.......cellular adaptation-converted.pptx

Jhh bsn

1. Unit-3 Cellular Adaptation & Aberrant Cell Growth Tariq Aziz Nursing Lecturer

2. When confronted with stresses that endanger its normal structure and function, the cell undergoes adaptive changes that permit survival and maintenance of function. It is only when the stress is overwhelming or adaptation is ineffective that cell injury and death occur

3. Cells that are atrophied reduce their oxygen consumption and other cellular functions by decreasing the number and size of their organelles and other structures . Mechanism of atrophy

4. Pathologic hypertrophy: Adaptive: thickening of the urinary bladder from long-continued obstruction of urinary outflow. Compensatory: if one kidney is removed, the remaining kidney enlarges to compensate for the loss Mechanism of Hypertrophy Hypertrophy occurs as a result of a number of variables – Mechanical Tension, Muscular Damage, and Metabolic Stress. This results in increased Testosterone and Growth Hormone levels that play a big role in triggering and maximizing protein synthesis needed for muscles repair and muscle growth to occur.

5. It occurs in tissues with cells that are capable of mitotic division, such as the epidermis, intestinal epithelium, and glandular tissue . Hyperplasia is a controlled process that occurs in response to an appropriate stimulus and ceases after the stimulus has been removed.

6. *Benign prostatic hyperplasia is an example of non physiologic hyperplasia Note: Hyperplasia is also an important response of connective tissue in wound healing.

7. TYPES: Squamous metaplasia: e.g squamous epithelial cells for the ciliated columnar epithelial cells in the trachea and large airways of a habitual cigarette smoker . Columnar metaplasia: e.g Barrett’s esophagus; The process of cell change from flat, layered squamous to tall columnar epithelium is an example of metaplasia

8. DYSPLASIA Dysplasia is characterized by deranged cell growth of a specific tissue that results in cells that vary in size, shape, and organization . Although dysplasia is abnormal, it is adaptive in that it is potentially reversible after the irritating cause has been removed. Dysplasia is strongly implicated as a precursor of cancer.

9. Examples of Atrophy NORMAL ATROPHIED

10. Examples of Hyperplasia

11. Left Normal breast Right Hyperplasia （ From ROBBINS BASIC PATHOLOGY ， 2003 ）

12. Examples of Metaplasia

13. Aberrant Cell Growth Normal tissue renewal and repair involves two components: cell proliferation and differentiation. Proliferation , or the process of cell division, is an inherent adaptive mechanism for cell replacement when old cells die or additional cells are needed, It maintains a balance between the number of cells dying and the number of cells actively dividing Differentiation is a pr o c e ss by which p r olifer a ti n g cells are transformed into different and more specialized cells for example RBCs takes the shape of a disc, becomes capable of carrying oxygen and is destined to die in 120 days .

14. Aberrant Cell Growth Aberrant cell growth is defined as any abnormal cell growth or new growth called neoplasm. Neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissue and persist in the same excessive manner after the cessation of the stimuli which evoked the change Apoptosis is a form of programmed cell death that eliminates senescent cells, cells with deoxyribonucleic acid ( DNA)

15. Cancer is the second leading cause of death in the United States. Cancer is not a single disease. It can originate in almost any organ. Cancer is a disorder of altered cell differentiation and growth. The resulting process is called neoplasia, meaning “new growth,” and the new growth is called a neoplasm . Unlike changes in tissue growth that occur with hypertrophy and hyperplasia, the growth of a neoplasm tends to be uncoordinated and relatively autonomous in that it lacks normal regulatory controls over cell growth and division. Continue

16. BENIGN & MALIGNANT NEOPLASM Benign neoplasm contain well differentiated cells that are clustered together in a single mass. Malignant neoplasm are less differentiated and have the ability to break loose, enter the circulatory or lymphatic system and form secondary malignant tumors at other sites. Cancer is a malignant neoplasm Word cancer is derived from the Greek word “Karkinos ” meaning crab. Malignancy is synonymous with the medical meaning of cancer.

17. DIFFERENCE BETWEEN BENIGN AND MALIGNANT NEOPLASM Benign neoplasm/Tumors Malignant neoplasm/Tumors Grow slowly Grow rapidly Less aggressive More Aggressive Have a well-defined capsule Are not encapsulated Are not invasive Invade local structure and tissues Well-differentiated; looks like the tissue from which it arises Poorly differentiated; may not be able to tell which tissue it arose from Have a low mitotic index; dividing cells are rare High mitotic index; many dividing cells Do not metastasize Can spreads distantly, often through blood vessels and lymphatics

18. NAMING OF BENIGN & MALIGNANT NEOPLASM Term carcinoma is used to designate a malignant tumor of epithelial tissue origin. E.g . malignant tumor of glandular epithelial origi n (producing fluids and mucus)is adenocarcinoma. Malignant tumor of parenchymal origin formed in bone and soft tissue, like muscle fat, blood & lymph vessels and fibrous tissue are called sarcomas (e.g. osteosarcoma is a malignant tumor of bone ) Tumors/neoplasm are named by adding the suffix- oma to parenchymal tissue type from which the growth originate. E.g. benign tumor of glandular epithelial origin is adenoma , of bone origin is osteoma .

