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Foundations exam 2 > Immunology II- Hypersensitivity reactions > Flashcards

Immunology II- Hypersensitivity reactions Flashcards

1
Q

Hypersensitivity reactions- definition

A

exaggerated, inappropriate immunologic reaction that is harmful to the host

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2
Q

Sensitization

A

First exposure to antigen with immune response (antibody) Subsequent exposures= hypersensitivity rxn

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3
Q

4 types of hypersensitivity rxns

A

A- Type I: Allergy or Anaphylaxis

C- Type II: antibody dependent or Cytotoxic

I- Type III: Immune complex

D- Type IV: Cell-mediated or Delayed type

“ACID”

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4
Q

Which type of hypersensitivity reaction involves Immune complex?

A

Type III

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5
Q

Which type of hypersensitivity reaction involves Cell-mediated or delayed type

A

Type IV

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6
Q

Which type of hypersensitivity reaction involves allergy or anaphylaxis

A

Type I This is immediate hypersensitivity

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7
Q

Which type of hypersensitivity reaction involves Antibody dependent or cytotoxic

A

Type II

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8
Q

Which types of reactions are antibody mediated

A

I= IgE II and III= IgG

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9
Q

Mechanism of Type I Hypersensitivity rxn

A
  • First exposure to antigen causes IgE formation
  • IgE binds to mast cells
  • Subsequent exposure- antigen binds to IgE bound-mast cell
  • Degranulation of mast cells
  • Release of mediators

*1st exposure is “priming”

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10
Q

What is the typical time of onset of type I

A

minutes

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11
Q

Antigens involved in Type I

A

substances that most people dont react to- pollen, animal dander, foods, drugs (things in environment)

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12
Q

Result of Type I hypersensitivity rxn

A

increased vascular permeability

edema

smooth muscle contraction

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13
Q

What are the clinical manifestations of Type I hypersensitivity rxn?

A

edema

erythema

itching

urticaria

eczema

rhinitis

conjunctivitis

asthma

most severe: systemic anaphylaxis (severe bronchoconstriction and hypotension)

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14
Q

What happens during an allergic response during sensitization

A
  1. During sensitization, an antigen presenting cell (APC) picks up the allergen and presents part of it to a Th2 cell, which helps a B cell become a plasma cell 2. Plasma cells produce allergen-specific antibodies called IgE, which binds to mast cells
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15
Q

What happens during an allergic response with re-exposure

A

When allergen returns, mast cells release histamine and other chemicals

Th2 cells release chemicals that attract inflammatory cells (i.e. eosinophils)

This results in allergy sxs (sneezing, mucus production, swelling, itching, runny nose, coughing and wheezing)

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16
Q

What is the mediator of a Type I hypersensitivity rxn and what is its effect?

A

Histamine

Effect- vasodilation, increased capillary permeability, smooth muscle contraction

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17
Q

What is the immunologic rxn involved in Type I hypersensitivity rxn?

A

Antigen (allergen) induces IgE antibody that binds to mast cells and basophils. When exposed to the allergen again, the allergen cross links the bound IgE on those cells. This causes degranulation and release of mediators (ex: histamine)

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18
Q

What is the emergency concern regarding anaphylaxis (Type I) nand what is the treatment?

A

low BP, bronchoconstriction treatment- Epi (bronchodilates and vasoconstricts–> increases BP)

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19
Q

What is the preventative medicaiton option for anaphylaxis (Type I)?

A

antihistimines, steroids

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20
Q

What infections can exacerbate a patients asthma (type I hypersensitivity rxn)

A

Bronchitis, influenza, pneumonia **can prevent with vaccines

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21
Q

What is the plan for a pt that presents with Type I Hypersensitivity rxn (anaphylaxis)?

