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Year 1 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

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?

A

Adrenalin constrict arterial smooth muscle

dilates bronchial smooth muscle

24
Q

Management IgE allergic disorders?

A 
Trigger (history!) avoid allergen
Block mast cell activation
prevent effects mast cell activation
Anti-inflammatory agents
Manage anaphylaxis
Immunottherapy
25
Q

What is sodium cromoglycate?

A

Mast cell stabilizer, blocks mast cell activation

26
Q

What are some drugs that block effects of mast cell activation?

A

Histamine receptor antagonist

Leukotriene receptor antagonist

27
Q

TRUE/FALSE

Histamine receptor antagonists are used prophylactically and to control symptoms

A

TRUE

28
Q

Step up treatment maximall y=

A

corticosteroids

29
Q

Immunotherapy allergic disease?

A

Controlled exposure to increasing amounts of allergen
Subcutaneous injection of tiny amounts of allergen
Followed by gradual increase in dose
RISK IS ANAPHYLAXIS

30
Q

Pathophysiology of Type II Hypersensitivity?

A

Antibody binds to CELL SURFACE antigen
IgG and IgM :Activation complement via classical pathway (cell lysis and release opsonins)
IgG: Summon NK cells

31
Q

What do fragments of C3a and C5a do after activation of complement system?

A

Increase permeability of blood vessels - anaphylotoxins

32
Q

What are the effects of antibody binding to cell membrane protein?

A
  • 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
Q

What are transfusion reactions?

A 
Antibodies binds to cells of transfused RBCs. 
Complement mediated lysis
-pyrexia/rigors
-tachycardia/pnoea
-hypotension
FATAL
34
Q

TRUE FALSE

Immediate Haemolytic Transfusion Reaction begins after at least 50mls of blood is transfused

A

FALSE!
May begin after only 1 ml blood is transfused
Overwhelming systemic inflammatory response

35
Q

What is Grave’s disease?

A

Antibodies bind to thyroid stimulating hormone RECEPTOR -> HYPERthyroidism
Popping eyes

36
Q

TRUE/FALSE

Many type II hypersensitivity diseases are associated with Autoimmune disease

A

TRUE

37
Q

TRUE/FALSE

Only mothers with mild or overt symptoms of autoimmune disease may pass on autoantibodies to neonatt

A

FALSE

mothers may have no symptoms

38
Q

How can Type II Hypersensitivity be managed?

A

Plasmapheresis

Immunosuppression to switch off B cell production

39
Q

What is plasmapheresis?

A

removal of pathogenic antibody, remove patient plasma and replace with someone else’s

40
Q

Major disadvantage of plasmapheresis?

A

Rebound antibody production

41
Q

What is the pathophysiology of Type 3 hypersensitivity reactions?

A

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
Q

TRUE/FALSE

Cheese worker’s lung due to mouldy cheese is a genuine Type III hypersensitivity

A

TRUE
Malt - mouldy maltings
Farmer’s lung - mouldy hay
Bird Fancier’s lung - avian excreta, feathers
Lung - accumulation and inflammation WITHIN alveoli

43
Q

TRUE/FALSE

Acute hypersensitivity pneumonitis and chronic hypersensitivity pneumonitis have the same pathophysiology

A

FALSE
Acute is a Type III hypersensitivity
Chronic causes fibrosis

44
Q

What are the features of acute hypersensitivity pneumonitis

A 
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
Q

What is SLE

A

Systemic lupus erythematosus
T 3 hypersesntiivity
Antibodies against contents of cell nuclei

46
Q

TRUE/FALSE

Immune complex deposition results in systemic small vessel vasculitis

A 
TRUE
Fever
renal impairment
vasculitic skin rash
arthralgias
47
Q

How to diagnose T 3 Hypersensitivity?

A

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
Q

How to manage T 3 Hypersensitivity?

A 
(Avoidance)
Decrease inflammation
Corticosteroids
Decrease production of antibody
Immunosuppression
49
Q

Type 4 hypersensitivity?

A

T CELL MEDIATED
Intial sensitization -> “primed” T effector cells
“DELAYED” hypersensitivity

50
Q

How long does T cell sensitization take?

A

7-10 days

51
Q

TRUE/FALSE

T cell sensitization results in dermatitis

A

FALSE

52
Q

What are the consequences of TH1 cell activation?

A
  • 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
Q

Sarcoidosis is characterized by?

A 
TYPE FOUR! T CELL MEDIATED = severe
unknown antigen
PERSISTANT STIMULATION
Leads to TISSUE DAMAGE and FIBROSIS
Leads to GRANULOMA formation
54
Q

What is a granuloma?

A

organised collection of activated macrophages and lymphocytes

55
Q

Management of sarcoidosis?

A 
Watchful waiting 
many patients undergo spontaneous remission
NSAIDS
For acute onset of disease
Systemic corticosteroids
Block T cell activation
Block macrophage activation

Year 1 (15 decks)

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