simple presentation especially for students

1. Cell injury , Cell Death and
Adaptation
DR ALIYA ZAMAN

2. PATHOLOGY
 Study of
structural
biochemical
functional
Changes in cell

3.  By using
morphological
microbiological
immunological
molecular
techniques

4. PATHOLOGY EXPLAIN
1. Causation
2. Biochemical and molecular
mechanism
3. Morphologic changes
4. Functional alterations

5. Etiology
Initiating cause of
disease
Genetics
Inherited or acquired
mutation
Polymorphism
Environmental
1,infectional
2,nutriional
3,chemical
Physical

6. Pathogenesis
 Sequence that leads to disease
• Molecular
• Biochemical
• Cellular events

7. Morphological changes

8. Clinical manifestation

9. Rudolf Virchow

10. Cellular basis of disease
A person is sick
because cell is sick

12. Cellular responses to stress and
noxious stimuli

14. CELL INJURY
If the limits of responses are
exceeded or if cells are exposed
to damaging insults ,deprived of
critical nutrients or compromised
by mutations that affects essential
cellular function a sequence of
events follows that termed as
CELL INJURY

15. Causes of cell injury
1, Oxygen deprivation
hypoxia
ischemia
CVS failure
Anemia
Severe blood loss
2, physical agents
mechanical trauma
extreme of temperature
atmospheric pressure
radiation
electric shock

16. 3, Chemical agents ,drugs
oxygen
arsenic,cyanide
eniv pollutants
insecticides
herbicides
CO, asbestos
alcohol
4, Infectious Agents
viruses, bactereia, tapeworm, fungi ,rickettsiae
5,Immunologic reaction
AUTOIMMUNE DISEASE
VIRUSES AND ENVIRONMENTAL

17. 6, Genetic abnormalities

18. 7, Nutritional imbalance
protein calorie deficiencies
anorexia nervosa
poor food diet
obesity
diet high in certain lipids

19. The progression of cell injury and
death

20. Outcome of cell injury

21. Reversible cell injury
It is characterized by functional
structural alterations in early stages or
mild forms of injury which are
correctable if the damaging stimulus is
removed

23. Morphological features of
reversible injury
1. Plasma membrane alterations
2. Mitochondrial changes
3. Accumulation of myelin figures
4. Dilation of ER with detachment of
polysomes
5. Nuclear alterations with
disaggregation of granular and fibrilar
elements

24. Cell Death

26. Necrosis
Characterized by denaturation of
cellular proteins ,leakage of cellular
contents through damaged
membranes, local inflammation and
enzymatic digestion of the lethally
injured cells
Inflammation
Detected in blood

27. Mechanisms of cell injury:
 Depletion of ATP
 Mitochondrial Damage
 Influx of Ca2+ and loss of Calcium
Homeostasis
 Accumulation of Oxygen Derived Free
Radicals (Oxidative Stress)
 Defects in Membrane Permeability
 Damage to DNA and Proteins

28. Mitochondrial damage
1, Mitochondrial damage often results in
the formation of a high-conductance
channel in the mitochondrial
membrane, called the mitochondrial
permeability transition pore

32.  Necrosis associated with leakage of
itracellular protein through damaged
plasma membranes and ultimately in
circulation
eg troponin from cardiac muscles
alkaline phosphatase from bile duct
transaminase from hepatocyte
Early diagnoses early management can
save life

35. Two points consistently observed
1. Inability to reverse mitochondrial
dysfunction
2. Profound disturbances of in
membrane function

36. Morphological patterns of
necrosis

37. Coagulative necrosis
 Architecture of dead tissue preserved
 A localized area of necrosis is called
an infarct
 Affected tissue has firm texture
 After some time these cells broken
down because of???

40. Liquefactive necrosis
 Digestion of dead cells
 Necrotic material become creamy
yellow called pus
 Hypoxic cells of brain often manifest
as liquefactive necrosis
 Contents of pus?

42. Gangrenous necrosis
 Specific pattern of cell death but term
used in clinical practice
 Usually applied to limb
 If superimposed by bacterial infection
there is more liquefactive necrosis
called wet gangrene

45. Caseous necrosis
Necrotic area appears as a
structureless collection of fragmented
or lysed cells and amorphous granular
debris enclosed within distinctive
inflammatory bodies this appearance
of a focus of inflammation known as
granuloma

49. Fat Necrosis
 Refer to focal area of fat destruction
typically due to release of pancreatic
enzymes
 It is grievous condition
 Pancreatic enzyme liquify the membrane
of fat cells in peritoneum releasing
triglyceride esters that are split by
pancreatic lipase
 Fatty acid produced that combine with
calcium to produce grossly visible chalky
white areas called fat saponification and
due to this underlying cause cant be
identefied

53. Fibrinoid necrosis
 Special type of vascular damage
occurs due to immune reaction in
blood vessels
 Complex of antigen antibodies formed
and deposit in wall
 These immune complexes along with
plasma protein that leaked out from
vessels