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56 Cards in this Set

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Trophic triggers for hypertrophy
Mechanical triggers: stretch


Trophic triggers: polypeptide growth factors and vasoactive agents
Common causes of pathologic atrophy
Decreased work load, loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, aging, pressure
Mechanisms of atrophy
Protein degradation (lysosomes, ubiquitin, proteasomes), glucocorticoids/thyroid hormone/cytokines (TNF) stimulate proteosome mediated degredtion, increases in autophagic vacuoles
Hallmarks of reversible cell injury
Reduced oxidative phosphorylation, ATP depletion, cellular swelling
general swelling of the cell/organelles, blebbing, ribosome detachment, chromatin clumping
Causes of cell injury
Hypoxia (ischemia, inadequate oxygenation, reduced oxygen carrying capacity), physical agents, chemical agents, infectious agents, immunologic reactions, genetic derangements, nutritional imbalances
Transition to irreversible injury: characteristics
Increased swelling, disruption of lysosomes, large amorphous densities in swollen mitochondria, disruption of cellular membranes, profound nuclear changes (pyknosis, karyorrhexis, karyolysis), laminated structures become more pronounced
Necrosis v. apoptosis:
cell size
N: enlarged
A: reduced
Necrosis v. apoptosis:
N: Pyknosis, karyorrhexis, karyolysis
A: Fragmentation into nucleosome size fragments
Necrosis v. apoptosis:
Plasma membrane
N: Disrupted
A: Intact; altered structure, esp. lipid orientation
Necrosis v. apoptosis:
Cellular contents
N: Enzymatic digestion
A: Intact
Cell injury results from abnormalities in one or more of which five essential cellular components
Aerobic cell respiration, maintenance of membrane integrity, protein synthesis, intracellular cytoskeleton, integrity of the genetic apparatus
Intracellular mechanisms of cell injury
ATP depletion, mitochondrial damage, loss of calcium homeostasis, accumulation of oxygen derived free radicals, defects in membrane permeability
ATP depletion effects
Sodium pump dysregulation (swelling, ER dilation, loss of microvilli), alteration of cellular energy metabolism (reduced pH; decreased enzyme activity, clumping of chromatin), failure of Ca pump, detachment of ribosomes (reduction in protein synthesis; lipid deposition), unfolded protein response
Causes of mitochondrial damage
Increases in cytosolic Ca, oxidative stress, breakdown of phospholipids through the phospholipase A2 and sphingomyelin pathways, lipid breakdown products
Free radical initiation
Radiant energy, enzymatic metabolism of exogenous chemicals, normal redox reactions, transition metals, nitric oxide
Relevant free radical effects
Lipid peroxidation of membranes, oxidative modifications to proteins, lesions in DNA
Systems that inactivate free radicals
Antioxidants, transition metal binding proteins, free radical scavenging enzymes: catalase, superoxide dismutase, glutathione peroxidase (hydrogen peroxide and superoxide anion)
Consistent irreversibility characteristics
Inability to reverse mitochondrial dysfunction, and profound disturbances in membrane function
Biochemical mechanisms that contribute to membrane damage
Mitochondrial dysfunction, loss of membrane phospholipids, cytoskeletal abnormalities, reactive oxygen species, lipid breakdown products
Morphologic features of reversible injury
Cell swelling and fatty change

