2. Alteration. Cell injury.Alteration. Cell injury.
AlterationAlteration is the pathological changes of cellular structure,is the pathological changes of cellular structure,
extracellular matrix, tissue and organs which areextracellular matrix, tissue and organs which are
accompanied by violation of their vital functions.accompanied by violation of their vital functions.
The cellular morphologic changes induced by variousThe cellular morphologic changes induced by various
stimuli can be divided into:stimuli can be divided into:
1.1. Patterns of acute cell injury — reversible and irreversiblePatterns of acute cell injury — reversible and irreversible
cell injury leading to necrosis or apoptosiscell injury leading to necrosis or apoptosis
2.2. Subcellular alterations that occur largely as a response toSubcellular alterations that occur largely as a response to
more chronic or persistent injurious stimulimore chronic or persistent injurious stimuli
3.3. Intracellular accumulations of a number of substances —Intracellular accumulations of a number of substances —
lipids, carbohydrates, proteins—as a result oflipids, carbohydrates, proteins—as a result of
derangements in cell metabolism or excessive storage.derangements in cell metabolism or excessive storage.
3. Reasons of development ofReasons of development of
alterationalteration
1.1. hypoxiahypoxia
2.2. chemical agents and drugschemical agents and drugs
3.3. physical agentsphysical agents
4.4. microbiological agents (bacteria, viruses,microbiological agents (bacteria, viruses,
fungies)fungies)
5.5. immune mechanismsimmune mechanisms
6.6. genetic defects (apoptosis)genetic defects (apoptosis)
7.7. nutritional imbalancesnutritional imbalances
8.8. agingaging
4. Classification of degenerationsClassification of degenerations
1.1. ССlassification in depending on localization of metabolism:lassification in depending on localization of metabolism:
parenchymalparenchymal
stromally - vascularstromally - vascular
mixedmixed
2. Classification in depending on deposition of protein, lipids,2. Classification in depending on deposition of protein, lipids,
carbohydrate , mineral (on predominance of the brokencarbohydrate , mineral (on predominance of the broken
exchange):exchange):
Proteinous (Dysproteinoses)Proteinous (Dysproteinoses)
Fatty (lipidoses)Fatty (lipidoses)
CarbohydrateCarbohydrate
MineralMineral
PigmentalPigmental
3. Classification in depending on prevalence of process:3. Classification in depending on prevalence of process:
LocalLocal
SystemSystem
4. Classification in depending on an origin:4. Classification in depending on an origin:
AcquiredAcquired
HereditaryHereditary
5. CategoriesCategories of intracellularof intracellular
accumulationsaccumulations
1.1. a normal cellular constituent accumulateda normal cellular constituent accumulated
in excess, such as water, lipid, protein,in excess, such as water, lipid, protein,
and carbohydrates;and carbohydrates;
2.2. an abnormal substance, eitheran abnormal substance, either
exogenous, such as a mineral, or aexogenous, such as a mineral, or a
product of abnormal metabolism;product of abnormal metabolism;
3.3. a pigment or an infectious product.a pigment or an infectious product.
6. Parenchymal dysproteinoses,Parenchymal dysproteinoses,
mechanisms.mechanisms.
CellCell
Denaturation andDenaturation and
coagulation ofcoagulation of
cytoplasmic proteinscytoplasmic proteins
Hyaline-drop dystrophyHyaline-drop dystrophy
Focal coagulativeFocal coagulative
necrosis of cellnecrosis of cell
Total coagulativeNecrosisTotal coagulativeNecrosis
of cellof cell
Hydratation andHydratation and
colliquation of cell’scolliquation of cell’s
cytoplasmcytoplasm
Hydropic dystrophyHydropic dystrophy
Focal colliquative
necrosis of cell
(balloon dystrophy)
Total colliquative
necrosis of cell
7. The most frequent localization of
intracellular accumulations of
proteins, lipids and
carbohydrates is
myocardium (cardiomyocytes),
liver (hepatocytes),
kidneys (nephrocytes).
8. Types of intracellularTypes of intracellular
parenhymatousparenhymatous
degenerationsdegenerations
GranularGranular
Hyaline-dropHyaline-drop
Hydropic (vacuolar, balloon)Hydropic (vacuolar, balloon)
Keratoid (horney)Keratoid (horney)
Here are Mallory bodies
9. ParenhymatousParenhymatous fatty degenerationsfatty degenerations
This liver is enlarged and has
a pale yellow appearance. It is
greasy to touch. It is called
“Goose liver”.
