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Sem 4: Immunity > 1a.) Hypersensitivity Reactions > Flashcards

1a.) Hypersensitivity Reactions Flashcards

1
Q

This just provides a brief summary of immune system

A
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2
Q

Define a hypersensitivity reaction

A

An antigen-specific immune response that is either inappropriate or excessive and results in harm to the host

“Hypersensitivity reactions are an overreaction of the immune system to an antigen which would not normally trigger an immune response”

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3
Q

When a patient presents with a hypersensitivity reaction what 3 questions should you ask yourself?

A
  • Trigger?
  • Mechanism?
  • Target tissue?
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4
Q

Antigens which trigger hypersensitivity reactions can be exogenous or endogenous; provide some broad examples for each

A

Exogenous:

  • Non-infectious substances (innocuous) e.g. in allergies
  • Infectious microbes e.g. in sepsis
  • Drugs e.g. penicillin

Endogenous

  • Infectious microbes leading to mimicry (idea that microbe and cells in body share similar antigenic sites hence once the body has mounted a response to the antigen of infectious microbe htat response will also acts against cells in body sharing similar antigenic site) e.g.Rheumatic fever
  • Self antigens e.g. autoimmunity
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5
Q

What is antigenic mimicry?

A

Idea that microbe and cells in body share similar antigenic sites hence once the body has mounted a response to the antigen of infectious microbe htat response will also acts against cells in body sharing similar antigenic site

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6
Q

State the 4 types of hypersensitivity reaction

A
  • Type I or immediate (allergy)
  • Type II or antibody mediated
  • Type III or immune complex mediated
  • Type IV or cell mediated (delayed)
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7
Q

What antigens are responsible for type I or immediate hypersensitivity reactions?

A

Environmental non infectious antigens e.g. in allergy

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8
Q

State which of the four hypersensitivity reactions are antibody mediated

A

Type I, II, III = antibody meditated

(Type IV is cell mediated)

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9
Q

Describe the difference between type II (or antibody mediated) and type III (immune complex mediated)

A
  • Type II: directed against membrane bound antigens hence often organ specific
  • Type III: directd agaisnt soluble antigens in the blood hence often systemic
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10
Q

Which antibodies or cells are respsonsbile for each of the hypersensitivity reactions

A

Type I: IgE

Type II: IgG (mostly) but also IgM

Type III: IgG (mostly) but also IgM

Type IV: lymphocytes & macrophages

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11
Q

Describe the two phases of hypersensitivity reactions

A
  • Sensitization phase: first encounter with the antigen. Antigen activates APCs and APCs carry antigen to nearest lymph node. Antigen is presented to and activates naive T cells. Naive T cells can then differentiated into primed T cells which can stimulate further immune response if they encounter the antigen again
  • Effector phase: pathological reaction upon re-exposure to the same antigen due to ativation of memory cells of the adapative immunity
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12
Q

Describe type II hypersensitivity reactions, include:

  • How long it takes for reaction to develop
  • Which antibodies it involves
  • What antigens it targets
  • What outcomes it induces
A
  • 5-12 hours after exposure
  • IgG (mostly) or IgM
  • Targets cell bound antigens
    • Exogenous: blood group antigens (in blood transfusion), Rhesus D antigens
    • Endogenous: self antigens
  • Induces different outcomes:
    • Tissue/cell damage
    • Physiological change
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13
Q

Describe the mechanism of action of a type II hypersensitivity reaction

A

A failure in the mechanism of central tolerance leads to the escape of self-reactive T and B cells. When self or innocuous antigens are presented to the T cells, an immune response is started, targeting the host cells to which the antigens are attached.

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14
Q

Type II hypersensitivity reactions can cause tissue/cell damage or physiological change. Describe how they can cause each

A
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15
Q

State some examples of type II hypersensitivity reactions

A
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16
Q

State the 4 blood group types in the ABO system

A
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17
Q

State:

  • The universal donor
  • The universal recipient

… for the ABO blood system

A
  • Universal donor= O-
  • Universal recipient= AB+
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18
Q

What does the +/- mean in the ABO blood groups?

A

+= Rhesus factor/protein D found on your RBCs

  • = Rhesus factor/protein D non found on your RBCs
  • *D antigen is strongly immunogenic and anti-D antiboies are the leading cause of haemolytic disease of the newborn*
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19
Q

Describe what happens in a haemolytic transfusion reaction

A
  • Mismatch of blood types(be this the ABO blood type or rehsus D antigens)
  • Destruction of donor RBCs by recipient alloantibodies and activation of complement system
  • Type II hypersensitivity involivng IgM
  • Leads to shock, kidney failure, circualtory collapse & death
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20
Q

How can we prevent haemolytic disease of the newborn?

