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Pathology > Immunity 1 > Flashcards

Immunity 1 Flashcards

1
Q

-A substance that can induce an immune response when introduced into an animal.

A

Antigen (Ag)

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2
Q

-A protein that is produced in response an antigen. It binds the antigen that stimulated its production. All are immunoglobulins.

A

Antibody (Ab)

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3
Q

-A glycoprotein composed of heavy and light chains that can function as an antibody.

A

Immunoglobulin (Ig)

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4
Q

•First immunoglobulin to appear in an immune response

A

IgM

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5
Q
  • Principal immunoglobulin of the secondary immune response

* Only immunoglobulin capable of crossing the placental barrier

A

IgG

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6
Q

•Principal immunoglobulin in mucosal secretions (ie. tears, saliva) and breast milk

A

IgA

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7
Q

•-plays an important role in immediate hypersensitivity reactions and parasitic infections•Low concentrations in circulation•Bound to tissue mast cells

A

IgE

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8
Q
  • -thought to activate the B-lymphocyte
  • Expressed on B cells
  • Not secreted
A

IgD

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9
Q

Only ____ undergo gene rearrangement

A

Lymphocyte

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10
Q

When there is class switching of antibodies, what portion of the Ig is changed?

A

Constant region

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11
Q
  • X-linked genetic disease: more common in males
  • A primary immunodeficiency disease
  • Can’t make antibody and are deficient in opsonization(primary function of antibody)
  • Recurrent bacterial infections
  • Treatment: intravenous infusions of immunoglobulin every 3-4 weeks for life (passive immunity)
A

X-linked Agammaglobulinemia

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12
Q 
Group of primary immune deficiency disorders 
Defective class switching
Elevated IgM levels; low levels of IgG, IgE, IgA
A

Hyper IgM Syndromes

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13
Q 
Antibodies are produced by which cell?
A Macrophage
B Mast Cell
C T lymphocyte
D B lymphocyte
E Neutrophil
A

B Lymphocyte

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14
Q 
Which is the first antibody to appear in an immune response?
AIgG
BIgM
CIgA
DIgE
A

IgM

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15
Q

Which is the antibody found in external secretions?

A

IgA

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16
Q

All lymphocytes arise in the ______

A

bone marrow

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17
Q

•_____ lymphoid organs–Bone marrow–Thymus

A

Primary

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18
Q

_____ lymphoid organs–Lymph nodes–Tonsils–Spleen–Mucosal-associated lymphoid tissue (MALT)

A

Secondary

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19
Q

B lymphocytes become _____ and secrete antibodies when challenged by antigen

A

plasma cells

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20
Q

Where do T cells become educated and learn self from non-self; self-reacting t cells are deleted

A

Thymus

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21
Q

_____ cells kill virus infected and damaged cells

A

CD8 T cells

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22
Q

____ cells help cytotoxic T cells and B cells in their immune functions

A

CD4 T cells

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23
Q

_____ cells produce antibodies

A

B Cells

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24
Q

Both _____ and _______ can be found near an infection

-The interaction between these cells is important in eliminating infection.

A

macrophages and lymphocytes

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25
Q

–A component of the innate immune system
–A type of cytotoxic lymphocyte
–Do not have markers for B or T cells

A

Natural Killer cells

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26
Q

–CD4+ (T Helper Cell) –quarterback
–CD8+( Cytotoxic T Cell) –effector
–Cell-mediated defense against intracellular pathogens
•Viruses, fungi and bacterial disease (tuberculosis)

A

•T lymphocytes

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27
Q

B lymphocytes leave the ________ and populate lymph nodes

A

bone marrow

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28
Q

T lymphocytes leave the ______ and populate lymph nodes

A

thymus

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29
Q

Are intracellular pathogens dealt with using cellular or humoral immunity?

A

Cellular immunity

30
Q

Are extracellular pathogens dealt with using cellular or humoral immunity?

