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Immune System > Hypersensitivity reactions > Flashcards

Hypersensitivity reactions Flashcards

1
Q

What is a hypersensitivity reaction?

A

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

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2
Q

Give some examples of hypersensitivity to exogenous antigens

A
  • Non infectious substances (innocuous) e.g. allergens to pollen, dust, food …
  • Infectious microbes e.g. over reaction of system
  • Drugs e.g penicillin
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3
Q

Give some examples of hypersensitivity to intrinsic antigens

A
  • Infectious microbes (mimickry)
  • Slef antigens (auto-immunity)
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4
Q

What is mimickry?

A

When the host triggers an immune reaction to an infectious microbes but due to host similarities the immune system begins to attack the host too e.g. Rheumatic fever

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5
Q

What are the 4 types of hypersensitivity reactions?

A
  • Type 1 (immediate) Allergy
    • IgE mediated
  • Type 2 antiBody mediated
    • IgG driven
    • Membrane bound antibdoies → organ specific
  • Type 3 or immune Complex mediated
    • IgG driven
    • Soluble antibodies → more systemic
  • Type 4 or cell mediated (Delayed)
    • environmental infectious agents and self antigens
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6
Q

What 2 phases must hypersensitivity reactions go through?

A
  1. Sensitisation phase
  2. Effector phase
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7
Q

What happens in the sensitisation phase of a hypersensitivity reaction?

A
  • First encounter with the antigen
  • APCs are activated and create memory effector cells
  • Previously exposed individal to the antigen is ‘sensitised’
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8
Q

What happens in the effector phase of a hypersensitivity reaction?

A

Pathological reactivation upon re-exposure to the same antigen and activation of the memory cells of the adaptive immunity

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9
Q

How long does it take for type 2 sensitivity reactions to develop after re-exposure?

A

5-12 hours

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10
Q

What antibodies are involved in type 2 hypersensitivity reactions

A

IgG (smaller) or IgM (larger)

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11
Q

Give some examples of type 2 hypersensitivity reactions that occure due to complement activation

A
  • Haemolytic disease of the newborn
    • Antigen to Rhesus D
  • Transfusion reactions
    • ABO blood system
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12
Q

Explain the mechanism of type 2 hypersensitivity reaction

A
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13
Q

Give examples of type 2 hypersensitivity reactions that occur due to antibody-dependent cell cytotoxicity

A
  • Autoimmune haemolytic anaemia (warm and cold)
  • Immune thrombocytopenia purpura
  • Goodpasture’s syndrome (Kidney glomerular nephritis)
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14
Q

Explain what happens in a haemolytic transfusion reaction

A
  • Type 2 hypersensitivity IgM related
  • Incompatibility in the ABO or rhesus D antigens leads to RBC lysis
  • Life threatening condition
  • Causes shock, kidney failure, circulatory collapse and even death
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15
Q

Which blood type is the universal donor?

A

O -

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16
Q

Which blood group is the universal plasma donor?

A

AB

(lacks A/B antibodies in plasma)

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17
Q

Explain the mechanism behind haemolytic disease of the newborn

A
  • Rhesus negative mother pregnant by a Rh+ father → first baby is Rh+
  • Mother develops antigens to the Rh D antigen from the developing fetus that can enter mothers blood during delivery → first baby is fine
  • These antibodies at IgG and can cross the placenta
  • On the 2nd pregnancy Rh+ baby, the anti-Rh antibodies can cross the placenta and attack the RBC of the fetus
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18
Q

Why does haemolytic disease of the newborn not occur in mismatch of mother and fetal ABO blood groups?

A

As ABO is IgM antibodies and these cannot cross the placenta

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19
Q

What symptoms happen to the baby in Haemolytic disease of the newborn?

A
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20
Q

What is kernicterus?

A

When bilirubin crosses the blood brain barrier

Can cause brain damage if not treated

Signs: increased tone, epilepsy, always tired

21
Q

What tests can be performedduring pregnancy to confirm destruction of red blood cells (of the fetus)

A

Amniocentesis: Hb, Reticulocytes, LFT, Bilirubin

Non invasive: Doppler ultrasound can tell you if baby is aneamic (measure middle cerebral artery)

22
Q

What can be given to pregnancy mothers who are Rh-?

A

RhoGAM administered 72hrs after birth

Stops the mother from becoming sensitised to Rh+ antigen

23
Q

Explain what the Coomb’s test is

A

A test for haemolytic anaemia, looks for agglutination of RBC

Direct: looks for antibodies on RBC

Indirect: looks for antibodies in serum

24
Q

What are the 2 types of haemolytic anaemia?

A

Warm: IgG mediated (optimally active at 37ºC)

Cold: IgM mediated (optimally active at 4ºC)

25
Q

Explain how type II hypersensitivity reactions can cause pysiological changes to receptors

A

Receptor stimulation: e.g GRAVE’s DISEASE

  • Increased thyroid activity
  • antigen TSH receptor

Receptor blockage: e.g. MYASTHENIA GRAVIS

  • antigen to Acetylcholine receptor
  • Impaired neuromuscular signalling
26
Q

Give some therapeutic approaches to dealing with the tissue damage caused by type II hypersensitivity reactions

A
  • Anti-inflammatory drugs
  • Plasmapheresis
  • Splenectomy → end up immuno compromised
  • Intravenous immunoglobin (IVIG)
    • IgG degredation provides temporary relief
27
Q

What is plasmapharesis therapy?

