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PHAR20400 > ALLERGIES AND ANTI-HISTAMINES > Flashcards

ALLERGIES AND ANTI-HISTAMINES Flashcards

1
Q

What is the definition of hypersensitivity?

A

Harmful immune response in which tissue damage is induced by exaggerated or inappropriate immune responses in a sensitized individual on re-exposure to the same antigen

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2
Q

What is central tolerance and how is it related to negative selection?

A
  • Central tolerance - a developing lymphocyte interacts with a self-antigen
  • Negative selection - the process of eliminating any developing T or B lymphocytes that are reactive to self
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3
Q

What is peripheral tolerance?

A

The removal of mature T cell that interacts with a self-antigen in peripheral tissues.

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4
Q

What are the 4 types of hypersensitivity reactions?

A
  1. Type I = IgE-mediated Hypersensitivity
  2. Type II = IgG-Mediated Cytotoxic Hypersensitivity
  3. Type III = Immune Complex-Mediated Hypersensitivity
  4. Type IV = Cell-Mediated Hypersensitivity
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5
Q

What is the meaning of immediate hypersensitivity reactions and what type of hypersensitivity reactions are included?

A
  • Antibody-mediated
  • Involves I,II, and III
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6
Q

What antibodies are involved in Type I hypersensitivity reaction?

A

IgE

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7
Q

Why are Type I hypersensitivity reactions rapid?

A

Because of the presence of performed mediators (histamine and vasoactive mediators) in the mast cells

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8
Q

What happens during a Type I hypersensitivity reaction?

A
  • On exposure to the antigen, TH2 cells specific to the antigen are activated
  • This stimulates B cells to produce IgE antibodies
  • IgE antibodies bind strongly to the Fc portion of mast and basophils cells
  • This stimulates the degranulation of granules of mast cells
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9
Q

What are the three types of responses that result from activation of mast cells in type I hypersensitivity?

A
  • Rapid degranulation (release of histamine and vasoactive mediators)
  • Synthesis and secretion of lipid mediators
  • Synthesis and secretion of cytokines
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10
Q

What do histamines do?

A

Dilate the small blood vessels, this increases vascular permeability and stimulates the contraction of smooth muscles

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11
Q

What does sensitisation mean? (in reference to cells)?

A

The mast cells have been coated with IgE antibodies

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12
Q

What are some examples of Type I hypersensitivity reactions?

A

Allergic rhinitis, allergic asthma, atopic dermatitis, and systemic anaphylaxis

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13
Q

Why are some people allergic to penicillin?

A
  • The β lactam ring of penicillin can be produce covalent conjugates with proteins of the body creating new foreign epitope
  • The TH2 cells recognise this epitote as foreign and activate B cells producing IgE antibodies and mast cells are degranulated
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14
Q

What drugs have been linked to Type II hypersensitivity and what can they cause?

A
  • Penicillin, quinidine, and methyldopa
  • haemolytic anaemia (destruction of red blood cells) thrombocytopenia (destruction of platelets)
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15
Q

Which antibodies are involved in type II hypersensitivity?

A

IgG and IgM

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16
Q

What happens during type II hypersensitivity?

A
  • IgM and IgG antibodies bind to the surface antigen, these antigens are structural components of cell surfaces
    • Antigen–antibody reaction leads to complement activation or ADCC (opsonisation)
17
Q

What are some examples of antibody mediated - complement dependent reactions? (3)

A

Transfusion reactions, reactions to certain drugs and autoimmune haemolytic anaemia

18
Q

How are the drugs cromlyn and ketotifin used in treatment of type I and II hypersensitivity?

A

They prevent mast cell degranulation, preventing allergic cascade from happening

19
Q

Which antibodies are involved in type III hypersensitivity?

A

IgA, IgE, IgG and IgM

20
Q

What happens during type III hypersensitivity reaction?

A
  • Accumulation of immune complexes (antibody-antigen complex),
    • immune complex isn’t removed by phagocytes
  • Immune complexes are deposited on blood vessel walls and joints
  • When IgG binds antigen, complement is activated
  • C5a (attracts neutrophils) and C3b (potent opsonin) are generated
  • This leads to phagocytosis and this leads to the release of enzymes and formation of oxygen radicals, resulting in tissue damage.
21
Q

How long does type IV hypersensitivity take to develop?

A

12 hours or more

22
Q

What happens during a Type IV hypersensitivity reaction?

A
  • First encounter: antigen is present on the surface of antigen-presenting cells, this activates the production of the TH1 cells.
  • At this point the immune system is said to be sensitised
  • Second contact with same antigen = sensitized TH1 cells react with antigen release cytokines that activate macrophages or Tc which can cause cellular damage
23
Q

Mycobacterium Tb can induce which type of hypersensitivity?

A

Type IV

24
Q

Which type of hypersensitivity does herpes simplex virus cause?

A

Type IV

25
Q

All four of histamine receptors subtypes are ligand gated ion channels. True or false?

A

False - GPC receptors

26
Q

Only H1 and H4 are of clinical interest. True or false?

A

False - H1 and H2

27
Q

What are the histamine physiological effects that are mediated by H1 receptors? (5)

A
  1. Contraction of bronchial smooth muscle
  2. Contraction of intestinal smooth muscle
  3. Stimulation of sensory nerve endings
  4. Enhancement of Ca2+ influx into cardiac myocytes leading to minor increases in force of contraction and rate of contraction
  5. Increased production of nasal mucus
28
Q

What effect does activation of H2 receptors have?

A

Signals for the stomach to make acid

29
Q

What are glucocorticoids?

A

Steroids synthesised in the adrenal cortex

30
Q

What are the cytokines that are inhibited by glucorticoids?

A

IL1 to IL6 and IL8

31
Q

Glucorticoids inhibit cell-mediated immunity. True or false?

A

True

32
Q

Inhibition of which cytokine by glucorticoids has the most crucial effect in immunosuppression?

A

IL2 - inhibits proliferation of Tcells and activation of cytotoxic T cells

33
Q

What is the definition of immunological tolerance?

A

Specific unresponsiveness to an antigen induced by exposure of lymphocytes to that antigen

34
Q

What is an auto-antibody?

A
  • An antibody produced to attack the host’s own cell or tissue components.
35
Q

What are the important stages in embryonic development (to prevent auto-immunity)? (2)

A
  • Isolation/removal of auto-antigens from the immune system
  • Deletion of auto-reactive TH-cell clones during development
36
Q

What is Myasthenia gravis and what is it an example of?

A

Example of autoimmune diseas

  • The patient with this disease produces autoantibodies that bind the acetylcholine receptors
  • These antibodies block the normal binding of acetylcholine and also induce complement-mediated lysis of the cells (reduction in number)
  • Na can’t enter cell = no muscle contraction
37
Q

How does maturity-onset diabetes relate to autoimmunity and how can it be treated?

A
  • Auto-antibody binds to insulin receptor site, so insulin cannot bind
  • This can be treated with injections of insulin = insulin outcompetes auto-antibodies
38
Q

How does insulin-dependent diabetes mellitus relate to auto-immunity?

A
  • Beta cells of pancreas producing insulin are targeted by cytotoxic T-cells
    • They are recognised as being infectious
  • So, insulin isn’t produced and this leads to increased glucose levels in blood
39
Q

How does multiple sclerosis relate to auto-immunity?

A
  • Antibodies target myelin and degrade it = no protective substance to facilitate transmission of signal
  • Problems in transmitting signals neurone to neurone
  • CNS doesn’t function normally = painful

PHAR20400 (20 decks)

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