Microscopically: there
are numerous lipid
vacuoles in the
cytoplasm of
hepatocytes.
11. Mucoid swellingMucoid swelling
It is disorganization and swelling ofIt is disorganization and swelling of
perivascular extracellular matrixperivascular extracellular matrix
(disorganization of connective(disorganization of connective
tissue) due to increased vasculartissue) due to increased vascular
permeability, plasmorrhagia andpermeability, plasmorrhagia and
deposition of glucosaminoglycansdeposition of glucosaminoglycans
(GAG).(GAG).
Microscopically:Microscopically: there is the phenomenon of metachromasia.there is the phenomenon of metachromasia.
That is basophylic color of basic substances. Collagen fibersThat is basophylic color of basic substances. Collagen fibers
save the structure, but swell and undergo to fibrillarsave the structure, but swell and undergo to fibrillar
destructure.destructure.
Gross appearanceGross appearance:: tissue or organ is saved.tissue or organ is saved.
Process is convertible.Process is convertible.
12. Fibrinoid changesFibrinoid changes
It is deep and irreversible disorganization ofIt is deep and irreversible disorganization of
connective tissue, in basis of which destruction ofconnective tissue, in basis of which destruction of
basic substances and fibers. It is accompaniedbasic substances and fibers. It is accompanied
by the sharp increase of permeability of vesselsby the sharp increase of permeability of vessels
and formation of fibrinoidand formation of fibrinoid
masses.masses.
Microscopically: the bands
of collagen fibers are
homogenous, impregnated
with plasma proteins.
Outcomes: fibrinoid
necrosis, hyalinosis,
sclerosis.
13. Hyaline changeHyaline change
It is an alteration within cells or in the extracellular
space, which gives a homogenous, glassy, pink
appearance in routine histologic sections
stained with H&E.H&E.
Hyalinosis is classified according
to its localization:
•Vascular hyalinosis (arteries are
thickened with sharply narrowed
or obliterated lumen)
•Hyalinosis of connective tissue is
usually localized; it develops in
scars, adhesions, in the areas of
chronic inflammation (e.g. “glazed
spleen”).
14. The outcome of hyalinosis is
irreversible.
Functional significance of hyalinosis
is different:
• Vascular hyalinosis may lead to
atrophy or sclerosis, infarction of
organs.
• Local hyalinosis in the cardiac
valves results in heart defects.
15. AmyloidosisAmyloidosis
AmyloidosisAmyloidosis is the term used for a group of diseasesis the term used for a group of diseases
characterized by extracellular deposition of febrillarcharacterized by extracellular deposition of febrillar
proteinaceous substance called amyloid.proteinaceous substance called amyloid.
Nature and etiologyNature and etiology
Amyloid is composed of 2 main types of complex proteins:Amyloid is composed of 2 main types of complex proteins:
Fibril proteinsFibril proteins comprising about 90% of amyloid.comprising about 90% of amyloid.
P-componentP-component comprising about 10% of amyloid.comprising about 10% of amyloid.
Of the 15 biochemically distinct forms of amyloidOf the 15 biochemically distinct forms of amyloid
proteins that have been identified, two are the mostproteins that have been identified, two are the most
common:common:
One, calledOne, called AL (amyloid light chain)AL (amyloid light chain) is derived fromis derived from
plasma cells (immunocytes) and contains immunoglobulinplasma cells (immunocytes) and contains immunoglobulin
light chains.light chains.
The other, designatedThe other, designated AA (amyloid-associated),AA (amyloid-associated), is ais a
unique nonimmunoglobulin protein synthesized by theunique nonimmunoglobulin protein synthesized by the
liver.liver.
16. Classification of amyloidosisClassification of amyloidosis
A. Systemic AmyloidosisA. Systemic Amyloidosis
1. Primary amyloidosis1. Primary amyloidosis (idiopathic) is the defect(idiopathic) is the defect
of primary mesodermal tissueof primary mesodermal tissue
2.2. Secondary amyloidosisSecondary amyloidosis ((acquired, reactive)acquired, reactive) isis
complication of chronic diseases (chroniccomplication of chronic diseases (chronic
infections, malignant tumors)infections, malignant tumors)
3. Familial amyloidosis3. Familial amyloidosis (inherited, genetic) is(inherited, genetic) is
predisposition of certain ethnic groups (periodicpredisposition of certain ethnic groups (periodic
illness).illness).
