CELL INJURY for physiotherapy students.pptx

About agents of cell injury

1. CELL INJURY Prepared by: Prof. O. O. K. Ibrahim

2. INTRODUCTION: Normal cell is in a fairly narrow range of function and structure by its genetic programs of metabolism, differentiation, and specialization. Constraints of neighbouring cells. And availability of metabolic substrates. It is in a steady state called homeostasis.

3. INRODUCTION CONTD More severe physiologic stresses and some pathologic stimuli may result in cellular adaptation – a new but altered steady state aim at preserving the viability of the cell. Cell injury results when the limits of the adaptive response to a stimulus are exceeded. Cell death is the ultimate result of cell injury.

4. CELLULAR ADAPTATIONS The adaptive responses are: Hyperplasia Hypertrophy Atrophy Metaplasia

5. HYPERPLASIA Increase in number of cells in an organ or tissue resulting in increased volume of the organ or tissue. Can be physiologic or pathologic Physiological can be hormonal (increase in breast glandular epithelial cells at puberty and during pregnancy) or compensatory. Pathological is caused by excessive (abnormal) hormonal stimulation (endometrial hyperplasia due to excessive oestrogen production.

6. HYPERTROPHY This refers to an increase in the size of the cells, resulting in the increase in the size of the organ. Can be physiologic (caused by increased functional demand) or pathologic (caused by specific hormonal stimulation).

7. ATROPHY Refers to shrinkage in the size of the cells and ultimately the size of the tissue or organ. Can be physiologic (decrease in the size of the uterus after parturition) Usually pathologic and caused by decreased workload (atrophy of disuse), loss of innervation , diminished blood supply, inadequate nutrition, loss of endocrine stimulation, aging, pressure, etc

8. METAPLASIA A reversible change in which one adult cell type is replaced by another adult cell type. Examples are: Squamous metaplasia in the respiratory tract as a result of chronic irritation in smokers (columnar to squamous ) Squamous metaplasia in the urinary bladder as a result of chronic schistosomiasis (transitional to squamous ) Squamous metaplasia of the endocervix as a result of repeated pregnancies (columnar to squamous ) Glandular metaplasia in the lower esophagus as a result of reflux of gastric secretion ( squamous to glandular epithelium). Metaplastic epithelium is at a great risk of malignant transformation

9. CAUSES OF CELL INJURY Cells are injured when their adaptive limits are exceeded by various injurious agents. Cell injury can be reversible or irreversible depending on the nature of the injurious agent, its intensity, duration of exposure, and the functional residual capacity of the cell. Reversible cell injury – it is manifested as functional and morphologic changes that are reversible if the damaging stimulus is removed. Irreversible cell injury and cell death – the injury becomes irreversible and the cell can not recover even if the injurious is removed.

10. CAUSES OF CELL INJURY Oxygen deprivation (Hypoxia and ischemia) Physical agents – mechanical trauma, extremes of temperature, radiation, electric shock, sudden changes in atmospheric pressure. Chemical agents and drugs (including toxins) Infectious agents – viruses, bacteria, fungi, parasites, etc Immunologic reactions – hypersensitivity reactions and autoimmune diseases

11. CAUSES OF CELL INJURY contd 6. Genetic derangements - 7. Nutritional imbalances – in form of deficiencies or excesses

12. Mechanisms of cell injury Depletion of ATP Mitochondrial damage Influx of intracellular calcium and loss of calcium homeostasis Accumulation of oxygen-derived free radicals Defects in membrane permeability

13. Mechanisms of cell death Apoptosis versus Necrosis APOPTOSIS This is a pathway of cell death that is tightly regulated. It involves intracellular program in which cells destined to die activate enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins.

14. APOPTOSIS Contd It is the mechanism of removing unwanted cells. It can be physiological or pathological Physiological apoptosis: Programmed destruction of cells during embryogenesis Hormone-dependent involution in adult Elimination of potentially harmful self reactive lymphocytes.

15. Pathological apoptosis Cell death produced by a variety of injurious agents. Cell injury in certain viral diseases. Cell death in tumors

16. NECROSIS This is another form of cell death. It is the spectrum of morphological changes that cell death in a living tissue. It results from denaturation of intracellular proteins and enzymatic digestion of the cells. There are 2 main forms of necrosis depending on the predominant mechanism.

17. NECROSIS Contd Coagulative necrosis Liquefactive necrosis (abscess formation) Variants of coagulative necrosis: Caseous necrosis Gangrenous necrosis Fat necrosis