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CELL INJURY and CELL DEATH

y  Local deficiency in the blood supply (ischemia) 

limited oxygen and glucose supply 

y  In the hypoxic state, the most commonly 

affected organelle is the mitochondrion (site of 

oxidative phosphorylation) 

y  mitochondrial activity will lead to  ATP

production

y  ATP will lead to a decreased level of activity 

of the ATP dependent Na-K pumps located at

the cell membrane Na remains in the cell andattracts water which leads to cellular swelling 

y  In the hypoxic state, the cell shifts to anaerobic 

glycolysis whose end product is pyruvate which

will be reduced to lactic acid thus resulting in a 

decrease in pH clumping of chromatin(ECF:

7.4; ICF:7-7.3) 

Reversible Injuries:

(Two types of changes can be gleaned using the

light microscope) 

  Cellular swelling (hydropic 

change/degeneration) 

o  e.g. Hydatidif orm mole

characterized by vesicle f ormation

  Fatty change (steatosis) 

o  e.g. f atty liver characterized grossly 

by an increase in weight f romnormally 1.1-1.3kg to 4-6kg and will 

appear yellowish and greasy 

o  histologically, accumulation of lipid

vacuoles pushing the nuclei to the

periphery signet ring sign; also 

has a sieve-like appearance

* Cell death can either be necrosis or apoptosis

which are distinct f rom one another 

Features Necrosis Apoptosis

Cell size Enlarged

(swelling) 

Reduced

(shrinkage) 

Subject: Pathology Pre-lab discussionTopic: Cell Injury and DeathLecturer: Dr. Kent ErmitaDate of Lecture: 06/16/2011Transcriptionist: porkanorPages: 2

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Nucleus Pyknosis

karyorrhexis

karyolysis

Fragmentation

into 

nucleosome-

size f ragments

Plasma

membrane

Disrupted Intact; altered

structure,

especially 

orientation of 

lipids

Cellular

contents

Enzymatic 

digestion; may 

leak out of cell 

Intact; may be

released in

apoptotic 

bodies

Adjacent

inflammation

Frequent No 

Physiologic

or Pathologic

role

Invariably 

pathologic 

(culmination of 

irreversible cell 

injury) 

Often

physiologic,

means of 

eliminating 

unwanted

cells; may be

pathologic 

after some

f orms of cell 

injury,especially 

DNA damage

*table taken f rom Robbins Basic Pathology 8th

ed. p.6 

Irreversible Injuries:

NECROSIS

  Increased eosinophilia 

  Nuclear changes

o  PYKNOSIS- shrinkage and increased

basophilia 

o  KARYOLYIS- dissolution and f ading of 

chromatin

o  KARYORRHEXIS- f ragmentation

  PATTERNS OF NECROSIS

o  Coagulation necrosis/ COAGULATIVE

necrosis

  Inf arction of solid organs except brain

  Denaturation of proteins as well as

enzymes blocking proteolysis of 

necrotic cells

  Basic tissue architecture is preserved

(tombstone) o  Liquef action necrosis/ LIQ UEFACTIVE

necrosis

-  CNS, f ocal bacterial infections with

accumulation of inf lammatory cells

-  Enzymatic digestion of dead cells

transf orming tissues into liquid viscous

mass

-  Obliteration of tissue architecture

o  Enzymatic f at necrosis

-  Release of activated pancreatic lipase

liquefies membranes of f at cells in the

peritoneum.

-  Fatty acid when combined with calcium

f orm chalky white areas

o  Caseous/ Caseation necrosis

-  Tuberculous infection

-  Complete obliteration of tissuearchitecture

-  Friable(crumbly) yellow-white areas of 

necrosis

-  Characteristic f ocus of inf lammation:

GRANULOMA

  collection of transf ormed

macrophages called

epitheloid cells (hallmark of 

granuloma f ormation) 

rimmed by lymphocytes

  may have Langhans type

giant cells

o  Gangrenous necrosis

-  e.g. Lower limb that has lost its blood

supply.

-  e.g. appendicitis

  there is obliteration of the

layers of the appendiceal 

wall 

-  Coagulative necrosis is transf ormed by 

liquef action action of enzymes released

by leukocytes when there is

superimposed bacterial infection

Intracellular Accumulations:

1. Lipids

A.  Fatty change, Liver 

B.  Atherosclerosis (Coronary Artery) 

2. Pigments

A.  Exogenous

  carbon (most common

exogenous pigment;

anthracotic pigment) 

B. Endogenous  lipofuscin (insoluble yellowish

brown granular material) 

  hemosiderin (golden yellow-

brown granular pigments

derived f rom hgb) 

  melanin (black-brown pigment

produced by melanocytes) 

3. Other cellular accumulations

A.  Dystrophic calcifications

o  Affinity of calcium to 

necrotic tissue

o  No disturbance in calcium

balance as opposed to 

metastatic calcification

B.  Hyaline change

 ____________END OF TRANSCRIPTION _________ Be strong and courageous. Do not be afraid or terrifiedbecause of them, for the LORD your God goes with you;he will never leave you nor forsake you." 

Deuteronomy 31:6

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