Surgical Pathology Fundamentals
Concorde Career College, Portland
ST120
Adapted from “Pathology” by Kansas State University
Terminology
Pathology:
The study of the structural and functional changes leading to
disease in:
• Cell
• Tissue
• Organs
Pathophysiology:
Is the abnormal function of organs or systems due to disease
Cell structure
Terminology
Pathology is divided
• General
• Special or systemic
General pathology:
Basic reaction of cells and tissue to normal stimuli
Specific pathology:
Specific response special organs to well defined stimuli
Four aspects of disease process
1.
2.
3.
4.
Etiology
Pathogenesis
Morphological changes
Clinical significance
1.Etiology

A) Determining cause


Specifically known to be the soul cause of
disease, such as a pathogenic organism,
e.g., HIV
B) Predisposing causes

Leading indirectly to disease such as
genetic predisposition
2.Pathogenesis
Is the mechanism by which a certain
etiological factor causes disease (In
Greek: pathos = disease, genesis =
development).
 Some forms of pathogenesis are:
 Inflammation
 Malignancy
 Tissue breakdown

2.Pathogenesis

The pathogenesis process leads to the formation of a
lesion

Lesion is derived from the Latin word "laesio" which
means "injury."

Lesions are a result of damage to tissues. For
example:

A cancerous tumor is an example of a lesion

The surrounding tissue damaged by a tumor is also termed a
lesion.
3.Morphological changes

Are the changes that occur in the cell tissue or
organ as a result of the pathological process

These changes can be Morbid:

Macroscopic appearance visible to the naked eye
3.Morphological changes

Are the changes that occur in the cell tissue or
organ as a result of the pathological process

Or Histological:

Microscopic appearance only visible under the
microscope
4.Clinical significance

What impact do these changes have on
the patient?
Progression of a disease

Complete cure

Death

Complication

Additional pathological changes which may
occur during or after the course of any
disease
Pathological investigation

During life





Surgical biopsy
Fine needle
aspiration biopsy
(FNAB)
Cytopathology
Molecular techniques
After death

Autopsy
Exposure to stress (irritant)
Mild irritant
 Moderate


Severe irritant
A) inflammation
B) Degeneration
Necrosis
Necrosis
Types of irritants

Living irritant:

Bacteria
 Pathogenic fungi
 Parasite
 Virus
 Helminths

Non-living irritant:

Physical


Chemical


Trauma, Burns, Radiation
Acids, Alkalies
Immunological
Ag-Ab reaction
 Hypersensitivity reaction

Chemical burns
Inflammation
It is the response of the living tissue to
mild to moderate irritant
 The response is directed to defend the
tissue for foreign irritants and to prevent
further damage
 The aim is to bring more blood to the
damaged area by acceleration of the
blood stream
 It is denoted by the suffix “itis”

Inflammation

Examples of inflammation
Tonsillitis
 Appendicitis
 Tendonitis ,………etc.


Lung?
Tonsillitis
Inflammation
Exudate

An exudate is any fluid that filters from
the circulatory system into lesions or
areas of inflammation

Its composition varies but generally
includes water and the dissolved solutes
of the blood, some or all plasma
proteins, white blood cells, platelets and
RBC
Transudate

A fluid that passes through a membrane which filters
out much of the protein and cellular elements to yield a
watery solution.

A transudate is due to increased pressure in the veins
and capillaries pressure forcing fluid through the
vessel walls or low levels of protein the blood serum

The transudated fluid accumulates in tissues outside
the blood vessels and can cause edema
Types of Exudate
1.
Serous exudate is usually seen in mild inflammation, with little protein content;
seen in certain disease states like tuberculosis
2.
Purulent or suppurative exudate consists of plasma with both active and dead
neutrophils, fibrinogen, and necrotic parenchymal cells; referred to as pus.
3.
Fibrinous exudate is composed mainly of fibrinogen and fibrin. It is characteristic
of rheumatic carditis, but is seen in all severe injuries such as strep throat and
bacterial pneumonia
4.
Hemorrhagic exudate is seen in injury that causes rupture of blood vessels.
5.
Pleural
6.
Catarrhal exudate is seen in the nose and throat and is characterized by a high
content of mucus.
Purulent Exudate
Inflammation
Effects of inflammation


Vascular phenomena
1.
2.
3.
4.
Transient vasoconstriction
rapidly followed by
Vasodilatation
Stasis
Migration of leucocytes
Inflammation

