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Micro and Immuno > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Despite its vital protective role against pathogens, the immune system is often responsible for ___ and is involved in the ___ of many diseases

A

tissue injury; pathogenesis

Ex: hypersensitivities, autoimmunity, transplant rejections

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2
Q

What are hypersensitivities?

A

Set of undesirable reactions by the normal immune system. “Over reaction” resulting in uncomfortable, damaging, and even fatal consequences.

Ex: allergies, autoimmune diseases

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3
Q

What state is required for hypersensitivities?

A

Pre-sensitized (immune) state; person is immune to a particular antigen before tissue damage occurs

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4
Q

What are the 4 types of hypersensitivities based on the triggering mechanism?

A
  1. Immediate (Type I)
  2. Antibody-mediated (Type II)
  3. Immune complex-mediated (Type III)
  4. Cell-mediated (Type IV)
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5
Q

Immediate (Type I) Hypersensitivity

A

Crosslinking of IgE antibodies bound to mast cells by an antigen (allergen)

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6
Q

Antibody-mediated (Type II) Hypersensitivity

A

Binding of IgG or IgM antibodies to antigens present on cells or basement membranes (our own cells/tissues) - basis for many autoimmune diseases

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7
Q

Immune complex-mediated (Type III) Hypersensitivity

A

Deposition of immune complexes (Ag/Ab) in tissues
Pre-reaction of Antigen and antibody occurs

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8
Q

Cell Mediated (Type IV) hypersensitivity

A

T cell-directed mechanisms of tissue injury

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9
Q

systemic anaphylaxis (type I hypersensitivity)

A

characterized by sudden respiratory and circulatory disruption that can be fatal within minutes due to airway blockage

Symptoms: swelling of the lips and periorbital areas, itching and erythema over wide areas of his body. This is followed by hypotension, tongue swelling and severe breathing difficulty with wheezing.

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10
Q

Mechanism behind Systemic Anaphylaxis (Type I Hypersensitivity) to anesthetic molecules

A

Reaction of anesthetic molecules with pre-existing specific IgE antibodies bound to the surface of mast cells, followed by release of vasoactive mediators (histamine).

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11
Q

majority of allergies are what type of hypersensitivity?

A

Type I (some type IV)

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12
Q

step-by-step mechanism of systemic anaphylaxis

A
  1. allergen gets into body
  2. Activation of Th2 cells and IgE class switching in B cells
  3. production of IgE
  4. binding of IgE to FceRI on mast cells
  5. repeat exposure to allergen
  6. activation of mast cell and cross linking; release of mediators: vasoactive amines, lipid mediators (all immediate), cytokines (later phase)
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13
Q

wheel and flare

A

Immediate reaction presentation with Type I hypersensitivity

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14
Q

acute phase of Type I hypersensitivity

A
  • 5-30 minutes
  • Subsides within 60 minutes
  • Vasodilation
  • Vascular leakage
  • Smooth muscle spasm

*all mediated by histamine

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15
Q

late phase of type I hypersensitivity

A
  • 2-24 hours
  • No additional exposure
  • Eosinophils, neutrophils, basophils, monocytes, and CD4+ T cells
  • Mucosal epithelial cell damage
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16
Q

Type I Hypersensitivity (Immediate) summarized

A
  • Rapid immune reaction (minutes)
  • Preformed antibodies (IgE) to allergen
  • IgE binds to FceRI on mast cells (stays until next allergen comes by)
  • Allergen crosslinks bound IgE molecules and triggers release of vasoactive mediators (histamine)(after second encounter with allergen)
  • Acute (< 1hr) and late phases (2 hr - days)
  • Local or systemic (anaphylaxis)
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17
Q

Key cells involved in type I hypersensitivities

A

CD4+ T cells (Th2 type), B cells making IgE antibodies

  • Mast cells, basophils (acute phase, contain histamine granules)
  • Eosinophils, neutrophils (late phase)
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18
Q

cytokines released from Th2 cells in Type I hypersensitivity

A

IL-4, IL-13, IL-5

*IL-4 and IL-13 is what tells B cells to make the IgE
*IL-5 activates cells of the late phase

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19
Q

What are the mast cell mediators of Type I hypersensitivity?

