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Pathology > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

What is a type I immune-type hypersensitivity?

A

IgE mediated hypersensitivity - allergy

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2
Q

What causes type I immune-type hypersensitivity?

A

Allergen hypersensitivity

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3
Q

What happens in a primary exposure in type I immune-type hypersensitivity?

A

Allergen presented to T helper cells

Selection of B-cells which generate B cells producing IgE

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4
Q

What determines ones propensity to develop IgE?

A

Genetics, T cell responsiveness and antigenic burden

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5
Q

What happens upon a secondary exposure in type I immune-type hypersensitivity?

A

IgE binds to high-affinity IgE receptors on the surfaces of mast cells and basophils, and these cells are now primed to react the next time the cells come into contact with the allergen

Cross-linking of IgE on the cell surface (via contact with allergen) causes rapid degranulation

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6
Q

What do mast cells/ basophils degranulate?

A

Highly potent inflammatory mediators such as histamines, PG, leukotrienes and PAF

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7
Q

What does histamine cause in the lungs?

A

Smooth muscle contraction

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8
Q

What does histamine cause in the skin?

A

Wheal and flare reaction

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9
Q

What does widespread activation of mast cells lead to?

A

Systemic effects - circulatory shock, hypotension, chest tightness and, in the most severe cases, respiratory arrest and death: this is anaphylactic shock.

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10
Q

How would you find out if your patient’s mast cells have degranulated?

A

The use of mast cell tryptase testing will confirm mast cell degranulation

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11
Q

What are anaphylactoid reactions?

A

Anaphylaxis-like reactions that also result from mast cell degranulation and widespread histamine release.

In these reactions the initial stimulation of mast cells does not occur through interaction of IgE with antigen.

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12
Q

What can mast cells be stimulated by in anaphylactoid reactions?

A

Examples include dextran starches, fluorescein and radio-opaque contrast media.

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13
Q

How do you treat anaphylactoid reactions?

A

The treatment of both anaphylactoid and anaphylactic reactions is the same and protocols for its management should be followed.

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14
Q

Does mast cell tryptase testing differentiate between anaphylaxis and anaphylactoid?

A

No

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15
Q

What is type II hypersensitivity?

A

Antibody mediated reactions - when an antibody is produced in response to non-harmful antigens resulting in an unwanted immune response. (with or without complement activation)

Autoimmune disease

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16
Q

When may type II hypersensitivity occur?

A

Type II hypersensitivity may occur when B-cells that produce immunoglobulin against native cells are not deleted during development.

Tolerance is not built up properly

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17
Q

What is stimulatory hypersensitivity type V? Example?

A

Autoantibody acting as agonists on cell surface receptors (graves disease)

18
Q

What is the immediate treatment for anaphylaxis?

A

Adrenaline, anti-histamines

19
Q

Long term anaphylaxis treatment?

A

Cromoglycate, leukotriene receptor antagonists, glucocorticoids and antihistamines

20
Q

What does cromoglycate do?

A

Cromoglycic acid (cromolyn sodium) is an anti-inflammatory agent that prevents mast cell activation and degranulation by inhibiting chloride transport and protein kinase C.

21
Q

What is haemolytic disease of the foetus and newborn (HDFN)?

A

Condition where antibodies in a pregnant woman’s blood destroy her baby’s blood cells.

22
Q

What does HDFN represent?

A

HDFN represents a breach of immune privilege for the fetus or some other form of impairment of the immune tolerance in pregnancy.

23
Q

What occurs in HDFN?

A

IgG antibodies are then able to cross the placenta into the fetal bloodstream to attach to the red blood cells and cause their destruction (hemolysis).

24
Q

Why does HDFN often occur?

A

Fetal-maternal hemorrhage

25
Q

How is HDFN prevented?

A

Rhesus-negative mothers who are pregnant with a rhesus-positive infant are offered Rho(D) immune globulin (RhIG, or RhoGam)

It works by binding any fetal red blood cells with the D antigen before the mother is able to produce an immune response and form anti-D IgG.

26
Q

What is type III hypersensitivity?

A

Deposition of immune complexes (antigen antibody complex), this results in complement activation and inflammation.

27
Q

In health, why are antigen antibody complexes not a problem? How are they cleared?

A

Complexes are maintained as soluble immune complexes in the blood by complement proteins C2 and C4.

Immune complexes bind to complement receptors on red blood cells allowing their transport to the spleen where complexes are removed and destroyed.

28
Q

Why does type III hypersensitivity occur?

A

When there is excessive production of immune complexes, precipitation may occur. This leads to complement activation, recruitment of immune cells and tissue damage through release of inflammatory mediators and free radicals.

29
Q

Which individuals may be predisposed to hypersensitivity?

A

Those with C2 or C4 complement protein deficiency.

30
Q

How is SLE a type III hypersensitivity?

A

This may be due to fewer complement receptors on RBCs leading to a reduced rate clearance of immune complexes.

31
Q

What hypersensitivity is SLE?

A

Type III and type II (autoantibodies)

32
Q

What induces Farmers lung?

A

High antigenic loads of organic dust particles - produce large amounts of immune complexes

33
Q

What type is farmers lung?

A

Type III

34
Q

What is the type III pathology of RA?

A

Immune complexes deposit in the synovium of joints

35
Q

What is type IV hypersensitivity?

A

Delayed type - actions of stimulated antigen specific T-cells. These reactions may take up to 12 hours to develop

36
Q

Do antibodies have a role in type IV hypersensitivity?

A

No

37
Q

Why does type IV take long to develop?

A

Cells take time to accumulate

38
Q

Describe the process of a type IV hypersensitivity?

A

Antigen is taken up by local innate immune cells such as macrophages and Langerhans cells.

These antigen presenting cells activate antigen specific CD4+ T-cells.

T-cells activated in this manner tend to adopt a Th1 profile and migrate to the area of high antigenic load where they release inflammatory cytokines such as interferon-γ (IFN-γ), IL-1, IL-2 and IL-6.

The result of cytokine release is local inflammation through an increase in vascular permeability and further immune cell migration and activation - destruction of the ECM

If an antigenic challenge is prolonged, the chronic inflammatory response can result in granuloma formation

39
Q

What type of hypersensitivity underpins contact sensitivity?

A

Type IV

40
Q

What mechanisms can contribute to multiple sclerosis and type I diabetes?

A

Type IV cell mediated

41
Q

The following clinical features are associated with a positive skin test for allergen at one hour

A

Oedema, pruritis and erythema

swelling, itching, redness

42
Q

Are Th1 T cells associated with allergens?

A

No

Pathology (21 decks)

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