FPP Block 1 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

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1
Q

What is hypersensitivity?

A

A harmful immunologic reaction developing in response to an otherwise harmless specific trigger

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2
Q

List the 4 types of hypersensitivity

A
  1. Type I- Immediate _Al_lergy: IgE mediated
  2. Type II- Direct antiBody mediated cytolytic
  3. Type III- Immune Complex mediated
  4. Type IV- Delayed type T cell mediated
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3
Q

What is the sensitization stage of hypersensitivity?

A
  1. Sensitization Stage
    1. development of the immune response
    2. symptoms silent
    3. requires adaptive immunity: antigen specific T and or B cell responses
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4
Q

What is the effector stage of hypersensitivity?

A
  • elicitation of the secondary immuen response
  • symptoms evident
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5
Q

What cells mediate Type I hypersensitivity and describe generally how this works?

A
  • Mast cells/basophils mediate the initial phase of anaphylaxis
    • Mast=tissue resident, basophils=tissue resident and ciruclating
  • IgE crosslinked by antigen trigger mast cell/basophil degranulation which causes the response
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6
Q

Describe the sensitization phase of Type I hypersensitivity

A
  1. first exposure: antigen binds to cognate B cell receptors on a naive B cell
  2. Antigen is processed by APCs (can be B cell) and presented to the cognate CD4 T cell
  3. the naive CD4 T helper cell matures into a Th2 antigen specific cell
  4. Th2 produces cytokines supporting B cell class switching to IgE
  5. B cells and plasma cells produce IgE
  6. Circulating IgE binds long term onto FCeRI on mast cells and basophils
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7
Q

Describe the Effector phase of Type I hypersensitivity reaction

A
  • second exposure: antigen crosslinks anti-IgE that is already bound to FCeRI on mast cells and basophils
  • this triggers rapid extracellular release of preformed mediators (degranulation)
  • symptoms of anaphylaxis develop immediately, and hours later delayed symptoms occur
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8
Q

What are the preformed mediators of a type I hypersensitivity reaction?

A
  • histamine and tryptase which can lead to vascular dilation, smooth muscle contraction and tissue damage
  • released within seconds to minutes
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9
Q

What are the rapidly produced mediators in a type I reaction and what do they lead to?

A
  • lipid mediators
    • Prostaglandins (PGD2)-vascular dilation
    • leukotrienes-smooth muscle contraction
    • Platelet activating factor (PAF)
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10
Q

What are the slowly produced mediators in a type I reaction?

A
  • cytokines! (hours to days)
    • inflammation (leukocyte recruitment)
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11
Q

What is the significance of the early and ate phase of a Type I hypersensitivity reaction?

A
  • the preformed mediators lead to symptoms right away, but some mediators are formed within minutes to days (PGD2, leukotrienes, cytokines) and therefore you can react again to the same stimulus hours later. therefore it is important to goto a hospital for observation after anaphylaxis
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12
Q

What are the physiologic changes associated with anaphylaxis?

A
  • leaky/ dilated blood vessels
    • angioedema, low BP, shock
  • Smooth muscle spasm
    • bronchospasm, GI/GU spasm, coronary spasm
  • Cardiac effects:
    • myocardial depression
    • tachy/bradycardia
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13
Q

What is histamine?

A
  • a preformed mediator of a type I reaction
  • short half-life in serum (minutes)
  • H1R
    • itching, increased vascular permeability: edema
    • smooth muscel contraction: bronchospams, cramping
  • H2R
    • gastric acid secretion
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14
Q

WHat is tryptase?

A
  • preformed mediator in type I hypersensitivity reaction
  • only in mast cells not basophils
  • immature: constituitively released (protryptase)
  • mature: only released during degranulation (b-tryptase)
  • found in serum only up to 4 hours after release, therefore it is the single best clinical marker of mast cell activation (bc histamine is too short lived)
  • leads to emodleing of tisse matrix
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15
Q

Describe the structure of an eosinophil

A

Crystalloid granule

matrix

core

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16
Q

what are the chemokines that are rapidly synthesized?

