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π“˜π“‚π“‚π“Šπ“ƒπ‘œπ“π‘œπ‘”π“Ž > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

What is hypersensitivity?

A

➝ An inappropriate immune response to non-infectious antigens that results in tissue damage and disese

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2
Q

How many types of hypersensitivity are there?

A

➝ 4

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3
Q

What is type 1 hypersensitivity?

A

➝ Immediate hypersensitivity

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4
Q

What is type 2 hypersensitivity?

A

➝ cytotoxic hypersensitivity

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5
Q

What is type 3 hypersensitivity?

A

➝ serum sickness and Arthus reaction

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6
Q

What is type 4 hypersensitivity?

A

➝ Delayed-type hypersensitivity

➝ contact dermatitis

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7
Q

Describe what happens in type 1 hypersensitivity?

A

➝ Type 1 results to being exposed to allergens in the environment
➝ the host generates an immune response characterised by the production of IgE antibodies
➝ The IgE antibodies become attached to immune cells called mast cells
➝ when someone is exposed to the allergen to which the IgE is specific the IgE is cross-linked and activates the inflammatory cells to release mediators causing inflammation

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8
Q

What type of conditions have type 1 reactions?

A

➝ Allergic rhinitis
➝ asthma
➝ anaphylaxis
➝ eczema

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9
Q

How can you induce immediate hypersensitivity?

A

➝ injecting an allergen onto the skin or by scratching the allergen onto the skin

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10
Q

How does the hypersensitivity reaction occur?

A

➝ If you have mast cells in the tissue that carry specific IgE
➝ the IgE will be cross-linked
➝ the mast cells are activated and release lots of inflammatory mediators that result in leakage of plasma and fluid into the surrounding tissues (wheal)
➝ vasodilation results in the flare response (erythema)

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11
Q

What is systemic anaphylaxis?

A

➝ Exaggerated response to an allergen

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12
Q

What occurs during systemic anaphylaxis?

A

➝ Someone is exposed to an allergen to which they are sensitised and develop a marked reaction to the allergen
➝ vasodilation and release of liquid into the tissue which causes edema

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13
Q

What is type II hypersensitivity caused by?

A

➝ an immune response generated against altered components of human cells

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14
Q

What is an example of type II hypersensitivity?

A

➝ people treated with penicillin
➝ drugs attach to the surface of RBCs
➝the attachment to the red cells is seen as an altered component

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15
Q

Describe how hypersensitivity type II occurs?

A

➝ a platelet or red cell is covered in a drug like penicillin
➝ the immune response recognises them as an allergen and generates an IgG response to that
➝ the red cell to which the drug is attached is coated by IgG
➝ this activates cells containing the IgG receptor causing activation of macrophages and activation of complement resulting in inflammation

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16
Q

What is an example of a type II response where IgG antibodies are directed at cell surface receptors?

A

➝ Myasthenia gravis

➝ Graves

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17
Q

Describe normal TSH function?

A

➝ pituitary releases TSH which acts on the thyroid and causes the release of thyroxine
➝ the levels of thyroxine in the blood cause negative feedback which reduces the TSH

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18
Q

What happens in Graves disease?

A

➝ Immune response is generated against TSH receptors
➝ this causes long term stimulation of the receptors which causes the thyroid to release thyroxine with no negative feedback

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19
Q

What happens in Myasthenia Gravis?

A

➝ There is an immune response directed against the post-synaptic receptors
➝ antibodies block or destroy nicotinic AcH receptors at the neuro-muscular junction
➝ this blocks nerve transmission resulting in paralysis

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20
Q

What type of hypersensitivity is haemolytic disease of the newborn?

A

➝ type II

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21
Q

Describe how haemolytic disease of the newborn occurs?

A

➝ if a rhesus negative mother has a rhesus positive child
➝ they can develop an immune response against the rhesus antigen
➝ during birth Rh+ fetal erythrocytes leak into maternal blood after breakage of the embryonic chorion which normally isolates fetal and maternal blood
➝ maternal B cells are activated by the Rh antigen and produce large amounts of anti-Rh antibodies
➝ during the second exposure (second pregnancy) the Rh antibody titer in the mother’s blood is elevated after first exposure
➝ Rh antibodies are small enough to cross the embryonic chorion and attack the fetal erythrocytes

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22
Q

Describe what happens during type III hypersensitivity?

