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Dr Ahmed Hassan
Cell Injury, Cell Death,
and Adaptations
OVERVIEW OF CELLULAR
RESPONSES TO STRESS AND
NOXIOUS STIMULI
 Cells are active participants in their environment,
constantly adjusting their structure and function to
accommodate changing demands and
extracellular stresses.
 Cells tend to maintain their intracellular milieu
within a fairly narrow range of physiologic
parameters; that is, they maintain normal
homeostasis.
 As cells encounter physiologic stresses or
pathologic stimuli, they can undergo adaptation,
achieving a new steady state and preserving
viability and function.
 The principal adaptive responses are
hypertrophy, hyperplasia, atrophy, and
metaplasia.
 If the adaptive capability is exceeded or if the
external stress is inherently harmful, cell injury
develops
 Within certain limits injury is reversible, and cells
return to a stable baseline; however, severe or
persistent stress results in irreversible injury
and death of the affected cells.
 Cell death is one of the most crucial events in the
evolution of disease in any tissue or organ.
 It results from diverse causes, including
ischemia (lack of blood flow), infections,
toxins, and immune reactions.
 Cell death is also a normal and essential process
in embryogenesis, the development of organs,
and the maintenance of homeostasis
 Hypertrophy and hyperplasia can also occur
together, and obviously both result in an enlarged
(hypertrophic) organ.
 Thus, the massive physiologic enlargement of
the uterus during pregnancy occurs as a
consequence of estrogen-stimulated smooth
muscle hypertrophy and smooth muscle
hyperplasia
 In contrast, the striated muscle cells in both the
skeletal muscle and the heart can undergo only
hypertrophy in response to increased demand
because in the adult they have limited capacity to
divide
 For example, after a normal menstrual period
there is a burst of uterine epithelial proliferation
that is normally tightly regulated by stimulation
through pituitary hormones and ovarian estrogen
and by inhibition through progesterone.
However, if the balance between estrogen and
progesterone is disturbed, endometrial
hyperplasia ensues, a common cause of
abnormal menstrual bleeding.
 Hyperplasia is also an important response of
connective tissue cells in wound healing, in
which proliferating fibroblasts and blood vessels
aid in repair
 Stimulation by growth factors is also involved in
the hyperplasia that is associated with certain
viral infections; for example, papillomaviruses
cause skin warts and mucosal lesions composed
of masses of hyperplastic epithelium.Here the
growth factors may be produced by the virus or
by infected cells.
 the hyperplastic process remains controlled; if
hormonal or growth factor stimulation abates, the
hyperplasia disappears. It is this sensitivity to
normal regulatory control mechanisms that
distinguishes benign pathologic hyperplasias from
cancer, in which the growth control mechanisms
become dysregulated or ineffective.
 Nevertheless, pathologic hyperplasia constitutes
a fertile soil in which cancerous proliferation may
eventually arise. Thus, patients with hyperplasia
of the endometrium are at increased risk of
developing endometrial cancer, and certain
papillomavirus infections predispose to cervical
cancers
 Atrophy results from decreased protein synthesis and
increased protein degradation in cells. Protein
synthesis decreases because of reduced metabolic
activity. The degradation of cellular proteins occurs
mainly by the ubiquitin-proteasome pathway.
 Nutrient deficiency and disuse may activate ubiquitin
ligases, which attach multiple copies of the small
peptide ubiquitin to cellular proteins and target these
proteins for degradation in proteasomes.
 This pathway is also thought to be responsible for the
accelerated proteolysis seen in a variety of catabolic
conditions, including cancer cachexia.
 The cellular response to injurious stimuli depends
on the type of injury, its duration, and its
severity. Thus, low doses of toxins or a brief
duration of ischemia may lead to reversible cell
injury, whereas larger toxin doses or longer
ischemic intervals may result in irreversible injury
and cell death
 The consequences of an injurious stimulus
depend on the type, status, adaptability, and
genetic makeup of the injured cell.
IMPORTANT TARGETS OF CELL
INJURY
 Aerobic respiration –
 ATP depletion or decreased synthesis.
 Cell membranes - plasma membranes,
mitochondrial, lysosomal and other organelle
membranes.
 Protein synthesis.
 Cytoskeleton.