A

MIP-1a (CCL3) and RANTES (CCL5) and Eoataxin (CCL11)

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17
Q

WHat are the lipid mediators that are rapidly synthesized?

A

Leukotrienes and Platelet activating factor PAF

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18
Q

What are the major mediators from eosinophils in type I hypersensitivity reactions?

A
  • Lysophospholipase
  • Major basic protein: mast cell activation
  • Eosinophilic cationic protein (ECP) (like MBP)
  • EDN (Eosinophil derived neurotoxin)
  • Platelet activating factor (PAF)
    • bronchoconstriction, activates platelets
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19
Q

What is the role of IL-5? What are some treatments for type I hypersensitivity reactions related to eosinophilia?

A
  • survival/ production of eosinophils!
  • it is produced by Th2 CD4 lymphocytes
    • when you hve IL-5 it can cause hypereosinophili syndrome
  • Anti-IL5 monoclonal antibodies and receptors
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20
Q

What is the therapeutic importance of corticosteroids in type I hypersensititivy reactions?

A
  • corticosteroids inhibit the production of IL-5
    • decrease release from marow and cause rapid apoptosis
    • steroids make eosinophils disapear!!
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21
Q

What are 3 type I hypersensitivity diseases?

A
  1. Allergic Rhinitis
    1. typical allergies, inhaled
  2. Drug, Food, Venom Allergies
    1. anaphylaxis or hives usually from ingestion not air
  3. Asthma
    1. cough, wheezing, shortness of breath, chest tightness
    2. inhaled aeroallergens
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22
Q

What are some Type I hypersensitivity reactions that are related to disorders of mast cells?

A
  • Utricaria/Angioedema (hives and swelling)
    • contact: dog licked hand
    • chronic: autoimmune
  • Mastocytosis (increases MC burden)
    • spontaneous anaphylaxis, osteoporosis, chronis diarrhea
    • KIT gene mutation leading to uncontrolled KIT activation thus mast cell proliferation
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23
Q

List the 3 tests to confirm sensitization

A
  • Prick/Scratch
    • first line test for confirmation of sensitization
    • balances sensitivity.specificity
  • Intradermal testing
    • 1000x more sensitive than prick/scratch, never used for food
  • Serum IgE ELISA
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24
Q

What is the clinical management for allergic rhinitis?

