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Pathology (272)
Craig Hall (18)
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Department
Pathology
Course
Pathology 3240A
Professor
Craig Hall
Semester
Winter

Description
Regeneration and Repair The restoration of damaged tissue ­ removal of exudate ­ removal of cellular and tissue debris ­ replacement of cells and tissues lost Replacement of Cells/tissues ­ Regeneration: replaced by IDENTICAL cells o physiologic/pathologic o tissues have different regenerative ability o atypical regeneration: cirrhosis  eventually kills ­ Repair: identical or different cells o Pathological o Involves granulation tissue and connective tissue ­ The Cell Cycle and Type of cells o Picture ** o Usually epithelial cells (labile cells)   Cells that are constantly cycling o Cells that leave the cycle:   Don’t need regeneration  If you need more of them, they can be recruited back into the cycle  Ie. Liver, kidney  STABLE cells o Cells that lose ability to mitosis  After brain is finished, neurons forget how to mitose   PERMANENT cells  Seizures – treatment is aggressive • Neurons are lost during seizure • Born with a  certain amount of neurons, but keep losing  them  • Run out of neurons • Not making new ones • Heart attack – no way to get more heart cells Type of Cells ­ according to their regenerative activity ­ labile: proliferate throughout life (epithelia, blood cells) o endometrium for ex.  Sheds, grows, etc.  Physiological o Cut/burn  Give time, new skin will grow  Pathological  ­ Stable: low normal replication rate, unless stimulated o Considered to be in G0 but recruited to G1 o Ie. Renal Tubular cells  Can be enticed ­ Permanent: unable to divide o Have left cell cycle o Ie. Neurons o Ie. Cardiac muscle Regeneration of Epithelium  ­ Atypical o Liver: cirrhosis  Hepatitis B/C  Liver cells die  Walls that hold liver cells die  Can be recruited back to grow, but problem will be that they  cannot grow  Lots of liver cells, just completely disorganized  Cells not functioning  Atypical regeneration o Mechanisms involved in Repair  Control of cell proliferation • And recruitment of G0 cells into cell cycle • Growth factors: o GH o Estrogen o Insulin o Progesterone o EGF, FGF, PGF o Int I and II o TNF o Tumor induceing GF o Macrophage derivatives o GF o All mitogenic • Loss of inhibit factors: negative growth inhibitory signals • Cell­cell or cell­matrix interactions:  o Contact inhibition o Integrins which are trans­membrane glycoproteins  Fibronectin and platelet surface receptors  Leukocyte adhesion molecules (CAMs)  Collagenization and acquisition of wound strength • Formation of a scar  Ie. Girl who couldn’t heal a paper cut • Couldn’t have a normal inflammatory response • Her leukocytes lacked the CAMS needed wound healing o Fibroblasts and Fibronectin  Fibroblasts are stars of healing • They make collagen • Very important for development of scar  Fibronectin • Fibres that organize process • Fibronectin is connected to collagen, and connect to the PM  that has receptors o Acts as a bridge • Anchors itself to collagen • Adhesive matrix proteins • Role in Wound healing: o Glue l
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