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Foundations > Immunology II > Flashcards

Immunology II Flashcards

1
Q

Define: hypersensitivity rxn

A
  • Exaggerated, inappropriate immunologic rxn that is harmful to the host
  • Subsequent exposure
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2
Q

Define: sensitivity

A

1st exposure to antigen w/ immune response (antibody)

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3
Q

Type I action

A
  • 1st exposure to antigen –> IgE formation
  • IgE binds to mast cells & basophils
  • Subsequent exposure – > antigen binds to IgE
  • Degranulation of mast cells
  • Release of mediators (histamine)
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4
Q

Type I result

A
  • Increased vascular permeability
  • Edema
  • SM contraction
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5
Q

Type I timing

A

Minutes

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6
Q

Type I manifestations

A
  • Edema
  • Erythema
  • Itching
  • Urticaria
  • Eczema
  • Rhinitis
  • Conjunctivitis
  • Asthma
  • Systemic anaphylaxis
  • Food/drug allergies
  • Hay fever
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7
Q

Allergic response

A
  • During sensitization, APC presents allergen presents to Th2 cell, which helps B cell become a plasma cell.
  • Plasma cells produce IgE, which binds to mast cells.
  • When allergen returns, mast cells release histamine
  • Th2 cells release chemicals that attract inflammatory cells
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8
Q

Allergic response results in what?

A

Allergy sx

  • Sneezing
  • Mucus, runny nose
  • Swelling
  • Itching
  • Coughing, wheezing
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9
Q

What is the effect of histamine?

A
  • Vasodilation
  • Increased capillary permeability
  • SM contraction
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10
Q

What is the emergency concern of anaphylaxis?

A
  • Airway
  • Hypotension
  • Shock
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11
Q

What is the emergency tx for anaphylaxis?

A
  • Epinephrine
  • Antihistamine
  • Steroid
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12
Q

Anaphylaxis prevention

A
  • Antihistamine
  • H2 blocker
  • Avoid allergen
  • Immunosuppression therapy w/ allergy shots
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13
Q

What is the rationale of desensitization?

A

Tiny amount of antigen over long period of time to blunt rxn

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14
Q

What infections may exacerbate asthma?

A
  • Flu

- PNA

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15
Q

Most common food allergies (90%)

A
  • Milk
  • Egg
  • Fish (bass, flounder, cod)
  • Shellfish (crab, lobster, shrimp)
  • Tree nuts (almonds, pecans, walnuts)
  • Wheat
  • Peanuts
  • Soybeans

*Also consider fruits, preservatives, dyes.

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16
Q

Type I hypersensitivity common presentation

A
  • Facial edema
  • Systemic histamine release in anaphylaxis:
    ˚ Hypotension
    ˚ Nausea
    ˚ Hives
    ˚ Swollen hands/feet
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17
Q

Type II (cytotoxic) hypersensitivity rxn

A
  • Antibody mediated cytotoxic rxn

- Antigens on cells or in ECM (endogenous or exogenously absorbed)

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18
Q

Type II action

A

Antigens on cell surface combine w/ IgG antibodies –> complement-mediated lysis of cells

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19
Q

Type II time of onset

A

Hours to days

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20
Q

Type II manifestations

A
  • Hemolytic anemia
  • Neutropenia
  • Thrombocytopenia
  • ABO transfusion rxns
  • Rh incompatibility (erythroblastosis fetalis, hemolytic disease of the newborn)
  • Rheumatic fever
  • Goodpasture’s syndrome
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21
Q

Hemolytic anemia (Type II)

A
  • Antibody attaches to antigen on RBC
  • Complement mediated lysis via MAC
  • Complement attracts phagocytes
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22
Q

Type III (Immune complex) hypersensitivity

A
  • Antigen–antibody immune complexes are deposited in tissues –> inflammatory response
  • Complement is activated & PMN cells are attracted to the site –> release of lysosomal enzymes –> tissue damage
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23
Q

Type III time of onset

A

2-3 wks

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24
Q

Type III manifestations

A
  • SLE
  • RA
  • Poststreptococcal glomerulonephritis
  • IgA nephropathy
  • Serum sickness
  • Hypersensitivity pneumonitis (farmer’s lung)
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25
Q

