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69 Cards in this Set
- Front
- Back
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What is the difference between hypertrophy and hyperplasia?
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In hypertrophy cells get larger as they increase the amount of structural proteins and organelles. Hyperplasia is characterized by an increase in cel number.
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What three groups characterize the various proliferative capacities of cellular tissues?
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Labile cells: continuously dividing cells; Stable tissues: quiescent, but proliferate in response to injury; Permanent tissues: non-proliferative.
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Will permanent cells be more likely to respond to stress through hypertrophy or hyperplasia? Labile cells?
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Permanent cells: hypertrophy (don't replicate); Labile cells: hyperplasia.
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What are examples of labile cells? stable tissues? permanent tissues?
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Labile: Hematopoietic cells, surface epithelia; Stable: organ parenchyma, endothelial cells, fibroblasts, SMCs; Permanent: neurons, cardiac myocytes.
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What are mechanical vs. trophic triggers of hypertrophy?
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An example of a mechanical trigger is stretch, while a trophic trigger would be alpha-adrenergic receptor activation.
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What is an example of hormonal hyperplasia? compensatory hyperplasia?
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Hormonal: proliferation of glandular epithelium during puberty or pregnancy; Compensatory: growth of remaining liver following resection.
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What distinguishes benign pathologic hyperplasias from cancer?
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Benign pathologic hyperplasias will be sensitive to the removal of the causal hormones or growth factors; cancers do not have that sensitivity or the growth control mechanisms are dysregulated.
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What is atrophy? Are atrophic cells "dead"?
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Atrophy is when cells shrink in size and atrophic cells are not dead but have diminished function (there is a new equilibrium for tissues perfusion and nutrition).
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What are some causes of atrophy?
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Decreased workload, loss of innervation, diminished blod supply, loss of endorine stimulation and aging.
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What intracellular changes result in atrophy?
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Decreased protein synthesis and increased protein degradation; degradation occurs primarily through the ubiquitin-proteasome pathway. Atrophy is also accompanied by autophagy.
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What s metaplasia?
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Metaplasia occurs when one adult cell type is replaced by another cell type; this often occurs because the latter cell type is better suited for some environmental stress. In addition its thought that the shift originates from stem cells not the adult cell.
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What s metaplasia?
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Metaplasia occurs when one adult cell type is replaced by another cell type; this often occurs because the latter cell type is better suited for some environmental stress. In addition its thought that the shift originates from stem cells not the adult cell.
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What s metaplasia?
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Metaplasia occurs when one adult cell type is replaced by another cell type; this often occurs because the latter cell type is better suited for some environmental stress. In addition its thought that the shift originates from stem cells not the adult cell.
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What are some examples of metaplasia?
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In common forms of lung cancer respiratory epithelium is replaced by stratified squamous epithelium; while this epithelia may be better able to survive it loses the ability to secrete mucous and ciliation. In chronic gastric reflux stratified squamous epithelium of the lower esophagus is replaced by gastric/intestinal type columnar epithelium.
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What changes occur in the cell nucleus during necrosis? Apoptosis?
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Necrosis: pyknosis (clumping of chromosomes and shrinking of nucleus), karyorrhexis (fragmentation of nucleus, breakup of chromatin into unstructured granules) and karyolysis (dissulution of the nucleus). Apoptosis: fragmentation of nucleus into nucleosome type fragments (eventually Karyorrhexis).
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What are the major differences between necrosis and apoptosis?
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In necrosis the cell swells and membrane integrity is lost, leaked lysosomal enzymes digest cellular components leading to cell death, while cellular contents pass through the damaged plasma membrane (which eventually disappears) and induce an inflammatory response; necrotic cells exhibit eosinophilia. Necrosis is always pathologic. In apoptosis the cell usually shrinks and fragments but the plasma membrane remains intact; the cell and its fragments (apoptotic bodies) are then phagocytosed. Apoptosis may not be pathologic.
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What 2 changes characterize irreversible cell injury?
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1. Irreversible mitochondrial damage resulting in lack of oxidative phosphorylation and ATP generation, 2. Disturbed membrane function (lysosomal enzyme release).
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What cellular changes characterize reversible cell injury?