plasma membrane alterations, mitochondrial changes, dilation of ER, nuclear alterations
General necrotic morphology
Increased eosinophilia, nuclear changes (p, k, k), glassy appearance (glycogen loss), vacuolated, may attract calcium salts
Morphologic appearance of necrosis is the result of?
Denaturation of intracellular proteins and enzymatic digestion of the cell
Coagulative necrosis
Protein denaturation, preservation of cell and tissue framework, characteristic of hypoxic death, either heterolysis or autolysis
Liquefactive necrosis
Autolysis/heterolysis predominates over protein denaturation, abcesses/brain tissue, focal bacterial/occasionally fungal
Caseous necrosis
TB lesions, eosinophilic amorphous material with cell debris, fragmented coagulated cells, distinctive inflammatory border
Fat necrosis
Lipase activation releases fatty acids from triglycerides, then complex with calcium
Wet gangrene
when bacterial infection is superimposed on coagulative necrosis
Ischemia: reversible injury
Na/K pump, Ca release, swelling, ER dilation, increase osmotic load, detachment of ribosomes, decreased protein synthesis, altered cellular metabolism
Ischemia: irreversible injury
MPT change, release of cytochrome c, activated membrane phospholipases, decreased ATP causes decreased phospholipid synthesis, activated intracellular proteases, accumulation of free fatty acids and lysophospholipids
Mechanisms underlying reperfusion injury
Increased generation of free radicals, MPT promotion, increased cytokine/adhesion molecule expression causes inflammation that is increased when blood flow resumes, deposition of IgM binds to complement proteins when flow resumes and cause injury and inflammation
Apoptosis in physiologic situations
embryogenesis, hormone dependent involution, cell deletion in proliferating cell populations, dead of host cells that have served their useful purpose, eliminations of self-reactive lymphocytes, cell death induced by cytotoxic T cells
Apoptosis in pathologic conditions
Death produced by a variety of injurious stimuli, injury in certain viral diseases, pathologic atrophy in parenchymal organs after duct obstruction, cell death in tumors
Biochemical features of apoptosis
Protein cleavage by caspases (may also activate DNAases), intranucleosomal cleavage of DNA (200 bp), plasma membrane alterations
Cytotoxic T lymphocytes and apoptosis
Secretes perforin, then secretes granzyme B, which enters the cell and cleaves proteins, activating caspases. also express FasL on their surface
Autophagic vacuole
Where intracellular organelles and portions of cytosol are sequestered, formed from ribosome-free regions of the ER; eventually fuse to form autophagolysosome
Lipofuscin pigment
Undigested material derived from intracellular lipid peroxidation. Composed of complex lipids, phospholipids, and protein
Mitochondrial alterations
Increase/decrease in number during hypertrophy/atrophy, megamitochondria, mitochondrial myopathies, oncocytomas
Microtubules, thin actin filaments, thick myosin filaments, intermediate filaments
Thin filaments
Leukocyte movement/phagocytosis
Sperm, cilia, leukocyte migration, phagocytosis
Intermediate filaments
Organizes cytoplasm
Abnormalities that result in accumulations
Normal, endogenous substance produced at normal/increased rate and rate of metabolism is inadequate; normal/abnormal endogenous compound accumulates bc of genetic/acquired defects in metabolism, packaging, transport, secretion; abnormal exogenous substance accumulates; can be reversible
Caused by alcohol abuse, protein malnutrition, diabetes, obesity, hepatotoxins, anoxia
Steatosis: causes
Excessive entry, excessive synthesis, decreased oxidation, increased esterification to triglycerides (due to alpha-glycerophosphate; alcohol), decreased apoprotein synthesis (carbon tetrachloride poisoning, starvation), impaired lipoprotein secretion (alcohol)
Cholesterol related pathologic states
atherosclerosis, xanthomas, inflammation and necrosis, cholesterolosis, niemann-pick disease type c
How altered protein folding causes disease
Defective intracellular transport and secretion of critical proteins, and toxicity of aggregated abnormally folded proteins, ER stress
Hyaline change
Any alteration that imparts a homogeneous, glassy pink appearance in routine H&E staining. Intracellular: proximal tubule epithelial protein droplets, russell bodies, viral inclusions, and aggregated intermediate filaments. Extracellular: damaged arterioles
How altered protein folding causes disease
Defective intracellular transport and secretion of critical proteins, and toxicity of aggregated abnormally folded proteins, ER stress
Hyaline change
Any alteration that imparts a homogeneous, glassy pink appearance in routine H&E staining. Intracellular: proximal tubule epithelial protein droplets, russell bodies, viral inclusions, and aggregated intermediate filaments. Extracellular: damaged arterioles
Hemoglobin derived, yellow-brown, composed of aggregated ferritin. Granules formed when there is a local or systemic excess of iron
Formed by enzymatic oxidation of tyrosine to dihydroxyphenylalanine in melanocytes
Increased absorption of dietary iron, impaired use of iron, hemolytic anemias, transfusions
Dystrophic intracellular calcification
Occurs in mitochondria
Dystrophic extracellular calcification
Calcium concentrates in membrane bound vesicles full of phospholipids. Calcium ion binds, phosphatases release phosphate groups which bind to calcium, cycle is repeated, structural change takes place that generates a microcrystal of calcium and phosphate which can perforate the membrane
Principal causes of hypercalcemia
Increased secretion of parathyroid hormone, destruction of bone tissue, vitamin D related disorders, renal failure
Morphologic alterations due to cell aging
Irregular and abnormally lobed nuclei, pleomorphic and vacuolated mitochondria, decreased ER, distorted golgi apparatus