chapter03 altered cell & tissue
TRANSCRIPT
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Altered Cellular and Tissue Physiology
BIO 300
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Tissue Regeneration and Replacement• Permanent Cells
– Neurons and cardiac muscle cells
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Tissue Regeneration and Replacement• Permanent Cells
– Neurons and cardiac muscle cells• Stable Cells (slow unless stimulated)
– Liver, smooth and skeletal muscle, cartilage, bone, endothelium
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Tissue Regeneration and Replacement• Permanent Cells
– Neurons and cardiac muscle cells• Stable Cells (slow unless stimulated)
– Liver, smooth and skeletal muscle, cartilage, bone, endothelium
• Labile Cells (continuous, often by stem cells)– Epidermal cells, GI epithelium, spermatazoa, blood
cells
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Chronic Inflammation
Continued tissue injury with release of growth factors
Altered growthAtrophy
HypertrophyHyperplasia
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Cellular Adaptation
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Adaptation in Cell Growth• Atrophy is a decrease or shrinkage in
cell size
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Adaptation in Cell Growth• Atrophy is a decrease or shrinkage in
cell size• Hypertrophy is an increase in cell
size
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Adaptation in Cell Growth• Atrophy is a decrease or shrinkage in cell size• Hypertrophy is an increase in cell size• Hyperplasia is an increase in the number of
cells via increased mitotic division– All of these can be caused by mechanical or
chemical stimuli
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Chronic Inflammation
Continued tissue injury with release of growth factors
Altered growthAtrophy
HypertrophyHyperplasia
Fibrosis
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Chronic Inflammation
Continued tissue injury with release of growth factors
Altered growthAtrophy
HypertrophyHyperplasia
Fibrosis
Altered differentiationMetaplasiaDysplasiaNeoplasia
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Adaptation in Cell Differentiation• Metaplasia is the replacement of
one cell by another as an adaptive response
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Adaptation in Cell Differentiation• Metaplasia is the replacement of one
cell by another as an adaptive response
• Dysplasia is the abnormal development of a tissue, often precancerous and in inflamed tissue
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Adaptation in Cell Differentiation• Neoplasia is the abnormal formation
of tissue, often poorly differentiated and unresponsive to growth control mechanisms.– Can be classified as benign or
malignant
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Benign Tumors• Similar to cell of origin• Encapsulated• Slow growth• Little or no vasculature• Seldom recur• Do not spread
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Benign Tumors• Similar to cell of origin• Encapsulated• Slow growth• Little or no vasculature• Seldom recur• Do not spread
Malignant Tumors• Poorly differentiated• Invades• Fast growth• Marked vasculature• Often recur• Metastic
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Metastic Tumor
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Adaptation in Cell Differentiation• Metastasis is the process of cancer
cells separate from the original tumor spreading to other organs.
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Biochemical changes from injury• 4 important sites in cell injury
–Mitochondria–Plasma membrane–Ionic channels–Cytoskeleton
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Biochemical changes from injury• ATP depletion• oxygen-derived free radicals• Ca+ alterations• Membrane permeability
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Manifestations of Injury• Ischemia
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Manifestations of Injury• < ATP production• Na-K pump dysfunction• Cellular edema
– ER and mitochondrial swelling, ribosomes detach, blebbing
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Cellular Injury
• Reversible
• Irreversible
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Reversible Cell Injury• Swelling of Cell, mitochondria, ER• Ribosome detachment• Loss of microvilli• Blebbing• Chromatin clumping
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Cellular Injury
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Reversible Cell Injury• Cloudy swelling
–Edema and pale, granular cytoplasm
–Also known as hydropic degeneration
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Hydropic Degeneration
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Reversible Cell Injury• Fatty changes
– Excess intracellular lipids within vacuoles in cytoplasm
– Most frequent in liver
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Irreversible Cell Injury• Lysosomal enzyme release• Protein digestion• Membrane disruption• Leakage of cell enzymes and proteins• Nuclear changes
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Cellular Injury
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Cellular Death
• Necrosis–Sudden change in cell leading to loss of function
and resulting in autodigestion•Changes in tissue are the result of the release of
denaturation and release of lysosomal denaturation
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Cellular Death• Processes
–Karyolysis•Nuclear dissolution and chromatin lysis
–Pyknosis •Clumping of the nucleus
–Karyorrhexis•Fragmentation of the nucleus
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Cellular Death
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Necrosis
• Coagulative necrosis–Kidneys, heart, and adrenal glands–Loss of nuclei and cell, but architecture remains–Lysosomal enzymes lost
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Coagulative Necrosis
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Necrosis
• Liquefactive necrosis–Neurons and glial cells of the
brain, bacterial infection–Hydrolytic enzymes produce
proteinaceous soup
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Liquefactive Necrosis
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Necrosis
• Caseous necrosis–Tuberculous pulmonary infection–Combination of coagulative and
liquefactive necrosis
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Caseous Necrosis
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Necrosis
• Fat necrosis–Breast, pancreas, and other
abdominal organs–Action of lipases
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Fat Necrosis
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Necrosis
• Gangrenous necrosis–Death of tissue from severe hypoxic injury
•Dry vs. wet gangrene–Dry = coagulative–Wet = liquefactive
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Gangrenous Necrosis
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Apoptosis
• Programmed cellular death• Physiologic vs. pathologic
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Apoptosis
• Physiological apoptosis is an important part of life.– Some examples include ….
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Apoptosis
• Apoptosis was originally known as shrinkage necrosis
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Signs of Apoptosis
• Loss of contact with neighboring cells• Nuclear fragmentation• Cytoplasmic shrinkage• Organelles parceled into vesicles• How is this different from necrosis?
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Apoptosis vs. Necrosis
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Apoptosis vs. Necrosis
• Which one requires energy?• Which one involves edema?• Which one produces localized inflammation?
– A = Necrosis– B = Apoptosis
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Aging and Altered Cellular and Tissue Biology
• Aging vs. disease• Normal life span• Gender differences
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Theories of Aging
• Accumulation of injurious events
• Genetically controlled program
• Theories– Genetic and environmental lifestyle
factors– Alterations of cellular control
mechanisms– Degenerative extracellular and vascular
changes
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Aging
• Cellular aging– Atrophy, decreased function, and loss of
cells
• Tissue and systemic aging– Progressive stiffness and rigidity– Sarcopenia
• Frailty– Mobility, balance, muscle strength, motor
activity, cognition, nutrition, endurance, falls, fractures, and bone density
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Somatic Death
• Death of an entire person
• Postmortem changes– Algor mortis– Livor mortis– Rigor mortis– Postmortem autolysis