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Gangrene and Apoptosis

Dr Aisha
Tabassum.

Gangrene
A form of necrosis of tissue with superadded
putrefaction.
Necrotizing inflammation provoked by virulent
bacteria
Dry gangrene
Wet gangrene
Gas gangrene

Dry gangrene
Begins in distal part of limb due to ischemia
Eg:dry gangrene of toe and foot in elderly people
due to atherosclerosis
Others;TAO,Raynauds disease,trauma,ergot
poisoning.
Starts in the toe farthest from blood supply
Spreads upwards untill the point of adequate
blood supply
Line of seperation is present

Dry gangrene

Wet gangrene
Occurs in naturally moist tissue;bowel,mouth
cervix,vulva,lung
Others : diabetic foot,bed sores in bed ridden
patient
Develops rapidly due to venous obstruction,less
commonly arterial
Effected part stuffed with blood,favours rapid
growth of putrifying bacteria
Lacks clear cut line of demarcation

Wet gangrene

S.NO

FEATURE

DRY GANGRENE WET


GANGRENE

SITE

COMMONLY
LIMBS

MORE COMMON
IN BOWEL

2.

MECHANISMS

ARTERIAL
OCCLUSION

VENOUS OBSTR.
MORE COMMON

3.

MACROSCOPY

ORGAN,DRY,
SHRUNKEN,
BLACK

MOIST,SOFT,
SWOLLEN

4.

PUTREFACTION

LITTLE

MARKED

5.

LINE OF
DEMARCATION

PRESENT

NO CLEAR LINE

6.

BACTERIA

FAIL TO SURVIVE

NUMEROUS

7.

PROGNOSIS

BETTER

POOR

Gas gangrene
A form of wet gangrene
Caused by gas forming clostridia
Gain entry into the tissue through open wounds ;
muscles,colonic surgery
Toxins produce necrosis and edema

Grossly; swollen ,edematous,painfull,crepitant


Subsequently becomes swollen and foul smelling
Microscopy;
Coagulative necrosis with liquifaction
Periphery;zone of leucocytic infilteration,edema
and congestion
Capillary and venous thrombi

Apoptosis : falling off


Apoptosis is a pathway of cell death that is
induced by a regulated intracellular programme
in which cells destined to die activate enzymes
that degrade the cells own nuclear DNA and
nuclear and cytoplasmic proteins.
APOPTOSIS can be both physiological and
pathological

Apoptosis in physiologic situations


Programmed destruction of cells during
embryogenesis
Hormone dependent involution in the adult
Cell deletion in proliferating cell populations
Host cell death after completion of function
Harmful self reactive lymphocytes
Cell death induced by cytotoxic T cells

Apoptosis in pathologic situations


Cell death by injurious stimuli
Cell injury in viral diseases
Pathologic atrophy in parenchymal organs after
duct obstruction
Cell death in tumors

Morphology
Cell shrinkage
Chromatin condensation
Formation of cytoplasmic blebs and apoptotic
bodies
Phagocytosis of apoptotic cells or cell
bodies,usually by macrophages

Histologic examination:apoptosis involves single


cells or small cluster of cells; round or oval mass of
intensely eosinophilic cytoplasm with dense nuclear
chromatin fragments.

Ultrastructural features :
some nuclear fragments with peripheral crescents
of compacted chromatin and others are uniformly
dense

Mechanisms of apoptosis
INITIATION PHASE
The extrinsic ( death-receptor-initiated) pathway
The intrinsic (mitochondrial) pathway
EXECUTION PHASE
REMOVAL OF DEAD CELLS

Extrinsic pathway

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