A
  1. avoidance
  2. suppression of mediators
    1. nasal steroid
    2. oral antihistamines
    3. ophthalmis antihistamine/mast cell inhibitors
    4. nasal antihistamines
    5. nasal mast cell inhibitors
  3. Immunotherapy
    1. SCIT (subQ allergy shots): result in production of IgG4 which outsompetes binding of allergen to IgE
    2. SLIT (sublingual allergy drops)
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25
Asthma is thought to be what type of hypersensitivity reaction? What is its prevalence, symptoms and mechanism?
Type I hypersensitivity Rxn * prevalence: 5% of ppl * Symptoms * NP cough * wheezing * SOB * chest tightness * Mechanism: * ***_Reversible airway obstruction_*** * ​smooth muscle bronchospasm increased mucus production and airway plugging/swelling. increased resistance hard to get air OUT of the lungs. * Sometimes due to IgE mediated inflammation
26
What are the pathologic airway changes associated with asthma?
* Edema * Mucus * Epithelial damage * airway smooth muscle * inflammatory cell infiltration
27
Basic treatment of asthma
* **Trigger avoidance** * viral infections, airborne irritants/pollutants, aeroallergens, cold/dry hot air * Corticosteroids * i**nhled corticosteroids**, oral IV steroids for exacerbations * Bronchodilators * short acting beta agonists (SABA)-albuterol (relax smooth muscle) * Note: antihistamines ineffectual
28
Second line treatment of asthma
* Anti-leukotrienes * **Montelukast** * Biologics * **Omalizumab** * Immunotherapy * **SCIT** * Bronchodilators * **Long acting beta agonists (LABA-only given with inhaled steroids too)**
29
WHat is Type II hypersensitivity?
* antiBody (IgM or IgG) binds cell or matric bound antigen leading to * future immunologic attack and or functional interference (inhibition or activation)
30
In type II hypersensitivity how does the antibody trigger pathology
1. complement activation 2. antibody dependent cellular cytotoxicity (ADCC) 3. phagocytosis (opsonization) 4. antibody alteration of normal function
31
What are the 4 types of Type II hypersensitivity?
1. complement 2. ADCC 3. opsonization 4. Anti-receptor
32
WHat are 6 diseases that are representative of Type II hypersensitivity?
1. Goodpasture 2. Bullous pephgold 3. Pernicious anemia 4. Vasculltides 5. Thombic phenomena 6. Actue rhuematic fever
33
What are the features and antibody specificity of goodpasture syndrome
* Features * nephritis and lung hemmorrhages * AB Specificity * Type IV collagen in basement membranes of glomeruli and lung alveoli
34
What are the features and specificity of Bullous pephigoid?
features: skin vesicles AB specificityL epidermal basement memebrane proteins
35
What are the features and specificity of pernicious anemia
features: megaloblastic anemia Ab specificity: intrinsic factor and gastric parietal cells
36
What are the features and specificity of vascultides
features: varied AB specificity: neutrophil cytoplasmic antibodies
37
What are the features and specificity of thrombotic phenomena
features: varied AB specificity: antiphosphoslipid antibodies
38
What are the features and specificity of acute rheumatic fever
features: carditis AB specificity: antibodies against streptococcal antigens cross-react with heart
39
What is an example of an ADCC representative type II hypersensitivity reaction?
Drug induced hemolytic anemia/thrombocytopenia * medicines become antigenic when bound to RBCs or platelets * IgG may target the combined drug-cell atigen ( called hapten formation) * Ab tagged blood cells/platelelets are targeted destruction (ADCC) in the spleen \*\*\*blood typing problems
40
Describe what happens when a B- person receives A- blood
* Anti-A IgM circulates in type B blood patients * Anti-A IgM binds to transfused blood's A antigen * complement activation, phagocytosis, and ADCC follows
41
What is fetal Rh incompatibility?
* Rh negative mother becomes sensitized to Rh factor during delivery of 1st child * mother develops IgG agains fetal Rh antigen * during next pregnancy * maternal anti-Rh IgG crosses the placenta, tagging fetal RBCs * feta RBC destruction leads to hydrops/stillbirth from severe anemia * treat mother with anti-Rh D antibody to prevent
42
What is type III hypersensitivity?
Immune Complex mediated * IgG targeted against a SOLUBLE foreign antigen can form large polymeric immune complexes ( linked antigen-antibody) (the big net) * immune complex formation and clearance by mononuclear phagocyte sytem is normal and uaually doesn't trigger pathology but in certan circustances can trigger self-injury
43
What is the zone of equivalence?
* immune complex formation is promoted in a range where the ratio of antigen to antibody is closer to 1:1 * this is necessary for type III hypersensitivity reaction to occur! (immune complex mediated)
44
How does an immune complex trigger injury in a type III hypersensitivity reaction?
1. actiavting FcyR expressing phagocytic cells ( the complex activates these phagocytes that cause damage) 2. activating complement at sites of deposition ( it deposits randomly)
