14 - Allergy and Hypersensitivity Flashcards

1
Q

What are hypersensitivities?

A

inappropriate immune response to antigens that pose little to no threat

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2
Q

Which antibodies are responsible for Type I hypersensitivities?

A

IgE antibodies

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3
Q

What are allergies initiated by?

A

interaction between an IgE and a multivalent antigen

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4
Q

What are the 6 common allergic reactions?

A

hay fever | asthma | eczema | bee stings | hives | food allergies

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5
Q

What are atopic individuals?

A

people who are susceptible to allergens

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6
Q

What is IgE only supposed to respond to?

A

pathogens specifically parasitic infections

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7
Q

What are 2 properties of allergens?

A

enzymatic protease = break through barriers | PAMPS = trigger activation and immune system

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8
Q

What are allergens?

A

non-parasitic antigens

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9
Q

In Type I hypersensitivity reactions, how do IgE antibodies act?

A

IgE = bound to mast cells | cross-linking Fce receptors on surfaces of innate immune cells (mast cells) = degranulation

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10
Q

What are in the granules of granulocytes?

A

histamine | heparin | proteases | leukotrines | prostaglandins | chemokines

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11
Q

If there is no allergen present during degranulation, what will happen to the contents of the granules?

A

will impact the tissue it is near = cause inflammation

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12
Q

What is the Fc receptor involved in Type I hypersensitivity?

A

FceR

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13
Q

On which cells are FceR only found on?

A

mast cells | eosinophils | basophils

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14
Q

What does histamine cause?

A

contraction of intestinal and bronchial smooth muscles | mucus secretion | increase vasopermeability and vasodilation | mast cell chemotaxis

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15
Q

What do prostaglandins and leukotrienes cause?

A

vascular permeability | mucus secretion | major cause of asthma symptoms

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16
Q

In Type I hypersensitivity, what does IL-5 do?

A

recruits and activates eosinophils

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17
Q

In Type I hypersensitivity, what does TNFa do?

A

contribute to shock in systemic anaphylaxis

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18
Q

What is CXCL-8?

A

chemotactic factor

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19
Q

In Type I hypersensitivity, what does IL-13 do?

A

helps with mucus secretion, goblet cells, hyperplasia

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20
Q

In Type I hypersensitivity, what does GM-CSF do?

A

helps with production of granulocytes

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21
Q

What is the early response during a Type I hypersensitivity reaction?

A

mast cells induce vasodilation | bronchoconstriction and goblet cells produce mucus = hard to breathe

22
Q

What is the late response during a Type I hypersensitivity?

A

more cells and inflammation to surrounding tissue | chemokine and cytokine production | eosinophil recruit neutrophils and induce degranulation

23
Q

What are the 3 categories of Type I hypersensitivity reactions?

A

systemic anaphylaxis | localized hypersensitivity reactions | food allergies

24
Q

What are 2 symptoms of systemic anaphylaxis? What is the treatment?

A

drop in BP = leads to shock | smooth muscles contract = bronchoconstriction | Tx = epinephrine

25
Q

What is the basis or cause for Type I hypersensitivity?

A

environmental factors | hygiene hypothesis | genetic factors

26
Q

What is the main idea of the hygiene hypothesis?

A

using Th2 cells at a younger age would help the body balance the Th1 response with Th2

27
Q

How can genetics cause Type I hypersensitivity?

A

increased IgE production and more of a Th2 response

28
Q

Which Th subsets counteract Th2 responses?

A

Treg and Th1

29
Q

What are the 2 diagnostic methods used for Type I hypersensitivity reactions?

A

skin test | allergen-specific IgE levels in serum

30
Q

What are 2 treatments for Type I hypersensitivity?

A

antagonists for the granule contents (anti-histamines, etc) | desensitization immunotherapy

31
Q

What is desensitization immunotherapy?

A

induce Th1 and Treg responses

32
Q

What is Type II sensitivity involved with?

A

complement activation (mostly) | ADCC = antibody-dependent cell cytotoxicity and NK cell-mediated

33
Q

What causes Type II sensitivity reactions?

A

blood incompatibilities such as transfusion reactions, autoimmune hemolytic anemia, HDN

34
Q

What are blood group antigens made out of?

A

carbohydrates

35
Q

How are antibodies involved with blood typing and how can this result in a Type II hypersensitivity reaction?

A

adults have antibodies against the blood group antigen they DON’T have

36
Q

Which is the universal blood group donor?

A

O

37
Q

Which is the universal blood group acceptor?

A

AB

38
Q

What is the hemolytic disease of a newborn (HDN)?

A

when mom is Rh- but baby is Rh+ = mom’s Abs will attack baby’s Rh+ RBCs | 2nd pregnancy = kills fetus

39
Q

What is the treatment for HDN?

A

UV lights = breaks down bilirubin

40
Q

What is a preventive measure for HDN?

A

rhogam shot = IgG abs against Rh-factor

41
Q

What is responsible for Type III hypersensitivity?

A

immune complexes = Ag/Ab complexes | complexes usually get cleared after a while if no autoimmune disease or drug inducing it to stay

42
Q

What does Type III hypersensitivity cause?

A

complement activation = inflammation and recruitment of neutrophils

43
Q

What are 3 key symptoms of Type III hypersensitivity?

A

joint pain due to complex deposits | proteinuria (protein in urine) | hematuria (blood in urine) due to complexes stuck on kidneys

44
Q

What can induce Type III hypersensitivity reactions?

A

autoimmune diseases | drug reactions | infectious diseases

45
Q

What is responsible for Type IV hypersensitivity reactions?

A

cell-mediated, initiated by T-cells, Th1 cells involved

46
Q

What is Type IV sensitivity also called?

A

delayed type hypersensitivity = needs time for the reaction to develop about 1-2 weeks

47
Q

What is Type IV hypersensitivity characterized by?

A

recruitment of macrophages at the inflammation site

48
Q

What is the most common example of Type IV hypersensitivity?

A

poison ivy contact dermatitis

49
Q

Why are macrophages important for Type IV hypersensitivity reactions?

A

macrophages = responsible for the inflammation

50
Q

What is the early phase of Type IV hypersensitivity reactions?

A

sensitization phase = initiation of reaction involves sensitization by antigen = trigger T-cell (Th) response

51
Q

What is the late phase of Type IV hypersensitivity reactions?

A

second exposure of antigen = induction of Th1 inflammatory cytokines = activate macrophages = granuloma formation