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Microbiology > 2. Hypersensitivity > Flashcards

2. Hypersensitivity Flashcards

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1
Q

common features of hypersensitivity reactions

A
  • immune reactions which are overtly injurious to the host
  • occurs in subjects previously exposed to an antigen and who developed an immune response to that antigen (sensitization)
  • clinical manifestations depend on host’s response, NOT on nature of antigen
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2
Q

hypersensitivity can basically occur anywhere

A

allergens can be anywhere
- upper resp tract: allergic rhinitis (hay fever)
- GI tract: cramps, nausea, vomiting, diarrhea
- skin: contact dermititis
- lower resp tract: asthma
- circulation: generalized anaphylaxis

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3
Q

common allergens

A
  • dust, pollen, animal dander, food, medications
  • substances that come in contact with skin (metals, plant compounds, latex, cosmetics)
  • venom of stinging insects
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4
Q

hypersensitivity reaction classifications

A
  • type I: IgE-mediated
  • type II: Ab-mediated cytotoxicity
  • type III: immune complex-mediated
  • type IV: cell-mediated
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5
Q

hypersensitivity reaction time course

A
  • type I: 2-30 mins (immediate)
  • type II: 5-8 hours
  • type III: 2-8 hours
  • type IV: 24-72 hours
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6
Q

classification of immunopathologic processes: type I

A
  • allergic/anaphylactic reactions
  • mainly IgE-mediated
  • clinical manifestations due to release of newly synthesized and preformed mediators from mast cells and basophils
  • reaction may be localized or generalized
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7
Q

harmless antigens that can specifically stimulate an IgE response are called ___. people are exposed to a variety of innocuous antigens on a daily basis.

A

allergens

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8
Q

clinical manifestations of type I hypersensitivity

A
  • due to the release of pre-formed and newly synthesized mediators from mast cells and basophils
  • designed to drive out potential parasitic pathogens or prevent their further entry:
    • by clearing the GI tract via vomiting and diarrhea
    • by contracting or blocking airways
    • by increasing fluids and blood flow to allow better access to immune and inflammatory components to the site of an attack
    • in places where parasitic infections are rare, the result of an IgE mediated response range from bothersome to life threatening
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9
Q

allergic reactions

A
  • allergic reactions cannot occur upon first exposure to the antigen (there must be sensitization)
    1. upon first exposure to an allergen, large amounts of IgE are produced
    2. antibodies bind to mast cells and basophils that have large numbers of receptors for the Fc portion of IgE on their surfaces (sensitization phase)
    3. bind to high affinity receptors for IgE, called FceRI, bind IgE without the Ig being bound to an antigen
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10
Q

IgE mechanism

A
  • once bound, IgE remains on the surface of the cell
  • activated only when a second exposure to the allergen causes the allergen to attach to cell-bound IgE molecule and cross-link different FceRI receptors
  • first exposure to an allergen “arms” a cell by coating it with IgE specific to that particular allergen
  • subsequent exposure activates the cell and leads to cascade of biochemical and cellular events which ultimately lead to allergic reaction
  • mast cells and basophils bind free circulating IgE via FceRI
  • binding of antigen and subsequent crosslinking of surface FceRI by antigen binding to bound IgE (activation phase)
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11
Q

when activated, mast cells and basophils immediately go through the process of ___, where contents of cellular granules are released into surrounding __. in this early phase, ___ mediators stored in the cell granules are released (histamines, prostaglandins, eosinophil chemotaxins, serotonin, proteases).

A

degranulation, environment, pre-formed

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12
Q

later phase of allergic reaction involves the synthesis and secretion of various ___, as well as some chemokines and leukotrienes

A

cytokines

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13
Q

majority of more severe clinical manifestations of type I hypersensitivity are due to __ phase response

A

early

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14
Q

late phase responses play a major role in more __ and __ manifestations of type I hypersensitivity

A

chronic, serious
ex: chronic asthma can be long lasting and cause problems even in absence of original allergen

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15
Q

degranulation

A

release of preformed mediators in a mast cell in type I hypersensitivity

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16
Q

altered phospholipid metabolism

A

occurs with release of newly synthesized mediators in mast cell in type I hypersensitivity

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17
Q

preformed mediators of mast cells and their functions

A
  • histamine: capillary permeability, smooth muscle contraction
  • ECF-A: eosinophil chemotaxin
  • serotonin: capillary permeability, smooth muscle contraction
  • HMW-NCF: neutrophil chemotaxin
  • proteases: degrade basement membranes, cleave complement proteins
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18
Q

newly synthesized mediators of mast cells and their functions

A
  • leukotrienes (C,D,E): capillary permeability, constricts bronchial smooth muscle
  • platelet-activating factor (PAF): aggregates platelets, constricts bronchial smooth muscle
  • prostaglandin D2: constricts bronchial smooth muscle
  • cytokines (IL-4,5,6): multiple actions
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19
Q

