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Unit 4 Flashcards

1
Q

Describe flow cytometry

A

-automated process that analyzes cells or beads in fluid suspensions for their light- scattering characteristics
-uses fluorochromes to identify cells by size, shape, and antigenic properties
- allows for rapid and accurate detection of cells found in small numbers

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2
Q

What is immunophenotyping

A

Identifying their surface and cytoplasmic antigen expression

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3
Q

What are fluorochcomes

A

Fluorescent molecule

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4
Q

What do fluorochromes do?

A

-absorbs light across a spectrum of wavelengths and emits light of lower energy across a spectrum of longer wavelengths

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5
Q

What is flow cytometry used to detect?

A
  • leukemia
  • lymphoma
  • AIDS
  • chronic granulomatous disease
  • leukocyte adhesion deficiency
  • fetal RBC
  • F-cell identification in maternal blood
  • identification of paroxysmal nocturnal hemoglobinuria
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6
Q

What is flow cytometry used for?

A
  • Enumerate hematopoietic stem cells
    -detect human leukocyte antigen (HLA) antibodies in transplantation
    -identify cells undergoing apoptosis
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7
Q

What is a significant advantage of flow cytometry?

A

Because the flow rate of cells is so rapid, thousands of events can be analyzed in seconds, allowing for accurate detection of cells that are present in very small numbers

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8
Q

What are the 4 parts of instrumentation of flow cytometry?

A

① fluidics
②laser light source
③optics and photodetectors
④ computer

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9
Q

Describe fluidics of flow cytometry

A
  • Allows for cell transport, one at a time
    -each time a cell passes in front of a laser beam, light is scattered,and the interruption o laser signal is recorded
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10
Q

Describe laser light source of flow cytometry

A
  • For cell illumination and identification
    -solid-state diode lasers are typically used
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11
Q

Describe optics and photodetectors of flow cytometry

A
  • Signal detection
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12
Q

Describe computers of flow cytometry

A
  • Data management
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13
Q

What colors are lasers?

A
  • Red
    -blue
    -violet
    -ultraviolet (UV)
  • yellow-green
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14
Q

What are the types of light scatter?

A

① forward scatter (FSC)
② side scatter (SSC)

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15
Q

Describe forward scatter

A

-an indicator of size

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16
Q

Describe side scatter

A
  • indicative of granularity or the intracellular complexity of the cell
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17
Q

What are the intrinsic parameters of the light sources of flow cytometry?

A
  • forward scatter
  • side scatter
    *light scattering properties
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18
Q

Describe extrinsic parameters in light source of flow cytometry

A

-require the addition of a fluorescent probe for their detection

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19
Q

Describe principle of hydronomically focusing
In flow cytometry

A
  • cells pass single file through the intersection of the laser light source
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20
Q

What are the sample types common in flow cytometry?

A
  • Whole blood
  • bone marrow
  • fluid aspirates
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21
Q

What WBCs can be differentiated based solely on their intrinsic parameters?

A
  • lymphocytes
  • monocytes
  • neutrophils
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22
Q

What is flow cytometry steps?

A

① celli are processed into a suspension, and the cytometer draws up the cell suspension and injects the sample inside a carrier stream of isotonic saline (sheath fluid) to form a laminar flow
② The sample stream is constrained by the carrier stream and is thus hydrodynamically focused so that the cells pass in a single file through the intersection of the laser light source
③ each cell is interrogated by a light source that typically consists of one or more small air-cooled lasers
④ cells are labeled with a fluorochrome or Fluorescent molecules, that absorbs light across a
Spectrum of wavelengths and emits light of lower energy pattern of absorption (excitation) and emission

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23
Q

What are common speciemens tested for
Flow cytometry?

A

Whole blood
Bone marrow
Fluid aspirates

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24
Q

What is the additive in the tube that is used for whole blood collection?

A

EDTA
Heparin can also be used

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25
Q

What is required for a sample that has a lot of RBCs for flow cytometry?

A

Requires erythrocytes removal to allow for efficient analysis of WBC

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26
Q

Describe single-parameter histogram

A
  • The y-axis consists of the number of events
  • usually extrinsic parameters (fluorescent-labeled) antibody
  • operator sets a marker to isolate the positive event!
    -will calculate the percentage of positive events within the designated markers
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27
Q

Describe dual-parameter dot plot

A
  • both parameters(axis) are chosen by operator
  • the operator then draws a “gate” or isolates the population of interestfor further analysis
  • gated cells are analyzed for fluorescence
  • suppurated into four quadrants
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28
Q

Describe quadrant 1 of a dual parameter dot plot

A

X - axis → negative for Fluorescence
Y - axis → positive for Fluorescence

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29
Q

Describe quadrant 2 of dual parameter dot plot

A

X-axis → positive for fluorescence
Y- axis → positive for fluorescence

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30
Q

Describe quadrant 3 of dual-parameter dot plot

A

X-axis→ negative of fluorescence
Y-axis→ negative of fluorescence

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31
Q

Describe quadrant 4 of dual-parameter dot plot

A

X-axis → positive for Fluorescence
Y-axis→ negative for Fluorescence

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32
Q

What are some applications of flow cytometry?

A

① identifies particular markers for diagnosis and monitoring of leukemias and lymphomas
② enumerates peripheral blood. CD4+ T cells to classify stages of HIV disease and guide treatment
③ enumerates CD34+ cells in stem cells transplantation
④determines DNA content or ploidy status of tumor cells
⑤ helps diagnosis inherited diseases

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33
Q

What is the significance of the presence of CD5+?

A

Indication of mantle cell lymphoma (CLL)

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34
Q

How is the HIV stage classified)

A

Enumeration of peripheral blood CD4+ T cells by flow cytometry

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35
Q

What are the advantages of immunoassay automation?

A
  • Reduces error
  • is more accurate and precise
  • requires fewer staff
  • saves on controls, duplicates, dilutes, and repeats
  • potential for better sample ID with use of bar coding
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36
Q

What are the two types of immunoassay analyzer?

A
  • batch
  • random-access analyzer
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37
Q

Describe batch analyzers

A
  • Can examine multiple samples
  • provide access to samples for formation of reaction mixture
  • permits one type of analysis at a time
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38
Q

Describe random access analyzers

A
  • Measure numerous analytes from multiple samples
  • can perform different tests on any one sample
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39
Q

What are the tasks performed by automated analyzers?

A
  • Introducing the sample
  • adding reagents
  • mixing reagents and sample
  • incubating
  • detecting reactions
  • calculating
  • reporting results
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40
Q

What does validation of immunoassay automation involve verification of?

A
  • accuracy
  • precision
  • analytic sensitivity
  • analytic specificity
  • determination of interfering substances, reportable range, reference intervals
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41
Q

What is accuracy?

