Degenerasi Dan Kematian Sel

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Transcript of Degenerasi Dan Kematian Sel

  • JAYUS INASTIAWAN

  • Page *

    Please mute Your cell!

  • Page *JEJAS SELSel merupakan partisipan aktif di lingkungannya, yg secara tetap menyesuaikan struktur & fungsinya untuk mengakomodasi tuntutan perubahan dan stres ekstrasel.Sel cenderung mempertahankan lingkungan segera dan intraselnya dalam rentang parameter fisiologis yang relatif sempit --- sel mempertahankan homeostasis normal.

  • KERUSAKAN SELCIDERA SEL / INJURY SELCidera reversible : cidera yg relative ringan dan kemungkinan sel kembali ke dalam bentuk semula Cidera irreversible, bila sel mati (cell death/apoptosis cellSel yang cidera tp tidak mati akan mengalami DEGENERASI yaitu perubahan morfologi / bentuk sel akibat kerusakan yang tidak fatal / reversibel.

  • *FIGURE 11 Stages of the cellular response to stress and injurious stimuli.

  • BENTUK-BENTUK PERUBAHAN DEGENERATIFDegenerasi bengkak keruh / Pembengkakan sel / cloudy swelling yaitu terjadinya penimbunan air di dalam sel-sel yang rusak (tp mrp kerusakan ringan).

    Secara makroskopis : terlihat pembesaran jaringan / organ yang terkena, dapat dideteksi dgn peningkatan sedikit BB.Perubahan / degenerasi hidropik / degenerasi vacuoler. Secara mikroskopis terlihat sitoplasma sel yang bervakuola (terdapat kantong-kantong yg berisi air pada RE), disebabkan oleh kegagalan pompa Na/K di dlm membran sel

  • Degenerasi lemak / infiltrasi lemak / steatosis / perlemakan hati, yaitu Penimbunan lipid didalam sel-sel yang rusak. Biasanya terjadi pada ginjal, jantung dan hati. (= hidropik, tapi isi vakuola adalah lipid bukan air).

    Secara makroskopis perubahan pada jaringan yg terkena meliputi pembengkakan jar, penambahan berat pada organ2 yg terkena, dan terlihat silinder berwarna kekuningan pada jaringan akibat adanya kandungan lipidPerlemakan hati dapat ditemukan pada pasien dgn malnutrisi, makan berlebihan, hipoksia, dan alkoholis

  • KEMATIAN SELJika pengaruh buruk pada sebuah sel cukup hebat atau terus berlangsung cukup lama, maka sel akan mencapai suatu titik dimana tidak lagi dapat mengompensasi dan tidak dapat melanjutkan metabolisme, proses tersebut menjadi irreversible, dan sel akan mati / NEKROSISJika sel yg telah mati masih tetap tinggal di dlm hospes, akan terjadi hal-hal brkt:Sewaktu sel hidup enzim-enzim yg terkandung didalam sel (umumnya litik) tidak menimbulkan kerusakan pada sel, tp enzim2 ini dilepaskan pada saat sel mati dan mulai melarutkan berbagai unsur selulerPada saat sel mati, terjadi perubahan secara kimiawi, jaringan hidup yg tepat disebelahnya memberikan respon terhadap perubahan itu dan menimbulkan reaksi peradangan akut dimana terjadinya pengiriman leukosit ke daerah tsb yg membantu pencernaan sel-sel yg sudah mati

  • APOPTOSIS : kematian sel yang terprogramBentuk kematian sel ini diprogram oleh informasi genetik yg telah ada di dalam sel, melibatkan sel-sel tunggal atau kelompok bbrp sel, dan bila sel tsb mati, akan membentuk fragmen mjd potongan-potongan yg terikat membran yg dgn cepat difagositosis oleh sel disebelahnya / oleh makrofagApoptosis diperlukan untuk:Pembentukan jari-jari tangan dan kaki pada janin meliputi pembuangan oleh apoptosis pada jaringan diantara jari-jari tsbPengelupasan endometrium pada saat awal menstruasi terjadi akibat apoptosis

  • Pembentukan hubungan yang sesuai (sinaps) diantara neuron didalam otak memerlukan penghilangan kelebihan sel oleh apoptosisKematian sel yg terprogram jg diperlukan untuk menghancurkan sel-sel yg merupakan ancaman bagi integritas organisme, spt:Sel-sel terinfeksi oleh virusSel-sel dgn kerusakan DNASel-sel sistem imunSel-sel kanker

  • Apoptosis merupakan bagian pusat perkembangan normal, berbeda dgn nekrosis, yg tidak tdp pada perkembangan normal dan merupakan respons terhadap cedera atau kerusakan toksik. Apoptosis secara khas mengenai sel-sel individu yg tersebar dan tidak mengakibatkan peradangan, berbeda dengan nekrosis yg biasanya mengenai jalur-jalur sel-sel disebelahnya dengan daerah yg dikelilingi oleh peradangan

  • Swollen kidney tubulesIncreased eosinophilic stainingDecreased basophilic staining (RNA) Plasma membrane rounding, blebbing, loss of cilia, due to loss of connections with cytoskeletonIntegrity of tubules degrading, but basement membranes intactNuclei largely intact, slightly narrowed, pyknotic

    *B, Early (reversible) ischemic injury showing surface blebs, increased eosinophilia of cytoplasm, and swelling of occasional cells.

