Introduction to pathology

introduction to pathology

1. Welcome

2. INTRODUCTION TO PATHOLOGY. JOMIN GEORGE LECTURER FACULTY OF HEALTH INFORMATION MANAGEMENT Email: [email protected]

3. Learning Objectives Upon completing this chapter students should be able to: 1. Define pathology and branches 2. Know the diagnostic techniques used in pathology 3.Discuss the core aspects of disease in pathology

4. What is Pathology? Pathology is the study of disease by scientific methods. The word pathology came from the Latin words “ patho ” & “logy”. ‘ Patho ’ means disease and ‘logy’ means study, therefore pathology is a scientific study of disease . It focuses on the structural, biochemical, and functional changes in cells, tissues, and organs in disease.

5. Branches of pathology General Pathology Systemic pathology. General pathology is concerned with the basic reactions of cells and tissues to abnormal stimuli that underlie all diseases. S ystemic (organ and organ system) pathology examines the specific responses of specialized organs and tissues to more or less well-defined stimuli. 

6. Techniques Explain the whys and wherefores of the signs and symptoms

7. Is it your Fault ?? Getting Sick The patient's own fault (for having sinned) or the effects of outside agents, such as bad smells, cold, evil spirits, two major classes of etiologic factors: Genetic and Acquired

8. Disease process Molecular and morphologic changes EP MC

9. Etiology Etiology of a disease means the cause of the disease. If the cause of a disease is known it is called primary etiology . If the cause of the disease is unknown it is called idiopathic . There are two major classes of etiologic factors:  G enetic and Acquired (infectious, nutritional, chemical, physical, etc ).

10. Pathogenesis Pathogenesis means the mechanism through which the cause operates to produce the pathological and clinical manifestations or structural and functional abnormalities. The incubation period, the time between exposure to the virus and the appearance of symptoms.

11. Morphologic Changes. The morphologic changes refer to the structural alterations in cells or tissues that occur following the pathogenetic mechanisms. The structural changes in the organ can be seen with the naked eye or they may only be seen under the microscope. GROSS MORPHOLOGIC CHANGES & MICROSCOPIC CHANGES.

12. Clinical Manifestations. The morphologic changes in the organ influence the normal function of the organ . By doing so , they determine the clinical features (symptoms and signs), course, and prognosis of the disease .

13. In summary, pathology studies:- Etiology Pathogenesis Morphologic changes Clinical features & Prognosis

14. Cellular response to stress and toxins:

15. Cell Injury & Cell Death

16. Objectives Upon completion of this lecture you will be able to : be a guide to cell injury and cell death Explain the difference between reversible and irreversible cell injury. List 7 common causes of cell injury. describe the morphological changes of cell injury/death Explain the difference between necrosis and apoptosis. Describe patterns of necrosis In tissues or organs.

17. Cell Injury. If the cells fail to adapt under stress, they undergo certain changes called cell injury .

18. Reversible and irreversible cell injury The affected cells may recover from the injury (reversible) or may die (irreversible). Adapt or die!

19. Objectives Upon completion of this lecture you will be able to : be a guide to cell injury and cell death Explain the difference between reversible and irreversible cell injury. List 7 common causes of cell injury. describe the morphological changes of cell injury/death Explain the difference between necrosis and apoptosis. Describe patterns of necrosis In tissues or organs.

20. Causes of cell Injury

21. Acquired Causes Nutritional imbalance

22. O2 Deprivation Hypoxia is a deficiency of oxygen, which causes cell injury by reducing aerobic oxidative respiration . Hypoxia is an extremely important and common cause of cell injury and cell death. Causes of hypoxia include reduced blood flow (celled ischemia ) Inadequate oxygenation due to cardiorespiratory failure. decreased oxygen-carrying capacity of the blood as in anemia after severe blood loss

23. Physical Agents . Physical agents capable of causing cell injury include mechanical trauma extremes of temperature radiation

24. Chemical Agents and Drugs. Poisons , such as arsenic, cyanide, or mercuric salts, may destroy sufficient numbers of cells within minutes or hours to cause death. Other potentially injurious substances as air pollutants, insecticides, and herbicides; industrial and occupational hazards, such as carbon monoxide and asbestos. Drugs ,alcohol and the ever-increasing variety of therapeutic drugs.

