4. “Necrosis is the morphological changes that follow
cell death in a living tissue or organ,
Resulting from the progressive degenerative action
of enzymes on the lethally injured cell.”
So,
Necrosis begins with an impairment of the cell’s
ability to maintain homeostasis, leading
to an influx of water and extracellular ions
5. Apoptosis vs Necrosis
The word apoptosis mean falling off.
“Apoptosis is a process of programmed and targeted
cause of cellular death”
Necrosis is differ from apoptosis:
6. Apoptosis Necrosis
Physiological or Always pathological
pathological
Cell shrinkage Cell swelling
Apoptotic bodies form Do not form
Dna cleavage No DNA cleavage
Beneficial Detrimental
Characteristic nuclear Nuclei lost
changes
No leak of lysosomal Leak of lysosomal enzymes
enzymes
8. Necrotic changes in tissues are caused By
Digestion of cell by enzymes
Denaturation of proteins
Digestion of cell by enzymes
This digestion is of two types
Autolysis: Digestion of cell by enzymes derived from
their own lyosomes
Heterolysis: Digestion of cell by enzymes derived from
lysosmes of leukocytes.
9. Denaturation of proteins caused by intracellular acidosis
and due to this result is that:
Injury to the cell membrane
Severe impairment of phosphorylation of cell
Increase permeability of the cell
Influx of Na+ and Ca+ in the cell
Decreased intracellular activity of the cell
10. Changes inside the cell
Changes in mitochondria
Changes in Nucleus
Changes in cytoplasm
11. Endoplasmic reticulum is disorganized
There is rupture of membrane
Ribosomes are shed off
Disorganization of polysomes & their structures
Mitochondria become swallon
Loss of interamitochondrial granules
Loss of cristae & change their shape
Rupture of outer membrane of Mitochondria
13. PYKNOSIS
“When the dna is broken down by endonucleases
fragments are formed & the nucleus becomes acid
and stains basophillic”
KARYORRHEXIS
“The pyknotic nucleus may break up into fragments
and disappear. This process is called karyorrhexis”
KARYOLYSIS
“The pyknotic nucleus may undergo lysis by the
enzyme DNAse”
14. Cytoplasm becomes more eosinophilic:
Due to loss of Rna & denaturation of cytoplasmic proteins
Cytoplasm becomes opaque.
16. “In this type of necrosis, the necrotic cell retains its
cellular outline for several days”
Coagulative necrosis typically occurs in solid organs
such as kidney, heart and adrenal gland usually as a
result of deficient blood supply and anoxia.
Examples
Myocardial infarction
17. Denaturation of protein is the basic mechanism of
coagulative necrosis
The injury and the subsequent increasing acidosis
denatures not only the structural proteins but also the
enzymic proteins, thus blocking the cellular proteolysis.
Morphology
Preservation of basic structural outline of the coagulated
cells
Appears as a mass of coagulated, pink staining
homogenous cytoplasm
18.
19.
20. It is the type of necrosis that occurs due to autolytic and
heterolytic actions of enzymes that convert the proteins
of cells into liquid.
It is characterized by softening and liquifaction of
tissue.
Examples
Ischemic necrosis of brain
Suppurative inflammation.
21. Enzymatic degradation of proteins is the basic
mechanism of liquefactive necrosis
Morphology
o Complete loss of cellular detail
o Cellular outline is also destroyed
22.
23.
24. Combination of coagulative and liquefactive necrosis
Characterized by the presence of soft, dry, cheesy
homogenous necrotic material.
It is not liquified
Examples
Principaly in the center of tuberculous granuloma
Morphology
Microscopically the necrotic focus is composed of
structureless amorphous granular debris enclosed
within a ring of granulomatous inflammation.
25.
26. Necrosis in special sites
It occurs in two forms:
Enzymatic fat necrosis
Traumatic fat necrosis
27. Most commenly seen in acute pancreatitis.
“Refers to the necrosis in adipose tissue, induced by the
action of pancreatic enzymes which are lead due to
trauma to the pancreas”
Morphology
Chalky white opaque spots surrounded by
inflammatory margins are seen
Necrotic area shows acute inflammatory changes with
dissolved fat cells
28. It occur following severe injury to the tissues with high
fat content such as the breast, subcutaneous tissue and
abdomen.
