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Pathology Exam 3 > Immunity Lecture > Flashcards

Immunity Lecture Flashcards

1
Q

What is the most numerous of all white blood cells

A

Neutrophils (40-87%)

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2
Q

What are neutrophils role?

A

Acute inflammatory cells

Involved in phagocytosis

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3
Q

Never Let Monkeys Eat Bananas

A 
N - Neutrophils (40-87%)
L - Lymphocytes (20-50%)
M - Monocytes (2-11%)
E - Eosinophils (0-6%)
B - Basophils (0-2%)
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4
Q

What are neutrophil markers?

A

CD45, CD11/18, CD13, CD15, CD33

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5
Q

What is the role of CD4+ T-Helper Cells

A

Activated by bind to class II MHC and secrete cytokines

Influence all other cells of immune system

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6
Q

What is the role of CD8+ Cytotoxic T-Cells

A

Activated by bind to Class I MHC

Directly kills virus-infected tumor cells

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7
Q

What are T-Cell Markers in Molecular testing

A

TCR, MHC-Peptide Antigen Complex

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8
Q

What are T-Cell markers in Flow Cytometry and Immunostains?

A

CD45, CD3, CD4, 8, 2, 5, 7

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9
Q

What is the role of B Cells?

A

Differentiate into plasma cells which secrete immunoglobulins

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10
Q

What are B Cells markers in Molecular testing?

A

BCR< immunoglobulin-subclasses IgM, IgA, IgD, IgG, IgE, Kappa and Lambda Light Chains

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11
Q

What are B cell markers in flow Cytometry

A

CD45, 19, 20 ,22, 79a

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12
Q

What are NK Cells Role

A

Lyse Tumor cells and virally infected cells

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13
Q

What are Nk Cell Markers in Molecular testing

A

KIR - inhibits NK cytolysis by recognition of self MHC

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14
Q

What are Macrophage roles

A

Antigen Presentation: MHC II

Phagocytosis - antigens w/complement

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15
Q

Macrophage markers for molecular testing

A

None

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16
Q

Macrophage markers for Flow Cytometry

A

CD45, 14, 64, 68, 163

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17
Q

Eosinophil Roles

A

Contains proinflammatory proteins involved in allergies

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18
Q

Flow Cytometry Eosinophil markers

A

CD45, 38, 123

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19
Q

Basophil roles

A

Contain proinflammatory granules involved in allergies

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20
Q

Basophil Flow Cytometry Markers

A

CD45, 38, 123

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21
Q

What HLA molecules are associated with MHC I?

A

HLA-A, B, C

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22
Q

How does MHC I molecules work?

A

They are present on all nucleated cells

Bind to peptides derived from proteins synthesized within cells and present them to CD8+ T-Cells

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23
Q

How does MHC Class I prevent lysis of a normal cell

A

By engaging KIRs on NKC

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24
Q

What HLA molecules are associated with MHC II

A

HLA-DR, DP, DQ

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25
Q

Where are MHC II cells present and how do they work?

A

Only present on antigen presenting cells

Binds to peptides derived from proteins outside the cells and present to CD4+

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26
Q

What HLA allele is involved in Ankylosing spondylitis?

A

B27

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27
Q

What is the classical complement pathways?

A

Initiation by interaction between IgM/IgG, and C1q

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28
Q

What is the alternate complement pathway?

A

Activation by bacterial cell walls, endotoxin, or venom binding to C3b absent of Ig

C3 –> C5 –> Membrane Attack
C3–> Opsonization, phagocytosis, B-lymphocyte activation

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29
Q

What cytokines mediate innate immunity?

A

IL-1, TNF, IL-6, interferons

Macrophages are major source

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30
Q

What cytokines activate inflammatory cells

A

IFN-y, TNF

Derived from T-Cells

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31
Q

What cytokines act to recruit inflammatory cells to sites of injury?

A

IL-8

Produced by macrophages and injured cells

32
Q

What cytokines regulate lymphocyte response?

A

IL-2, IL-4, IL-5, IL-12

33
Q

What cytokines stimulate hematopoiesis?

A

Colony Stimulating Factors (CSF)

34
Q

What 2 global tests are used for the immune system?

A

WBC Count with differentials

Peripheral Smear Examination

35
Q

How is B-Cell function tested?

A

Ig levels and isotope titer

Flow Cytometry

36
Q

How is T-Cell function tested?

A

Delayed type hypersensitivity testing

Flow cytometry

37
Q

What are the key uses for flow cytometry?

A

Blood cell population analysis, Cancer diagnostics, cell sorting

38
Q

What are the 2 steps in interpreting flow cytometry dot plots?

A
  1. Establish clonality of B-Cells

2. Subclassify the disease

39
Q

How do you test neutrophil function?

A

Neutrophil count and smear

MPO Staining

Nitroblue tetrazolium (NBT)

40
Q

Define hypersensitivity reactions

A

Excessive Immune responses that cause tissue injury and diseases

Dependent on adaptive immune system

41
Q

What is required in hypersensitivity reactions to prime the adaptive immune response?

A

Prior Antigen exposure

42
Q

What are causes of Hypersensitivity reactions

A

Failure of self-tolerance to self

Uncontrolled responses against foreign antigens

43
Q

What is Type 1 hypersensitivity?

A

Allergies - IgE

44
Q

What is Type 2 Hypersensitivity

A

Antibody-mediated - IgG, IgM

phagocytosis and lysis of cells

Autoimmune disease

45
Q

What is Type 3 Hypersensitivity

A

Immune Complex Mediated - Ag-Ab

inflammation, necrotizing vasculitis

Systemic lupus erthematosus, glomerulonephritis, serum sickness

46
Q

What is Type 4 Hypersensitivity

A

Cell Mediated - T-Lymphocytes

Perivascular cellular infiltrates, edema

Contact dermatitis, multiple sclerosis

47
Q

What does ACID stand for?

