Pathology Of Inflammation

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6 classifications for chronic inflammation

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Fibrous, Suppurative (chronic abscesses), Eosinophilic, Necrotizing/Ulcerative (little exudate), Lymphocytic/hyperplastic, Granulomatous

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Pathophysiologic problems of chronic inflammation

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progressive tissue dysfunction, poor weight gain/performance insufficiency, recurrent or persistent fever, leukocytosis/hyperfibrinogenemia, anemia

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sequelae of chronic inflammation

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resolution/tissue repair (destruction of inflammatory stimulus) OR persistence until somatic death (as opposed to necrosis)

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granulomatous inflammation

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inflammatory process dominated by macrophages or specialized macrophages (epitheliod/giant cells)

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granuloma

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compact, organized collection of mononuclear inflammatory cells (macrophages, lymphocytes,and plasma cells) - macrophages dominant

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granulomatous inflammation

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inflammation marked by macrophages

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inciting stimuli of chronic inflammation

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particulate and resistant to lysosomal degredation/inactivation; may induce T-cell hypersensitivity. Always starts as acute inflammation - persistance leads to macrophage dominated response.

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cells present during granulomatous inflammatory reaction

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monocytes, macrophages, epithelioid cells, giant cells, T-lymphocytes

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gross morphology of granulomatous inflammation

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thickening of affected tissue, or solid/firm lesions that compress adjacent tissues. lesions often difficult to distinguish from neoplasms. possibly necrotic or suppurative in centers.

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microscopic morphology of granulomatous inflammation

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dense accumulations of macrophages and lymphocytes. possibly epithelioid, neutrophils, giant cells, plasma cells. if neutrophils present = pyogranulomatous inflammation.

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simple granuloma

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organized and compact aggregate of macrophages and possibly other cells

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complex granuloma

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central necrosis, possible calcification (e.g. tubercles)

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tissue repair

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process by which necrotic or dead cells are replaced by vital cells; includes regeneration and//or replacement

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regeneration of tissue

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replacement of cells by cells of the same type

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replacement of tissue

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replacement of cells by connective tissue (fibrosis)

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fibrosis

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process resulting in increase of collagen in tissue; usually results in increase of fibrous connective tissue (collagen and fibroblasts)

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organization by fibrous connective tissue

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process where large defects in tissue caused by injury or accumulation of fibrin/necrotic debris is removed by macrophages and replaced by fibrovascular tissue rich in collagen (granulation tissue)

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cell cycle phases

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G0 - quiescent phase
G1 - presynthetic phase
S - DNA synthesis
G2 - Premitotic phase
M - Mitotic

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labile cell; examples?

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cells that multiply throughout life (no G0 phase in cell cycle); replenish due to normal turnover; examples - epidermal, intestinal epithelial, lymphoid, hematopoitic cells

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stabile cell; examples?

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latent capacity to regenerate (normally in G0 phase); do not turnover quickly; after injury will rapidly enter G1 and divide; examples - epithelial cells in liver/kidney/lung/endocrine glands, smooth muscle cells, fibroblasts, endothelial cells, skeletal muscle (to small extent); terminally differentiated cells (ciliated) not capable of repair

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permanent cell; examples?

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no capacity to regenerate additional cells; examples - neurons, cardiac myocytes; fibrosis replaces these cells (or glial cells in nervous system); these cells CAN regenerate portions of lost cells

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Epidermal Growth Factor

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produced by macrophages; epithelial proliferation and repair

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Platelet derived growth Factor

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produced by macrophages; stimulates smooth muscle proliferation and fibrosis

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Basic fibroblast growth factor

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produced by macrophages; induces endothelial cell proliferation and angiogenesis

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transforming growth factor

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produced by macrophages; promotes fibrosis and inhibits epithelial regeneration

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vascular endothelial growth factor

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produced by macrophages and by many malignant tumor cells and assists in neoplasm angiogenesis

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tumor necrosis factor

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produced by macrophages; thrombogenic, endogenous pyrogen, induces acute phase reaction proteins, causes cachexia

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determinants of fibrosis - favoring factors

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severe/prolonged tissue injury, loss of tissue framework (basement membranes), large amounts of exudates (fibrin, necrotic debris), lack of renewable cell population (permanent cells)

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Healing by first intention

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little exudate, tissues closely approximated - edges bind easily

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Healing by second intention

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edges of wound widely separated; defect may contain exudate and necrotic debris; fills in by granulation tissue and leaves large area of fibrosis

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Scar contraction mechanism

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fibroblasts in scar modify into contractile cells (myofibroblasts with actin and dense bodies)

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granulation tissue

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highly organized fibrovascular tissue with orderly episodes of macrophage infiltration, stimulation of angiogenesis and fibrosis, and maturation to a dense CT scar. If poor epithelial regeneration (lower limbs of horses), this can produce proliferative lesions - proud flesh.

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granulation zones, top to bottom

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1.zone of necrotic debris and fibrin (fibrin on top)
2. zone of macrophages and ingrowing capillaries
3. zone of proliferating capillaries and fibroblasts
4. zone of maturing fibrous connective tissue (thicker blood vessels, fibroblasts)

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consequences of fibrosis

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loss of functional parenchyma and alteration of physical properties of tissue (skin may tear more easily, lung may be less compliant)