Composition and function of
inflammatory fluid exudates

Fluid exudates
Dilution of bacterial toxins
 fibrin threads : help the movement of leucocytes
and limit the spread of infection
 Also contain antibodies

Inflammation

Composition and function of
inflammatory fluid exudates

Cellular part

Phagocytosis: engulfing of and
destruction of bacteria and necrotic
tissue by phagocytes and PNL
Inflammation
 Chemotaxis:
the movment of WBCs in
the area of inflammation towards the
irritant
 Emigration
of leukocytes: the migration of
WBC from within the blood vessel
towards the inflammation site
 Diapedesis:
the passage and movement
of RBCs from within the blood vessel
towards the inflamed area
Cardinal signs of inflammation

Redness (rubor)

Hotness (calor)

Edema (tumor) swelling due to inflammatory exudate

Pain (dolor) due to pressure of edema on nerves and
irritation of nerve endings by metabolites

Loss of function (functio laesa) this is to make the
inflamed part of tissue rest and heal
Types of inflammation

Acute inflammation


Acute non-suppurative inflammation: acute without
the formation of pus
Acute suppurative inflammation: with pus



Localized : Abscess, Furuncle, Carbuncle
Diffused : cellulitis, septic meningitis
Chronic inflammation


Chronic specific : TB
Chronic non-specific: follows acute or chronic from
the beginning
Cells of inflammation
Acute inflammation cells:
1- RBC
2- PNL (leukocyte)
Eosinophils
Basophils
Neutrophils
Chronic inflammation cells
1- lymphocytes
2- Plasma cells
3- Histocytes
4- fibroblasts
Leukocyte review
http://en.wikipedia.org/wiki/
White_blood_cell
Neutrophil engulfing
anthrax bacteria
Cells of inflammation
Fate of acute inflammation
1- Regression: by resolution, for example when the body
(immune system) overcomes bacterial infection
2- Progression: can lead to chronic inflammation and
spread; the bacteria overcome the immune system
and can spread by:
Blood: septicemia, bacteremia, toxemia pyemia
Lymphatyic: lymphangitis, lymphadenitis
Direct: to other surrounding tissue
Type of cells
Labile cells: epithelium, haematopoietic (blood)
Quiescent (Stable): hepatic, kidney and
pancreas
Non-dividing (Permanent): nerve cells and
skeletal muscle cells
Cell development

Proliferation: increased number

Differentiation: development through
stages
Healing
Tissue repair involves replacement of damaged tissue with new healthy living tissue
when resolution cannot occur
Types
Usually involves two separate but coordinated components
A)
Regeneration:
healing by the same type of tissue cells from surrounding healthy living cells; this
occurs following damage to labile cells and stable cells, for example, liver
cirrhosis and bone fractures
B)
Fibrous (scar tissue):
healing by granulation tissue (fibroblast with new capillaries formed) which mature into
vascular fibrous tissue (scar); this occurs in the healing process of permanent
cells and stable cells with extensive damage, for example, myocardial
infraction and open wounds
Introduction to wound healing

Healing is a complex and dynamic process of
restoring cellular structures and tissue layers.

The adult wound healing process can be
divided into 4 distinct phases:




Hemostasis phase
Inflammatory phase
Proliferative phase
Remodeling phase
Sequence of events in healing
Initial phase - Hemostasis

Following vasoconstriction, platelets adhere to damaged endothelium
and discharge adenosine diphosphate (ADP), promoting thrombocyte
clumping, which dams the wound.

The inflammatory phase is initiated by the release of numerous cytokines
by platelets.

Fibrinogen is cleaved into fibrin and the framework for completion of the
coagulation process is formed. Fibrin provides the structural support for
cellular constituents of inflammation.

This process starts immediately after the insult and may continue for a
few days.
Sequence of events in healing
Second phase - Inflammation

Within the first 6-8 hours, the next phase of the healing process is underway, with
polymorphonuclear leukocytes (PMNs) or PNLs engorging the wound

These cells “cleanse” the wound, clearing it of debris. The PMNs attain their
maximal numbers in 24-48 hours and commence their departure by hour 72.

As the process continues, monocytes also exude from the vessels. These are
termed macrophages. The macrophages continue the cleansing process and
manufacture various growth factors during days 3-4.

Many factors influencing the wound healing process are secreted by
macrophages.
Sequence of events in healing
Third phase – Proliferation
This phase consists of different subphases.