  • Necrotic kidney tubulesCellular fragmentationLoss and fading of nuclei--karyolysisBurst membranesLoss of tissue architecture

    * C, Necrosis (irreversible injury) of epithelial cells, with loss of nuclei, fragmentation of cells, and leakage of contents. The ultra structural features of these stages of cell injury are shown in Figure 110. (Courtesy of Drs. Neal Pinckard and M.A. Venkatachalam, University of Texas Health Sciences Center, San Antonio, TX.)

  • *FIGURE 2025 Acute kidney injury. Some of the tubular epithelial cells in the tubules are necrotic, and many have become detached (from their basement membranes) and been sloughed into the tubular lumens, whereas others are swollen, vacuolated, and regenerating. (Courtesy of Dr. Agnes Fogo, Vanderbilt University, Nashville, TN.)

    Look to see where the patterns emerge, starting with one of the two well-defined tubules. Swollen cells will have clear areas of vacuolarization due to ER smoothing, dilation, pinching. Necrotic cells are more eosinophilic (deeper pink) due to accumulation of denatured proteins and loss of RNA. Dead cells without nuclei are sloughed into tubular lumen. Dying cells have either fading, karyolytic nuclei; or condensed, pyknotic nuclei.

  • Tissue necrosisCoagulative necrosisProteins denature and aggregate rather than degradeDry gangreneLiquefactive necrosisEnzymatic digestion of cellular componentsWet gangreneCaseous necrosisEnd result of tuberculous infections, granulomaFatty necrosisEnd result of pancreatic lipases digesting fat cells resulting in calcium soapsFibrinoid necrosisAg-Ab complexes and fibrin accumulate in arteries or other vessels

  • Coagulative necrosisCellular proteins denature (unstick and unwind) due to altered osmotic environment and acidosisAnuclear cells stain more deeply pink, tissue retains gross architectureCells burst and are cleared by phagocytesResults from hypoxia in tissues other than brain (which liquifies instead)

  • Coagulative necrosismyocardial infarctionWhen there is marked cellular injury, there is cell death and necrosis. This microscopic appearance of myocardium shown here is a mess because so many cells have died that the tissue is not recognizable. Many nuclei have become pyknotic (shrunken and dark) and have then undergone karyorrhexis (fragmentation) and karyolysis (dissolution). The cytoplasm and cell borders are no longer recognizable. In this case, loss of the blood supply from a major coronary artery led to ischemia and cell death.

    *http://library.med.utah.edu/WebPath/CINJHTML/CINJ012.html

    Although the structure of the tissue is no longer recognizable, there are some dense, eosinophilic areas, and there are no large pools of pus or aqueous, hydrolytic areas. This is not yet, then, liquefactive necrosis.

  • Coagulative necrosismyocardial infarctionHere is myocardium in which the cells are dying as a result of ischemic injury from coronary artery occlusion. This is early in the process of necrosis. The nuclei of the myocardial fibers are being lost. The cytoplasm is losing its structure, because no well-defined cross-striations are seen.

    *http://library.med.utah.edu/WebPath/CINJHTML/CINJ013.html

    These cells still clearly resemble muscle.

  • Coagulative necrosismyocardial infarctionGross, cross section: A pale, whitish infarct is surrounded by a zone of hyperemia (vascular dilatation).

    Very low power glass slide: The area of coagulative necrosis is bright pink compared to the lighter pink viable myocardium. The bluish areas on each side of the necrotic zone represent the granulation tissue response to the necrosis.

    *ExpertConsult > Case Studies > Begin > Cell Injury > Introductory Images > Image 11 and 12

  • *The small intestine is infarcted. The dark red to grey infarcted bowel contrasts with the pale pink normal bowel at the bottom. Some organs such as bowel with anastomosing blood supplies, or liver with a dual blood suppy, are hard to infarct. This bowel was caught in a hernia and the mesenteric blood supply was constricted by the small opening to the hernia sac. http://library.med.utah.edu/WebPath/CINJHTML/CINJ019.html

    GRIPE Image: 234 Item: 72-41-003-1 Organ/System: Small Intestine Diagnosis: infarct Description: coagulation necrosis transmural, submucosal edema, marked vascular congestion

  • Coagulative necrosiskidney infarctionThis is the typical pattern with ischemia and infarction (loss of blood supply and resultant tissue anoxia). Here, there is a wedge-shaped pale area of coagulative necrosis (infarction) in the renal cortex of the kidney. Microscopically, the renal cortex has undergone anoxic injury at the left so that the cells appear pale and ghost-like. There is a hemorrhagic zone in the middle where the cells are dying or have not quite died, and then normal renal parenchyma at the far right.

    *http://library.med.utah.edu/WebPath/CINJHTML/CINJ015.htmlhttp://library.med.utah.edu/WebPath/CINJHTML/CINJ016.html

  • *Gangrenous necrosis involves the tissues of a body part. The inflammation seen here is extending beneath the skin of a toe to involve soft tissue (fat and connective tissue) and bone. Because multiple tissues are non-viable, amputation of such areas is necessary. WebP