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BLD 434 > BLD section 6 quiz > Flashcards

BLD section 6 quiz Flashcards

1
Q

Type 1 hypersensitivity

A

IgE mediated, typically environmental allergens

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2
Q

Type 2 hypersensitivity

A

IgG, antibody cell mediated causes cytotoxicity, complement activation, drug response creates novel antigen, which causes hypersensitive response at next exposure

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3
Q

Type 3 hypersensitivity

A

IgG, immune complex mediated, complement activation, Immune complex activating complement which acts in an autoimmune fashion

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4
Q

Type 4 hypersensitivity

A

Cell mediated, sensitized T cells (typically cytotoxic, can be Th1), activated macrophages, Contact dermatitis, bacterial infection IgE

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5
Q

How does immediate hypersensitivity differ from delayed type hypersensitivity

A

Immediate hypersensitivity is type 1 while delayed is type 4 and usually 1-3 days after exposure

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6
Q

What type of hypersensitivity is associated with histamine release

A

type 1

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7
Q

Describe the utility of total serum IgE testing

A

RIST. Elevated total serum IgE

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8
Q

What are advantages to total serum IgE testing

A

inexpensive and suggests further testing

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9
Q

What are disadvantages to total serum IgE testing

A

not sensitive and doesn’t identify allergen

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10
Q

Describe the utility of skin prick testing

A

wheal reaction

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11
Q

What are advantages to skin prick testing

A

positive test is clinically significant

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12
Q

What are disadvantages to skin prick testing

A

danger of systemic reaction, traumatic to the patient, and only tests limited individual allergens

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13
Q

Describe the utility of allergen specific testing

A

RAST

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14
Q

What are advantages to allergen specific testing

A

can be taken with antihistamines and only require single skin puncture to draw blood for serum testing

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15
Q

What are disadvantages to allergen specific testing

A

lower specificity than skin testing and only tells if IgE is present not if its responsible for current allergic symptoms

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16
Q

Identify common examples of type II hypersensitivities

A

Hemolytic anemia and hemolytic disease of fetus and newborn (HDFN)

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17
Q

Identify the type of hypersensitivity for: Serum sickness

A

Type 3

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18
Q

Identify the type of hypersensitivity for: Celiac disease

A

Type 4

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19
Q

Identify the type of hypersensitivity for: Poison ivy

A

Type 4

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20
Q

Identify the type of hypersensitivity for: Allergic asthma

A

Type 1

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21
Q

Identify the type of hypersensitivity for: Food allergies

A

Type 1

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22
Q

Identify which hypersensitivity responses involve complement activation

A

Type 2 and type 3 hypersensitivity involves complement activation

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23
Q

Identify whether CD4+ T cells, CD8+ T cells, and/or B cells are responsible for autoimmune disease

A

Both autoimmune antibodies and Tc have been found to be responsible for eliciting autoimmunity - usually one or the other cell type dominates

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24
Q

Identify two proteins involved in T lymphocyte self-tolerance that when defective in humans lead to generalized autoimmune disease

A

Homozygous deletion mutations of AIRE (autoimmune response element) or FoxP3 cause generalized autoimmunity

-AIRE - produces proteins for negative selection
- FoxP3 - a transcription factor that maintains Treg phenotype

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25
Q

Explain the role of HLA alleles in development of autoimmunity (i.e. what are the HLA molecules doing exactly to trigger autoimmunity?)

A

Linked more commonly to increased susceptibility to autoimmunity to due their ability to present self-antigen

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26
Q

Define “relative risk” and the ultimate effect that it has on an individual’s likelihood to develop any given autoimmune disease.

