Alterations in immunity: immune disorders and immunodeficiency Flashcards

1
Q

what is a hypersensitivity?

A
  • an EXTREAM or dramatic reaction to something
  • someone is VERY sensitive to something
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2
Q

What are the 4 types of immune mechanisms?

IMMUNE MECHANISMS !! NOT ANTIBODIES

A
  • TYPE 1: IgE mediated
  • TYPE 2: tissue specific / blood reactions
  • TYPE 3: immune complex mediated
  • Type 4: cell mediated
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3
Q

what is an allergy and is it a hypersensitivity?

A
  • yes! its an hypersensitivity
  • its due to IgE
  • deleterious effects of hypersensitivity to Enviromental (exogenous) antigens
  • has to do with something outside of the body to have a reaction
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4
Q

what is an autoimmunity and is it an hypersensitivity

A
  • yes it is
  • autoimmunity is a disturbance in the immunologic tolerance of self antigens antinuclear antibodies
  • aka self attacking self (or your own immune system attacking itself)
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5
Q

what is an alloimmunity?

A
  • immune reaction to tissue of another individual
  • immunity reacting to SOMEONE else
  • ex: blood transfusions or organ transplantation
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6
Q

when do hypersensitivities occur?

A
  • they occur after sensitization, meaning they don’t happen the first time someone comes into contact with something making them a SECONDARY immune response
  • for example, an allergic reaction will happen during the second bee sting, not first
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7
Q

are hypersensitivities a primary or secondary immune response?

A
  • secondary
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8
Q

what is immediate hypersensitivity?

A
  • it takes minutes to hours for a reaction
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9
Q

what is anaphylaxis?

A
  • the most rapid and severe allergic reaction that occurs in minutes
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10
Q

what is a delayed hypersensitivity

A
  • the reaction is hours to days after exposure
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11
Q

For type 1: whats the effector cell, the antibody, what the onset is, and the example:

A
  • type 1 = IgE mediated
  • effector cell = Mast cell
  • antibody = IgE
  • onset = immediate
  • example = seasonal allergies (or anaphylaxis)
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12
Q

For type 2: whats the type of hypersensitivity whats the effector cell, the antibody, what the onset is, and the example:

A
  • type 2 = tissue specific
  • effector cell = tissue macrophages
  • antibody = IgG & IgM
  • onset: immediate
  • example: graves’ disease, blood transfusion reaction
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13
Q

what do I need to know about graves disease for the exam?

A
  • that its an autoimmune disease and that it effects the thyroid, and is genetic typically
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14
Q

For type 3: whats the type of hypersensitivity whats the effector cell, the antibody, what the onset is, and the example:

A
  • type 3: is immune complex mediated
  • effector cells: neutrophils
  • antibody: IgM & IgG
  • onset: immediate
  • example: LUPUS (SLE) and Raynaud’s
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15
Q

For type 4: whats the type of hypersensitivity whats the effector cell, the antibody, what the onset is, and the example:

A
  • type 4 = cell mediated
  • effector cell: lymphocytes & macrophages
  • antibody: none
  • onset: delayed
  • example: poison ivy, contact dermatitis, contact sensitivity
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16
Q

what hypersensitivity is type 1

A
  • IgE mediated
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17
Q

what is type 1 hypersensitivity against?

A
  • environmental antigens
  • allergies
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18
Q

is type 1 an immediate hypersensitivity or late?

A
  • immediate (its allergies)
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19
Q

what does type 1 hypersensitivity trigger?

A
  • mast cells to degranulate to give us histamine
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20
Q

is type 1 hypersensitivity worse on the first exposure or second

A
  • second bc the body had never had it before the first exposure to know it was bad
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21
Q

what are the first symptoms of anaphylaxis?

A
  • nausea and vomiting, diarrhea
  • hives, swelling, itching, redness
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22
Q

in anaphylaxis what does histamine do?

A
  • bronchoconstriction = drop in BP
  • unable to breath
  • vascular = hypotension and then shock bc of vasodilation -
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23
Q

what are the common examples of type 1 hypersensitivity?

A
  • Enviromental antigens
  • pollens, mold, food, pollution, foods, animals
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24
Q

in allergies what are the two types of histamine receptors

A
  • H1
  • H2
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25
Q

what clinical symptoms is the H1 receptors responsible for?

