Cell Injury and Death, Pigmentation, Necrosis

cell injury

the underlying principle of pathology is that all disease is due to:

lethal

causing necrosis/cell death

sublethal

cell function is altered but cell is not destroyed

cell degeneration

deterioration of cell function

labile

cells that divide frequently to replace lost cells

stable

cells that are fully differentiated and don't divide often

permanent

cells that lose the ability to divide after birth

hypertrophy

increase in cell size without an increase in cell numbers, generally seen in stable or permanent cells

hyperplasia

increase in cell number usually seen in labile cells

agenesis

complete failure of an organ or tissue to develop

aplasia

only a rudimentary form of an organ is present

hypoplasia

occurs during development, the result of a deficiency of growth and a diminution of size

atrophy

reduction in size of a fully formed tissue due to reduction in cell size

metaplasia

replacement of one fully differentiated cell type into another where it is normally not found

dysplasia

abnormal differentiation or development of a tissue with distorted architecture

calcification

the abnormal deposition of calcium and other minerals within a tissue

dystrophic

type of calcification where calcium is deposited in injured, degenerating, or dead tissue

metastatic

type of calcification where calcium deposits in tissues that are not the site of previous damage, associated with hypercalcemia

circumscripta

type of calcinosis calcification that consists of localized deposits, usually found on the extremities (such as elbows of large dogs) as a result of pressure

universalis

type of calcinosis calcification that is widespread

cutis

type of calcinosis calcification that has mineralization of dermal collagen in dogs with hyperadrenocorticism

exogenous

type of pigmentation that results in conditions that fall under "occupational hazards" category

endogenous

pigmentation made by body

lipochromes

yellow/brown pigment made from breakdown of fatty acids and cell membranes

ischemia

lack of blood and therefore O2

pyknosis

nucleus shrinks and becomes dense

karyorrhexis

nucleus breaks down into small fragments and the chromatin breaks up into unstructured granules throughout the cytoplasm

karyolysis

nucleus dissolves (with a loss of its affinity for basic stains)

coagulation

type of necrosis where cytoplasm thickens and details within the cell are lost

liquefaction

type of necrosis that contains dead and dying tissue cells that are partially liquefied and the WBCs made by the body to clean up the process

caseous

type of necrosis that is slow and progressive. associated with the effects of hydrolytic enzymes released by inflammatory cells. production of dry, white, cheesy, granular material; common in rabbits, birds, reptiles and animals with TB

fat

type of necrosis that usually occurs as a result of injury to fat, as in pancreatitis

soaps

fatty acids are converted into:

gangrenous

type of necrosis that is a combo of ischemia and a bacterial infection. two types: wet and dry