A

Tests ability to measure what it claims to measure

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42
Q

What is precision?

A

Ability to consistently reproduce a result on repeated testing of the same sample

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43
Q

What is analytic sensitivity?

A

The lowest measurable amount of an analyte

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44
Q

What is analytic specificity?

A

An assays ability to generate a negative result when the analyze is not present

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45
Q

What is a reportable range?

A

The range of values that will generate a positive result for the specimens assayed by the test procedure

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46
Q

What is reference interval?

A

Range of values found in healthy individuals

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47
Q

What is the single most important requirement for samples to be analyzed on a flow cytometer?

A

Cells must be in a single-call suspension

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48
Q

It an analyzer consistently indicates a positive test when the analyte in question is not present, this represents a problem with what?

A

Specificity

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49
Q

The various signals generated by cells intersecting with a flow cytometry laser are captured by what?

A

Photomultiplier tubes

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50
Q

If an analyzer gets different results each time the same sample is tested, what type of problem dues this represent?

A

Precision

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51
Q

What is flow cytometry most commonly used method?

A

Immunophenotyping of lymphoid and myloid

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52
Q

Describe hypersensitivity

A
  • Exaggerated immune response to a typically harmless antigen
  • results in tissue injury and disease
  • 4 types
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53
Q

Describe the immediate reaction of hypersensitivity

A
  • develop minutes to hours after antigen exposure
  • type I,II, and III
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54
Q

Describe the delay reaction of hypersensitivity

A
  • develop 24 to 48 hours after antigen exposure
    -type IV
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55
Q

Describe type I hypersensitivity,

A
  • cell bound antibodies react with antigen to release physiologically active substances
  • complement is not involved
  • known as “allergies”
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56
Q

Describe type II hypersensitivity

A
  • Free antibody reacts with antigen associated with cell surfaces
  • complement plays major role in producing tissue damage
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57
Q

Describe type III hypersensitivity

A
  • Antibody reacts with soluble antigen to form complexes that precipitate in tissues
  • complement plays major role in producing tissue damage
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58
Q

Describe type IV hypersensitivity

A
  • not seen until 24-48 hours
  • differs from the other three because sensitized T cells rather than antibody are responsible for symptoms
  • complement not involved
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59
Q

What is another name for type I hypersensitivity?

A

Anaphylactic hypersensitivity

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60
Q

What is another name for type II hypersensitivity?

A

Antibody-mediated cytotoxic hypersensitivity

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61
Q

What is another name for type III hypersensitivity?

A

Complex-mediated hypersensitivity

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62
Q

What is another name for type IV hypersensitivity?

A

Cell-mediated hypersensitivity

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63
Q

What are the key components of type I hypersensitivity?

A
  • IgE
  • mast cells
  • basophils
  • eosinophils
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64
Q

Describe the sensitization phase of hypersensitivity

A
  • APCs process allergens and present them to Th cells
  • Th2 cells induce production of allergen-specific IgE
  • IgE binds to FceRI receptors on most cells and basophils
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65
Q

Describe the activation phase of hypersensitivity I

A
  • Allergen cross-links adjacent cell-bound IgEs
  • mast cells and basophils degranulate
  • chemical mediators are released and bind to target organs
  • allergy symptoms produced
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66
Q

What are the type I preformed/primary mediators?

A
  • Histamine
  • heparin
  • eosinophil chemomatic factor of anaphylaxis (ECF-A)
  • neutrophil chemotactic factor
  • proteases
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67
Q

What are the type I newly formed mediators?

A
  • Platelet activating factor (PAF)
  • prostaglandin (PG) D2
  • Leukotrienes (LT) → B2, C4, D4 and E4
  • cytokines
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68
Q

What are some common allergens?

A
  • Pollen ‘’
  • mold spores
  • animal danders
  • dust mites
  • insect venom
  • certain foods
  • certain dogs
  • latex
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69
Q

What are the clinical manifestations of type I?

A
  • Rhinitis (hay fever)
  • allergic asthma
  • food allergies
  • urticaria (hives) → wheal and flare
  • eczema
    -systemic anaphylaxis → potentially fatal
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70
Q

What are treatments for type I?

A
  • Avoid allergens ‘
  • drug therapy → antihistamines, bronchodilators, most cell stabilizers, corticosteroids epinephrine
  • monoclonal anti-lgE antibody
  • allergy immunotherapy (AIT)→administer gradually, increasing doses of allergen
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71
Q

What are the in vivo skin tests of type I?

A

-percutaneous or intradermal

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72
Q

Describe process of percutaneous and intradermal of type I

A

① apply a panel of allergens to separate sites on the skin
② wait 15 to 20 minutes
* positive test = wheal and flare at the site of application

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73
Q

Describe allergen specific IgE testing of type I?

A
  • RAST (radioallergosorbent test) was the first type of test to be used for specific IgE
    -enzyme methods are now used to detect IgEt specific allergen in patient serum
    -safer than skin testing
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74
Q

What are the in vitro tests of type I?

A
  • Allergen-specific IgE testing
  • total IgE
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75
Q

Describe the total IgE test of type I

A

-RIST (radioimmunosorbent test) was first type of test method for total IgE
-enzymes are now use to detect total concentration of IgE in patient serum

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76
Q

What are allergens?

A

Antigens that trigger type I

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77
Q

What is passive cutaneous anaphylaxis?

A

Redness and swelling at site that was injected with serum (from patient who is allergic to allergen) and later exposed to allergen

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78
Q

What is atopy?

A
  • refers to an inherited tendency to develop classic allergic responses to naturally occurring inhaled or ingested allergens
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79
Q

How long does it take for type I to occur?

A

30-60 minutes

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80
Q

What regulates IgE production ?

A

Th2 cells

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81
Q

What is predominant in people with allergies? What does this cause to be produce?

A

-Th2
- IL-4 and IL-13

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82
Q

What are IL-4 and IL-13 responsible for?

A
  • Final differentiation that occurs in B cells, initiating the transcription of the genes that codes for the epsilon heavy chain of immunoglobulin molecules belonging to the IgE
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83
Q

Describe allergic rhinitis

A
  • Most common form of atopy
  • hay fever
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84
Q

What are symptoms of Hay Feveri?

A
  • paroxysmal sneering
  • rhinorrhea (runny nose)
  • nasal congestion
  • itchy eyes and nose
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85
Q

What is angioedema?

A

Skin reactions that occur deeper in the skin

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86
Q

What can hives and hay fever be treated with?

A

Decongestants and antihistamines

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87
Q

What is used to treat severe asthma?

A

Anti-lgE monoclonal antibodies

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88
Q

Describe allergy immunotherapy (AIT)

A
  • Goal is to induce immune tolerance to a specific allergen by administering gradually increasing doses of the allergen over time
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89
Q

How is the allergic reaction scored?

