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Veterinary Pathology > Diseases of Immunity (Part 2) > Flashcards

Diseases of Immunity (Part 2) Flashcards

1
Q

What are autoimmune diseases?

A

immune response to self-antigens

loss of “immune tolerance”

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2
Q

Many autoimmune diseases are _____ and/or have a _____ component

A

multifactorial; genetic component

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3
Q

Most autoimmune diseases are characterized by _____

A

alternating clinical disease and convalescence

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4
Q

What is very important when trying to diagnose an autoimmune disease?

A

history!

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5
Q

What is immunologic tolerance?

A

failure of the immune system to respond to a specific antigen AFTER previous exposure to that antigen

misdirected response

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6
Q

Immunologic tolerance is the absence of a [response entirely / functional response]

A

immunologic tolerance: functional response

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7
Q

How does one maintain tolerance?

A

deletion
- self tolerance: clonal elimination of self-reactive lymphocytes

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8
Q

Where is central tolerance? Peripheral?

A

central: thymus

peripheral: peripheral tissue

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9
Q

What is autoimmunity? Which tolerance influences this more?

A

failure of immunologic tolerance

peripheral tolerance

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10
Q

What are mechanisms of peripheral tolerance?

A

anergy

suppression

antigen sequestration

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11
Q

What is anergy? In what context?

A

functional INactivation of lymphocytes that encounter antigen

peripheral tolerance mechanism

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12
Q

What does an anergia cell lack?

A

co-stimulatory protein from APC

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13
Q

What is suppression mechanism? In what context?

A

inhibition of lymphocyte activation & effector function

activation of regulatory cells to prevent immune reactions to self-antigens
- which keep lymphocytes in check

peripheral tolerance

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14
Q

What are antigen sequestration mechanisms? In what context?

A

immune-privileged sites - DO NOT go through tolerance

peripheral tolerance

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15
Q

List some immune-privileged sites

A

BBB
testes
eye

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16
Q

What are the two forms of lupus erythematosus?

A

systemic lupus erythematous (SLE)

discoid lupus erythematous (DLE)

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17
Q

What is SLE?

A

multisystemic, including the skin

fatal! - 40% die within 1 year

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18
Q

What is DLE?

A

localized to the skin

low morbidity (good prognosis)

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19
Q

What is the problem with differentiating DLE and SLE? What do we need to help determine which one?

A

they look almost identical

history!

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20
Q

What is the predominant autoantibody for SLE?

A

antinuclear antibody (ANA): target = nuclear antigens

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21
Q

What can trigger SLE?

A

drugs
viruses
UV light

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22
Q

SLE is which hypersensitivity?

A

type III
lesser type II and IV

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23
Q

What are some causes of SLE?

A

definitive cause: unknown

genetic, environmental (UV), transmissible factors implication

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24
Q

What does SLE have antibodies against?

A

antibodies against a range of nuclear and cytoplasmic components of the cell

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25
Q

What are some symptoms of SLE?

A

polyarthritis
fever of unknown origin
anemia
thrombocytopenia
stomatitis
glomerulonephritis
dermatitis

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26
Q

For SLE, _________ signs occur in approximately 1/3 of cases

A

dermatologic signs

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27
Q

What are some symptoms of DLE?

A

depigmentation, erythema, scaling, erosion, ulceration, crusting

skin of the nasal plane, nose
- less commonly: pinnae, lips, periocular region, and rarely in oral mucosa

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28
Q

The blood panel of [SLE/DLE] should be normal

A

DLE

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29
Q

What is the cause of rheumatoid arthritis?

A

rheumatoid factor - anti-IgG antibody

fibroblasts in the pannus enzymatically degrade cartilage

due to chronic injury - fibrous CT, chronic inflammatory cells

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30
Q

What is the pannus?

A

abnormal layer of fibrovascular tissue or granulation tissue (joints, cornea)

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31
Q

What are clinical signs of rheumatoid arthritis?

A

lameness
joint laxity

32
Q

What is Sjögren-Like Syndrome?

A

influx of lymphocytes and plasma cells

stuff gets pushed in and glandular tissue can’t work

possible link to viral infection

33
Q

What are the lesions in Sjögren-Like Syndrome?

A

keratoconjunctivitis sicca: dry eyes, conjunctivitis, and keratitis

xerostomia: dry mouth, gingivitis and stomatitis

lymphoplasmacytic sialoadenitis: inflammation of salivary glands

34
Q

What is the clinical pathology for Sjögren-Like Syndrome?

A

hypergammaglobulinemic

might have ANA titer

might have positive RF (rheumatoid factor)

35
Q

What is Inflammatory Bowel Disease?

A

cats and some dogs

bowels get thicker because of influx of inflammatory cells into lamina propria
- infiltrate and affect tissue and job

36
Q

What can Inflammatory Bowel Disease lead to?

A

malabsorption and chronic protein losing enteropathy (PLE)

cats: may be caused by dietary antigens and progress into lymphoma

37
Q

Regarding Inflammatory Bowel Disease, chronic irritation can lead to ______

A

neoplasia

38
Q

What are the type of lesions in Uveodermatologic Syndrome (Vogt-Koyanagi-Harada-like Syndrome)?

A

skin lesions
ocular lesions

39
Q

What kinds of dogs are affected with Uveodermatologic Syndrome (Vogt-Koyanagi-Harada-like Syndrome)?

