Immunology- Hypersensitivity Flashcards

1
Q

What is a hypersensitivity reaction

A

Excessive immune responses that cause damage

Can respond to different types of antigens:

  • infectious agents
  • environmental substances
  • self antigens
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2
Q

Cytokines role in hypersensitivity

A

any of a number of substances, such as interferon, interleukin, and growth factors, which are secreted by certain cells of the immune system and have an effect on other cells eg attract leukocytes

High levels of leukocytes can cause cytokines storm

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3
Q

What are happens

A

Small molecule irritants that bind to proteins and elicit an immune response

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4
Q

What type of reaction in type 1 hypersensitivity

A

ALLergy

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5
Q

What cells mediate type 1 hypersensitivity

A

Mast cells
Eosinophils
IgE

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6
Q

Define atopy

A

Immediate hypersensitivity reaction to environmental antigens mediated by IgE
Develops within minutes of exposure

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7
Q

Atopy presentation

A
Anaphylaxis 
Angiooedema 
Urticaria 
Rhinitis 
Asthma 
Dermatitis 
Eczema
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8
Q

Describe the allergens peanut and penicillin

A

Peanut

  • allergy to peanut protein ARA h2
  • allergy to ARA h8

Penicillin
-allergen to B-lactam

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9
Q

When do B cells release IgE

A

When costimulated with IL-4

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10
Q

Mast cell roles

A

Degranulating cells

Mast cells initiate allergic symptoms after allergen and IgE interact

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11
Q

Example of type 1 hypersensitivity disease

A

Asthma
Rhinitis
Anaphylaxis is

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12
Q

What is filaggrin

A

Expressed by keratinocytes and involved in maintaining epithelial barriers and moisturising surfaces and controlling pH

Associated with severe eczema

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13
Q

Presentation of anaphylaxis

A

Mast cells produce prostaglandins and leukotrienes through cyclooxygenase and lipoxygenase pathways

=vasodilation
Increased vascular permeability
Fall in vascular tone
Severe blood pressure drop

Histamine release

=wellling
Fluid shift

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14
Q

treatment of type 1 hypersensitivity

A
B2-adrenergic agonists
Epinephrine 
Antihistamines 
Leukotriene specific receptor blocker 
Corticosteroids
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15
Q

Investgation for type 1 hypersensitivity

A

Skin prick

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16
Q

Type 2 hypersensitivity

A

(B)
AntiBody mediated
IgG or IgM react with antigen present on surface of cells
Results in immune mediated haemolysis (takes several hours)

17
Q

Example of type 2 hypersensitivity

A

Blood groups
Rhesus blood groups (IgG develops and crosses placenta= alloimmune haemolysis)
SLE

(all above = autoimmune haemolysis)
(Below= autoimmune against solid tissue)

Goodpasture syndrome (nephritis, pulmonary haemorrhage)

(Below= autoimmune against cell function)

Graves’ disease
Myasthenia gravies

18
Q

What are type 3 hypersensitivity reactions

A

C
immune Complex disease
IgG is responsible

Immune complexes of antigen and antibody form and cause damage at site of protection or circulate and cause damage elsewhere

Complexes take some time to form

19
Q

When do complexes form between antigens and antibodies?

A

When antibody exceeds antigen levels

20
Q

How does the body clear complexes

A

Complement breaks down large complexes

Complement receptor 1 transfers complexes to phagocytes

Failure of clearance leads to immune complex disease and activation of innate immune system

21
Q

Examples of type 3 hypersensitivity diseases?

A
Nephrotic syndrome, 
Nephritis,
Glomerulonephritis ,
SLE, 
Polyarteritis nodosa,
Poststreptococcal glomerulonephritis,
Serum sickness
22
Q

What is type 4 hypersensitivity reactions

A

D
Delayed hypersensitivity
T cell mediated

Tissue macrophages initiate inflammatory response
T cells stimulated
And secrete TNF

23
Q

Examples of diseases caused by type 4 hypersensitivity

A

RA (TH1 and TH17)
(RA antigens= Citrullinated proteins)

MS

Type 1 DM

IBD

Psoriasis

24
Q

Treatment of delayed hypersensitivity

A
Avoiding antigens 
Anti-inflammatory drugs:
-NSAID
-Corticosteroids 
-drugs that block TNF and IL-6
-antibodies against B cells 

Immunosuppressive drugs

25
Q

Mechanism of tissue injury in Type 1 hypersensitivity

A

Mast cells,
Eosinophils
Their mediators (vasoactive amines, lipid mediators, cytokines)

26
Q

Mechanism of tissue injury in Type 2 hypersensitivity

A

Opsonisation and phagocytosis of cells

Complement and FC receptor medicated recruitment and activation of leukocytes (neutrophils, macrophages)

Abnormalities in cellular function eg hormone receptor, signaling, neurotransmitter receptor blockade

27
Q

Mechanism of tissue injury in Type 3 hypersensitivity

A

Complement and Fc receptor mediated recruitment and activation of leukocytes

28
Q

Mechanism of tissue injury in Type 4 hypersensitivity

A

1-cytokines mediated inflammation and macrophage activation

2- direct target cell killing, cytokines mediated