A
  1. IM/SQ Epinephrine x1 now 2. IV corticosteroids 3. IV fluids for hydration and to increase BP 4. IV diphenhydramine (Benadryl)–> antihistamine 5. IV promethazine (Phenergan)–> antiemetic 6. observation
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22
Q

What foods cause 90% of food allergies

A

milk

egg

fish (bass, flounder, cod)

shellfish (crab, lobster, shrimp)

Tree nuts (almonds, pecans, walnuts

wheat

peanuts

soybeans

**also a consideration: fruits, preservatives, dyes

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23
Q

What results when there is systemic histamine release in anaphylaxis (type I hypersensitivity)

A

Hypotension

nausea

hives

swollen hands/feet

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24
Q

What is the other name for Type II: cytotoxic hypersensitivity

A

antibody dependent

antibody= IgG

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25
Q

Antigens involved in Type II hypersensitivity rxn

A

on cells or in extracellular matrix

can be endogenous or exogenous antigens

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26
Q

Antibody involved in Type II hypersensitivity rxn

A

IgG

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27
Q

Immunologic rxn of Type II hypersensitivity rxn

A

Antigens on a cell surface combine with IgG antibody this leads to complement-mediated lysis of the cells (ex: transfusion or Rh reactions or autoimmune hemolytic anemia)

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28
Q

What is the typical time of onset of a Type II cytotoxic hypersensitivity rxn?

A

hours to days

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29
Q

What are the clinical manifestations of Type II hypersensitivity rxn

A

Hemolytic anemia

neutropenia

thrombocytopenia

ABO transfusion rxns

Rh incompatibility (erythroblastosis fetalis, hemolytic disease of the newborn)

rheumatic fever

Goodpasture syndrome

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30
Q

What is hemolytic anemia

A

Example of Type II cytotoxic hypersensitivity 1. antibody attaches to antigen on RBC 2. Complement mediated lysis via MAC 3. complement also attracts phagocytes

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31
Q

What is the antibody associated with Type III Immune complex hypersensitivity?

A

IgG

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32
Q

What is the immunologic rxn associated with Type III Immune complex hypersensitivity?

A

-antigen-antibody immune complexes are deposited in tissues, complement is activated, and polymorphonuclear cells are attracted to the side -They release lysosomal enzymes, causing tissue damage

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33
Q

What is the typical time of onset of Type III Immune complex hypersensitivity?

A

2-3 weeks

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34
Q

What is the clinical manifestations of Type III Immune complex hypersensitivity?

A

Systemic lupus erythematosus

rheumatoid arthritis

poststreptococcal glomerulonephritis

IgA nephropathy

serum sickness

hypersensitivity pneumonitis (Farmers lung)

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35
Q

What is the mechanism of Type III Immune complex hypersensitivity?

A
  1. Antigen-antibody immune complexes form and deposit in tissue
  2. Inflammatory response induced in tissue
  3. Complement activated, and PMNs attracted to the site -Lysosomal enzymes released -tissue damage
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36
Q

Systemic Lupus erythematosus

A

Example of Type III Immune complex hypersensitivity.

  • Antibodies formed to DNA and cell nucleaus (ANA=antinuclear antibody)
  • antibodies form immune complexes that activate complement
  • Complement activation produces C5a, which attracts neutrophils that release enzymes, thereby damaging tissue

***butterfly rash on face

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37
Q

Rheumatoid Arthritis

A

Example of Type III Immune complex hypersensitivity

  • Serum and synovial fluid of pt contain “rheumatoid factor” (i.e. IgM and IgG antibodies that bind to the Fc fragment of normal human IgG)
  • Deposits of immune complexes (containing the normal IgG and rheumatoid factor) on synovial membranes in blood vessels
  • Activate complement and attract polymorphonuclear cells, causing inflammation
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38
Q

What is seen on labs of patients with Rheumatoid arthritis?

A

-Pts have high titers of rheumatoid factor and low titers of complement in serum, especially during periods when their dz is most active.

**this is an example of Type III Immune complex hypersensitivity

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39
Q

Immunologic reaction of Type IV Delayed (cell mediated) hypersensitivity

A

T lymphocytes, activated/sensitized by an antigen, release lymphokines upon second contact with the same antigen

-The lymphokines induce inflammation and activate macrophages, which in turn, release various inflammatory mediators (and causes damage)

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40
Q

What is the typical time of onset of Type IV Delayed (cell mediated) hypersensitivity?

A

2-3 days

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41
Q

What are the clinical manifestations of Type IV Delayed (cell mediated) hypersensitivity

A

Contact dermatitis, poison oak/ivy, tuberculin skin test reaction, drug rash, stevens-johnson syndrome, toxic epidermal necrolysis, erythema multiforme

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42
Q

Mechanism of Type IV Delayed (cell mediated) hypersensitivity

A
  • The macrophage ingests the antigen, processes it, and presents an epitope on its surface in association with class II major histocompatibility complex (MHC) protein
  • the helper T (Th-1) cell is activated and produces gamma interferon, which activates macrophages
  • these two types of cells mediate delayed hypersensitivity
43
Q

Important clinical aspects of delayed hypersensitivities- What are the main immune cells involved?

