Immunological Diseases Flashcards

1
Q

What are the two main Immune system reasons for Immunological disease?

A
  • Immune system may fail to control infection
    • Pathogen factors (evasion mechanisms)
    • Host factors (immunodeficiency)
  • Immune system may cause disease directly
    • Failure of tolerance (eg allergy/ autoimmunity)
    • Immune system inappropriately activated for unknown reasons (eg inflammatory bowel disease) or
    • for reasons that are known but poorly understood (eg asbestos or cigarette smoke) or during infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How are Immunological diseases classified?

A
  • Gell and Coombes system
    • Gell and Coombes hypersensitivity reactions types 1-4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain what Type 1 Hypersensitivity is

  • how is it clinically relevant
A

IgE- mediated allergy

  • B cells class switch to IgE antibody. Secreted IgE is picked up by tissue mast cells and circulating basophils
  • Cross-linking of allergen-specific IgE antibodies by allergen activates the mast cell
  • Mast cell rapidly ‘degranulates’ releasing histamine, tryptase and other pre-formed mediators
  • Pharmacological effects of histamine lead to symptoms in the affected organ(s)
  • In health, believed to assist with parasite immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give examples Type 2 hypersensitivity diseases

A

- AB blood system and transfusion medicine

- Haemolytic disease of the newborn

- Autoimmune haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AB blood system and transfusion medicine

A

a Type 2 hypersensitivity disease

  • Refers to pathology directly mediated by antibodies
  • Mismatch blood transfusion reactions are an example of type II hypersensitivity
  • IgM antibodies against AB antigens develop during first year of life
  • The antibodies are an example of is antibodies – develop against similar antigens on surface of gut bacteria and cross-react with red cell antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Haemolytic Disease of the Newborn?

  • Treatment
A
  • a Type 2 hypersensitive immunological disease
  • a Rhesus -ve mother may be sensitised to Rhesus D antigens due to exposure from fetal red cells during pregnancy
    • parturition
    • trauma
  • they then develop antibodies that will cause this disease in subsequent pregnancies
    • Growth retardation, cardiovascular failure, ‘hydrops fetalis’, neurotoxicity from high bilirubin levels

Rhesus-negative mothers with rhesus+ partner are given anti-D IgG during pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is Haemolytic disease of the newborn treated/ managed?

A
  • Rhesus-negative mothers with rhesus+ partner are given anti-D IgG during pregnancy
    • At 28 weeks routinely
    • After accidents, miscarriage or surgical delivery
  • Binds to fetal red cells entering circulation; fetal red cells then destroyed, preventing sensitisation
  • Risk of maternal sensitisation reduced from 16% per pregnancy to 0.1%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is autoimmune haemolysis?

  • clincical effect?
A
  • spontansous formation of anti-RBC autoantibodies
  • results in jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Type 3 hypersensitivity?

  • when would this occur
A
  • Describes disease caused by complexes of antibody and antigen
  • Such complexes are a normal phenomenon
    • Usually soluble, removed in spleen
  • In some situations (below) they become insoluble and cause disease
    • Large quantity of antigen
    • Large quantity of antibody
    • Interaction between the two is very strong
    • Complexes are of the correct size
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a hand sign of type 3 sensitivity?

  • which diseases would this sign be seen in?
A
  • Painful lesions in the fingertip pulp due to deposition of circulating immune complexes
  • May be seen in infective endocarditis (Osler’s nodes)
  • May be seen in other diseases with immune complex deposition eg SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Serum Sickness?

  • presentation
A
  • A ‘generalised’ transient immune complex-mediated syndrome
    • type 3 sensitivity on gell coombs classification
  • Mainly results from injection of certain immunogenic drugs or anti-sera produced in animals eg after snake envenomation
  • after many doses of the antivenom, the body can become sensitized as it is derived from animal Ig
    • Rash
    • Fever
    • Arthritis
    • Glomerulonephritis
      • due to immune complex deposition in the kidneys - once cleared it will clear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Hypersensitivity pneumonitis?

  • caused by?
  • effect?
A
  • Patient becomes sensitised to an environmental antigen by repeated exposure, producing large quantities of IgG antibodies
  • Immune complexes form in the lung upon re-exposure causing shortness of breath and cough
    • Mould spores in hay (farmers lung)
    • Pigeon feathers and stool (pigeon-fanciers lung)
  • Initially transient, lung scarring with repeated exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Type 4 Hypersensitivity?

A
  • Delayed type hypersensitivity
  • Reactions are mediated by antigen-specific effector T cells
  • Because it takes time to process and present antigen, these reactions do not develop for at least 24 hours following exposure
  • When it occurs in the skin it is known as contact dermatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Explain how Contact dermatitis sensitisation occurs

  • what can cause this sensitisation
A
  • Sensitising agents are typically highly reactive small molecules that can penetrate the skin
  • These react with self-proteins to create protein-hapten* complexes that are picked up by Langerhans cells, which migrate to regional lymph nodes
  • Examples are nickel and molecules in perfume/ cosmetics
  • The Langerhans cells process and present the antigen together with MHCII
  • In some susceptible individuals, the complexes are recognised as foreign
  • The activated T cells then migrate to the dermis

*small molecule which cannot produce an immune response by itself, but can bind to a protein to alter its immunogenicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can an individual know if they are sensitized to something Type 4 sensitization?

A
  • Get a patch test for contact dermatitis
    • antigen-impregnated patch placed on the back
    • nickel, chrome, cobalt, epoxy resin, lanolin
    • results read after 2 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain what a Tuberculin skin test is (TST)

A
  • a type 4 hypersensitivity reaction
  • Used to determine previous EXPOSURE to TB
  • Tuberculin injected intradermally (tuberculin=complex mixture of antigens derived from MTB)
  • Local inflammatory response evolves over 24-72 hours if previously exposed
  • Mediated by Th1 cells
17
Q

What is the alternative for Tuberculin Skin Test?

  • hoe does the test work
  • what would the results show +ve and -ve
A

using in vitro mechanisms - interferon gamma release assay (IGRA)

  • mycobacterium peptides (MTB) are added to blood in the lab
  • antigen-presenting cell presents with MHC2 and secretes IL-12

Previous Exposure to TB

  • memory Th1 cell recognises the antigen
  • they are primed and release cytokines within the short time frame

No Previous TB Exposure

  • there are no primed memory T cells specific for MTB
  • no IFN-gamma produced in the short time frame
18
Q

What are other ways to use the IFN-gamma release assay to test for TB?

A
  • ELISPOT method (T-SPOT)
  • ELISA method (Quantiferon Gold)