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Cellular swelling, membrane blebs, loss of microvilli, mitochondrial swelling, clumping of chromatin, some eosinophilia, and a distended endoplasmic reticulum which lead to hydropic/vacuolar change/degeneration (swollen compartments forcing nucleus to periphery). Fatty change (appearance of lipid vacuoles in cytoplasm) primarily seen in fat dependent cells (hepatocytes and cardiac myocytes).
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ATP depletion is generally associated with which type of cell death?
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Necrosis
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What happens in coagulative necrosis?
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Usually ischemia or hypoxia cause a loss in function of the cell's structural proteins and enzymes. The cell outline remains because lysosomal enzymes are non-functional. Eventually leukocytes will digest the eosinophilic, anucleate cell.
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Where does coagulative necrosis occur/not occur?
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Solid organs; NOT the brain though.
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Dry gangrenous necrosis is actually a form of what necrosis type? Wet gangrene?
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Dry gangrene is coagulative necrosis of the limbs. Wet gangrene is when there is coagulative necrosis and liquefactive necrosis of the limb.
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What happens in liquefactive necrosis?
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Microbes induce inflammation (WBCs) and complete cellular digestion into a liquid puss composed of necrotic and inflammatory cells. This occurs in the brain due to hypoxia.
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What happens in caseous necrosis?
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Usually a tuberculous infection causes the obliteration of cells, which are seen surrounded by inflammatory cells (granuloma).
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What events occur in fat necrosis?
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Usually acute pancreatitis causes the release of pancreatic lipases, which digest fat cells. Fat saponification then occurs with calcium exposure leaving chalky observable areas.
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What happens in fibrinoid necrosis?
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Antigens, antibodies and fibrin are deposited in the arterial walls, resulting in a bright pink appearance. Occurs in vasculitis.
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What is autophagy?
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Autophagy occurs when the cell is nutrient depleted and must digest its own organelles for energy through autophagic vacuoles made from a ribosome free part of the RER which will merge with a lysosome.
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What is Lipofuscin?
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Lipids in lysosomes that cannot be digested and get peroxidated.
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What happens intracellularly when the cell is chronically exposed to toxins (P-450 detox)?
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Hypertrophy of the SER (where cyt P-450 is located) to deal with the toxins
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What happens to mitochondria nutrient deficiency? cellular hypertrophy? chronic alcohol exposure? myopathy?
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1. Decrease in number, 2. Increase in number, 3. Enlarge, 4. Increase in number and enlarge
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Why does ATP depletion result in cellular swelling?
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Reduced activity of the Na-K pump, results in K efflux and Na, Ca influx for a net accumulation of solutes; this draws in water.
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If ATP is depleted where will the cell find energy?
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Anaerobic metabolism is increased, glycogen stores are used; lactic acid accumulates (decreased pH and enzyme activity).
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How does depletion of ATP affect protein synthesis?
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It causes the dissociation of ribosomes from the ER and protein synthetic apparatus.
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What are 3 things that can cause mitochondrial damage?
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1. High intracellular Ca (activates phospholipases), 2. ROS, 3. lipid peroxidation (all damage mito. membrane).
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What are the two main consequences of mitochondrial membrane damage?
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1. Reduced ATP production (formation of mito. permeability transition pore leads to loss of mito. membrane potential), 2. Release of cyt. c and apoptosis activation.
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How does high intracellular Ca cause damage?
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Activation of enzymes: ATPases, Phospholipases, proteases, endonucleases.
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How do ROS cause damage?
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1. Lipid peroxidation (disrupt membranes), 2. Oxidize/cross-link proteins (abnormal enzyme activity), 3. Damage DNA
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What can eliminate ROS?
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1. Superoxide dismutases, 2. Glutathione peroxidase, 3. Catalase in peroxisomes.
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How does high intracellular Ca damage membranes?
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1. Protease activation: damage cytoskeleton, 2. phospholipase activation increase phospholipid degradation, the products of which disrupt the membrane.
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What 2 mechanisms cause reperfusion injury?
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1. Increased free radical generation (xanthine oxidase), 2. Increased inflammatory cell and protein exposure to site.
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What is the difference between dystrophic and metastatic calcification?