A

➝ presence of a soluble antigen such as a vaccine (tetanus toxoid)
➝ there is an IgG response to the antigen
➝ because there are large amounts of antibody and antigen at the site of injection, immune complexes form
➝ immune complexes can activate the cells around the capillaries causing an inflammatory response and activating the complement

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23
Q

What is type III hypersensitivity also called?

A

➝ Arthus reaction/serum sickness

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24
Q

What do the immune complexes cause activation of?

A

➝ mast cells

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25
Q

Why does haemorrhage and purpura occur in type III?

A

➝ blood vessel permeability and blood flow are increased

➝ platelets accumulate leading to the occlusion of small blood vessels, haemorrhage and purpura

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26
Q

What is serum sickness caused by?

A

➝ large IV doses of soluble antigens

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27
Q

What happens during serum sickness and how does tissue damage occur?

A

➝ IgG antibodies produced form small immune complexes with the antigen in excess
➝ immune complexes are deposited in the tissues e.g blood vessel walls
➝ tissue damage is caused by complement activation and the subsequent inflammatory response

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28
Q

How is antivenom made?

A

➝ Injecting a horse with venom and collecting the serum

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29
Q

What can injecting people with horse immunoglobulin cause?

A

➝ Serum sickness

➝ nephritis if the immune complexes are deposited in the kidney

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30
Q

How does farmers lung happen?

A

➝ Farmers are exposed to hay
➝ hay has moulds in it which are inhaled
➝ they cause localised inflammation in the lung and immune complex reaction
➝ IgG and antigen gets complexed

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31
Q

What mold is found in sugarcane?

A

➝ actinomycosis

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32
Q

What type of a reaction can inhaling actinomycosis cause?

A

➝ type III reaction

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33
Q

What happens if you inhale actinomycosis?

A

➝ fibrosis, granulation and inflammation

➝ interstitial pneumonitis - non caseating granulomas

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34
Q

What are the resulting 3 diseases caused if antigens are given IV and where do the immune complexes deposit?

A

➝ Vasculitis - immune complexes deposit in the blood vessel walls
➝ Nephritis - immune complexes deposit in the renal glomeruli
➝ Joint spaces -immune complexes deposit in the joint spaces

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35
Q

What disease occurs if antigens are given subcutaneously and where do the immune complexes deposit?

A

➝ Arthus disease

➝ perivascular area

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36
Q

What disease occurs if antigens are inhaled and where do the immune complexes deposit?

A

➝ Farmers lung

➝ alveolar/capillary interface

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37
Q

What are the two forms of type IV hypersensitivity?

A

➝ related to the immune cells that are produced

➝TH1 and TH2

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38
Q

What is TH1 associated with?

A

➝ response to intracellular bacteria

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39
Q

What is TH2 associated with?

A

➝ responses to worm infections

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40
Q

Describe how TH1 type IV delayed hypersensitivity to tuberculin happens?

A

➝ tuberculin stimulates TH1 cells to produce cytokines such as IFN gamma and IL-12 which stimulate macrophages to release cytokines and chemokines which recruit cells to the site of infection
➝ a granuloma is formed (tuberculin granuloma) which takes 2-3 days

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41
Q

What is the mantoux test?

A

➝ Inject an extract of dead tuberculin subcutaneously

➝ wait to see if there is a reaction within 2-3 days

42
Q

Describe how TH2 delayed type hypersensitivity occurs?

A

➝ TH2 cells produce cytokines such as IL-4 and IL-5 which are important in IgE production and eosinophil recruitment
➝ this causes production of basic proteins, enzymes and cytokines

43
Q

What is TH2 mediated hypersensitivity associated with?

A

➝ allergic contact dermatitis

44
Q

What is the tuberculoid response?

A

➝ strong TH1 response to the presence of leprosy bacilli resulting in granuloma and DTH type response

45
Q

How does IgE mediated hypersensitivity happen and what type is this?

