is enhanced when it is
confined within a solid organ or rigid medium such as a fibrin
network; where conditions are looser and more fluid, activity is
diminished.

67. • CHEMICAL MEDIATORS:
Various chemical mediators have roles in the inflammatory
process. They may be circulating in plasma and require activation
or they may be secreted by inflammatory cells. Many of these
mediators have overlapping actions.

68. Mediators derived from:
1. Inflammatory cells

69. 2. Plasma. These pathways are all interrelated.

70. SEQUELS OF ACUTE INFLAMMATION

71. Types of acute inflammation
1. Suppurative inflammation: associated with pus
formation.
• Localized: abscess.
• Diffuse: cellulitis.

72. cellulitis

73. 2. Non suppurative inflammation: with no pus
formation. It includes:
Catarrhal inflammation Catarrha rhinitis
Membranous inflammation Diphtheria
Fibrinous inflammation Lobar pneumonia
Serous inflammation Mild burns
Sero- fibrinous inflammation Pleurisy
Haemorrhagic inflammation Streptococcal
Necrotizing inflammation Infective gangrene
Allergic inflammation Bronchial asthma

74. Catarrhal inflammation

75. Serous inflammation

76. Pleurisy
Sero- fibrinous inflammation

77. A-Right cranial lobe, lobar pneumonia (arrow), dorsal appearance, B-Right cranial
lobe with medial lobe, lobar pneumonia (arrow), dorsal appearance, C-Medial lobe
lobular pneumonia (arrow), adhesion on visceral pleura (thin arrow), dorsal
appearance, D-.The cut section of pneumonic areas

78. Membranous inflammation
Diphtheria

79. Haemorrhagic inflammation
Streptococcal

80. Necrotizing inflammation

81. Allergic inflammation Bronchial asthma

82. CHRONIC INFLAMMATION
Definition:
Chronic inflammation can be defined as a prolonged
inflammatory process (weeks or months) where an
active inflammation, tissue destruction and attempts at
repair are proceeding simultaneously.

83. Causes of chronic inflammation:
 Persistent infections Certain microorganisms associated with
intracellular infection such as tuberculosis, leprosy, certain
fungi etc characteristically cause chronic inflammation.
 These organisms are of low toxicity and evoke delayed
hypersensitivity reactions.
 Prolonged exposure to nondegradable but partially toxic
substances either endogenous lipid components which result
in atherosclerosis or exogenous substances such as silica,
asbestos.
 Progression from acute inflammation: Acute inflammation
almost always progresses to chronic inflammation following:
a. Persistent suppuration as a result of uncollapsed abscess
cavities, foreign body materials (dirt, cloth, wool, etc),
sequesterum in osteomylitis, or a sinus/fistula from chronic
abscesses.
 Autoimmuniy. Autoimmune diseases such as rheumatoid
arthritis and systemic lupus erythematosis are chronic
inflammations from the outset.

84. Cells of chronic inflammation:

85. Classification of chronic inflammation:
1. Non specific chronic inflammation:
This involves a diffuse accumulation of macrophages and lymphocytes at
site of injury that is usually productive with new fibrous tissue formations.
E.g. Chronic cholecystitis.
2. Specific inflammation (granulomatous inflammation):
Definition: Granulomatous inflammation is characterized by the presence
of granuloma. A granuloma is a microscopic aggregate of epithelioid cells.
Epithelioid cell is an activated macrophage, with a modified epithelial cell-
like appearance (hence the name epithelioid). The epitheloid cells can fuse
with each other & form multinucleated giant cells. So, even though, a
granuloma is basically a collection of epithelioid cells, it also usually
contains multinucleated giant cell & is usually surrounded by a cuff of
lymphocytes and occasional plasma cells. There are two types of giant
cells:

86. a. Foreign body-type giant cells which have irregularly
scattered nuclei in presence of indigestible materials.
b. Langhans giant cells in which the nuclei are arranged
peripherally in a horse -shoe pattern which is seen
typically in tuberculosis, sarcoidosis etc… Giant cells are
formed by fusion of macrophages perhaps by a concerted
attempt of two or more cells to engulf a single particle.