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Dystrophic: damaged/dead tissue, normal calcium (i.e. aortic valves); Metastatic: normal tissues, hypercalcemia (i.e. high parathyroid, renal failure), often occurs in lung, kidney, gut (interstitial tissues).
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What are some of the causes of cellular aging?
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DNA damage, decreased cellular replication, reduced stem cell regenerative activity, ROS accumulation
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What are the major components of acute inflammation?
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Vasodilation, increased vascular permeability (leakage of plasma protein aids edema) and leukocyte recruitment and activation.
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How does lymph flow change during acute inflammation?
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It increases to drain edema.
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What is the difference between transudate and exudate?
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Transudate is hypocellular and protein poor and is caused by hydrostatic or osmotic imbalances. Exudate is cellular and protein rich caused by increased permeability (i.e. inflammation)
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What are the types of adhesion molecules that aid in leukocyte margination and adhesion?
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Selectins for loose attachment (expressed on endothelial cells, platelets and leuk. only when induced by mediators like histamines and thrombins) and integrins for stable attachment (on leukocytes, expressed with chemokine activation).
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What is a common surface molecule that ads in diapedesis?
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CD31 (PECAM1)
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What is the role of opsonins?
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Opsonins (i.e. Ig, complement, lectins) coat microbes and help WBCs recognize them.
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What are some examples of conditions where the inflammatory response damages nearby tissues?
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Asthma, tuberculosis of the lung
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What are some conditions where leukocyte adhesion is impaired?
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Diabetes and hemodialysis
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What is the underlying etiology of chronic granulomatous disease? Chediak-Higashi syndrome?
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1. Cannot produce the ROS to degrade phagolysosome contents, 2. Cannot form a phagolysosome
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Inflammation where the ECM is damaged results in...
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...fibrosis, scarring, potential loss of function
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What are the vascular functions of histamine and seratonin? What cells release them?
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Vasodilation and increase vascular permeability (especially for early acute inflammation); released primarily by platelets (histamine by mast/basophils) in response to injury anaphylatoxins, neuropeptides and cytokines.
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Cyclooxygenase stimulates synthesis of ...
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Prostaglandins and thromboxanes
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Lypoxygenase stimulates synthesis of ...
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Leukotrienes and lipoxins
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Which cells are the primary releasers of arachidonic acid derivatives (Eicosanoids)?
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Leukocytes, endothelial cells and platelets
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What are some of the effects TNF and IL-1 have on endothelial cells?
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Increase cellular adhesion, increase coagulation activity, induce IL-1, IL-8, PDGF, PGE2 and PGI2 production.
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What are some of the systemic effects of TNF and IL-1?
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Increase fever, sleep, acute phase proteins, decrease appetite.
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What lysosomal enzymes in macrophages and neutrophils are important mediators of inflammation?
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Acid proteases, elastase, cathepsin and collagenase.
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Describe serous inflammation
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Characterized by an outpouring of thin fluid forming serosal cavity effusions (i.e. skin blisters)
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What characterizes fibrinous inflammation?
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Vascular leakage of fibrinogen which forms fibrin: occurs in meninges, pleura and pericardium.
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What characterizes suppurative inflammation?
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Large amounts of pus with WBCs, necrotic cells, bacteria and edema fluid: an abscess may form with localized purulent material.
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What characterizes an ulcer?
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Usually on an organ where a local defect has resulted in the sloughing of necrotic cells
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What are some of the main pathologic categories that involve chronic inflammation?
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persistent infections, toxins, autoimmune diseases.
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In general what cells and processes are involved in chronic inflammation?
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Persistent WBCs and macrophages in the tissues lead to damage. Meanwhile repair occurs through fibrosis and angiogenesis.
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What characterizes granulomatous inflammation?
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Macrophages with epithelial characteristics, multinucleated giant cells induced by IFN-g, collar of lymphocytes and plasma cells and surrounding fibrosis.
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Leukocytosis is stimulated primarily by (in inflammation)?
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IL-1 and TNF induce the left shift in bacterial infections (more immature neutrophils), (lymphocytosis in viral infection, eosinophilia with allergies/parasites)
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What is required for complete parenchyma repair?
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integrity of supporting stroma/ECM and existing cells must be able to divide
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What are some of the important growth factors?
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TGF-b and VEGF
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