A

Anaphylactic
Cytotoxic
Immune Complex
Delayed-Type Hypersensitivity

48
Q

What are primary immunodeficiency disease

A

BCS, TC, X-Linked WAS

49
Q

What are secondary immunodeficiency disease

A

Infection, malnutrition, aging, chemoradiation, immunosuppression, autoimmunity

50
Q

What are manifestations Defect in Ig, Completement or phagocytic cells

A

Recurrent pyogenic bacterial infections

51
Q

What are manifestations of Cell-mediated Immunity

A

Viral, Fungal, and intracellular bacterial infections

52
Q

What are 4 B Cell Defects?

A

B- Bruton (x-linked) agammaglobulinemia

C- Common Variable Immunodeficiency (CVID)

S - Selective IgA Deficiency

H - Hyper IgM syndrome

53
Q

What are T cell Defects (2)

A

Thymic Hypoplasia - Digeorge Syndrome

Chronic mucocutaneous candidiasis

54
Q

What are Combined B & T Cell Defects?

A

X-linked WAS –>

X-linked lymphoproliferative disorder
WAS
Ataxia Telangiectasia
Severe Combined Immunodeficiency

55
Q

Bruton (X-linked) Agammaglobulinemia Characteristics

A

Prevalence: 1/100K

Gene Defect (Xq21.3022): Mutant Bruton’s tyrosine kinase involved in pre-B cell signal transduction

B-Cell maturation stops after the initial heavy chain rearrangement: light chains not produced

56
Q

What age does Bruton (X-linked) Agammaglobulinemia manifest

A

6 months of age as maternal immunoglobulin depletes

57
Q

How do infections occur in Bruton (X-linked) Agammaglobulinemia

A

By encapsulated bacteria, cleared by antibody opsonization

Susceptible to certain viral infections and guard

Prone to autoimmune disease

58
Q

What are the characteristics of peripheral blood in Bruton (X-linked) Agammaglobulinemia

A

Absent or decreased mature B-Cells and depressed serum levels of all Ig classes

59
Q

What are the characteristics of lymph nodes in Bruton (X-linked) Agammaglobulinemia

A

Absent/Rudimentary germinal centers and absence of plasma cells

60
Q

What are the characters if the GI tract in Bruton (X-linked) Agammaglobulinemia

A

Absence of plasma cells and possible giardia infection

61
Q

What is the treatment for Bruton (X-linked) Agammaglobulinemia

A

IVIg, antibiotics, gene therapy

62
Q

What is the prevalence, gene defects and general characteristics of CVID?

A

Prevalence: 1/50K
Gene Defect: Heterogenous (ICOS, TACI) - leads to insufficient activation to Ig plasma cells
Normal B cells - absent plasma
Low IgG, IgA, IgM

63
Q

What is the onset of CVID

A

15-35 years in both M and F

64
Q

What are symptoms/signs of CVID

A

Impaired antibody response to infection: Pneumonia, Sinusitis, GI infection

Weakened T Cell Immunity

lymphoid Malignancy

65
Q

Treatment for CVID

A

IVIg

66
Q

What is the prevalence and gene defects of Selective IgA deficiency

A

Most Common primary immunodeficiency: 1/700

Defect: Intrinsic B Cell Defects or altered T-Cell Cytokine Production

Low IgA

67
Q

What is the presentation of selective IgA deficiency?

A

Recurrent Sinopulmonary infections, diarrhea, autoimmune diseases, anaphylaxis during blood transfusion

68
Q

Hyper-IgM Syndrome Characteristics

A

Failure to isotype switch

70% due to defective CD154 on x chromosome

Low levels of opsonizing IgG

Increased susceptibility to pathogens that require intact DTH responses

69
Q

What are the gene defects in DiGeorge Syndrome

A

90% due to 22q11 depletion

Malformation in 3rd and 4th pharyngeal pouches - form thymus

Absent T-Cells

70
Q

What is the presentation of DiGeorge Syndrome?

A 
Catch-22: 
C- Cardiac Defect
A - Abnormal Facies
T - Thymic Hypoplasia
C - Cleft Palate
H - HypoCa2+
71
Q

Characteristics of Chronic Mucocutaneous Candidiasis

A

Selective T-Cell Immunodeficiency against Cadida Species

Presents: Chronic, Recalcitrant mucocutaneous candidal infections

Does not represent specific disease, but a phenotypic spectrum

72
Q

X-Linked Lymphoproliferative Disease Gene Defects

A

Xq25 mutation –> Deletion in the SH2D1A gene which codes for SH2 domain on a SAP protein

73
Q

What does a deletion in SH2D1A gene in X-Linked Lymphoproliferative Disease cause?

A

leads to lack of modulation of IFN-y, causing uncontrolled cell proliferation

74
Q

What is the presentation of X-Linked Lymphoproliferative Disease

A

Overwhelming T-cell mediated response to EBV

Death from bone marrow failure
Irreversible hepatitis
Malignant Lymphoma

75
Q

WAS gene defects

A

Wiskott-Adrich Syndrome

X-linked recessive mutation of WASP - responsible for cytoskeletal malleability

Responsible for intracellular signaling

76
Q

Presentation of WAS

A

WIPE:

W - WAS

I - Immunodeficiency: progressive age-related depletion of T-Cells, decreased IgM

P - Purpura

E - Eczema

Lymphoid Malignancy

Pathology Exam 3 (4 decks)

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