A
  • If we know mum is Rh- and baby is Rh+ then we can give the mum RhoGam (commonly known as anti-D) once during pregnancy at about 28 weeks and then again within 72 hours of birth of the child (given intramuscularly)
  • Rho-Gam is a purified polyclonal antibody against the rhesus D antigen hence it destroys any of the rhesus D antigens that may have enter mums circulation (in first pregnancy)
  • This prevents her forming IgG antibodies against rhesus D hence the second baby won’t be born with haemolytic disease of the newborn
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21
Q

Which immunoglobulin is responsible for haemolytic transfusion reaction (an example of a type II hypersensitivity)

A

IgM

22
Q

Describe what happens to cause haemolytic disease of the newborn

A
  • When a Rh- woman carreis a Rh+ fetus, small amounts of D+ RBCs can enter her cirulation during the pregnany. The most likley time for them to enter her circulation is during birth when the placenta ruptures/comes away from uterus
  • Her body then produces anti-D IgG antibodies
  • If she becomes pregnant again in the future with a Rh+ fetus the antibodies will cross the placenta (as they are IgG) and attakc the RBCs of the fetus
23
Q

Which immunoglobulin is responsible for haemolytic disease of the newborn?

A

IgG

24
Q

Describe how we can treat type II hypersensitivity reactions. NOTE: treatment is dependent on whether the reaction has caused tissue/cell damage or physiological change

A
25
Q

Describe how plasmapheresis therapy works for type II hypersensitivity reactions

A
  • Remove blood (like for dialysis)
  • Blood separated into RBCs, WBCs, platelets & plasma
  • Remove plasma (which is where circulating IgG, IgM and immune complexes are)
  • Replace plasma with substitute (most common) or filter plasma and return it
  • Provides short term relief and allows healing of damaged tissue for diseases such as myasthenia gravis, goodpasture’s syndrome, Grave’s disease
26
Q

State 3 diseases plasmapheresis therapy can be used for

A
27
Q

Describe the clinical features of haemolytic disease of the newborn

A

Remember: when baby in utero placenta clears bilirubin. Bilirubin mainly accumlates after birth as placenta is not getting rid of it and baby’s liver cannot cope

  • Jaundice
  • Anaemic
  • Hypotonia
  • Lacking in energy (anaemia)
  • Pale skin (anaemia)
  • Increased resp rate (anaemia)
  • Oedema/hydrops fetalis when born
28
Q

What is the main complication of increased bilirubin levels for baby?

A

Kernicterus

Bilirubin crosses blood brain barrier and can cause brain damage

29
Q

Remind yourself, from ICPP, how neuromuscular junctions work

A
  • Action potential propagated down motoneurone until presynaptic terminal is depolarised
  • Depolarisation of pre-synaptic terminal cuased voltage gated Ca2+ channels to open
  • Ca2+ flows into nerve terminal
  • Uptake of Ca2+ causes exocytosis of stored ACh into synaptic cleft
  • ACh diffuses across synaptic clrft o muscle end plate
  • Binds to nAChR
  • nAChR are also ion channels permeable to Na+ and K+
  • Influx of Na+ and efflux of K+ through nAChR causing depolarisation (end plate potential)
  • Depolarisation spreads to neighbouring region of muscle fibre and opens voltage gated Na+ channels
  • Further influx of Na+ causing depolarisation to threshold and action potential generated
  • After ACh binds to nAChR it is degraded by acetylcholinesterase (present on motor encd plate) into choline & acetate- AP is terminated
  • Choline is taken up into motoneuron to be recycled into syntehsis of more ACh
30
Q

Describe the pathophysiology of myasthenia gravis

A
  • Abnormal antibodies to AChR are produced
  • They ciruclate in blood and bind to nAChR on muscle end plates
  • When antibodies are bound the receptors are not available to be activaated by ACh
  • Hence ACh cannot depolarise muscle end plates
  • No action potential
  • No muscle contraction
31
Q