SLE (Type III)

A
  • Antibodies formed to DNA & nucleus
  • Antibodies form immune complexes that activate complement –> production of C5a –> attracts neutrophils –> release enzymes –> damage tissue
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26
Q

RA (Type III)

A
  • Serum & synovial fluid contain “rheumatoid factor” (IgM & IgG antibodies that bind to the Fc fragment IgG)
  • Deposits of immune complexes (containing the normal IgG & Rh) on synovial membranes & in blood vessels
  • Activate complement & attract PMN cells –> inflammation.
  • Pts have high titers of Rh & low titers of complement in serum (esp. during periods when disease is most active)
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27
Q

Type IV: Delayed (Cell-mediated) hypersensitivity

A
  • T lymphocytes, activated/sensitized by an antigen, release lymphokines upon 2nd contact w/ same antigen
  • Lymphokines induce inflammation & activate macrophages –> release of inflammatory mediators.
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28
Q

Type IV time of onset

A

2-3 days

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29
Q

Type IV manifestations

A
  • Contact dermatitis
  • Poison oak/ivy
  • TB skin test rxn
  • Drug rash
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
  • Erythema multiforme
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30
Q

Type IV continued

A
  • Macrophage ingests antigen, processes it, & presents an epitope on its surface in association w/ class II MHC
  • Helper T (Th-1) cell is activated & produces gamma interferon –> activates macrophages
  • These 2 cells mediate delayed hypersensitivity
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31
Q

Hereditary angioedema

A
  • Congenital immunodeficiency (deficiency of C1 protease inhibitor, autosomal dominant)
  • Excess C3a, C4a, C5a
32
Q

Hereditary angioedema result

A

Capillary permeability & edema

33
Q

Hereditary angioedema dx

A
  • Family hx
  • Lack of pruritis & urticarial lesions
  • Recurrent abdominal colic &/or laryngeal edema
  • Labs: decreased C1 inhibitor levels (or decreased fxn, or mutation in C1 inhibitor gene altering synthesis/fxn)
34
Q

Fxn of immune system

A

Provide a protective response against infective organisms & foreign cells, while avoiding damage to self

35
Q

Markers of self

A
  • Distinctive surface proteins that identify “self”
  • Able to coexist w/ immune system
  • Unique markers on human cells are the MHC proteins (type I = all cells, type II = specialized cells)
36
Q

Markers of non-self

A
  • Non-self substance (antigen) can trigger the immune system
  • Epitope: area on the antigen that triggers a response
  • Ex: transplanted tissues are recognized as foreign & attract antibodies
37
Q

Self-antigens

A

Mechanisms for avoiding damage to self

  • Sequestration
  • Tolerance of relevant T or B cells
  • Regulatory cells
38
Q

What is an autoimmune disease?

A

A trigger interferes w/ normal mechanisms protecting antigens against immune response –> tissue injury

39
Q

Types of autoimmune triggers

A
  • Exogenous
  • Endogenous
  • Molecular mimicry (pathogen derived antigen)
40
Q

Autoimmunity criteria

A
  • Autoantibodies
  • Self-reactive T lymphocytes
  • Imbalance btwn T & B cell & regulatory factors
41
Q

Etiologies of autoimmune disease

A
  • Genetic susceptibility
  • Environmental immune stimulants
  • Infectious agents
  • Loss of T regulatory cells
  • Decreased clearance of apoptotic material
  • Antibodies that react w/ apoptotic material
42
Q

Graves disease - Environmental & genetic factors

A
  • Stress
  • Smoking (minor risk, but major risk for opthalmopathy)
  • Sudden increased iodine intake
  • Post-partum
43
Q

Graves disease

A
  • Autoantibody stimulation of TSH receptor (TSI)

- Thyroid associated ophthalmopathy (T cells activate cytokine infiltration)

44
Q

Rheumatic fever

A
  • Autoimmune rxn to infection w/ group A streptococcus

- Molecular mimicry

45
Q

Rheumatic fever susceptibility

A
  • Inherited
  • Human leukocyte antigen class II alleles – some associated w/ susceptibility & some are protective
  • Cardiac valve damage = rheumatic heart disease
46
Q