A

-based on presence or absence of erythema
-diameter of the wheal

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90
Q

What has largely replaced RIST?

A
  • Noncompetive solid-phase immunoassays
  • nephelometry assays
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91
Q

When is total serum IgE testing most beneficial?

A

In evaluating patients with other conditions in which IgE levels may be elevated

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92
Q

What are the key components of type II?

A
  • IgG and IgM directed against cell surface antigen
  • complement
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93
Q

What effects can type II have on antibodies?

A
  • Cell destruction
  • inhibition of cell function
  • increase in cell function
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94
Q

What can cause cell damage for type II?

A
  • Activation of classical pathway of complement and cell lysis
  • opsinozation and phagocytosis of the cell
  • antibody
  • antibody-dependent cell-mediated cytotoxicity (ADCC)
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95
Q

What are clinical examples of type II?

A
  • transfusion reactions
  • hemolytic disease of the newborn (HDN)
  • autoimmune hemolytic anemia
  • anti-GBM disease
  • hashimotos disease
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96
Q

How long dues it take type II to occur?

A

A few hours after exposare antigen

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97
Q

What is a isohemagglutinin?

A

When anti-a and anti-B antibodies are naturally occurring antibodies which are probably triggered by contact with similar antigenic determinants

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98
Q

What happens when sensitized mast cells and basophils become activated?

A

Release chemicals that induce symptoms

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99
Q

Describe mast cells of the sensitization phase of type I?

A

-have abundant cytoplasmic granules that store numerous preformed inflammatory mediators

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100
Q

Describe binding of IgE to mast cells or basophils

A
  • increase half life from 2-3 days to 10 days atleast
    Once IgE binds, functions as an antigen receptor on mast cells and basophils
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101
Q

What are the effector calls of type I?

A

Mast cells

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102
Q

Describe hemolytic disease of the newborn (HDN)

A

-pregnant woman produces antibodies to Rh antigens (usually RhD) on fetal RBCs
- IgG cross placenta and and destroy fetal RBCs

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103
Q

Describe autoimmune hemolytic anemia

A
  • type II reaction
  • directed against self-antigens because this disease forms antibodies to their own RBCs
    -2 kinds of antibodies → warm reactive antibodies and cold agglutinins
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104
Q

What are the symptoms of autoimmune hemolytic anemia?

A
  • Malaise ‘
  • lightheadedness
  • weakness
  • unexplained fever
  • pallor
  • mild jaundice
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105
Q

What temperature does warm reactive antibodies react at?

A

37°C

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106
Q

What temperature does cold agglutinins react to?

A

Below 30°C

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107
Q

Describe the warm autoimmune hemolytic anemia

A
  • account for more than 70% of autoimmune anemias
  • characterized by formation of IgG antibody
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108
Q

Describe cold agglutinins

A
  • autoantibodies that cause RBCs to clump together at cold temperatures
  • below 37°C
  • belong to IgM class
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109
Q

What are the harmful effects of cold agglutinins that are active in vitro up to temperatures of 30°C or more?

A
  • Blocking of small vessels on exposure to cold
  • RBC agglutination
  • production of hemolytic anemia
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110
Q

Describe chronic cold agglutinin syndrome

A
  • Usually has a gradual onset and chronic course
  • usually seen in elderly
    -agglutinins usually contain monoclonal kappa light chains
  • condition may also be due to presence of lymphoma in some individuals
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111
Q

Describe postinfection cold agglutinin syndrome

A
  • Commonly follows infection with mycoplasma pneumoniae or infectious mononucleosis
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112
Q

What is found in those affected with cold agglutinin syndrome?

A
  • high titer of cold agglutinins
  • large amounts of C3d resulting in a positive direct antiglobulintest
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113
Q

What are high-titer monoclonal cold agglutinins associated with?

A
  • B-cell CLL
  • B cell lymphoma s
  • Hodgkin disease
  • Waldenstrom macroglobulinemia
  • SLE
  • cold agglutinin syndrome
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114
Q

Describe paroxysmal cold hemoglobinuria

A
  • Can cause autoimmune hemolytic anemia
  • occurs after certain infections (measels, mumps, chickenpox, and infections mononucleosis)
  • agglutinate at cold temperatures
  • activates complement at 37°c to produce intermittent hemolysis.
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115
Q

Describe mycoplasma pneumoniae

A
  • Cold agglutinins found in approximately 55% of patients
  • cold agglutinius appear around week 2 or 3 after onset
    -reoccurring respiratory infections
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116
Q

What are the symptoms of mycoplasma pneumoniae?

A
  • increasing pallor
  • jaundice
  • enlarged spleen (splenomegaly)
  • hemoglobinogluria
  • if hemolytic anemia occurs, proceeds at alarming rate and may be fatal
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117
Q

Describe infectious mononucleosis

A
  • 50% of patients with disease have anti-i present
  • antibody normally detectable in vitro up to a temperature of about 25°C
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118
Q

Describe direct antiglobulin test (DAT)

A
  • detects RBCs coated with complement components or IgG antibody in vivo
  • patient RBCs are incubated with a poly-specific anti human Ig directed against IgG and C’
  • if positive (agglutination), the test is repeated with mono-specific anti-IgG, anti-C3b, and anti-C3d
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119
Q

Describe indirect antiglobulin test (IAT)

A
  • Coombs test
  • test patient serum for antibodies to RBC antigens
  • positive test → agglutination
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120
Q

Describe the process of indirect antiglobuun test

A

① incubate reagent RBCs with patient serum at 37°C, wash to remove excess
② add anti-human globulin

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121
Q

What is DAT used to detect?

A
  • Transfusion reactions
  • HDFN
  • autoimmune hemolytic anemia
  • drug induced hemolytic anemia
  • detects in vivo binding
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122
Q

What is IAT used for?

A
  • Cross matching of blood to prevent a transfusion reaction
  • determine the presence of a particular antibody in patient plasma
  • type patient RBCs for specific blood group antigens
  • detects in vitro binding
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123
Q

Describe type III hypersensitivity

A
  • keys components are IgG and IgM directed against a soluble antigen
  • small antigen-antibody complexes precipitate out and deposit in tissues
  • C’ binds → vasodilation and vasopermeability increase
  • macrophages and neutrophils migrate to affected areas and release lysosomal enzymes, resulting in tissue damage
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124
Q

How long does type III take to occur!

A

A few hours after exposure

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125
Q

Describe Arthus reaction

A
  • Skin reaction caused by type III hypersensitivity
  • localized inflammation characterized by redness and edema
  • peaks at 3 to 8 hours
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126
Q

Describe serum sickness

A
  • Generalized type III hypersensitivity reaction
  • caused by passive immunization of humans with animal serum
  • produces antibodies against the foreign animal proteins in patients
  • causes immune complexes to form and deposit in tissues
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127
Q

What are the symptoms of Serum sickness?

