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Year 1 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

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1
Q

What is an allergy?

A

IgE mediated antibody response to external antigen (allergen)

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2
Q

What are the clinical features of Type 1 allergic disease?

A
  • quick after exposure to antigen (minutes-hours)
  • site of contact related to
    site of presentation
  • More than one organ system
  • threshold influenced by other things (alcohol, excersise, infection)
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3
Q

Which vasoactive substance to mast cells synthesize on demand?

A

Leukotrienes
Prostaglandin
Cytokines: TNF & IL4

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4
Q

Why is there no allergic reaction the first time host exposed to allergen/antigen?

A

Because the allergen-specific IgE antibody is synthesized by B cells the first time.
Allergen is cleared before IgE binds to mast cells..

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5
Q

What is the role of mast cells in allergic reaction?

A

Body has previously been exposed to allergen and B cells have synthesize allergen-specific IgE antibodies…
Antigen binding to IgE COATED MAST CELLS stimulates:
Release of preformed vasoactive mediators
Increased transcription of leukotrienes and cytokines (IL4 & TNFa)

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6
Q

How does IgE bind to mast cells?

A

Via Fc receptors (bottom of Y bit)

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7
Q

What are the two types of asthma?

A

Intrinsic: “non-allergic” non IgE mediated
Extrinsic: IgE mediated, external allergen

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8
Q

Pathophysiology of asthma?

A

Mast cell degranulation results in

  • Muscle spasm: broncoconstriction: wheeze
  • Mucosal inflammation: mucosal oedema: sputum production
  • Inflammatory cell (eosinophils & lymphocytes) infiltrates bronchioles: yellow sputum
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9
Q

What are some manifestations of allergic reactions?

A

Urticaria (wheals)
Angioedema (swelling of subcutaneous tissue)
Diarrhoea, vomiting
Anaphylaxis

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10
Q

What is anaphylaxis?

A

characterized by low blood pressure - type of hypovolemic shock
SOB, itchy rash, swollen tongue

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11
Q

What else (other than IgE) causes spontaneous mast cell degranulation?

A

Drugs (morphine, aspirin) - can induce asthma
Thyroid disease
Physical urticaria due to pressure or heat

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12
Q

How can you test for allergic disease?

A
  • Skin prick
  • Measure amount of IgE primed against allergen
  • Supervised exposure to antigen
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13
Q

TRUE/FALSE

Skin testing is the “gold standard” to support a diagnosis of allergy

A

TRUE

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14
Q

What is skin prick test?

A

Expose patient to standardised solution of allergen extract through a skin prick to the forearm
Positive reaction = Local wheal and flare response

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15
Q

TRUE/FALSE

Corticosteroids do influence skin prick tests

A

FALSE

they do not

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16
Q

TRUE/FALSE

Antihistamines do not influence skin prick tests

A

FALSE

they do, should be discontinued 48hrs before testing

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17
Q

What are the pros of skin prick testing?

A

Cheap
Quick (15 minutes)
Unrivalled sensitivity for the majority of allergens, particularly aeroallergens
Patient can see the result

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18
Q

What are the cons of skin prick testing?

A

Requires experience for interpretation

Very rarely may induce anaphylaxis (1:3000)

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19
Q

TRUE/FALSE

Measuring total IgE is useful for diagnosing/investigating allergic disease

A

FALSE

There are many causes of raising total IgE e.g. vasculitis, drugs etc.

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20
Q

When should specific IgE tests be used (RAST)?

A

Skin test not available

75% specificity /sensitivity comp skin prick

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21
Q

What is the investigation used during acute anaphylactic episode?

A

Serum tryptase levels (tryptase product mast cell granules)

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22
Q

TRUE/FALSE

Rise in tryptase level only occurs in anaphylaxis, and not in local reactions

A

TRUE

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23
Q

Treatment anaphylaxis?

Study These Flashcards
A

Adrenalin constrict arterial smooth muscle

dilates bronchial smooth muscle

24
Q

Management IgE allergic disorders?

