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Pathology > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

1) List five stimulations that can lead to mast cell degranulation.

A
  1. IgE -mediated lectin and antigen
  2. C3a & C5a
  3. amines
  4. Interleukins 1, 3 & 8
  5. physical stimulation (vibration, heat, cold)
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2
Q

2) Explain how IgE leads to mast cell activation.

A
  1. antigen is processed by a dendritic cell, presented to a TH2 cell, which “helps” B cell convert to a plasma cell to produce IgE. IgE binds to FcRe on mast cell. when antigen is again presented, it binds to IgE on mast cell&raquo_space; degranulation.
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3
Q

3) Name the preformed and synthesized mediators produced by an activated mast cell.

A
  1. primary: histamines, proteases, chemotactic factors, oxidase enzymes
    secondary (synthesized) : secreted cytokines, leukotrienes, prostaglandins
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4
Q

4) Give three examples of localized and two of systemic type I hypersensitivity reactions.

A
  1. localized: urticaria; atopic keratoconjunctivitis

systemic: anaphylaxis due to bee stings, drug reaction

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5
Q

5) Explain the basic mechanism active in type II hypersensitivity reactions.

A
  1. antigen binds to antibody, activates cytotoxic effect and causes cellular damage
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6
Q

6) Explain the difference between acute and delayed transfusion reactions.

A
  1. acute: Ab already high, > intravascular hemolysis

delayed: rising Ab titer, > extravascular hemolysis

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7
Q

7) Explain the etiology and pathogenic mechanism of erythroblastosis fetalis.

A

7.

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8
Q

8) Explain the mechanism and distinctions between thyrotoxicosis (Grave’s disease) and
myasthenia gravis.

A
  1. Grave’s: mimics hyperthyroid. Thyroid Stimulating Immunoglobulins recognizes and binds to the thyrotropin receptor (TSH receptor). It mimics the TSH to that receptor and activates the secretion of thyroxine (T4) and triiodothyronine (T3), and the actual TSH level will decrease in the blood plasma.
    Myasthenia gravis: Muscle weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors at neuromuscular junctions.
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9
Q

9) Name the Streptococcal antigens that cross react with human tissues in producing the
phenomena of rheumatic fever.

A
  1. hyaluronidase > cartilage > arthritis
  2. M protein > heart muscle > myocarditis
  3. Cell wall antigen > basal ganglia > chorea
  4. Carbohydrate A > heart valves > endocarditis
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10
Q

10) Describe the immunological phenomena causing type III hypersensitivity reactions.

A

antigen-antibody complexes (systemic or deposited locally) cause recruitment of neutrophils that cause tissue damage

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11
Q

11) List four diseases that are type III hypersensitivity diseases.

A
  1. Systemic: serum sickness, some drug reactions

Localized: glomerulonephritis, arthritis, Arthus reaction,

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12
Q

12) Discuss the role of complement in hypersensitivity diseases.

A
  1. Activated complement forms MACs and recruits neutrophils to site to produce cellular damage, also = anaphylatoxins that&raquo_space; edema and vasodilation
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13
Q

13) Explain the basic mechanism underlying type IV hypersensitivity.

A
  1. T-cell mediated. sensitized T-cells respond to antigen (delayed-type hypersensitivity)
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14
Q

14) Give three examples of type IV hypersensitivity disorders.

A
  1. granulomas (miliary tuberculosis), allograft rejection, Graft-v-host, Hashimoto’s thyroiditis
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15
Q

15) Explain the underlying mechanisms of hyperacute, acute and chronic allograft rejection.

A
  1. hyperacute: preformed antibodies (Antigen mismatch)
    acute: due to minor antigen mismatch. antibodies develop over time (weeks to months)
    chronic: loss of function in transplanted organs via fibrosis of the transplanted tissue’s blood vessels.
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16
Q

16) Describe the cause of graft versus host disease.

A
  1. graft lymphocytes attack host’s tissues in response to host’s antigens. Typically if host is immunocompromised. Does not occur in infants b/c don’t have antigens.
17
Q

1) Define the mechanisms that lead to immunological tolerance.

