2. DEGENERATION
Definition : It is defined as a retrogressive change in the
cell following a cell injury , more so in the cytoplasm than
the nucleus, caused by a factor which is not stong enough
to cause cell death.
It is a reversible cell injury.
4. CELLULAR SWELLING
It is the most common and earliest form of cell injury .
Results from impaired regulation of cellular volume
GROSS: The affected organ is enlarged , pale , the cut surface
bulges out .
MICROSCOPY :The cells are swollen with cytoplasmic granularity
and they compress the surrounding microvasculature.
HYDROPIC CHANGE : Small clear vacuoles are seen in the cells
Organs affected:
Kidney (Large white kidney ) , islets of Langerhans in DM
5.
6. FATTY CHANGE
Occurs due to intracellular accumulation of neutral
fats.
CAUSES:
Excess alcohol consumption,obesity malnutrition
,starvation ,diabetes mellitus, chronic ilnesses , late
pregnancy, hypoxia , hepatotoxins [ carbontetra
chloride , chloroform , ether,aflatoxins ] certain
drugslike estrogen steroids tetracycline etc.
Liver is the most common organ affected . Other
organs affected are heart, kidney and skeletal muscle.
7. FATTY LIVER
Gross :The organ is enlarged yellow tense glistening capsule and rounded
margins. C/S – bulges and pale yellow and greasy to touch.
8. MICROSCOPY
Fat in the cytoplasm of the hepatocytes is seen as
clear area which may vary from minute droplets in the
cytoplasm of a few hepatocytes [microvesicular] to
distension of the entire cytoplasm of most cells by
coaslesced droplets [macrovesicular] pushing the
nucleus to the periphery of the cell.
Occ. the adjacent cell containing fat, rupture
producing fatty cysts
Special stains such Sudan III & IV,Sudan black Oil
red O can be employed to demonstrate fat in the
tissue
9.
10. HYALINE CHANGE
Hyaline is a glassy homogenous material that stains pink in
H&E sections.
Two types :
1. Intra cellular (epithelial )
2. Extra cellular (connective tissue)
11. Intra cellular (epithelial ) hyaline :
1. Zenkers degeneration in typhoid.
2. Mallory’s hyaline in ALD
3. Russel bodies in plasma cells
Extra cellular (connective tissue) hyaline
1. Hyaline degeneration of splenic capsule , leiomyomas of uterus.
2. Hyaline arterisclerosis in HT and DM.
3. Copora amylacea in prostate.
13. DEF OF NECROSIS
Focal death along with degradation of
tissue by hydrolytic enzymes liberated
by cells. accompanied by
inflammatory reaction.
14. NECROSIS
DEF.-It refers to spectrum of morphological
changes that follows cell death in living tissue
largely resulting from progressive degradative
action of enzymes on lethally injured cell.
Irreversible cell injury.
Nucleus – pyknosis, karyolysis, karyorrhexis.
Cytoplasm – homogenous ,intensely eosinphilic.
16. COAGULATIVE
NECROSIS
Mc , caused by sudden cessatiion of blood flow.
Organs commonly affected are kidney , heart , spleen.
17. Gross :they are pale or anemic & wedge shaped with the
base resting under the capsule & apex pointing towards the
medulla.
18. Microscopy: the hallmark
of coagulative necrosis is
that architectural outlines
of cells may be preserved
although the cellular
details are lost.
19. LIQUEFACTIVE
NECROSIS
Occurs commonly due to ischemic injury and bacterial
and fungal infections.
Due to degradation of tissue by the action of powerful
hydrolytic enzymes.
Eg : infarct brain , abcess cavity
20. well defined,soft with
liquified centre
containing necrotic
debris later a cyst wall
is formed
-
The cystic space contains necrotic
cell debris & macrophages
containing phagocytosed material.
The cyst wall is formed by
proliferating capillaries
,inflammatory cells and
proliferating glials cells.
21. CASEOUS NECROSIS
It is found in the centre of tuberculous foci
It combines features of both coagulative ana liquefactive
necrosis.
23. Microscopy :The necrosed foci are
structureless ,granular eosinophilic
The surrounding tissue shows chacteristic
granulomatous
reaction
24. CAUSES hypoxia,chemical and physical agents.
Microbial agents and immunologic injury.
Changes---cell digestion by lytic enzymes.& denaturation of proteins.
manifested morphologically by changes in nucleus &cytoplasm.
CYTOPLASM ---EOSINOPHILIC/WITH
VACUOLATION OR DYSTROPHIC
CALCIFICATION.
NUCLEUS—
PYKNOSIS/KARYOLYSIS/KARYORRHEXIS.
25. Types of necrosis
5 types.
1)Coagulative necrosis---common type. caused by ischaemia. less
commonly by bacterial or chemical agents.
Organs—HEART,KIDNEY & SPLEEN.
GROSS: Focii of coagulative necrosis ;pale firm &slightly swollen. With
progression, becomes yellowish softer & shrunken .
26. Microscopy — cells can be recognized as
merely having ghost architecture. the
nuclear and cytoplasmic characters are
lost. Cells swollen &more eosinophilic
along with nuclear changes described. It is
infiltrated by inflammatory cells.
Dead cells are phagocytosed./granular
debris/fragments of cells.
