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Heart, Lungs and Blood > Allergy and Hypersensitivity > Flashcards

Allergy and Hypersensitivity Flashcards

1
Q

what is hypersensitivity

A

immune disorder caused by an inappropriate response to antigens that are not necessarily pathogens.

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2
Q

how are the 4 classes of hypersensitivity differentiated

A
  • differ by the immune molecules and cells which cause them
  • by the way they induce damage
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3
Q

what is allgery

A

a damaging immune response by the body to a substance (allergen) to which it has become hypersensitive.

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4
Q

what does allergy trigger

A

unnecessary increases in vascular permeability and inflammation that lead to tissue damage with little benefit.

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5
Q

what are local allergic responses

A

the symptoms are restricted to the site where the antigen interacts with the body

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6
Q

what kind of response is anaphylaxis

A

system wide

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7
Q

when does anaphylaxis occur

A

if the same antigens are more widely disseminated

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8
Q

can Anaphylactic shock can be fatal

A

yes

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9
Q

what is a description of type I hypersensitivity

A

allergy and atopy/ immediate hypersensitivity

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10
Q

what is an overview of the mechanism of type I hypersensitivity

A

IgE driven, involves degranulation of mast cells and basophils

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11
Q

what are clinical examples of type I hypersensitivity

A

asthma
hay fever
anaphylaxis

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12
Q

what is a description of type II hypersensitivity

A

antibody mediated

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13
Q

what is the overall mechanism for type II hypersensitivity

A

IgG driven, involved the complement system and cytotoxic cells

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14
Q

what are clinical examples of type II hypersensitivity

A

blood transfusion reactions
hemolytic anemia

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15
Q

what is a description of type III hypersensitivity

A

immune complex-mediated

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16
Q

what is the overall mechanism for type III hypersensitivity

A

antigen-antibody complexes complement system, neutrophils/inflammation

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17
Q

what are clinical examples of type III hypersensitivity

A

rheumatoid arthritis
systemic lupus

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18
Q

what is a description of type IV hypersensitivity

A

cell-mediated delayed-type hypersensitivity

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19
Q

what is an overall mechanism of type IV hypersensitivity

A

sensitised t cells, cytokines, activated machrophages

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20
Q

what are clincial examples of type IV hypersensitivity

A

contact dermatitis

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21
Q

what is atopy

A

predisposition to an immune response against diverse antigens and allergens leading overproduction of immunoglobulin E (IgE).

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22
Q

what can atopy lead to

A

an increased likelihood of developing a hypersensitivityreaction.

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23
Q

what is an allergen

A

An allergen is a type of antigen that produces an abnormally vigorous immune response in which the immune system fights off a perceived threat that would otherwise be harmless to the body

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24
Q

How do IgE antibodies recognise an antigen

A
  • via their variable region.
    • IgE antibodies bind to one of two types of Fc receptors (FcR) via their constant regions.
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25
Q

what immune cells express the FcεRI receptor and what does it do

A

Mast cells, basophils, and eosinophils
main mediators of allergy symptoms

26
Q

what does the cross-linking of FcεRI receptors by allergen/IgE complexes initiate

A

signalling cascades that resemble those initiated by antigen receptors

27
Q

what does the signalling cascade initiated by the cross-linking of FcεRI receptors result in

A

mast cell/basophil degranulation with the release of inflammatory mediators.

28
Q

what is mediated by IgE antibodies

A

Allergy is a type I hypersensitivity reaction that is mediated by IgE antibodies.

29
Q

when do individuals without allergies generally produce IgE antibodies

A

in response to parasitic infections

30
Q

for the cross-linking of FcεRI, what Is a requirement of the allergen

A

The allergen needs to be multivalent (have multiple epitopes) in order to cause cross-linking

31
Q

what happens during the first exposure of an allergen in type I hypersensitivity

A

triggers a standard immune response with the production of IgE.

32
Q

what happens during re-exposure of an allergen in type I hypersensitivity

A

triggers mast cell degranulation with the associated inflammatory responses.

