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Clinical Pathology - > CP10 - Allergy > Flashcards

CP10 - Allergy Flashcards

1
Q

what is allergy/hypersensitivity?

A

undesirable, damaging, discomfort producing and sometimes fatal reactions produced by the normal immune system directed against innocuous antigens in a pre-sensitised host.

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2
Q

what does atopic mean?

A

allergic

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3
Q

what does innocuous mean?

A

not harmful

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4
Q

which types of hypersensitivity are most commonly observed in a clinical context?

A

types I and IV

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5
Q

which types of hypersensitivity are mediated by antibodies?

A

I, II, III

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6
Q

which types of hypersensitivity are cell mediated?

A

IV

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7
Q

what is the immunopathology of type I hypersensitivity?

A
  1. processed by APC
  2. presented to T cells
  3. t cell activation to form Th1,2,17 or Treg (in allergies, thought to only activate the
  4. the cells generate IL4
  5. IL4 stimulates B cells to produce IgE
  6. IgE binds to the allergen
  7. next time, IgE is already in the system bound to the receptors on sensitised mast cells
  8. binding of allergen to IgE causes cross linking
  9. sends the signal to mast cells to release mediators eg. histamine
  10. 2,d stage is regulated by the arachidonic acid pathway which produces leukotrienes and prostaglandins (late phase)
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8
Q

what are the clinical features oh type I hypersensitivity?

A

fast onset - 15-30 mins

called wheal and flare, but short lived

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9
Q

what is the immunopathogenesis of type II hypersensitivity?

A

IgG/IgM response against self or foreign antigen that has adhered to the cell surface (solid medium) , leading to complement activation and phagocytosis or ADCC (antibody dependent cell-mediated cytotoxicity)

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10
Q

what are the clinical features of type II hypersensitivity?

A

slightly delayed onset - minutes to hours. causes cell lysis and necrosis

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11
Q

which antigen commonly causes type II hypersensitivity?

A

penecillin

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12
Q

which diseases are associated with type II hypersensitivity?

A
  1. Erythroblastosis fetalis - difference in Rh between mum and fetes sensitises her in the first pregnancy and in the second pregnancy, if there is a difference too, her body will react
  2. Goodpasture’s nephritis
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13
Q

what is the immunopathogenesis of type III hypersensitivity?

A

IgG/IgM against soluble antigen, not bound to cell leads to formation of immune complexes, which are unable to pass into small blood vessels, causing vasculitis and cell damage in that area

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14
Q

what are the clinical features of type III hypersensitivity?

A

delayed onset of 3-8 hours, causes vasculitis

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15
Q

what are the common triggers of type III hypersensitivity?

A

serum sickness, when they injected horse serum as protection from tetanus

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16
Q

which autoimmune condition is associated with type III hypersensitivity?

A

Systemic Lupus Erythematosus (SLE)

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17
Q

what is the immunopathophysiology of type IV hypersensitivity reactions?

A

no antibodies involved. APC presents antigen to T cells which develop defences against the antigen and learn to recognise it in later stages

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18
Q

what are the clinical features of a type IV hypersensitivity reaction?

A

delayed response, 48-72h

erythema induration

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19
Q

which antigens can trigger a type IV hypersensitivity reaction?

A

metals eg. nickel, causing a tuberculin reaction

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20
Q

which condition is associated with type IV hypersensitivity?

A

contact dermatitis - reaction caused due to patch testing carried out by dermatologists

21
Q

how does genetics affect allergies?

A
  1. at the level of sensing allergens
  2. poor barriers (SPINK5 for eczema)
  3. immune response
  4. tissue response
22
Q

are allergies genetic or environmental disorders?

A

multifactorial, genetics only increases susceptibility

23
Q

which organs respond to allergens?

