Cellular Growth Adaptations, Cellular Injury, Cell Death
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Cellular Growth Adaptations, Cellular Injury, Cell Death - Marcador
Cellular Growth Adaptations, Cellular Injury, Cell Death - Detalles
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| Increased cell production from stem cells | Hyperplasia |
| Ubiquitin attaches to intermediate filaments of cytoskeleton -> degradation by proteasome | Ubiquitin-proteasome pathway |
| Night blindness; Decreased immunity (decreased maturation of leukocytes); Keratomalacia | Vitamin A deficiency |
| T(15;17); Disrupted vitamin A receptor-> Cells trapped in blast state -> decreased immunity | Acute Promyelocytic Leukemia |
| Associated with Fibrocystic changes of the breast, no increased risk for cancer | Apocrine metaplasia of breast |
| Thrombosis of hepatic vain | Budd-Chiari Syndrome |
| Polycythemia vera | MC cause of Budd Chiari Syndrome |
| FiO2-> PAO2 -> PaO2 -> SpO2 | Pathway of oxygen partial pressure |
| High altitude, Hypoventilation, Diffusion defect, V/Q mismatch | Causes of hypoxemia |
| Anemia, CO poisoning, Methemoglobinemia | Decreased O2-carrying capacity |
| Cherry red appearance of skin | Classic finding for CO poisoning |
| Headache | Earliest sign of CO exposure |
| Iron in heme is oxidized to Fe3+ which cannot bind O2 | Methemoglobinemia |
| Fe 2+ ("Fe two binds O two") | Normal iron in heme |
| Cyanosis with chocolate colored blood | Classic finding for methemoglobinemia |
| IV methylene blue | Treatment for methemoglobinemia |
| No Na-K pump-> Na and water retention in cell; No Ca++ pump-> inc cytosolic Ca++; Shift to anaerobic glycolysis -> lactic acidosis -> protein denaturation | Effects of low ATP |
| Cellular swelling | Hallmark of reversible injury |
| Loss of microvilli; membrane blebbing; dissociation of ribosome from RER -> decreased protein synthesis | Effects of cellular swelling |
| Membrane damage (plasma membrane, mitochondrial membrane, lysosomal membrane) | Hallmark of irreversible injury |
| Cytosolic enzyme leakage (eg. cardiac biomarkers), increased intracellular [Ca++] | Plasma membrane damage |
| Loss of electron transport chain; leakage of cytochrome c -> apoptosis | Mitochondrial membrane damage |
| Leakage of hydrolytic enzymes into cytosol with activation by calcium | Lysosomal membrane damage |
| Inner mitochondrial membrane | Location of electron transport chain |
| Cell death | End result of irreversible injury |
| Loss of nucleus | Morphologic hallmark of cell death |
| Breaking up/fragmentation of nucleus | Karyorrhexis |
| Necrosis and apoptosis | Mechanisms of cell death |
| Death of large group of cells followed by inflammation brought about by pathologic processes | Necrosis |
| Firm necrotic tissue with absent nuclei and preserved cell shape and organ structure due to protein coagulation | Coagulative Necrosis |
| Associated with coagulative necrosis (Exception: Brain) | Ischemic infarction |
| Liquefied necrotic tissue due to enzymatic lysis of cells and protein | Liquefactive necrosis |
| Liquefactive necrosis due to proteolytic enzymes from microglia | Brain infarction |
| Coagulative + Liquefactive necrosis; characteristic of granulomatous inflammation from TB and fungal infection | Caseous necrosis |
| Caseous necrosis | Cottage cheese-like appearance |
| Fat necrosis; appearance brought about by calcium deposition | Chalky white appearance |
| Normal calcium and phosphate levels; necrotic tissue forms nidus for calcium deposit | Dystrophic calcification |
| High calcium and phosphate levels lead to calcium deposition in normal tissue | Metastatic calcification |
| Mediator of apoptosis | Caspase |
| Breaks down cytoskeleton | Protease |
| Breaks down DNA | Endonuclease |
| Cellular injury, DNA damage and loss of hormonal stimulation cause inactivation of Bcl2 -> cytochrome c release -> caspase activation | Intrinsic mitochondrial pathway |
| Activator of caspases | Cytochrome c |
| FAS ligand, TNF binds to corresponding receptors, activating caspases | Extrinsic receptor-ligand pathway |
| FAS ligand-mediated apoptosis of T-cells which have too avid or strong binding of self antigen | Negative selection (Thymus) |
| CD8+ T cells release perforin and granzyme to stimulate apoptosis (eg. virally infected cells) | Cytotoxic CD8 + T-cell mediated pathway |
| During oxidative phosphorylation through partial reduction of O2 via cytochrome c oxidase (complex IV) | Physiologic generation of free radicals |
| Superoxide (O2-), Hydrogen peroxide (H2O2), Hydroxyl free radical (OH-) | Free radical species in the body |
| Hydroxyl free radical | Most damaging free radical |
| Hydrolyzes water to hydroxyl free radical | Ionizing radiation |
| Drug metabolism generates free radicals | CYP450 system |
| Peroxidation of lipids and DNA damage | Mechanism of cellular injury by free radicals |
| O2- -> H2O2 (mitochondria) | Superoxide dismutase |
| Utilizes glutathione to convert a free radical to water in mitochondria | Glutathione peroxidase |
| H2O2 -> O2 + H2O (peroxisome) | Catalase |
| Iron-binding protein in blood | Transferrin |
| Copper-binding protein in blood | Cerulopasmin |
| Coverted to CCl3- by CYP450 -> cellular injury -> decreased apolipoprotein synthesis -> fatty changes in liver | Carbon tetrachloride (CCl4) |
| Leads to continued rise in cardiac enzymes post-reperfusion | Reperfusion injury |
| Beta pleated sheets, Congo red staining and apple green birefringence under polarized light | Features of amyloid proteins |
| Congo red stain | Staining used to visualize amyloid |
| Apple green birefringence | Characteristic finding under polarized light |
| Beta pleated sheet | Protein configuration of amyloid |
| Overproduction of immunoglobulin light chain; associated with plasma cell dyscrasia (eg. multiple myeloma) | Primary amyloidosis |
| Primary amyloidosis | AL amyloid |
| Secondary amyloidosis | AA amyloid |