45
Where do immune complexes deposit in type IIIhypersensitivity reactions?
* preferential sites (kidneys, vessels, joints, and skin) * increased vascular permeability * hemodynamic features support deposition ( bifurcations or pressure gradients...basically they get stuck where it makes sense for them to clog) * sites of high antigen concentration
46
WHat is serum sickness?
* type III hypersensitivity reaction * systemic reaction classically following large quantities of foreign protein * antivenom from horse, antithymocyte globin (ATG), streptokinase ("clot buster"), post infectious antigens * flu-like symptoms with rash, arthritis, and glomerulonephritis * onset 7-10 days after initial exposure time: IgM to IgG class switch
47
What is arthus reaction?
* a skin rxn when sensitized individuals are re-exposed to specific antigen * hemorrhage/edema develops within 4-10 hours * commong after vaccination (antigen) in pts recently vaccinated ( with high IgG titiers already) * edema, induration, hemorrhage, necrosis of skin
48
what are some sources of "foreign" antigen in type III hypersensitivity reactions
1. Exogenous 1. **Infectious agents** 2. **Drugs or chemicals** 2. Endogenous 1. immunoglobins, tumor anitgens, nuclear antigens
49
Why would someone with SLE (lupus) develop disease in joints, and skin?
* places they can deposit/ get lodged! * favorable locations for immune complex deposition *
50
Would it be helpful to removeantibodies during a lupus crisis? Why or why not?
Yes possibly bc in order to make the immune complex you need to have a 1:1 ratio of antigen to antibody. if you remove antibody you mess up the ratio and move away from the zone of equivalence. this may stop immune complex formation
51
WHat is a type IV hypersensitivity reaction?
* "cell mediated" delayed * Involves **T cells** not antibody * Antigen binds to self creating a haptenated self-protein which is processed by antigen presenting cells to T cells * T cells then proliferate and secrete mediators
52
What mediators do T cellse secrete during Type IV hypersensitivity reactions and what does that cause?
* IFNg * induces expression of adhesion molecules and activates **macrophages** * **TNFa** and lymphotoxin * local tissue destruction, induces expression of adhesion molecules * IL-3 and GM-CSF * Chemokines * recruit **macrophages** to site
53
What is an example of a type IV hypersensitivity reaction?
Allergic contact dermatitis * caused by reactive chemical sensitizer exposure * hapten binds to self protein **(haptenization)** creating a foreign protein presented by APC and recognized by TCRs * this trigger extensive macrophage mediated inflammation
54
Give a very common example of allergic contact dermatitis and a few others..... Also what type of hypersensitivity reaction is this?
* ***_Poison ivy rash_***- nearly universal sensitizer * other commons: * formaldehyde, methacrylates, nickel, gold, cobalt, fragrances, preservatives, rubber accelerators
55
How do you confirm allergic contact dermatitis and what improves it
* confirmed by patch testing * **slow** to test positive (24-72 hours) * adhesive pathces impregnated with sensitizer applied to skin and interpreted 2-3 days and 1 week later * induration/erythema interpreted by clinician * improved by topical corticosteroids
56
What is the tuberculin test?
type IV hypersensitivity intradermal diagnostic testing * PPD injected intradermally with a fine needle * a good screening test of prior sensitization to TB
57
Describe type IV hypersensitivity reactions and what they activate
* antigen is processed by tissue macrophages and stimulates Th1 cell * Chemokines * IFNy * TNFa TNFb * IL-3/GM-CSF: stimulate monocyte production by bone marrow stem cells
58
Type I reaction Reactor antigen effector echanism exaples
* Reactor : IgE * antigen: soluble * effector mechanism: mast cell activation * examples allergic rhinitis, asthma, anaphylaxis
59
Type II Reactor antigen effector echanism exaples
* Reactor: IgG or IgM * antigen: cell or matric associated * effector mechamism: FcR+ cells (phagocytes and NK) * examples: Penicilin induced thrombocytopenia
60
Type III ## Footnote Reactor antigen effector mechanism examples
* Reactor: IgG antigen: soluble (large quantities 1:1) effector mechanism: FcR+ cells, complement examples: serum sickness, arthus reaction
61
Type IV: Th1 ## Footnote Reactor antigen effector mechanism examples
Reactor: Th1 cells antigen: soluble effector mechanism: macrophage activation examples: contact dermatitis, tuberculin reaction
62
Type IV CD8 CTL ## Footnote Reactor antigen effector mechanism examples
Reactor: CD8 CTL antigen: Cell associated effector mechanism: cytotoxicity examples: contact dermatitis
63
autoimmunity
* reactivity to self antigens * lupus, rheumatoid arthritis, thyroiditis, MS
64
Allergy
* reactivity to harmless foreign antigens * food/drug/venom/allergic rhinitis
65
Anergy
* ignorance or failure to clear harmful self/foreign antigens * cancer, HIV, TB
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