A

CD4 (helper) T cells and macrophages

CD8 (cytotoxic) T cells

44
Q

Important clinical aspects of delayed hypersensitivities- What are the important diseases/ skin tests having to do with CD4 (helper) T cells and macrophages?

A
  1. Tuberculosis, coccidioidomycosis
  2. Tuberculin or coccidioidin (or spherullin) skin tests
45
Q

Important clinical aspects of delayed hypersensitivities- What are the important diseases/ skin tests having to do with CD8 (cytotoxic) T cells

A
  1. Contact dermatitis
  2. Erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis
46
Q

Overview of Important clinical aspects of delayed hypersensitivities (graph)

A
47
Q

Type IV hypersensitivity- Repeat exposure

A

•T lymphocytes activated/sensitized by an antigen release of lymphokines upon second contact with the same antigen.

-The lymphokines induce inflammation and activate macrophages–>release various inflammatory mediators

48
Q

What is Hereditary Angioedema

A

A congenital immunodeficiency of C1 protease inhibitor

Autosomal dominant

-Patient has excess C3a, C4a, C5a

49
Q

What is the typical time of onset of Type IV hypersensitivity reaction

A

2-3 days

50
Q

What is the result of Hereditary angioedema?

A
  • capillary permeability and edema
  • Episodic local subcutaneous and submucosal edema typically involving GI and upper respiratory tracts

**essentially an overdrive of the complement cascade (deficiency of C1 protease= increased complement)

51
Q

How do you make a diagnose Hereditary Angioedema?

A
  • Family history
  • Lack of pruritis (NOT histamine dependent) and urticarial lesions
  • Recurrent abdominal colic and/or laryngeal edema
  • Labs: decreased C1 inhibitor levels (or decreased function, or mutation in C1 inhibitor gene altering synthesis/function)
52
Q

What is the function of the immune system?

A

•Provide a protective response against infective organisms and foreign cells WHILE Avoiding damage to self

53
Q

What are the targets of the immune system?

A
  • Infectious organisms (bacteria, viruses, fungi, parasites)
  • Foreign bodies
  • Toxins
  • Cancer
54
Q

What are “markers of self”?

A
  • Distinctive surface proteins that identify “self”
  • Able to coexist with your immune system
  • Unique markers on human cells–> the major histocompatibility complex (MHC) proteins
  • MHC Class I proteins found on all cells
  • MHC Class II proteins found only on certain specialized cells
55
Q

What are markers of “non-self”?

A
  • Non-self substance (antigen) can trigger the immune system
  • Area on the antigen that triggers a response is the epitope
  • Example: Transplanted tissues are recognized as foreign and attract antibodies
56
Q

What is the purpose of Self-antigens?

A

Mechanisms for avoiding damage to self (preventing autoimmunity):

  1. Sequestration
  2. Tolerance
  3. Regulation
57
Q

Mechanisms of preventing autoimmunity: Generation and maintenance of tolerance

A
  • Central deletion of autoreactive lymphocytes
  • peripheral anergy of autoreactive lymphocytes
  • receptor replacement in autoreactive lymphocytes
58
Q
A
59
Q

Mechanisms of preventing Autoimmunity: Regulatory mechanisms

A
  • Regulatory T cells
  • Regulatory B cells
  • Regulartory mesenchymal cells
  • regulatory cytokines
  • idotype work
60
Q

What is an autoimmune disease?

A

a trigger interferes with normal mechanisms protecting auto-antigens against an immunologic response causing tissue injury

61
Q

Types of triggers of autoimmune disease

A

Exogenous

endogenous

molecular mimicry (infection/pathogen gets into system and has very similar mechanism to self so antibodies released that also attack self)

62
Q

Criteria of an autoimmune disease

A

Autoantibodies

self-reactive T lymphocytes

Imbalance b/w T and B cell pathogenic factors and regulatory factors that control immune response

63
Q

What are examples of Exogenous triggers of autoimmunity?

