cell injury and cell death

Question 1

Cell injury results when

Answer 1

Cells are stressed so severely that they are no longer able to adapt
 When cells are exposed to inherently damaging agents
 Suffer from intrinsic abnormalities

Question 2

Reversible cell injury

Answer 2

Only if the damaging stimulus is removed

Question 3

Hallmarks of reversible injury

Answer 3

Reduced oxidative phosphorylation with depletion of energy stores (ATP –
adenosine triphosphate)
 Cell swelling – caused by changes in ion concentrations and water influx
- a.k.a: hydrophic change

Question 4

Fatty change

- a.k.a steatosis

Answer 4

Refers to the abnormal accumulation of lipid droplets (triglycerides) in the
parenchymal cells of organs

Question 5

Fatty change causes

Answer 5

Toxins
 Protein malnutrition
 Diabetes mellitus
 Obesity
 Hypoxia
 Alcohol

Question 6

MECHANISMS OF FATTY CHANGE

Answer 6

excessive entry of lipids

 defective metabolism and/or export of lipids

Question 7

Two phenomena consistently characterize irreversibility:

Answer 7

Irreversible mitochondrial dysfunction

 Profound disturbances in membrane function

Question 8

Causes of Cell Injury

Answer 8

Oxygen deprivation 
Physical Agents
Infectious Agents
Immunological reactions
Genetic Derangements
Nutritional Imbalances

Question 9

Hypoxia

Answer 9

is a deficiency of oxygen, which causes cell injury by reducing aerobic
oxidative respiration
o Causes of hypoxia
 Reduced blood flow (ischemia)

Question 10

NECROSIS

Answer 10

the death of tissues following bioenergetic failure & loss of plasma membrane
integrity.
It is always a pathologic process

Question 11

necrosis Morphology cytoplasm

Answer 11

Increased eosinophilia
• Glassy & homogenous
• Vacuolated, moth-eaten

Question 12

necrosis Morphology nucleus

Answer 12

Karyolysis
• Pyknosis
• Karyorrhexis

Question 13

Coagulative necrosis

Answer 13

Localised area of coagulative necrosis = infarct
o The injury denatures structural proteins AND degradative enzymes therefore blocking
enzymatic digestion of the cell enabling cells to retain their outlines.
o Macroscopic Findings:
 Initially: organ may appear firm
 With time: organ becomes soft (due to digestion by macrophages)
 Often a wedge-shaped infarct
o Microscopic Findings:
 eosinophilic, anucleate cells may persist for days or week

Question 14

Liquefactive necrosis

Answer 14

digestion of the dead cells, resulting in transformation of the tissue into
a liquid viscous mass

Question 15

Gangrenous necrosis

Answer 15

Usually applies to a limb that has lost its blood supply and undergone necrosis (coagulative
type)

Question 16

Caseous necrosis

Answer 16

Tuberculous infection

Question 17

Fat necrosis

Answer 17

Refers to focal areas of fat destruction

o Direct trauma to adipocytes and extracellular liberation of fat

Question 18

Fibrinoid necrosis

Answer 18

A special form of necrosis usually seen in immune reactions involving blood vessel

Question 19

APOPTOSIS

Answer 19

a pathway of cell death induced by a tightly regulated suicide program in which
cells destined to die activate intrinsic enzymes that degrade the cells own DNA & proteins
“Programmed cell death”

Question 20

apoptosis morphology

Answer 20

Cell shrinkage
• Chromatin condensation
• Formation of cytoplasmic blebs & apoptotic bodies
• Phagocytosis of apoptotic bodies
• Appears as a mass of intensely eosinophilic cytoplasm with fragments of dense nuclear
chromati

Question 21

AUTOPHAGY

Answer 21

A process in which a cell eats its own contents