A

If you have the associated HLA gene, relative risk is the increased risk you have over the general population to get the disease. However, just because you have HLA susceptibility does not mean that you will get the disease

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27
Q

Interpret a relative risk score

A
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28
Q

Define epitope spreading

A

a common feature of autoimmune disease that refers to the amount of autoantigen that is recognized by the immune system

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29
Q

How is linked recognition responsible for epitope spreading

A

Epitope spreading is responsible for the ↑ in disease severity in autoimmune diseases
- When a patient is first diagnosed, auto-antibodies are limited
- as the disease progresses, the patient develops auto-antibodies against more & more antigens
- Result of “sloppiness” of T cell help to B cells - in the production of high affinity isotype switched antibody

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30
Q

Describe the usefulness IVIg in therapeutic treatment

A

IVIg - “intravenous immunoglobulin”
- Concentrated human IgG pooled from multiple “normal” healthy donors to treat primary Ab immune deficiency
- Now used as interfering anti-idiotypic Ab to block autoantibodies, inhibit naïve B cells, and overwhelm FcγR

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31
Q

Describe the usefulness RhoGAM in therapeutic treatment

A

RhoGAM - used in prevention of hemolytic disease of the newborn
- Polyclonal IgG purified from pooled serum taken from Rh-negative moms who have anti-Rh Ab

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32
Q

discuss the general usefulness of other antibody preparations in therapeutic treatment

A

monoclonal antibody (recombinant protein “therapies”) used to target and kill tumor cells or acts as immunosuppressants

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33
Q

Describe how monoclonal antibody preparations differ from polyclonal antibody preparations (aka, antiserum)

A

Monoclonal antibodies are antibody preparations in which antibody is all identical and is produced by a cell clone called a hybridoma

34
Q

Identify specific monoclonal antibody therapies used to treat Rheumatoid Arthritis and other destructive autoimmune disorders (Anti-TNF alpha)

A

Anti-TNF alpha is a blocking monoclonal antibody that is used to treat rheumatoid arthritis (it blocks joint destruction)

35
Q

Identify specific monoclonal antibody therapies used to treat Rheumatoid Arthritis and other destructive autoimmune disorders (Anti-ɑ 4)

A

Anti-ɑ 4 integrin blocks the homing of inflammatory cells which prevents autoimmune tissue destruction

36
Q

Identify specific monoclonal antibody therapies used to treat Rheumatoid Arthritis and other destructive autoimmune disorders (Anti-IL-1 or Anti-IL-6)

A

Anti-IL-1 or anti-IL-6 antibodies interfere with macrophage inflammatory cytokines with anti-TNF ɑ doesn’t work

37
Q

Identify which types of hypersensitivity responses can cause autoimmune disorders, and which of these is most commonly encountered.

A

Type II-IV hypersensitivity responses causes autoimmune disorders, most commonly encountered is: Type II

38
Q

Identify four autoimmune diseases that have a much higher incidence rate (> 5 times) in women than in men

A
  1. hashimoto’s thyroiditis
  2. Grave’s disease
  3. systemic lupus erythematosis
  4. Addison’s disease
39
Q

Describe the general cause of Celiac disease

A

During digestion, tissue transglutaminase (TTG) delaminates the gliadin component of gluten, and the modified gliadin stimulates a T cell response against new antigen

40
Q

What are the auto-antibodies that can be used to diagnose celiac disease

A

IgA anti-TTG antibodies, IgA anti-gliadin antibodies, and IgA anti-endomysium

41
Q

Why dermatitis herpetiformis is associated with celiac disease

A

high IgA anti-tissue transglutaminase

42
Q

Identify the two forms of Inflammatory Bowel Disease in humans

A
  1. ulcerative colitis - only inflames large intestine
  2. crohns disease- can inflame all of intestinal tract from mouth to anus
43
Q

Which of the two forms of IBD can be associated with ANCA, and which ANCA pattern is associated with (cANCA or pANCA)?