A

molecular mimicry

superantigenic stimulation

microbial and tissue damage-associated adjuvanticity

64
Q

What are examples of Endogenous triggers of autoimmunity?

A
  1. Altered antigen presentation
  2. Increased T cell help
  3. increased B cell function
  4. Apoptotic defects or defects in clearance of apoptotic material
  5. Cytokine imbalance
65
Q

Endogenous triggers of autoimmunity- altered antigen presentation

A
  1. Loss of immunologic privelege
  2. Presentation of novel or cryptic epitopes (epitope spreading)
  3. Alteration of self-antigen
  4. Enhanced function of antigen-presenting cells (Costimulatory molecule expression and cytokine production)
66
Q

example of Endogenous triggers of autoimmunity- Increased T cell help

A
  1. Cytokine production
  2. Costimulatroy molecules
67
Q

Example of Endogenous triggers of autoimmunity- Increased B cell function

A
  1. B cell activating factor
  2. Costimulatroy molecules
68
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 with apoptotic material
69
Q

Triggers of imbalance that leads to autoimmune disease

A

Bacteria-

  1. Streptococcus pyogenes (Strep throat)–> Rheumatic fever
  2. Borrelia burgdorferi–> Lyme Arthritis

Viruses-

  1. Hepatitis B virus–> Multiple Sclerosis
70
Q

Graves disease

A

Autoimmune disease

Hyperactive thyroid disorder- Involves autoantibody stimulation of the TSH receptor–> Thyroid stimulating immunoglobulin (TSI)

(TSI is the antibody that reacts with TSH receptor and causes it to be hyperactive)

71
Q

Environmental and genetic factors of autoimmune disease Grave’s Disease

A
  • Stress
  • Smoking (minor risk factor; but major risk factor for ophthalmopathy)–> dont have to have this risk factor
  • Sudden increased iodine intake
  • Post-partum
72
Q

Myasthenia Gravis

A

Autoimmune disease

  • Autoantibody blocking/inactivation of the alpha-chain of the nicotinic acetylcholine receptor at neuromuscular junctions
  • Causes Abnormalities of the thymus
  • Anti-AChR antibodies

This is an inhibitory reaction (As opposed to Graves Disease which is hyperactive)

73
Q

What happens if you have Graves Disease and have Thyroid associated opthalmopathy?

A

T cells will activate cytokine infiltration of extraocular muscles

74
Q

What is the role of Anti-AChR antibodies in Myasthenia gravis?

A
  • Increases receptor turnover
  • Damage to postsynaptic muscle membrane by antibody and complement
  • Blockage of AChR active site that normally binds acetylcholine
75
Q

What thyroid abnormalities are involved in Myasthenia gravis?

A
  • Hyperplastic
  • Tumors (thymoma)
  • Muscle-like cells within the thymus – these cells have AChRs on their surface which may be a source of autoantigen triggering the autoimmune reaction within the thymus
76
Q

Rheumatic fever

A
  • Autoimmune reaction to infection with group A streptococcus —>Molecular mimicry – immune response against streptococcal antigens also recognizes human tissues causing cross-reactive antibodies
  • Cardiac valve damage – rheumatic heart disease
77
Q

Susceptibility of rheumatic fever

A

•Human leukocyte antigen class II alleles – some are associated with susceptibility and some are protective

78
Q

Systemic lupus erythematosus (SLE)

A

Autoimmune disease

  • Type III hypersensitivity reaction
  • Immune complex formation targeting double-stranded DNA
  • Genetic susceptibility and environmental factors result in abnormal immune responses
  • Immune cell activation leads to sustained autoantibody and immune complex production, activation of complement, release of chemical mediators
  • Chronic inflammation leads to irreversible tissue damage (fibrosis/sclerosis of glomeruli, arteries, lungs, and other tissue)
79
Q

Which specific antibodies are involved in the autoimmune disease Systemic Lupus Erythematosus?

A

Anti-dsDNA

anti-Smith

80
Q

Type I Diabetes mellitus

A

Autoimmune disease

  • Genetic (genes that code for MHC II) and environmental factors (perinatal, viruses, dietary)
  • Insulin and islet cell autoantibodies
  • T cell cytokine production and cellular cytotoxicity (destruction of pancreatic beta cells)
81
Q

Which autoantibodies are involved in Type I diabetes mellitus?

