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Immunology > Lecture 19 +20: Immunotherapies > Flashcards

Lecture 19 +20: Immunotherapies Flashcards

1
Q

Immune mediated or autoimmune: failure of immune regulation- self or non-self antigens inciting a pathologic immune response

A

Immune mediated disease

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2
Q

How are immune mediated diseases classified

A

Usually acquired/secondary- caused by another disease process

Multifactorial in etiology

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3
Q

Immune mediated or autoimmune:
Organ specific, start in one place

Antigen/antibody complexes can cause multi-organ dysfunction

A

Immune mediated

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4
Q

Autoimmune disease is a failure of ____

A

Self tolerance, known self antigen inciting a pathologic immune response

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5
Q

What is the classification for an autoimmune disease

A

Primary- acquired through germ line

Secondary

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6
Q

Immune mediated or autoimmune: organ specific, cell type specific effects

A

Autoimmune

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7
Q

What are some common immune mediated diseases of dogs and cats

A

Atopic dermatitis, osteoarthritis, chronic bronchitis/asthma/RAO, lymphoplasmacytic rhinitis, IBD, inflammatory/reactive hepatitis, glomerulonephritis, granulomatous meningoencephalitis

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8
Q

What are some common autoimmune diseases of dogs and cats

A

Immune mediated hemolytic anemia, immune mediated thrombocytopenia, systemic lupus erythematosus, immune mediated poly-arthritis, masticatory mastitis, autoimmune myasthenia Travis, type I DM (dogs)

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9
Q

What is pharmacodynamics

A

What drugs do to the body, what receptors drug target, how drugs act (antagonist, agonist, competitive vs non-competitive binding), adverse effects (off target or overextension)

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10
Q

What is pharmacokinetics

A

What the body does to the drug

Absorption
Distribution
Metabolism
Elimination

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11
Q

What is required for a drug to be labeled use

A

FDA approved

defines a drug (ex: ketoprofen)

given dose/internval and duration (2.2mg/kg q24, 5 days)

Given by a specified route (IV)

For a particular species (horses)

Has been shown by manufacturer to be effective for indicated disease (inflammation and pain with musculoskeletal disorders)

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12
Q

What makes something extra-label use of drug

A

Allows for us of veterinary FDA approved drug in a non-approved way (ketoprofen use in birds)

Allows for use of human FDA approved drug that lacks veterinary approval (aspirin)

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13
Q

What are some mediators of acute inflammation

A

Histamine, serotonin, bradykinin, prostaglandins, leukotrienes

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14
Q

Does histamine cause the following: vasodilation, vascular permeability, chemotaxis, and/or pain

A

Vasodilation: ++
Vascular permeability +++
Chemotaxis: -
Pain: -

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15
Q

Does serotonin cause the following: vasodilation, vascular permeability, chemotaxis, pain

A

Vasodilation: +/-
Vascular permeability: +
Chemotaxis: -
Pain: -

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16
Q

Does bradykinin cause the following: vasodilation, vascular permeability, chemotaxis, pain

A

Vasodilation: +++
Vascular permeability: +
Chemotaxis: -
Pain: +++

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17
Q

Do prostaglandins cause the following: vasodilation, vascular permeability, chemotaxis, pain

A

Vasodilation: +++
Vascular permeability: +
Chemotaxis: +++
Pain: +

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18
Q

Do leukotrienes cause the following: vasodilation, vascular permeability, chemotaxis, pain

A

Vasodilation: -
Vascular permeability: +++
Chemotaxis: +++
Pain: -

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19
Q

What two things can be used to synthesize arachidonic acid

A

Phospholipids via PLA2
Diacyglycerols via DG lipase

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20
Q

How is arachidonic acid made into prostaglandins

A

Via COX-1 and COX-2

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21
Q

COX-1 or COX-2:

Always expressed, generates prostanoids needed for maintenance of normal physiology (ex: gastric cytoprotection and normal renal vasoconstriction)

