1- cell and tissue injury. ppt

7/30/2019 1- Cell and Tissue Injury. Ppt

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By: Dr Tarek Atia

Introduction

ofPathology


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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) tounderstand Pathology.

"Pathology deals with knowledge of what causes

disease, how disease starts, progresses & it explains

the reason for signs and symptoms of patient"


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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'.


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Factors causing disease are mainly two types.

Environmental (or external) factors and Genetic (or

Internal) factors.

Diseases which present since birth are calledCongenital diseases and all other diseases are

known as Acquired diseases.

Diseases which occur in families are known as

Familial diseases.


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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.


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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.


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Cell & Tissue Injury


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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.

Principles


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Visual changes in the cell

or tissue morphology is

seen under microscopy

when cells are stained.


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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.


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Stages in the cellular response to stress and

injurious stimuli


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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.


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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.


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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.


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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).


17/51Hypertrophy versus Necrosis


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Uterine hypertrophy


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Muscular hypertrophy


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Diagram of columnar to squamous metaplasia.

Metaplasia


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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


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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.


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Reversible Cell Injury

1. Cell swellingusually 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.


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3. Fatty change in liver. Vacuoles of fat accumulate

within the liver cell following many types of injury:

alcohol intoxication, chronic illness, diabetes

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.


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Vulnerable Sites of the Cell

1. Cell membranes

2. Mitochondria

3. Endoplasmic reticulum

4. Nucleus


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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


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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


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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


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Cell Death

Apoptosis

Necrosis


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Apoptosis


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Morphology of Necrosis


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Pyknosis

Shrunken nucleus with dark staining

Seen in a necrotic (dead) cell


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Karyorrhexis

Fragmentation of pyknotic nucleus


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Karyolysis

Extensive hydrolysis of pyknotic nucleus with

loss of staining

Represents breakdown of the denatured

chromatin


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Karyolysis


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Types of Necrosis


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1- Coagulative Necrosis

Dead cells remain as ghost-like remnants of

their former self

Classically seen in an MI

C di l fib


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Cardiac muscle fibers


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Kidney (necrotic renal tubules)


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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.


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Liquefactive

Necrosis


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(A) Coagulative vs. (B) Liquefactive Necrosis


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3- Caseous Necrosis (caseum -cheesy)

Resembles cottage cheese

Soft, friable, whitish-grey

Present within infected tissues

Seen in Tuberculosis (Mycobacterium tuberculosis)


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Caseous Necrosis


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Caseous Necrosis


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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


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1- cell and tissue injury. ppt

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