87. Pathogenesis:
There are two types of granulomas, which differ
in their pathogenesis.
A. Foreign body granuloma
These granulomas are initiated by inert foreign
bodies such as talc, sutures (nonabsorbable),
fibers, etc… that are large enough to preclude
phagocytosis by a single macrophage and do not
incite an immune response.

88. B. Immune granulomas
Antigen presenting cells (macrophages) engulf a poorly
soluble inciting agent. Then, the macrophage processes and
presents part of the antigen (in association with MHC type2
molecules) to CD4+T helper 1 cells which become activated.
The activated CD4+ T-cells produce cytokines (IL-2 and
interferon gamma).The IL-2 activates other CD4+T helper
cells and perpetuates the response while IFN-γ is important in
transforming macrophages into epitheloid cells and
multinucleated giant cells. The cytokines have been implicated
not only in the formation but also in the maintenance of
granuloma.
Macrophage inhibitory factor helps to localize activated
macrophages and epitheloid cells.

89. SYSTEMIC EFFECTS OF INFLAMMATIONS
• The systemic effects of inflammation include:
a. Fever
b. Endocrine & metabolic responses
c. Autonomic responses
d. Behavioral responses
e. Leukocytosis
f. Leukopenia
g. Weight loss

90. Repair
Definition: repair is the replacement of the
damaged tissue by new healthy one.
Types:
1. Regeneration: replacement of damaged cells by
cells of the same kind. Regeneration means the
ability of the cells to divide and reproduce
themselves.
2. Fibrosis: replacement of damaged tissue by
granulation tissue which matures to fibrous tissue.

91. HEALING
I. Definition of healing
The word healing, used in a pathological context, refers to
the body‘s replacement of destroyed tissue by living tissue.
II. Processes of healing
The healing process involves two distinct processes:
- Regeneration, the replacement of lost tissue by tissues
similar in type and
- Repair (healing by scaring), the replacement of lost tissue
by granulation tissue which matures to form scar tissue.
Healing by fibrosis is inevitable when the surrounding
specialized cells do not possess the capacity to proliferate.

92. • Tissue → Inflammation → Removal of dead
tissue & Damage

93. • Processes of healing: Removal of dead tissue &
injurious agent and replacement occur simultaneously.
Whether healing takes place by regeneration or by repair
(scarring) is determined partly by the type of cells in the
damaged organ & partly by the destruction or the
intactness of the stromal frame work of the organ. Hence,
it is important to know the types of cells in the body.

94. • Types of cells:
Based on their proliferative capacity there are three types
of cells.
1. Labile cells
These are cells which have a continuous turn over by
programmed division of stem cells. They are found in the
surface epithelium of the gastrointestinal tract, urinary
tract or the skin. The cells of lymphoid and haemopoietic
systems are further examples of labile cells. The chances
of regeneration are excellent.

95. 2. Stable cells
Tissues which have such type of cells have normally a much
lower level of replication and there are few stem cells.
However, the cells of such tissues can undergo rapid
division in response to injury. For example, mesenchymal
cells such as smooth muscle cells, fibroblasts, osteoblasts
and endothelial cells are stable cells which can proliferate.
Liver, endocrine glands and renal tubular epithelium has
also such type of cells which can regenerate. Their chances
of regeneration are good.

96. 3. Permanent cells
These are non-dividing cells. If lost, permanent cells
cannot be replaced, because they don not have the
capacity to proliferate. For example: adult neurons,
striated muscle cells, and cells of the lens.

98. • REGENERATION involves Two PROCESSES:
1. PROLIFERATION of SURVIVING CELLS to
replace lost tissue.
2. MIGRATION of SURVIVING CELLS into the
vacant space.

