Fate of dead cells

1. ‫الرحيم‬‫الرحمن‬‫هللا‬ ‫بسم‬

2. Fate of dead cells
Supervision : Dr. Nahla Kamel
2017-2018

3. NECROSIS
Done by: Anas Darwish
ID: 1432

4. NECROSIS
Necrosis result mainly from:
I. Denaturation of proteins
II. degradative action of enzymes on lethally injured cells
 The enzymes responsible for digestion of the cell may
be derived from:
a. The lysosomes of the dying cells themselves
b. The lysosomes of leukocytes that are recruited
as part of the inflammatory reaction to the
dead cells.

5. Morphological changes of necrosis:
 GROSSLY

6. 1-Cytoplasmic changes:
 MICROSCOPICALY

8. 2-Nuclear changes

10. types of necrosis
 COAGULATIVE Necrosis
 Liquefactive Necrosis
 Caseous Necrosis
 Gummatus Necrosis
 Fat Necrosis
 Fibrinoid Necrosis

11. Coagulation Necrosis
 Done by: Amjad Elloh
ID: 1434

12. COAGULATIVE NECROSIS
• “In this type of necrosis, the necrotic cell retains its cellular outline for
several days”
Examples
A-solid organs "heart, adrenals, kidney" in blood supply & anoxia.
B-liver cells in viruses or toxic chemicals
C-Skin in burns.
D-Ischemic infarcts except brain & spinal cord

13. Morphology
1-Gross
• opaque
• Pale
• Firm
• Triangular, cone, fan
shaped dt distribution of
arterial blood supply.
• Base to out side.
• Apex toward occluded
vessels (hilum of organ(
Necrotic area

14. • Coagulated mass .
• Acidophilic or eosinophilic .
• Pink homogenous cytoplasm .
• Retains its cellular outlines .
• Nucleus changes & disappears
• Preservation of tissue architecture.
2-Microscopic Necrotic cell

15. Liquefactive necrosis
Done by:Mansour balla
ID: 1433

16. Liquefactive necrosis
• Description, Causes and Risk Factors:
A type of necrosis characterized by a fairly well-circumscribed, microscopically or
macroscopically visible lesion that consists of the dull, opaque or turbid, gray-white to
yellow-gray, soft or boggy, partly or completely fluid remains of tissue that became
necrotic and was digested by enzymes, especially proteolytic enzymes liberated from
disintegrating leukocytes;
liquefactive necrosis is a type of necrosis which results in a transformation of the
tissue into a liquid viscous mass. Often it is associated with focal bacterial or fungal
infections.

17. In liquefactive necrosis, the affected cell is completely digested by hydrolytic
enzymes, resulting in a soft, circumscribed lesion consisting of pus and the fluid
remains of necrotic tissue. Dead leukocytes will remain as a creamy yellow pus. After
the removal of cell debris by white blood cells, a fluid filled space is left. It is generally
associated with abscess formation and is commonly found in the central nervous system
(CNS).
Liquefactive necrosis develops when enzymatic digestion is the dominant pattern.
It is due to the destructive effects of lytic enzymes generated by neutrophils and
macrophages in infected tissues. The ultimate result of proteolytic digestion is
liquefaction of Liquef

18. • necrotic tissue. A bacterial abscess filled with collections of fluid pus is an
example of liquefactive necrosis. Bacterial infection is the principal cause of
liquefactive necrosis but not the only one. For obscure reasons, ischemic injury
within the central nervous system after arterial occlusion evokes liquefactive
necrosis
The dead brain tissue is softened and converted into a liquid viscous mass. As time
passes, there develops a cystic space filled with clear fluid, the walls of which are
defined by non-necrotic tissue

19. Denaturation of protein < Enzymatic digestion
Characteristics:
rapid liquefaction of necrotic cell by lysosomal enzyme
Mechanism :
Increase role of digestive lysosomal enzymes on necrotic cells

20. Gross:
necrotic tissue :
softened.
liquefied.
whole tissue
semi liquid.

21. In irreversible cell injury :
when enzymatic digestion is the cause of the death
This causes cell destruction in one of two ways
Autolysis : lysosomes of dead cell itself
Hetrolysis : lysosomes of invading inflammatory cells
TISSUE ARCHITECTURE IS LOST

22. Examples:-
Brain and spinal cord following ischemia
“autolysis“
due to very sensitive and fragile structure.
suppurative inflammation " heterolysis“
cellular lysis by enzymes derived from a source
Specific type of cell
specific cause of death

23. Caseous Necrosis&
Gummatus Necrosis
Done by: Majd Emad
ID: 1435

24. Caseous Necrosis
• found in the centre of foci of tuberculous infections.
• It combines features of both coagulative and liquefactive necrosis.
• term "caseous" (cheeselike) is derived from the friable yellow-white
appearance of the area of necrosis.

25. Morphology
The necrotic areas appear dry,
cheesy, soft and
yellowish
GROSS

26. The necrosed foci are structureless ,granular eosinophilic The
surrounding tissue shows chacteristic granulomatous reaction
Microscopy

27. Gummatus Necrosis
Characteristics: as caseous coagulative combined &
followed by Liquefactive necrosis.
Cause : 3rd stage syphilis affecting anywhere as liver,tongue & testis .