A
  1. Ignorance - innaccessible antigen
  2. Negative & Positive selection - priming T Cells and B cells to respond to foreign antigen and eliminating cells that attack self-antigen
  3. Supression by T regs
  4. Anergy in absence of signal indicating foreign antigen
18
Q

2) Describe positive selection and negative selection.

A
  1. Positive selection: T lymphocytes must interact with MHC and B cells with their ligand with sufficient strength
    Negative selection: lymphocytes that bind self-antigen too strongly are eliminated
    (Goldilocks - not too strong or weak)
19
Q

3) Name possible mechanisms in autoimmunity.

A

molecular mimicry, release of sequestered antigen, escape of negatively self-reactive lymphocytes, epitope spreading, polyclonal B cell activation

20
Q

4) List genes/loci known or strongly suspected to be associated with autoimmunity in humans.

A
  1. PTPN-22: rheumatoid arthritis. inability to down-regulate tyrosine kinase > overreactive T cells
    NOD2: Crohn’s disease - encodes sensor in epithelial cells disease allele fails to notice microbial invasion. Invading microbes initiate inflammatory response against commensal bacteria
  2. Cytokine receptors: Il-2 alpha Il-7 a: associated with MS. control development of T-regs.
21
Q

5) Describe 4 mechanisms by which infection can lead to autoimmunity.

A
  1. adjuvant effect: increased activation of lymphocytes breaks down self-tolerance
  2. molecular mimicry: invading pathogen antigens resemble self-antigen and cross-reactivity initiates autoimmune response (myocarditis after strep)
  3. polyclonal B cell activation: ex EBV augments autoantibodie production
  4. tissue damage: > release of self-antigen or modified self-antigen from sequestered area
22
Q

6) Describe the role of regulatory T cells in controlling autoimmunity.

A
  1. T Reg cells suppress reactive T cells. Low T cell count > autoimmune disease due to loss of T regs. CD25+ is a good marker of T reg cells. Undetermined whether cell-cell contact is required or if suppression if via cytokine release.
23
Q

7) Identify diseases mediated by antibodies and diseases mediated by T cells

A
  1. antibody-immune complex: autohemolytic anemia
    SLE (Lupus) - antigen-antibody complexes
    T Cell: diabetes mellitus, rheumatoid arthritis
    Rheumatoid arthritis - CCP (anti-cyclic citrullinated peptide) reacts w/ T cells
24
Q

8) Describe the manifestations, etiology, pathogenesis, genetic factors, immunologic factors,
environmental factors, and pathologic changes associated with systemic lupus
erythematosus.

A
  1. Wide range of organs affected. Symptoms heterogeneous.
    Genetic: contributions from MHC, deficiency in complement (impairs removal of antigen/antibody complexes). HLA-DQ alleles associated with anti-DS DNA
    Immunologic: defective elimination of self-reactive B cells. nuclear DNA and RNA in immune complexes activate TLRs > aggregation of immune response. peripheral leukocytes show overreaction to Type 1 interferons that would normally react to virions
    Environmental: UV light, reproductive years in women, drug reactions may mimic SLE.
25
Q

9) Describe the signs and symptoms, morphologic alterations, and the genetic, immunological,
and environmental factors associated with rheumatoid arthritis.

A
  1. 1% diagnosed. women more frequent. Late middle age to elderly. Affects joints and visceral organs. non-suppurative.
    fatigue, myalgias, morning stiffness.
    Infiltration by dense inflammatory filtrate. Fibrin, neutrophils in synovial fluid, osteoclastic activity, Pannus formation: mass of synovium and stroma, inflammatory cells, etc.
    Genetic: MHC loci, HLA-DR4 alleles, PTPN-21 allele
    Environmental: unknown. citrulinated proteins.
    Immunologic: immune complexes activate complement. CD 4+ cells appear early. rheumatoid bodies: autoantibodies to Fc portion of IgG. antibodies bind other antibodies. Don’t cause disease but are a marker of it. Players: TGF-beta, TNF important,
26
Q

10) Define factors associated with the development of type I diabetes mellitus.

A
  1. T-cell mediated immune destruction of beta cells of pancreatic islet. Detect anti-insulin antibodies.
27
Q

What is FoxP3?