B. Localized AmyloidosisB. Localized Amyloidosis
1. Senile amyloidosis1. Senile amyloidosis
2. Endocrine amyloidosis2. Endocrine amyloidosis
17. Diagnosis of amyloidosisDiagnosis of amyloidosis
Histologic examination of biopsy materialHistologic examination of biopsy material
is the commonest and confirmatoryis the commonest and confirmatory
method for diagnosis in a suspected casemethod for diagnosis in a suspected case
of amyloidosis.of amyloidosis.
If renal manifestations are present, kidneyIf renal manifestations are present, kidney
is the preferred site for biopsy.is the preferred site for biopsy.
Other sites such as rectum, gingiva, andOther sites such as rectum, gingiva, and
more recently abdominal fat, are biopsiedmore recently abdominal fat, are biopsied
and are followed byand are followed by Congo red stainingCongo red staining forfor
confirmation.confirmation.
18. PathologyPathology
Systemic amyloidosis (AA) related to chronic inflammationSystemic amyloidosis (AA) related to chronic inflammation
tends to involve parenchymatous organs, such astends to involve parenchymatous organs, such as kidneys,kidneys,
spleen, liver, and adrenals.spleen, liver, and adrenals.
While amyloidosis (AL) related to myeloma tends to affectWhile amyloidosis (AL) related to myeloma tends to affect
mesodermal or other tissues, such as heart, gastrointestinalmesodermal or other tissues, such as heart, gastrointestinal
tract, peripheral nerves, skin, and tongue.tract, peripheral nerves, skin, and tongue.
Grossly:Grossly:
Organs extensively infiltrated by amyloid are usually enlargedOrgans extensively infiltrated by amyloid are usually enlarged
and have a pale, waxy ("lardaceous") or varnished appearanceand have a pale, waxy ("lardaceous") or varnished appearance
and firm consistency.and firm consistency.
The iodine test for amyloid is done by applying iodine solutionThe iodine test for amyloid is done by applying iodine solution
to the washed cut surface of the organ: amyloid typically stainsto the washed cut surface of the organ: amyloid typically stains
mahogany-brown, and this color reaction changes to blue ( amahogany-brown, and this color reaction changes to blue ( a
"starch-like" reaction) after the application of dilute sulfuric acid"starch-like" reaction) after the application of dilute sulfuric acid
19. Primary amyloidosis ofPrimary amyloidosis of
kidneys.kidneys.
Grossly, amyloid kidneysGrossly, amyloid kidneys
are usually enlarged,are usually enlarged,
pale, and smoothpale, and smooth
surfaced and have a firmsurfaced and have a firm
consistency. On corticalconsistency. On cortical
transaction, the glomerulitransaction, the glomeruli
(visible as pink dots in the(visible as pink dots in the
normal kidney) may benormal kidney) may be
seen as enlarged, waxy,seen as enlarged, waxy,
gray dots.gray dots.
20. Microscopically: the amorphous
pink deposition of amyloid may
be found in and around
arteries, in interstitium, or in
glomeruli. A Congo red stain
will demonstrate the red
material to be amyloid.
21. This section of
myocardium
demonstrates
amorphous deposits of
pale pink (H&E ) or red
(Congo red) material
between myocardial
fibers. Amyloidosis is a
cause for "infiltrative" or
"restrictive"
cardiomyopathy.
H&E
Congo red
Amyloidosis of
myocardium
22. Amyloidosis of the spleenAmyloidosis of the spleen
Amyloidosis of the spleen has
two different anatomical
patterns. Most commonly, the
amyloid deposits is limited to
the splenic follicles, resulting in
the gross appearance of a
moderately enlarged spleen
dotted with gray nodules (so
called "sago" spleen).
Alternatively, the amyloid
deposits may spare the follicles
and mainly infiltrate the red
pulp sinuses, producing a
large, firm spleen mottled with
waxy discolorations
("lardaceous" spleen).
23. Amyloidosis of adrenal glandAmyloidosis of adrenal gland
Amyloid depositsAmyloid deposits
surround,surround,
compress, andcompress, and
replace somereplace some
cortical cells andcortical cells and
infiltrate the wallinfiltrate the wall
of a small bloodof a small blood
vessel. Congo redvessel. Congo red..
