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Pathophysiology > Alterations in Immunity and Inflammation ‏ > Flashcards

Alterations in Immunity and Inflammation ‏ Flashcards

1
Q

4 types of inappropriate immune response

A

allergy, autoimmunity, alloimmunity, immune deficiency

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2
Q

allergy

A

exaggerated response against environmental Ags

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3
Q

autoimmunity

A

misdirected against host’s own cells

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4
Q

alloimmunity

A

directed against beneficial foreign tissues, such as transfusions or transplants

a.k.a. isoimmunity

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5
Q

immune deficiency

A

insufficient to protect host

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6
Q

2 classifications for hypersensitivity

A
  • source of Ag (allergy, autoimmunity, alloimmunity)
  • mechanism of Dz (Types I, II, III, IV)

mechanism of onset not understood

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7
Q

Hypersensitivity Types

A
  • Type I: immunoglobulin E mediated
  • Type II: Tissue specific
  • Type III: Immune complex mediated
  • Type IV: cell-mediated/delayed

artificial. Rarely just one.

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8
Q

Sensitization to an antigen

A

when adequate # of Abs or T cells to cause noticeable reaction on reexposure

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9
Q

Immediate vs delayed hypersensitivity

A

Immediate: minutes to hours

Delayed: several hours to days

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10
Q

Type I: name

A

IgE-mediated reaction

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11
Q

Type I: rate of development

A

immediate

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12
Q

Type I: Class of Ab involved

A

IgE

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13
Q

Type I: Principal effector cells

A

Mast

release histamine –> vasodilation, mucous secretion, bronchoconstriction, itch

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14
Q

Type I: complement participation?

A

No

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15
Q

Type I: example d/os

A

allergic rhinitis, urticaria, asthma, anaphylaxis

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16
Q

Type II: name

A

Tissue-specific reaction

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17
Q

Type II: rate of dvpt

A

Immediate

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18
Q

Type II: Ab

A

IgG, IgM

dissolved by complement

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19
Q

Type II: effector cells

A

Macrophages in tissues

(damaged by lymphocytes, uptaken by macrophages)

Ab directed against cell surface Ags mediates cell destruction via complement activation or ADCC

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20
Q

Type II: complement participation

A

frequently

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21
Q

Type II: example d/os

A

autoimmune thrombocytopenic purpura, Graves dz, autoimmune hemolytic anemia,

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22
Q

Type III: Name

A

Immune complex-mediated reaction

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23
Q

Type III: Rate of dvpt

A

immediate

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24
Q

Type III: Ab

A

IgG, IgM

Ag-Ab complex deposited in various tissues induce complement activation and an ensuing inflammatory response mediated by massive infiltration of neutrophils

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25
Q

Type III: effector cells

A

neutrophils

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26
Q

Type III: complement participation

A

Yes

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27
Q

Type III: example d/os

A

SLE, RA, hemolytic anemia, hypersensitivity pneumonia

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28
Q

Type IV: name

A

cell-mediated reaction

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29
Q

Type IV: Rate of dvpt

A

delayed

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30
Q

Type IV: Ab

A

None

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31
Q

Type IV: effector cells

A

lymphocytes, macrophages

sensitized Th1 cells release cytokines that activate macrophages or Tc cells which mediate cell damage

32
Q

Type IV: complement?

A

No

33
Q

Type IV: examples of d/os

A

contact sensitivity/dermatitis to poison ivy and metals (jewelry), liver damage d/t drug allergy

34
Q

Mechanism of Type I IgE mediated reactions

A
35
Q

Type I IGE mediated reaction: initial exposure, ___ cells activate ___ cells.

And what is the result?

A
  1. Antigen Presenting dendritic cells activate Th2 cells
  2. Th2 produce cytokines IL-3, IL-4, IL-5 and GM-CSF (granulocyte macrophage colony stimulating factor)
    • ​IL-3, IL-5, and GM-CSF attract and promote survival of eosinophils
    • other cytokines, e.g., IL-4, induce B cells to class-switch to IgE producing plasma cells
      • IgE coats surface of mast cell by binding w/IgE specific Fc receptors on mast cell’s PM (sensitization)
36
Q

