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Vet Derm Review > Pharmacology - Immunomodulatory agents > Flashcards

Pharmacology - Immunomodulatory agents Flashcards

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1
Q

What are the major metabolic effects of glucocorticoids?

A

gluconeogenesis, protein catabolism and lipolysis

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2
Q

How do glucocorticoids cause an increase in glucose?

A

enhance gluconeogenesis in extrahepatic tissues, increase hepatic storage of glycogen, reduce uptake and utilization of glucose by tissues, may decrease expression of insulin receptor by target cells

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3
Q

What effect do glucocorticoids have on plasma protein levels?

A

increased levels of plasma and liver protein levels –> due to reduced tissue protein synthesis and increased protein catabolism; results in muscle atrophy

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4
Q

How do glucocorticoids suppress the inflammatory function of leukocytes?

A

stabilizing the membranes of those cells (specifically granulocytes, mast cells, and monocyte-macrophages) –> prevents release of inflammatory mediators such as histamine and arachidonic acid metabolites

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5
Q

Glucocorticoids suppress production of what pro-inflammatory cytokines?

A

IL-1, IL-6, TNF-alpha

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6
Q

What effect do glucocorticoids have on macrophages?

A

downregulate expression of Fc receptors on macrophages –> decreases phagocytosis of opsonized particles

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7
Q

T/F: Glucocorticoids directly inhibit antibody production by B lymphocytes.

A

False - B lymphocytes are more resistant to the suppressive effects of glucocorticoids, BUT they can indirectly suppress antibody production through the effect on T cells

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8
Q

T/F: Glucocorticoids inhibit complement.

A

TRUE

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9
Q

Why are glucocorticoids bound to esters of acetate, diacetate, tebutate, phenylpropionate, or isonicotinate released over days to weeks?

A

moderately insoluble

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10
Q

Glucocorticoids bound to esters of acetonide, hexacetate, pivalate, or diproprionate are short-acting or long-acting?

A

long-acting, are poorly soluble which allows steroid release over a period of weeks to months

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11
Q

Examples of topical cutaneous glucocorticoids - formulated as acetonide or valerate esters

A

hydrocortisone, prednisolone, betamethasone, dexamethasone

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12
Q

T/F: Endogenous cortisol has greater glucocorticoid and mineralocorticoid activity than synthetic glucocorticoids.

A

False - synthetic glucocorticoids have greater glucocorticoid activity and less mineralocorticoid activity than endogenous cortisol

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13
Q

What are the only synthetic glucocorticoids with mineralocorticoid activity?

A

hydrocortisone, cortisone, and prednisolone

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14
Q

Which diffuses more readily into tissues: endogenous cortisol or synthetic glucocorticoids?

A

synthetic glucocorticoids - bind with less avidity to serum proteins

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15
Q

Which has a greater affinity for the cytoplasmic steroid receptor: endogenous cortisol or synthetic glucocorticoids?

A

synthetic glucocorticoids - and are less rapidly degraded

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16
Q

Prednisone and cortisone require activation in the liver to what compounds?

A

prednisolone and cortisol

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17
Q

T/F: Increasd ALP with glucocorticoid treatment indicates hepatic damage and should prompt discontinuation of therapy.

A

False - increase in ALP is due to activation of the corticosteroid-induced alkaline phosphatase gene within canine hepatocytes. This does not have any pathological consequences

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18
Q

Concurrent administration of glucocorticoids and cyclosporine has what effect on the metabolism of each drug?

A

reduced hepatic metabolism of each drug –> elevated blood levels of both agents

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19
Q

What antibiotic REDUCES hepatic metabolism of methylprednisolone?

A

erythromycin

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20
Q

There is an increased risk of hypokalemia when glucocorticoids are used concurrently with what drugs?

A

acetazolamide, amphotericin B, potassium-depleting diuretics (furosemide, thiazides)

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21
Q

What drugs may accelerate the metabolism of glucocorticoids?

A

phenobarbital, primidone, rifampin

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22
Q

What is the cause of the leukocytosis seen with glucocorticoid administration?

A

glucocorticoids inhibit expression of adhesion molecules on endothelial cells (ELAM-1 and ICAM-1) and thereby interfere with movement of leukocytes from the vasculature into inflamed tissues

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23
Q

What is the cause of the mature neutrophilia seen with glucocorticoid administration?

A

increased release of mature neutrophils from the bone marrow, decreased margination, decreased migration of neutrophils out of the blood vessels

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24
Q

What is the cause of the lymphopenia seen with glucocorticoid administration?

A

redistribution of circulating lymphocytes to nonvascular lymphatic compartments such as lymph nodes

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25
Q

How is the arachidonic acid cycle inhibited with glucocorticoid administration?

