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immunology > hypersensitivity > Flashcards

hypersensitivity Flashcards

1
Q

what are hypersensitive reactions?

A

excessive immune responses that cause damage

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2
Q

what are examples of antigens involved in hypersensitive reactions?

A
  • infectious agents
  • environmental substances
  • self-antigens
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3
Q

what are the 4 different types of hypersensitivity?

A
  • type I (Immediate)
  • type II (cell-bound antigen)
  • type III (immune complex)
  • type IV (delayed)
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4
Q

describe the process of influenza causing hypersensitivity?

A
  • damaged respiratory tract epithelial cells
  • exaggerated immune response
  • cytokine storm
  • attract leukocytes to the lungs (hypotension and coagulation)

severe influenza

  • inflammatory cytokines spill into systemic circulation causing effects in remote parts of body, such as brain
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5
Q

describe the process of dust causing hypersensitivity?

A

enters lower extremities of respiratory tract and mimics parasites to stimulate an antibody response

IgE: triggers immediate hypersensitivity → allergy symptoms (asthma or rhinitis)

IgG: different kind of hypersensitivity eg farmer’s lung

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6
Q

describe the lower extremities of respiratory tract

A

rich in adaptive immune response cells

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7
Q

what are haptens?

A

small molecule irritants that bind to proteins and elicit immune response

example is nickel causing contact dermaititis

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8
Q

describe type I hypersensitivity

A

immediate hypersensitivity reaction to environmental antigens

degranulation of mast cells and eosinophils

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9
Q

how quick is the onset of type I hypersensitivity?

A

within minutes of exposure

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10
Q

what is type I hypersensitivity basically?

A

an allergy

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11
Q

what is another word for allergy?

A

atopy

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12
Q

presentations of type I hypersensitivity?

A
  • anaphylaxis
  • angioedema
  • asthma
  • dermatitis, eczema, urticaria
  • rhinitis
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13
Q

atopic march

A

different presentations of type I hypersensitivity come and go at different ages

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14
Q

allergens

A

antigens that trigger allergic reactions

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15
Q

how can people be exposed to allergens

A
  • inhalation
  • ingestion
  • contact
  • administered as drugs
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16
Q

what immunoglobulin mediates type I hypersensitivity?

A

IgE

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17
Q

what is IgE produced by

A

B cells when co-stimulated with IL-4 (secreted by TH2 cells)

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18
Q

describe the mechanism of type I hypersensitivity?

A
  • release of mediators that cause allergic symptoms
  • mast cells are resident in many tissues
  • eosinophils migrate to tissues
  • mast cells initiate allergic symptoms after allergen and IgE interact
  • mast cells have receptors for IgE and FcεRI
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19
Q

anaphylaxis symptoms

A
  • low blood pressure
  • angioedema
  • airway obstruction
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20
Q

asthma symptoms

A

reversible airway obstruction in bronchi

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21
Q

rhinitis symptoms

A
  • discharge
  • sneezing
  • nasal obstruction
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22
Q

urticaria symptoms

A

acute, itchy oedema of subcutaneous tissue

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23
Q

angioedema symptoms

A

acute, non-itchy oedema of subcutaneous tissue

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24
Q

atopic eczema symptoms

A

chronic, itchy inflammation of skin

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25
Q

epidemiology of allergies

A

very common, up to 40% population

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26
Q

describe the genetics of allergies

A

filaggrin is expressed by keratinocytes

  • maintains epithelial barrier
  • moisturises surfaces
  • controls pH

polymorphism in filaggrin → allergy

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27
Q

what is the role of environmental factors in allergy

A
  • urbanisation
  • hygiene hypothesis: reduced exposure to microorganisms in early life
  • infections: increase/decrease risk of allergies
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28
Q

what is the most serious type of allergy?