Type I IgE mediated reaction: subsequent exposure

A
  1. cross-links the surface bound IgE and activates signals from teh cytoplasmic portion of the IgE Fc receptors
    • ​this initiates 2 parallell and interdependent processes
      • mast cell degranulation and discharge of preformed mediatory (e.g., histamine, eosinophil chemotactic factor of anaphylaxis)
      • production of newly formed mediators such as arachidonic metabolites (leukotrienes, PGs)
37
Q

Type I IgE mediated reactions: 2 phases

A
  1. Initial phase: vasodilation, vascular leakage, and, depending on location, smooth muscle spasm or glandular secretions (5-30 min post-exposure)
  2. Late phase: 2-8hrs later w/o additional exposure. more intense infiltration of tissues w/eosinophils, neutrophils, basophils, monocytes, Th cells, and tissue destruction in form of mucosal epithelial damage
38
Q

IgE mediated reactions: what happens when mast cells are activated?

A

degranulation of preformed mediators (primary mediators) and synthesis of newly formed (de novo) mediators (secondary mediators)

39
Q

what characterizes a Type II hypersensitivity reaction?

A

specific cell or tissue targeted. MHC locus antigens (HLAs) or other tissue specific Ags

some TSAs only on certain cells

40
Q

IgE mediated reactions: primary mediators

A

Granule contents: histamine, proteases, chemotactic factors (ECF, NCF)

41
Q

IgE mediated reactions: secondary mediators

A

membrane phospolipids lead to arachidonic acid (leukotrienes and PGs) and PAF (plt activating factor)

42
Q

Mechanisms of Type II reactions

A
  1. destruction via Ab/Ag binding
  2. phagocytosis by macrophages in tissue
  3. neutrophil mediated immune destruction
  4. ADCC
  5. Modulaton or blocking the normal function of receptors by antireceptor Ab
43
Q

Type II reaction: Ab/Ag destruction

A

complement mediated

44
Q

Type II reaction: Phagocytosis

A

opsonization (IgG and C3b) & eating by macrophages

e.g., Abs against PLT-specific Ags or RBC Ags of Rh system coat and they’re removed in spleen

45
Q

Type II: neutrophil mediated damage

A

Ag deposition -> Ab binds _> complement cascade -> C3a & C5a –> neutrophil chemotaxis -> neutrophil adhereance (bia Fc portion of Ab or C3bR) and degranulation (enzymes, ROS) into healty tissue!

46
Q

Type II reaction: ADCC

A
  • Ab dependent cell mediated cytotoxicity
  • apoptosis of target cells is induced
  • FcR on NK cell recognizes Ab on target cell
  • by granzymes and perforin produced by NK cells and interactions of FasL - FasR)
47
Q

Type II: antireceptor Ab

e.g., hyperthyroidism of Graves dz - binds and activates TSH

A

blocks normal function of receptors. Not destroy, just malfunction

48
Q

Myasthenia gravis - what type of hypersensitivity and what does it do?

A

Type II

acetylcholine receptor Abs block acetylcholine from attaching to receptors on motor end plates of skeletal muscle, thereby impairing neuromuscular transmission and causing muscle weakness

49
Q

autoimmune hemolytic anemia: what type and why?

A

Type II

d/t alloimmune reaction to ABO mismatched transfused blood cells - Ag/Ab reaction w/complement cascade

50
Q

What characterizes Type III

A
  • Ag-Ab immune complexes formed in circulation and deposited later in vessel walls or extravascular tissues
  • Not organ specific and Sx not to do w/particular antigenic target.
  • harmful effects d/t complement activation - esp through chemotactic factors for neutrophils
51
Q

Primary difference from type II and Type III

A

Type II Ab binds to Ag on cell surface

Type III: Ab binds to soluble Ag that was rleased into blood or body fluids and complex is then deposited in tissues.

52
Q

Why are neutrophils usually unsuccessful at ingesting immune complexes in Type III?

A

bound to large areas of tissue - deposit bad stuff into tissue instead of phagolysosomes

53
Q

Type III: how do immune complexes form?

A

in blood from circulating Ag and Ab

54
Q

Type III: What happens to small and large immune complexes?