28. Morphology
.
Gross : necrotic area pale yellow-gray & rubbery in consistrncy
Microscopic: Amorphous , graunlra , structure less , eophilic debris surrounded sinoby inflammatory reaction

29. Fat necrosis&
Fibrinoid necrosis
Done by: Abd EL Rahman Odeh
ID: 1436

30. Fat necrosis
Affected tissue: Adipose tissue.
Etiology :
•physical trauma
•release of lipases from the affected tissue
•history of radiation to a particular area of tissue
•history of surgery to a particular area
•history of removal of breast implants.
Types:
•Enzymatic
•Traumatic

31. Enzymatic Fat Necrosis
focal enzyme necrosis of pancreatic fat and vessels necrosis - hemorrhage-
occur after acute hemorrhagic pancreatitis due to release of lipases.
Morphology:
Grossly Microscopically

32. Traumatic Fat Necrosis
This type is common in the breast and subcutaneous fat after trauma, like a
punch or knock to the breast . The trauma cause disruption of the cell
membrane leading to release of the fatty acids.
Morphology:
Grossly Microscopically

33. Fibrinoid necrosis
Is a special form of necrosis, visible by light microscopy, usually in immune reactions, in
which complexes of antigens and antibodies are deposited in the walls of arteries.
Fibrinoid necrosis is usually seen in immune reactions involving blood vessels, known as
Type III hypersensitivity reactions.
Affected tissue: Connective tissue.
Common sites undergoing fibrinoid necrosis are
SLE, polyarteritis nodosa , poststreptococcal glomerulonephritis, hyperacute rejected
grafts.

34. Morphology:
The deposited immune complexes,
together with fibrin that has leaked
out of vessels, produce a bright pink
and amorphous appearance on H&E
preparations called fibrinoid (fibrin
like)

35. Diagnosis and fate of
Necrosis
Done by:• Diab Diab
ID: 1437

36. Diagnosis
Necrosis is a type of irreversible cell injury which results in the
premature death of cells in living tissue by autolysis.

37. Fate of nectosis

40. Apoptosis
Done by:Layan Mohammad
ID: 1438

41. Apoptosis

42. Definition
a process of active self destruction and
programmed cell death affecting scattered single
cell which are aged or abnormal with rapid
elimination of it.

44. Why should a cell commit suicide?
There are two different reasons.
1. Programmed cell death is as needed for proper development as mitosis is.
Example
2. Programmed cell death is needed to destroy cells that represent a
threat to the integrity of the organism.
Example

45. Mechanism of Apoptosis:
Apoptosis is results from the activation of enzymes called caspases.
Caspases can be activated by two pathways
i. Mitochondrial/Cytochrome pathway:
ii. Tumour-necrosis factor-receptor (TNF)
pathway:
In this pathway the ligation of members
of the TNF-receptors takes place,
activating caspase-8 and then caspase-3
which leads to apoptosis.

46. Differentiation between
Necrosis and Apoptosis
Done by:Saqr Obeid
ID: 1439

47. Differentiation between Necrosis and Apoptosis
• Necrosis
1. Premature cell death and living tissue.
2. Cellular enzymes leak out and ultimately digest the cell.
3. Enzymes responsible for digestion of the cell are derived from lysosomes and may come from the dying
cells themselves or from leukocytes recruited as part of the inflammatory reaction.
• Apoptosis:
1. Programmed cell death.
2. cells activate enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins.
3. Fragmentation of the apoptotic cells into apoptotic bodies.
4. The dead cell and its fragments are cleared by phagocytosis.

48. 1. Pathologic
(culmination of
irreversible cell injury)
1. Often physiologic, may
be pathologic after some
forms of cell injury
2. Frequently
accompanied by
inflammation
2. NOT accompanied by
inflammation
3. Enlarged (Swelling)
cell
3. Shrinkage of cell
4. Nucleus:
Pyknosis - Karyorrhexis
- Karyolysis
4. Nucleus:
Karyorrhexis
5. Disrupted plasma
membrane
5. Intact plasma membrane.
(Cell fragmented into
Apoptotic bodies)
6. Enzymatic digestion of
the cellular contents.
(May leak out of the
cell)
6. Intact cellular
components. (May be
released in apoptotic
bodies)
Necrosis Apoptosis

49. Feature Necrosis Apoptosis
Cell size Enlarged (swelling) Reduced (shrinkage)
Nucleus Pyknosis which may be followed by
Karyorrhexis and ultimately Karyolysis.
Fragmentation into
nucleosome-sized
fragments (Karyorrhexis)
Plasma membrane Disrupted
Intact
Cellular contents Enzymatic digestion; may leak out of
cell.
Intact; may be released in apoptotic bodies.
Adjacent inflammation Frequent No
Physiologic or pathologic role Invariably pathologic (culmination of
irreversible cell injury)
Often physiologic means of eliminating unwanted
cells; may be pathologic after some forms of cell
injury, especially DNA and protein damage.