A

glucocorticoids increase production of lipocortin 1 lipomodulin –> causes a reduction in the action of phospholipase A2 on cell membranes –> inhibits AA cycle

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26
Q

Why can synthetic glucocorticoids be more potent at low doses?

A

poorly protein bound – only free glucocorticoid is metabolically active

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27
Q

What effect does adding a methyl or fluoride group to the basic steroid molecule have on potency and duration of action?

A

increases potency and duration of action

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28
Q

What effect does hypoalbuminemia have on glucocorticoid activity?

A

animals with low serum albumin levels have a lower binding capacity of glucorticoids –> excessive unbound glucocorticoid becomes freely available –> increases toxicity

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29
Q

Glucocorticoid effect on: eosinophils

A

decrease formation in bone marrow; increase apoptosis and inhibit prolongation of eosinophil survival and function from IL-3 and IL-5

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30
Q

Glucocorticoid effect on: lymphocytes and monocytes

A

redistribution of circulating lymphocytes to nonvascular lymphatic compartments such as lymph nodes/bone marrow; reduced number of lymphocytes and monocytes that bear low-affinity IgE and IgG receptors; Decreased serum immunoglobulin levels; Decrease all lymphocyte subpopulations (T > B lymphocytes), CD4+ decreased more than CD8+; Decreased lymphocyte production of IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, and IFN-gamma; Inhibit release of IL-1 and TNF-alpha from monocytes

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31
Q

Glucocorticoid effect on: mast cells

A

May decrease number o mast cells and synthesis of histamine

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32
Q

Glucocorticoid effect on: neutrophils

A

neutrophilia due to release from bone marrow as well as decreased margination and diapedesis of neutrophils into tissues; decreased chemotaxis, adherence, and enzyme secretion

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33
Q

Glucocorticoid effect on: lipocortin 1

A

Causes upregulation of lipocortin 1 (phospholipid binding protein) – potent anti-inflammatory effects; inhibition of phospholipase A2; Decrased production of AA metabolites from COX and LOX pathways; Decreased production of platelet-activating factor

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34
Q

Glucocorticoid effect on: humoral immunity

A

decreased antibody synthesis only after high dose, long-term therapy; reduces degree of suppression of B-lymphocyte proliferation in response to mitogens

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35
Q

Glucocorticoid effect on: cellular immunity

A

decreased antigen survival, uptake, and migration; decreased maturation of dendritic cells; inhibition of transcriptional activators (NF-kB and AP-1); decreased macrophages expression of some inflammatory cytokines (IL-1, TNF-alpha); increased expression of some anti-inflammatory cytokines (IL-10), decreased T-lymphocyte proliferation in response to mitogens; decreased T-cell activation; Decreased T-cell cytokines (IL-2 and IFN-gamma); Decreased NK-cell-mediated lysis of target cells)

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36
Q

Local areas of alopecia, pigmentary changes, and epidermal and dermal atrophy are more commonly induced when glucocorticoids are administered via what route?

A

subcutaneous injection

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37
Q

What long-acting injectable glucocorticoids are available for use in dogs?

A

betamethasone acetate, methylprednisolone acetate, triamcinolone acetonide

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38
Q

What long-acting injectable glucocorticoids are available for use in cats?

A

methylprednisolone acetate, triamcinolone acetonide

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39
Q

Unique side effect of glucocorticoids in cats

A

curling of the pinnae, alopecia, thin and easily torn skin, hypertrophic cardiomyopathy, diabetes mellitus, steroid hepatopathy

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40
Q

Common side effects of glucocorticoids

A

PU, PD, PP (weight gain), behavioral changes (depression, hyperactivity, aggression), panting, diarrhea, risk of infections

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41
Q

What is the mechanism of PU/PD in dogs with glucocorticoids?

A

interference of glucocorticoids with ADH –> polyuria and compensatory polydipsia

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42
Q

What is the mechanism of PU/PD in cats with glucocorticoids?

A

glucosuria and osmotic diuresis; most cases commonly maintain normal USG

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43
Q

What steroid may have a greater diabetogenic effect in cats?

A

dexamethasone

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44
Q

Arachidonic acid is stored in cells and released by the action of what enzyme?

A

phospholipase A2

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45
Q

What is the proposed mechanism of action of how fatty acids function in controlling pruritus?

A

inhibition of AA metabolism (competing for COX and LOX enzymes), alteration of metabolic byproducts of fatty acid metabolism (produce less inflammatory byproducts)

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46
Q

Gamma-linolenic acid is found in what oils?