A

anaphylaxis

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29
Q

describe the mechanism of anaphylaxis

A

mast cells degranulate to produce histamine and leukotrienes

  • vasodilation
  • increased vascular permeability → hypotension
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30
Q

describe the mechanism of rhinitis

A

mast cells degranulation and leukotrienes

  • vasodilation & oedema (nasal stuffiness and sneezing)
  • mucous secretion (nasal discharge)
31
Q

describe the mechanism of asthma

A

leukotrienes cause smooth muscle contraction → airflow reduction

32
Q

describe the treatment of allergies?

A

prevention

desensitisation (allergen immunotherapy)

drug treatment

  • beta 2 adrenergic agonists
  • epinephrine
  • antihistamines
  • corticosteroids
33
Q

test to determine what antigen someone is allergic to

A

skin prick test

34
Q

what immunoglobulins mediate type II hypersensitivity

A

IgG or IgM

react with antigen present on surface of cell

bound IgG then interacts with complement or with Fc receptor on macrophages

35
Q

effects of type II hypersensitivity

A

damage to red cells

damage to solid tissues

functional effects

36
Q

examples of damage to red blood cells

A

autoimmune haemolytic anaemia

  • rhesus disease
  • mismatched blood transfusion (ABO compatibility)
  • infections: hep c, hiv, cmv, vzv
  • diseases: SLE, CVID
  • drugs
37
Q

examples of damage to solid tissues

A

good pastures syndrome

38
Q

examples of functional effects

A

graves disease

39
Q

what are the different variations of blood type?

A
  • rhesus positive or negative
  • I positive or negative
  • group A, B or O
40
Q

what is a consequence of A and B blood group antigens being oligosaccharides which are similar to molecule exposed by bacteria?

A

antibodies recognise A and B blood group

  • anti A and anti B are IgM antibodies naturally occurring

group O have antibodies against both A and B

41
Q

People who are group O have antibodies against what groups?

A

A and B

42
Q

People who are group AB have antibodies against what groups?

A

None

43
Q

What type of antibodies are anti-A and anti-B?

A

IgM antibodies

44
Q

What is unique about IgM?

A

IgM antibodies are multivariant (can combine to multiple antigens)

45
Q

What is a complication of IgM being multivariant?

A

IgM antibodies are multivariant (can combine to multiple antigens):

  1. causes agglutinate of red blood cells
  2. IgM activates complement
  3. membrane attack complex destroying RBC
46
Q

How does IgG lead to destruction of red cells?

A

IgG does not damage circulating red cells:

  1. Fc receptors on splenic macrophages bind IgG coated red cells, which are then destroyed
47
Q

What can autoimmune haemolysis occur due to?

A
  • Rhesus antigen (IgG develops during pregnancy and crosses the placenta and causes haemolytic disease
  • Incompatibility in the ABO system during blood transfusion
48
Q

What can autoimmune haemolytic anaemia be caused by?

A
  • Induced by infections or drugs
  • Part of systematic autoimmune disease (SLE)
  • Autoantibodies produced by malignant B cells
49
Q

Describe the pathophysiology of Goodpasture syndrome?

A
  1. IgG autoantibodies bind a glycoprotein in basement membrane of lung and glomeruli
  2. Anti-basement membrane antibody activates complement, triggering inflammatory response
50
Q

Describe the genetics of Graves disease?

A
  • Family history
  • HLA allele DR3
51
Q

Describe the epidemiology of Graves disease?

A
  • Most common cause of hyperthyroidism
  • Young woman
52
Q

Describe the pathophysiology of Graves disease?

A

thyroid-stimulating autoantibody binds TSH receptors and stimulates thyroxine secretion

53
Q

What is type III hypersensitivity?

A
  • IgG responsible
  • Immune complexes of antigen and antibody form and cause damage at site of production or circulate and cause damage elsewhere
  • Take time to form and initiate tissue damage
54
Q

What Ig mediates type III hypersensitivty?

A

IgG

55
Q
A
56
Q

Antigens that form complexes must be what?

A
  • Polyvalent
  • Present long enough to start an antibody response
57
Q

Why is the antigen:antibody ratio important for type III hypersensitivity?

