Cell Injury II Death and Adaptation by murplelake82

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									Cell Injury II: Death and Adaptation
Questions
   1. What are the 2 types of cell death? What is associated with nonprogrammed cell death?
   2. What are the 4 types of cellular adaptation?
   3. What are the 2 major processes in necrosis? Which is associated with liquefaction, and which is
        associated with coagulation necrosis?
   4. What are other patterns of necrosis?
   5. What is the usual cause of coagulation necrosis, and what tissue is exempt from this?
   6. What is the usual cause of liquefactive necrosis? What tissue liquefies in response to hypoxic
        injury?
   7. What are the histological characteristics of coagulation necrosis, and what is the time table of
        their appearance.
   8. Liquefactive necrosis often involves pus, which is a mixture of what?
   9. What causes gangrene, and what is wet gangrene?
   10. What is caseous necrosis?
   11. What are the 2 usual causes of fat necrosis, and what is the resulting material?
   12. What are the 2 types of calcification?
   13. What is the usual site of calcification in the heart?
   14. What are the main differences between necrosis and apotosis?
   15. What are possible causes for apoptosis?
   16. What is the intrinsic and extrinsic apoptotic pathway?
   17. What are the regulatory intracellular signals for apoptosis? Which are proapoptotic and which
        are anti-apoptotic? How do they act?
   18. What is the morphological progression of apoptosis?
   19. What are the 3 pathways for intracellular accumulation?
   20. Where does steatosis form? Is it reversible? What is the progression?
   21. What are the causes of steatosis, and what do they affect?
   22. What may cause protein accumulation in the kidneys, and what part is most affected? What
        about multiple myeloma?
   23. What is the difference between type I and II glycogen storage disease?
   24. What are foam cells, and what happens when they rupture?
   25. What are 2 exogenous pigment accumulations?
   26. What are the 4 types of endogenous pigment accumulation? Which a normal process associated
        with aging?
   27. Above what level of bilirubin does jaundice develop?
   28. What is hemosiderin? What is the extreme form of hemosiderin accumulation when Fe cannot
        be excreted adequately?
   29. How is melanin formed, and what is a benign and malignant accumulation of melanin?
   30. Contrast atrophy and hypertrophy. What is hyperplasia?
   31. What is an example of metaplasia in the lung (usually due to smoke irritation), and the
        esophagus (due to acid reflux)?
Answers
   1. Necrosis and apoptosis. Inflammation accompanies necrosis.
   2. cellular adaptation
           a. Atrophy,
           b. Hypertrophy,
           c. Hyperplasia
           d. Metaplasia.
   3. Necrosis:
           a. Enzymatic auto- and heterolysis,
           b. Protein denaturation.
           c. Enzymatic processes area associated with liquefactive necrosis, and denaturation
               processes are associated with coagulation necrosis.
   4. Gangrenous, caseous, and fat necrosis.
   5. Hypoxia causes coagulative necrosis, except for CNS tissue.
   6. Liquefactive necrosis is caused by bacterial or fungal infection. CNS tissue liquefies on hypoxic
       injury.
   7. Eosinophilic, anuclear cells, with intact structure and white blood cell infiltrate in 12-18 hours.
       By 4-5 days a pale infarct with hyperemic border develops, especially in myocardial infarction.
   8. Dead and a few alive inflammatory cells and pathogens, liquefied tissue, and exoenzymes.
   9. Coagulation necrosis cuts off the vascular supply for gangrene, and infection causes liquefactive
       wet gangrene.
   10. TB creates a form of coagulative necrosis which results in obliterated structure, and a
       white/cheesy structure.
   11. Pancreatic enzyme release by trauma or pancreatitis, and breast trauma, cause fat liquefaction by
       lipases, and fat saponification after combination with calcium.
   12. Dystrophic (local and post necrosis) and metastatic due to hypercalcemia.
   13. Valves
   14. Necrosis is due to injury, unregulated, involves a large number of cells, is always pathological,
       and initiates inflammation. Apoptosis is highly-regulated, occurs in many adult tissues and
       embryogenesis, in isolated cells, and does not initiate an inflammatory response.
