Term
| What are the 5 possible cell adaptations? |
|
Definition
1) metaplasia
2) atrphy
3) hyperplasia
4) hypertrophy
5) neoplasia |
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Term
| Which of the possible cell adaptations are the reversible? |
|
Definition
-Reversible: metaplasia, atrophy, hyperplasia, hypertrophy
-Irreversible: neoplasia |
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Term
|
Definition
-cell becomes completely different cell type
-occurs when cell undergoes repeated stress and there is a need to change via reprommaing of stem cells
-NO GENETIC CHANGE |
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Term
|
Definition
| -dec metabolism and inc catabolism |
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Term
| What are the causes of atrophy? |
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Definition
-disuse (like in a cast)
-reduced innervation
-reduced endocrine stimulation
-pressure like an expanded mas that kills cells
-age |
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Term
|
Definition
| -much more cells, some cells can replicate more easily (ex: myocytes) |
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Term
| What are the possible causes of hypertrophy? |
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Definition
-inc workload
-inc endocrine stimulation
-compensation for hypertrophy (one kidney is so bad that the other works harder)
-causes higher efficiently |
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Term
|
Definition
-cancer
-REQUIRES GENETIC CHANGE, THUS IRREVERSIBLE |
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Term
| When does cell injury occur? |
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Definition
| -occurs when cell's ability to adapt is exceeded |
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Term
| What are the two types of cell injury? |
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Definition
|
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Term
|
Definition
| -cell membrane becomes leaky and thus cell explodes |
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Term
| What is apoptosis? How was it first ID'd? |
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Definition
-can be stimulated by toxins (lower doses stimulate it than necrosis)
-first identified with keratin |
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Term
|
Definition
| -cell injury occurs=> acute cell swelling (uptake of water)=> membrane degrades=> spills into ECF=>causes inflammatory response |
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Term
|
Definition
| -cell injury occurs=>cell condenses (nuc fragments, membrane blebs form=>cell fragments=> pagocytized, thus no inflammation |
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Term
| What are the possible etiologic agents of necrosis? |
|
Definition
-infection
-toxic
-immune
-physical
-nutrition |
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Term
| The extent of necrosis depends on what factors? |
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Definition
-cell type that is injured (ex: neurons are most susceptible to low pO2 and cerebral cortex more susceptible than brainstem called DIFFERENTIAL SUSCEPTIBILITY)
-dose of etiologic agent
-duration of exposure
-multiplicity of etiologic agents |
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Term
| The outcome of necrosis depends on what factors? |
|
Definition
-type of cell
-state oc cell (ex: some viruses only target rapidly dividing cells (Parvo)
-adaptability of a cell (ex" neurons are not very adaptable) |
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Term
| Necrosis results from damage to.... |
|
Definition
-protein synth
-DNA: cell cannot repair itself
-mitochondria: dec in cell resp
-membranes: leads to inflammation (influx of Na into cell=water intake=swelling) |
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Term
| Necrosis and Apoptosis both leads to what? |
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Definition
| -the production of Oxygen free radicals |
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|
Term
| What is an Oxygen free radical? What occurs if this happen? |
|
Definition
-O2 with one unpaired election
-these mols will go attach to other electrons on other cpds (like superoxide anion and hydroxyl radical)
-they especially attach to lipids (lipid peroxidases): dec lipid solidity which leads to breakdown
-can potentially cause breaks in DNA= focal disruptions= necrosis or apoptosis |
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Term
| How does the body handle oxygen free radicals? |
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Definition
|
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Term
| What are the 3 main methods of antioxidant use? |
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Definition
-use enzyme: superoxide dismutase: breaks down superoxide anions
-Glutathione peroxidase: breaks down hydrogen peroxide (mech used by phagocytes to kill bacteria)
-intracellular catalase
-Vit E and Vit C |
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Term
| What are the 3 ways that the nucleus breaks down? And define them. |
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Definition
-pyknosis: nuc condenses
-karyorrexesis: nuc exploded
-karyolysis: nuc fades away (mem ruptures) |
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