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Immunology > 1.1.1 Type II Hypersensitivity Reactions > Flashcards

1.1.1 Type II Hypersensitivity Reactions Flashcards

1
Q

What is the most common primary immunodeficiency?

A

Di George Syndrome
Deletion of part of chromosome 22q11.2

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2
Q

What is the main cause of immunodeficiency in the UK?

A

Malnutrition

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3
Q

What effects can the immune system have on the body in an autoimmune reaction?

A

Organ specific
Non-organ specific

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4
Q

What are some examples of organ specific autoimmune diseases?

A

Goodpasture’s syndrome
Haemolytic anaemia
Myasthenia gravis
Grave’s disease

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5
Q

What are some examples of non-organ specific disease?

A

Systemic lupus erythematosus
Rheumatoid arthritis

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6
Q

Define hypersensitivity

A

Antigen specific immune responses that are either inappropriate or excessive and result in harm to the host

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7
Q

What are the types of triggers for hypersensitivity reactions?

A

Exogenous antigens
Intrinsic antigens

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8
Q

Give 3 examples of exogenous antigens causing hypersensitivity reactions

A
  • Non-infectious substances (innocuous, allergens)
  • Infectious microbes
  • Drugs (e.g. penicillin)
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9
Q

Give 2 examples of intrinsic antigens causing hypersensitivity reactions

A
  • Infectious microbes (mimicry)
  • Self antigens (auto-immunity)
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10
Q

What are the 4 types of hypersensitivity reactions?

A
  • Type I- or immediate Allergy, environmental non-infectious antigens
  • Type II- or antibody mediated
  • Type III- or immune Complexes mediated
  • Type IV- or cell mediated (Delayed), environmental infectious agents and self antigens
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11
Q

What antibody drives Type I reactions?

A

IgE mediated (Allergy)

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12
Q

What antibody drives type II and III reactions and how are they different?

A

IgG and IgM

Type II- antibodies against tissue bound antigens

Type III- antibodies against soluble antigens

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13
Q

What antibody drives type IV reactions?

A

Not antibody driven, cell mediated therefore T cells and macrophages mostly

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14
Q

What are the two phases of hypersensitivity reactions?

A

Sensitisation phase - First encounter with antigen, activation of APCs and memory effector cells

Clinically silent phase, asymptomatic

Effector phase -Pathologic reaction upon re-exposure to same antigen and activation of memory cells

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15
Q

Features of Type II hypersensitivity

A
  • Develops 5-12 hours after re-encounter with infection
  • Involves IgG (chronic infection) or IgM (acute infection) antibodies
  • Targets cell bound antigens
  • Induces different outcomes
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16
Q

What are the targets of type II hypersensitivity?

A

Exogenous
-Blood group antigens
-Rhesus D antigens

Endogenous
-Self antigens

17
Q

What are the different induced outcomes of type II hypersensitivity reactions?

A

Tissue / cell damage
Physiological change in function

18
Q

What immune mechanisms are involved in type II hypersensitivity reactions causing tissue/ cell damage?

A

Complement activation
-Cell lysis
-Neutrophil recruitment/ activation (C3a/ C5a)
-Opsonisation (C3b)

Antibody-dependent cell cytotoxicity
-NK cells- part of innate immunity

19
Q

How do natural killer cells work?

A

NK cells have receptors for IgG, NK cell binds and releases its granules

20
Q

What are two clinical examples of type II hypersensitivity reactions causing tissue damage? -complement activation

A
  • Haemolytic disease of the newborn, -Rhesus D antigen
  • Transfusion reactions, ABO system (mainly due to human error)
21
Q

What are three clinical examples of type II hypersensitivity reactions causing tissue damage? -Antibody-dependent cell cytotoxicity

A
  • Autoimmune haemolytic anaemia, RBC
  • Immune thrombocytopenic purpura, Platelet
  • Goodpasture’s syndrome, collagen in the basement membrane of the lung and glomerulus of the kidney
22
Q

Give an example of a hypersensitivity type II reaction driven by IgM

A

Haemolytic transfusion reaction (ATR)
-Medical emergency (carry out ABC approach)
-Caused mainly by human error e.g. mislabled specimen

23
Q

What is the immune mechanism behind haemolytic transfusion reaction?

A
  • Incompatibility in the ABO antigens on RBCs
  • Donor RBC lysis induced by type II hypersensitivity involving recipients IGM
24
Q

What is the clinical outcome of haemolytic transfusion reaction?

A

Shock
Respiratory distress
Kidney failure
Death

25
Q

What blood type can donate to all other blood types and what blood type is the universal plasma donor?

A

O- for whole blood
AB- for plasma

26
Q

What is the pathophysiology of haemolytic disease of the newborn?

A
  1. Rhesus positive father
  2. Rhesus negative mother carrying rhesus positive foetus
  3. During delivery rhesus positive antigens from foetus enter maternal circulation
  4. Mother then produces anti-Rh +ve antibodies
  5. If the woman becomes pregnant with another Rh +ve foetus, anti-Rh antibodies will cross the placenta and destroy foetal RBCs

First encounter no effects as sensitisation occurs only affects the second baby

Anti-Rh antibodies cross the placenta as they are IgG

27
Q

What complications arise as a result of haemolytic disease of the newborn?

A
  • Hydrops fetalis- (fluid accumulation) liver failure, resulting in reduced albumin production, fluid moves into interstitium
  • Liver/splenomegaly
  • Severe hyperbilirubinaemia
  • Kernicterus- brain damage due to bilirubin accumulation in brain
28
Q

What is given to prevent anti-Rh antibodies forming, preventing the sensitisation phase?

A

RhoGAM
Rh0(D) immune globulin

  • Give within 72 hours of giving birth
  • 0.1% of mothers are not protected- too much blood enters maternal circulation?
29
Q

How can we treat high antibody titres with Rh positive foetus?

A

Treat with plasmapheresis- removal of plasma which is replaced removing the anti-Rh antibodies

High dose of IV immunoglobulin

Intrauterine transfusions to ensure adequate blood supply to foetus through umbilical vein (not artery don’t make that mistake again)

30
Q

How can haemolytic disease of newborn be diagnosed before birth?

A

-Check mother and fathers Rh antigens
-Check if mother and father had a child previously
- Indirect Coombs Test-antiglobulin test, used to check for anti-Rh antibodies
-Doppler scan of foetus to check for anaemia
-Foetal blood sample from umbilical vein for bilirubin

31
Q

What physiological changes are caused by type II hypersensitivity reactions?

A
  • Receptor stimulation,eg Graves disease, TSH receptor is the antigen that the antibody binds to
  • Receptor blockade,eg Myasthenia gravis antigen is AChR
  • Protein blockade, eg Pernicious anaemia, antigen is intrinsic factor in gastric parietal cells
32
Q

What are the therapeutic approaches of type II hypersensitivity reactions?

A

Tissue/cell damage:
-Corticosteroids - anti-inflammatory
-Plasmapheresis - remove circulating antibodies and inflammatory mediators
-Splenectomy - removal of opsonised material
-IV immunoglobulin - blocks Fc receptor

Physiological change:
-Correct metabolism - antithyroid drugs in Graves
-Replacement therapy eg Pyridostigmine (Ach esterase inhibitor) in Myasthenia gravis,Vit B12 (IM) in pernicious anaemia

Immunology (14 decks)

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