32. 2)Liquifactive necrosis--- combination of ischemic injury and
bacterial or fungal infection. action of strong powerful hydrolytic
enzymes. eg; infarct brain, abscess.
Gross— soft with liquefied centre containing necrotic debris. Later
cyst wall is formed.
Microscopy— necrotic cell debris/macrophages with phagocytosed
material. Cyst wall—proliferating capillaries, inflammatory cells, and
gliosis in case of brain. fibroblasts.
39. 4)fat necrosis —acute pancreatic
necrosis,traumatic fat necrosis.
Gross-yellowish white &firm deposits.micro
—cloudy appearance with inflammatory
cells.
5)Fibrinoid necrosis —fibrin like
material.seen in examples of immunologic
injury.
Micro—brighitly eosinophilic hyaline
material in vessel walls etc.
42. PATHOLOGIC CALCIFICATION
When calcium getrs deposited at sites other than bone
and enamel it is called as pathologic or heterotopic
calcification.
Two types :
1. Dystrophic
2. Metastatic
43. DYSTROPHIC
Deposits of Ca salts in dead and
degenerated tissue.
Ca metab . is normal
Sr Ca levels normal
Causes : necrosis,infarcts,
thrombi,atheromas , Monckebergs
sclerosis etc
METASTATIC
Deposits of Ca salts in normal
tissue
Deranged
Hypercalcemia
Hyperparthyroidism,bony
destructive lesions ,prolonged
immobilisation etc
46. “ A FORM OF CELL DEATH DESIGNED TO ELIMINATEA FORM OF CELL DEATH DESIGNED TO ELIMINATE
UNWANTED HOST CELLS THROUGH ACTIVATION OFUNWANTED HOST CELLS THROUGH ACTIVATION OF
COORDINATED , INTERNALLY PROGRAMMED SERIESCOORDINATED , INTERNALLY PROGRAMMED SERIES
OF EVENTS REGULATED BY A SET OF GENE PRODUCTSOF EVENTS REGULATED BY A SET OF GENE PRODUCTS ”
DEFINITION
51. CELL DELETION IN INTESTINAL CRYPT EPITHELIA
CELL DEATH IN TUMORS
DEATH OF NEUTROPHILS IN ACUTE INFLAMMATION
DEATH OF IMMUNE CELLS
IN DUCT OBSTRUCTION
VIRAL HEPATITIS ( Councilman bodies )
CELL DEATH PRODUCED BY INJURIOUS STIMULI
( In low doses )
63. APOPTOSIS NECROSIS
Cell shrinkage Cell swelling
No inflammatory response Inflammatory response
Death of single cells Death of many contiguous cells
Cytoplasmic blebbing Plasma membrane disruption
Chromatin condensation Nuclear swelling & lysis
Intact lysosomes & other Lysosomal breakdown
organelles
Fragmentation of nucleus & Cell lysis & disentegration
cytoplasm
Phagocytosis by adj ‘ cells Phagocytosis by infl ‘ cells
Physiological & path ‘ stimuli Hypoxia , toxins mainly
Apoptotic bodies Damaged organelles
Programmed cell death Cell death by ATP depletion
64.
65.
66.
67. Necrosis Apoptosis
Morphological changes
Loss of membrane integrity
Begins with swelling of cytoplasm and
mitochondria
Ends with total cell lysis
No vesicle formation, complete lysis
Disintegration (swelling) of organelles
Membrane blebbing, but no loss of integrity
Aggregation of chromatin at the nuclear
membrane
Begins with shrinking of cytoplasm and
condensation of nucleus
Ends with fragmentation of cell into smaller
bodies
Formation of membrane bound vesicles
(apoptotic bodies)
Mitochondria become leaky due to pore
formation involving
proteins of the bcl-2 family.
68. Necrosis Apoptosis
Physiological significance
Affects groups of contiguous cells
Evoked by non-physiological
disturbances (complement
attack, lytic viruses, hypothermia,
hypoxia, ischemica,
metabolic poisons)
Phagocytosis by macrophages
Significant inflammatory response
Affects individual cells
Induced by physiological stimuli (lack of
growth
factors, changes in hormonal
environment)
Phagocytosis by adjacent cells or
macrophages
No inflammatory response
69. GANGRENE necrosis of tissue with superadded putrifaction.usually coagulative.
3types.
DRY GANGREN—seen in distal part of limb due to
ischemia. eg toes & FEET IN ATHEROSCLEROSIS
THROMBOANGITISOBLITERANCE.RAYNAUDS.
GROSS-DRY,SHRUNKEN,DARK BLACK.MICRO—
SMUDGING OF TISSUE/INFL.GRANULATION
TISSUE.
71. Wet gangrene —moist tissues. Diabetic foot.high
growth of bacteria.bed sores.venous blockage
commonly than arterial.due to
thrombosis,embolism.
Gross —soft swollen ,putrid rotten dark. eg-
bowel gangrene.
Micro —coagulative necrosis with blood,.
uleration, inflammatory infiltrate. No clear line of
demarcation.
72. P – 779/83. Extensive Gangrene of small intestine.
73.
74.
75.
76. Gas gangrene
special form of wet gangrene—gas forming clostridia
infectswounds. ms., colonic operation.
GROSS—Swollen, oedematous, crepitant/ dark black,
foul smelling.
Microscopy—ms. fibres show coagulative necrosis with
liquefaction. gm +bacilli can be identified.