A

associated with IPEX (immunodysregulation polyendocrinopathy enteropathy X-linked syndrome). Critically related to development of T regs

28
Q

Define what is meant by “immunodeficiency” and name the two categories into which it is divided.

A

primary: born w/ disease
secondary: acquire in lifetime

X-linked: typically recessive. defects associated with X chromosome. affects males more frequently.
Autosomal

29
Q

2) List 4 X-linked and 2 autosome-linked diseases that cause immunodeficiency.

A

X - linked:
1. XLA (bruton’s):
2. X-linked SCID: defect in IL-2 receptor on T cells
3. IPEX
4. Wiskott-Aldrich - inability to mount IgM response to capsular polysaccharides of bacteria. Defect in ability of T cells to help B cells
80:20: Chronic Granulomatous Disease: cat + infections reoccur. Lack of NADPH oxidase activity > no oxidative burst = organisms not killed.
Autosomal:
1. Hereditary Angioedema
2.

30
Q

3) List three causes of acquired immunodeficiencies.

A

Malnutrition - reduces synthesis of IgG
HIV - kills CD4+ cells
Common variable hypogammaglobulinemia: recurrent infections caused by pygoenic bacteria (H. influenza. S. pneumoniae). Failure to produce IgG.

31
Q

4) Discuss the cause of Bruton’s X-linked agammaglobulinemia.

A

4.b-cell precursors don’t fully develop. Plenty of T cells. A mutation occurs at the Bruton’s tyrosine kinase (Btk) gene that leads to a severe block in B cell developmentand a reduced Immunoglobulin (antibody) production in the serum.

32
Q

5) Identify the anatomic abnormalities associated with DiGeorge Syndrome.

A

Thymic aplasia > defect in differentiation of T cells. Embryologic failure of development of 3/4 pharyngeal pouches. No T-cell mediated immunity. Also have congenital heart defects. 22Q11 deletion. Susceptible to: viral infection, fungal and parasitic infections.

33
Q

6) Name the life-threatening condition associated with IgA deficiency.

A

Anaphylactic transfusion reaction (rxn to IgA in transfused blood)

34
Q

7) Describe severe combined immunodeficiency syndrome (SCID) and name two molecular
etiologies for it.

A

no or non-reactive B and T cells. Don’t make antibodies. hypogammagobulinemia.

  1. Cytokine receptor deficiency, X-linked
  2. Adenosine deaminase deficiency > toxic derivatives impacting immature lymphocytes
35
Q

8) Describe the disease hereditary angioneurotic edema and discuss its etiology.

A

recurrent attacks of marked, diffuse, nonpitting and nonpruritic skin swellings, painful abdominal attacks, and laryngeal edema. Deficiency in C1 inhibitor: causes mast cell degranulation.

36
Q

9) Diagram the HIV genome and name the functions of the genes encoded therein.

A 
Three Typical retroviral genes: 
Gag = internal "core' proteins inc. antigenic p24, 
Pol  = reverse transcriptase for genome RNA > DNA, inc. protease, integrase, RNase 
Env = gp120 & gp41
Six regulatory genes: 
tat = enhance initaiation/elongation of viral mRNA transcription
rev = controls late mRNA passage from nucleus to cytoplasm 
nef, vif, vpr, vpu = accessory. nef supresses MHC class I proteins.
37
Q

10) Discuss the natural evolution of HIV-1 infection in an untreated host.

A

Early acute: mono-like fever, lethargy, sore throat, lympahedenopathy. CD4 cell count normal
Middle, latent stage: long latent period. 7 to 11 years. asymptomatic. HIV sequestered within lymph nodes. AIDS-related complex can occur, leads to AIDS.
Late, immunodeficiency stage: AIDS. Decline in CD4+ cells below 400/uL. Opportunistic infections.

38
Q

Describe Hyper-IgM syndrome:

A

recurrent pyogenic bacterial infections. High [IgM] but little IgG, IgA, and IgE. Normal T and B cells but mutation in gene encoding CD40 ligand = inedibility to induce class switching in B cells.

Pathology (10 decks)

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