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NEOPLASIA
Pathophysiology of tumors

Neoplasm – a type of tumor – group of neoplasic cells

Study of tumors is oncology from Greek for tumor
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Objectives
• 1. Have concept regarding neoplasia.
• 2. Know different causes of tumors.
• 3. Understand clinical manifestations, diagnosis and
treatment of cancer.
• 4. Understand mechanism of local & systemic
inflammation.
• 5. Know resolution and repair occurring in the body.
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Cells normally differentiate, grow, mature and

divide. These are regulated processes, balanced in a
healthy system

Any increase in tissue size is not necessarily neoplasia.

Here is an example of left ventricular cardiac hypertrophy
in which there has been an increase in the size of the
myocardial fibers in response to an increased pressure
load from hypertension.
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Two major types: Benign and Malignant:

Benign tumours:
• grow slowly
• low mitotic rate
• well differentiated
• not invasive; well-defined borders
• remain localized; do not metastasize

Malignant tumours (cancer):

• Grow rapidly ;
• high mitotic index,
• poorly differentiated;
• do not have a capsule;
• invade surrounding structures;
• can metastasize from the primary to a secondary site
(metastasis).
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Tissue of origin + “-oma” indicates a benign

tumor

Malignant tumors – use embryonic origin

of tissue

Carcinomas come from ectoderm and

Endoderm - epithelial and glandular tissue
Sarcomas arise from mesoderm connective
tissue, muscle, nerve and endothelial
tissues
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causes of cancer:
•Viral causes of cancer:
•viruses assoc. with about 15 % of cancers world wide. e.g viral
hepatitis B or C.

•Bacterial causes:
• e.g Helicobacter pylori infects >1/2 world’s population assoc. with
B cell lymphomas of the stomach.

• Environmental factors:
• Smoking.
• Diet.
• alcohol up use.
• Air pollution
• Occupation hazards
• radiation
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• Stage 1 – confined to
site of origin
Stages • Stage 2- cancer is
of locally invasive
cancer • Stage 3 – cancer has
spread spread to regional
structures
: • Stage 4- cancer has
spread to distant sites
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Clinical manifestations of Cancer

• Pain: Due to pressure, obstruction, stretching, tissue
damage or inflammation, usually late.

• Fatigue
• Cachexia – wasting
• anorexia
• early satiety
• weight loss
• Anemia, Leukopenia and thrombocytopenia.
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Diagnosis:

• screening procedures and blood tests:

• Tumor markers
• substances on plasma membranes in blood, spinal fluid or
urine ,hormones, genes antigens or antibodies
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Cancer Treatment
• Chemotherapy:
• by Cytotoxic drugs.
• Radiation:
• Immunotherapy: Nonspecific enhancement of the
immune system – interferons or interleukins
• Surgery with adjuvant chemotherapy or radiation
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Side effects of treatment

• Gastrointestinal tract:
• Oral ulcers, Malabsorption, Diarrhea and Vomiting.
• Bone marrow:
• chemo and radiation suppress bone marrow: decrease in
red blood cells, white blood cells and platelets.
• Hair and skin: alopecia and skin dryness.
• Reproductive tract: affects gametes
• premature menopause.
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INFLAMMATION
AND FEVER
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Immunity
First line of defense
• Innate resistance – physical (skin/epithelial layer, GI & Resp
Tract)
• mechanical (Cough, sneeze, vomit, cilia action in trachea)
• biochemical barriers (antimicrobial peptides, lung secretions,
mucus, saliva, tears, earwax)
Second line of defense
• Inflammation – vascular response – dilation, histamines
increase vessel leakage, wbc action, cytokines, leucokines,
fever. Usually redness and heat with swelling.
Third line of defense
• Adaptive (acquired) immunity – antibody production
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Inflammation:
A non-specific response to injury or necrosis that occurs in a vascularized tissue.

• Limit and control the

inflammatory process
• Prevent and limit infection
Goal and further damage
• Interact with components of
s the adaptive immune
system
• Prepare the area of injury
for healing
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Stages of Inflammation
1. Vascular stage
2. Cellular stage
3. Tissue repair
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Phagocytosis
Process by which a cell ingests and disposes of foreign
material

Production of adhesion molecules

Margination (pavementing)
• Adherence of leukocytes to endothelial cells

Diapedesis
• Emigration of cells through the endothelial junctions
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Phagocytosis
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Phagocytosis

• Opsonization, recognition,
and adherence
Step • Engulfment
• Phagosome formation
s • Fusion with lysosomal
granules
• Destruction of the target
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Phagocytes

Neutrophils (polymorphonuclear
leucocyte)

• Predominate in early inflammatory

responses
• Ingest bacteria, dead cells, and cellular
debris
• Cells are short lived and become a
component of the purulent exudate
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Phagocytes

Monocytes and
macrophages
• Monocytes are produced in the
bone marrow, enter the
circulation, and migrate to the
inflammatory site, where they
develop into macrophages
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Monocytes and Macrophages

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Phagocytes

Eosinophils
• Mildly phagocytic
• against parasites and
regulation of vascular
mediators
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Phagocytes

Natural killer (NK)

cells
• Function is to recognize
and kill cells infected with
viruses and cancer cells.
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Cytokines
• Interleukins:
• Produced by macrophages and lymphocytes in response
to a pathogen.
• Interferon:
• Protects against viral infections Produced by virally
infected host cells.
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Local Manifestations of Inflammation

Results from vascular changes

and corresponding leakage of
circulating components into the
tissue
• Hotness
• Redness
• Swelling
• Pain
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Exudative Fluids
Serous exudate (Watery).

Purulent exudate (Pus) in

bacterial infection.

Hemorrhagic exudate (contains

blood).
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Systemic Manifestations of Inflammation

Fever
• Caused by exogenous and endogenous pyrogens
• Act directly on the hypothalamus

Leukocytosis
• Increased numbers of circulating leukocytes

Increased plasma protein synthesis

• Acute-phase reactants:
• C-reactive protein, fibrinogen, haptoglobin, amyloid,
ceruloplasmin, etc.
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Chronic Inflammation
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Resolution and Repair

Regeneration

Resolution
• Returning injured tissue to the original
structure and function
Repair
• Replacement of destroyed tissue with scar
tissue
• Scar tissue Composed primarily of collagen
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Resolution and Repair

Débridement
• Cleaning up the dissolved clots,
microorganisms, erythrocytes, and dead
tissue cells
Healing
• Filling in the wound
• Sealing the wound (epithelialization)
• Shrinking the wound (contraction)
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Healing

Primary intention
• Wounds that heal under conditions of
minimal tissue loss
Secondary intention
• Wounds that require a great deal
more tissue replacement
• Open wound
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Healing
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Dysfunctional Wound Healing

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Dysfunctional Wound Healing

Wound disruption
• Dehiscence
• Wound pulls apart at the suture
line
• Excessive strain and obesity
are causes
• Increases risk of wound sepsis
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References
• 1. Porth’s Pathophysiology: Concepts of Altered
Health States. 9th ed. J.B. Lippincott Comp.
Pennsylvania
• 2.Sue E.Huether ,Kathryn L.
McCance,2016,Understanding pathophysiology ,6th
edition ,Elsevier Mosby