Flashcards in Cell Growth And Neoplasia Deck (28):
What are the results of Cellular Adaptation?
Hypertrophic (inc. in size)
-Hyperplasia (inc. #)
The replacement of adult cells to another TYPE of cell that can be reversed is called _____?
What is an example of Dysplasia, deranged cell growth of a specific tissue?
Crevical epithelial cells growing into cancer cells
-Dysplasia is only in epithelial cells
What are sources of intracellular accumulations?
1. Normal body substances (triglycerides produced at a rate that exceeds removal —> fatty liver disease)
2. Abnormal endogenous products
(Inborn errors of metabolism/ genetic defect OR accumulation of pigments)
3. Exogenous Products (environmental agents)
How do inborn errors of metabolism result in intracellular accumulations? For example Tay Sach disease?
- abnormal lipids accumulate in the the brain —> motor and mental deterioration
Explain how dystrophic calcification and metastatic calcification are different?
Dystrophic: in injured, dead or dying tissue
Metastatic: in normal tissue
-calcium levels increase secondary to disease (cancer, hyperparathyroid, pagers, excess CA++ ingestion)
What are 3 mechanisms of cellular injury?
1. Free radical formation
2. Hypoxica/ ischemia —> ATP depletion
3. Disruption of intracellular calcium homeostasis.
Explain pathological conditions leading to free radical formation?
1. Ionizing ration (bombs, CA treatment)
2. Inflammation (trauma/ electrical forces)
4. Drugs and chemicals (ex: acetomenophen —> inc. P450 metabolism —> inc. free radicals
What are the bodies defenses against free radicals?
1. Antioxidants: donate electrons to unstable free radicals to make stable
2. Metal carrier proteins: transferrants bind to metals
3. Enzymes: (-tase) bind to electrons. Hopefully reverse oxidative modifications of proteins
Explain how hypoxia cell injury can lead to irreversible cellular injury OR oxidative stress?
1. Hypoxia —> injury —> deprivation of oxygen —> decrease generation of ATP —> swelling —> if untreated —> irreversible cellular injury
2. Hypoxia —> Injury —> repair —> flood with O2 —> oxidative stress —> oxygen free radicals —> affects protein synthesis
How do cells lose protein syntheses through hypoxic cell injury?
1. Injury —> dec. ATP b/c of dec. mitochondrial action —> sodium potassium pump stops working —> more NA into the cell —> more H2O follows —> cells swell —> “bleb” —> rough ER swells —> DEC. PROTEIN SYNTHESIS
2. Injury —> hypoxia —> anaerobic glycolysis —> inc. lactic acid —> DENATURING OF PROTEINS
3. Injury —> dec. ATP —> dec calcium pump —> dec activation of enzymes
Which types of cell injury are reversible?
1. Cellular swelling ( Na+/K+ ATPase pump)
2. Fatty changes
What is the difference between apoptosis and necrosis?
Apoptosis - planned for cells that are ineffective, damaged, worn out
Necrosis- unplanned in living person
Gangrene = large amount of necrotic tissue
Dry gangrene vs wet gangrene?
DRY: dry, shrinks —> dark brown or black —> slowly spreads
WET: infection —> cold, swollen, pulse less —> moist black w/ tension —> liquefaction —> odor —> spread is rapid
What are treatments of gangrene?
What are characteristics of cell differentiation?
- orderly steps
- more specialized = less differentiated
- more specialized neurons unable to divide and reproduce
- parent cells can continue to divide and reproduce
What are characteristics of cancer?
- disordered differentiation and growth
- uncoordinated and autonomous growth (no growth factor)
- no regulatory controls over growth or division (rate)
Which type of neoplasm resembles cells in tissue of origin, progresses at a slow rate, and does not spread by metastasis into surrounding tissue?
How do malignant neoplasms metastasize?
Primary solid tumor grows —> cells detach —> invade surrounding tissue —> enter blood and lymph systems —> spread to distant sites
What is the process of angiogenesis?
Normal cells —> Dysplasia —> neoplasia —> invasive neoplasia ( new blood vessels created to feed) —> angiogenesis (into blood stream)
What are cancer cell characteristics?
1. Anaplasia: cant change/ differentiate in cancerous tissue
2. Pleomorpism: various size and shape
3. Genetic instability: lots of mutations
3. No growth factors
4. Grow rampantly w/o density-dependent inhibition (no spatial considerations)
5. Don’t stick together & shed
6. Multiply w/o attachements (anchorage), survive in micro environments
7. Impaired cell to cell communication
9. Antigen expression - foreign markers
10. Change cytoskeleton to facilitate metastasis
11. Produce substances others do not
How is CA spread?
1. Direct invasion
2. Seeding into body cavities
3. Through blood or lymph pathways
What are 2 reasons for CA causing genes?
1. Single nucleotide base change —> Mutation of normal genes
2. Loss of tumor suppressor gene —> unregulated growth begins
Initiation: susceptible to malignant transformation
Promotion: accelerated growth
-promotes invasive ness, metastasis, autonomous growth, inc. genetic instability
What oncogenes viruses can lead to CA?
What are nursing clinical manifestations of cancer?
1. Impaired tissue integrity (effusions, ulceration, necrosis, compressed BV, hemorrhage)
2. Anorexia & chachexia
3. Fatigue and sleep disorders
What are paraneoplastic syndromes that have inappropriate hormone relapse —> circulating factors that produce hematopoietic, neurological, and dermatological syndromes?