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Cell Injury, Cell...
| Question | Answer |
|---|---|
| What are the 3 cellular responses to stress? | 1) Adaption 2) Reversible Injury 3)Irreversible Injury leading to cell death |
| What are the adaptive cell responses? | Hypertrophy, Hyperplasia, Atrophy, Metaplasia |
| Name the two main type of cell death? | Necrosis and Apoptosis |
| What is hypertrophy? | It is an increase in the SIZE of a cell without an increase in cell number. |
| What is hyperplasia? | It is an increase in cell NUMBER |
| What are the 2 types of cellular changes that may occur for cellular adaptations or reversible changes? | Physiologic - these are cell responses to hormones or chemical mediators. Pathologic - these are cell changes to allow the cell to exist in its altered environment and escape injury. |
| What types of hyperplasia exist? | Compensatory – portion of the tissue is removed or diseased (eg. When liver is resected) and proliferation of glandular epi (eg. Female breast at puberty and pregnancy). Pathologic – Hyperplastic squamous epi caused by hpv, also can develop into cancer. |
| What is atrophy? | A decrease in the size of a cell |
| What causes atrophy? | Decreased workload, loss of innervation, diminished blood supply, poor nutrition, loss of endocrine stimulation, and aging. |
| What accompanies atrophy in many situations? | An INCREASE in the number of autophagic vacuoles - a fusion of lysosomes and organelles. |
| What is Metaplasia? | When one type of adult cell changes into another type of adult cell, to better withstand the environment. |
| Name the 4 different types of Metaplasia. | Squamous Metaplasia, Oncocytic Metaplasia, Osseous and Cartilaginous Metaplasia. |
| Squamous Metaplasia | Occurs in the respiratory epithelium of cigarette smokers. Ciliated Columnar epithelial cells replaced by stratified squamous epithelial cells. |
| Oncocytic Metaplasia | Occurs in salivary gland parenchyma, brightly eosinophilic, granular cytoplasm packed with mitochondria. (can be due to aging but seen secondary to inflammatory changes with in the gland. |
| Osseous and Cartilaginous Metaplasia | Seen in association with inflammatory fibrous hyperplasia secondary to an ill-fitting denture. |
| Barrett Esophagus | Chronic gastric reflux, normal stratified squamous epithelium of the esophagus undergo metaplastic transformation to gastric or intestinal type columnar epithelium. This transformation is linked to the development of Esophageal Adenocarcinoma. |
| Agenesis | Failure of an organ to develop during embryonic growth due to absence of primordial tissue. |
| Aplasia | Defective development or congenital absence of a structure or organ |
| Hypoplasia | Underdevelopment of a structure or organ due to an inadequate or below normal number of cells. |
| What is hypoxia? | A reduction in the oxygen supply to tissues. |
| What is ischemia? | A loss of blood supply to tissues. |
| Name some causes of cell injury. | 1)Hypoxia 2)Chemical agents 3)Physical agents 4)Infectious agents 5)Immune reactions 6)Genetic defects 7)Nutritional imbalances 8)Aging |
| What are the steps of change in cells following injury? | 1) Biochemical or molecular 2) Functional 3) Morphologic |
| What 2 phenomena characterize IRREVERSIBLE cell injury? | Inability to reverse mitochondrial dysfunction and disturbances of membrane function |
| What are the 3 types of MORPHOLOGIC changes that an injured cell may experience? | Reversible Cell Injury. Necrosis. Apoptosis. |
| What are the LIGHT MICROSCOPE expressions of Reversible injury? | 1) cellular swelling 2) Fatty change |
| Cellular Swelling | “Cloudy Swelling” May produce small clear vacuoles in the cytoplasm, sometimes referred to as Hydropic change or Vacuolar degeneration. |
| Fatty Change | Sign of more severe cell injury, commonly seen in the liver, kidney, and heart, and may impair function. |
| What is Necrosis? | Necrosis is the cell death of living tissue. Membrane integrity is lost and contents spill out. |
| Where do the enzymes that breakdown cells in Necrosis originate? | Inside the cell itself = AUTOLYSIS. Or from invading inflammatory cells. |
| What characterizes necrosis? | Increased EOSINOPHILIA, breakdown of membranes and: loss of basophilia (karyolysis), shrinking nucleus with increased basophilia (pyknosis) or nuclear fragmentation (karyorrhexis). |
| What is coagulation necrosis? | Cells maintain their shape and outline for some time. This is typical for HYPOXIC cells. Ex. seen in Myocardial Infarctions (Heart Attack). |
| What is liquefaction necrosis? | Necrotic cells are digested and leave a cavity(abscess) filled with contents and WBC (pus). Ex. Hypoxia of the brain. |
