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kefah zaben
Cellular Adaptation, Injury, and Death
Dr. Kefah zaben
Cellular Adaptation, Injury, and Death
 Cells adapt to changes in the internal environment, just as the total organism
adapts to changes in the external environment.
kefah zaben
 Cells may adapt by undergoing
1. Changes in size
2. Changes in number
3. Changes in type.
Cellular Adaptation, Injury, and Death
 Cell changes occurring singly or in combination and may lead to
1.Atrophy
2.Hypertrophy
kefah zaben
3.Hyperplasia
4. Metaplasia
5. Dysplasia
 Adaptive cellular responses also include
1. Intracellular accumulations
2. Storage of products in abnormal amounts.
Cellular Adaptation, Injury, and Death
kefah zaben
 There are several molecular mechanisms mediating cellular adaptation,
including factors produced by other cells or by the cells themselves.
 The molecular mechanisms depend on : signals transmitted by chemical
messengers that exert their effects by changing gene function.
kefah zaben
Atrophy
Atrophy; When confronted with a decrease in work demands or adverse
environmental conditions, most cells are able to return to a smaller size and
a lower and more efficient level of functioning that is compatible with
survival.
This decrease in cell size is called atrophy.
kefah zaben
Atrophy
 Cells that are atrophied reduce their oxygen consumption and other cellular
functions by decreasing the number and size of their organelles and other
structures.
There are fewer mitochondria, myofilaments, and endoplasmic reticulum structures.
 When a sufficient number of cells are involved, the entire tissue or muscle
atrophies.
kefah zaben
Cell Cycle
 Multiplication of the somatic (mitosis) and germ (meiosis) cells is the most
complex of all cell functions.
 Mitosis is controlled by genes which encode for release of specific proteins
molecules that promote or inhibit the process of mitosis at different steps.
 Mitosis - promoting protein molecules are cyclins A, B and E.
kefah zaben
Cell Cycle
 These cyclins activate cyclin dependent kinases (CDKs) which act in conjunction
with cyclins.
 After the mitosis is complete, cyclins and CDKs are degraded and the remains of
used molecules are taken up by cytoplasmic caretaker proteins, ubiquitin, to the
peroxisome for further degradation.
 Ubiquitin: a compound found in living cells which plays a role in the degradation
of defective and superfluous proteins. It is a single-chain polypeptide.
kefah zaben
Cell Cycle
Period between the mitosis is called interphase.
The cell cycle is the phase between two consecutive divisions (Fig. 3.5).
There are 4 in sequence phases in the cell cycle:
1. G1 (Gap 1) Phase
2. S (Synthesis) Phase
3. G2 (Gap 2) Phase
kefah zaben
4. M (Mitotic) Phase.
Cell Cycle
1. G1 (Pre-mitotic gap) phase is the stage when messenger RNAs for the
proteins and the proteins themselves required for DNA synthesis (e.g. DNA
polymerase) are synthesized.
The process is under control of cyclin E and cyclin dependent kinases (CDKs)
2. S (Synthesis) phase involves replication of nuclear DNA.
kefah zaben
Cyclin A and cyclin dependent kinases (CDKs) control it.
Cell Cycle
3- G2 (Pre-mitotic gap) phase is the short gap phase in which correctness of DNA
synthesized is assessed.
This stage is promoted by cyclin B and cyclin dependent kinases (CDKs) .
4- M (Mitotic) phase is the stage in which process of mitosis to form two daughter
cells is completed.
kefah zaben
M (Mitotic) phase occurs in 4 sequential stages: prophase, metaphase, anaphase, and
telophase (abbreviation= PMAT)
Cell Cycle
M (Mitotic) phase occurs in 4 sequential stages:(abbreviation= PMAT)
1. Prophase
2. Metaphase
kefah zaben
3. Anaphase
4. Telophase
Cell Cycle
M phase occurs in 4 sequential stages
Prophase:
Each chromosome divides into 2 chromatids which are held together by centromere.
The centriole divides and the two daughter centrioles move towards opposite poles
of the nucleus and the nuclear membrane disintegrates.
kefah zaben
Metaphase:
The microtubules become arranged between the two centrioles forming spindle,
while the chromosomes line up at the equatorial plate of the spindle.
