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11.20 (dr. yasmeen hashim) apoptosis (mechanism in normal tissues. programmed cell death) necrosis cancer cell growth
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11.20 (dr. yasmeen hashim) apoptosis (mechanism in normal tissues. programmed cell death) necrosis cancer cell growth

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  • 1. APOPTOSIS, NECROSIS and CANCER
  • 2. LEARNING OBJECTIVES
    • At the end of the lecture, students should be able to:
    • Know the importance of cell death.
    • Define various modes of cell death.
    • Identify features of necrosis, apoptosis.
    • Differentiate between necrosis and apoptosis.
    • Define cancer
    • Describe the mechanism
    • of cancer development
  • 3. CELL DEATH
    • Cells are born,
    • live for a given period of time
    • an d then die
    • Bowen, 1998
  • 4. Cell Injury
    • A cell maintaining a steady state called Homeostasis
  • 5. Cell Injury
    • Altered Homeostasis
  • 6. To die or not to die?
    • Integrated balance between positive survival factors and negative death signals decides fate of cell
  • 7.  
  • 8. CELL DEATH
    • The 100 trillion cells of the body are members of a highly organized community
    • The total number of cells is regulated by ;
    • controlling the rate of cell division and
    • controlling the rate of cell death.
    • Cells die by one of two mechanisms
    • Necrosis or
    • Apoptosis
    • Two physiologically different processes
    • Apoptosis and necrosis have different characteristics
  • 9. APOPTOSIS
    • Apoptosis is an energy dependent
    • programmed cell death
    • for removal of unwanted individual cells
  • 10.
    • Programmed cell death during embryogenesis
    • Formation of free and independent digits
    • Development of the brain
    • Development of
    • reproductive organs
    • Programmed cell death
    • during adult stage
    • Cell loss in proliferating
    • cell populations
    • Death of cells that have served
    • their useful purpose
    • Elimination of harmful self- reacttive lymphocytes
    APOPTOSIS IN PHYSIOLOGIC SITUATIONS
  • 11.
    • Chronic viral diseases
    • Neurodegenerative diseases
    • Reperfusion injury
    • Insulin-dependent Diabetes
    • Atherosclerosis
    • Myo c ard ial Infarction
    • AIDS
    • Development and Treatment of Malignancies
    • onic viral diseases
    • ...
    APOPTOSIS IN PATHOLOGICAL SITUATIONS
  • 12. THE MECHANISMS OF APOPTOSIS
    • This process involves a specific proteolytic cascade
    • There are 3 different mechanisms by which a cell commits suicide by apoptosis
    • by signals arising within the cell;
    • by death activators binding to receptors at the cell surface:
      • TNF-α
      • Lymphotoxin
      • Fas ligand ( FasL )
    • third that may be triggered by dangerous reactive oxygen species.
  • 13. APOPTOSIS ; MORPHOLOGIC CHANGES
    • Early : Chromosome condensation, cell body shrink
    • Later : Membranes become irregular- Blebbing ;
    • Nucleus and cytoplasm fragment- Apoptotic bodies
    • At last : Phagocytosed
  • 14. Membrane blebs during apoptosis
  • 15. THE ENZYMATIC REGULATION OF APOPTOSIS
    • Apoptosis is initiated by activation of a family of
    • proteases called caspases.
    • These are enzymes that are synthesized and stored in the cell as inactive procaspases.
    • once activated, the enzymes cleave and activate other procaspases, triggering a cascade that rapidly breaks down proteins within the cell
    • The cell thus dismantles itself, and its remains are rapidly digested by neighboring phagocytic cells .
  • 16.
    • Excessive apoptosis
    • Uncontrolled cell loss
  • 17. Diseases featuring excessive apoptosis
    • Neurodegenerative
      • Parkinson’s disease
      • Alzheimer's disease
      • Amyotrophic lateral sclerosis (ALS)
      • Huntingdon’s disease
  • 18.
    • Uncontrolled growth of cells
    • Insufficient apoptosis
  • 19. Diseases featuring insufficient apoptosis
    • Many cancers
    • Autoimmune Lymphoproliferative Syndrome (ALPS)
  • 20. CLINICAL IMPORTANCE OF APOPTOSIS
    • Recent studies suggest that abnormalities of apoptosis may play a key role in neurodegenerative diseases such as Alzheimer’s disease, as well as in cancer a nd autoimmune disorders .
    • Some drugs that have been used successfully for chemotherapy appear to induce apoptosis in cancer cells.
    • Cancer
    • Loss of the ability to undergo apoptosis leads to cancer.
  • 21. NECROSIS death by injury
    • cell death as the result of injury, disease, or pathological state
    • usually involves large numbers of cells.
    • Necrotic cells may spill their contents, causing inflammation and injury to neighboring cells.
  • 22. COAGULATIVE NECROSIS
    • Cell outlines remain intact after cell death and can be observed by light microscopy
    • is typically seen in hypoxic(low-oxygen) environments
    • Examples;
    • infarcts of solid organs,
    • heart, spleen, kidney.
