Patho Week 4 Immunity.txt

  1. What are other names for a Type I hypersensitivity reaction?
    Anaphylaxis, Allergy, Immediate
  2. List four type one local hypersensitivity reactions?
    • 1. Allergic Asthma
    • 2. allergic Rhinitis
    • 3. Allergic Dermatitis
    • 4. Allergic Gastroenteropathy
  3. What is the antibody involved with Type I Hypersensitivities?
  4. Allergic Rhinitis is a local Type I reaction. Where does it occur and what causes the symptoms.
    Allergic Rhinitis occurs in the upper respiratory. Vasodilation and WBC infiltration cause stuffiness and exudate formation causes a runny nose.
  5. Allergic Dermatitis is a local Type I reaction. How does it manifest and when is it common?
    Allergic Dermatitis manifest as rashes or hives on the skin after you ingest or breath the antigen. It is most common with food allergies.
  6. Allergic Gastroenteropathy is a local Type I reaction. Describe it.
    Allergic gastroenteropathy is usually from something you ingest and it usually affects the lining of the gut. it causes vasodilation in the gut wall and the exudate formation causes sloughing-off of gut wall which can lead to diarrhea.
  7. How does generalized anaphylactic disease (type I) differ from the local type I?
    Generalized anaphylaxis is a type I response that is systemic. The vascular volume is constricted which causes intervascular fluid to escape to the ECF, so IV volume is shrinking. It also causes bronchospasms so patient can't breathe.
  8. Describe the sequence of events in Type I Hypersensitivity response.
    • 1. Allergen enters body
    • 2. T4 helper cells bind to allergen and release IL so B cells can bind as well
    • 3. Bcell binds to allergen; some become memory cells and some become plasma cells that secrete IgE
    • 4. The IgE binds to mast cells and causes them to degranulate and release their contents to kill the antigen
  9. What are the four types of hypersensitivity responses?
    • Type I = Allergic/Anaphylactic
    • Type II = Cytotoxic
    • Type III = Immune Complex
    • Type IV = Delayed (DTH)
  10. What are antigens called in a Type I response? What are they called in other responses?
    • Type I = allergens
    • Type II = antigens
  11. Where are the antigens located in Type I and Type II hyperactivity responses?
    Allergens are free floating in Type I; Antigens are FIXED on a cell/tissue in Type II.
  12. Type II hyperactivity is compliment activated. What activates the compliment?
    When the antigen creates a crosslink between two antibodies on the surface of the mast cell. That activates compliment.
  13. Why is Type II called Cytotoxic?
    Type II is called Cytotoxic because the antigen is fixed on a cell/tissue. In order to get rid of it, the cell must die.
  14. What are the two ways to get rid of an antigen in a Type II hyperactivity reaction?
    Once compliment has been activated, the compliment can either drill holes in the membrane wall to lyse it, or the compliment can coat the antigen in opsonins which will facilitate phagocytosis.
  15. Describe Myasthenia Gravis
    Autoimmune disorder, classified as Type II, but there is no cytotoxicity so there is no tissue damage. The ACH receptors are blocked at the neuromuscular junction which results in decreased muscle contraction and muscle weakness. This is an example of how with tissue bound antigens we can make antibodies against the receptor not the antigen. This is autoimmune so the body things the ACH receptors are foreign.
  16. Describe Graves' Disease
    The antibody binds with the TSH receptor, but instead of inhibiting production, it stimulates the TSH to produce a lot of Thyroid Hormone
  17. What is Erythroblastosis Fetalis, how is it prevented?
    Rh- mom has Rh+ baby, mix of circulation happens during pregnancy. Mom's immunity builds memory cells as she destroys the newborns Rh+ in her. Second pregnancy, there is a mix of circulation and the anti-RH antibodies end up in fetus killing its RBCs. This is prevented by giving the mother Rhogam after 1st pregnancy so her immune system will not develop memory cells.
  18. List three diseases associated with Type II: Cytotoxic Hypersensitivity Reactions
    Myasthenia Gravis, Graves', Erythroblastosis Fetalis
  19. What is different about the antigens between Type I and Type II hypersensitivity reactions?
    • Type II = fixed antigen
    • Type III = free floating
  20. What do the free floating antigen create in Type III?
    Immune Complexes
  21. How are small and large immune complexes taken care of in the body?
    Small immune complexes are small enough to cross the glomerular membrane and be voided out, which large immune complexes are large enough to attract phagocytes and get eaten up.
