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Year 1: Respiratory > Respiratory Immunology Hypersensitivity > Flashcards

Respiratory Immunology Hypersensitivity Flashcards

1
Q

Gel and Coomb’s classification

A

Type I: immediate hypersensitivity (allergy)
Type II: direct cell killing (antibody mediated)
Type III: Immune Complex mediated
Type IV: Delayed hypersensitivity

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2
Q

define allergy

A

IgE mediated antibody response to external antigen (allergen).

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3
Q

urticarial (hives)

A

sign of an allergic reaction

skin rash with raised, red itchy bumps that may burn or sting

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4
Q

angioedema

A

sign of an allergic reaction
rapid swelling of dermis, subcutaneous tissue, mucosa, and submucosal tissues. Very similar to urticarial, but urticarial occurs in the upper dermis, and angioedema in the dermis
angioedema is self-limiting, non-pitting oedema, not itchy unless associated with urticaria

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5
Q

which T cell is involved mainly in the allergic response? Which cytokines does it produce?

A

Th2 cells
They produce IL-4, IL-5, IL-10 (anti-inflammatory), and IL-13
These instruct activated B cells to use epsilon heavy chains to secrete IgE

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6
Q

what are some examples of adverse reactions that are NOT allergies?

A

Ones that are not IgE mediated!
e.g.
coeliac disease, lactose intolerance, bacterial food poisoning caffeine, irritable bowel syndrome, eating disorders

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7
Q

clinical features of Type I allergic disease

A
  • occurs quickly after exposure to allergen (minutes to 1/2 hours)
  • responses are stereotyped
  • may be associated with more than one organ system
  • urticarial, angioedema, asthma, allergic rhinitis and conjunctivitis, anaphylaxis
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8
Q

role of B lymphocytes, T lymphocytes and mast cells in allergic disease?

A

B lymphocytes: recognise antigen, produce antigen-specific IgE
T lymphocytes: help B lymphocytes to make IgE
Mast cells: inflammatory cells that release vasoactive substances

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9
Q

role of mast cells in allergic reactions?

A
  • express receptors for Fc region of IgE
  • on encounter with allergen, B cells produce antigen-specific IgE
  • allergen is cleared
  • residual IgE binds to circulating mast cells via Fc receptors
  • upon SECONDARY exposure: allergen binds to IgE coated mast cells and disrupts cell membrane
  • release of vasoactive mediators (histamine, tryptase)
  • increased cytokines and leukotriene transcription
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10
Q

Intrinsic asthma is IgE mediated. True/ False?

A

False.
Intrinsic asthma is “non-allergic” asthma - so it is NOT IgE mediated.
EXTRINSIC asthma is IgE mediated and is allergic disease

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11
Q

What happens clinically when an allergic reaction occurs in the lung? (First: release of histamine and other inflammatory mediators…)

A
  • muscle spasm (causes bronchoconstriction, this manifests as a wheeze)
  • mucosal inflammation (causes mucosal oedema and increases secretions, manifests as sputum production)
  • inflammatory cell infiltrate (infiltration of lymphocytes and eosinophils into bronchioles - making sputum yellow. Infiltration is associated with chronicity).
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12
Q

apart from being mediated by IgE, what else can cause mast cell degranulation?

A
  • drugs: morphine, opiates, aspirin and non-steroidal anti-inflammatories
  • thyroid disease
  • idiopathic
  • physical urticarial (urticarial in response to heat/ pressure)
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13
Q

aspirin-induced asthma

A

This affects 20% asthmatics

wheeze 0.5-3 hours after ingestion

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14
Q

Non-steroidal anti-inflammatories (NSAIDs)

A

this is a drug class that groups together drugs that provide analgesia (pain-killing) and antipyretic effects, and, in higher doses, anti-inflammatory effects

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15
Q

Samter’s triad

A

This is aspirin-exacerbated respiratory disease, which is a condition consisting of:
-asthma
-recurrent sinus disease with nasal polyps
-sensitivity to aspirin and other NSAIDs
Samter’s triad may require diet modification

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16
Q

What is the investigation that can be done to find evidence of mast cell degranulation during anaphylactic episode?