Morphology
Foam cells and gaint cells are seen.
necrotic foci contain a lot of phagocytes containing fat
known as foam cells
29.
30. Type of connective tissue necrosis especially affecting
arterial walls.
Mostly seen in two conditions
Auto immune diseases e.g
Rheumaic fever
SLE
Malignant hypertension
31.
32. Gangrene is the necrosis of tissue with superadded
putrefaction (enzymatic decomposition).
It is the clinical condition in which extensive tissue
necrosis is complicated to a variable degree by
secondary bacterial infection.
Gangree= Necrosis + infection + putrefaction
33.
34. Arterial obstructon due to:
Thrombosis of atherosclerotic artery
Embolus
Diabetes:- atherosclerotic artery , loss of sensation
results reapeted trauma & increase chances of infection
Infection
Gas gangrene
Gangrene of scrotum
Trauma
Crush injuries
Physical agents
Burns
Chemicals
36. It is usually secondary to slow occlusive vascular disease
Etiology
Gradual loss of arterial supply to an organ or tissue as
happens in
Arteriosclerosis
Atherosclerosis
Trauma
Ergot poisoning
Common sites
limbs; especially foot
37. Pathogenesis
It is a traditional term used to describe the infarction
of the limbs.
It is not true gangrene because the infection in
necrotic tissue is insignificant and putrefaction is
absent or minimal.
The necrotic area becomes black due to breakdown of
hemoglobin and formation of iron sulfide
38.
39. It is a type of gangrene in which tissue appears moist.
It results from severe bacterial infection superimposed on
necrosis
Pathogenesis
It is a true gangrene because it shows the severe infection and
putrefaction of tissue with edema and foul smell.
Arterial obstruction present.
blackening of the tissue is due to formation of iron sulphide
It is not clearly demarcated from adjacent healthy tissues.
Common sites
Intestine
Appendix
Limbs
41. “In this type of gangrene bacterial infection causes necrosis
and then gangrene with abundant gas formation in the tissue”
Gas gangrene=wet gangrene + gas formation
Predisposing factors
Foreign bodies in wound cause tissue ischemia
Foreign bodies favour infection
Contamination of wound by soil is dangerous bqz its ionisable
calcium salts and silicic acid may lead to tissue necrosis.
Infection by aerobic organisms at the same time serve to
produce anaerobic environment that is favourable for
anaerobic clostridia.
42. Two groups of clostridia cause gas gangrene
Saccharolytic:
Clostridia profringes
Proteolytic:
Clostridia isolyticum
Pathogenesis
Deep wound----anerobic condition---caused by spores of
clostridia
Necrosis of muscle fiber occur
Fermentation of muscle carbohydrate occur with formation of
lactic acid and gas.
Arterial supply of the area is cut down
Muscles become greenish- black due to iron sulphide & foul
smell
43. Muscles
Liver
Complicatons
Rapidly spreading gangrene
Shock and hemolytic anemia
Treatment of gangrene
Treatment of predisposing factor:
Amputation:
Surgical removal of gangrene tissue to prevent spreading of
the infection to the healthy tissue.
45. “It is wet type of gangrene in which necrosis is superadded
by infection and putrefaction”
Predisposing factors:
Sensory neuropathy
Ischemia
Lower resistance to infection
Management:
Control diabetes
Keep the tissue dry and clean
Antibiotics
Surgical drainage of necrotic tissue
46.
47. Referances:
http://www.diffen.com/difference/Apoptosis_vs_Necr
osis
http://www.qub.ac.uk/cm/pat/undergraduate/Basicca
ncer/necrosis_v_apoptosis.htm
www.roche-applied-science.com
http://en.wikipedia.org/wiki/Necrosis
Gross pathology By Dr. jawad ahmed.
Text book of pathology by inam danish
Text book illustrated pathology by peter
s.macfarlane/robin reid/robin callander.