A
  • primary: biogenic amines: histamine
  • secondary: leukotrienes, prostaglandins, platelet activating factor, cytokines
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20
Q

effects of histamine release

A
  • Increased vascular permeability
  • Smooth muscle contraction (airways)
  • Increased mucous gland secretion
  • Produced by mast cells, basophils, platelets
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21
Q

Secondary mediators in mast cells

A
  • Leukotrienes (C4 & D4): what inhalers inhibit
  • Prostaglandins (D2)
  • Platelet Activating Factor (PAF)
  • Cytokines
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22
Q

describe the histamine receptors

A
  • Histamine Receptors (H1, H2, H3)
  • Acute allergic reactions mediated by H1 receptors on

smooth muscle and endothelial cells: this is why allergy leads to smooth muscle contraction and vasodilation

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23
Q

what do antihistamines do?

A

Antihistamines (prevent binding to H1 receptors) are a main line of treatment for allergic reactions

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24
Q

what are Arachidonic Acid Metabolites (AA)?

A
  • Derived from arachidonic acid (20 carbon unsaturated fatty acid - eicosanoids). Present in phospholipids of cell membranes.
  • Release of AA is mediated by phospholipases(activated by inflammatory stimuli)
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25
Q

two main pathways of Arachidonic Acid Metabolites (AA)

A
  • Cyclooxygenases (COX-1, COX-2) (Prostaglandins and

Thromboxanes) – Target of many NSAIDs

  • Lipooxygenases (Leukotrienes and Lipoxins)

*many anti-inflammatory meds block production of prostaglandins

*leukotriene inhibitors used for asthma

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26
Q

what are the effects of mediators?

A
  • Preformed mediators responsible for early phase (edema, itching, smooth muscle contraction).
  • Later, synthesized mediators (prostaglandins and cytokines) and recruited cells for late phase.
  • Combined effect is to attract circulating eosinophils, basophils, neutrophils, monocytes, lymphocytes (Th2) to site of mast-cell activation
  • Beneficial in parasite immunity but damaging in allergic reactions (today’s immune systems not used to reacting to these antigens so now overreact)
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27
Q

IgE-crosslinking is the main trigger of Type I hypersensitivity, but mast cell degranulation can also be induced by…

i.e. mast cells induced to release granules without IgE

A
  • Complement anaphylatoxins (C3a, C5a)
  • Certain drugs/chemicals (codeine, morphine,
    adenosine, mellitin, local anesthetics, contrast media)
  • Calcium ionophores
  • Eosinophil products (eosinophil basic protein)
  • Certain cytokines (IL-8)
  • Excess cold, heat, environmental irritants
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28
Q

What factors are responsible for the clinical Presentation of Type I Hypersensitivities?

A
  • Amount of allergen-specific IgE present (bound to mast cells) (people with a lot of allergies have more IgE)
  • Amount/dose of allergen encountered
  • Route of allergen contact/entry into the body: local vs. systemic contact
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29
Q

Clinical Manifestations of Allergens in Skin

A
  • Urticaria, hives
  • Angioedema
  • Atopic dermatitis or eczema
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30
Q

urticaria

A

allergic reaction of the skin characterized by the eruption of pale red, elevated patches called wheals or hives

*cutaneous tissue

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31
Q

Angioedema

A

swelling of the blood vessels;

*subcutaneous tissue

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32
Q

Atopic dermatitis or eczema

A

erythematous papules and vesicles with weeping, oozing crusts. allergies, asthma.

*chronic form

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33
Q

Clinical Manifestations of Inhaled Allergens

A
  • Allergic rhinitis, conjunctivitis
  • Allergic asthma
  • Chronic inflammation in allergic asthma can be perpetuated in absence of allergen
  • Development of airway hyper-responsiveness

*airway can become full of inflammatory cells and mucous, resulting in closing of airway and death

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34
Q

Clinical Manifestations of Allergens in Blood

A

Most severe: systemic anaphylaxis

  • Injections, insect bites, rapidly absorbed ingested

allergens (e.g., penicillin, wasp venom, eating peanuts)

  • IgE-independent reactions can be caused by certain drugs, chemicals, exercise (Anaphylactoid reactions)
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35
Q

treatment for systemic anaphylaxis

A

epinephrine: relaxes smooth muscle of bronchi to allow person to breathe again

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36
Q

In systemic anaphylaxis, an antigen enters the bloodstream then tissues and activates CT mast cells throughout the body. How does mast-cell degranulation and release of inflammatory mediators affect the tissues?

A
  • heart and vascular system: swelling, loss of BP, anaphylactic shock
  • respiratory tract: contraction of smooth muscle
  • GI tract: contraction of smooth muscle, cramps, vomiting, diarrhea
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37
Q

Why do some people get allergic reactions and others don’t?