A

Separation of the cells and plasma to remove the circulating antibodies

Useful in:

  • Myaesthenia gravis
  • Goodpasture’s syndrome
  • Grave’s disease
28
Q

What can you give to treat myaesthenia gravis?

A

Pyridostigmine

AChesterase inhibitor → increases levels of ACh at NMJ

29
Q

What happens in myaesthenia gravis?

A
  • Autoantibodies to the AChR produced and bind to nicotinic receptors at muscle end plates
  • ACh cannot bind and cause normal depolarisation → action potentials
30
Q

How long does it take for a type III hypersensitivity reaction to develop?

A

Usually 3-8 hours after exposure

31
Q

Explain what happens in a type III hypersensitivity reaction?

A
  • Immune complexes of IgG or IgM
  • Targets soluble antigens
    • immune complex will travel to target either foreign antigens (infection) or endogenous (self antigens)
  • Causes tissue damage by deposition of the immune complexes in host tissue
32
Q

How does the size of the immune complex alter its ability to create a reaction?

A
  • Small and large size immune complexes are cleared
  • Intermediate sized immune complexes aren’t → difficult to get rid of → clinically problematic
33
Q

What kind of reaction will you always get if you have a deficiency in complement?

A

Type III reactions → cannot opsonise large complexes for degredation

34
Q

Which body systems do immune complexes usually affect?

A

Multisystemic:

  • Joint
  • Kidney
  • Small vessels
  • Skin
35
Q

Give 3 examples of dieases caused by type 3 hypersensitivity reactions?

A
  • Rhemuatoid Arthritis (self-antigen)
  • Glomerulonephritis (infectious)
    • Bacterial endocarditis
    • Hepatitis B infection
  • Systemic lupus erythematosus
36
Q

Explain the immune background of Rheumatoid arthritis

A
  • Antigen to the Fc portion of IgG (Rheumatoid Factor)
  • Get articular and extra-articular features
  • Episodes of inflammation and remission
37
Q

What factors give poorer prognosis of rheumatoid arhritis?

A
  • <30 years old
  • High titre of rheumatoid factor
  • Female
  • DR4 allele
  • Joint erosions
38
Q

What is the immune background to systemic lupus erythematosus?

A
  • Antigen to Ds-DNA
  • Most prevelant immune complex disease
  • Affected Females: Males 9:1
  • 40-60% of patients have cardiac, respiratory, joint, neurological features
  • Repeated miscarriage
39
Q

What are some of the common symptoms of systemic lupus erythematosus?

A
40
Q

What is a type 4 hypersensitivity reaction?

A
  • Cell mediated reaction that develops within 24-72hrs
  • Involves lymphocytes and macrophages
41
Q

What are the different subtypes of type IV hypersensitivity reactions?

A
  • Contact hypersensitivity
  • Tuberculin hypersensitivity
  • Granulomatous hypersensitivity
42
Q

How do type IV hypersensitivity reactions cause tissue destruction?

A
  • Sensitisation phase
    • APCs present antigen to TH cells
    • Causes a TH1 response
  • Effector phase
    • TH1 cells activate resting macrophages
    • Macrophage activation recruit more TH1 → granuloma
43
Q

What is contact hypersensitivity?

A
  • Occurs 48-72hr post exposure
  • Epidermal reaction
  • Requires endogenous proteins
  • Examples
    • Nickel
    • Poison ivy
    • Organic chemicals
44
Q

What happens in granulomatous hypersensitivity reaction?

A
  • Occurs 21-48 days post-exposure
  • Granuloma forms when host can’t get rid of the microbe → helps seal off infection as long as granuloma is intact
  • Tissue damage
  • Examples
    • TB
    • Leprosy
    • Schistosomiasis
    • Sarcoidosis
45
Q

What diseases can be caused by type 4 hypersensitivity reactions?

A
  • Pancreatic islet cells → insulin dependent diabetes mellitus
  • Thyroid gland → Hashimoto’s thyroiditis
  • Fc portion of IgG→ Rheumatoid arthritis
46
Q

What is the difference immunologically between Grave’s and Hashimotos disease?

A

Hashimotos: B cell and CD8 T cell activation causes necrosis/ apoptosis of thryroid cells → hypothyroidism

Grave’s: CD4+ tell cell reaction causes overstimulation of the TSH receptor → hyperthyroidism

47
Q

How can you treat type III and IV hypersensitivity reactions?

A

Anti-inflammatory drugs

  • Non steroidals
  • Corticosteroids
  • Steroid sparing agents
    • Azathioprine
    • Mycophenolate mofetil
    • Cyclophosphamide

Monoclonal antibodies

  • B and T cells
  • Cytokine network
  • APCs
48
Q

Newborn infants from mothers with myaesthenia gravis can exhibit symtpoms of myaesthenia ravis at birth. Explain the immune mechanism why and why the disease eventually dissapears?

A
  • Mother transfers antibodies to nAChR across the placenta to the baby
  • Maternal antibodies will dissapear on their own as they are replaced by babies own antibodies
49
Q

What are some of the side effects of treating myaesthenia gravis with an AChesterase inhibitor?

A
  • stomach pain
  • muscle cramps
  • twitching
  • sweating
  • blurred vision
  • cough with mucus

Immune System (7 decks)

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