Pathoma: Growth Adaptations, Cellular Injury, and Cell Death
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Increase in the size of cells
Increase in the # of cells
3 Permanent Tissues
- Cardiac Muscle
- Skeletal Muscle
(Undergo hypertrophy only! No hyperplasia!)
Most hyperplasia is capable of progressing to dysplasia and cancer. Name one form of hyperplasia that does NOT have an increased cancer risk.
Benign Prostatic Hyperplasia
Involves gene activation, protein synthesis, and production of organelles.
(Bigger cells need more protein for cytoskeleteon, increase protein synthesis by gene activation. Bigger cell needs more organelles)
Decrease in organ size, occurs via a decrease in the size and # of cells
Decrease in cell size (in atrophy) occurs via
- 1) Ubiquitin-protosome degradation of the cytoskeleton
- 2) Autophagy of cellular components
Fibers that are targeted for degradation via ubiquitin-proteosome degradation
Int. filaments of the cytoskeleton (tagged w/ ubiquitin and destroyed by proteosomes)
Change in cell type due to stress on an organ
- Normal: Nonkeratinizing Squamous Epi.
- Metaplasia: Non-ciliated mucin-producing columnar cells
Due to acid reflux
Metaplasia is reversible; for example, tx of GERD may reverse Barrett's esophagus
Under constant stress, metaplasia can progress to dysplasia and eventually cancer; for example, Barrett's esophagus may progress to adenocarcinoma of the esophagus
(Exception: Fibrocystic change of breast (apocrine metaplasia) carries no increased risk for cancer.)
Deficiency of what Vit. can result in metaplasia?
Vit. A, necessary for differentiation of specialized epithelial surfaces
(Example: Keratomalacia- Vit. A deficiency causes the thin squamous lining of the conjunctiva to undergo metaplasia into stratified keratinizing squamous epithelium.)
Vit. A deficiency; Eye conjunctiva goes from squamous --> stratified keratinizing squamous epithelium
Metaplasia: muscle to bone (occurs during healing after trauma)
Disordered cellular growth, proliferation of precancerous cells
Metaplasia and Dysplasia are both
Failure of cell production during embryogenesis
Decrease in cell production during embryogenesis, resulting in small organs
Hypoplasia (e.g. streak ovary in Turner Syndrome)
Skeletal Muscles vs. Neurons: More susceptible to hypoxia
Neurons (can only endure hypoxia for 3-5 minutes).
Skeletal muscle can endure hypoxia for a long time.
3 causes of Hypoxia
Hypoxia= low oxygen delivery to tissues
- Ischemia= low blood flow through an organ
- Hypoxemia= low pp of oxygen in the blood (PaO2 < 60 mm Hg, SaO2 < 90%)
- Decreased O2-carrying capacity= arises w/ Hb loss or dysfunction
Iron in heme is oxidized to Fe3+, which cannot bind oxygen
2 types of drugs that can cause methemoglobinemia
Sulfa and nitrate drugs (they oxidize Fe in Hb to Fe3+)
Chocolate-colored blood, cyanosis
IV methylene blue
How does hypoxia result in decreased ATP?
Impairs oxidative phosphorylation
Name 3 cellular functions that low ATP disrupts
- Na+-K+ pump: results in sodium and water build-up in cell --> cell swelling
- Ca2+ pump: Ca2+ build-up in cytosol of cell
- Aerobic glycolysis: results in switch to anaerobic glycolysis --> lactic acid build-up --> low pH --> denatures proteins and DNA
Hallmark of reversible cellular injury
- *Cytopasmic swelling= loss of microvilli and increased membrane blebbing
- *RER swelling= dissassociation of ribosomes -> decreased protein synthesis
Hallmark of irreversible cellular injury
- *Plasma Membrane damage= Cytosolic enzymes leaking into the serum (e.g. cardiac troponin), additional Ca2+ enters the cell
- *Mitochondiral Membrane damage= Loss of ETC (inner mitochondrial membrane); Cytochrome C leaks into cytosol (activates apoptosis)
- *Lysosome Membrane damge= Hydrolytic enzymes leak into cytosol, these are activated by high intracellular calcium
Protein that leaks into cytosol due to mitochondrial membrane damage; activates apoptosis
Hallmark of cell death
Loss of nucleus (pyknosis, karyorrhexis, karyolysis)
Loss of nucleus mechanism:
- pyknosis: nuclear condensation
- karyorrhexis: fragmentation
- karyolysis: dissolution of nucleus
2 Mechanism of cell death
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