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Principles of Science BVetMed 3 > Immune-mediated disease - overview > Flashcards

Immune-mediated disease - overview Flashcards

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1
Q

What is the spectrum of immune-mediated disease?

A
  • organ specific to non-organ specific (vasculitis)

- primary (‘idiopathic’) vs secondary

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2
Q

What underlying factors should be eliminated when considering immune-mediated disease?

A
  • drug use
  • neoplasia
  • infxn
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3
Q

Example - non-organ specific immune dz

A

SLE

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4
Q

Example: organ specific immune dz

A

Myasthenisa gravis (MG)

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5
Q

What goes wrong in immune-mediated dz?

A

Immune system (I.S.) overreacts to normal body tissues or harmless exogenous protein. aka loss of tolerance

  • humoral and cellular mechanisms
  • loss of self-tolerance needed to perpetuate +/- start dz
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6
Q

Trigger factors - immune-mediated dz

A
  • release of sequestered Ag
  • abnormal immunoregulation
  • molecular mimicry
  • polycloncal activation of BCs and TCs
  • exposure of cryptic epitopes or haptenisation of foreign molecules to self antigens
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7
Q

What is haptenisation?

A

small molecules bind to larger carreir molecules and these complexes elicit an immune response, directed against the carrier molecule.

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8
Q

How is infxn thought to influence autoimmune dz?

A
  • breakdown of vascular/cellular barriers allowing exposire of self-antigens
  • promotion of cell death by necrosis, causes inflammation –> bystander sactionation
  • polyclonal activation of TCs by bacterial superantigens
  • molecular mimicry leading to cross-reactivity
  • vector-borne pathogens may be important in some parts of the world (r/o by different tests)
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9
Q

Name 3 main vector-borne pathogens that can be important in influencing autoimmune dz

A
  • protozoa
  • rickettsia
  • bacteria
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10
Q

Aetiology - autoimmune dx

A
  • of many is unclear, likely mutlifactorial often

- genetic, infectious, hormonal influences

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11
Q

Give canine autoimmune dz examples of aetiology

A
  • SLE: genetics (DLA-A7, C4,4), c-type viruses (retroviruses)
  • IMHA: vaccinal Ag?
  • IMPA: vaccinal Ag?
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12
Q

Signalment - idiopathic immune-mediated disease

A
  • over-represented in juvenile to middle-aged patients
  • any age or dog/cat though
  • SLE: Dogs 2mo-13yo, GSD, shelties, collies, beagles, poodles. Cats 1-11 yo, Siamese, Persian, Persian-related breeds
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13
Q

Hx and PE - immune-mediated dz characteristics

A
  • remission and exacerbation
  • lameness, mucocutaneous lesions, lethargy, dyspnoea, wt loss, PUPD, +/- seizures or behavioural changes
  • effusive, painful joint, cutaneous erythema, macules, papules, pustules, erosion etc, pallor +/- petechiae, cardiac arrhythmias, lymphadenomegaly +/- splenomegaly
  • Hx and PE are PIVOTAL to a DIAGNOSIS
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14
Q

How can CBC/coags tests help make diagnosis? 4

A
  • ANAEMIA: regenerative (IMHA) or non-regenerative (ifxn, uraemia, chronic bleeding, attack of precursors)
  • THROMBOCYTOPAENIA: I-M thrombocytopaenia
  • LEUCOPAENIA? anti-leukocyte Abs (e.g. SLE, I-M neutropaenia)
  • COAGULATION ABNORMALITIES: increased APTT, PT, anticoagulant Ab (SLE), DIC
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15
Q

On a blood smear, what is the hallmark of extravascular haemolysis?

A

spherocytes

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16
Q

What do chromatophils suggest on smear?

A

rengerative anaemia

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17
Q

What is rubricytosis?

A
  • presence of immature RBCs

- suggests regenerative anaemia

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18
Q

What do ghost cells represent on a smear?

A

intravascular haemolysis

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19
Q

How can biochem. help make I-M dz diagnosis? 5

A
  • AZOTAEMIA, increased inorganic phosphate (chronic glomerular lesions)
  • HYPOALBUMINAEMIA, HYPERCHOLESTEROLAEMIA: e.g. PLN
  • HYPERBILIRUBINAEMIA: pre-hepatic/ haemolysis
  • HYPERGLOBULINAEMIA; inflammatory disease, polyclonal BC activation
  • INCREASED CK and (LACTATE DEHYDROGENASE); polymyositis and/or myocarditis
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20
Q

How can UA make an I-M diagnosis?

A
  • PROTEINURIA: with PLN r/o UTI and occult infections
  • HAEMATURIA, POLYURIA, ERYTHROCYTE CASTS: r/o UTI and occult infxn, compatible with membranoproliferative glomerulonephritis (GN)
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21
Q

Features - radiography for I-M dz

A
  • erosive lesions suggest an overlap syndrome

- arthritis is not always clinically obvious

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22
Q

Define pauciarthropathy

A

where a few joints are affected, >1 but

23
Q

How common are joint lesions in polysystemic I-M dz?

A
  • common

- usually a non-erosive pauciarthropathy

24
Q

Describe synovial fluid of I-M dz

A
  • increased WBC
  • increased neutrophil %
    +/- increased protein content
  • decreased viscosity
  • poor mucin clot formation
25
Q

Describe synovial fluid of I-M dz

A
  • increased WBC
  • increased neutrophil %
    +/- increased protein content
  • decreased viscosity
  • poor mucin clot formation
26
Q

Which joint space do you aim for in carpus?

