1. Introduction to Basic Pathology; Cellular Reaction to Injuries`
Dr. ROOPA
Pathophysiology
Premed 2

2. Basic Pathophysiology
Basic Pathology
Basic Microbiology
Bacteriology
Virology
Mycology
Immunology
Basic Pharmacology

3. What is Pathology?

4. Pathology Branch of Medicine Studies the underlying causes of diseases
“etiology”
Mechanisms that result in the signs and symptoms of the patient
“pathogenesis”

5. Pathology Bridge between basic science and clinical practice
“study of suffering”
Divisions:
General Pathology
Systemic Pathology

6. The Cell

7. How do cells react to environmental stress?
Hypertrophy
Hyperplasia
Aplasia
Hypoplasia
Atrophy
Metaplasia

8. Hypertrophy Increase in protein synthesis/ organelles
Increase in size of cells
Increase in organ/tissue size

9. Hypertrophy

10. Hyperplasia Increase in NUMBER of cells
Increase in size of organ/tissue
Similar end result as hypertrophy
May occur with hypertrophy

11. Hyperplasia

12. Aplasia Failure of cell production
Agenesis or absence of an organ:fetus
Loss of precursor cells:adults

13. Aplasia

14. Hypoplasia
Decrease in cell production

15. Atrophy Decrease in mass of preexisting cells Smaller tissue/organ
Most common causes:
disuse
poor nutrition
lack of oxygen
lack of endocrine stimulation
aging
injury of the nerves

16. Atrophy

17. Metaplasia Replacement of one tissue by another tissue Several forms:
Squamous metaplasia
Cartilaginous metaplasia
osseous metaplasia
myeloid metaplasia

18. Metaplasia

19. DEFINITION- DYSPLASIA
Dysplasia means disordered growth, most commonly seen in squamous epithelial cells following chronic injury.

20. What are the causes of injury/stress?
Hypoxic cell injury
Free radical injury
Chemical cell injury

21. Hypoxic cell injury Complete lack of oxygen/ decreased oxygen
Anoxia or hypoxia
Causes:
ischemia
anemia
carbon monoxide poisoning
decrease tissue perfusion
poorly-oxygenated blood

22. Hypoxic cell injury

23. Early stage Hypoxic cell injury
Decrease in production of ATP
Changes in cell membrane
Cellular swelling
endoplasmic reticulum
mitochondria
Ribosomes disaggregate
Failure of protein synthesis
Clumping of chromatin

24. Late stage
Cell membrane damage
myelin blebs
cell blebs

25. Cell Death Irreversible damage to the cell membranes Calcium influx
Mitochondria calcifies
Release of cellular enzymes
Most vulnerable cells:
neurons

26. Free radicals: superoxide and hydroxyl radicals
Seen in:
normal metabolism
oxygen toxicity
ionizing radiation
UV light
drugs/chemicals
ischemia

27. Mechanisms to detoxify free radicals
Glutathione
Catalase
Superoxide dismutase
Vitamin A, C, E
Cysteine,glutathione, selenium, ceruloplasmin
Spontaneous decay

28. Chemical Injury
Carbon tetrachloride and liver damage

29. NECROSIS AND APOPTOSIS
sum of the morphologic changes that follow cellular death in the tissue or organs.
Mainly 2 processes cause the morphologic changes of necrosis;
Denaturation of proteins
Enzymatic digestion of organelles n other cytosolic components.

30. Autolysis – cell digestion due to hydralytic enzymes derived from dead cells.
Heterolysis ; derived from invading inflammatory cells.

31. Types of necrosis Coagulative necrosis Liquefactive necrosis
Caseous necrosis
Gangrenous necrosis
Fibrinoid necrosis
Fat necrosis

32. Coagulative necrosis Interruption of the blood supply
Commonest form of necrosis
Poor collateral circulation
heart
kidney
Characteristic nuclear changes
pyknosis
karyorrhexis
karyolysis
disappearance of a nuclei

33. NUCLEAR CHANGES
Karyolysis- disintegration and dissolution of a cell nucleus when a cell dies
Due to DNA se activity
Basophilia of chromatin fade

34. NUCLEAR CHANGES Pyknosis – a degenerative state of the cell nucleus
-Nuclear shrinkage
- Increased basophilia
Karyorrhexis – nuclear fragmentation
within 1 or 2 days nucleus disappears.

35. Coagulative Necrosis

36. Liquefactive necrosis
Is typically found in the brain or in an abscess. Tissue is softened through the action of enzymes released from brain or in the case of an abscess, PMN.

37. Liquefactive necrosis

38. Caseous necrosis Coagulative + liquefactive “cheese - like”
Part of granulomatous inflammation
Classic picture:
Tuberculosis

39. Caseous necrosis

40. Gangrenous necrosis
Interuption of the blood supply to the lower extremities or bowels
Wet type: complicated by liquefactive necrosis
Dry type: complicated by coagulative necrosis

41. Gangrenous necrosis

42. Fibrinoid necrosis Immune-mediated vascular damage
Protein – like material in the blood vessel walls

43. Fat necrosis Traumatic fat necrosis – after injury Breast
Enzymatic fat necrosis – after inflammation
Pancreas

44. FAT NECROSIS

45. APOPTOSIS -”Programmed cell death”
Occurs when a cell dies through the activation of an internal suicide program.
This is mainly useful in eliminating the unwanted cells with minimal disruption of the surronunding tissue.
Can be seen mainly in the elimination of unwanted cells during embryogenesis.

46. Necrosis versus apoptosis
Gross irreversible cell injury
Passive form of cell death
Does not require genes, protein synthesis
Marked inflammatory reaction
Physiologic programmed cell removal
Active form of cell death
Requires genes, proteins, energy
No inflammatory reaction

47. Genes affecting apoptosis
Inhibits:
bcl-2
Facilitates:
bax
p53

48. Morphological features in apoptosis
Involves small clusters of cells only
No inflammatory cells
Cell membrane blebs
Cytoplasmic shrinkage
Chromatin condensation
Phagocytosis of apoptotic bodies