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Terms in this set (21)
What is hyperplasia?
Increase in number of cells in organ or tissue.
Cells that are capable of mitotic division.
- Hormonal (e.g. breast enlargement)
- Compensatory (e.g. liver hyperplasia after partial removal)
Important response in wound healing (proliferating fibroblasts and blood vessels contribute)
- excessive hormonal stimulation or effects of growth factors on target tissues. e.g. skin warts due to growth factors produced by certain viruses.
What is metaplasia?
Reversible change in which one adult cell type is replaced by another.
Thought to involve reprogramming of undifferentiated stem cells.
Often occurs in chronic irritation and inflammation.
What is dysplasia
Deranged cell growth of a specific tissue that results in cells that vary in size, shape, and organization. Associated with chronic irritation and inflammation.
Strong indicator for cancer.
Hypoxic cell injury
Deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP.
Stimulates red blood cell formation and angiogenesis.
Can be a result of decreased oxygen amount in air, ischemia, respiratory disease, decreased BF, edema, anemia, inability of the cells to use oxygen.
- Ischemia: impaired oxygen delivery and impaired removal of metabolic end products (e.g. lactic acid).
- Edema: if the oxygen delivery is limited by distance
The cell reverts to anaerobic metabolism, using limited glycogen stores. pH falls due to lactic acid accumulation -> chromatin clumping and cell shrinkage.
Reduced ATP: failure of the energy dependent sodium/potassium ATPase -> water accumulation in the cell -> injury to lysosomal membranes -> lysosomal enzymes into the cytoplasm.
Highly selective process that eliminates injured and aged cells.
1) Shrinking of the cell.
2) condensation of the nucleus and cytoplasm. Chromatin aggregates in nuclear envelope.
3) The cell becomes fragmented, but maintains integrity of the plasma membrane. Hence, does not initiate inflammation.
4) Macrophages engulf the fragments.
1) Fas ligand expressed on cells. When a ligand binds, death-initiating complex is formed.
2) Procaspase-8 is converted to caspase-8 activating a cascade of caspases -> apoptosis.
Mitochondrion induced. Activated by e.g. DNA damage, hypoxia. Opening of the mitochondrial membrane pores --> cytochrome c released to cytoplasm, which activates campases.
Limit seems to be related to the length of the telomeres (at the end of chromosomes), shortening every time a cell divides.
Why Acute Inflammation?
Aimed at removing the injurious agent and limiting the extent of tissue damage.
Cells involved in acute inflammation
- Endothelial cells lining the blood vessels
- connective tissue cells (mast cells, fibroblasts, tissue macrophages, lymphocytes)
- ECM (consists of firbrous proteins collagen and elastin, glycoproteins and proteoglycans.)
Acute inflammation STEP BY STEP
1) VASCULAR PHASE
momentary vasoconstriction followed rapidly by vasodilation.
This causes increase in BF -> heat and redness
Increase in permeability -> exudate into extravascular spaces -> swelling, pain and impaired function.
2) CELLULAR PHASE
Neutrophiles (and other leukocytes) arrive at the site of injury.
- endothelial activation, adhesion and margination (facilitated by slow BF)
- transmigration: the neutrophil leaves the blood into the extravascular tissue
- chemotaxis: the guiding of the leukocytes once they have left the blood. Substances like protein fragments generated due to activation of complement system, chemotactic cytokines etc.
3) LEUKOCYTE ACTIVATION AND PHAGOCYTOSIS
Products generated by tissue damage trigger response from leukocytes: phagocytosis and cell killing.
Endocytosis by macrophages of foreign material
1) Those with vasoactive and smooth muscle constricting properties (histamine, arachidonic acids: prostaglandins and LT)
2) Plasma proteases activating members of the complement system, coagulation factors and vasoactive peptides of the kinin system
3) chemotactic factors: complement fragments and chemokines
4) reactive molekyles and cytokines from leukocytes
Chemical stored in mast cells that triggers dilation and increased permeability of capillaries.
Arachidonic Acid Metabolites
Found in phospholipids of cell membranes. Release --> production of prostaglandins and Leukotrienes.
Prostaglandins and thromboxane A2: promote platelet aggregation + vasoconstriction. Aspirin inhibits this pathway.
Leukotrienes: Induces smooth muscle contraction, constricts pulmonary airways, increases microvascular permeability.
Cytokines and chemokines
TNF-alpha and interleukin-1: major inflammatory mediators. Source: macrophages
IL-1 also produced by neutrophils, endothelial cells.
They stimulate endothelial cells to produce adhesion molekyles and release cytokines and reactive oxygen species. This causes fever, hypotension, increased HR, anorexia, release of neutrophils into circulation and increase levels of corticosteroids.
Nitric oxide & oxygen-derived free radicals
Smooth muscle relaxation
Local manifestations of acute inflammation
Exudates: serous (watery, plasma entering the inflammatory site), hemorrhagic, fibrinous (thick and sticky meshwork like blood clot), membranous (on mucous membrane surfaces with necrotic cells), purulent (pus).
Characteristic: infiltration of macrophages and lymphocytes instead of neutrophils (as in acute)
Proliferation of fibroblasts instead of exudates
Nonspecific chronic inflammation
Diffuse accumulation of macrophages and lymphocytes at injury site
-Macrophages mass together around foreign bodies
Associated with splinters, asbestos etc.
Acute phase response in systemic inflammation
Why? To enable optimal host response
Begins within hours or days of the onset of inflammation or infection.
- Increased acute phase proteins (e.g. C reactive protein, prod. in liver. Upregulated by cytokines)
- Increase in white blood cells
- Skeletal muscle catabolism
- negative nitrogen balance
- elevated erythrocyte sedimentation ratel
- cytokines release: IL-1, IL-6, TNF-alpha: affect the thermoregulatory center in hypothalamus -> fever.
- IL-1: increase number of circulating neutrophils by stimulating production in bone marrow
- anorexia, somnolence, malaise: due to actions of IL-1 and TNF-alpha on CNS.
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