A
  • Susceptibility to type I reactions has a strong genetic component
  • Not completely understood
  • Involves genes controlling IgE antibodies, Th2 differentiation, Th2 cytokines, mast cell production and activation (stronger activation/production)
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38
Q

diagnostic tests for allergies

A
  • skin testing
  • RadioImmunoSorbentTest(RIST)
  • RadioAllergoSorbent Test (RAST)
39
Q

Skin testing

A

Scratch the allergen on the skin and examine for a wheal and flare reaction appearing within minutes.

Subcutaneous antigen given in a low dose, causing mast-cell activation. Increased vascular permeability leads to localized swelling.

40
Q

RadioImmunoSorbentTest(RIST)

A

A quantitative test for total serum IgE.

People who suffer from allergies usually have a lot more IgE

41
Q

RadioAllergoSorbent Test (RAST)

A

A quantitative test for IgE antibody reactive with a particular allergen.

42
Q

Treatment of Allergic Reactions

A
  • Avoidance of allergen
  • Pharmacological
  • Immunological
43
Q

Pharmacological treatment of allergies

A
  • Antihistamines
  • Cyclo/Lipooxygenase inhibitors (e.g., leukotrienes): for asthma
  • Corticosteroids
  • Chromolyn sodium (prevents degranulation)
  • b2 agonists (e.g., epinephrine, albuterol) for systemic anaphylaxis
44
Q

immunological treatment of allergic reactions

A
  • Desensitization (promotion of IgG antibodies)
  • Anti-IgE: gets to mast cells before IgE
  • Cytokine-based (IFNg, Inhibitors of IL-4, IL-5)
45
Q

Allergy to Local Anesthetics

A
  • True allergies are very rare (<1%). Psychogenic and toxic reactions are more common, but sometimes labelled as “allergies”
  • True allergies are more likely to develop to ester- type anesthetics because they are metabolized to p-aminobenzoic acid (PABA), which is an allergenic compound.
  • Type I or type IV
46
Q

types of local anesthetics

A
  • Amides (e.g., lidocaine, bupivacaine, prilocaine)
  • Esters (e.g., benzocaine, procaine, tetracaine)
47
Q

Symptoms of True Allergic Reactions

A
  • Type I Allergies tend to occur within minutes of giving the injection.
  • Swelling of the lips and periorbital areas (angioedema)
  • The patient may become agitated and there is generalised urticaria (‘hives’) and pruritus (itchiness), particularly of the hands and feet. Other symptoms include abdominal cramps, nausea and diarrhea.
  • Tightness of the chest, with wheezing. Dyspnea (difficulty in breathing) may occur.
  • There may be a fall in blood pressure & tachycardia, which may be accompanied by flushing of the skin or rash.

*treat right away with Epinephrine

48
Q

Allergic reactions to anesthetics may be directed against other constituents rather than the anesthetic molecule itself, such as…

A

preservatives(benzoates), anti-oxidants (meta-bisulfites)

49
Q

In an allergic reaction in the dental office, what other allergy should be considered besides LA?

A

Allergy to latex must be considered

50
Q

The use of the term ___ for any adverse effect must be avoided unless actually proven.

A

“allergic reaction”

51
Q

prototype disorders of hypersensitivities

A

Anaphylaxis
allergies
bronchial asthma

52
Q

immune mechanisms behind type I hypersensitivity

A

Production of IgE antibody -> immediate release of vasoactive amines (histamine) and other mediators from mast cells; recruitment of inflammatory cells (late-phase reaction)

53
Q

pathologic lesion in type I hypersensitivities

A

Vascular dilation, edema, smooth muscle contraction, mucus production, inflammation

54
Q

What are Type II Hypersensitivity Reactions caused by?

A
  • IgG or IgM antibodies reacting with antigens on cells or basement membranes.
  • This mechanism is responsible for many antibody- mediated autoimmune diseases.
55
Q

Antigens involved in type II hypersensitivity reactions can be:

A
  • Foreign antigens (e.g., a drug) that bind to cells and act as haptens
  • Pathogen antigens that happen to cross-react with self antigens (e.g., Streptococcus antigens and rheumatic fever) – Molecular mimicry
  • Alloantigens (e.g., blood group antigens in transfusion reactions, erythroblastosis fetalis)
  • Self antigens (e.g., Auto-antigens in Autoimmune diseases)
56
Q

Haptens

A

antigens too small to provoke immune responses; attach to carrier molecules/bigger protein/cell to induce an antibody response

57
Q

molecular mimicry

A

close resemblance between foreign and self-antigen; mimic out own antigens

Ex: Streptococcus have antigens that look like those in our heart valves and joints, so immune system antibodies attack our own tissue. Basis for rheumatic fever

