Gen patho - Cell injury, Necrosis, Apoptosis - PL

Results when cells are stressed that they are no longer able to adapt or when cells are exposed to inherently damaging agents or suffer from intrinsic abnormalities

CELL INJURY

•During early stages or mild forms of injury - the functional and morphologic changes are reversible if the damaging stimulus is removed

Reversible Cell Injury

•The first manifestation of almost all forms injury to cells.

•The result of failure of energy-dependent ion pumps in the plasma membrane that leads to inability to maintain ionic and fluid homeostasis.

•Causes pallor, increased turgor and increased weight of the organ

Cellular swelling

•Mirco examination reveals small, clear vacuoles within the cytoplasm - represents pinched-off portions of ER.

This pattern of non-lethal injury is called

hydropic change or vacuole degeneration

•Occurs in hypoxic, toxic, and metabolic injury.

•Manifested by the appearance of small or large lipid vacuoles in the cytoplasm.

•Encountered in cells participating in fat metabolism - hepatocytes and myocardial cells.

Fatty change

time the cell cannot recover and it dies

Irreversible Cell Injury: Cell Death

A form of cell death in which cellular membranes fall apart and cellular enzymes leak out and, ultimately, digest the cell.

Necrosis

•Elicits a local host reaction (inflammation) that is induced by substances released from dying or dead cells.

•Often the culmination of irreversible cell injury that cannot be corrected.

Necrosis

nuclear shrinkage

Pyknosis

fragmentation of the pyknotic nuclei

Karyorrhexis

nucleus and DNA fades due to DNAse activity

Karyolysis

•Seen in focal bacterial and fungal infections

•Because microbes stimulate the accumulation of inflammatory cells.

•The dead cells are completely digested, transforming the tissue into a liquid viscous mass.

•If the process was initiated by acute inflammation - the material is creamy yellow Pus

•Seen in abscesses

•Ischemic destruction of brain tissue

Liquefactive Necrosis

•This is a combination of coagulative and liquefactive necrosis encountered principally in the center of tuberculous infections.

•Characteristic appearance is that of a soft, friable, whitish-gray debris resembling clumped cheesy material.

Caseous Necrosis

•is due to the action of lipases on triglycerides resulting to saponification.

•The released fatty acids combine with calcium to produce the visible chalky white areas.

Enzymatic Fat Necrosis

•occurs in the female breast, mesenteries and in the omentum.

•There is no enzymatic lipolysis but there is apparent rupture of the cell membrane with release of neutral fat. Subsequent phagocytosis of the fat follows.

Traumatic fat necrosis

If Gangrenous Necrosis is produced by ischemia with a superimposed saprophytic bacterial infections

wet gangrene

may be cause by: arteriosclerosis, Buerger's disease, Raynaud's disease, Ergot poisoning

Dry gangrene

it is marked by deposition of fibrin-like proteinaceous material in arterial walls

appears smudgy and eosinophilic on light microscopy

Fibrinoid Necrosis

"falling off", fragments of apoptotic cells break off

Apoptosis

•A pathway of cell death in which cells activate enzymes that degrade the cells' own nuclear DNA and nuclear and cytoplasmic proteins.

Apoptosis

•Replacement of worn out cells.

•Highly proliferative and hormone responsive tissues undergo cycles of proliferation and cell loss.

•In immunity, elimination of excess leukocytes left at the end of an immune response.

Physiologic Apoptosis

•When DNA is severely damaged.

•Accumulation of misfolded proteins

Some viruses induce apoptotic death of infected cells

Pathologic Apoptosis

formation of calcium soaps is identified in the tissue sections as amorphous, granular, and basophilic material

Fat necrosis