50. Gangrene
Done by: Esraa Ibrahim
ID: 1440

51. Gangrene
TypesDefinition
Causes

52. *Gangrene
• It is a localized death with putrefaction of body tissue resulting from obstructed
circulation or bacterial infection.
Causes
Atherosclerosis Obesity

53. Peripheral
arterial disease Smoking
Diabetes
mellitus

54. Trauma or
serious injury
Raynaud’s
Disease

55. Types of gangrene
Dry gangrene Gas gangreneWet gangrene

56. -More common in people with atherosclerosis
Dry gangrene
-This happen when blood flow is blocked in given area of the body ( poor
circulation ).
-Morphology:
-May be brown to purplish-blue to black & often falls off.
-Infection NOT present.

57. Symptoms
Dry and
shriveled skin
Cold and numb
skin
foul odour

58. Lines of Demarcation & Separation
Demarcation line Separation line
It is the line the dead & living
tissue.
It is the line appears toward the
gangerous part which is responsible
for autoamputation.

59. Demarcation line
Separation line
Treatment
-Surgery (Amputation)

60. Done by: Hussam Akkash
ID: 1441
Wet Gangrene

61. Wet gangrene(moist gangrene)
Causes:
Due to sudden complete obstruction of arterial supply usually
preceded by obstruction of veins and lymphatics, Resulting from :
burning by heat or acid .
severe freezing .
physical accident that destroys the tissue (cut) .
embolism
intussusception
embolism

62. also it may be results from a gradual decrease in the blood supply (as from
tumor, diabetes or arteriosclerosis).
arteriosclerosis
tumor

63. It is mostly found in naturally moist tissue and organ ( internal organs) where
there is excessive tissue fluids such as :
Site:
intestine, lung, cervix and mouth . also it may occur in limbs and skin of back ( bedsores) , in diabetic
patients

64. Type of wet gangrene :
1-Moist gangrene of intestine .
2-Moist gangrene of alimb .
3-Moist gangrene of the skin of the back
(bed_sores).
4-Cancrum oris .
5-Moist gangrne of lung .

65. What are bed sores?
It also called pressure sores, it is an injury to the skin caused by constant pressure
over a period of time. The constant pressure blocks the blood supply to the skin.
This causes skin cells to die and creates a sore.
Moist gangrene of the skine of back
(bed sore)

66. Site:
bedsores usually occur over bony areas, such as the hips, lower back,
elbows, heels, and shoulders. Pressure sores can also occur in places
where the skin folds over on itself.

67. Stages of bedsores:
appear as sun burn on the skin formulation of a blister and open sore.
involves a hole, or a depression in the skin Excessive tissue damage , exposure of bone , muscles or nerve

68. Done by:Ismail Khaled Sa’adeh
ID: 1442
Moist Gangrene of intestine
and limbs

69. Moist gangrene of intestine
•Definition: it occurs due to compression of the blood
vessels, the lymphatic's and veins are compressed before the
arterial occlusion as in strangulated hernia, volvulus, or
intussusceptions.

70. Morphologic feature:
1.Grossly:

71. Histologically:

72. Moist gangrene of limbs
•Definition: it usually occurs in diabetic
patients, initiated by mild trauma that starts in
big toe, its dry but soon becomes wet due to
hyperglycemia and diminished resistance.

73. Grossly:

74. cancrum oris&
Differences between dry
& wet gangrene
Done by: Mohammed Ayham
ID: 1443

75. cancrum oris
• A devastating disease which destroys the soft
and hard tissues of the oral and Para-oral
structures.
• Involve the mandible, maxilla, and nose, and
it occasionally extends to the infra orbital
margins .

76. Etiology
Bad oral hygiene Weak immune system Measles
Typhoid Malaria HIV

77. Clinical feature :
1. A tender, small red spot on the gingiva , which quickly becomes indurated, ulcerated
and then becomes necrotic .
2. Sore mouth with focal edema having fetid odour and taste .

78. 3. Purulent oral discharge is associated with profuse salivation.
4. Anorexia

79. Differences between dry & wet gangrene
Feature Dry Wet (moist)
Site Commonly limbs More common in bowel
mechanism Arterial occlusion arterial obstruction preceded
by venous occlusion
Microscopy Organ : dry , shrunken and
black
Part : moist , soft , swollen ,
rotten and dark
Line of
demarcation
Present at the junction between
healthy and gangrenous part
No clear line of demarcation

80. Gas Gangrene
Done by: Qusai Sayah
ID: 1444

81. What is gas gangrene ?
• Special form of wet gangrene caused by bacteria.
• Occurs mainly in muscles & wounds.
• Fast progression with toxemia.

82. Morphology
• Grossly:
• Swelling
• Oedematous
• Crepitant
• Painful
• Black + bad smelling

83. Microscopically:
• Coagulative necrosis
• Gram + bacilli
• Leucocytic infiltration

84. Fate
• Myonecrosis
• Sepsis
• Shock
• Treatment : amputation

85. THANK YOU