A
  • headache
  • fever
  • nausea
  • joint pain
  • rashes
  • lymphadenopathy
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128
Q

What are other conditions (besides Arthus and serum sickness) associated with type III?

A
  • SLE
  • RA
  • reactions to bee sting
  • Drug reactions (penicillin)
    -sequelae to infection (post streptococcal glomerulonephiritis)
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129
Q

What are the laboratory tests of type III?

A
  • Testing ANAs
  • fluorescent staining of tissue sections to detect deposited immune complexes
  • testing for rheumatoid factor (anti-IgG)
  • testing complement levels
130
Q

When are complement levels decreased in serum?

A
  • During periods of nigh disease activity
131
Q

When do symptoms of a type IV reaction peak?

A

48-72 hours after exposure

132
Q

What methods detect antinuclear antibodies in SLE and RA?

A
  • indirect immunofluorescence
  • ELISA
  • fluorescent microsphere multiplex immunoassay
133
Q

What methods can detect RF?

A
  • Latex agglutination
  • nephelometry
  • other immunoassays
134
Q

Describe Type IV hypersensitivity

A
  • Th1 and macrophages are involved
  • APCs present antigen to naive T helper cells, which differentiate into Th1 cells
  • Th1 cells release cytokines that attract and activate macrophages
  • macrophages induce inflammation
  • cytotoxic t lymphocytes are recruited and destroyed target cells
135
Q

What are triggers of type IV ?

A
  • Mycobacterium tuberculosis ‘
  • myobacterium leprae
  • pneumocystis carinil
  • leishmania species
  • herpes simplexvirus
    (intracellular pathogens)
  • contact dermatitis
  • hypersensitivity pneumonitis
136
Q

Describe hypersensitivity pneumonitis

A
  • Allergic diseases of lungs
  • caused by inhalation of bacterial and fungal spores
  • ## primarily mediated by sensitized T cells that respond to inhaled allergens
137
Q

What are some examples of hypersensitivity pneumonitis

A
  • Farmers lung disease
  • birds breeders lung disease
  • humidifier lung disease
138
Q

Describe contact dermatitis

A
  • Low-molecular weight compounds contact the skin and act as haptens to sensitive Th1 cells
139
Q

What are triggers of contact dermatitis?

A
  • Poison ivy ‘
  • poison oak
  • Nickle salts
  • cosmetics
  • hair dyes
  • latex
140
Q

What are the symptoms of contact dermatitis?

A
  • Skin eruptions
  • erythema -
  • Swelling
  • papules
141
Q

What are granoulomas?

A
  • Cluster of cells produced by chronic persistence of antigen
  • can function to wall off the organism in contained area, preventing spread.
142
Q

What are the skin tests for type IV?

A
  • Patch test
  • skin testing for immunodeficiency (inject common antigens intradermally)
  • mantoux method
143
Q

Describe the patch test

A
  • Antigen applied to skin surface
  • test for contact dermatitis
  • positive test → redness with papules or blisters
144
Q

Describe mantoux method

A
  • Antigen injected intradermally
  • test for tuberculosis exposure (PPD) or T cell function)
  • positive test→ induration
145
Q

What are types of interferon gamma release assays

A
  • Quantiferon TB gold plus assay
  • T- spot-TB test
146
Q

Describe interferon gramma release assays (IGRA)

A
  • Measures production of IFN- gamma by patient T cells stimulated with MTB antigens
147
Q

Describe T-SPOT-TB test

A
  • Patient mononuclear cells are incubated with MTB antigens and tested for IFN- gamma by ELISPOT
148
Q

What is the gold standard testing for contact dermatitis?

A

Patch test

149
Q

What could a positive result in DAT show?

A
  • Presence of IgG on RBCs
  • presence of C3b or C3d on RBCs
  • A transfusion reaction caused by preformed antibody
150
Q

What is the best test to perform if an allergy to ryegrass is expected:

A

Skin prick test

151
Q

What is the immune phenomenon associated with the Arthus reaction?

A

Deposition of immune complexes in blood vessels

152
Q

What conclusion should be drawn about a patient whose total IgE level was determined to be 150 IU/mL?

A

Antigen- specific testing should be done

153
Q

What is the difference between type I and type II?

A

Type II involves cellular antigens

154
Q

A young woman developed red, itchy papules on her wrist 2 days after wearing a new bracelet. What is this reaction caused by?

A

An inflammatory response induced by cytokines released from Th1

155
Q

What are reactions to latex caused by?

A
  • type I
  • type IV
  • skin irritation
156
Q

How is the cold agglutinin titer determined?

A
  • Patient serum should be seperated from whole blood at 37°C and tested at 4°C
157
Q

What is the principle of the tuberculin test

A
  • PPD is injected into the forearm and stimulates a delayed type hypersensitivity response mediated by T cells.in patients with prior exposure causes induration at the injection site within 48-72 hours
158
Q

Describe auto immune diseases

A
  • humoral and cell-mediated immune responses directed toward self-antigens
  • cause tissue or organ damage
  • systemic or organ-specific
    .due to loss of self tolerance
159
Q

What is self tolerance

A

Ability of the immune system to accept self-antigens and not initiate an immune response against them

160
Q

Describe mechanisms of central and peripheral tolerance

A
  • during maturation process of T cells, the great majority of undifferentiated lymphocytes that are processed through the thymus do not survive
  • The process is not totally effective, however, as normal individuals do possess self-reactive lymphocytes
161
Q

What does autoimmunity result from?

A
  • Complex interactions between genetic and environmental factors
  • inheritance of certain genes can make some individuals more susceptible
  • hormones can influence autoimmunity (women are three times as likely to acquire an autoimmune disease)
  • tissue injury
  • microbial infections
  • environmental factor that can alter gene expression
162
Q

What are microbial infections that can trigger autoimmunity?

A
  • Molecular Mimicry
  • epitope spreading
  • superantigens
163
Q

Why does molecular mimicry trigger autoimmunity?

A

Bacteria or viruses possess antigens that are like a self antigen

164
Q

Why does epitope spreading trigger autoimmunity?

A

-immune response to a microbe expands to activate immune response to other antigens, including self antigens

165
Q

Why do superantigens trigger autoimmunity?

A

Can activate numerous clones of T cells, or through certain viruses, which can cause polyclonal B cells activation

166
Q

What are systemic diseases of autoimmunity?

A
  • SLE, RA, and other SARDs, GPA
167
Q

What are organ specific diseases of autoimmunity?