Cell Cycle
M phase occurs in 4 sequential stages
Anaphase :
The centromeres divide and each set of separated chromosomes moves towards
the opposite poles of the spindle. Cell membrane also begins to divide.
kefah zaben
Telophase :
There is formation of nuclear membrane around each set of chromosomes and
reconstitution of the nucleus.
The cytoplasm of the two daughter cells completely separates.
Cell Cycle
G0 Phase.
kefah zaben
The daughter cells may continue to remain in the cell cycle and divide further, or
may go out of the cell cycle into resting phase, called G0 phase.
Stimulation of mitosis can be studied in a number of ways as under:
1. Compensatory stimulation of mitosis : by removal of part of an organ.
2. Reparative stimulation of mitosis occurs when a tissue is injured.
kefah zaben
adaptation stimulus example
Hypertrophy-increase in cell size leading
to increase in organ size
Increased workload Leg muscles of runner Arm muscles in tennis
player Cardiac muscle in person with
hypertension
Atrophy-shrinkage in size of cell, leading
to decrease in organ size
Decrease in:
Use
Blood supply
Nutrition
Hormonal stimulation
Innervation
Secondary sex organs in aging person
Extremity immobilized in plas-ter cast
Hyperplasia-increase in number of new
cells (increase in mitosis)
Hormonal influence Breast changes of a girl in pu-berty or of a
pregnant woman
Regeneration of liver cells New red blood
cells in blood loss
Dysplasia-change in the ap- pearance of
cells after they have been subjected to
chronic irritation
Reproduction of cells with
re- sulting alteration of
their size and shape
Alterations in epithelial cells of the skin or the
cervix, pro- ducing irregular tissue changes
that could be the precursors of a malignancy
Metaplasia-transformation of one adult
cell type to another (reversible)
Stress applied to highly
spe-cialized cell
Changes in epithelial cells lin- ing bronchi in
response to smoke irritation (cells be- come
less specialized
kefah zaben

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ilovepdf_merged-4.pdf

  • 1. kefah zaben Cellular Adaptation, Injury, and Death Dr. Kefah zaben Cellular Adaptation, Injury, and Death  Cells adapt to changes in the internal environment, just as the total organism adapts to changes in the external environment.
  • 2. kefah zaben  Cells may adapt by undergoing 1. Changes in size 2. Changes in number 3. Changes in type. Cellular Adaptation, Injury, and Death  Cell changes occurring singly or in combination and may lead to 1.Atrophy 2.Hypertrophy
  • 3. kefah zaben 3.Hyperplasia 4. Metaplasia 5. Dysplasia  Adaptive cellular responses also include 1. Intracellular accumulations 2. Storage of products in abnormal amounts. Cellular Adaptation, Injury, and Death
  • 4. kefah zaben  There are several molecular mechanisms mediating cellular adaptation, including factors produced by other cells or by the cells themselves.  The molecular mechanisms depend on : signals transmitted by chemical messengers that exert their effects by changing gene function.
  • 5. kefah zaben Atrophy Atrophy; When confronted with a decrease in work demands or adverse environmental conditions, most cells are able to return to a smaller size and a lower and more efficient level of functioning that is compatible with survival. This decrease in cell size is called atrophy.
  • 6. kefah zaben Atrophy  Cells that are atrophied reduce their oxygen consumption and other cellular functions by decreasing the number and size of their organelles and other structures. There are fewer mitochondria, myofilaments, and endoplasmic reticulum structures.  When a sufficient number of cells are involved, the entire tissue or muscle atrophies.
  • 7. kefah zaben Cell Cycle  Multiplication of the somatic (mitosis) and germ (meiosis) cells is the most complex of all cell functions.  Mitosis is controlled by genes which encode for release of specific proteins molecules that promote or inhibit the process of mitosis at different steps.  Mitosis - promoting protein molecules are cyclins A, B and E.
