Micro Exam 3: Hypersensitivity – Flashcards
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Unlock answers| What is the term used to describe an immune response which is in excess of the norm? (may result from "accidental" triggering of immune system) |
| hypersensitivity; damage to host |
| Allergies are categorized into what type of hypersensitivity? |
| Type 1 or Immediate hypersensitivity |
What does IgE do on re-exposure in Type 1 or Immediate Hypersensitivity? What else is released during this process? |
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| Runny nose, red watery eyes, skin redness and asthma are all symptoms of what type of hypersensitivity? What is the most severe symptome of this type of hypersensitivity? |
Type 1/Immediate Hypersensitivity most severe = anaphylaxis (systemic) |
| "wheal and flare" is what? |
type 1/immediate hypersensitivity reaction in the skin
flare - wheal - flare |
| What are the biological effects of mast cell mediators? (What do activated mast or basophils produce and what do they cause) |
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| What type of hypersensitivity causes transfusion reactions, haemolytic disease of newborns and some autoimmune diseases? |
| Type 2 or Antibody Mediated Hypersensitivity |
| Describe the process of type 2 hypersensitivity. What is the reaction onset time? |
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| What are the three types of Type 2 or antibody mediated hypersensitivity (cytotoxic reactions)? |
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| Cytotoxic hypersensitivity is what 3 things? |
Type II IgG Fast |
| How does haemolytic disease in newborns work? |
the mother is RhD negative but fetus is RhD positive; when first birth, RhD positive cells in mothers blood stream and mother makes anti-RhD IgG antibodies
For the next pregnancy; the anti-RhD IgG attack fetus |
| What type of hypersensitivity causes serum sickness, glomerulonephritis in endocarditis, autoimmune disease like rheumatoid arthritis, SLE? |
| Type 3 or Immune Complex Mediated Hypersensitivity |
How does Type 3 (or Immune Complex Mediated Hypersensitivity) work?
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large amount of soluble antigen in plasma reacts with antibody and forms large antigen-antibody complexes these overwhelm normal ability of RBC to take them up for transport and removal in liver |
| What happens to the immune complexes in Type 3 hypersensitivity? What does PMN do? What is onset rate? |
trapped in capillaries (esp. kidneys and lungs) and activate complement cascade - PMN are attracted but unable to phagocytose complex; release granules of damaging enzymes (cause local tissue damage) - mast cell degranulate and cause inflammation - rxn onset within 6 hrs of exposure
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| 3 things about Immune Complex Mediated. |
Type III IgG Slow |
List examples of Type III hypersensitivity
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| What type of hypersensitivity is seen in tuberculin skin tests, contact dermatitis and granuloma formation? |
| Type 4 or Delayed Type Hypersensitivity |
| Why is Type 4 hypersensitivity slow to develop? |
| because it is mediated by CELLS and not antibodies |
| When does sensitization occur in Type 4 hypersensitivity? What occurs on re-exposure? |
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| 3 things about delayed type hypersensitivity |
Type IV (4) T cell Delayed |
| Are antibodies involved in Type 4/Delayed Type Hypersensitivity? |
| No. |
| How long does it take for Type 4 Sensitivity to occur? What happens if it is chronic |
occurs in 24-48 hours - if chronic (antigen cannot be cleared), area surrounded by macrophages with lymphocytes and fibrosis occurs = granuloma |
| what type of cancer in particular is responsible for secondary immunodeficiency states? |
| hematological malignancies |
| How sufficient is pregnancy to secondary immunodeficiency states? |
| mild, but sufficient enough to increase susceptibility to malaria and TB (for example) |
| What are the types of immunodeficient states? |
1. Primary = genetic 2. Secondary = therapy, cancer, preggers, etc |
| What may happens in complement deficiencies of genetic (primary) immunodeficiency states? |
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| What does loss of early components of complement system (genetic) result in? |
| results in increased staphylococcal and streptococcal infections |
| loss of late components of complement system (genetic) results in? |
| increased Neisseria infections |
| What results from genetic (primary) defect in phagocytic cell function? What organisms tend to cause infections? |
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| What is Subacute Combined Immune Deficiency (SCID)? |
a group of diseases in which there are low antibody levels, and lack of lymphoid tissue becuase failure of development
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| When will patients with lymphocytic malfunction (genetic - primary immunodeficiency) present with infections? |
as maternal immunity transferred at birth wears off ex. SCID and others |
| What immunodeficiency causes the individual to tend to get infected with viruses (especially herpes family), intracellular bacteria and fungi? |
| T cell deficiency (primary - genetic) |
| What type of immunodeficiencty causes patients to tend to get bacterial infections? |
| B cell deficiencies (primary - genetic) |
| What does chemotherapy do to the immune system? |
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| How long do the levels of PMN and other blood cells drop for after chemotherapy? |
| 1-4 weeks depending on therapy |
| What type of immunodeficiency are corticosteroids? What are some examples of them? What do they do? |
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What are the commonly used post transplant medications? What do they do? What type of cell is then predisposed to infection? |
cyclosporin A, tacrolimus, serolimus - inhibit lymphocyte function - immunosuppressed w/ predisposition to infection of T cell deficiency |
| What is the main site of production of opsonizing antibody? |
| spleen! |
Why might a spleen be removed? What does it do?