A

measure the serum mast cell tryptase levels (tryptase is a marker for mast cell activation as its levels only rise in anaphylaxis, and not in local reactions)

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17
Q

skin prick test

A

a few drops of purified allergen are gently pricked onto the skin
a positive response is a local wheal and flare response
(Drugs can influence the response! The person should discontinue anti-histamines at least 48 hours before test)
This test is cheap, quick
BUT: requires experience for interpretation, and may (rarely) induce anaphylaxis

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18
Q

What’s a specific IgE test (RAST test - radioallergosorbent test)

A

amount of IgE in serum against a specific allergen is measured
Sensitivity of this test is about 70% compared to skin prick test

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19
Q

How useful is measuring total IgE when investigating allergic disease?

A
  • not useful in the diagnosis / investigation usually
  • other things (vasculitis, lymphoma, drugs) can cause elevated IgE
  • also, significant allergic disease can occur in absence of elevated IgE
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20
Q

management of type I hypersensitivity?

A
  • allergen avoidance
  • block mast cell activation
  • prevent effects of mast cell activation
  • anti-inflammatory agents
  • management of anaphylaxis
  • immunotherapy
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21
Q

what can be used to block mast cell activation?

A
  • sodium cromoglicate (mast cell stabiliser)

- It has poor oral absorption, can be used as a topical spray when allergen exposure is predicted

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22
Q

what can prevent the effects of mast cell activation?

A

-anti-histamines
-These are H1 receptor antagonists and are the main treatment of allergic disease
They block bronchoconstriction, bronchial smooth muscle contraction, vasodilation, and block the promotion of visceral hypersensitivity involved in itch perception
ALSO: leukotriene receptor antagonists
These block effects of leukotrienes which are synthesised by mast cells after activation. e.g, montelukast
They block the early and late phase

23
Q

what anti-inflammatory agents can be used to treat allergic disease?

A

-corticosteroids

They inhibit formation of many different inflammatory mediators

24
Q

what does an epi-pen do and what’s it for?

A

it’s a self-injectable adrenaline syringe, to use in anaphylaxis
It acts on B2 receptors to constrict arterial smooth muscle- increasing BP and therefore limiting vascular leakage, dilating bronchial smooth muscle- and so decreasing airflow obstruction

25
Q

what is immunotherapy?

A

In a controlled manner: exposing more and more of the allergen the patient to train their immune system to not overreact. This induces regulator T cells (which produce IL-0 - an anti-inflammatory cytokine).

26
Q

Type II hypersensitivity

A

Direct cell killing
Antibody binds to cell-surface antigen, resulting in activation of complement (leading to cell lysis/ opsonisation), and opsonisation (leading to antibody-mediated phagocytosis)
IgG and IgM are important here: they are good at activating complement - their conformational change allows them to activate C1

27
Q

What happened if elimination of self-reactive B cells is not working, and a type II response is initiated?

A

Complement will be activated, and there is no pathogen: so tissue damage will occur

28
Q

Which components of complement are known as “anaphylotoxins”?

A

C3a and C5a fragments
They are released after activation, and increase permeability of blood vessels - increasing traffic of cells to sites of infections
(They can also act indirectly to induce the same effects by activating mast cells (resulting in mast cell degranulation and release of histamine, tryptase, leukotrienes, and other pro-inflammatory mediators)

29
Q

In type II hypersensitivity, how is there regulation of the process of complement activation?

A

Fragments of complement can dissolve the immune complexes which triggered them: switching off the process of complement activation

30
Q

what time after antigen exposure does type II hypersensitivity occur?

A

12-18 hours

31
Q

What is ADCC (antibody dependent cellular cytotoxicity)

A

a mechanism of cell-mediated immune defence whereby an effector cell of the immune system actively lyses a target cell, whose membrane-surface antigens have been bound by specific antibodies

32
Q

examples of type II hypersensitivity conditions?