19. NOMENCLATURE Benign Malignant Epithelial Tumor Surface Glandular Papilloma Adenoma Squamous cell carcinoma Adenocarcinoma Connective tissue Fibrous Fibroma Fibro sarcoma Adipose Lipoma Liposarcoma Cartilage Chondroma Chondrosarcoma Bone Osteoma Osteosarcoma Blood vessels Hemangioma Hemangiosarcoma

20. Lymph Vessels Lymphangioma Lymphangiosarcoma Muscle tumors Smooth Leiomyoma Leiomyosarcoma Striated Rhabdomyoma Rhabdomyosarcoma Nerve Cell Tumors Nerve cell Neuroma Glial tissue Glioma Hematologic tumors Granulocytic Myelocytic leukemia Erythrocytic Erythroleukemia Plasma Cell Multiple Myeloma Lymphoid L y m phocytic leukemia

21. Cancer cell fail to undergo normal cell proliferation and differentiation. ( more differentiation less malignant) Loss of normal arrangement of cells(cohesiveness and adhesiveness) Alteration in contact inhibition. Altered cell responsiveness to growth factor. Impaired cell to cell communication (Fibronectin , Anchoring molecule) Expression of altered tissue antigens Tumor/biologic markers on P. membrane, blood ,spinal fluid & urine (hormones, enzymes, antigens, antibodies, genes) Elaboration of degradative enzymes that participate in invasion and metastatic spreads. Escape from tissue of origin by releasing enzymes (collagenase and protease ) that digest basement membrane. CHARACTERISTICS OF CANCER CELL

22. CANCER IS DRIVEN BY:

23. Cancer-associated genes: Two broad categories based on whether gene over activity or underactivity increases the risk for cancer. The category associated with gene over activity involves proto-oncogenes, which are normal genes that become cancer-causing oncogenes if mutated. Proto-oncogenes encode for normal cell proteins such as growth factors , growth factor receptors, growth factor signaling molecules, and transcription factors that promote cell growth or increase growth factor–dependent signaling.

24. Cancer-associated genes: The category associated with gene underactivity comprises the tumor suppressor genes, which, by being less active, create an environment in which cancer is promoted. Tumor suppressor genes include the retinoblastoma ( RB ) gene, which normally prevents cell division, and the TP53 gene, which normally becomes activated in DNA-damaged cells to initiate apoptosis. Loss of RB activity may accelerate the cell cycle and lead to increased cell proliferation, whereas inactivity of TP53 may increase the survival of DNA-damaged cells.

25. DOES APOPTOSIS OCCUR IN CANCER CELLS

26. CANCER “GRADING” Tumor grade is the description of a tumor based on how abnormal the tumor cells and the tumor tissue look under a microscope. It is an indicator of how quickly a tumor is likely to grow and spread. Based on the appearance of cells and the organization of the tumor tissue (well differentiated and poorly differentiated) and other differences the pathologist assign numerical grade to most cancers

27. CLASSIFICATION OF TUMOR GRADES One classification of Cancer Grading uses numbers (0, 1, 2, 3 and 4). Grade X: Gra d e 1 : Grade 2 : Grade cannot be assessed (undetermined grade) Well differentiated (low grade). Moderately differentiated. (intermediate grade) Grade 3: Poorly differentiated (high grade) Grade 5 : Undifferentiated. (high grade)

28. CA N CER S T AGING Stage of cancer refers to the extent of cancer, such as how small or large the tumor is and if it has spread to other parts of the body. TNM ( T umor, N odes, M etastasis) staging system is widely used.  The T refers to the size and extent of the main tumor. The main tumor is usually called the primary tumor.  The N refers to the number of nearby lymph nodes that have cancer.  The M refers to whether the cancer has metastasized. This means that the cancer has spread from the primary tumor to other parts of the body.

29. T (tumor) Cancer Staging Tx Main Tumor cannot be measured T0 Main tumor cannot be found T1—4 Progressive increase in tumor size or involvement N (nodes) Nx Cancer in nearby regional lymph nodes cannot be measured N0 No cancer in regional node N1—3 Increasing involvement of regional lymph nodes

30. M (metastasis) Mx Matastasis cannot be measured M0 Cancer has not spread to other parts of body M1 Cancer has spread to other parts of body

31. Predisposing factors of aberrant cell growth

32. R e ferenc e s Cancer epidemiology bookmark prev 2001 may 10(5):489-93 Int j cancer 2010 nov 15;42(5) 677-80. Porth M. Carol (2009), Pathophysiology concept of Altered Health States (new , edition). Philadelphia J.B. Lippincott . Huether E. Sue (2005). Understanding Pathophysiology . New York, Mosby. Sylvia A. Price & Lorraine M. Wilson (2002). Clinical Concepts of Disease processes, ( 5th ed.) Mosby. Kumar. Vinay (2002), Robins Basic Pathology . Philadelphia: Saunders