Myasthenia Gravis

A
  • Autoantibody blocking/inactivation of alpha-chain of nicotinic acetylcholine receptor at neuromuscular junctions
47
Q

Abnormalities of the thymus (Myasthenia Gravis)

A
  • Hyperplastic
  • Tumors
  • Muscle-like cells within thymus (have AChRs on surface - may be source of auto antigen triggering)
48
Q

Myasthenia Gravis antibodies

A

Anti-AChR

  • Increases receptor turnover
  • Damage to postsynaptic muscle membrane by antibody & complement
  • Blockage of AChR active site that normally binds Ach
49
Q

SLE

A
  • Type III
  • Immune complex formation targeting DNA
  • Genetic susceptibility & environmental factors –> abnormal immune response
  • Immune cell activation –> sustained autoantibody & immune complex production, activation of complement, release of chemical mediators
50
Q

SLE antibodies

A

Anti-dsDNA, anti-Smith

51
Q

SLE chronic inflammation

A

Leads to irreversible tissue damage

52
Q

Type I DM genetic susceptibility

A

Genes that code for MHC class II molecules

53
Q

Type I DM environmental factors

A
  • Perinatal
  • Viruses
  • Dietary
54
Q

Type I DM autoantibodies

A
  • Insulin

- Islet cell

55
Q

Type I DM destruction of pancreatic cells

A

Caused by T cell cytokine production and cytotoxicity

56
Q

Rheumatoid arthritis

A
  • Type III
  • Genetic factors
  • Pro-inflammatory cytokines
57
Q

RA environmental factors

A
  • Tobacco smoke exposure

- Exposure to silicone dust & mineral oil

58
Q

RA autoantibodies

A
  • Rheumatoid factor

- Anti-CCP antibodies

59
Q

Multiple sclerosis

A
  • Genetic susceptibility

- Pro-inflammatory autoimmune response –> destruction of CNS myelin (both T & B cell involvement)

60
Q

Immunizations

A

Exploit adaptive immune response

  • Uninfected individuals given controlled infection or exposed to antigen that elicits an immune response
  • When exposed to pathogen in environment, memory T & B cells mount immune response before pathogen can spread
61
Q

Passive immunity

A

Antibody transferred from immune individual to nonimmune individual

62
Q

Advantage & disadvantage of passive immunity

A
  • Advantage: immediate availability

- Disadvantage: short duration (months)

63
Q

Active immunity

A
  • Artificial antigens administered to elicit controlled immune response
  • Mediators: Antibody and T cells
64
Q

Active immunity: Advantage & disadvantage

A
  • Advantage: long duration

- Disadvantage: Slow onset

65
Q

Live attenuated vaccines

A
  • Weakened form of virus
  • Antigens stimulate immune response
  • Must be refrigerated
  • Possible to become virulent again if mutates in host (rare)
  • Not for immune compromised or pregnancy
66
Q

Examples of live attenuated vaccines

A 
Measles 
Mumps 
Rubella 
Varicella 
Rotavirus 
Influenza
67
Q

Inactivated vaccines

A
  • Pathogens killed – isolates antigenic material
  • Freeze-dried, don’t require refrigeration
  • Induce weaker immune response
  • Need multiple doses to sustain immunity
68
Q

Examples of inactivated vaccines

A

Poliovirus
Hep A
Japanese encephalitis

69
Q

Subunit vaccine

A
  • Use component of the pathogen as vaccine antigen to mimic exposure
  • Weaker immune response than live attenuated
70
Q

Recombinant subunit vaccine

A

Antigens manufactured via recombinant DNA technology

71
Q

Polysaccharide subunit vaccine

A

Utilize polysaccharide antigens

72
Q

Surface protein subunit

A

Utilize purified proteins from the pathogen

73
Q

Toxoids

A

Inactivated or killed toxins used to elicit immune response –> antibodies that can neutralize toxins (Diphtheria)

74
Q

Conjugate subunit vaccine

A
  • Technology binds polysaccharide from bacterial capsule to a carrier protein
  • This antigen combo induces long-term protection
75
Q

Conjugate subunit vaccine examples

A

Hib, Pneumococcal (PCV), meningococcal

Foundations (9 decks)

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