 Genetic apparatus.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 4 April 2005 06:11 PM)
© 2005 Elsevier
ATP DEPLETION - HYPOXIA/ISCHAEMIA
 Mitochondria - reduced oxidative phosphorylation.
 Cell membrane - reduced sodium pump.
 Sodium and water enter the cell; potassium exits.
 Endoplasmic reticulum dilates, the cell swells, blebs
appear.
 Anaerobic glycolysis occurs with loss of glycogen,
accumulation of lactic acid, acid pH which interferes with
enzymes.
 Failure of the calcium pump leads to influx of Ca++ into
the cell, activate various enzymes to the detriment of the
cell.
 RER loses ribosomes and protein synthesis falls -
structural proteins (membranes,cytoskeleton) and
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 4 April 2005 06:11 PM)
© 2005 Elsevier
THE IMPORTANCE OF CALCIUM
 Influx of calcium to the cytosol comes from the
extracellular fluid and stores in mitochondria and
endoplasmic reticulum.
 Ca++ activates phospholipases (damages cell
membranes),proteases (damages cell membranes
and cytoskeleton) and endonucleases (damages
DNA).
 This is one of the main mechanisms of cell death,
either through severe damage to membranes of
lysosomes and leakage of lysosomal enzymes or
triggering apoptosis.
 Occurs particularly in hypoxia and ischaemia and with
certain toxins. Preventing the rise in Ca++ or
restoring to normal levels prevents cell death.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 4 April 2005 06:11 PM)
© 2005 Elsevier
MEMBRANE DAMAGE
 Mitochondria –
 mitochondrial permeability transition; this non-selective
pore may be reversible or become permanent leading to
cell death.
 Leakage of cytochrome c can trigger apoptosis.
 Plasma membrane –
 mechanisms include those occuring with
hypoxia/ischaemia and free radicals, but also immune
mechanisms as with complement activation and perforin
from lymphocyte attack on cells infected with a virus.
 All membranes may be damaged and ruptured by
 mechanical force as in trauma, or by ice crystals as in
extreme cold.
 Damage to lysosomal membranes can lead to cell death
by necrosis.
cell adaptation and cell injury - Copy-4 copy.pptx
cell adaptation and cell injury - Copy-4 copy.pptx
cell adaptation and cell injury - Copy-4 copy.pptx

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cell adaptation and cell injury - Copy-4 copy.pptx

  • 1. Dr Ahmed Hassan Cell Injury, Cell Death, and Adaptations
  • 2. OVERVIEW OF CELLULAR RESPONSES TO STRESS AND NOXIOUS STIMULI  Cells are active participants in their environment, constantly adjusting their structure and function to accommodate changing demands and extracellular stresses.  Cells tend to maintain their intracellular milieu within a fairly narrow range of physiologic parameters; that is, they maintain normal homeostasis.
  • 3.  As cells encounter physiologic stresses or pathologic stimuli, they can undergo adaptation, achieving a new steady state and preserving viability and function.  The principal adaptive responses are hypertrophy, hyperplasia, atrophy, and metaplasia.  If the adaptive capability is exceeded or if the external stress is inherently harmful, cell injury develops
  • 4.  Within certain limits injury is reversible, and cells return to a stable baseline; however, severe or persistent stress results in irreversible injury and death of the affected cells.  Cell death is one of the most crucial events in the evolution of disease in any tissue or organ.  It results from diverse causes, including ischemia (lack of blood flow), infections, toxins, and immune reactions.  Cell death is also a normal and essential process in embryogenesis, the development of organs, and the maintenance of homeostasis
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  • 8.  Hypertrophy and hyperplasia can also occur together, and obviously both result in an enlarged (hypertrophic) organ.  Thus, the massive physiologic enlargement of the uterus during pregnancy occurs as a consequence of estrogen-stimulated smooth muscle hypertrophy and smooth muscle hyperplasia  In contrast, the striated muscle cells in both the skeletal muscle and the heart can undergo only hypertrophy in response to increased demand because in the adult they have limited capacity to divide
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  • 13.  For example, after a normal menstrual period there is a burst of uterine epithelial proliferation that is normally tightly regulated by stimulation through pituitary hormones and ovarian estrogen and by inhibition through progesterone. However, if the balance between estrogen and progesterone is disturbed, endometrial hyperplasia ensues, a common cause of abnormal menstrual bleeding.  Hyperplasia is also an important response of connective tissue cells in wound healing, in which proliferating fibroblasts and blood vessels aid in repair
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  • 15.  Stimulation by growth factors is also involved in the hyperplasia that is associated with certain viral infections; for example, papillomaviruses cause skin warts and mucosal lesions composed of masses of hyperplastic epithelium.Here the growth factors may be produced by the virus or by infected cells.
