c

Cell injury: Mechanisms:

Reversible/ Irreversible Increased local production of GF,
increased level of GF receptors, act of
Cell death ʹ cell injury; ischemia, particular intracellular signaling pathways
infection, toxins, and immune reactions. = cellular proliferation.

Necrosis- abnormal stresses; ischemia and Pathologic hyperplasia:

chemical injury Caused by excessive hormonal stimulation
or growth factors.
Apoptosis- controlled suicide; eliminate Useful in wound healing where connective
unwanted cells tissue cells (fibroblasts) and blood vessels
aid in repair.
Cellular adaptations of growth and
differentiation- for increased demand and
external stimulation, reduced supple of Hyperthrophy
nutrients and growth factors. Increase in size of cells resulting in
increase in the size of organ; no new cells,
Hyperplasia just larger cells. Cause by synthesis of
An increase in the number of cells in an more structural components. Cells may be
organ or tissue : increased volume. dividing and nondividing cells (where
(hypertrophy may occur with hyperplasia nuclei have a higher dna content because
as the same external stimulus triggers it is arrested in the cell cycle without
both ie growth in uterus) mitosis).
Requires cells to synthesize dna for For muscle; increased workload
mitotic division. (heart/skeletal muscles) to permit at a
higher level of activity. Balances demand
Physiologic Hyperplasia and functional capacity.
Hormonal hyperplasia: increases Hormone induced: during pregnancy by
functional capacity (breasts at puberty estrogenic hormones increases muscle
and pregnancy, and uterus) where cell size. Prolactin and estrogen increase
hormones may acts as GF that trigger breasts for lact.
transcription of various cell genes.
Mechanisms:
Compensatory hyperplasia: increases Genes the encode transcription factors;
tissue mass after damage of partial growth factors; fibroblast growth factors;
resection (liver regeneration) proliferation vasoactive agents. Reinduction of genes
of remaining cells and devt of new cells expressed during early devt.
from stem cells.
Atrophy Irreversible /cell death:
Shrinkage in cell size by loss of cell Structural changes and functional changes
substance/structural components of the that are recognized as cell death.
cell.
Physiologic: fetal devt notochord and Causes of cell injury
thyroglossal duct; uteral size decrease Oxygen deprivation:
after parturition. Hypoxia- loss of oxygen carrying ability of
Pathologic: the blood (CO poiso ning or anemia)
Decreased workload Ischemia more sever as both nutrients
Loss of innervation and metabolites are cut off from the
Diminished blood supply (ischemia) tissue.
Malnutrition Physical agents:
Loss of endocrine stimulation (ie Mech trauma, temperature, pressure,
menopause) radiation, shock.
Aging (cell loss in brain and heart) Chemical agents:
Pressure (ischemia to surrounding tissue Poisons, toxic chemicals
from pressure from tumours, etc.) Infectious agents:
Submicroscopic viruses to large
Mechanisms: tapeworms, bacteria, fungi, etc.
Increased protein degradation (ubiquitin - Immunologic reactions:
proteasome pathway) -- glucocorticoids Hypersensitivity, anaphylactic shock,
and thyroid hormone stimulation; TNF. autoimmune disease
Increased autophagic vacuoles- vacuoles Genetic derangements:
where cell fragments are digested. Malformations, etc.
Nutritional imbalances:
Metaplasia Anorexia, starvation, hyperlidiemia, etc.
Reversible change where an adult cell
type is replaced by another cell type Ie
columnar to squamous in respiratory tract Mechanisms of cell injury:
(barret esophagus from gastric reflux). Type of injury, duration, and severity.
Type, state, and adaptability of injured
Mechanisms: cell (vulnerability).
Reprogamming of stem cells in normal Functional and biochemical abnormalities
cells/undifferentiated mesenchymal cells in one or more of several essential cellular
in connective tissue. components.

Cell injury and cell death: ATP depletion

Reversible: reduced oxidative mc NA accumulation in cell ʹ
phosphorylation, atp depletion, and isosmotic gain of water ʹ cell
cellular swelling (ion conc and water swelling and dilation of the er.
influx.
 mc Anaerobic metabolism (glycolysis) Defect in membrane permeability
ʹ glycogen stores depletion ʹ lactic mc Mitochondrial dysfunction ʹ
acid and inorganic phosphate decreased phospholipid synthesis
accumulation- reduction of ʹ faulty cell membrane
intracell pH ʹ decreased cellular mc Loss of membrane phospholipids ʹ
enzyme activity. activation of phopholipases by ca
mc Ca pump failure- influx of Ca ʹ influx
cellular component damage mc Cytoskeletal abnormality ʹ
mc Prolonged depletion of ATP ʹ stretching nad rupture
structural disruption of protein mc Reactive oxygen species
synthetic apparatus ʹ ribosome mc Lipid breakdown products-
detachment from rer ʹ reduction changes in permeability
of protein synthesis.
mc Protein misfolding. Reversible injury
Cellular swelling, hydropi change/
Mitochondrial damage vacuolar degeneration. Swelling is
Cytochrome c leakage into cytosol. reversible
1. c Plasma membrane alteration-
Influx of Ca and loss of Ca homeostasis bebbing
Increase in membrane permeability- 2. c Mitochondrial changes-swelling
activates enzymes (ATPases, 3. c Dilation of er- detachment and
phopholipases, proteases, and disaggregation of polysomes
endonucleases. 4. c Nuclear alterations- granular and
fibrillar elements
Accumulation of O2 derived free radicals
Reactive oxygen species from Necrosis
mitochondrial respiration- oxidative Morphologic changes from progressive
stress. Free radicals have a single degradative action of enzymes on cells.
unpaired electron in the outer orbit which May elicit inflammation in surrounding
may react with adjacent molecules. cells as contents leak out.
mc Absorption of radiant energy (UV,
xray)
mc Dnzymatic metabolism of
exogenous chemicals or drugs.
mc Redox reaction occur during
normal metabolic processes.
(superoxide)
mc Transition metals
mc Nitric oxide