A

➝ Ag induces cross-linking of IgE bound to mast cells and basophils with release of vasoactive mediators
➝ Type I

46
Q

How does IgM or IgG mediated hypersensitivity happen and what type is this?

A

➝ Ab directed against cell surface antigens mediates cell destruction via complement activation or ADCC
➝ type II

47
Q

How does Immune complex mediated hypersensitivity happen and what type is this?

A

➝ Ag-Ab complexes deposited in various tissues induce complement activation and an ensuring inflammatory response mediated by massive infiltration of neutrophils
➝ type III

48
Q

How does cell mediated hypersensitivity happen and what type is this?

A

➝ sensitised Th1 cells release cytokiens that activate macrophages or Tc cells that mediate direct cellular damage
➝ Th2 cells and CTLs mediate similar responses
➝ Type IV

49
Q

What are 4 allergens that cause systemic anaphylaxis?

A

➝ drugs
➝ serums
➝ venom
➝ peanuts

50
Q

What are 3 allergens that cause acute urticaria (wheal and flare)?

A

➝ animal hair
➝ insect bites
➝ allergy testing

51
Q

What are 2 allergens that cause allergic rhinitis?

A

➝ pollens

➝ dust mite feces

52
Q

What are 3 allergens that cause asthma?

A

➝ Danders (cat)
➝ pollens
➝ dust mite feces

53
Q

What are 6 allergens that cause food allergy?

A 
➝  peanuts
➝  tree nuts
➝  shellfish
➝  milk
➝  eggs
➝  fish
54
Q

What is IgE used against?

A

➝ worms

55
Q

How is IgE different to IgG?

A

➝ it has one extra domain in the heavy chain compared to IgG

56
Q

What does IgE bind to on mast cells?

A

➝ FcΡR1 receptor

57
Q

What do IgE cells do to mast cells and inflammatory cells?

A

➝ pre-arms them to react in the presence of an antigen

➝ coats inflammatory cells and basophils

58
Q

Describe allergen specific (pollen) IgE production?

A

➝ the first exposure to pollen causes activation of the immune response
➝ APC picks up pollen and takes it to the local lymph nodes where they activate immune cells
➝ they activate TH2 cells
➝ TH2 cells release IL-4 which induces B cells that have the same specificity to allergens to produce IgE
➝ the IgE is released in circulation on mast cells, ready for the next exposure to the allergen

59
Q

What causes allergic sensitisation?

A

➝ Exposure to the allergen including dosage, timing, location of priming
➝ genetic pre disposition

60
Q

How are allergens named?

A

➝ after the source organism and the order they were discovered

61
Q

What happens in high dose vs low dose exposure to an allergen?

A

➝ high dose - tolerance

➝ low dose - sensitisation

62
Q

What is the link between filaggrin and atopic dermatitis?

A

➝ filaggrin granules form a barrier on skin

➝ when it is defective atopic dermatitis is greater

63
Q

What makes a dendritic cell pro-allergic?

A

➝ a protein called TSLP which can switch DC to a pro-allergic state
➝ TSLP : thymic stromal lymphopoietin

64
Q

What do activated mast cells release?

A

➝ releases its granules (histamines and leukotrienes)

65
Q

What are the two phases of an allergic response?

A

➝ Early and late phase

66
Q

What is the early phase mediated by?

A

➝ mast cells

67
Q

What is the late phase mediated by?

A

➝ T cells

68
Q

What happens during the early response?

A

➝ activation of mast cells and release of mediators

69
Q

Describe what happens during primary exposure to an allergen?

A

➝ Sensitisation
➝ dendritic cells present antigens to the T cells
➝ Activated T cells produce IL-13 and IL-4
➝ this causes B cells to release IgE
➝ IgE lines the mast cells

70
Q

What happens during secondary exposure to an allergen?

A

➝ The mast cells release histamine and lipid mediators

➝ T cells recruit eosinophils and other mast cells

71
Q

What happens in an acute allergic reaction?

A

➝ Wheezing
➝ Urticaria
➝ Sneezing, rhinorrhoea
➝ conjunctivitis

72
Q

What happens in a chronic allergic reaction?

A

➝ Further wheezing
➝ sustained blockage of the nose
➝ Eczema

73
Q

What is the function of histamine?