Fibroplasia

Matrix deposition

Angiogenesis

Reepithelialization

During days 5-7, fibroblasts have migrated into the wound, laying down new collagen.

The wound is suffused with GAGs and fibronectin that are bonded to a protein core and
contribute to matrix deposition.

Angiogenesis is the product of parent vessel offshoots. The formation of new vasculature
requires extracellular matrix and basement membrane degradation followed by migration,
mitosis, and maturation of endothelial cells.

Re-epithelization occurs with the migration of cells from the periphery of the wound and
adnexal structures. This process commences with the spreading of cells within 24 hours.
Division of peripheral cells occurs in hours 48-72, resulting in a thin epithelial cell layer, which
bridges the wound.
This succession of subphases can last up to 4 weeks in the clean and uncontaminated wound.
Sequence of events in healing
Fourth phase - Remodeling
After the third week, the wound undergoes constant alterations,
known as remodeling.

This can last for years after the initial injury occurred. Collagen is
degraded and deposited in an equilibrium-producing fashion.

The collagen deposition in normal wound healing reaches a peak
by the third week after the wound is created.

Contraction of the wound is an ongoing process resulting in part
from the proliferation of the specialized fibroblasts termed
myofibroblasts, which resemble contractile smooth muscle cells.
Stages of wound healing
Resolution/ Remodeling
Vessel regression, Collagen remodeling
Proliferation
Reepithelialization, Angiogenesis, Fibrogenesis,
Inflammation
PMNs, Macrophages, Lymphocytes
Hemostasis
Fibrin clot, platelet
deposition
1D 3D
1wk
Time after injury
6wk
8wk
Types of healing
Primary vs. secondary healing
Complications of the healing process

This process can go wrong and
produce an increase of fibroblastic
proliferation with a resultant
hypertrophic scar

Further exuberance can result in
keloid formation where scar
production extends beyond the area
of the original insult. Conversely,
insufficient healing can result in
atrophic scar formation.
Hypertrophic scar
Keloid
Complications of the healing process









Weak scar: this may lead to hernia
Cicatrisation: contracture of the size of the scar
Implantation epidermoid cyst
Stump neuroma: following amputation causing a painful
coiled mass of nerves
Sinus: is a track of septic granulation tissue connecting a
cavity to the outside and has one blind end, e.g. pilonidal
sinus
Fistula: is a tract of septic granulation tissue connecting 2
epithelial surfaces
Infection : leading to delayed healing
Rarely scars may develop squamous cell carcinoma
Ulcers: discontinuity of cover epithelium or muscle
membrane
Anal fistula
Bone

Bone is a dynamic tissue
 Osteoblasts
 Osteocytes
 Osteoclasts
Osteogenic cells
Bone anatomy











Diaphysis
Metaphysis
Epiphysis – Prox/Dist
Epiphyseal line
Periosteum
Compact cortical bone
Spongy bone
Articular Cartilage
Medullary cavity
Marrow
Nutrient artery
The histologic types





Compact bone
Trabecular bone
Lamellar bone
Woven bone
Callus
The matrix of bone
Contains inorganic salt Calcium
Hydroxyapatite in collagen framework.
 Osteoblasts - Calcification Mineralization
 Minerals  hardness
 Collagen fibres  Tensile strength.
 Collagen is necessary for Calcification.

Fractures
Break in the bone
 Simple / Compound – infection
 Single - Horizontal, oblique, spiral,
 Comminuted – multiple
 Greenstick – partial children
 Torus (buckle) – compression of cortex
– children

Types of fractures
Compound fracture
Bone remodeling
Healing in bone





Day 1 - Hematoma formation (fibrin mesh)
Day 3 - Inflammation
Week 1 - Soft callus – granulation, matrix
Week 3-6 - Callus – ossification, woven bone
Week 8+ - Re-modeling – absorb/deposit,
strengthen, lamellate
Healing in bone
Healing in bone
Healing in bone
Healing in bone
Healing in bone
Callus formation
Following mid-shaft humeral
fracture
Factors affecting healing





Systemic & local
factors
Immobilization
Improper reduction –
abnormal position
Infection: debris &
dead tissue in wound
Joint involvement
Complications
Delayed healing
 Non healing
 Joint involvement - ankylosis
 Abnormal position – arthritis
 Bone necrosis – nutrient artery


Avascular necrosis
Involucrum formation
 Pseudarthrosis

Involucrum