A

ANA( anti-neutrophil antibodies) are most common seen in patients with ulcerative colitis that have vasculitis. These patients usually have a pANCA (peripheral) pattern

44
Q

Identify the autoantibodies associated with Pernicious Anemia and the vitamin deficiency they can cause

A

Autoantibodies: anti-intrinsic factor antibody (most common) and anti-Parietal cell antibody.
Causes megaloblastic anemia due to cobalamin deficiency (vitamin B12)

45
Q

Identify the auto-antigen that is targeted in Myasthenia gravis

A

ACH receptor

46
Q

Disease pathophysiology of Myasthenia gravis

A

Antibody blocks binding to ACH-R and increased receptor uptake by muscle cell so that an action potential cannot occur

47
Q

Immune mechanisms responsible for Myasthenia gravis

A

Anti-ACH-R antibodies increase ACH-R recycling (remove it from cell surface) and blood ACR binding to ACH-R

48
Q

Laboratory test used for Myasthenia gravis diagnosis

A

Detection of anti-ACH-R antibody by precipitation radioimmunoassay

49
Q

Identify the auto-antigens that are targeted in Multiple sclerosis

A

MBP (myelin basic protein) and MOG (myelin oligodendrocyte glycoprotein)

50
Q

Disease pathophysiology of Multiple sclerosis

A

Inflammatory autoimmune disease of myelin located in the CNS).

51
Q

Immune mechanisms responsible for Multiple sclerosis

A

Auto-antigens are targeted by both antibody and T cells (Th1 and Tc) and they both play a role in myelin destruction

52
Q

Identify the two most common rheumatologic diseases that are considered autoimmune diseases.

A

systemic lupus erythematosus and rheumatoid arthritis

53
Q

Explain why autoimmune rheumatologic diseases are difficult to diagnose

A

There can be an overlap in symptoms from one disease to another, and on overlap in laboratory results (no one test is 100% specific or sensitive for a particular disease)

54
Q

Define FANA and the staining patterns that may be observed

A

fluorescent antinuclear antibody testing. Results include titer and pattern of antibody binding including: homogenous, speckled, nucleolar, peripheral, and mixed. Positive FANA indicates a follow up with ENA testing for specific antibodies to ENA

55
Q

Define ANA

A

antinuclear antibodies test is a classical screening test for SLE/ Lupus

56
Q

Define ENA and identify the two specific ENAs that are diagnostic for Systemic Lupus Erythematosus (SLE or Lupus)

A

Extractable nuclear antigen antibodies
Anti-dsDNA (antibody to double stranded DNA) and Anti-Sm (antibody to Smith antigen). They are specific but not sensitive

57
Q

Categorize the autoimmune mechanism responsible for Lupus as one of the Type I-IV hypersensitivity responses.

A

Caused by autoantibodies to nuclear components, IgG autoantibodies form immune complexes with soluble proteins/nucleic acids and deposit in tissues where complement activation occurs in blood vessels, joints, and kidneys.
Complement activation is indicative of Type II and Type III hypersensitivity; however, Type III hypersensitivity is due to immune complex deposition activating complement which leads to inflammation. Causes vasculitis, kidney and joint damage in autoimmune disorders such as lupus and rheumatoid arthritis

58
Q

Identify other diseases that may show a low positive titer in a FANA test, as well as other “non-disease” states

A

A positive FANA test doesn’t diagnose SLE. 5% of healthy individuals has low positive, up to 70% of elderly have low positive. Low positive titers in RA (about 50%), scleroderma (60-90%), Sjorgen’s syndrome (80%)

59
Q

Identify the specific ENA that is associated with drug-induced lupus

A

Anti-histone antibody is only ENA positive in drug-induced lupus, and if you take the patient off of that drug the lupus will disappear

60
Q

Explain why lupus patients can have a false positive syphilis test. Choose whether this false positive would be in either the non-treponemal or treponemal test for syphilis, or both

A

lupus patients may have a false positive because of the anti-cardiolipin antibody that can develop in some lupus patients. Cardiolipin is the target in non-treponemal syphilis testing

61
Q

Define “rheumatoid factor” (RF) and identify what diseases it may be found in, and for which disease it is considered most significant

A

IgM, IgG, or IgA antibody to the Fc portion of IgG (i.e. anti-immunoglobulin antibodies)
Can be found in patients with syphilis, lupus, hepatitis, TB, mono, and Sjoren’s syndrome. Most common in rheumatoid arthritis

62
Q

Describe how the screening test for IgM isotype RF differs from the specific tests for IgG and IgA isotypes of RF. Which is/are most specific for diagnosis of RA?