99. The FACTORS which CONTROL healing and repair are
complex: they include the production of a large variety of growth
factors.

100. WOUND HEALING
Healing of a wound shows both epithelial
regeneration (healing of the epidermis) and
repair by scarring (healing of the dermis). Two
patterns are described depending on the amount
of tissue damage. These are the same process
varying only in amount.

101. 1. Healing by first intention (primary union)
This occurs in clean, incised wounds with good
apposition of the edges – particularly planned
surgical incisions.

103. 2. Healing by second intention (secondary union) This
occurs in open wounds, particularly when there has
been significant loss of tissue, necrosis or infection.

105. FIBROSIS: is the end result of WOUND HEALING, CHRONIC
INFLAMMATION and ORGANISATION.
Formation of fibrous tissue:
REMODELLING follows: Action of
COLLAGENASE SCAR TISSUE + secretion of
COLLAGEN
REMODELLING follows: Action of COLLAGENASE SCAR TISSUE
+ secretion of COLLAGEN

107. NEOPLASIA
• NEOPLASIA definition:
NEOPLASIA = new growth.
Oncology = onco =tumor = neoplasm. Logy: science
Neoplasm: abnormal mass of tissue due to uncontrolled
proliferation of the cells.
Benign neoplasm : innocent behavior
Malignant: cancer ( behave like crab)

109. Nomenclature
• Neoplasms are named based upon two factors
1. The histologic types : mesenchymal and
epithelial.
2. Behavioral patterns : benign and malignant
neoplasms.

110. • Benign neoplasms
Thus, the suffix -oma denotes a benign neoplasm.
Benign mesenchymal neoplasms originating from muscle, bone,
fat, blood vessel nerve, fibrous tissue and cartilages are named as
Rhabdomyoma, osteoma, lipoma, hemangioma, neuroma, fibroma
and chondroma respectively. Benign epithelial neoplasms are
classified on the basis of cell of origin for example adenoma is the
term for benign epithelial neoplasm that form glandular pattern or
on basis of microscopic or macroscopic patterns for example
visible finger like or warty projection from epithelial surface are
referred to as papillomas.

111. • This nomenclature has, however, some
exceptions (I) Non neoplastic misnomers
hematoma, granuloma, hamartoma.
(II) Malignant misnomers melanoma, lymphoma,
seminoma, glioma, hepatoma.

112. • Malignant neoplasm nomenclature:
essentially follows the same scheme used for benign
neoplasm with certain additions. Malignant neoplasms
arising from mesenchymal tissues are called sarcomas
(Greed sar =fleshy). Thus, it is a fleshy tumour. These
neoplasms are named as fibrosarcoma, liposarcoma,
osteosarcoma, hemangiosarcoma etc.

113. • Malignant neoplasms of epithelial cell origin derived
from any of the three germ layers are called carcinomas.
Eg. Ectodermal origin: skin (epidermis squamous cell carcinoma, basal
cell carcinoma)Mesodermal origin: renal tubules (renal cell
carcinoma).Endodermal origin: linings of the gastrointestinal tract
(colonic carcinoma) Carcinomas can be furtherly classified those
producing glandular microscopic pictures are called Aden carcinomas
and those producing recognizable squamous cells are designated as
squamous cell carcinoma etc furthermore, when possible the carcinoma
can be specified by naming the origin of the tumour such as renal cell
adenocarcinoma etc.

114. • Tumors that arise from more than tissue components:-
Teratomas contain representative of parenchyma cells of more
than one germ layer, usually all three layers. They arise from
totipotential cells and so are principally encountered in ovary
and testis.
- Mixed tumors containing both epithelial and mesenchymal
components Examples include pleomorphic adenoma and
fibroadenoma

115. III. Characteristics of Benign and Malignant
Neoplasms
• The difference in characteristics of these
neoplasms can be conveniently discussed
under the following headings:
1. Differentiation & anaplasia
2. Rate of growth
3. Local invasion
4. Metastasis

116. Microscopical features of malignant cells
1- pleomorphism ( marked variation in shape and size of
cell).
2- hyperchromatic ( dark staining) and large nuclei.
3- increase nuclear cytoplasmic ratio 1:1 ( normal 1:4 or
1:6).
4- numerous atypical mitosis.
5- giant cell.
6- lose of orientation to each other.

