32 thoughts on “Questions and answers – Inflammation

  1. The difference between acute and chronic inflammation is given by the dominating cell type in the inflammatory exudate. When neutrophils predominate: acute inflammation; when lymphocytes / plasma cells predominate: chronic inflammation. The difference between acute and chronic inflammation is thus not unambiguously defined by the time aspect of the inflammatory process (start and duration). For example, all clinical acute viral and parasitic infections are always chronic inflammations.

  2. Dear all, I was wondering whether anyone has an overview of what the consequences of complement activation are? I find it a bit confusing…

  3. Complement activation–it results in the formation of biologically active substances which are :
    a) fragments (e.g. C3a,C5b etc), or
    b)complexes ( eg. 567, or the terminal complex with membrane attach complec (MAC) activity.
    These active products could have 4actions:
    a. Opsonization (important for phagocytosis of bacteria)
    b.chemotaxis ( important for attraction of inflammatory cells to the site of inflammation)
    c. Cytotoxic effects ( e.g. lysis of RBC in autoimmune hemolysis with antibodies)
    d. Effect on blood vessels–increased permeability=edema.This is usually indirect.

    Does that make more sense now.Ivan D.(Kansas)

  4. Mayu:
    The pathological changes are aneurisms typically located in the thoracic part of the aorta (arcus aorta) due to proliferation and ingrowth of the vasa vasorum facilitated by the syphilitic infection.

  5. In relation to acute pericarditis:
    Is its ethiology the preceding AMI or the viral infection leading to the AMI?

  6. Camilla,
    Acute myocardial infarction (AMI) is not a viral infection, although it is discusses whether the aterosclerotic changes in the coronary arteries have viral origin. AMI is initiated by impeded blood flow to the heart muscle, causing heart muscle necrosis. This necrosis might be transmural (i.e. involving the entire heart muscle thickness), which will induce an inflammatory response on the outer surface, i.e. the pericardium. This is called acute pericarditis. AMI is the primary cause of this disorder, but it can also be caused by more systemic changes such as chronic kidney failure.
    An unspecific acute pericarditis that is mild and most often symptomless may have viral etiology as a sign of systemic involvement.

  7. No one knows for sure, however, two theories dominate this field: The first theory is that cells fuse, the second theory states that giant cells arise as a consequence of incomplete mitosis (that is the cell replicates its nucleus, organelles etc. but does not undergo division into a mother and a daughter cell).

  8. I have two questions:
    1) What is the exact difference between transudate and exudate?
    Which pathophysiologic conditions are seen with transudate and exudate fluid?

    2) What is the definition of ulceration and why can’t it occur in the brain?

    Thanks in advance!

  9. exudate: extravascular fluid with high protein content (inflammatory response)
    transudate: extravascular fluid with low protein content due to increased hydrostatic pressure (fx in venous outflow obstruction in congestive heart failure) or decrease osmotic pressure (fx due to decreased protein synthesis in case of liver failure)

    ulceration describes originally the discontinuity of skin with a total loss of epidermis. with an extra word it is also used to describe loss of epithelium, wounds or inflammation in other tissues (eg gastric ulver, venous ulcer, etc). Extra- or intracerebral ulceration describe wounds in the head and brain region.

  10. Hi! I find it difficult to distinguish between neutrophils and lymphocytes in microscopic preparations. How can I tell the difference?

  11. I find this very hard too.

    Are there any other characteristics to distinguish lymphocytes from neutrophils?

    Is the cell concentration of neutrophils larger than the concentration of lymphocytes during chronic inflammation?

  12. AL:
    The main characteristic is the nucleus.

    The tissue in which chronic inflammation occurs is dominated by all inflammatory cells OTHER than neutrophils. Neutrophils dominate the tissue when acute inflammation occurs.

  13. The description of mic preparation 37 on Mirax states that amyloidosis can induce an inflammatory response. However, page 171 in Robbins book on pathology clearly states that amyloidosis does not induce an inflammatory response – which is correct?

