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Pathology > Hypersensitivities > Flashcards

Hypersensitivities Flashcards

1
Q

IgE mediated degranulation of mast cells is a key effector mechanism of which of the following inflammatory events?

A

Type I Hypersensitivity

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2
Q

What are 4 features of type I hypersensitivity?

A

Increased vascular permeability
Oedema
Acute inflammation
Infiltrate of eosinophils

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3
Q

What do type one hypersensitivies require first?

A

Prior sensitiziation -> TH2 switches on B cells via ILs

B cell produces IgE antibodies that bind to mast cell (now are armed and will degranulate next time)

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4
Q

Can type I hypersensitivites be triggered by opioids or drugs?

A

Yes - things we have never been exposed to before can cause this

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5
Q

What are preformed mediators in mast cells?

A

Histamine, heparin and tryptase

Serine proteases activate complement (anaphylotoxins)

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6
Q

What are rapidly synthesised mediators in type I reactions?

A

Prostaglandins + leukotrienes - bronchospasm + vasodilation

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7
Q

What happens in late phase type I?

A

Cellular infiltrate - onset 4-8h lasts 24h

Mast cells release chemokines -> TFN-a, IL1,3,4,5,6

Epithelial cells release eotaxin, IL6 and IL8

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8
Q

What are some examples of type I?

A

Allergic rhinitis, acute bronchial asthma, food hypersensitivity, flea bite HS

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9
Q

What is a milk allergy?

A

Milking delayed - a-casein into blood treated as foregin causing systemic anapyhylaxis and multifocal cutaneous oedema

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10
Q

What is canine and feline atopy?

A

Allergic dermatitis - from ingested or inhaled antigen

Genetic predisposition (increased IL4) to develop Ag-specigic IgE and IgG against environmental antigens and antibodies attach to cutaneous mast cells

Re-exposure to antigens by any route provokes cutaneous type I hypersensitivity

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11
Q

How does desensitisation work?

A

High dose of antigen stimulates TH1 response = IgG production

Activates macrophages to produce IL12 and present antigens to CD4

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12
Q

How is type II described?

A

IgG and IgM mediated - IgG binds to self or foreign agntigens coated onto cells stimulating phagocytosis

NKC, copmlement mediated lysis of cell = tissue damage against own cells

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13
Q

What is antibody dependent cytotoxicity?

A

Involved in type II

IgG binds with complement -> MAC -> opsonins + chemotaxis for neutrophils + eosinophils damaging accidentally targeted cells

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14
Q

What is drug induced immune mediated haemolytic anaemia?

A

Type II reaction

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15
Q

What is haemolytic anaemia?

A

Type II - maternal IgG attack fetus erythrocytes (by colostrum)

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16
Q

What are myasthenia gravis and pemphigus vulagaris part of?

A

Type II hypersensitivity

Myasthenia - response against nicotinic acetylcholine receptor

Pemphigus - keratinocyte antigens

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17
Q

What are two types of immune mediated haemolysis?

A

Extravascular - rbc agglutination and rbc phagocytosis by splenic macrophage = jaundice + anaemia

Intravascular - complement binding + activation rbc lysis and red urine

18
Q

what is type III response?

A

Lots of antigen -> excess antigen and IgG and IgM complexes form in blood that precipitate in tissues (glomeruli, vessel walls)

Activates complement

Usually chronic disease

Neutrophils attracted to complex causing inflammation

19
Q

What can stimulate type III?

A 
Large doses of antigen
Pyometra
Persistent infectious agents
Repeatedly inhaled things
Persistently available self antigen (lupis)
20
Q

Examples of Immune complex diseases (Type III)

A 
EIA
Adrican swine fever
Liver fluke in cattle
Pyometra
Infectious canine hepatitis
21
Q

What is immune complex glomerulonephritis?

A

Circulating Ab:Ag complex deposits in glomerulus

Antibodies leave circulation and complex with glomerular self antigens or endo/exogenous antigens in glomerulus

African swine fever

22
Q

Membranoproliferative glomerulonephritis

A

Subendothelial immune complex deposited

Reactive prolferation of mesangial cells

Thickened glomerular capillary BM and amyloid deposits

23
Q

What is type IV?