A
  • Blood cells (transfusion reactions, autoimmune haemolytic anaemia, idiopathic thrombocytopaenia purpura)
  • kidney: Goodpasture’s syndrome (Ig binds to glomerular basement membrane)
  • Nervous system: myasthenia gravis (antibodies bind to acetylcholine receptor), Guillain Barre syndrome (antibodies bind to peripheral nerve glycoprotein)
  • endocrine system: Graves’ disease (antibodies bind to TSH receptor)
  • Skin: pemphigus vulgaris (antibodies bind to epithelial cell cement)
33
Q

Transfusion reactions

A

This is an example of Type II hypersensitivity
Depends on ABO group and Rhesus antigens on donor and recipient
If not a match: there is complement mediated lysis followed by haemolysis of transfused RBCs

34
Q

Immediate Haemolytic transfusion reaction

A

This may begin after just 1ml blood if transfused:
-overwhelming systemic inflammatory response (pyrexia, rigors, tachycardia, tachpnoea, hypotension, dizziness, headaches, chest/ lumbar pain, may be fatal)

35
Q

Graves’ Disease

A 
Antibodies bind to TSH receptor
Leading cause of hyperthyroidism - an example of an autoimmune disease
Abnormal antibodies (autoantibodies) are released by the body, and these mimic TSH. These false signals spur the thyroid hormone production
36
Q

Many type II hypersensitivity diseases are associated with autoimmune diseases. True/ False?

A

True.
Type II diseases which are also autoimmune diseases are: autoimmune haemolytic anaemia, idiopathic thrombocytopaenia purpura, goodpasture’s syndrome, myasthenia gravis, guillan barre syndrome, graves’ disease, pemphigus vulgaris

37
Q

Name some type II hypersensitivity disease which are NOT autoimmune

A
  • transfusion reactions

- haemolytic disease of the newborn

38
Q

how can it be proved that many type II hypersensitivity diseases are mediated by autoantibodies?

A

Show that serum causes disease when transferred into another host
e.g. myasthenia gravis, idiopathic thrombocytopaenia purpura, and rhesus disease can be transferred

39
Q

management of type II hypersensitivity?

A
  • plasmapheresis (patient blood plasma removed, replaced by plasma from someone else - fresh frozen plasma - or from pooled immunoglobulin)
  • immunosuppression (rebound Ig production limits efficacy of plasmapheresis, so usually given immunosuppressive agent to switch off B cell production of Ig)
40
Q

type III hypersensitivity

A

there are antibodies to soluble antigens. In the presence of excess antigen, Ig binds, forming small immune complexes. These immune complexes are trapped in small blood vessels, joints and glomeruli.
The immune complexes are deposited in the wall of a blood vessel. The presence of immune complexes activates complement and attracts inflammatory cells e.g. neutrophils. Enzymes are released from neutrophils and these cause damage to endothelial cells of the basement membrane

41
Q

examples of local type III hypersensitivity conditions

A
  • farmer’s lung (inhaled fungal particles from hay are deposited in lung, stimulate Ig formation, Ig forms immune complexes with antigen, resulting in complement activation, inflammation, recruitment of other leukocytes)
  • bird fancier’s lung (avian serum proteins)
  • malt worker’s lung (mouldy maltings: aspergillus clavatus)
  • cheese worker’s lung (mouldy cheese: aspergillus clavatus, penicillum casei)
  • maple bark stripper’s lung (bark from stored maple: cryptostroma corticale)
42
Q

clinical features of a type III hypersensitivity reaction

A
  • wheezing and malaise 4-8 hours after exposure
  • may have dry cough, pyrexia, breathlessness
  • examination is often normal
43
Q

Which type of hypersensitivity is ACUTE hypersensitivity pneumonitis (AKA acute extrinsic allergic alveolitis mediated by?

A

Type III

EAA can come in subacute and chronic forms too: but these are different!

44
Q

examples of type III hypersensitivity conditions?

