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Y2 MCD - PP SAQs > Immunology > Flashcards

Immunology Flashcards

1
Q

What is a transplantation between different individuals of the same species, and between different species? (2)

A

Allograft  same species

Xenograft  different species

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2
Q

What are risks of immunosuppression? (4)

A
  • Increase risk of getting infection both conventional infections and opportunistic, or activation of dormant pathogen such as TB
  • Increase risk of malignancy
  • Cardiac toxicity
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3
Q

Transplantation between different individuals of the same species is called: (1 mark)

A

Allograft

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4
Q

Transplantation between individuals of the different species is called: (1 mark)

A

Xenograft

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5
Q

Name two clinically useful drugs that are used to help prevent graft rejection, and state how they work (4 marks) / What are 2 drugs used in transplantation and their mechanism of action? (4)

A
  • Tacrolimus - inhibit t lymphocyte signal transduction (CNI inhibitor)
  • Cyclosporin - inhibit t lymphocyte signal transduction (CNI inhibitor)
  • Rapamycin - inhibit t lymphocyte signal transduction (mTOR inhibitor)
  • Azathioprine - antiproliferative agent - purine synthesis inhibitor
  • Corticosteroids
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6
Q

Name two common complications that usually arise from using these drugs, and name an example for each (2 marks)

A
  • Tacrolimus - side effects include cardiac damage, nephrotoxicity, lung damage, increased chance of malignancy
  • Cyclosporin - side effects include convulsions, pancreatitis, kidney and liver dysfunction
  • Rapamycin - side effects include lung toxicity, DM
  • Azathioprine - side effects include nausea, vomiting anaemia
  • Corticosteroids - cushing’s
  • All would cause decreased immune system so increased chance of infection and cancer
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7
Q

Name 3 things that could cause anaphylactic shock (5)

A

Food e.g. peanuts, insect sting e.g. wasp, medication e.g. penicillin

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8
Q

what is atopy (2)

A

Tendency to produce abnormally high IgE responses to otherwise harmless foreign substances
Genetic tendency to develop allergic diseases, e.g. rhinitis, asthma, eczema

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9
Q

Explain what happens during an anaphylaxis. You may use diagrams.

A

Allergen –> severe generalised allergic reaction due to generalised mass degranulation of IgE sensitised mast cells
• Vasodilation and cardiovascular collapse
• Respiratory effects are bronchospasm and laryngeal oedema
• Skin effects are vasodilation, erythema, urticaria and angioedema

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10
Q

What are the three types of kidney transplant rejection? Give their type, onset and cause.

A

Hyperacute –> mins/hours –> due to pre-existin B cell antibodies eg. wrong blood type transfused
Acute –> days –> due to B/T cells –> body develops antibodies to foreign body for transplant etc. –> tissue destroyed
Chronic –> months/years –> B/T cell mediated

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11
Q

Explain/describe the immunological occurrences in asthma (3)

A

Sensitisation to antigen. Antigen taken by dendritic cells to Th 2 cells - release IL-5 (activates eosinophils) and IL-4 and IL-13 to cause IgE production. Reexposure to antigen - crosslinks IgE on mast cell causing degranulation - histamine release, leukotriene production, prostanoid production. Results in increased permeability of capillaries -> oedema. Also bronchoconstriction and increase mucus production

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12
Q

Give the 3 main clinical features of asthma (3)

A
  • Difficulty breathing
  • Chest tightness
  • Wheezing
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13
Q

Give 4 treatments in managing asthma in order of severity (4)

A

1- Short acting B2 agonist eg. salbutamol
2- Low dose of inhaled corticosteroids eg. budesonide
3- Long acting B2 agonist and high dose inhaled corticosteroids
4- Oral corticosteroids eg. prednisone

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14
Q

Name 3 autoimmune diseases and state the organ they affect (3)

A
  • Hashimoto’s disease – thyroid
  • rheumatoid arthritis - joints(particularly small joints)
  • T1DM - pancreatic B cells
  • Graves - thyroid, pernicious anaemia - stomach
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15
Q