A

Insulin autoantibodies

Islet cell autoantibodies (likely target proinsulin/insulin)

82
Q

Which type of Hypersensitvity reaction is Rheumatoid Arthritis

A

Type III hypersensitivity rxn

Autoimmune disease

83
Q

Rheumatoid arthritis

A
  • Type III hypersensitivity reaction
  • Genetic and environmantal factors
  • Environmental factors (ex: tobacco smoke exposure, Exposure to silicone dust and mineral oil)

-Involves autoantibodies and pro-inflammatory cytokines

84
Q

What are the autoantibodies involved in Rheumatoid arthritis?

A

Rheumatoid factor

anti-CCP antibodies

**RA also has cytokine involvement

85
Q

Multiple Sclerosis

A
  • Genetic susceptibility
  • Pro-inflammatory autoimmune response causing destruction of CNS myelin–> Both T and B cell involvement

**No specific antibody involvement

86
Q

What is the effector of Graves Disease in addition to its mechanism and target?

A

Effector= autoantibody

mechanism= stimulation

target= TSH receptor (LATS)

87
Q

What is the effector of Myasthenia Gravis in addition to its mechanism and target?

A

Effector= Autoantibody

Mechanism= Blocking or inactivation

Target= alpha chain of the nicotinic acetylcholine receptor

88
Q

What is the effector of Systemic lupus erythematosus in addition to its mechanism and target?

A

effector- autoantibody

mechanism- immune complex formation

target- ds DNA

89
Q

What is the effector of Rheumatoid arthritis in addition to its mechanism and target?

A

Effector- autoantibody

Mechanism= immune complex formation

Target- immunoglobulin

Effector #2= T cells

Mechanism- cytokine production

90
Q

What is the effector of Type I DM, Multiple sclerosis and rheumatoid arthritis in addition to its mechanism and target?

A

Effector= T cells

Mechanism= cytokine production

target= ?

91
Q

What is the effectors of DM type I in addition to its mechanism and target?

A

Effector: T cells

Mechanisms: Cytokine production and cellular cytotoxicity

Target: ?

92
Q

What is the concept of immunizations in relation to the immune system?

A

Vaccinations exploit the 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 and B cells can quickly mount immune response before pathogen can spread
93
Q

What are active immunity vaccinations?

A

-These are your traditional vaccines

  • Artificial antigens administered to elicit controlled immune response
  • Mediators: Antibody and T cells
  • Advantage: Long duration (years)
  • Disadvantage: slow onset
94
Q

Passive immunity vaccinations

A
  • Antibody transferred from immune individual to nonimmune individual
  • Advantage: immediate protection
  • Disadvantage: short duration (months)

**You would give immunoglobulin with known exposure

95
Q

Active vs passive immunity- Specifcity vs memory

A

Active immunity provides memory and specificity

Passive immunity DOES have specificity but DOESNT have memory

96
Q

Live attenuated vaccine

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
  • Examples: measles, mumps, rubella, varicella, rotavirus, influenza (intranasal) yellow fever
97
Q

Inactivated vaccines

A
  • Pathogens killed to inactivate them – can isolate antigenic material
  • Freeze-dried, don’t require refrigeration
  • Induce weaker immune response
  • Need multiple doses to sustain immunity
  • Examples: poliovirus, hepatitis A, Japanese encephalitis
98
Q

Subunit vaccines

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

Types:

  • recombinant subunit vaccine
  • polysaccharide subunit vaccine
  • Surface protein subunit
  • Toxoids
99
Q

Subunit vaccines–> Recombinant subunit vaccine

A

•antigens manufactured via recombinant DNA technology

100
Q

Subunit vaccines- polysaccharide subunit vaccine

A

utilize polysaccharide antigens (meningococcal, pneumococcal PPSV)

101
Q

Subunit vaccines- Surface protein subunit

A

utilize purified proteins from the pathogen

102
Q

Subunit vaccines–> Toxoids

A

Inactivated or killed toxins used to elicit immune response resulting in antibodies that can neutralize toxins (Diptheria)

103
Q

Conjugate subunit vaccine

A
  • Technology binds polysaccharide from bacterial capsule to a carrier protein
  • This antigen combination induces long-term protection in infants and adults
  • Examples: Hib, Pneumococcal (PCV), meningococcal

Foundations exam 2 (2 decks)

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