A
  • Autoimmune thyroid disease
  • type I diabetes
  • celiac disease
  • autoimmune liver diseases
  • multiple sclerosis
  • myasthenia gravis
  • anti-glomerular basement membrane disease
168
Q

Describe immunologic tolerance

A

A state or immune unresponsiveness that is directed against a specific antigen

169
Q

Describe central tolerance

A

Occurs in central or primary lymphoid organs, thymus, and bone marrow

170
Q

What is anergy?

A

Absence of the normal immune response to a particular antigen or allergen

171
Q

Describe peripheral tolerance

A

Lymphocytes that recognize self-antigens in the secondary lymphoid organs are rendered incapable of reacting with those antigens

172
Q

What are the classifications of autoimmune diseases?

A

① systemic
② organ specific

173
Q

What are the a groups of systemic diseases?

A
  • Systemic autoimmune rheumatic diseases (SARDs)
  • anti-neutrophil cytoplasmic antibodies ( ANCAs)
174
Q

Describe SARDs

A

-involve inflammation of the joints and their associated structures

175
Q

Describe ANCAs

A

Characterized by inflammation of the blood vessel

176
Q

Describe systemic lupus erythematosus (SLE)

A
  • Chronic systemic inflammatory disease that affects multiple organ systems
  • pathology caused by type III, tissue damage occurs at the sites in the body where immune complexes have deposited
  • develop numerous autoantibodies
177
Q

What happens when immune complexes form within a patient with SLE?

A

Trigger
- complement activation
- chemotaxis of neutrophils
- inflammation

178
Q

What autoantibodies develop in patients with SLE?

A
  • dsDNA and other nuclear components
  • lymphocytes
  • RBCs
  • platelets
179
Q

What are symptoms of SLE?

A
  • Fatigue
  • malaise
  • weight loss
  • Joint involvement (most frequently reported-90%)
  • skin rashes (80%)
  • renal involvement (50%)
  • neurological symptoms
  • anemia, leukopenia, thrombocytopenia
180
Q

Describe the skin rash that occurs on patients with SLE

A
  • A classic butterfly rash across the nose and cheeks
    -this is where lupus comes from, meaning wolf-like
181
Q

What was the first clue in the mystery of lupus?

A

Discovery of LE cell

182
Q

Who discovered LE cells?

A

Malcolm Hargraves (1948)

183
Q

Describe the LE cell

A
  • It is a neutrophil that have engulfed the antibody- coated nucleus of another neutrophil, mainly in vitro
184
Q

What was the second discovery of SLE?

A
  • It is associated with more than 25 autoantibodies
  • this reflects a generalized dysregulation of the immune system in SLE
185
Q

What are the laboratory tests to diagnose SLE?

A
  • CBC
  • urinalysis
  • CRP/ESR (elevated during flare-ups)
  • complement quantitation (C3 levels can be decreased during inflammation)
  • ANAs
186
Q

What test is typically done first if SLE is suspected?

A
  • Screening test for antinuclear antibodies (ANAs)
187
Q

What treatment is recommended for all SLE patients?

A

Anti-malarial drug→hydroxychloroquine

188
Q

What is the most common cause of death In lupus?

A

Renal failure and infection

189
Q

Describe ANAs

A
  • Directed against antigens in cell nuclei
  • present in move than 95% of lupus patients
  • heterogenous group of antibodies ‘
  • includes:
    -anti-dsDNA (lupus specific)
    -anti-ssDNA
    -anti-histones and nucleosomes
    -antibodies to centromere or nuclear components
    -anti-ENA (anti-sm, anti-RNP, anti-ss-A, and anti-ss-B)
190
Q

What antibody (ANA) is most specific for SLE?

A
  • dsDNA
  • especially found in combination with low levels of complement component C3
191
Q

What anti-histories are detected in almost all patients with drug-induced lupus?

A

H2A and H2B

192
Q

What is a nucleolus?

A

Prominent structure within the nucleus where transcription and processing of ribosomal RNA and assembly of ribosomes takes place

193
Q

What are methods usedto detect ANAs in patient serum?

A
  • Indirect immunofluorescence (IIF)
  • ELISA
  • microsphere multiplex immunoassay (MIA)
  • immunodiffusion
194
Q

What is the dsDNA immune fluorescent pattern?

A

Homogenous on IIF

195
Q

What is the immunofluorescent pattern of anti-histones?

A

Homogenous in IIF assay

196
Q

What is the immunofluorescent pattern of nucleosome antibodies?

A

Homogenous in IIF assay

197
Q

What are the immunofluorescent patterns of anti-sm and anti-RNP?

A

Coarse speckled

198
Q

What testing is most widely used to detect ANAs?

A

Fluorescent antinuclear antibody

199
Q

What is the FANA test principle?

A

① incubate patient serum with hep-2 cells fixed onto microscope side
② wash and incubate with fluorescein- labeled anti-human IgG
③ wash and view under-fluorescent microscope

200
Q

Describe immunofluorence using crithidia luciliae

A
  • An IIF using C. Luciliae as substrate
  • contains circular organelle called a kinetoplast (rich in dsDNA)
  • used to detect antibodies to dsDNA antibody titers
201
Q

Describe ENA Ouchterlony test

A
  • Immunodiffusion test detects antibodies to specific ENA
  • patient serum in outer wells react with ENA antigens in center well
  • in this example, patient A has antibody to Sm
  • anti-sm is diagnostic for SLE
  • positive reactions indicated by immunoprecipitation lines of serologicalidentity
  • not as sensitive
  • long turnaround times
202
Q

Describe ELISA testing of SLE

A
  • Has come into wider use for detection of: anti-dsDNA, antihistone antibodies, anti-ss A, and anti-ss-B
  • quantitative
  • less subjective
203
Q

Describe phospholipid antibodies found in SLE patients

A
  • Heterogenous group of antibodies that bird to phospholipids
  • Found in about 60% of lupus patients
  • associated with deep vein and arterial thrombosis
  • increased risk of reoccurring pregnancy loss
  • can cause false positive results in nontreponemal tests for syphilis
204
Q

What is an example of a phospholipid antibody?

A

The lupus anticoagulant → produces prolonged APTT and PT

205
Q

What are the three main applications of IIF?

A

① as initial test to determine the presence or absence of ANAs in patients with SARDs, aiding in diagnosis
② to provide guidance in selection of follow-up tests based on the immunofluorescence patterns obtained
③ to determine ANA titer because moderate to high titers have been better correlated with disease

206
Q

Why are HEp-2 cells used in IIF?

A

-they have large nuclei with high antigen expression, allowing for high sensitivity and facilitating visualization of results

207
Q

What are the 4 major nuclear pattern groups?

A

① homogenous
② speckled
③ centromere
④ nucleolar

208
Q

Describe homogenous nuclear pattern

A
  • Characterized by uniform staining of entire nucleus in interphase cells and of condensed chromosomal region in metaphase cells
  • associated with dsDNA, histones, and nucleosomes
209
Q

When is homogenous nuclear patterns presents?