A

evening primrose, borage, and black currant oils

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47
Q

How can EPA be supplied?

A

cold water marine fish oils or krill oil, conversion of alpha-linolenic acid to EPA and DHA

48
Q

Dogs with seborrhea sicca have what alterations in their cutaneous fatty acids?

A

low cutaneous levels of linoleic acid and increased levels of cutaneous oleic acid

49
Q

Adverse effects of fatty acid supplementation

A

pancreatitis, diarrhea, weight increase, unpleasant odor or eructation

50
Q

What are the immunomodulatory and rheologic effects of pentoxifylline?

A

1) increased leukocyte deformability and chemotaxis, 2) Decreased platelet aggregation, 3) Decrased leukocyte responsiveness to IL-1 and TNF-alpha, 4) Decreased production of TNF-alpha from macrophages, 5) Decreased production of IL-1, IL-4, and IL-12, 6) Inhibition of T- and B-lymphocyte activation, 7) Decreased NK cell activity

51
Q

How does pentoxifylline affect wound healing?

A

Increased production of collagenase and decreased production of collagen, fibronectin, and glycosaminoglycans

52
Q

Adverse effects of pentoxifylline

A

vomiting, diarrhea, dizziness and headaches reported in humans

53
Q

T/F: Retinoids enhance wound healing by stimulating fibroblasts to produce TGF-beta.

A

TRUE

54
Q

Adverse effects of isoretinoin

A

conjunctivitis, hyperactivity, pruritus, pedal and mucocu- taneous junction erythema, stiffness, vomiting, diarrhea, and keratoconjunctivitis; Laboratory abnormalities that are generally not associated with clinical signs include hyper- triglyceridemia, hypercholesterolemia, and increased levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase.

55
Q

T/F: Retinoids are teratogenic.

A

TRUE

56
Q

Does isotretinoin need to be given with food?

A

yes, otherwise absorption is variable

57
Q

What monitoring should be done with synthetic retinoids?

A

pretreatment measurement of tear production, hemogram, chemistry profile, and urinalysis. Repeated in 1-2 months then as needed

58
Q

Mechanism of action of synthetic retinoids

A

egulation of epithelial cell proliferation and differentiation; although its exact mechanism of action is unknown. It affects monocyte and lymphocyte function, which can cause changes in cellular immune responses. The effects on skin include reduction of sebaceous gland size and activity, thereby reducing sebum production. It also has anti-keratinization and anti-inflammatory activity and may indirectly reduce bacterial populations in sebaceous pores.

59
Q

What is cyclosporine derived from?

A

fat-soluble cyclic polypeptide metabolite of the fungus Tolypocladium inflatum gams

60
Q

What cytokine does cyclosporine block transcription of?

A

IL-2&raquo_space; IFN-alpha

61
Q

By blocking IFN-alpha transcription, cyclosporine has effects on activation of what cells?

A

macrophages and monocytes

62
Q

T/F: Microemulsified cyclosporine is completely absorbed from the GI tract.

A

False - although it is better absorbed than emulsified CsA, it is still poorly and erratically absorbed - bioavailability varies from 23-45%

63
Q

Adverse effects of cyclosporine

A

vomiting, diarrhea, gingival overgrowth and papillomatosis, vomiting, diarrhea, bacteriuria, bacterial skin infection, anorexia, hirsutism, involuntary shaking, nephropathy, bone marrow suppression, and lymphoplasmacytoid dermatosis

64
Q

T/F: Cyclosporine increases Toxoplasma gondii shedding in infected cats.

A

FALSE

65
Q

Mechanism of action: Cyclosporine

A

binds to cyclophilin (cytoplasmic molecule) - expressed in high concentration in T lymphocytes; the ciclosporin-cylophilin complex binds to calcineurin (cytoplasmic molecule) –> blocks activation of nuclear factor of activated T cells & transcription factor AP-1 –> blocks transcription of IL-2

66
Q

T/F: Cyclosporine reduces clonal proliferation of B lymphocytes.

A

True - reduces production of IL-4

67
Q

T/F: Cyclosporine inhibits histamine release.

A

TRUE

68
Q

Mechanism of action: Tacrolimus

A

tacrolimus binds the T-cell cytoplasmic molecules known as FK-binding proteins –> the FKBP-tacrolimus complex binds and inhibits calcineurin

69
Q

Method of excretion: Cyclosporine

A

metabolites are largely excreted in bile, with some minor (5%) urinary loss

70
Q

FDA-approved indication for cyclosporine in dogs

A

control of atopic dermatitis

71
Q

FDA-approved indication for cyclosporine in cats

A

control of feline allergic dermatitis as manifested by excoriations (including facial and neck), miliary dermatitis, eosinophilic plaques, and self-induced alopecia

72
Q

Cyclosporine is found at highest levels in what tissues?