A

Screening tests for RF are agglutination tests with either RBC or latex particles coated with IgG. Only IgM RF will cause agglutination due to the fact that it is a pentamer. As monomers IgA and IgG are unable to cause agglutination. Specific isotype testing including IgG RF and IgA RF are much more disease-specific and are present in nearly 100% of patients

63
Q

Define the antigen used for anti-CCP testing, the disease this antibody is associated with, and its usefulness in relation to RF testing

A

Anti-CCP= anti cyclic citrullinated peptide
Anti-CCP test is paired with RF for diagnosis of rheumatoid arthritis (and is 98% sensitive). Citrulline is a non-standard amino acid that is created by deamination of arginine by peptidylarginine deiminase. This process is post-translational modification of joint proteins filaggrin, vimentin, and fibrin

64
Q

Recognize the laboratory tests that may be used to follow the course of SLE/lupus and whether the results will be abnormally high or abnormally low in uncontrolled disease flares

A

Disease activity correlates with a rise in: C-reactive protein, erythrocyte sedimentation rate, and urine protein. Disease activity also correlates with a decrease in: CBC (WBC, RBC, and platelet counts resulting from destruction), complement (C3 and C4), and serum albumin

65
Q

Recognize the laboratory tests that may be used to follow the course of RA and whether the results will be abnormally high or abnormally low in uncontrolled disease flares

A

Increased erythrocyte sedimentation rate, increased C-reactive protein, and decreased complement components (C3 and C4)

66
Q

Chronic immune thyroiditis
Auto-antibodies observed:

A

anti-thyroglobulin and anti-thyroid peroxidase (aka thyroid microsomal antigen)

67
Q

Chronic immune thyroiditis
Serologic testing done:

A

enzyme immunoassay (most common), particle agglutination, or indirect immunofluorescence

68
Q

Chronic immune thyroiditis
Immune mechanism responsible for tissue destruction

A

thyroid gland is infiltrated w/ lymphocytes, macrophages, and plasma cells, and germinal centers actually form in gland. Although auto- antibody is found, Tc destruction of thyroid epithelial cells is thought to ultimately cause the disease

69
Q

Chronic immune thyroiditis
Hypersensitivity type

A

Type 4

70
Q

Grave’s disease
Auto antibodies observed

A

antibody to thyroid stimulating hormone receptor (anti-TSH-R)

71
Q

Grave’s disease
Serological testing done to diagnose

A

Most commonly done without serological testing- Assays for T3, T4, and TSH performed

72
Q

Grave’s disease
Immune mechanism responsible for tissue destruction

A

antibody acts as a receptor ligand (mimics TSH) and stimulates excessive T3 and T4 secretion

73
Q

Addison’s disease:
Auto antibodies observed

A

anti-21-hydroxylase antibody

74
Q

Addison’s disease
Serological testing done to diagnose

A

Not serological testing- chemistry tests for elevated serum ACTH and plasma renin

75
Q

Addison’s disease
Immune mechanism responsible for tissue destruction

A

autoantibodies destroy the adrenal cortex (type II hypersensitivity)

76
Q

Type 1 diabetes mellitus
Auto antibodies observed

A

anti-GAD (glutamic acid decarboxylase) antibody, anti-IA-2 (transmembrane tyrosine phosphate protein) antibody, and IAA (insulin antibody)

77
Q

Type 1 diabetes mellitus
Immune mechanism responsible for tissue destruction

A

Autoimmune Tc destruction of pancreatic beta cells that normally secrete insulin (Type IV hypersensitivity)

78
Q

Type 1 diabetes mellitus
Serological testing done to diagnose

A

Not serological testing- Fasting hyperglycemia and elevated hemoglobin A1C

79
Q

RAST

A

radioallergosorbent test
evaluates total serum levels of IgE, regardless of antigen specificity

80
Q

RIST

A

radioimmunosorbent test
evaluates total serum levels of IgE, regardless of antigen specificity

BLD 434 (3 decks)

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