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22 Cards in this Set
- Front
- Back
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Regeneration
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Physiologic
One to one replication of cells Eg: endothelial cells in blood vessels after angioplasty regenerate to form new lining |
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Hyperplasia (2 examples)
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Physiologic or pathologic
Increase in # of fully functional cells Eg: if after angioplasty if endothelial cells don't regenerate, smooth cells will replicate and become hyperplastic (also RBC physiologic hyperplasia in bone marrow at high alt) |
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Graves Disease
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Hyperthyroidism
Too many differentiated thyroid cells |
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Metaplasia
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Pathologic
Adaptive substitution of one cell for another Eg: delicate endocervical epithelial cells are too delicate to withstand inflammation and are replaced by squamous epithelium (similar situation in lungs due to smoking) |
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Dysplasia
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Pathologic
Disorientation of cells in tissue and increase in # and loss of uniformity of shape (pleiotropy) Eg: exocervical dysplasia is a precursor to cervical cancer (detect by pap smear) |
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Neoplasia
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Only irreversible proliferative state
Benign - only lost proliferative control, still has positional control. Proliferation in absence of external stimulus. Eg: uterine fibroids Malignant - lost proliferation and positional control. |
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Restriction (R) point (2)
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G1 checkpoint: proceed through cell cycle or enter quiescent phase
Cells are insensitive to external signals after R-point |
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Cyclin and Cdk (eg M-cyclin)
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Phosphorylate other proteins
Have inhibitory and activating phosphorylation sites M-cyclin (cyclin B/cdk1) rises at beginning of M phase, declines at end, active enzyme functions as a kinase with lamins and histones as key substrates |
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Retinoblastoma (cell cycle and signal transduction)
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Active RB is hypo phosphorylated
Signal transduction: Mitogens activate receptors -> activate cyclin D+E (push cell thru R point) -> cyclins partner with cdks(4/6-D, 2-E) complex -> phosphorylate Rb to inactivate -> loss of repression of cell cycle genes |
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Necrosis (4)
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Necrosis: triggered by ischemia, physical/chemical trauma, cells swell+lyse, organelles are damaged/destroyed, chromatin randomly degraded, leads to inflammation
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Apoptosis: main features (6)
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Triggered by specific signals that activate specific genes
Cells shrink Organelles remain intact Chromatin degraded systematically Membrane blebs off cell contents ->Phagocytosis DNA laddering due to breaks between nucleosomes |
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Apoptosis: 3 phases
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Induction
Modulation Execution |
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Apoptosis: Induction (3 main ways)
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Physiologic (TNF-α, FAS-L), disease-related (viral infection, heat shock, tumor suppressors, toxins), therapy associated factors (UV/γ radiation, chemo drugs)
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Apoptosis: Modulators
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Bcl family has pro and anti apoptosis members
Balance of the presence of these members dictates apoptosis Burkitt's lymphoma has high apoptosis rate due to Blc2 |
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Polycistic kidney disease
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Uncontrolled apoptosis of kidney cells leading to cysts
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Intrinsic pathway
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Caused by insufficient growth factors or injuries like viruses
Through mitochondria Activation of caspase cascade via Bcl modulators binding mitochondrial cytochrome |
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Extrinsic pathway
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Receptor-mediated: TNF-α/FasL
Activation of caspases |
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Immunologic privilege
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The immune system can't attack certain systems (eye, testes)
Lymphocytes express Fas Blood vessels leading to these systems have endothelial cells expression Fas-L ligand which binds lymphocytes before they can enter |
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Endostatin (3)
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Fragment of collagen XVIII
Cleaved by an MMP Induces apoptosis in endothelial cells (newly developing blood vessels) |
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Proteoglycans (3)
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Regulate hydration state of tissues (cartilage)
Provide resistance to impact Chondrodysplasias affect chondroitin sulfate |
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Apoptosis in oocyte atresia
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Loss of oocytes with advancing maternal age
Due to proapoptotic modulation |
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Apoptosis in stroke
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Apoptosis inhibitors in stroke could save neurons
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