1. CELL DEATH
or
NECROSIS
Lecture No. 3

2. What is Necrosis?
• Necrosis is the sum total of morphologic
changes that follow cell death in a living
tissue or organ
• Dead cells usually show changes in both the
cytolasm and in the nucleus.
• Cytoplasmic changes are: increases
eosinohilia, glassy appearance, granular or
vacuolated cytolasm, swollen mitochondria,
may also show calcification
• Nuclear changes: pyknosis, karyorrhexis,
karyolysis

6. What are the types of necrosis?
• Coagulation Necrosis
• Liquefactive or Colliquative Necrosis
• Fat Necrosis
• Caseous Necrosis
• Gangrenous Necrosis
• Fibrinoid Necrosis

7. COAGULATION NECROSIS
A photomicrograph of the
heart in a patient with an
acute myocardial infarction.
In the center, the deeply
eosinophillic necrotic cells
have lost their nuclei.
The necrotic focus is
surrounded by paler-staining,
viable cardiac myocytes.

8. COAGULATION NECROSIS-HEART

9. Coagulation Necrosis-wedge
shaped infarct in kidney

10. Enzymatic and Traumatic Fat
Necrosis
• Enzymatic fat necrosis is due to the action of
lipases on triglycerides resulting to
saponification.
• Adipose tissue is damaged in pancreatitis
and occasionally due to trauma
• Traumatic fat necrosis occurs in the female
breast, mesenteries and in the omentum.
There is no enzymatic lipolysis but there is
apparent rupture of the cell membrane with
release of neutral fat. Subsequent
phagocytosis of the fat follows.

11. ENZYMATIC FAT NECROSIS

12. CASEOUS NECROSIS
• This is a combination of coagulative
and liquefactive necrosis encountered
principally in the center of tuberculous
infections.
• Characteristic appearance is that of a
soft, friable, whitish-gray debris
resembling clumped cheesy material

13. CASEOUS NECROSIS

14. CASEOUS NECROSIS-LUNGS

15. TUBERCLE
• A tubercle or follicle is the diagnostic lesion
of both caseous and tuberculous conditions.
• It has 4 components:
1. A central caseous necrotic core
2. Concentrically arranged eithelioid-like cells
3. Peripheral zone of lymphocytes
4. Presence of 2 or more Langhan’s giant
cells

16. LIQUEFACTIVE NECROSIS

17. LIQUEFACTIVE NECROSIS
• Results from the action of powerful
hydrolytic enzymes and occurs when
autolysis and heterolysis prevail over
conditions that favor denaturation of
proteins
• This necrosis is characteristic of
ischemic destruction of brain tissue.
• Commonly encountered in all focal
bacterial lesions like abscesses.

19. LIQUEFACTIVE NECROSIS-
BRAIN ABSCESS

20. ABSCESS-HEART

21. DRY GANGRENE
(Raynaud’s disease and diabetic gangrene)

22. GANGRENE
• It is produced by ischemia with a superimposed
saprophytic bacterial infections
• Two types: Dry gangrene and Wet or moist
gangrene
• Dry gangrene or mummification occurs when
bacterial infection does not supervene.
• Dry gangrene may be cause by: arteriosclerosis,
Buerger’s disease, Raynaud’s disease, Ergot
poisoning

23. GANGRENOUS NECROSIS

24. Examples of Dry and Wet Gangrene
• Raynaud’s disease is more common in females and is
caused by spasmodic contraction of the arteries.
• Ergot poisoning – is caused by ergot from certain
plants that often cause dry gangrene of the extremities
• Escharotic drugs like strong acid or alkali cause dry
and moist gangrenes respectively.
• Frost bite – may cause gangrene of the fingers, toes,
nose and ears
• Carbolic acid application to a finger can cause cell
death followed by gangrene.
• Wet gangrene is seen when there is obstruction to the
venous return flow. Seen in moist areas like infections of
the mouth or the vagina. It may also result when the
mesentery of the intestines becomes twisted at the roots.

26. Apoptosis in Health
• In embryogenesis and development:
1. Loss of autoreactive response of T cells
in the thymus preventing auto-immune
attack;
2. in atrophy and involution, often on
withdrawal of hormones, e.g. menstrual
breakdown of endometrium

27. APOPTOSIS-LIVER

28. POSTMORTEM CHANGES
• Somatic death is the death of the organism or the
human body as a whole.
• Changes that occur after somatic death are:
• Algor mortis – first demontrable change. It is the
cooling of the body.
• Rigor mortis – rigidity or stiffening of the skeletal
muscles. It occurs approxiamtely 6-10 hours after
death
• Livor mortis – is the reddish discoloration of the
dependent portions of the body to a red blue color.
Blood slowly flows by gravity into the dependent
vessels which dilate because of the loss of their
muscular tone. Also caused by postmorten hemolysis.
• Autolysis and putrefaction – or softening of the
body. Eventually all the tissues of the body undergo
self-digestion at varying rates of speed called
autolysis.

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