A

➝ Increases vascular permeability

➝ causes smooth muscle contraction

74
Q

What is the function of Leukotrienes?

A

➝ increases vascular permeability
➝ causes smooth muscle contraction
➝ stimulates mucus secretion

75
Q

What is the function of Prostaglandins?

A

➝ Chemoattractants for T cells, eosinophils and basophils

76
Q

What does IL-4 and IL-13 promote?

A

➝ TH2

➝ IgE

77
Q

What does TNF alpha promote?

A

➝ Promotes tissue inflammation

78
Q

What three substances are released during the early phase of an allergic reaction?

A

➝ Histamine
➝ leukotriene
➝ prostaglandins

79
Q

What does mast cell activation and granule release cause in the GI tract?

A

➝ Increased fluid secretion and increased peristalsis

➝ expulsion of GI contents (vomiting & diarrhoea)

80
Q

What does mast cell activation and granule release cause in the airways?

A

➝ Decreased diameter and increased mucus secretion
➝ congestion and blockage of airways (wheezing), coughing and phlegm
➝ swelling and mucus secretion in nasal passages

81
Q

What does mast cell activation and granule release cause in the blood vessels?

A

➝ Increased blood flow, increased permeability
➝ increased fluid in tissues causing increased lymph to lymph nodes, increased cells and proteins in tissues, increased effector response in tissues

82
Q

Where are eosinophils located and where are they recruited to?

A

➝ located in tissues

➝ recruited to sites of allergic reactions

83
Q

What do eosinophils express upon activation?

A

➝ FcΡR1

84
Q

What are the two effector functions of eosinophils?

A

➝Release highly toxic granule proteins and free radicals upon activation to kill microorganisms/parasites and cause tissue damage in allergic reactions
➝Synthesise and release prostaglandins, leukotrienes and cytokines in order to amplify the inflammatory response by activating epithelial cells and recruiting leukocytes

85
Q

What is the late phase of the allergic reaction dependent on?

A

➝ allergen dose

86
Q

What is chronic allergic inflammation caused by?

A

➝ TH2 cells

87
Q

What is asthma?

A

➝ a state of reversible bronchial hyper reactivity resulting from a persistent inflammatory process in response to a number of stimuli in a genetically susceptible individuals

88
Q

What are the two types of asthma?

A

➝ atopic and non-atopic

89
Q

What are the 4 causes of asthma?

A

➝ Occupational
➝ exercise induced
➝ nocturnal asthma
➝ post-bronchiolitic wheeze

90
Q

What are the 3 characteristics of allergic asthma?

A

➝ Episodes of wheezy breathing
➝ narrowing of the airways
➝ rapid changes in airway obstruction

91
Q

What does the acute response to asthma cause and within what timeframe?

A

➝ occurs within seconds of allergen exposure

➝ results in airway obstruction and breathing difficulties

92
Q

What is acute asthma caused by?

A

➝ allergen induced mast cell degranulation in the submucosa of airways

93
Q

What is the chronic response to asthma caused by?

A

➝ activation of eosinophils, neutrophils, T cells and other leukocytes

94
Q

What does the chronic response to asthma cause?

A

➝ Airway remodelling, permanent narrowing of the airways and further tissue damage

95
Q

What are the 6 treatment options for asthma?

A

➝ Inhibit effects of mediators on specific receptors - antihistamines
➝ inhibit mast cell degranulation - mast cell stabilisers
➝ inhibit synthesis of specific mediators - lipoxygenase inhibitors
➝ steroids
➝bronchodilators
➝ immunotherapy

96
Q

What is an example of a lipoxygenase inhibitor?

A

➝ montelukast

97
Q

What is an example of a mast cell stabiliser?

A

➝ chromoglycate

98
Q

What effect do steroids have on asthma?

A

➝ act directly on DNA to increase transcription of anti-inflammatory mediators such as IL-10 and decrease transcription of pro-inflammatory mediators

99
Q

What is a steroid used to treat asthma?

A

➝ prednisolone

100
Q

What is an example of a bronchodilator?

A

➝ Salbutamol

π“˜π“‚π“‚π“Šπ“ƒπ‘œπ“π‘œπ‘”π“Ž (14 decks)

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