Intro to Patho by medicine 2 lecture files

med 2 lecture file

1. Introduction to Pathology
Cell Adaptation, Injury and Death
By Noel C. Santos, M.D.

2. LEARNING OBJECTIVES

3. Introduction to Pathology
•Define Pathology
•Give the two main divisions of
Pathology
•Give the four aspects of
disease process

4. Cell Adaptation
•Define and review the concept
of normal homeostasis
•Define cellular adaptation
•Give the six types of adaptive
response that may occur in a
cell

5. Cell Injury
•Define cell injury
•Enumerate the general categories of the cause of cell injury
•Give the two main phase of cell injury
•Give the basic principles of cell injury
•Give the general biochemical mechanisms of cell injury
•Discuss the events that occur during ischemia with hypoxia
•Discuss the events that occur during ischemia with
reperfusion
•Discuss the events that occur in free radical-induced cell injury
•Discuss the mechanisms of chemical injury
•Give the morphologic changes that occur during reversible cell
injury
•Enumerate and discuss each of the subcellular responses to
cell injury

6. Cell Death
•Define cell death
•Give the principal patterns of cell death in response to
lethal and/or acute cell injury
•Discuss the causes, biochemical features and
mechanisms of apoptosis
•Give examples of apoptosis
•Give the morphologic changes of cells that undergo
apoptosis
•Give the morphologic changes that occur during
irreversible cell injury and cell death
•Enumerate the morphologic types of necrosis, and give
examples
•Give the morphologic cellular alterations in response to
sublethal and/or chronic cell injury

7. Pathology
Definition:
“pathos” = “suffering” or “disease”
“logos” = “study”
“study of diseases”
-study of the structural and
functional causes of human
disease.

8. Main Divisions of Pathology
1.BASIC or GENERAL PATHOLOGY
2.SYSTEMIC PATHOLOGY
-CLINICAL PATHOLOGY
-ANATOMIC PATHOLOGY
-PATHOPHYSIOLOGY
-SURGICAL PATHOLOGY

9. Four Aspects of Disease Process
1.ETIOLOGY –cause of a disease
2.PATHOGENESIS –mechanism/s of
disease development
3.MORPHOLOGIC CHANGE –
structural alterations induced in cells,
tissues, organs, systems, body
4.FUNCTIONAL DERANGEMENT and
CLINICAL SIGNIFICANCE –
functional consequences of the
morphologic changes

10. PATHOLOGY……..

11. HOMEOSTASIS
“steady state –normal function where
there is a balance between
physiologic demands and the
constraints of cell structure and
metabolic capacity.”
MAINTAINED STATE OF VIABILITY
OR VITALITY

12. THE CELL
-Can alter their functional state in
response to modest stress, maintain
the steady state
-More excessive physiologic stresses
or adverse pathologic stimuli
-ADAPTATION
-INJURY: Reversible or Irreversible
-DEATH

13. Normal
Cell
Cell
Adaptation
Cell Injury
Reversible Irreversible
Cell Death
Hypoxia
Infectious
Chemical
Physical
Immunologic
Genetic
Nutritional Imbalance

15. ADAPTATION
-Stressful stimuli induce a new state
that changes the cell
-Preserves the cell’s viability
-HYPERPLASIA
-HYPERTROPHY
-ATROPHY
-INVOLUTION
-METAPLASIA
-DYSPLASIA

18. Muscle -ischemic atrophy:

20. LVH -Heart in
Hypertension:
Left Ventricular Hypertrophy

21. Goitre –Iodine Deficiency

22. Renal Artery stenosis -Atrophy
Nephrosclerosis Atrophic Kidney

23. CELL INJURY
-REVERSIBLE
-Pathologic cell changes that can be
restored to normal state
-IRREVERSIBLE
-Stress exceeds the capacity to adapt
-“point of no return”
-Permanent changes –DEATH

33. CELL DEATH
-2 patterns
-NECROSIS
-Always pathologic
-Severe cell swelling
-Denaturation and coagulation of proteins
-Breakdown of cellular organelles
-Cell rupture
-Large number cells in the adjoining tissue are
affected
-APOPTOSIS
-May be physiologic
-Activation of internal “suicide” program
-Orchestrated disassembly of cell components
-Minimal disruption of the surrounding tissue
-Chromatin condensation/fragmentation

35. Morphologic Types of Necrosis
•Coagulation
•Liquefaction
•Caseation
•Enzymatic Fat

39. Cerebral Infarction (Stroke) :
Haemorrhagic
Necrosis

40. Normal & Ischemic -kidney tubule
Microvilli

41. Renal Infarction -Coagulative

42. Infarct Adrenal gland:

43. Caseous necrosis
Tuberculosis
hilar lymphnode

44. Extensive
Caseous necrosis
Tuberculosis

45. Splenic Infarction -Coagulative necrosis

46. Stroke-Liquifactive necrosis

47. Liver abscess: Liquifactive necrosis

48. Gangrene Intestine -Thrombosis.

49. Gangrene -Diabetic foot

50. Gangrene -Amputated Diabetic foot

51. Ageing

52. Ageing:
“Progressive time related loss of
structural and functional capacity of
cells leading to death”
•Senescence, Senility, Senile changes.
•Ageing of a person is intimately related
to cellular ageing.
•Countdown starts with birth…!

53. Factors affecting Ageing:
•Genetic –Clock genes,
(fibroblasts)
•Diet –malnutrition, obesity etc.
•Social conditions -
•Diseases –Atherosclerosis,
diabetes etc.
•Genetic disease -Werner’s
syndrome.

54. Telomerase in ageing:
Germ
Cells
Somatic
Cells

55. Cellular ageing mechanisms:
•Nuclear:
–Reduced synthesis of nucleic acids
–Telomere shortening
–Clock genes
•Metabolic:
–Reduced Mitochondrial oxidative reactions
–Reduced protein synthesis, Protein cross
linking.
–Decreased cell receptors, transcription factors.
–Oxidative peroxidation of organelles.

56. Ageing –Morphologic
changes:
•Loss of skin elasticity
•Easy bruising –fragile capillaries.
•Glycosylation of lens proteins –
•Accumulation of Lipofuscinpigment
–Brown atrophy.

57. Normal Brain surface:

58. Cerebral atrophy -Alzheimers:

59. Elastosis of skin:

60. Pathology
of Ageing

61. Conclusions:
•Cellular Injury -Various causes
•Reversible Injury -Adaptations
–Hypertrophy, Hyperplasia, Atrophy
–Accumulations -Hydropic, hyaline, fat..
•Irreversible Injury -Necrosis
–Coagulative, Liquifactive, Caseous, fat…
•Ageing: Physiological & pathological.
–Time related, several theories.

62. Thank You