A

cell mediated/delayed type

No antibody involvement

depends on Ag specific sensitised T cells to be present to react (infiltration of tissue by monocytes + lymphocytes)

Intensity delayed until 48-72h

24
Q

Cell mediated vs delayed type

A

Protective CMI beneficial

Normal immune respone to poorly digestible antigen

Immunopathological DTH deleterious + causing chronic lymphocyte + granulomatous inflammation

25
Q

What is tuberculin reaction?

A

Type IV

26
Q

What is canine allergic contact dermatitis?

A

Type IV - intitiated by transdermal absorbed haptens (formaldehyde)

IFN-g from CD8+ and CD4+ cells attracts monocytes + lymphocytes

27
Q

Self tolerance

A

Central clonal deletion of self-reactive T cells and B cells in fetal thymus and bone marrow - t cell receptors on trial in thymus (self react = deleted)

28
Q

What are anatomically sequestered antigens?

A

Exposed by tissue damage - milk allergy, post traumatic sympathetic uveitis, sperm granulomas

29
Q

What is molecularly sequesered antigen?

A

exposure of epitopes normally hidden in globular proteins

30
Q

What is bacterial superantigens?

A

+++ immunostimulatory proteins = bind to MHC and T cell receptor domains, activating large % of bodies APCs and T lymphocytes

31
Q

Which of the following protects spermatozoa from immune attack?

a. High background levels of IL-1a, Il-6 and TGF-b and Activin-A in the testis.
b. Immune tolerance generated by Hassall’s corpuscles during thymus development.
c. Low expression of MHC-I by spermatogonia.
d. Down-regulation of IL-17 by spermatogonia and spermatocytes.

A

a. High background levels of IL-1a, IL6 and TGF-b and activin-A in the testis

32
Q

What is canine phemigus?

A

Bullous vesicular disease - lesions appear at mucocutaneous junctions

33
Q

What are two examples of inherited immunodeficiency?

A

Chediak-higashi syndrome

Severe combined immune deficiency of arabs

34
Q
  1. Chédiak-Higashi Syndrome results in:
    a. Normal CD8+ cytotoxicity & NK functions but impaired B-cells.
    b. Failure of phagolysosome formation in neutrophils and macrophages.
    c. Failure of phagocytosis by neutrophils.
    d. Normal circulating neutrophil numbers but abnormal neutrophil granules.
    e. A defective adaptive immune system due to a defective immunoglobin gene.
A

d. Normal circulating neutrophil numbers but abnormal neutrophil granules.

35
Q

Chediak-higashi syndrome

A

Neutropaenia and partial albinism

Neutrophils, macrophages, lymphocytes and melanocytes have defective giant intracellular granules due to microtubule effect

Neutrophils and macrophages can phagocytose but phagolysosome fusion is delayed

Cd8+ cytotocivity and NK impaired - B cells are fine

36
Q
  1. Severe Combined Immune Deficiency (SCID) in Arabian foals has which of the following features?
    a. There is partial failure of adaptive immune responses.
    b. Antibody response is retained.
    c. Defective Ig gene results in loss of B and T cell receptors.
    d. They can be diagnosed at age 1 week by measuring plasma IgG.
    e. Haematology at 1 week of age reveals an absence of circulating lymphocytes (absolute lymphocytopaenia).
A

c. Defective Ig gene results in loss of B and T cell receptors.

37
Q

SIDS

A

Complete failure of adaptive response - coat linked autosomal recessive

Defective B and T cell receptors

Normal at birth, fine until 1-3 months surviving on colostrum - rely only on neutrophils

Dead by 5 months

38
Q

Acquired immunodeficiency examples

A

Retrovirus/lentivirus

AIDS like - decreased T cell function (FIV, SIV)

T-2 toxin, corticosteroids

39
Q
  1. In older animals which of the following is a recognised feature of immunosenescence?
    a. There is a random deletion of CD4 lymphocytes
    b. Phagocytes increase in number to counteract a decline in lymphocytes.
    c. Response to vaccination is usually still strong.
    d. There is an increase in CD4:CD8 lymphocyte ratio
    e. There is diminished self-renewal capacity of haematopoietic stem cells.
A

e. There is diminished self-renewal capacity of haematopoietic stem cells.

40
Q

Immunosenescence

A

Gradual deterioration of immune system with aging

Decreased self-renewal of haematopoietic stem cells

Less phagocytes

NK cells less cytotoxocity function

Decline in humoral immunity

Reduction in CD4:CD8 ratio

Pathology (6 decks)

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