Cell Adaptation Cell Injury PDF

Cell Adaptation, Cell Injury and Cell Death
Pathology:- is the study of structural and functional abnormalities that are expressed as
diseases of organs and systems. Modern pathology, proposed that injury to the smallest
living unit of the body, the cell, is the basis of all disease.
The plasma membrane establish a structural and functional barrier between its
internal milieu and a hostile environment. in several ways:
1-It maintains a constant internal ionic composition against very large chemical gradients
between the interior and exterior compartments.
2- It selectively admits some molecules while excluding or extruding others.
3- It provides a structural envelope to contain the informational, synthetic and catabolic -
constituents of the cell.
4- It provides an environment to house signal transduction molecules that mediate
communication between the external and internal milieus.
At the same time, to survive, a cell must be able to adapt to adverse environmental
conditions, such as changes in temperature, solute concentrations or oxygen supply, cells
encounter many stresses because of changes in their internal and external environments,
and this patterns of response to such stresses comprise the cellular basis of disease.
1-Reactions to Persistent Stress and Cell Injury:
*Reduced Functional Demand *Inadequate Supply of Oxygen

*Insufficient Nutrients *Interruption of Trophic Signals
*Persistent Cell Injury *Increased Pressure
*Aging *Chronic Disease
Cell injury (cell death): it is the variable changes in morphological and functional
properties of cell occurs due to internal or external causes (ex. Chemical, physical,
infectious and genetic agents), that obligate cell to respond for preserving normal
hemostasis (adaptation) or death (necrosis) when the injury factors sever cell unable to
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adept, cell may also killed by another pathway even when it have the ability to adept for
saving other cells and tissue by programed cell death (apoptosis).
Mechanisms and Morphology of Cell Injury:

All cells have efficient mechanisms to deal with shifts in environmental conditions. Thus,
ion channels open or close, harmful chemicals are detoxified, metabolic stores such as fat
or glycogen may be mobilized and catabolic processes lead to the segregation of internal
particulate materials.
Types of cell damages:

1-Reversable (adaptable) (fatty change, cellular swelling).
2-Irreversable (non-adaptable) (necrosis, apoptosis).
A) Adaptation:
1-Atrophy:- Is an Active Response to an Altered Environment That Results in Reduced
Function orSize of Cells or Organs, atrophy is often noted as decreased size or function of
an organ, which may occur under both pathologic and physiologic circumstances. Adipose
tissue and skeletal muscle, which respond rapidly to changes in demand for energy storage
and contractile force, respectively.
When a muscle is immobilized and the need for contraction decreases (“unloading”),
myocytes institute selective adaptive mechanisms include:
Protein synthesis: Shortly after unloading, protein synthesis Decreases

Protein degradation: Particular ubiquitin-related specific protein degradation pathways
Gene expression: There are selective decreases in transcription of genes
Signaling: The checks and balances that control the levels of upregulation and
downregulation of intracellular signaling species change.
Energy utilization: A selective decrease
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2-Hypertrophy Is an Increase in Cell Size and Functional Capacity, When trophic signals
or functional demand increases, adaptive changes to satisfy these needs lead to increased
cellular size (hypertrophy) and, in some cases, increased cellular number (hyperplasia).
Mechanisms of Cellular Hypertrophy

*Cellular Remodeling in Hypertrophy: enhanced proteasomal degradation
*Signaling Mechanisms in Hypertrophy: many types of signaling may lead to cell
hypertrophy
3-Hyperplasia Is an Increase in the Number of Cells in an Organ or Tissue. Hormonal

Stimulation: Changes in hormone concentrations can elicit proliferation of responsive
cells.
4-Metaplasia Is conversion of one differentiated cell type to another. usually an adaptive
response to chronic injury, persistent and usually fully reversible.
5-Dysplasia Is Disordered Growth and Maturation of the Cellular Components of a
Tissue, it is a preneoplastic lesion, in that it is a necessarystage in the multistep cellular
evolution to cancer.
6-Calcification May Occur as Part of Normal Development or as a Reflection of an
Abnormal Process, “Metastatic” calcification reflects deranged calcium metabolism, in
contrast to dystrophic calcification, which has its origin in cell injury.
7-Hyaline Refers to any material that has a reddish, homogeneous appearance when
stained with Hematoxylin and Eosin.
8-Hydropic Swelling Is a reversible increase in cell volume, characterized by a large, pale