  14. Amyloidosis does typically not display an inflammatory response.

    However, amyloidosis results in cell death and thus provokes responses related to inflammation, e.g. invasion of macrophages (cytokine-mediated recruitment).

  15. How do you describe the inflammatory process occurring in the pulp of teeth?
    For example: When preparing a crown for a tooth the pulp gets irritated. This causes infiltration of neutrophils (acute inflammation). Since no bacteria are present, the neutrophils quickly die. If the tooth is later exposed to bacteria, the response includes infiltration of lymphocytes and plasma cells (chronic inflammation).
    Is this correct?

  16. MM:
    Yes you can describe it briefly like that! The crucial point for further progress would be that the massive dead of the inflammatory cells will create focal areas of necrotic tissue, and then the point of no return has arisen as the bacterial growth will be able to continue undisturbed within these areas ending with a total necrotic and infected root canal producing apical periodontitis !
    Now a days we would prefer to involve details of the immune system a little bit more with the onset of primary as well as secondary antigen exposure along the tubules within the dentine! F.ex we have the dendrite cell very close to the odontoblast cells along the dentinal tubules being an antigen-presenting cell – you could say first line of defense -yes!

    For further interest I could suggest Text book of Endodontology edited by Bergenholtz et al. second ed. 2010. Wiley-Blackwell.

  17. What is the definition of resolution, regeneration and scarring/fibrosis in relation to the healing process and inflammation?

    When do each process occur?

    Are there any examples of complete healing processes where no sign of the damage remains, e.g. apoptosis?

  18. Resolution refers to the complete restoration of the tissue structure and function. This includes the terms regeneration (of the damaged parenchyma), macrophage phagocytosis of cellular debris, and edema resorption. Two conditions must be met in order for complete resolution to occur: 1) The parenchyma has proliferative capacity. 2) The tissue damage is limited and does not include larger stromal areas.

  19. Robbins: Hyperemia is an active process in which arterioles dilate to increase blood flow to a given tissue. The tissue thus becomes red due to engorgement with oxygenated blood.

    I also wonder whether this process is associated with increased transudation of fluid, does anyone know anything about this?

  20. I have three questions:
    1) Can peptic ulcers develop outside the stomach and duodenum?
    2) Can brain ulceration occur?
    3) Which bacteria causes colitis with pseudomembranes?

  21. Answer to:
    1) Peptic ulceration may occur in the ileum in rare cases (http://www.springerlink.com/content/q7u554604876jx38/fulltext.pdf)

    2) Yes, although it is very rare – e.g. see: “… ulcer invading the… brain is quite exceptional. A case is presented of a patient with a massive Marjolin’s ulcer arising in chronic scarring …” (scielo.isciii.es/pdf/neuro/v20n5/7.pdf)

    3) Pseudomembranous colitis is caused by the bacterium Clostridium difficile (http://en.wikipedia.org/wiki/Pseudomembranous_colitis).

  22. Hey Tooni,

    Try to read the very first comment at the top of this page (a student named Anders from last year asked the same question).

    Please write back if this doesn’t answer your question 🙂

  23. With regards to pathological terminology/categorization:

    Are abscess, flegmone and empyem three DIFFERENT types of acute inflammation or are they all categorized as a SINGLE type of acute inflammation (purulent)?

  24. Acute inflammation is defined as inflammation dominated by neutrophil granulocytes. Morphology (gross os microscopically) can be used as undercategorisation, e.g. abscess formation, phlegmone and empyema. However, the cellular contents are identical.
    The term purulent is used when neutrophil granulocytes forms an amorph substance together with cell debris and fibrin.

  25. In recent years, there has been a growing realization that mast cells are key components of inflammation. They can respond to pathogens, such as bacteria and viruses, through multiple Toll-like receptors expressed on their cell surface. They can furthermore mediate inflammation through the binding of antigen-specific antibodies. These, as well as other stimuli, result in degranulation (e.g. histamine) and cytokine production.

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