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PH2113 Disease & Drugs 1 > U3 L2 Hypersensitivity I > Flashcards

U3 L2 Hypersensitivity I Flashcards

1
Q

What is the definition of hypersensitivity?

A

a set of undesirable reactions (exaggerated response) produced by the normal immune system in response to an antigen

causes tissue damage

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2
Q

What is hypersensitivity mediated by?

A

adaptive immune system - cannot be manifested upon the very first contact with an antigen

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3
Q

What is the common term for type I hypersensitivity?

A

immediate

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4
Q

What antibody mediates type I hypersensitivity?

A

IgE monomers

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5
Q

What are examples of type I hypersensitivity?

A

atopy, anaphylaxis (extreme end) (allergies)

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6
Q

What is another term for Type II hypersensitivity?

What antibodies mediate type II?

A

Cytotoxic

IgG/IgM monomers

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7
Q

What is another term for Type III hypersensitivity?

What antibodies mediate type III?

A

Immune Complex

IgG/IgM complexes

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8
Q

What is another term for Type IV hypersensitivity?

What cells mediate Type IV?

A

Delayed

T-cells

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9
Q

How long can the first exposure to an antigen have occurred before hypersensitivity reactions happen?

How?

A

Over 10 years previously

immunologic memory sensitisation

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10
Q

Why do hypersensitivity reactions have to involve a protein?

A

humoral adaptive system involved in hypersensitivity is acted upon by T cells which cause class switching
T cells only respond to proteins and peptides

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11
Q

What is the role of the protein (or peptide) during hypersensitivity reactions?

A
  • protein itself is target perceived as foreign or
  • protein serves as carrier molecule for hapten molecules which are covalently bound to its surface
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12
Q

What is a hapten?

A

a small molecule that is not immunogenic by itself, but can trigger an immune response when combined with a larger carrier molecule

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13
Q

How do IgE antibodies mediate allergies? (type 1 hypersensitivity)

A

sensitised individuals have pre-formed IgE reacting against the antigen

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14
Q

What is the role of mast cells (or less commonly basophils) during allergic reactions?

A
  • Fc receptors on mast cell surface bind IgE antibodies
  • IgEs sit on mast cell surface and undertake surveillance
  • specific antigen will bind to IgE and cause IgEs to crosslink
  • causes mast cell to degranulate, release its contents, driving inflammatory response
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15
Q

Why are IgE antibodies synthesised?

A

Because the body is having a reaction against an allergen/antigen

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16
Q

What do mast cells release immediately during degranulation?

A

Histamine

preformed cytokines

bioactive lipids

pro-inflammatory bradykinin

proteases e.g. tryptase

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17
Q

What are some examples of early-phase inflammatory mediators that are synthesised and released by mast cells?

How long after degranulation are they released?

A

bioactive lipids e.g. leukotrienes e.g. LTB4, LTC4
prostaglandins

Released minutes after degranulation

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18
Q

What is the time frame in terms of exposure and consequent degranulation from the mast cell and the presence of symptoms of an allergic reaction?

A

can occur within seconds to minutes of an exposure

(from irritating to fatal)

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19
Q

Why does tendency for individuals to have an IgE-mediated response to antigens vary?

A

‘atopic’ individuals e.g. those with allergic rhinitis, atopic eczema have inherited predisposition to display IgE responses

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20
Q

What does ‘atopic’ mean?

A

refers to the genetic tendency to develop allergic diseases (sometimes a family history)

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21
Q

What is the value for the half life of serum IgE?

A

2 days

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22
Q

What is the value for the half life of serum IgG?

A

21 days

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23
Q

What is the process of having an allergic reaction?

A
  1. sensitisation (see immunology recap for reminder of initial exposure and adaptive immunity)
  2. elicitation (re-exposure)
  3. immediate release of preformed mediators
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24
Q

What is an example of a marker used when analysing serum to confirm allergic reaction?

A

tryptase

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25
Q

What are some examples of late-phase inflammatory mediators synthesised and released by mast cells?

How long after initial degranulation are they released?

A

Pro-inflammatory cytokines e.g. TNF, IL-3,-4,-5,-10,-13
Leukotrienes and prostaglandins

Released 6+ hours after initial degranulation

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26
Q

What will happen at the tissue site after degranulation and release of further inflammatory mediators?

A
  • smooth muscle contraction, vasodilation and leaking of plasma water and plasma proteins
  • Increased GI motility, mucus secretion and sensory nerve activation
  • chemotaxis of immune cells e.g. granulocytes, lymphocytes
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27
Q

What are the consequent symptoms of the immune activity at the site of inflammation?

A

smooth muscle contraction e.g. of lungs causes bronchoconstriction

vascular leak - swelling

Increased GI motility - nausea

Increased mucus secretion - impact breathing, congestion

sensory nerve activation - pain, rash, itchiness

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28
Q

What is a major consequence of widespread mast cell degranulation?

How would treatment for such consequence look during anaphylaxis?