   15. Hormonal changes (endometrium, prostate post castration), control of proliferating populations
       (intestinal crypts, even tumors, etc.) DNA damage, other unrepairable cellular stress that does
       not cause necrosis.
   16. Apoptosis
           a. Intrinsic is more closely related to p53 (stops in G1 with DNA damage, causes apotosis
               if repair is impossible. Apaf-1 complexes with cytochrome c, causes procaspase 9 to
               caspase 9, which causes procaspase 3 to caspase 3, which is executive, causing
               endonuclease, protease, and other apoptotic activation.
           b. Extrinsic pathway is related to TNF and FAS, which bind Death Domain Receptors,
               cause procaspase 8 to caspase 8, which causes procaspase 3 to caspase 3, as above.
   17. Bcl-2 is anti-apoptotic, and Bax is proapoptotic. The regulators dimerize, and the regulator with
       the majority determines the cell fate, by interacting with Apaf-1 to open (apoptosis) or close
       mitochondrial permeability pores.
           a. Bax: Bcl-XS, Bad, Bid, Bim, Bak.
           b. Bcl-2: Bcl-XL, Bcl-W.
18. Nuclear DNA is cut into segment, and the nucleus forms distinct segments, while the membrane
    blebs, and buds off apoptotic bodies which are phagocytosed immediately.
19. Intracellular accumulation
        a. (Inadequate removal) Endogenous
        b. Abnormal (Defective metabolism) Endogenous
        c. Exogenous (no process for degradation or transport).
20. In heart and skeletal muscle, and liver. Steatosis progresses from small peri-nuclear vesicles to
    coalesced vesicles pressing the nucleus, to cell rupture. The process is reversible.
21. In the liver steatosis may be caused by starvation causing massive FFA mobilization, CCl4
    disruption of apoprotein, alcohol damage to the triglyceride pathway and liver stroma, and
    anoxia blocking oxidation to ketone bodies and CO2. Muscle steatosis is caused by hypoxia.
22. Glomerulonephritis releases proteins which must be reabsorbed in the proximal tubules, forming
    pink hyaline droplets. Multiple myeloma causes the accumulation of protein in the RER known
    as Russell bodies because of immunoglobulin light chain overproduction.
23. glycogen storage disease
        a. Type I glycogen storage disease is a defect in glucose-6-phosphatase causing liver
             intracytoplasmic and intranuclear glycogen deposition.
        b. Type II is a defect in lysosomal glucosidase, causing cardiomegaly, and muscle
             accumulation of cytoplasmic and membrane bound glycogen.
24. Foam cells are subendothelial macrophages laden with cholesterol and lipid following
    endothelial injury. They may rupture, releasing cholesterol which will crystallize.
25. Carbon anthracosis in the lungs, from macrophages transporting C to tracheobronchial nodes.
    Tattoo ink.
26. From Hb bilirubin and hemosiderin, lipofuscin, and melanin. Lipofuscin is normally
    accumulated with age with free radical injury.
27. Above 2.0 mg/dL.
28. Hemosiderin is Hb derived ferritin micelles in macrophages and parenchymal cells.
    Hemosiderosis is more local, hemochromatosis is systemic. Dietary iron, hemolytic anemia,
    hemolysis, and repeated transfusions can cause elevated hemosiderin.
29. Melanin is oxidized tyrosine, which normally accumulated in benign nevi (moles), and
    pathologically accumulates in malignant melanoma.
30. Atrophy is a decrease in cell size, hypertrophy is an increase in cell size. Hyperplasia is an
    increase in cell number.
31. Columnar to stratified squamous metaplasia is observed in respiratory epithelium in smokers,
    while stratified squamous to columnar metaplasia is observed in the esophagus following acid
    reflux, in a condition known as Barrett’s esophagus.

								
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