A

high levels into the liver, fat, and blood cells (granulocytes, 5-12%; lymphocytes, 5-9%); significantly accumulates in the skin

73
Q

T/F: Dogs with diabetes may have a reduced response to cyclosporine.

A

True - due to increased clearance and reduced elimination half-life

74
Q

T/F: Food in the GI tract reduces bioavailability of cyclosporine by ~20% in both dogs and cats.

A

False - true for the dog, but absorption is not altered in the cat when given with food

75
Q

Contraindications for administration of cyclosporine in the cat

A

cats infected with FeLV or FIV; history of malignant neoplasia; less than 6 months of age; weight <1.4 kg

76
Q

What sample should be submitted for cyclosporine therapeutic drug monitoring?

A

whole blood (NOT plasma) - as cyclosporine concentrates in blood cells

77
Q

What are the type II IFNs? What cells produce them?

A

IFN-gamma; NK cells, CD4+ helper T cells; Cd8+ cytotoxic T cells

78
Q

What are the type I IFNs?

A

IFN-alpha, IFN-beta, IFN-omega, IFN-delta, IFN-tau

79
Q

How is melatonin synthesized in the body?

A

synthesized in the pineal gland from L-tryptophan

80
Q

When is melatonin secretion the greatest?

A

during dark hours

81
Q

What effect does melatonin have on estradiol levels? Why?

A

reduced estradiol levels - inhibits adrenal 21-hydroxylase and aromatase

82
Q

What are phytoestrogens?

A

isoflavones, lignans, genistein

83
Q

What enzyme do phytoestrogens inhibit?

A

3-beta-hydroxysteroid dehydrogenase

84
Q

What is melatonin FDA approved for?

A

accelerate the fur priming cycle in mink

85
Q

Adverse effect of melatonin implants in dogs

A

sterile abscesses

86
Q

What effect can melatonin have on TT4 concentration?

A

decreased TT3 and TT4 - no effect on free T3 or free T4

87
Q

Mechanism of action: Azathioprine

A

antagonizes purine metabolism –> interferes with DNA and RNA synthesis

88
Q

What cells does azathioprine target?

A

primarily affects rapidly proliferating cells, with its greatest effects on cell-mediated immunity and T lymphocyte–dependent antibody synthesis. Primary antibody synthesis is affected more than secondary antibody synthesis.

89
Q

Adverse effects of azathioprine

A

diarrhea; anemia, leukopenia, thrombocytopenia, vomiting, hypersensitivity reactions (especially of the liver), pancreatitis, elevated serum alkaline phosphatase concentra- tions, rashes, and alopecia.

90
Q

What monitoring should be done with azathioprine?

A

CBC and platelet q2 weeks

91
Q

Azathioprine is an imidazole prodrug of what?

A

6-mercaptopurine

92
Q

Administration of azathioprine with what other drug increases the risk of azathioprine toxicity? Why?

A

allopurinol – allopurinal inhibits xanthine oxidase, which is one of the enzymes that metabolizes azathioprine

93
Q

How is azathioprine metabolized and excreted?

A

Pharmacokinetics
Azathioprine is poorly absorbed from the GI tract. It is rapidly metabolized to 6-mercaptopurine (6-MP), which is then taken up by lymphocytes and erythrocytes. The remaining drug in the plasma is further metabolized in the liver and GI tract and excreted by the kidneys. Only minimal amounts of either azathioprine or mercaptopurine are excreted unchanged.

94
Q

Azathioprine has a similar mechanism of action to what other immunosuppressant?

A

mycophenolate - both are purine antagonists

95
Q

How is chlorambucil metabolized? How is it excreted?

A

Chlorambucil is extensively metabolized in the liver primarily to the active metabolite phenylacetic acid mustard. Phenylacetic acid mustard is further metabolized to other metabolites that are excreted in the urine.

96
Q

Mechanism of action: Colchicine

A

suppresses neutrophil chemotactic and phagocytic functions via disruption of microtubule assembly and elongation; increases cellular cAMP levels; inhibitins lysosomal degranulation; inhibits Ig secretion, IL-1 production, histamine release; inhibits cell division during metaphase

97
Q

Adverse effects of colchicine

A

nausea, vomiting, and diarrhea in dogs, particularly at higher dosages. Rarely, bone marrow depression (neutropenia), renal toxicity, and peripheral neuropathy can occur.

