8. Necrosis

Question 1

Necrosis: Cell Size

Answer 1

Enlarged (swelling)

Question 2

Necrosis: Nucleus

Answer 2

Pyknosis to karyorrhexis to karyolyis

Question 3

Necrosis: Plasma Membrane

Answer 3

Disrupted

Question 4

Necrosis: Cellular Contents

Answer 4

Enzymatic digestion; may leak out of cell

Question 5

Necrosis: Adjacent Inflammation

Answer 5

Frequent

Question 6

Necrosis: Physiologic or Pathologic Role

Answer 6

Invariably pathologic (culmination of irreversible cell injury)

Question 7

Reversible Cell Injury (structural changes)

Answer 7

1. Plasma membrane alterations: blebbing, blunting, loss of microvilli
2. Mitochondrial changes: swelling and the appearance of small amorphous densities
3. Dilation of the ER: detachment of polysomes, intracytoplasmic myelin figures may be there.
4. Nuclear alterations: disaggregation of granular and fibrillar elements.

Question 8

Necrosis Morphology

Answer 8

• Show increased eosinophelia (attributable to loss of cytoplasmic RNA and denatured cytoplasmic proteins)
• more glassy homogenous (loss of glycogen particles)
• when enzymes digest organelles, cytoplasm becomes vacuolated and appears moth-eaten
• dead cells may be replaced by large phospholipid masses called myelin figures (from damaged cell membranes)
• nuclear changes: karyolysis (basophilia of chromatin fades), pyknosis (nuclear shrinkage and increased basophilia), karyorrhexis (pyknotic nucleus undergoes fragmentation)

Question 9

Coagulative necrosis

Answer 9

Architecture of dead tissues is preserved for a span of at least some days.

• tissues exhibit firm texture
• injury denatures structural proteins and enzymes (blocks proteolysis of dead cells)
• eosinophilic, anucleate cells may persist for days
• ultimately, removed by phagocytosis by leukocytes

-Ischemia caused by obstruction in a vessel may lead to this (except in brain)
Infarct: localized area of coagulative necrosis

Question 10

Liquefactive necrosis

Answer 10

Digestion of the dead cells, resulting in tissue becoming liquid viscous mass

• Focal bacteria or fungal infections
• necrotic material is creamy yellow (presence of dead leukocytes and is called pus)
• hypoxic death of cells within CNS manifests often as liquefactive necrosis

Question 11

Gangrenous necrosis

Answer 11

Term usually applied to limb (lower leg that has lost its blood supply and undergone necrosis, typically coagulative necrosis in multiple tissue planes)
-when bacterial infection superimposed, there is more liquefactive necrosis (giving rise to so-called wet gangrene)

Question 12

Caseous necrosis

Answer 12

Most often in foci of tuberculous infection

• caseous means “cheese-like,” from the friable white appearance
• necrotic area appears as structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within distinctive inflammatory border (characteristic of a focus of inflammation known as granuloma)

Question 13

Fat necrosis

Answer 13

Focal areas of fat destruction (resulting from release of activated pancreatic lipases into the substance of the pancreas and peritoneal cavity), happens in acute pancreatitis.

• chalky-white areas (fat saponification)
• foci of shadowy outlines of necrotic fat cells, with basophillic calcium deposits, surrounded by inflammatory reaction.

Question 14

Fibrinoid necrosis

Answer 14

Immune reactions involving blood vessels

• when complexes of antigens and antibodies are deposited in walls of arteries
• bright pink and amorphous appearance (called fibrinoid)

Question 15

If necrotic cells aren’t removed

Answer 15

Provide nidus for the dystrophic calcification