A

High levels of vascular leakage, causes drop in blood pressure

saline drip to maintain blood flow, pressure

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29
Q

What is urticaria?

A

itchy, raised rash (hives)

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30
Q

what are the common symptoms of allergic reactions?

A
  1. allergic rhinitis - sneezing and itchy, runny or blocked nose
  2. allergic conjunctivitis - itchy, red, watery eyes
  3. allergic asthma - wheezing, chest tightness, shortness of breath, cough
  4. urticaria or hives - raised itchy rash
  5. angiodema - swollen lips, tongue, eyes, face
  6. general issues - abdominal pain, nausea, vomiting, diarrhoea, dry/red cracked skin
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31
Q

what do allergic conditions often reflect?

A

where the antigen and mast cells are coming into contact

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32
Q

What are some allergens causing allergic rhinitis and asthma?

A

mould
house dust mites
cleaning products
animals (all inhaled)

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33
Q

What are some common allergens in relation to skin reactions?

A
  • chemicals
  • light
  • metals
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34
Q

What are common symptoms of anaphylaxis?

A

throat and mouth swelling, swallowing difficulties
vomiting
drop in BP, breathing difficulties
confusion, loss of consciousness
rashes

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35
Q

atopic dermatitis AKA

A

atopic eczema

36
Q

What are the symptoms of atopic dermatitis?

Who is it most common in and in what stage of life does it most commonly develop?

A
  • skin is itchy, dry, cracked
  • presents as small vesicles on red plaques which will ooze when scratched

Most common type in children, often before first birthday

37
Q

What are the symptoms of urticaria?

A

very itchy, raised red rash
swollen rash resembling nettle stings

38
Q

Which mediators of inflammation are mostly responsible for angioedema?

A

histamine and bradykinin

39
Q

What is one mechanism by which vasoactive bradykinin is broken down?

What sorts of medicines are therefore considered a main cause of angioedoema?

A

ACE

ACE inhibitors prevent breakdown of bradykinin,

40
Q

What happens during Stage 1 anaphylaxis?

Is it always present?

A

Mild - symptoms like skin rash, itching, hives

Missing in some cases

41
Q

What happens during Stage 2 anaphylaxis?

Is it always present?

A

Moderate - widespread and extensive symptoms
- spreading rash, hives
- mild swelling of lips, tongue

Missing in some cases

42
Q

What happens during Stage 3 anaphylaxis?

A

Severe - anaphylactic shock
- signs of difficulty breathing
- extensive swelling
- dizziness, weak pulse

43
Q

What happens during Stage 4 anaphylaxis?

A

Life-threatening
- loss of consciousness
- inability to breathe
- inadequate blood flow to vital organs

44
Q

What are some common triggers of anaphylaxis?

A

foods e.g. nuts, fish, dairy, eggs

medicines - greater risk with IV route
- antibiotics e.g. penicillin
- NSAIDs
- general anaesthetics
- N-acetyl cysteine (paracetamol overdose)

wasps and bee stings

45
Q

When do anaphylaxis symptoms start after allergen exposure?

A

5-30 minutes after

46
Q

what is biphasic anaphylaxis?

how common is this?

A

initial reaction that is not so severe
second wave reaction - could be hours or 2-3 days after

occurs in 20% of patients

47
Q

what is idiopathic anaphylaxis?

A

anaphylaxis with no known trigger

48
Q

How does penicillin cause mast cell degranulation?

A

causes cross-linking of IgE antibodies

49
Q

How do other agents cause mast cell degranulation?

what are the examples of this?

A

act directly on membrane, destabilises mast cell (non-IgE mechanism)
e.g. codeine, morphine

C3a and C5a can act on mast cell receptors in response to anaphylatoxins and cause degranulation

50
Q

what is the name for the reactions causing anaphylaxis that do not start with IgE cross-linking?

A

anaphylactoid reactions

51
Q

What are some ways of managing anaphylaxis outside of hospital?

A
  1. adrenaline auto-injector (epipen)
  2. call 999 even if feeling better
  3. remove any triggers if possible e.g. stingers
  4. lie flat (unless breathing difficulties - sit up)
    - if unconscious lie patient flat on side
  5. inject again after 5-15 minutes if no improvement of symptoms and is available
52
Q

How is anaphylaxis treated within medical care facilities?

A
  • IV adrenaline
  • IV fluids
  • IV medication e.g. strengthen heart function and respiratory function
  • Oxygen
  • IV steroids e.g. methylprednisolone and anti-histamines
53
Q

What are three types of autoinjectors?

A
  1. EpiPen
  2. Jext
  3. Emerade
54
Q

What percent of people will show reactions to intradermal injection of common environmental allergens?

A

> 30%

55
Q

What percent of people actually have symptomatic allergic diseases?

A

15-20%

56
Q

How is atopy tested for?

A

allergen is introduced to the skin - intradermal
leads to mast cell degranulation

57
Q

what will a positive atopy test look like?

