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WEEK 4:
Building Bodies 2: Organs + Systems
| Question | Answer |
|---|---|
| parenchyma | cells that perform main function in organ |
| stroma | support cells (eg connective tissue + blood vessels) in organ |
| 4 layers from inside to outside | inner lining, support, muscle layers, outer wrapping |
| inner lining | epithelium + basement membrane + thin layer of connective tissue (for mechanical support + nutrition) + mucosa |
| support layer | connective tissue (biggest layer) + submucosa |
| outer wrapping | connective tissue (in body cavities coated with single epithelium layer) |
| simple tissue | collection of similar cells |
| compound tissue | mix of cells + ECM |
| atheroma | build up of fatty deposits in arteries |
| thrombus | blood clot formed in bloodstream |
| embolism | blood clot, air, fat travelling in bloodstream and gets stuck as vessels get smaller |
| ischaemia | reduction in blood flow to part of body, one of the main causes of cell death via necrosis |
| necrosis | premature cell death where severe damage to membranes causes enzymes to leak from lysosomes into cytoplasm + digests cell (pathologic) |
| stenosis | narrowing of blood vessel |
| there is a balance of pro and anti-thrombotics in the blood, what happens if the balance tips in favour of prothrombotics | clot can form in interior blood vessel causing stenosis leading to decreased blood flow and reduction in oxygen and nutrients to tissues |
| Virchows triad | 3 factors involved in thrombus formation: hypercoagulability, circulatory statis, vascular damage |
| what 2 things can a thrombus do | cause critical stenosis or break off and travel in the bloodstream until it gets stuck in a smaller vessel preventing blood flow |
| causes of cell injury | physical agents, chemical + biological agents eg poison, blockage of metabolic pathways, damage/disruption membrane integrity, DNA damage/loss |
| sub lethal injury in cells | severe cell damage that doesn't "kill it" but eventually leads to cell death |
| when sub lethal injury occurs what does the cell do to recover | removal of damaged components via autophagy |
| autophagy | digestion of body's own tissues |
| if a cell cannot recover after sub lethal injury, what happens | initially loss of nucleolus + no ribosomes + swelling of all mitochondria and ER, nuclear condensation membrane blebs + holes + lysosome rupture, fragmentation of inner membranes |
| all thrombus, embolism, atheroma lead to | ischaemia and eventually necrosis |
| PARP | poly (ADP-ribose) polymerase |
| AIF | apoptosis-inducing factor |
| BNIP3 | BLC2 interacting protein 3 |
| BLC2 | B-lymphoma/leukemia protein 2 |
| effects of ischaemia can be reversible depending on | (1- duration: brief ischaemic episodes ma be recoverable) (2- metabolic demands of tissue: cardiac myocytes + cerebral neurones most vulnerable) |
| explain cellular events leading to necrosis | |
| how can proteins/enzymes from dead tissue be detected in blood | must be specific + low conc |
| apoptosis | cell kills self due to lack of growth hormones/ damage to DNA/proteins, changing intact membrane to initiate phagocytosis (active, regulated, energy dependent, physiologic + pathologic) |
| physiologic apoptosis | embyrological development (GI lumen), involution of hormone dependant tissues (breast), maintenance of cell number in tissues with high turnover (eg intestinal epithelium) |
| pathological apoptosis | DNA damage (eg radiation), misfolding proteins (accumulate in RER = stress), growth factor deprivation, apoptosis of lymphocytes directed against host antigens |
| example of diseases with increased apoptosis | aids, neurodegenerative diseases eg Alzeheimer's |
| example of disease with inhibited apoptosis | cancer, autoimmune disorders, viral infection |
Created by:
kablooey
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