  • 23. CASEOUS NECROSIS
    • Tissues bear soft, granular,
    • friable appearance
    • cream-cheesy(caseous) material
    • Architecture completely destroyed .
    • Examples;
    • Tuberculosis,
    • some systemic fungal infection
    A tuberculous lung with a large area of caseous necrosis
  • 24. LIQUEFACTIVE NECROSIS (OR COLLIQUATIVE NECROSIS)
    • Necrotic degradation of tissue that softens and liquify tissues grossly.
    • Examples
    • Infarction of central nervous system
    • Abscess in bacterial infection
  • 25. FAT NECROSIS
    • results from the action of lipases on fatty tissues
    • Chalky yellow white deposits formed
    • Basophilic calcified areas
    • Examples:
    • acute pancreatitis
    • traumatic breast tissue necrosis
  • 26. FIBRINOID NECROSIS
    • It is marked by deposition of fibrin-like proteinaceous material in arterial walls ,
    • appears smudgy and eosinophilic on light microscopy.
    • Examples;
    • Immune vasculitis
    • Malignant hypertension
  • 27. DIFFERENCE B/W APOPTOSIS AND NECROSIS
    • APOPTOSIS
    • Chromatin condensation
    • • Cell shrinkage
    • • Preservation of organelles
    • and cell membranes
    • • Rapid engulfment by
    • neighboring cells
    • preventing inflammation
    • • Biochemical hallmark -
    • DNA fragmentation
    • NECROSIS
    • Nuclear swelling
    • • Cell swelling
    • • Disruption of organelles
    • • Rupture of cell and
    • Release of cellular
    • contents
    • • Inflammatory response
  • 28. DIFFERENCE B/W APOPTOSIS AND NECROSIS
  • 29. CANCER; INTRODUCTION
    • Neoplasm - (new growth) abnormal mass of tissue, the growth of which exceeds and is uncoordinated with the normal tissues
    • Tumor - a non-specific term meaning lump or swelling. Often syn. for neoplasm
    • Cancer - malignant neoplasm or tumor
    • Metastasis - discontinuous spread
    • of a malignant neoplasm
    • to distant sites
  • 30. Diseases featuring excessive apoptosis
    • Neurodegenerative
      • Parkinson’s disease
      • Alzheimer's disease
      • Amyotrophic lateral sclerosis (ALS)
      • Huntingdon’s disease
  • 31. CANCER
    • Cancer is a disorder of cellular homeostasis disease in which there is uncontrolled cell division caused by:
    • by mutation
    • or by some other abnormal activation of cellular genes that control cell growth and cell mitosis .
  • 32. CANCER
    • The abnormal genes are called oncogenes.
    • Also present in all cells are antioncogenes , which suppress the activation of specific oncogenes.
    • Therefore, loss of or inactivation of antioncogenes can allow activation of oncogenes that lead to cancer.
    • A factor which brings about a mutation is called a mutagen.
    • Any agent that causes cancer is called a carcinogen and is described as carcinogenic.
  • 33. CARCINOGENS
    • Ionising radiation – X Rays, UV light
    • Chemicals – asbestos,
    • tar from cigarettes
    • Virus infection – papilloma virus can be responsible for cervical cancer.
    • Hereditary predisposition –
    • Some families are more susceptible
    • to getting certain cancers.
    carcinogen sign
  • 34. HALLMARKS OF CANCER
  • 35. BENIGN OR MALIGNANT?
    • Benign tumours
    • do not spread from their site of origin
    • can crowd out (squash) surrounding cells
    • slow growing
    • well differentiated
  • 36.
    • Malignant tumours
    • can spread from the original site and cause secondary tumours .
    • This is called metastasis .
    • Fast growing
    • Poorly differentiated
    • They interfere with neighbouring cells and can block blood vessel, gut etc.
    BENIGN OR MALIGNANT?
  • 37. GENERAL AND LOCAL EFFECTS OF CANCER
    • Cancer can kill the patient by:
    • Local effects
    • Systemic effects
    • Why Do Cancer Cells Kill?
    • Cancer tissue competes with normal tissues for nutrients .
    • Because cancer cells continue to proliferate indefinitely, cancer cells soon demand essentially all the nutrition available to the body or to an essential part of the body.
    • As a result, normal tissues gradually suffer nutritive death .
  • 38. REFERENCES
    • Text book of medical physiology , Guyton and Hall
    • Robbins & Cotran Pathologic Basis of Disease
    • Rapid Review Pathology, By Edward F. Goljan, MD
    • http://users.rcn.com/jkimball.ma.ultranet/BiologyPages
  • 39. SELF ASSESSMENT
    • Q1. Is cell death necessary? why?
    • Q2. Which type of cell death is called programmed cell death?
    • Q3. Identify the processes labeled as A & B.
    A B
  • 40. SELF ASSESSMENT
    • Q4. Identify the type of necrosis in fig A& B
    • A B
  • 41.
    • Q5. Name some of the common carcinogens.
    • Q6. Differentiate b/w benign and malignant tumors.
    SELF ASSESSMENT
  • 42.