A
  • itching
  • hives
  • eyes
  • rhinitis = nose
  • hypotension
  • bronchospasm
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26
Q

what clinical symptoms is the H2 receptor responsible for

A
  • GI cramps & mal - absorption
  • dysrhythmias
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27
Q

what is a treatment for allergies?

A
  • antihistamines
  • anti-inflammatory
  • epinephrine for severe
  • desensitization
  • cautiously
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28
Q

what causes anaphylaxis?

A
  • severity depends on the level of sensitization
  • can be small (skin test)
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29
Q

what do allergenic desesnitization do?

A
  • they are injections @ home that have IgG blocking antibodies
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30
Q

what is the type 2 hypersensitivity tagreting?

A
  • tissue specific
  • specific cell or tissue is the target of immune response
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31
Q

what antibody is type 2 hypersensitivity?

A
  • IgG and IgM mediated !
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32
Q

what are the different mechanisms of type 2 hypersensitivity?

A
  • cell is destroyed by antibodies and complement
  • cells are destroyed through phagocytosis
  • antibody dependent cell mediated cytotoxicity (ADDCC)
33
Q

what do natural killer cells do?

A
  • causes target cell malfunction (graves disease)
  • kills cancer cells
34
Q

what is alloimmunity?

A
  • immune system reacts with antigens on the tissue surface of other genetically dissimilar humans
35
Q

what are the examples of alloimmunity?

A
  • transplant rejection
  • transfusion injection
  • Rh incompatibility
  • graft rejection
36
Q

are the signs & symptom with an ABO transfusion reaction?

A
  • back pain
  • blood in urine
  • chills
  • fever
  • jaundice
37
Q

what labs are run with ABO incompatible transfusing reactions? & what hypersensitivity is it?

A
  • CBC = complete blood count
  • bilirubin
  • type 2
38
Q

what is the treatment for ABO transfusion rejection?

A
  • fluids
  • symptom management
39
Q

what is HND and what immunity malfunction is it?

A
  • alloimmunity
  • if a Rh-negative mother has a Rh positive baby and the second pregnancy the fetus is also Rh positive the mother’s antibodies with the blood will enter through the placenta and attack the babies blood and break it down
  • only on second pregnancy
  • only when mom is Rh negative and baby is Rh positive
  • type 2
40
Q

in HND what causes destruction?

A
  • direct destruction of macrophages
41
Q

what are the 3 types of graft rejection?

A
  • hyperacute
  • acute
    -chronic
42
Q

what do I need to know ab hyperacute graft rejection?

A
  • its immediate
  • its rare
  • due to preexistent antibodies to the antigens of the graft
43
Q

what do I need to know about acute graft rejection?

A
  • cell mediated immune response against unmatched HLA antigen
44
Q

How long does chronic graft rejection take?

A
  • months or years
45
Q

what is chronic graft rejection due to?

A
  • inflammatory damage to endothelial cells of vessels as a result of weak cell mediated reaction against minor HLA antigens
45
Q

what is graves disease due to? what type of hypersensitivity is it?

A
  • hypersensitivity type 2
  • autoantibodies bind to the surface of antigens in thyroid and continually stimulate thyroid cell receptors
  • hyperthyroid
45
Q

what is type 3 hypersensitivity named? what antibodies are apart of it?

A
  • named: immune complex mediated
  • antibodies: IgG and IgM
45
Q

what happens in type 3 hypersensitivity?

A
  • antigen - antibody complexes are formed in the circulation and are later deposited into the blood in the vessel walls or extravascular tissues
45
Q

what are the two main examples type 3 hypersensitivity?

A
  • Raynaud’s phenomenon
  • Lupus
46
Q

what disease is SLE? or lupus?

A
  • chronic multisystem inflammatory disease
46
Q

what is the effector are used for type 3 hypersensitivity?

A
  • neutrophils
46
Q

what are the autoantibodies against in autoimmunity’s?

A
  • body sees its own antigens as a foreign so they attack
46
Q

what are the treatments for lupus?

A
  • NSAIDS = non steroids and anti - inflammatory’s
  • corticosteroids for seriou disease
  • immunosuppressants
  • protective from sun exposures
  • IV Ig (Iv immunoglobulins)
46
Q

what is the clinical presentation of SLE? (lupus)

A
  • more common in females, especially young (20 - 40)
  • black people then white
  • they have flair ups
  • arthralgias = joint pain
  • have vasculitis and a rash (mallards/ butterfly rash or discoed rash)
  • possible renal disease
  • hematologic changes (increases/easy brushing)
  • cardiovascular disease
  • presence of antinuclear antibodies (ANA) due to lupus
  • need at least 4 for a diagnosis
47
Q

what is the name of the 4th hypersensitivity? and what antibodies are included? response time? examples?