Study These Flashcards
A 
Trigger (history!) avoid allergen
Block mast cell activation
prevent effects mast cell activation
Anti-inflammatory agents
Manage anaphylaxis
Immunottherapy
25
What is sodium cromoglycate?
Mast cell stabilizer, blocks mast cell activation
26
What are some drugs that block effects of mast cell activation?
Histamine receptor antagonist | Leukotriene receptor antagonist
27
TRUE/FALSE | Histamine receptor antagonists are used prophylactically and to control symptoms
TRUE
28
Step up treatment maximall y=
corticosteroids
29
Immunotherapy allergic disease?
Controlled exposure to increasing amounts of allergen Subcutaneous injection of tiny amounts of allergen Followed by gradual increase in dose RISK IS ANAPHYLAXIS
30
Pathophysiology of Type II Hypersensitivity?
Antibody binds to CELL SURFACE antigen IgG and IgM :Activation complement via classical pathway (cell lysis and release opsonins) IgG: Summon NK cells
31
What do fragments of C3a and C5a do after activation of complement system?
Increase permeability of blood vessels - anaphylotoxins
32
What are the effects of antibody binding to cell membrane protein?
- complement activation and osmotic lysis of cell via Massive Attack Complex - NK and eosinophil activation - Antibody acts as opsonin - complement acts as opsonin2 - Phagocytosis of antigen +ve cells
33
What are transfusion reactions?
``` Antibodies binds to cells of transfused RBCs. Complement mediated lysis -pyrexia/rigors -tachycardia/pnoea -hypotension FATAL ```
34
TRUE FALSE | Immediate Haemolytic Transfusion Reaction begins after at least 50mls of blood is transfused
FALSE! May begin after only 1 ml blood is transfused Overwhelming systemic inflammatory response
35
What is Grave's disease?
Antibodies bind to thyroid stimulating hormone RECEPTOR -> HYPERthyroidism Popping eyes
36
TRUE/FALSE | Many type II hypersensitivity diseases are associated with Autoimmune disease
TRUE
37
TRUE/FALSE | Only mothers with mild or overt symptoms of autoimmune disease may pass on autoantibodies to neonatt
FALSE | mothers may have no symptoms
38
How can Type II Hypersensitivity be managed?
Plasmapheresis | Immunosuppression to switch off B cell production
39
What is plasmapheresis?
removal of pathogenic antibody, remove patient plasma and replace with someone else's
40
Major disadvantage of plasmapheresis?
Rebound antibody production
41
What is the pathophysiology of Type 3 hypersensitivity reactions?
Antibody SOLUBLE in antigens due to EXCESS antigens Forms small immune complexes which trapped in small blood vessels/joints/glomeruli This activates complement and attracts neutrophils - damage endothelial cells and basement membranes
42
TRUE/FALSE | Cheese worker's lung due to mouldy cheese is a genuine Type III hypersensitivity
TRUE Malt - mouldy maltings Farmer's lung - mouldy hay Bird Fancier's lung - avian excreta, feathers Lung - accumulation and inflammation WITHIN alveoli
43
TRUE/FALSE | Acute hypersensitivity pneumonitis and chronic hypersensitivity pneumonitis have the same pathophysiology
FALSE Acute is a Type III hypersensitivity Chronic causes fibrosis
44
What are the features of acute hypersensitivity pneumonitis
``` Symptoms 4-8hrs after exposure Wheezing - inflammation terminal bronchi Malaise, pyrexia - systemic inflammation Dry cough, breathlessness - alveolitis, decreased efficiency of gas transfer Examination often normal ```
45
What is SLE
Systemic lupus erythematosus T 3 hypersesntiivity Antibodies against contents of cell nuclei
46
TRUE/FALSE | Immune complex deposition results in systemic small vessel vasculitis
``` TRUE Fever renal impairment vasculitic skin rash arthralgias ```
47
How to diagnose T 3 Hypersensitivity?
Test for presence of specific IgG antibodies that are reactive to putative antigen For example: Anti-DNA binding antibodies (SLE), Antibodies to Aspergillus (Farmer’s lung)
48
How to manage T 3 Hypersensitivity?
``` (Avoidance) Decrease inflammation Corticosteroids Decrease production of antibody Immunosuppression ```
49
Type 4 hypersensitivity?
T CELL MEDIATED Intial sensitization -> "primed" T effector cells "DELAYED" hypersensitivity
50
How long does T cell sensitization take?
7-10 days
51
TRUE/FALSE | T cell sensitization results in dermatitis
FALSE
52
What are the consequences of TH1 cell activation?
- Chemotaxi = Macrophage recruitment site of antigen - IFNy secretion = activates macrophages, releases TNFa - TNFa secretion = Local tissue destruction - Release GM- CSF(granulocyte-macrophage colony stimulating factor) stimulates maturation of neutrophils in bone marrow
53
Sarcoidosis is characterized by?
``` TYPE FOUR! T CELL MEDIATED = severe unknown antigen PERSISTANT STIMULATION Leads to TISSUE DAMAGE and FIBROSIS Leads to GRANULOMA formation ```
54
What is a granuloma?
organised collection of activated macrophages and lymphocytes
55
Management of sarcoidosis?
``` Watchful waiting many patients undergo spontaneous remission NSAIDS For acute onset of disease Systemic corticosteroids Block T cell activation Block macrophage activation ```

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