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Cell injury: Pathologic calcification and Cell aging
This document discusses various types of calcification and cell aging. It describes dystrophic calcification as abnormal calcium deposition in dead or degenerated tissues. Metastatic calcification occurs when calcium deposits in normal tissues, often due to disturbances in calcium metabolism. Cellular aging results from genetic abnormalities and accumulated damage over time. Telomeres protect chromosome ends but shorten with each cell division, ultimately leading to cell death. Telomerase can extend telomeres and allow cells to divide indefinitely, playing a role in cancer and aging. Calorie restriction may prolong lifespan by activating sirtuin proteins.
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Cell injury: Pathologic calcification and Cell aging
- 2. Learning objectives • Pathologiccalcification • Hyaline change • Cell aging!
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- 4. • Abnormal tissuedeposition of calcium salts, together with smaller amounts of iron, magnesium, and other mineral salts
- 5. DYSTROPHIC CALCIFICATION METASTATIC CALCIFICATION 1. Occurs locallyin dead and degenerated tissues 2. Normal levels of serum calcium 3. Absence of derangements in calcium metabolism Examples – Psammoma bodies in papillary cancers, Asbestos bodies Can cause organ dysfunction (heart valves, Atherosclerosis) 1. Deposition in normal tissues 2. Increased levels of serum calcium 3. Disturbance in calcium metabolism (in hyperparathyroidism, bone damage or diseases, William’s syndrome
- 6. CALCIFICATION IN DEAD TISSUES 1.Necrosis 2. Infarcts 3. Thrombi 4. Hematomas 5. Dead parasites CALCIFICATION IN DEGENERATED TISSUES 1. Dense old scars 2. Atheromas 3. Monckeberg’s sclerosis 4. Stroma of tumors 5. Cyst walls DYSTROPHIC CALCIFICATION
- 7. DYSTROPHIC CALCIFICATION 1. 2Phases 1. Initiation – occurs in the mitochondria of necrotic cells with the creation of a microcrystal 2. Propagation – accumulation of Ca+2 phosphate salts Although it may just be a sign of past injury it often results in organ dysfunction
- 8. Dystrophic Calcification Dystrophic calcification inthe Achilles tendon after repeated traumatic injury.
- 9. • Morphology =Basophilic,amorphous or granular appearance intracellular, extracellular or both in H & E stained sections
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- 12. METASTATIC CALCIFICATION 1. 4Primary causes 1. Elevated PTH causing bone resoption 1. Primary hyperparathyroidism 2. Secondary hyperparathyroidism 2. Destruction of bone 3. Vitamin D related disorders intoxication, Sarcoidosis (macrophages turn on Vita D receptor) 4. Renal failure (phosphate retention so increased PTH) 2. Occurs throughout the body but favors tissues that lose acid (alkali) favoring calcium deposition (gastric mucosa, lungs, kidneys)
- 13. PATHOGENESIS • Excessive bindingof inorganic phosphate ions with the calcium ions • Precipitation of calcium phosphates
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- 16. • This isan alteration • within cells or extracellular space • Homogeneous glassy pink appearance in H& E stains
- 17. • Its justa descriptive term • rather than a specific marker of cell injury!!
- 18. Intracellular • Mallory body •Russel body • Zenkers degeneration in rectus muscle .. In typhoid Extracelular • Collagenous fibrous tissue • Change in leiomyoma • Hyaline membrane • Hyalinization in chronic glomerulonephritis • Corpora amylaceae
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- 20. • There isgood evidence that aging-induced alterations in cells are an important component of the aging of the organism
- 21. • Cellular agingis the result of a progressive decline in cellular function and viability – caused by genetic abnormalities & – the accumulation of cellular and molecular damage due to the effects of exposure to exogenous influences
- 22. changes that contributeto cellular aging • Decreased cellular replication. • Accumulation of metabolic and genetic damage.
- 23. Telomeres and Aging: Isthere a connection?
- 24. What are telomeres? •Telomeres are… – Repetitive DNA sequences at the ends of all human chromosomes – They contain thousands of repeats of the six- nucleotide sequence, TTAGGG – In humans there are 46 chromosomes and thus 92 telomeres (one at each end)
- 25. What do telomeresdo? • They protect the chromosomes. • They separate one chromosome from another in the DNA sequence • Without telomeres, the ends of the chromosomes would be "repaired", leading to chromosome fusion and massive genomic instability.
- 26. Telomere function, cont’. •Telomeres are also thought to be the "clock" that regulates how many times an individual cell can divide. • Telomeric sequences shorten each time the DNA replicates.
- 27. How are telomereslinked to aging? • Once the telomere shrinks to a certain level, the cell can no longer divide. Its metabolism slows down, it ages, and dies. • SENESCENCE
- 28. Telomeres & Aging •Healthy human cells are MORTAL because they can divide only a finite number of times, growing older each time they divide. Thus cells in an elderly person are much older than cells in an infant.
- 29. What is telomerase,anyway? • Telomerase (TEE-LÓM-ER-ACE) is a ribonucleoprotein enzyme complex (a cellular reverse transcriptase) that has been referred to as a cellular IMMORTALIZING enzyme. • It stabilizes telomere length by adding hexameric (TTAGGG) repeats onto the telomeric ends of the chromosomes, thus compensating for the erosion of telomeres that occurs in its absence.
- 30. How Does TelomeraseWork? • Telomerase works by adding back telomeric DNA to the ends of chromosomes, thus compensating for the loss of telomeres that normally occurs as cells divide. • Most normal cells do not have this enzyme and thus they lose telomeres with each division.
- 31. How Does TelomeraseWork? • In humans, telomerase is active in germ cells, in vitro immortalized cells, the vast majority of cancer cells and, possibly, in some stem cells. • High telomerase activity exists in germ cells, stem cells, epidermal skin cells, follicular hair cells, and cancer cells.
- 32. HOW TO PROLONG LIFESPAN !!!!!!
- 33. CALORIE RESTRICTION!!! • YES! •Studies in model organisms, from yeasts to mammals • HOW?
- 34. • Mediated byfamily of proteins called SIRTUINS! • Promotes expression of several genes whose products increase longevity • Increase metabolism, reduce apoptosis, decrease the effects of free radicals
- 35. • constituent ofred wine may activate SIRTUINS and thus increase life span!
- 36. • Relevance ofthese findings to aging in humans is an area of active investigation!!!!.
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