Immuno II Flashcards

1
Q

Exaggerated, inappropriate immunologic rxns that are harmful to the host

A

Hypersensitivity reactions

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2
Q

Sensitization

A

first exposure to antigen with an immune response (antibody)

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3
Q

Subsequent exposures to an antigen:

A

cause a hypersensitivity reaction

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4
Q

Four types of hypersensitivity reactions:

A

Type I - allergy/anaphylaxis
Type II - antibody-dependent/cytotoxic
Type III - immuno-complex
Type IV - T-cell mediated/delayed

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5
Q

Which hypersensitivity reactions are mediated by antibodies and what antibodies are they?

A

I (IgE)

II and III (IgG)

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6
Q

Biggest chemical mediator in a type I rxn?

A

histamine

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7
Q

What is a type I reaction?

A

Immediate anaphylactic (IgE)

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8
Q

What is a type II rxn?

A

antibody-mediated cytotoxic reaction to antigens (IgG)

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9
Q

T/F: type II rxns are complement-dependent.

A

True - MACs destroy the foreign cell membrane and cause lysis

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10
Q

Examples of type I rxns:

A
Systemic anaphylaxis
Urticaria
Asthma
Hay Fever
Allergic rhinitis/conjunctivitis
Food or drug allergies
Atopic dermatitis (eczema)
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11
Q

Examples of type II rxns:

A
Transfusion rxns
Rh incompatibility
Hemolytic dx of the newborn
Rheumatic fever
Autoimmune hemolytic anemia
Goodpasture syndrome
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12
Q

What is the onset timing of a type I rxn?

A

minutes

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13
Q

What is the onset timing of a type II rxn?

A

hours to days

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14
Q

What is a type III rxn?

A

1) Ag-Ab immune complexes form and deposit in tissues
2) Inflammatory response is induced in the tissues
3) Activates complement, causing tissue damage and lysosomal enzyme release

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15
Q

Onset time of a type III rxn?

A

2 to 3 weeks

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16
Q

Examples of type III rxns:

A
SLE (lupus)
Rheumatoid arthritis
Poststreptococcal glomerulonephritis
IgA nephropathy
Serum sickness
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17
Q

A patient with SLE forms what kind of auto-antibodies?

A

antinuclear antibodies (ANAs)

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18
Q

Complement activation in type III rxns (i.e. SLE) produces what complement protein that attracts neutrophils?

A

C5a

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19
Q

Body fluids of pts with RA contain what factor and where does it bind?

A

Rheumatoid factor (IgM and IgG) that binds to the Fc fragment of normal host IgG

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20
Q

Patients with RA have ___ titers of RF and ___ titers of complement in serum when their disease is active.

A

High RF

Low complement

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21
Q

What is a type IV rxn?

A

Delayed cell-mediated rxn where:

1) Macrophage ingests and presents the foreign antigen on a MHC-II complex
2) T cells are activated and produce IFN-gamma –> activates macrophages and cause inflammation

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22
Q

What kinds of cells mediate type IV reactions?

A

CD4 (helper) and CD8 (cytotoxic)

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23
Q

Examples of type IV rxns:

A
Contact dermatitis
Poison oak/ivy
TB skin test rxn
Drug rash
Steven-Johnson syndrome
Toxic epidermal necrolysis
Erythema multiforme
24
Q

Pathologic features of type IV rxns using CD4 and macros:

A

ex: TB, cocci
Disease produces granuloma
Skin test produce an induration

25
Q

Pathologic features of type IV rxns using CD8 cells:

A

ex: contact dermatitis (pruritic vesicular rash)

EM, SJS, TEN: target lesion

26
Q

Time of onset for type IV rxns:

A

2-3 days

27
Q

Hereditary angioedema (HAE)

A

congenital immunodeficiency of C1 protease inhibitor (complement cascade can’t be turned off)

28
Q

What complement proteins does a person with HAE have in excess?

A

C3a, C4a, C5a

29
Q

What are the main symptoms of HAE?

A

Episodic local significant capillary permeability and subcutaneous and submucosal edema (usually GI and UR tracts)

30
Q

How do you differentiate between a type I HS reaction and HAE?

A

HAE lacks itchiness and urticaria

31
Q

Biggest red flag symptom for HAE:

A

recurrent abdominal colic

32
Q

Treatment for HAE

A

Replace the missing C1 esterase inhibitor

33
Q

What the surface proteins that are markers of “self” on cells?

A

MHC I and MHC II

34
Q

What are the non-self substances that trigger the immune system?

A

Epitope (trigger area on the antigen)

35
Q

Autoimmunity mechanisms for avoiding damage to self-cells:

A

1) Sequestration
2) Tolerance
3) Regulation

36
Q

What autoimmunity mechanism has the body keeping bad cells from being released into the bloodstream before destroying them?

A

sequestration

37
Q

What autoimmunity mechanism involves the body not reacting to self-reactive B and T cells?

A

tolerance

38
Q

What autoimmunity mechanism involves regulatory cells preventing self-reactive cells from being activated?

A

regulation

39
Q

Exogenous autoimmune triggers:

A

bacterial or viral infections
T1D
Medications
Smoking/toxins

40
Q

Endogenous autoimmune triggers:

A

autoantibodies

41
Q

Example of molecular mimicry autoimmune triggers:

A

Strep antigen is similar to the body’s own and the body attacks cardiac tissue because it looks similar

42
Q

Criteria for autoimmune disease diagnosis

A

1) autoantibodies
2) self-reactive T cells
3) Imbalance between T and B cell pathogenic factors and regulatory factors that control immune response

43
Q

T/F: people only have autoantibodies if they have an autoimmune dx?

A

False

44
Q

What dx is characterized by autoantibody stimulation (thyroid stimulating immunoglobulin [TSI]) of the TSH receptor?

A

Graves disease

45
Q

What disease is an autoimmune reaction to infection with GAS?

A

Rheumatic fever

46
Q

What disease involves autoantibody blocking and inactivation (anti-AcHR) of the alpha-chain of the nicotinic AcH receptors in neuromuscular jxns?

A

Myasthenia gravis

47
Q

What disease has immune complex formation that targets dsDNA?

A

SLE

48
Q

What are the autoantibodies associated with SLE?

A

anti-dsDNA

anti-Smith

49
Q

What disease is characterized by insulin and islet cell autoantibodies, as well as T cell cytokine production and cellular toxicity?

A

Type I diabetes

50
Q

What disease is characterized by RF and anti-CCP?

A

Rheumatoid arthritis

51
Q

What disease is characterized by a pro-inflammatory autoimmune response causing destruction of CNS myelin?

A

Multiple sclerosis

52
Q

Immunizations exploit the _____ immune response.

A

adaptive

53
Q

A vaccine that contains the weakened form of the virus.

A

live attenuated

54
Q

A vaccine that contains killed pathogens.

A

inactivated

55
Q

A vaccine that uses a component of the pathogen as a vaccine antigen to mimic exposure.

A

Subunit

56
Q

A vaccine where the polysaccharide from the bacterial capsule is bound to a carrier protein.

A

conjugate subunit vaccine