Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/34

Click to flip

34 Cards in this Set

  • Front
  • Back
6 classifications for chronic inflammation
Fibrous, Suppurative (chronic abscesses), Eosinophilic, Necrotizing/Ulcerative (little exudate), Lymphocytic/hyperplastic, Granulomatous
Pathophysiologic problems of chronic inflammation
progressive tissue dysfunction, poor weight gain/performance insufficiency, recurrent or persistent fever, leukocytosis/hyperfibrinogenemia, anemia
sequelae of chronic inflammation
resolution/tissue repair (destruction of inflammatory stimulus) OR persistence until somatic death (as opposed to necrosis)
granulomatous inflammation
inflammatory process dominated by macrophages or specialized macrophages (epitheliod/giant cells)
granuloma
compact, organized collection of mononuclear inflammatory cells (macrophages, lymphocytes,and plasma cells) - macrophages dominant
granulomatous inflammation
inflammation marked by macrophages
inciting stimuli of chronic inflammation
particulate and resistant to lysosomal degredation/inactivation; may induce T-cell hypersensitivity. Always starts as acute inflammation - persistance leads to macrophage dominated response.
cells present during granulomatous inflammatory reaction
monocytes, macrophages, epithelioid cells, giant cells, T-lymphocytes
gross morphology of granulomatous inflammation
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.
microscopic morphology of granulomatous inflammation
dense accumulations of macrophages and lymphocytes. possibly epithelioid, neutrophils, giant cells, plasma cells. if neutrophils present = pyogranulomatous inflammation.
simple granuloma
organized and compact aggregate of macrophages and possibly other cells
complex granuloma
central necrosis, possible calcification (e.g. tubercles)
tissue repair
process by which necrotic or dead cells are replaced by vital cells; includes regeneration and//or replacement
regeneration of tissue
replacement of cells by cells of the same type
replacement of tissue
replacement of cells by connective tissue (fibrosis)
fibrosis
process resulting in increase of collagen in tissue; usually results in increase of fibrous connective tissue (collagen and fibroblasts)
organization by fibrous connective tissue
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)
cell cycle phases
G0 - quiescent phase
G1 - presynthetic phase
S - DNA synthesis
G2 - Premitotic phase
M - Mitotic
labile cell; examples?
cells that multiply throughout life (no G0 phase in cell cycle); replenish due to normal turnover; examples - epidermal, intestinal epithelial, lymphoid, hematopoitic cells
stabile cell; examples?
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
permanent cell; examples?
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
Epidermal Growth Factor
produced by macrophages; epithelial proliferation and repair
Platelet derived growth Factor
produced by macrophages; stimulates smooth muscle proliferation and fibrosis
Basic fibroblast growth factor
produced by macrophages; induces endothelial cell proliferation and angiogenesis
transforming growth factor
produced by macrophages; promotes fibrosis and inhibits epithelial regeneration
vascular endothelial growth factor
produced by macrophages and by many malignant tumor cells and assists in neoplasm angiogenesis
tumor necrosis factor
produced by macrophages; thrombogenic, endogenous pyrogen, induces acute phase reaction proteins, causes cachexia
determinants of fibrosis - favoring factors
severe/prolonged tissue injury, loss of tissue framework (basement membranes), large amounts of exudates (fibrin, necrotic debris), lack of renewable cell population (permanent cells)
Healing by first intention
little exudate, tissues closely approximated - edges bind easily
Healing by second intention
edges of wound widely separated; defect may contain exudate and necrotic debris; fills in by granulation tissue and leaves large area of fibrosis
Scar contraction mechanism
fibroblasts in scar modify into contractile cells (myofibroblasts with actin and dense bodies)
granulation tissue
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.
granulation zones, top to bottom
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)
consequences of fibrosis
loss of functional parenchyma and alteration of physical properties of tissue (skin may tear more easily, lung may be less compliant)