  • 16.  the hyperplastic process remains controlled; if hormonal or growth factor stimulation abates, the hyperplasia disappears. It is this sensitivity to normal regulatory control mechanisms that distinguishes benign pathologic hyperplasias from cancer, in which the growth control mechanisms become dysregulated or ineffective.  Nevertheless, pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise. Thus, patients with hyperplasia of the endometrium are at increased risk of developing endometrial cancer, and certain papillomavirus infections predispose to cervical cancers
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  • 18.  Atrophy results from decreased protein synthesis and increased protein degradation in cells. Protein synthesis decreases because of reduced metabolic activity. The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway.  Nutrient deficiency and disuse may activate ubiquitin ligases, which attach multiple copies of the small peptide ubiquitin to cellular proteins and target these proteins for degradation in proteasomes.  This pathway is also thought to be responsible for the accelerated proteolysis seen in a variety of catabolic conditions, including cancer cachexia.
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  • 31.  The cellular response to injurious stimuli depends on the type of injury, its duration, and its severity. Thus, low doses of toxins or a brief duration of ischemia may lead to reversible cell injury, whereas larger toxin doses or longer ischemic intervals may result in irreversible injury and cell death  The consequences of an injurious stimulus depend on the type, status, adaptability, and genetic makeup of the injured cell.
  • 32. IMPORTANT TARGETS OF CELL INJURY  Aerobic respiration –  ATP depletion or decreased synthesis.  Cell membranes - plasma membranes, mitochondrial, lysosomal and other organelle membranes.  Protein synthesis.  Cytoskeleton.  Genetic apparatus.
  • 33. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 4 April 2005 06:11 PM) © 2005 Elsevier
  • 34. ATP DEPLETION - HYPOXIA/ISCHAEMIA  Mitochondria - reduced oxidative phosphorylation.  Cell membrane - reduced sodium pump.  Sodium and water enter the cell; potassium exits.  Endoplasmic reticulum dilates, the cell swells, blebs appear.  Anaerobic glycolysis occurs with loss of glycogen, accumulation of lactic acid, acid pH which interferes with enzymes.  Failure of the calcium pump leads to influx of Ca++ into the cell, activate various enzymes to the detriment of the cell.  RER loses ribosomes and protein synthesis falls - structural proteins (membranes,cytoskeleton) and
  • 35. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 4 April 2005 06:11 PM) © 2005 Elsevier
  • 36. THE IMPORTANCE OF CALCIUM  Influx of calcium to the cytosol comes from the extracellular fluid and stores in mitochondria and endoplasmic reticulum.  Ca++ activates phospholipases (damages cell membranes),proteases (damages cell membranes and cytoskeleton) and endonucleases (damages DNA).  This is one of the main mechanisms of cell death, either through severe damage to membranes of lysosomes and leakage of lysosomal enzymes or triggering apoptosis.  Occurs particularly in hypoxia and ischaemia and with certain toxins. Preventing the rise in Ca++ or restoring to normal levels prevents cell death.
  • 37. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 4 April 2005 06:11 PM) © 2005 Elsevier
  • 38. MEMBRANE DAMAGE  Mitochondria –  mitochondrial permeability transition; this non-selective pore may be reversible or become permanent leading to cell death.  Leakage of cytochrome c can trigger apoptosis.  Plasma membrane –  mechanisms include those occuring with hypoxia/ischaemia and free radicals, but also immune mechanisms as with complement activation and perforin from lymphocyte attack on cells infected with a virus.  All membranes may be damaged and ruptured by  mechanical force as in trauma, or by ice crystals as in extreme cold.  Damage to lysosomal membranes can lead to cell death by necrosis.