A
  • Systemic lupus erythematosus (SLE): As tissues undergo normal lifecycle and die - contents of the nuclei are released into ECF and immune system starts to recognise it as non-self. This is an autoimmune driven process. Ig produced against contents of nuclei, forms immune complexes which are deposited in small vessels in skin, joints, kidneys, resulting is complement activation, inflammation, recruitment of other cells. There is a characteristic butterfly pattern in 30% lupus patients.
  • Systemic small vessel vasculitis: fever, renal impairment, vasculitic skin rash, arthralgias (due to immune complex deposition in joints, in glomeruli - renal dysfunction, in skin - causing vasculitic purpura
45
Q

tests to diagnose Type III hypersensitivity?

A
  • test for presence of specific IgG that are reactive to a putative antigen (e.g. anti-DNA Ig - indicating SLE, or Ig reactive to aspergillus - indicating Farmer’s Lung
  • test complement
46
Q

management of type III hypesensitivity?

A
  • antigen avoidance
  • use corticosteroids to decrease inflammation
  • use immunosuppression drugs to decrease Ig production
47
Q

Which respiratory disease can be treated with corticosteroids?

A
  • obstructive lung diseases (COPD, asthma)
  • restrictive lung diseases (sarcoid, pulmonary fibrosis)
  • infective lung diseases (if evidence of severe inflammation)
  • cancer (some types)
48
Q

Which respiratory disease CANNOT be treated with corticosteroids?

A
  • sleep apnoea

- uncomplicated infection

49
Q

type IV hypersensitivity

A

delayed hypersensitivity
T-cell mediated hypersensitivity
First, there is initial sensitisation to antigen: generating “primed” effector Th1 cells and memory cells
Then, subsequent exposure: activation of previously primed T cells, recruitment of macrophages, other lymphocytes, neutrophils, release of proteolytic enzymes, persistent inflammation

50
Q

examples of type IV hypersensitivity?

A
  • Autoimmune: type 1 diabetes, psoriasis, rheumatoid arthritis
  • Non-autoimmune: nickel hypersensitivity, TB, leprosy, sarcoidosis, cellular rejection of solid organ transplant
51
Q

What type of hypersensitivity reaction does poison ivy cause?

A

Chemical antigens in leaves initiate activation, proliferation and differentiation of antigen-specific T cells, leading to production of effector TH1 cells and memory T cells
There is no skin reaction on first encounter
Subsequent encounter after this initial sensitization step results in the activation of skin-resident TH1 cells that initiate an inflammatory response, resulting in dermatitis (rash) on the affected area
In delayed type IV hypersensitivity reactions, secondary presentation of the initiating antigen by APCs to these TH1 cells results in secretion of cytokines that stimulate inflammation and activate macrophages and other leukocytes, leading to tissue damage.
In some type IV diseases, CD8+ effector cells (CTLs) are also involved, directly kill antigen positive host cells.

52
Q

Sarcoidosis
What is it?
What type of hypersensitivity reaction is it?

A

Type IV hypersensitivity
It’s a multisystem granulomatous disease of unknown aetiology
Characterised by presence of granulomas
Underlying pathophysiology is type IV delayed hypersensitivity response to unknown antigen
Can affect any part of body, but 90% cases involve the lungs
(Granuloma = an organised collection of activated macrophages and lymphocytes. A non-specific inflammatory response is triggered by diverse antigenic agents or by inert foreign materials, resulting in activation of T lymphocytes and macrophages, failure to remove stimulus ends up in persistent production of activated cytokines, end result is an organised collection of persistently activated cells

53
Q

Name some disease characterised by type IV hypersensitivity and granuloma formation

A
  • sarcoidosis
  • TB
  • leprosy (some forms)
  • Berylliosis, Silicosis, and other dust diseases
  • chronic stage of hypersensitivity pneumonitis (EAA)
54
Q

management of sarcoid

A
  • wait: many patients undergo spontaneous remission
  • NSAIDs: for acute onset of the disease
  • systemic corticosteroids: for blocking T cell activation, and blocking macrophage activation

Year 1: Respiratory (25 decks)

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