A

Humoral immunity

31
Q

_____ immunity
–Early
–Physical and chemical barriers: epithelium and antimicrobial substances
–All phagocytic cells: neutrophils, macrophages, NK cells
–Complement proteins
–Cytokines: TNF, IL-1, interferon

A

Innate immunity

32
Q 
\_\_\_\_\_ immunity
–Later
–Antibodies
–Lymphocytes
–Cytokines (IL-2, IL-12)
A

Adaptive immunity

33
Q

_______
–First line of defense against extracellular pathogens
–Antibody dependant

A

Humoral immunity

34
Q

______
–First line of defense against intracellular pathogens
–Antibody independent

A

Cellular immunity

35
Q

What is the critical step in the complement system?

A

Cleavage of C3

36
Q
  • Originally discovered on leukocytes and called Human Leukocyte Antigens (HLA)
  • All cells of the body have these molecules
  • These molecules are recognition molecules that allow the immune system to distinguish self from non-self
A

MHC molecules

37
Q
  • The recognition arm of cellular immunity –the “bloodhounds”
  • Role is to look at all the MHC-2 molecules in the body (on APCs) to determine if they’re “clean” or “dirty”
A

CD4+ T Helper Lymphocyte

38
Q

CD4+ T helper cells secretes what cytokine that signals naïve lymphocytes to differentiate into CD8+ Cytotoxic lymphocytes?

A

IL-2

39
Q
  • The effector arm of cellular immunity
  • Role is to scout the body for dirty MHC-1 molecules on somatic cells and kill them
  • AKA: Cytolytic T-cells, Killer T cells, Cytotoxic lymphocytes, CTL
A

CD8 Killer T cells

40
Q

CD8 Killer T-Lymphocytes kills hepatocyte via ______, exposing virus to humoral immune system

A

perforins

41
Q

______ are recognition molecules that allow the immune system to distinguish self from non-self.

A

MHC molecules

42
Q 
Defects in \_\_\_\_\_\_\_\_ immunity
•Bruton X-linked agammaglobulinemia
•IgA deficiency
•Hyper IgM syndrome
•Common variable immune deficiency (CVID)
A

humoral immunity

43
Q 
Defects in \_\_\_\_ immunity
•DiGeorge syndrome
•Bare lymphocyte syndrome
•Severe combined immunodeficiency (SCID)
•Acquired immunodeficiency syndrome (AIDS)
A

cellular immunity

44
Q
  • Failure of B cell maturation to plasma cells
  • No plasma cells
  • No antibodies
  • Recurrent bacterial infections
  • X-linked inheritance: affects only males–Lyonization
A

Bruton X-Linked Agammaglobulinemia - XLA

45
Q
  • Common immune deficiency (1:700)
  • Defect in differentiation of IgA secreting plasma cells
  • Low levels of circulating and secretory IgA
  • Low morbidity
  • Recurring infections of respiratory and gastrointestinal tracts
A

IgA deficiency

46
Q
  • Defect in class switching from IgM to IgG and IgA antibody production
  • High levels of IgM
  • No IgG or IgA
  • Recurring bacterial infections
  • X-linked inheritance
A

Hyper IgM syndrome

47
Q
  • Common primary immunodeficiency
  • A heterogenous group of 20–30 immunodeficiencies
  • Symptoms: all exhibit hypogammaglobulinemia due to different causes
  • Recurring bacterial infections
  • Treatment: intravenous infusion of immunoglobulins
A

Common Variable Immune Deficiency (CVID)

48
Q
  • Congenital absence of structures derived from the 3rd and 4th branchial pouches
  • Thymic and parathyroid aplasia
  • No cellular immunity -no T Cells (neither CD4 nor CD8)
  • Hypoparathyroidism
  • Defects in humoral immunity
A

DiGeorge Syndrome - Thymic Aplasia

49
Q

______

APC don’t express MHC Class II molecules

A

Bare Lymphocyte Syndrome

50
Q
  • A heterogenous group of diseases caused by defective development of both T and B cells
  • No T cells
  • No B cells
  • No humoral and cellular immunity -lethal
A

Severe Combined Immune Deficiency (SCID)