A

wheal-and-flare response - raised, red and itchy

lasts up to 30 min post injection

58
Q

What % of children are atopic where both parents are non-allergic?

A

10%

59
Q

What % of children are atopic where 1 parent has allergy history?

A

30%

60
Q

What % of children are atopic where both parents have allergy history (any allergy)?

A

50%

61
Q

other than genetics, what factors can contribute towards atopy?

A

environmental factors

62
Q

What factors could be contributing to the increased prevalence of allergic disease e.g. asthma in the last 20 years?

A
  1. altered barrier function - increased exposure to allergens
  2. sensitisation - greater allergen levels in homes ie. increase in house dust mite populations
  3. hygiene hypothesis
63
Q

What could be causing altered barrier function in people?

What could the effect of this be?

A

due to pollutants

could be altering mucosal permeabilities

64
Q

What is the hygiene hypothesis?

A

reduced contact with infectious agents decreases Th1 activity and results in increased Th2 activity, hallmark of allergic disorders

65
Q

What % of people that believe they are penicillin allergic are TRULY allergic?

What is the percentage prevalence to penicillin allergy?

A

10-20% ; many people have intolerances e.g. GI upset but not allergic

<1%

66
Q

What is the most common cause of both general and fatal anaphylactic reactions?

What is the estimated %?

A

penicillin - 75%

67
Q

What are the antigenic determinants (allergens) for penicillin allergy?

A

degradation products of penicillin

beta lactam ring opens up; allows covalent linkage between penicilloyl metabolite (acts as hapten) and one of own host proteins (acts as carrier) - will cause degranulation upon binding to IgE

68
Q

What sorts of drugs have similar antigenic determinants?

What does this mean for patients with a penicillin allergy?

A

Cephalosporins

increased chance of suffering allergic reaction to cephalosporin antibiotics

69
Q

What are the most common symptoms of allergy to penicillin?

A
  • rash
  • urticaria
  • diarrhoea
  • nausea
70
Q

What are the infrequent symptoms of allergy to penicillin?

A
  • fever
  • atopic dermatitis
  • erythema
  • angioedema
71
Q

What interventions may be used to manage allergies to penicillin?

A
  • discontinuation of the drug
  • treatment of acute symptoms if needed
72
Q

what sorts of antibiotics could be offered to someone who is penicillin allergic?

A

macrolides e.g. clarithromycin

73
Q

what sorts of drugs could be used to treat some of the acute symptoms of penicillin allergy?

A
  • epipen
  • antihistamines
  • mast cell stabilisers
  • leukotriene receptor antagonists
  • corticosteroids
74
Q

What are desensitising vaccines?

What are they used for?

A

Typically low dose of an allergen given weekly to monthly over 2-3 years

to induce tolerance to allergen

75
Q

What is an example of a desensitising vaccine?

A
  1. Pharmelgen - bee and wasp venom
  2. Pollinex - grass pollen
76
Q

What other sort of immunotherapy is also available for grass pollen?

A

sublingual

77
Q

For people with known allergies e.g. to a foreign insect, what short term approach can be taken to induce some form of tolerance?

A

injection of insect venom; multiple low dose administrations at greater frequency over a few months

78
Q

What is Palforzia, available in UK and EU?

how is it given?

A

oral powder immunotherapy; peanut powder
only approved food-based hyposensitisation therapy

  • mixed with semi-solid foods e.g. yoghurt
  • for 4-17 year olds only
  • powder taken daily over months, years
79
Q

Hyposensitisation therapies are contra-indicated with what?

Why?

A
  1. beta-adrenergic blockers
  2. ACE inhibitors

because these meds can mask AND mimic the symptoms of anaphylaxis e.g. masking of increased HR
OR Can cause bronchoconstriction not related to allergen

Also reduce threshold by which mast cells degranulate

80
Q

What is the general mechanism of action of hyposensitisation methods?

A

inducing populations of Tregulator T cells

81
Q

What is the role of Tregulators in relation to allergies?

A

suppress allergen-specific IgE, suppress effector Th1, Th2, Th17 responses

therefore increasing IgG

82
Q

What is the role of Th17 cells?

A

pro-inflammatory, defence against extracellular pathogens

83
Q

What is the role of Th1 cells?

A
  • pro-inflammatory
  • surveillance of cancer cells
  • stimulate humoral response and B cell production of IgM and IgG
84
Q

What is the role of Th2 cells?

A

inflammatory but have more of an anti-inflammatory profile than Th1, 17

stimulate humoral immune responses, induce antibody class switching, specifically IgE class switching

85
Q

How does class switching of IgE to IgG impact allergic responses/lead to hyposensitisation?

A

IgG can inhibit IgE-mediated mast cell activation by competing with IgE for allergen binding

therefore reduces cross-linking of IgE receptors and mast cell degranulation

  • reduces immediate allergic reactions
  • contributes to long-term immune tolerance

PH2113 Disease & Drugs 1 (5 decks)

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