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