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What does a splenectomy increase the risk of? List some examples. |
life threatening infections with encapsulated organisms ex. Strept pneumo, Haemophilus influenzae, Neisseria Meningitidis, salmonella, etc |
| Does infections after a splenectomy progress slow or rapidly? |
| rapidly! health to death in <24 hrs |
| Immunization is recommended for patients undergoing which procedure? What are bugs are they immunizing for? |
splenectomy S. pneumoniae, H. influenzae, N. meningitidis |
| List the 4 Classic features of inflammation: |
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| First exposure - initial response? |
microorganism gain entry (breach in innate defense) phagocytose bacteria and present antigen to T cells (local lymph nodes) complement activated = MAC = punch holes in cell membrane |
| What are some examples of inflammatory mediators? what do they do? |
histamine, tumor necrosis factor α (TNF-α) - release cells that increase vascular permeability and increase blood flow
part of first exposure response |
| what is: migration of cells in response to concentration gradients of certain factors? |
| chemotaxis |
| what is: movement of blood cells between endothelial cells lining blood vessels |
| diapedesis |
| Describe the arrival of PMN |
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| what resutls in oxidative burst? |
| fusion with granules that contain reactive oxygen radicals (hydrogen peroxide) generated within the PMN |
| Accumulation of PMN forms what? |
| pus |
| What causes proliferation of lymphocytes and lymph node enlargement and tenderness? |
| T cell activation |
| What happens when T cells are activated? What about B cells? |
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| what does class switching entail |
| switch from IgM to IgG |
| What happens in the lymph node after activation of the specific response? How long does this take? |
T cells activate macrophages so become more effective at kililng organism by producing more reactive substance to fuse to phagocytic vacuoles - 1-3 days after infection arrive at site |
| True or false: initially, opsonization/phagocytosis and complement activation occurs in blood with IgM, but later in tissues with IgG |
| true |
If organisms have spilled into the blood, what will clear them?
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| macrophages in the spleen clear them |
| What happens in severe reaction? |
production of cytokines = fever and production of acute phase reactants - bone marrow produces more PMN = increase WBCs |
| Memory cells are |
| long lived and able to repond to reexposure by generating IgG antibodies rapidly (others too) |
| What happens as the infection subsides (acute)? Is anything left behind? |
| T cells suppress immune response = conditions return to normal; may be residual tissue damage manifested by fibrosis + scaring |
| What happens if infection is chronic? |
| macrophages and lymphocytes at site = form granuloma = walled off by fibroblasts |
| What is produced locally at the site of a viral infection? What does this result in? |
interferon; results in inhibition of viral replication, "warns" adjoining cells, renders them resistant to infection, activates immune system, host experiences malais and muscle aches and fever
may activate NK killer cells (eliminate infected cells) |
| How does a fever help fight against viral infection? |
| inhibits many viruses unable to multiply at raised temperatures |
| True or false: infection may be extinguished before the host becomes aware of symptoms. |
| true |
| which antibody is produced more rapidly on re-exposure? |
| IgG |
| How might bacteria evade the immune response? |
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| Which bacteria are not killed by the usual mechanisms inside the cell phagocytic vacuole and can multiply? |
| salmonella |
| What bacteria may prevent the phagocytic cell from killing them? |
| M. Tuberculosis |
| Which bacteria evades the bodys immune response by destroyign complement components? |
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| Which bacteria evades the bodies immune response by destroying immunoglobulin? |
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| Which bacteria evades the host immune response by preventing phagocytosis? |
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| Which bacteria evade the hosts immune response by growing in the cytoplasms of cells protected? |
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