A

COX-1

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22
Q

COX-1 or COX-2:Conditionally expressed (inducible), produced in response to cytokines, tumor promoters, growth factors, generates positive feedback loop with cytokines–> cox–> prostaglandins

A

COX-2

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23
Q

What 3 drugs/classes inhibit COX

A

Acetaminophen, aspirin, NSAIDS

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24
Q

What are the therapeutic effects of acetaminophen

A

Analgesia, anti-pyretic

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25
Q

What are the therapeutic effects of aspirin

A

Analgesia, anti-pyretic anti-inflammatory, anti-thrombotic

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26
Q

What are the therapeutic effects of NSAIDS

A

Analgesia, anti-pyretic, anti-inflammatory

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27
Q

_____ and ____ are effects from acetaminophen, aspirin, and NSAIDS are due to actions on the nervous system not anti-inflammatory effects

A

Analgesic and anti-pyretic

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28
Q

What COX inhibitor drug is “added-in” for pain control in dogs but rarely

A

Acetaminophen

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29
Q

What COX inhibitor drug is highly toxic in cats

A

Acetaminophen

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30
Q

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

A

Aspirin

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31
Q

What COX inhibitor drug has minor and variable anti-thrombotic effects

A

NSAIDS

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32
Q

What are the three classes of NSAIDS in regards to COX inhbition

A

Non-specific cox inhibitor, COX-2 preferential, and COX-2 exclusive

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33
Q

What are some examples of nonspecific COX inhibitors

A

Ketoprofen

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34
Q

What are some examples of COX-2 preferential inhibitors

A

Phenybutazone (bute), flunixin meglumine (banamine), carporfen (rimadyl), meloxicam (metacam)

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35
Q

What are some examples of COX-2 exclusive inhibitors

A

Firocoxib (previcox)
Robenacoxib (onisor)
Deracoxib (deramaxx)

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36
Q

Why can’t preference/exclusivity of a drug be guaranteed

A

Because of differences in COX-1 and -2 genes between species that can lead to slightly different binding sites for the drugs

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37
Q

Why are drugs that have increased COX-2 specificity better/safer

A

Reduce inflammation but also have less effect on prostanoids because COX-1 can still generate normal prostaglandins needed for normal physiological function so fewer adverse effects

38
Q

What is the most common chronic labeled use of NSAIDS

A

Osteoarthritis

39
Q

What do NSAID’s target in treating OA

A

Inflammation occurring in synovium (synovitis membrane) and degradation of articular cartilage

40
Q

What is the mechanism of action of NSAID’s in treating OA

A

NSAID’s reduce the production of PGE2 by synoviocytes and chondrocytes

41
Q

How does PGE2 negatively impact joints in osteoarthritis

A

PGE2 directly contributes to inducing apoptosis of chondrocytes and also

PGE2 promotes secretion of other cytokines like IL-1, NO and TNF-alpha that contribute to cartilage breakdown leading to synovitis and chondrocyte apoptosis

42
Q

What are the three greatest side effects of NSAID toxicities

A

Gastric ulcers
Nephrotoxicity
Hepatotoxicity

43
Q

What are some signs of gastric ulcers

A

Pain and bleeding, diarrhea
Result of decreased secretion of mucous to protect stomach from acid by inhibiting COX-1 and therefore prostaglandins that produce mucous

44
Q

What are the signs of nephrotoxicity

A

Acute renal failure, interstitial nephritis, glomerularnephropathy

Prostaglandins blocked by COX-1 inhibitors so can’t control vasoconstriction at kidney by inducing vasodilation

45
Q

What are some other, less common effects of NSAID toxicities

A

Bronchoconstriction, pancreatitis, agranulocytosis, aplastic anemia, headache, dizziness, confusion, depression, hypersensitivity reactions

46
Q

What class of drug is grapiprant (galliprant) and what is the labeled use

A

Class: NSAID

Labeled only for pain and inflammation associated with OA in dogs

47
Q

What are the pharmacodynamics of grapiprant (galliprant)