A

arctic breeds (sled dogs)

40
Q

Describe the pathogenesis of Uveodermatologic Syndrome (Vogt-Koyanagi-Harada-like Syndrome)

A

breakdown of blood-retinal barrier —> exposure of retina-specific antigen —> production of anti-retinal antibodies —> blindness

41
Q

What are the skin lesions in Uveodermatologic Syndrome (Vogt-Koyanagi-Harada-like Syndrome) mediated by?

A

T cells, macrophages (Th1 immunity)

42
Q

What are the ocular lesions in Uveodermatologic Syndrome (Vogt-Koyanagi-Harada-like Syndrome) mediated by?

A

more consistent with B cell and macrophage response (Th2 immunity)

43
Q

In Uveodermatologic Syndrome (Vogt-Koyanagi-Harada-like Syndrome), [skin/ocular] lesions commonly precede or are recognized prior to the other

A

ocular before

44
Q

What is the clinical syndrome of Uveodermatologic Syndrome (Vogt-Koyanagi-Harada-like Syndrome)?

A

facial dermal depigmentation

severe generally bilaterally symmetric uveitis

45
Q

What is an immunodeficiency?

A

failure of the immune system to protect the host from infectious organisms or cancer

46
Q

What are the types of immunodeficiencies?

A

primary: congenital (something happened in utero) or genetic defect

secondary: loss of immune function due to infections, malnutrition, irradiation, chemotherapy

47
Q

Just look at this immunodeficiency chart

A
48
Q

What is SCID (severe combined immunodeficiency disease)?

A

a primary immunodeficiency

deficiencies in humoral and cell-mediated immunity

49
Q

What does SCID (severe combined immunodeficiency disease) have defects in?

A

T lymphocytes

or T and B lymphocytes

50
Q

What is the common sequelae to SCID?

A

fungal or vira infections

bacterial: if not reliant on passive humoral immunity from colostrum

51
Q

What does SCID cause in horses? Which breeds?

A

hypoplasia of lymphoid tissue

spontaneous mutation in the catalytic subunit of DNA-dependent protein kinase (DNA-Pkcs) on chromosome 9 - also Jack Russell terriers

arabian or arabian cross

52
Q

What can happen if a horse with SCID has a secondary infection?

A

death resultant from equine adenovirus, pneumocystis carinii, cryptosporidium parvum

53
Q

Heterozygous foals with SCIDS can live longer but are prone to develop _____

A

sarcoids

54
Q

What is SCID in dogs? Which breeds?

A

X-linked defect

basset hounds

55
Q

What is the cause and effect of SCID in dogs?

A

cause: mutation on common gamma subunit of IL-2, 4, 7, 9, 15 receptors (type I cytokine family)

lymphoPENIA, severe lymphoid hypoplasia

56
Q

What is SCID in mice?

A

absence of mature B and T lymphocytes

CB-17 strain, autosomal recessive

57
Q

What is the exception regarding mice?

A

survive with SCIDs if kept in sterile facilities

58
Q

Which thymus most likely has SCID

A

right: causes thymic hypoplasia (morophologic diagnosis)

59
Q

What is Agammaglobulinemia? Who is affected?

A

x-linked recessive

absence of B lymphocytes (and plasma cells) —> inability to produce immunoglobulins

young colts - thoroughbred, quarter horse, Standardbreds

60
Q

What are some lesions in Agammaglobulinemia?

A

pneumonia - lungs an easy entrance

arthritis

others in picture

61
Q

What is Chèdiak-Higashi Syndrome?

A

inherited - autosomal recessive

defective lysosomes, melanosomes, platelet-dense granules, & cytolytic granules

62
Q

Describe what is happening here regarding Chèdiak-Higashi Syndrome

A

the lymphocyte contains a large red-purple granule

63
Q

What do you see microscopically regarding Chèdiak-Higashi Syndrome?

A

enlarged granules in melanocytes, neutrophils, eosinophils, monocytes

64
Q

What are clinical signs of Chèdiak-Higashi Syndrome?

A

hypopigmentation, bleeding problems, ocular abnormalities, recurrent infections

65
Q

What are LADs?

A

leukocyte ahesion deficiency

defective expression of beta-2 integrins

66
Q

What is this an example of?

A

leukocyte adhesion deficiency

67
Q

What is Amyloidosis? List the types

A

defect in beta-pleated sheet - leads to deposition in blood vessels, basement membranes, spaces of disse, spleen

AL amyloid
AA amyloid
B amyloid

68
Q

What is AL type of Amyloidosis?

A

secreted in B cell proliferative disorders

more so horses affected

69
Q

What is AA type of Amyloidosis?

A

liver secretes SAA during inflammation

AA synthesized from SAA

70
Q

Which stain is for fresh tissue and which stain is for fixed tissue?

A

fresh: iodine - not specific for amyloid

special: formalin-fixed tissue
- congo red
- apple green perfringence under polarized light

71
Q

What is the problem with Amyloidosis?

A

targets capillaries

deposition of material cannot be broken down

compression, occlusion of spaces

72
Q

What are the most affected organs regarding Amyloidosis?

A

kidney: glomerulonephropathy

liver: birds

spleen

73
Q

Identify what has accumulated in these H&E and congo red stains

A

amyloid

74
Q

How does amyloid affect the liver?

A

goes down lobule of liver —> starts to compress hepatocytes —> pressure atrophy

75
Q

Review table regarding Amyloidosis

A

Veterinary Pathology (11 decks)

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