| What is caseous necrosis? | Common in TB. A form of coagulation necrosis with chees-like appearance. |
| What is fat necrosis? | Seen in pancreatitis. Lipid breakdown in peritoneal cavity |
| What is fibrinoid necrosis? | Unusual - only seen in immune reaction to blood vessels. |
| What is Apoptosis? | The energy-dependent, tightly regulated form of cell death. ** Cells maintain integrity so there is NO local inflammation. “Programmed cell death” |
| What is Physiologic apoptosis? | Normal phenomenon to eliminate cells from a population where they are no longer needed. |
| What is Pathogenic apoptosis? | Eliminates cells that are genetically altered or injured beyond repair. |
| (Mechanism of Cell Injury) What is the Most Important targets of injurious stimuli? | 1.Mitochondria, sites of ATP generation 2. Cell membranes 3. Protein Synthesis 4. Cytoskeleton 5. Genetic apparatus. |
| Describe the Mechanism of Cell Injury | Damage to Mitochondria leads to depletion of ATP. Depletion of ATP leads to reduced activity of plasma membrane sodium pump with increased sodium and water accumulation in the cell (Cloudy Swelling). Compensatory increase in anaerobic glycolysis... |
| ...Describe the Mechanism of Cell Injury | ...Failure of calcium pump = influx of calcium ions which activate enzyme that cause cell damage. Depletion of ATP causes detachment of ribosome from RER = disruption of protein. Mitochondrial damage cause leakage of Cytochrome C which leads to apoptosis. |
| Reactive Oxygen Species | Oxygen derived free radicals which results in lipid peroxidation of membranes, cross-linking of proteins, and fragmenting nuclear and mitochondrial DNA. |
| What is the most important sites of Membrane Damage? | 1) Mitochondrial membranes = decrease production of ATP. 2) Plasma membranes = loss of cellular content and influx of fluids. 3) Lysosomal = Enzyme in cytoplasm leading to digestion of cell content and necrosis. |
| What are some examples of REVERSIBLE cell injury? | Ischemia and Hypoxia. Ischemia and Reperfusion - due to ROS (reactive oxygen species) from returning leukocytes. Chemical injury - Toxicity directly or indirectly. |
| Chemical (Toxic) Injury | Chemical induced cell injury, directly combining with critical molecular component or cellular organelle (Mercury poisoning) or indirectly convert of reactive toxic metabolites (free radicals) acting on target cells (Carbon Tetrachloride poisoning) |
| What are the normal pathways of cellular buildup? | 1. Buildup w/o clearing 2. Defect in folding 3. Genetic lack of metabolism 4. Abnormal substance buildup |
| What is Autophagy? | "Self-eating", represents lysosomal digestion of cell's own content. When cell cannot cope, autophagy signals cell death by apoptosis. |
| Intracellular Accumulation (4 general pathways) | 1. Inadequate metabolic removal(Fatty change in liver) 2. Acquired or genetic defects(Alpha-Antitrypsin Deficiency) 3. Inherited defects of enzymatic metabolism(Storage Disease) 4. Exogenous substance cannot be degraded or transported(Carbon and Silica) |
| What is fatty change build up called? | STEATOSIS - common with alcohol abuse or diabetes |
| What is cholesterol build up called? | ATHEROSCLEROSIS - usually vascular smooth muscle |
| Give three examples of protein build up | Russell bodies - found in newly formed Ig. Mallory bodies - aggregates of prekeratin in liver (common in EtOH abuse). Neurofibrillary tangle - Alzheimer disease |
| What is glycogen build up called? | Glycogen storage disease - common for poorly controlled diabetes |
| What is Anthracosis? | Build up of CARBON in lungs and lymph nodes |
| What is Hemosiderin? | Accumulation of IRON pigment in the tissues |
| What is Hemochromatosis? | A hereditary systemic iron overload disorder. It damages parenchymal cells (liver, heart, and pancreas). |
| What pigment builds up in Jaundice? | Bilirubin |
| What pigment is noted as the "wear and tear" pigment from previous injury(Marker of past free radical injury)? | Lipofuscin |
| What is the pigment of skin? | Melanin |
| Pathological Calcification | Abnormal deposition of calcium salts with other minerals. (Dystrophic and Metastatic) |
| Dystrophic Calcification | Pathologic calcification in dead or dying tissue. |
| Metastatic Calcification | Deposition of calcium salt in normal tissue. |
| What are the common causes of hypercalcemia? | 1) Increased parathyroid function. 2) Bone destruction 3) Vitamin D disorders 4) Renal failure |
| What are the mechanisms of cellular aging? | 1) DNA damage *** 2) Decreased replication 3) Reduced capacity of tissue stem cells 4) Accumulation of metabolic damage. |
Created by:
ddde227
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