2 types of anaphylactic reactions in humans

A
  • systemic anaphylaxis
  • localized anaphylactic reactions
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20
Q

3 localized anaphylactic reactions

A
  • allergic rhinitis (hay fever)
  • asthma
  • atopic dermatitis
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21
Q

systemic anaphylaxis

A
  • increased blood vessel permeability
    • when systemic can result in disastrous loss of blood pressure and cardiovascular collapse
  • smooth muscle contraction cause respiratory difficulties
  • severe swelling of upper airway can lead to asphyxia, but most of these cases are localized not systemic
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22
Q

common allergens that cause systemic anaphylaxis

A
  • venom from bees and wasps
  • food products with peanuts or peanut-derived components
  • certain shell fish and antibiotics with penicillin (penicillin can link to host cells or proteins and function as hapten; can activate IgE coated mast cells and basophils in allergic individuals and generate systemic response)
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23
Q

asthma

A

varying degrees of reversible airway obstruction in association with exaggerated airway responsiveness to a wide variety of physical and pharmacologic stimuli

24
Q

intrinsic vs extrinsic asthma

A

extrinsic: allergic/atopic
- < 20 y/o
- 1.6M:1F
- seasonal pattern often
- family history often
- allergen identified sometimes
- total serum IgE elevated

intrinsic: non allergic
- > 30 y/o
- 1M:1F
- no seasonal pattern
- no family history
- no allergen identified
- normal total serum IgE

25
Q

early phase response in allergic asthma

A
  • peaks in 10-20 mins
  • smooth muscle contraction
  • vascular leakage
  • mucus secretion
26
Q

late phase response in allergic asthma

A
  • peaks in 2-8 hours
  • eosinophil and PMN infiltration
  • fibrin and deposition
  • later infiltration with macrophages and fibroblasts
27
Q

two pathways of activated mast cell

A

min:
1. degranulation (histamine, PG, leukotrienes)
2. early reaction
3. chemotaxis
4. cell influx
5. mediators
6. late phase reaction

hours:
1. secretion
2. cytokines
3. late phase reaction

28
Q

variable airflow obstruction in asthma due to combination of:

A
  • edema of bronchial mucosa
  • spasm of bronchial smooth muscle
  • mucus plugging of bronchial lumen
29
Q

why are some antigens allergenic?

A
  • small protein antigens on dry particles (such as pollen grains) become wet in mucosa and elute protein into it
  • very low concentrations of these proteins (often enzymes) tend to stimulate an IgE response
  • since an IgE response is usually generated against various parasites:
    • certain parasites use particular enzymes to break down and penetrate host tissue
    • IgE response to allergenic proteins may be due to enzyme recognition mechanisms originally designed to fight parasites
    • allergen in the feces of common dust is similar in structure to enzyme papain
    • not all allergens are enzymes
30
Q

testing for type I hypersensitivity 2 basic approaches

A
  • evaluating levels of components of immune response to an allergen (ex: total IgE or allergen-specific IgE)
  • evaluating actual physiological reaction of an individual to a particular antigen (ex: skin test)
31
Q

two early tests that exemplify the first approach of testing type I hypersensitivity (evaluating levels of components of IR to an antigen) are the __ and __

A

RIST (radioimmunosorbent test) and RAST (radioallergosorbent test)

32
Q

RIST

A
  • measures total serum IgE level (how much IgE is is in the bloodstream)
  1. solid phase antihuman IgE (antihuman IgE)
  2. capture IgE in patient serum (human IgE)
  3. detect captured IgE with radiolabeled anti IgE (radiolabeled antihuman IgE)
33
Q

RAST

A
  • measures allergen-specific IgE activity
  1. disk coated with test allergen
  2. incubate with test serum (specific IgE bound)
  3. radiolabeled antihuman IgE (antihuman IgE)
34
Q

skin testing

A
  • RIST, RAST, evaluate levels of IgE
  • skin tests evaluate the in vivo response of that individual to test an allergen
  • two types: prick and intradermal
35
Q

advantages of skin testing

A
  • simple and easy
  • very sensitive
  • very specific to particular antigen
  • examines final reaction of an individual to that allergen in vivo
36
Q

prick test

A
  • small amount of sample allergen is injected into skin and the area of injection is observed for a localized reaction
  • negative control: saline without allergen (shouldn’t have any reaction)
  • positive control: histamine (should cause localized reaction)
  • different allergens can be tested on large surface of skin (arm or back)
  • positive reaction indicated by appearance 15-30 mins later of red area and inflammation at site of injection
37
Q

intradermal test

A
  • conducted if positive control results in prick test were no different from negative control but suspicious of patient being allergic to particular antigen
  • allergen is used at lower dose than prick test (100-1000 times less) but injected between different layers of skin
  • exercise caution as not to stimulate anaphylactic reaction
  • administered on limb (arm) that can be isolated with tourniquet to avoid spreading the allergen systemically
38
Q

why are only certain people allergic

A
  • genetic basis to susceptibility to allergy
    • allergy/atopic individuals more prone to stimulation of Th2 cells (have higher level of circulating IgE)
  • genetically associated
    • MHC haplotypes that favor a strong Th2 response
    • specific genetic variations that encode for cytokines that promote or favor an IgE-selected antibody response
    • some have specific genetic variations in the genes that encode for cytokines that promote an IgE-selected antibody response
    • genetic variation in IL-4 gene has been reported for certain atopic individuals
39
Q