A

Found in patients with:
- SLE
- drug induced lupus
- chronic autoimmune hepatitis (AIH)
- juvenile idiopathic arthritis

210
Q

Describe the speckled nuclear pattern

A
  • Characterized by discrete fluorescent specks throughout the nuclei of interphase cells
  • 3 groups: dense fine, tiny/fine, and large/course
211
Q

What are fine or coarse speckles associated with?

A
  • Antibodies to ENAs ‘
    -SLE
    -Sjogren’s syndrome
    -SSc
  • other SARDs
212
Q

What are the dense fine speckles associated with?

A
  • Antibodies to the DFS70/LEDGF antigen
  • correlated with absence of a SARD upon confirmatory test
213
Q

Describe the centromere nuclear pattern

A
  • Numerous discrete speckles are seen in nuclei of interphase cells and the chromatin of dividing cells
  • 46 speckles, represents each chromosome
  • found mainly in patients with CREST syndrome
214
Q

Describe the nucleolar nuclear pattern

A
  • Prominent staining of the nucleoli within nuclei of interphase cells is seen in this pattern
  • seen in patients with SSc but also can be present in other SARDs
215
Q

Describe rheumatoid arthritis (RA)

A
  • Chronic arthritis of the peripheral joints that can progress to joint deformity and disability
  • 25% of patients have osteoporosis
  • some patients also develop:
    -subcutaneous nodules
    -pericarditis
    -interstitial lung disease
    -vasculitis
216
Q

Describe pathology of RA

A
  • Inflammation destroys the bone and cartilage
  • TNF-alpha plays key role in the process
  • overly active osteoclasts absorb the bone
  • autoantibodies combine with antigens to form immune complexes
217
Q

Describe treatments for RA

A
  • NSAIDS
  • disease-modifying anti-rheumatic drugs (DMARDs)
  • biological agent that target TNF-alpha
218
Q

What are some laboratory tests for RA?

A
  • Rheumatoid factor
  • anti-CCP
  • ANAs
  • ESRs, CRP, and C’
219
Q

Describe rheumatoid factor

A

-autoantibody (usually IgM) that reacts with Fc portion of IgG
-found in approximately 80% of patients with RA, not specific for RA

220
Q

Describe anti-CCP

A
  • autoantibody directed against cyclic citrullinated peptide (containing modified Arginine)
  • highly specific RA
  • best for early detection of RA
221
Q

What is pannus?

A

A sheet of inflammatory granulation tissue that grows into the joint space and invades the cartilage

222
Q

What are the cytokines found in synovial fluid that contribute to inflammation?

A
  • IL-1
  • IL-6
  • IL-17
  • TNF-alpha→ key role in stimulating cytokine production and facilitate transport of WBC to affected area
223
Q

What is the gold standard for ANA testing?

224
Q

What are the symptoms of rheumatoid arthritis?

A

-malaise ‘’
- fatigue
- fever
- weight loss
- transient joint pain in hands and feet
- muscle spasm
- limitation of movement

225
Q

What autoimmune disease is characterized by dry mouth and eyes?

A

Sjögren’s syndrome

226
Q

What is the most common cause of death in RA?

A

Cardiovascular disease

227
Q

What are the criteria for identification of RA?

A
  • number and Type of joints involved
  • duration of symptoms
  • serology results for RF and anti-CCP
  • serum level of the acute phase reactant
  • CRP
    -ESR
228
Q

What are the components of RF?

A

Patients with RA and specific HLA-DRB1 alleles or PTPN22 gene polymorphism

229
Q

What are other systemic autoimmune rheumatic diseases (SARDs)?

A
  • Sjorgren syndrome
  • Systemic sclerosis (SSc)
  • mixed connective tissue disease
  • inflammatory myopathies
230
Q

Describe sjogren syndrome

A
  • Dry eyes and mouth
  • ss-A and ss-B antibodies
  • characterized by chronic inflammation of the exocrine glands, most notably → the ocular and salivary gland
  • have primary (solo) and secondary (other diseases) categories
231
Q

Describe systemic sclerosis (SSc)

A
  • Fibrosis and vasculitis affecting skin, joints, other organs
  • includes CREST syndrome and many ANAs
232
Q

What are the symptoms of systemic sclerosis?

A
  • tightening and hardening of skin
  • musculoskeletal pain
  • raynaud’s phenomenon
  • heartburn
233
Q

Describe mixed connective tissue disease

A
  • Overlap of limited cutaneous SSc and other SARDs; anti-u1-RNP
234
Q

Describe inflammatory myopathies

A
  • Polymyositis and dermatomyostis
  • progressive muscle weakness; many ANAs
  • characterized by chronic inflammation of the skeletal muscles and progressive muscle weakness
235
Q

Describe granulomatosis with polyangitis

A
  • Wegners granulomatosis
  • rare autoimmune disease involving inflammation of small-to-medium sized blood vessels and respiratory tract
  • progresses to more systemic disease involving other organs (kidneys, joints, skin)
  • most patients have antibodies to neutrophil cytoplasmic antigens such as proteinase 3
  • neutrophil activation results in damage to vascular endothelium and Th1 response
236
Q

What are symptoms of granulomatosis with polyangitis? (GPA)

A
  • Fever
  • malaise
  • joint pain
  • anorexia
  • weight loss
  • persistent runny nose
  • rhinitis
  • sinusitis
  • oral or nasal ulcers
  • gingivitis
  • hearing loss
  • collapsed nose bridge
  • renal involvement
  • pain and arthritis of large joints
  • skin lesions
237
Q

What alleles are associated with GPA?

A
  • HLA-DRB1*0401 (Caucasian)
  • HLA-DRB1*0901 (Asian and African American)
  • HLA-DRB*1501 (Asian and African American)
238
Q

What is the treatment for GPA?

A
  • combo of glucocorticoid drugs and cyclophosphamide ( severe forms)
  • monoclonal antibody rituximab
    -immune suppressive therapy
239
Q

Describe anti-neutrophil cytoplasmic antibodies (ANCA)

A
  • Produced against proteins in neutrophil granules
  • strongly associated with syndromes involving vascular inflammation
  • detected by IIF on ethanol-fixed leukocytes
  • ELISA and chemo luminescent assays are also available
240
Q

Describe ANCA detected by IIF on ethanol fixed leukocytes procedure

A

① patient serum incubated with microscope slide containing ethanol- fixed leukocytes
② wash and add FITC- labeled anti-lgG conjugate
③ Wash and view fluorescence in neutrophils under fluorescent microscope

241
Q

What are the 3 syndromes involving vascular inflammation associated with ANCAs?

A
  • GPA
    -microscopic polyangitis (MPA)
  • eosinophilic granulomatosis with polyangitis ( EGPA)
242
Q

What are the two patterns that can be observed with ANCAs?

