Morphologic Response of the Cell PDF

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StylizedVitality6510

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Vision Colleges

Dr. Amal Abd El-hafez

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cell biology morphology pathology cellular responses

Summary

This document is a lecture on the morphologic responses of cells to various conditions, including intracellular accumulations, aging, adaptations, reversible and irreversible cell injury, and malignant cell changes. It outlines the morphological characteristics of these different cellular states.

Full Transcript

## Morphologic Response of the Cell **Dr. Amal Abd El-hafez** Associate Professor of Histopathology & Consultant Pathologist ### Objectives: By the end of this lecture, the student will be able to: 1. Outline the morphology of common intracellular accumulations. 2. Discuss morphological cell ch...

## Morphologic Response of the Cell **Dr. Amal Abd El-hafez** Associate Professor of Histopathology & Consultant Pathologist ### Objectives: By the end of this lecture, the student will be able to: 1. Outline the morphology of common intracellular accumulations. 2. Discuss morphological cell changes in response to aging. 3. Discuss the morphology of cellular adaptations with examples. 4. Compare the morphology of reversible and irreversible cell injury. 5. Enumerate the morphologic changes of malignant cells. ### Morphologic Responses of the Cell Are changes in the shape of the cells in response to different conditions. - **Intracellular Accumulations** - metabolic disturbance - **Cellular Aging** - long life span - **Normal Cell (homeostasis)** - **Stress** - injurious stimulus - **Adaptation** - inability to adapt - **Reversible Injury** - mild, transient - **Cell Injury** - severe, progressive - **Irreversible Injury** - **Necrosis** - **Cell Death** - **Apoptosis** ### Types of Cell Responses #### Intracellular Accumulations - **Abnormal accumulation of materials inside cells due to excessive intake or defective transport or defective catabolism (metabolic disturbance).** - **Triglycerides** - accumulation of triglycerides in cells (e.g. fatty liver) - **Cholesterol** - accumulates in macrophages and smooth muscle cells of vessel walls in atherosclerosis. - **Proteins** - immunoglobulins accumulate in plasma cells in immune response. - **Glycogen** - accumulates in liver and muscle in glycogen storage diseases. - **Pigments** - **From outside the body or from inside the body:** - Carbon (anthracosis) - Lipofuscin (aging pigment) - Iron (in hemosiderosis) - **From inside the body:** - Inside cells of liver - Inside cells - From outside the body. #### Cellular Aging - **Morphologic and functional changes of the cell due to prolonged life-span. (The age of cells)** - **Caused by many factors:** 1. Accumulating genetic cellular damage. 2. Reduced ability to repair damaged DNA. 3. Reduced capacity to divide (senescence). 4. Defective protein homeostasis. 5. Effect of high caloric intake. - **Morphologic responses to aging include:** 1. Abnormal shaped nuclei, mitochondria, Golgi apparatus. 2. Decreased endoplasmic reticulum, ribosomes. 3. Accumulation of cytoplasmic lipofuscin pigment (aging pigment). - **Examples:** - Lipofuscin in neurons - Lipofuscin in Cardiac Muscle - **Autophagy is the main mechanism of cellular aging:** - It is engulfment of cell organelles into cytoplasmic vacuoles that fuses with lysosomes to digest the engulfed organelle. - Autophagy also occurs in cancers. #### Cellular Adaptations - **Hypertrophy:** Increased cell size and organ size, in response to increased workload, growth. - **Example:** - Hypertrophy of smooth muscle cells of the uterus during pregnancy. - **Hyperplasia:** Increased cell numbers due to hormone and growth factor stimulation. Occurs in tissues whose cells are able to divide or contain tissue stem cells. - **Example:** Hormonal hyperplasia of female breast during puberty. - **Atrophy:** Decreased cell size and organ size, due to decreased nutrient and blood supply or disuse. - **Mechanism:** Decreased synthesis of cellular proteins and organelles and increased breakdown of cellular proteins and organelles. - **Example:** Senile brain atrophy. - **Metaplasia:** Replacement of one differentiated cell type by another differentiated cell type of the same category (e.g. epithelium to another epithelium), often in response to chronic irritation. This change makes cells able to resist the stress. - **Example:** Squamous metaplasia of respiratory epithelium in cigarette smokers. #### Reversible Cell Injury - **Includes:** 1. Cellular swelling (cloudy swelling; hydropic degeneration) - intracellular accumulation of water e.g. kidney tubules lining epithelium. 2. Fatty change - intracellular accumulation of fat e.g. hepatocytes. - **Morphology:** - Cell swelling - Cell membrane blebs - Mitochondrial swelling - Swelling of the endoplasmic reticulum. - **Keep the shape. Back after injury.** #### Irreversible Cell Injury - **A- Necrosis** - **Death of group of cells or tissues.** - **Morphology:** - The dead cells and tissue become more eosinophilic. - Nuclear dissolution. - Breakdown of plasma membrane and organelle membranes forming myelin figures. - Enzymatic digestion of cellular contents. - Surrounding inflammation. - **B- Apoptosis** - **Programmed single-cell death. It removes unwanted or genetically damaged cells.** - **Mechanism:** 1. Activation of cellular enzymes called 'caspases'. 2. Cell fragmentation into apoptotic bodies (nuclear fragments + cytoplasm). 3. Engulfment of fragmented cells by phagocytes. - **Pathways:** 1. Mitochondrial (intrinsic) pathway: initiated inside the cell. 2. Death receptor (extrinsic) pathway: initiated by signals from outside the cell.) - **Light microscope findings of apoptosis:** 1. Cell shrinkage and eosinophilia. 2. Nuclear condensation, Cell fragmentation. ### Morphologic Changes of Malignant Cells - **Cells of malignant tumors are characterized by:** 1. Marked variation in cell size and shape. 2. Loss of polarity i.e. loss of orientation to one another. 3. Nuclei are hyperchromatic, large variable in size and shape. 4. High nucleo-cytoplasmic ratio. 5. Giant cells and bizarre cells with multiple nuclei. 6. Coarse (condensed) chromatin. 7. Large prominent nucleoli. 8. Frequent mitoses and abnormal mitotic figures. ### Recommended References, Websites - Robbins & Cotran Pathologic Basis of Disease, 9e (Robbins Pathology), 2014 - ISBN-13: 978-1455726134 - ISBN-10: 1455726133 - PATHMAX: http://www.pathmax.com/

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