Differences between type 2 and type 3 hypersensitivity reactions (2)

A

Type 2 - insoluble receptors, antibody mediated

Type 3 - soluble receptors, immune complex mediated

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16
Q

Name 4 ways in which pathogenic infections can predispose to hypersensitivity reactions/allergy (2)

A

Can reduce ignorance through damage- expose immunologically privileged sites
Immune shift/deviation e.g. Th1 to th2 response
Increased costimulatory molecules- pro inflammatory
Molecular mimicry of self: If pathogen expresses molecule that is very similar to self molecule then induces immune response against self

17
Q

Define hypersensitivity

A

Hypersensitivity reactions are inappropriate immune responses mounted against harmless foreign antigens, autoantigens or alloantigens

18
Q

Explain the mechanism of T1 hypersensitivity + give an example.

A

Type I = immediate, IgE mediated. Need sensitisation - primary exposure to form IgE. Then secondary exposure antigen can cross link IgE -> mast cell degranulation, eosinophil and basophil recruitment. Anaphylaxis

19
Q

Explain the mechanism of T2 hypersensitivity + give an example.

A

Type 2 = Ab-dependent cytotoxicity. Tissue damage. e.g. Pernicious anemia. Hemolytic anemia.

20
Q

Explain the mechanism of T3 hypersensitivity + give an example.

A

Type 3 = Immune complex. Antigen-antibody complexes form in blood - deposition in tissue. Complement, cell activation/recruitment, activation of other cascades Causes vasculitis. SLE

21
Q

Explain the mechanism of T4 hypersensitivity + give an example.

A

Type 4= T-cell, delayed. Transient/persistent antigen causes T cell activation of macrophages, CTLs causes tissue damage - dependant on TNF alpha. Th1 or CTLs release TNFa. Contact dermatitis, chronic graft rejection

22
Q

Give an example of a disease for type II and III and state what antigen is targeted(4)

A

Type II - Graves - TSH receptor, with Anti-ACh R, Pernicious anaemia - intrinsic factor
Type III - SLE - dsDNA, nucleosome. Antibodies in SLE are anti dsDNA, anti cardiolipin –> cardiolipin is antigen

23
Q

What is tolerance? In what kind of immune cells does it occur?

A

Tolerance - Defined as the acquired inability to respond to an antigenic stimulus
Involves cells of the acquired/adaptive immune system

24
Q

What are central and peripheral tolerance?

A

Central - lymphocytes that respond to self antigens in the bone marrow for B cells or in the thymus for T cells will undergo apoptosis so they are not exposed to the body. T cells exposed to MHC - if can’t detect it or detect it too strongly -> apoptosis. B cell exposed to multivalent molecule - has many of bodies antigens - if generates response -> apoptosis. Crosslinking of surface immunoglobulin by polyvalent antigens expressed on bone marrow stromal cells facilitates deletion
Peripheral - anergy - need costimulation to produce response

25
Q

What are two differences between central and peripheral tolerance?

A

Central tolerance occurs during lymphocyte development, involves T cell selection in the thymus and B cell selection in the bone marrow. Peripheral tolerance - mechanisms to generate tolerance once mature lymphocytes have been developed - involves anergy, immune privilege and regulation

26
Q

2 mechanisms by which failures in tolerance can lead to autoimmune disease.

A

Failure in tolerance - centrally - e.g. mutation of transcription factor AIRE - important in expression of ‘tissue-specific’ genes in thymus - involved in negative selection of T cells results in APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy) - affects endocrine glands.
Failure of tolerance - peripherally IPEX - costimulation of self antigen. Trauma to privileged site - increase amount of antigen - immune attack. Defect of T reg

27
Q

Define each type of hypersensitivity briefly

A
  • Type 1  immediate hypersensitivity
  • Type 2  antibody-dependent cytotoxicity
  • Type 3  immune complex mediated
  • Type 4  delayed cell mediated

Y2 MCD - PP SAQs (5 decks)

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