A
  • antebrachial joint as this is the 1st joint space and this is the largest joint space
  • aim for middle (to avoid nn, tendons, BVs)
27
Q

List some tests for specific I-M dz

A
  • coomb’s test
  • anti-platelet Ab
  • rheumatoid factor
  • T3, T4, TG autoAb
  • ACh receptor autoAb
  • 2M myofibre autoAb
  • ANA
  • biopsies
28
Q

What to do if IMHA is suspected

A
  • in-saline agglutination and ostmotic fragility tests to be performed
  • Ab associated with surface of RBC may also be detected with Coomb’s test
  • primary reagent: polyvalent anti-dog or anti-cat IgG, IgM and C3 antiserum (direct antiglobulin test)
  • false positive and negatives may occur
29
Q

What is the commonest I-M neuromuscular disorder?

A

Acquired MG (various forms: focal, generalised, acute fulminating, paraneoplastic)

30
Q

Gold standard diagnosis for acquired MG

A
  • documentation of nicotinic AChR autoAb by immunoprecipitation RIA
31
Q

Sensitivity/specificity of nicotinic AChR autoAb by immunoprecipitation radioimmunoassay (RIA)

A
  • false positives v rare: 2% dogs with generalised MG may be seronegative
32
Q

What part of PE may cause you to suspect MG?

A

you will be able to fatigue the palpebral response in MG patients after 10-20 stimulations

33
Q

Outline antinuclear antibodies (ANA)

A
  • serum ANA = hallmark of human/canine/feline SLE, occasional ANA-negative cases
  • indirect immunofluorescene or immuno-peroxidase test
  • substrate tissues have included rat liver, vero and Hep-2 cells: various patterns of staining
  • false positives /negatives may occur
34
Q

How are biopsies useful for I-M dz?

A
  • often signal immune mediation of lesionsin organ-specific and polysystemic diseases
  • mucocutaneous lesions should be sampled across interface with normal tissue
  • lesions may not be specific for one disease but helps you localise lesion (e.g. dermis vs. epidermis)
  • immune deposits in lesional tissue may be demonstrated by immunoperoxidase or immunofluorescence techniques.
35
Q

T/F: I-M dz are a major cuse of morbidity and mortality in SA

A

True

36
Q

T/F: various vector-borne dz have immunopathological sequelae

A

True

37
Q

Define anergy

A

the absence of a normal immune response to a particular Ag

38
Q

What determines central tolerance?

A

thymic selection

39
Q

What determines peripheral tolerance?

A
  • intrinsic and extrinsic components
40
Q

What can be the physiological response to degranulation?

A
  • inflammatory mediators
  • pruritus
  • bronchoconstriction
  • vasodilation
  • oedema
  • eosinophil chemotaxis
41
Q

Define MMM

A

Masticatory Muscle Mysositis

42
Q

What is MMM?
CS?
Dx?

A
  • idiopathic I-M dz of 2M myofibres, directed specifically at myosin
  • CS include swelling +/- eventual atrophy of mm of mastication
  • Dx by demonstrating autoAb against 2M myofibres of temporalis mm in immunocytochemical assay
43
Q

What is the anti-platelet Ab test?

A
  • considered when I-M thrombocytopaenia is a ddx
  • indirect immuofluorescence test: substrate comprises PLTs from healthy donor
  • reagent is fluoresceinated and goat anti-dog or anti-cat IgG antiserum: micrscopic and flow cytometric assays are described
  • false positive/negatives may occur
44
Q

What is rheumatoid factor?

A
  • considered when erosive arthritis documented
  • RF is a non-specific autoAb to IgG that may be found at low titre in animals with a range of infectious, inflammatory neoplastic diseases
  • high titres characterise RA
  • assayed by ELISA or Rose-Waaler test, in which RF agglutinates IgG-coated substrate RBCs
45
Q

What are T3, T4 and thyroglobulin autoAb used for?

A
  • lymphocytic thyroiditis thought to represent an autoimmune disease: Ab against thyroid Ag are released during ensuing inflammation
  • 50-60% hypothyorid dogs have TG-autoAb
  • 20% euthyroid dogs with TG-autoAb develop additional signs within a year
  • T3-autoAb observed in 33% hypothyroid dogs, T4-autoAb observed in 15% cases
46
Q

Define TT4

A

total T4

47
Q

Define fT4d

A

free T4 by dialysis (baseline)

48
Q

What is suggested with normal FT4D and TSH

A

healthy euthyroid

49
Q

What is suggested with low TT4 or FT4D with increased TSH

A

hypothyroidism

50
Q

What is suggested by TG-autoAb with no other abnormalities?

A

impending hypothyroidism?

51
Q

What does low TT3 suggest?

A

it is of limited diagnositic value, except in sight hounds, which have low TT4 and FT4D based on generic canine reference ranges

52
Q

What can be the physiological response to degranulation?

A
  • inflammatory mediators
  • pruritus
  • bronchoconstriction
  • vasodilation
  • oedema
  • eosinophil chemotaxis
53
Q

Define MMM

A

Masticatory Muscle Mysositis

54
Q

What is MMM?
CS?
Dx?

A
  • idiopathic I-M dz of 2M myofibres, directed specifically at myosin
  • CS include swelling +/- eventual atrophy of mm of mastication
  • Dx by demonstrating autoAb against 2M myofibres of temporalis mm in immunocytochemical assay

Principles of Science BVetMed 3 (110 decks)

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