D r Mays Ibrahim C ell injury and adaptation learning objectives introduction to pathology knows the type of cell response to stress and injury be able to define adaptation and its types ID: 1042857
Download Presentation The PPT/PDF document "C ell injury and adaptation" is the property of its rightful owner. Permission is granted to download and print the materials on this web site for personal, non-commercial use only, and to display it on your personal computer provided you do not modify the materials and that you retain all copyright notices contained in the materials. By downloading content from our website, you accept the terms of this agreement.
1. Cell injury and adaptation Dr Mays Ibrahim
2. Cell injury and adaptation learning objectives:introduction to pathologyknows the type of cell response to stress and injury be able to define adaptation and its types
3. Introduction Pathology is the study of suffering.In pathology, any disease we will be studied from the following aspects:Its causation: etiology Mechanism of its development: pathogenesis The structural changes: morphologic changes (gross and microscopic changes)Clinical significance: the resulting sign and symptoms, prognosis of disease.
4. Homeostasis Cell response to change CELLULAR RESPONSES TO STRESS AND NOXIOUS STIMULI
5. The Question is Adapt or die????The duration of injury The severity and intensity of injury The type of cell injured The cell ability to adapt
6.
7. Cell response to cell injury Adaptation Reversible cell injury Irreversible cell injury and cell death (necrosis/ apoptosis)
8.
9. Adaptationreversible changes in the number, size, phenotype ,metabolic activity or functions of cells in response to change in their environment during which new but steady states are achieved, allowing the cell to survive and continue to function. The adaptive responses are. Types of adaptation HypertrophyHyperplasiaatrophy metaplasiaCells capable of division may respond to stress by undergoing both hyperplasia (described later) and hypertrophy, whereas nondividing cells (e.g., myocardial fibers) increase tissue mass due to hypertrophy only.
10. Hypertrophy is an increase in the size of cells that results in an increase in the size of the affected organ. Physiologic hypertrophy. Gravid uterus: smooth muscle fiber stimulated by estrogenic hormoneBody builder muscles: stimulated in response to increased demand. Pathologic hypertrophy. enlargement of the heart in response to pressure overload (hypertension or valvular disease). Mechanism: The increased size of the cells is due to the synthesis and assembly of additional intracellular structural components.
11. Physiologic hypertrophy of the uterus during pregnancy. (A) Gross appearance of a normal uterus (right) and a gravid uterus (removed for postpartum bleeding) (left). (B) Small spindle-shaped uterine smooth muscle cells from a normal uterus, compared with (C) large plump cells from the gravid uterus, at the same magnification
12. myocardial hypertrophy caused by increased blood pressure requiring greater mechanical effort by myocardial cells
13. Hyperplasia is an increase in the number of cells in an organ or tissue in response to a stimulus. Hyperplasia can only take place if the tissue contains cells capable of dividing.It can be physiologic or pathologic. • Physiologic hyperplasia.Hormonal hyperplasia: occur in response to hormones or growth factorsfemale breast glandular epithelium proliferation at puberty and during pregnancy compensatory hyperplasia liver regeneration after partial hepatectomy The bone marrow hyperplasia in response to a deficiency of mature blood cells. In case of acute bleeding and (hemolysis)
14. Lactating breast hyperplasia in glandular epithelium
15. Pathologic hyperplasia. Most forms of pathologic hyper- plasia are caused by excessive or inappropriate actions of hormones or growth factors acting on target cells. Endometrial hyperplasia due to estrogen stimulation/ increase risk of endometrial adenocarcinoma Benign prostatic hyperplasia stimulation by androgens Mechanisms of Hyperplasia Hyperplasia is the result of growth factor–driven proliferation of mature cells and, in some cases, by increased output of new cells from tissue stem cells
16. Endometrial hyperplasia , due to estrogen stimulation, carry a high risk of malignancy
17. Atrophy is a reduction in the size of an organ or tissue due to a decrease in cell size and number. associated with decreased synthesis of cellular building blocks and increased breakdown of cellular organelles by increased autophagy Atrophy can be physiologic or pathologic. Physiologic atrophyduring fetal development: Some embryonic structures, such as the thyroglossal duct atrophy. The decrease in the size of the uterus that occurs shortly after delivery
18. Pathologic atrophy Decreased workload (disuse atrophy).e.g Skeletal muscle atrophy after bone fracture Loss of innervation (denervation atrophy). Inadequate nutrition. Loss of endocrine stimulation. Endometrium atrophy following the loss of estrogen stimulation after menopause prostrate atrophies following chemical or surgical castration (e.g., for treatment of prostate cancer).Pressure atrophy Diminished blood supply (chronic ischemia)- the brain may undergo progressive atrophy,called senile atrophy.
19. Brain atrophy
20. Metaplasia Metaplasia is a reversible change in which one differentiated cell type is replaced by another cell type It often represents an adaptive response to make tissue able to withstand the adverse environment. ExamplesEpithelial metaplasia Metaplasia from columnar to squamous as occurs in the respiratory tract in response to (smoking)In the respiratory tract, for example, although the epithelial lining becomes more durable, important mechanisms of protection against infection—mucus secretion and the ciliary action of the columnar epithelium—are lost. Can be associated with the development of squamous cell carcinoma Metaplasia from squamous to columnar type may also occur, as in Barrett esophagus, in which the esophageal squamous epithelium is replaced by intestinal-like columnar cells under the influence of refluxed gastric acid. Can be associated with the development of adenocarcinomas of the esophagus.
21. Barret esophagus
22. Barrett esophagus. (A) Normal gastroesophageal junction. (B) Barrett esophagus. (C) barret, Note the transition between esophageal squamous mucosa (left) and Barrett metaplasia, with abundant metaplastic goblet cells (right).
23. Mesenchymal metaplasia is the formation of cartilage, bone, or adipose cells (mesenchymal tissues) in tissues that normally do not contain these elements. Like in myositis ossificans (bone formation inside muscle affected by hemorrhage) this type has no malignant transformation risk.Mechanisms of Metaplasia Metaplasia does not result from a change in the phenotype of an already differentiated cell type; rather, it results from either reprogramming of local tissue stem cells or, alternatively, colonization by differentiated cell popula- tions from adjacent sites.
24. Take home message Note: If the stress is eliminated, the cell can return to its original state without having suffered any harmful consequences. However, if the stimulus continues these adaptations may be inadequate and the cell may become permanently injured or die.
25.