58
Q

erythroblastosis fetalis

A

a disorder that results from the incompatibility of a fetus with Rh-positive blood and a mother with Rh-negative blood, causing red blood cell destruction in the fetus; a blood transfusion is necessary to save the fetus

59
Q

Complement-Dependent Type mechanism for Type II Hypersensitivity

A
  • Opsonization for digestion by phagocytes - phagocytes destroy the cell
  • Hemolytic anemias (antibodies against own RBCs, antibody-coated RBC are destroyed in the spleen or liver by phagocytes)
  • Transfusion Rx
60
Q

Antibody Dependent Cell-Mediated Cytotoxicity (ADCC) mechanism for Type II Hypersensitivity

A
  • antibodies reacting with a larger structure, like a membrane. Neutrophil enzymes and reactive oxygen intermediates get released, leading to inflammation and tissue injury
  • Targets are lysed by leukocytes with Fcg receptors (e.g., neutrophils)
  • Graft rejection
61
Q

Antibody mediated cellular dysfunction mechanism of Type II Hypersensitivity

A
  • Antibodies directed against cell-surface receptors
  • GravesDisease (agonistic Abs)
  • Myasthenia Gravis (antagonistic Abs)
62
Q

Grave’s disease

A

an autoimmune disorder that is caused by hyperthyroidism.
One of the most common autoimmune disorders.
More common in women.
- antibody binds to TSH receptor, activating the thyroid cell to secrete thyroid hormone: antibody stimulates receptor without hormone

63
Q

Myasthenia Gravis

A

autoimmune disorder with descending muscle weakness
- antibody inhibits binding of neurotransmitter ACh to receptor, so muscle cannot contract (antagonistic)

64
Q

Describe how penicillin can act as a hapten

A
  • normally binds to bacterial transpeptidase to inactivate it
  • as a hapten, penicillin modifies proteins on human RBCs to create foreign epitopes
  • B cells stimulated to make IgG antibodies, penicillin-specific IgG binds to penicillin-modified proteins on erythrocytes
  • activation of complement and activation of macrophages causes RBC destruction
65
Q

what type of hypersensitivity is blood transfusion reactions?

A

Type II Hypersensitivity
- Structural polymorphisms in carbohydrates of glycolipids in surface of RBCs

66
Q

How do antibodies cause lung and kidney damage in Goodpasture syndrome?

A
  1. Reaction of autoantibodies with basement membrane
  2. complement activation
  3. Anaphylatoxin production (C3a, C5a)
  4. Recruitment of leukocytes (PMNs) (CRs, FcgRs)
  5. Degranulation, Production of ROS
  6. Tissue damage (Lung, Kidney)
67
Q

prototype disorders of Type II hypersensitivity

A

Autoimmune hemolytic anemia
Goodpasture syndrome

68
Q

Immune mechanism of Type II hypersensitivity

A

Production of IgG, IgM -> binds to antigen on target cell or tissue -> phagocytosis or lysis of target cell by activated complement or Fc receptors; recruitment of leukocytes

69
Q

Pathologic lesions of Type II hypersensitivity

A

Cell lysis; inflammation

70
Q

What happens in Type III Hypersensitivity?

A
  • Immune Complex Disease
  • Antibodies (IgM, IgG) bind soluble antigen (not present on cells), activate complement and are normally cleared by phagocytic cells in liver and spleen
  • Complexes that cannot be easily cleared deposit in tissues, creating inflammation
71
Q

what is an immune complex?

A

an antibody bound to an antigen

72
Q

Examples of Type III Hypersensitivity

A
  • Systemic (Serum sickness, SLE)
  • Localized (Arthus reaction)
  • Diverse Antigens (exogenous, endogenous)
73
Q

SLE

A

systemic lupus erythematosus
- deposition of immune complexes
- antigens against DNA, which then deposit and cause problems

74
Q

Antigens involved in Type III Hypersensitivity reactions can be:

A
  • Autoantigens (e.g., SLE)
  • Pathogen antigens (e.g., Post-streptococcal
    glomerulonephritis (too many antigens to be cleared so they get deposited), Hepatitis B virus)
  • Tumor antigens
  • Foreign proteins (e.g., antisera, antibodies)
  • Environmental antigens (e.g., Aspergillus in Farmer’s Lung)
75
Q

