APOPTOSIS , DESCRIPTION, CELL INJURY, Cell injury that damage DNA , loss of growth factors. , Direct action of cytokines (e.g., tumor necrosis factor) , Immune system action (e.g., natural killer cells or cytotoxic T lymphocytes). Viral infection (eg HIV, Hepatitis) , Sublethal damage to the cells , by ionizing radiation, hyperthermia, toxins

1. CELL INJURY

2.  Greek word “falling off”
 Good cell death
 Is a programmed cell death without inflammatory reaction
having significance in a variety of physiological and
pathological conditions.

3.  Involvement of single cells or small clusters of cells in the
background of viable cells.
 Round to oval intensely eosinophilic cytoplasm.
 Nuclear chromatin is condensed(pyknosis) or
fragmented(karyorrehexis).
 Unlike necrosis, there are no inflammatory reaction around
apoptosis.

4.  Cell shrinkage
 Chromatin condensation
 Formation of cytoplasmic blebs and
apoptotic bodies
 Phagocytosis of apoptotic cells or cell bodies

6.  Cell injury that damage DNA
 loss of growth factors.
 Direct action of cytokines (e.g., tumor necrosis factor)
 Immune system action (e.g., natural killer cells or cytotoxicT
lymphocytes).
 Viral infection (eg HIV, Hepatitis)
 Sublethal damage to the cells (e.g., by ionizing radiation,
hyperthermia, toxins)

7. 1.Programmed cell death during embryogenesis.
2. Hormone dependent cell involution in case of
endometrial cell break down during menstrual
cycle.

8. 1.Cell death in tumours during regression induced by
cytotoxic drugs or irradiation.
2. In some viral disease e.g. viral hepatitis in which
apoptotic cells are known as councilman bodies

9. Feature Apoptosis Necrosis
Definition Programmed cell death Cell death by hydrolytic
enzyme
Cause Physiologic and pathologic Hypoxia,Toxins
Morphology •No inflammatory rxn
• Death of single cells
• Cell shrinkage
• Cytoplasmic blebs on
membrane
• Apoptotic bodies
•Chromatin condensation
•Phagocytosis of apoptotic
bodies by macrophages
•Inflammatory rxn present
•Death of many cells
•Cell swelling initially
•Membrane disruption
•Damaged organells
•Nuclear disruption
•Phagocytosis of cell debris by
macrophages

10.  Intracellular accumulation of substance in abnormal
amounts within the cytoplasm (esp.lysosomes) or nucleus of
the cell.
 Causes reversible and irreversible cell injury.
Some abnormal intracellular accumulations can be divided into
3 groups
1. Accumulation of constituents of normal metabolism
produced in excess: eg lipids, proteins and carbohydrates
2. Accumulation of abnormal substance due to lack of enzyme
3. Accumulation of pigments

11.  Steatosis (Fatty Change):The terms steatosis and fatty
change describe abnormal accumulations of triglycerides
within parenchymal cells.
 Liver is the most common organ to involved but kidney,
heart, skeletal muscles are also involved.
 The causes of steatosis include toxins, protein malnutrition,
diabetes mellitus, obesity, and anoxia.

12.  Free fatty acids enters the hepatocytes
 Fatty acids metabolize into mainly tryglyceride and enters
blood as lipoprotein with the help of the receptor
apoprotein
 In absence of apoprotein tryglyceride accumulates.
 several factors like alcohol consumption, hepatotoxins and
protein malnutrition causes accumulation of tryglyceride in
the liver

14.  In all organs fatty change appears as clear vacuoles within
parenchymal cells.
 Nucleus is squeezed into the displaced rim of cytoplasm
about the fat vacuole.
Liver:
mild –no change,
if progressive accumulation: bright yellow, soft greasy organ,
two to four times than normal weight.

15.  prolonged moderate hypoxia: causes intracellular deposits of fat
 Gross: apparent bands of yellowed myocardium alternating with
bands of darker, red-brown, uninvolved myocardium
 profound hypoxia: uniformly affected hypoxia

16.  Atherosclerosis:Tunica intima is covered with cholesterol
esters.
 Xanthomas: clusters of foamy cells are found in the
subepithelial connective tissue of the skin and in tendons,
producing tumorous masses known as xanthomas.
 Cholesterolosis: accumulations of cholesterol-laden
macrophages in the lamina propria of the gallbladder .

17.  In proteinuria protein
accumulates in the
proximal convoluted
tubules.
 Russells bodies:
intracytoplasmic
accumulation of
immunoglobulin in
plasma cells.

18.  Diabetes mellitis: proximal tubule, loop of Henle,
hepatocytes
 Glycogen storage disease: defect in the enzyme for
synthesis and breakdown of glycogen.
 ACCUMULATION OF PIGMENTS:
Exogenous: carbon, tatooing
Endogenous: Lipofuscin, melanin, hemosiderin, bilirubin

19.  Lipofuscin:lipo= fat, fuscus= brown
insoluble pigment, Wear and tear pigment
Tissue section: coarse, golden-brown granular pigment present
 Hemosiderin: hemoglobin-derived, golden yellow-to-brown,
granular or crystalline pigment that serves as one of the major
storage forms of iron.
visualised by prussian blue stain
 Bilirubin: derived from bile, excessive accumulation causes
jaundice.
 Melanin: is an endogenous, non-hemoglobin-derived, brown-black
pigment. Eg alkaptonuria

20. H&E STAIN PRUSSIAN BLUE STAIN

21.  Pathologic calcification is the abnormal tissue deposition of
calcium salts, together with smaller amounts of iron,
magnesium, and other mineral salts
 Two types of calcification
1. Dystrophic calcification
2. Metastatic calcification

22.  encountered in areas of necrosis. commonly develops in
aging or damaged heart valves, further hampering their
function.
 Macroscopically: fine, white granules or clumps
 Microscopically: basophilic, amorphous granular sometimes
clump appearance.
 lamellated configurations, of calcium deposits called
psammoma bodies seen in meningioma, papillary
carcinoma of thyroid and ovary

24. precipitant of calcium phosphate in normal tissue due to
hypercalcemia
1. increased secretion of parathyroid hormone
2. destruction of bone tissue
3. vitamin D–related disorders
4. renal failure