A
  • At low levels of antibody, each antigen binds several immunoglobulin molecules
  • When antibody and antigen levels are equal, or antibody in slight excess, large complexes can form
  • When antibody exceeds antigen small complexes form
58
Q

When do small and when do large complexes form?

A
  • When antibody and antigen levels are equal, or antibody in slight excess, large complexes can form
  • When antibody exceeds antigen small complexes form
59
Q

Describe the process of clearing complexes?

A
  1. Done by compliment system
  2. Complement receptor 1 (CR1) transfers complexes to phagocytes
60
Q

What does failure of clearance of complexes lead to?

A

Failure of clearance leads to immune complex disease:

  • Activation of innate immune system
61
Q

What are two diseases type III hypersensitivty is involved in?

A

Glomerulonephritis

Farmer’s lung

62
Q

What is the presentation of glomerulonephritis due to hypersensitivity?

A
  • Nephrotic syndrome (protein leaks into urine) with gradual development of renal failure
  • Nephritis with rapid onset renal failure, blood and protein in the urine and hypertension
63
Q

What is Farmer’s lung?

A

Hypersensitivity reaction to fungal spores:

  1. Precipitating IgG antibodies against mold proteins
  2. If patient inhales mold protein, insoluble immune complexes form in lung tissues
64
Q

What is type IV hypersensitivity?

A

Delayed hypersensitivity reaction:

  • Mediated by T cells
  • Takes 2-3 days to develop
65
Q

What mediates type IV hypersensitivity?

A

T cells

66
Q

How long is the onset of type IV hypersensitivity?

A
  • Takes 2-3 days to develop
67
Q

What are the main diseases of type IV hypersensitivity?

A
  • Rheumatoid arthritis
  • Multiple sclerosis
68
Q

Describe the mechanism of type IV hypersensitivity?

A
  1. Initiated when tissue macrophages recognise danger signals and initiate an inflammatory response
  2. Dendritic cells loaded with antigen migrate to local lymph node, where present antigen to T cells
  3. Specific T-cell clones proliferate in response to antigens, which migrate to site of inflammation
  4. Tumour necrosis factor (TNF) is secreted by both macrophages and T cells and stimulates much of the damage in delayed hypersensitivities
69
Q

Describe the presentation of rheumatoid arthritis?

A
  • Symptoms arise in joints and tendons, but also affects skin, lungs and eyes
70
Q

Describe the mechanism behind rheumatoid arthritis?

A
  • Antigens that drive RA are citrullinated proteins (citrullination is the conversion of amino acid arginine to the amimo acid citrulline)
  • Autoreactive T and B cells recognise citrullinated proteins, causing production of antibodies against the protein
    • Referred to as anti-cyclic citrullinated peptide (CCP) antibodies
  • Synovium becomes infiltrated by T cells (TH1 and TH17) and macrophages
  • TNF and IL-17 attracts and activates neutrophils that cause damage to synovium
  • Osteoclasts are activated and destroy bone at the joint margins, creating erosions
  • Persistent IL-6 secretion triggers an acute-phase response
71
Q

What are risk factors for rheumatoid arthritis?

A
  • Family history
    • Associated with HLA-DR4
  • Smokers
  • Infection with porphyromonas
72
Q

Describe the mechanism behind MS?

A
  1. Initially, acute attacks occur during which inflammatory lesions consisting of TH1 and TH17 cells and macrophages develop in the affected nervous tissue
  2. Lesions are reversible, relapsing disability typical of early MS
  3. Myelin loss impairs ability of neurons to conduct impulses, resulting in neurological symptoms
  4. Once inflammation settles the disability improves
73
Q

Describe the treatment for delayed hypersensitivity?

A
  • Prevention through avoiding antigens
  • Anti-inflammatory drugs
    • NSAID
    • Corticosteroids
    • Drugs that block TNF and IL-6
    • Antibodies against B cells
  • Immunosuppressive drugs

immunology (11 decks)

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