cytoplasm and a normally located nucleus reflects acute reversible cell injury. Subcellular
changes include Endoplasmic reticulum, Mitochondria, Plasma membrane and Nucleus.
9-Fatty change: accumulation of fat and triglyceride in cellular cytoplasm, sever fatty
changer can effect cellular function.
10-Ischemic Cell Injury Usually Results From Obstruction to the Flow of Blood
3
Oxidative Stress Is a key trigger for cell injury and adaptive responses. Included Reactive
Oxygen Species (OH), Hydroxyl Radical H2O2 with ferrous iron (Fe2_), Peroxynitrite
interaction of two free radicals,
The effectiveness of cellular defenses against oxygen free radicals may determine the
outcome of oxidative injury it depends on
* Detoxifying Enzymes
* Scavengers of ROS
11-Mutations my impair cell function without causing cell death
12-Intracellular storage is retention of materials within the cell (Nutrients, Degraded

phospholipids, Substances that cannot be metabolized, Overload of normal body
constituents, Abnormal proteins/ ex. Fat, Glycogen, Inherited Lysosomal Storage Diseases,
Cholesterol, Abnormal Proteins, Lipofuscin, Melanin, Exogenous Pigments eg.
Anthracosis refers to the storage of carbon particles in the lung and regional lymph nodes)
B)-Cell Death (Necrosis)
Stages of necrosis:-
1-pyknosis; clumping of chromosomes and shrinking of the nucleus of the cell,
2-karyorrhexis; fragmentation of the nucleus and break up of the chromatin into
unstructured granules
3-karyolysis; dissolution of the cell nucleus
Necrotic Cell Death results from exogenous cell injury and is reflected in geographic
areas of cell death.
1-Coagulative necrosis is a morphologic term that refers to light microscopic alterations
in dead or dying cells shortly after a cell’s death, its outline is maintained.
2-Liquefactive Necrosis when the rate of dissolution of necrotic cells is considerably
faster than the rate of repair
4
3-Fat necrosis specifically affects adipose tissue and most commonly results from
pancreatitis or trauma. The unique feature determining this type of necrosis is the presence
of triglycerides in adipose tissue.
4-Caseous necrosis is characteristic of tuberculosis, in caseous necrosis, unlike
coagulative necrosis, the necrotic cells fail to retain their cellular outlines.
5-Fibrinoid Necrosis is an alteration of injured blood vessels, in which insudation and

accumulation of plasma proteins cause the wall to stain intensely with eosin.
Cells May Participate Actively in their own death (apoptosis)

Apoptosis is a form of cellular suicide in which the cell participates actively in its own
demise. a mechanism by which individual cells utilize their own signaling systems to
sacrifice themselves for the preservation of the organism. removal of apoptotic cells by
Tissue Macrophages occurs without an inflammatory reaction. Apoptosis participates in
developmental and physiologic processes, deletes mutant cells, defense against
dissemination of Infection.
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Qestions:-
1-Define pathology, cell injury, cellular necrosis, apoptosis.

2-Enumerate five reactions to persistent stress and cell injury.
3- Enumerate five cellular adaptable changes and discuss one.
4- Enumerate five cellular non-adaptable changes and discuss one.
5-Write briefly with draw the stages of necrosis.
6- The effectiveness of cellular defenses against oxygen free radicals may determine the
outcome of oxidative injury it depends on.
7-________ Refers to any material that has a reddish, homogeneous appearance when
stained with Hematoxylin and Eosin.
8- In _________ necrosis cellular outline is maintained.
9- _________ necrosis fail to retain their cellular outlines.
10- In _________ necrosis the dissolution faster than repairing.

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Cell Adaptation, Cell Injury and Cell Death

1-Reactions to Persistent Stress and Cell Injury:

Reduced Functional Demand Inadequate Supply of Oxygen

Mechanisms and Morphology of Cell Injury:

Types of cell damages:

Protein synthesis: Shortly after unloading, protein synthesis Decreases

Mechanisms of Cellular Hypertrophy

3-Hyperplasia Is an Increase in the Number of Cells in an Organ or Tissue. Hormonal

8-Hydropic Swelling Is a reversible increase in cell volume, characterized by a large, pale

11-Mutations my impair cell function without causing cell death

12-Intracellular storage is retention of materials within the cell (Nutrients, Degraded

B)-Cell Death (Necrosis)

5-Fibrinoid Necrosis is an alteration of injured blood vessels, in which insudation and

Cells May Participate Actively in their own death (apoptosis)

1-Define pathology, cell injury, cellular necrosis, apoptosis.

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