Describe how pyridostigmine is an effective treatment for myasthenia gravis

A
  • Pyridostigmine= acetylcholineesterase inhibitor
  • Binds to ACh esterase and reduces binding and degradation of ACh at muscle end plate
  • This increases synaptic concentration of ACh and prolongs its action
  • Longer muscle end plate is exposed to high ACh more likely it is that an ation potential, and hence muslce contraction, will be generated
32
Q

Describe type III hypersensitivity reactions, include:

  • How long it takes for them to develop
  • What immunoglobulins it involves
  • What antigens it targets
  • How tissue damage is caused
A
  • 3-8 hours
  • Immune complexes between IgG or IgM and antigens
  • Targets soluble antigens
    • Foreign (infection)
    • Endogenous (self antigens)
  • Tissue damage caused by deposition of immune complexes in host tissues. Once deposited they activate complement system causing local inflammation and attraction of leukocytes. Activation of complement results in increased vasopermeability, the attraction and degranulation of neutrophils, and the release of oxygen free radicals which can severely damage surrounding cells
33
Q

There aer som key factors that affect immunecomplex pathogenesis, elaborate on each of the following:

  • Complex size
  • Host reponse
  • Local tissue factors
A
  • Complex size
    • Small & large ICs cleared
    • Intermediate size ICs are difficult to clear
  • Host reponse
    • Low affinity antibody
    • Complement deficiency
  • Local tissue factors
    • Haemodynamic factors
    • Physiochemical factors
34
Q

State some common places for immune complexes to deposit

A
35
Q
A
36
Q

State 3 examples of diseases caused by type III hypersensitivity reactions

A
  • Rheumatoid arthritis (self-antigen)
  • Glomerulonephritis (infectious)
  • SLE
37
Q

Describe the pathophysiology of rheumatoid arthritis, include:

  • Antigen
  • Course of disease
  • Poor prognosis factors
A

NOTE: rheumatiod factor is the antibody against the Fc portion of IgG

38
Q

Describe the pathophysiology of SLE, include:

  • Antigen
  • Symptoms
A
39
Q

Describe type IV hypersensitivity reactions, include:

  • How long it usually takes for them to develop
  • What immune cells are involved
  • State the 3 different subtypes
A
  • 24-72 hour
  • Lymphocytes & macrophages
  • Subtypes:
    • Contact hypersensitivity
    • Tuberculin hypersensitivity
    • Granulomatous hypersensitivity
40
Q

Describe how type IV hyper sensitivity reaction scan lead to tissue destruction

A

Type 4 hypersensitivity reactions are the only kind that do not involve antibodies in any way- instead, they are mediated by T-cells. When the antigen enters the system, it is picked up by an antigen-presenting cell and presented on the MHC region to a T-helper cell.

If the T-helper cell recognises the antigen, it will differentiate into a Th1 cell and release IL-2 and interferon-gamma, leading to proliferation of further Th1 cells and also causing the activation of macrophages and their differentiation in CD4+ and CD8+ cells.

41
Q

Contact dermatitis is an example of type IV hypersensitivity:

  • State some examples of materials that commonly cuase contact dermatitis
  • State how long post-exposure rash appears
A
42
Q

Granulomatous hypersensitivity is an example of type IV hypersensitivity; state some examples of diseases which have granulomatous hypersensitivity

How long following exposure does this reaction happen?

A
43
Q

State 3 diseases caused by type IV hypersensitivity to endogenousu antigens

A
44
Q

Compare Hashimotos and Grave’s in terms of what type of hypersensitivity reaction each one is

A
45
Q

State some treatment options for type III and type IV hypersensitivity reactions

A
46
Q

A disease may involve more than on type of hypersensitivty mechanism; true or false?

A

True e.g. RA is type III and type IV

47
Q

Why does the mismatch of ABO system rarely cause HDN (haemolytic disease of newborn)?

A

Anti-A and anti-B antibodies are IgM and only IgG crosses placenta

48
Q

What lab tests can be performed during pregnancy to confirm desruction of RBCs?

A
  • Sample of amniotic fluid and check for bilirubin
  • Doppler ultrasound of babies middlel cerebral artery to check for anaemia
49
Q

Describe the direct Coombs test

A

This is used for patients with suspected autoimmune haemolytic anaemias or those who may have delaed haemolytic tranfusion reactions

50
Q

Describe the indirect Coombs test

A

This is used when a pt requires a blood transfusion to ensure a compatible match is found. First, RBCs tested for presence of A,B and D antigens. Next an antibody screen is performed using indirect Coombs test

Sem 4: Immunity (6 decks)

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