A

Removed successfully from circulation, not deposited

55
Q

What happens to intermediate sized immune complexes (type III)

A

deposited in certain target tissues in which circulation is slow or filtration of blood occurs. They activate the complement cascade through C1 and generate fragments, e.g., C5a, C3b

C5a brings neutrophils which attach to IgG and C3b in immune complexes. These fail at phagocytizing and instead destroy healthy tissue

56
Q

Complement & Type III

A

Only type in which complement levels may be depleted

57
Q

Serum Sickness

A

Type III. foreign serum introduced. Typically affect blood vessels, joints, kidneys. +fever, LAD, rash, pain

58
Q

Raynaud phenomenon

A

Type III. Form of serum sickenss. Temperature dependent deposition of immune complexes

59
Q

Arthus reaction

A

Localized immune complex mediated inflammatory response. Type III.

Repeated exposure to Ag reacts w/preformed Ab and forms immune complexes on walls of local blood vessels.

Sx 1 hour of exposure and peak 6-12

60
Q

Characterize Type IV

A

No Ab. Delayed.

61
Q

Mechanism of Type IV

A
  • Ags from target cells stimulate T cells to differentiate into
    • Tc cells (direct cytotoxic) and
    • Th1 cells (delayed hypersensitivity)
      • produce lymphokines (esp IFN-gamma) that activate macrophage through specific receptors (IFN-gammaR).
        • Macrophage can attach to targets and release enzymes and ROS responsible for most tissue destruction
62
Q

ABO: surface of erythrocytes blood group O

A

core H antigenic carbohydrate - not Abs against it, so universal donor

63
Q

O blood serum, Abs against

A

IgM against A and B carbohydrates

64
Q

A blood type, what type of Ag?

A

Some H modified into A Ags by addition of N-acetylgalactosamine (NAGA)

65
Q

Serum Abs of Type A blood

A

IgM against B antigen

66
Q

B blood group, antigens

A

Some H modified to B antigens by addition of galactose (Gal)

67
Q

B blood group, Abs against

A

IgM Abs against A antigen

68
Q

AB blood group, antigens

A

Some Ags modified into both A and B

69
Q

AB blood group, antibodies

A

no Abs to A or B antigens – universal recipient

70
Q

Brutons agammaglobulinemia:

A
  • agammaglobulinemia = antibodies are almost totally absent
  • most severe B lymphocyte deficiency
  • X linked, mutation in the gene for Bruton’s tyrosine kinase (Btk).
    • enzyme is involved in intracellular signaling from several B cell receptors (IgM B antigen receptors, IL-5 receptor & IL-6.
    • Ineffective signaling – arrest of development in bursal-equivalent tissue (bone marrow) of early cells in the B cell maturation process.
  • Few circulating B cells, IgM and IgA are almost absent
71
Q

DiGeorge’s

A
  • Congenial thymic aplasia or hypoplasia: Lack/ partial lack of thymus
  • Decreased T cells and functioning
  • Usually due to deletions on chromosome 22
  • May have partial or complete absence of the parathyroid: decreased blood Ca levels, structural defects in heart & aorta, abnormal facial features- underdeveloped chin, low-set ears, shortened structure of upper lip
72
Q

Reticular Dysgenesis

A
  • Combined B & T cell deficiency
  • Failure of blood cells to develop- a common stem cell for all WBCs is absent so B/T and phagocytic cells never develop
  • Baby usually dies in utero or after birth
73
Q

ADA deficiency: Adenosine Deaminase (ADA)

A
  • Enzyme involved in purine metabolism
  • Autosomal recessive
  • Accumulation of toxic levels or purine metabolites which affects rapidly dividing cells like lymphocytes
  • Development of B, T & NK cells arrested very early, very few lymphocytic cells found in blood
74
Q

TB SKIN TEST (TST):

A

aka PPD, purified protein derivative; the first type IV hypersensitivity reaction described (1890s); intradermal injection of the tuberculin antigen –> in a sensitized individual (someone previously exposed to the Ag), the site becomes infiltrated with T cells and macrophages, leading to a clear hard center (induration) and a reddish surrounding area (erythema); DELAYED hypersensitivity RXN –> reaches peak intensity at 24-72 hours; measurement of the induration diameter guides test interpretation

75
Q

Atopy:

A

genetic predisposition to developing type I allergies; 40% chance if one parent has an allergy; atopic individuals tend to produce ↑ IgE, have ↑ Fc receptors on their mast cells, and more responsive skin / airways

Pathophysiology (10 decks)

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