A

EP4 receptor antagonist, EP4 is one of the four PGE2 receptors that mediate inflammation in OA

48
Q

Why is grapiprant (galliprant) a safer NSAID

A

Only blocks one of four PGE2 receptors and doesn’t block production of prostaglandins so at less risk of affecting normal physiology

49
Q

What are some adverse effects of grapiprant (galliprant)

A

Vomiting, diarrhea, anorexia, buccal ulcers, IMHA

50
Q

What is the mechanism of action (rapid onset) for gluocorticoids

A

Blocks synthesis of arachidonic acid by inhibiting PLA2 which is needed to make arachidonic acid from phospholipids

51
Q

What is the mechanism of action (delayed onset) for glucocorticoids

A

Increased transcription of anti-inflammatory genes and decreased transcription of pro-inflammatory genes

52
Q

What is the most commonly used and efficacious anti-inflammatory drugs that suppresses virtually every component of the inflammatory process and inhibit more mediators of inflammation than any other drug

A

Glucocorticoids

53
Q

What is the endogenous glucocorticoid

A

Hydrocortisone

54
Q

Some glucocorticoids are inactive precursors, where must they be processed to become active and what is an example

A

Must be processed by liver
Example: prednisone must be converted to prednisolone by liver 1

55
Q

Which species can’t absorb nor convert prednisone effectively

A

Cats, must be given prednisolone

56
Q

What drug is used to treat hypoadrenocorticism (addion’s disease)

A

Glucocorticoids

57
Q

What are three drugs that have labeled use for musculoskeletal/joint injections

A

Triamcinolone
Isoflupredone
Flumethasone

58
Q

What species can triamcinolone be used for to be considered labeled use

A

Dogs, cats, horses

59
Q

What species can isoflupredone be used in to be considered labeled use

A

Cattle and swine

60
Q

What species can flumethasone be used in to be considered labeled use

A

Dogs and horses

61
Q

What are some adverse effects of the drugs used for musculoskeletal/joint injections

A

Causes muscle atrophy due to increased circulating amino acids, inhibits fibrocartilage growth, causes osteoporosis- increased Ca+ excretion and decreased vitamin D activation, inhibits osteoblasts

62
Q

What animals should just injections not be used in

A

Growing animals because the drugs inhibit fibrocartilage growth

63
Q

Glucocorticoids and treating OA

A

Reduce production of PGE2 by synoviocytes and chondrocytes

Glucocorticoids directly suppress production of IL-1 and TNF-alpha

64
Q

What drug type is fluticasone (Flovent)

A

Glucocorticoids

65
Q

What are the labeled uses of fluticasone (Flovent)

A

Dogs: upper tracheobronchial disease
Cats: asthma
Horses: RAO (expensive so prednisolone, dexamethasone, and isoflupredone are alternatives

66
Q

What are the pharmacodynamics of Fluticasone (flovent)

A

Local, pulmonary immunosuppression reducing inflammation and epithelial damage

67
Q

What are some adverse effects of fluticasone (Flovent)

A

Pharyngitis and URI’s
May decrease production of endogenous corticosteroids (systemic effect), lethargy, bradycardia, anemia, hypovolemic shock(latrogenic addisonian crisis)

68
Q

What drug should not be used in acute asthma attacks that can even cause bronchospasms

A

Fluticasone (Flovent)

69
Q

What are the five major glucocorticoids

A

Dexamethasone, hydrocortisone, isoflupredone, prednisolone, triamcinolone

70
Q

What are some major reasons not to use glucocorticoids

A

Cutaneous food allergies (adjust diet first)
Infectious or parasitic infections (don’t want to suppress immune system when trying to fight infection)

71
Q

What are the most important adverse effects of systemic use of glucocorticoids that are most common with treatment > 2 weeks

A

Gastric ulcers and colonic perforation (messing with AA not Prostgladins to produce mucous)

