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24 Cards in this Set
- Front
- Back
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What are the variables that limit cardiac hypertrophy and what is the end result when the limit is reached?
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- vasculature limited to supplythe enlarged fibers
- limit of mitochondria to supply ATP - limit of biosynth machinery to provide contractile proteins or other cytoskeletal elements Net result = ventricular dilation and ultimately cardiac failure |
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What are the 2 types of physiologic hyperplasia?
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1. hormonal - ex prolif of glandular epithelium of female breast at puberty and pregnancy
2. compensatory - occurs when portion of tissue is removed or diseased (ex. when liver partially resected, grows back via mitosis of remaining cells) |
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what are most forms of pathological hyperplasia caused by?
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excessive hormonal or GF stimulation
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what distinguishes between benign pathological hyperplasia and cancer
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hyperplasia - process remians controlled; due to excessive hormonal or GF stim, but if those stims stop, hyperplasia disappears
cancer = growth control mechanisms become dysregulated or ineffective |
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what are the causes of atrophy?
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1. decreased workload
2. loss of innervation 3.. diminished blood supply 4. loss of endocrine fn 5. aging (senile atrophy) 6. inadequatae nutrition |
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autophagy
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process by which the starved cell eats its own components in an attempt to find nutrients and survive
- will see increases in autophagic vacuoles - often accompanies atrophy |
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metaplasia
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reversible change in which one adult cell type is replaced by another adult cell type
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what type of adaptive response occurs in the respiratory system of smokers?
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epithelial metaplasia
- normal ciliated columnar epithelial cells of trachea and bronchi are replaced by stratified squamous epithelium |
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what conditions induce metaplasia in the respiratory epithelium? in the epithelium of the lower esophagus?
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1. smoking (ciliated colunar to stratified squamous)
2. Vit A defiency Gastric metaplasia = chronic gastric reflux (stratified squamous to gastric or intestinal type columnar epithelium) |
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what is the major pathway of death for many common injuries such as ischemia, trauma, exposure to toxins, infections?
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necrosis
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what is the most common cause of hypoxia?
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ischemia
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what are examples of chemical agents that can cause cell injury?
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1. oxygen at sufficiently high partial pressures
2. poisons 3. air pollutants 4. insectisides 5. CO 6. therapeutic drugs etc etc |
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What is the chronological order of events and observations in reversible and irreversible cell injury?
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1. loss of cellular fn (can still be reversible)
2. cell death (irreversible) 3. ultrastructural changes (EM) 4. Light microscopic changes 5. gross morphologic changes |
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What 2 phenomena consistently characterize irreversibility?
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1. inability to reverse mitochrondrial dysfunction (lack of ox phosphor and ATP generation)
2. profound disturbances in membrane fn |
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what are the 2 main morphologic correlates of reversible cell injury? What are they due to?
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1. cellular swelling - due to failure of energy-dep ion pumps in the plasma membrane --> inability to maintain ionic and fluid homeostasis
2. fatty change - hypoxic injury, toxic or metabolic injury |
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what are the key morphological characteristics of fatty change? what types of cells is it found in?
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1. appearance of small or large lipid vacuoles in the cytoplasm
- most often found in hepatocytes and myocardial cells (participate in fat metabolism) |
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hydropic change/vacuolar degeneration
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pattern of nonlethal injury in which small, clear vacuoles are visible within the cytoplasm --> represent distended and pinched-off segments of the ER
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What are common ultrastructural changes of reversible cell injury?
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1. plasma membrane alterations (blebbing, blunting or distortion of microvilli, loosening of intercelllular attachments)
2. mitochondrial changes (swelling, appearance of PL-rich amorphous densities) 3. dilation of the ER w/ detachment of ribosomes and dissociation of polysomes 4. nuclear alterations w/ clumping of chromatin 5. INCREASED EOSINOPHILIA |
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what is the reason for increased eosinophilia in necrotic cells?
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- increased binding of eosin to denatured cytoplasmic proteins
- loss of basophilia that is normally imparted by the RNA in the cytoplasm |
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myelin figures
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large, whorled phospholipid masses that replace dead cells
- derived from damaged cellular membranes - result from dissociation of lipoproteins w/ ummasking of phosphatide groups --> promotes uptake and intercalation of water bet lamellar stacks of membranes |
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what are the 3 different patterns of nuclear changes due to the breakdown of DNA and chromatin?
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1. karyolysis - basophilia of chromatin fades
2. pyknosis - nuclear shrinkage and increase basophilia (DNA condenses) 3. karyorrhexis - pyknotic nucleus undergoes fragmentation |
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what are the different patterns of tissue necrosis and their morphological characteristics?
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1. coagulative - component cells dead but basic tissue architecture is preserved for several days
- enzymes are denatured so proteolysis of dead cells is blocked 2. liquefactive- microbes stimulate accumulation of inflamm cells and enzymes of leukocytes digest tissue - tissue transformed to viscous liquid mass 3. gangrenous - limb that's lost blood supply and undergone coag necrosis involving multiple tissue layers 4. caseous - yellow-white apperance of area of necrosis - tissue architecture completely obliterated and cellular outlines cannot be discerned - often enclosed w/in a distinctive inflammatory border 5. fat - from release of pancreative lipases into the substance of the 6. fibrinoid |
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what are the 3 different patterns of nuclear changes due to the breakdown of DNA and chromatin?
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1. karyolysis - basophilia of chromatin fades
2. pyknosis - nuclear shrinkage and increase basophilia (DNA condenses) 3. karyorrhexis - pyknotic nucleus undergoes fragmentation |
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what are the different patterns of tissue necrosis and their morphological characteristics?
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1. coagulative - component cells dead but basic tissue architecture is preserved for several days
- enzymes are denatured so proteolysis of dead cells is blocked 2. liquefactive- microbes stimulate accumulation of inflamm cells and enzymes of leukocytes digest tissue - tissue transformed to viscous liquid mass 3. gangrenous - limb that's lost blood supply and undergone coag necrosis involving multiple tissue layers 4. caseous - yellow-white apperance of area of necrosis - tissue architecture completely obliterated and cellular outlines cannot be discerned - often enclosed w/in a distinctive inflammatory border 5. fat - from release of pancreative lipases into the substance of the 6. fibrinoid |