A
  1. eye - allergic conjunctivitis
  2. nose - allergic rhinitis
  3. mouth - oral allergy syndrome
  4. airways - allergic asthma
  5. skin - atopic dermatitis
  6. GI tract - food allergy
24
Q

what was the initial function of IgE in our body?

A

to fight parasitic infections

25
Q

why does our body exhibit severe symptoms when faced with a parasitic infection?

A

D&V to quickly get rid of an organism that would have otherwise been difficult to remove from the body

26
Q

what is thought to increase the prevalence of allergies?

A

less infectious drive

27
Q

how does parasitic disease impact blood?

A
  1. eosinophilia
  2. mastocytosis - abnormal increase of mast cells in multiple organs
  3. basophil infiltration
  4. tissue inflammation
  5. secretion of IL4, IL5, IL13, by CD4 t cells
28
Q

what is the hygiene hypothesis?

A

stimulation of the immune system by microbes is protective. competition between allergens and infectious agent and the absence of infectious agents is thought to make allergies more predominant

29
Q

which types of t helper cells manage which conditions?

A

th1 - infections

th2 - allergies

30
Q

what is immunoregulation?

A

a method by which the body controls the response of the immunee system and prevents it from doing too much damage

31
Q

what are allergens?

A

antigens that initiate an IgE mediated response. the first encounter leads to sensitisation rather than an actual response

32
Q

what is the role of the th2 cell?

A
  1. releases multiple cytokines which activate other cells
  2. activates innatee cells eg. macrophages via cytokines
  3. supports b cells to produce IgE
33
Q

what is the atopic triad?

A

a triad of 3 commonly seen conditions -

  1. asthma - type I
  2. Rhinitis - type I
  3. Eczema - type IV
34
Q

what happens in asthma and rhinitis?

A

allergens cause irritation in the mast cells within the nasal mucosa and airway epithelium

35
Q

what are the 2 types of rhinitis?

A
  1. allergic
    i. perennial
    ii. seasonal
    depending on the occurrence of allergens
  2. non-allergic
36
Q

what is the clinical presentation of allergic rhinitis?

A

blocked nose
runny nose
often eye symptoms

37
Q

what are the triggers of allergic rhinitis?

A

house dust mites
animal danders
pollens

38
Q

how is allergic rhinitis treated?

A

antihistamines

nasal steroids

39
Q

what is the clinical presentation of asthma?

A

bronchoconstriction of airways due to hyper-reactive response to allergic stimuli

40
Q

what are the triggers to asthma?

A

similar to allergic rhinitis, but house dust mite is key

41
Q

what is the clinical presentation of dermatitis?

A

intense itching, blistering, cracking of skin

clue is in the history

42
Q

why does the itching cause a vicious cycle in dermatitis?

A

development of th2 cells stimulates the release of IL31 (t cell derived itch-mediator), which makes one want to scratch, causing barrier disruption

43
Q

what are the types of dermatitis?

A
  1. atopic - idiopathic, commonly eczema
  2. contact
    a. allergic - type IV
    b. non-allergic - irritant
44
Q

what is anaphylaxis?

A

acute potentially life threatening, IgE mediated systemic hypersensitivity reaction. it is a multi systemic syndrome, with an immediate onset.

45
Q

how is allergy diagnosed in clinics?

A
  1. history - important to gauge time relation between exposure and onset of symptoms
  2. specific IgE levels measuring >0.35 signifies allergy, but patient may be tolerant to substances with a higher IgE count too
  3. skin prick tests
  4. intradermal tests
  5. oral challenge test
  6. basophil activation test
46
Q

what happens in an intradermal test?

A

going deeper into the skin. high sensitivity, low specificity

47
Q

what is an oral challenge test?

A

gold standard, if skin prick and intradermal are inconclusive. give increasing concentrations of the substance to patients and check for a reaction

48
Q

what are the advantages of a specific IgE test?

A

safe

49
Q

what are the advantages of a skin prick test?

A

quick

satisfies the patient

Clinical Pathology - (15 decks)

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