A
  • cytoplasmic (c-ANCA)
  • pernicular (p- ANCA)
243
Q

Describe c-ANCA pattern

A
  • primarily caused by PR3-ANCA and appears as a diffuse, granular staining in cytoplasm of neutrophils
244
Q

Describe p-ANCA pattern

A

-fluorescence surrounds the lobes of the nucleus, blending them together so that individual lobes cannot be distinguished

245
Q

What is the autoantigen of c-ANCA?

A

PR3 antigen

246
Q

What disease is associated with c-ANCA?

247
Q

What is the autoantigen of p-ANCA?

A

Positively charged antigens, including myeloperoxidase (MPO)

248
Q

What are diseases associated with p-ANCA?

249
Q

What test should be run if the initial IIF test results are positive for ANCA?

A

Confirmed by PR3- and MPO-specific immanoassays

250
Q

What diseases can ANCA be detected in?

A
  • SARDs, such as SLE and RA ‘
  • autoimmune gastrointestinal disease
  • liver disease
  • HIV
  • hepatitis C
    -malignancy
251
Q

Describe autoimmune thyroid diseases (AITDs)

A
  • thyroid hormone synthesis is carefully regulated by endocrine feedback loop
  • autoantibodies produced in AITDs can lead to decreased or increased production of thyroid hormones
252
Q

What diseases are AITDs?

A
  • Hashimotos thyroiditis
  • graves disease
253
Q

What is the target tissue of graves disease and hashimotos disease?

A

Thyroid grand

254
Q

Describe hashimotos thyroïditis

A
  • immune destruction of the thyroid gland produces hypothyroidism
  • lab results:
    -normal or high TSH
    -low free T4
    -anti-TPO
  • anti-Tg
255
Q

What are hashímotos thyroiditis symptoms?

A
  • fatigue
  • dry skin
  • weight gain
  • brittle hair
    -formation of goiter
256
Q

What is hypothyroidism?

A

Decreased thyroid function

257
Q

What are symptoms of hypothyroidism?

A

-dry skin
- decreased sweating
- puffy face with edematous eyelids
- pallor with a yellow tinge
- weight gain
- fatigue
- brittle hair

258
Q

Describe Graves’ disease

A
  • AITD characterized by hyperthyroidism
  • TRAbs produced
  • low TSH and high FT4; antibodies to TPO and Tg may be produced
259
Q

What are autoantibodies of Hashimoto’s thyroiditis?

A
  • Anti-thyroglobulin
  • anti-thyroid peroxides
260
Q

What are the autoantibodies of Graves’ disease?

A

-thyroid-stimulating hormone receptor antibodies (TRAbs)
-anti-thyroglobulin
- anti-thyroid peroxides (TPO)

261
Q

What is hyperthyroidism?

A
  • State of excess thyroid function
  • associated with Graves’ disease
262
Q

What are symptoms of Graves’ disease?

A
  • nervousness
  • insomnia
  • depression
  • weight loss
  • heat intolerance
  • sweating
  • rapid heartbeat
  • palpitations
  • breathlessness
  • fatigue
  • cardiac dysrhythmias
  • bulging eyes
  • restlessness
  • lower leg edema
263
Q

What are treatments for hashimotos thyroïditis?

A

-daily oral thyroid hormone replacement therapy, levothyroxine (T4)

264
Q

What are the treatments for Graves’ disease?

A
  • Radio active iodine
265
Q

What are most commonly used to detect thyroid antibodies?

A
  • Sensitive ELISA
  • chemiluminescent immunoassays
266
Q

What is the best indicator for hashimotos thyroiditis?

A

Antibodies to TPO

267
Q

What is highly indicative of Graves’ disease?

268
Q

What are the two types of tests for TRAbs?

A
  • Binding assay
  • bioassay
269
Q

Describe binding assays for TRAbs

A
  • Automated solid-phase ELISA
  • chemoluminescent immunoassays
  • labeled TRAbs reagent competes with the patient antibody for TSH receptor bound to solid phase
  • unable to distinguish between TSI and TRAbs
270
Q

Describe bioassay for TRAbs

A
  • Require tissue culture
  • difficult to perform
  • specifically measure the function of TSI
271
Q

Describe type I diabetes mellitus (T1D)

A
  • Endocrine disorder characterized by hyperglycemia
  • type I destruction of beta cells in pancreas results in insulin deficiency
  • genetic susceptibility to the disease
272
Q

What are the long term effects of type I diabetes mellitus?

A
  • Cardiovascular disease
  • kidney dysfunction
  • nerve damage
  • blindness
  • infections
273
Q

What would the results look like for a patient with type I diabetes mellitus?

A
  • increased glucose blood level
  • elevated HbA1c
  • autoantibodies to GAD and IA-2, ICA
274
Q

What is hyperglycemia?

A

A high level of glucose in the blood

275
Q

What are the four types of diabetes?

A

-type I
- type II
- gestational
- for other reasons (neonatal, Pancreatitis)

276
Q

What is the treatment for type I diabetes mellitus

A
  • lifelong insulin injections to control glucose levels
277
Q

What genes are usually carried by patients with type I diabetes mellitus?

A
  • HLA-DR3
  • DR4
  • increased risk if both are present
278
Q

What leads to fibrosis and destruction of most beta cells in patients with type I diabetes mellitus?

A
  • Progressive inflammation of the islets of langerhans in pancreas
279
Q

What are the four criteria that is used to diagnose type I diabetes mellitus?

A

*only one is required
① fasting glucose greater than 126 mg/dL on more than one occasion
② a random plasma glucose level of 200 mg/dL or more with classic symptoms of diabetes
③oral glucose tolerance test of 200 mg/dL or more in a 2-hour samplewith a 75 g glucose load
④ a hemoglobin A1c value (HbA1c) greater than 6.5%

280
Q

Describe celiac disease

A
  • Affects small intestine and other organs
  • triggered by gluten
281
Q

What are the symptoms of celiac disease?

A
  • Diarrhea
  • abdominal pain
  • bloating
282
Q

What is the treatment for celiacs disease?

A

Gluten-free diet

283
Q

In celiacs disease, autoantibodies form in HLA-DQ2 or HLA-DQ8 positive people to what?

A
  • gliadin (component of gluten)
  • tissue transglutaminase (IgA is screening test of choice)
    -endomysium (EMA)
284
Q

What environmental factors are believed to play a role in development of celiac disease?

A
  • gluten administered at 4 months or younger in absence of breast feeding
    -rotavirus infection
    -overgrowth of pathogenic bacteria in the gut
285
Q

What is the diagnosis of celiac disease based in?

