Irreversiblecellinjury 15thseptpatho121 090915142909 Phpapp02

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Irreversiblecellinjury 15thseptpatho121 090915142909 Phpapp02

  1. 1. PATHOLOGY LAB<br />DATE:- 15TH SEPT<br />RAVI A PATEL<br />CELL INJURY-2IRREVERSIBLE CELL INJURY & INFLAMMATORY CELLS<br />
  2. 2. GEOGRAPHY OF THE SLIDES SHOWN IN THE PATHO LAB- 9:00 AM 15TH SEPT<br />
  3. 3. TABLE#1<br />1<br />2<br />3<br />4<br />Slides of Irreversible Cell injury <br />5<br />7<br />8<br />6<br />TABLE #2<br />9<br />10<br />11<br />12<br />Slides of<br />Inflammatory cells<br />13<br />14<br />15<br />
  4. 4. Reversible injury slides<br />
  5. 5. LUNG ABSCESS<br />TYPE OF NECROSIS:- LIQUEFACTIVE<br /> HALL MARK:- <br />Grossly:- Purulent Exudate(PUS)<br />Microscopically:- Complete destruction of the tissue and loss of the architecture(We can see Cell debris, infiltrates of lymphocytes, and Fibres)- <br /> Though alveoli and other pulmonary structures can be differentiated depending on the level of lung absess<br />TYPE OF INFLAMMATION:-CAN BE ACUTE OR CHRONIC<br />
  6. 6. LEVELS OF LUNG ABSCESS<br />MINIMAL:- We can appreciate the Pulmonary struct.<br />MODERATE:- Most of the pulmonary parenchyma are involved in the necrosis<br />LATENT:- We can rarely appreciate the Pulmonary structures(Most of the tissue has been destroyed)<br />***Commonest cause is aspiration of infected particles****<br />
  7. 7. NORMAL LUNG TISSUE<br />Organ : Lung<br />Alveolar duct<br />Alveolar sac<br />
  8. 8. LPO<br />GRANULAR DEBRIS<br />NEUTROPHIL AND OTHER <br />INFLAMMATORY CELLS<br />1<br />HPO<br />
  9. 9. MYOCARDIAL INFARCTION<br />TYPE OF NECROSIS:- COAGULATIVE<br /> HALLMARK:- The necrosed Cells appear more eosinophilic(Dark pinkish) <br /> Infiltrates and PMNs become prominent(Neutrophils Spec)<br />PYKNOSIS:- Nuclear condensation<br />KARYOLYSIS:- Nuclear Dissolution<br />KARYORRHEXIS:- Fragmentation of nucleus into granules<br />Type Of inflammation:- Acute<br />
  10. 10. MYOCARDIAL INFARCTION<br />Kidneys and Heart have only one blood supply unlike other organs<br /> Because of this reason these organs are very sensitive to oxygen deprivation and due to this they usually undergo infarction in any ischemic conditions…..<br />When we think of infarction its Most commonly HEART AND KIDNEYS<br />
  11. 11. 2<br />The nucleus seems to have undergone <br />Pyknosis<br />Karyorrhexis<br />MI is Acute type of Inflammation<br />So there are a lot of PMNs <br />Notice that the Architecture of the <br />Myocardium is still preserved<br />But the Structures within the cells (Nucleus <br />And cytoplasmic) are not clear..<br />
  12. 12. Acute Pancreatitis<br />Type of Necrosis:- Enzymatic Fat Necrosis<br />Hallmark:- Necrotic fat cells have cloudy appearance<br />The necrotic area is surrounded by inflammatory reactions<br />Type of inflammation:- Acute<br />Notice the Architecture being still intact<br />
  13. 13. Noramal Pancreas<br />No<br />Islet of Langerhans<br />
  14. 14. 3<br />Site of Necrosis<br />Necrotic Tissue <br />Cloudy appearace<br />due to Autodigestion<br />by <br />Lipase <br />Inflammatory Reaction<br />
  15. 15. Pulmonary Tuberculosis<br />Type of Necrosis:- Caseous( Coagulative+Liqufaction)<br /> Hallmark:- Chessy appearance<br />Granuloma<br />Epitheliod cells(they are simply modified macrophages)<br />Giant Cells:-(Many macrophages combine and form Giant cell)<br /> Two types---Langhans and Foreign body Giant cells<br />CAUSE:- Mycobacterium tuberculosis<br />Type of inflammation:- Chronic<br />
  16. 16. 4<br />GRANULOMA<br />Surrounding the Granuloma<br /> we can see inflammatory reaction<br />
  17. 17. TB of the Lymph nodes<br />Type of Necrosis:- Caseous<br /> HALLMARK:- <br />Purple color- Epithelioid cells<br />Pink Color:- Granuloma<br />M. Tuberculosis if not removed from the lungs is taken up by the lymph…<br />Through Lympho-Heamtogenous distribution M. Tuberculosis is spread to different organs<br />