51
Q

•HIV ______ is a perfect fit for the CD4 receptor on T cells

A

gp 120

52
Q

•HIV _______ promotes fusion

A

gp 41

53
Q
  • As CD4 cells are killed, cellular immunity fails, followed by humoral immunity
  • Infections by intracellular pathogens as cellular immunity fails
  • Infections by extracellular pathogens as humoral immunity fails
  • Neoplasms
A

HIV/AIDS

54
Q
  • Aphthous ulcers
  • Candidiasis
  • Human papilloma virus lesions -papillomas
  • Herpes simplex virus lesions
  • Hairy leukoplakia (Epstein Barr virus)
  • Accelerated periodontitis
  • Necrotizing ulcerative gingivitis, periodontitis, stomatitis
  • Kaposi sarcoma (HHV-8)
  • Other Neoplasms (squamous cell carcinoma, lymphoma)
A

Oral lesions in ______

55
Q

Defects in _______:
•Abnormalities in leukocyte adhesion molecules(LFA-1 and MAC-1)
•Defect in actin molecules(lazy leukocytes)
•Defects in microtubule assembly(Chediak-Higashi)
•Defect in NADPH oxidase(Chronic granulomatous disease of childhood)
•Myeloperoxidase deficiency
* Diabetes mellitus

A

Leukocytes defects

56
Q
  • Advanced periodontitis
  • Early loss of primary teeth
  • Palmar-plantar hyperkeratosis
  • Mutations of the Cathepsin C gene
  • Autosomal recessive inheritance
A

Papillon Lefevre Syndrome

57
Q

–Immediate Hypersensitivity

A

–Type I hypersensitivity

58
Q

–Type ____immune injury –Antibody-Mediated Hypersensitivity

A

Type 2 hypersensitivity

59
Q

–Type ___ immune injury –Immune Complex-Mediated Hypersensitivity

A

Type 3 hypersensitivity

60
Q

–Type___ immune injury –Cell-Mediated Hypersensitivity

A

Type 4 hypersensitivity

61
Q

•Type ____ hypersensitivity –FAST: immediate hypersensitivity–hives in 10 minutes secondary to antigen exposure–Mediated by IgE antibodies and Mast cells–May be genetic•Allergic rhinitis, allergies run in families •Familial but not a single gene characteristic. No tissue damage

A

Type 1

62
Q

What 3 things make up the type 1 hypersensitivity?

A

Antigen
IgE antibodies
Mast cells

63
Q

What are the primary mediators of mast cells?

A

Histamine
Proteases
Chemotactic factors

64
Q

What are the secondary mediators of mast cells?

A

Prostaglandins

Leukotrienes

65
Q

During the _____ encounter to an allergen:
•IgE antibody is induced by allergen
•Mast cells have high affinity receptors for the Fc end of IgE
•IgE binds via its Fc receptor to mast cells

A

FIRST ENCOUNTER

66
Q

During the _____ encounter to an allergen:
•Antigen cross-links the fixed IgE
•Mast cell degranulation
•Pharmacologic effects of histamine, leukotrienes

A

SECOND ENCOUNTER

67
Q

HOw does histamine affect bp, vasodilation, and permeability?

A

Decreases bp
Increases vasodilation
Increases permeability which lead to edema

68
Q

During the _____ exposure to penicillin:
–PCN dose bridges Fab ends of two adjacent molecules •sends signal into mast cell cytoplasm to degranulate–Bronchioles constrict•Histamine, prostaglandins and leukotrienes cause smooth muscle contraction–If recognize in time –shot of epi –relax smooth muscle in bronchioles and vasoconstriction

A

Second exposure

69
Q

During the _____ exposure to penicillin: –no reaction–May trigger an immune response by stimulating the Th2 pathway–Cytokines IL-4 (IgE molecules), IL-5 (recruits eosinophils)–Lots of IgE antibodies and eosinophils–IgE AB circulate have a high affinity for Mast cells in the skin and mucosa (Fc end of IgG)

A

FIRST EXPOSURE

70
Q

Is anaphylactic shock a systemic or localized immediate hypersensitivity?

A

Systemic

71
Q

Is angioedema a systemic or localized immediate hypersensitivity?

A

Localized

Pathology (26 decks)

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