A
  • clinical symptoms
  • serological test findings
  • duodenal biopsy
  • presence of HLA-DQ2 or HLA-DQ8 haplotype
286
Q

Describe autoimmune liver diseases

A
  • Immune-mediated liver diseasesthat can lead to end-stage liverfailure if left untreated
  • includes:
    -autoimmune hepatitis (AIH)
    -primary biliary cholangitis (PBC)
287
Q

Describe autoimmune hepatitis

A
  • hepatocytes targeted
  • AIH-1- positive for SMA, ANAs
  • AIH-2- positive for LKM-1 or LC-1 antibodies
  • affects small interlobular bile ducts
288
Q

What are symptoms of AIH?

A

-25% are asymptomatic
- fatigue
- nauseous
- weight loss
- abdominal pain
- itching
- maculopopular rashes
- jaundice

289
Q

What alleles are associated with AIH-1?

A

HLA-DR-3 and HLA-DR4

290
Q

What alleles are associated with AIH-2?

A
  • HLA-DRB1 and HLA-DQB1
291
Q

What would lab results look like of a patient with AIH?

A
  • Elevated levels of the liver enzymes asparate aminotransferase (AST) and alanine aminotransferase (ALT)
    -increase in serum bilirubin and alkaline phosphate
  • IgG are high
292
Q

What is necessary to confirm AIH?

A

Liver biopsy

293
Q

What is the treatment for AIH?

A
  • immunosuppressant treatment of prednisolone
  • arathioprine to maintain remission
294
Q

Describe PBC

A
  • Destruction of intrahepatic bile ducts; cholestasis
  • inflammation of portal vein in liver
  • accumulation of scar tissue that can lead to cirrhosis and liver failure
  • majority of patients produce mitochondrial Abs (AMAs)
295
Q

What is the most common autoimmune liver disease?

296
Q

What is cholestasis

A

A condition in whichthe flow of bile is slowed or blocked

297
Q

What are the symptoms of PBC?

A
  • Some can be asymptomatic
  • fatigue
  • itchy skin (pruritis)
  • abdominal pain
  • dry eyes
  • dry mouth
  • jaundice
  • greasy stools
298
Q

What is the standard initial therapy of PBC?

A

-ursodeoxycholic acid (UDCA) → bile acid that helps move bile through the liver

299
Q

What are the 3 criteria of PBC diagnosing?

A
  • AMAs present
  • serum alkaline phosphates level elevated at least 1.5 times the upper limit of normal for 6 months
  • liver biopsy showing nonsuppurative destruction cholangitis andinterlobular bile duct injury
  • 2out of 3 needed
300
Q

What methods are there to detect AMAs?

A

-IIF
- immunoblotting with mitochondrial preparations from mammal tissues
- ELISA
- fluorescent microbead immunoassay

301
Q

Describe multiple sclerosis (MS)

A
  • Involves inflammation and destruction of the central nervous system.
  • most patients produce antibodies against myelin basic protein
  • plaques form in while matter of the brain and spinal Cord, causing destruction of the myelin sheath of axons
302
Q

What are the symptoms of multiple sclerosis?

A
  • Visual disturbances
  • weakness in limps
  • dizziness
  • sensory abnormalities ( pins and needles tingling)
  • facial palsy
303
Q

What would be the laboratory findings of a patient with multiple sclerosis?

A

-lesions on magnetic resonance imaging (MRI)
-increased immunoglobulins in spinal fluid and increased IgG index
-oligocional bands on protein electrophoresis of CSF

304
Q

What gene is closely associated with inheritance of MS

305
Q

What are environmental factors that have been associated with MS?

A
  • Reduced exposure to sunlight
  • vitamin D deficiency
  • cigarette smoking
  • infection with EBV after early childhood
306
Q

What is the treatment of MS?

A
  • Glucocorticoids
  • disease modifying therapy
307
Q

Describe myasthenia gravis

A
  • Affects neuromuscular junction, resulting in weak skeletal muscles
  • most patients have antibodies to acetylcholine receptors (ACHR) which block binding of ACH to receptor and transmission of nerve impulses that activate muscles
  • heterogenous
308
Q

What are symptoms of myasthenia Gravis?

A
  • Drooping eyelids
  • inability to retract corners of mouth
  • Difficulty speaking, chewing,and swallowing
  • inability to support think, neck or head
  • respiratory muscle weakness
  • associated with several HLA antigen abnormalities
309
Q

What is the main contributor to pathogenosis of MG?

A
  • Antibody to ACH receptors
  • 80-85% patients have antibody
310
Q

What other diseases are associated with presence of MG?

A
  • SLE
  • RA
  • pernicious anemia
  • thyroïditis
311
Q

Describe laboratory testing for MG

A
  • RIA is used to detect antibody, based on assays that block the binding of receptors by anti-ACH receptor (ACHR) antibody
  • radio labeled snake venom called alpha-bungarotoxin is used to irreversibly bind to ACHRs
  • precipitation of receptors caused by combination with antibody is then measured
  • a quick immunostick ELISA has also been developed for testing
312
Q

What is the treatment for MG?

A
  • Anti-cholinsterase agents to prevent destruction of neurotransmitter Ah
    -thymectomy
    -high doses of glucocorticoid drugs
  • immunosuppressive drugs
313
Q

What is the gold standard for detecting binding AChRs?

A

Quantitative radioimmunoassay that have radio-labeledsnake venous

314
Q

In MG, if the patient tests negative for AChRs, what should be tested for?

A

-MuSK antibodies
-this can be done by quantitative RIA

315
Q

Describe anti-glomerular basement membrane disease

A
  • formerly known as good pasture syndrome
  • patients produce autoantibodies to basement membranes living the renal glomeruli and lung alveoli
  • immune complexes bind to basement membranes, attract complement, and cause damage by type II hypersensitivity
  • antibodies to GBM found in most patient s
316
Q

Describe testing of anti-glomemlar basement membrane disease

A
  • Detected by IIF on frozen kidney sections or ELISA for antibody to a 3-subunit
  • tissue-bound anti-GBM detected by direct immunofluorence on kidney biopsy sections; produces a smooth, linear, ribbon-like fluorescence along the GBM
317
Q

What are the symptoms of Anti-glomerular basement membrane disease?

A

-fatigue
- malaise
- edema
- hypertension
- Can progress to renal failure and respiratory problems ( cough, shortness of breathe, hemoptysis

318
Q

What is the treatment for anti -GBM disease?

A

-high doses of corticosteroids
- immunos oppressive drugs
- plasmapheresis is performed
-

319
Q

What allele has a strong association with anti-GBM disease?

A

HLA-DRB1-15

320
Q

What detects GBM antibodies currently?

A
  • ELISA
    -fluorescent microbead immunoassay that uses recombinant alpha -3(IV) antigen substrates
  • confirmation → western blot

MLT immunology (7 decks)

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