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Introduction of Pathology By: Dr Tarek Atia


• Pathology is "Scientific study of disease“ Study of structural and functional changes in disease. • You need to have a basic knowledge of normal

Anatomy (structure) and Physiology (function) to understand Pathology. • "Pathology deals with knowledge of what causes disease, how disease starts, progresses & it explains the reason for signs and symptoms of patient"


• Diseases is an expression of "discomfort" due to structural or functional abnormality. • This abnormality can be caused by various agents Eg. Bacteria, virus, heat, radiation etc. collectively called 'etiology'.


• Factors causing disease are mainly two types. Environmental (or external) factors and Genetic (or Internal) factors. • Diseases which present since birth are called Congenital diseases and all other diseases are known as Acquired diseases. • Diseases which occur in families are known as

Familial diseases.


Pathology of a disease is formally studied under four subdivisions.

- Etiology - Study of cause / causative agent of disease - Pathogenesis- Study of disease progression or

evolution. - Morphology - Study of structural changes in disease (Gross & microscopic) - Clinical Significance - Study of how clinical features are related to changes.


Major groups of diseases are Inflammatory, Degenerative & Neoplastic.

Inflammatory disorders are due to damage to tissues by

various injuries (physical, chemical, infections etc.) Degenerative disorders are due to lack of growth or

ageing. Neoplastic disorders are due to excess cell division forming tumours.


Cell & Tissue Injury


Principles • Human disease occurs because of injury to cells / tissue. • Most human disease results from injury to epithelium. • Injury to one tissue usually affects the adjacent or

underlying tissue as well. • Cell injury produces morphologic changes.


Visual changes in the cell or tissue morphology is

seen

under microscopy

when cells are stained.


Cell Injury Damage or alteration of one or more cellular components

1. Many types of injury are tissue-specific because of anatomic relationships and tissue response to chemical and infectious agents.

2. Cell injury disrupt cell physiology; so the cell does not function at full capacity.


Stages in the cellular response to stress and

injurious stimuli


Consequences of Injury 1. (Reversible): No long term effects- the cell damage is repaired, the effects of the injury are reversible. 2. The cell “adapts� to the damaging stimulus. 3. (Irreversible): The cell dies, undergoing necrosis.

The damage is irreversible.


Adaptation to injury 1. Atrophy: decrease in the size and functional capacity of the cell. after normal growth has been attained. ( O2, blood, nerve supply) 2. Hypertrophy: an increase in the size of the cell secondary to an increase in cell function. Increase in the number of mitochondria and ER, etc.


3. Hyperplasia: an increase in the number of cells of a tissue in response to a stimulus or injury.

4. Metaplasia: replacement of one type of tissue with

another in response to an injury.


5.

Hypoplasia:

underdevelopment

or

incomplete

development of an organ / tissue (less severe in degree than aplasia). 6. Aplasia: lack of development of an organ or tissue (may have a rudimentary organ). can also refer to lack of production of cells from an organ or tissue (eg aplastic anemia).


Hypertrophy versus Necrosis


Uterine hypertrophy


Muscular hypertrophy


Metaplasia

Diagram of columnar to squamous metaplasia.


Cell Atrophy Causes 1. Loss of blood supply or innervations 2. Loss of endocrine factors (eg. TSH)

3. Decrease in the workload 4. Aging, chronic illness


Outcomes from cell injury depend upon: 1.

Type of injury

2.

Severity of the injury

3.

Duration of the injury

4.

Type of cell being injured- Some cell types sustain injury better than others; some tissues (e.g. liver) have a capacity to regenerate.


Reversible Cell Injury 1. Cell swelling– usually accompanies all types of injury. Results from an increase in water permeability. Reverses once membrane function is restored 2. Increase in extracellular metabolite- Because of a biochemical derangement. i.e.: Increase in extracellular glycogen in diabetes.


3. Fatty change in liver. Vacuoles of fat accumulate within the liver cell following many types of injury:

alcohol

intoxication,

chronic

illness,

mellitus, etc.

This may be due to: •

An increase in entry of free fatty acids.

An increase in synthesis of free fatty acids.

A decrease in fatty acid oxidation.

diabetes


Vulnerable Sites of the Cell 1. Cell membranes 2. Mitochondria

3. Endoplasmic reticulum 4. Nucleus


Causes of Cell and Tissue Injury 1. Physical agents 2. Chemicals and drugs 3. Infectious pathogens

4. Immunologic reactions 5. Genetic mutations 6. Nutritional imbalances


7. Hypoxia and Ischemia: cell injury resulting from inadequate levels of oxygen. Causes:

A. Inadequate blood supply B. Lung disease C. Heart failure D. Shock


Susceptibility of specific cells to ischemic injury • Neurons: 3 to 5 min.

• Cardiac myocytes, hepatocytes, renal epithelium: 30 min. to 2 hr. • Cells of soft tissue, skin, skeletal muscle: many hours


Cell Death • Apoptosis • Necrosis


Apoptosis


Morphology of Necrosis


Pyknosis • Shrunken nucleus with dark staining • Seen in a necrotic (dead) cell


Karyorrhexis • Fragmentation of pyknotic nucleus


Karyolysis • Extensive hydrolysis of pyknotic nucleus with loss of staining

• Represents breakdown of the denatured chromatin


Karyolysis


Types of Necrosis


1- Coagulative Necrosis • Dead cells remain as ghost-like remnants of their former self • Classically seen in an MI


Cardiac muscle fibers


Kidney (necrotic renal tubules)


2- Liquefactive Necrosis • The dead cell undergoes extensive autolysis, caused by the release of lysosomal hydrolases (proteinases, DNases, RNases, lipases, etc.)

• Seen classically in the spleen and brain following

infarction.


Liquefactive Necrosis


(A) Coagulative vs. (B) Liquefactive Necrosis


3- Caseous Necrosis (caseum cheesy) • Resembles cottage cheese • Soft, friable, whitish-grey • Present within infected tissues • Seen in Tuberculosis (Mycobacterium tuberculosis)


Caseous Necrosis


Caseous Necrosis


4- Fat Necrosis  Leakage of lipases from dead cells attack triglycerides in surrounding fat tissue and generate free fatty acids and calcium soaps

 These soaps have a chalky-white appearance  Seen in the pancreas following acute inflammation



1 cell and tissue injury ppt