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IMMUNOLOGY > Lecture 19+20: Immunotherapies > Flashcards

Lecture 19+20: Immunotherapies Flashcards

1
Q

immune-mediated diseases are a failure of immune ______

A

regulation
- self or non-self antigens inciting a pathologic immune response

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2
Q

auto-immune diseases are a failure of….

A

self tolerance
- usually a known self antigen inciting a pathogenic immune response

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3
Q

what are some common immune-mediated diseases of dogs & cats

A
  • atopic dermatitis
  • osteoarthirits
  • chronic bronchitis /asthma / recurrent airway obstruction
  • lymphoplasmacytic rhinitis
  • IBS
  • Glomerulonephritis
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4
Q

common auto-immune diseases in dogs+cats

A
  • immune mediated hemolytic anemia (IMHA)
  • immune mediated thrombocytopenia (ITP)
  • systemic lupus erythematosus (SLE)
  • immune mediated poly-arthiritis (IMPA)
  • Type I DI (dogs)
  • Autoimmune myasthenia gravis
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5
Q

pharmacodynamics is…

A

what drugs to do the body

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6
Q

pharmacokinetics is ….

A

what body does to drugs

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7
Q

what is responsible for the conversion of Arachidonate into prostaglandin H2 (PGH2)

A

COX 1 + 2

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8
Q

COX metabolizes the first step in….

A

arachidonic acid metabolism to prostanoids

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9
Q

COX I is constitutive meaning

A

it is always expressed

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10
Q

COX 2 is inducible meaning

A

it is conditionally expressed
COX-2 is produced in response to cytokines, tumor promoters, growth factors, etc.

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11
Q

what is COX 2 produced in response to

A

cytokines, tumor promoters, growth factors, etc
- generates a positive inflammatory feedback loop

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12
Q

what species is acetaminophen highly toxic to

A

cats

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13
Q

what are the main COX inhibitor drugs that are analgesic and anti-pyretic

A
  • acetaminophen
  • aspirin
  • NSAIDs
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14
Q

what are the 3 classes of NSAIDs

A

Nonspecific (COX 1+2)
COX-2 Preferential
COX-2 Exclusive (99% specific for COX2)

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15
Q

what class of NSAID is ketoprofen

A

Nonspecific (COX 1 and 2)

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16
Q

what class of NSAID is phenybutazone

A

COX 2 Preferential

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17
Q

what class of NSAID is flunixin meglumine (‘Banamine’)

A

COX 2 Preferential

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18
Q

what class of NSAID is carprofen

A

COX 2 Preferential

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19
Q

what class of NSAID is meloxicam

A

COX 2 Preferential

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20
Q

what class of NSAID is firocoxib

A

COX 2 Exclusive

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21
Q

what class of NSAID is robenacoxib (‘Onsior’)

A

COX 2 Exclusive

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22
Q

what class of NSAID is deracoxib

A

COX 2 Exclusive

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23
Q

NSAIDs target inflammation occurring primarily in the….

A

synovium (synovitis membrane) and articular cartilage

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24
Q

NSAIDs reduce the production of…

A

PGE2 by synoviocytes + chondrocytes

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25
Q

PGE2 directly contributes to inducing ________ of chondrocytes

A

apoptosis

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26
Q

what does PGE2 promote the secretion of

A
  • other cytokines (IL-1, NO, TNF-a) that contribute to the cartilage breakdown leading to synovitis and chondrocyte apoptosis
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27
Q

major NSAID toxicities

A
  • gastric ulcers (pain, bleeding, diarrhea)
  • nephrotoxicity (acute renal failure, interstitial nephritis, glomerular nephropathy)
  • Hepatotoxicity (enzyme elevation + hepatitis)

also… bronchoconstriction, pancreatitis, agranulocytosis, aplastic anemia

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28
Q

Grapiprant use

A

pain and inflammation for osteoarthiritis

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29
Q

Grapiprant is a _____ receptor antagonist

A

EP4

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30
Q

EP4 is one of four ______ receptors that mediate inflammation in osteoarthritis

A

PGE2

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31
Q

what are the most commonly used and efficacious anti-inflammatory drugs

A

glucocorticoids
- suppress essentially every component of the inflammatory process, inhibit more mediators of inflammation than any other drug

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32
Q

what is the early effect of glucocorticoids?

A

inhibition of phospholipase A2

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33
Q

what are the late effects of glucocorticoids?

A
  • increases the synthesis of anti-inflammatory ILs
  • decreased synthesis of pro-inflammatory ILs and cytokines
  • decreased production of leukocytes
  • decreased opsonization
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34
Q

what is the endogenous glucocorticoid?