24. Amyloidosis of theAmyloidosis of the
tonguetongue
Amyloid infiltrates theAmyloid infiltrates the
capillary walls andcapillary walls and
narrows the lumensnarrows the lumens
of some of them. H&E.of some of them. H&E.
Amyloidosis of the liverAmyloidosis of the liver
The hepatic parenchymaThe hepatic parenchyma
is infiltrated andis infiltrated and
replaced by nodularreplaced by nodular
accumulations ofaccumulations of
amyloid (pink). H&E.amyloid (pink). H&E.
26. Stromal vascular fatty degenerations
•Stromal fatty infiltration is the deposition of mature adipose cells in the
stromal connective tissue.
•The condition occurs most often in patients with obesity.
Classifications of Obesity
1. According to the etiology : Primary (idiopathic) and
Secondary.
2. There are several types of secondary obesity: Alimentary,
Cerebral, Endocrine, Hereditary in Gierke’s disease.
3. According to the patient's appearance: symmetrical,
upper, medial, and lower.
4. According to morphological peculiarities of adipose
tissue:
•In hypertrophic type adipose tissue enlarges due to
increased volume of fatty cells
•In hyperplastic due to increase in their number.
27. PATHOLOGY OF PIGMENTSPATHOLOGY OF PIGMENTS
PigmentsPigments are colored substances, some of which areare colored substances, some of which are
normal constituents of cells where as others are abnormalnormal constituents of cells where as others are abnormal
and collect in cells only under special circumstances.and collect in cells only under special circumstances.
Pigments are generally classified into two broad categories:Pigments are generally classified into two broad categories:
1.1. Endogenous pigments, which are normal constituents ofEndogenous pigments, which are normal constituents of
cells and tissues;cells and tissues;
2.2. Exogenous pigments introduced into the body fromExogenous pigments introduced into the body from
environment.environment.
Classification of endogenous pigmentsClassification of endogenous pigments
1.1. Hemoglobinogenic pigments:Hemoglobinogenic pigments:
Physiologic pigments:Physiologic pigments: Ferritin, Hemosiderin,Ferritin, Hemosiderin, BilirubinBilirubin
Pathologic pigments:Pathologic pigments: Hematoidin,Hematoidin, Hematin, PorfirinHematin, Porfirin
2.2. Proteinogenic (melanin).Proteinogenic (melanin).
3.3. Lipidogenic (lipofuscin).Lipidogenic (lipofuscin).
28. HemosiderosisHemosiderosis
Local hemosiderosisLocal hemosiderosis isis
characterized by localcharacterized by local
breakdown of red cells inbreakdown of red cells in
tissues, e.g. in internaltissues, e.g. in internal
hemorrhage.hemorrhage.
Mechanism of localMechanism of local
hemosiderosis ishemosiderosis is
extravascular hemolysis.extravascular hemolysis.
It occurs regularly aroundIt occurs regularly around
areas of bruising andareas of bruising and
hemorrhage.hemorrhage.
In the lungs hemosiderin-ladenIn the lungs hemosiderin-laden
macrophages (siderophages)macrophages (siderophages)
are appropriately referred to asare appropriately referred to as
“heart failure cells”.“heart failure cells”.
29. Visceral siderosis (systemic hemosiderosis).Visceral siderosis (systemic hemosiderosis).
Mechanism of systemicMechanism of systemic
hemosiderosis is intravascularhemosiderosis is intravascular
hemolysis.hemolysis.
It is seen in the liver, spleenIt is seen in the liver, spleen
and sometimes in kidneys inand sometimes in kidneys in
cases of hemolytic anemia, incases of hemolytic anemia, in
patients requiring repeatedpatients requiring repeated
blood transfusion, in patientsblood transfusion, in patients
with chronic ineffectivewith chronic ineffective
erythropoiesis. The pigmenterythropoiesis. The pigment
imparts a deep brown color toimparts a deep brown color to
tissues and organs when it istissues and organs when it is
present in highpresent in high
concentrations.concentrations.
A Prussian blue reaction is seen
in this iron stain of the liver to
demonstrate large amounts of
hemosiderin that are present in
hepatocytes and Kupffer cells.
30. Pathology of bilirubin’s
metabolism.