117. • Sequential steps in mechanisms of tumor
invasion & metastasis:
a. Carcinoma in-situ b. Malignant cell surface receptors bind to
basement membrane components (ex laminin). c. Malignant
cell disrupt and invade basement membrane by releasing
collagenase type IV and other protease. d. Invasion of the
extracellular matrix e. Detachment f. Embolization g.
Survival in the circulation h. Arrest i. Extravasation j. Evasion
of host defense k. Progressive growth l. Metastasis

118. Epidemiology of cancer
The incidence of cancer varies with:
1. Age
2. Race
3. Geographic
4. Genetic factors.

119. Etiology of neoplasm ( carcinogenic agents)
• Four classes of carcinogenic agent have been
identified:
1. Genetic causes
2. Chemical causes
3. Radiation
4. Microbial agents ( viruses)

120. Clinical effects of neoplasm
• Clinical effects of benign neoplasms:
 pressure atrophy
Obstructions
Hemorrhage
Hormonal over secretion
 deformity

121. • Clinical effects of malignant neoplasms:
 Pressure atrophy
 Obstruction
 Ulceration
 Distraction of tissue
 Hemorrhage
 Hormonal over secretion
 Infection
 Starvation and anemia
 Pain
 Carcinomatous syndrome
 Cachaxia or wasting
 Effect of metastasis

122. Staging of malignancy
• Staging: measuring the size of neoplasm and extent of
spread.
• Staging is the functions of physician, surgeon,
pathologist and oncologist.
• Staging based on:
1) Size of primary lesion
2) Regional lymph node
3) Distant of metastasis

123. • Significance of staging: assessing prognosis and
treatment.
• System of staging:
 TNM system: T = tumor N= lymph node
statues
M = metastasis
So the stage take the following degree I, II, III,
IV)
2- AJC American joint committee

124. Example for staging of malignancy
Stage Definition
T0 In situ, non-invasive (confined to epithelium)
T1 Small, minimally invasive within primary organ site
T2 Large, more invasive within primary organ
T3 Large and invasive beyond primary organ.
T4 Very large and or very invasive , spread to adjacent
organ
N0 No lymph node involvement
N1 Regional lymph node involvement
N2 extensive regional LN involvement
N3 more distance LN involvement
M0 No distances metastasis

125. Grading of malignancy:
Grading: measuring the extent and degree of
differentiation. It is the function of pathologist.
Significance of grading: assessing aggressiveness
of neoplasm.
Grading based in:
1- degree of differentiation
2- pleomorphism
3- mitotic activities

126. • System of grading:
1. Grade I, II, III, IV.
2. Low grade, intermediate grade and high grade
3. Well- differentiated (WD), moderately
differentiated (MD), poorly differentiated (PD)
and undifferentiated – anaplastic (UD).
Staging: progression or spread in the body.
Grading: cell differentiation and rate of growth –
microscopy.

127. Diagnosis of neoplasm
• Clinical data, radiology, and ultrasound
• Cytology
• Histological study
• Biochemical study( seromarkers)
• ICC or IHC
• Flow cytometers
• Molecular diagnosis

128. Cancer prevention
1. Avoid tobacco 2- avoid alcohol
3- limit fat and calories 4- avoid khat
5- protect yourself from excessive sunlight
6- breast, prostate, ovarian, colorectal, and
cervical cancer screening ( early detection)
7- consumed fruited and vegetable
8- avoid cancer viruses
9- treat bacteria predispose to gastric cancer.