A

Hydrocortisone (Cortisol)

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35
Q

can cats utilize prednisone

A

no b/c they cannot absorb nor convert prednisone effectively

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36
Q

glucocorticoid replacement is used to treat ?

A

hypoadrenocorticism (addison’s)

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37
Q

glucocorticoids used for musculoskeletal / joint infections

A

triamcinolone: dogs, cats, horses
isoflupredone: cattle and pigs
flumethasone: dogs and horses

38
Q

adverse effects of glucocorticoids used for musculoskeletal / joint infections

A
  • muscle atrophy
  • inhibits fibrocartilage growth
    * DON’T USE IN GROWING ANIMALS
  • causes osteoperosis
39
Q

use of Fluticasone

A
  • upper tracheobronchial disease in dogs
  • asthma in cats
  • RAO in horses ($$$)
40
Q

effect of Fluticosane

A

local pulmonary immunosuppression to reduce inflammation and epithelial damage

41
Q

adverse effects of Fluticosane

A
  • pharyngitis and upper resp. infections
  • may decrease the production of endogenous corticosteroids = systemic effect
  • risk of lethargy, bradycardia, anemia, hypovolemic shock
  • not for use in acute asthmatic attacks
42
Q

what are the 5 most common glucocorticoids used for skin, eyes, ears (Don’t Honk I’ll Tinkle Pee)

A
  • dexamethasone
  • hydrocortisone
  • isoflupredone
  • triamcinolone
  • prednisolone
43
Q

main reasons to NOT use glucocorticoids

A
  • cutaneous food allergies (rare in herbivores)
  • infectious or parasitic (bacterial or fungal skin infections….flea allergy dermatitis)
44
Q

what is the common length of txt time w/ glucocorticoids

A

> 2 weeks

45
Q

main adverse effects of glucocorticoid use

A
  • gastric ulcers and colonic perforation
  • infections
    —> increases susceptibility to infections b/c of immune suppression & inhibition of inflammation masks signs of disease
  • polyuria, polydipsia, polyphagia
  • muscle atrophy
  • laminitis in horses
46
Q

adverse effects caused by the systemic
use of glucocorticoids

A
  • chronically high exogenous glucocorticoids suppress the HPA axis
  • adrenals reduce glucocorticoid and mineralocorticoid production
  • adrenals may atrophy
  • slowly reduce exogenous glucocorticoid dose over time to allows HPA axis to recover
47
Q

what are the itch cytokines

A

IL- 2
IL-4
IL-6
IL-13
IL-31

48
Q

what does Cyclosporin A (‘Atopica’) do

A
  • binds cyclophilin to calcineurin
  • inhibits all T-cell response by blocking the transcription of IL-2 and INF-y
49
Q

what is Cyclosporin A used for

A
  • atopic dermatitis
  • keratoconjunctivitis sicca and autoimmune disorders (extra-label)
50
Q

adverse effects of Cyclosporin A

A
  • V+/D+, anorexia
  • hypersensitivity
  • gingival hyperplasia
  • DM (dogs)
  • hepatic lipidosis (cats)
51
Q

when should Cyclosporin A NOT be used

A
  • history of malignant neoplasia
  • use of live Vx
  • FIV or FeLV positive
  • latent Toxoplasma gondii infection
52
Q

what is the use of Oclacitinib (‘Apoquel’)

A

txt of atopic dermatitis in dogs >1yr

53
Q

what are the adverse effects of Oclacitinib?

A
  • D+/V+
  • polydipsia
  • lethargy
  • immunosuppression, neoplasia, skin disorders
54
Q

what is the MOA of Oclacitinib?

A

competitive inhibitor of Janus kinases (JAK1 primarily)

55
Q

what is Lokivetmab (‘Cytopoint’), how does it work

A
  • “caninized” (only works in dogs) monoclonal antibody
  • Neutralizes IL-31 (a pro-pruritic cytokine acting through JAK1/2 pathway)
56
Q

Adverse effects of Lokivetmab

A
  • lethargy
  • V+
  • hyperexcitability
  • injection site pain
  • urinary incontinence
57
Q

how are monoclonal antibodies traditionally produced?