Th2 response is always associated with __ response and leads to __ response

A

antibody, IgE

40
Q

cross-regulation of T helper subsets

A
  • cytokines downregulate development of opposing Th
  • ex: if you have Th1, IFNgamma will downregulate Th2. if you have Th2, IL-4,10 will downregulate Th1
41
Q

true or false: if family members have allergies you are more likely to have those allergies

A

true

42
Q

prophylaxis and treatment

A
  • allergen avoidance
  • downregulation of inflammatory process
  • relief of symptoms
  • hyposensitization
43
Q

hyposensitization

A
  • extremely small amounts of allergen are administered to an allergic individual (ex: allergy shots)
  • switches the response of the individual to that allergen from IgE to IgG
  • IgG blocking antibodies that block antigen binding with IgE
  • repeated administration of antigen may stimulate regulatory T cells to downregulate the response (tolerization)
  • IgG will compete with IgE for antigens and won’t bind mast cells (no allergic reaction)
44
Q

classification of immunopathologic processes: type II

A
  • antibody-mediated cytotoxicity
  • mediated by IgG and IgM antibodies
  • Abs directed to tissue or cell surface Ags
  • pathologic changes due to complement activation, PMN, and macrophage recruitment and activation
45
Q

types of type II reactions

A
  • transfusion reactions
  • hemolytic anemias
  • hemolytic disease of newborn (erythroblastosis fetalis)
46
Q

erthroblastosis fetalis (Rh incompatibility)

A
  1. Rh- mother carries Rh+ fetus
  2. fetal rbc enter maternal circulation during delivery
  3. mother sensitized to Rh antigen, with activation of Rh-specific B cells (mom makes Rh antibodies now and is immunized to Rh)
  4. during subsequent pregnancies with Rh+ fetuses, maternal IgG anti-Rh antibodies cross placenta
  5. anti Rh- IgG attack Rh+ fetal rbc, leading to hemolysis and anemia

*Rh component is highly immunogenic

47
Q

rhesus prophylaxis

A
  • anti-RhD antibodies are given to the Rh- mother immediately after delivery of Rh+ infants
  • led to decrease in HDNB incidence
  • assumed that prevention of sensitization is due to destruction of fetal red cells in mother
48
Q

classification of immunopathologic processes: type III

A
  • immune complex-mediated
  • IgG or IgM containing immune complexes formed in large quantities, either locally or systematically
  • ICs trigger complement, leading to vascular permeability and PMN recruitment/activation
  • ex: arthus reaction and post-streptococcal glomerulonephritis
49
Q

immune complexes

A

antibodies and antigens binding together to form a lattice structure

50
Q

classification of immunopathologic processes: type IV

A
  • cell-mediated
  • involves Ag-sensitized CD4+ T cells (DTH reactions) or CD8+ T cells (cell-mediated cytolysis)
  • pathology due to release of T cell-derived cytokines, with recruitment/activation of macrophages, or CD8 - mediated cytolysis
  • ex: contact dermatitis and tuberculin reactions
51
Q

steps of contact dermatitis (type IV delayed)

A
  1. antigen (cosmetics, poison ivy, nickel)
  2. formation of complexes with proteins in skin
  3. antigen presenting cell (APC) processing
  4. CD4+ T cell (Th1 phenotype)
  5. cytokine release (IL-2, IFNgamma)
52
Q

contact dermatitis

A
  • usually initiated by small substances that get in contact with the skin and penetrate it
    • once absorbed into the skin, these molecules attach to host proteins acting as haptens, forming hapten-protein complexes, and rendering those self proteins “foreign looking” and thus immunogenic
  • small compounds can cause CD (urushiol in poison ivy/oak, components in cosmetics, metals in jewelry, topical medications like local anesthetic/antiseptic)
53
Q

latex hypersensitivity

A
  • natural rubber latex contains at least 5 allergenic proteins
  • sensitization occurs via contact with skin or mucosa
  • inhalation of rubber proteins bound to powders are important in sensitization
  • repeated exposure is primary risk factor
54
Q

risk of latex hypersensitivity

A
  • risk among latex industry and health care workers who wear natural rubber latex gloves
  • ~1% allergy in general population
  • ~3-9% allergy among health care workers
55
Q

latex hypersensitivity prevention

A
  • vinyl gloves (not as effective against HIV though)
  • cotton or vinyl glove liners under latex gloves
  • gore-tex liners, in combo with unpowdered latex gloves

Microbiology (7 decks)

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