98
Q

Indications for colchicine in dogs

A

epidermolysis bullosa acquisita, junctional epidermolysis bullosa, amyloidosis, Shar-Pei fever syndrome

99
Q

Cyclophosphamide is more effective against which cell types?

A

B cells > T cells

100
Q

Mechanism of action: Mycophenolate Mofetil

A

Prodrug of the antiproliferative agent mycophenolic acid. 1) Specifically and reversibly inhibits inosine monophosphate dehydrogenase –> inhibits synthesis of guanine nucleotides, blocks synthesis of purine, prevents maturation of T and B lymphocytes, 2) Induces T-lymphocyte apoptosis, 3) Induces dendritic cell maturation, 4) Decreases expression of IL-1, Increases expression of IL-1 receptor antagonist

101
Q

How is mycophenolate metabolized and excreted?

A

metabolized by the liver, primarily via glucuronidation; metabolites are primarily eliminated via the kidneys

102
Q

Mechanism of action: Gold salts

A

1) Inhibition of lymphocyte proliferation (possibly T-helper cells), 2) Inhibition of Ig production, 3) Inhibition of complement component C1, 4) Inhibition of neutrophil and monocyte-macrophage function (particularly the release of lysosomal enzymes and prostaglandins), 5) Inhibition of connective tissue enzymes (elastase, collagenase, hyaluronidase), 6) Protection from oxygen radicals

103
Q

Where do gold salts concentrate?

A

liver, kidney, spleen, lungs, adrenal glands, and macrophages

104
Q

How is gold excreted?

A

absorbed gold is excreted in urine, unabsorbed gold is excreted in feces

105
Q

Recommended monitoring for gold salts

A

CBC and renal (urinalysis) at baseline, then q2 weeks, then q1-2 months

106
Q

Gold salts are contraindicated for what condition as it exacerbates the disease?

A

systemic lupus erythematosus

107
Q

Mechanism of action: IVIG

A

1) saturation of Fc receptors on macrophages, prevent-
ing binding of cell-bound autoantibody. IVIG inhi- bits the binding of canine IgG to monocytes and inhibits phagocytosis of antibody-coated canine erythrocytes in vitro. 2) modulation of T- and B-lymphocyte function via binding of immunoglobulin to molecules on the surface membrane of these cells. IVIG has been shown to bind to canine T (CD4+ and CD8+) and B lymphocytes in vitro. In humans, there is evidence that the immunoglobulin in IVIG blocks the interac- tion between the molecules Fas (CD95) and Fas- ligand (CD95R) which are involved in the induction of apoptosis in lymphocyte-mediated cytotoxic destruction of target cells.

108
Q

Mechanism of action: leflunomide

A

selective inhibition of dihydro-orotate dehydrogenase, a mitochondrial enzyme essential for de novo pyrimidine biosynthesis (particularly affects T and B lymphocytes that lack a pyrimidine salvage pathway)

109
Q

How is leflunomide metabolized and excreted?

A

metabolized by liver, undergoes enterohepatic recycling; excreted by both biliary and renal routes

110
Q

What is megestrol acetate?

A

oral progestin

111
Q

Adverse effects of megestrol acetate?

A

PP, weight gain, depression/lethargy, mammary gland hyperplasia and carcinoma, DM, bone marrow suppression, endometrial hyperplasia, pyometria, adrenocortical suppression, thinning and increased fragility of the skin

112
Q

What is the active metabolite of leflunomide?

A

teriflunomide

113
Q

Adverse effects of leflunomide

A

diarrhea, decreased appetite, lethargy, vomiting, respiratory signs (ie, dyspnea, cough), increased liver enzymes, unexplained hemorrhage, leukocytopenia, lymphopenia, thrombocytopenia, hypercholesterolemia, and anemia.

114
Q

Recommended monitoring for leflunomide

A

CBC prior to starting therapy, then q2 weeks for the first 2 months; Liver enzymes q2 weeks for the first 2 months

115
Q

Immunomodulatory properties of levamisole

A

1) Enhancement of T-lymphocyte number and function (no direct effect on B lymphocytes or antibody production); 2) Enhanced chemotaxis, phagocytosis, and intracellular killing by granulocytes and monocytes

116
Q

Method of metabolism and excretion: levamisole

A

metabolized in liver and excreted in urine (primarily) and feces

117
Q

Adverse effects of levamisole

A

dog: lethargy, vomiting, diarrhea, panting, shaking, agitation, behavioral changes, hemolytic anemia, agranulocytosis, dyspnea, pulmonary edema and cutaneous drug eruption (particularly of the erythema multiforme–toxic epidermal necrolysis spectrum); cat: hypersalivation, excitement, mydriasis and vomiting

Vet Derm Review (44 decks)

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