A

using an in vitro cell culture known as hybridoma that uses mouse cells

58
Q

immune-mediated diseases are usually acquired or secondary, this means that…

A

they are caused by another disease process
- multifactoral etiology

59
Q

autoimmune diseases are primary mostly, this mean…

A

diseases are acquired through the germ line

60
Q

what does it mean for effects to be off-target

A

they can end up binding something else somewhere else in the body

61
Q

what does it mean for drug effects to be overextended

A

the drug causes more of an effect than expected

62
Q

what do labeled use drugs (FDA-approved for veterinary use) require

A
  1. defines a drug
  2. defines dose/interval and duration of the drug
  3. is given by a specified route
  4. given for a particular species
  5. has been shown (by manufacturer) to be effective for the indicated disease
63
Q

what is extra-label use of a drug?

A

drug itself is FDA approved but the way it used isn’t - however using it is still allowed legally

also allows for use of Human FDA approved drugs that lack veterinary approval

64
Q

using ketoprofen in birds is an example of what type of drug use (labeled vs extra labeled)

A

Extra label use

65
Q

what does COX-1 produce

A

prostanoids needed for the maintenance of normal physiology

ex: gastric cytoprotection and normal renal vasoconstriction

66
Q

the analgesic and anti-pyretic properties of COX inhibitors are due to actions of the ________, not anti-inflammatory effects

A

Nervous system

67
Q

COX inhibitor that is an investigational drug for cats at risk of saddle thrombi

A

Aspirin

68
Q

what are the most common chronic, labeled indications for NSAIDs usage?

A

musculoskeletal pain and inflammation and osteoarthritis

69
Q

what is one of the major differences b/w indications for glucocorticoid use

A

different doses

70
Q

can you give Cylosporin A to a cat who is positive for FIV or FeLV ?

A

naur

71
Q

what can result from using murine (human) antibodies to treat other species?

A

can cause an immune response against the therapeutic antibody

patients endogenous immune system opsonizes the therapeutic antibody = HAMA respnse = Human Anti-Mouse Antibody

72
Q

what is a HAMA response

A

Human Anti-Mouse Antibody
occurs when a murine antibody is used to treat other species and the patients endogenous immune system ends up opsonizes the therapeutic antibody

73
Q

what is the effect of Mycophenylate mofetil

A

reduces DNA synthesis by inhibiting production of guanine nucleotides

74
Q

what is the effect of Azathioprine

A

reduces DNA synthesis by…
- introducing thio-guanine bases into elongating DNA strands
- inhibiting adenosine and guanine (purine) production

75
Q

how does Azathioprine promote T-cell apoptosis

A

by inhibiting Rac stimulation from CD28

76
Q

what drug can be used in combination w/ corticosteroids to reduce corticosteroid dose

A

Azathioprine

77
Q

adverse effects caused by Mycophenylate mofetil

A

V+/D+, anorexia

lymphopenia w/ increased skin infections

78
Q

adverse effects caused by Azathioprine

A

in dogs…
-V+/D+, anorexia
-leukopenia and thrombocytopenia
-pancreatitis
-hepatopathy

in cats…
bone marrow suppression b/c they have lower capacity to metabolize the drug

79
Q

if a drug ends in “-coxib”, it is a COX-2 _________ NSDAID

A

COX 2 exclusive

80
Q

if a drug ends in ‘-one’ it is probably a glucocorticoid… but there are 2 exceptions what are they

A

Phenylbutazone (COX 2 Preferential NSAID)
Budenoside is a glucocorticoid

81
Q

cyclosporine, oclacitinib and lokivetmab all act on ________ function

A

Cytokine function

82
Q

what is Triamcinolone, what is its use, and in what species?

A

glucocorticoid used in musculoskeletal/joint infections

dogs, cats, horses

83
Q

what is Isoflupredone, what is its use, and in what species?

A

glucocorticoid used in musculoskeletal/joint infections

cattle, pigs

84
Q

what is Flumethasone, what is its use, and in what species?

A

glucocorticoid used in musculoskeletal/joint infections

dogs, horses

85
Q

what drug is a treatment for atopic dermatitis and works by inhibiting all T-cell response by blocking the transcription of IL-2 and INF-y

A

Cyclosporin A

86
Q

what drug is a treatment for atopic dermatitis and can cause hepatic lipidosis in cats

A

Cyclosporin A

87
Q

what drug promotes T-cell apoptosis by inhibiting Rac stimulation from CD28

A

Azathioprine

88
Q

symptoms of gastric ulcers (an NSAID toxicity)

A

pain, bleeding, diarrhea

89
Q

symptoms of hepatotoxicity (NSAID toxicity)

A

enzyme elevation + hepatitis

90
Q

symptoms of nephrotoxicity (NSAID toxicity)

A

acute renal failure, interstitial nephritis, glomerular nephropathy

IMMUNOLOGY (26 decks)

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