Jaundice.Types of jaundice:
1. Prehepatic jaundice (Hemolytic jaundice) is
characterized by lysis of the red blood cells in a variety of
conditions.
2. Intrahepatic jaundice (Hepatocellular jaundice) - results
from failure both of hepatocytes to conjugate bilirubin and
of bilirubin to pass through the liver into the intestine. Both
of conjugated bilirubin and unconjugated bilirubin increase
its amount in blood. The liver is light yellowish-green color
of saffron (“saffron liver”).
3. Posthepatic jaundice (Obstructive jaundice) - results
from an obstruction of the passage of conjugated bilirubin
from hepatocytes to the intestine. Conjugated bilirubin is
water-soluble and is excreted in the urine. The liver is dark
green.
31. In the liver, bile pigments may appear:
• As bile pigment droplets in the hepatocytes.
• As bile impregnations in necrotic areas.
• As bile casts (bile capillaries, cholangioles, or bile
canaliculi).
• In Kupffer’s cells.
The yellow-green globular
material seen in small bile
ductules in the liver here is
bilirubin pigment.
32. This is dystrophic calcification in
the wall of the stomach. At the far
left is an artery with calcification
in its wall. There are also
irregular bluish-purple deposits of
calcium in the submucosa.
Calcium is more likely to be
deposited in tissues that are
damaged.
Here is so-called
"metastatic calcification" in
the lung of a patient with a
very high serum calcium
level (hypercalcemia).
Calcium metabolism disturbances
33. Cells DeathCells Death
It is the premature death and destruction ofIt is the premature death and destruction of
cell in the living organism under action ofcell in the living organism under action of
factors of critical damagefactors of critical damage
Classification of Cells Death, based on theClassification of Cells Death, based on the
mechanism of development:mechanism of development:
necrosisnecrosis
pathogenic inducted apoptosispathogenic inducted apoptosis
immunological elimination of cells.immunological elimination of cells.
34. NECROSISNECROSIS
If the acute or chronic injury to whichIf the acute or chronic injury to which
a cell must react is too great, thea cell must react is too great, the
resulting changes in structure andresulting changes in structure and
function lead to the death of cells.function lead to the death of cells.
Death of the cells and tissues in aDeath of the cells and tissues in a
living organism is called Necrosis.living organism is called Necrosis.
35. According to the cause ofAccording to the cause of
necrosis there are the followingnecrosis there are the following
types of necrosis:types of necrosis:
traumatic necrosis;traumatic necrosis;
toxic necrosis;toxic necrosis;
trophoneurotic necrosis;trophoneurotic necrosis;
allergic necrosis;allergic necrosis;
vascular or ischemic necrosis.vascular or ischemic necrosis.
36. Two essential changes bring about irreversible cellTwo essential changes bring about irreversible cell
injury in necrosis - cell digestion by denaturation ofinjury in necrosis - cell digestion by denaturation of
proteins and lytic enzymes.proteins and lytic enzymes.
coagulative necrosiscoagulative necrosis develops (during denaturation ofdevelops (during denaturation of
proteins ).proteins ).
liquefactive necrosisliquefactive necrosis is a progressive catalysis of cellis a progressive catalysis of cell
structures (during enzymic digestion)structures (during enzymic digestion).. Liquefactive
necrosis is typical of organs in which the tissues have a
lot of lipid (such as brain) or when there is an abscess
with lots of acute inflammatory cells whose release of
proteolytic
Both of these processes require hours to developBoth of these processes require hours to develop
Main types of necrosisMain types of necrosis
37. Clinic-morphological forms ofClinic-morphological forms of
necrosis of organs:necrosis of organs:
1)1) GangreneGangrene – total necrosis of the organ, reported with the– total necrosis of the organ, reported with the
external environment:external environment:
drydry – at the thrombosis of arteries, an organ acquires the black coloring– at the thrombosis of arteries, an organ acquires the black coloring
moist (wet) –moist (wet) – at the thrombosis of arteries and veins + influencing of putridat the thrombosis of arteries and veins + influencing of putrid
bacteria.bacteria.
gas gangrenegas gangrene
bedsorebedsore is a type of gangrene, death of the tissue under the influence ofis a type of gangrene, death of the tissue under the influence of
pressure (sacral area, buttocks, great trochanter). It is trophoneuroticpressure (sacral area, buttocks, great trochanter). It is trophoneurotic
necrosis of the bed- patientsnecrosis of the bed- patients
nomanoma – widespread necrosis of soft tissue of person.– widespread necrosis of soft tissue of person.
