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Altered Cellular and Tissue Physiology
BIO 300
Tissue Regeneration and Replacement• Permanent Cells
– Neurons and cardiac muscle cells
Tissue Regeneration and Replacement• Permanent Cells
– Neurons and cardiac muscle cells• Stable Cells (slow unless stimulated)
– Liver, smooth and skeletal muscle, cartilage, bone, endothelium
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
Chronic Inflammation
Continued tissue injury with release of growth factors
Altered growthAtrophy
HypertrophyHyperplasia
Cellular Adaptation
Adaptation in Cell Growth• Atrophy is a decrease or shrinkage in
cell size
Adaptation in Cell Growth• Atrophy is a decrease or shrinkage in
cell size• Hypertrophy is an increase in cell
size
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
Chronic Inflammation
Continued tissue injury with release of growth factors
Altered growthAtrophy
HypertrophyHyperplasia
Fibrosis
Chronic Inflammation
Continued tissue injury with release of growth factors
Altered growthAtrophy
HypertrophyHyperplasia
Fibrosis
Altered differentiationMetaplasiaDysplasiaNeoplasia
Adaptation in Cell Differentiation• Metaplasia is the replacement of
one cell by another as an adaptive response
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
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
Benign Tumors• Similar to cell of origin• Encapsulated• Slow growth• Little or no vasculature• Seldom recur• Do not spread
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
Metastic Tumor
Adaptation in Cell Differentiation• Metastasis is the process of cancer
cells separate from the original tumor spreading to other organs.
Biochemical changes from injury• 4 important sites in cell injury
–Mitochondria–Plasma membrane–Ionic channels–Cytoskeleton
Biochemical changes from injury• ATP depletion• oxygen-derived free radicals• Ca+ alterations• Membrane permeability
Manifestations of Injury• Ischemia
Manifestations of Injury• < ATP production• Na-K pump dysfunction• Cellular edema
– ER and mitochondrial swelling, ribosomes detach, blebbing
Cellular Injury
• Reversible
• Irreversible
Reversible Cell Injury• Swelling of Cell, mitochondria, ER• Ribosome detachment• Loss of microvilli• Blebbing• Chromatin clumping
Cellular Injury
Reversible Cell Injury• Cloudy swelling
–Edema and pale, granular cytoplasm
–Also known as hydropic degeneration
Hydropic Degeneration
Reversible Cell Injury• Fatty changes
– Excess intracellular lipids within vacuoles in cytoplasm
– Most frequent in liver
Irreversible Cell Injury• Lysosomal enzyme release• Protein digestion• Membrane disruption• Leakage of cell enzymes and proteins• Nuclear changes
Cellular Injury
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
Cellular Death• Processes
–Karyolysis•Nuclear dissolution and chromatin lysis
–Pyknosis •Clumping of the nucleus
–Karyorrhexis•Fragmentation of the nucleus
Cellular Death
Necrosis
• Coagulative necrosis–Kidneys, heart, and adrenal glands–Loss of nuclei and cell, but architecture remains–Lysosomal enzymes lost
Coagulative Necrosis
Necrosis
• Liquefactive necrosis–Neurons and glial cells of the
brain, bacterial infection–Hydrolytic enzymes produce
proteinaceous soup
Liquefactive Necrosis
Necrosis
• Caseous necrosis–Tuberculous pulmonary infection–Combination of coagulative and
liquefactive necrosis
Caseous Necrosis
Necrosis
• Fat necrosis–Breast, pancreas, and other
abdominal organs–Action of lipases
Fat Necrosis
Necrosis
• Gangrenous necrosis–Death of tissue from severe hypoxic injury
•Dry vs. wet gangrene–Dry = coagulative–Wet = liquefactive
Gangrenous Necrosis
Apoptosis
• Programmed cellular death• Physiologic vs. pathologic
Apoptosis
• Physiological apoptosis is an important part of life.– Some examples include ….
Apoptosis
• Apoptosis was originally known as shrinkage necrosis
Signs of Apoptosis
• Loss of contact with neighboring cells• Nuclear fragmentation• Cytoplasmic shrinkage• Organelles parceled into vesicles• How is this different from necrosis?
Apoptosis vs. Necrosis
Apoptosis vs. Necrosis
• Which one requires energy?• Which one involves edema?• Which one produces localized inflammation?
– A = Necrosis– B = Apoptosis
Aging and Altered Cellular and Tissue Biology
• Aging vs. disease• Normal life span• Gender differences
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
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
Somatic Death
• Death of an entire person
• Postmortem changes– Algor mortis– Livor mortis– Rigor mortis– Postmortem autolysis