Factors that affect immune complex deposition

A
  • Amount of antigen (the more antigen is present, the more likely this can happen)
  • Physicochemical properties of antigen and
    antibody (some antigens more prone to cause this than others due to size, charge, etc.)
  • Ratio of antigen/antibodies (e.g., antigen excess, equivalence, antibody excess)
  • Inability of phagocytes to remove circulating immune complexes
76
Q

Describe serum sickness

A
  • Antigen-antibody complexes in circulation
  • Deposition of immune complexes
  • Inflammatory reaction at sites of immune complex deposition. Fibrinoid necrosis
77
Q

Step-by-stem what happens in an example of a person who has a reaction to Horse anti-venom? (serum sickness)

A
  1. horse SVA recognized by immune system as foreign
  2. primary immunization occurs (if is the first exposure), resulting in plasma cell secretion of immunoglobulins specific to horse SVA
  3. immunoglobulins bind to r-ATG resulting in immune complexes (antibody-antigen complexes)
  4. immune complexes deposit in tissues and blood vessels
  5. complement activation results in release of anaphylatoxins and neutrophil recruitment (which releases damaging enzymes)
78
Q

when do symptoms of Type III hypersensitivities develop?

A

After around 7 days: antigen:antibody complexes reaching equilibrium around this time

79
Q

Prototype disorder of Type III hypersensitivity

A

Lupus
Some forms of glomerulonephritis
Serum sickness
Arthus reaction

80
Q

Type III immune mechanism

A

Deposition of antigen-antibody complexes -> complement activation -> recruitment of leukocytes by complement products and Fc receptors -> release of enzymes and other toxic molecules

81
Q

Pathologic lesions of Type III hypersentivities

A

Necrotizing vasculitis (fibrinoid necrosis)
Inflammation

82
Q

cells involved in Type IV Hypersensitivity

A
  • Mediated by Antigen-specific effector T cells
  • Both CD4+ and CD8+ T cells may be involved
  • CD4+ T cells act through cytokines and activation of other cells (e.g. macrophages).
  • CD8+ T cells act through cytotoxicity
83
Q

Why is Type IV hypersensitivity also known as Delayed-type Hypersensitivity (DTH)

A
  • takes several days to develop as opposed to minutes
  • takes days for T cells to get activated and response going

Ex: Tuberculin reaction (TB test)

84
Q

mechanism behind Type IV Hypersensitivity

A
  • CD4 T cell activated by APC makes cytokines
  • cytokines activate phagocytes
  • phagocytes cause tissue injury
  • CD8 cells will directly damage the cells
85
Q

pentadecacatechol

A

This chemical acts as a hapten, binding covalently with proteins in the skin to elicit a delayed sensitivity reaction

Poison ivy

86
Q

step-by-step Delayed Type Hypersensitivity (DTH)

A
  1. antigen is introduced into subcutaneous tissue and processed by local antigen-presenting cells
  2. a Th1 effector cell recognizes antigen and releases cytokines which act on vascular endothelium
  3. recruitment of T cells, phagocytes, fluid, and protein to site of antigen injection causes visible lesion (inflammation)

*24-72 hours

87
Q

describe contact hypersensitivity

A
  • Type IV Hypersensitivity reactions against environmental antigens: pentadecacathecol (poison ivy), small metal ions (Ni, CrO3, Ti, Co, V)
  • Antigens act as haptens, modifying host proteins, eliciting a T cell response
  • May involve both CD4+ and CD8+ T cells. Edema resulting from cytokines made by T cells
88
Q

Type IV hypersensitivity prototype disorders

A

Contact dermatitis
Multiple sclerosis
Type I diabetes
Transplant rejection
Tuberculosis

89
Q

Type IV hypersensitivity mechanism

A

Activated T lymphocytes -> release of cytokines and macrophage activation -> T cell-mediated cytotoxicity

90
Q

Type IV pathologic lesions

A

Perivascular cellular infiltrates
Edema
Cell destruction
Granuloma formation

91
Q

Hypersensitivities to Medications or Materials used in Dentistry

A
  • Hypersensitivities to antibiotics, anesthetics, analgesics (Type I, IgE-dependent (classical) and independent (anaphylactoid) reactions
  • Hypersensitivities to materials; e.g., certain metals such as Ti, V, Cr, Co, Ni, Mo (Type IV-contact Hypersensitivity type -T cell-mediated)
  • Allergies to latex products (may involve both type I and IV hypersensitivities)
92
Q

MELISA

A

Assay to detect hypersensitivity to metals; measures reactivity of T cells

93
Q

What actually is involved in an allergy to latex?

A

Chemicals applied during manufacturing process are what the person is allergic to

Micro and Immuno (17 decks)

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