  22. What is "frustrated phagocytosis" and how does it relate to hypersensitivity reactions?
    Frustrated phagocytosis occurs in a Type III response. The medium immune complexes are not big enough to attract phagocytes, but are too big to cross glomerular membrane to be voided out. Therefore, they get stuck in the membrane and since they are too big for the neutrophils to wrap around, the neutrophils release contents to lyse the cell and antigen. This causes tissue damage in that area.
  23. List some differences between Type IV and the other types of hypersensitivity reactions.
    • Type IV:
    • - Tcell mediated
    • - no Bcells
    • - no antigen
  24. When the Tcell binds directly to an antigen in Type IV, what two things can it become?
    • T1 Helper Tcell or
    • a Cytotoxic Tcell
  25. What two ways to Tcells kill in Type IV?
    • 1. Lysis/Apoptosis
    • 2. Delayed
  26. When Tcells kill by apoptosis or lysis in a Type IV reaction, how do they do that?
    The Tcell is bound to the antigen, it can drill holes in the membrane and kill it that way, or it can promote apoptosis.
  27. What is an autoantibody or an autoreactive Tcell?
    Produced in response to self-antigen, even though the antigen isn't actually foreign
  28. What is an auto- or self-antigen?
    An antigen that is perceived as foreign but is not, it is part of the host
  29. What is tolerance?
    The reason our immune system doesn't normally react to our own cells/tissue. The immune system "tolerates" the components of "self".
  30. Where does the antigen parade take place?
  31. What is the difference between negative and positive selection?
    • Negative selection is the process where in the antigen parade we actively send death signals to clones that had a response that was too strong to a self-antigen.
    • Positive selection is when we actively decided to keep the moderate or intermediate reacting clones
  32. What are the four parts of peripheral tolerance?
    • 1. Ignorance
    • 2. Deletion
    • 3. Inhibition
    • 4. Suppressor
  33. Is the antigen parade classified as Central or Peripheral tolerance?
  34. Why do we have peripheral tolerance?
    In case there is a leak in central tolerance
  35. What is another name for cytotoxic hypersensitivity?
    Tissue Specific
  36. What are the main effector cells for Type I?
    Mast Cells and Basophils because this is an allergic reaction, they both release histamine.
  37. What is ADCC?
    Antibody Dependent Cell Mediated Cytotoxicity: these are null cells, K cells and Natural Killer Cells, they can directly lyse hole immune complexes but it doesn't get compliment involved so there is no opsonization. This is Type II
  38. List three examples of delayed hypesensitivities
    • - granulomatos diseases like TB. TB test; it takes 48-72 hours for the hard, fibrous bump to develop on your arm. This is Type IV. This causes caseous necrosis.
    • - skin graft
    • - contact dermatitis
  39. In delayed hypersensitivity, what do TH1 helper cells release to attract macrophages.
  40. If T8 cells are involved with Type IV hypersensitivity, is that quick or delayed? What about Th1 helper cells?
    If T8 cells are involved, those are the cytotoxic Tcells so they can lyse immediately. TH1 cells are helper cells and release lymphkines to attract macrophages. This is Delayed Hypersensitivity and takes longer.
  41. What happens to Tcells that have a weak response in the antigen parade?
    They just live their little lives and then apoptosis happens.
  42. What selection happens to Tcells that have a strong reaction to self-antigens in the antigen parade?
    Negative Selection; they get a death signal
  43. What selection happens to Tcells that have an intermediate reaction to self-antigens in the antigen parade?
    Positive Selection; they get a survival/live signal.
  44. What is the primary signal in peripheral tolerance?
  45. What is the secondary signal in peripheral tolerance?
  46. If there is a Fas Ligand receptor on a Tcell that presents itself first to the APC, what happens?
  47. If the second signal in peripheral tolerance is CD 152 instead of of CD 28, what happens?
  48. If T-suppressor cells release interleukin 10 and TGFbeta to stop a Tcell from being activated, what happens?
  49. If there is a hypersensitivity to a blood transfusion, what type is that?
    Type II
  50. Describe SLE, including what it stands for, eitiology and symptoms.
    • Systemic Lupus Erythromatosis
    • - something on clotting factor 8 looks foreign, autoimmune
    • - bleeding, clotting issues
    • - Arithritis/joint issue: MOST COMMON, followed by Malar butterfly rash
    • - Thrombocytopenia, neutropenia occur because they get destroyed.
    • - neutropenia causes increased risk of infection
    • - involves Type II and Type III hypersensitivities
    • - anytime blood disorder is involved it is Type II
    • - the rash, gangrene, vascullitis and diarrhea are type III
    • - must have 4 symptoms at once or back-to-back to be SLE
    • - Anemia occurs because of RBC destruction
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Patho Week 4 Immunity.txt
Patho: Immunity