Infections- immune suppression so increased susceptibility to infection and masks signs of disease

72
Q

Systemic use of glucocorticoids and HPA axis

A

Chronically high exogenous glucocorticoids suppress HPA axis so adrenals will reduce glucocorticoid and mineralcorticoid production, adrenals can atrophy so must slowly reduce exogenous glucocorticoid dose over time via a taper to allow HPA axis to recover

73
Q

What are some therapeutic options for atopic dermatitis

A

Cyclosporine A, lokivetmab, oclacitinib, glucocorticoids

74
Q

What are the itch cytokines

A

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

75
Q

What are the pharmacodynamics of cyclosporine A (atopica)

A

Binds cyclophilin to calcineurin, inhibits all T cell responses by blocking transcription of IL-2 and INF-gamma

76
Q

What is the labeled use for cyclosporin A (atopica)

A

Atopic dermatitis in dogs and cats

77
Q

What are some extra lable uses of cyclosporin A (atopica)

A

Keratoconjunctivitis sicca and autoimmune disorders

78
Q

What are the adverse effects of cyclosporin A (atopica)

A

Vomiting, diarrhea, anorexia, hypersensitivity, gingival hyperplasia, hypertrichosis, DM (dogs), hepatic lipidosis (cats)

79
Q

What are some contraindications for cyclosporin A (atopica)

A

History of malignant neoplasia, use of live vaccines, FIV or FeLV +, latent toxoplasma gondii infection

80
Q

What is the labeled use of olacitinib (Apoquel)

A

Treatment of atopic dermatitis in dogs > 1yr

81
Q

What are the pharmacodynamics of olcacitinib (Apoquel)

A

Competitive inhibitor of JAK1, competes with histamine and cytokines released from mast cells and basophils

82
Q

Why is specificity of olcacitnib (Apoquel) for JAK1 important

A

JAK2 is needed for erythropoietin—> RBC

83
Q

What are some adverse effects of olcacitnib (Apoquel)

A

Diarrhea, vomiting, anorexia, polydipsia, and lethargy, immunosuppression, neoplasia, skin disorders, anemia

84
Q

What are the pharmacodynamics of lokivetmab (cytopoint)

A

Canonized monoclonal antibody for dogs
Neutralizes IL-31 which is a pro-itch cytokine working through JAK1/2 pathways

85
Q

What are some adverse effects of lokivetmab (apoquel)

A

Lethargy, vomiting, hyper excitability, injection site pain, urinary incontinence

86
Q

What is the process of caninization

A

Genetically engineering the therapeutic antibody from mouse to be structurally closer to endogenous antibodies of target species to decrease immunogenecity (decrease opsonization)

87
Q

A small number of dogs have a declining response to lokivetmab over time, why?

A

caninization is not 100%, overtime many develop immune response to antibodies so lose efficacy, develop response to mouse parts

88
Q

What are the pharmacodynamics of mycophenylate mofetil (cellcept)

A

Reduces DNA synthesis by inhibiting production of guanine nucleotides

89
Q

What are the pharmacodynamics of Azathioprine (imuran)

A

Reduces DNA synthesis by two mechanisms:
1. Introduces this-guanine bases into elongating DNA Strands
2. Inhibits adenine and guanine (purine) production

Promotes T cell apoptosis by inhibiting RAC stimulation from CD28

90
Q

What are some adverse effects of mycophenylate mofetil (cellcept)

A

Dogs:
Vomiting, diarrhea, anorexia, lymphopenia associated with increased occurrence of skin infection

Cats???

91
Q

What are some adverse side effects of azathioprine in dogs

A

Vomiting, diarrhea, anorexia, leukopenia and thrombocytopenia, pancreatitis, hepatopathy

92
Q

What are some adverse side effects of azathioprine in cats

A

More marked bone marrow suppression, because of lower capacity to metabolize drug (thiopurine methyltranferase)

Immunology (22 decks)

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