A
  • DOES NOT INVOLVED antibodies
  • cell mediated immunity
  • local
  • delayed response
  • ex: skin TB test, dermatitis, poison Ivy, contact allergic dermatitis
48
Q

what cells are involved in type 4 hypersensitivity?

A
  • mediated by T LYMPHOCYTES
  • destruction of the tissues are caused by defect killing by toxins from Tc cells
49
Q

what is an immune deficiency?

A
  • failure of immune or inflammatory response that makes us increasingly susceptible to infections
50
Q

what is a primary immunodeficiency?

A
  • born with
  • found early in life
  • not attributable to any outside cause
  • genetic anomaly
51
Q

what is an acquired immunodeficiency?

A
  • something that you get from life
  • ex: radiation that damaged bone marrow
52
Q

what is a secondary immunodeficiency? how do you get it?

A
  • consequence of non - immune system disorders or treatments that secondary affect immune function
  • something else causing bad immune response
  • more common
53
Q

how do immunodeficiencies present clinically?

A
  • development of unusual or recurrent, severe infections
  • ex: super sever recurrent pneumonia
54
Q

what cells do immunodeficiencies lack?

A
  • T cells
  • both T helper and T cytotoxic cells
  • B cells
  • phagocytes and compliment system
55
Q

what clinical diseases do T cell defiance’s affect?

A
  • viruses (eg. varicella, herpes, ect)
  • fungus
  • yeast
56
Q

what clinical diseases do B cell & phagocyte defiance’s affect?

A
  • bacteria and virus
57
Q

whats the difference between lymphocytes and leukocytes

A
  • leukocytes are white blood cells in the blood
  • lymphocytes = blood cells in adaptive immunity, made of T cells, B cells, and NK cells
58
Q

what is the effect of a B lymphocyte deficiency?

A
  • decrease in antibody production
59
Q

what is the effect of a T lymphocyte deficiency?

A
  • defect in Developpement and function of the cell mediated immunity
  • B lymphocyte response impeached
60
Q

what is the impact of combined T and B cell deficiencies?

A
  • defected that affect development of both T and B lymphocytes
  • SEVERE COMBINED IMMUNODEFICENCIES
  • worst kind
  • can cause failure of all WBC development
61
Q

how to determine if someone has a immunodeficiency

A
  • Obtain history = recurrent infections? what ones?
  • Lab tests = CBC w/ differential, quantitative determination of antibodies
  • skin test = Pt reaction to previously encountered antigens
62
Q

what is the treatment for immunodeficiencies?

A
  • replace missing component
  • B cell insufficiency: = IVIg (gamma-globulin therapy
  • stem cell transplantation = bone marrow transplant, umbilical cord stem cells
  • gene therapy
  • be careful w/ immunizations (don’t get one where u could get some of the antigens)
63
Q

where can you get aids from?

A
  • blood born pathogen!
  • blood
  • blood products
  • IV drug use
  • sexual activity
  • perinatal transmission
64
Q

what kind of virus is AIDs?

A
  • retrovirus made from RNA, and it reverse transcriptase’s to be constantly mutating
65
Q

what cells does AIDS destroy

A
  • CD 4 Th cells
66
Q

what is the seroconversion for AIDS?

A
  • the time between infection and antibody appearance
  • 3 weeks to 6 months but can be 14
67
Q

How is AIDS diagnosed?

A
  • with CD 4 cells less than 200 !!
  • atypical or opportunist infections = cancer & pneumonia
  • severely diminished response to pathogens & tumors
68
Q

What tests are used to diagnose AIDS?

A
  • antibody screening test = immunoassay
69
Q

what does a serologically negative AIDS result mean

A
  • no detectable antibody = no aids
70
Q

what drug therapy can be used for AIDS?

A
  • active antiretroviral therapy (ART)
71
Q

what is active antiretroviral therapy (ART)

A
  • combo of 3 + meds from 2 classes to attack virus in different ways
  • effective antiviral therapies have made HIV chronic disease which people are rare to convert AIDS