  18. 18. 5<br />PINK COLORED<br />GRANULOMA IS THE<br />SITE OF NECROSIS<br />PURPLE COLORED ARE THE EPITHELIOD CELLS <br />
  19. 19. Tuberculosis of Intestines<br />Type of Necrosis:- Caseous<br /> Hallmark:- In intestines there is Tunica muscularis which helps in differentiating lung and intesting TB<br />Granuloma<br />Epithelioid cells<br />Giant cells<br />
  20. 20. 6<br />Site of necrosis<br />(Granuloma)<br />Inflammatory Reaction<br />Where epithelioid cells are visible<br />
  21. 21. ACUTE APPENDICITIS<br />HALLMARK:- PMNs(NEUTROPHILS)<br />MOST COMMON CAUSE:- Enterococcusfeacalis<br />
  22. 22. 4<br />3<br />2<br />1<br />NORMAL APPENDIX<br />Organ : Appendix<br />4 layers<br /> 1. Mucosa<br />2. Submucosa<br /> 3. Tunica muscularis<br /> 4. Tunica serosa<br />
  23. 23. 7<br />IMPT HALL MARK OF <br />ACUTE APPENDICITIS<br />PMNs <br />SPECIALLY NEUTROPHILS<br />Tunica <br />Muscularis<br />
  24. 24. TUBERCULOID LEPROSY-SKIN<br />It is a Chronic type of Inflammation<br />Cause:- Infection by Mycobacterium leprae<br /> Hallmark:- <br />Granuloma in Dermis<br />Foamy cells or Leprae cells in Dermis<br />Epithelioid cells <br />
  25. 25. NORMAL SKIN<br />
  26. 26. 8<br />Giant cells<br />Foam cells or Leprae cells<br />Granuloma in<br /> the Dermis<br />Epithelioid cells<br />
  27. 27. Renal infarction<br />Kidney and Heart have only one main blood supply<br /> Because of this reason these organs are very sensitive to oxygen deprivation and due to this they usually undergo infarction in any ischemic conditions…..<br />Hallmark:- <br />The cells look more eosinophilic,karyolysis<br />And karyorrhexis can be seen<br />When we think of infarction its Most commonly HEART AND KIDNEYS<br />
  28. 28. Normal Kidney<br />
  29. 29. Renal infarction which we couldnot see during our Demo slides<br />Notice that the structures of Glomerulus and the tubules are still intact <br />But due to protein degeneration which took place due to the ischaemic infarction the nucleus are fragmented and infiltrates of the PMNs can be seen(This make it more eosinophilic)<br />
  30. 30. Inflammatory cells<br />
  31. 31. Cells elevated in different kinds of infections<br />Bacterial infection:- Neutrophils<br />Neutrophils contain Myeloperixidase which helps in the O2 dependant pathogen destruction by forming free radicals<br /> (Neutrophils will convert into monocytes after their action due to their short life span)<br />Viral Infection:-Lymphocytes<br /> Lymphocytes will release interferons which in turn will help makes the process of virus recognizition through receptors more effective<br />Parasitic infection:-Eosinophils<br /> There are granules in Eosinophils which contains neurotoxins,andeosionophilperoxidase– neurotoxins are harmful to parasites <br />
  32. 32. 9<br />
  33. 33. 10<br />
  34. 34. 11<br />
  35. 35. 12<br />
  36. 36. <ul><li>Organ- Liver
  37. 37. Pathology::- Fibrosis</li></ul> due to liver cirrhosis<br /><ul><li>Precursor cells</li></ul> leading to fibrosis:-<br /> Fibroblasts<br />13<br />
  38. 38. 14<br />
  39. 39. TYPICAL LANGHAN’S CELL<br />HORSE SHOE SHAPED<br />Nucleus are arranged on the <br />Periphery so the the infection does<br />Not spread further<br />GIANT CELLS <br />Foreign body <br />Giant cell<br />TYPICAL FOREIGN BODY GIANT CELL<br />NUCLEUS ARE SCATTERED<br />
  40. 40. 15<br />SLIDE MADE FROM BLOOD TISSUE<br />PATHOLOGY:-<br /> MULTIPLE MYELOMA<br />PLASMA CELLS CONTINUE<br /> TO BE IN G-2 PHASE <br /> SO WE SEE SO MANY PLASMA CELLS <br />IN BLOOD DURING THIS CODITION<br />HPO<br />TYPICAL PLASMA CELL<br />CART/<br />WHEEL <br />SHAPE NUCLES<br />LPO<br />RUSSLE BODIES<br />
  41. 41. Thanking to the entire Universe<br />

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