25. Infectious Agents. T he rickettsiae , bacteria, fungi, and higher forms of parasites.

26. Immunologic Reactions. Autoimmunity Hypersensitivity Alopecia areata

27. Genetic Derangements. Disease may result from abnormal mutated genes or chromosomal abnormalities. 46

28. Nutritional Imbalances. Nutritional Deficiencies N utritional excesses

29. In summary , cell injury:- O2 Deprivation Physical Agents . Chemical Agents and Drugs. Infectious Agents. Immunologic Reactions. Genetic Derangements Nutritional Imbalances.

30. Morphologic Alterations in Cell Injury Swelling of the cell and its organelles Blebbing of the plasma membrane Detachment of ribosomes from the ER Clumping of nuclear chromatin. Loss of cell membrane integrity, defects in protein synthesis, cytoskeletal Damage DNA damage.

31. Reversible cell injury Cellular swelling Acute and mid Fatty changes Hypoxia Fatty liver

32. Cell Death For every cell, there is a time to live and a time to die.

33. How many times you die?

34. Clinical & biologic death Clinical death is the reversible transmission between life and biologic death. Clinical death is defined as the period of respiratory, circulatory and brain arrest during which initiation of resuscitation can lead to recovery .

35. Signs indicating clinical death are The patient is without pulse or blood pressure and is completely unresponsive to the most painful stimulus. The pupils are widely dilated Some reflex reactions to external stimulation are preserved. For example, during intubations , respiration may be restored in response to stimulation of the receptors of the superior laryngeal nerve, the nucleus of which is located in the medulla oblongata near the respiratory center. Recovery can occur with resuscitation.

36. Biological Death Biological death (sure sign of death), which sets in after clinical death, is an irreversible state of cellular destruction. It manifests with irreversible cessation of circulatory and respiratory functions , or irreversible cessation of all functions of the entire brain, including brain stem.

37. Irreversible cell injury Persistent or excessive injury “point of no return”

38. Necrosis Necrosis = Death / premature death of cells in living tissue. In necrosis, excess fluid enters the cell, swells it, & ruptures its membrane which kills it. After the cell has died, intracellular degradative reactions occur within a living organism. Narcosis???

39. In an average adult human, between 50 billion and 70 billion cells die off and are replaced every day, but necrosis refers to cell death that is unprogrammed and results from atypical body conditions, such as infections, cancer, serious injury, the presence of venom, severe inflammation , and a variety of diseases.

40. How it happens ?? I N F L A M M A T I O N

41. Necrosis does not occur in dead organisms. In dead organisms, autolysis & heterolysis take place

42. The brown recluse spider, whose bite can cause necrotic lesions up to 10 inches (25 centimeters) in diameter. Loxoscelism

43. Morphology changes Necrotic cells show increased eosinophilia. H ave a more glassy homogeneous appearance than do normal cells, mainly as a result of the loss of glycogen particles. the cytoplasm becomes vacuolated and appears moth-eaten . Dead cells may be replaced by large, myelin figures . the dead cells may ultimately become calcified.

44. Types of necrosis The types of necrosis include: 1. Coagulative necrosis 2. Liquefactive necrosis 3. Fat necrosis 4. Caseous necrosis 5. Gangrenous necrosis

45. Morphological patterns of Necrosis Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction . In coagulative necrosis the architecture of dead tissue is preserved for at least a couple of days.

46. A localized area of coagulative necrosis is called an infarct.

47. Liquefactive necrosis Liquefactive necrosis (or colliquative necrosis ) is a type of necrosis which results in a transformation of the tissue into a liquid viscous mass.. It is seen in focal bacterial or, occasionally, fungal infections. The necrotic material is frequently creamy yellow because of the presence of dead leukocytes and is called pus . For unknown reasons, hypoxic death of cells within the central nervous system often manifests as liquefactive necrosis

48. Gangrenous necrosis It is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone necrosis (typically coagulative necrosis) When bacterial infection is superimposed there is more liquefactive necrosis because of the actions of degradative enzymes in the bacteria and the attracted leukocytes (giving rise to so-called wet gangrene ).

