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Steady state of a cell is called?
Homeostatis
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Acute and transient cell damage leads to
reversible cellular swelling, fatty change
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Progressive and severe damage will lead to
irreversible damage like necrosis or apoptosis
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Hyperplasia or hypertrophy
inc demand or inc stimulation
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Atrophy?
dec nutrients or decreased stimulation
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Chronic irritation (physical or chemical) leads to?
Metaplasia
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Adaptation can be divided into?
PHysiologic: hormone induced hypertrophy of breast and uterus during pregnancy.
Pathologic: response to stress to escape injury
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Increase in cell size
Hypertrophy
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Increase in cell number
Hyperplasia
Example: Benign prostatic hyperplasia
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Pathologic hypertrophy example?
HTN or aortic stenosis results in stretching of the cardiac muscle (mechanical or trophic triggers)
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Pathologic hyperplasia example?
Hyperplasia of fibroplasts in response to a wound stress (growth factors)
Acanthosis nigricans: excess epidermal growth factor production of malignant tumor
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Gingival hyperplasia causes?
Dilantin, Cyclosporine
Epulis fissuratum, Parulis (sinus tract), pulpal hyerplasia, hypekeratosis (linea alba)
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Hyperplasia of some tissues can lead to malignant neoplasia, example?
Endometrium
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Define atrophy?
shrinkage in size of the cell by loss of cell substance, dec protein synthesis, inc protein degradation
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Define metaplasia?
Reversible change from one adult cell type (epithelial or mesenchymal) to another
reprogrammed to differentiate along a new path
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List some causes of atrophy?
- 1. aging
- 2. dec workload
- 3. loss of innervation
- 4. dec blood supply
- 5. dec nutrition
- 6. dec endocrine stimulation
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What is autophagy?
in time of nutrient deprivation, proteins are degraded by lysosomes after being packaged into autophagosomes.
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What two cellular changes can be premalignant in some tissues?
Metaplasia and Dysplasia
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What are some mechanisms leading to intracellular accumulations?
- 1. Abnormal metabolism (fatty liver cells)
- 2. Lack of enzyme
- 3. Defective protein folding, transport
- 4. Uptake of indigestible material
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Another name for fatty change in liver?
Steatosis
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Dystrophic calcification?
deposition of calcium at sites of injury
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Metastatic calcification?
deposition of calcium in normal tissues (hypercalcemia, high PTH)
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Telomere shortening leads to ?
Replicative senescene
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What are some principle mechanism of cellular injury?
- 1. ROS
- 2. dec ATP
- 3. Mitochondrial damage
- 4. Membrane damage
- 5. Protein misfolding
- 6. Entry or Calcium
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Cell injuries leading to necrosis?
Ischemia or hypoxia: ischemia faster damage
Ischemia and reperfusion: inflammatory cells add insult
Chemical
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Difference in cell size from necrosis to apoptosis?
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Difference in nucleus in necrosis vs. apoptosis?
- N: pyknosis, karyorrhexis (nuclear fading), karyolysis
- A: fragmentation into nucelosome-size fragments
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Difference in plasma membrane necrosis vs. apoptosis?
- N: disrupted
- A: Intact, but reorganized
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Difference in cellular contents necrosis vs. apoptosis?
- N: Enzymatic digestion, leakage
- A: Intact; may be released in apopotic bodies
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Difference in inflammation necrosis vs. apoptosis?
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Necrosis is always from pathology (irreversible cell injury)
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Apoptosis can be pathologic (DNA damage) or physiologic (unwanted cells)
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Consequence of chronic inflammation or inflammatory exudate?
Fibrosis and scarring, deposition of fibrous connective tissue in place of original cells
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