33
Q

what is degranulation

A

a cellular process that releases antimicrobial cytotoxic or other molecules from secretory vesicles called granules found inside some cells

34
Q

what happens when vasoactive amines are released

A

vascular dilation
smooth muscle contraction

35
Q

what happens when proteases are released

A

tissue damage

36
Q

what happens when lipid mediators act on prostaglandins

A

vascular dilation

37
Q

what happens when leukotrienes are secreted

A

smooth muscle contraction

38
Q

what happens when cytokines are released

A

inflammation

39
Q

what are the 3 things that can get released through IgE binding in type I hypersensitivity

A

granule exocytosis
- vasoactive amines
-proteases
lipid mediators secretion
-prostaglandins
-leukotrienes
cytokine secretion

40
Q

what is the initial contraction of the bronchial and tracheal smooth muscle mediated by

A

histamines

41
Q

when is histamines released in the initial contraction of bronchial and tracheal smooth muscle

A

minutes of release as a result of mast cell degranulation

42
Q

what happens when histamines bind to the H1 receptor

A

induces increased vascular permeability and mucous secretion

43
Q

what do phospholipase released by degranulation initiate

A

enzymatic breakdown of phospholipids in the plasma membrane leading eventually to the release of leukotrienes and prostaglandins

44
Q

what do cytokines released by mast cells do

A

increase the expression of adhesion molecules on endothelial cells, and this facilitates the influx of neutrophils, eosinophils and helper T cells

45
Q

what does type II hypersensitivity reactions involve

A

antibody-mediated destruction of cells by antibody classes other than IgE (IgG or IgM).

46
Q

what are the 3 mechanisms of type II hypersensitivity

A
  • Activation of the complement cascade.
  • Antibody-dependent cell-mediated cytotoxicity (ADCC).
  • Antibody bound to the target cell attracts and activates phagocytic cells that kill by the process known as opsonization.
47
Q

how does type II hypersensitivity transfusion reactions manifest

A

antigens on transfused blood cells generate antibodies in people with a different blood group lacking those antigens resulting in intravascular haemolysis

48
Q

how does type II hypersensitivity haemolytic disease of the newborn manifest

A

maternal IgG specific for fetal Rhesus (Rh) antigens cross the placenta and destroy fetal red blood cells if mother is Rh- and father is Rh+

49
Q

how does type II hypersensitivity malaria manifest

A

red blood cells pick up antigens from the parasite and antibodies trigger haemolysis

50
Q

how does type II hypersensitivity drug-induced haemolytic anaemia manifest

A

red blood cells that have bound drug molecules trigger antibody responses

51
Q

what do uncleared immune complexes induce

A

degranulation of mast cells and inflammation triggered by complement activation and attraction and activation of neutrophils at the site of the immune complex.

52
Q

where can immune complexes be deposited

A

in tissues and capillary beds where they induce more innate immune activity, blood vessel inflammation (vasculitis) and tissue damage.

53
Q

what can deposition of immune complexes in the kidney lead to

A

glomerulonephritis, and in the joints to arthritis.

54
Q

what does type IV hypersensitivity response require

A

It requires T cells to be sensitized to antigen (Sensitization phase), and subsequent re-exposure results in cytokine production, inflammation and recruitment of macrophages (Effector phase).

55
Q

what happens in the sensitisation stage of type IV hypersensitivity

A

nitial contact with antigen presented by an antigen presenting cell triggers the activation, clonal expansion and differentiation of T helper cells bearing appropriately shaped T cell receptors.

56
Q

what happens during the effector phase of type IV hypersensitivity

A
  • On re-exposure to antigen, the sensitized T cell produces a variety of cytokines and chemokines.
  • These in turn attract and activate macrophages and other non-specific inflammatory cells.
  • Activated macrophages are very good antigen presenting cells, so this perpetuates the immune response.
57
Q

what are red flag symptoms

A

Red flags are signs and symptoms found in the patient history and clinical evaluation that may tie a disorder to a serious pathology, and therefore require further investigation.

58
Q

what is the antigen form of type I hypersensitivity

A

soluble antigen

59
Q

what is the antigen form of type II hypersensitivity

A

cell bound antigen

60
Q

what is the antigen form of type III hypersensitivity

A

soluble antigen

61
Q

what is the antigen form of type IV hypersensitivity

A

soluble or cell bound antigen

Heart, Lungs and Blood (51 decks)

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