49. Nuclear changes Karyolysis  a change that presumably reflects loss of DNA because of enzymatic degradation by endonucleases Pyknosis  characterized by nuclear shrinkage and increased basophilia . the chromatin condenses into a solid,shrunken basophilic mass. Karyorrhexis  the pyknotic nucleus undergoes fragmentation.

50. Apoptosis It is type of cell death which helps to eliminate unwanted cells--an internally SUICIDE PROGRAM series of events effected by dedicated gene products Apoptosis is the death of single cells within clusters of other cells.

51. Apoptotic cells break up into fragments, called apoptotic bodies , which contain portions of the cytoplasm and nucleus . The plasma membrane of the apoptotic cell and bodies remains intact, but its structure is altered in such a way that these become “tasty” targets for phagocytes.

52. When a cell is compelled to commit suicide , proteins called caspases go into action. They break down the cellular components needed for survival.

53. Apoptosis is not followed by inflammation or calcification. Examples: The resorption of the tadpole tail at the time of its metamorphosis into a frog occurs by apoptosis. The formation of the fingers and toes of the fetus requires the removal, by apoptosis, of the tissue between them. The sloughing off of the inner lining of the uterus (the endometrium) at the start of menstruation occurs by apoptosis

54. CAUSES OF APOPTOSIS Apoptosis occurs normally both during development and throughout adulthood, and serves to eliminate unwanted, aged or potentially harmful cells. It is also a pathologic event when diseased cells become damaged beyond repair and are eliminated.

55. Apoptosis in Physiologic Situations During development for removal of excess cells during embryogenesis To maintain cell population in tissues with high turnover of cells, such as skin, bowels. Hormone-dependent involution - Endometrium, ovary, breasts etc . Elimination of potentially harmful self reactive lymphocytes.

56. To remove damaged cells by virus To eliminate cells with DNA damage by radiation, cytotoxic agents etc. Cell death in tumours Apoptosis in Pathologic Situations

57. Features of Necrosis and Apoptosis Table – 12 . Refer it.

58. In summary , cell Death:- cell death Necrosis Types. M&N changes Apoptosis P&P situation Features.

59. Autophagy Autophagy is a process in which a cell eats its own contents. It is a survival mechanism in times of nutrient deprivation. In this process intracellular organelles and portions of cytosol are first sequestered from the cytoplasm in an autophagic vacuole, which subsequently fuses with lysosomes to form an autophagolysosome , and the cellular components are digested by lysosomal enzymes

60. Intracellular Accumulations DEFINITION : Accumulation of abnormal amounts of various substances due to manifestations of metabolic derangements in the cell.

61. CATEGORIES: 1. Normal cellular constituents e.g., water, lipids, CHO. 2. Abnormal substances a) Exogenous  Substance accumulate because the cell can neither degrade the substance nor the ability to transport it to other sites. e.g., mineral or products of infectious agents

62. b) Endogenous  Substance that cannot be metabolized because of deficiency or defect of the enzyme and accumulate in cells. e.g., products of abnormal synthesis or metabolism

63. CHLOASMA  Tan or brown pigmentation commonly associated with pregnancy or the use of oral contraceptives . Also called the mask of pregnancy or melasma .

64. Steatosis ( Fatty Changes) The terms steatosis and fatty change describe abnormal accumulations of triglycerides within parenchymal cells.

65. Organs Involved & Causes Fatty change is often seen in the liver because it is the major organ involved in fat metabolism, but it also occurs in heart, muscle, and kidney. Disorder with heoatocyte damage. The causes of steatosis include toxins, protein malnutrition, alcohol and anoxia Disorder with Hyperlipidemia. diabetes mellitus and obesity.

66. Assignment. proteins, Glycogen, Pigments ,Hyaline Change Endogenous and Exogenous Constituents