  • 8. kefah zaben Cell Cycle  These cyclins activate cyclin dependent kinases (CDKs) which act in conjunction with cyclins.  After the mitosis is complete, cyclins and CDKs are degraded and the remains of used molecules are taken up by cytoplasmic caretaker proteins, ubiquitin, to the peroxisome for further degradation.  Ubiquitin: a compound found in living cells which plays a role in the degradation of defective and superfluous proteins. It is a single-chain polypeptide.
  • 9. kefah zaben Cell Cycle Period between the mitosis is called interphase. The cell cycle is the phase between two consecutive divisions (Fig. 3.5). There are 4 in sequence phases in the cell cycle: 1. G1 (Gap 1) Phase 2. S (Synthesis) Phase 3. G2 (Gap 2) Phase
  • 10. kefah zaben 4. M (Mitotic) Phase. Cell Cycle 1. G1 (Pre-mitotic gap) phase is the stage when messenger RNAs for the proteins and the proteins themselves required for DNA synthesis (e.g. DNA polymerase) are synthesized. The process is under control of cyclin E and cyclin dependent kinases (CDKs) 2. S (Synthesis) phase involves replication of nuclear DNA.
  • 11. kefah zaben Cyclin A and cyclin dependent kinases (CDKs) control it. Cell Cycle 3- G2 (Pre-mitotic gap) phase is the short gap phase in which correctness of DNA synthesized is assessed. This stage is promoted by cyclin B and cyclin dependent kinases (CDKs) . 4- M (Mitotic) phase is the stage in which process of mitosis to form two daughter cells is completed.
  • 12. kefah zaben M (Mitotic) phase occurs in 4 sequential stages: prophase, metaphase, anaphase, and telophase (abbreviation= PMAT) Cell Cycle M (Mitotic) phase occurs in 4 sequential stages:(abbreviation= PMAT) 1. Prophase 2. Metaphase
  • 13. kefah zaben 3. Anaphase 4. Telophase Cell Cycle M phase occurs in 4 sequential stages Prophase: Each chromosome divides into 2 chromatids which are held together by centromere. The centriole divides and the two daughter centrioles move towards opposite poles of the nucleus and the nuclear membrane disintegrates.
  • 14. kefah zaben Metaphase: The microtubules become arranged between the two centrioles forming spindle, while the chromosomes line up at the equatorial plate of the spindle. Cell Cycle M phase occurs in 4 sequential stages Anaphase : The centromeres divide and each set of separated chromosomes moves towards the opposite poles of the spindle. Cell membrane also begins to divide.
  • 15. kefah zaben Telophase : There is formation of nuclear membrane around each set of chromosomes and reconstitution of the nucleus. The cytoplasm of the two daughter cells completely separates. Cell Cycle G0 Phase.
  • 16. kefah zaben The daughter cells may continue to remain in the cell cycle and divide further, or may go out of the cell cycle into resting phase, called G0 phase. Stimulation of mitosis can be studied in a number of ways as under: 1. Compensatory stimulation of mitosis : by removal of part of an organ. 2. Reparative stimulation of mitosis occurs when a tissue is injured.
  • 17. kefah zaben adaptation stimulus example Hypertrophy-increase in cell size leading to increase in organ size Increased workload Leg muscles of runner Arm muscles in tennis player Cardiac muscle in person with hypertension Atrophy-shrinkage in size of cell, leading to decrease in organ size Decrease in: Use Blood supply Nutrition Hormonal stimulation Innervation Secondary sex organs in aging person Extremity immobilized in plas-ter cast Hyperplasia-increase in number of new cells (increase in mitosis) Hormonal influence Breast changes of a girl in pu-berty or of a pregnant woman Regeneration of liver cells New red blood cells in blood loss Dysplasia-change in the ap- pearance of cells after they have been subjected to chronic irritation Reproduction of cells with re- sulting alteration of their size and shape Alterations in epithelial cells of the skin or the cervix, pro- ducing irregular tissue changes that could be the precursors of a malignancy Metaplasia-transformation of one adult cell type to another (reversible) Stress applied to highly spe-cialized cell Changes in epithelial cells lin- ing bronchi in response to smoke irritation (cells be- come less specialized