2)2) SequesterSequester – fragment of dead tissue, which can’t be autolysed,– fragment of dead tissue, which can’t be autolysed,
replaced by connective tissue and which is localized amongreplaced by connective tissue and which is localized among
alive tissuealive tissue
3)3) InfarctionInfarction – vascular or ischemic necrosis;– vascular or ischemic necrosis;
4)4) Fat necrosisFat necrosis
5)5) Caseous necrosisCaseous necrosis
6)6) Fibrinoid necrosisFibrinoid necrosis..
38. This is an example of coagulative
necrosis. This is the typical pattern
with ischemia and infarction (loss of
blood supply and resultant tissue
anoxia). Here, there is a wedge-
shaped pale area of coagulative
necrosis (infarction) in the renal
cortex of the kidney.
The contrast between normal adrenal
cortex and the small pale infarct is
good. The area just under the capsule
is spared because of blood supply
from capsular arterial branches. This
picture illustrates the shape and
appearance of an ischemic (pale)
infarct well.
Infarction
39. At high magnification, liquefactive
necrosis of the brain demonstrates
many macrophages at the right which
are cleaning up the necrotic cellular
debris.
Grossly, the cerebral infarction at
the upper left here demonstrates
liquefactive necrosis. Eventually, the
removal of the dead tissue leaves
behind a cavity
Liquefactive necrosisLiquefactive necrosis
40. This is gangrene. In this case, the
toes were involved in a frostbite
injury. This is an example of "dry"
gangrene in which there is mainly
coagulative necrosis from the
anoxic injury.
This is gangrene of the lower
extremity. In this case the term
"wet" gangrene is more applicable
because of the liquefactive
component from superimposed
infection in addition to the
coagulative necrosis from loss of
blood supply. This patient had
diabetes mellitus.
Gangrene
41. This is fat necrosis of the pancreas.
Cellular injury to the pancreatic acini
leads to release of powerful enzymes
which damage fat by the production of
soaps, and these appear grossly as
the soft, chalky white areas seen here
on the cut surfaces.
Microscopically, fat necrosis is
seen here. Though the cellular
outlines vaguely remain, the fat
cells have lost their peripheral
nuclei and their cytoplasm has
become a pink amorphous mass
of necrotic material.
Fat necrosis
42. This is more extensive caseous
necrosis, with confluent cheesy tan
granulomas in the upper portion of
this lung in a patient with tuberculosis.
The tissue destruction is so extensive
that there are areas of cavitation
(cystic spaces) being formed as the
necrotic (mainly liquefied) debris
drains out via the bronchi.
Microscopically, caseous necrosis is
characterized by acellular pink areas
of necrosis, as seen here at the upper
right, surrounded by a granulomatous
inflammatory process.
Caseous necrosis
43. Sometimes the small arteries and arterioles can be
damaged so severely in malignant hypertension that they
demonstrate necrosis with a pink fibrin-like quality that gives
this process its name - fibrinoid necrosis.
Fibrinoid necrosis
44. Phase of necrosisPhase of necrosis
Many nuclei have become
pyknotic (shrunken and dark). ItIt
process is calledprocess is called
karyopicnosiskaryopicnosis..
After thatAfter that karyorrhexiskaryorrhexis
(fragmentation) develops.develops.
Nucleus is decomposed intoNucleus is decomposed into
small granules.small granules.
Also mayAlso may bebe developsdevelops
karyolysiskaryolysis,, when the nucleuswhen the nucleus
dissolves.dissolves.
The cytoplasm and cell borders
are not recognizable.
45. Regeneration of tissues – replacement of the dead tissue with a
new one;
Incapsulation – formation of the connective tissue capsula around
necrotic area;
Organization – replacement of the dead tissue with connective
tissue;
Petrification – replacement of the dead tissue with calcium salts;
Incrustation – replacement of the dead tissue with any other salts
exept calcium;
Ossification – the formation of the bone tissue in the necrotic area;
Hyaline change – the appearance of the hyaline-like substance in
the necrotic area;
Sequestration – formation of sequester;
Mutilation – spontaneous tearing away of the dead tissue;
Cystic formation.
Suppuration fusion of necrotic tissues
The outcomes of necrosis
